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<title>Digital Commons</title>
<copyright>Copyright (c) 2012 Berkeley Electronic Press All rights reserved.</copyright>
<link>http://digitalcommons.bepress.com</link>
<description>Recent documents in Digital Commons</description>
<language>en-us</language>
<lastBuildDate>Wed, 09 May 2012 12:04:16 PDT</lastBuildDate>
<ttl>3600</ttl>


	



<item>
<title>Refining estimates of pollinator efficiencies calculated using delivered stigmatic loads: a cranberry model</title>
<link>http://digitalcommons.usu.edu/piru_pubs/511</link>
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<pubDate>Wed, 09 May 2012 12:05:51 PDT</pubDate>
<description>
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Managing non-social bees for agriculture</title>
<link>http://digitalcommons.usu.edu/piru_pubs/510</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/510</guid>
<pubDate>Wed, 09 May 2012 12:05:35 PDT</pubDate>
<description>
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</description>

<author>James H. Cane</author>


<category>Bee management</category>

</item>


<item>
<title>Exposing their progeny: using x-rays and observation nests to study and manipulate cavity-nesting bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/509</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/509</guid>
<pubDate>Wed, 09 May 2012 12:05:20 PDT</pubDate>
<description>
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</description>

<author>James H. Cane</author>


<category>Bee management</category>

</item>


<item>
<title>The Invention of Glory: The Pastrana Tapestries of King Afonso V of Portugal</title>
<link>http://digitalrepository.smu.edu/meadowsmuseum_programs/1</link>
<guid isPermaLink="true">http://digitalrepository.smu.edu/meadowsmuseum_programs/1</guid>
<pubDate>Wed, 09 May 2012 12:05:17 PDT</pubDate>
<description>
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</description>

<author>Robert Walker</author>


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<item>
<title>Bees and seed production for native plant restoration in wildlands</title>
<link>http://digitalcommons.usu.edu/piru_pubs/508</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/508</guid>
<pubDate>Wed, 09 May 2012 12:05:01 PDT</pubDate>
<description>
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Florida: Citizens Bank Building in Tampa</title>
<link>http://digitalcommons.ric.edu/smolski_images/838</link>
<guid isPermaLink="true">http://digitalcommons.ric.edu/smolski_images/838</guid>
<pubDate>Wed, 09 May 2012 12:04:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pictured is a shopping district in downtown Tampa, Florida. To the far right of this picture is the Citizens Bank Building. Built in 1913 with a height of 145 feet tall, this building was considered the tallest building in Tampa until 1915 when the Tampa City Hall surpassed it. The building was built in the renaissance revival architectural style with a steel structure and a brick facade. Unfortunately, this building no longer stands as it was demolished in 1978.</p>

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</description>

<author>Chet Smolski</author>


</item>


<item>
<title>Bees for seeds of rehabilitation forbs in the Great Basin</title>
<link>http://digitalcommons.usu.edu/piru_pubs/507</link>
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<pubDate>Wed, 09 May 2012 12:04:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Ecology &amp; conservation</category>

</item>


<item>
<title>Using non-social bees to pollinate crops: a case study to evaluate and manage the bee Osmia aglaia for raspberry pollination</title>
<link>http://digitalcommons.usu.edu/piru_pubs/506</link>
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<pubDate>Wed, 09 May 2012 12:04:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Bee management</category>

</item>


<item>
<title>Pollination promise and manageability of the bee Osmia aglaia for cultivated cane fruits (Rubus: Rosaceae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/505</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/505</guid>
<pubDate>Wed, 09 May 2012 12:04:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Options and considerations for managed pollinators in seed alfalfa</title>
<link>http://digitalcommons.usu.edu/piru_pubs/504</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/504</guid>
<pubDate>Wed, 09 May 2012 12:03:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>How much pollen and nectar constitute larval provisions of the alfalfa leaf-cutting bee?</title>
<link>http://digitalcommons.usu.edu/piru_pubs/503</link>
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<pubDate>Wed, 09 May 2012 12:03:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


</item>


<item>
<title>Pollinating and growing desert wildflowers for seed to ecological restoration</title>
<link>http://digitalcommons.usu.edu/piru_pubs/502</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/502</guid>
<pubDate>Wed, 09 May 2012 12:03:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Bees and the seeds that their pollination breeds</title>
<link>http://digitalcommons.usu.edu/piru_pubs/501</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/501</guid>
<pubDate>Wed, 09 May 2012 12:03:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Feed’em and reap: Linking bloom, foraging tempos and reproduction by alkali bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/500</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/500</guid>
<pubDate>Wed, 09 May 2012 12:02:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Blue orchard bee for almond pollination</title>
<link>http://digitalcommons.usu.edu/piru_pubs/499</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/499</guid>
<pubDate>Wed, 09 May 2012 12:02:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Bee mediated Pollen Flow and Isolation Distances for GMO Alfalfa</title>
<link>http://digitalcommons.usu.edu/piru_pubs/498</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/498</guid>
<pubDate>Wed, 09 May 2012 12:02:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Teaching Law Students to Be Policymakers: The Health and Science Policy Workshop on Genomic Research</title>
<link>http://digitalcommons.law.umaryland.edu/fac_pubs/1198</link>
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<pubDate>Wed, 09 May 2012 12:02:06 PDT</pubDate>
<description>
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</description>

<author>Benjamin E. Berkman et al.</author>


</item>


<item>
<title>Bee Pollination of Farmed Wildflowers for Habitat Restoration Seed</title>
<link>http://digitalcommons.usu.edu/piru_pubs/497</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/497</guid>
<pubDate>Wed, 09 May 2012 12:02:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Bee Pollination of Farmed Wildflowers for Habitat Restoration Seed</title>
<link>http://digitalcommons.usu.edu/piru_pubs/496</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/496</guid>
<pubDate>Wed, 09 May 2012 12:01:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Bee Pollination of Farmed Wildflowers for Habitat Restoration Seed</title>
<link>http://digitalcommons.usu.edu/piru_pubs/495</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/495</guid>
<pubDate>Wed, 09 May 2012 12:01:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Pollinating Great Basin forbs for seed to rehabilitate western rangelands</title>
<link>http://digitalcommons.usu.edu/piru_pubs/494</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/494</guid>
<pubDate>Wed, 09 May 2012 12:01:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Climatically tuned Blue Orchard Bee development and how to manage it for almond pollination</title>
<link>http://digitalcommons.usu.edu/piru_pubs/493</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/493</guid>
<pubDate>Wed, 09 May 2012 12:01:06 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Bee management</category>

</item>


<item>
<title>Biscuitroots needing bees, heady progress with a sweetvetch pollinator</title>
<link>http://digitalcommons.usu.edu/piru_pubs/492</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/492</guid>
<pubDate>Wed, 09 May 2012 12:00:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Pollen tube attrition in cranberries</title>
<link>http://digitalcommons.usu.edu/piru_pubs/491</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/491</guid>
<pubDate>Wed, 09 May 2012 12:00:39 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Pollinating Great Basin forbs for seed to rehabilitate western rangelands</title>
<link>http://digitalcommons.usu.edu/piru_pubs/490</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/490</guid>
<pubDate>Wed, 09 May 2012 12:00:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Ecology &amp; conservation</category>

</item>


<item>
<title>Investigation of Inter-Diffusion in Bilayer GeTe/SnSe Phase Change Memory Films</title>
<link>http://scholarworks.boisestate.edu/electrical_facpubs/190</link>
<guid isPermaLink="true">http://scholarworks.boisestate.edu/electrical_facpubs/190</guid>
<pubDate>Wed, 09 May 2012 12:00:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>A metal-chalcogenide layer, SnSe, is inserted between the memory layer GeTe and the top electrode to form a phase change memory cell. The GeTe layer exhibits ovonic threshold switching at a threshold field of ~ 110 V/μm. For subsequent implementation into applications and reliability, material inter-diffusion and sublimation are examined in bilayer phase change films of GeTe/SnSe. Transmission electron microscopy and parallel electron energy loss spectroscopy analyses reveal Sn migration to the GeTe layer, which is responsible for lowering the rhombohedral to cubic structural transformation temperature in GeTe. Incongruent sublimation of SnSe and GeTe is observed at temperatures higher than 500 °C. Severe volatilization of Se results in the separation of a metallic Sn phase. The use of Al<sub>2</sub>O<sub>3</sub> as a capping layer has been found to mitigate these effects.</p>

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</description>

<author>Archana Devasia et al.</author>


</item>


<item>
<title>Pollinators for restoration seed production</title>
<link>http://digitalcommons.usu.edu/piru_pubs/489</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/489</guid>
<pubDate>Wed, 09 May 2012 12:00:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Pollinators and climate change</title>
<link>http://digitalcommons.usu.edu/piru_pubs/488</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/488</guid>
<pubDate>Wed, 09 May 2012 11:59:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Do Specialist Bees Better Discriminate Among Their Hybridizing Balsamorhiza Floral Hosts?</title>
<link>http://digitalcommons.usu.edu/piru_pubs/487</link>
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<pubDate>Wed, 09 May 2012 11:59:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Ecology &amp; conservation</category>

</item>


<item>
<title>Contrasting self-fertilities of a biscuitroot and 3 globemallows, with prospects for their pollination</title>
<link>http://digitalcommons.usu.edu/piru_pubs/486</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/486</guid>
<pubDate>Wed, 09 May 2012 11:59:33 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Contrasting roles for host plant recognition in Group IX Ips and solitary bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/485</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/485</guid>
<pubDate>Wed, 09 May 2012 11:59:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Natural history</category>

</item>


<item>
<title>For wildflower seed, bees are key</title>
<link>http://digitalcommons.usu.edu/piru_pubs/484</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/484</guid>
<pubDate>Wed, 09 May 2012 11:59:09 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Pollination and pollinators for wildflower seed farming and post-fire wildland rehabilitation</title>
<link>http://digitalcommons.usu.edu/piru_pubs/483</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/483</guid>
<pubDate>Wed, 09 May 2012 11:58:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Peculiar factors enable sustained mass-production of native alkali bees for alfalfa pollination</title>
<link>http://digitalcommons.usu.edu/piru_pubs/482</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/482</guid>
<pubDate>Wed, 09 May 2012 11:58:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Bees are key for producing native forb seed</title>
<link>http://digitalcommons.usu.edu/piru_pubs/481</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/481</guid>
<pubDate>Wed, 09 May 2012 11:58:30 PDT</pubDate>
<description>
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>On-farm pollinator surprises ease some pollination challenges for native forb production</title>
<link>http://digitalcommons.usu.edu/piru_pubs/480</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/480</guid>
<pubDate>Wed, 09 May 2012 11:58:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Specialist Peponapis bees prevail in pollinating U.S. squash crops</title>
<link>http://digitalcommons.usu.edu/piru_pubs/479</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/479</guid>
<pubDate>Wed, 09 May 2012 11:58:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Alkali bees: Great pollinators with management limitations</title>
<link>http://digitalcommons.usu.edu/piru_pubs/478</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/478</guid>
<pubDate>Wed, 09 May 2012 11:57:52 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


</item>


<item>
<title>Habitat Gardens: Birds, Bees, and Butterflies</title>
<link>http://digitalcommons.usu.edu/piru_pubs/477</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/477</guid>
<pubDate>Wed, 09 May 2012 11:57:40 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


</item>


<item>
<title>Post-fire fates and on-farm use of wild bees for native forb seed production</title>
<link>http://digitalcommons.usu.edu/piru_pubs/476</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/476</guid>
<pubDate>Wed, 09 May 2012 11:57:29 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Ecology &amp; conservation</category>

</item>


<item>
<title>Florida: Kress Building in Downtown Tampa</title>
<link>http://digitalcommons.ric.edu/smolski_images/837</link>
<guid isPermaLink="true">http://digitalcommons.ric.edu/smolski_images/837</guid>
<pubDate>Wed, 09 May 2012 11:57:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The four story building to the left of this photo is known as the Kress Building in downtown Tampa, Florida. Originally opened in 1900 on Franklin Street, the store was soon relocated to Florida Avenue in 1908. That store was demolished in 1929. That same year, the most recent building was built in the Renaissance Revival architectural style by G. E. McKay. Known for its two identical Renaissance Revival terra-cotta facades, the building is styled with bronze marquees, coats of arms. This historic building was once part of the S.H. Kress & Co. department store chain.</p>
<p>In more recent years, the building has sat downtown vacant and worn down.</p>

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</description>

<author>Chet Smolski et al.</author>


</item>


<item>
<title>On-farm needs and post-fire fates of bees that pollinate our restoration forbs</title>
<link>http://digitalcommons.usu.edu/piru_pubs/475</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/475</guid>
<pubDate>Wed, 09 May 2012 11:57:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Native wildflowers for native bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/474</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/474</guid>
<pubDate>Wed, 09 May 2012 11:57:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Ecology &amp; conservation</category>

</item>


<item>
<title>Another Move away from Title VII: Why Gross Got It Right</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss3/7</link>
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<pubDate>Wed, 09 May 2012 11:56:57 PDT</pubDate>
<description>
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</description>

<author>Jacqueline Go</author>


</item>


<item>
<title>Menu-Labeling Laws: A Move from Local to National Regulation</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss3/6</link>
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<pubDate>Wed, 09 May 2012 11:56:55 PDT</pubDate>
<description>
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</description>

<author>Christine Cusick</author>


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<item>
<title>Greenhouse Gas Emission Targets and Mass Transit: Can the Government Successfully Accomplish Both without a Conflict</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss3/5</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss3/5</guid>
<pubDate>Wed, 09 May 2012 11:56:54 PDT</pubDate>
<description>
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</description>

<author>Darren A. Prum et al.</author>


</item>


<item>
<title>Making Sense of State Action</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss3/4</link>
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<pubDate>Wed, 09 May 2012 11:56:53 PDT</pubDate>
<description>
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</description>

<author>John Dorsett Niles et al.</author>


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<item>
<title>Should Substitute Private Attorneys General Enforce Public Environmental Actions - Balancing the Costs and Benefits of the Contingency Fee Environmental Special Counsel Arrangement</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss3/3</link>
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<pubDate>Wed, 09 May 2012 11:56:52 PDT</pubDate>
<description>
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</description>

<author>Julie E. Steiner</author>


</item>


<item>
<title>Bee communities and wildfire: Thermal tolerances, soil heat conduction and nesting depths</title>
<link>http://digitalcommons.usu.edu/piru_pubs/473</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/473</guid>
<pubDate>Wed, 09 May 2012 11:56:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Ecology &amp; conservation</category>

</item>


<item>
<title>Restoring the Founders&apos; Ideal of the Independent Jury in Criminal Cases</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss3/2</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss3/2</guid>
<pubDate>Wed, 09 May 2012 11:56:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Thomas Regnier</author>


</item>


<item>
<title>The Influence of Justice John Paul Stevens: Opinion Assignments by the Senator Associate Justice</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss3/1</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss3/1</guid>
<pubDate>Wed, 09 May 2012 11:56:50 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Charles F. Jacobs et al.</author>


</item>


<item>
<title>Alkali Bee Research Projects</title>
<link>http://digitalcommons.usu.edu/piru_pubs/472</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/472</guid>
<pubDate>Wed, 09 May 2012 11:56:37 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


</item>


<item>
<title>Breeding Biology and Pollinators of Dusty Maiden, Chaenactis douglasii</title>
<link>http://digitalcommons.usu.edu/piru_pubs/471</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/471</guid>
<pubDate>Wed, 09 May 2012 11:56:23 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Gardening and Landscaping for Native Bee</title>
<link>http://digitalcommons.usu.edu/piru_pubs/470</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/470</guid>
<pubDate>Wed, 09 May 2012 11:56:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Native bees for wildflower seed farming and large-scale wildland restoration in the western USA</title>
<link>http://digitalcommons.usu.edu/piru_pubs/469</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/469</guid>
<pubDate>Wed, 09 May 2012 11:55:56 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Structural examination of the Dufour’s gland of the cavity-nesting bees Osmia lignaria Say and Megachile rotundata (Fabricius) (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/468</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/468</guid>
<pubDate>Wed, 09 May 2012 11:55:42 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>The long summer: pre-wintering temperatures affect metabolic expenditure and winter survival in a solitary bee</title>
<link>http://digitalcommons.usu.edu/piru_pubs/467</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/467</guid>
<pubDate>Wed, 09 May 2012 11:55:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>F. Sgolastra et al.</author>


<category>Bee management</category>

</item>


<item>
<title>Attraction to old nest cues during nest selection by the solitary bee Megachile rotundata (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/466</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/466</guid>
<pubDate>Wed, 09 May 2012 11:55:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. Stanley et al.</author>


</item>


<item>
<title>Influence of rough handling on Osmia lignaria (Hymenoptera: Megachilidae) retention in commercial orchards</title>
<link>http://digitalcommons.usu.edu/piru_pubs/465</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/465</guid>
<pubDate>Wed, 09 May 2012 11:55:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. Stanley et al.</author>


</item>


<item>
<title>Effects of the insect growth regulator, novaluron on immature alfalfa leafcutting bees, Megachile rotundata</title>
<link>http://digitalcommons.usu.edu/piru_pubs/464</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/464</guid>
<pubDate>Wed, 09 May 2012 11:54:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E. W. Hodgson et al.</author>


</item>


<item>
<title>Sexual harassment by males reduces female fecundity in the alfalfa leafcutting bee (Megachile rotundata)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/463</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/463</guid>
<pubDate>Wed, 09 May 2012 11:54:31 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>B. H. Rossi et al.</author>


<category>Bee management</category>

</item>


<item>
<title>Nest establishment, pollination efficiency, and reproductive success of Megachile rotundata (Hymenoptera: Megachilidae) in relation to resource availability in field enclosures</title>
<link>http://digitalcommons.usu.edu/piru_pubs/462</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/462</guid>
<pubDate>Wed, 09 May 2012 11:54:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>The proboscis extension reflex not elicited in megachilid bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/461</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/461</guid>
<pubDate>Wed, 09 May 2012 11:54:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. Vorel et al.</author>


</item>


<item>
<title>Prewinter management affects Megachile rotundata (Hymenoptera: Megachilidae) prepupal physiology and adult emergence and survival</title>
<link>http://digitalcommons.usu.edu/piru_pubs/460</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/460</guid>
<pubDate>Wed, 09 May 2012 11:53:48 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Cuticular lipids of female solitary bees, Megachile rotundata (F.) and Osmia lignaria Say (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/459</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/459</guid>
<pubDate>Wed, 09 May 2012 11:53:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J. S. Buckner et al.</author>


</item>


<item>
<title>Do weather conditions correlate with findings in failed, provision-filled nest cells of Megachile rotundata (Hymenoptera: Megachilidae) in western North America?</title>
<link>http://digitalcommons.usu.edu/piru_pubs/458</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/458</guid>
<pubDate>Wed, 09 May 2012 11:53:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>The future of agricultural pollination</title>
<link>http://digitalcommons.usu.edu/piru_pubs/457</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/457</guid>
<pubDate>Wed, 09 May 2012 11:53:06 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R. R. James et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Bees in nature and on the farm</title>
<link>http://digitalcommons.usu.edu/piru_pubs/456</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/456</guid>
<pubDate>Wed, 09 May 2012 11:52:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Past and present management of alfalfa bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/455</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/455</guid>
<pubDate>Wed, 09 May 2012 11:52:37 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer</author>


<category>Bee management</category>

</item>


<item>
<title>Field use of an incubation box for improved emergence timing of Osmia lignaria populations used for orchard pollination</title>
<link>http://digitalcommons.usu.edu/piru_pubs/454</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/454</guid>
<pubDate>Wed, 09 May 2012 11:52:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Nest demographics and foraging behavior of Apterostigma collare Emery (Hymenoptera, Formicidae) provide evidence of colony independence</title>
<link>http://digitalcommons.usu.edu/piru_pubs/453</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/453</guid>
<pubDate>Wed, 09 May 2012 11:52:12 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Olfactory response of megachilid bees, Osmia lignaria, Megachile rotundata and M. pugnata, to individual cues from old nest cavities</title>
<link>http://digitalcommons.usu.edu/piru_pubs/452</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/452</guid>
<pubDate>Wed, 09 May 2012 11:52:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer</author>


</item>


<item>
<title>Leafcutting Bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/451</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/451</guid>
<pubDate>Wed, 09 May 2012 11:51:49 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer</author>


</item>


<item>
<title>Emergence success and sex ratio of commercial alfalfa leafcutting bees from the United States and Canada</title>
<link>http://digitalcommons.usu.edu/piru_pubs/450</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/450</guid>
<pubDate>Wed, 09 May 2012 11:51:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Ascosphaera aggregata contamination on alfalfa leafcutting bees in a loose cell incubation system</title>
<link>http://digitalcommons.usu.edu/piru_pubs/449</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/449</guid>
<pubDate>Wed, 09 May 2012 11:51:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R. R. James et al.</author>


</item>


<item>
<title>Hybrid and environment effects on popcorn kernel
physiochemical properties and their relationship to
microwave popping performance</title>
<link>http://digitalcommons.unl.edu/foodsciefacpub/115</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/foodsciefacpub/115</guid>
<pubDate>Wed, 09 May 2012 11:51:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>The objective of this study was to characterize the effect of hybrid and environment on physical and chemical characteristics of popcorn kernels that have shown importance in predicting end-use quality. Three popcorn hybrids grown in three different environments were tested for physiochemical attributes and popping performance. Hybrid had a significant effect on kernel sphericity, time-to-grind, dietary fiber, sugars, and starch. Environment effect alone affected total mineral content. Hybrid and environment main effects influenced test weight, tangential abrasive dehulling device index, thousand-kernel weight, total carbohydrates, and kernel protein content. Oil adherence to the bag averaged 15.8% and was proportional to oil amount added prior to microwave popping. Unpopped kernels averaged 11.4 ± 5.3%. Most unpopped kernels were observed to successfully pop when heated a second time in microwave tests. Expansion volume was 44.7 ± 3.7 and 47.3 ± 6.4 cm3/g, depending on the method of determination. Expansion volume was correlated (p < 0.05) with several kernel physiochemical parameters that were influenced by hybrid effect. Sphericity, thousand-weight, and total fat are physiochemical characteristics that appear to be good predictors (p < 0.05) of expansion volume.</p>

	]]>
</description>

<author>Jess C. Sweley et al.</author>


</item>


<item>
<title>Examination of “pollen balls” in nests of the alfalfa leafcutting bee, Megachile rotundata</title>
<link>http://digitalcommons.usu.edu/piru_pubs/448</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/448</guid>
<pubDate>Wed, 09 May 2012 11:51:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer</author>


</item>


<item>
<title>A review of the Sphaeropthalma uro species-group (Hymenoptera: Mutillidae), with taxonomic changes</title>
<link>http://digitalcommons.usu.edu/piru_pubs/447</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/447</guid>
<pubDate>Wed, 09 May 2012 11:51:04 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J. P. Pitts et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

</item>


<item>
<title>Centennial Library E-News, March/April 2011</title>
<link>http://digitalcommons.cedarville.edu/library_enews/4</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/library_enews/4</guid>
<pubDate>Wed, 09 May 2012 11:50:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Articles in this issue: Library staff members move on, New Director appointed, Library scholarship awarded, Library staff honored, Library Sunday hours added, Collection development recognitions, Commemorative Bible received, National library week celebrated, University faculty in print, University alumni in print, Library summer schedule</p>

	]]>
</description>

<author>Centennial Library</author>


</item>


<item>
<title>Insect pollinators of three rare plants in a Florida longleaf pine forest</title>
<link>http://digitalcommons.usu.edu/piru_pubs/446</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/446</guid>
<pubDate>Wed, 09 May 2012 11:50:53 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>A new host record for Pseudodacteon crawfordi (Diptera: Phoridae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/445</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/445</guid>
<pubDate>Wed, 09 May 2012 11:50:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J. P. Pitts et al.</author>


<category>Pathogens &amp; parasites</category>

</item>


<item>
<title>Influence of guidelines and passageways on tunneling behavior of Reticulitermes flavipes (Kollar) and R. virginicus (Banks) (Isoptera: Rhinotermitidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/444</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/444</guid>
<pubDate>Wed, 09 May 2012 11:50:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Nest and nestmate recognition by a fungus-growing ant, Apterostigma collare Emery (Hymenoptera: Formicidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/443</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/443</guid>
<pubDate>Wed, 09 May 2012 11:50:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Roles of hydrocarbons in the recognition systems of insects</title>
<link>http://digitalcommons.usu.edu/piru_pubs/442</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/442</guid>
<pubDate>Wed, 09 May 2012 11:50:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer</author>


</item>


<item>
<title>Nest and nestmate discrimination in independent-founding paper wasps</title>
<link>http://digitalcommons.usu.edu/piru_pubs/441</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/441</guid>
<pubDate>Wed, 09 May 2012 11:49:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Exposure to nest paper hydrocarbons is important for nest recognition by a social wasp, Polistes metricus Say (Hymenoptera, Vespidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/440</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/440</guid>
<pubDate>Wed, 09 May 2012 11:49:42 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Nest surface hydrocarbons facilitate nestmate recognition for the social wasp, Polistes metricus Say (Hymenoptera: Vespidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/439</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/439</guid>
<pubDate>Wed, 09 May 2012 11:49:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Social wasps use nest paper hydrocarbons for nestmate recognition</title>
<link>http://digitalcommons.usu.edu/piru_pubs/438</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/438</guid>
<pubDate>Wed, 09 May 2012 11:49:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Discriminant analysis of the cuticular hydrocarbons of social wasp Polistes exclamans Viereck and the surface hydrocarbons of its nest paper and pedicel</title>
<link>http://digitalcommons.usu.edu/piru_pubs/437</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/437</guid>
<pubDate>Wed, 09 May 2012 11:49:08 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Ultrastructural and chemical examination of paper and pedicel from laboratory and field nests of the social wasp Polistes metricus Say</title>
<link>http://digitalcommons.usu.edu/piru_pubs/436</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/436</guid>
<pubDate>Wed, 09 May 2012 11:48:56 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. L. Pitts-Singer et al.</author>


</item>


<item>
<title>Timing of eclosion affects diapause development, fat body consumption and longevity in Osmia lignaria, a univoltine, adult-wintering solitary bee</title>
<link>http://digitalcommons.usu.edu/piru_pubs/435</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/435</guid>
<pubDate>Wed, 09 May 2012 11:48:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Jordi Bosch et al.</author>


</item>


<item>
<title>Florida: Franklin Exchange Building in Tampa</title>
<link>http://digitalcommons.ric.edu/smolski_images/836</link>
<guid isPermaLink="true">http://digitalcommons.ric.edu/smolski_images/836</guid>
<pubDate>Wed, 09 May 2012 11:48:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Built in 1957 by the MacEwen Group, this building was formerly known as the Exchange National Bank Building. This skyscraper towers over many surrounding buildings at 280 feet and 22 stories. This piece of architecture was built in the international style with its structure made of steel and a white facade. Along with the Exchange National Bank and 7-story annex, this skyscraper is considered part of the “new Franklin Exchange” area and occupies a full city block in Tampa.</p>

	]]>
</description>

<author>Chet Smolski</author>


</item>


<item>
<title>Effect of temperature regime on diapause intensity in an adult-wintering Hymenopteran with obligate diapause</title>
<link>http://digitalcommons.usu.edu/piru_pubs/434</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/434</guid>
<pubDate>Wed, 09 May 2012 11:48:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>F. Sgolastra et al.</author>


</item>


<item>
<title>Foraging and nesting behavior of the mason bee Osmia lignaria (Hymenoptera; Megachilidae) in the presence of fungicides: cage studies</title>
<link>http://digitalcommons.usu.edu/piru_pubs/433</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/433</guid>
<pubDate>Wed, 09 May 2012 11:48:23 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E. Ladurner et al.</author>


</item>


<item>
<title>Effect of three dimension and color contrast on nest localization performance of two solitary bees (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/432</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/432</guid>
<pubDate>Wed, 09 May 2012 11:48:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. Guédot et al.</author>


</item>


<item>
<title>Thermal history influences diapause development in the solitary bee Megachile rotundata</title>
<link>http://digitalcommons.usu.edu/piru_pubs/431</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/431</guid>
<pubDate>Wed, 09 May 2012 11:47:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>G. D. Yocum et al.</author>


</item>


<item>
<title>Effects of three-dimensional and color patterns on nest location and progeny mortality in alfalfa leafcutting bee (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/430</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/430</guid>
<pubDate>Wed, 09 May 2012 11:47:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. Guédot et al.</author>


</item>


<item>
<title>Bee population returns and cherry yields in an orchard pollinated with Osmia lignaria (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/429</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/429</guid>
<pubDate>Wed, 09 May 2012 11:47:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jordi Bosch et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Olfactory cues and nest recognition in the solitary bee Osmia lignaria Say (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/428</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/428</guid>
<pubDate>Wed, 09 May 2012 11:47:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>C. Guédot et al.</author>


</item>


<item>
<title>Sex allocation in the solitary bee Osmia cornuta: do females behave in agreement with Fisher´s theory?</title>
<link>http://digitalcommons.usu.edu/piru_pubs/427</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/427</guid>
<pubDate>Wed, 09 May 2012 11:47:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jordi Bosch et al.</author>


</item>


<item>
<title>The relative importance of vertical and horizontal visual cues in nest location by Megachile rotundata (F.) (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/426</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/426</guid>
<pubDate>Wed, 09 May 2012 11:46:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>C. Guédot et al.</author>


</item>


<item>
<title>Effects of temperature on Osmia lignaria (Hymenoptera: Megachilidae) prepupa-adult development, survival, and emergence</title>
<link>http://digitalcommons.usu.edu/piru_pubs/425</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/425</guid>
<pubDate>Wed, 09 May 2012 11:46:39 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. P. Kemp et al.</author>


</item>


<item>
<title>Assessing chronic and acute toxicity of five fungicides to Osmia lignaria and Apis mellifera</title>
<link>http://digitalcommons.usu.edu/piru_pubs/424</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/424</guid>
<pubDate>Wed, 09 May 2012 11:46:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>E. Ladurner et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Alfalfa leafcutting bee population dynamics, flower availability, and pollination rates in two Oregon alfalfa fields</title>
<link>http://digitalcommons.usu.edu/piru_pubs/423</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/423</guid>
<pubDate>Wed, 09 May 2012 11:46:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Jordi Bosch et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Evaluation of a standard artificial flower design to feed individual bees known amounts of pesticides</title>
<link>http://digitalcommons.usu.edu/piru_pubs/422</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/422</guid>
<pubDate>Wed, 09 May 2012 11:45:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>E. Ladurner et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Maintaining Incentives for Bioprospecting: The Occasional Need for a Right to Lie</title>
<link>http://www.repository.law.indiana.edu/facpub/535</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/535</guid>
<pubDate>Wed, 09 May 2012 11:45:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Building on a model by Anthony Kronman, the author argues that biotechnological researchers searching for valuable cells should occasionally be allowed to deceive research subjects whose cells prove valuable. The wish to preserve proper incentives for these searches justifies this exception to the law's usual abhorrence of deception. The subject's ability to "hold up" the researcher once the subject learns of his cells' value combined with the law's likely refusal to force an unwilling subject to continue his cooperation with the researcher poses risks for biotechnologists that other producers of information do not face and that the right to deceive helps to alleviate. The author explains the variables that limit the proposed right to deceive, examines arguments against the proposed rule, and describes the current law.</p>
<p>Bioprospecting, the search for valuable cells, also presents three related issues on which the author comments. One issue is whether the subject's assignment of all his rights in his cell samples to the researcher should be enforced ex post when the cells prove valuable. A second issue is whether, in the absence of a clear assignment of rights to the cell samples, the subject or patient should possess a claim against the researcher to a share of revenues derived from those cell samples. A third issue is whether a patient whose samples are used for research or commercial purposes without his express consent should possess some dignitary claim against the researcher regardless of whether the samples have proven valuable. On each issue, the author supports an approach that favors the biotechnological researcher.</p>

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</description>

<author>Robert H. Heidt</author>


</item>


<item>
<title>Temporal variation in overwintering gene expression and respiration in the solitary bee Megachile rotundata</title>
<link>http://digitalcommons.usu.edu/piru_pubs/421</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/421</guid>
<pubDate>Wed, 09 May 2012 11:45:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>G. D. Yocum et al.</author>


</item>


<item>
<title>On Game Theory and the Law</title>
<link>http://www.repository.law.indiana.edu/facpub/534</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/534</guid>
<pubDate>Wed, 09 May 2012 11:45:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kenneth G. Dau-Schmidt et al.</author>


</item>


<item>
<title>Misrepresentation in the Sale of Stock: Which Buyers Are Protected?</title>
<link>http://www.repository.law.indiana.edu/facpub/533</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/533</guid>
<pubDate>Wed, 09 May 2012 11:45:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>This case concerns the civil liability of persons who misrepresent material facts in a privately negotiated sale of securities. The Supreme Court will decide  whether Section 12(2) of the Securities Act of 1933 provides a buyer of securities with a right to rescind the purchase both in public and private offerings.</p>

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</description>

<author>J. William Hicks</author>


</item>


<item>
<title>Characterization of triacylglycerols from overwintering prepupae of the alfalfa pollinator Megachile rotundata (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/420</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/420</guid>
<pubDate>Wed, 09 May 2012 11:45:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J. S. Buckner et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>National Security and Environmental Laws: A Clear and Present Danger?</title>
<link>http://scholarship.law.georgetown.edu/facpub/953</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/953</guid>
<pubDate>Wed, 09 May 2012 11:45:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Without question, life in the United States has changed significantly since September 11, 2001. The attacks launched from within the United States in broad daylight against non-military targets and innocent civilians, followed by the intentional dispersal of the biological agent anthrax, ushered in an era of uncertainty and fear in this country unlike any in recent memory. The visible manifestations of this fear are still with us--concrete barriers and the closing of public spaces around public buildings, heightened security at airports and train stations subjecting people to invasive searches of their persons and belongings, the sudden, seemingly random appearance of fighter planes over major cities, previously benign colors taking on a whole new and frightening appearance, and the detention of persons who were our neighbors and, we thought, our friends.</p>
<p>This is also a war unlike any other the United States has experienced. No nation-states are threatening our shores. Therefore, it is unlikely that there will be a clear signal that the war is over as no armistice will be signed. Instead, the country appears to be now perpetually at war with "shadowy groups, often fluid in nature, motivated by a distorted Islamist ideology and only sometimes in association with established governments." The methods and weapons these groups use are "unconventional" and "intended to disrupt civil society rather than conquer it with large-scale military means." In response to the horrors of that day, the country is newly and fervently patriotic, and "the military is popular again."</p>
<p>The events of 9/11 have also brought into sharp focus a conflict that this country has not witnessed since the Cold War: the clash between the safety and continuation of the Republic and other values we hold dear, among them a healthy environment. That conflict is the subject of this article.</p>
<p>Unavoidable conflicts between the requirements of environmental laws and protecting national security exist, although some like Stephen Dycus believe that they are avoidable with proper planning and foresight. No one understands this situation better than the military.</p>
<p>In time of war, the resolution of these conflicts may favor national security over the environment. According to Lawrence Gostin, in a constitutional democracy, however, "[t]he state acts at its lowest level of legitimacy when the risk [of harm] is low and the means are ill-suited to achieve legitimate ends." Even in high-risk situations, if "the means . . . exceed the scope of the threat," Gostin suggests the government's actions will be "unacceptable." The challenge is to find a workable balance in this new, and perhaps unending, era of terror without undercutting the national defense and the government's legitimacy. This article posits that the proper balance has not been found, at least with respect to laws protecting the environment and public health.</p>
<p>The first section of the article describes the ways in which pre-9/11 environmental laws protected the country's national security interests. To provide a broader context for understanding the more narrowly focused changes to environmental laws after 9/11, the article next briefly describes the USA PATRIOT Act and the fundamental changes it has made to basic civil liberties. The third part of the article describes changes made to wildlife laws in the immediate aftermath of 9/11, and pending revisions to pollution control laws, which have not moved as swiftly. This part of the article also contains a discussion of modifications made to public disclosure laws and policies, including those curtailing the release of information to the public about environmental risks. The article concludes by discussing why these initiatives should be of concern and asks whether they are a necessary response to the perceived terrorist threat to the country; a question made all the more urgent by the fact that war now appears to be "continually on the horizon." The article concludes that the military is using the "war on terrorism" as a Trojan horse to get out from under thirty years of constraining environmental laws it has never fully accepted.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>A Civic-Republican Vision of &quot;Domestic Dependent Nations&quot; in the Twenty-First Century: Tribal Sovereignty Re-Envisioned, Reinvigorated, and Re-Empowered</title>
<link>http://scholarship.law.georgetown.edu/facpub/952</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/952</guid>
<pubDate>Wed, 09 May 2012 11:45:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>As a cure for what ails democracy in a pluralistic modem society, such as ours, Michael Sandel recommends "dispersing" sovereignty to a "multiplicity of [civic republican] communities--some more, some less extensive than nations." He intimates that doing this "may entail according greater cultural and political autonomy to subnational communities," which, in turn might "ease the strife that arises when state sovereignty is an all-or-nothing affair, absolute and indivisible, the only meaningful form of self-determination." He sees in federalism not just a "theory of intergovernmental relations," but a "political vision" that "self-government works best when sovereignty is dispersed and citizenship formed across multiple sites of civic engagement." Although Sandel appears not to have had American Indian tribes in mind when he made these comments, his thoughts have interesting implications for tribes, whose members have retained separate cultural and political identities despite concerted efforts to assimilate them into American society.</p>
<p>This article uses Michael J. Sandel's twin concepts of a civic republican polity and dispersed sovereignty as a starting point for developing a theoretical justification for returning greater political and cultural autonomy to tribes. Republican thinking contains some very useful principles for the cause of enhanced tribal sovereignty. These principles should be persuasive because of the important role they played in the founding of this nation and their continuing relevance to theoreticians struggling to find a harmonic place for difference in our democratic society. However, there is a need to find a way to do this without destabilizing the country's capacity to govern or creating separate racial homelands for tribes. The article suggests that granting tribes a constrained power to nullify laws and policies that diminish their sovereignty may offer a structural solution that assures the continuation not only of Indian tribes as vibrant, unique cultures, but also of the United States as a nation and as a robust, pluralistic, tolerant democratic society. "[T]he moral independence of local nomic communities is not a burden to be tolerated or overcome, but is, instead, an essential part of how we build personal integrity and moral freedom as rooted, situated, and well-constituted selves." In order to reach the article's goal of proposing a new theoretical foundation upon which to build solutions to the <em>problem</em> of tribal sovereignty, much ground must be covered. Part II starts this journey by looking briefly at modern conceptions of sovereignty to see whether granting tribes enhanced sovereignty within the United States would offend archetypical notions of sovereignty. Finding it would not, part II concludes that there is much to be gained by tribes, if they were to succeed in their quest. Part III discusses the basic elements of tribal sovereignty, identifies its principal theoretical sources, and then briefly describes its status at the start of the fifth century of contact with non-Indians. Part III concludes that, despite centuries of ill-conceived federal policies and destructive Supreme Court decisions that have weakened the theoretical sources of tribal sovereignty, Indian tribes have retained sufficient core elements of what it means to be sovereign, as described in part II, to qualify objectively as sovereign entities. Part IV acquaints the reader with classical and contemporary republican principles and discusses three such principles that provide particular support for a more robust tribal sovereignty than exists today, as well as one that might undermine it. Part IV of the article shows that Indian tribes not only deserve and need enhanced self-governing authority to protect what is unique about their communities, it also demonstrates that, despite everything that has happened to them, the tribes have retained sufficient cultural, political, and even territorial separation to qualify as repositories of Sandel's downward dispersed sovereign authority. Part V acknowledges the problems that recognizing difference as a basis for separate sovereignty pose to our national norm of a blended society--as well as to any notion of territorial integrity. However, it argues that modem republican thinking, particularly Sandel's multiply-situated citizen and Frank Michelman's dialogic deliberation, assures the survival of both.</p>
<p>It is not enough to establish a theoretical basis for reinvigorated tribal sovereignty. A practical means for its exercise must be found. Otherwise, the painful history of Indian tribes in this country may still end with their disappearance. Accordingly, part VI examines various practical solutions to the problem of tribal sovereignty and finds each of them wanting in some aspect. The article proposes that tribes be allowed to exercise a constrained power to nullify (or opt out of) laws that diminish their sovereignty. Part VI ends with a brief discussion of how the application of republican principles might make this result palatable to both Congress and the Court.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>The Effect of the Supreme Court&apos;s Eleventh Amendment Jurisprudence on Environmental Citizen Suits: Gotcha!</title>
<link>http://scholarship.law.georgetown.edu/facpub/951</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/951</guid>
<pubDate>Wed, 09 May 2012 11:45:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The current Supreme Court has substantially expanded the scope of protection from lawsuits accorded to states by the Eleventh Amendment and narrowed the exceptions to its application. As a result, many people are finding they are unable to vindicate federal rights in any court when the defendant is a state or a state agency. The most recent example of this is the Court's decision in <em>South Carolina State Ports Authority v. Federal Maritime Commission</em>, in which the Court extended the reach of the Eleventh Amendment to private <em>administrative</em> enforcement actions against states, thus forsaking completely any connection to the text of the Amendment.</p>
<p>This trend in the Court's application of the Eleventh Amendment to shield states from injured private citizens has potentially ominous implications for citizens seeking to enforce federal environmental laws against states, as Justice Breyer warned in his dissent in <em>College Savings Bank v. Florida Prepaid Post-secondary Education Expense Board</em>. States are important players in the administration of many environmental laws, as recipients of delegated federal regulatory authority. States also own, operate, and construct potentially polluting facilities, such as hazardous waste landfills, hospitals, prisons, airports, roads, and reservoirs that may violate federal law. Thus, they are often targets of citizen suits.</p>
<p>An examination of the effect of the Court's sovereign immunity jurisprudence on the private enforcement of environmental laws against states, therefore, is no mere academic exercise. In an atmosphere in which states are assuming a more central place in the administration of federal environmental laws and federal oversight of state performance is lessening, any initiative that insulates states from legal challenge takes on grave significance for environmentalists. If environmental plaintiffs cannot enforce federally mandated standards and programmatic requirements against the states that run these programs, history advises that the states may under-perform. Thus, a reinvigorated Eleventh Amendment applied to citizen suits brought to enforce federal environmental laws can as effectively undercut the impact of those laws as if Congress had amended them to achieve the same result.</p>
<p>This paper focuses upon the impact of the Court's Eleventh Amendment jurisprudence on citizen suits authorized under the Clean Water Act (CWA) because that law's cooperative federalism structure is typical of many other environmental laws and because citizens suits have historically played a critical role in its implementation. The Act's citizen suit provision (section 505), which specifically incorporates the Eleventh Amendment, has brought to bear on citizen suits the full force and effect of the Court's current state sovereign immunity jurisprudence. The prevailing wisdom is that that jurisprudence will not bar CWA citizen suits against states. The author shows that she is not persuaded for the reasons set out in this paper.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>Looking Ahead: The Future of Affirmative Action</title>
<link>http://scholarship.law.georgetown.edu/facpub/950</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/950</guid>
<pubDate>Wed, 09 May 2012 11:45:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fifty years after <em>Brown v. Board of Education</em>, race is still a serious issue in this country. Fortunately, we no longer debate whether it is legal for the government to operate segregated schools or to treat blacks as second-class citizens. We finally answered that question correctly—it is unconstitutional for the law to segregate and to treat blacks worse than whites.</p>
<p>Today, we face the more difficult question of ascertaining the constitutionality of “affirmative action” or “benign discrimination” programs. The Supreme Court first addressed this issue in 1978 in the landmark case <em>Regents of the University of California v. Bakke</em>. In a confusing set of six opinions, four Justices concluded that the program was constitutional, while four others held that it violated federal law. Justice Powell alone stated that the consideration of race was not necessarily unconstitutional, but that the use of quotas was. As a result, with Justice Powell’s vote controlling, there were five Justices who said race could be considered in school admissions, but also five Justices who struck down the particular program at issue.</p>
<p>In 2003, the Supreme Court had the opportunity to tell us more in the cases challenging the University of Michigan’s affirmative action programs. But before discussing the Michigan cases, the author sets the stage by giving the views of the man who brought us <em>Brown v. Board of Education</em>, Thurgood Marshall.</p>
<p>Justice Marshall started with the premise that the ultimate goal for our country is to be a “colorblind” society in which race is irrelevant. However, Marshall pointed out that this commonly accepted goal has led to two very different conclusions. Some people conclude that, because what is ultimately desired is a colorblind society, race-conscious remedies <em>should not</em> and <em>cannot</em> be used to eliminate the effects of past discrimination. Others, however, believe that the vestiges of racial bias in America are, in Marshall’s words, “so pernicious and difficult to remove that we must take advantage of all the remedial measures at our disposal.” Which of these conclusions one adopts, said Marshall, depends on how close one believes this country is to the desired colorblind society.</p>

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</description>

<author>Susan Low Bloch</author>


</item>


<item>
<title>Foraging behavior and pollinating effectiveness of Osmia cornuta and Apis mellifera (Hymenoptera: Megachilidae, Apidae) on &apos;Comice&apos; pear</title>
<link>http://digitalcommons.usu.edu/piru_pubs/419</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/419</guid>
<pubDate>Wed, 09 May 2012 11:45:23 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>V. H. Monzon et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Effect of pre-wintering and wintering temperature regimes on weight loss, survival, and emergence time in the mason bee Osmia cornuta (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/418</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/418</guid>
<pubDate>Wed, 09 May 2012 11:45:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Jordi Bosch et al.</author>


</item>


<item>
<title>Oxygen consumption during the life cycle of the prepupa-wintering bee Megachile rotundata (F.) and the adult-wintering bee Osmia lignaria Say (Hymenoptera: Megachilidae).</title>
<link>http://digitalcommons.usu.edu/piru_pubs/417</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/417</guid>
<pubDate>Wed, 09 May 2012 11:44:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. P. Kemp et al.</author>


</item>


<item>
<title>A method to feed bees known amounts of pesticides</title>
<link>http://digitalcommons.usu.edu/piru_pubs/416</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/416</guid>
<pubDate>Wed, 09 May 2012 11:44:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E. Ladurner et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Effect of wintering duration and temperature on survival and emergence time in males of the orchard pollinator Osmia lignaria (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/415</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/415</guid>
<pubDate>Wed, 09 May 2012 11:44:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jordi Bosch et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Blue orchard bees – Another six-legged secret to improved fruit tree pollination</title>
<link>http://digitalcommons.usu.edu/piru_pubs/414</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/414</guid>
<pubDate>Wed, 09 May 2012 11:44:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. P. Kemp et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Developing and establishing bee species as crop pollinators: the example of Osmia spp. and fruit trees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/413</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/413</guid>
<pubDate>Wed, 09 May 2012 11:44:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Jordi Bosch et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Body size as an estimator of production costs in a solitary bee</title>
<link>http://digitalcommons.usu.edu/piru_pubs/412</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/412</guid>
<pubDate>Wed, 09 May 2012 11:44:08 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jordi Bosch et al.</author>


</item>


<item>
<title>Bees in your backyard</title>
<link>http://digitalcommons.usu.edu/piru_pubs/411</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/411</guid>
<pubDate>Wed, 09 May 2012 11:43:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. P. Kemp et al.</author>


<category>Bee Management</category>

</item>


<item>
<title>The Effect of the Hydrogen Ion and Light on the Membrane Properties of Nitella</title>
<link>http://digitalcommons.brockport.edu/env_theses/14</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_theses/14</guid>
<pubDate>Wed, 09 May 2012 11:43:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Using the Kitasato hypothesis as a basis, the effect of H<sup>+</sup>and light on Nitella was investigated. Upon a light to dark transition, the cell resting potential at pH 5.7 depolarized, whereas at pH 4.7 the membrane became hyperpolarized. Membrane conductance and H<sup>+</sup> extrusion were not significantly affected by the pH change 5.7 to 4.7. Light promoted increases in both membrane conductance and H<sup>+</sup> fluxes. All cells except those having extreme resting potential values, either high or low, were responsive to light. The action spectra for H<sup>+</sup> flux, resting potential and membrane conductance is not the same as that for photosynthesis suggesting the possibility of another more complex mechanism(s) being involved with the light effects on Nitella.</p>

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</description>

<author>Danley F. Brown</author>


</item>


<item>
<title>A phylogenetic analysis of nesting behavior in the genus Osmia (Insecta, Hymenoptera, Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/410</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/410</guid>
<pubDate>Wed, 09 May 2012 11:43:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jordi Bosch et al.</author>


</item>


<item>
<title>Post-cocooning temperatures and diapause in the alfalfa pollinator Megachile rotundata (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/409</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/409</guid>
<pubDate>Wed, 09 May 2012 11:43:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. P. Kemp et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Management of Osmia lignaria (Hymenoptera, Megachilidae) populations for almond pollination: methods to advance bee emergence</title>
<link>http://digitalcommons.usu.edu/piru_pubs/408</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/408</guid>
<pubDate>Wed, 09 May 2012 11:43:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Jordi Bosch et al.</author>


<category>Bee Management</category>

</item>


<item>
<title>Development and emergence of the alfalfa pollinator, Megachile rotundata (Hymenoptera, Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/407</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/407</guid>
<pubDate>Wed, 09 May 2012 11:43:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. P. Kemp et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Weather-dependent pollinator activity in an apple orchard, with special reference to Osmia cornuta and Apis mellifera (Hymenoptera, Megachilidae and Apidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/406</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/406</guid>
<pubDate>Wed, 09 May 2012 11:42:59 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>N. Vincens et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Pollinating efficacy of Osmia cornuta and Apis mellifera (Hymenoptera, Megachilidae, Apidae) on ‘Red Delicious’ apple</title>
<link>http://digitalcommons.usu.edu/piru_pubs/405</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/405</guid>
<pubDate>Wed, 09 May 2012 11:42:48 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>N. Vincens et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Nest site orientation and relocation of populations of the orchard pollinator Osmia cornuta (Hymenoptera, Megachilidae</title>
<link>http://digitalcommons.usu.edu/piru_pubs/404</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/404</guid>
<pubDate>Wed, 09 May 2012 11:42:37 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>N. Vincens et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Development and emergence of the orchard pollinator, Osmia lignaria (Hymenoptera, Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/403</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/403</guid>
<pubDate>Wed, 09 May 2012 11:42:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Jordi Bosch et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Exceptional cherry production in a cherry orchard pollinated with blue orchard bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/402</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/402</guid>
<pubDate>Wed, 09 May 2012 11:42:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Jordi Bosch et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Substrates and materials used for nesting by North American Osmia bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/401</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/401</guid>
<pubDate>Wed, 09 May 2012 11:42:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nesting substrates and construction materials are compared for 65 of North America's 139 described native species of Osmia bees. Most accounts report Osmia bees nesting in preexisting cavities in dead wood or pithy stems such as elderberry (Sambucus spp.), with cell partitions and plugs made from a pulp of finely masticated leaf tissue. Mud is widely used by species constructing free-form clumps of nest cells against stone surfaces. Some Osmia bees adopt abandoned nests of other Hymenoptera, particularly those of mud dauber wasps (Sceliphron spp.) and larger ground-nesting bees (e.g., Anthophora spp.). Reports of subterranean nesting by Osmia species are uncommon but possibly under-represent the habit, because subterranean nests are obscure and likely to be scattered. Ground- or surface-nesting habits are suspected for species that are absent from intensive trap-nesting programs in their native ranges but that otherwise have been commonly taken at flowers. The range of nesting habits and materials of European species are largely comparable, although records indicate that far more European species may nest in empty snail shells</p>

	]]>
</description>

<author>James H. Cane et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Stelis rozeni (new species) the first record of the parasitic bee genus Stelis from southern Africa (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/400</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/400</guid>
<pubDate>Wed, 09 May 2012 11:41:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>The first record of Stelis from southern Africa is described as Stelis rozeni. This distinctive species does not fit any recognized subgenus. Its systematic position is discussed and comparison made to the rare subgenus Malanthidium</p>

	]]>
</description>

<author>Terry L. Griswold et al.</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Bee pollination of Cuphea (Lythraceae) species in greenhouse and field</title>
<link>http://digitalcommons.usu.edu/piru_pubs/399</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/399</guid>
<pubDate>Wed, 09 May 2012 11:41:41 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Nest clustering as a means of managing Osmia sanrafaelae (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/398</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/398</guid>
<pubDate>Wed, 09 May 2012 11:41:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adults lived 30 d, provisioned cells with 99% alfalfa and sweet clover, no aggresive behavior seen when nesting side by side</p>

	]]>
</description>

<author>Frank D. Parker</author>


<category>Bee management</category>

</item>


<item>
<title>Alternation of sex ratio in a partially bivoltine bee, Megachile rotundata (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/397</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/397</guid>
<pubDate>Wed, 09 May 2012 11:41:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Parental investment and sex ratio theory. Spring-emergent adults produce two types of offspring: those that develop directly to adult stage by mid-summer, and those that diapause to the following spring. Sex ratio of summer-emergent progeny biased toward females (because some spring-emergent males should still be around, although they found this to be highly unlikely), sex ratio of diapausing progeny biased toward males (regardless of whether they came from spring or summer generation). Importantly, diapausing progeny are 50% larger than summer-emergent brood</p>

	]]>
</description>

<author>Vincent J. Tepedino et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Influence of wood, paper and plastic nesting units on efficiacy of three candidate fungicides for control of chalkbrood in the alfalfa leafcutting bee (Hymenoptera, Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/396</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/396</guid>
<pubDate>Wed, 09 May 2012 11:41:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Bee management</category>

</item>


<item>
<title>Nesting biology of two North American species of Chelostoma, Hymenoptera: Megachilidae</title>
<link>http://digitalcommons.usu.edu/piru_pubs/395</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/395</guid>
<pubDate>Wed, 09 May 2012 11:41:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>Knowledge-Assisted Sequential Pattern Analysis: An Application in Labor Contraction Prediction</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/757</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/757</guid>
<pubDate>Wed, 09 May 2012 11:40:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although neuraxial techniques, such as spinal and epidural, are still considered as the gold standard for labor analgesia, there are some parturients who cannot receive neuraxial analgesia because of pre-existing conditions, or who request analgesia other than epidural block. An alternative analgesia is remifentanil, which is a relatively new, very potent and short-acting opioid. It has been shown to be effective in the relief of labor pain, but reports to date have failed to find the optimal dosing regimen. A challenge to a systemic opioid is that it must match the unique time course of labor pain. A continuous infusion is not ideal, as the parturient experiences no pain between contractions. Moreover, a continuous infusion during times in which the patient does not experience pain, may increase the risks of respiratory depression, sedation and nausea. The continuous infusion also increases the amount of the drug to which the fetus is exposed. Designing an optimal dosing regimen necessitates the prediction of the pace of contractions, so that the drug can be given shortly before the pain of the contraction begins. The prediction and thus drug administration should be made early enough to allow for the administration of intravenous analgesia that will have maximal efficacy during contractions, little effect between contractions, and minimal impact on the fetus. Towards such a need, we propose a knowledge-assisted sequential pattern analysis framework to predict the changes in intrauterine pressure, which indicate the occurrence of labor contractions. The proposed framework predicts in real time and provides a prediction multiple seconds before a contraction occurs, so as to assist in designing optimal administration strategies of remifentanil in labor. The proposed framework first selects a group of patients, from the stored record, who share similar demographic and obstetrical information with the current patient of interest. Second, it develops a sequential association rule mining approach to learn the patterns of the contractions from the historical patient tracings of the selected patients. Third, a sequential association rule-based collaborative filtering strategy is designed to dynamically select a training dataset from the historical patient tracings, as well as from the most recent training time series of the patient of interest. The training set is used for training a set of prediction models. A k-nearest neighbors (k-NN) based least squares support vector machine (LS-SVM) approach with heuristic parameter tuning is proposed to conduct the long-term time series prediction. A post-prediction process is also incorporated to further enhance the prediction results. Because to the best of our knowledge, there has been no previous study to predict future contractions, this work can be considered as a pioneer in the field. We evaluate the performance of the proposed framework using actual data from anonymous patients with varied contraction patterns. The data include patient demographic and obstetrical information, and measured intrauterine pressure time series. Overall, the proposed framework outperforms several well-known prediction methods, and it accomplishes that in real time. Meanwhile, experiments that compare each component with some other famous algorithms are conducted. The promising experimental results show that all proposed components improve the prediction precision, and the proposed framework achieves the effectiveness, robustness and efficiency that are needed for designing the optimal dosing regimen of remifentanil.</p>

	]]>
</description>

<author>Zifang Huang</author>


</item>


<item>
<title>New Perdita (Perdita) oligoleges of Mentzelia, with notes on related species of the Ventralis group (Hymenoptera: Andrenidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/394</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/394</guid>
<pubDate>Wed, 09 May 2012 11:40:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Terry L. Griswold et al.</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>The xylophilous bees and wasps of a high, cold desert: Leslie Gulch, Oregon (Hymenoptera: Apoidea, Vespoidea)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/393</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/393</guid>
<pubDate>Wed, 09 May 2012 11:40:41 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D. R. Frohlich et al.</author>


</item>


<item>
<title>Nests of Callanthidium from block traps (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/392</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/392</guid>
<pubDate>Wed, 09 May 2012 11:40:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>New pollinators for our crops</title>
<link>http://digitalcommons.usu.edu/piru_pubs/391</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/391</guid>
<pubDate>Wed, 09 May 2012 11:40:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Host records and nest entry by Dolichostelis, a kleptoparasitic anthidiine bee (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/390</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/390</guid>
<pubDate>Wed, 09 May 2012 11:40:05 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Further studies on the use of fungicides for control of chalkbrood of the alfalfa leafcutting bee</title>
<link>http://digitalcommons.usu.edu/piru_pubs/389</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/389</guid>
<pubDate>Wed, 09 May 2012 11:39:53 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Bee management</category>

</item>


<item>
<title>A new species of Protosmia Ducke from Spain with notes on related species (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/388</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/388</guid>
<pubDate>Wed, 09 May 2012 11:39:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Terry L. Griswold et al.</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Biological Notes on Nomia heteropoda Say (Hymenoptera: Halictidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/387</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/387</guid>
<pubDate>Wed, 09 May 2012 11:39:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Field Studies With Osmia sanrafaelae Parker, a Pollinator of Alfalfa (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/386</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/386</guid>
<pubDate>Wed, 09 May 2012 11:39:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Factors Influencing Mortality and Nesting in Managed Populations of the Sunflower Leafcutter Bee (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/385</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/385</guid>
<pubDate>Wed, 09 May 2012 11:39:14 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


</item>


<item>
<title>Nesting, Associates, and Mortality of Osmia sanrafaelae Parker</title>
<link>http://digitalcommons.usu.edu/piru_pubs/384</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/384</guid>
<pubDate>Wed, 09 May 2012 11:39:05 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>Pollination Efficiency of Honey Bees and Wild Bees as Pollinators of Sunflowers</title>
<link>http://digitalcommons.usu.edu/piru_pubs/383</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/383</guid>
<pubDate>Wed, 09 May 2012 11:38:55 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Studies on Management of the Sunflower Leafcutter Bee (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/382</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/382</guid>
<pubDate>Wed, 09 May 2012 11:38:45 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker et al.</author>


<category>Bee management</category>

</item>


<item>
<title>Observations on the Nest Building and Reproductive Behavior of a Resin Gathering Bee: Dianthidium ulkei (Cresson)(Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/381</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/381</guid>
<pubDate>Wed, 09 May 2012 11:38:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D. R. Frohlich et al.</author>


<category>Natural history</category>

</item>


<item>
<title>An Effective Fungicide Treatment for Controlling Chalkbrood Disease of the Alfalfa Leafcutting Bee in Field Populations (Hymenoptera: Megachilidae) (Ascomycetes: Ascosphaeraceae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/380</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/380</guid>
<pubDate>Wed, 09 May 2012 11:38:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Sunflower Bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/379</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/379</guid>
<pubDate>Wed, 09 May 2012 11:38:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Louise Martin Brown et al.</author>


</item>


<item>
<title>Nesting Habits of Osmia grinnelli Cockerell (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/378</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/378</guid>
<pubDate>Wed, 09 May 2012 11:38:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>Osmia sanrafaelae, a New Species From Utah&apos;s San Rafael Desert (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/377</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/377</guid>
<pubDate>Wed, 09 May 2012 11:37:59 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Nest Selection, Mortality and Sex Ratio in Hoplitis fulgida (Cresson) (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/376</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/376</guid>
<pubDate>Wed, 09 May 2012 11:37:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Vincent J. Tepedino et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Nests and nest associates of two &quot;red&quot; Odynerus wasps (Hymenoptera: Eumenidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/375</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/375</guid>
<pubDate>Wed, 09 May 2012 11:37:42 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>Effect of fungicide treatments on incidence of chalkbrood disease in nests of the alfalfa leafcutting bee (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/374</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/374</guid>
<pubDate>Wed, 09 May 2012 11:37:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Biological Notes on the Bee Exomalopsis Crenulata Timberlake (Hymenoptera: Anthophoridae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/373</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/373</guid>
<pubDate>Wed, 09 May 2012 11:37:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>A candidate legume pollinator, Osmia sanrafaelae Parker (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/372</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/372</guid>
<pubDate>Wed, 09 May 2012 11:37:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>The nesting biology of Osmia (Trichinosmia) latisulcata Michener</title>
<link>http://digitalcommons.usu.edu/piru_pubs/371</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/371</guid>
<pubDate>Wed, 09 May 2012 11:37:03 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>Nest building behavior and development of the sunflower leafcutter bee: Eumeachile (Sayapis) pugnata (Say) (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/370</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/370</guid>
<pubDate>Wed, 09 May 2012 11:36:53 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D. R. Frohlich et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Nest size, mortality and sex ratio in Osmia marginata Michener</title>
<link>http://digitalcommons.usu.edu/piru_pubs/369</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/369</guid>
<pubDate>Wed, 09 May 2012 11:36:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Vincent J. Tepedino et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Influence of attractants on nest establishment by the alfalfa leafcutting bee (Hymenoptera: Megachilidae) in styrofoam and rolled paper</title>
<link>http://digitalcommons.usu.edu/piru_pubs/368</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/368</guid>
<pubDate>Wed, 09 May 2012 11:36:31 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker et al.</author>


<category>Bee management</category>

</item>


<item>
<title>A New Perdita From Utah&apos;s San Rafael Desert (Hymenoptera: Andrenidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/367</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/367</guid>
<pubDate>Wed, 09 May 2012 11:36:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Hybrid sunflower pollination by a manageable composite specialist: The sunflower leafcutter bee (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/366</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/366</guid>
<pubDate>Wed, 09 May 2012 11:36:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Pollination and &quot;non-apis&quot; pollinators, pp. 77-81</title>
<link>http://digitalcommons.usu.edu/piru_pubs/365</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/365</guid>
<pubDate>Wed, 09 May 2012 11:35:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Florida: Publix Super Markets, Inc.</title>
<link>http://digitalcommons.ric.edu/smolski_images/835</link>
<guid isPermaLink="true">http://digitalcommons.ric.edu/smolski_images/835</guid>
<pubDate>Wed, 09 May 2012 11:35:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Publix Super Markets, Inc. is one of the leading privately owned grocery stores in the states of Florida, Georgia, South Carolina, Alabama, and Tennessee. The first store was opened in Winter Haven, FL in the 1930s by George Jenkins. Starting out with purchasing a chain of just 19 grocery stores, Jenkins was able to make the Publix name known. It has since grown to include over 1,000 stores in the states listed above. Being so big, it has gained the name of being one of the 10 largest volume supermarket chains in the United States.</p>

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</description>

<author>Chet Smolski</author>


</item>


<item>
<title>Florida: Tin City in South Naples</title>
<link>http://digitalcommons.ric.edu/smolski_images/834</link>
<guid isPermaLink="true">http://digitalcommons.ric.edu/smolski_images/834</guid>
<pubDate>Wed, 09 May 2012 11:35:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pictured is the entrance to historic Tin City, named for its distinguishable tin roofed buildings. Ever since the 1880s, this area of waterfront has attracted many tourists. In earlier times, access to this area was rather difficult;  passengers has to disembark at Back Bay. In 1887, Walter N. Haldeman wanted to make this area more accessible, so he and a team built a 600 foot pier into the Gulf of Mexico.</p>
<p>In more recent years, Tin City includes more than 30 shops, 2 waterfront restaurants, and access to the water for the general public.</p>

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</description>

<author>Chet Smolski</author>


</item>


<item>
<title>Introduction of alfalfa leafcutting bees to new areas and selection development</title>
<link>http://digitalcommons.usu.edu/piru_pubs/364</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/364</guid>
<pubDate>Wed, 09 May 2012 11:35:42 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frank D. Parker</author>


<category>Bee management</category>

</item>


<item>
<title>&quot;Go now and tell them&quot;: Bulgarian folksongs and political resistance to the Turkish &quot;yoke&quot;</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/270</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/270</guid>
<pubDate>Wed, 09 May 2012 11:35:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Senior Project submitted to The Division of Languages and Literature and the Division of Social Sciences of Bard College.</p>

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</description>

<author>Thea Piltzecker</author>


</item>


<item>
<title>Biological notes on Andrena (Callandrena) haynesi Viereck and Cockerell (Hymenoptera: Andrenidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/363</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/363</guid>
<pubDate>Wed, 09 May 2012 11:35:30 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Further On and Further Up</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/269</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/269</guid>
<pubDate>Wed, 09 May 2012 11:35:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Senior Project submitted to The Division of Arts of Bard College.</p>

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</description>

<author>Stefan J. Superti</author>


</item>


<item>
<title>Crying &quot;Theater&quot; in a Crowded Fire: Audience Performer Relations and Using Theater for Social Change</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/268</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/268</guid>
<pubDate>Wed, 09 May 2012 11:35:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Senior Project submitted to The Division of Arts of Bard College.</p>

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</description>

<author>Eva Steinmetz</author>


</item>


<item>
<title>Behavior of Osmia (Nothosmia) marginata Michener in the nest (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/362</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/362</guid>
<pubDate>Wed, 09 May 2012 11:35:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Natural history</category>

</item>


<item>
<title>&apos;Bring on the Cats&apos; and &apos;Mozart with a Hint of Strauss&apos;</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/267</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/267</guid>
<pubDate>Wed, 09 May 2012 11:35:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Senior Project submitted to The Division of Arts of Bard College.</p>

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</description>

<author>Rosina B. Williams</author>


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<item>
<title>DANCE UNTIL YOU DIE</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/266</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/266</guid>
<pubDate>Wed, 09 May 2012 11:35:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>When I started working on <em>DANCE UNTIL YOU DIE</em>, I did not expect the project that I ultimately produced.  I allowed the process of editing to sculpt my thoughts and to take me to unforeseen places.  In this way, editing became an extremely meditative act which in part reflected the subject matter I focused on in my senior project: dance.</p>
<p><br>I find dance to be an overwhelmingly personal, spiritual, and meditative art form.  It can be an incredible outlet for individual expression granting the mind and body freedom in perhaps its most essential state.   Yet simultaneously, dance as it exists in today’s society can be surprisingly oppressive.  The most obvious example of this lies in the drill team or cheerleading dance aesthetic where individual expression is nearly forbidden.  The image of the group must be upheld at all costs and is done so through a very strict and limited movement vocabulary.  Here we start to see how contradictory dance can be; it is introspective yet communicative, both thoughtful and performative.</p>
<p>My project is meant to explore the complicated and often contrary place of dance in the modern world.  I chose to use American and North Korean culture as a platform for this discussion.  Both the United States and North Korea are obsessively devoted to pop culture icons.  While this devotion is both theatrical and over-the-top, it is often extremely serious and even religious.  The love for their respective deities exists in the same confusing place that dance lives in: intensely personal and oddly performative.  This is evidenced in the footage of the North Koreans mourning the death of Kim Il-sung and in video of American mourners grieving the death of Michael Jackson.  In both cases there is truth and reality in their emotions and yet I can't help but also see a performative quality or affectedness in their grief.</p>
<p>Americans and North Koreans also share a veneration for those who are able to move well and with dexterity.   In my project the American example of this idea is featured in clips of Michael Jackson.  The "King of Pop" was recognized at a young age for his amazing ability to dance and eventually became famous for such moves as the "moon walk" and the "robot."  North Koreans also share a respect for skillful dancers as seen in the epic dance and gymnastic spectacles that make up their Mass Games.  Thousands of young North Korean children train and rehearse for months in order to perfect the movements.  All of this training is done in order to please the Great Leader (Kim Il-sung) and prove true loyalty to communism.  In both instances the body acts as a signifier though in decidedly different contexts.  The transmission of meaning through dance and the body is partially contingent on these contexts and when juxtaposed an intriguing tension is built.</p>
<p>In terms of movement specifically it’s interesting how dance can in some ways define us as humans and our ability to move fluidly, making quick personal choices through improvisation while in other ways it can strip us of our individualism through the generalizing aesthetic of popular culture. There is certainly an undeniable power to bodies moving in unison, but at times it seems this power is exploited.  Movements within this context begin to appear militaristic.  We see this most literally in the North Korean footage of their Mass Games, where performers are often dressed as soldiers, but it’s also apparent in American cheerleading routines as well.  Individual bodies become lost to a greater image, a larger machine.</p>
<p>This tension between the individual expressive self and the massive group dynamic demonstrated within the dance aesthetic is reflected in the installation of my project.  Each of the videos were made independently to exist on their own but when played side by side on several monitors the intent is to unlock meanings and call attention to images through comparison and juxtaposition.  In the same way that several bodies moving together convey different messages than a single dancer might express so too are the videos meant to indicate other connotations through simultaneous play.</p>
<p>Both film-making and dance serve a self-reflective purpose in my life.  <em>DANCE UNTIL YOU DIE</em> is meant to show the mirror-like qualities both art forms have to me as well as to our society as a whole.</p>
<p>Rachael Williams</p>
<p>April 2011</p>

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</description>

<author>Rachael Marie Williams</author>


</item>


<item>
<title>Dream Lover</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/265</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/265</guid>
<pubDate>Wed, 09 May 2012 11:35:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dream  Lover is a High School musical about a boy named Bobby, and the new  girl in town, Brenda.  Brenda is not your average 16 year old girl, but a  teenage Succubus in search of a mate, or a “dream lover”, to take back  with her into her dream world.  As soon as Bobby sees Brenda, he falls  under her spell.  Brenda takes advantage of her new found zombie; using  him for milkshakes and as arm candy.</p>
<p>Bobby knows nothing about Brenda, he asks her where she is from, and  she responds “Wisconsin”, a place she had to leave due to the death of  her last boyfriend.  Much of the information given about the characters  is vague or false.  Most of what Brenda says is part of her cover story.   She pushes Bobby around, manipulating him into inviting her to the  dance, so she can lure him back to her house for her 16th birthday cake.   Brenda has chosen Bobby as the boy she will spend the rest of her  demon life with, living happily together back in her dream world.</p>
<p>However,  not everything goes according to Brenda’s plan.  on the night of  Brenda’s 16th birthday, just before Bobby is hers forever, Bobby manages  to  snap out of  Brenda’s  spell.  He  takes the cake knife and cuts  off Brenda’s head.  He head lands in the cake, where it lives on,  singing “It’s my Party (and I’ll die if I Want to)”, while her body  chases Bobby through an alternate dimension.  Brenda’s body stabs Bobby,  and continues to dance along to Brenda’s head’s tune.  She doesn’t go  down too easily.</p>
<p>Dream  Lover is a video made by, and starring, me, Melissa Wynne.  This piece  is a personal exploration of the American Dream as it exists today in a  YouTube world.  Throughout the making of this movie, I jokingly told  myself, “I’m gonna make me a star”.  Brenda is a character who lives a  life that I do not, and cannot.  She looks like me, but lives without  boundaries.  She can seduce a boy with the flip of her hair, she sings  like a siren, and has a license to kill.  She goes from saccharine sweet  to sour in an instant, and offers no apologies.  I use Brenda as a venue  to be a star.  Brenda is a character that lives out my fantasies on  screen.  I consider stars like Justin Bieber and Katy Perry, who found  fame by posting videos of themselves on YouTube.  The idea that you can  become famous by making yourself into some marketable character, and  putting it on the internet, is incredibly fascinating.  I don’t think of  YouTube as the exclusive venue for my project, but know that parts of  it are going to end up there.  YouTube allows for a kind of  unsurpassed self-indulgence.  12 year-old girls and 45 year-old men  alike are posting video diaries about the most mundane bullshit  imaginable, staring at themselves in the computer screen as they do it.   I basically allowed myself to indulge in all of my worldly pleasures;  mixing my love of 60’s pop music and 80’s slasher films, as well as  fashion and glamor.  I played the role of a high school sweet heart, a  lead singer in a 60’s girl group, and last but most definitely not  least, a bad ass demon bitch.  Brenda is a survivor, and even though she  loses her head in the final scene, she lives on.  After all, I’m too  pretty to die.</p>

	]]>
</description>

<author>Melissa E. Wynne</author>


</item>


<item>
<title>Maternal influence on diapause in the alfalfa leafcutting bee (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/361</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/361</guid>
<pubDate>Wed, 09 May 2012 11:35:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


</item>


<item>
<title>Res Cogitans</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/264</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/264</guid>
<pubDate>Wed, 09 May 2012 11:35:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Senior Project submitted to The Division of Arts of Bard College.</p>

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</description>

<author>Nicholas Peet</author>


</item>


<item>
<title>A nest and pollen-collection records of Osmia sculleni sandhouse, a bee with hooked hairs on the mouthparts (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/360</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/360</guid>
<pubDate>Wed, 09 May 2012 11:34:52 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Notes on the Biology of Andrena (Callandrena) Helianthi Robertson (Hymenoptera: andrenidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/359</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/359</guid>
<pubDate>Wed, 09 May 2012 11:34:39 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Interspecific differences in the relative importance of pollen and nectar to bee species foraging on sunflowers</title>
<link>http://digitalcommons.usu.edu/piru_pubs/358</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/358</guid>
<pubDate>Wed, 09 May 2012 11:34:27 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Vincent J. Tepedino et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Notes on the biology of Odynerus dilectus (Hym.: Eumenidae), a predator of the alfalfa weevil, Hypera Postica (Col.: Curculionidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/357</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/357</guid>
<pubDate>Wed, 09 May 2012 11:34:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>George E. Bohart et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Efficiency of bees in pollinating onion flowers</title>
<link>http://digitalcommons.usu.edu/piru_pubs/356</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/356</guid>
<pubDate>Wed, 09 May 2012 11:34:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>The Effect of Flower Occupancy on the Foraging of Flower-visiting Insects</title>
<link>http://digitalcommons.usu.edu/piru_pubs/355</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/355</guid>
<pubDate>Wed, 09 May 2012 11:33:49 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Vincent J. Tepedino et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Volatile Components of Alfalfa Leaf-cutter Bee Cells</title>
<link>http://digitalcommons.usu.edu/piru_pubs/354</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/354</guid>
<pubDate>Wed, 09 May 2012 11:33:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ron G. Buttery et al.</author>


</item>


<item>
<title>Nests and nest associates of a desert bee, Osmia marginata Michener</title>
<link>http://digitalcommons.usu.edu/piru_pubs/353</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/353</guid>
<pubDate>Wed, 09 May 2012 11:33:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>Navigating through the Legal Minefield of State and Federal Filing for Perfecting Security Interests in Intellectual Property</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/8</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/8</guid>
<pubDate>Wed, 09 May 2012 11:33:18 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Christina Lui</author>


</item>


<item>
<title>CIRM&apos;s Consolidated IP Policy: Will It Promote Collaboration</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/7</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/7</guid>
<pubDate>Wed, 09 May 2012 11:33:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James Langston</author>


</item>


<item>
<title>Apportioning Cleanup Costs in the New Era of Joint and Several CERCLA Liability</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/6</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/6</guid>
<pubDate>Wed, 09 May 2012 11:33:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Michael Foy</author>


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<item>
<title>Process, Outcomes and the Invention of Tradition: The Growing Importance of the Appearance of Judicial Neutrality</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/5</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/5</guid>
<pubDate>Wed, 09 May 2012 11:33:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Anne Richardson Oakes et al.</author>


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<item>
<title>Dangerous Criminals, the Search for the Truth and Effective Law Enforcement: How the Supreme Court Overestimates the Social Costs of the Exclusionary Rule</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/4</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/4</guid>
<pubDate>Wed, 09 May 2012 11:33:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John P. Gross</author>


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<item>
<title>Federal Disability Discrimination Law and the Toxic Workplace: A Critique of ADA and Section 504 Case Law Addressing Impairments Caused or Exacerbated by the Work Environment</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/3</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/3</guid>
<pubDate>Wed, 09 May 2012 11:33:12 PDT</pubDate>
<description>
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</description>

<author>John E. Rumel</author>


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<item>
<title>The FCC&apos;s New Theory of the First Amendment</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/2</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/2</guid>
<pubDate>Wed, 09 May 2012 11:33:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Hannibal Travis</author>


</item>


<item>
<title>Sunflower Pollination: Abundance, Diversity and Seasonality of Bees on Male-Sterile and Male-Fertile Cultivars</title>
<link>http://digitalcommons.usu.edu/piru_pubs/352</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/352</guid>
<pubDate>Wed, 09 May 2012 11:33:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Physical Takings, Regulatory Takings, and Water Rights</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/1</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss2/1</guid>
<pubDate>Wed, 09 May 2012 11:33:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Josh Patashnik</author>


</item>


<item>
<title>Sunflower Pollination: Abundance, Diversity and Seasonality of Bees and Their Effect on Seed Yields</title>
<link>http://digitalcommons.usu.edu/piru_pubs/351</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/351</guid>
<pubDate>Wed, 09 May 2012 11:32:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>How efficient are bees in pollinating sunflowers?</title>
<link>http://digitalcommons.usu.edu/piru_pubs/350</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/350</guid>
<pubDate>Wed, 09 May 2012 11:32:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>A Candidate Red Clover Pollinator Osmia Coerulescens (L.)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/349</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/349</guid>
<pubDate>Wed, 09 May 2012 11:32:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Notes on the Biology of a Common Sunflower Bee, Milissodes (Eumelissodes) Agilis Cresson</title>
<link>http://digitalcommons.usu.edu/piru_pubs/348</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/348</guid>
<pubDate>Wed, 09 May 2012 11:32:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Observations on the Provisioning Behavior of Ammophila Aberti Haldeman (Hymenoptera: Sphecidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/347</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/347</guid>
<pubDate>Wed, 09 May 2012 11:32:12 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Nest of Osmia marginipennis Cresson With a Description of the Female (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/346</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/346</guid>
<pubDate>Wed, 09 May 2012 11:32:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>Management of wild bees. Beekeeping in the United States</title>
<link>http://digitalcommons.usu.edu/piru_pubs/345</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/345</guid>
<pubDate>Wed, 09 May 2012 11:31:49 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Bee Management</category>

</item>


<item>
<title>Alfalfa leafcutter bee: origin of the female and its influence on diapause</title>
<link>http://digitalcommons.usu.edu/piru_pubs/344</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/344</guid>
<pubDate>Wed, 09 May 2012 11:31:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


</item>


<item>
<title>A New Proteriades With Distributional Notes and a Key to its Subgenus Hoplitina</title>
<link>http://digitalcommons.usu.edu/piru_pubs/343</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/343</guid>
<pubDate>Wed, 09 May 2012 11:31:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Research at the Bee Biology and Systematics Laboratory</title>
<link>http://digitalcommons.usu.edu/piru_pubs/342</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/342</guid>
<pubDate>Wed, 09 May 2012 11:31:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


</item>


<item>
<title>Alfalfa leafcutter bee: reducing parasitism of loose cells during incubation</title>
<link>http://digitalcommons.usu.edu/piru_pubs/341</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/341</guid>
<pubDate>Wed, 09 May 2012 11:31:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>An illustrated key to alfalfa leafcutter bees Eutricharaea</title>
<link>http://digitalcommons.usu.edu/piru_pubs/340</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/340</guid>
<pubDate>Wed, 09 May 2012 11:30:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Biology of the bee genus Proteriades Titus</title>
<link>http://digitalcommons.usu.edu/piru_pubs/339</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/339</guid>
<pubDate>Wed, 09 May 2012 11:30:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>A new Proteriades (Xerosomia) from New Mexico with biological notes</title>
<link>http://digitalcommons.usu.edu/piru_pubs/338</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/338</guid>
<pubDate>Wed, 09 May 2012 11:30:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>A new Ashmeadiella from Arizona</title>
<link>http://digitalcommons.usu.edu/piru_pubs/337</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/337</guid>
<pubDate>Wed, 09 May 2012 11:30:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Biological notes on some Mexican bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/336</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/336</guid>
<pubDate>Wed, 09 May 2012 11:30:12 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>Centennial Library E-News, November/December 2010</title>
<link>http://digitalcommons.cedarville.edu/library_enews/3</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/library_enews/3</guid>
<pubDate>Wed, 09 May 2012 11:30:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Articles in this issue: Canoe race victory, Mobile apps coming, Book cart drill team performs, Health Sciences Center planning, Library science dinner, Library scholarship available, Instructional team sets record, University faculty in print, University alumni in print, Semester break hours</p>

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</description>

<author>Centennial Library</author>


</item>


<item>
<title>U. S. National Pollinating Insects Collection</title>
<link>http://digitalcommons.usu.edu/piru_pubs/335</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/335</guid>
<pubDate>Wed, 09 May 2012 11:29:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Nests of Anthocopa enceliae (Cockerell) and A. elongata (Michener)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/334</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/334</guid>
<pubDate>Wed, 09 May 2012 11:29:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>Potentials of European alfalfa polliantors</title>
<link>http://digitalcommons.usu.edu/piru_pubs/333</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/333</guid>
<pubDate>Wed, 09 May 2012 11:29:31 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Asymmetries Among the Members of Mercosur</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/327</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/327</guid>
<pubDate>Wed, 09 May 2012 11:29:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mercosur countries are very different in terms of their economic size and dimension, their level of development, their population, and the size of their market. Taking into account GDP, population and territory, Uruguay and Paraguay are clearly the smaller Mercosur members and they do not represent even 5% of any of these variables, while Brazil accounts for 70%. At the same time, there are other political and regulatory differences, such as a lack of coordinated macroeconomic policies and incentive policies, in particular. Each member has its own investment promotion policies, as well as policies to support the productive sectors and exports, which alters the conditions for competition between firms even more depending on their country of origin. This combination of structural and politicies asymmetries can be considered an obstacle to deeper integration within Mercosur. This paper addresses considerations on asymmetries and growth, and then moves onto asymmetries and integration and the different ways of addressing and treating this problem in the European Union and in Mercosur. Finally, it considers possible policy impacts.</p>

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</description>

<author>Hadi Hijazi</author>


</item>


<item>
<title>Spechid Wasps of the World</title>
<link>http://digitalcommons.usu.edu/piru_pubs/332</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/332</guid>
<pubDate>Wed, 09 May 2012 11:29:19 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>A new proteriades reared from trap stems, its biology and nest associates</title>
<link>http://digitalcommons.usu.edu/piru_pubs/331</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/331</guid>
<pubDate>Wed, 09 May 2012 11:29:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


</item>


<item>
<title>Nests of the Mason Bees Osmia tanner Sandhouse and O. lingual Cresson with a Description of the Female of O. tenneri (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/330</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/330</guid>
<pubDate>Wed, 09 May 2012 11:28:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>Nest Descriptions and Associates of Three American Bees of the Genus Anthocopa Lepeletier</title>
<link>http://digitalcommons.usu.edu/piru_pubs/329</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/329</guid>
<pubDate>Wed, 09 May 2012 11:28:41 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Natural history</category>

</item>


<item>
<title>First Get the Seeds</title>
<link>http://digitalcommons.usu.edu/piru_pubs/328</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/328</guid>
<pubDate>Wed, 09 May 2012 11:28:28 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>P. F. Torchia et al.</author>


</item>


<item>
<title>Alfalfa leafcutter bee: Effect of alfalfa saponins on larval mortality</title>
<link>http://digitalcommons.usu.edu/piru_pubs/327</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/327</guid>
<pubDate>Wed, 09 May 2012 11:28:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


</item>


<item>
<title>Alfalfa pollinators abroad and candidates for introduction into the United States</title>
<link>http://digitalcommons.usu.edu/piru_pubs/326</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/326</guid>
<pubDate>Wed, 09 May 2012 11:28:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Effectiveness of Triahogramma spp. in parasitizing eggs of Pieris rapae and Triahoplusia ni in the laboratory</title>
<link>http://digitalcommons.usu.edu/piru_pubs/325</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/325</guid>
<pubDate>Wed, 09 May 2012 11:27:49 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Chumming on the Chesapeake Bay and Complexity Theory: Why the Precautionary Principle, Not Cost-Benefit Analysis, Makes More Sense as a Regulatory Approach</title>
<link>http://scholarship.law.georgetown.edu/facpub/949</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/949</guid>
<pubDate>Wed, 09 May 2012 11:27:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Estuaries like the Chesapeake Bay ("Bay") and Puget Sound are in grave trouble. They each suffer from poor water quality, loss of habitat, and declining biodiversity, and efforts to restore their health are straining both public and private resources. While accomplishments are often recorded in the fight against these ills, it is clear these accomplishments "are not yet equal to the scale of the problems." The focus of this article is on the nation's largest estuary, the Bay. Despite the investment of billions of dollars to improve water quality, the Bay continues to suffer from severe environmental degradation that impairs statutorily protected uses such as "[t]he growth and propagation of fish (other than trout), other aquatic life, and wildlife."</p>
<p>Among the most serious of the ills afflicting the Bay's water quality is nutrification. Nutrification, which lowers dissolved oxygen levels in the water, sets off positive feedback loops further eroding the Bay's health. This article brings to the fore a largely overlooked source of the Bay's nutrification problem: the practice of chumming. Chumming involves dumping a slurry of decomposed or decomposing baitfish, usually menhaden, over the side of a boat to attract highly-prized game species like striped bass. The practice is widely used by Maryland's recreational fishing industry, which is an important part of Maryland's economy.</p>
<p>Chum contributes to the Bay's serious nutrient enrichment problem by increasing biological oxygen demand, resulting in lower dissolved oxygen levels in the water. It also increases water turbidity and may be a source of bacterial disease in striped bass. The use of menhaden as baitfish is also contributing to the decline in populations of that critically important food and filter fish. Even though chumming adversely affects the Bay's water quality and threatens its biodiversity, neither the federal government nor Maryland currently regulates the practice. While Bay area regulators may believe that they have made an economically rational decision to attend to larger targets of opportunity such as nutrient discharges from sewage treatment plants and farm fields, the high cost and political flashpoints of addressing those large sources of nutrients have largely paralyzed legislators and regulators for nearly two decades. The result is that the Bay's nutrification problem is getting worse, and the bill for addressing the problem is getting bigger.</p>
<p>The reluctance of regulators to address small sources of environmental problems, or even small environmental problems, is not unusual and is what makes the chumming story relevant to those who live outside the Bay's watershed. The premise of this article is that the failure of regulators to regulate chumming originates through a misapprehension about how complex natural systems like estuaries behave and also in an over-dependence on economic analytical methodologies, like bioeconomics and cost-benefit analysis. Economic approaches measure success based on the amount of pollutants taken out of the waste stream and undervalue broader, more difficult-to-quantify improvements to the receiving environment. Because economic approaches depend on factors remaining stable, they are also singularly ill-suited to constantly changing natural systems. Precautionary principles are better suited to the preservation of biodiversity in these systems, where so much is scientifically uncertain and where the goal is to avoid irreversible and catastrophic consequences regardless of the economic sense in taking the precautionary steps. These same conclusions apply to other complex, evolving natural systems and other types of low volume, but ultimately highly detrimental environmental harms to them.</p>
<p>To assist in the development of this thesis, part I of the article presents background information on the Bay and the serious problem of nutrient enrichment. Part II introduces the reader to the practice of chumming and its contribution to the Bay's over-enrichment problems. Part III explores how the misguided reliance of regulators on choosing an economically rational target, usually the largest sources of environmental problems, misapprehends the capacity of smaller sources in complex natural systems like estuaries to cause potentially irreversible and catastrophic positive feedback loops. This misguided approach, in turn, may lead to loss of biodiversity. Part III also describes the precautionary principle, and how its application would direct regulators to prohibit the practice of chumming in the Bay.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>The National Environmental Policy Act in the Urban Environment: Oxymoron or a Useful Tool to Combat the Destruction of Neighborhoods and Urban Sprawl?</title>
<link>http://scholarship.law.georgetown.edu/facpub/948</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/948</guid>
<pubDate>Wed, 09 May 2012 11:27:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>To some, applying the National Environmental Policy Act (NEPA) to decisions affecting land use in an urban or built environment is an oxymoron. Cities have historically not been seen “as natural entities but as foreign impositions upon the native landscape,” places where the physical environment is already largely destroyed or reduced to insignificant remnants. Moreover, detecting the required federal presence to trigger NEPA may initially seem difficult when decisions affecting urban resources appear to be principally made by local or state agencies.</p>
<p>At the Institute for Public Representation (IPR) at the Georgetown University Law Center, the author has learned that many kinds of environments, including the built environment, are worthy of protection because of their importance on a local, if not regional or national, level. She also has repeatedly encountered federal agencies that permit or fund activities that threaten these environments. In some cases, such as national parks or monuments, these agencies actually own or manage the threatened resource. Accordingly, the IPR has used NEPA as one of its basic tools to protect the urban environment.</p>
<p>This is not to say that the fit between NEPA and the urban environment is necessarily perfect. Quite the contrary, an urban environment can both test the effectiveness of NEPA and suggest ways in which the Act might be improved. For example, relevant case law demonstrates that finding a sufficiently large federal handle to warrant the application of NEPA to urban land use decisions can be challenging. Despite this federal-presence challenge and other flaws, NEPA adds unique analytical tools to the web of federal laws protecting the urban landscape. These tools are particularly suited to addressing two problems that are plaguing metropolitan areas today: loss of neighborhood viability leading to urban blight and white flight, and the phenomenon of urban sprawl.</p>
<p>The first tool is NEPA’s mandate that federal agencies consider their proposed actions impact on social and cultural resources. This requirement can be used to help assess the extent to which federal projects may lessen the diversity and sustainability of urban neighborhoods by adversely affecting their “social capital,” that complex web of interlocking and mutually supportive networks of social and economic relationships that binds communities together.</p>
<p>The second tool compels proponents of federally authorized or funded projects to consider their proposed actions’ indirect and cumulative impacts. This requirement offers a mechanism for addressing problems raised by urban sprawl. The effectiveness of both of these tools may be limited when an urban land use change appears too small to trigger NEPA’s applicability or seemingly will have only a minor impact on the physical environment. Overcoming these challenges is the focus of this article.</p>
<p>In responding to these challenges, this article first takes a brief look at cities, their positive and negative features, and the importance of vibrant, healthy neighborhoods to good quality urban life. Part I also discusses the phenomenon of urban sprawl and its environmental impacts. Part II examines how government decisions that negatively affect seemingly isolated, small uses of urban land, such as a corner bodega, can ripple out into the greater metropolitan area and lead to economic blight, white flight, and urban sprawl. In addition, part II introduces the concept of social capital and explains why it is a central component of healthy neighborhoods, especially for those that are less financially secure.</p>
<p>Part III turns to NEPA and looks at the statute’s use in the urban environment. This part identifies particular features of NEPA that give city residents, particularly those who live in less financially stable areas, unique tools to resist non-desirable changes to their neighborhoods. The last part of the article shows how the principles of conservation biology and social capital can be combined to translate principally socio-economic impacts from isolated land use changes into large-scale physical impacts. The final part then demonstrates how these physical consequences can be sufficiently magnified to warrant the preparation of an environmental impact statement (EIS). In case this rationale should fail, the article explores informal means of communicating with agencies during the preparation of an environmental assessment (EA) that offer communities another way of influencing neighborhood land use decisions.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>Dual Regulation, Collaborative Management, or Layered Federalism: Can Cooperative Federalism Models from Other Laws Save Our Public Lands?</title>
<link>http://scholarship.law.georgetown.edu/facpub/947</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/947</guid>
<pubDate>Wed, 09 May 2012 11:27:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>To realize the goals of conservation biology and ecosystem management, the institutions that govern these systems must be able to work together harmoniously, across political boundary lines and into a biologically uncertain future. The rigidity of the current public lands model creates substantial barriers to the achievement of these goals.</p>
<p>This article's working premise is that unless the current governance structure for the management of public lands changes, the political conflicts over their use and management will continue to blight their future, just as it has marred their past. Further, failing to adapt the management of public lands to our changing perceptions about the nature and needs of the biological and social communities that depend upon them will only engender a new generation of conflicts and further diminish the vitality of those communities. Nowhere are these conflicts more intense and the risks and consequences of failure higher than on the "public domain" lands; those lands managed by the Bureau of Land Management (BLM) under the authority of the Federal Land Policy & Management Act (FLPMA).</p>
<p>The purpose of this article is to determine whether there are alternatives models of federalism, which might improve the management of public domain lands. None of the models discussed here, however, proposes complete rescission of federal authority over public lands; rather they offer an enhanced role for states in the federal decision-making process. A continuing federal presence is assumed to be necessary to prevent inter-state distribution inequities from arising or economic discrimination from occurring. Only the federal government can correct market failures when they occur and uniformly protect national norms, such as our natural heritage. And even if the Western states are becoming more supportive of these norms as some assert, serious questions would remain about the ability of those states to take on sole responsibility for management of these lands without an infusion of new funds.</p>
<p>The article examines three models of governance ("dual regulation," "collaborative management," and "layered federalism") found in other areas of environmental law to determine whether their application to public domain lands might lessen the federalism tensions inherent in the current model and enhance the land manager's ability to make decisions that are both ecologically sound and reflect the new voices populating these lands. Achieving rational ecosystem management and a more democratic mode of decision-making may be of greater importance than attaining non-fractious governance. Intergovernmental friction may be a necessary, unavoidable, even welcome byproduct of our "compound republic" form of government; a transaction costs of a federal structure that relies on overlapping and sometimes conflicting jurisdictions of governance to safeguard those liberties not protected by the explicit constitutional guarantees. No such benefit accrues from the other two problems.</p>
<p>The structure of the article is straightforward. Part II examines the current federalism model on public domain lands and concludes, despite some of its virtues, the model has caused inter-governmental friction and created barriers to rational ecosystem management and community-based participation in the decision-making process. Part III describes and then critiques each of the alternative federalism designs against the same three criteria. The article concludes by suggesting which, if any of the models holds the greatest promise for resolving the problems besetting public lands management. While the author recognizes that these problems may be too complex, diverse and endogenous to the public lands experience or a specific geographic area to enable a "single size fits all solution," she hopes that the analytical exercise of examining these models may enrich the storehouse of ideas we draw from in the search for solutions.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>Civic Republicanism Provides Theoretical Support for Making Individuals More Environmentally Responsible</title>
<link>http://scholarship.law.georgetown.edu/facpub/946</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/946</guid>
<pubDate>Wed, 09 May 2012 11:27:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genesis for this essay is the recognition that individual behavior is contributing in a significant way to the remaining environmental problems we have. For a variety of reasons, ranging from the difficulty of trying to identify and then regulate all of these individual sources to the political backlash that might result if such regulation was tried, efforts to control that behavior have either failed or not been tried. The phenomenon of individuals as irresponsible environmental actors seems counter-intuitive given the durability of the environmental protection norm and polls that consistently show that people contribute to environmental causes, are willing to pay more to protect environmental resources, and consider protecting the environment among their highest priorities. This conflict between thought and deed and its serious effect, if not resolved, is the puzzle that has sent me on this quest.</p>
<p>This essay is the author's third attempt at unraveling the problem of irresponsible individual environmental behavior and at suggesting possible ways to reform how people behave toward the environment. The first article proposed expanding the abstract environmental protection norm to include individual environmental responsibility as the approach most likely to overcome barriers to behavioral change. The article recommended enlisting environmental groups as the most effective "norm entrepreneurs" to achieve widespread change in personal environmental conduct. In that piece, she concluded that the best way to change norms and thus change behavior was through education, but additional measures might be necessary.</p>
<p>The second article expanded on the earlier discussion of norms and their influence on behavior, and why changing norms, though difficult, is more effective than other means of inciting behavioral change. However, given the difficulty inherent in creating or changing norms, the second article also identified and evaluated other norm and behavior-changing tactics, such as shaming, public education, and market-based incentives, which might supplement norms as a means of changing behavior. The article concluded that no one approach alone is sufficient to secure both norm and behavior change, but a combination of any or all of them when properly tailored to the source and nature of the harm and when accompanied by public education can lead to both norm and behavioral changes.</p>
<p>Thus, both articles concluded that public education plays a critical role in any effort to alter public behavior through changing norms. This essay examines how republican theory supports that conclusion and provides the theoretical framework within which norm change can occur.</p>
<p>All three pieces start with the premise that the current crisis over global climate change has created the circumstances in which norm change can occur--circumstances that collectively have created what the author calls a second environmental republican moment. This second republican moment, like the first one in the 1970s, might result in widespread public support for a variety of environmentally protective legislative and regulatory initiatives and offers a rare, albeit brief, opportunity in which to educate the public about its contribution to environmental harm. This essay develops the republican aspect of that thought further, demonstrating how the overlapping strands of republican thought and norm development support the creation of a new norm of personal environmental responsibility. The essay also shows how, during republican moments, the public is more amenable to being educated about civic matters, including their responsibilities as environmental citizens. It is particularly during republican moments that people acquire information that may influence their "expressed preferences," lending a sense of urgency to the present moment we find ourselves in.</p>
<p>This essay begins by discussing the concept of an environmental republican moment, and why the public's response to the crisis of global climate change appears to be such a moment. The essay then identifies the key features of republican theory and shows how those features replicate many of the elements necessary for norm and behavioral change. The essay concludes by showing how republicanism--with its emphasis on public education, civic involvement, and achieving the common good through civic virtue--provides a useful construct for thinking about how to make people behave in more environmentally responsible ways.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>The Public Trust Doctrine: What a Tall Tale They Tell</title>
<link>http://scholarship.law.georgetown.edu/facpub/945</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/945</guid>
<pubDate>Wed, 09 May 2012 11:27:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite continuing hostility towards the public trust doctrine because of its potential to defeat private property rights and the will of elected representatives, the doctrine refuses to die. It continues to assure public access to and protection of certain natural resources of communal value; in fact, the doctrine's geographic reach and the activities it protects have expanded beyond its original conception. It is this doctrinal accretion that has drawn the attention of Professor James Huffman, who in a recent article criticizes the "ambitions" of public trust scholars who see in "an expansive public trust doctrine . . . a powerful tool for the protection and preservation of natural resources and the environment" because, among other failings, they rely on a "mythological history of the doctrine." This essay is intended as a response to Professor Huffman's critique.</p>
<p>Professor Huffinan's critical assessment of the alleged mythological history of the public trust doctrine is beside the point. Indeed, as he suggests, he is "tilting at windmills in trying to set the story straight." The story he criticizes has become a "fact" in the minds of judges who use it to justify a particular application of the doctrine. Retelling the story to prevent future applications of the doctrine could destabilize property law, which has embraced the doctrine for centuries. Even if the doctrine is a myth invented by legal scholars and judges, the legal fiction doctrine, which Professor Huffman's argument implicates, justifies it. Indeed, this essay argues that the public trust doctrine is a good legal fiction because it enables new uses of the doctrine to perform a gap-filling function in the absence of positive law and, therefore, that it deserves to continue unchallenged.</p>
<p>Because much has been written on the topic of the public trust doctrine, part II of the essay very briefly describes the doctrine's origins, its major features, and its most common uses. Part III sets out Professor Huffman's critique of the doctrine's origins and poses as a rejoinder the legal fiction doctrine, which justifies the use of fictions in similar situations. Part IV of the essay looks specifically at the Exclusive Economic Zone (EEZ), where numbers of wild fish are in a free fall because there is no coherent, comprehensive program to regulate activities in the area. This part of the essay also discusses the phenomenon of a regulatory commons, which, according to Professor William Buzbee, arises when there is not "a matching political-legal regime," leaving the underlying social ill unattended. The essay suggests that the public trust doctrine can fill the regulatory gap on the EEZ by offering an interim management regime with protective normative standards and other management tools, and thus end the stasis created by the regulatory commons that has left the EEZ's resources unprotected. By highlighting the underlying social ill, application of the doctrine may actually encourage the enactment of positive law that can displace the stop gap common law regime and bring more regulatory certainty and uniformity to the area.</p>
<p>The essay closes by asserting that, for these reasons, the public trust doctrine is a good legal fiction. Not only is the doctrine doing no harm, but its potential expansion could fill gaps in positive law and offer much needed protection for vulnerable resources of communal value. Therefore, Professor Huffman's cavil against further expansion of the doctrine because of its "mythic" origins deserves no more attention than it has been given here.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>The Problem with Particularized Injury: The Disjuncture Between Broad-Based Environmental Harm and Standing Jurisprudence</title>
<link>http://scholarship.law.georgetown.edu/facpub/944</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/944</guid>
<pubDate>Wed, 09 May 2012 11:27:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Several recent events harmonically converged into the topic for this article. The first was a posting on Georgetown Law’s environmental law professors’ listserv by Professor John Bonine, which raised a number of questions about whether and how standing doctrine might be rethought in light of the Supreme Court’s opinion in <em>Massachusetts v. EPA</em>. That opinion relaxed the states’ standing burden because of the unique sovereign interests, finding that federalism bargaining earned states “special solicitude” when it came to meeting the Court’s standing requirements.</p>
<p>The second was a complaint filed by a consortium of regional environmental organizations, Chesapeake Bay Foundation, Inc., and individuals against the Environmental Protection Agency (EPA) for failing to achieve the goals of the Chesapeake Bay Agreements. EPA is one of five signatories to the Agreements, which contains a variety of goals, deadlines, and recommended actions, and which has failed miserably to halt the Chesapeake Bay’s decline. This complaint led to a reflection on work done in the clinic several years ago, where bringing a lawsuit on behalf of a commercial fisherman challenging the practice of chumming on the Bay was thought about long and hard. Chumming involves depositing a slurry of decomposed fish parts, usually menhaden, over the side of a fishing boat to attract game fish like striped bass. While chumming contributes to the Bay’s nutrification, by itself it has little discernible impact on the Bay’s overall health given the much larger sources of nutrients like sewage treatment plants, runoff from farm fields, and confined animal feeding operations. Ultimately it was determined, in part on standing grounds, that such a lawsuit could not succeed.</p>
<p>The last event was a recent conversation with a retired Washington attorney about his decision to start a new organization that would supply pro bono assistance to property owners concerned about relatively discrete, highly localized harms to the Bay such as leaking septic systems or permit violations by industrial dischargers. Collectively, these separate events congealed into a somewhat amorphous concern about the extent to which the Supreme Court’s standing jurisprudence and its insistence on a showing of a particularized injury-in-fact are ill-suited to the types of broad-based, generalized harms from which complex, constantly changing ecosystems suffer.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>Responsible Environmental Behavior, Energy Conservation, and Compact Fluorescent Bulbs: You Can Lead a Horse to Water, But Can You Make It Drink?</title>
<link>http://scholarship.law.georgetown.edu/facpub/943</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/943</guid>
<pubDate>Wed, 09 May 2012 11:27:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite professing to care about the environment and supporting environmental causes, individuals behave in environmentally irresponsible ways like driving when they can take public transportation, littering, or disposing of toxic materials in unsound ways. This is the author's fourth exploration of how to encourage individuals to stop behaving irresponsibly about the environment they allege to care deeply about. The prior three articles all explored how the norm of environmental protection could be enlisted in this effort; this article applies those theoretical conclusions to the very practical task of getting people to switch the type of light bulb they use.</p>
<p>To accomplish this, the article synthesizes the previous articles into an assumption about the critical role of norms in changing personal behavior and tests that assumption by exploring how to make individuals more responsible consumers of electricity and adhere to the concrete norm of energy conservation by swapping out their incandescent light bulbs for compact fluorescent lights (“CFLs”). The agreed upon goal behind energy conservation is to reduce the country’s reliance on fossil fuel-based energy production, thus reducing the emission of harmful airborne pollutants and greenhouse gases as well as the related environmental harms associated with coal production. One way to reduce residential energy consumption is to persuade individuals to switch to CFLs. Up to ninety percent of energy produced by incandescent bulbs is lost as heat; switching to CFLs is one way to prevent this energy loss.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>Assuming Personal Responsibility for Improving the Environment: Moving Toward a New Environmental Norm</title>
<link>http://scholarship.law.georgetown.edu/facpub/942</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/942</guid>
<pubDate>Wed, 09 May 2012 11:27:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is general agreement that we are nearing the end of achieving major gains in pollution abatement from traditional sources, that a significant portion of the remaining environmental problems facing this country is caused by individual behavior, and that efforts to control that behavior have either failed or not even been made.</p>
<p>The phenomenon of individuals as irresponsible environmental actors seems counterintuitive when polls show that people consistently rate protecting the environment among their highest priorities, contribute to environmental causes, and are willing to pay more to protect environmental resources.</p>
<p>This article is the author's second effort at understanding why people who consider themselves to be “environmentalists” or support environmental causes behave in environmentally destructive ways, and what, if anything, can be done to change that behavior. The first article endorsed expansion of the abstract environmental protection norm to include individual environmental responsibility and concluded that doing this is the most promising approach to overcoming barriers to behavioral change. That article also identified environmental groups as the most effective “norm entrepreneurs” that can bring about widespread change in personal environmental conduct through carefully tailored information campaigns. This article expands on the earlier article’s discussion of the role norms play in influencing personal behavior and why changing them is a critical part of any campaign to make individuals more environmentally responsible.</p>
<p>The best way to change norms is through education, as the first article acknowledged, but supplemental measures may be necessary. This article identifies what those additional measures might be and assesses their effectiveness. A third article will explore how republican theory supports the critical role that education performs in altering public behavior through changing norms. All three articles rest on the premise that the global climate change crisis has created circumstances in which norm change can take place, namely the occurrence of a second environmental republican moment, in which people are open to being educated about their civic responsibilities, including those pertaining to the environment.</p>
<p>To develop these ideas, section II provides background information about individual contributions to environmental problems. Section III discusses various barriers to changing personal environmental behavior, such as the role federal laws play in perpetuating the myth that only industry is responsible for environmental harm. That section also explores certain cognitive heuristics that influence how people process information and personal barriers to changing behavior such as habits, inconvenience, cost, unavailability of alternatives, and self-interest. The role of norms in influencing behavior and how norms are formed and changed are examined in section IV. Next, section V investigates how a new norm of environmental responsibility might arise and displace competing norms. However, that section recognizes that the development of a new norm may not be an easy task because of some of the same barriers identified in section III. In section VI, acknowledging that neither norms nor the happenstance of an environmental republican moment will inexorably lead to changes in personal behavior, various norm and behavior-changing tools, such as public education, shaming and other sanctions, and market-based incentives are identified. Section VI examines the inherent strengths and weaknesses of these tools, as well as particular problems with their application to individual behavior. Section VII concludes that no single approach will work, but a combination of any or all of the above, depending on the source and nature of the problem, is called for. However, any combination of tools must include public education if a permanent new environmental norm is to emerge and change individual behavior in the long term.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>Methods of transferring and establishing the alkali bee</title>
<link>http://digitalcommons.usu.edu/piru_pubs/324</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/324</guid>
<pubDate>Wed, 09 May 2012 11:27:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Bee management</category>

</item>


<item>
<title>The Stories We Tell, and Have Told, About Tribal Sovereignty: Legal Fictions at Their Most Pernicious</title>
<link>http://scholarship.law.georgetown.edu/facpub/941</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/941</guid>
<pubDate>Wed, 09 May 2012 11:27:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Starting with Chief Justice John Marshall and continuing through to the present Supreme Court, the story of Indian sovereignty has been consistent—it exists only in the most diminished form. Some reasons for this have been premised on the incapacity of Indians to self-govern; others on theories of federalism; while still others on the ambitions of non-Indians. However, the factual premises behind the concept of diminished sovereignty are baseless—legal fictions about the conquest of Indians and their nature. These fictions originated in Chief Justice Marshall’s Indian Law Trilogy and should have vanished long ago when their original purposes were fulfilled, like other legal fictions that are no longer useful. This article examines the reasons for the persistence of Marshall’s fictions in the face of contradictory evidence and the harm they have done to the cause of tribal sovereignty and Indians in general. The author's conclusion is that their endurance has less to do with serving some intellectual purpose or maintaining stability in the law—traditional justifications for the continuation of a legal fiction—than with hiding a normative judgment that Indians should not exists as a separate people.</p>
<p>In support of that thesis, this article briefly discusses the origin of the modern concept of diminished tribal sovereignty in Marshall’s Indian Law Trilogy. This discussion points out the dissonance between the fictions Marshall propounded in support of that concept and the actual record he should have considered in reaching his decisions. The article then turns to the legal fiction doctrine and briefly identifies the traditional functions it performs as well as the doctrine’s hidden dangers. This part of the article shows how Marshall used legal fictions in his Trilogy and speculates about why he used them. The third part of the article describes the harm that Marshall’s use of the legal fiction doctrine has done to the cause of tribal sovereignty and Indians in general. Based on their pernicious effect, the article concludes that Marshall’s fictions are “bad” legal fictions that should, and can, be expunged from federal Indian jurisprudence; their momentary usefulness, long outlived.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>How Judicial Hostility Toward Environmental Claims and Intimidation Tactics by Lawyers Have Formed the Perfect Storm Against Environmental Clinics: What&apos;s the Big Deal About Students and Chickens Anyway?</title>
<link>http://scholarship.law.georgetown.edu/facpub/940</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/940</guid>
<pubDate>Wed, 09 May 2012 11:27:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Since 1976, when the first environmental clinic was started at the University of Oregon’s law school, clinics have proliferated. Today, approximately one out of five law schools has an environmental clinic. With respect to clinics in general, the <i>Association of American Law Schools Directory of Law Teachers</i> lists “nearly 1400 full-time faculty teaching clinical courses.” Yet far from being an uncontroverted part of the academic landscape, clinics—particularly environmental clinics—have endured political blowback from challenging the environmentally destructive behavior of major economic interests. The effectiveness of environmental clinics is no greater than established environmental organizations—perhaps less effective given the length of time it takes for law students guided by faculty to mount a legal challenge and the complexity and difficulty of the cases these clinics take on. Nonetheless, environmental clinics repeatedly find themselves the target of efforts to shut them down, restricted in the types of cases and/or clients they can take on, and limited by supervisory boards with the power of case approval. Why is this? What is it about law students working for credits and grades that powerful interests find so threatening that they spend their resources on eliminating clinics instead of confronting them in court? Is the attack on clinics part of a broader attack on public access to the courts for righting environmental wrongs? Do these attacks reflect something about the nature of the attacker and her victim?</p>
<p>This article seeks to answer those questions, and concludes that clinics, like environmental organizations, function in an environment that is exceptionally hostile to the types of clients they represent and the cases they bring. This means that the claims environmental clinics file, like those filed by the national groups, will be met with a barrage of opposing filings based on a number of jurisdictional and other challenges enabled by the U.S. Supreme Court’s anti-public interest jurisprudence. Unlike the well-funded, publicly visible, and widely supported national organizations, environmental clinics are more vulnerable to less conspicuous attacks brought directly by the economic interests they challenge and their political supporters. Perhaps clinics unwittingly invite these attacks that in turn weaken their ability to function in this already hostile environment. The combination of the two can create a perfect storm for environmental clinics.</p>
<p>Even more curious is the role that lawyers play in attacks on clinics and the bullying techniques they use to discourage clinic-initiated litigation. There is something about students that brings the bully out in those who face them across the table that goes beyond the usual reasons given for these attacks—namely, that environmental clinics empower people who are otherwise without power to confront those who disregard their interest, that they are successful, and that they have enormous staying power and endless student enthusiasm. This behavior, although part of the general incivility problem afflicting the legal profession, is something more, and has to do with the nature of today’s lawyers and the context in which they learned how to be lawyers and practice law. Although many articles have been written about attacks on environmental clinics, none has identified this second reason—the milieu in which lawyers are educated and trained—and placed it in the broader context of judicial hostility toward environmental claims brought against established economic interests.</p>
<p>This article lays the groundwork for these conclusions by first briefly discussing the origins of clinics and clinical pedagogy in general. Then it describes the various attacks on the clinics, some consequences of those attacks, and how certain responses to those attacks run afoul of basic ethical precepts as well as notions of academic freedom. The third part of the article, after briefly listing some of the conventional reasons for these attacks, focuses on a less conventional one—namely, that they are fueled by the asocial behavior of lawyers who are in the vanguard of many of these attacks. It shows how such behavior is akin to that of a schoolyard bully who, in sensing a weaker opponent, acts out in ways that have been fodder for psychological literature. This part of the article also describes the various barriers the Court has erected that make it difficult for public interest litigants, particularly poorly funded and understaffed environmental clinics, to prosecute legal claims representing individuals who threaten the economic and political status quo. The article concludes that the more conventional explanation for the attacks against clinics are incomplete because they neither explain the persistence of the attacks nor show how the combination of intimidation and hostile judicial doctrine make it extremely difficult for environmental clinics to do their job.</p>

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</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>Another look at the alkali bee</title>
<link>http://digitalcommons.usu.edu/piru_pubs/323</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/323</guid>
<pubDate>Wed, 09 May 2012 11:27:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


</item>


<item>
<title>Biological Notes on Lithurgus apicalis Cresson (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/322</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/322</guid>
<pubDate>Wed, 09 May 2012 11:27:09 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Natural history</category>

</item>


<item>
<title>Field Stability of the Heliothis Nucleopolyhedrosis Virus on Corn Silks</title>
<link>http://digitalcommons.usu.edu/piru_pubs/321</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/321</guid>
<pubDate>Wed, 09 May 2012 11:26:58 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>C. M. Ignoffo et al.</author>


</item>


<item>
<title>Effect on food consumption of the imported cabbageworm when parasitized by two species of Apanteles</title>
<link>http://digitalcommons.usu.edu/piru_pubs/320</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/320</guid>
<pubDate>Wed, 09 May 2012 11:26:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Effectiveness of Trichogramma spp. in Parasitizing Eggs of Pieris rapae and Trichoplusia ni. 1. Field Studies</title>
<link>http://digitalcommons.usu.edu/piru_pubs/319</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/319</guid>
<pubDate>Wed, 09 May 2012 11:26:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


</item>


<item>
<title>On the Subfamily Astatinae. Part VII. The Genus Diploplectron Fox (Hymenoptera: Specidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/318</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/318</guid>
<pubDate>Wed, 09 May 2012 11:26:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Further studies of the biological control of Pieris papae using supplemental host and parasite releases</title>
<link>http://digitalcommons.usu.edu/piru_pubs/317</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/317</guid>
<pubDate>Wed, 09 May 2012 11:26:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Suppression of Pieris rapae (L.) using a new control system: Mass releases of both the pest and its parasites</title>
<link>http://digitalcommons.usu.edu/piru_pubs/316</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/316</guid>
<pubDate>Wed, 09 May 2012 11:26:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Stock Option Backdating: Is the Government&apos;s Response Enough to Eliminate the Problem or is It Still a Work in Progress</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/7</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/7</guid>
<pubDate>Wed, 09 May 2012 11:25:50 PDT</pubDate>
<description>
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</description>

<author>Lara E. Muller</author>


</item>


<item>
<title>The Key to the Courthouse Door: The Effect of Ashcroft v. Iqbal and the Heightened Pleading Standard</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/6</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/6</guid>
<pubDate>Wed, 09 May 2012 11:25:49 PDT</pubDate>
<description>
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</description>

<author>Michael Eaton</author>


</item>


<item>
<title>Climate Change: A New Realm of Tort Litigation, and How to Recover When the Litigation Heats Up</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/5</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/5</guid>
<pubDate>Wed, 09 May 2012 11:25:48 PDT</pubDate>
<description>
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</description>

<author>Lauren Case</author>


</item>


<item>
<title>Measuring a Degree of Deference Institutional Academic Freedom in a Post-Grutter World</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/4</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/4</guid>
<pubDate>Wed, 09 May 2012 11:25:47 PDT</pubDate>
<description>
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</description>

<author>Erica Goldberg et al.</author>


</item>


<item>
<title>Overwintering of Some Trichogramma spp. in Missouri</title>
<link>http://digitalcommons.usu.edu/piru_pubs/315</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/315</guid>
<pubDate>Wed, 09 May 2012 11:25:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


</item>


<item>
<title>The Trillion Dollar Problem of Underwater Homeowners: Avoiding a New Surge of Foreclosures by Encouraging Principal-Reducing Loan Modifications</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/3</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/3</guid>
<pubDate>Wed, 09 May 2012 11:25:45 PDT</pubDate>
<description>
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</description>

<author>Gregory Scott Crespi</author>


</item>


<item>
<title>The Future of Corporate Aiding and Abetting Liability under the Alien Tort Statute: A Roadmap</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/2</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/2</guid>
<pubDate>Wed, 09 May 2012 11:25:44 PDT</pubDate>
<description>
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</description>

<author>Andrei Mamolea</author>


</item>


<item>
<title>Apprendi Land Becomes Bizarro World: Policy Nullification and Other Surreal Doctrines in the New Constitutional Law of Sentencing</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/1</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol51/iss1/1</guid>
<pubDate>Wed, 09 May 2012 11:25:42 PDT</pubDate>
<description>
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</description>

<author>Benjamin J. Priester</author>


</item>


<item>
<title>Management of pest populations by manipulating densities of both hosts and parasites through periodic releases</title>
<link>http://digitalcommons.usu.edu/piru_pubs/314</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/314</guid>
<pubDate>Wed, 09 May 2012 11:25:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Rearing the Imported Cabbageworm Parasite, Aparteles rubecula, in the Laboratory</title>
<link>http://digitalcommons.usu.edu/piru_pubs/313</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/313</guid>
<pubDate>Wed, 09 May 2012 11:25:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker et al.</author>


</item>


<item>
<title>Seasonal Mortality and Survival of Pieris rapae (L.) in Missouri and the Effect of Introducing an Egg Parasite, Trichogramma evanescens Westwood</title>
<link>http://digitalcommons.usu.edu/piru_pubs/312</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/312</guid>
<pubDate>Wed, 09 May 2012 11:25:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


</item>


<item>
<title>New North American Microdynerus With Notes on the Nests of Two Species</title>
<link>http://digitalcommons.usu.edu/piru_pubs/311</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/311</guid>
<pubDate>Wed, 09 May 2012 11:24:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>The introduction of Apanteles rubecula into the United States as a parasite of the imported cabbageworm</title>
<link>http://digitalcommons.usu.edu/piru_pubs/310</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/310</guid>
<pubDate>Wed, 09 May 2012 11:24:47 PDT</pubDate>
<description>
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</description>

<author>B. Puttler et al.</author>


</item>


<item>
<title>On the subfamily Astatinae . Part VI. The Arnerican species in the genus Dryudella Spinola (Hymenoptera: Sphecidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/309</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/309</guid>
<pubDate>Wed, 09 May 2012 11:24:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank D. Parker</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>On the subfamily Astatinae. Part IV. The South American species in the genus Astata Latreille</title>
<link>http://digitalcommons.usu.edu/piru_pubs/308</link>
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<author>Lynn F. James et al.</author>


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<author>George E. Bohart et al.</author>


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<author>N. S. Shasha&apos;a et al.</author>


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<author>William P. Nye</author>


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<author>W. F. Campbell et al.</author>


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<author>William P. Nye</author>


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<author>William P. Nye et al.</author>


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<author>William P. Nye</author>


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<author>William P. Nye</author>


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<author>William P. Nye</author>


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<author>William P. Nye</author>


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<author>William P. Nye</author>


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	<![CDATA[
	
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<author>William P. Nye</author>


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<author>J. A. Kefuss et al.</author>


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<author>George E. Bohart et al.</author>


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<author>William P. Nye et al.</author>


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<author>O. Mackensen et al.</author>


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<author>William P. Nye</author>


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<author>William P. Nye</author>


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<author>O. Mackensen et al.</author>


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<author>William P. Nye et al.</author>


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<author>William P. Nye et al.</author>


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<link>http://digitalcommons.usu.edu/piru_pubs/256</link>
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<pubDate>Wed, 09 May 2012 11:15:53 PDT</pubDate>
<description>
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</description>

<author>William P. Nye et al.</author>


<category>Bee Management</category>

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<item>
<title>How to WInter Colonies</title>
<link>http://digitalcommons.usu.edu/piru_pubs/255</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/255</guid>
<pubDate>Wed, 09 May 2012 11:15:41 PDT</pubDate>
<description>
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</description>

<author>William P. Nye et al.</author>


<category>Bee Management</category>

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<item>
<title>Preliminary Report on Selection and Breeding of Honeybees for Alfalfa Pollen Collection</title>
<link>http://digitalcommons.usu.edu/piru_pubs/254</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/254</guid>
<pubDate>Wed, 09 May 2012 11:15:31 PDT</pubDate>
<description>
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<author>William P. Nye et al.</author>


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<item>
<title>How to Destroy Bees in the Home</title>
<link>http://digitalcommons.usu.edu/piru_pubs/253</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/253</guid>
<pubDate>Wed, 09 May 2012 11:15:20 PDT</pubDate>
<description>
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</description>

<author>William P. Nye et al.</author>


<category>Bee Management</category>

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<item>
<title>Nesting Shelters for Alfalfa Pollinators (Alfalfa Leaf-cutting Bee, Megachile rotundata F.)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/252</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/252</guid>
<pubDate>Wed, 09 May 2012 11:15:06 PDT</pubDate>
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</description>

<author>George E. Bohart et al.</author>


<category>Pollination and foraging</category>

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<item>
<title>Birds of Ohio</title>
<link>http://digitalcommons.fiu.edu/etd/608</link>
<guid isPermaLink="true">http://digitalcommons.fiu.edu/etd/608</guid>
<pubDate>Wed, 09 May 2012 11:14:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>BIRDS OF OHIO is a collection of lyrical and narrative poems that explore the interior nature of domestic life. These poems peer below the surface of ideas like home, family, faith, and marriage to reveal the complex contradictions and particular moments of love, fear, pain, and grace that create the domestic world of the speaker. Rooted in natural landscapes and often drawing on religious language, the poems point to the meeting of the physical and spiritual worlds, at times blurring the distinction between them. The collection is not divided into sections; rather, the different themes are braided together to create a portrait of domestic life where experiences of love and death, questions of faith and meaning, and conflict concerning marriage, family, addiction, and the idea of <em>home</em> are inextricable from one another.</p>

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</description>

<author>Amy L. Hughes</author>


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<item>
<title>Alfalfa Seed Production Studies</title>
<link>http://digitalcommons.usu.edu/piru_pubs/251</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/251</guid>
<pubDate>Wed, 09 May 2012 11:14:52 PDT</pubDate>
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<author>M. W. Pedersen et al.</author>


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<item>
<title>Nectar Sugar Concentration as a Measure of Pollination of Alfalfa (Medicago sativa L.)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/250</link>
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<pubDate>Wed, 09 May 2012 11:14:40 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William P. Nye et al.</author>


<category>Pollination and foraging</category>

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<item>
<title>Observations on the Behavior of Bees in a Controlled-environment room</title>
<link>http://digitalcommons.usu.edu/piru_pubs/249</link>
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<pubDate>Wed, 09 May 2012 11:14:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William P. Nye</author>


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<item>
<title>Management of Honeybee Colonies for Pollination in Cages</title>
<link>http://digitalcommons.usu.edu/piru_pubs/248</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/248</guid>
<pubDate>Wed, 09 May 2012 11:14:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William P. Nye</author>


<category>Pollination and foraging</category>

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<item>
<title>Extra Supering and Shading as Factors in Honey Production in Northern Utah</title>
<link>http://digitalcommons.usu.edu/piru_pubs/247</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/247</guid>
<pubDate>Wed, 09 May 2012 11:13:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William P. Nye</author>


<category>bee management</category>

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<item>
<title>The Art of Mugging: A Collection of 16mm Portraits</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/263</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/263</guid>
<pubDate>Wed, 09 May 2012 11:13:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>I love old things. I constantly find myself drawn to stories and artifacts from a time way before my own. I can’t explain why—I’m just an old soul.</p>
<p>Of all the old things I collect, my collection of 16mm film prints are by far the most precious to me. I have been collecting them since the age of fifteen. From newsreels to cartoons; to features, travelogues, and home movies—I have a varied, self-facilitated archive of over fifty films dating from the 1920’s to the 1970’s. My Senior Project, <em>The Art of Mugging</em>,<em> </em>started with this archive.</p>
<p>I had no qualms about using the footage from my collection. A lot of it was in extremely poor condition when I received it—among the worst affected were the home movies. The footage I used for <em>The Art of Mugging </em>was riddled with torn sprocket holes and faulty splices; and was slowly warping due to Vinegar Syndrome—a virus that attacks the chemical compounds in film stock. I wanted to do something with the footage before it became completely unwatchable. I was saddened by the prospect of losing them.</p>
<p>Home movies are extremely fun to watch. Even though I had no idea who made these movies or who appeared in them, I got hours of enjoyment watching the unnamed figures mug for the camera. I was the most attracted to these funny, loving, and sometimes awkward moments. Something so wonderful and weird happens in home movies. The amateur-filmmaker films what they find interesting. The result often comes out like a moving portrait.</p>
<p>Isolating these precious, portrait-like shots within the home movies in my collection, I set out to create something simple and beautiful. Inspired by the duration and style of the earliest moving pictures—which like home movies, were often experimental and documentary in their subject matter—I created sixteen, 16mm portraits.</p>
<p>The movies that comprise <em>The Art of Mugging</em>, are not only movies—they are paintings, collages, artifacts, and oddities.<em> </em> Film is beautiful to me because of its physicality. I left in imperfections, like scratches, lint, and dirt which age the film nicely. Manipulating each scene, frame-by-frame, by slathering a cocktail of fast-drying top coat, ink, bleach, toluene, and finger print grease, each film becomes twenty-four paintings per second. All of these alterations made the film strip itself even more physical and wonderful to touch. Each movie was optically printed and digitally edited, allowing me even more ways to add my love to films that were originally made with so much love.</p>
<p>Each movie in <em>The Art of Mugging</em> was designed to work as a standalone piece within a larger collection. I wanted to start a project that I could keep adding to. I also liked the idea of having a collection of little movies that viewers could watch (and re-watch) in a variety of different orders. Most of all, I wanted to make pieces that were delightful for the sake of being delightful. But, delightful and fun as they may be, they also bring up other deeper feelings and thoughts on love, sentimentality, relationships, domesticity, and even death.</p>
<p>The films contained within <em>The Art of Mugging </em>are little oddities that exist within a particular moment in time where they will forever remain to bring comfort and a smile for those who watch them.</p>

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</description>

<author>Amy Strumbly</author>


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<item>
<title>Maternity</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/262</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/262</guid>
<pubDate>Wed, 09 May 2012 11:13:49 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Maternity</em></p>
<p>It isn't physically possible for me to have a child. I'm gay. I don't want to have children. I don't think I will ever be able to financially support a child the way it deserves to be taken care of. My mother is dead. We have a history of mental illness in my family. I have bad genes. I don't think I would make a good mother; I'm too selfish. I'm the oldest living woman in my family. Who do I look to for advice?</p>
<p>Motherhood, pregnancy, and birth function together as major points of female experience, for some. Experiencing a connection to a life inside of you, be it fleeting or sustained can profoundly affect an individual in seemingly inexpressible ways. For some women senses and internal rhythms fall into place, creating bodily harmonies they never could have conceived of. Others find themselves at war, struggling to stay on an even keel, confronted constantly with new sensitivities and obstacles. Some even pass through a great deal of it relatively unscathed and unchanged, but most experience at one point or another all of these expressions of pregnancy. In the first trimester, the connection between mother and child seems almost hallucinatory, with the woman conjuring feelings for a fetus just starting to gestate, mentally forging a state of maternity out of the knowledge of this truth about her body.</p>
<p>The symptoms that tip a woman off to the truth about her body, the cessation of her period/an overly long period, bloating, changes in her breasts, fatigue, and nausea, are all symptoms that can also express themselves in hysterical pregnancies as well. Hysterical pregnancy is the manifestation in a woman of a belief that she is pregnant accompanied by the symptoms of pregnancy, but the woman does not have an actual fetus inside of her. Some very rare cases persist all the way through the nine months culminating in a hysterical birth. It is possible for these women to experience a first trimester the same way women who are actually pregnant do, even forming the early bond of maternity with their imaginary child.</p>
<p>My desire not to have children, does to preclude me from wanting to explore the female experiences of motherhood, pregnancy, and birth. The desire to explore maternity, searching for how it might change me, open me up to seeing in new ways, and finding a way to express the meaning I hoped to find within it, pushed me to seek access through the blurring of truth and delusion in the first trimester. I set out on a nine month performance of non-biological pregnancy hoping ti would help me shape my own connection with maternity. Following in the footsteps of hysterical pregnancy, I was pregnant for nine months. I lived healthily, worried about our future and stability, informed my family and friends, took care of myself, walked slowly and with great deliberation on icy days, experienced total 180 mood swings, and thought a lot about the future and the past. At the same time, I couldn't pee positive, didn't look pregnant without a false belly on to anyone but myself, kept getting my period erratically, didn't experience quickening until much later than it should have come, lost confidence in myself, and struggled with the dichotomy I experienced between my body and my mind.</p>
<p>I found myself drawn to the friction between analog and digital video technologies over the nine months. Something in the frenetic glitches I was making within unstable analog to digital conversions reminded me of how my pregnancy was being shaped by the clash of my mental and physical states. I amassed children's videos and instructional pregnancy VHS ranging from pregnancy massage to preparing your car safely for your upcoming newborn, along with home movies of my childhood and my mother's pregnancy with my sister, while shooting my own home videos as well, with the help of my friends.</p>
<p>My video installation, <em>Maternity</em>, springs from and serves as a reconstitution of the nine month performance, the play and experimentation with creating glitches through degradation and manipulation between analog and digital systems, and the amassing of media and images that were part of the conception of maternity I was forging in myself.</p>

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</description>

<author>Sarah Timberlake Taylor</author>


</item>


<item>
<title>&quot;North South,&quot; and &quot;Portiranges&quot; (two films)</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/261</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/261</guid>
<pubDate>Wed, 09 May 2012 11:13:45 PDT</pubDate>
<description>
	<![CDATA[
	<p><a></a><a></a><a></a><a></a><a></a><a>For a number of years before I started my education at Bard, I had been documenting friends, family, and places, but had no intentions of editing the material. My approach to filming was identical to my journal writing, and the same problems arose; my documentation lacked expression, and though I wrote about and filmed personal subjects,<em> </em>there was no catharsis to my efforts. This wasn’t an issue of introspection, it was a limitation I faced in my comprehension of the language of both mediums. It was when I began my film studies at Bard and saw the diary films of Jonas Mekas that I realized the potential in my footage for personal reflection. Mekas’ “Walden” in particular taught me that the implications of an image are determined by the editing, which he views as a means of reflection. The structuring of his segments—which are akin to diary entries, with poetic text that explains what is happening—creates a collection of memories that explore periods of his life. To distance myself from documentation, I approach the editing process as a way to reflect through the reinterpretation of what I’ve lensed. Looking through my footage, I distance myself from my initial attachment to the material and use the people and places as symbols of the sentiment I want to explore. In this way, my films become more lyrical than diaristic. Each film reflects upon a single idea, through the use of reconsidered material.</a></p>
<p>“Portiragnes” is a portrait of a small working-class town in the south of France where I spent a month every summer for fifteen years. It was shot over the summer and winter, 2010-11.</p>
<p>“North South” is a travel log of a two-month cross-country trip I took in the summer of 2009.</p>

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</description>

<author>Max Weinman</author>


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<item>
<title>A Modified Pollen Trap for Honey Bee Hives</title>
<link>http://digitalcommons.usu.edu/piru_pubs/246</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/246</guid>
<pubDate>Wed, 09 May 2012 11:13:45 PDT</pubDate>
<description>
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</description>

<author>William P. Nye</author>


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<item>
<title>Additional Studies on the Effect of Field Applications of Insecticides on Honey Bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/245</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/245</guid>
<pubDate>Wed, 09 May 2012 11:13:34 PDT</pubDate>
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</description>

<author>F. V. Lieberman et al.</author>


<category>Pathogens and Parasites</category>

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<item>
<title>Feeding Pollen Supplement and Pollen Substitute to Honey Bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/244</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/244</guid>
<pubDate>Wed, 09 May 2012 11:13:23 PDT</pubDate>
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</description>

<author>M. D. Levin et al.</author>


<category>Bee Management</category>

</item>


<item>
<title>Raising Bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/243</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/243</guid>
<pubDate>Wed, 09 May 2012 11:13:13 PDT</pubDate>
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</description>

<author>G. F. Knowlton et al.</author>


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<item>
<title>The Effect of Field Application of DDT, Chlordane, Parathion, and Chorinated Camphene Dusts on Honey Bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/242</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/242</guid>
<pubDate>Wed, 09 May 2012 11:13:02 PDT</pubDate>
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</description>

<author>F. E. Todd et al.</author>


<category>Pathogens and Parasites</category>

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<item>
<title>Insect Food of the Vesper Sparrow</title>
<link>http://digitalcommons.usu.edu/piru_pubs/241</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/241</guid>
<pubDate>Wed, 09 May 2012 11:12:51 PDT</pubDate>
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</description>

<author>G. F. Knowlton et al.</author>


<category>Natural History</category>

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<item>
<title>The Relationship Between Arsenic in the Blossoms of White Sweet Clover and in the Soil</title>
<link>http://digitalcommons.usu.edu/piru_pubs/240</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/240</guid>
<pubDate>Wed, 09 May 2012 11:12:42 PDT</pubDate>
<description>
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</description>

<author>William P. Nye</author>


<category>Pathogens and Parasites</category>

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<item>
<title>An Arsenic Survey in Utah</title>
<link>http://digitalcommons.usu.edu/piru_pubs/239</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/239</guid>
<pubDate>Wed, 09 May 2012 11:12:33 PDT</pubDate>
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</description>

<author>G. F. Knowlton et al.</author>


<category>Pathogens and Parasites</category>

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<item>
<title>A Simple Method for Mounting Aphids</title>
<link>http://digitalcommons.usu.edu/piru_pubs/238</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/238</guid>
<pubDate>Wed, 09 May 2012 11:12:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William P. Nye</author>


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<item>
<title>Some Insect Food of the Sage Sparrow</title>
<link>http://digitalcommons.usu.edu/piru_pubs/237</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/237</guid>
<pubDate>Wed, 09 May 2012 11:12:14 PDT</pubDate>
<description>
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</description>

<author>G. F. Knowlton et al.</author>


<category>Natural History</category>

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<item>
<title>Lizards Feeding on Ants in Utah</title>
<link>http://digitalcommons.usu.edu/piru_pubs/236</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/236</guid>
<pubDate>Wed, 09 May 2012 11:12:04 PDT</pubDate>
<description>
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</description>

<author>G. F. Knowlton et al.</author>


<category>Natural History</category>

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<item>
<title>A Report of Investigations of the Extent and Causes of Heavy Losses of Adult Honey Bees in Utah</title>
<link>http://digitalcommons.usu.edu/piru_pubs/235</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/235</guid>
<pubDate>Wed, 09 May 2012 11:11:53 PDT</pubDate>
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</description>

<author>A. P. Sturtevant et al.</author>


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<item>
<title>Utah Coleoptera, a List of Buprestidae, Cerambycidae, and Scolytidae</title>
<link>http://digitalcommons.usu.edu/piru_pubs/234</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/234</guid>
<pubDate>Wed, 09 May 2012 11:11:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William P. Nye et al.</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Interspecific geographic distribution and variation of the pathogens Nosema bombi and Crithidia species in United States bumble bee populations</title>
<link>http://digitalcommons.usu.edu/piru_pubs/233</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/233</guid>
<pubDate>Wed, 09 May 2012 11:11:32 PDT</pubDate>
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</description>

<author>N. Cordes et al.</author>


<category>Pathogens and Parasites</category>

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<item>
<title>Host Range Expansion of Black Queen Cell Virus in the Bumble Bee, Bombus huntii</title>
<link>http://digitalcommons.usu.edu/piru_pubs/232</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/232</guid>
<pubDate>Wed, 09 May 2012 11:11:21 PDT</pubDate>
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<author>W. Peng et al.</author>


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<item>
<title>Patterns of range-wide genetic variation in six North American bumble bee (Apidae: Bombus) species</title>
<link>http://digitalcommons.usu.edu/piru_pubs/231</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/231</guid>
<pubDate>Wed, 09 May 2012 11:11:11 PDT</pubDate>
<description>
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</description>

<author>J. D. Lozier et al.</author>


<category>Ecology &amp; conservation</category>

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<item>
<title>Global invasion by Anthidium manicatum (Linnaeus) (Hymenoptera: Megachilidae): assessing potential distribution in North America and beyond</title>
<link>http://digitalcommons.usu.edu/piru_pubs/230</link>
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<pubDate>Wed, 09 May 2012 11:11:00 PDT</pubDate>
<description>
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</description>

<author>James P. Strange et al.</author>


<category>Ecology &amp; conservation</category>

</item>


<item>
<title>Recent widespread population declines of some North American bumble bees: Current status and causal factors</title>
<link>http://digitalcommons.usu.edu/piru_pubs/229</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/229</guid>
<pubDate>Wed, 09 May 2012 11:10:49 PDT</pubDate>
<description>
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</description>

<author>S. C. Cameron et al.</author>


<category>Ecology &amp; conservation</category>

</item>


<item>
<title>Nest initiation in three North American bumble bees (Bombus): Gyne number and presence of honey bee workers influence establishment success and colony size</title>
<link>http://digitalcommons.usu.edu/piru_pubs/228</link>
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<pubDate>Wed, 09 May 2012 11:10:39 PDT</pubDate>
<description>
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</description>

<author>James P. Strange</author>


</item>


<item>
<title>Constructing a species database and historic range maps for North American bumble bees (Bombus sensu stricto Latreille) to inform conservation decisions</title>
<link>http://digitalcommons.usu.edu/piru_pubs/227</link>
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<pubDate>Wed, 09 May 2012 11:10:28 PDT</pubDate>
<description>
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</description>

<author>J. B. Koch et al.</author>


<category>Taxonomy, systematics, biogeography</category>

</item>


<item>
<title>Evaluation of apicultural characteristics of first year colonies initiated from packaged honey bees (Hymenoptera: Apidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/226</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/226</guid>
<pubDate>Wed, 09 May 2012 11:10:17 PDT</pubDate>
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</description>

<author>James P. Strange et al.</author>


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<item>
<title>Corporate Environmental Social Responsibility: Corporate &quot;Greenwashing&quot; or a Corporate Culture Game Changer?</title>
<link>http://scholarship.law.georgetown.edu/facpub/939</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/939</guid>
<pubDate>Wed, 09 May 2012 11:10:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>This article focuses on the extent to which unenforceable voluntary initiatives undertaken by corporations can change corporate behavior to make businesses more environmentally responsible, i.e. not only comply with the law, but to do more than the law actually requires of them. These initiatives, loosely gathered under the umbrella of a movement called corporate social responsibility (CSR), are often proposed by the government as a way to fill regulatory and enforcement gaps or by industry, often as an alternative to regulatory requirements. In each case, their goal is to improve the compliance record of businesses and, in some cases, to achieve a higher level of environmental performance. Based on a closer look at some of these initiatives and their design flaws, this article concludes that these voluntary programs, even when properly designed, should only function as supplements, not replacements, to existing regulatory programs and will only be effective if judicially enforceable by third parties.</p>
<p>To develop this idea, the first part of the article very briefly discusses the regulatory problems, including the ineffectiveness of federal enforcement, that have, to some extent, spurred a turn towards corporate self-regulation and the emergence of the concept of CSR. The second part of the article looks more closely at corporate culture and asks what about it makes businesses seemingly indifferent to being seen as "good environmental citizens." One thing that emerges from this discussion is that shame and compliance sanctions levied against the corporations are imperfect motivators when it comes to overcoming the institutional pressure on firms to make a profit for their shareholders.</p>
<p>The third part of the article discusses the CSR movement more broadly, its origins and the likelihood that it is not disappearing any time soon; while the fourth part discusses some of the potential benefits of CSR programs to corporations and society as a whole, including their latent capacity to change corporate attitudes towards the environment. The fifth part of the article turns to three examples of voluntary CSR programs: information disclosure programs; voluntary performance standards; and environmental management systems (EMSs). Studies show that these programs have been largely ineffective, creating the perception that firms undertake them principally for public relations purposes and not to achieve any real change in corporate behavior let alone social benefit. This part examines three principle problems with these programs; specifically, the absence of any internal or external monitoring of their effectiveness, their lack of public transparency, and the absence of sanctions or other consequences for businesses or their employees who promise to undertake a CSR initiative and then fail to do so or only support the initiative in a half-hearted way. However, given the problems with regulatory programs set out in part I, properly designed and enforceable CSR programs that function as supplements to existing regulatory programs may be the best way to change corporate culture because they work within, not outside, the corporation.</p>
<p>The sixth part of the article reviews possible design changes that might be made in these initiatives to overcome the flaws identified in part V; however, as this part shows, it is unlikely that businesses, without being ordered, will change their CSR programs because of the attendant costs. Accordingly, the final part of the article discusses the importance of litigation as a means to improve the design of CSR programs and compel their implementation. Two types of lawsuits are discussed: one, the typical citizen enforcement suit, which presumes the inclusion of the company's CSR initiative into its regulatory permit when undertaken to gain the benefits of some Environmental Protection Agency (EPA) CSR program; the other, a suit brought in state court employing contract principles. Neither approach is without problems. Yet, both offer the opportunity for real reform. Indeed the mere threat of such lawsuits can induce companies to change their behavior to avoid the costs of defending against them and the unwanted publicity; once filed, there is a possibility of settlement, where structural changes can be made to the business' operation to include a more robust CSR program.</p>

	]]>
</description>

<author>Hope M. Babcock</author>


</item>


<item>
<title>DNA amplification from pin-mounted bumble bees (Bombus) in a museum collection:  effects of fragment size and specimen age on successful PCR</title>
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<author>James P. Strange et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>What’s in that package? An evaluation of quality of package honey bee (Hymenoptera: Apidae) shipments in the United States</title>
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<author>James P. Strange et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<author>James P. Strange et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<author>W. S. Sheppard et al.</author>


<category>Pathogens and Parasites</category>

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<author>C. Perrier et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<item>
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<author>S. Kamel et al.</author>


<category>Pathogens and Parasites</category>

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<title>Optimum treatment timing of fluvalinate for the control of Varroa destructor (Acari: Varroidae) in Apis mellifera in Washington State</title>
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<author>James P. Strange et al.</author>


<category>Pathogens and Parasites</category>

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<author>James P. Strange</author>


<category>Natural History</category>

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<author>R. C. Zack et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<author>James H. Cane et al.</author>


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<title>The hind tibiotarsal and tibial spur articulations in bees (Hymenoptera: Apoidea)</title>
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<author>James H. Cane</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>Nest defense and foraging ethology of a neotropical sand wasp, Bembix multipicta (Hymenoptera: Sphecidae)</title>
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<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

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<title>Notes on the reproductive behavior of a Costa Rica population of Hyla ebraccata</title>
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<author>M. M. Miyamoto et al.</author>


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<title>Behavioral observations of non-calling males in Costa Rican Hyla ebraccata</title>
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<author>M. M. Miyamoto et al.</author>


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<title>Pheromonal cues direct mate-seeking behaviors of male Colletes cunicularius (Hymenoptera: Colletidae)</title>
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<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

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<title>Dufour&apos;s gland secretion in the cell linings of bees (Hymenoptera: Apoidea)</title>
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<author>James H. Cane</author>


<category>Ecology and conservation</category>

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<title>A field method for sampling chemicals released by active insects</title>
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<author>James H. Cane et al.</author>


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<author>R. M. Duffield et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>A comparative study of the exocrine products of clepto-parasitic bees (Holcopasites) and their hosts (Calliopsis) (Hymenoptera: Anthophoridae, Andrenidae)</title>
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<author>A. Hefetz et al.</author>


<category>Pathogens and Parasites</category>

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<item>
<title>Olfactory evaluation of Andrena host nest suitability by kleptoparasitic Nomada bees (Hymenoptera: Apoidea)</title>
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<author>James H. Cane</author>


<category>Pathogens and Parasites</category>

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<item>
<title>Mandibular gland secretions of solitary bees (Hymenoptera; Apoidea): Potential for nest cell disinfection</title>
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<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

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<title>Dufour&apos;s gland lipids of three species of Centris bees (Hymenoptera: Apoidea, Anthophoridae)</title>
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<author>James H. Cane et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

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<author>James H. Cane</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>Preliminary chemosystematics of the Andrenidae and exocrine lipid evolution of the short-tongued bees (Hymenoptera: Apoidea)</title>
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<author>James H. Cane</author>


<category>Taxonomy, systematics, and biogeography</category>

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<author>James H. Cane et al.</author>


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<author>R. W. Brooks et al.</author>


<category>Ecology and conservation</category>

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<title>Dufour&apos;s gland glycerides from Anthophora, Emphoropsis (Anthophoridae) and Megachile (Megachilidae) bees (Hymenoptera: Apoidea)</title>
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<author>James H. Cane et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

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<title>Predator deterrence by mandibular gland secretions of bees (Hymenoptera:Apoidea)</title>
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<author>James H. Cane</author>


<category>Ecology and conservation</category>

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<author>James H. Cane</author>


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<title>Male competition and mating behavior within mating aggregations of Glenostictia satan Gillaspy (Hymenoptera: Sphecidae)</title>
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<author>R. W. Longair et al.</author>


<category>Natural History</category>

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<title>Host records and nest entry by Dolichostelis, a kleptoparasitic anthidiine bee (Hymenoptera: Megachilidae)</title>
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<author>F. D. Parker et al.</author>


<category>Pathogens and Parasites</category>

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<item>
<title>Foraging ecology of the bee Habropoda laboriosa (Hymenoptera: Anthophoridae), an oligolege of blueberries (Ericaceae: Vaccinium) in the southeastern United States</title>
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<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

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<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

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<title>Nesting biology notes for Perdita (Alloperdita) bradleyi Viereck (Hymenoptera: Andrenidae)</title>
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<author>James H. Cane</author>


<category>Natural History</category>

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<author>J. A. Payne et al.</author>


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<author>S. L. Buchmann et al.</author>


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<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

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<author>James H. Cane et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<author>James H. Cane et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>Real Objects, Real Spaces, Real Expertise: An Undergraduate Seminar Curates an Exhibition on the Medieval Book of Hours</title>
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<author>Marianne Hansen</author>


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<title>Pheromonal specificity of Southeastern Ips pine bark beetles reflects phylogenetic divergence (Coleoptera: Scolytidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/183</link>
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<pubDate>Wed, 09 May 2012 11:01:29 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>E. E. Lewis et al.</author>


</item>


<item>
<title>Stridulation as a primary antipredator defence of a beetle</title>
<link>http://digitalcommons.usu.edu/piru_pubs/182</link>
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<pubDate>Wed, 09 May 2012 11:01:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>E. E. Lewis et al.</author>


</item>


<item>
<title>Aggregation pheromones induce interspecific pairing between two sibling Ips species (Coleoptera: Scolytidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/181</link>
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<pubDate>Wed, 09 May 2012 11:01:02 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J. W. Fox et al.</author>


</item>


<item>
<title>Soils of ground-nesting bees (Hymneoptera: Apoidea): Texture, moisture, cell depth and climate</title>
<link>http://digitalcommons.usu.edu/piru_pubs/180</link>
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<pubDate>Wed, 09 May 2012 11:00:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Bee management</category>

</item>


<item>
<title>Nest cell lining of the solitary bee Hylaeus bisinuatus (Hymenoptera: Colletidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/179</link>
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<pubDate>Wed, 09 May 2012 11:00:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K. E. Espelie et al.</author>


</item>


<item>
<title>The solitary bee Melissodes thelypodii thelypodii Cockerell (Anthophoridae) collects pollen from wind-pollinated Amaranthus palmeri Watson</title>
<link>http://digitalcommons.usu.edu/piru_pubs/178</link>
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<pubDate>Wed, 09 May 2012 11:00:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Inefficacy of courtship stridulation as a pre-zygotic ethological mating barrier for Ips bark beetles (Coleoptera: Scolytidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/177</link>
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<pubDate>Wed, 09 May 2012 11:00:03 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>E. E. Lewis et al.</author>


</item>


<item>
<title>Temporal patterns of floral visitation for two bee species foraging on Solanum</title>
<link>http://digitalcommons.usu.edu/piru_pubs/176</link>
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<pubDate>Wed, 09 May 2012 10:59:50 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>T. E. Shelley et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Honey bees harvest pollen from the porose anthers of cranberries (Vaccinium macrocarpon) (Ericaceae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/175</link>
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<pubDate>Wed, 09 May 2012 10:59:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Reproductive role of sterile pollen in cryptically dioecious species of flowering plants</title>
<link>http://digitalcommons.usu.edu/piru_pubs/174</link>
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<pubDate>Wed, 09 May 2012 10:59:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Regional, annual and seasonal variation in pollinator guilds: intrinsic traits of bees (Hymenoptera: Apoidea) underlie their patterns of abundance at Vaccinium ashei (Ericaceae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/173</link>
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<pubDate>Wed, 09 May 2012 10:59:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Reproductive role of sterile pollen in Saurauia (Actinidiaceae), a cryptically dioecious neotropical tree</title>
<link>http://digitalcommons.usu.edu/piru_pubs/172</link>
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<pubDate>Wed, 09 May 2012 10:59:03 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Nesting biology and mating behavior of the southeastern blueberry bee, Habropoda laboriosa (Hymenoptera: Apoidea)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/171</link>
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<pubDate>Wed, 09 May 2012 10:58:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Natural History</category>

</item>


<item>
<title>Notes on the nesting biology of Svastra atripes (Hymenoptera: Apoidea)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/170</link>
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<pubDate>Wed, 09 May 2012 10:58:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Natural History</category>

</item>


<item>
<title>Susceptibility of Ips calligraphus (Germar) and Dendroctonus frontalis Zimmermann (Coleoptera: Scolytidae) to coleopteran-active Bacillus thuringiensis, a bacterial metabolite, and Avermectin B1</title>
<link>http://digitalcommons.usu.edu/piru_pubs/169</link>
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<pubDate>Wed, 09 May 2012 10:58:28 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Nesting resins obtained from pollen host by an oligolectic bee, Trachusa larreae (Cockerell) (Hymenoptera: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/168</link>
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<pubDate>Wed, 09 May 2012 10:58:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Natural History</category>

</item>


<item>
<title>A new monolectic coastal bee, Hesperapis oraria Snelling and Stage (Hymenoptera: Melittidae), with a review of desert and Neotropical disjunctives in the Southeastern U.S.</title>
<link>http://digitalcommons.usu.edu/piru_pubs/167</link>
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<pubDate>Wed, 09 May 2012 10:58:06 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

</item>


<item>
<title>Pollination, foraging and nesting ecology of the leaf-cutting bee, Megachile (Delomegachile) addenda (Hymenoptera: Megachilidae) on cranberry beds (Vaccinium macrocarpon)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/166</link>
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<pubDate>Wed, 09 May 2012 10:57:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Floral resource utilization by solitary bees (Hymenoptera: Apoidea) and exploitation of their stored foods by natural enemies</title>
<link>http://digitalcommons.usu.edu/piru_pubs/165</link>
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<pubDate>Wed, 09 May 2012 10:57:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. T. Wcislo et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Violent weather and bees: Populations of the barrier island endemic, Hesperapis oraria (Hymenoptera:  Melittidae) survive a category 3 hurricane</title>
<link>http://digitalcommons.usu.edu/piru_pubs/164</link>
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<pubDate>Wed, 09 May 2012 10:57:33 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>President Herbert and Executive Staff</title>
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<pubDate>Wed, 09 May 2012 10:57:27 PDT</pubDate>
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	<![CDATA[
	<p>Back row l-r: Karen Stone, Ed Johnson, Roland Buck, Alan Ling.</p>
<p>Front row l-r: Curtis Bullock, President Adam Herbert.</p>
<p>August 3, 1994</p>

	]]>
</description>


</item>


<item>
<title>Nectar production of cranberries: genotypic differences and insensitivity to soil fertility</title>
<link>http://digitalcommons.usu.edu/piru_pubs/163</link>
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<pubDate>Wed, 09 May 2012 10:57:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


</item>


<item>
<title>Ground-nesting bees: the neglected pollinator resource for agriculture</title>
<link>http://digitalcommons.usu.edu/piru_pubs/162</link>
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<pubDate>Wed, 09 May 2012 10:57:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Bee management</category>

</item>


<item>
<title>Lifetime monetary value of individual pollinators: the bee Habropoda laboriosa at rabbiteye blueberry (Vaccinium ashei)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/161</link>
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<pubDate>Wed, 09 May 2012 10:57:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>The potential consequences of pollinator declines on the conservation of biodiversity and stability of food crops</title>
<link>http://digitalcommons.usu.edu/piru_pubs/160</link>
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<pubDate>Wed, 09 May 2012 10:56:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Impact of intensified ultraviolet-B radiation on flower, pollen and nectar production</title>
<link>http://digitalcommons.usu.edu/piru_pubs/159</link>
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<pubDate>Wed, 09 May 2012 10:56:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B. Sampson et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Spatial predictability and resource specialization of bees (Hymenoptera: Apoidea) at a superabundant, widespread resource</title>
<link>http://digitalcommons.usu.edu/piru_pubs/158</link>
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<pubDate>Wed, 09 May 2012 10:56:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>R. L. Minckley et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Origins and ecological consequences of pollen specialization among desert bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/157</link>
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<pubDate>Wed, 09 May 2012 10:56:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>R. L. Minckley et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Pollen  nutritional content and digestibility for animals</title>
<link>http://digitalcommons.usu.edu/piru_pubs/156</link>
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<pubDate>Wed, 09 May 2012 10:56:15 PDT</pubDate>
<description>
	<![CDATA[
	
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<author>T. J. Roulston et al.</author>


</item>


<item>
<title>What governs protein content of pollen: Pollinator preferences, pollen-pistil interactions, or phylogeny?</title>
<link>http://digitalcommons.usu.edu/piru_pubs/155</link>
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<pubDate>Wed, 09 May 2012 10:56:06 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. J. Roulston et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Pollinator genetics and pollination: do honey bee colonies selected for pollen-hoarding field better pollinators of cranberry Vaccinium macrocarpon Ait?</title>
<link>http://digitalcommons.usu.edu/piru_pubs/154</link>
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<pubDate>Wed, 09 May 2012 10:55:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Pollination efficiencies for three bee species (Hymenoptera: Apoidea) visiting rabbiteye blueberry, Vaccinium ashei Reade (Ericaceae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/153</link>
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<pubDate>Wed, 09 May 2012 10:55:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B. Sampson et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Causes and extent of declines among native North American invertebrate pollinators: detection, evidence, and consequences</title>
<link>http://digitalcommons.usu.edu/piru_pubs/152</link>
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<pubDate>Wed, 09 May 2012 10:55:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Habitat fragmentation and native bees: a premature verdict?</title>
<link>http://digitalcommons.usu.edu/piru_pubs/151</link>
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<pubDate>Wed, 09 May 2012 10:55:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>The effect of diet breadth and nesting ecology on body size variation in bees (Apoidea)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/150</link>
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<pubDate>Wed, 09 May 2012 10:55:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. H. Roulston et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Sampling bees (Hymenoptera: Apiformes) for pollinator community studies: pitfalls of pan-trapping</title>
<link>http://digitalcommons.usu.edu/piru_pubs/149</link>
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<pubDate>Wed, 09 May 2012 10:55:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Host-switching does not circumvent the Ni-based defence of the Ni hyperaccumulator Streptanthus polygaloides (Brassicaceae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/148</link>
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<pubDate>Wed, 09 May 2012 10:54:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>M. A. Davis et al.</author>


</item>


<item>
<title>Pollinators of U.S. alfalfa (Medicago sativa L.) compared for rates of pod and seed set</title>
<link>http://digitalcommons.usu.edu/piru_pubs/147</link>
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<pubDate>Wed, 09 May 2012 10:54:50 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Biological impediments to measures of competition among introduced honey bees and desert bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/146</link>
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<pubDate>Wed, 09 May 2012 10:54:41 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R. L. Minckley et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Annual displacement of soil in nest tumuli of alkali bees (Nomia melanderi)(Hymenoptera: Apiformes) across a Washington landscape</title>
<link>http://digitalcommons.usu.edu/piru_pubs/145</link>
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<pubDate>Wed, 09 May 2012 10:54:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Bee Management</category>

</item>


<item>
<title>Introduction in For Non-native Crops, Whence Pollinators for the Future?</title>
<link>http://digitalcommons.usu.edu/piru_pubs/144</link>
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<pubDate>Wed, 09 May 2012 10:54:23 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K. V. Strickler et al.</author>


<category>Bee Management</category>

</item>


<item>
<title>Exotic non-social bees  (Hymenoptera: Apoidea) in North America: Ecological implications</title>
<link>http://digitalcommons.usu.edu/piru_pubs/143</link>
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<pubDate>Wed, 09 May 2012 10:54:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Dose-response relationships between pollination and fruiting refine pollinator comparisons for cranberry (Vaccinium  macrocarpon Ait.)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/142</link>
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<pubDate>Wed, 09 May 2012 10:54:05 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Screenhouse evaluations of a mason bee Osmia ribifloris (Hymenoptera: Megachilidae) as a pollinator of blueberries in the southeastern United States</title>
<link>http://digitalcommons.usu.edu/piru_pubs/141</link>
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<pubDate>Wed, 09 May 2012 10:53:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>B. J. Sampson et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Temporally persistent patterns of incidence and abundance in a pollinator guild at annual and decadal scales: the bees of Larrea tridentata</title>
<link>http://digitalcommons.usu.edu/piru_pubs/140</link>
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<pubDate>Wed, 09 May 2012 10:53:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Pollination needs of arrowleaf balsamroot, Balsamorhiza sagittata (Heliantheae: Asteraceae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/139</link>
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<pubDate>Wed, 09 May 2012 10:53:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

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<item>
<title>63 Mulberry Way</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/260</link>
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<pubDate>Wed, 09 May 2012 10:53:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>My senior project is about creating a fictional reality. Over the course of my time making photographs at Bard, I became disenchanted with documenting the deteriorating world around me and instead became fascinated by photography's capability to lie-- to present fiction as though it is fact. And so I began with simple narrative images, creating characters that lived and died within a series of still frame images. However, given the opportunity, as I was this year, to spend two semesters on a project, I thought bigger, and about expanding this idea of fictional reality out of the frame and into space.</p>
<p>For my project, I made an installation that is a construction of a house-- a fictional house in which a fictional family resides. There are four elements that I employed in the piece: photography, sculpture, video, and sound. The photos serve to portray the family that lives in the house, remnants of them, glimpses into their life so you get a sense of character, despite their absence. These photos are meant to allude to the role of photography in a domestic “non-art” space by charging the space with emotional content. The sculptural element is to give a sense of space, and to introduce familiar household architecture. Video's will be employed to give glimpses of reality: eggs cooking, a fire burning--elements of home life that can only be experienced through the use of time. The audio component will be installed but hidden speakers throughout the "house" that have familiar house sounds, dishes being washed, music being listened to from a room upstairs, etc. All four of these elements serve to transform the space that the viewer enters, in hopes of reminding them of their families, and their houses and homes as compared to the archetype I have constructed.</p>
<p>63 Mulberry Way is an entire fictional address; it is a house that resides on no particular street in no particular town, because it is on every street in every town. As I embark upon my “adult” life upon graduation, constructing my own home is an issue more pertinent than ever. This installation is a culmination of everything I’ve learned from my family, from TV, and from the world around my about how a happy home is to be constructed…a failed attempt some might say.</p>

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</description>

<author>Kiah D. Vidyarthi</author>


</item>


<item>
<title>The Inherent Possibility of Achieving a State of Balance with Nature: An Analysis of Terrence Malick&apos;s The New World</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/259</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/259</guid>
<pubDate>Wed, 09 May 2012 10:53:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Senior Project submitted to The Division of Arts of Bard College.</p>

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</description>

<author>Chase A. Sinzer</author>


</item>


<item>
<title>Look/See</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/258</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/258</guid>
<pubDate>Wed, 09 May 2012 10:53:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Kim Shifrin</p>
<p>Artist’s Statement</p>
<p>Senior Project Title:  Look/See</p>
<p>April 27th, 2011</p>
<p>When on my way to sleep early in my life, I would stare at the white ceiling above my bed and pick out faces created from the creases in the paint.  After many nights of staring I developed a habit of seeing the same faces over and over again.  It became hard to see anything new in the ceiling, the forms traced in my mind were less free and more automatic; there, again, was profile of the same man with the long nose and extended brow as the night before etc.  When attempting to alter the familiar faces I was dissatisfied with my new creations and quickly disregarded them for what now seemed like the instinctual forms.  These faces were so obvious to me that I even found it odd when no one else could see what I was talking about in pointing out the faces.  This same sort of looking game is played frequently with clouds.  People seem to naturally create associations from abstract forms found in everyday life, and this seeing process is subjective and behaves differently in everyone’s mind.  This sort of gaze is similar to the way in which a viewer first confronts an abstract work of art.  The initial sight is like a choice of what the mind will make of the piece, and only further observation can alter this primary sentiment.  The pieces in the collection “Look/See” are intended to serve foremost as objects of free association and meditation.  No references within the work are directly intended, the mind is left free to categorize and think.  The way I have manipulated the surface with paint and fabric should trap the eye within the painting.</p>
<p>On a material level, over the past year I have been working on my way of relating to art making.  I wanted to develop a new form of mark making and remove evidence of my hand more from the final pieces.  I accomplished this by using sewing to create line and using fabric to create planes of color and texture.  Subtle shifts in color have become much more important to me, so I sewed large pieces of color on the back of the of some of the paintings as a substitute for washes.  My interest in fabric stemmed from its complicated history and beauty as a material on and off the canvas.</p>
<p>It is not difficult for me to imagine that everyone sees something different when looking at a piece of abstract art.  In this way the works exists on two planes; the piece has a physical existence in the world and metaphysical existence (an emotional reaction) in the brain.  For me the work symbolizes this process in two steps; the first glance one recognizes the piece as an abstract painting, and in the second closer glance, one sees that some of the paint is actually fabric, and the illusion is undone.  In this way the pieces hopefully trip up that instinct reaction in order to gain a deeper level of insight from one’s own eye in the painting.</p>
<p>There is a difference between looking and seeing. One either sees and understands the intention of the artist, sees it for what it is on its own, or disregards it, looking but seeing nothing and probably walking away.  Art often exists in the world and as a debate in our minds.  Sometimes art is instinctually appreciated at first glance and sometimes it grows into liking.  I hope I have created work that people find accessible, relatable, and worthy of contemplation, and I hope others may find something of themselves in the work.</p>

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</description>

<author>Kimberly L. Shifrin</author>


</item>


<item>
<title>Bees, pollination, and the challenges of sprawl</title>
<link>http://digitalcommons.usu.edu/piru_pubs/138</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/138</guid>
<pubDate>Wed, 09 May 2012 10:53:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Worked Collections</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/257</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/257</guid>
<pubDate>Wed, 09 May 2012 10:53:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>It would be near impossible to demonstrate every aspect of my music studies. My second senior project is meant as a sampler; the concert is a platform to best display the wide array of projects (musical and non-musical) that I am involved in.</p>
<p>I will demonstrate my work with singers, movies, trios, and large ensembles. I am young and would be be disillusioned with my studies if i claimed to have a complete and confident artist's statement. These four years have aced as a time to gain the tools and skills necessary shape a clear and useful artist's statement during the years to come.</p>
<p>It is my goal to work with as many people as possible. Music is (for the most part) a social activity; practicing musicians play with other practicing musicians. It is easy to be isolated when living the lifestyle of an artist. Often, art is confined to a complete and cut off head world. While this is certainly an important aspect of creating, it is only one half of the whole. The other half is the social side of creating. This social side of creating is important for me. It is often other people that create excitement and energy for me. My senior project (particularly this last concert) has enabled me to create a balance between isolation and inclusion. I isolate myself in anticipation of including others.</p>
<p>This last concert demonstrates my commitment to collaboration. In preparation for this concert I worked with singers, dancers, sculptors, film makers, actors, performance artists, and many varieties of musicians.</p>

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</description>

<author>zachary seman</author>


</item>


<item>
<title>Gunslinger</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/256</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/256</guid>
<pubDate>Wed, 09 May 2012 10:53:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Senior Project short film “Gunslinger,” explores the idea of leaving home, combined with the internal struggle of making so personal a decision as enlisting in the army regardless of the opinions of those around you.  The story follows Colin’s walk from his house to the train station where he is to ship out for the army.  Along the way different landmarks in his small town trigger flashbacks from his past that tell the story of how he came to make his decision and the effect it has had on those closest to him.   Drawing from the personal experiences of close friends who have gone through the process of enlistment, as well as the first hand accounts of others, I tried to convey the stress and isolation present in those who make the decision to give their life over to an idea, regardless of the consequences.</p>
<p>Producing the film almost entirely by myself, with little to no budget, my goal was to make the piece seem as internal as possible—setting my characters against empty backgrounds, and remaining close where another film maker might have used a wider, more expansive shot.  Though the film was about the relation of the characters to the space, the internal nature of the decisions being made led me to the aesthetic choice to keep the shots closer in.  There are wider establishing shots used to convey the isolation of the main character, but these are almost exclusively used in the present tense sections where the character is reflecting on his past.  This coupled with the use of warmer colors during the flashbacks juxtaposed with cooler colors during the present tense scenes leads the viewer to understand the warmth that Colin is leaving behind, as it becomes more apparent to him as he leaves the only home he’s known.</p>

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</description>

<author>William Sarno</author>


</item>


<item>
<title>Pollination promise of the bee Osmia aglaia for cultivated raspberries and blackberries (Rubus: Rosaceae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/137</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/137</guid>
<pubDate>Wed, 09 May 2012 10:53:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Drawn Animations: Animeditation and Golden Ears</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/255</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/255</guid>
<pubDate>Wed, 09 May 2012 10:53:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>My Senior Project consists of two short hand-drawn animations, Animeditation and Golden Ears. In Animeditation I visualize a meditation, illustrating a surge of thought-images, and their inevitable retreat back to a pure and simple circle, a buzzing mantra. Golden Ears is a moral fable about a “Mountainear” (a fellow with mountains for ears) who is visited by a succession of foreboding intruders: an “Electionear,” an “Enginear” and an Auctionear.” Golden Ears speaks to my love of the wilderness, as well as my affection for drawing strange and silly characters. Both pieces are experiments in classical animation, an aging form in which every frame is drawn on paper, hand-colored and individually photographed using an enormous animation stand. My decision to attempt this medium was a natural one; animation seems to activate all aspects of my creativity. I have been drawing since I was old enough to grip a pencil. I remember drawing a Grizzly Bear eating a camper when I was very young, my grandmother standing over me, instructing me to draw bigger. I don’t really think I ever internalized her advice; throughout the course of this year I’ve drawn at least three thousand tiny images. But I guess if they’re projected on a big screen, it’s sort of like a big drawing. When I reached twelve or so I turned my attention towards filmmaking, creating silly movies of little value to anybody except for myself, that is to say, anybody who doesn’t find the sight of me jumping into bushes or mouthing along to Public Enemy particularly compelling. Animation blends filmmaking and drawing, empowering the animator with an infinite number of possibilities. The bond of these two forms imbue them with opportunities that each lacks on their own. When your drawings are filmed the imagination is rendered viewable. When you film your drawings you can devise your own system of movement, doing what a camera cannot do. For a chunk of the day you get to play God, creating a world complete with its own rules, its own aesthetic, its own proportions and physics. Through teaching myself how to animate, I happened upon several lessons that I cannot help applying to some sort of broader system of living. Every frame in an animation influences the next. If drawings began to morph or warp, I would embrace them and just try to follow along. As soon as I got comfortable working on a segment, a new one would suddenly appear. I caught on, and learned to appreciate those little pockets of familiarity while they still lasted, knowing all the while that the micro-habits and muscle-memories of the hand and wrist navigating the page would soon be refreshed. Often times, segments of the animation became so complex and intricate that I seemed only to exist within that little 9 x 12 universe, executing the drawings like an entranced servant to the page itself. A few months ago I was riding on the back of a friend’s motorcycle. The rider was telling me about his experience riding across the U.S. on a motorcycle, how you really feel every mile on a motorcycle. The same is true for animation. When you personally create every single frame by hand, there is a strong sensation of feeling the work, of earning it. Looking back at any given clip from my animations, I can explicitly recall the moment in which it was created. For every drawing there is the memory of the song I was listening to at the time, the people I was with, a vague recollection of the quality of light, the time of day, snowstorm or sunshine, irritated or mellow. This is perhaps my favorite feature of animating, and in a broader sense, my favorite feature of producing art; I am not satisfied unless the piece faithfully encapsulates that time of my life.</p>

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</description>

<author>Jonathan Rosen</author>


</item>


<item>
<title>Floral specialization by bees: analytical methodologies and a revised lexicon for oligolecty</title>
<link>http://digitalcommons.usu.edu/piru_pubs/136</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/136</guid>
<pubDate>Wed, 09 May 2012 10:53:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Complex responses within a desert bee guild (Hymenoptera: Apiformes) to urban habitat fragmentation</title>
<link>http://digitalcommons.usu.edu/piru_pubs/135</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/135</guid>
<pubDate>Wed, 09 May 2012 10:52:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>An evaluation of pollination mechanisms for purple prairie-clover, Dalea purpurea (Fabaceae: Amorpheae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/134</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/134</guid>
<pubDate>Wed, 09 May 2012 10:52:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>The Logan Beemail shelter: a practical, portable unit for managing cavity-nesting agricultural pollinators</title>
<link>http://digitalcommons.usu.edu/piru_pubs/133</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/133</guid>
<pubDate>Wed, 09 May 2012 10:52:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Bee Management</category>

</item>


<item>
<title>Importance of crop pollination in changing landscapes</title>
<link>http://digitalcommons.usu.edu/piru_pubs/132</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/132</guid>
<pubDate>Wed, 09 May 2012 10:52:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>A. M. Klein et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Foraging behavior, pollinator effectiveness, and management potential of the new world squash bees Peponapis pruinosa and Xenoglossa strenua (Apidae: Eucerini)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/131</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/131</guid>
<pubDate>Wed, 09 May 2012 10:52:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B. J. Sampson et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>An effective, manageable bee for pollinating Rubus cane fruits, Osmia aglaia</title>
<link>http://digitalcommons.usu.edu/piru_pubs/130</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/130</guid>
<pubDate>Wed, 09 May 2012 10:52:06 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Bee Management</category>

</item>


<item>
<title>Pollinating bees crucial to farming wildflower seed for U.S. habitat restoration</title>
<link>http://digitalcommons.usu.edu/piru_pubs/129</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/129</guid>
<pubDate>Wed, 09 May 2012 10:51:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>A native ground-nesting bee (Nomia melanderi) sustainably managed to pollinate alfalfa across an intensively agricultural landscape</title>
<link>http://digitalcommons.usu.edu/piru_pubs/128</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/128</guid>
<pubDate>Wed, 09 May 2012 10:51:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>James H. Cane</author>


<category>Bee Management</category>

</item>


<item>
<title>Breeding biologies, pollinating bees and seed production of Cleome lutea and C. serrulata (Cleomaceae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/127</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/127</guid>
<pubDate>Wed, 09 May 2012 10:51:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Biology and management potential for three orchard bee species (Hymenoptera: Megachilidae): Osmia ribifloris Cockerell, O. lignaria (Say) and O. chalybea Smith, with emphasis on the former</title>
<link>http://digitalcommons.usu.edu/piru_pubs/126</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/126</guid>
<pubDate>Wed, 09 May 2012 10:51:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B. J. Sampson et al.</author>


<category>Bee Management</category>

</item>


<item>
<title>Pollen viability and pollen tube attrition in cranberry (Vaccinium macrocarpon)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/125</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/125</guid>
<pubDate>Wed, 09 May 2012 10:51:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Resurrecting the bee Osmia aglaia Sandhouse from synonymy (Hymenoptera: Apiformes: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/124</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/124</guid>
<pubDate>Wed, 09 May 2012 10:51:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

</item>


<item>
<title>Visiting bees of Cucurbita flowers (Cucurbitaceae) with emphasis on the presence of Peponapis fervens Smith (Eucerini - Apidae) - Santa Catarina, southern Brasil</title>
<link>http://digitalcommons.usu.edu/piru_pubs/123</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/123</guid>
<pubDate>Wed, 09 May 2012 10:50:58 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>C. Krug et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>The alfalfa leaf-cutting bee, Megachile rotundata: The world’s most intensively managed solitary bee</title>
<link>http://digitalcommons.usu.edu/piru_pubs/122</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/122</guid>
<pubDate>Wed, 09 May 2012 10:50:50 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>T. L. Pitts-Singer et al.</author>


<category>Bee Management</category>

</item>


<item>
<title>Breeding biology of the Threadstalk Milkvetch, Astragalus filipes (Fabaceae), with a review of the genus</title>
<link>http://digitalcommons.usu.edu/piru_pubs/121</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/121</guid>
<pubDate>Wed, 09 May 2012 10:50:41 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K. Watrous et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Nectar and pollen sugars constituting larval provisions of the alfalfa leaf-cutting bee (Megachile rotundata) (Hymenoptera: Apiformes: Megachilidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/120</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/120</guid>
<pubDate>Wed, 09 May 2012 10:50:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


</item>


<item>
<title>Meeting wild bees’ needs on rangelands</title>
<link>http://digitalcommons.usu.edu/piru_pubs/119</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/119</guid>
<pubDate>Wed, 09 May 2012 10:50:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Pollination value of male bees: the specialist bee Peponapis pruinosa (Apidae) at cultivated summer squash (Cucurbita pepo)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/118</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/118</guid>
<pubDate>Wed, 09 May 2012 10:50:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Specialist Osmia bees forage indiscriminately among hybridizing Balsamorhiza floral hosts</title>
<link>http://digitalcommons.usu.edu/piru_pubs/117</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/117</guid>
<pubDate>Wed, 09 May 2012 10:50:03 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Predicted fates of ground-nesting bees in soil heated by wildfire: Thermal tolerances of life stages and a survey of nesting depths</title>
<link>http://digitalcommons.usu.edu/piru_pubs/116</link>
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<pubDate>Wed, 09 May 2012 10:49:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Breeding biology and incremental benefits of outcrossing for the restoration wildflower, Hedysarum boreale Nutt. (Fabaceae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/115</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/115</guid>
<pubDate>Wed, 09 May 2012 10:49:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K. A. Swoboda et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Breeding biologies, pollinators and seed beetles of two prairie-clovers, Dalea ornata and D. searlsiae (Fabaceae: Amorpheae), from the Intermountain West USA</title>
<link>http://digitalcommons.usu.edu/piru_pubs/114</link>
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<pubDate>Wed, 09 May 2012 10:49:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James H. Cane et al.</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>The pollination Requirements of Insect-pollinated Seed Crops</title>
<link>http://digitalcommons.usu.edu/piru_pubs/113</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/113</guid>
<pubDate>Wed, 09 May 2012 10:49:30 PDT</pubDate>
<description>
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</description>

<author>George E. Bohart</author>


<category>Pollination and foraging</category>

</item>


<item>
<title>Brood Care in Halictid Bees</title>
<link>http://digitalcommons.usu.edu/piru_pubs/112</link>
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<pubDate>Wed, 09 May 2012 10:49:22 PDT</pubDate>
<description>
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</description>

<author>S. W.T. Batra et al.</author>


<category>Natural History</category>

</item>


<item>
<title>Should Beekeepers Keep Wild Bees for Pollination?</title>
<link>http://digitalcommons.usu.edu/piru_pubs/111</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/111</guid>
<pubDate>Wed, 09 May 2012 10:49:12 PDT</pubDate>
<description>
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	]]>
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<author>Nabil N. Youssef et al.</author>


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<author>William P. Nye et al.</author>


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<author>George E. Bohart</author>


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<author>George E. Bohart</author>


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<author>Earle A. Cross et al.</author>


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<author>George E. Bohart</author>


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<author>Pedersen M. W. et al.</author>


<category>Pollination and foraging</category>

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<title>Bees Make Alfalfa Seed</title>
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<author>George E. Bohart</author>


<category>Bee Management</category>

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<title>Time Relationships in the Nest Construction and Life Cycle of the Alkali Bee</title>
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<author>George E. Bohart et al.</author>


<category>Bee Management</category>

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<title>Notes on the Habits of Osmia (Nothosmia) seclude Sandhouse</title>
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<author>George E. Bohart</author>


<category>Natural History</category>

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<title>Selection of Pollens by Honey Bees</title>
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<author>M. D. Levin et al.</author>


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<title>Gradual Nest Supersedure Within the Genus Osmia</title>
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<author>George E. Bohart</author>


<category>Natural History</category>

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<item>
<title>New Records of Hornia minutipennis Riley, With Notes on its Biology (Coleoptera, Meloidae)</title>
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<pubDate>Wed, 09 May 2012 10:39:55 PDT</pubDate>
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<author>George E. Bohart et al.</author>


<category>Pathogens and Parasites</category>

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<title>Alkali Bees vs. Drainage</title>
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<pubDate>Wed, 09 May 2012 10:39:45 PDT</pubDate>
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<author>George E. Bohart</author>


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<title>Pollination (in Growing Alfalfa for Seed)</title>
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<pubDate>Wed, 09 May 2012 10:39:33 PDT</pubDate>
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<author>George E. Bohart et al.</author>


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<title>Additional Studies of the Effect of Field Application of Insecticides on Honey Bees</title>
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<pubDate>Wed, 09 May 2012 10:39:21 PDT</pubDate>
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<author>F. V. Lieberman et al.</author>


<category>Ecology and conservation</category>

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<item>
<title>The Effect of Competing Pollen Sources on the Number of Honey Bees Collecting Alfalfa Pollen</title>
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<pubDate>Wed, 09 May 2012 10:39:10 PDT</pubDate>
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<author>George E. Bohart</author>


<category>Pollination and foraging</category>

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<item>
<title>The Biology of Zonitis atripennis flavida Leconte (Coleoptera: Meloidae)</title>
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<pubDate>Wed, 09 May 2012 10:38:58 PDT</pubDate>
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<author>Richard B. Selander et al.</author>


<category>Pathogens and Parasites</category>

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<item>
<title>Honey Bees Attacked at Their Hive Entrance by the Wast Philanthus flavifrons Cresson</title>
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<pubDate>Wed, 09 May 2012 10:38:47 PDT</pubDate>
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<author>George E. Bohart</author>


<category>Pathogens and Parasites</category>

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<item>
<title>Factors Responsible for the Attractiveness of Various Clones of Alfalfa to Pollen-collecting Bumble Bees</title>
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<pubDate>Wed, 09 May 2012 10:38:36 PDT</pubDate>
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<author>M. W. Pedersen et al.</author>


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<title>Notes on Food Habits of the Western Harvester Ant</title>
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<pubDate>Wed, 09 May 2012 10:38:23 PDT</pubDate>
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<author>George E. Bohart et al.</author>


<category>Natural History</category>

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<pubDate>Wed, 09 May 2012 10:38:12 PDT</pubDate>
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<author>George E. Bohart et al.</author>


<category>Natural History</category>

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<author>William P. Nye et al.</author>


<category>Pathogens and Parasites</category>

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<title>Pollination by Native Insects (in Insects, The Yearbook of Agriculture)</title>
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<pubDate>Wed, 09 May 2012 10:37:49 PDT</pubDate>
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<author>George E. Bohart</author>


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<title>Yearly Population Fluctuation of Bombus morrisoni at Fredonia, Arizona</title>
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<author>George E. Bohart et al.</author>


<category>Ecology and conservation</category>

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<title>Wild Bees for Pollination of the Alfalfa Seed Crop in Utah</title>
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<pubDate>Wed, 09 May 2012 10:37:29 PDT</pubDate>
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<author>George E. Bohart et al.</author>


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<title>Tribe Larrini (in Hymenoptera of America North of Mexico)</title>
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<pubDate>Wed, 09 May 2012 10:37:19 PDT</pubDate>
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<author>George E. Bohart</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>Filth-inhabiting flies of Guam</title>
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<pubDate>Wed, 09 May 2012 10:37:09 PDT</pubDate>
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<author>George E. Bohart et al.</author>


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<title>Honey Bees for Higher Yields of Alfalfa Seed in Utah</title>
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<pubDate>Wed, 09 May 2012 10:36:58 PDT</pubDate>
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<author>George E. Bohart et al.</author>


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<title>Alfalfa Seed Growers of Utah Should Protect their Wild Bees</title>
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<pubDate>Wed, 09 May 2012 10:36:49 PDT</pubDate>
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<author>George E. Bohart</author>


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<title>New insecticides. What is their effect on bees when applied to flowering alfalfa?</title>
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<pubDate>Wed, 09 May 2012 10:36:40 PDT</pubDate>
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<author>George F. Knowlton et al.</author>


<category>Bee Management</category>

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<title>Using Bumble Bees in Cages as Pollinators for Small Seed Plots</title>
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<author>M. W. Pedersen et al.</author>


<category>Pollination and foraging</category>

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<title>Some Wild Bees of Utah</title>
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<pubDate>Wed, 09 May 2012 10:36:21 PDT</pubDate>
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<author>George E. Bohart et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>The Alkali Bee, Nomia melanderi Ckll., a Native Pollinator of Alfalfa</title>
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<pubDate>Wed, 09 May 2012 10:36:13 PDT</pubDate>
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<author>George E. Bohart</author>


<category>Natural History</category>

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<title>Pollination (in Growing Alfalfa for Seed in Utah)</title>
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<pubDate>Wed, 09 May 2012 10:36:05 PDT</pubDate>
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<author>F. E. Todd et al.</author>


<category>Pollination and foraging</category>

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<title>Observations on the Mating Habits of Halictid Bees</title>
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<pubDate>Wed, 09 May 2012 10:35:55 PDT</pubDate>
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<author>George E. Bohart</author>


<category>Natural History</category>

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<title>Effect of an Experimental Field Application of DDT Dust on Nomia melanderi Ckll</title>
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<pubDate>Wed, 09 May 2012 10:35:46 PDT</pubDate>
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<author>George E. Bohart et al.</author>


<category>Ecology and conservation</category>

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<title>Record of a Fungus Outbreak Among Adult Bees of the Genus Andrena</title>
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<pubDate>Wed, 09 May 2012 10:35:36 PDT</pubDate>
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<author>George E. Bohart</author>


<category>Pathogens and Parasites</category>

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<title>New North American Bees of the Genus Dufourea (Apoidea: Halictidae) Part III</title>
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<pubDate>Wed, 09 May 2012 10:35:26 PDT</pubDate>
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<author>George E. Bohart</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>The Sarcophagidae of Guam (Diptera)</title>
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<author>David G. Hall et al.</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>New North American Bees of the Genus Dufourea (Apoidea: Halictidae) Part II</title>
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<author>George E. Bohart</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>Beneficial Insects in Relation to Alfalfa-seed Production in Utah</title>
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<pubDate>Wed, 09 May 2012 10:34:57 PDT</pubDate>
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<author>George E. Bohart</author>


<category>Pollination and foraging</category>

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<title>Wild Bees in Relation to Alfalfa Pollination</title>
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<pubDate>Wed, 09 May 2012 10:34:47 PDT</pubDate>
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<author>George E. Bohart</author>


<category>Bee Management</category>

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<title>New North American Bees of the Genus Dufourea (Apoidea; Halictidae) Part I</title>
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<author>George E. Bohart</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>Some Records of Parasitism of Solitary Bees by Conopid Flies</title>
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<author>John W. MacSwain et al.</author>


<category>Pathogens and Parasites</category>

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<title>The Phorid Flies of Guam</title>
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<author>George E. Bohart</author>


<category>Taxonomy, systematics, and biogeography</category>

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<title>Three New Muscoid Flies from Guam</title>
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<author>George E. Bohart et al.</author>


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<author>A. A. Weathersbee et al.</author>


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<title>Keys to the mosquitoes of the Australasian Region</title>
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<author>K. L. Knight et al.</author>


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<author>George E. Bohart</author>


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<title>Notes on Some Feeding and Hibernation Habits of California Polistes (Hymenoptera, Vespidae)</title>
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<author>George E. Bohart</author>


<category>Natural History</category>

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<title>A Review of the Genus Physocephala of the Western United States (Diptera, Conopidae)</title>
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<author>George E. Bohart</author>


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<title>Winter Insect Collecting in Mexico</title>
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<author>George E. Bohart et al.</author>


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<author>George E. Bohart</author>


<category>Pathogens and Parasites</category>

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<title>Notes on Two Chrysidids Parasitic on Western Bembicid Wasps (Hymenoptera)</title>
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<author>George E. Bohart et al.</author>


<category>Pathogens and Parasites</category>

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</description>

<author>George E. Bohart et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>A record of Physocephala affinis Williston as a parasite of adult Bembix comata Parker</title>
<link>http://digitalcommons.usu.edu/piru_pubs/9</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/9</guid>
<pubDate>Wed, 09 May 2012 10:32:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>George E. Bohart et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>The Life History of the Sand Wasp, Bembix occidentalis beutenmuelleri Fox, and its Parasites</title>
<link>http://digitalcommons.usu.edu/piru_pubs/8</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/8</guid>
<pubDate>Wed, 09 May 2012 10:32:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>George E. Bohart et al.</author>


<category>Natural History</category>

</item>


<item>
<title>Synopsis of the Genus Dalmannia in North America (Diptera, Conopidae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/7</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/7</guid>
<pubDate>Wed, 09 May 2012 10:32:06 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>George E. Bohart</author>


<category>Taxonomy, systematics, and biogeography</category>

</item>


<item>
<title>Field Comparisons of Attractants for the Screwworm Fly (Diptera, Calliphoridae) in A Tropical Dry Forest in Costa-Rica</title>
<link>http://digitalcommons.usu.edu/piru_pubs/6</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/6</guid>
<pubDate>Wed, 09 May 2012 10:31:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Field trials were conducted to determine the best attractant for adults of the screwworm, Cochliomyia hominivorax (Coquerel), in Costa Rica. The five attractants were wounded sentinel sheep, decayed fruit, rotted beef liver, rotted fish, and medium used to rear larvae of this blow fly. Significantly more adults came to rotted liver than any other attractant. No adults were captured in traps baited with rotted fruit. Significantly more males came to beef liver than were captured at other baits; males were rarely encountered at wounds. Ovarian development of females obtained with different attractants indicated that proportionally more gravid females visited wounded animals than were caught in traps with proteinaceous baits. Most females had mated by egg stage five and mating and and parity in the populations that visited different attractants were similar. Significantly more females (81%) marked initially at wounds returned to wounds than visited traps baited with liver or fish</p>

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</description>

<author>Frank D. Parker et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Alternative to Sentinel Animals for Collecting Egg Masses from Wild Females of the Screwworm (Diptera, Calliphoridae)</title>
<link>http://digitalcommons.usu.edu/piru_pubs/5</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/5</guid>
<pubDate>Wed, 09 May 2012 10:31:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Egg masses from wild populations of the screwworm, Cochliomyia hominivorax (Coquerel), were obtained by collecting females from rotted liver, holding them for 3 d until egg maturation and then placing them on heated ground beef for oviposition. Nearly 50% of the females oviposited. Fertility of egg masses was 66 and 95% at the two collection sites. Decreased fertility was associated with collections of virgin females. Average weight +/- SD of the egg masses was 13.7 +/- 1.40 mg; the number of eggs per mass averaged 343. This method of obtaining egg masses from wild screwworm females is a cost-effective, sensitive alternative to the use of sentinel animals in the field. The use of rotted liver costs less, takes less time, and takes less equipment than the traditional sentinel animal technique</p>

	]]>
</description>

<author>Frank D. Parker et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Influence of Attractants on Behavior of Screwworms (Diptera, Calliphoridae) in A Tropical Wet Forest in Costa-Rica</title>
<link>http://digitalcommons.usu.edu/piru_pubs/4</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/4</guid>
<pubDate>Wed, 09 May 2012 10:31:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>In a mark-release-recapture study, sheep wounds and rotted liver were used as attractants to study movements of the screwworm fly, Cochliomyia hominivorax (Coquerel), in a Costa Rican tropical wet forest in the wet season. When sites were monitored for < 1 h, liver attracted between 3 and 12.2 times more flies of both sexes than did wounds, but proportionately fewer gravid and parous females. Only 24.6% of females marked at liver sites were recaptured; seldom (3.1%) did they visit sheep wounds. Females originally marked at sheep wounds remained at the study site longer, visited both sheep and liver sites, and > 50% were recaptured. Some females were observed for 16 d and one laid four clutches of eggs. Only 8% of the marked males were recaptured and none was recaptured < 2 d later. Only a small proportion of the adult screwworms at a locality visited wounds on sentinel sheep; the majority of the adults were transient</p>

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</description>

<author>Frank D. Parker et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Monitoring Adult-Populations of the Screwworm (Diptera, Calliphoridae) with Feeding Stations Baited with Liver</title>
<link>http://digitalcommons.usu.edu/piru_pubs/3</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/3</guid>
<pubDate>Wed, 09 May 2012 10:31:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Populations of the screwworm, Cochliomyia hominivorax (Coquerel), were monitored by capturing adults with hand nets from rotted liver set on the ground. Adults were marked and released. During the 61-d study conducted in a tropical dry forest in the dry season January to March 1989), 2,640 individual females and 460 individual males were recorded at the four liver-baited stations. The total number of visits by females was 5,769 and by males 510. The mean number of unmarked adults per day was 44.1 females and 7.6 males in an area of almost-equal-to 2.59 km2. The mean percentage of marked flies that were recovered was 64.3%. The mean number of feeding stations visited, times recaptured, and days in the study area by individual females was 2.1, 2.4, and 4.5, respectively. Daily visitational patterns by both sexes at the feeding stations were bimodal with peaks occurring between the hours of 0730 to 0859 and 1500 to 1629. Flies were most active when the mean temperature was 29.8-degrees-C; the majority of the visits occurred when air temperatures were between 26 and 33-degrees-C. Most females attracted to feeding stations were nulliparous (70.7%) and mated (69.7%). Our results suggest that observing adults at feeding stations is a reliable method of obtaining data on the behavior and population dynamics of indigenous populations of screwworm adults in tropical habitats. Although this method was labor intensive, the amount of data gleaned from the manipulation of wild populations more than compensated for such costs</p>

	]]>
</description>

<author>Frank D. Parker et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Influence of Habitat, Season, and Attractant on Adult Behavior of the Screwworm (Diptera, Calliphoridae) in A Tropical Dry Zone in Costa-Rica</title>
<link>http://digitalcommons.usu.edu/piru_pubs/2</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/2</guid>
<pubDate>Wed, 09 May 2012 10:31:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Influence of attractant, season, habitat, temperature, and physiological state of the screwworm, Cochliomyia hominivorax (Coquerel), on daily activity and oviposition were examined during a 122 d study in a tropical dry forest in Costa Rica. Flies were marked and released. Numbers of flies visiting baits increased during the wet season and decreased during the dry season; 3 times more flies were observed a baits during the wet season than were observed during the dry season. An average of 33 females and 3 males was observed per day during the study. More flies (3.6 times) were attracted to liver than to sentinel sheep; many flies originally marked at liver failed to return and few of them oviposited on sentinel sheep. Females marked at sheep were recaptured more times and remained in the study area longer. More females marked at sheep sites were recaptured (51.4-54.1%) than those marked at liver sites (32.3-44.7). More than 6 times as many flies were observed at forest than at pasture sites. The physiological state of the female influenced daily activity. High temperatures during midday (>31-degrees-C) depressed activity and decreased the number of foraging hours available for flies during the dry season. Decreasing host resources and number of hours available for foraging may be factors that limit screwworm populations in the dry season</p>

	]]>
</description>

<author>Frank D. Parker et al.</author>


<category>Pathogens and Parasites</category>

</item>


<item>
<title>Autoimmunity&apos;s next top models.</title>
<link>http://mouseion.jax.org/stfb2012/18</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2012/18</guid>
<pubDate>Wed, 09 May 2012 10:31:03 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Hartmut Wekerle et al.</author>


<category>Animals</category>

<category>Animals, Genetically Modified</category>

<category>Autoimmune Diseases</category>

<category>Autoimmunity</category>

<category>Brain</category>

<category>Disease Models, Animal</category>

<category>Humans</category>

<category>Joints</category>

<category>Mice</category>

<category>Translational Medical Research</category>

</item>


<item>
<title>Estimating Population Density Per Unit Area From Mark, Release, Recapture Data</title>
<link>http://digitalcommons.usu.edu/piru_pubs/1</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/piru_pubs/1</guid>
<pubDate>Wed, 09 May 2012 10:30:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this paper, we describe a method for estimating animal population density per unit area from mark, release, recapture (MRR) data. Standard procedures are available for estimating population size from MRR data, but not density per unit area, which is often of more practical value. If data on dispersal movements are available in addition to capture/recapture records, they can be used to estimate the area over which the study population ranges. These area estimates can then be combined with MRR abundances to yield estimates of population density. As a concrete example of how these methods can be applied, we calculated population density estimates for seven MRR data sets for the screwworm, Cochliomyia hominivorax (Diptera: Calliphoridae), from Costa Rica. As a standard of comparison, we also used a different method to calculate estimates of screwworm density for five sets of USDA APHIS Screwworm Eradication Program data from Mexico. Mean densities for both sets of analyses were similar, ranging from 10 to 120 adult flies/km(2). General agreement between the Mexican and Costa Rican estimates lends support to the dispersal approach we propose here. Although we have applied these methods to the screwworm as a specific example, they are entirely general and can be applied to virtually any organism for which both MRR records and dispersal data are available</p>

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</description>

<author>R. B. Matlock et al.</author>


<category>Ecology and conservation</category>

</item>


<item>
<title>Centennial Library E-News, March/April 2012</title>
<link>http://digitalcommons.cedarville.edu/library_enews/2</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/library_enews/2</guid>
<pubDate>Wed, 09 May 2012 10:29:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Articles in this issue: Library staff members retire, New faculty position filled, Community work recognized, Name added to Honor roll, Library scholarship awarded, Library staff honored, National library week celebrated, University faculty in print, University alumni in print, Library summer schedule  <ul> </ul></p>

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</description>

<author>Centennial Library</author>


</item>


<item>
<title> Precipitation of phreatic overgrowths at the water table of meteoric-marine mixing zones in coastal cave systems:   a useful tool in sea level change reconstruction</title>
<link>http://scholarcommons.usf.edu/gly_facpub/116</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/116</guid>
<pubDate>Wed, 09 May 2012 10:29:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Precipitation of carbonates within coastal karst caves at the present-day water table has been extensively documented in Mallorca and Sardinia. These depositions frequently occur either as calcite rafts floating at the brackish waters surface or, more commonly, as horizontal bulbous belts of calcite or aragonite overgrowths that develop over the walls of the caves or whatever suitable support is available (stalactites, stalagmites, columns) in correspondence to current sea level. The water table in the coastal caves is at about the same elevation as sea level and undergoes analogous daily fluctuations. Therefore, the presentday precipitates, known as Phreatic Overgrowths on Speleothems (POS), mark the current position of sea level and provide an excellent analogue for interpreting past bands of precipitates now located above or below modern sea level. With the aim of testing the strength of POS as indicators of present and past sea levels, some overgrowths, now located at current water table in Mallorca, have been dated by U-series methods. The results indicate that the phreatic carbonate precipitation took place sometimes between ~2,800 and ~600 years BP. The discovery of a drowned prehistoric construction, at a depth of 1 m below current sea level in a cave from the same area, and its temporal chronological attribution to about 3,700 - 3,000 years BP seem to be in good agreement with the obtained age of calcite precipitation at the current water table. The geographical distribution of POS is restricted to some very specific geochemical environments, always related to coastal caves characterized by low-range tidal fluctuations.</p>

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</description>

<author>Paola Tuccimei et al.</author>


</item>


<item>
<title> Mineralogical and stable isotope investigations of minerals from caves on Cerna Valley (Romania)</title>
<link>http://scholarcommons.usf.edu/gly_facpub/115</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/115</guid>
<pubDate>Wed, 09 May 2012 10:29:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The caves from Cerna Valley, southwest Romania, are ideal for mineralogical studies because the reaction between hot ascending thermal water or steam with the bedrock or cave sediments enabled a number of minerogenic processes (e.g., replacement, steam-condensate weathering) that ultimately led to the deposition of a unique suite of cave minerals. The mineral species identified in caves along Cerna Valley are: calcite, aragonite, gypsum, anhydrite, epsomite, pickeringite, halotrichite, apjonite, tamaragite, alunite, aluminite, chalcanthite, apatite-(CaOH), brushite, darapskite, and nitratine. Although the speleothems are not extremely spectacular, their mineralogy and stable isotope signature provides a wealth of information with respect to the environment in which they were precipitated. Combining this information with particular cave morphology observations, tectonic, and structural data, we document at least one episode of hypogenic activity within this karst area of Romania.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Depositi di gesso nelle grotte del Monte Cucco e della Gola di Frasassi - Considerazioni sulla speleogenesi</title>
<link>http://scholarcommons.usf.edu/gly_facpub/114</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/114</guid>
<pubDate>Wed, 09 May 2012 10:29:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>M Menichetti et al.</author>


</item>


<item>
<title> Sea-level position at ~80 ka based on speleothems from Mallorca</title>
<link>http://scholarcommons.usf.edu/gly_facpub/113</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/113</guid>
<pubDate>Wed, 09 May 2012 10:28:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Pestera Humpleu. Nouvelle topographie d’une des plus importantes cavités roumaines</title>
<link>http://scholarcommons.usf.edu/gly_facpub/112</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/112</guid>
<pubDate>Wed, 09 May 2012 10:28:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>P Häuselmann et al.</author>


</item>


<item>
<title> Unusual types of secondary cave calcite from the Scarisoara Ice Cave, Bihor Mts., Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/111</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/111</guid>
<pubDate>Wed, 09 May 2012 10:28:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K Zak et al.</author>


</item>


<item>
<title> Mineralogical reconnaissance of caves from Mallorca Island</title>
<link>http://scholarcommons.usf.edu/gly_facpub/110</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/110</guid>
<pubDate>Wed, 09 May 2012 10:28:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Eighteen caves on the Mallorca Island were investigated with respect to their mineralogy. Sixteen minerals, divided into four chemical groups, were identified and described using X-ray diffraction, infrared, thermal, and scanning electron microscope analyses. Calcite is the only mineral found in every sampled cave. Aragonite, gypsum, and hydroxylapatite occur in speleothems from four different caves. In addition, a few other carbonates, phosphates, and silicates were identified in crusts, minute crystals, and earthy masses. The mechanisms responsible for deposition of minerals in the Majorcan caves are: (i) precipitation from percolating water, (ii) precipitation in the freshwater/seawater mixing zone, (iii) reaction between the bedrock and various speleothems, and the phosphate-rich solutions derived from bat guano, and (iv) mineral phase transition.</p>
<p>Cova de sa Guitarreta and Cova de ses Rates Pinyades were confirmed to be two outstanding cavities with respect to their mineralogy, both hosting eight true cave minerals. Their phosphate association is diverse and interesting.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Assessing the palaeoclimate potential of cave glaciers:   the example of the Scărişoara Ice Cave (Romania)</title>
<link>http://scholarcommons.usf.edu/gly_facpub/109</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/109</guid>
<pubDate>Wed, 09 May 2012 10:28:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ice block in Sc_ri­oara Cave, NW Romania, is preserved due to unusual climate and permafrost conditions within the cave. The air temperature in the cave is governed by the winter cold, the cooling effect of the ice block, and only to a minor extent influenced by summer temperatures. At present, the ice block is slowly thinning, but the present-day climate is sufficiently cold to preserve the permafrost conditions caused by the cold air trapped in the cave. In February 2003 a 22.5 m long ice core was recovered from the ice block. Approximately 200 ice layers have been identified by visual examination. Ice crystallographic analyses indicate a steady growth of ice crystals with depth and there is no sign of deformation. Carbon-14 dates on wood-related samples collected from a natural vertical exposure of the ice block indicate that the ice spans more than 1000 years. Observations on the exposure indicate that a basal melting phase may have occurred in the past.</p>

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</description>

<author>P Holmlund et al.</author>


</item>


<item>
<title>Lateglacial-Middle Holocene stable isotope records in two coeval stalagmites from the Bihor Mountains, NW Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/108</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/108</guid>
<pubDate>Wed, 09 May 2012 10:28:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Oxygen and carbon stable isotope records of two stalagmites from NW Romania provide a continuous climatic record between 14.8 and 5.6 ka BP. The chronology is established by 21 TIMS uranium series ages. Uncertainties in the isotope chronology range between ą20 and ą100 yr. The d18 O values are positively correlated with temperature, whereas d13 C fluctuations suggest changes in soil CO2 production. Lateglacial deposition of both stalagmites started at ~14.8 ka BP. The d18 O records subsequently show a slow decline in temperatures until 12.6 ka BP. Three warmer periods with increased soil productivity occurred at 14.5-13.9 ka BP, 13.6-13.2 ka BP, and 12.9-12.6 ka BP. Lower d18 O and high d13 C values between 12.6 and 11.4 (11.7) ka BP indicate a cold and dry climate during the Younger Dryas (GS-1). During the Early Holocene, three short cold intervals are marked on the d18 O profiles at 11.0-10.6, 10.5-10.2 and 9.4-9.1 ka BP. For the remainder of the Holocene sequence, the d18 O records show less variation between 9 and 7.8 ka BP and gradual warming from 7.6-5.6 ka BP. The speleothem records correlate with the Greenland ice core records and with other proxies throughout Europe and the North Atlantic region.</p>

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</description>

<author>T Tămaş et al.</author>


</item>


<item>
<title> A modern, guano-related occurrence of foggite, CaAl(PO4)(OH)2·H2O and churchite-(Y), YPO4·2H2O in Cioclovina Cave, Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/107</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/107</guid>
<pubDate>Wed, 09 May 2012 10:28:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study reports foggite and churchite-(Y) from two spatially separate locations in the guano-related phosphate deposit from the Cioclovina Cave, Romania. Optical microscope observations, powder X-ray diffraction, electron microprobe analyses, and FTIR were used in the analysis of the two minerals. The chemical composition of foggite was determined to be Ca0.925(Al0.91Fe2+0.016)Σ0.926(P0.991Si0.043)Σ1.034O3.74(OH)2.26 · H2O and churchite-(Y) [(Y0.830Dy0.043Er0.033Gd0.029Yb0.022)Σ0.957Ca0.009]P1.023O4.00 · 2H2O. Chemical analyses of Cioclovina churchite-(Y) clearly revealed enrichment in lanthanides of even atomic number. The refined unit-cell parameters are for foggite (orthorhombic) a = 9.264(1) Å, b = 21.334(8) Å, c = 5.197(7) Å, and V = 1027.13(8) Å3 (Z = 8); for churchite-(Y) (monoclinic): a = 5.578(8) Å, b = 15.013(6) Å, c = 6.277(8) Å, β = 117.94(4)°, and V = 464.38(5) Å3 (Z = 4). FTIR spectrum of churchite-(Y) exhibits all the bands assigned to the vibrations of PO4, OH, and water groups.</p>
<p>Unlike other documented occurrences of foggite and churchite-(Y), in Cioclovina Cave, the occurrence of these minerals are related to a process that phosphatized subjacent limestone and various cave sediments (sand, clay, and limy mud) to form a complex phosphate assemblage. The minerals are presumably derived from phosphate-rich solutions that reacted with clay earth while moving downward through the sediments. Foggite was formed at the expense of the originally precipitated crandallite. Locally concentrated yttrium, REE, and dissolved phosphate are probably responsible for the precipitation of churchite-(Y).</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> U-Th ages constraining the Neanderthal footprint at Vârtop Cave, Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/106</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/106</guid>
<pubDate>Wed, 09 May 2012 10:28:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Early human footprints are rare in the fossil record. A survey of the literature reveals very few well documented and dated cases. Here, we report the first clear Homo neanderthalensisfootprint. It was found in VârtopCave, Romania. The individual stepped into calcareous mud that later hardened. The 22 cm long print suggests a body height of ∼1.46 m; a gap of 1.6 cm marks the separation of big and second toes. The date of the footprint is constrained by three coeval dates of ∼62 kyr on sub-samples from the basal layer of a nearby stalagmite that grew on top of the layer of calc-tufa covering the footprint. The lower constraint is a poorly constrained uranium (U)–thorium (Th) isochron date of ∼97 kyr on the calc-tufa layer in which the footprint is embedded. Thus, the VârtopCave individual lived in Romania sometime before 62 kyr, long before the appearance of Homo sapiens in Central and Eastern Europe, the earliest records of which date from only ∼35 kyr. To our knowledge, this is the first recognised and dated Homo neanderthalensisfootprint.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Hydroxylellastadite from Cioclovina Cave (Romania),  microanalytical,  structural, and vibrational spectroscopy data</title>
<link>http://scholarcommons.usf.edu/gly_facpub/105</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/105</guid>
<pubDate>Wed, 09 May 2012 10:28:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Electron-microprobe analyses of hydroxylellestadite from the Cioclovina Cave (Romania) gave the composition Ca10.27[(SiO4)2.53(SO4)2.17(PO4)1.27]∑=5.97[(OH)1.66F0.21Cl0.16]∑=2.03. The mineral is translucent to transparent, light orange, slightly fluorescent, has a vitreous luster and <1.5 mm in length. A single-crystal X-ray structure investigation gave the average space-group symmetry P63/m [R1(F) = 0.038 for 783 reflections up to 2�MoKα = 70° and 42 variables, a = 9.496(2), c = 6.920(2) Å, V = 540.4 Å3, and Z = 2]. Some atoms exhibit large anisotropic displacements. Ordering of atoms along with a symmetry reduction is not verified. Fourier-transformed infrared (FT-IR) and micro-Raman spectra exhibit a distinct contribution from (PO4)3− modes along with the characteristic (SO4)2− and (SiO4)4− modes. The occurrence is quite unusual and suggests that an intense thermal process affected a restricted area within the cave. Hydroxylellestadite is associated with berlinite, another high-temperature mineral. It is likely to have formed within highly phosphatized, silicate-rich, carbonate-mudstone sediments heavily compacted and thermally transformed due to in situ bat guano combustion.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> The relationship between the mineralization of breccia pipes and mineral composition of speleothems:   evidence from Corkscrew Cave,  Arizona</title>
<link>http://scholarcommons.usf.edu/gly_facpub/104</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/104</guid>
<pubDate>Wed, 09 May 2012 10:28:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Solution-collapse breccia pipes are common features in northwestern Arizona. They were mineralized with uranium, but associated with it are a suite of elements (e.g., As, Mo, V, Ba, Cu, Pb, and Fe) that may form other ore minerals. Breccia bodies are in some cases cut by cave passages, such as at Corkscrew Cave, Arizona, where such structures are exposed along the walls and on the cave ceilings. The abundance of gypsum and barite throughout the cave and their isotopically light δ34S value (−11 to −7‰) suggest deposition from warm sulfidic solutions that were also responsible, at least in part, for development of the recent cave passages that dissect older paleokarst breccia bodies. The presence of calcite showing depleted δ18O values (−11.3 and −16.9‰) is considered indicative of a low-temperature hydrothermal episode in the deposition history of cave minerals. Groundwater percolating through the breccia-pipe bodies mobilized and transported ore-related ions into the cave, where they formed a unique assemblage of minerals (i.e., hörnesite, talmessite, carnotite, tyuyamunite, claudetite, and powellite) that mirror breccia-pipe mineralization.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Younger Dryas to mid-Holocene environmental history of the lowlands of NW Transylvania, Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/103</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/103</guid>
<pubDate>Wed, 09 May 2012 10:28:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pollen, micro-charcoal and total carbon analyses on sediments from the Turbuta palaeolake, in the Transylvanian Basin of NWRomania, reveal YoungerDryas to mid-Holoceneenvironmental changes. The chronostratigraphy relies on AMS 14C measurements on organic matter and U/Th TIMS datings of snail shells. Results indicate the presence of Pinus and Betula open woodlands with small populations of Picea, Ulmus, Alnus and Salix before 12,000 cal yr BP. A fairly abrupt replacement of Pinus and Betula by Ulmus-dominated woodlands at ca. 11,900 cal. yr BP likely represents competition effects of vegetation driven by climate warming at the onset of the Holocene. By 11,000 cal yr BP, the woodlands were increasingly diverse and dense with the expansion of Quercus, Fraxinus and Tilia, the establishment of Corylus and the decline of upland herbaceous and shrubs taxa. The marked expansion of Quercus accompanied by Tilia between 10,500 and 8000 cal yr BP could be the result of low effective moisture associated with both low elevation of the site and with regional change towards a drier climate. At 10,000 cal yr BP, Corylus spread across the region, and by 8000 cal yr BP it replaced Quercus as a dominant forest constituent, with only little representation of Picea abies. Carpinus became established around 5500 cal yr BP, but it was only a minor constituent in local woodlands until ca. 5000 cal yr BP. Results from this study also indicate that the woodlands in the lowlands of Turbuta were never closed.</p>

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</description>

<author>A Feurdean et al.</author>


</item>


<item>
<title> Re-examination of berlinite from Cioclovina Cave, Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/102</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/102</guid>
<pubDate>Wed, 09 May 2012 10:28:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Berlinite is a mineral indicative of high-temperature formation and, therefore, it would not be expected to be present in a sedimentary environment. In this study, we review the characteristics of a berlinite-bearing deposit and present a single-crystal structure investigation based on X-ray data: the refinement converged at R1(F) = 0.0276, wR2(F2) = 0.0657 for 677 reflections (2θMoKα ≤ 70°) and 31 variables in space-group P3121 [a = 4.9458(10), c = 10.9526(20) Å, V = 232.0 Å3, Z = 3{AlPO4}]. The average  bond distances within the two crystallographically unique TO4 tetrahedra are 1.734 and 1.526 Å, respectively. From the scattering power at these T sites and the stereochemistry, the presence of an AlO4 tetrahedron linked to a PO4 tetrahedron is established. Consequently, the sample from Cioclovina Cave is verified as AlPO4 (modification berlinite), reconfirming the first description of this mineral from a sedimentary occurrence, which underwent an obvious natural heating process.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Cryogenic carbonates in cave environments:  a review</title>
<link>http://scholarcommons.usf.edu/gly_facpub/101</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/101</guid>
<pubDate>Wed, 09 May 2012 10:28:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K Zak et al.</author>


</item>


<item>
<title> Archives of Climate and Environmental Change in Karst</title>
<link>http://scholarcommons.usf.edu/gly_facpub/100</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/100</guid>
<pubDate>Wed, 09 May 2012 10:28:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Stable isotope study of precipitation and cave drip water in Florida (USA):  implications for speleothem-based paleoclimate studies</title>
<link>http://scholarcommons.usf.edu/gly_facpub/99</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/99</guid>
<pubDate>Wed, 09 May 2012 10:28:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Stable isotopes of hydrogen and oxygen were used to examine how the isotopic signal of meteoric water is modified as it travels through soil and epikarst into two caves in Florida. Surface and cave water samples were collected every week from February 2006 until March 2007. The isotopic composition of precipitation at the investigated sites is highly variable and shows little seasonal control. The δ18O vs. δ2H plot shows a mixing line having a slope of 5.63, suggesting evaporation effects dominate the isotopic composition of most rainfall events of less than 8 cm/day, as indicated by their low d-excess values. The δ18O values of the drip water show little variability (<0.6‰), which is loosely tied to local variations in the seasonal amount of precipitation. This is only seen during wintertime at the Florida Caverns site.</p>
<p>The lag time of over two months and the lack of any relationship between rainfall amount and the increase in drip rate indicate a dominance of matrix flow relative to fracture/conduit flow at each site. The long residence time of the vadose seepage waters allows for an effective isotopic homogenisation of individual and seasonal rainfall events. We find no correlation between rainfall and drip water δ18O at any site. The isotopic composition of drip water in both caves consistently tends to resemble the amount-weighted monthly mean rainfall input. This implies that the δ18O of speleothems from these two caves in Florida cannot record seasonal cycle in rainfall δ18O, but are suitable for paleoclimate reconstructions at inter-annual time scales.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Apatite-(CaOH) in the fossil bat guano deposit from the “Dry” Cioclovina Cave, Sureanu Mountains, Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/98</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/98</guid>
<pubDate>Wed, 09 May 2012 10:28:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Apatite-(CaOH) is the most abundant phosphate in the deposit of fossil bat guano in the “dry” Cioclovina Cave, Şureanu Mountains, South Carpathians, Romania. Initial deposits, of both biogenic and authigenic origin, were chemically equilibrated during diagenesis. Individual crystals are tabular, roughly hexagonal, platy on (0001) and usually between 3 and 15 μm across and up to 1 μm thick. The mean indices of refraction measured for 10 representative samples are ε 1.645(2) and ω 1.653(1). The mean measured density [Dm = 3.17(2) g/cm3] is in good agreement with the individual calculated values. The unit-cell parameters calculated as an average of 20 sets of values are a 9.436(13), c 6.868(8) Å. The mineral is Ca-deficient, carbonate- and sulfate-bearing. Less than 2.26% of the phosphate groups are protonated, and less than 4.66% are replaced by sulfate. The cumulative incorporation of other cations in the Ca sites accounts for only 0.71 to 4.07% (mean 2.07%). Both unit-cell parameters and thermal behavior are characteristic for a hydrous A-type carbonated apatite-(CaOH), with molecular H2O and carbonate substituting for hydroxyl in the structural channels. The multiplicity of the bands in the infrared absorption spectrum (3ν3 + 1ν1 + 3ν4 + 2ν2) is consistent with a C6 point symmetry of the phosphate anion. Whitlockite obtained by thermal breakdown at 1000°C is sulfate-bearing. The authigenesis of the Cioclovina apatite-(CaOH) involved a reaction between calcium carbonate from the moonmilk flows or the cave floor and phosphoric solutions derived from guano, with brushite or an X-ray amorphous phase as a precursor.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Raman study of natural berlinite from the Cioclovina Cave phosphate deposit</title>
<link>http://scholarcommons.usf.edu/gly_facpub/97</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/97</guid>
<pubDate>Wed, 09 May 2012 10:28:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Naturalberlinite from a heated sedimentary sequence in CioclovinaCave (Romania) was studied using Raman spectroscopy complemented with infrared techniques. Vibrational data acquired at room temperature were compared with those reported for synthetic berlinite in ambient conditions. The symmetry of the (PO4)3− units is confirmed by the observation of characteristic bands attributed to the ν1(PO4)3− stretching mode, both the ν4 and ν2 bending regions at 500–595 cm−1, and 350–500 cm−1, respectively. The berliniteRaman fingerprint was unambiguously identified at 1111 and 1104 cm−1, confirming the identity of the species and elucidating some controversial reports in the mineralogy field.</p>
<p>The vibrational data of naturalberlinite relates to its crystallography, and along with the spectra–structure correlation, confirmed an almost ideal naturalberlinite crystal.</p>

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</description>

<author>Cinta et al.</author>


</item>


<item>
<title> Authigenic burbankite in the Cioclovina Cave sediments (Romania)</title>
<link>http://scholarcommons.usf.edu/gly_facpub/96</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/96</guid>
<pubDate>Wed, 09 May 2012 10:28:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>The complex rare-earth-bearing anhydrous carbonate burbankite, A3B3(CO3)5, occurs as microcrystalline yellow greyish aggregates in the lower part of a lacustrine-like sediment sequence in the Cioclovina Cave, Romania. From this occurrence, foggite, churchite-(Y) and colourless or milky-white needle-like brushite and gypsum were also documented. The empirical formula (calculated from the electron-microprobe results on the basis of five carbonate groups pfu) is (Na2.46Ca0.98Sr1.71Ba0.32Y0.05Ce0.17La0.08Nd0.08Pr0.02Th0.09)Σ = 5.96(CO3)5. Single-crystal X-ray investigations gave a = 10.514(3) and c = 6.477(2) Å, space group P63mc, Z = 2. The structural refinement converged at R1 = 0.030 for 827 F0 > 4σ(F0). The crystal structure refinement was performed to verify ordering at the two sites, A and B. The A site is [6 + 2] coordinated with an average A—O bond length of 2.491 Å; the B site is [10] coordinated, the average B—O bond length is 2.678 Å. As expected the Na and Ca atoms are concentrated in the smaller AO8 polyhedron whereas the larger cations occupy the B site. The three crystallographically different carbonate groups are planar within the accuracy of structure refinement, C—O bonds vary from 1.268(4) to 1.294(3) Å. The δ13C and δ18O values for Cioclovina burbankite compare to other low-temperature cave carbonates, and thus clearly distinguish it from the more common burbankite occurring in igneous alkaline rocks. Precipitation of burbankite in cave settings is attributed to the reaction between percolating REEs, Sr- and Na-rich solutions and carbon dioxide, in an alkali-balanced environment, under dry and poor or no drainage conditions.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> The relationship between cave minerals and hypogene activity along the Cerna Valley (SW Romania)</title>
<link>http://scholarcommons.usf.edu/gly_facpub/95</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/95</guid>
<pubDate>Wed, 09 May 2012 10:28:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Over 100 caves are known to develop in the Jurassic and Cretaceous limestone that outcrops on both sides of the Cerna Valley in southwestern Romania. High temperature anomalies are rather uncommon in the cave environment; however, in certain caves in the lower part of Cerna Valley one can measure air temperatures as high as 40°C. This situation is due to the presence of thermal water pooling or flowing through the caves or to the hot steam that rises along fractures from deeper thermal water pools. During the long evolution of the thermo-mineral activity along the Cerna Valley interaction has occurred on a wide scale between the cave host rock or/and cave sediments and the ascending hot steam or/and thermal solutions of all types (mainly sulfide-rich). The present work documents the products of these processes and record the occurrence of twenty-four secondary cave minerals (both of primarily or replacement origin) precipitated under particular cave environments. Among these, glauberite, apjonite, halotrichite, pickeringite, rapidcreekite, tamarugite, and darapskite are the most interesting. The mineral samples were investigated by means of X-ray diffraction, electron microprobe, Fourier-transformed infrared spectroscopy, and scanning electron microscope analyses with the scope of linking the cave minerals with possible hypogene speleogenetic processes. The isotopic measurements (δ34S) performed on sulfate speleothems contribute valuable information on both minerals and caves origin. Apart from two minerals (i.e., calcite and gypsum), which were identified in every cave investigated so far, all the others fall into three distinct associations that have resulted from specific reactions under highly particular settings in Diana (sulfate-dominated association), Adam (phosphate-dominated), and Great Sălitrari (sulfate/phosphate/nitrate-rich association) caves. These three remarkable cave occurrences are presented along with morphological features that confirm the sulfidic hypogenic origin of these caves.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Tracing groundwater geochemistry using δ13C on San Salvador Island (southeastern Bahamas):  implications for carbonate hydrogeology and dissolution</title>
<link>http://scholarcommons.usf.edu/gly_facpub/94</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/94</guid>
<pubDate>Wed, 09 May 2012 10:28:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mixing dissolution is a widely accepted process of karstification on carbonate platforms, but regional differences in climate and geology indicate that a universal application of this model is insufficient to assess water– limestone interactions in more specific island settings. A two-phase study investigating d13C, carbon concentration, and other geochemical parameters took place on San Salvador Island, The Bahamas, to better understand its hydrologic characteristics and identify local controls on dissolution. In the initial phase, Crescent Pond and adjacent Crescent Top Cave, both with conduit connections to one another and to open marine water, were monitored over 1.5 normal tidal cycles and found to have little geochemical variation. Contrasting geochemical compositions between these two sites and the ocean illustrates the complexity of subsurface hydrology, while lower pH and d13CDIC values in the cave suggest the potential for bacterially mediated dissolution. The second phase included a more comprehensive geochemical survey of 12 of the island’s surface/ subsurface water bodies, and found that water geochemistry was governed primarily by connectivity to the ocean and secondarily by topographic and vegetative settings. Geochemical relationships illustrated by regression analyses showed that biologic activity exerted additional controls over water geochemistry, with photosynthesis removing biotically respired CO2 and elevating organic carbon in surface waters, while biotically respired CO2 accumulates and supports dissolution in the subsurface. These data underscore the importance of including the role of biotic processes with climate and geologic settings when identifying dissolution mechanisms and using them to estimate modern and historical dissolution processes.</p>

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</description>

<author>D K. McGee et al.</author>


</item>


<item>
<title> Speleogenesis and deposition of sediments in Cioclovina Uscata Cave, Sureanu Mountains, Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/93</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/93</guid>
<pubDate>Wed, 09 May 2012 10:28:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>The sedimentary deposits from Cioclovina Uscată Cave yielded numerous paleontological, anthropological and mineralogical findings. However, until now, a study of the sediments and their depositional features and environment had not been conducted. Here, we present a complete study of the sediments within the Main Gallery with the purpose of documenting their origin, depositional mode and processes, and direction of the paleodrainages. Seventeen sedimentary profiles were mapped and analyzed. A complete map was drawn, based on the lithological description, laboratory analyses, and the exact position of the profiles in the sedimentary deposit and their location along the gallery. Although the deposition mode of the sediments is very complex, the distribution of three main complexes (silt, sand and pebbles) can be clearly distinguished, indicating a typical cave channel lithofacies. We recognize seven stages in the evolution of the cave; the third one indicates a sudden change in the climatic conditions at the surface.</p>

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</description>

<author>A D. Häuselmann et al.</author>


</item>


<item>
<title> The mineral assemblage of caves within Şălitrari Mountain (Cerna Valley, SW Romania):  depositional environment and speleogenetic implications</title>
<link>http://scholarcommons.usf.edu/gly_facpub/92</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/92</guid>
<pubDate>Wed, 09 May 2012 10:28:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Eighteen minerals belonging to eight chemical groups were identified from three caves within Şălitrari Mountain, in the upper Cerna River basin (Romania) by means of scanning electron microscopy, electron microprobe analysis, and X-ray powder diffraction. One passage in the Great Cave from Şălitrari Mountain, the largest cave investigated, exhibits abnormal relative humidity and temperature ranges, allowing for a particular depositional environment. The cave floor is covered by alluvial sediments (ranging from cobble, sand, and clay to silt-sized material), bear bones, bat guano, and rubble. These materials reacted with percolating meteoric water and hydrogen sulfide-rich hypogene hot solutions, precipitating a variety of secondary minerals. Most of these minerals are common in caves (e.g. calcite, gypsum, brushite), however, some of them (alunite, aluminite, and darapskite) require very particular environments in order to form and persist. Cave passage morphologies suggest a complex speleogenetic history that includes changes from phreatic to vadose conditions. The latter was punctuated by a sulfuric acid dissolution/precipitation phase, partly overprinted by present-day vadose processes. The cave morphology and the secondary minerals associated with the alluvial sediments in these caves are used to unravel the region’s speleogenetic history.</p>

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</description>

<author>C M. Puscaş et al.</author>


</item>


<item>
<title> Sulfur isotopic composition and the source of dissolved sulfur species in thermo-mineral springs of the Cerna Valley, Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/91</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/91</guid>
<pubDate>Wed, 09 May 2012 10:28:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Documenting the source and processes controlling dissolved sulfur (S) mineralization in thermo-mineral waters of the Cerna Valley, Romania is important to understanding speleogenesis in this karst region, in addition to understanding hydrogeological controls, therapeutic qualities and sustainability of the region's historic spas. Stable S and carbon (C) isotopic results reported here elucidate controls on redox processes, the source of dissolved S mineralization, and sulfur-bearing mineral precipitation in this unique karst hydrothermal system. At reservoir temperatures that occur in the Cerna Valley aquifers, it is likely that thermochemical sulfate reduction (TSR) is the dominant S reduction pathway. However the apparent isotope enrichment that we observed between coexisting dissolved sulfate and sulfide is higher than normally associated with TSR—a fact that likely reflects rapid redox cycling at low grade hydrothermal temperatures. δ13C values of dissolved inorganic carbon (DIC) are consistent with TSR using methane as an electron donor. δ34S values of total dissolved S (sum of sulfide and sulfate) in all springs sampled and particularly in those for which closed-system conditions can be demonstrated, is greater than + 16‰, consistently pointing to dissolved S that derives from marine-derived sulfate mineral sources. To this combined S–C isotope data set, we apply a model of Rayleigh distillation which describes exponentially increasing δ34S values of a diminishing sulfate reservoir during TSR, and linearly decreasing δ13C values of DIC indicating mixing of C from the electron donor involved in TSR. Comparison of our results to this model shows two distinct stages of TSR during transport of fresh water from karst aquifers towards the local geothermal anomaly. In an up-gradient group of springs and wells, incomplete TSR progress that is limited by energy from electron donors is evident from: low concentrations of dissolved sulfide with low δ34S values (as low as − 21.9‰), a large balance of remaining as SO42− similar in isotopic composition to its source (∼ + 17.4‰), and δ13C values showing little methane-derived DIC. Conversely, in a downstream group of springs and wells, excess concentration of methane provides abundant energy for near-complete TSR, and this near complete reaction progress is evident from: high δ34S values of remaining SO42− (up to + 71.8‰), high dissolved sulfide concentrations (> 32 mg/L as S2−) with δ34S values that take on the approximate isotopic signature of the total dissolved S (mean + 17.4‰), and low δ13C values of additional DIC derived from methane (as low as − 30‰). Thus the unique hydrogeology of the Cerna Valley allows the observation of two end-members of TSR (energy- and sulfate-limited) demonstrating wide boundary conditions of stable isotopic composition of dissolved S and C produced by TSR in a single natural system.</p>

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</description>

<author>J G. Wynn et al.</author>


</item>


<item>
<title> Sea-level highstand 81,000 years ago in Mallorca</title>
<link>http://scholarcommons.usf.edu/gly_facpub/90</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/90</guid>
<pubDate>Wed, 09 May 2012 10:27:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Global sea level and Earth’s climate are closely linked. Using speleothem encrustations from coastal caves on the island of Mallorca, we determined that western Mediterranean relative sea level was ~1 meter above modern sea level ~81,000 years ago during marine isotope stage (MIS) 5a. Although our findings seemingly conflict with the eustatic sea-level curve of far-field sites, they corroborate an alternative view that MIS 5a was at least as ice-free as the present, and they challenge the prevailing view of MIS 5 sea-level history and certain facets of ice-age theory.</p>

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</description>

<author>J A. Dorale et al.</author>


</item>


<item>
<title> Evaluating the palaeoecological potential of pollen recovered from ice in caves:   a case study from Scărişoara,  Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/89</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/89</guid>
<pubDate>Wed, 09 May 2012 10:27:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Scărişoara Ice Cave (NW Romania) contains the world's largest underground perennial ice deposit. In this paper we present the results from pollen, micro- and macro-charcoal, and plant macrofossil investigations of a vertical ice exposure spanning the past ca. 1000 years in the Little Reservation from this cave. These results are then compared with three peat sequences close to the study area in order to evaluate the potential of using biotic remains preserved in the ice block for past vegetation, environment and climatic reconstructions. Pollen data from Scărişoara Ice Cave suggest that each impurity-poor layer is likely to include a smaller number of years, compared to organic-rich layers in which repeated, multi-annual melting events may have concentrated a higher amount of organic matter. However, layers with abundant presence of organic matter and also containing plant macro-remains, micro- and macro-charcoal particles appear to indicate a rapid wash-in of surface material into the cave. Evidence from the pollen record suggests the prevalence of close forest dominated by Fagus sylvatica between ca. AD 1200 and 1500 and by Picea abies between ca. AD 1000 and 1500 and from AD 1550 onwards. Contrary to the pollen records from the surface, the pollen assemblages from Scărişoara Ice Cave are characterized by low frequencies and diversity of pollen of herbaceous plants (non-arboreal pollen, NAP) and coprophilous spores. However, there are fluctuating frequencies in these taxa, which appear to track changes in climate conditions (higher during the Medieval Warm Period and lower during the Little Ice Age), which suggest that land-use changes were likely modulated by the climate. High amounts of micro- and macro-charcoal particles between AD 1600 and 1850, when climate conditions were cool and wet, suggests that the charcoal was washed into the cave during times of extreme rainfall events, rather than associated with increased burning regime. A comparison with pollen records from the surface shows analogous forest development and fluctuations in the NAP, therefore supporting the hypothesis that the cave ice can be a valuable paleoecological archive.</p>

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</description>

<author>A Feurdean et al.</author>


</item>


<item>
<title> The interplay between air temperature and ice mass balance changes in Scarisoara Ice Cave, Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/88</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/88</guid>
<pubDate>Wed, 09 May 2012 10:27:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper examines the short-term relations established between external and cave air temperature in Scărişoara Ice Cave (Romania) and the role they play upon ice genesis and mass balance changes. Geothermal heat and external climate are the main drivers of the cave’s air temperature, but the ice forming and ablation processes modulate its spatial and temporal characteristics. In the winter half-year, cold air inflow leads to the overcooling of the cave atmosphere and walls and ice formation; while in summer, melting of ice acts as strong thermal sink, keeping the air temperature at 0 °C. In autumn and winter, dynamic cooling of the cave atmosphere leads to ice build-up, whereas in summer, the causality is overturned, the cave air temperature being controlled by the melting ice. The existence of a net heat sink in the cave (melting ice in summer in this case), leads to the overcooling of the non-glaciated parts of the cave as well, a phenomenon that can hamper paleoclimatic reconstructions based on stable isotope studies in speleothems.</p>

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</description>

<author>A Perşoiu et al.</author>


</item>


<item>
<title> Stable isotopes behavior during cave ice formation by water freezing</title>
<link>http://scholarcommons.usf.edu/gly_facpub/87</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/87</guid>
<pubDate>Wed, 09 May 2012 10:27:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recently, a series of studies have targeted the stable isotopic composition of cave ice as a possible source of paleoclimatic information, but none presented an explanation for the way in which the external climatic signal is transferred to cave ice. While the relation between the stable isotopic composition of precipitation and drip water can be relatively easily determined, a more complex problem arises, i.e., the possible alteration of the primary climatic signal recorded by the oxygen and hydrogen stable isotopes during the freezing of water to form cave ice. Here we report the results of the first detailed investigations of the oxygen and hydrogen stable isotope behavior during the formation of ice in Scărişoara Ice Cave. Samples of ice align on a straight line with a slope lower than 8 in a δ18O-δ2H plot, characteristic for ice formed by the freezing of water. A model is presented for the reconstruction of the initial isotopic composition of water, despite the complexity induced by kinetic effects during early stages of freezing. These results are consistent with ice that forms by the downward freezing of a stagnant pool of water, under kinetic conditions in the initial stages of the process, and isotopic equilibrium thereafter. As ice caves are described in many parts of the world, otherwise poorly represented in ice-based paleoclimatology, the results of this study could open a new direction in paleoclimatic research so that an array of significant paleoclimate data can be developed on the basis of their study.</p>

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</description>

<author>A Perşoiu et al.</author>


</item>


<item>
<title> Large-scale climate anomaly patterns associated to temperature variability inside Scarisoara Ice Cave</title>
<link>http://scholarcommons.usf.edu/gly_facpub/86</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/86</guid>
<pubDate>Wed, 09 May 2012 10:27:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The relationship between temperature variability inside Scarisoara Ice Cave (NW Romania) and large-scale atmospheric circulation and sea surface temperature (SST) anomalies is investigated. A composite analysis reveals that high (low) temperatures inside the cave are associated with high (low) air temperature over a large area that covers central and Eastern Europe. Coherent large-scale patterns are identified in the field of SST anomalies. The corresponding atmospheric circulation patterns favour relatively warm (cold) air advection towards the cave region during high (low) temperatures inside the cave. A correlation analysis reveals that the atmospheric circulation patterns associated with cave temperature variability is mainly the result of the East Atlantic-Western Russia (r = −0.38) teleconnection pattern. Our results have strong implications for the interpretation of climate variability in the region as recorded by the ice block within the Scarisoara Ice Cave, which is more than 3000 years old.</p>

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</description>

<author>N Rimbu et al.</author>


</item>


<item>
<title>US-Soviet  Relations And The Nuclear strategic Factor 1945-1984: Crisis management and Confronting The Nuclear Dilemma.</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6944</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6944</guid>
<pubDate>Wed, 09 May 2012 10:27:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis explores the often-troubled relationship between the US and the USSR during the period 1945-1984. Interjected into this relationship has been a juggernaut- like nuclear strategic arms race that seemingly defies control an potentially threatens the destruction of the entire world. it has, in effect, created a mutual hostage relationship which neither superpower seems capable of resolving. Also, to be examined are the effects that possession of such nuclear weapons by the superpowers has had on the reordering of the post World War II world. Each, it will be pointed out, had its own messianic goals and negative stereotype images of the other which were characterized by high levels of fear, mistrust and misperceptions. Both superpowers have come to regard nuclear weapons not only as instruments of unimaginable mass destructive capabilities; but also as political-psychological weapons, whose threatened use alone, often-times, is sufficient to achieve certain political goals. Moreover efforts at achieving significant nuclear strategic arms control have, to date, been relatively ineffective. In the absence of such agreements, crisis management principles continue to be stresses in order to avoid any destabilizing superpower confrontation. Time, however, is running out. The US and the USSR must choose to accept mutual co-existence and significant nuclear strategic arms control or face the danger of worldwide nuclear annihilation. A political solution is deemed to be the only way out of this grave problem. Potentially, complex computers and telecommunications networks threaten to usurp control over their nuclear deterrents. The study argues that absolute control must remain in the hands of he respective national political leaders.</p>

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</description>

<author>Ken Robertson</author>


</item>


<item>
<title> Tracing the sources of cave sulfates:   a unique case from Cerna Valley,  Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/85</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/85</guid>
<pubDate>Wed, 09 May 2012 10:27:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>In order to reliably distinguish between different genetic processes of cave sulfate formation and to quantify the role of thermo-mineral waters on mineral deposition and cave morphology, it is critical to understand sulfur (S) sources and S transformations during hydrological and speleogenetic processes. Previous work has shown that sulfuric acid speleogenesis (SAS) often produces sulfate deposits with 34S-depleted isotopic signatures compared to those of the original source of S in sulfate rocks. However, 34S-depleted isotopic composition of S-bearing minerals alone does not provide enough information to clearly distinguish SAS from other speleogenetic processes driven by carbonic acid, geothermal heat, or other processes. The isotopic composition (δ18O and δ34S) of sulfate minerals (mainly gypsum) from seven caves of the Cerna Valley (Romania) defines three distinct populations, and demonstrates that the δ34S values of SAS-precipitated cave sulfates depend not only on the source of the S, but also on the H2S:SO42− ratio during aqueous S species reactions and mineral precipitation. Population 1 includes sulfates that are characterized by relatively low δ34S values (− 19.4 to − 27.9‰) with δ18O values between 0.2 and 4.3‰ that are consistent with oxidation of dissolved sulfide produced during methane-limited thermochemical sulfate reduction (TSR) that presently characterizes the chemistry of springs in the upper Cerna Valley. Population 2 of cave sulfates has 34S-enriched δ34S values (14.3 to 19.4‰) and more 18O-depleted δ18O values (from − 1.8 to − 10.0‰). These values argue for oxidation of dissolved sulfide produced during sulfate-limited TSR that presently characterizes the chemistry of springs further downstream in the Cerna Valley. The δ18O values of cave sulfates from Population 1 are consistent with oxidation under more oxic aqueous conditions than those of Population 2. δ34S values of cave sulfates within Population 3 (δ34S: 5.8 to 6.5‰) may be consistent with several scenarios (i.e., pyrite oxidation, oxidation of dissolved sulfide produced during methane-limited TSR coupled with O2-limited oxidation during SAS). However, comparatively 18O-enriched δ18OSO4 values (11.9 to 13.9‰) suggest the majority of this sulfate O was derived from atmospheric O2 in gas-phase oxidation prior to hydration. Thus, the combined use of oxygen- and sulfur-isotope systematics of sulfate minerals precipitated in a variety of cave settings along Cerna Valley may serve as an example of how more complex cave systems can be deconvoluted to allow for more complete recognition of the range of processes and parameters that may be involved in SAS.</p>

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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Decoding last interglacial sea-level variations in the Western Mediterranean using speleothem encrustations from coastal caves in Mallorca and Sardinia:   A field data - model comparison</title>
<link>http://scholarcommons.usf.edu/gly_facpub/84</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/84</guid>
<pubDate>Wed, 09 May 2012 10:27:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>P Tuccimei et al.</author>


</item>


<item>
<title> Cryogenic cave pearls in the periglacial zone of ice caves. Journal of Sedimentary Research (in review)</title>
<link>http://scholarcommons.usf.edu/gly_facpub/83</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/83</guid>
<pubDate>Wed, 09 May 2012 10:27:40 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K Zak et al.</author>


</item>


<item>
<title> Caves of Romania. A worthy treasure / Peşteri din România </title>
<link>http://scholarcommons.usf.edu/gly_facpub/82</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/82</guid>
<pubDate>Wed, 09 May 2012 10:27:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B P. Onac</author>


</item>


<item>
<title> Ponor Plateau (south-eastern Plopis Mountains)</title>
<link>http://scholarcommons.usf.edu/gly_facpub/81</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/81</guid>
<pubDate>Wed, 09 May 2012 10:27:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>I Gabrian et al.</author>


</item>


<item>
<title> The hydrogeology of Cuciulat-Purcaret-Boiu Mare karst area, northern part of the Somes Plateau, Romania</title>
<link>http://scholarcommons.usf.edu/gly_facpub/80</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/80</guid>
<pubDate>Wed, 09 May 2012 10:27:33 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Ice in Caves</title>
<link>http://scholarcommons.usf.edu/gly_facpub/79</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/79</guid>
<pubDate>Wed, 09 May 2012 10:27:30 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>A Persoiu et al.</author>


</item>


<item>
<title> Minerals</title>
<link>http://scholarcommons.usf.edu/gly_facpub/78</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/78</guid>
<pubDate>Wed, 09 May 2012 10:27:27 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B P. Onac</author>


</item>


<item>
<title> Archives of Climate Change in Karst</title>
<link>http://scholarcommons.usf.edu/gly_facpub/77</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/77</guid>
<pubDate>Wed, 09 May 2012 10:27:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Scărişoara</title>
<link>http://scholarcommons.usf.edu/gly_facpub/76</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/76</guid>
<pubDate>Wed, 09 May 2012 10:27:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title> Atlasul pesterilor din Munții Apuseni. Munții Bihor - 1. Bazinul Arieșului Mare</title>
<link>http://scholarcommons.usf.edu/gly_facpub/75</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/75</guid>
<pubDate>Wed, 09 May 2012 10:27:19 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B P. Onac et al.</author>


</item>


<item>
<title>Book Review. The Supreme Court and Constitutional Theory: 1953-1993</title>
<link>http://www.repository.law.indiana.edu/facpub/532</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/532</guid>
<pubDate>Wed, 09 May 2012 10:16:18 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Donald H. Gjerdingen</author>


</item>


<item>
<title>Developments in the Law of Evidence</title>
<link>http://www.repository.law.indiana.edu/facpub/531</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/531</guid>
<pubDate>Wed, 09 May 2012 10:16:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this Article is to alert Indiana practitioners to significant 1991 developments in the law of evidence. The Article first discusses Indiana developments. It then briefly highlights Seventh Circuit and United States Supreme Court decisions of note.</p>

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</description>

<author>Sophia Goodman et al.</author>


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<item>
<title>Equitable Discretion to Dismiss Congressional-Plaintiff Suits: A Reassessment</title>
<link>http://www.repository.law.indiana.edu/facpub/530</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/530</guid>
<pubDate>Wed, 09 May 2012 10:16:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>The United States Court of Appeals for the District of Columbia Circuit has devised a doctrine called equitable <br>discretion to screen congressional-plaintiff suits. The Author argues that the doctrine should be abandoned. She proposes that the courts be guided by existing standng principles in deciding whether to hear these cases.</p>

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</description>

<author>Sophia Goodman</author>


</item>


<item>
<title>Personality and Positive Psychology in Social Media and Post-Secondary Education</title>
<link>http://digitalcommons.mcmaster.ca/cmst_grad_research/12</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/cmst_grad_research/12</guid>
<pubDate>Wed, 09 May 2012 10:10:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study combines the fields of communication studies and psychology in order to determine the relationship between personality type, academic background, and social media content. Ten participants from each of McMaster University’s seven undergraduate faculties completed a Myers-Briggs Type Indicator (MBTI) to determine their personality type, and submitted 10 personally written status updates or comments from the social media platforms of Twitter or Facebook. The Content Analysis of Verbatim Explanation (CAVE) method was used to analyze 630 social media content to determine overall positive or negative explanatory style.</p>
<p>The dominant personality types at McMaster University as determined by the 70 participants are: INFP, ENFJ, and ISTJ. In type preference it was found that 68% of the participants prefer the attitude of Introversion (I), 70% prefer the perceptive function of Intuition (N), 54.3% prefer the judging function of Thinking (T), and 61.4% prefer the orientation of Judging (J). The following personality preferences were found to be correlated with the CAVE’s explanatory dichotomies: Internal/External with Sensing (S) / Judging (J), Stable/Unstable with Extraversion (E) / Sensing, Global/Specific with Sensing/Thinking, and Controllable/Uncontrollable with Sensing.</p>
<p>Of the 630 submitted social media content, 68.4% of them were found describing positive events. It was found that 92.1% of the social media content contained an optimistic explanatory style. These findings strongly suggest that the majority of content written and uploaded on social media is positive and that personality type plays a minor role in content and explanations produced. It is concluded from these results that social media is an inherently positive medium for university students. The primary reason for this is believed to be a result of social media being an immensely public sphere forcing all individuals, regardless of personality type, to engage in higher levels of self-monitoring.</p>

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</description>

<author>Dustin P. Manley</author>


</item>


<item>
<title>Questionable Coverage: Canadian Online News Media And The Representation Of The Oil Sands</title>
<link>http://digitalcommons.mcmaster.ca/cmst_grad_research/11</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/cmst_grad_research/11</guid>
<pubDate>Wed, 09 May 2012 10:10:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Some of the most pressing environmental issues, such as climate change and global warming, have been discussed, examined and contested in online news media. However, little research has been completed on the reporting styles of Canadian media, and in particular, Canadian online news media’s coverage of the oil sands. This paper examines media content and discusses the concept of media bias by examining the differences in reporting styles of the online formats of the CBC, the National Post, and The Globe and Mail, and discusses to what degree these news websites are providing balanced coverage from an environmental point of view. Through a content analysis of a collection of news articles, this study allows for an in-depth examination of which oil sands voices, such as oil companies, and environmental or government organizations, for example, are given a balanced amount of coverage. The study finds that stories on the oil sands are very limited and that there are a number of different news frames that are missing from the coverage, including the oil sands’ potential harm to humans and wildlife. The oil sands have become a pressing issue for Canadian oil companies, environment groups, and oil consumers, and as the sands continue to take a large toll on the environment, the sands will only become more contested and questioned.</p>

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</description>

<author>Josh Willard</author>


</item>


<item>
<title>The Polish Baptist Identity in Historical Context</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6943</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6943</guid>
<pubDate>Wed, 09 May 2012 09:52:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jerzy Rogaczewski</author>


</item>


<item>
<title>An Experiment on the Effect of Construal Level and Small Wins Framing on Environmental Sustainability Goal Commitment</title>
<link>http://digitalarchive.gsu.edu/bus_admin_diss/5</link>
<guid isPermaLink="true">http://digitalarchive.gsu.edu/bus_admin_diss/5</guid>
<pubDate>Wed, 09 May 2012 09:52:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Companies are under increasing pressure from every category of stakeholder, from government and community to supply chain and consumer, to improve the environmental sustainability of their operations, products and services.  To be most successful with environmental sustainability improvement initiatives, a company must have the commitment and effort of its employees.  The purpose of this research is to study the effect of the company’s approach to the initiative on the level of employee commitment to the company’s environmental sustainability goals.</p>
<p>This research was conducted with a two-factor, factorial experiment.  The experimental factors were construal level and small wins framing.  Each of these factors had two levels, creating a 2x2 design with four treatment level combinations.  A third study factor was environmental concern.  Four other variables, goal difficulty, perceived organizational efficacy, gender and age, were included in the model as control variables.  The dependent variable was goal commitment.  Approximately 150 participants were recruited for the experiment and randomly assigned to one of the four fixed, treatment combinations.  Hierarchical regression was used to estimate the factors’ main and interaction effects, as well as the significance of the control variables.</p>
<p>Neither of the two manipulated variables, construal level and small wins, was found to have a significant main effect on goal commitment. There were, however, significant interactions between environmental concern and construal level, and between environmental concern and small wins framing, on goal commitment.   At high levels of environmental concern, the effects of construal level and small wins were as hypothesized, but at low levels of environmental concern, the effects of construal level and small wins were opposite of what was expected.  Additionally, both organizational efficacy and gender were found to significantly affect one’s goal commitment.</p>

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</description>

<author>James O&apos;Connor</author>


</item>


<item>
<title>The Effect Of Organizational Knowledge Creation On Firm Performance:  An Operational Capabilities-Mediated Model</title>
<link>http://digitalarchive.gsu.edu/bus_admin_diss/4</link>
<guid isPermaLink="true">http://digitalarchive.gsu.edu/bus_admin_diss/4</guid>
<pubDate>Wed, 09 May 2012 09:52:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>What operational factors can explain the performance differences between manufacturing firms?  Scholars have produced a significant volume of research that examines the linkages between operational factors (resources and practices) and firm performance. There is agreement that organizational capabilities mediate the relationship between operational factors and firm performance. However, due to the numerous and sometimes contradictory definitions of organizational capabilities in the literature and because organizational capabilities includes non-operational factors, it has been suggested that operational capabilities, as a sub construct of organizational capabilities, is more appropriate for establishing an empirical relationship between operational factors and firm performance. Scholars have argued that process improvement practices facilitate the development of operational capabilities, which can consequently lead to improved firm performance. Other scholars have argued that process improvement practices facilitate organizational knowledge creation, which can also influence firm performance. We integrate these two theoretical perspectives into a single conceptual model that better explains the relationship between knowledge-creating practices and firm operational performance. Specifically, we argue that knowledge-creating practices play a significant role in developing a firm’s operational capabilities, which in turn, influence firm operational performance. This research investigates the existence of a relationship between organizational knowledge creation and firm operational performance that is mediated by operational capabilities.</p>

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</description>

<author>Michael S. Jordan</author>


</item>


<item>
<title>Effect of Nitrogen Fertilizer Rate and Harvest Season on Forage Yield, Quality, and Macronutrient Concentrations in Midland Bermuda grass</title>
<link>http://digitalcommons.unl.edu/agronomyfacpub/555</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/agronomyfacpub/555</guid>
<pubDate>Wed, 09 May 2012 09:51:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bermuda grass [<em>Cynodon dactylon</em> (L.) Pers.] is a major forage for grazing and hay production in the southern United States. The objectives of this study were to determine effects of nitrogen (N) fertilization rate (0, 112, 224, 336, and 448 kg ha<sup>−1</sup>), split spring and summer applications of N at the 224 and 448 kg ha<sup>−1</sup> rates, and harvest periods (spring and summer) on forage yield, crude protein (CP), acid detergent fiber (ADF), neutral detergent fiber (NDF), total digestible nutrients (TDN), and concentrations of phosphorus (P), potassium (K), magnesium (Mg), and calcium (Ca) in Midland Bermuda grass. Data were collected from 2002 to 2008 as part of an ongoing, long-term soil fertility experiment in southern Oklahoma. Repeated measures analysis of these long-term data showed that forage yield responses to N rate varied with year and harvest time with up to 2.5-fold yield differences among years. Nitrogen fertilization increased CP, TDN, and macronutrient P and Mg and decreased ADF and NDF. Crude protein was increased by ≥50%, and ADF and NDF dropped by up to 25% with the greatest N rate. In general, split N applications did not affect forage yield but produced low-quality forage compared to single N application in spring. Split application of 448 kg N ha<sup>−1</sup> gave forage with CP, TDN, ADF, and NDF similar to the Bermuda grass receiving 336 or 448 kg N ha<sup>−1</sup> as a single application. Spring forage had better forage quality than summer harvests. While N fertilization increased forage Mg and P concentrations by more than 50% during both spring and summer, it had no effect or slight increased K and Ca concentrations. In the southern Great Plains, despite the weather-dependent variability in forage yield of Bermuda grass, N application increase forage quality.</p>

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</description>

<author>Maru K. Kering et al.</author>


</item>


<item>
<title>Alice in Wonderland</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/24</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/24</guid>
<pubDate>Wed, 09 May 2012 09:51:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>A puzzle.</p>

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</description>


</item>


<item>
<title>Instructions to Authors</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/23</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/23</guid>
<pubDate>Wed, 09 May 2012 09:51:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Instructions to authors wishing to contribute to Word Ways.</p>

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</description>


</item>


<item>
<title>Answers and Solutions</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/22</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/22</guid>
<pubDate>Wed, 09 May 2012 09:51:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Answers and solutions to the puzzles and games contained in this issue.</p>

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</description>


</item>


<item>
<title>Some New Results on King- and Queen- Graphable Words</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/21</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/21</guid>
<pubDate>Wed, 09 May 2012 09:51:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>A word (or phrase, sentence, etc.) is said to be <em>king-graphable</em> (KG) if each of its distinct letters can be placed on a square of an infinite chessboard such that the entire word or pharase can be spelled out by starting on the first letter and making only the moves of a chess king to get from letter to letter.</p>

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</description>

<author>Mike Keith</author>


</item>


<item>
<title>Punk Whiz 18</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/20</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/20</guid>
<pubDate>Wed, 09 May 2012 09:51:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>More pun quiz misdefinitions.</p>

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</description>

<author>. Anil</author>


</item>


<item>
<title>Statue of Limitations</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/19</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/19</guid>
<pubDate>Wed, 09 May 2012 09:50:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>More funny bloopers and witty retorts.</p>

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</description>

<author>Don Hauptman</author>


</item>


<item>
<title>Funny Words 4</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/18</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/18</guid>
<pubDate>Wed, 09 May 2012 09:50:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>No abstract available.</p>

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</description>

<author>. Anil</author>


</item>


<item>
<title>Exchanging Antonyms</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/17</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/17</guid>
<pubDate>Wed, 09 May 2012 09:50:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Antonyms have long been favourites of the readers of Word Ways, either as themselves (ODD-EVEN) or in disguise. In the latter case, they may be hidden in other word pairs such as in <strong>FAT</strong>E - <strong>THIN</strong>E, SH<strong>IN</strong> - SH<strong>OUT</strong> and B<strong>AND</strong>ED -B<strong>OR</strong>ED where they occur at the beginnings, ends and in the middles of the word pairs respectively, <strong>the other letters remaining the same. </strong></p>

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</description>

<author>Susan Thorpe</author>


</item>


<item>
<title>Tripartitle Numerical Tautonyms</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/16</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/16</guid>
<pubDate>Wed, 09 May 2012 09:50:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>A numerical tautonym is traditionally defined as a word which can be divided into a sequence of at least two (adjacent) parts, where each part has both the same number of letters as well as the same alphabetic value sum (see David Morice, <em>The Dictionary of Wordplay</em>).  For example, the four letters in the word THIS can be transposed into the corresponding numbers 20-8-9-19 (where A = 1, B = 2...Z = 26), which can be divided in the two parts 20-8 and 9-19.  If the numbers in the first part are added together, then we obtain 28, which is precisely the sum of the two numbers in the second part.  Note that the two-part numerical tautonym THIS is 'balanced' in two respects:  The numerical value of each of the two parts is identical, as is the number of letters in each part.</p>

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</description>

<author>T.A. Hall</author>


</item>


<item>
<title>Book Review - Steven Kahan</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/15</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/15</guid>
<pubDate>Wed, 09 May 2012 09:50:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>A book review of <em>You Can Take My Word For It: Another Sixty Adventures in Logology For the Connoisseur</em> by Steven Kahan (Esskay Publishing Company, Hollis Hills, New York 2012).</p>

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</description>

<author>Karen Farrell</author>


</item>


<item>
<title>An Alice Puzzle</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/14</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/14</guid>
<pubDate>Wed, 09 May 2012 09:50:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>I have been sitting in on an honor's class about Lewis Carroll being taught this spring semester at my old college haunt Butler University in Indianapolis.  Among the many new puzzles and games being introduced in the class I offer the following based on the ten different letters in "Alice in Wonderland". These ten are ALICE and DROWN, perhaps referring the the 2nd Wonderland chapter "A Pool of Tears" where Alice thought she might drown in her own tears.</p>

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</description>

<author>Oscar Thumpbindle</author>


</item>


<item>
<title>Anagram Quiz 6</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/13</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/13</guid>
<pubDate>Wed, 09 May 2012 09:50:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>No abstract available.</p>

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</description>

<author>. Anil</author>


</item>


<item>
<title>Kickshaws</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/12</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/12</guid>
<pubDate>Wed, 09 May 2012 09:50:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>A collection of linguistic kickshaws.</p>

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</description>

<author>David Morice</author>


</item>


<item>
<title>More Martin Magic</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/11</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/11</guid>
<pubDate>Wed, 09 May 2012 09:50:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Martin is Martin Gardner of course and the magic is his "The 3-by-3 Matix" which first appeared in <em>Scientific American</em> (August, 1966) and is reprinted in his <em>Martin Gardner Presents</em>, 1993, Kaufman and Greenburg, p.149.  Word Ways subscriber Max Maven has written a fine introduction to this book and has himself developed a new version of  the effect.</p>

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</description>

<author>Jeremiah Farrell</author>


</item>


<item>
<title>Crossword</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/10</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/10</guid>
<pubDate>Wed, 09 May 2012 09:50:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>A crossword puzzle.</p>

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</description>

<author>Derrick Niederman</author>


</item>


<item>
<title>This Rugged World</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/9</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/9</guid>
<pubDate>Wed, 09 May 2012 09:50:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>A poem.</p>

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</description>

<author>Sir Jeremy Morse</author>


</item>


<item>
<title>Typoclycemic Anaphoric Verse</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/8</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/8</guid>
<pubDate>Wed, 09 May 2012 09:50:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Anaphoric verse - a term taken from the word 'Anaphora' - is poetry that involves the "repetition of a word at the beginning of successive utterances," Motte 2007 pp. 209. Inspired by the power that such technique lends to a text, each repetition potentially a reiteration, I sought to employ it with a further constraint that I believed would serve to even better illustrate the anophora's potential for stern, powerful imagery through accretion.</p>

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</description>

<author>Dave Drayton</author>


</item>


<item>
<title>Hebrew or Japanese?</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/7</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/7</guid>
<pubDate>Wed, 09 May 2012 09:50:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>1. INTRODUCTION</p>
<p>It is quite common that, for any two languages, there will be words that look or sound alike, but with different meanings.  French words that look like English words but with different meanings in the two languages are called <em>faux amis</em> ("false friends").  In some cases they are from unrelated roots (e.g. French <em>pain</em> means "bread" and <em>rue</em> means "street".  In other cases, words that began the same evolved different meanings. From its Latin roots, <em>concurrence</em> basically means "running along side of", which in English came to mean "agreement", but in French it means "competition."</p>

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</description>

<author>Solomon W. Golomb</author>


</item>


<item>
<title>Gerunding</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/6</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/6</guid>
<pubDate>Wed, 09 May 2012 09:50:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>A Poem</p>

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</description>

<author>Ron Singer</author>


</item>


<item>
<title>Spanning the Globe With Scrabble Tiles</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/5</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/5</guid>
<pubDate>Wed, 09 May 2012 09:50:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Here is a puzzle that's simple to state but not so easy to solve.  Take a set of English Scabble tiles with its standard complement of 98 letters and two blanks (that can be used to stand for any letter).  Use all 100 tiles to make a list of names of countries in the world, all different.  For the acceptable list of country names use the current list of 192 member states of the United Nations.</p>

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</description>

<author>Mike Keith</author>


</item>


<item>
<title>Colloquy</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/4</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/4</guid>
<pubDate>Wed, 09 May 2012 09:50:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>A collection of responses to previously published articles.</p>

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</description>


</item>


<item>
<title>Banananames</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/3</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/3</guid>
<pubDate>Wed, 09 May 2012 09:50:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Words like LOGOLOGICAL, which alternate vowels and sonsonanats could use a succinct name. David Morice's <em>The Dictionary of Word Play</em> cites them only with reference to numbers, as "alternating vowel-consonant number name", a wordful description rather than a handy name.  May we suggest "banananames", in the spirit of Agamemnon, Albuquerque and Miami words which are named after prime examples.</p>

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</description>

<author>. Anil et al.</author>


</item>


<item>
<title>Party Smarty</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/2</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/2</guid>
<pubDate>Wed, 09 May 2012 09:50:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>A Poem.</p>

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</description>

<author>Martin Gardner</author>


</item>


<item>
<title>Front Cover and Publication Information, Volume 45, Number 2</title>
<link>http://digitalcommons.butler.edu/wordways/vol45/iss2/1</link>
<guid isPermaLink="true">http://digitalcommons.butler.edu/wordways/vol45/iss2/1</guid>
<pubDate>Wed, 09 May 2012 09:50:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Front cover and publication information for this issue.</p>

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</description>


</item>


<item>
<title>Journaling as a Test Preparatory Measure in Secondary Mathematics: Successful Student Strategies</title>
<link>http://digitalcommons.cedarville.edu/education_theses/15</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/15</guid>
<pubDate>Wed, 09 May 2012 09:37:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study examines a math journal writing assignment comparing how high school (grades 10 through 12) algebra students who performed well and students who performed poorly on traditional mathematics tests constructed their corresponding journal entries. Statistically significant differences found indicated that students who performed well on the tests were more likely to have originally composed the text and examples in their journal entries, and students who performed poorly were more likely to have copied much of the mathematical language and examples in their journal entries from their textbooks. Students who performed well on the test were also more likely to include examples accompanied by explanation for each step toward a solution. An assignment involving several such explanatory examples could perform a same or similar function as the longer journal assignment examined in this study.</p>

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</description>

<author>Lloyd E. Nickerson II</author>


</item>


<item>
<title>Negotiating Federalism: State Bargaining and the Dormant Treaty Power</title>
<link>http://scholarship.law.gwu.edu/faculty_publications/9</link>
<guid isPermaLink="true">http://scholarship.law.gwu.edu/faculty_publications/9</guid>
<pubDate>Wed, 09 May 2012 09:36:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The orthodox view that states have no role in U.S. foreign relations is not only inconsistent with their place in the modern global economy, but the constitutional basis for a "dormant" bar on state participation - that is, absent a controlling federal statute or treaty - is obscure. Revisionist scholarship, and recent Supreme Court case law, suggest that Congress alone should decide when the states must stay out of foreign relations.</p>
<p>In this article, I argue that both the orthodox and revisionist views neglect an alternative basis for a judicial role - the Treaty Clause, enforced through the dormant treaty power. The text, structure, and original understanding of the treaty power establish two important principles of continuing validity. First, the President was to have an independent and substantive authority to negotiate on behalf of the United States, the better to secure advantageous treaties and avoid perilous entanglements. Second, state interference with this negotiating authority, even prior to the conclusive adoption of a federal treaty or statute, was unlawful.</p>
<p>Treaty Clause exclusivity is best maintained by a judicially-enforced dormant treaty power barring the states from bargaining with foreign powers, including indirect bargaining through measures that are contingent on foreign government policies - such as the Massachusetts law targeting companies doing business with Burma. However, state activities that incidentally have effects overseas would not be precluded, and the jurisprudence must be informed by the original rationales for federal exclusivity and by the President's discretion to exempt state activities posing no threat to federal functions.</p>

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</description>

<author>Edward T. Swaine</author>


</item>


<item>
<title>SEX DETERMINATION AND AGE ESTIMATION: SKELETAL EVIDENCE FROM ST. THOMAS&apos; CEMETERY BELLEVILLE, ONTARIO</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6942</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6942</guid>
<pubDate>Wed, 09 May 2012 09:30:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>The precision and accuracy of 17 pelvic an 17 cranial features commonly used to assess adult skeletal sex and three systems of adult pelvic age estimation were tested on a sample of 278 individuals from the 19th century St. Thomas' Anglican church Cemetery in Belleville, Ontario. Documentation in the form of parish burial, marriage and baptismal records exists for the entire cemetery, but only fifty-five individuals over 17 years  of age are personally identified. Both the pelvic an cranial methods of morphological sex determination produce sex ratios indistinguishable from the documented ratio. on a individual basis, the precision and accuracy of the pelvic approach is superior to that of the cranial approach. The most reliable and accurate pelvic results may be obtained from an examination of the following six criteria: ventral arc, obturator foramen, true pelvis shape, sacrum shape, subpubic concavity and pubis shape. the following eight cranial criteria produced the least amount of intraobserver error and the greatest degree of accuracy: superaorbital ridges, mastoid size, malar size and shape, occipital markings, chin form, general size, zygomatic root extension and mandible shape. Three features, posterior view of the sacrum, zygomatic root extension and occipital muscle markings, exhibit increases accuracy with age. There is no age-related affect on accuracy when the complete trait lists are employed. Pelvic assessments appear to be biased in favour of males while cranial assessments seem biased in favour of females. Of the Phenice (1969) criteria, the ventral arc is the single most useful trait exhibiting both high precision (0% intraobserver error) and high accuracy (86.9%). The subpubic concavity ranked second and the ischiopubic ramus last. None of the age techniques examined in this investigation are precise and accurate enough to be employed exclusive of other systems. When both precision and accuracy are taken into account, the auricular surface technique of estimating skeletal age-at-death produces the best results for individual cases. One major problem with this method is its tendency to overage individuals less than 40 years and underage indviduals greater than 40 years. The accuracies of the Suchey methods are acceptable mainly ecause of the wide age ranges covered by each phase. The estimates provided by these methods are too broad to be useful in individual cases. When used to produce an age profile the Suchey systems (with the Jackes (1985) distribution method) are better than the auricular surface method. The pattern is slightly distorted by problems associated with phases  III (2), IV (1) and IV.</p>

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</description>

<author>Tracy Rogers</author>


</item>


<item>
<title>Finite Element Modeling of Full Depth Precast Concrete Bridge Deck Connections in Bending and Shear</title>
<link>http://digitalcommons.usu.edu/gradreports/128</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/128</guid>
<pubDate>Wed, 09 May 2012 09:28:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The need for reduced construction times of highway bridges has become more important recently. Precast concrete panels used for the bridge deck replacements are being used more frequently in order to achieve this reduced construction time and to also reduce the cost of the construction. Bridges can also be repaired quickly and with less cost if individual panels can be replaced when needed instead of replacing the entire bridge deck. The problem at hand is the structural integrity of these individual precast bridge deck panels. The joints in-between these panels often crack due to service stresses. These cracks expose the steel in the deck and lead to corrosion of the girders. Various transverse connections have been tested at Utah State University to address this problem. These tested connections supply post-tensioning of the panels along the joints to reduce cracking and increase flexural and shear capacity. Among these tested connections include the standard Utah Department of Transportation connections. Also several variations of a curved bolt connection have been tested. To further analyze these connections and compare with the laboratory test results, finite element models were created using the finite element software ANSYS. The finite element models were used to create load-deflection curves and figures to show failure. These were compared with the results from the laboratory testing. The finite element analyses and laboratory testing produced similar results. The new curved strand method tested in this research was found to be more satisfactory than the old curved bolt method.</p>

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</description>

<author>Patrick H. James</author>


</item>


<item>
<title>Development of Methods for Assessing the Effect of Moisture and Aging On Sliceability of Cheese</title>
<link>http://digitalcommons.usu.edu/gradreports/127</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/127</guid>
<pubDate>Wed, 09 May 2012 09:28:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sliceability is a cheese’s ability to cut cleanly into thin slices, resist breakage or fracture at slices edges, and undergo a high level of bending before breaking. Intuitively, sliceability depends on the chemistry, microstructural, and rheological properties of the casein network. Currently there is no reported scientific research investigating evaluation methods of cheese slice quality, as well as properties that influence a cheese’s ability to slice. In this study, a method for slice quality evaluation was developed on purchased cheese and performed on commercial cheeses and experimental cheeses manufactured at three different moisture contents (40.6%, 37.0%, and 33.9%). In addition, tack force, tack energy, flexibility force, G’, G”, and G* were examined to determine whether or not moisture content influences cheese sliceability. Overall, slice quality at all three moisture contents improved as storage time increased, and the high moisture cheeses produced the worst quality slices and the low moisture cheeses produced the best. Both tack energy and tack force increased with increasing moisture content, and G’, G”, and G* decreased This work made publicly available electronically on May 9, 2012. with increasing moisture and did not change over time. Tack energy and G” were found to be slightly correlated with cheese slice quality. Flexibility force was not correlated with cheese slice quality. Moisture and storage time, as well their interaction, had significant effects on dependent variables, potentially indicating that a higher moisture cheese texture changes differently compared to medium and low moisture cheeses during storage. Correlation tests did not express a strong connection between moisture content, age, and cheese slice quality, overall. This research lays the foundation for future slice quality evaluation, and is a starting point upon which other companies and scientists can build.</p>

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</description>

<author>Jess Renee Perrie</author>


</item>


<item>
<title>Preschool Nutrition Education and Influence On Food Neophobia</title>
<link>http://digitalcommons.usu.edu/gradreports/126</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/126</guid>
<pubDate>Wed, 09 May 2012 09:28:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Food neophobia, the fear of new foods, has been identified as a significant barrier to the intake of healthy foods, including fruits and vegetables in young children. Food neophobia can hinder dietary quality as well as dietary variety by limiting the development of food preferences. It has also been suggested that neophobia is linked to the development of childhood obesity, and due to the escalating epidemic of childhood obesity that is known to be associated with serious health complications, interventions that target food neophobia in preschool aged children may be successful in improving healthy eating habits and potentially reversing the obesity trend.</p>
<p>This thesis includes data collected from the testing of an interactive nutrition education curriculum, Food $ense Kids, that specifically targeted neophobia in 3 to 5-year-old children. It was implemented at two child care facilities using baseline and post-intervention surveys and included 51 participants. The curriculum was evaluated on its ability to engage children, be effective across multiple settings, and be easily implemented into a variety of preschool programs. The curriculum was also examined to determine its influence on food neophobia, food knowledge, and food preferences when implemented in its entirety.</p>
<p>Results indicate that the curriculum was engaging, equally effective across multiple settings, and easily implemented into a variety of programs. In addition, teachers were positive about the program and its effect on their students. Food knowledge increased significantly as a result of participation in the program at both facilities. Overall, no significant changes in neophobia or food preferences occurred as a result of participation in the curriculum. This lack of impact may be explained by not including multiple exposures to each food. Future application of the Food sense Kids curriculum could include selecting a smaller number of lessons from the overall curriculum to implement over time in order to include multiple exposures to each food, which may lead to beneficial effects on food neophobia and food preferences.</p>

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</description>

<author>Kelsey Eller</author>


</item>


<item>
<title>Effect of Orifice Shape on Synthetic Jet Efficiency</title>
<link>http://digitalcommons.usu.edu/gradreports/125</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/125</guid>
<pubDate>Wed, 09 May 2012 09:28:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>David J. Nani</author>


</item>


<item>
<title>A Novel and Effective Short Track Speed Skating Tracking System</title>
<link>http://digitalcommons.usu.edu/gradreports/124</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/124</guid>
<pubDate>Wed, 09 May 2012 09:28:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation proposes a novel and effective system for tracking high-speed skaters. A novel registration method is employed to automatically discover key frames to build the panorama. Then, the homography between a frame and the real world rink can be generated accordingly. Aimed at several challenging tracking problems of short track skating, a novel multiple-objects tracking approach is proposed which includes: Gaussian mixture models (GMMs), evolving templates, constrained dynamical model, fuzzy model, multiple templates initialization, and evolution. The outputs of the system include spatialtemporal trajectories, velocity analysis, and 2D reconstruction animations. The tracking accuracy is about 10 cm (2 pixels). Such information is invaluable for sports experts. Experimental results demonstrate the effectiveness and robustness of the proposed system.</p>

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</description>

<author>Yuxuan Wang</author>


</item>


<item>
<title>Ethnic Disparities in Prenatal Care Utilization in Vietnam</title>
<link>http://digitalcommons.usu.edu/gradreports/123</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/123</guid>
<pubDate>Wed, 09 May 2012 09:28:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Prenatal care is credited with reducing neonatal, perinatal, and maternal mortality and morbidity. The main purpose of the thesis is to examine the ethnic disparities between majority and ethnic minority women in prenatal care usage. The thesis also analyzes the effects of age, education attainment, female employment, and region on prenatal care utilization in Vietnam. I employ the Demographic and Health Survey 2002 in Vietnam. Descriptive statistic and logistic regression are the two statistical tests employed in this research. Results exhibit evidence of ethnic disparities in type of prenatal care utilization. Although ethnic minority women are likely to enter prenatal checkups at the same time as ethnic majority women, they are less likely to receive three or more prenatal checkups. Ethnic minority women are also less likely to receive prenatal checkups from professionals. When giving birth, minority women are less likely to deliver with a professional birth attendant, in a hospital or health facility. When controlling for other independent variables, education attainment and region show significant effects on prenatal care usage. Uneducated women, or women with less than secondary education, and women residing outside the Red River Delta consumed less professional prenatal care usage.</p>

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</description>

<author>Ha Ngoc Trinh</author>


</item>


<item>
<title>The Effectiveness of an Adapted SNAP-Ed (Supplemental Nutrition Assistance Program-Education) Curriculum for Adults with Intellectual or Developmental Disabilities</title>
<link>http://digitalcommons.usu.edu/gradreports/122</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/122</guid>
<pubDate>Wed, 09 May 2012 09:28:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rates of overweight and obese adults with intellectual or developmental disabilities in the United States are high and associated with increased risk of chronic diseases. Many of these adults are trying to become more independent in the community and live in group homes where care is managed by a paid employee. Group home managers assist clients with daily living such as shopping and meal preparation and play an important role in their care. Nutrition and healthy behavior choices are important to help keep this population independent and decrease risks of excess weight and related diseases. Many group home managers and clients have limited nutrition knowledge. Few nutrition education programs are available to either group home managers or their clients.</p>
<p>This study adapted a Supplemental Nutrition Assistance Program-Education (SNAP-Ed) curriculum to teach adults with intellectual or developmental disabilities living in group homes. SNAP-Ed is a government food assistance program targeted at providing basic nutrition education to low-income persons. The study’s objectives were to develop, implement, and evaluate the effectiveness of the adapted SNAP-Ed curriculum by measuring nutrition knowledge among group home managers and clients and managers’ intent for behavior change. Extension paraprofessionals taught the original SNAP-Ed lessons to group home managers and trained them on the adapted curriculum (n=33). The trained managers then taught the adapted SNAP-Ed lessons to their clients (n=83).</p>
<p>Results from the study showed both group home managers and adults with intellectual or developmental disabilities improved nutrition knowledge from pre to post tests. Group home managers reported intent to change behavior for 12 of 18 behaviors examined. The curriculum was seen to be adaptable to fit various needs of group homes in different teaching settings, learning levels, and interests for participants.</p>
<p>Overall, the adapted SNAP-Ed curriculum for managers and clients living in group homes appears to increase knowledge of nutrition and may improve food behavior. Increased nutritional knowledge among group home managers and adults with intellectual or developmental disabilities may help decrease risk of nutritional related diseases.</p>

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</description>

<author>Amanda Panting</author>


</item>


<item>
<title>Using Short-Term Environmental Education Programs to Increase Student Learning and Elicit Positive Attitude Change</title>
<link>http://digitalcommons.usu.edu/gradreports/121</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/121</guid>
<pubDate>Wed, 09 May 2012 09:28:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Short-term environmental education programs such as water festivals and field days are a common outreach tool for watershed programs, yet little is known about their effectiveness at increasing knowledge and environmental awareness. To address this question, I conducted a formal assessment by pre- and post-testing 1400 fourth-grade students who participated in a field day at a Forest Service campground in northern Utah. During the day, each child spent approximately one hour engaged in water-related activities, with an emphasis on aquatic macroinvertebrates and water quality. My research focused on whether this single hour was sufficient to change both knowledge and interest in protecting water and aquatic organisms.</p>
<p>The study also compared student learning in those classes that participated only in the single event with classes that had additional water-related lessons and activities prior to and after the field day. I also examined how well variables such as teacher knowledge and attitude, socio-demographics and type of outdoor activities enjoyed by students were correlated with student knowledge and attitude.</p>
<p>Results demonstrated that short-term events, especially those that include additional classroom experiences, can result in knowledge gain and changes in attitudes in young children. Teacher knowledge and attitude were not correlated with student knowledge and attitude; however, school district and type of outdoor activities enjoyed by students were both good predictors of knowledge and attitude scores.</p>

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</description>

<author>Tiffany Kinder</author>


</item>


<item>
<title>Social Implications of Adolescent Text Messaging</title>
<link>http://digitalcommons.usu.edu/gradreports/120</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/120</guid>
<pubDate>Wed, 09 May 2012 09:28:44 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sarah S. Tulane</author>


</item>


<item>
<title>G-PLEX PSI</title>
<link>http://scholarship.claremont.edu/cgu_mfatheses/58</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_mfatheses/58</guid>
<pubDate>Wed, 09 May 2012 09:24:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Monumental metal sculpture that incidentally creates sound. Heaviness and lightness displayed via large, heavy, metal sculptures of abstract geometric forms suspended from the ceiling by seemingly fragile wires that not only appear to defy gravity but provide tonal expression when plucked, hammered, or bowed. Further conversation associated with the micro to the macro is easily revealed when the sounds and shapes are compared to the vibration of life identified with imagined subatomic movement.</p>

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</description>

<author>Jacques Louis David</author>


</item>


<item>
<title>The Darkness is Passing</title>
<link>http://scholarship.claremont.edu/cgu_mfatheses/57</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_mfatheses/57</guid>
<pubDate>Wed, 09 May 2012 09:24:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>My work is about the interplay of light, darkness and space. I express illumination of space and penetrating light with abstract painting. I use the white of canvas and thick application of black paint to create frames and to break rules of defined dimensions. Through my paintings, I challenge the perception of space and question the boundaries between two and three dimensions.</p>

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</description>

<author>Grace Heeeun Park</author>


</item>


<item>
<title>Tutti Frutti</title>
<link>http://scholarship.claremont.edu/cgu_mfatheses/56</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_mfatheses/56</guid>
<pubDate>Wed, 09 May 2012 09:24:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>My reliance on the exhibition space as an activator for art has become a vehicle for addressing the building as the art not the backdrop for the art. If the gallery is white and unpleasant it can be covered like a canvas or a body. Dressing the building, like dressing my body is an extension of my person as mark making is to the painter. Art without true utilitarian function resulting from material desire is analogous to the body and its lack of political power. Why should the objectified body be worse off than the object? I can make the Cartier bracelet, which sits on the wrist, be seen as no different than the (fill-in-the-blank) painting above the couch.</p>

	]]>
</description>

<author>Damaris G. Rivera</author>


</item>


<item>
<title>Marginalia no. 31</title>
<link>http://digitalcommons.usu.edu/marginalia/30</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/marginalia/30</guid>
<pubDate>Wed, 09 May 2012 09:24:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Next Chapter: Is the Book Extinct?</p>
<p>2011 Arrington Writing Award Winners</p>
<p>Book of Hours</p>
<p>Founder’s Day: 150 Years. “Democracy Enrolls at the College”</p>
<p>Common Literature Experience 2012: The Beast in the Garden</p>
<p>‘Forgotten Photographs of the Union Pacific Railroad’</p>
<p>Jack London Society coming to Logan</p>
<p>Spring: Library Academia</p>

	]]>
</description>

<author>Merrill-Cazier Library</author>


</item>


<item>
<title>Notebook - April-June 1985</title>
<link>http://scholarcommons.sc.edu/notebook/58</link>
<guid isPermaLink="true">http://scholarcommons.sc.edu/notebook/58</guid>
<pubDate>Wed, 09 May 2012 09:20:12 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Contents:</strong></p>
<p>Private Artifact Collections Revisted: the Fourth Phase.....p. 1</p>

	]]>
</description>

<author>South Carolina Institute of Archaeology and Anthropology--University of South Carolina</author>


</item>


<item>
<title>No-Yes</title>
<link>http://digitalcommons.library.umaine.edu/services/6</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/services/6</guid>
<pubDate>Wed, 09 May 2012 09:20:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>No-Yes is an example of a poster highlighting our services and resources. It is an example of a poster that serves as a reminder about library policies.</p>

	]]>
</description>

<author>Brad Finch</author>


</item>


<item>
<title>On One Only</title>
<link>http://digitalcommons.library.umaine.edu/services/5</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/services/5</guid>
<pubDate>Wed, 09 May 2012 09:20:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>On One Only is an example of a poster highlighting our services and resources. It is an example of a poster that serves as a reminder about library policies.</p>

	]]>
</description>

<author>Jerry Lund</author>


</item>


<item>
<title>Light Therapy: The Effectiveness of Light Therapy on Pain and Swelling of Acute Lower Extremity Sprains and Strains of Collegiate Athletes</title>
<link>http://digitalcommons.cedarville.edu/education_theses/14</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/14</guid>
<pubDate>Wed, 09 May 2012 09:19:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis investigated light therapy to discover if this therapeutic modality had any effect on pain and swelling in acute lower extremity sprains and strains of collegiate athletes. The subjects were 18-22 year old male and female collegiate athletes from Cedarville University. The study was a blind study using experimental and sham treatment groups. The researcher used the Dynatron 709 Solaris unit with a superluminous diode cluster probe with wavelengths from 660 nm to 880 nm. The dosage was 10 J/cm² of continuous strength for 1 minute and 40 seconds at each injury site. The conclusion of this study was that light therapy decreased pain in the experimental group although it was not found to be significant. There was no significance in the decrease of swelling. My research found that light therapy is an effective modality for use with acute pain of acute lower extremity sprains and strains.</p>

	]]>
</description>

<author>Elisabeth A. Martin</author>


</item>


<item>
<title>HOW LOCAL SCHOOLS CAN PROMOTE CIVICS EDUCATION</title>
<link>http://opensiuc.lib.siu.edu/ppi_papers/31</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/ppi_papers/31</guid>
<pubDate>Wed, 09 May 2012 09:19:05 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Suzanne Schmitz</author>


</item>


<item>
<title>Imagine - Somewhere Cool</title>
<link>http://digitalcommons.library.umaine.edu/services/4</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/services/4</guid>
<pubDate>Wed, 09 May 2012 09:13:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Imagine - Somewhere Cool is an example of a poster highlighting our services and resources. The “imagine a library…” posters were both part of a multifaceted outreach initiative.</p>

	]]>
</description>

<author>Stephen Fadel</author>


</item>


<item>
<title>Imagine - Online Journals</title>
<link>http://digitalcommons.library.umaine.edu/services/3</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/services/3</guid>
<pubDate>Wed, 09 May 2012 09:13:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Imagine - Online Journals is an example of a poster highlighting our services and resources. The “imagine a library…” posters were both part of a multifaceted outreach initiative.</p>

	]]>
</description>

<author>Kjerste Christensen</author>


</item>


<item>
<title>Outside Consultants: When,
Who, and How to Use Them</title>
<link>http://digitalcommons.unl.edu/podimproveacad/222</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/222</guid>
<pubDate>Wed, 09 May 2012 09:13:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>How Do You Know When You Need A Consultant?</p>
<p>1. Before initiating a new program</p>
<p>2. When effectiveness is hampered by interpersonal difficulties</p>
<p>3. When budget problems are hampering effectiveness</p>
<p>4. When in-house staff doesn't have time to do vital work</p>
<p>5. When a more objective viewpoint is is needed</p>
<p>How Do You Find the Right Consultant?</p>
<p>How Do You Ensure Maximum Benefit at Minimum Cost?</p>
<p>1. Before the initial phone call, define with care the problem to be addressed by the consultant</p>
<p>2. The initial phone call focuses on refining the definition of the problem(s) to be addressed and on identifying the information needed to develop a solution</p>
<p>3. The information is collected and used to develop the first draft of an action plan</p>
<p>4. The first-draft action plan is presented in a teleconference attended by all affected constituencies</p>
<p>5. The action plan is revised and implemented</p>
<p>5a. Follow-up</p>
<p>On-site Consultation</p>
<p>Before The Visit</p>
<p>The Visit</p>
<p>Summary</p>
<p>Conclusion</p>
<p>References</p>

	]]>
</description>

<author>Martin Nemko</author>


</item>


<item>
<title>Notebook - January-March 1985</title>
<link>http://scholarcommons.sc.edu/notebook/57</link>
<guid isPermaLink="true">http://scholarcommons.sc.edu/notebook/57</guid>
<pubDate>Wed, 09 May 2012 09:12:22 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Contents:</strong></p>
<p>Table of Contents.....p. i<br> Editorial Notes.....p. iii<br> Small Watercraft Research Project Update.....p. 1<br> A Site History of 1927, 1919 Pickens Street.....p. 7<br> Wachesaw Archaeological Field Trip.....p. 13<br> Appendix I: Subject Index, Volumes 6-16, Notebook 1974-1984.....p. 17<br> Appendix II: Author Index, Volumes 6-16, Notebook 1974-1984.....p. 21</p>

	]]>
</description>

<author>South Carolina Institute of Archaeology and Anthropology--University of South Carolina</author>


</item>


<item>
<title>Review of Feminists Doing Ethics</title>
<link>http://epublications.marquette.edu/phil_fac/204</link>
<guid isPermaLink="true">http://epublications.marquette.edu/phil_fac/204</guid>
<pubDate>Wed, 09 May 2012 09:09:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Theresa Weynand Tobin</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1897-1898</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/14</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/14</guid>
<pubDate>Wed, 09 May 2012 09:08:31 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1898-1899</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/13</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/13</guid>
<pubDate>Wed, 09 May 2012 09:08:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1899-1900</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/12</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/12</guid>
<pubDate>Wed, 09 May 2012 09:08:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Place of Narrative in the
Study and Practice of Adult
Development</title>
<link>http://digitalcommons.unl.edu/podimproveacad/221</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/221</guid>
<pubDate>Wed, 09 May 2012 09:06:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Introduction</p>
<p>Narrative in Several Disciplines</p>
<p>Shifts in Ways of Knowing in the Social Sciences</p>
<p>Narrative Methods: A Personal Response</p>
<p>Narrative Methods in Adult Development Activities</p>
<p>Conclusion</p>
<p>References</p>

	]]>
</description>

<author>Diane E. Morrison</author>


</item>


<item>
<title>Putting the Teaching Portfolio
in Context</title>
<link>http://digitalcommons.unl.edu/podimproveacad/220</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/220</guid>
<pubDate>Wed, 09 May 2012 09:02:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>What is the Teaching Portfolio?</p>
<p>Five Reasons for the Viability of the Teaching Portfolio</p>
<p>The Teaching Portfolio and the New Scholarship</p>
<p>Conclusion</p>
<p>References</p>
<p>Appendix A</p>
<p>Appendix B</p>

	]]>
</description>

<author>Barbara J. Millis</author>


</item>


<item>
<title>View Your Own Record</title>
<link>http://digitalcommons.library.umaine.edu/services/2</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/services/2</guid>
<pubDate>Wed, 09 May 2012 09:01:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>View Your Own Record is an example of a poster highlighting our services and resources. Our series of letter from studies was part of a multifaceted outreach initiative.</p>

	]]>
</description>

<author>Jerry Lund</author>


</item>


<item>
<title>eReserves</title>
<link>http://digitalcommons.library.umaine.edu/services/1</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/services/1</guid>
<pubDate>Wed, 09 May 2012 09:01:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>eReserves is an example of a poster highlighting our services and resources. Our series of letter from studies was part of a multifaceted outreach initiative.</p>

	]]>
</description>

<author>Jerry Lund</author>


</item>


<item>
<title>What Theories Underlie the
Practice of Faculty
Development?</title>
<link>http://digitalcommons.unl.edu/podimproveacad/219</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/219</guid>
<pubDate>Wed, 09 May 2012 08:59:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Do We Need a Theory?</p>
<p>What Theories Did We Start With?</p>
<p>What of the Future?</p>
<p>Conclusion</p>
<p>References</p>

	]]>
</description>

<author>Wilbert J. McKeachie</author>


</item>


<item>
<title>How Attitudes Change: A
Primer for Faculty Developers</title>
<link>http://digitalcommons.unl.edu/podimproveacad/218</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/218</guid>
<pubDate>Wed, 09 May 2012 08:56:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Nature of Attitude</p>
<p>Theories of Attitude Change</p>
<p>Classical Conditioning Theory</p>
<p>Reinforcement (Behaviorist) Theory</p>
<p>Modelling Theory</p>
<p>Message Learning Theory</p>
<p>Balance Theory</p>
<p>Impression Management Theory</p>
<p>Cognitive Dissonance Theory</p>
<p>Self-Persuasion Theory</p>
<p>Probabilogical Theory</p>
<p>The Foot-in-the-Door Effect</p>
<p>Conclusion</p>
<p>References</p>

	]]>
</description>

<author>Richard F. Lewis</author>


</item>


<item>
<title>Teaching Grammar: The most Effective Strategies to use in a Middle School Classroom</title>
<link>http://scholar.valpo.edu/sarp/20</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/20</guid>
<pubDate>Wed, 09 May 2012 08:53:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>My action research explores the most effective strategies for grammar instruction to middle school students, specifically at the sixth grade level. The purpose of this research is to help myself and other educators teach grammar in the most effective way. Data will consist of student work samples from differentiated lessons and surveys from students and teachers (sixth grade). The method of research is simple—every grammar lesson I teach will be differentiated and will implement a different strategy. Student work samples will be taken from these lessons for analysis. Student improvement and/or declination will decide the best teaching strategies. Student/ teacher survey answers will also be factors in the decision. Key findings from this research are still inconclusive, since my research is incomplete. The significance of this research is to educate and assist educators with the instruction of grammar and to ensure all students have the opportunity to reach success.</p>

	]]>
</description>

<author>Heather Zaharias</author>


</item>


<item>
<title>A Community of Prophets</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/399</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/399</guid>
<pubDate>Wed, 09 May 2012 08:53:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Tom Tumblin</author>


</item>


<item>
<title>University Faculty Attitudes
Towards Teaching and
Research</title>
<link>http://digitalcommons.unl.edu/podimproveacad/217</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/217</guid>
<pubDate>Wed, 09 May 2012 08:51:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Method and Sample</p>
<p>Results</p>
<p>Descriptive Statistics</p>
<p>Teaching and Research</p>
<p>Morale</p>
<p>Inferential Statistics</p>
<p>Interest and Satisfaction in Research</p>
<p>Interest and Satisfaction in Teaching</p>
<p>Perceived Institutional Support for Teaching</p>
<p>Discussion</p>
<p>Conclusion</p>
<p>References</p>

	]]>
</description>

<author>Russell Lee et al.</author>


</item>


<item>
<title>The Relationship between TRP (Total Physical Response) with Memory of Chinese Characters</title>
<link>http://scholar.valpo.edu/sarp/16</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/16</guid>
<pubDate>Wed, 09 May 2012 08:50:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chinese characters are considered by many people as one of the most difficult words to read. The purpose of this project is to exam if Total Physical Response (TPR) strategy improves non-native speakers’ memory of Chinese characters. The action research took place in a high school class which was composed by 4 girls and 5 boys. In the first two weeks, regular vocabulary teaching methods were offered and several vocabulary quizzes were taken by students. For the next two weeks, TPR strategy was added to the vocabulary teaching and students took a couple quizzes again. The comparisons between the two groups of data show the vocabulary learning with TPR strategy was more efficient than without it. The research project supports the belief that TPR strategy should be used for Chinese vocabulary teaching in Chinese classrooms.</p>

	]]>
</description>

<author>Shuyi Feng</author>


</item>


<item>
<title>The Response of High School Students in a Trimester Term</title>
<link>http://scholar.valpo.edu/sarp/19</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/19</guid>
<pubDate>Wed, 09 May 2012 08:50:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>These days, most high schools are usually on semester terms. However, there are still some that use trimester terms, three 12-week trimesters, compared to two 17-week semesters. This research takes a look at how students handle a transition or routine change in the middle of the trimester. The 2<sup>nd</sup> trimester had their routine changed mid-trimester and observations were made on their behavior. A survey was also given to them questioning how their transition went from having the regular teacher and a student teacher. The 3<sup>rd</sup> trimester classes were also observed and given a survey. It was a little different for the 3<sup>rd</sup> trimester because they started off the trimester with the student teacher and were used to the rules and did not experience a transitional period.</p>

	]]>
</description>

<author>Amy Ketchum</author>


</item>


<item>
<title>Adding Music to the Math Equation</title>
<link>http://scholar.valpo.edu/sarp/18</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/18</guid>
<pubDate>Wed, 09 May 2012 08:49:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Depending on the material covered on any particular day, students may end up with anywhere from 5 minutes to 35 minutes to do their homework in class. Unfortunately, students will only stay on task for so long before they get off task. This research project will investigate the effects of playing classical music during in-class work time on the work ethic and environment of the classroom.</p>

	]]>
</description>

<author>Phil Luster-Bartz</author>


</item>


<item>
<title>Name Those Notes</title>
<link>http://scholar.valpo.edu/sarp/17</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/17</guid>
<pubDate>Wed, 09 May 2012 08:49:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>The names of the notes on the treble clef staff are not currently taught in the Indiana State Music Curriculum.  This concept is essential to the understanding, reading, and writing of music.  Therefore, it is important that research based curriculum is developed for this topic.  Fourth grade students will complete a pre-test and series of lessons about learning the note names.  These lessons will include direct instruction, activities, and homework assignments.  A different method or unit plan will be used at each school.  Upon the conclusion of each unit, the students will re-take the pre-test as a post-test.  Scores from both schools will be compared to analyze which method seemed to produce higher test scores.</p>

	]]>
</description>

<author>Emily Prough</author>


</item>


<item>
<title>We Grew Up Together : Brothers and Sisters in Nineteenth-century America</title>
<link>http://digitalcommons.csbsju.edu/history_books/1</link>
<guid isPermaLink="true">http://digitalcommons.csbsju.edu/history_books/1</guid>
<pubDate>Wed, 09 May 2012 08:49:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>"While much attention has been devoted to connections in American families between husbands and wives and between parents and children, We Grew Up Together speaks to an area that has been largely neglected until now: the emotional relationships among siblings." "Through close readings of the letters brothers and sisters wrote to each other over the course of nearly a century (1840-1920), Annette Atkins reveals the inner workings, everyday lives, and central relationships of ten nineteenth-century families. She looks at families located in various regions, families headed to the frontier, obscure families, and prominent families such as the Blairs of Washington, D.C. Drawing on the insights of Alfred Adler and others, Atkins examines the varying dynamics of "warm" and "cool" families and shows how siblings tutored each other in friendship, authority, cooperation and competition, dependence and independence."--BOOK JACKET.</p>

	]]>
</description>

<author>Annette Atkins</author>


</item>


<item>
<title>Instructional Development
Programs for International
TAs: A Systems Analysis
Approach</title>
<link>http://digitalcommons.unl.edu/podimproveacad/216</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/216</guid>
<pubDate>Wed, 09 May 2012 08:47:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Introduction</p>
<p>A Research University as a System</p>
<p>The Culture Audit</p>
<p>The University as a System</p>
<p>ITA Program Design</p>
<p>Orientation</p>
<p>Pre-term/Pre-teach</p>
<p>Concurrent</p>
<p>Curriculum Design</p>
<p>Program Implementation</p>
<p>Issues in ITA Assessment</p>
<p>ITA Tests</p>
<p>1. Pre-recorded Speaking Tests</p>
<p>2. Oral Interviews</p>
<p>3. Oral Communicative Performance Tests</p>
<p>4. Teaching Simulations</p>
<p>Models of ITA Assessment</p>
<p>Conclusion</p>
<p>References</p>

	]]>
</description>

<author>Rosslyn Smith et al.</author>


</item>


<item>
<title>Advent Within Us</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/398</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/398</guid>
<pubDate>Wed, 09 May 2012 08:43:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alice Ward</author>


</item>


<item>
<title>Front Line Faculty
Development: Chairs
Constructively Critiquing
Colleagues in the Classroom</title>
<link>http://digitalcommons.unl.edu/podimproveacad/215</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/215</guid>
<pubDate>Wed, 09 May 2012 08:41:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Peer Observation and Peer Evaluation: Formative and Summative Evaluation</p>
<p>Anxieties of Both Tenured and Untenured Faculty Working Together</p>
<p>Random Versus Focused Observation and Descriptive Versus Judgmental Observation</p>
<p>Underlying Value Systems That Propel Instruction</p>
<p>Factors That Contribute to Effective and Not-so-effective Teaching</p>
<p>Common Teaching Vocabulary</p>
<p>Observation Through Videotape and Microteaching Process</p>
<p>Microteaching Process</p>
<p>Classroom Observation Triads</p>
<p>Conclusions</p>
<p>Agenda for Peer Observation Training Groups</p>
<p>References</p>
<p>Appendix A</p>
<p>Tabs</p>
<p>Appendix B</p>

	]]>
</description>

<author>Linda Hilsen et al.</author>


</item>


<item>
<title>The Emptiness of Majority Rule</title>
<link>http://www.repository.law.indiana.edu/facpub/529</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/529</guid>
<pubDate>Wed, 09 May 2012 08:37:37 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Luis Fuentes-Rohwer</author>


</item>


<item>
<title>The Independence of the Judicial Branch in the New Republic</title>
<link>http://www.repository.law.indiana.edu/facpub/528</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/528</guid>
<pubDate>Wed, 09 May 2012 08:37:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Charles G. Geyh et al.</author>


</item>


<item>
<title>Book Review. Courts, Congress, and the Constitutional Politics of Interbranch Restraint</title>
<link>http://www.repository.law.indiana.edu/facpub/527</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/527</guid>
<pubDate>Wed, 09 May 2012 08:37:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Charles G. Geyh</author>


</item>


<item>
<title>What about the Quiet Students?: Investigating Students&apos; and Teachers&apos; Perceptions of Non-Participatory Students</title>
<link>http://scholar.valpo.edu/sarp/15</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/15</guid>
<pubDate>Wed, 09 May 2012 08:37:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>As a student teacher, I already have a fair idea of how classroom discussion works: some students participate but most sit quietly. If I use discussion to indicate student learning, what data do I have available to gauge the "quiet" students? My research will survey students about reasons they have for not participating and suggestions they have for involving everyone in discussion. Also, I will be surveying middle school teachers to compare their ideas of discussion. This research is knowledge I hope to take with me to my first teaching position to be implemented into my own classroom.</p>

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</description>

<author>Elise Appold</author>


</item>


<item>
<title>Secondary Student Metacognition Compared to Actual Participation in the Classroom</title>
<link>http://scholar.valpo.edu/sarp/14</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/14</guid>
<pubDate>Wed, 09 May 2012 08:37:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many times in a conflict there are three different accounts of what happened: person one’s side, person two’s side, and the truth. As often as this saying gets made and joked about, it does reveal truth about how perception and truth don’t always align. With this thought, I want to compare a student’s perceived participation in comparison with actual class participation. In many secondary and collegiate level classrooms, course grades are partially determined on class participation. Because of this, it would seem relevant to consider perceptions with reality so that students can better understand themselves. When a student has a good grasp on his or herself, then he or she is more likely to modify behavior for improvement. As for the actual measuring of data, a survey will be given out after one session of recording, then to also be followed by a second session. During each recording session, the primary principal/co-principal investigator will record how often each student raises their hand, how often each student is called on with and without their hand raised separately by tallies. The students will also turn in their assignment, not for a grade but for a completion of finished, half finished, or not finished as a score. Assignments will be tallied on two different situations: one prior to the survey and one after the survey. After all data has been collected and coded to protect identities, surveys will be compared to before and after survey recordings and then compared through mean, mode and median.</p>

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</description>

<author>Kristin Buch</author>


</item>


<item>
<title>The City Filled with S(e)oul</title>
<link>http://digitalcommons.linfield.edu/intl_postcards_1112/16</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/intl_postcards_1112/16</guid>
<pubDate>Wed, 09 May 2012 08:37:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Postcard from Dana Hellie, during the Linfield College Semester Abroad Program at Yonsei University in Seoul, South Korea</p>

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</description>

<author>Dana Hellie</author>


</item>


<item>
<title>Spring Break and More!</title>
<link>http://digitalcommons.linfield.edu/intl_postcards_1112/15</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/intl_postcards_1112/15</guid>
<pubDate>Wed, 09 May 2012 08:36:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Postcard from Emmy Elliott, during the Linfield College Semester Abroad Program at Instituto Cultural A.C. in Oaxaca, Mexico</p>

	]]>
</description>

<author>Emmylu Elliott</author>


</item>


<item>
<title>Sunshine in Galway and the End of Classes</title>
<link>http://digitalcommons.linfield.edu/intl_postcards_1112/14</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/intl_postcards_1112/14</guid>
<pubDate>Wed, 09 May 2012 08:36:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Postcard from Abby Lundberg, during the Linfield College Semester Abroad Program at the National University of Ireland, Galway</p>

	]]>
</description>

<author>Abigail Lundberg</author>


</item>


<item>
<title>Floods, Beetles, and Soccer</title>
<link>http://digitalcommons.linfield.edu/intl_postcards_1112/13</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/intl_postcards_1112/13</guid>
<pubDate>Wed, 09 May 2012 08:36:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Postcard from Mary Robertson, during the Linfield College Semester Abroad Program at James Cook University in Australia</p>

	]]>
</description>

<author>Mary Robertson</author>


</item>


<item>
<title>Class/Schedule</title>
<link>http://digitalcommons.linfield.edu/intl_postcards_1112/12</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/intl_postcards_1112/12</guid>
<pubDate>Wed, 09 May 2012 08:36:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Postcard from Nora Burnfield, during the Linfield College Semester Abroad Program at Telemark University in Bø, Norway</p>

	]]>
</description>

<author>Nora Burnfield</author>


</item>


<item>
<title>Best Month Yet</title>
<link>http://digitalcommons.linfield.edu/intl_postcards_1112/11</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/intl_postcards_1112/11</guid>
<pubDate>Wed, 09 May 2012 08:36:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Postcard from Elizabeth Dadoly, during the Linfield College Year Abroad Program at American University Center of Provence in Aix en Provence, France</p>

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</description>

<author>Elizabeth Dadoly</author>


</item>


<item>
<title>Sociology of Medicine for Whom?: Feminist Perspectives in a Multi-Paradigmatic Sociology of Medicine</title>
<link>http://scholars.wlu.ca/soci_faculty/8</link>
<guid isPermaLink="true">http://scholars.wlu.ca/soci_faculty/8</guid>
<pubDate>Wed, 09 May 2012 08:36:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>My mother was a nurse, always called on when the neighbor’s child fell out of a high chair, woke up with spots or red eyes or had a fever. But, like others with whom I’ve talked whose parents offer health care services, I learned to feel that sickness was a weakness. I grew to feel ashamed of being sick; to have to rationalize and justify my own indisposition or to ignore or hide it. Through this, I learned that sickness and health were not biological events only but were constructed out of a web of social relations and meanings. And I developed an interest in the social-psychological aspects of health and illness. Later, I was swept away with feminist awareness and concerns and asked myself in what ways women and men and health and illness intersected. From these experiences and my academic education came thoughts such as those explored in this paper.</p>

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</description>

<author>Juanne Nancarrow Clarke</author>


</item>


<item>
<title>Competing Paradigms? The Use of DNA Powers in Youth Justice</title>
<link>http://digitalcommons.law.umaryland.edu/fac_pubs/1197</link>
<guid isPermaLink="true">http://digitalcommons.law.umaryland.edu/fac_pubs/1197</guid>
<pubDate>Wed, 09 May 2012 08:35:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Collecting deoxyribonucleic acid (DNA) from crime scenes and individuals is now regarded as a critical element of effective criminal investigation and prosecution. Numerous benefits are said to accrue from the gathering and comparison of DNA evidence: suspects may be speedily identified, innocent parties ruled out, the wrongfully convicted exonerated and some would-be criminal actors deterred. Retention of DNA in state controlled databases allows for speculative searching to identify subsequent offending and to provide leads for unsolved crimes. The collection and retention of convicted adults’ DNA has been held by European and US courts to be a proportionate incursion on human rights given the need to tackle crime effectively, although the law relating to un-convicted persons is more contentious (Campbell, 2010a). The application of DNA powers to young people in the youth justice system has received less attention.</p>
<p>This article considers the application and expansion of DNA powers in the youth justice system, and identifies the ‘competing paradigms’ at play. New Zealand and Scotland, often cited as having progressive and sensitive approaches to youth justice, are used to illustrate the tension between the perceived need for expanded powers of investigation and prosecution of crime and the rights and interests of young people.<sup>2</sup> Both jurisdictions are recognised for their established emphasis on diversionary and non-stigmatising processes in youth justice but more recently, are experiencing broader trends away from a rights-oriented paradigm towards a more populist and punitive model. This article examines the recent expansion of DNA powers in both countries which illustrates a comparable trajectory away from conventional youth justice precepts. It assesses the safeguards, if any, that have been introduced to mitigate this ‘ratcheting up’ of crime control, which is particularly problematic in the context of young people. In doing so, we draw on our respective work on DNA and human rights (Campbell, 2011; 2010a; 2010b; 2010c) and the rights of young people in the youth justice system (Lynch, 2007; 2008; 2010a; 2010b). Our analysis of legislative developments has a wider application as many jurisdictions have adopted elements of the New Zealand and Scottish approaches to youth justice, and can also contribute to a wider discussion about compliance with international standards for youth justice in the context of DNA collection and storage.</p>

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</description>

<author>Liz Campbell</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1894-1895</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/11</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/11</guid>
<pubDate>Wed, 09 May 2012 08:34:47 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1895-1896</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/10</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/10</guid>
<pubDate>Wed, 09 May 2012 08:34:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1896-1897</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/9</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/9</guid>
<pubDate>Wed, 09 May 2012 08:34:45 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Medicine Wheel:
Emotions and Connections in
the Classroom</title>
<link>http://digitalcommons.unl.edu/podimproveacad/214</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/214</guid>
<pubDate>Wed, 09 May 2012 08:33:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Emotions in the Classroom</p>
<p>Connections in the Classroom</p>
<p>The Medicine Wheel in the Classroom</p>
<p>References</p>
<p>Appendix A</p>

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</description>

<author>Peter J. Frederick</author>


</item>


<item>
<title>Worship Fuels the Flame</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/397</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/397</guid>
<pubDate>Wed, 09 May 2012 08:30:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Doris Khalaf</author>


</item>


<item>
<title>Coping with the Academic
&quot;Tragedy of the Commons&quot;:
Renovating Classrooms at
Carnegie Mellon University</title>
<link>http://digitalcommons.unl.edu/podimproveacad/213</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/213</guid>
<pubDate>Wed, 09 May 2012 08:30:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Carnegie Mellon: A Case Study</p>
<p>The situation</p>
<p>1. An action plan and its recommendations</p>
<p>2. The Educational Facilities Committee</p>
<p>3. The results: improved facilities and enhanced learning</p>
<p>4. What we have learned</p>
<p>Conclusion</p>
<p>References</p>

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</description>

<author>Edwin Fenton</author>


</item>


<item>
<title>Starting Out: Experiences of
New Faculty at a Teaching
University</title>
<link>http://digitalcommons.unl.edu/podimproveacad/212</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/212</guid>
<pubDate>Wed, 09 May 2012 08:26:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Methods</p>
<p>Subjects</p>
<p>Interview Protocol</p>
<p>Data Analysis</p>
<p>Results</p>
<p>Workloads</p>
<p>Collegial Support</p>
<p>Teaching</p>
<p>Scholarly Writing</p>
<p>Discussion</p>
<p>Workloads</p>
<p>Collegial Support</p>
<p>Teaching</p>
<p>Scholarly Writing</p>
<p>Summary</p>
<p>References</p>

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</description>

<author>Virginia van der Bogert</author>


</item>


<item>
<title>Trade Primer: Qs and As on Trade Concepts, Performance, and Policy</title>
<link>http://digitalcommons.ilr.cornell.edu/key_workplace/915</link>
<guid isPermaLink="true">http://digitalcommons.ilr.cornell.edu/key_workplace/915</guid>
<pubDate>Wed, 09 May 2012 08:24:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>[Excerpt] The 112th Congress has a full legislative and oversight agenda on international trade. The agenda so far has included approval of legislation to implement free trade agreements with Colombia, Panama, and South Korea, and may take up enhanced enforcement of U.S. trade agreements, as well as Russia’s accession to the World Trade Organization (WTO) and Permanent Normal Trade Relations (PNTR) status, oversight of the World Trade Organization’s Doha Round, and trade relations with China. This report provides information and context for many of these topics. It is intended to assist members and staff who may be new to trade issues.</p>
<p>This report is divided into four sections in a question-and-answer format: trade concepts; U.S. trade performance; formulation of U.S. trade policy; and trade and investment issues. Additional suggested readings are provided in an appendix.</p>

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</description>

<author>J. F. Hornbeck</author>


</item>


<item>
<title>A Six Year Follow-up of the Cavan/Monaghan First Episode Psychosis Study</title>
<link>http://epubs.rcsi.ie/mdtheses/23</link>
<guid isPermaLink="true">http://epubs.rcsi.ie/mdtheses/23</guid>
<pubDate>Wed, 09 May 2012 08:22:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Aspects of outcome in first episode psychosis require clarification. In doing so, boundaries between diagnoses within the psychosis spectrum of disorders may be better understood, thus contributing to improvement in operational diagnoses of psychotic disorders. In addition, the place within the spectrum of psychotic disorders of lesser studied diagnoses, such as major depressive disorder with psychotic features, is unclear. This study is a six year follow-up of the CavanMonaghan First Episode Psychosis Study, and investigates outcomes in a cohort characterised by substantive ethnic and socioeconomic homogeneity and stability. This study examines key aspects and predictors of outcome, including diagnostic stability, psychopathology, social and occupational functioning, quality of life and service-engagement. Three major diagnostic nodes, schizophrenia, bipolar disorder and major depressive disorder with psychotic features emerge from the data. Schizoaffective disorder appears to inhabit the territory between these three nodes. Schizophreniform disorder appears primarily a progenitor of schizophrenia, while delusional disorder appears primarily a variant progenitor of schizophrenia and schizoaffective disorder. Brief psychotic disorder appears to be related prospectively to bipolar disorder and major depressive disorder, while substance-induced psychosis and psychosis not otherwise specified appear to be related prospectively to schizophrenia and schizoaffective disorder. Follow-up data on psychopathology, functioning, QOL and service engagement result in an overall picture of SZ having the most adverse outcome of all the diagnoses within the psychotic spectrum. Systematic comparisons are made with SA, BD and MDDP. Additionally, the study illuminates rarely considered aspects of SF, DD, BrPsy, PNOS, SIP, SIM, PGMC and MGMC. Extent of psychopathology has a notably adverse effect on outcome for all diagnoses, whereas an ability to maintain social integration and a more 'normal' life course appears to have a positive effect on outcome. These fmdings have implications for the approach to treatment across psychotic disorders: broader symptom management, whether via pharmacological or psychotherapeutic approaches, may prevent particularly adverse outcomes, and interventions that promote occupational and social integration are key in raising outcomes beyond the level achievable by symptom management alone.</p>

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</description>

<author>Tara Kingston</author>


</item>


<item>
<title>Editorial Matter 1991</title>
<link>http://digitalcommons.unl.edu/podimproveacad/211</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/podimproveacad/211</guid>
<pubDate>Wed, 09 May 2012 08:21:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Foreword, by Kenneth J. Zahorski, Editor</p>
<p>Mission Statement</p>
<p>Contents</p>

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</description>


</item>


<item>
<title>Effects of Prlor Processlng on Judging Gynnastlcs</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6941</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6941</guid>
<pubDate>Wed, 09 May 2012 08:21:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Three experiments are reported that examined the lnfluence of prior judgements on implicit and expliclt tests of memory in gymnastic judging. The rationale was that if gymnastlc Judging ls affected by the memory for prior eplsodes, then the accuracy of judgements should change as a result of the prior episode. The results of Experiment 1 revealed that perceptual judgements dlffered as a functlon of an item's relationship between the study phase and the perceptual test phase. Moves that had the same performance ln both phases resulted ln the hlghest level of accuracy (M = 79%). New moves were less accurate (M = 75%). The lowest level of accuracy was achieved for items where the performance was altered between study and the perceptual test (M = 72%) . Similarly, recognition judgements differed as a functlon of an item's relationship between the study phase and recognition test phase. Novlce and expert Judges revealed similar memory lnfluences for perceptual and recognition Judgements (Experiment 1). Memory influences were reduced, but still evident when subjects were given prior knowledge of these effects and procedural changes were adopted (Experiment 2). Spacing of repetitions dld not enhance prior processlng effects of perceptual Judgements, but superior retention was noted for spaced repetitions in the recognition test phase (Experiment 3). These findings are discussed in terms of memory influences on subjective experience and the practical implications of Judges' exposure to an athlete's performance prlor to competition.</p>

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</description>

<author>Dlane Ste-Marie</author>


</item>


<item>
<title>Determining the Effect of One-On-One Education in Addition to Written Material on Breastfeeding Initiation Rates in the Hospital Setting</title>
<link>http://digitalcommons.usu.edu/gradreports/119</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/119</guid>
<pubDate>Wed, 09 May 2012 08:20:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>The objective of this research was to determine the breastfeeding initiation rate among healthy, term infants at a select hospital, the effect of one-on-one breastfeeding education, in addition to written material on breastfeeding initiation rates in the hospital setting, and if other factors from available data are associated with differences in breastfeeding initiation. This was a quasi-experimental convenience sample study with subjects assigned to a control group (written education) or intervention group (written and one-on-one education). The setting was the obstetrics unit at Siloam Springs Memorial Hospital (Benton County, Arkansas). Subjects were women delivering infants without complication between March and August 2011. 120 charts were reviewed (60 control and 60 experimental). The experimental group n=60 participants were mothers who received one-on-one instruction about breastfeeding iv topics from a certified breastfeeding educator in addition to a written education booklet. The education was completed within 24 hours either before or after delivery in the patient’s hospital room. The control group mothers n=60 received a written education booklet only. Each infant’s logged intake data was recorded from reviewed medical records for ever breastfed, formula fed or both. Other infant and maternal criteria collected in the chart review included demographics, insurance status, smoking status, obstetric physician, as well as infant birth order, birth type, and weight. Logistical regression analysis was used to determine the effect of certain maternal factors on breastfeeding initiation. Statistical significance was determined at a p-value of <0.05. Chi squared tests were used to further verify the significance of these variables. Descriptive statistics were performed on the demographic data for means. 61.7% of infants initiated breastfeeding in the hospital. This study revealed 5 main factors that influenced breastfeeding initiation at the significant level: maternal intention to breast feed, maternal education level, maternal smoking, infant birth order, and in-hospital one-on-one breastfeeding education. One-on-one breastfeeding education along with written education is a promising intervention for increasing breastfeeding initiation in the hospital setting. Partial implementation of the BFHI was successful increasing breastfeeding rates by introducing step 5- showing mothers how to breastfeed and maintain lactation.</p>

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</description>

<author>Carly Elizabeth Grace</author>


</item>


<item>
<title>Racial Profiling: Legal and Constitutional Issues</title>
<link>http://digitalcommons.ilr.cornell.edu/key_workplace/914</link>
<guid isPermaLink="true">http://digitalcommons.ilr.cornell.edu/key_workplace/914</guid>
<pubDate>Wed, 09 May 2012 08:15:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>[Excerpt] Racial profiling is the practice of targeting individuals for police or security detention based on their race or ethnicity in the belief that certain minority groups are more likely to engage in unlawful behavior. Examples of racial profiling by federal, state, and local law enforcement agencies are illustrated in legal settlements and data collected by governmental agencies and private groups, suggesting that minorities are disproportionately the subject of routine traffic stops and other security-related practices. The issue has periodically attracted congressional interest, particularly with regard to existing and proposed legislative safeguards, which include the proposed End Racial Profiling Act of 2011 (H.R. 3618/S. 1670) in the 112th Congress. Several courts have considered the constitutional ramifications of the practice as an “unreasonable search and seizure” under the Fourth Amendment and, more recently, as a denial of the Fourteenth Amendment’s equal protection guarantee. A variety of federal and state statutes provide potential relief to individuals who claim that their rights are violated by race-based law enforcement practices and policies.</p>

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</description>

<author>Jody Feder</author>


</item>


<item>
<title>A Comparative Analysis of the Jewish Law and the Secular Perspective on International Human Rights (part of the article, “Human Rights in the Bible, an Exchange of Ideas”).</title>
<link>http://digitalcommons.tourolaw.edu/scholarlyworks/425</link>
<guid isPermaLink="true">http://digitalcommons.tourolaw.edu/scholarlyworks/425</guid>
<pubDate>Wed, 09 May 2012 08:13:19 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Richard Klein et al.</author>


</item>


<item>
<title>GVSU Art Gallery Meets iOS: How To Cram 10K+ Works of Art Into Your Pocket</title>
<link>http://scholarworks.gvsu.edu/cistechlib/144</link>
<guid isPermaLink="true">http://scholarworks.gvsu.edu/cistechlib/144</guid>
<pubDate>Wed, 09 May 2012 08:11:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Grand Valley State University Art Gallery has over ten thousand works of original art, including paintings, sculptures, ceramics, and more.  A large portion of this collection is displayed across GVSU's campuses. These pieces of art are used by students for courses and research and are also simply enjoyed by people each day as they encounter them on campus.  Although each individual work has a placard describing it and its artist, these do not help people locate specific works of art around the different campuses and buildings. Furthermore, the amount of information that can be displayed on a work of art is limited to the size of the placard.  Another difficulty is that there is no way for a person to share or comment on a work of art that they really appreciate. This project addressed these problems by developing and deploying a mobile application that allows users to browse and locate works of art using their iPhone and its network connection and GPS capabilities.  Furthermore, users can use the application to go on virtual art tours, and they can interact with their friends around a piece of art via integration with Facebook, Twitter, and other social networks, all from their iPhone.</p>

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</description>

<author>Andres Solano</author>


</item>


<item>
<title>Mandatory Minimalism</title>
<link>http://scholarlycommons.law.wlu.edu/wlufac/96</link>
<guid isPermaLink="true">http://scholarlycommons.law.wlu.edu/wlufac/96</guid>
<pubDate>Wed, 09 May 2012 08:09:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>One of us (Cassell) is a former federal judge nominated by President George W. Bush, now a “conservative” scholar whose work is often supportive of law enforcement, the death penalty, and the rights of crime victims. The other (Luna) is a “libertarian” who tends to be suspicious of government and adamant about abuses of power, including those by police and prosecutors, and his scholarship has expressed the need for wholesale criminal justice reform (especially in the federal system). If we could find common ground on ways to modify federal mandatory minimums, we hoped that policymakers might share this agreement, perhaps sowing the seeds of further reforms. Whether or not modest congressional action spurs greater feats, however, our proposal is far from death defying. It is instead a fairly unpretentious yet principled modification. <br><br>Part I of this Article begins by briefly describing the background of mandatory minimum sentencing, including arguments for and against mandatory minimums and an analysis of their enactment in the federal system. Part II considers the resilience of mandatory minimums from a behavioral science perspective and then sketches a potential process of reform in light of the relevant phenomena. Part III discusses the concept of minimalism in philosophy and legal theory, proposing the idea of “political minimalism” as a justification for reform efforts that seeks consensus on basic principles accompanied by small legislative steps. Part IV provides specific changes to federal law consistent with a minimalist approach to statutory modification. Finally, Part V offers some suggestions for further reforms, with the hope of inspiring dialogue on the propriety of legislatively compelled, judicially unavoidable punishment.</p>

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</description>

<author>Erik Luna et al.</author>


</item>


<item>
<title>The God-World Relationship Between Joseph Bracken, Philip Clayton, and the Open Theism</title>
<link>http://scholarship.claremont.edu/cgu_etd/43</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/43</guid>
<pubDate>Wed, 09 May 2012 08:08:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation investigates the God-world relationship between Joseph Bracken as a process theologian, Philip Clayton as a panentheist, and the open theism. They have affinities and differences as conversational partners in their multilayered relations. Their common question must be as follows: “What does it mean to believe in God today?” In this dissertation I compare their respectively theological perspectives and explore their affinities and differences. Many scholars have already noted more affinities than untenable differences among Bracken’s theology, Clayton’s panentheism, and the open theism. On the one hand, even though theological perspectives of Bracken and Clayton are obviously different from each other, they are both influenced in specific ways by Whitehead. On the other hand, open theism is a movement that emphasizes “the openness of God,” from within evangelical theism. The fact that there is even within classical theism the pursuit of new models of God such as revised classical theism or modified classical theism might suggest the need for contemporary models of God in philosophical theology.</p>
<p>This dissertation will thus explore philosophical theologies that are proper both to the biblical faith and intellectual earnestness, that is, 居敬窮理 (geo (to live) kyeong (piety) kung (to acknowledge) li (reason)) in Eastern philosophy, which means distinctions but not separation between piety and intelligence, and that stand between classical theism and “orthodox” process theism. If there is no consistency among biblical, rational and existential descriptions of God, how can we establish philosophical theologies? Our theological task is to frame a new constructive theology whose primary aspect must synthesize both classical theism and process theology in the hermeneutical circle. For example, this new theism admits an infinitely qualitative difference between God and the world, as well as a really radical relation between God and the world. Aspects and domains do not encroach upon each other.</p>

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</description>

<author>Dong-Sik Park</author>


</item>


<item>
<title>Autonomic Nervous System Functioning as a Correlate to Health and Recovery</title>
<link>http://scholarship.shu.edu/petersheim-expo/petersheim-2012/Presentations/6</link>
<guid isPermaLink="true">http://scholarship.shu.edu/petersheim-expo/petersheim-2012/Presentations/6</guid>
<pubDate>Wed, 18 Apr 2012 12:00:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Thomas J. Mernar, PhD, OTR et al.</author>


</item>


<item>
<title>Keynote Speaker - Generational Crossroads: When X, Y, &amp; Boomers Collide!</title>
<link>http://scholarworks.uno.edu/academicsummit/2012/day1/2</link>
<guid isPermaLink="true">http://scholarworks.uno.edu/academicsummit/2012/day1/2</guid>
<pubDate>Thu, 19 Apr 2012 12:15:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>What do each of these generations have in common?  And just as important, what makes them so different—in the workplace, in the community, in their day-to-day lives? This POWERFUL presentation helps deepen the connection and communication across the ages.</p>

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</description>

<author>Eric Rowles</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1890-1891</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/8</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/8</guid>
<pubDate>Wed, 09 May 2012 08:04:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1891-1892</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/7</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/7</guid>
<pubDate>Wed, 09 May 2012 08:04:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1892-1893</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/6</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/6</guid>
<pubDate>Wed, 09 May 2012 08:04:08 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1893-1894</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/5</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/5</guid>
<pubDate>Wed, 09 May 2012 08:04:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>Insourcing Functions Performed by Federal Contractors: An Overview of the Legal Issues</title>
<link>http://digitalcommons.ilr.cornell.edu/key_workplace/913</link>
<guid isPermaLink="true">http://digitalcommons.ilr.cornell.edu/key_workplace/913</guid>
<pubDate>Wed, 09 May 2012 08:02:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>[Excerpt] While agencies are prohibited by federal law and policy from contracting out functions that are “inherently governmental,” other functions could potentially be contracted out. There has long been debate over both general government policies promoting the use of the private sector to perform “commercial functions” and whether specific functions should be performed by government personnel or contractors. However, since 2008, the insourcing initiatives of recent Congresses and the Obama Administration have caused particular controversy. Several lawsuits have been filed challenging agencies’ determinations to insource particular functions, and broader questions have been raised as to whether agencies’ implementation of insourcing runs afoul of civil service, ethics, or small business laws. This report provides a brief overview of key legal issues related to recent insourcing initiatives. It will be updated as developments occur.</p>

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</description>

<author>Kate M. Manuel et al.</author>


</item>


<item>
<title>Jesus: Master Change Theorist</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/396</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/396</guid>
<pubDate>Wed, 09 May 2012 08:00:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J. D. Walt</author>


</item>


<item>
<title>Gossypol Induced Cell Death in DU 145 Prostate Cancer Cells</title>
<link>http://epubs.rcsi.ie/mscrestheses/10</link>
<guid isPermaLink="true">http://epubs.rcsi.ie/mscrestheses/10</guid>
<pubDate>Wed, 09 May 2012 07:58:47 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Cancer Biology</em></p>
<p>Tumourigenesis is a multistep process which includes the transformation of healthy cells into extremely malignant cells, caused by the disruption of normal tissue homeostasis. Hanahan and Weinberg propose that there are a common set of 'acquired capabilities' that most if not all cancers posses's in order to survive and proliferate despite changes in their normal cell physiology during cancer development (Hanahan and Weinberg, 2000). These "Hallmarks of Cancer", according to Hanahan and Weinberg, are the six essential physiological alterations which lead to malignant growth: self-sufficiency in growth signals, insensitivity to growth inhibitory signals, evasion of apoptosis, limitless replicative potential, sustained angiogenesis and tissue invasion and metastasis.</p>
<p>Evasion of apoptosis is a cleverly employed alteration by cancer to enhance their survival and proliferation. Most tumours have defective apoptotic machinery and for this reason therapies which are specifically targeted at promoting apoptosis are particularly effective in the treatment of cancer. This aspect of cancer biology will be the primary focus of this thesis.</p>
<p><em>Prostate cancer</em></p>
<p>It is estimated around 913,000 cases of prostate cancer were diagnosed worldwide in 2008. Of these, 338,000 cases were diagnosed in the EU with the highest incidence in Ireland (Ferlay et <em>a/., </em>2008). Although there are several etiological factors (genetics, environment etc.) associated with prostate cancer, the most prominent risk factor is age with a rapid steep rise in incidences, more than any other cancer (Jemal eta/., 2003; Wang et a/., 2008).</p>
<p>There are several treatment options for prostate cancer including surgery, radiotherapy, hormone therapy and chemotherapy. Some patients can avail of surgery to remove the prostate-nerve sparing prostatectomy, but this is not option for every patient. Brachytherapy is another option which involves the placement of hundreds of radioactive seeds into the prostate. Ultrasound technology is used to ensure careful placement and to better control the effect on surrounding healthy tissue. The most common therapy for prostate cancer is Androgen Deprivation Therapy (ADT), as this cancer is highly reliant on androgens for proliferation (Miyamoto <em>et </em>a/., 2004). ADT can prolong patient's life expectancy, but nearly all patients progress to an androgen independent state which has no current effective therapy (Assikis and Simons, 2004).</p>
<p>In prostate cancer, chemotherapy is used to treat advanced cancers usually after radiotherapy or surgery have failed, or when the cancer progresses to a hormone refractory state and no longer responds to ADT. Docetaxel is one such chemotherapeutic drug used to treat advanced prostate cancer. Docetaxel is a member of the taxane class of drugs and acts by binding to microtubules causing them to become hyper-stabilized (Mollinedo and Gajate, 2003; Stein, 1999). This prevents depolymerisation of the microtubules, inhibiting mitotic cell division. It is cytotoxic to all quickly dividing cells including bone marrow and hair follicles as well as the cancer cells. Due to this extensive cytotoxicity which is not localised to cancer cells, there are adverse side effects associated with all chemotherapy, with alopecia being a very common side effect.</p>
<p>There is constant on-going research to develop new treatments that more specifically target cancer cells. This is likely to be a much more effective approach; it will try to limit the damage to surrounding healthy cells and help reduce the side effects associated with standard chemotherapy while still providing effective treatment to the patient. One of these promising new class of drugs currently in trials are the BH3 mimetics. They aim to promote apoptosis in cells with defective apoptotic machinery. These drugs will be discussed in more detail in section 1.4.</p>
<p>The Androgen Independent DU 145 prostate cancer cell line is one of the "classical" cell lines used to study prostate cancer (Alimirah <em>et </em>a/., 2006). It was originally derived from a 69 year old male with metastatic prostate cancer (Stone <em>et </em>a/., 1978). The DU 145 cell line completely lacks Bax expression.</p>

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</description>

<author>Susan Kennelly</author>


</item>


<item>
<title>Adam W. Herbert</title>
<link>http://digitalcommons.unf.edu/unf_pres/36</link>
<guid isPermaLink="true">http://digitalcommons.unf.edu/unf_pres/36</guid>
<pubDate>Wed, 09 May 2012 07:57:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>President Herbert, circa 1990</p>

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</description>


</item>


<item>
<title>Meta-analysis of subchorionic hemorrhage and adverse pregnancy outcomes</title>
<link>http://ir.uiowa.edu/pog_in_press/1</link>
<guid isPermaLink="true">http://ir.uiowa.edu/pog_in_press/1</guid>
<pubDate>Wed, 09 May 2012 07:54:10 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong></strong>The purpose of this study was to determine whether subchorionic hemorrhage is associated with increased adverse pregnancy outcomes of preterm delivery, spontaneous abortion, and abruption. PUBMED databases were searched for case control, cohort, and cross-sectional human studies that investigated the relationship of ultrasound detected subchorionic hemorrhage and adverse outcomes of preterm delivery, spontaneous abortion, and abruption. Data were extracted by two independent investigators. Nine studies were included in the pooled meta-analysis. Relative risk estimates (RR) and 95% confidence intervals (CI) were pooled across studies. Subchorionic hemorrhage was associated with preterm delivery (pooled RR = 1.64; 95%CI 1.41-1.89), spontaneous abortion (pooled RR = 2.59; 95% CI 2.34-3.25), and abruption (pooled RR = 3.16; 95% CI 2.32 – 4.31). This study suggests that early pregnancy subchorionic hemorrhage may increase the risk of preterm delivery, spontaneous abortion, and abruption.<strong> </strong>Women may be advised of increased adverse outcomes associated with subchorionic hemorrhage.</p>

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</description>

<author>Kathy L. Kyser</author>


</item>


<item>
<title>Waiting is Hard for the Rich</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/395</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/395</guid>
<pubDate>Wed, 09 May 2012 07:53:12 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kandace Brooks</author>


</item>


<item>
<title>Ethnoterritorial Conflict in the Western World: Northern Ireland and the Basque Region in Spain</title>
<link>http://digitalrepository.trincoll.edu/theses/235</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/235</guid>
<pubDate>Wed, 09 May 2012 07:47:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper examines two classic cases of ethnoterritorial groups demanding greater political autonomy: Northern Ireland and the Basque Country in Spain. Although the cases are very similar, Northern Ireland has reached a political settlement with the British government, while Basque nationalists have struggled to do so in Spain. In this thesis, I argue that four variables co-mingle to affect the prospects of a successful political settlement: the overall level of ethnoterritorial violence; concessions offered by the central government; the process of negotiations to end the violence; and the economic environment of the ethnoterritory.</p>

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</description>

<author>Meghan Mahder</author>


</item>


<item>
<title>The challenges that membership in the European Union has posed to national identity and citizenship policy in the Eastern European and Baltic states participant in the 2004 and 2007 enlargement processes.</title>
<link>http://digitalrepository.trincoll.edu/theses/234</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/234</guid>
<pubDate>Wed, 09 May 2012 07:47:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Adrian Jul Garcia</author>


</item>


<item>
<title>Conversing with the Ashes</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/394</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/394</guid>
<pubDate>Wed, 09 May 2012 07:36:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kandace Brooks</author>


</item>


<item>
<title>The &apos;worthy&apos; unemployed: societal stratification and unemployment insurance programs in China and the United States</title>
<link>http://iris.lib.neu.edu/slaw_fac_pubs/94</link>
<guid isPermaLink="true">http://iris.lib.neu.edu/slaw_fac_pubs/94</guid>
<pubDate>Wed, 09 May 2012 07:34:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>This is a comparative study of the unemployment compensation schemes in China and in the U.S. The article emphasizes how the structure of unemployment scheme can add to or detract from the view of the unemployed as “worthy” or “unworthy.”</p>

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</description>

<author>Lucy A. Williams et al.</author>


</item>


<item>
<title>Penalty and Proportionality in Deportation for Crimes</title>
<link>http://digitalcommons.law.umaryland.edu/fac_pubs/1196</link>
<guid isPermaLink="true">http://digitalcommons.law.umaryland.edu/fac_pubs/1196</guid>
<pubDate>Wed, 09 May 2012 07:33:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Maureen A. Sweeney et al.</author>


</item>


<item>
<title>LANGUAGE AND CHANGE: THE IMMLINITY-TO-CHANGE LANGUAGE TECHNOLOGY AS A TOOL FOR INTEGRATING THE ECCLESIAL VISION OF THE CENTRE FOR MINISTRY FORMATION INTO ITS MINISTRY FORMATION PROCESS</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6940</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6940</guid>
<pubDate>Wed, 09 May 2012 07:32:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation explores the relationship between language and change and assesses the effectiveness of the immunity-to-change language technology for integrating the ecclesial vision of the Centre for Ministry Formation (Saint Paul University in Ottawa) into its ministry formation process. The Centre offers pastoral leadership education for candidates for both lay and ordained ministry in the Roman Catholic Church and its ecclesial vision is a post-Vatican II model of church as communion. In order to ground this exploration of language and change in the context of the Centre's ecclesial vision, I draw upon evolutionary and feminist thought, trinitarian theology, ecclesiology, psychology, education theory, leadership education and organizational development. The immunity-to-change language technology is a language form for deep structural change. Deep structural change is epistemologic change, change in our ways of knowing. The language form is intended to help people make changes to which they are truly committed. In the qualitative research process, I presented the immunity-to-change language technology to persons actively engaged in a variety of pastoral ministries and who are affiliated to the Centre. The ultimate goal of my research process was to assess the potential usefulness of this language form for enabling the Centre's candidates for ministry to identify and work toward changing their built-in resistances to integrating the Centre's ecclesial vision into their own pastoral practice. The findings of this research indicate that the immunity-to-change language is a powerful process for deep structural change. It has the potential to be an effective tool for integrating the Centre's vision into its ministry formation process, if the process includes the appropriate follow-up stages and built-in supports after the initial presentation of the diagnostic phase.</p>

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</description>

<author>Lorraine Ste-Marie</author>


</item>


<item>
<title>Accessorized Therapeutic Game Experiences for Touch-Enabled Devices</title>
<link>http://scholarworks.gvsu.edu/cistechlib/143</link>
<guid isPermaLink="true">http://scholarworks.gvsu.edu/cistechlib/143</guid>
<pubDate>Wed, 09 May 2012 07:31:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the world of physical therapy, a number of consumer gaming devices have been used with various levels of success. Most commercially available video games are designed for the general population and are, in most cases, overwhelming and difficult for traumatic brain injury (TBI) or stroke patients to use. Specialized therapeutic medical devices are not only expensive and non-portable, they also make limited use of gamification techniques to better engage and motivate the patient. This thesis aims to study the use of inexpensive, portable handheld devices, together with a custom sensor accessory in order to drive a set of therapist designed and configured, short video games. The games are intended to elicit specific therapeutic movements from the patient, and also to produce clinical output for the therapists to use.</p>

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</description>

<author>Alex Restrepo</author>


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<item>
<title>The Originalist Case for the “Individual Mandate”: Rounding out the Government’s Argument in the Health Care Case</title>
<link>http://digitalcommons.law.uga.edu/fac_wp/83</link>
<guid isPermaLink="true">http://digitalcommons.law.uga.edu/fac_wp/83</guid>
<pubDate>Wed, 09 May 2012 07:29:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Supreme Court has now received the briefs and heard the oral arguments in the landmark case that concerns the federal health care law. Much attention has focused on the law’s minimum coverage provision, or so-called “individual mandate,” and in particular its constitutionality under the Commerce Clause and the Necessary and Proper Clause. This Article offers two observations about the arguments made to the Court on that issue. First, it shows that the challengers of the minimum coverage provision adopted a strategy of emphasizing originalist reasoning, while the federal government focused its defense of the law on practical considerations and modern precedents. This difference in tactics, it is suggested, may prove to be of great consequence to the outcome of the case in light of the current Court’s marked receptivity to originalist analysis. Second, the Article suggests that – contrary to the impression created by the submissions of the parties – there are in fact powerful originalism-based reasons for concluding that the minimum coverage provision is constitutional. Indeed, according to the treatment offered here, these arguments have their roots in in all key elements of originalist discourse – the text of the Constitution, the background understandings that gave rise to the relevant clauses, and early congressional and judicial precedents. To be sure, different observers who take different views of constitutional analysis will reach different conclusions about the constitutionality of minimum coverage provision. But this Article contends that originalism-based arguments that were not fully aired before the Court cut strongly in favor of the provision’s constitutionality.</p>

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</description>

<author>Dan T. Coenen</author>


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<item>
<title>Some Preliminary Thoughts on the Law of Neighbors</title>
<link>http://digitalcommons.law.uga.edu/fac_artchop/764</link>
<guid isPermaLink="true">http://digitalcommons.law.uga.edu/fac_artchop/764</guid>
<pubDate>Wed, 09 May 2012 07:25:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>A fundamental characteristic of real property law, one that is definitional in nature, is that its subject matter consists of land parcels. A land parcel, in contrast to an ownership interest such as a fee simple estate, is not an abstraction. Each land parcel has a physical reality, and virtually all land parcels abut other parcels. Each parcel has one particular location, defined by its proximity to other pieces of property. The value of a land parcel depends heavily upon its location, and the nature of neighboring parcels has a major impact in determining that value.</p>
<p>Owners of neighboring parcels have sets of rights, privileges, and duties that define their legal relationships with neighbors. In Anglo-American law, those rights, privileges, and duties are components of real property law, but they are not a recognized category of real property law. Rather, they represent the application of general doctrines and rules to neighbors, instead of a distinct and cohesive body of law of its own. Other legal systems have developed distinct bodies of law to govern relations among neighbors.</p>
<p>The law of neighbors or “neighborhood law” is not presently a recognized type of law practice in the United States, and it will not likely become one anytime in the near future. In part this is the case because neighbor law disputes typically do not involve high financial stakes and resulting incentives for lawyers to market themselves as experts in the area. This Article suggests that if the field of neighbor law develops in the United States, academics will have to lead the way.</p>
<p>This Article does three things. First, it introduces the “stranger model” and the “friend model” of neighbors law, using these models as a frame for describing three components of existing U.S. law applicable to neighboring landowners. Second, it briefly describes the extent to which South Africa and Scotland have come to describe neighbors law as a discrete legal category, which correlates to the stranger model and friend model. Third, it concludes by making several suggestions on how the models may help in the construction of a coherent law of neighbors.</p>

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</description>

<author>Jim Smith</author>


</item>


<item>
<title>UA3/1/7/2 Henry Bosworth Campaign Letter</title>
<link>http://digitalcommons.wku.edu/dlsc_ua_records/1064</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_ua_records/1064</guid>
<pubDate>Wed, 09 May 2012 07:24:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Form letter created by Henry Bosworth's gubenatorial campaign.  This document is part of the Henry Cherry Political Papers.</p>

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</description>

<author>Henry Bosworth</author>


</item>


<item>
<title>Conversations in a Bar</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/393</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/393</guid>
<pubDate>Wed, 09 May 2012 07:24:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Daryl Smith</author>


</item>


<item>
<title>UA3/1/7/2 Edward McDermott Campaign Letter</title>
<link>http://digitalcommons.wku.edu/dlsc_ua_records/1063</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_ua_records/1063</guid>
<pubDate>Wed, 09 May 2012 07:23:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Form letter created by the Edward McDermott gubernatorial campaign.  This document is found in the Henry Cherry Political Papers.</p>

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</description>

<author>Edward McDermott</author>


</item>


<item>
<title>The Impact of Education and Gender on Perception of Borderline Personality Disorder</title>
<link>http://scholarship.shu.edu/theses/214</link>
<guid isPermaLink="true">http://scholarship.shu.edu/theses/214</guid>
<pubDate>Wed, 09 May 2012 07:21:08 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jennifer J. Noonan</author>


</item>


<item>
<title>Alteration of Protein Kinases&apos; Activities by Hypoxic Mimic Compounds</title>
<link>http://scholarship.shu.edu/theses/213</link>
<guid isPermaLink="true">http://scholarship.shu.edu/theses/213</guid>
<pubDate>Wed, 09 May 2012 07:21:06 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Lawerence Rasmussen</author>


</item>


<item>
<title>UA3/1/7/2 Henry Cherry Campaign Letter</title>
<link>http://digitalcommons.wku.edu/dlsc_ua_records/1062</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_ua_records/1062</guid>
<pubDate>Wed, 09 May 2012 07:19:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Form letter created by Henry Cherry's gubernatorial campaign headquarters.</p>

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</description>

<author>Henry Cherry</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1888-1889</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/4</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/4</guid>
<pubDate>Wed, 09 May 2012 07:12:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1889-1890</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/3</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/3</guid>
<pubDate>Wed, 09 May 2012 07:12:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>Culturally Sensitive Palliative Care For Native Seniors: A Case Study</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6939</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6939</guid>
<pubDate>Wed, 09 May 2012 07:10:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis is based on fieldwork done in a native palliative care institution, band run and staffed by native caregivers, located in a expansive native community. The purpose of the present study is to understand how an individual's sense of Self can be affirmed in an institution providing 'culturally sensitive care', defined as interactions and activities that enable the individual to preserve a strong sense of culture, community and family. A strong sense of self should be reflected in the best possible state of physical, psychological and spiritual well-being given the chronic condition of the individual.</p>

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</description>

<author>Deborah Truscott</author>


</item>


<item>
<title>President Adam Herbert and Vice President of Academic Affairs Alan Ling</title>
<link>http://digitalcommons.unf.edu/unf_pres/35</link>
<guid isPermaLink="true">http://digitalcommons.unf.edu/unf_pres/35</guid>
<pubDate>Wed, 09 May 2012 07:10:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>UNF Commencement Ceremony, May 6, 1994.</p>

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</description>


</item>


<item>
<title>For Such A Time As This</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/392</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/392</guid>
<pubDate>Wed, 09 May 2012 07:02:42 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Victor Artreche</author>


</item>


<item>
<title>Racial and Ethnic Group Variations in Service Use among Medicare Home Health Care Beneficiaries with Type 2 Diabetes Mellitus</title>
<link>http://digitalcommons.uconn.edu/gs_theses/247</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/247</guid>
<pubDate>Wed, 09 May 2012 07:01:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Purpose: Due to the importance of Medicare home health care (HHC) to beneficiaries when complications of diabetes mellitus result in the need for skilled home care and consistent with efforts to better understand and minimize racial disparities in patterns of HHC service use, we compared racial and ethnic groups across measures of HHC service use in a nationally representative sample of Medicare HHC beneficiaries with a primary diagnosis of type 2 diabetes mellitus. Methods: Medicare HHC claims were linked to Outcome and Assessment Information Set data in a 20% stratified random sample of Medicare beneficiaries who completed HHC episodes in 2002. Inclusion criteria for this study were self-reported identity as White, African American, Hispanic, or Asian; and a primary HHC diagnosis of type 2 diabetes mellitus. HHC use measures were: visits per week by nursing, physical therapy, home health aide, and all HHC clinicians combined (including occupational therapy, speech therapy, and medical social work). Results: Racial and ethnic group distribution of study sample (N=9,838) was: 62% White, 22% African American, 12% Hispanic, and 3% Asian. Controlling for numerous health-related and sociodemographic covariates, African Americans as compared to Whites received fewer nurse visits per week and fewer visits per week from all clinical staff combined (p < 0.001); Hispanics as compared to Whites were less likely to receive physical therapy (adjusted odds ratio (AOR) = 0.640, 95% confidence interval (CI) = 0.543-0.754, p < 0.001) or home health aide (AOR = 0.716, 95% CI = 0.582-0.880, p = 0.002) services. There were no statistically significant differences in service use measures between African Americans and Hispanics. Conclusions: Hispanic and African American Medicare HHC beneficiaries with type 2 diabetes mellitus received less rehabilitation and fewer skilled nursing services.</p>

	]]>
</description>

<author>Amoah Yeboah-Korang</author>


</item>


<item>
<title>Student Scholarship Day 2001</title>
<link>http://scholarworks.gvsu.edu/ssd_archives/5</link>
<guid isPermaLink="true">http://scholarworks.gvsu.edu/ssd_archives/5</guid>
<pubDate>Wed, 09 May 2012 07:00:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Grand Valley State University</author>


</item>


<item>
<title>Student Scholarship Day 2002</title>
<link>http://scholarworks.gvsu.edu/ssd_archives/4</link>
<guid isPermaLink="true">http://scholarworks.gvsu.edu/ssd_archives/4</guid>
<pubDate>Wed, 09 May 2012 07:00:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Grand Valley State University</author>


</item>


<item>
<title>Student Scholarship Day 2004</title>
<link>http://scholarworks.gvsu.edu/ssd_archives/3</link>
<guid isPermaLink="true">http://scholarworks.gvsu.edu/ssd_archives/3</guid>
<pubDate>Wed, 09 May 2012 07:00:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Grand Valley State University</author>


</item>


<item>
<title>Student Scholarship Day 2005</title>
<link>http://scholarworks.gvsu.edu/ssd_archives/2</link>
<guid isPermaLink="true">http://scholarworks.gvsu.edu/ssd_archives/2</guid>
<pubDate>Wed, 09 May 2012 07:00:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Grand Valley State University</author>


</item>


<item>
<title>Student Scholarship Day 2006</title>
<link>http://scholarworks.gvsu.edu/ssd_archives/1</link>
<guid isPermaLink="true">http://scholarworks.gvsu.edu/ssd_archives/1</guid>
<pubDate>Wed, 09 May 2012 07:00:16 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Grand Valley State University</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1886-1887</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/2</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/2</guid>
<pubDate>Wed, 09 May 2012 06:59:04 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>St. Ignatius Catalogue, 1887-1888</title>
<link>http://collected.jcu.edu/stignatiuscatalogues/1</link>
<guid isPermaLink="true">http://collected.jcu.edu/stignatiuscatalogues/1</guid>
<pubDate>Wed, 09 May 2012 06:59:03 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>An Examination of the Ability of Christian Schools to Prevent Deterioration of Doctrinal Integrity in Postmodern Christian Youth</title>
<link>http://digitalcommons.cedarville.edu/education_theses/13</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/13</guid>
<pubDate>Wed, 09 May 2012 06:52:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Can Christian schools prevent the deterioration of doctrinal integrity, or do factors such as the church and family have a greater impact? Sixty young adults were surveyed that had attended Christian school for four or more years during seventh through twelfth grades as were thirty-one that had not. The purpose was to assess the influence that Christian school, church, and family have had on the doctrinal integrity of eighteen to twenty-one year-old Christians. Upon completion of the study, it was found that there was not a statistically significant difference in the doctrinal integrity of the two groups of students. However, a statistically significant correlation was found between doctrinal integrity and both church involvement and family influence. It was also found that among those surveyed, the degree of doctrinal “confusion” was not nearly as severe as that which had been presented in other research.</p>

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</description>

<author>David H. Bryant</author>


</item>


<item>
<title>Tables</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/28</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/28</guid>
<pubDate>Wed, 09 May 2012 06:52:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Index</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/29</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/29</guid>
<pubDate>Wed, 09 May 2012 06:52:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Chapter 22: Evidence</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/26</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/26</guid>
<pubDate>Wed, 09 May 2012 06:52:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frederick A. McDermott</author>


</item>


<item>
<title>Chapter 23: Administration of Justice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/27</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/27</guid>
<pubDate>Wed, 09 May 2012 06:52:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan J. Dimond</author>


</item>


<item>
<title>Chapter 20: Workmen&apos;s Compensation</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/24</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/24</guid>
<pubDate>Wed, 09 May 2012 06:52:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Maurice F. Shaughnessy</author>


</item>


<item>
<title>Chapter 21: Civil Procedure and Practice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/25</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/25</guid>
<pubDate>Wed, 09 May 2012 06:52:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Wendell F. Grimes</author>


</item>


<item>
<title>Chapter 19: State and Municipal Government</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/23</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/23</guid>
<pubDate>Wed, 09 May 2012 06:52:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph C. Duggan</author>


</item>


<item>
<title>Chapter 18: Insurance</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/22</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/22</guid>
<pubDate>Wed, 09 May 2012 06:52:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J. Albert Burgoyne</author>


</item>


<item>
<title>Chapter 16: Public Utilities</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/20</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/20</guid>
<pubDate>Wed, 09 May 2012 06:52:12 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Herbert Baer</author>


</item>


<item>
<title>Chapter 17: State Taxation</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/21</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/21</guid>
<pubDate>Wed, 09 May 2012 06:52:12 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>David Flower Jr.</author>


</item>


<item>
<title>Chapter 14: Zoning and Land Use</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/18</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/18</guid>
<pubDate>Wed, 09 May 2012 06:52:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Richard G. Huber</author>


</item>


<item>
<title>Chapter 15: Labor Relations</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/19</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/19</guid>
<pubDate>Wed, 09 May 2012 06:52:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Lawrence M. Kearns</author>


</item>


<item>
<title>Chapter 13: Administrative Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/17</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/17</guid>
<pubDate>Wed, 09 May 2012 06:52:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>George N. Welch</author>


</item>


<item>
<title>Chapter 11: Constitutional Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/15</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/15</guid>
<pubDate>Wed, 09 May 2012 06:52:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John D. O&apos;Reilly Jr.</author>


</item>


<item>
<title>Chapter 12: Criminal Law, Procedure, and Administration</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/16</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/16</guid>
<pubDate>Wed, 09 May 2012 06:52:09 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J. Edward Collins</author>


</item>


<item>
<title>Chapter 9: Security and Mortgages</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/13</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/13</guid>
<pubDate>Wed, 09 May 2012 06:52:08 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Austin T. Stickells</author>


</item>


<item>
<title>Chapter 10: Conflict of Laws</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/14</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/14</guid>
<pubDate>Wed, 09 May 2012 06:52:08 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Monroe Inker</author>


</item>


<item>
<title>Chapter 7: Commercial Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/11</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/11</guid>
<pubDate>Wed, 09 May 2012 06:52:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William E. Hogan</author>


</item>


<item>
<title>Chapter 8: Domestic Relations and Persons</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/12</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/12</guid>
<pubDate>Wed, 09 May 2012 06:52:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William J. Greenler Jr.</author>


</item>


<item>
<title>Chapter 6: Corporations</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/10</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/10</guid>
<pubDate>Wed, 09 May 2012 06:52:06 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bertram H. Loewenberg</author>


</item>


<item>
<title>Chapter 4: Contracts and Agency</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/8</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/8</guid>
<pubDate>Wed, 09 May 2012 06:52:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kenneth B. Hughes</author>


</item>


<item>
<title>Chapter 5: Equity and Equity Practice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/9</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/9</guid>
<pubDate>Wed, 09 May 2012 06:52:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Harry Zarrow</author>


</item>


<item>
<title>Chapter 2: Trusts and Estates</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/6</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/6</guid>
<pubDate>Wed, 09 May 2012 06:52:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Emil Slizewski</author>


</item>


<item>
<title>Chapter 3: Torts</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/7</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/7</guid>
<pubDate>Wed, 09 May 2012 06:52:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Robert E. Keeton</author>


</item>


<item>
<title>Chapter 1: Property and Conveyancing</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/5</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/5</guid>
<pubDate>Wed, 09 May 2012 06:52:03 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Cornelius J. Moynihan</author>


</item>


<item>
<title>Summary of Contents</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/3</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/3</guid>
<pubDate>Wed, 09 May 2012 06:52:02 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Table of Contents</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/4</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/4</guid>
<pubDate>Wed, 09 May 2012 06:52:02 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Foreword</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/2</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/2</guid>
<pubDate>Wed, 09 May 2012 06:52:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Calvert Magruder</author>


</item>


<item>
<title>Masthead</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/1</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1958/iss1/1</guid>
<pubDate>Wed, 09 May 2012 06:52:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>The State of Research on Multinationals and Emerging Markets</title>
<link>http://scholarship.rollins.edu/as_facpub/44</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/as_facpub/44</guid>
<pubDate>Wed, 09 May 2012 06:46:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Emerging markets are increasingly becoming the growth drivers of the global economy and there is increased scrutiny and interest in emerging markets since the 1990s. The interest can be viewed from a demand and supply perspective. With a huge population and increasing income, emerging economies provide a big market for goods and services. Also, with talented manpower and low costs, emerging economies are supplying more and more goods and services to the world (Pillania, 2009). Multinational corporations (MNCs) play a very important role in global business and economy. There is an increased interest in research and explanation for emerging markets and MNCs (London and Hart, 2004; Meyer, 2004; Ramamurti, 2004; Khanan et al., 2005, Pillania, 2009).</p>
<p>This article contributes to a better understanding of the research field of multinationals and emerging markets as well as knowledge on key disciplines, journals, and articles. Bibliometric analysis represents a relatively new form of meta-analytical research or “meta-review” of the literature (Kim and McMillan, 2008). It is valuable in illustrating the links between and among scholarly works and the nature of development in a given research field or discipline by measuring and analyzing published materials (Borgman, 2000). Citation analysis is a bibliometric technique that considers a citation as the basic unit of analysis (Kim and McMillan, 2008). Initially, it has been used in diverse range of disciplines in the science and humanities (Price, 1976; White and McCain, 1989; Wiberley, 2003), and only recently in social science (Glanzel 1996) such as communications (Pasadeos et al., 1999), advertising (Kim and McMillan, 2008), marketing (Arnott, 2007), and international management (Acedo and Casilla, 2005).</p>

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</description>

<author>Rajesh K. Pillania et al.</author>


</item>


<item>
<title>A Tribute to Nicholas</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/391</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/391</guid>
<pubDate>Wed, 09 May 2012 06:42:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Dalles</author>


</item>


<item>
<title>Geomorphological Approach to Toxic Trace Metal Distribution Across a Medial Bar Deposit in the Trout Brook of the Park River Watershed, Hartford, CT</title>
<link>http://digitalrepository.trincoll.edu/theses/233</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/233</guid>
<pubDate>Wed, 09 May 2012 06:27:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Trout Brook, a major tributary of the Park River watershed, was sampled for heavy metals in sediment with a focus on Pb, Cu, Cd, and Zn. These metals are known to be contaminating the river due to a history of discharge from metal finishing industries. In a watershed-wide survey conducted in September 2011, high concentrations of metals were found in the Trout Brook, with some sites exceeding the probable effect concentration (PEC). The Trout Brook contains a Sanitary Sewer Overflow (SSO) and a vegetated medial bar that may be trapping sediment. Based on the results of the earlier studies, this site was chosen for an in depth analysis. In 2010, a detailed sediment study was performed at the landfill site, located on the north bank of the Trout Brook further downstream from the SSO site, which contained a landfill point source and a sand bar. It was unclear what lead to the high heavy metals values: the SSO or the effects of sediment transport around the bar. The Trout Brook SSO site provides the opportunity for a more detailed analysis of the relationship between a potential point source and a vegetated bar and resulting sediment contamination. The purpose of the study was to determine the degree to which the SSO and the medial bar affect the distribution of heavy metals. Forty-nine samples were taken on the north and south banks of the Trout Brook SSO site and on either side of the vegetated bar. Five sediment cores were taken from the bar to determine if trace metals are accumulated within the river’s older deposits. Trace metals in sediments were analyzed using a weak-acid digestion method and an Inductively Coupled Plasma-OES (ICP-OES). Highest concentrations of metals were found at the SSO and therefore it is concluded that the SSO acts as the main source of heavy metal contamination, and that the medial bar has no effect on the distribution of metals in sediment.</p>

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</description>

<author>Kelsey Semrod</author>


</item>


<item>
<title>Computable Linear Orders and Turing Reductions</title>
<link>http://digitalcommons.uconn.edu/gs_theses/246</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/246</guid>
<pubDate>Wed, 09 May 2012 06:26:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis explores computable linear orders through Turing Reductions and codes zero jump and zero double jump into linear orders using discrete, dense, and block linear relations.</p>

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</description>

<author>Whitney P. Turner</author>


</item>


<item>
<title>The Truth Shall Set You Free: The Bible, the Revolution, and the Debate over Slavery in the American South</title>
<link>http://digitalcommons.liberty.edu/masters/239</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/masters/239</guid>
<pubDate>Wed, 09 May 2012 06:18:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Before the slavery debate pushed a divided American nation to the brink of civil war, the argument divided the family of God.  By the time cannon fire erupted at Fort Sumter, Christians had already staked out positions based on sophisticated lines of argument they used to justify or condemn chattel slavery.  The generation coming of age during the Civil War era witnessed a debate more intense and contentious than their ancestors had seen, but in terms of the arguments employed, it broke very little fresh ground.  Contrary to the assumption that antebellum apologists in the South invented the defense of slavery as a positive good, the attempt to defend chattel slavery began long before ministers argued for the benefits of the institution in the 1830s.   People of God largely supported the growth and virtue of slavery based on a narrow perception informed by their own personal experience.  The slavery they knew was benevolent, not the degrading aberration described by abolitionists.  The blacks they knew were not the social or intellectual equals of whites and thus, would benefit from being enslaved.  The Bible they knew afforded proslavery Christians enough justification to support their preconceived notions.  These factors combined to create a defense of slavery they viewed as consistent and justifiable. Christians committed to the same Bible, arrived at completely different conclusions regarding the biblical sanction of slavery.  Their willingness to make Scripture fit their preconceived notions concerning the nature of slavery in the American South helped widen the disagreement.  Common misconceptions over the racial inferiority of blacks evidenced an intellectual blind-spot that led both sides to equate race slavery with biblical slavery.  These misconceptions caused many to claim the Bible sanctioned slavery even as they dismissed any possible scriptural distinction between servitude regulated by the Almighty and the brutal, demeaning brand of race slavery practiced primarily by southerners.  Thinkers on both sides commonly considered biblical references, Enlightenment concepts of the natural rights of man, and pragmatic economic and social arguments to construct a formidable polemic. The early arguments informed the later debate, and a common thread wound its way through the dialogue, from colonial days through the national challenge of Reconstruction.  While Christians disagreed regarding what Scripture proscribed, they chose to contextualize the Bible and define slavery in a manner best suited to their argument.  The debate simmered for over a century.  Ironically, it was agreement regarding the racial inferiority of the black that enabled some men to accept slavery while it prevented others from drawing a clear distinction between biblical servitude and race slavery.  The volatile combination of misrepresentation, misinterpretation, and ignorance could only remain dormant for so long.  The emotionally charged atmosphere of the mid-nineteenth century became the incubator that released the contagion of disunion upon the nation.  Many lamented the coming of that dreaded day; others wondered how the nation had maintained a semblance of unity for so long.</p>

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</description>

<author>Kevin Simon</author>


<category>Black Studies</category>

<category>Religion, General</category>

<category>Religion, Clergy</category>

<category>History, Black</category>

<category>History, United States</category>

<category>History, Church</category>

</item>


<item>
<title>Valuating Brand Equity and Product Related Attributes in the Context of the German Automobile Market</title>
<link>http://scholarship.rollins.edu/as_facpub/43</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/as_facpub/43</guid>
<pubDate>Wed, 09 May 2012 06:17:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The concept of consumer-based brand equity has been discussed widely in the literature and there are a wide variety of both quantitative and qualitative measures used to assess it. For the most part, previous research has studied the way a brand and product attributes are <em>perceived</em> in a consumer’s mind and the empirical data used in most studies is based on self-reported survey data. In this research, objective data from the largest German Automobile Association, including <em>actual</em> prices, objective quality ratings of product attributes and market share of brands are used to estimate their effect on the actual price set by the manufacturer and paid by consumers for those automobiles in Germany. By conducting multiple hedonic regressions we are able to explain the actual price of a car on the basis of it’s product attributes, brand and the market share of that brand. Our results show that five out of the eight product attribute categories used in this research (chassis, interior, comfort, engine, and safety) influence the price paid by consumers. In addition, when brand dummy variables are added to the model the explanatory power of the proposed model increases. The paper also shows that product variety is positively related and market share negatively related to the price. Therefore, this paper provides an important contribution to existing literature on modeling and measuring the effect of product related attributes, market share and especially brand equity on price. It further provides important managerial insight as it shows which product attributes and how they are valued by consumers. In addition, the proposed model can be used by automotive manufacturers to approximate the price of existing and new automobiles.</p>

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</description>

<author>Marc Fetscherin et al.</author>


</item>


<item>
<title>Educational Structures of the 50 States</title>
<link>http://diginole.lib.fsu.edu/ecs/6</link>
<guid isPermaLink="true">http://diginole.lib.fsu.edu/ecs/6</guid>
<pubDate>Wed, 09 May 2012 06:16:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper is part of a substantial amount of research work which was defined and solicited by the Governors Commission on the Structure and Governance of Education in Maryland (the Rosenberg Commission) from many scholarly people working throughout the Maryland system of education.</p>
<p>This publication briefly outlines the educational structures in all 50 states and the District of Columbia. The Organizational chart form restricted the amount of information that could be used. Also, because changes in educational structure are constantly being made, some information may be obsolete.</p>

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</description>

<author>Governor&apos;s Commission on the Structure and Governance of Education in Maryland</author>


</item>


<item>
<title>Sermon</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/390</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/390</guid>
<pubDate>Wed, 09 May 2012 06:13:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jeff Peppers</author>


</item>


<item>
<title>Adult Perceptions of the Experience of Being Identified &quot;Talented and Gifted&quot; as Children: A Phenomenological Study</title>
<link>http://digitalcommons.liberty.edu/doctoral/558</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/doctoral/558</guid>
<pubDate>Wed, 09 May 2012 06:10:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>This is a phenomenological study of adult perceptions of the experience of being identified "talented and gifted" as children.  Data were gathered by transcribing the video recordings of adults who were students of the Talented and Gifted (TAG) education program in Fairfield, Ohio during 1978-1983.  The phenomenological method was used to discover perceptions of a unique population of adults who shared life experiences during elementary and middle school.  Analysis of the data resulted in the identification of four main themes: Growth, Interpersonal, Future, and Thankfulness.  Three facilitating and three challenging subthemes were identified under each main theme.  These were: Internal Validation of TAG Identity, Opportunity to Channel Talents and Gifts, Broadminded Thinking for Problem Solving, Overcoming Self-criticism, Setting Priorities Relative to the TAG Identity, Persuading Others, Positive Bonding Within TAG, Respect from Others, Social Confidence, Feelings of Isolation, Being Misunderstood, Ongoing Intellectual Insecurity, TAG Career Preparation, Optimism, Awareness of Responsibility to Achieve Potential, Career Indecision, Boredom With the Status Quo, How to Achieve Potential, Creative Outlet, Positive Memories, Love for Enthusiastic Teachers, Need for Creative Outlet Post-TAG, Creating New Memories, and Disappointed with Other Education.  Implications for future practice and research include an eclectic approach to counseling and education with the TAG identity in mind.  Cognitive Behavioral, Adlerian, and Existentialist theories and therapies are recommended as a resource for therapists and educators to help gifted people discover what they want out of life, and to help them focus on positive action in the present moment.</p>

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</description>

<author>Bradford Summers</author>


<category>Education, Educational Psychology</category>

<category>Education, General</category>

<category>Education, Sociology of</category>

<category>Psychology, General</category>

</item>


<item>
<title>Ministry of Memories: Keys to Pastoral Care of Non-Cognitive Persons</title>
<link>http://digitalcommons.liberty.edu/doctoral/557</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/doctoral/557</guid>
<pubDate>Wed, 09 May 2012 06:09:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>This work is intended to examine and study the theological and moral reasons to provide pastoral care to persons who have limited or no cognition. Dementia, Alzheimer's, certain other medical conditions and the aging process cause a loss of brain function that affects memory, thinking, behavior and judgment. Most Clergy wrestle with the fact as to whether there is any purpose in ministering to such persons especially when there is no verbal or non-verbal response.  This paper involves surveys, research, collection of historical and biblical data and medical science to evaluate the disease process and explore ways in which to communicate with them and in turn help them connect with God.   This thesis will also help families of non-cognitive persons, caregivers, peers and the writer to better understand ways in which to love and care for these marginalized people.</p>

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</description>

<author>Reginald Corfield</author>


<category>Religion, General</category>

<category>Religion, Clergy</category>

<category>Religion, Philosophy of</category>

<category>Psychology, Cognitive</category>

<category>Health Sciences, General</category>

<category>Gerontology</category>

</item>


<item>
<title>Forgiveness Fundamentals</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/389</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/389</guid>
<pubDate>Wed, 09 May 2012 06:00:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Toddy Holeman</author>


</item>


<item>
<title>The Ethics of Conducting Ex Parte Interviews</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss2/8</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss2/8</guid>
<pubDate>Wed, 09 May 2012 05:59:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Eugene P. Gurr</author>


</item>


<item>
<title>Direct Mail Solicitation by Attorneys</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss2/6</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss2/6</guid>
<pubDate>Wed, 09 May 2012 05:59:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Philip Franke</author>


</item>


<item>
<title>Residency Requirements for Admission to the Bar</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss2/7</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss2/7</guid>
<pubDate>Wed, 09 May 2012 05:59:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Robert Cote</author>


</item>


<item>
<title>Chambers v. Omaha Girls Club, Inc.: The Eighth Circuit Opens the Door to Pregnancy Based Discrimination</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss2/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss2/5</guid>
<pubDate>Wed, 09 May 2012 05:59:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Patricia K. Hart</author>


</item>


<item>
<title>Section 17(a) of the Securities Act of 1933 and an Implied Action: An Answer Is In Sight</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss2/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss2/3</guid>
<pubDate>Wed, 09 May 2012 05:59:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Julianne Gennuso</author>


</item>


<item>
<title>Can the IRS &quot;Whiteout&quot; a Surrogate&apos;s Court Decision on the Deductability of Administration Expenses Under I.R.C. § 2053? United States v. White</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss2/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss2/4</guid>
<pubDate>Wed, 09 May 2012 05:59:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph P. Gaffney</author>


</item>


<item>
<title>The Constitutionality of Attorney Fee Forfeiture Under the Comprehensive Forfeiture Act</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss2/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss2/1</guid>
<pubDate>Wed, 09 May 2012 05:59:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Andrea E. Forman et al.</author>


</item>


<item>
<title>Hazlewood School District v. Kuhlmeier: Has the Schoolhouse Gate Shut on the Marketplace of Ideas?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss2/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss2/2</guid>
<pubDate>Wed, 09 May 2012 05:59:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bennett R. Katz</author>


</item>


<item>
<title>Scaling Approach to Spin-Glass Phenomena</title>
<link>http://scholarlyrepository.miami.edu/physics_articles/62</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/physics_articles/62</guid>
<pubDate>Wed, 09 May 2012 05:36:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>The scaling model of spin-glass phenomena is extended to consider both longitudinal and transverse order parameters q<sub>1</sub> and q<sub>t</sub>. The lowest-order coupling in the free energy goes as q<sub>l</sub><sup>2</sup>q<sub>t</sub><sup>2</sup>. The field (h) dependence of the reduced temperature t for transverse freezing is found to be t∼h<sup>4/δ</sup> where δ is the conventional nonlinear susceptibility field exponent (χ∼h<sup>2/δ</sup>). While the transverse correlation length diverges at t=0, the longitudinal correlation length remains finite.</p>

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</description>

<author>S. E. Barnes et al.</author>


</item>


<item>
<title>Derivation of Exact Results for the Single-Ion Kondo Problem with the Use of Diagrammatic Methods</title>
<link>http://scholarlyrepository.miami.edu/physics_articles/61</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/physics_articles/61</guid>
<pubDate>Wed, 09 May 2012 05:36:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>It is shown that exact results for the single-impurity Kondo problem can be obtained by diagrammatic methods. The results for the susceptibility and specific heat agree with those obtained by Wilson’s numerical methods. In particular, the crossover W’=(π/e)<sup>1/2</sup> and Wilson R=2 ratios are reproduced exactly. Conduction-electron scattering from the impurity reaches the unitarity limit corresponding to a phase shift δ=π/2. Both this and the compensation of the impurity spin are also exact results. The methods described are relatively easily extended to the Anderson model and the corresponding lattice problems.</p>

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</description>

<author>S. E. Barnes</author>


</item>


<item>
<title>Theory of in situ Measurement of Wave-Vector-Dependent Dynamic Susceptibility and ESR Spectroscopy Using the AC Josephson Effect</title>
<link>http://scholarlyrepository.miami.edu/physics_articles/60</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/physics_articles/60</guid>
<pubDate>Wed, 09 May 2012 05:36:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The elementary theory of in situ measurements of the wave-vector-dependent dynamic susceptibility χ(q,ω) in superconductor-insulator-superconductor (SIS) and superconductor–normal-metal–superconductor (SNS) Josephson junctions is presented in some detail. The theory for more complicated SISN and SINS junctions is also described. In addition, the theory of point-contact and superconducting quantum interference device geometries, relevant to the recent experiments of Baberschke, Bures, and Barnes is developed. Involved is a detailed application of the Maxwell and London equations along with the distributed Josephson effect. In a measurement of χ(q,ω), the frequency ω is determined by the relation 2eV<sub>0</sub>=ħω where V<sub>0</sub> is the voltage applied across the junction, and the wave vector q is determined by the relation 2edB<sub>0</sub>=ħq where d is the effective width of the junction and B<sub>0</sub> is the magnetic field applied perpendicular to the direction of the current. The relative merits of the different types of junctions are discussed and the expected signal strengths are estimated. The limitations for the maximum measurable frequency and wave vector are also given. It seems probable that the proposed technique can be used to measure spin-wave branches from zero wave vector up to about 10% of the way to the Brillouin zone edge. The electron-spin resonance (ESR) of dilute magnetic systems can be measured as in the experiments of Baberschke, Bures, and Barnes. Estimates and experiment suggest that this method of performing ESR is better than an order of magnitude more sensitive than conventional methods. Some applications are discussed.</p>

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</description>

<author>S. E. Barnes et al.</author>


</item>


<item>
<title>Paramagnetic Resonance of Cu&lt;sup&gt;2+&lt;/sup&gt; Ions in the Superconductor Y&lt;sub&gt;0.2&lt;/sub&gt;Ba&lt;sub&gt;0.8&lt;/sub&gt;CuO&lt;sub&gt;x&lt;/sub&gt;</title>
<link>http://scholarlyrepository.miami.edu/physics_articles/59</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/physics_articles/59</guid>
<pubDate>Wed, 09 May 2012 05:36:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>A strong paramagnetic resonance signal characteristic of Cu<sup>2+</sup> ions in ‖x<sup>2</sup>-y<sup>2</sup>〉 states is observed in the high-T<sub>c</sub>≊90 K superconductor Y<sub>0.2</sub>Ba<sub>0.8</sub>CuO<sub>x</sub>. The line intensity of the ioniclike signal shows a deviation from Curie behavior at T≳T<sub>c</sub>. It is speculated that the phase that is responsible for the signal is an example of an Anderson lattice with an unusually high Kondo temperature.</p>

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</description>

<author>F. Mehran et al.</author>


</item>


<item>
<title>Seeing only Jesus</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/388</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/388</guid>
<pubDate>Wed, 09 May 2012 05:27:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mike Watson</author>


</item>


<item>
<title>Willy Widmer</title>
<link>http://arrow.dit.ie/scthebk/28</link>
<guid isPermaLink="true">http://arrow.dit.ie/scthebk/28</guid>
<pubDate>Wed, 09 May 2012 04:52:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Willy Widmer</author>


</item>


<item>
<title>Evaluation of outcomes of elderly patients at 3 and 15 months post hip fracture</title>
<link>http://epubs.rcsi.ie/mscrestheses/9</link>
<guid isPermaLink="true">http://epubs.rcsi.ie/mscrestheses/9</guid>
<pubDate>Wed, 09 May 2012 04:44:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>The aim of this study was to observe the functional abilities of hip fracture patients at two time points post hip fracture.</p>
<p>Falls and fractures are a major concern for the elderly population as they can result in decreased functional abilities and more dependence to complete activities of daily living within the community.</p>
<p>The use of valid, reliable and sensitive outcome measures is essential to observe functional abilities over time and assess the risk of falls in the future. Eighty-one patients consented to participate in this study with thirty three participating in the early assessment group; these patients were assessed at three and 15 months. For the 81 subjects, the average age was 81 years with a standard deviation of 8.00 years (60 - 96 years). The average age of the 33 subjects was 81 years (sd 8.00, range 65 - 94). A range of measures assessing movement, strength, balance, endurance and extended activities of daily living were applied.</p>
<p>The types of fracture, surgery, length of stay to surgery, types of anaesthesia used, surgical approach used, pain reported, discharge plan from the acute hospital, length of stay were reviewed in both the acute hospital and rehabilitation facility.</p>
<p>At three months the mean Berg balance score was 39.16 (sd12.98, range 18 - 56) and 15 months 38.44 (sd 14.04; range 11 -55) but no significant differences were found (p>0.05).</p>
<p>The mean Timed Up and Go score was 29.90 (sd 18.99; range 0 - 69.18) at three months and 27.27 (sd 18.76; range 0 - 66.38) at fifteen months but no significant differences were found (p>0.05).</p>
<p>The mean six minute walk test scores for the early assessment group were 165.84m (sd 85.34; range 0 - 359.20) at three months and at 15-months 193.72m (sd 110.98; range 0 - 3 84.69), the change was not significant (p>0.05).</p>
<p>At three months the right hand dynamometry mean score was 25.56 (sd 13.57; range 0 - 65) lbs and left hand mean score was 25.48 (sd 10.88; range 6.00 - 46.00) lbs. At fifteen months the right hand dynamometry score was 23.80 (sd 12.67 range 8.67 - 59.33) lbs and left hand dynamometry score was 25.48 (sd 8.47; range 11 - 37.67) lbs. No significant differences were found in grip strength (p>0.05).</p>
<p>The mean pre-fracture Nottingham Extended activities of daily living (NEADL) score was 47.61 (sd 13.14; range 18 - 63) while at three months the mean score was 32.55 (sd 17.26; range 3 - 63) and at fifteen months was 39.45 (sd 18.45; range 1 - 63). Significant differences were found between pre fracture and 3 months (p</p>
<p>In conclusion, no significant functional improvements were observed after 3 months despite significant in-patient input (compared with other countries) and further physiotherapy/rehabilitation input post discharge. Therefore, the findings from this study highlight the need to re-evaluate the current model of care for elderly post hip fracture patients.</p>

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</description>

<author>Sheila McCarthy</author>


</item>


<item>
<title>Herbert (Sonny) Geldof</title>
<link>http://arrow.dit.ie/scthebk/27</link>
<guid isPermaLink="true">http://arrow.dit.ie/scthebk/27</guid>
<pubDate>Wed, 09 May 2012 04:30:33 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Herbert (Sonny) Geldof</author>


</item>


<item>
<title>Geology of National Parks Modules for the Spreadsheets Across the Curriculum Library</title>
<link>http://scholarcommons.usf.edu/gly_facpub/74</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/74</guid>
<pubDate>Wed, 09 May 2012 03:56:27 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>H. Len Vacher et al.</author>


</item>


<item>
<title>Featured Collection: Headwaters Hydrology</title>
<link>http://scholarcommons.usf.edu/gly_facpub/73</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/73</guid>
<pubDate>Wed, 09 May 2012 03:56:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>In January 2001, the U.S. Supreme Court issued a ruling in the case of Solid Waste Agency of Northern Cook County v. U.S. Army Corps of Engineers, 531 U.S. 159 (2001) (SWANCC). The SWANCC case presented the Court with two issues: (1) whether an isolated water could be considered part of the “waters of the United States,” protected under the Clean Water Act (CWA) – and thus subject to the U.S. Army Corps of Engineers’ (Corps) regulatory authority under Section 404 of the CWA – solely based on its use by migratory birds; and, if so, (2) whether Congress had the constitutional authority under the Commerce Clause to include these as waters of the United States. In particular, the Court considered the Corps’ Migratory Bird Rule – which deemed waters of the United States to include isolated intrastate waters that provide habitat for migratory birds. In a 5-4 decision, the Court found that the Migratory Bird Rule exceeded the Corps’ authority under the CWA [531 U.S., 159 (2001)], and held that the CWA is not intended to protect isolated, intrastate, non-navigable waters based solely on their use by migratory birds. While the Court’s decision did not create a bright line test for what Congress intended to regulate under the CWA, the Court’s reasoning implies that the CWA intended some “connection” to navigability, and that isolated waters need a “significant nexus” to navigable waters to be jurisdictional.</p>

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</description>

<author>T. L. Nadeau et al.</author>


</item>


<item>
<title>The role of groundwater in resource conservation efforts</title>
<link>http://scholarcommons.usf.edu/gly_facpub/72</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/72</guid>
<pubDate>Wed, 09 May 2012 03:56:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is something mysterious about groundwater that befuddles some of my brightest colleagues. Surface water is so much easier to comprehend. The presence and behavior of surface water is easily observed, and the environmental and economic benefits of surface water are easily quantified. Yet fresh surface water is a small component of the global water budget, which is composed of 125,000 km3 of fresh surface water and 8,500,000 km3 of fresh groundwater. More important, fresh surface water is an integral part of a hydrological cycle linking the oceans, atmosphere, and fresh surface water and groundwater. The linkages between fresh surface water and groundwater are particularly pronounced; indeed, the distinction between the two often is blurred. Thus, one cannot be altered without concomitantly altering the other. In Water Follies: Groundwater Pumping and the Fate of America's Fresh Waters by Robert Glennon, we finally have a general-interest book that tells us why and that details the consequences.</p>

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</description>

<author>Mark Cable Rains</author>


</item>


<item>
<title>Hydrogeologic principles useful in predicting the effects of stream flow alterations on shallow groundwater and associated riparian vegetation</title>
<link>http://scholarcommons.usf.edu/gly_facpub/71</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/71</guid>
<pubDate>Wed, 09 May 2012 03:56:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Numerous studies have shown that stream water and shallow groundwater are tightly linked in alluvial settings, and that changes in stream stage are propagated rapidly across alluvial aquifers (Castro and Hornberger 1991, Sophocleous 1991). Thus, many researchers have assumed that stream stages approximate water tables in alluvial aquifers (Auble et al. 1994, Stromberg and Patten 1996). This assumption is valid in some cases but invalid in other cases, particularly in arid basin terrain and more humid mountain terrain. Even when this assumption is valid, this relationship only implies correlation and not causation so the potential effects of stream flow alterations on shallow groundwater and associated riparian vegetation remain unknown.</p>

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</description>

<author>Mark Cable Rains</author>


</item>


<item>
<title>Simulated changes in shallow groundwater and vegetation distributions under different reservoir operations scenarios</title>
<link>http://scholarcommons.usf.edu/gly_facpub/70</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/70</guid>
<pubDate>Wed, 09 May 2012 03:56:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>The objectives of this study were to develop and use a linked groundwater and vegetation model to simulate groundwater and vegetation distributions in a riverine and reservoir-fringe system under different reservoir operations scenarios. This study was conducted where Little Stony Creek flows into East Park Reservoir on the east front of the Coast Range, northern California. A numerical groundwater model was used to model mean depth to groundwater during the growing season for water years 1980–1999 for each of five community types identified on the study site. Multiple vegetation models were developed, each of which described the probability that a given community type would occur primarily as a function of modeled mean depth to groundwater during the growing season and secondarily as a function of flooding. Four scenarios representing four different reservoir operations were simulated: existing condition, existing condition with late drawdown, full drawdown, and full pool. A groundwater backwater effect caused by the imposed reservoir stage extends to portions of the terrace, but the most pronounced effects occur on the delta. Consequently, the most pronounced changes in vegetation distributions also occur on the delta. Compared to the existing-condition scenario, modeled vegetation distributions do not change under the existing condition with late-drawdown scenario, a xeric herbaceous community type is greatly expanded under the full-drawdown scenario, and mesic herbaceous, scrub-shrub, and forested community types are greatly expanded under the full-pool scenario. The results of this study are twofold. First, the linked groundwater and vegetation model is relatively simple to construct and can be used to efficiently simulate multiple surface-water and groundwater management scenarios. Second, changes in reservoir operations can have pronounced effects on shallow groundwater and associated vegetation distributions in riverine and reservoir-fringe systems. Thus, the effects of changing reservoir operations must be considered if the management of shallow groundwater and associated plant and wildlife habitat resources is to be successful.</p>

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</description>

<author>Mark Cable Rains et al.</author>


</item>


<item>
<title>The role of perched aquifers in hydrological connectivity and biogeochemical processes in vernal pool landscapes</title>
<link>http://scholarcommons.usf.edu/gly_facpub/68</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/68</guid>
<pubDate>Wed, 09 May 2012 03:56:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mark Cable Rains et al.</author>


</item>


<item>
<title>Local shallow groundwater drawdown and baseflow cessation due to regional groundwater pumping.  In Lowrance, R. (Ed.), Riparian Ecosystems and Buffers: Multi-Scale Structure, Function, and Management</title>
<link>http://scholarcommons.usf.edu/gly_facpub/69</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/69</guid>
<pubDate>Wed, 09 May 2012 03:56:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mark Cable Rains et al.</author>


</item>


<item>
<title>Hydrological connectivity of headwaters to downstream waters: State-of-the-science and future directions</title>
<link>http://scholarcommons.usf.edu/gly_facpub/67</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/67</guid>
<pubDate>Wed, 09 May 2012 03:56:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>In January 2001, the U.S. Supreme Court ruled that the U.S. Army Corps of Engineers exceeded its statutory authority by asserting Clean Water Act (CWA) jurisdiction over non-navigable, isolated, intrastate waters based solely on their use by migratory birds. The Supreme Court’s majority opinion addressed broader issues of CWA jurisdiction by implying that the CWA intended some “connection” to navigability and that isolated waters need a “significant nexus” to navigable waters to be jurisdictional. Subsequent to this decision (SWANCC), there have been many lawsuits challenging CWA jurisdiction, many of which are focused on headwater, intermittent, and ephemeral streams. To inform the legal and policy debate surrounding this issue, we present information on the geographic distribution of headwater streams and intermittent and ephemeral streams throughout the U.S., summarize major findings from the scientific literature in considering hydrological connectivity between headwater streams and downstream waters, and relate the scientific information presented to policy issues surrounding the scope of waters protected under the CWA. Headwater streams comprise approximately 53% (2,900,000 km) of the total stream length in the U.S., excluding Alaska, and intermittent and ephemeral streams comprise approximately 59% (3,200,000 km) of the total stream length and approximately 50% (1,460,000 km) of the headwater stream length in the U.S., excluding Alaska. Hillslopes, headwater streams, and downstream waters are best described as individual elements of integrated hydrological systems. Hydrological connectivity allows for the exchange of mass, momentum, energy, and organisms longitudinally, laterally, vertically, and temporally between headwater streams and downstream waters. Via hydrological connectivity, headwater, intermittent and ephemeral streams cumulatively contribute to the functional integrity of downstream waters; hydrologically and ecologically, they are a part of the tributary system. As this debate continues, scientific input from multiple fields will be important for policymaking at the federal, state, and local levels and to inform water resource management regardless of the level at which those decisions are being made. Strengthening the interface between science, policy, and public participation is critical if we are going to achieve effective water resource management.</p>

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</description>

<author>T. L. Nadeau et al.</author>


</item>


<item>
<title>Non-navigable streams and adjacent wetlands: Addressing science needs following the Supreme Court&apos;s Rapanos decision</title>
<link>http://scholarcommons.usf.edu/gly_facpub/65</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/65</guid>
<pubDate>Wed, 09 May 2012 03:56:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>S. G. Leibowitz et al.</author>


</item>


<item>
<title>Contribution of headwaters to downstream integrity: Introduction to the JAWRA special issue</title>
<link>http://scholarcommons.usf.edu/gly_facpub/66</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/66</guid>
<pubDate>Wed, 09 May 2012 03:56:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>T. L. Nadeau et al.</author>


</item>


<item>
<title>Quantifying the hydrologic effects of stream restoration in a montane meadow environment</title>
<link>http://scholarcommons.usf.edu/gly_facpub/64</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/64</guid>
<pubDate>Wed, 09 May 2012 03:56:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>C. T. Hammersmark et al.</author>


</item>


<item>
<title>Geological control of physical and chemical hydrology in vernal pools, Central Valley, California</title>
<link>http://scholarcommons.usf.edu/gly_facpub/63</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/63</guid>
<pubDate>Wed, 09 May 2012 03:56:19 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mark Cable Rains et al.</author>


</item>


<item>
<title>Vegetation – water-table relationships in a hydrologically-restored riparian meadow</title>
<link>http://scholarcommons.usf.edu/gly_facpub/61</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/61</guid>
<pubDate>Wed, 09 May 2012 03:56:18 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>C. T. Hammersmark et al.</author>


</item>


<item>
<title>Hydrological connectivity between clay settling areas and surrounding hydrological landscapes in the phosphate mining district, peninsular Florida, USA</title>
<link>http://scholarcommons.usf.edu/gly_facpub/62</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/62</guid>
<pubDate>Wed, 09 May 2012 03:56:18 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K. E. Murphy et al.</author>


</item>


<item>
<title>Wetland assessment alphabet soup: How to choose (or not choose) the right assessment method</title>
<link>http://scholarcommons.usf.edu/gly_facpub/60</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/60</guid>
<pubDate>Wed, 09 May 2012 03:56:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>For more than 25 years wetland scientists have been striving to develop scientifically defensible wetland assessment methods that are robust, easily applied, affordable, and provide sufficient discrimination to guide management or regulatory decision making. While each generation of methods attempts to build upon the concepts and techniques developed in the previous generation, the fundamental goal remains to evaluate wetland(s) relative to a gradient of condition ranging from natural and undisturbed to extremely perturbed or altered. The progression from one method to the next is a natural and healthy indication that wetland science continues to advance and society learns. However, each generational transition is often accompanied by discourse about the benefits of various methods/approaches and the need or desirability to alter the assessment approach. Such was the case when the Corps of Engineers shifted from the Wetland Evaluation Technique (WET) to the Hydrogeomorphic Assessment Method (HGM). More recently, similar discussions have arisen around the development and application of Rapid Assessment Methods (RAMs) for wetland condition. The recent release of the Corps/EPA rule that strongly promotes use of condition or functional assessment in mitigation monitoring and performance evaluation (U.S. Army Corps and Engineers and Environmental Protection Agency 2008) has once again intensified debates about the efficacy of various assessment approaches.</p>
<p>We assert that debate over the utility of HGM, indices of biotic integrity (IBIs) the various RAMs, and other wetland assessment methods is somewhat misdirected. Rather than focusing on details of one specific method or debating the merits of one method over another, discussion should focus on the institutional structure and goals for which the methods are developed, tested, and ultimately implemented. Although wetland assessment methods vary in the scale of assessment and quantitative detail of the data collected and the assessment output, they are all designed to achieve a common objective: to evaluate the complex ecological condition of a wetland using a finite set of observable field indicators, and to express the relative condition of a particular site in a manner that informs ecosystem management (Figure 1). The design of an assessment method should be based on the information required to make management decisions and what resources (e.g., time, expertise, and equipment) are available to obtain that information? It is critical that management needs drive the selection of an assessment approach and not the other way around.</p>

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</description>

<author>E D. Stein et al.</author>


</item>


<item>
<title>A response to Tom Hruby.  (Response to “A reply by Tom Hruby” to “Wetland assessment alphabet soup: How to choose (or not choose) the right assessment method”</title>
<link>http://scholarcommons.usf.edu/gly_facpub/59</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/59</guid>
<pubDate>Wed, 09 May 2012 03:56:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>E D. Stein et al.</author>


</item>


<item>
<title>A case study on the accuracy and cost/effectiveness in simulating reference evapotranspiration in west-central Florida</title>
<link>http://scholarcommons.usf.edu/gly_facpub/57</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/57</guid>
<pubDate>Wed, 09 May 2012 03:56:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>M. G. Exner-Kittridge et al.</author>


</item>


<item>
<title>A Geochemical Mass-Balance Method for Base-Flow Separation, Upper Hillsborough River Watershed, West-Central Florida, 2003-2005 and 2009</title>
<link>http://scholarcommons.usf.edu/gly_facpub/58</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/58</guid>
<pubDate>Wed, 09 May 2012 03:56:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>G. R. Kish et al.</author>


</item>


<item>
<title>HGM is a rapid assessment: Clearing the confusion</title>
<link>http://scholarcommons.usf.edu/gly_facpub/55</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/55</guid>
<pubDate>Wed, 09 May 2012 03:56:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. Kleindl et al.</author>


</item>


<item>
<title>Controls on water levels and salinity in a barrier island mangrove, Indian River Lagoon, Florida</title>
<link>http://scholarcommons.usf.edu/gly_facpub/56</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/56</guid>
<pubDate>Wed, 09 May 2012 03:56:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>C. E. Stringer et al.</author>


</item>


<item>
<title>Simulated effects of stream restoration on herbaceous vegetation distribution</title>
<link>http://scholarcommons.usf.edu/gly_facpub/54</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/54</guid>
<pubDate>Wed, 09 May 2012 03:56:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Meadow restoration efforts typically involve the modification of stream channels to re-establish hydrologic conditions necessary for the maintenance of native vegetation. To predict change in the distribution of common meadow plant species in response to meadow restoration, a hydrologic model was loosely coupled to a suite of individual plant species distribution models. The approach was tested on a well-documented meadow/stream restoration project on Bear Creek, a tributary to the Fall River in northeastern California, U.S.A. We developed a surface-water and groundwater hydrologic model for the meadow. Vegetation presence and absence data from 170 plots were combined with simulated water-table depth time series to develop habitat-suitability models for 11 herbaceous plant species. In each model, the habitat suitability is predicted as a function of growing-season, water-table depth, and range. The hydrologic model was used to simulate water-table depth time series for the pre- and post-restoration conditions. These results were used to predict the spatial distribution of habitat suitability for the 11 herbaceous plant species. Model results indicate that restoration changed water levels throughout the study area, extending well beyond the near-stream region. Model results also indicate an increase in the spatial distribution of suitable habitat for mesic vegetation and a concomitant decrease in the spatial distribution of suitable habitat for xeric vegetation. The methods utilized in this study could be used to improve setting of objective and performance measures in restoration projects in similar environments, in addition to providing a quantitative, science-based approach to guide riparian restoration and active revegetation efforts.</p>

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</description>

<author>C. T. Hammersmark et al.</author>


</item>


<item>
<title>Water sources and hydrodynamics of closed-basin depressions</title>
<link>http://scholarcommons.usf.edu/gly_facpub/53</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/53</guid>
<pubDate>Wed, 09 May 2012 03:56:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mark Cable Rains</author>


</item>


<item>
<title>Hydrologic characterization of 56
geographically isolated wetlands in west-central Florida using a probabilistic method</title>
<link>http://scholarcommons.usf.edu/gly_facpub/52</link>
<guid isPermaLink="true">http://scholarcommons.usf.edu/gly_facpub/52</guid>
<pubDate>Wed, 09 May 2012 03:56:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K. A. Nilsson et al.</author>


</item>


<item>
<title>論李碧華小說“神怪敘述模式”的效果與作用</title>
<link>http://commons.ln.edu.hk/chi_diss/22</link>
<guid isPermaLink="true">http://commons.ln.edu.hk/chi_diss/22</guid>
<pubDate>Wed, 09 May 2012 02:26:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>評析李碧華小說的文章，向來多以歷史、社會、文化等方面作為觀察角度，即集中探討其小說與(香港)歷史、社會和文化之間的關係。1 原因大抵是論者認為李碧華小說在上述各方面的意義比她的文字更有論述價值。2然而，小說作為一件藝術成品(object)，除了從歷史、社會、文化等 "外在背景"去研究外，亦應多加注意作品本身的藝術成就，即所謂文本(text)的分析。李碧華的小說，在文字上，或許真是 "無足觀處" (事實上，一個作者的遣詞用字，很多時關乎他的閱讀和寫作習慣，有一定的客</p>
<p>觀因素影響)，但在敘述手法上，本文認為確有值得討論的地方。學者王德成指出：</p>
<p>她(李碧華)的想像穿梭於古今生死之間，探勘情慾輪迴，冤孽消長，每每有扣人心弦之處。3</p>
<p>能夠做到 "每每有扣人心弦之處"，本文認為正是由於李碧華慣用了一種敘述方式所致，而我們稱這種敘述方式為 "神怪敘述模式"。</p>
<p>"神怪" 一詞在這種要作為一個專門概念理解，本義即英語中的 "Supernatural"。據《英漢大詞典》 (繁體字縮印本)，"Supernatural" 作為形容詞，解釋是:</p>
<p>超自然的、自然規律所無法解釋的；神奇的、不可思議的、異常的。4</p>
<p>其中 "自然規律所無法解釋" 一項最值得注意《英漢辭海》關於這點說得更詳細，指出“Supematural" 超自然)</p>
<p>指、屬於、關於或來源於超越可觀察的、通過日常段可經驗到的物理宇宙之外存在秩序的：在程度和種類上都超越自然或同超越自然的東西相關的。5</p>
<p>因此其名詞解釋就是 "超自然物" 即：</p>
<p>存在的超自然的秩序：神聖的作用、影響或干預 ( ......超自然的東西就其終極的本質來說是我們存在水平上所不能理解的)。6</p>
<p>一般來說，我們所謂的超自然物，是指神、仙、魔、鬼、妖、怪等一類統稱 "神怪" 的東西，亦即孔子所不語的 "怪力亂神" 而 "神怪敘述模式"，就是以 "神怪" 作為主要角色發展故事的寫作模式。</p>
<p>香港作家李碧華的小說充滿著鬼怪異人，如《胭脂扣》的女鬼如花、《青蛇》的青白二蛇精、《潘金蓮之前世今生》前生是海金蓮的單玉蓮、《秦俑》的不死人蒙天放等。這些形象角色，全都可以列入 "神怪" (Supernatural)一類。由於這樣，其作品自成體系，成功營造了一個鬼氣、神秘、暖昧、異乎尋常的小說世界。</p>
<p>李碧華以 "神怪" 作為故事主要角色的這種敘述模式，並非偶然出現，而是佔了她所有小說作品一半的比例。我們相信，除了作者個人趣味導致這個現象外，選取這種敘述方式，還有其他作用。本文嘗試就這點進行分析。</p>
<p>在分析之前，有一點必先要說明。本文討論的重點雖然是李碧華的小說作品，但在論證過程中，會多有引用其雜文文章，原因如李焯雄所說：</p>
<p>談李碧華的小說，不能不拿她的專欄文章來並讀一一不是指由此愈發可見李的作品萬變不離其宗，特式不外有二 (或詭異或犬儒)，而是說讀李的專欄往往有助了解她的作品。8</p>
<p>到目前為止 (1997年4月)，李碧華總共出版了十二本小說，分別是你《胭脂扣》、《霸王別姬》(1985年初版，1992年修訂版)、《青蛇》(1986年初版，1993年修訂版) 、9《潘金蓮之前世今生》、《生死橋》、《秦俑》、《滿洲國妖艷――川島芳子》、《誘僧》(長篇)、10《糾纏》、《誘僧》(短篇) 、《天安門舊魂新魄》及《基情十一刀》。除去四部短篇結集 (《糾纏》、《誘僧》(短篇)、《天安門舊魂新魄》和《基情十一刀》)，李碧箏的小說故事，依內容區分，大致可歸為三類：一、再世輪迴的故事 (《胭脂扣》、《秦俑》、《潘金蓮之前世今生》)；二、舊故事重新演繹，(《青蛇》、《潘金蓮之前世今生》)；三、人物傳奇(《誘僧》(長篇)、《滿洲國妖艷――川島芳子》、《霸王別姬》、《秦俑》等)。11</p>
<p>前兩類故事，作者都是採用了 "神怪敘述模式"。12依此敘述模式，很可以發展成為 "超現實" 或 "靈幻" 內容的故事，然而李碧華顯然並沒有這個意思；反之，其小說內容都是經過多方考證、資料搜集，背景以及很多細節都有所依據，13因此有論者評她的作品 "有強烈現實主義"。14故事內容既力求真實、有所參照，卻採用 "神怪" 這種不現實的敘述模式，作者是如何將兩者有機地結合在一起?或者當我們明白李碧華作品中 "神怪敘述模式" 所發揮的一些效果和作用，便可幫助了解這問題，而闕於這一點，我們發現最少有四個解答。</p>

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</description>

<author>李 子翹</author>


</item>


<item>
<title>Colin O&apos;Daly</title>
<link>http://arrow.dit.ie/scthebk/26</link>
<guid isPermaLink="true">http://arrow.dit.ie/scthebk/26</guid>
<pubDate>Wed, 09 May 2012 02:22:19 PDT</pubDate>
<description>
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</description>

<author>Colin O&apos;Daly</author>


</item>


<item>
<title>從《紅高粱》試論小說改編成電影的問題</title>
<link>http://commons.ln.edu.hk/chi_diss/21</link>
<guid isPermaLink="true">http://commons.ln.edu.hk/chi_diss/21</guid>
<pubDate>Wed, 09 May 2012 02:12:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>電影事業蓬勃發展，令電影故事題材的發掘亦顯得十分重要。小說作品一直是電影故事題材的主要來源之一，不少的小說家同時也是電影編劇家。當我們把小說搬上銀幕，以電影的形式去表現，卻發現這原來是個相當微妙而又可以廣為討論的問題。小說作品改編成電影故事，固然可以豐當電影故事的題材，也可藉原著小說的知名度，為電影的宣傳增強效果。一部不為人熟悉的小說作品，亦能因為改編成電影故事，而更使人注意。當然，這要取決於電影改編的成功與否。小說和電影，通過改編使二者存在彼此帶動的關係，它們儘管是不同的媒體，其表達的方式也各有各的特性，但二者的聯繫又似乎是分不開的。</p>
<p>作為中國電影史上第一部獲得國際一級影展(柏林)首獎的影片，《紅高梁》也是一部改編自小說的作品。莫言的《紅高梁》和《高梁酒》，劉恆的《伏義伏羲》，蘇童的《妻妾成群》，陳源斌的《萬家訴訟》，余華的《活著》等等，這些小說作品都被張藝謀改成電影，而且獲得了成功。可以這樣說，張藝謀的電影的成功，是離不開小說的。本論文將以《紅高梁》這部電影為文本，試論小說改編成電影的問題。</p>

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</description>

<author>李 彥</author>


</item>


<item>
<title>Reducing Whole Body Vibration Levels in Off-road, Heavy-duty Vehicles: A Case Study with Computer Modelling</title>
<link>http://arrow.dit.ie/engschmeccon/52</link>
<guid isPermaLink="true">http://arrow.dit.ie/engschmeccon/52</guid>
<pubDate>Wed, 09 May 2012 01:22:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper describes a case study involving the dynamic ride performance of a 30-ton, articulated dumper vehicle. The vehicle in question was originally fitted with a front-end, solid axle with leading arm mechanism. After an engineering design program, the vehicle was custom-fitted with a Timoney Independent suspension system. Extensive testing and modelling activities using LMS Virtual.lab Motion® were undertaken to determine the productivity levels of each vehicle. It was demonstrated that the vehicle fitted with a Timoney suspension could achieve a productivity increase of up to 50%. A health analysis is also presented which shows the Timoney Independent suspension system reduces the potential health risk.</p>

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</description>

<author>Shaun McFadden et al.</author>


</item>


<item>
<title>小說《青蛇》中小青的性格分析</title>
<link>http://commons.ln.edu.hk/chi_diss/20</link>
<guid isPermaLink="true">http://commons.ln.edu.hk/chi_diss/20</guid>
<pubDate>Wed, 09 May 2012 01:02:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>白蛇故事，家傳戶曉。這個浪漫淒美的傳奇故事，以各種不同的文學形式流傳下來，一直為人們所歌頌。這個古老的傳說源遠流長，自宋、元以來流傳不衰，並衍生各類的民間故事。1 有說其淵源可追溯自唐，2 或見於宋代的話本，其實有關白蛇故事的最重要記載，應是明馮夢龍(1574-1646) 的《警世通言》中〈白娘子永鎮雷峰塔〉一卷，之後陸續有不同版本的話本、小說、彈詞、京劇、講唱等出現。無論白蛇故事是以何種形式出現，故事的情節總離不開遊湖借傘，訂親贈銀、發配蘇州、戲弄道士、瑰服招禍、發配鎮江、水漫金山、法海收妖、被鎮雷峰等基本骨榦。</p>
<p>人們慣於將焦點放在幾個方面：1.稱讚白娘子對愛情的執著、熱情、專一、堅持和爭取的精神；2.認為許仙寡情薄倖、怯弱畏縮；3.怪法海身為佛門高僧，不但沒慈悲為懷的善心. 倒反要拆散許白二人的姻緣。往往被忽略了的，是一直對白娘子忠心耿耿，為許白二人盡力盡心的青蛇。其實在整個白蛇故事裏，青蛇是一個不可缺少的重要角色，若沒有她，可能整個白蛇故事都要改寫。</p>
<p>第一次看李碧華所寫的小說《青蛇》，挺佩服作者的獨特創見，嘗試以小青的角度，重看整個白蛇故事。既能保留一般白蛇故事的情節，但又能以一個嶄新的角度去側寫詐白二人的感情。從前，青蛇一直是許白二人的侍俾、紅娘、朋友，而在李碧箏的筆下，小青終被釋放出來，成為一個突出獨立而性格鮮明的角色。這讓人發現到，小青一角其實同樣有值得研究的價值。後來《青蛇》改編成電影，在李碧華任編劇的情況下，大刀闊斧的將故事情節刪減，加重了小青在故事裏的重要性，亦著墨於她的性格描寫，為這角色賦予了生命。本論文並不妄想能為小青平反或確定些甚麼，只嘗試對這角色加以發掘及研究。</p>
<p>在撰寫論文的過程中，遇到不少困難。因為李氏的《青蛇》及一九八六年出版的坊間流行小說，在短短幾年間，並沒有太多關於此本小說的分析或研究資料，故在資料搜集上有一定的困難。而前人對白蛇故事加以研究時，亦偏重在白素貞、許仙、甚至法海身上，有關小青的研究實在不多，尤其是關於性格及心理描寫的文章，就更是乏善足陳。</p>
<p>本論文共分五個部分，首先是追溯一些關於白蛇故事的原始素材及重要素材；然後是交代李碧華筆下的白蛇故事；第三部分將集中探究小青的身份及替這角色加以定位；從而進一步分析這個角色的性格；最後更會就《青蛇》小說改編成電影後，小青一角性格上的分野作進一步研究。</p>

	]]>
</description>

<author>胡 幗明</author>


</item>


<item>
<title>The emergence of &apos;The HUGO Journal&apos;.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2107</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2107</guid>
<pubDate>Tue, 08 May 2012 23:55:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D Kumar et al.</author>


</item>


<item>
<title>The Human Genome Organisation (HUGO).</title>
<link>http://mouseion.jax.org/stfb2000_2009/2106</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2106</guid>
<pubDate>Tue, 08 May 2012 23:55:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E T. Liu</author>


</item>


<item>
<title>Integrating text mining into the MGI biocuration workflow.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2105</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2105</guid>
<pubDate>Tue, 08 May 2012 23:55:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>A major challenge for functional and comparative genomics resource development is the extraction of data from the biomedical literature. Although text mining for biological data is an active research field, few applications have    been integrated into production literature curation systems such as those of the model organism databases (MODs). Not only are most available biological natural language (bioNLP) and information retrieval and extraction solutions difficult to    adapt to existing MOD curation workflows, but many also have high error rates or are unable to process documents available in those formats preferred by scientific journals.In September 2008, Mouse Genome Informatics (MGI) at The Jackson    Laboratory initiated a search for dictionary-based text mining tools that we could integrate into our biocuration workflow. MGI has rigorous document triage and annotation procedures designed to identify appropriate articles about mouse genetics    and genome biology. We currently screen approximately 1000 journal articles a month for Gene Ontology terms, gene mapping, gene expression, phenotype data and other key biological information. Although we do not foresee that curation tasks will    ever be fully automated, we are eager to implement named entity recognition (NER) tools for gene tagging that can help streamline our curation workflow and simplify gene indexing tasks within the MGI system. Gene indexing is an MGI-specific    curation function that involves identifying which mouse genes are being studied in an article, then associating the appropriate gene symbols with the article reference number in the MGI database.Here, we discuss our search process, performance    metrics and success criteria, and how we identified a short list of potential text mining tools for further evaluation. We provide an overview of our pilot projects with NCBO's Open Biomedical Annotator and Fraunhofer SCAI's ProMiner. In doing    so, we prove the potential for the further incorporation of semi-automated processes into the curation of the biomedical literature.</p>

	]]>
</description>

<author>K G. Dowell et al.</author>


</item>


<item>
<title>Four additional mouse crosses improve the lipid QTL landscape and identify Lipg as a QTL gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2104</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2104</guid>
<pubDate>Tue, 08 May 2012 23:54:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>To identify genes controlling plasma HDL and triglyceride levels, quantitative trait locus (QTL) analysis was performed in one backcross, (NZO/H1Lt x NON/LtJ) x NON/LtJ, and three intercrosses, C57BL/6J x DBA/2J, C57BL/6J x C3H/HeJ,    and NZB/B1NJ x NZW/LacJ. HDL concentrations were affected by 25 QTL distributed on most chromosomes (Chrs); those on Chrs 1, 8, 12, and 16 were newly identified, and the remainder were replications of previously identified QTL. Triglyceride    concentrations were controlled by nine loci; those on Chrs 1, 2, 3, 7, 16, and 18 were newly identified QTL, and the remainder were replications. Combining mouse crosses with haplotype analysis for the HDL QTL on Chr 18 reduced the list of    candidates to six genes. Further expression analysis, sequencing, and quantitative complementation testing of these six genes identified Lipg as the HDL QTL gene on distal Chr 18. The data from these crosses further increase the ability to    perform haplotype analyses that can lead to the identification of causal lipid genes.</p>

	]]>
</description>

<author>Z Su et al.</author>


</item>


<item>
<title>Maximal extraction of biological information from genetic interaction data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2103</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2103</guid>
<pubDate>Tue, 08 May 2012 23:54:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Extraction of all the biological information inherent in large-scale genetic interaction datasets remains a significant challenge for systems biology. The core problem is essentially that of classification of the relationships among    phenotypes of mutant strains into biologically informative "rules" of gene interaction. Geneticists have determined such classifications based on insights from biological examples, but it is not clear that there is a systematic, unsupervised way    to extract this information. In this paper we describe such a method that depends on maximizing a previously described context-dependent information measure to obtain maximally informative biological networks. We have successfully validated this    method on two examples from yeast by demonstrating that more biological information is obtained when analysis is guided by this information measure. The context-dependent information measure is a function only of phenotype data and a set of    interaction rules, involving no prior biological knowledge. Analysis of the resulting networks reveals that the most biologically informative networks are those with the greatest context-dependent information scores. We propose that these    high-complexity networks reveal genetic architecture at a modular level, in contrast to classical genetic interaction rules that order genes in pathways. We suggest that our analysis represents a powerful, data-driven, and general approach to    genetic interaction analysis, with particular potential in the study of mammalian systems in which interactions are complex and gene annotation data are sparse.</p>

	]]>
</description>

<author>G W. Carter et al.</author>


</item>


<item>
<title>Cytoscape: a community-based framework for network modeling.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2102</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2102</guid>
<pubDate>Tue, 08 May 2012 23:54:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cytoscape is a general network visualization, data integration, and analysis software package. Its development and use has been focused on the modeling requirements of systems biology, though it has been used in other fields.     Cytoscape's flexibility has encouraged many users to adopt it and adapt it to their own research by using the plugin framework offered to specialize data analysis, data integration, or visualization. Plugins represent collections of    community-contributed functionality and can be used to dynamically extend Cytoscape functionality. This community of users and developers has worked together since Cytoscape's initial release to improve the basic project through contributions to    the core code and public offerings of plugin modules. This chapter discusses what Cytoscape does, why it was developed, and the extensions numerous groups have made available to the public. It also describes the development of a plugin used to    investigate a particular research question in systems biology and walks through an example analysis using Cytoscape.</p>

	]]>
</description>

<author>S Killcoyne et al.</author>


</item>


<item>
<title>Hematopoietic cell types: Prototype for a revised cell ontology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2101</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2101</guid>
<pubDate>Tue, 08 May 2012 23:54:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Cell Ontology (CL) aims for the representation of in vivo and in vitro cell types from all of biology. The CL is a candidate reference ontology of the OBO Foundry and requires extensive revision to bring it up to current    standards for biomedical ontologies, both in its structure and its coverage of various subfields of biology. We have now addressed the specific content of one area of the CL, the section of the ontology dealing with hematopoietic cells. This    section has been extensively revised to improve its content and eliminate multiple inheritance in the asserted hierarchy, and the groundwork has been laid for structuring the hematopoietic cell type terms as cross-products incorporating logical    definitions built from relationships to external ontologies, such as the Protein Ontology and the Gene Ontology. The methods and improvements to the CL in this area represent a paradigm for improvement of the entire ontology over    time.</p>

	]]>
</description>

<author>A D. Diehl et al.</author>


</item>


<item>
<title>Automated annotation-based bio-ontology alignment with structural validation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2100</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2100</guid>
<pubDate>Tue, 08 May 2012 23:54:14 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C A. Joslyn et al.</author>


</item>


<item>
<title>Light-induced dark states of organic fluochromes enable 30 nm resolution imaging in standard media.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2099</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2099</guid>
<pubDate>Tue, 08 May 2012 23:54:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>We show that high quantum efficiency fluorophores can exhibit reversible photobleaching. This observation provides the basis for an imaging technique we call reversible photobleaching microscopy. We demonstrate applicability of this    technique using antibody labeled biological samples in standard aqueous (or glycerol based) media to produce far-field images at approximately 30 nm resolution. Our novel method relies on intense illumination to reversibly induce a very    long-lived (>10 s) dark state from which single fluorochromes slowly return stochastically. As in other localization microscopy methods, reversible photobleaching microscopy localizes single fluorochromes, but has the advantage that specialized    photoactivatible and photoswitchable molecules or special immersion/embedding media are not required.</p>

	]]>
</description>

<author>D Baddeley et al.</author>


</item>


<item>
<title>Integrating text mining into the MGI biocuration workflow.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2098</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2098</guid>
<pubDate>Tue, 08 May 2012 23:53:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>A major challenge for functional and comparative genomics resource development is the extraction of data from the biomedical literature. Although text mining for biological data is an active research field, few applications have    been integrated into production literature curation systems such as those of the model organism databases (MODs). Not only are most available biological natural language (bioNLP) and information retrieval and extraction solutions difficult to    adapt to existing MOD curation workflows, but many also have high error rates or are unable to process documents available in those formats preferred by scientific journals.In September 2008, Mouse Genome Informatics (MGI) at The Jackson    Laboratory initiated a search for dictionary-based text mining tools that we could integrate into our biocuration workflow. MGI has rigorous document triage and annotation procedures designed to identify appropriate articles about mouse genetics    and genome biology. We currently screen approximately 1000 journal articles a month for Gene Ontology terms, gene mapping, gene expression, phenotype data and other key biological information. Although we do not foresee that curation tasks will    ever be fully automated, we are eager to implement named entity recognition (NER) tools for gene tagging that can help streamline our curation workflow and simplify gene indexing tasks within the MGI system. Gene indexing is an MGI-specific    curation function that involves identifying which mouse genes are being studied in an article, then associating the appropriate gene symbols with the article reference number in the MGI database.Here, we discuss our search process, performance    metrics and success criteria, and how we identified a short list of potential text mining tools for further evaluation. We provide an overview of our pilot projects with NCBO's Open Biomedical Annotator and Fraunhofer SCAI's ProMiner. In doing    so, we prove the potential for the further incorporation of semi-automated processes into the curation of the biomedical literature.</p>

	]]>
</description>

<author>K G. Dowell et al.</author>


</item>


<item>
<title>Where&apos;s the mouse info?</title>
<link>http://mouseion.jax.org/stfb2000_2009/2097</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2097</guid>
<pubDate>Tue, 08 May 2012 23:53:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title>A data-capture tool for mouse pathology phenotyping.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2096</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2096</guid>
<pubDate>Tue, 08 May 2012 23:53:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Disease Information System is a free Microsoft Access database (http://research.jax.org/faculty/sundberg/index.html) designed by veterinary pathologists to aid veterinary pathologists in data acquisition, analysis, and    coordination of tissue-sample archives. Linking the system to the Mouse Anatomy and Mouse Pathology Ontologies provides controlled vocabulary (and spelling) for organ, tissue, and diagnosis. Severity scores provide a quantitative assessment of    all lesions to enable quantitative trait locus analysis for large-scale studies. Individual diagnoses can be verified for their definition by online linkage to Pathbase.net. Histologic images can be accessed from Pathbase by using the Mouse    Pathology Ontology directly for comparison with slides being viewed at the time of data entry and providing the user with a reference and a "virtual second opinion."</p>

	]]>
</description>

<author>B A. Sundberg et al.</author>


</item>


<item>
<title>RPGRIP1 is essential for normal rod photoreceptor outer segment elaboration and morphogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2095</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2095</guid>
<pubDate>Tue, 08 May 2012 23:53:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The function of the retinitis pigmentosa GTPase regulator interacting protein 1 (RPGRIP1) gene is currently not known. However, mutations within the gene lead to Leber Congenital Amaurosis and autosomal recessive retinitis    pigmentosa in human patients. In a previously described knockout mouse model of the long splice variant of Rpgrip1, herein referred to as Rpgrip1(tm1Tili) mice, mislocalization of key outer segment proteins and dysmorphogenesis of outer segment    discs preceded subsequent photoreceptor degeneration. In this report, we describe a new mouse model carrying a splice acceptor site mutation in Rpgrip1, herein referred to as Rpgrip1(nmf247) that is phenotypically distinct from Rpgrip1(tm1Tili)    mice.  Photoreceptor degeneration in homozygous Rpgrip1(nmf247) mice is earlier in onset and more severe when compared with Rpgrip1(tm1Tili) mice. Also, ultrastructural studies reveal that whereas Rpgrip1(nmf247) mutants have a normal structure    and number of connecting cilia, unlike Rpgrip1(tm1Tili) mice, they do not elaborate rod outer segments (OS). Therefore, in addition to its role in OS disc morphogenesis, RPGRIP1 is essential for rod OS formation. Our study indicates the absence    of multiple Rpgrip1 isoforms in Rpgrip1(nmf247) mice, suggesting different isoforms may play different roles in photoreceptors and underscores the importance of considering splice variants when generating targeted null mutations.</p>

	]]>
</description>

<author>J Won et al.</author>


</item>


<item>
<title>Bioluminescent imaging demonstrates that transplanted human embryonic stem cell-derived CD34(+) cells preferentially develop into endothelial cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2094</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2094</guid>
<pubDate>Tue, 08 May 2012 23:53:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human embryonic stem cells (hESCs) provide an important resource for novel regenerative medicine therapies and have been used to derive diverse cell populations, including hematopoietic and endothelial cells. However, it remains a    challenge to achieve significant engraftment of hESC-derived blood cells when transplanted into animal models. To better understand mechanisms that enhance or limit the in vivo developmental potential of hESC-derived cells, we utilized hESCs that    express firefly luciferase (luc) to allow noninvasive, real-time bioluminescent imaging of hESC-derived CD34(+) cells transplanted into the liver of neonatal immunodeficient mice. Serial imaging demonstrated stable engraftment and expansion of    the luc(+) hESC-derived cells in vivo over several months. While we found that these hESC-derived CD34(+) cells have bipotential ability to generate both hematopoietic and endothelial lineages in vitro, these studies demonstrate preferential    differentiation into endothelial cells in vivo, with only low levels of hematopoietic cell engraftment. Therefore, these studies reveal key differences in the developmental potential of hESC-derived cells using in vitro and in vivo analyses.    Although transplanted hESC-derived CD34(+) cells are well-suited for revascularization therapies, additional measures are needed to provide higher levels of long-term hematopoietic engraftment.</p>

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</description>

<author>X Tian et al.</author>


</item>


<item>
<title>Animal models of diabetic uropathy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2093</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2093</guid>
<pubDate>Tue, 08 May 2012 23:53:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Diabetes mellitus is a group of debilitating and costly diseases with multiple serious complications. Lower urinary tract complications or diabetic uropathy are among the most common complications of diabetes mellitus,    surpassing widely recognized complications such as neuropathy and nephropathy. Diabetic uropathy develops in individuals with types 1 and 2 diabetes, and little is known about the natural history of these common and troublesome complications.    Animal models have the potential to reveal mechanisms and aid in the development of treatment strategies. MATERIALS AND METHODS: We present a review of available animal models of diabetes mellitus relative to their use in the study of diabetic    uropathy. RESULTS: Large and small animal models of diabetes mellitus are available. While large animals such as dogs and swine may closely mirror the human disease in size and phenotype, the time between diabetic complication onset and    development, and associated husbandry expenditures can make acquiring data on statistically valid sample sizes prohibitively expensive. In contrast, small animal models (rats and mice) have much lower expenditures for a larger number of animals    and compressed observation time due to a shorter life span. Also, mice are readily manipulated genetically to facilitate the isolation of the effect of single genes (transgenic and knockout mice). Type 1 diabetes mellitus can be induced    chemically with streptozotocin, which is selectively toxic to pancreatic beta cells. Type 2 diabetes mellitus models have been developed by selective breeding for hyperglycemia with or without associated obesity. Diabetic uropathy has been noted    in several well characterized, predictable animal models of diabetes mellitus. CONCLUSIONS: Diabetic uropathy, including diabetic bladder dysfunction, has been more frequently studied in small animals with type I diabetes. The recent availability    of transgenic models provides a new opportunity for further studies of diabetic uropathy in mouse models of types I and II diabetes mellitus.</p>

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</description>

<author>F Daneshgari et al.</author>


</item>


<item>
<title>Bone: serotonin, leptin and the central control of bone remodeling.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2092</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2092</guid>
<pubDate>Tue, 08 May 2012 23:52:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title>Bone loss or lost bone: rationale and recommendations for the diagnosis and treatment of early postmenopausal bone loss.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2091</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2091</guid>
<pubDate>Tue, 08 May 2012 23:52:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recent reports suggest that bone loss begins during late perimenopause at a dramatic rate, even before estrogen levels plummet. During the ensuing 5 years, there is evidence of the beginnings of microarchitectural deterioration,    which impacts bone strength and ultimately enhances its propensity to fracture. The diagnosis of osteoporosis based on T-scores alone, or through stratification for a high fracture risk by FRAX, excludes these women who are rapidly losing bone.     Because all antiosteoporosis therapies, in particular bisphosphonates, reduce bone loss, we propose aggressive, likely short-term therapy with a goal to reduce bone loss, stabilize bone density, and prevent microarchitectural    deterioration.</p>

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</description>

<author>M Zaidi et al.</author>


</item>


<item>
<title>Human nasal polyp microenvironments maintained in a viable and functional state as xenografts in NOD-scid IL2rgamma(null) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2090</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2090</guid>
<pubDate>Tue, 08 May 2012 23:52:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVES: The objective was to develop a model with which to study the cellular and molecular events associated with nasal polyp progression. To accomplish this, we undertook to develop a system in which nondisrupted human nasal    polyp tissue could be successfully implanted into severely immunocompromised mice, in which the histopathology of the original nasal polyp tissue, including inflammatory lymphocytes, epithelial and goblet cell hyperplasia, and subepithelial    fibrosis, could be preserved for prolonged periods. METHODS: Small, non-disrupted pieces of human nasal polyp tissues were subcutaneously implanted into NOD-scid IL2rgamma(null) mice. Xenografts at 8 to 12 weeks after implantation were examined    histologically and immunohistochemically to identify human inflammatory leukocytes and to determine whether the characteristic histopathologic characteristics of the nasal polyps were maintained for a prolonged period. The xenografts, spleen,    lung, liver, and kidneys were examined histologically and immunohistochemically and were evaluated for changes in volume. The sera of these mice were assayed for human cytokines and immunoglobulin. RESULTS: Xenografts of human nasal polyp tissues    were established after their subcutaneous implantation into NOD-scid IL2rgamma(null) mice. The xenografts were maintained in a viable and functional state for up to 3 months, and retained a histopathologic appearance similar to that of the    original tissue, with a noticeable increase in goblet cell hyperplasia and marked mucus accumulation in the submucosal glands compared to the original nasal polyp tissue. Inflammatory lymphocytes present in the polyp microenvironment were    predominantly human CD8+ T cells with an effector memory phenotype. Human CD4+ T cells, CD138+ plasma cells, and CD68+ macrophages were also observed in the xenografts. Human immunoglobulin and interferon-gamma were detected in the sera of    xenograft-bearing mice. The polyp-associated lymphocytes proliferated and were found to migrate from the xenografts to the spleens of the recipient mice, resulting in a significant splenomegaly. A progressive increase in the volume of the    xenografts was observed with little or no evidence of mouse cell infiltration into the human leukocyte antigen-positive human tissue. An average twofold increase in polyp volume was found at 3 months after engraftment. CONCLUSIONS: The use of    innate and adaptive immunodeficient NOD-scid mice homozygous for targeted mutations in the interleukin-2 receptor gamma-chain locus NOD-scid IL2rgamma(null) for establishing xenografts of nondisrupted pieces of human nasal polyp tissues    represents a significant improvement over the previously reported xenograft model that used partially immunoincompetent CB17-scid mice as tissue recipients. The absence of the interleukin-2 receptor gamma-chain results in complete  elimination of    natural killer cell development, as well as severe impairments in T and B cell development. These mice, lacking both innate and adaptive immune responses, significantly improve upon the long-term engraftment of human nasal polyp tissues and    provide a model with which to study how nasal polyp-associated lymphocytes and their secreted biologically active products contribute to the histopathology and progression of this chronic inflammatory disease.</p>

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</description>

<author>J M. Bernstein et al.</author>


</item>


<item>
<title>Extracellular matrix molecules in neuromuscular junctions and central nervous system synapses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2089</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2089</guid>
<pubDate>Tue, 08 May 2012 23:52:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>L Burgess R. Bogdanik</author>


</item>


<item>
<title>The Mammalian Phenotype Ontology: enabling robust annotation and comparative analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2088</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2088</guid>
<pubDate>Tue, 08 May 2012 23:52:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse has long been an important model for the study of human genetic disease. Through the application of genetic engineering and mutagenesis techniques, the number of unique mutant mouse models and the amount of phenotypic data    describing them are growing exponentially. Describing phenotypes of mutant mice in a computationally useful manner that will facilitate data mining is a major challenge for bioinformatics. Here we describe a tool, the Mammalian Phenotype Ontology    (MP), for classifying and organizing phenotypic information related to the mouse and other mammalian species. The MP Ontology has been applied to mouse phenotype descriptions in the Mouse Genome Informatics Database (MGI,    http://www.informatics.jax.org/), the Rat Genome Database (RGD, http://rgd.mcw.edu), the Online Mendelian Inheritance in Animals (OMIA, http://omia.angis.org.au/) and elsewhere. Use of this ontology allows comparisons of data from diverse    sources, can facilitate comparisons across mammalian species, assists in identifying appropriate experimental disease models, and aids in the discovery of candidate disease genes and molecular signaling pathways.</p>

	]]>
</description>

<author>C L. Smith et al.</author>


</item>


<item>
<title>Effects of atherogenic diet on hepatic gene expression across mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2087</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2087</guid>
<pubDate>Tue, 08 May 2012 23:51:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Diets high in fat and cholesterol are associated with increased obesity and metabolic disease in mice and humans. To study the molecular basis of the metabolic response to dietary fat, 10 inbred strains of mice were fed atherogenic    high-fat and control low-fat diets. Liver gene expression and whole animal phenotypes were measured and analyzed in both sexes. The effects of diet, strain, and sex on gene expression were determined irrespective of complex processes, such as    feedback mechanisms, that could have mediated the genomic responses.  Global gene expression analyses demonstrated that animals of the same strain and sex have similar transcriptional profiles on a low-fat diet, but strains may show considerable    variability in response to high-fat diet. Functional profiling indicated that high-fat feeding induced genes in the immune response, indicating liver damage, and repressed cholesterol biosynthesis. The physiological significance of the    transcriptional changes was confirmed by a correlation analysis of transcript levels with whole animal phenotypes. The results found here were used to confirm a previously identified quantitative trait locus on chromosome 17 identified in males    fed a high-fat diet in two crosses, PERA x DBA/2 and PERA x I/Ln. The gene expression data and phenotype data have been made publicly available as an online tool for exploring the effects of atherogenic diet in inbred mouse strains    (http://cgd-array.jax.org/DietStrainSurvey).</p>

	]]>
</description>

<author>K R. Shockley et al.</author>


</item>


<item>
<title>Meiotic behavior of aneuploid chromatin in mouse models of Down syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2086</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2086</guid>
<pubDate>Tue, 08 May 2012 23:51:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Aneuploidy, which leads to unpaired chromosomal axes during meiosis, is frequently accompanied by infertility. We previously showed, using three mouse models of Down syndrome, that it is an extra chromosome, but not extra gene dose,    that is associated with male infertility and virtual absence of post-meiotic gem cells. Here, we test the hypothesis that aneuploid segments are differentially modified and expressed during meiosis, depending on whether they are present as an    extra chromosome or not. In all three models examined, the trisomic region lacks a pairing partner, but in one case, spermatocytes have an extra (and unpaired) chromosome, while the two other models involve translocation of the trisomic region    rather than an extra chromosome. An extra unpaired chromosome was always modified by phosphorylation of histone H2AX and lacked RNA PolII. But in the case of trisomic regions attached to a paired chromosome, assembly of these protein    modifications was affected by the position of a trisomic region relative to a centromere and the physical extent of the unpaired chromatin. Analysis of gene expression in testes revealed that extra copy number alone was not sufficient for meiotic    upregulation of genes in the trisomic interval.  Additionally and unexpectedly, presence of meiotic gene silencing chromatin modifications was not sufficient for downregulation of genes in unpaired trisomic chromatin. Thus, the meiotic chromatin    modifications that are cytologically visible are unlikely to be directly involved in sterility versus fertility of DS models. Finally, the presence of an extra unpaired chromosome, but not the presence of extra (trisomic) genes, caused global    deregulation of transcription in spermatocytes. These results reveal mechanisms by which an extra chromosome, but not trisomic gene dose, impact on meiotic progress and infertility.</p>

	]]>
</description>

<author>L G. Reinholdt et al.</author>


</item>


<item>
<title>The response of C57BL/6J and BALB/cJ mice to increased housing density.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2085</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2085</guid>
<pubDate>Tue, 08 May 2012 23:51:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Increased numbers of mice housed per cage (that is, increased housing density) is seen as 1 way to reduce the costs of conducting biomedical research. Current empirically derived guidelines are based on the area provided per mouse    depending on body weight as documented in the Guide for the Care and Use of Laboratory Animals. The current study aimed to provide a more scientific basis for housing density by examining the response of C57BL/6J and BALB/cJ mice to increased    housing density from weaning to 5 mo of age, to determine those parameters most useful for future larger-scale studies. A wide range of phenotypic characteristics--including growth rate, body composition, hematology, serum biochemistry, hormone    and metabolite measurements, in-cage telemetry, behavior, and cage microenvironment--was examined at various time points. The parameters showing greatest changes were: growth rate, which was significantly reduced in animals at the highest    density; adrenal gland size, the proportion of adrenal cortex, and concentration of fecal corticosterone metabolites, all of which were increased at higher densities; and anxiety and barbering, which were more pronounced at higher densities. Cage    microenvironment deteriorated with increasing density, but the increases in measured parameters were small, and their biologic impact, if any, was not apparent. The current findings indicate that mouse housing density can be increased 50% to 100%    above the current recommendations (as floor area per mouse) with no or few apparent affects on mouse overall wellbeing. However, weight gain, fecal corticosterone metabolite levels, and barbering differed significantly with housing density and    therefore are suggested as good measures of the response to alterations in housing.</p>

	]]>
</description>

<author>A Nicholson et al.</author>


</item>


<item>
<title>Retinoblastoma protein plays multiple essential roles in the terminal differentiation of Sertoli cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2084</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2084</guid>
<pubDate>Tue, 08 May 2012 23:51:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Retinoblastoma protein (RB) plays crucial roles in cell cycle control and cellular differentiation. Specifically, RB impairs the G(1) to S phase transition by acting as a repressor of the E2F family of transcriptional activators    while also contributing towards terminal differentiation by modulating the activity of tissue-specific transcription factors. To examine the role of RB in Sertoli cells, the androgen-dependent somatic support cell of the testis, we created a    Sertoli cell-specific conditional knockout of Rb. Initially, loss of RB has no gross effect on Sertoli cell function because the mice are fertile with normal testis weights at 6 wk of age. However, by 10-14 wk of age, mutant mice demonstrate    severe Sertoli cell dysfunction and infertility. We show that mutant mature Sertoli cells continue cycling with defective regulation of multiple E2F1- and androgen-regulated genes and concurrent activation of apoptotic and p53-regulated genes.    The most striking defects in mature Sertoli cell function are increased permeability of the blood-testis barrier, impaired tissue remodeling, and defective germ cell-Sertoli cell interactions. Our results demonstrate that RB is essential for    proper terminal differentiation of Sertoli cells.</p>

	]]>
</description>

<author>R L. Nalam et al.</author>


</item>


<item>
<title>Devastation of bone tissue in the appendicular skeleton parallels the progression of neuromuscular disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2083</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2083</guid>
<pubDate>Tue, 08 May 2012 23:51:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>A mouse model of spinal muscular atrophy with respiratory distress (SMARD1) was used to study the consequences of neuromuscular degenerative disease on bone quantity and morphology. Histomorphometry and micro-computed tomography    were used to assess the cortical and cancellous bone in the tibia, femur and humerus of adult neuromuscular degeneration (nmd) mice (up to 21w) and age-matched wild-type controls (WT). At 21w, the average lengths of the humerus, tibia and femur    were 15%, 10%, and 10% shorter in the nmd mice, respectively. The midshaft of the humerus, tibia and femur of nmd mice had 41%, 47% and 34% less cortical bone than the WT. In the humeral, tibial, and femoral metaphyses of the nmd mice, there was    50%, 78%, and 85% less trabecular bone volume, and 58%, 92%, and 94% less trabecular connectivity than the WT. NMD cortical bone had less than half of the 42% active surface measured in the WT, yet the mineral apposition rate of those surfaces    were similar between strains (nmd: 1.80 microm x day(-1); WT: 2.05 microm x day(-1)). Osteoclast number and activity levels did not differ across strains. These data emphasize that neuromuscular degeneration as a result of immunoglobulin S-mu    binding protein-2 (Ighmbp2) mutation will compromise several critical parameters of bone quantity and architecture, the most severe occurring in the trabecular compartment.</p>

	]]>
</description>

<author>B J. Lee et al.</author>


</item>


<item>
<title>Dysferlin deficiency and the development of cardiomyopathy in a mouse model of limb-girdle muscular dystrophy 2B.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2082</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2082</guid>
<pubDate>Tue, 08 May 2012 23:51:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Limb-girdle muscular dystrophy 2B, Miyoshi myopathy, and distal myopathy of anterior tibialis are severely debilitating muscular dystrophies caused by genetically determined dysferlin deficiency. In these muscular dystrophies, it is    the repair, not the structure, of the plasma membrane that is impaired. Though much is known about the effects of dysferlin deficiency in skeletal muscle, little is known about the role of dysferlin in maintenance of cardiomyocytes.  Recent    evidence suggests that dysferlin deficiency affects cardiac muscle, leading to cardiomyopathy when stressed. However, neither the morphological location of dysferlin in the cardiomyocyte nor the progression of the disease with age are known. In    this study, we examined a mouse model of dysferlinopathy using light and electron microscopy as well as echocardiography and conscious electrocardiography. We determined that dysferlin is normally localized to the intercalated disk and sarcoplasm    of the cardiomyocytes. In the absence of dysferlin, cardiomyocyte membrane damage occurs and is localized to the intercalated disk and sarcoplasm. This damage results in transient functional deficits at 10 months of age, but, unlike in skeletal    muscle, the cell injury is sublethal and causes only mild cardiomyopathy even at advanced ages.</p>

	]]>
</description>

<author>T H. Chase et al.</author>


</item>


<item>
<title>Comparison of threshold selection methods for microarray gene co-expression matrices.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2081</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2081</guid>
<pubDate>Tue, 08 May 2012 23:50:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>ABSTRACT: BACKGROUND: Network and clustering analyses of microarray co-expression correlation data often require application of a threshold to discard small correlations, thus reducing computational demands and decreasing the number    of uninformative correlations. This study investigated threshold selection in the context of combinatorial network analysis of transcriptome data. FINDINGS: Six conceptually diverse methods - based on number of maximal cliques, correlation of    control spots with expressed genes, top 1% of correlations, spectral graph clustering, Bonferroni correction of p-values, and statistical power - were used to estimate a correlation threshold for three time-series microarray datasets.  The    validity of thresholds was tested by comparison to thresholds derived from Gene Ontology information. Stability and reliability of the best methods were evaluated with block bootstrapping.Two threshold methods, number of maximal cliques and    spectral graph, used information in the correlation matrix structure and performed well in terms of stability. Comparison to Gene Ontology found thresholds from number of maximal cliques extracted from a co-expression matrix were the most    biologically valid. Approaches to improve both methods were suggested. CONCLUSION: Threshold selection approaches based on network structure of gene relationships gave thresholds with greater relevance to curated biological relationships than    approaches based on statistical pair-wise relationships.</p>

	]]>
</description>

<author>B R. Borate et al.</author>


</item>


<item>
<title>B Cell IgD Deletion Prevents Alveolar Bone Loss Following Murine Oral Infection.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2080</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2080</guid>
<pubDate>Tue, 08 May 2012 23:50:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Periodontal disease is one of the most common infectious diseases of humans.  Immune responses to infection trigger loss of alveolar bone from the jaw and eventual tooth loss. We investigated the contribution of B cell IgD to    alveolar bone loss by comparing the response of B cell normal BALB/cJ mice and IgD deficient BALB/c-Igh-5(-/-J) mice to oral infection with Porphyromonas gingivalis, a gram-negative periodontopathic bacterium from humans. P. gingivalis-infected    normal mice lost bone. Specific antibody to P. gingivalis was lower and oral colonization was higher in IgD deficient mice; yet bone loss was completely absent. Infection increased the proportion of CD69(+) activated B cells and CD4(+) T cells in    immune normal mice compared to IgD deficient mice.  These data suggest that IgD is an important mediator of alveolar bone resorption, possibly through antigen-specific coactivation of B cells and CD4(+) T cells.</p>

	]]>
</description>

<author>P J. Baker et al.</author>


</item>


<item>
<title>Ontological Discovery Environment: a system for integrating gene-phenotype associations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2079</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2079</guid>
<pubDate>Tue, 08 May 2012 23:50:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>The wealth of genomic technologies has enabled biologists to rapidly ascribe phenotypic characters to biological substrates. Central to effective biological investigation is the operational definition of the process under    investigation.  We propose an elucidation of categories of biological characters, including disease relevant traits, based on natural endogenous processes and experimentally observed biological networks, pathways and systems rather than on    externally manifested constructs and current semantics such as disease names and processes.  The Ontological Discovery Environment (ODE) is an Internet accessible resource for the storage, sharing, retrieval and analysis of phenotype-centered    genomic data sets across species and experimental model systems. Any type of data set representing gene-phenotype relationships, such quantitative trait loci (QTL) positional candidates, literature reviews, microarray experiments, ontological or    even meta-data, may serve as inputs. To demonstrate a use case leveraging the homology capabilities of ODE and its ability to synthesize diverse data sets, we conducted an analysis of genomic studies related to alcoholism. The core of ODE's gene    set similarity, distance and hierarchical analysis is the creation of a bipartite network of gene-phenotype relations, a unique discrete graph approach to analysis that enables set-set matching of non-referential data. Gene sets are annotated    with several levels of metadata, including community ontologies, while gene set translations compare models across species. Computationally derived gene sets are integrated into hierarchical trees based on gene-derived phenotype    interdependencies. Automated set identifications are augmented by statistical tools which enable users to interpret the confidence of modeled results. This approach allows data integration and hypothesis discovery across multiple experimental    contexts, regardless of the face similarity and semantic annotation of the experimental systems or species domain.</p>

	]]>
</description>

<author>E J. Baker et al.</author>


</item>


<item>
<title>Using ontology visualization to facilitate access to knowledge about human disease genes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2078</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2078</guid>
<pubDate>Tue, 08 May 2012 23:50:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M E Blake Dolan</author>


</item>


<item>
<title>Reconstructing generalized logical networks of transcriptional regulation in mouse brain from temporal gene expression data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2077</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2077</guid>
<pubDate>Tue, 08 May 2012 23:50:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gene expression time course data can be used not only to detect differentially expressed genes but also to find temporal associations among genes. The problem of reconstructing generalized logical networks to account for temporal    dependencies among genes and environmental stimuli from transcriptomic data is addressed. A network reconstruction algorithm was developed that uses statistical significance as a criterion for network selection to avoid false-positive    interactions arising from pure chance. The multinomial hypothesis testing-based network reconstruction allows for explicit specification of the false-positive rate, unique from all extant network inference algorithms. The method is superior to    dynamic Bayesian network modeling in a simulation study. Temporal gene expression data from the brains of alcohol-treated mice in an analysis of the molecular response to alcohol are used for modeling. Genes from major neuronal pathways are    identified as putative components of the alcohol response mechanism.  Nine of these genes have associations with alcohol reported in literature.  Several other potentially relevant genes, compatible with independent results from literature    mining, may play a role in the response to alcohol. Additional, previously unknown gene interactions were discovered that, subject to biological verification, may offer new clues in the search for the elusive molecular mechanisms of    alcoholism.</p>

	]]>
</description>

<author>M J. Song et al.</author>


</item>


<item>
<title>Four additional mouse crosses improve the lipid QTL landscape and identify Lipg as a QTL gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2076</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2076</guid>
<pubDate>Tue, 08 May 2012 23:50:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>To identify genes controlling plasma high-density lipoprotein cholesterol (HDL) and triglyceride levels, quantitative trait locus (QTL) analysis was performed in one backcross, (NZO/H1Lt x NON/LtJ) x NON/LtJ, and three intercrosses;    C57BL/6J x DBA/2J, C57BL/6J x C3H/HeJ, and NZB/B1NJ x NZW/LacJ. HDL concentrations were affected by 25 QTL distributed on most chromosomes (Chr); those on Chrs 1, 8, 12, and 16 were newly identified and the remainder were replications of    previously identified QTL. Triglyceride concentrations were controlled by nine loci; those on Chrs 1, 2, 3, 7, 16 and 18 were newly identified QTL and the remainder were replications. Combining mouse crosses with haplotype analysis for the HDL    QTL on Chr 18 reduced the list of candidates to six genes. Further expression analysis, sequencing, and quantitative complementation testing of these six genes identified Lipg as the HDL QTL gene on distal Chr 18. The data from these crosses    further increases the ability to perform haplotype analyses that can lead to the identification of causal lipid genes.</p>

	]]>
</description>

<author>Z Su et al.</author>


</item>


<item>
<title>Fibroblast growth factors and epidermal growth factor cooperate with oocyte-derived members of the TGFbeta superfamily to regulate Spry2 mRNA levels in mouse cumulus cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2075</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2075</guid>
<pubDate>Tue, 08 May 2012 23:49:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mouse oocytes produce members of the transforming growth factor beta (TGFbeta) superfamily, including bone morphogenetic protein 15 (BMP15) and growth differentiation factor 9 (GDF9), as well as fibroblast growth factors (FGFs).     These growth factors cooperate to regulate cumulus cell function. To identify potential mechanisms involved in these interactions, the ability of fully grown oocytes to regulate expression of BMP or FGF antagonists in cumulus cells was examined.    Oocytes promoted cumulus cell expression of transcripts encoding antagonists to TGFbeta superfamily members, including Grem2, Htra1, Htra3, and Nog mRNAs. In contrast, oocytes suppressed cumulus cell expression of Spry2 mRNA, which encodes a    regulator of receptor tyrosine kinase signals, such as FGF and epidermal growth factor (EGF) receptor signals. The regulation of Spry2 mRNA levels in cumulus cells was studied further as a model for analysis of potential mechanisms for    cooperativity of FGF/EGF signaling with oocyte-derived members of the TGFbeta superfamily. Oocytes suppressed basal and FGF-stimulated Spry2 mRNA levels in cumulus cells but promoted EGF-stimulated levels. Furthermore, recombinant TGFbeta    superfamily proteins, including BMP15 and GDF9, mimicked these effects of oocytes. Elevated expression of Spry2 mRNA in cumulus and mural granulosa cells correlated with human chorionic gonadotropin-induced expression of mRNAs encoding EGF-like    peptides. Therefore, oocyte-derived members of the TGFbeta superfamily suppress FGF-stimulated Spry2 mRNA levels before the luteinizing hormone surge but promote Spry2 mRNA levels stimulated by EGF receptor-mediated signals after the    surge.</p>

	]]>
</description>

<author>K Sugiura et al.</author>


</item>


<item>
<title>Identification of genetic loci involved in diabetes using a rat model of depression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2074</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2074</guid>
<pubDate>Tue, 08 May 2012 23:49:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>While diabetic patients often present with comorbid depression, the underlying mechanisms linking diabetes and depression are unknown. The Wistar Kyoto (WKY) rat is a well-known animal model of depression and stress hyperreactivity.    In addition, the WKY rat is glucose intolerant and likely harbors diabetes susceptibility alleles. We conducted a quantitative trait loci (QTL) analysis in the segregating F(2) population of a WKY x Fischer 344 (F344) intercross. We previously    published QTL analyses for depressive behavior and hypothalamic-pituitary-adrenal (HPA) activity in this cross. In this study we report results from the QTL analysis for multiple metabolic phenotypes, including fasting glucose, post-restraint    stress glucose, postprandial glucose and insulin, and body weight. We identified multiple QTLs for each trait and many of the QTLs overlap with those previously identified using inbred models of type 2 diabetes (T2D). Significant correlations    were found between metabolic traits and HPA axis measures, as well as forced swim test behavior. Several metabolic loci overlap with loci previously identified for HPA activity and forced swim behavior in this F(2) intercross, suggesting that the    genetic mechanisms underlying these traits may be similar. These results indicate that WKY rats harbor diabetes susceptibility alleles and suggest that this strain may be useful for dissecting the underlying genetic mechanisms linking diabetes,    HPA activity, and depression.</p>

	]]>
</description>

<author>Woods L. Solberg et al.</author>


</item>


<item>
<title>Quantitative trait locus analysis using J/qtl.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2073</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2073</guid>
<pubDate>Tue, 08 May 2012 23:49:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Quantitative trait locus (QTL) analysis is a statistical method to link phenotypes with regions of the genome that affect the phenotypes in a mapping population. R/qtl is a powerful statistical program commonly used for analyzing    rodent QTL crosses, but R/qtl is a command line program that can be difficult for novice users to run. J/qtl was developed as an R/qtl graphical user interface that enables even novice users to utilize R/qtl for QTL analyses. In this chapter, we    describe the process for analyzing rodent cross data with J/qtl, including data formatting, data quality control, main scan QTL analysis, pair scan QTL analysis, and multiple regression modeling; this information should enable new users to    identify QTL affecting phenotypes of interest within their rodent cross datasets.</p>

	]]>
</description>

<author>R Smith et al.</author>


</item>


<item>
<title>Haplotype association mapping in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2072</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2072</guid>
<pubDate>Tue, 08 May 2012 23:49:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Haplotype Association Mapping (HAM) is a novel phenotype-driven approach to identify genetic loci and was originally developed for mice. This method, which is similar to Genome-Wide Association (GWA) studies in humans, looks for    associations between the phenotype and the haplotypes of mouse inbred strains, treating inbred strains as individuals. Although this approach is still in development, we review the current literature, present the different methods and    applications that are in use, and provide a glimpse of what is to come in the near future.</p>

	]]>
</description>

<author>S W. Tsaih et al.</author>


</item>


<item>
<title>Global changes in processing of mRNA 3&apos; untranslated regions characterize clinically distinct cancer subtypes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2071</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2071</guid>
<pubDate>Tue, 08 May 2012 23:49:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Molecular cancer diagnostics are an important clinical advance in cancer management, but new methods are still needed. In this context, gene expression signatures obtained by microarray represent a useful molecular diagnostic. Here,    we describe novel probe-level microarray analyses that reveal connections between mRNA processing and neoplasia in multiple tumor types, with diagnostic potential.  We now show that characteristic differences in mRNA processing, primarily in the    3'-untranslated region, define molecular signatures that can distinguish similar tumor subtypes with different survival characteristics, with at least 74% accuracy. Using a mouse model of B-cell leukemia/lymphoma, we find that differences in    transcript isoform abundance are likely due to both alternative polyadenylation (APA) and differential degradation. While truncation of the 3'-UTR is the most common observed pattern, genes with elongated transcripts were also observed, and    distinct groups of affected genes are found in related but distinct tumor types. Genes with elongated transcripts are overrepresented in ontology categories related to cell-cell adhesion and morphology. Analysis of microarray data from human    primary tumor samples revealed similar phenomena.  Western blot analysis of selected proteins confirms that changes in the 3'-UTR can correlate with changes in protein expression. Our work suggests that alternative mRNA processing, particularly    APA, can be a powerful molecular biomarker with prognostic potential. Finally, these findings provide insights into the molecular mechanisms of gene deregulation in tumorigenesis.</p>

	]]>
</description>

<author>P Singh et al.</author>


</item>


<item>
<title>Epilepsy genes that do not encode ion channels.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2070</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2070</guid>
<pubDate>Tue, 08 May 2012 23:49:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W N. Frankel</author>


</item>


<item>
<title>Human epilepsy as a complex genetic trait: lessons from animal models and prospects for the future.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2069</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2069</guid>
<pubDate>Tue, 08 May 2012 23:48:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W N. Frankel</author>


</item>


<item>
<title>Experimental characterization of 3D localization techniques for particle-tracking and super-resolution microscopy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2068</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2068</guid>
<pubDate>Tue, 08 May 2012 23:48:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Three-dimensional (3D) particle localization at the nanometer scale plays a central role in 3D particle tracking and 3D localization-based super-resolution microscopy. Here we introduce a localization algorithm that is independent    of theoretical models and therefore generally applicable to a large number of experimental realizations. Applying this algorithm and a convertible experimental setup we compare the performance of the two major 3D techniques based on astigmatic    distortions and on multiplane detection. In both methods we obtain experimental 3D localization accuracies in agreement with theoretical predictions and characterize the depth dependence of the localization accuracy in detail.</p>

	]]>
</description>

<author>M J. Mlodzianoski et al.</author>


</item>


<item>
<title>A Cmv2 QTL on chromosome X affects MCMV resistance in New Zealand male mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2067</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2067</guid>
<pubDate>Tue, 08 May 2012 23:48:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>NK cell-mediated resistance to viruses is subject to genetic control in humans and mice. Here we used classical and quantitative genetic strategies to examine NK-mediated murine cytomegalovirus (MCMV) control in genealogically    related New Zealand white (NZW) and black (NZB) mice. NZW mice display NK cell-dependent MCMV resistance while NZB NK cells fail to limit viral replication after infection.  Unlike Ly49H(+) NK resistance in C57BL/6 mice, NZW NK-mediated MCMV    control was Ly49H-independent. Instead, MCMV resistance in NZW (Cmv2) involves multiple genetic factors. To establish the genetic basis of Cmv2 resistance, we further characterized a major chromosome X-linked resistance locus (DXMit216)    responsible for innate MCMV control in NZW x NZB crosses. We found that the DXMit216 locus affects early MCMV control in New Zealand F(2) crosses and demonstrate that the NZB-derived DXMit216 allele enhances viral resistance in F(2) males. The    evolutionary conservation of the DXMit216 region in mice and humans suggests that a Cmv2-related mechanism may affect human antiviral responses.</p>

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</description>

<author>M R. Rodriguez et al.</author>


</item>


<item>
<title>Leptin&apos;s RIGHT turn to the brain stem.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2066</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2066</guid>
<pubDate>Tue, 08 May 2012 23:48:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>In a paper by Yadav and colleagues, a novel pathway linking the central nervous system effects of leptin on bone mass and energy expenditure to serotonin signaling in brainstem circuits is described. The data from those studies    strengthen the tenet that skeletal remodeling is intimately connected to central regulation of metabolism.</p>

	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 3 No 1</title>
<link>http://ro.uow.edu.au/uowgazette/14</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/14</guid>
<pubDate>Tue, 08 May 2012 23:48:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 3 No 2</title>
<link>http://ro.uow.edu.au/uowgazette/13</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/13</guid>
<pubDate>Tue, 08 May 2012 23:48:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 3 No 3</title>
<link>http://ro.uow.edu.au/uowgazette/12</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/12</guid>
<pubDate>Tue, 08 May 2012 23:48:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 3 No 4</title>
<link>http://ro.uow.edu.au/uowgazette/11</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/11</guid>
<pubDate>Tue, 08 May 2012 23:48:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 3 No 5</title>
<link>http://ro.uow.edu.au/uowgazette/10</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/10</guid>
<pubDate>Tue, 08 May 2012 23:48:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>Probe-level analysis of expression microarrays characterizes isoform-specific degradation during mouse oocyte maturation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2065</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2065</guid>
<pubDate>Tue, 08 May 2012 23:48:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Gene expression microarrays have provided many insights into changes in gene expression patterns between different tissue types, developmental stages, and disease states. Analyses of these data focused primarily    measuring the relative abundance of transcripts of a gene, while treating most or all transcript isoforms as equivalent. Differences in the selection between transcript isoforms can, however, represent critical changes to either the protein    product or the posttranscriptional regulation of the transcript. Novel analyses on existing microarray data provide fresh insights and new interpretations into transcriptome-wide changes in expression. METHODOLOGY: A probe-level analysis of    existing gene expression arrays revealed differences in mRNA processing, primarily affecting the 3'-untranslated region. Working with the example of microarrays drawn from a transcriptionally silent period of mouse oocyte development, probe-level    analysis (implemented here as rmodel) identified genes whose transcript isoforms have differing stabilities. Comparison of micorarrays measuring cDNA generated from oligo-dT and random primers revealed further differences in the polyadenylation    status of some transcripts. Additional analysis provided evidence for sequence-targeted cleavage, including putative targeting sequences, as one mechanism of degradation for several hundred transcripts in the maturing oocyte. CONCLUSIONS: The    capability of probe-level analysis to elicit novel findings from existing expression microarray data was demonstrated. The characterization of differences in stability between transcript isoforms in maturing mouse oocytes provided some    mechanistic details of degradation. Similar analysis of existing archives of expression microarray data will likely provide similar discoveries.</p>

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</description>

<author>J Salisbury et al.</author>


</item>


<item>
<title>The impact of incomplete knowledge on evaluation: an experimental benchmark for protein function prediction.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2064</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2064</guid>
<pubDate>Tue, 08 May 2012 23:48:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>MOTIVATION: Rapidly expanding repositories of highly informative genomic data have generated increasing interest in methods for protein function prediction and inference of biological networks. The successful application of    supervised machine learning to these tasks requires a gold standard for protein function: a trusted set of correct examples, which can be used to assess performance through cross-validation or other statistical approaches. Since gene annotation    is incomplete for even the best studied model organisms, the biological reliability of such evaluations may be called into question. RESULTS: We address this concern by constructing and analyzing an experimentally based gold standard through    comprehensive validation of protein function predictions for mitochondrion biogenesis in Saccharomyces cerevisiae. Specifically, we determine that (i) current machine learning approaches are able to generalize and predict novel biology from an    incomplete gold standard and (ii) incomplete functional annotations adversely affect the evaluation of machine learning performance.  While computational approaches performed better than predicted in the face of incomplete data, relative    comparison of competing approaches-even those employing the same training data-is problematic with a sparse gold standard. Incomplete knowledge causes individual methods' performances to be differentially underestimated, resulting in misleading    performance evaluations. We provide a benchmark gold standard for yeast mitochondria to complement current databases and an analysis of our experimental results in the hopes of mitigating these effects in future comparative evaluations.    AVAILABILITY: The mitochondrial benchmark gold standard, as well as experimental results and additional data, is available at http://function.princeton.edu/mitochondria.</p>

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</description>

<author>C Huttenhower et al.</author>


</item>


<item>
<title>Validation of a noninvasive dynamic spinal stiffness assessment methodology in an animal model of intervertebral disc degeneration.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2063</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2063</guid>
<pubDate>Tue, 08 May 2012 23:48:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>STUDY DESIGN: An experimental in vivo ovine model of intervertebral disc degeneration was used to quantify the dynamic motion response of the lumbar spine. OBJECTIVE: The purpose of this study was to: (1) compare invasively measured    lumbar vertebral bone acceleration responses to noninvasive displacement responses, and (2) determine the effects of a single level degenerative intervertebral disc lesion on these responses. SUMMARY OF BACKGROUND DATA: Biomechanical techniques    have been established to quantify vertebral motion responses, yet their invasiveness limits their use in a clinical setting.  METHODS: Twenty-five Merino sheep were examined; 15 with surgically induced disc degeneration at L1-L2 and 10 controls.    Triaxial accelerometers were rigidly fixed to the L1 and L2 spinous processes and dorsoventral (DV) mechanical excitation (20-80 N, 100 milliseconds) was applied to L3 using a spinal dynamometer. Peak force and displacement and peak-peak    acceleration responses were computed for each trial and a least squares regression analysis assessed the correlation between L3 displacement and adjacent (L2) segment acceleration responses. An analysis of covariance (ANCOVA) was performed to    test the homogeneity of slopes derived from the regression analysis and to assess the mean differences. RESULTS: A significant, positive, linear correlation was found between the DV displacement of L3 and the DV acceleration measured at L2 for    both normal (R = 0.482, P < 0.001) and degenerated disc groups (R = 0.831, P < 0.001). The L3 DV displacement was significantly lower (ANCOVA, P < 0.001) for the degenerated group (mean: 10.39 mm) in comparison to the normal group (mean: 9.07    mm). Mean peak-peak L2-L1 DV acceleration transfer was also significantly reduced from 12.40 m/s to 5.50 m/s in the degenerated animal group (ANCOVA, P < 0.001). CONCLUSION: The findings indicate that noninvasive displacement measurements of the    prone-lying animal can be used to estimate the segmental and intersegmental motions in both normal and pathologic spines.</p>

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</description>

<author>C J. Colloca et al.</author>


</item>


<item>
<title>Emu-BCL10 mice exhibit constitutive activation of both canonical and noncanonical NF-kappaB pathways generating marginal zone (MZ) B-cell expansion as a precursor to splenic MZ lymphoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2062</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2062</guid>
<pubDate>Tue, 08 May 2012 23:47:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>BCL10, required for nuclear factor kappaB (NF-kappaB) activation during antigen-driven lymphocyte responses, is aberrantly expressed in mucosa-associated lymphoid tissue-type marginal zone (MZ) lymphomas because of chromosomal    translocations. Emu-driven human BCL10 transgenic (Tg) mice, which we created and characterize here, had expanded populations of MZ B cells and reduced follicular and B1a cells. Splenic B cells from Tg mice exhibited constitutive activation of    both canonical and noncanonical NF-kappaB signaling pathways is associated with increased expression of NF-kappaB target genes. These genes included Tnfsf13b, which encodes the B-cell activating factor (BAFF). In addition, levels of BAFF were    significantly increased in sera from Tg mice. MZ B cells of Tg mice exhibited reduced turnover in vivo and enhanced survival in vitro, indicative of lymphoaccumulation rather than lymphoproliferation as the cause of MZ expansion.  In vivo    antibody responses to both T-independent, and especially T-dependent, antigens were significantly reduced in Tg mice. Mortality was accelerated in Tg animals, and some mice older than 8 months had histologic and molecular findings indicative of    clonal splenic MZ lymphoma. These results suggest that, in addition to constitutive activation of BCL10 in MZ B cells, other genetic factors or environmental influences are required for short latency oncogenic transformation.</p>

	]]>
</description>

<author>Z Li et al.</author>


</item>


<item>
<title>Functional interchangeability of rod and cone transducin alpha-subunits.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2061</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2061</guid>
<pubDate>Tue, 08 May 2012 23:47:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rod and cone photoreceptors use similar but distinct sets of phototransduction proteins to achieve different functional properties, suitable for their role as dim and bright light receptors, respectively. For example, rod and cone    visual pigments couple to distinct variants of the heterotrimeric G protein transducin.  However, the role of the structural differences between rod and cone transducin alpha subunits (Talpha) in determining the functional differences between    rods and cones is unknown. To address this question, we studied the translocation and signaling properties of rod Talpha expressed in cones and cone Talpha expressed in rods in three mouse strains: rod Talpha knockout, cone Talpha GNAT2(cpfl3)    mutant, and rod and cone Talpha double mutant rd17 mouse. Surprisingly, although the rod/cone Talpha are only 79% identical, exogenously expressed rod or cone Talpha localized and translocated identically to endogenous Talpha in each    photoreceptor type. Moreover, exogenously expressed rod or cone Talpha rescued electroretinogram responses (ERGs) in mice lacking functional cone or rod Talpha, respectively. Ex vivo transretinal ERG and single-cell recordings from rd17 retinas    treated with rod or cone Talpha showed comparable rod sensitivity and response kinetics. These results demonstrate that cone Talpha forms a functional heterotrimeric G protein complex in rods and that rod and cone Talpha couple equally well to    the rod phototransduction cascade. Thus, rod and cone transducin alpha-subunits are functionally interchangeable and their signaling properties do not contribute to the intrinsic light sensitivity differences between rods and cones. Additionally,    the technology used here could be adapted for any such homologue swap desired.</p>

	]]>
</description>

<author>W T. Deng et al.</author>


</item>


<item>
<title>A homologous genetic basis of the murine cpfl1 mutant and human achromatopsia linked to mutations in the PDE6C gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2060</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2060</guid>
<pubDate>Tue, 08 May 2012 23:47:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Retinal cone photoreceptors mediate fine visual acuity, daylight vision, and color vision. Congenital hereditary conditions in which there is a lack of cone function in humans cause achromatopsia, an autosomal recessive trait,    characterized by low vision, photophobia, and lack of color discrimination.  Herein we report the identification of mutations in the PDE6C gene encoding the catalytic subunit of the cone photoreceptor phosphodiesterase as a cause of autosomal    recessive achromatopsia. Moreover, we show that the spontaneous mouse mutant cpfl1 that features a lack of cone function and rapid degeneration of the cone photoreceptors represents a homologous mouse model for PDE6C associated    achromatopsia.</p>

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</description>

<author>B Chang et al.</author>


</item>


<item>
<title>A feedback loop involving the Phd3 prolyl hydroxylase tunes the mammalian hypoxic response in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2059</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2059</guid>
<pubDate>Tue, 08 May 2012 23:47:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hypoxia-inducible factor (HIF), consisting of a labile alpha subunit and a stable beta subunit, is a master regulator of hypoxia-responsive mRNAs. HIF alpha undergoes oxygen-dependent prolyl hydroxylation, which marks it for    polyubiquitination by a complex containing the von Hippel-Lindau protein (pVHL).  Among the three Phd family members, Phd2 appears to be the primary HIF prolyl hydroxylase. Phd3 is induced by HIF and, based on findings from in vitro studies, may    participate in a HIF-regulatory feedback loop. Here, we report that Phd3 loss exacerbates the HIF activation, hepatic steatosis, dilated cardiomyopathy, and premature mortality observed in mice lacking Phd2 alone and produces a closer phenocopy    of the changes seen in mice lacking pVHL than the loss of Phd2 alone.  Importantly, the degree to which Phd3 can compensate for Phd2 loss and the degree to which the combined loss of Phd2 and Phd3 resembles pVHL loss appear to differ for    different HIF-responsive genes and in different tissues. These findings highlight that the responses of different HIF target genes to changes in prolyl hydroxylase activity differ, quantitatively and qualitatively, in vivo and have implications    for the development of paralog-specific prolyl hydroxylase inhibitors as therapeutic agents.</p>

	]]>
</description>

<author>Y A. Minamishima et al.</author>


</item>


<item>
<title>Transcriptome analysis reveals an unexpected role of a collagen tyrosine kinase receptor gene, Ddr2, as a regulator of ovarian function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2058</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2058</guid>
<pubDate>Tue, 08 May 2012 23:47:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice homozygous for the smallie (slie) mutation lack a collagen receptor, discoidin domain receptor 2 (DDR2), and are dwarfed and infertile due to peripheral dysregulation of the endocrine system of unknown etiology. We used a    systems biology approach to identify biological networks affected by Ddr2(slie/slie) mutation in ovaries using microarray analysis and validate findings using molecular, cellular, and functional biological assays.  Transcriptome analysis    indicated several altered gene categories in Ddr2(slie/slie) mutants, including gonadal development, ovulation, antiapoptosis, and steroid hormones. Subsequent biological experiments confirmed the transcriptome analysis predictions. For instance,    a significant increase of TUNEL-positive follicles was found in Ddr2(slie/slie) mutants vs. wild type, which confirm the transcriptome prediction for decreased chromatin maintenance and antiapoptosis. Decreases in gene expression were confirmed    by RT-PCR and/or qPCR; luteinizing hormone receptor and prostaglandin type E and F receptors in Ddr2(slie/slie) mutants, compared with wild type, confirm hormonal signaling pathways involved in ovulation. Furthermore, deficiencies in    immunohistochemistry for DDR2 and luteinizing hormone receptor in the somatic cells, but not the oocytes, of Ddr2(slie/slie) mutant ovaries suggest against an intrinsic defect in germ cells. Indeed, Ddr2(slie/slie) mutants ovulated significantly    fewer oocytes; their oocytes were competent to complete meiosis and fertilization in vitro.  Taken together, our convergent data signify DDR2 as a novel critical player in ovarian function, which acts upon classical endocrine pathways in somatic,    rather than germline, cells.</p>

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</description>

<author>H Matsumura et al.</author>


</item>


<item>
<title>The podosomal-adaptor protein SH3PXD2B is essential for normal postnatal development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2057</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2057</guid>
<pubDate>Tue, 08 May 2012 23:47:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Podosome-type adhesions are actin-based membrane protrusions involved in cell-matrix adhesion and extracellular matrix degradation. Despite growing knowledge of many proteins associated with podosome-type adhesions, much remains    unknown concerning the function of podosomal proteins at the level of the whole animal. In this study, the spontaneous mouse mutant nee was used to identify a component of podosome-type adhesions that is essential for normal postnatal growth and    development. Mice homozygous for the nee allele exhibited runted growth, craniofacial and skeletal abnormalities, ocular anterior segment dysgenesis, and hearing impairment. Adults also exhibited infertility and a form of lipodystrophy. Using    genetic mapping and DNA sequencing, the cause of nee phenotypes was identified as a 1-bp deletion within the Sh3pxd2b gene on mouse Chromosome 11. Whereas the wild-type Sh3pxd2b gene is predicted to encode a protein with one PX domain and four    SH3 domains, the nee mutation is predicted to cause a frameshift and a protein truncation altering a portion of the third SH3 domain and deleting all of the fourth SH3 domain. The SH3PXD2B protein is believed to be an important component of    podosomes likely to mediate protein-protein interactions with membrane-spanning metalloproteinases. Testing this directly, SH3PXD2B localized to podosomes in constitutively active Src-transfected fibroblasts and through its last SH3 domain    associated with a transmembrane member of a disintegrin and metalloproteinase family of proteins, ADAM15. These results identify SH3PXD2B as a podosomal-adaptor protein required for postnatal growth and development, particularly within    physiologic contexts involving extracellular matrix regulation.</p>

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</description>

<author>M Mao et al.</author>


</item>


<item>
<title>Selecting the &quot;right&quot; mouse model for metabolic syndrome and type 2 diabetes research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2056</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2056</guid>
<pubDate>Tue, 08 May 2012 23:46:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>This is not a "Methods" chapter in the traditional sense. Rather, it is an essay designed to help address one of the most frequently asked questions by investigators about to embark on a study requiring an animal model of diabetes -    what is the "right" model for the reader's specific research application. Because genetic heterogeneity and the requirement for complex gene-environment interaction characterize the various mouse models of Type 2 diabetes as well as the human    disease manifestations, the readers may come to share the author's conclusion that more than one model is required if the investigator is interested in knowing how broadly effective a given compound with putative therapeutic efficacy might    be.</p>

	]]>
</description>

<author>E H. Leiter</author>


</item>


<item>
<title>Development of immunoglobulin lambda-chain-positive B cells, but not editing of immunoglobulin kappa-chain, depends on NF-kappaB signals.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2055</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2055</guid>
<pubDate>Tue, 08 May 2012 23:46:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>By genetically ablating IkappaB kinase (IKK)-mediated activation of the transcription factor NF-kappaB in the B cell lineage and by analyzing a mouse mutant in which immunoglobulin lambda-chain-positive B cells are generated in the    absence of rearrangements in the locus encoding immunoglobulin kappa-chain, we define here two distinct, consecutive phases of early B cell development that differ in their dependence on IKK-mediated NF-kappaB signaling. During the first phase,    in which NF-kappaB signaling is dispensable, predominantly kappa-chain-positive B cells are generated, which undergo efficient receptor editing. In the second phase, predominantly lambda-chain-positive B cells are generated whose development is    ontogenetically timed to occur after rearrangements of the locus encoding kappa-chain. This second phase of development is dependent on NF-kappaB signals, which can be substituted by transgenic expression of the prosurvival factor    Bcl-2.</p>

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</description>

<author>E Derudder et al.</author>


</item>


<item>
<title>Understanding the muscular dystrophy caused by deletion of choline kinase beta in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2054</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2054</guid>
<pubDate>Tue, 08 May 2012 23:46:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Choline kinase in mice is encoded by two genes, Chka and Chkb. Disruption of murine Chka leads to embryonic lethality, whereas a spontaneously occurring genomic deletion in murine Chkb results in neonatal bone deformity and hindlimb    muscular dystrophy. We have investigated the mechanism by which a lack of choline kinase beta, encoded by Chkb, causes hindlimb muscular dystrophy. The biosynthesis of phosphatidylcholine (PC) is impaired in the hindlimbs of Chkb -/- mice, with    an accumulation of choline and decreased amount of phosphocholine. The activity of CTP: phosphocholine cytidylyltransferase is also decreased in the hindlimb muscle of mutant mice. Concomitantly, the activities of PC phospholipase C and    phospholipase A2 are increased. The mitochondria in Chkb -/- mice are abnormally large and exhibit decreased inner membrane potential. Despite the muscular dystrophy in Chkb -/- mice, we observed increased expression of insulin like growth factor    1 and proliferating cell nuclear antigen. However, regeneration of hindlimb muscles of Chkb -/- mice was impaired when challenged with cardiotoxin. Injection of CDP-choline increased PC content of hindlimb muscle and decreased creatine kinase    activity in plasma of Chkb -/- mice. We conclude that the hindlimb muscular dystrophy in Chkb -/- mice is due to attenuated PC biosynthesis and enhanced catabolism of PC.</p>

	]]>
</description>

<author>G Wu et al.</author>


</item>


<item>
<title>Complex oncogenic translocations with gene amplification are initiated by specific DNA breaks in lymphocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2053</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2053</guid>
<pubDate>Tue, 08 May 2012 23:46:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chromosomal instability is a hallmark of many tumor types. Complex chromosomal rearrangements with associated gene amplification, known as complicons, characterize many hematologic and solid cancers. Whereas chromosomal aberrations,    including complicons, are useful diagnostic and prognostic cancer markers, their molecular origins are not known. Although accumulating evidence has implicated DNA double-strand break repair in suppression of oncogenic genome instability, the    genomic elements required for chromosome rearrangements, especially complex lesions, have not been elucidated. Using a mouse model of B-lineage lymphoma, characterized by complicon formation involving the immunoglobulin heavy chain (Igh) locus    and the c-myc oncogene, we have now investigated the requirement for specific genomic segments as donors for complex rearrangements. We now show that specific DNA double-strand breaks, occurring within a narrow segment of Igh, are necessary to    initiate complicon formation. By contrast, neither specific DNA breaks nor the powerful intronic enhancer Emu are required for complicon-independent oncogenesis. This study is the first to delineate mechanisms of complex versus simple instability    and the first to identify specific chromosomal elements required for complex chromosomal aberrations. These findings will illuminate genomic cancer susceptibility and risk factors.</p>

	]]>
</description>

<author>S M. Wright et al.</author>


</item>


<item>
<title>Importance of randomization in microarray experimental designs with Illumina platforms.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2052</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2052</guid>
<pubDate>Tue, 08 May 2012 23:46:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Measurements of gene expression from microarray experiments are highly dependent on experimental design. Systematic noise can be introduced into the data at numerous steps. On Illumina BeadChips, multiple samples are assayed in an    ordered series of arrays. Two experiments were performed using the same samples but different hybridization designs. An experiment confounding genotype with BeadChip and treatment with array position was compared to another experiment in which    these factors were randomized to BeadChip and array position. An ordinal effect of array position on intensity values was observed in both experiments. We demonstrate that there is increased rate of false-positive results in the confounded design    and that attempts to correct for confounded effects by statistical modeling reduce power of detection for true differential expression.  Simple analysis models without post hoc corrections provide the best results possible for a given    experimental design. Normalization improved differential expression testing in both experiments but randomization was the most important factor for establishing accurate results. We conclude that lack of randomization cannot be corrected by    normalization or by analytical methods. Proper randomization is essential for successful microarray experiments.</p>

	]]>
</description>

<author>R A. Verdugo et al.</author>


</item>


<item>
<title>Novel ENU-induced point mutation in scavenger receptor class B, member 1, results in liver specific loss of SCARB1 protein.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2051</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2051</guid>
<pubDate>Tue, 08 May 2012 23:46:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cardiovascular disease (CVD) is the largest cause of premature death in human populations throughout the world. Circulating plasma lipid levels, specifically high levels of LDL or low levels of HDL, are predictive of susceptibility    to CVD.  The scavenger receptor class B member 1 (SCARB1) is the primary receptor for the selective uptake of HDL cholesterol by liver and steroidogenic tissues. Hepatic SCARB1 influences plasma HDL-cholesterol levels and is vital for reverse    cholesterol transport. Here we describe the mapping of a novel N-ethyl-N-nitrosourea (ENU) induced point mutation in the Scarb1 gene identified in a C57BL/6J background. The mutation is located in a highly conserved amino acid in the    extracellular loop and leads to the conversion of an isoleucine to an asparagine (I179N). Homozygous mutant mice express normal Scarb1 mRNA levels and are fertile. SCARB1 protein levels are markedly reduced in liver (approximately 90%), but not    in steroidogenic tissues. This leads to approximately 70% increased plasma HDL levels due to reduced HDL cholesteryl ester selective uptake. Pdzk1 knockout mice have liver-specific reduction of SCARB1 protein as does this mutant; however, in    vitro analysis of the mutation indicates that the regulation of SCARB1 protein in this mutant is independent of PDZK1. This new Scarb1 model may help further our understanding of post-translational and tissue-specific regulation of SCARB1 that    may aid the important clinical goal of raising functional HDL.</p>

	]]>
</description>

<author>I M. Stylianou et al.</author>


</item>


<item>
<title>An experimental assessment of in silico haplotype association mapping in laboratory mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2050</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2050</guid>
<pubDate>Tue, 08 May 2012 23:46:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: To assess the utility of haplotype association mapping (HAM) as a quantitative trait locus (QTL) discovery tool, we conducted HAM analyses for red blood cell count (RBC) and high density lipoprotein cholesterol (HDL) in    mice. We then experimentally tested each HAM QTL using published crosses or new F2 intercrosses guided by the haplotype at the HAM peaks. RESULTS: The HAM for RBC, using 33 classic inbred lines, revealed 8 QTLs; 2 of these were true positives as    shown by published crosses. A HAM-guided (C57BL/6J x CBA/J)F2 intercross we carried out verified 2 more as true positives and 4 as false positives. The HAM for HDL, using 81 strains including recombinant inbred lines and chromosome substitution    strains, detected 46 QTLs. Of these, 36 were true positives as shown by published crosses. A HAM-guided (C57BL/6J x A/J)F2 intercross that we carried out verified 2 more as true positives and 8 as false positives. By testing each HAM QTL for RBC    and HDL, we demonstrated that 78% of the 54 HAM peaks were true positives and 22% were false positives. Interestingly, all false positives were in significant allelic association with one or more real QTL. CONCLUSION: Because type I errors (false    positives) can be detected experimentally, we conclude that HAM is useful for QTL detection and narrowing. We advocate the powerful and economical combined approach demonstrated here: the use of HAM for QTL discovery, followed by mitigation of    the false positive problem by testing the HAM-predicted QTLs with small HAM-guided experimental crosses.</p>

	]]>
</description>

<author>Herbert S. Burgess et al.</author>


</item>


<item>
<title>Alcohol alters whole body composition, inhibits bone formation, and increases bone marrow adiposity in rats.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2049</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2049</guid>
<pubDate>Tue, 08 May 2012 23:45:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chronic alcohol abuse is a risk factor for osteoporosis and sarcopenia, but the long-term effects of alcohol on the immature musculoskeletal system are less clear. The present investigation in growing rats was designed to determine    the effects of alcohol consumption on body composition, muscle mass, and bone mass, architecture, and turnover. INTRODUCTION: Few studies have focused on the long-term effects of drinking on bone and muscle during skeletal maturation.  METHODS:    Alcohol was included in the diet of 4-week-old male Sprague-Dawley rats (35% caloric intake) for 3 months. The controls were fed an isocaloric alcohol-free liquid diet ad libitum. A second study was performed in which the controls were pair-fed    to the alcohol-fed animals. RESULTS: Compared to ad libitum-fed age-matched controls, alcohol-fed rats weighed less and had lower lean mass, fat mass, and percent body fat. In addition, they had lower slow- and fast-twitch muscle mass, lower    total body bone mineral content and bone mineral density, and lower cancellous bone volume in the lumbar vertebra and proximal tibia. The effects of alcohol consumption on body composition were reduced when compared to the pair-fed control diet,    indicating that caloric restriction was a comorbidity factor. In contrast, the effects of alcohol to decrease bone formation and serum leptin and IGF-I levels and to increase bone marrow adiposity appeared independent of caloric restriction.    CONCLUSIONS: The skeletal abnormalities in growing alcohol-fed rats were due to a combination of effects specific to alcohol consumption and alcohol-induced caloric restriction.</p>

	]]>
</description>

<author>G F. Maddalozzo et al.</author>


</item>


<item>
<title>Mechanical stimulation of mesenchymal stem cell proliferation and differentiation promotes osteogenesis while preventing dietary-induced obesity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2048</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2048</guid>
<pubDate>Tue, 08 May 2012 23:45:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mesenchymal stem cells (MSCs) are defined by their ability to self-renew and differentiate into the cells that form mesodermal tissues such as bone and fat.  Low magnitude mechanical signals (LMMS) have been shown to be anabolic to    bone and have been recently reported to suppress the development of fat in normal animals fed a regular diet. Using male C57BL/6J mice, the ability of LMMS (0.2g, 90-Hz signal applied for 15 min/d, 5 d/wk) to simultaneously promote bone formation    and prevent diet-induced obesity was correlated to mechanical influences on the molecular environment of the bone marrow, as indicated by the population dynamics and lineage commitment of MSCs. Six weeks of LMMS increased the overall marrow-based    stem cell population by 37% and the number of MSCs by 46%. Concomitant with the increase in stem cell number, the differentiation potential of MSCs in the bone marrow was biased toward osteoblastic and against adipogenic differentiation, as    reflected by upregulation of the transcription factor Runx2 by 72% and downregulation of PPARgamma by 27%. The phenotypic impact of LMMS on MSC lineage determination was evident at 14 wk, where visceral adipose tissue formation was suppressed by    28%, whereas trabecular bone volume fraction in the tibia was increased by 11%. Translating this to the clinic, a 1-yr trial in young women (15-20 yr; n = 48) with osteopenia showed that LMMS increased trabecular bone in the spine and kept    visceral fat at baseline levels, whereas control subjects showed no change in BMD, yet an increase in visceral fat.  Mechanical modulation of stem cell proliferation and differentiation indicates a unique therapeutic target to aid in tissue    regeneration and repair and may represent the basis of a nonpharmacologic strategy to simultaneously prevent obesity and osteoporosis.</p>

	]]>
</description>

<author>Y K. Luu et al.</author>


</item>


<item>
<title>The nuclear periphery of embryonic stem cells is a transcriptionally permissive and repressive compartment.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2047</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2047</guid>
<pubDate>Tue, 08 May 2012 23:45:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chromatin adapts a distinct structure and epigenetic state in embryonic stem cells (ESCs), but how chromatin is three-dimensionally organized within the ESC nucleus is poorly understood. Because nuclear location can influence gene    expression, we examined the nuclear distributions of chromatin with key epigenetic marks in ESC nuclei. We focused on chromatin at the nuclear periphery, a compartment that represses some but not all associated genes and accumulates facultative    heterochromatin in differentiated cells. Using a quantitative, cytological approach, we measured the nuclear distributions of genes in undifferentiated mouse ESCs according to epigenetic state and transcriptional activity. We found that trimethyl    histone H3 lysine 27 (H3K27-Me(3)), which marks repressed gene promoters, is enriched at the ESC nuclear periphery. In addition, this compartment contains 10-15% of chromatin with active epigenetic marks and hundreds of transcription sites.    Surprisingly, comparisons with differentiated cell types revealed similar nuclear distributions of active chromatin. By contrast, H3K27-Me(3) was less concentrated at the nuclear peripheries of differentiated cells. These findings demonstrate    that the nuclear periphery is an epigenetically dynamic compartment that might be distinctly marked in pluripotent ESCs. In addition, our data indicate that the nuclear peripheries of multiple cell types can contain a significant fraction of both    active and repressed genes.</p>

	]]>
</description>

<author>L Luo et al.</author>


</item>


<item>
<title>Epiblast-specific Snai1 deletion results in embryonic lethality due to multiple vascular defects.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2046</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2046</guid>
<pubDate>Tue, 08 May 2012 23:45:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Members of the Snail gene family, which encode zinc finger proteins that function as transcriptional repressors, play essential roles during embryonic development in vertebrates. Mouse embryos with conditional deletion    of the Snail1 (Snai1) gene in the epiblast, but not in most extraembryonic membranes, exhibit defects in left-right asymmetry specification and migration of mesoderm cells through the posterior primitive streak. Here we describe phenotypic    defects that result in death of the mutant embryos by 9.5 days of gestation. FINDINGS: Endothelial cells differentiated in epiblast-specific Snai1-deficient embryos, but formation of an interconnected vascular network was abnormal. To determine    whether the observed vascular defects were dependent on disruption of blood flow, we analyzed vascular remodeling in cultured allantois explants from the mutant embryos. Similar vascular defects were observed in the mutant allantois explants.    CONCLUSION: These studies demonstrate that lethality in the Snai1-conditional mutant embryos is caused by multiple defects in the cardiovascular system.</p>

	]]>
</description>

<author>H Lomeli et al.</author>


</item>


<item>
<title>Improved murine model of malaria using Plasmodium falciparum competent strains and non-myelodepleted NOD-scid IL2Rgammanull mice engrafted with human erythrocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2045</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2045</guid>
<pubDate>Tue, 08 May 2012 23:45:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Murine models of Plasmodium falciparum malaria may become crucial tools in drug discovery. Here we show that non-myelodepleted NOD-scid IL2Rgamma(null) mice engrafted with human erythrocytes support an infectious burden up to    tenfold higher than that supported by engrafted NOD-scid beta2microglobulin(null) mice.  The new model was validated for drug discovery and was used to assess the therapeutic efficacy of 4-pyridones, selective inhibitors of P. falciparum    cytochrome bc1.</p>

	]]>
</description>

<author>Diaz M. Jimenez et al.</author>


</item>


<item>
<title>Dengue virus infection and virus-specific HLA-A2 restricted immune responses in humanized NOD-scid IL2rgammanull mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2044</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2044</guid>
<pubDate>Tue, 08 May 2012 23:45:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The lack of a suitable animal model to study viral and immunological mechanisms of human dengue disease has been a deterrent to dengue research.  METHODOLOGY/PRINCIPAL FINDINGS: We sought to establish an animal model for    dengue virus (DENV) infection and immunity using non-obese diabetic/severe combined immunodeficiency interleukin-2 receptor gamma-chain knockout (NOD-scid IL2rgamma(null)) mice engrafted with human hematopoietic stem cells. Human CD45(+) cells in    the bone marrow of engrafted mice were susceptible to in vitro infection using low passage clinical and established strains of DENV. Engrafted mice were infected with DENV type 2 by different routes and at multiple time points post infection, we    detected DENV antigen and RNA in the sera, bone marrow, spleen and liver of infected engrafted mice. Anti-dengue IgM antibodies directed against the envelope protein of DENV peaked in the sera of mice at 1 week post infection. Human T cells that    developed following engraftment of HLA-A2 transgenic NOD-scid IL2rgamma(null) mice with HLA-A2(+) human cord blood hematopoietic stem cells, were able to secrete IFN-gamma, IL-2 and TNF-alpha in response to stimulation with three previously    identified A2 restricted dengue peptides NS4b 2353((111-119)), NS4b 2423((181-189)), and NS4a 2148((56-64)).  CONCLUSIONS/SIGNIFICANCE: This is the first study to demonstrate infection of human cells and functional DENV-specific T cell responses    in DENV-infected humanized mice. Overall, these mice should be a valuable tool to study the role of prior immunity on subsequent DENV infections.</p>

	]]>
</description>

<author>S Jaiswal et al.</author>


</item>


<item>
<title>Computational analysis of the yeast proteome: understanding and exploiting functional specificity in genomic data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2043</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2043</guid>
<pubDate>Tue, 08 May 2012 23:44:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Modern experimental techniques have produced a wealth of high-throughput data that has enabled the ongoing genomic revolution. As the field continues to integrate experimental and computational analyzes of this data, it is essential    that performance evaluations of high-throughput results be carried out in a consistent and biologically informative manner. Here, we present an overview of evaluation techniques for high-throughput experimental data and computational methods, and    we discuss a number of potential pitfalls in this process. These primarily involve the biological diversity of genomic data, which can be masked or misrepresented in overly simplified global evaluations. We describe systems for preserving    information about biological context during dataset evaluation, which can help to ensure that multiple different evaluations are more directly comparable. This biological variety in high-throughput data can also be taken advantage of    computationally through data integration and process specificity to produce richer systems-level predictions of cellular function. An awareness of these considerations can greatly improve the evaluation and analysis of any high-throughput    experimental dataset.</p>

	]]>
</description>

<author>C Huttenhower et al.</author>


</item>


<item>
<title>Exploring the human genome with functional maps.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2042</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2042</guid>
<pubDate>Tue, 08 May 2012 23:44:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human genomic data of many types are readily available, but the complexity and scale of human molecular biology make it difficult to integrate this body of data, understand it from a systems level, and apply it to the study of    specific pathways or genetic disorders. An investigator could best explore a particular protein, pathway, or disease if given a functional map summarizing the data and interactions most relevant to his or her area of interest. Using a regularized    Bayesian integration system, we provide maps of functional activity and interaction networks in over 200 areas of human cellular biology, each including information from approximately 30,000 genome-scale experiments pertaining to approximately    25,000 human genes. Key to these analyses is the ability to efficiently summarize this large data collection from a variety of biologically informative perspectives: prediction of protein function and functional modules, cross-talk among    biological processes, and association of novel genes and pathways with known genetic disorders. In addition to providing maps of each of these areas, we also identify biological processes active in each data set.  Experimental investigation of    five specific genes, AP3B1, ATP6AP1, BLOC1S1, LAMP2, and RAB11A, has confirmed novel roles for these proteins in the proper initiation of macroautophagy in amino acid-starved human fibroblasts. Our functional maps can be explored using HEFalMp    (Human Experimental/Functional Mapper), a web interface allowing interactive visualization and investigation of this large body of information.</p>

	]]>
</description>

<author>C Huttenhower et al.</author>


</item>


<item>
<title>Mouse population-guided resequencing reveals that variants in CD44 contribute to acetaminophen-induced liver injury in humans.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2041</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2041</guid>
<pubDate>Tue, 08 May 2012 23:44:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Interindividual variability in response to chemicals and drugs is a common regulatory concern. It is assumed that xenobiotic-induced adverse reactions have a strong genetic basis, but many mechanism-based investigations have not    been successful in identifying susceptible individuals. While recent advances in pharmacogenetics of adverse drug reactions show promise, the small size of the populations susceptible to important adverse events limits the utility of whole-genome    association studies conducted entirely in humans. We present a strategy to identify genetic polymorphisms that may underlie susceptibility to adverse drug reactions. First, in a cohort of healthy adults who received the maximum recommended dose    of acetaminophen (4 g/d x 7 d), we confirm that about one third of subjects develop elevations in serum alanine aminotransferase, indicative of liver injury. To identify the genetic basis for this susceptibility, a panel of 36 inbred mouse    strains was used to model genetic diversity. Mice were treated with 300 mg/kg or a range of additional acetaminophen doses, and the extent of liver injury was quantified. We then employed whole-genome association analysis and targeted sequencing    to determine that polymorphisms in Ly86, Cd44, Cd59a, and Capn8 correlate strongly with liver injury and demonstrated that dose-curves vary with background. Finally, we demonstrated that variation in the orthologous human gene, CD44, is    associated with susceptibility to acetaminophen in two independent cohorts. Our results indicate a role for CD44 in modulation of susceptibility to acetaminophen hepatotoxicity. These studies demonstrate that a diverse mouse population can be    used to understand and predict adverse toxicity in heterogeneous human populations through guided resequencing.</p>

	]]>
</description>

<author>A H. Harrill et al.</author>


</item>


<item>
<title>Rab3 dynamically controls protein composition at active zones.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2040</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2040</guid>
<pubDate>Tue, 08 May 2012 23:44:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Synaptic transmission requires the localization of presynaptic release machinery to active zones. Mechanisms regulating the abundance of such synaptic proteins at individual release sites are likely determinants of site-specific    synaptic efficacy. We now identify a role for the small GTPase Rab3 in regulating the distribution of presynaptic components to active zones. At Drosophila rab3 mutant NMJs, the presynaptic protein Bruchpilot, calcium channels, and electron-dense    T bars are concentrated at a fraction of available active zones, leaving the majority of sites devoid of these key presynaptic release components. Late addition of Rab3 to mutant NMJs rapidly reverses this phenotype by recruiting Brp to sites    previously lacking the protein, demonstrating that Rab3 can dynamically control the composition of the presynaptic release machinery. While previous studies of Rab3 have focused on its role in the synaptic vesicle cycle, these findings    demonstrate an additional and unexpected function for Rab3 in the localization of presynaptic proteins to active zones.</p>

	]]>
</description>

<author>E R. Graf et al.</author>


</item>


<item>
<title>Mouse models of diabetic nephropathy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2039</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2039</guid>
<pubDate>Tue, 08 May 2012 23:44:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Diabetic nephropathy is a major cause of ESRD worldwide. Despite its prevalence, a lack of reliable animal models that mimic human disease has delayed the identification of specific factors that cause or predict diabetic    nephropathy.  The Animal Models of Diabetic Complications Consortium (AMDCC) was created in 2001 by the National Institutes of Health to develop and characterize models of diabetic nephropathy and other complications. This interim report and our    online supplement detail the progress made toward that goal, specifically in the development and testing of murine models. Updates are provided on validation criteria for early and advanced diabetic nephropathy, phenotyping methods, the effect of    background strain on nephropathy, current best models of diabetic nephropathy, negative models, and views of future directions. AMDCC investigators and other investigators in the field have yet to validate a complete murine model of human    diabetic kidney disease. Nonetheless, the critical analysis of existing murine models substantially enhances our understanding of this disease process.</p>

	]]>
</description>

<author>F C. Brosius et al.</author>


</item>


<item>
<title>Nr2e3-directed transcriptional regulation of genes involved in photoreceptor development and cell-type specific phototransduction.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2038</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2038</guid>
<pubDate>Tue, 08 May 2012 23:44:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The retinal transcription factor Nr2e3 plays a key role in photoreceptor development and function. In this study we examine gene expression in the retina of Nr2e3(rd7/rd7) mutants with respect to wild-type control mice, to identify    genes that are misregulated and hence potentially function in the Nr2e3 transcriptional network. Quantitative candidate gene real time PCR and subtractive hybridization approaches were used to identify transcripts that were misregulated in    Nr2e3(rd7/rd7) mice. Chromatin immunoprecipitation assays were then used to determine which of the misregulated transcripts were direct targets of NR2E3. We identified 24 potential targets of NR2E3. In the developing retina, NR2E3 targets    transcription factors such as Ror1, Rorg, and the nuclear hormone receptors Nr1d1 and Nr2c1. In the mature retina NR2E3 targets several genes including the rod specific gene Gnb1 and cone specific genes blue opsin, and two of the cone transducin    subunits, Gnat2 and Gnb3. In addition, we identified 5 novel transcripts that are targeted by NR2E3. While mislocalization of proteins between rods and cones was not observed, we did observe diminished concentration of GNB1 protein in adult    Nr2e3(rd7/rd7) retinas. These studies identified novel transcriptional pathways that are potentially targeted by Nr2e3 in the retina and specifically demonstrate a novel role for NR2E3 in regulating genes involved in    phototransduction.</p>

	]]>
</description>

<author>N B. Haider et al.</author>


</item>


<item>
<title>Dual color localization microscopy of cellular nanostructures.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2037</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2037</guid>
<pubDate>Tue, 08 May 2012 23:44:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The dual color localization microscopy (2CLM) presented here is based on the principles of spectral precision distance microscopy (SPDM) with conventional autofluorescent proteins under special physical conditions. This technique    allows us to measure the spatial distribution of single fluorescently labeled molecules in entire cells with an effective optical resolution comparable to macromolecular dimensions. Here, we describe the application of the 2CLM approach to the    simultaneous nanoimaging of cellular structures using two fluorochrome types distinguished by different fluorescence emission wavelengths. The capabilities of 2CLM for studying the spatial organization of the genome in the mammalian cell nucleus    are demonstrated for the relative distributions of two chromosomal proteins labeled with autofluorescent GFP and mRFP1 domains. The 2CLM images revealed quantitative information on their spatial relationships down to length-scales of 30    nm.</p>

	]]>
</description>

<author>M Gunkel et al.</author>


</item>


<item>
<title>Genetics of complex neurological disease: challenges and opportunities for modeling epilepsy in mice and rats.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2036</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2036</guid>
<pubDate>Tue, 08 May 2012 23:43:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Currently, approximately 20 genetic variants are known to cause Mendelian forms of human epilepsy, leaving a vast heritability undefined. Rodent models for genetically complex epilepsy have been studied for many years, but only    recently have strong candidate genes emerged, including Cacna1 g in the GAERS rat model of absence epilepsy and Kcnj10 in the low seizure threshold of DBA/2 mice. In parallel, a growing number of mouse mutations studied on multiple strain    backgrounds reveal the impact of genetic modifiers on seizure severity, incidence or form--perhaps mimicking the complexity seen in humans. The field of experimental genetics in rodents is poised to study discrete epilepsy mutations on a diverse    choice of strain backgrounds to develop better models and identify modifiers. But, it must find the right balance between embracing the strain diversity available, with the ability to detect and characterize genetic effects.  Using alternative    strain backgrounds when studying epilepsy mutations will enhance the modeling of epilepsy as a complex genetic disease.</p>

	]]>
</description>

<author>W N. Frankel</author>


</item>


<item>
<title>Otitis media in a mouse model for Down syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2035</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2035</guid>
<pubDate>Tue, 08 May 2012 23:43:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Ts65Dn mouse shares many phenotypic characteristics of human Down syndrome.  Here, we report that otitis media, characterized by effusion in the middle ear and hearing loss, was prevalent in Ts65Dn mice. Of the 53 Ts65Dn mice    tested, 81.1% had high auditory-evoked brainstem response (ABR) thresholds for at least one of the stimulus frequencies (click, 8 kHz, 16 kHz and 32 kHz), in at least one ear. The ABR thresholds were variable and showed no tendency toward    increase with age, from 2 to 7 months of age. Observation of pathology in mice, aged 3-4 months, revealed middle ear effusion in 11 of 15 Ts65Dn mice examined, but only in two of 11 wild-type mice. The effusion in each mouse varied substantially    in volume and inflammatory cell content. The middle ear mucosae were generally thickened and goblet cells were distributed with higher density in the epithelium of the middle ear cavity of Ts65Dn mice as compared with those of wild-type controls.    Bacteria of pathogenic importance to humans also were identified in the Ts65Dn mice. This is the first report of otitis media in the Ts65Dn mouse as a model characteristic of human Down syndrome.</p>

	]]>
</description>

<author>F Han et al.</author>


</item>


<item>
<title>DSCAM and DSCAML1 function in self-avoidance in multiple cell types in the developing mouse retina.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2034</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2034</guid>
<pubDate>Tue, 08 May 2012 23:43:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>DSCAM and DSCAM-LIKE1 (DSCAML1) serve diverse neurodevelopmental functions, including axon guidance, synaptic adhesion, and self-avoidance, depending on the species, cell type, and gene family member studied. We examined the    function of DSCAM and DSCAML1 in the developing mouse retina. In addition to a subset of amacrine cells, Dscam was expressed in most retinal ganglion cells (RGCs). RGCs had fasciculated dendrites and clumped cell bodies in Dscam(-/-) mice,    suggesting a role in self-avoidance. Dscaml1 was expressed in the rod circuit, and mice lacking Dscaml1 had fasciculated rod bipolar cell dendrites and clumped AII amacrine cell bodies, also indicating a role in self-avoidance. Neurons in Dscam    or Dscaml1 mutant retinas stratified their processes appropriately in synaptic laminae in the inner plexiform layer, and functional synapses formed in the rod circuit in mice lacking Dscaml1. Therefore, DSCAM and DSCAML1 function similarly in    self-avoidance, and are not essential for synaptic specificity in the mouse retina.</p>

	]]>
</description>

<author>P G. Fuerst et al.</author>


</item>


<item>
<title>Gene expression during the oocyte-to-embryo transition in mammals.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2033</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2033</guid>
<pubDate>Tue, 08 May 2012 23:43:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The seminal question in modern developmental biology is the origins of new life arising from the unification of sperm and egg. The roots of this question begin from 19th to 20th century embryologists studying fertilization and    embryogenesis.  Although the revolution of molecular biology has yielded significant insight into the complexity of this process, the overall orchestration of genes, molecules, and cells is still not fully formed. Early mammalian development,    specifically the oocyte-to-embryo transition, is essentially under "maternal command" from factors deposited in the cytoplasm during oocyte growth, independent of de novo transcription from the nascent embryo. Many of the advances in    understanding this developmental period occurred in tandem with application of new methods and techniques from molecular biology, from protein electrophoresis to sequencing and assemblies of whole genomes. From this bed of knowledge, it appears    that precise control of mRNA translation is a key regulator coordinating the molecular and cellular events occurring during oocyte-to-embryo transition. Notably, oocyte transcriptomes share, yet retain some uniqueness, common genetic motifs among    all chordates. The common genetic motifs typically define fundamental processes critical for cellular maintenance, whereas the unique genetic features may be a source of variation and a substrate for sexual selection, genetic drift, or gene flow.    One purpose for this complex interplay among genes, proteins, and cells may allow for evolution to transform and act upon the underlying processes, at molecular, structural and organismal levels, to increase diversity, which is the ultimate goal    of sexual reproduction.</p>

	]]>
</description>

<author>A V. Evsikov et al.</author>


</item>


<item>
<title>A new standard genetic map for the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2032</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2032</guid>
<pubDate>Tue, 08 May 2012 23:43:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic maps provide a means to estimate the probability of the co-inheritance of linked loci as they are transmitted across generations in both experimental and natural populations. However, in the age of whole-genome sequences,    physical distances measured in base pairs of DNA provide the standard coordinates for navigating the myriad features of genomes. Although genetic and physical maps are colinear, there are well-characterized and sometimes dramatic heterogeneities    in the average frequency of meiotic recombination events that occur along the physical extent of chromosomes. There also are documented differences in the recombination landscape between the two sexes. We have revisited high-resolution genetic    map data from a large heterogeneous mouse population and have constructed a revised genetic map of the mouse genome, incorporating 10,195 single nucleotide polymorphisms using a set of 47 families comprising 3546 meioses. The revised map provides    a different picture of recombination in the mouse from that reported previously. We have further integrated the genetic and physical maps of the genome and incorporated SSLP markers from other genetic maps into this new framework. We demonstrate    that utilization of the revised genetic map improves QTL mapping, partially due to the resolution of previously undetected errors in marker ordering along the chromosome.</p>

	]]>
</description>

<author>A Cox et al.</author>


</item>


<item>
<title>IGF-1:tetanus toxin fragment C fusion protein improves delivery of IGF-1 to spinal cord but fails to prolong survival of ALS mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2031</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2031</guid>
<pubDate>Tue, 08 May 2012 23:43:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>To improve delivery of human insulin-like growth factor-1 (hIGF-1) to brain and spinal cord, we generated a soluble IGF-1:tetanus toxin fragment C fusion protein (IGF-1:TTC) as a secreted product from insect cells. IGF-1:TTC    exhibited IGF-1 and TTC activity in vitro; it increased levels of immunoreactive phosphoAkt in treated MCF-7 cells and bound to immobilized ganglioside GT1b. In mice, the fusion protein underwent retrograde transport by spinal cord motor neurons    following intramuscular injection, and exhibited both TTC- and IGF-1 activity in the CNS following intrathecal infusion. Analogous to the case with TTC, intrathecal infusion of the fusion protein resulted in substantial levels of IGF-1:TTC in    spinal cord tissue extracts. Tissue concentrations of hIGF-1 in lumbar spinal cords of mice infused with IGF-1:TTC were estimated to be approximately 500-fold higher than those in mice treated with unmodified recombinant hIGF-1 (rhIGF-1). Like    rhIGF-1, infusion of IGF-1:TTC reduced levels of IGF-1 receptor immunoreactivity in the same extracts. Despite raising levels of exogenous hIGF-1 in spinal cord, intramuscular- or intrathecal administration of IGF-1:TTC had no significant effect    on disease progression or survival of high-expressing SOD1(G93A) transgenic mice. IGF-1:TTC may prove to be neuroprotective in other animal models of CNS disease or injury known to be responsive to unmodified IGF-1.</p>

	]]>
</description>

<author>R J. Chian et al.</author>


</item>


<item>
<title>Differential induction of apoptosis in HER2 and EGFR addicted cancers following PI3K inhibition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2030</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2030</guid>
<pubDate>Tue, 08 May 2012 23:42:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Non-small cell lung cancers with activating mutations in the epidermal growth factor receptor (EGFR) are highly responsive to EGFR tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib. Such cancers are "addicted" to    EGFR, and treatment with a TKI invariably leads to down-regulation of the PI3K-AKT-mTOR and MEK-ERK signaling pathways, resulting in apoptosis. Using a dual PI3K-mTOR inhibitor, NVP-BEZ235, we evaluated whether PI3K-mTOR inhibition alone induced    apoptosis in these cancers. In contrast to HER2-amplified breast cancers, we found that PI3K-mTOR inhibition did not promote substantial apoptosis in the EGFR mutant lung cancers. However, blocking both PI3K-mTOR and MEK simultaneously led to    apoptosis to similar levels as the EGFR TKIs, suggesting that down-regulation of these pathways may account for much of the apoptosis promoted by EGFR inhibition. In EGFR mutant lung cancers, down-regulation of both intracellular pathways    converged on the BH3 family of proteins regulating apoptosis. PI3K inhibition led to down-regulation of Mcl-1, and MEK inhibition led to up-regulation of BIM. In fact, down-regulation of Mcl-1 by siRNA was sufficient to sensitize these cancers to    single-agent MEK inhibitors. Surprisingly, an AKT inhibitor did not decrease Mcl-1 levels, and when combined with MEK inhibitors, failed to induce apoptosis. Importantly, we observed that the combination of PI3K-mTOR and MEK inhibitors    effectively shrunk tumors in a transgenic and xenograft model of EGFR T790M-L858R cancers. These data indicate simultaneous inhibition of PI3K-mTOR and MEK signaling is an effective strategy for treating EGFR mutant lung cancers, including those    with acquired resistance to EGFR TKIs.</p>

	]]>
</description>

<author>A C. Faber et al.</author>


</item>


<item>
<title>A locus on distal chromosome 10 (ahl4) affecting age-related hearing loss in A/J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2029</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2029</guid>
<pubDate>Tue, 08 May 2012 23:42:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ahl locus, shown to be a strain-specific Cdh23 dimorphism, contributes to age-related hearing loss in many inbred mouse strains. A/J mice begin to lose hearing by 4 weeks of age, much earlier than C57BL/6J (B6) mice, although    both strains have the same Cdh23(ahl) variant. Here, we use recombinant inbred strains, chromosome substitution strains, and a linkage backcross to map a locus on distal Chromosome 10, designated ahl4, that contributes to the early-onset hearing    loss of A/J mice. Cochleae of 9-week-old A/J mice exhibit inner and outer hair cell loss from the basal turn through the apical turn, with outer hair cell loss at the base being severest. To quantify the progression of hair cell loss,    cytocochleograms were evaluated from 0 to 20 weeks of age. A/J mice showed evidence of hair cell loss in the base of the cochlea as early as 14 days of age and the magnitude and extent of loss increased rapidly during the following 2-5 months.    Hair cell loss occurred earlier and was much more severe and widespread in A/J mice than in B6 mice during the first 5 months of age. Spiral ganglion neurons, cells of the stria vascularis, and vestibular hair cell densities, however, appeared    normal in 20-week-old A/J mice.</p>

	]]>
</description>

<author>Q Y. Zheng et al.</author>


</item>


<item>
<title>Distinguishing mouse strains by proteomic analysis of pelage hair.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2028</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2028</guid>
<pubDate>Tue, 08 May 2012 23:42:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>AKR/J mice display a hair interior defect (hid) phenotype for which the molecular basis is unknown. To investigate the application of hair-shaft proteomics to the study of such diseases, pelage from AKR/J and two other mouse strains    without this defect was analyzed by shotgun proteomics. The results permitted the identification of 111 proteins from tryptic digests of total hair from AKR/J-hid/hid mice, which were predominantly keratins (Krts) and Krt-associated proteins    (Krtaps). From the non-solubilizable (crosslinked) fraction of the hair remaining after extensive detergent extraction, 58 proteins were identified. The majority were Krts and Krtaps, but junctional and other membrane proteins, cytoplasmic    proteins, and histones were also identified. The results indicate the incorporation of a multitude of proteins into highly crosslinked material.  Comparison of unique peptides generated among hair samples from AKR/J-hid/hid, FVB/NJ+/+, and    LP/J+/+ mice indicated that these inbred strains could be distinguished by their proteomic patterns. Transmission electron microscopy after mild treatment in detergent and reducing agent permitted the visualization of projections of cortex cells,    with characteristic filament patterns, into adjoining medulla cells. Hair shafts from AKR/J mice were deficient in these projections and also exhibited relatively low levels of trichohyalin, a possible contributor to or marker for the hid    phenotype.</p>

	]]>
</description>

<author>R H. Rice et al.</author>


</item>


<item>
<title>Ultrahigh resolution imaging of biomolecules by fluorescence photoactivation localization microscopy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2027</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2027</guid>
<pubDate>Tue, 08 May 2012 23:42:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Diffraction limits the biological structures that can be imaged by normal light microscopy. However, recently developed techniques are breaking the limits that diffraction poses and allowing imaging of biological samples at the    molecular length scale. Fluorescence photoactivation localization microscopy (FPALM) and related methods can now image molecular distributions in fixed and living cells with measured resolution better than 30 nm. Based on localization of single    photoactivatable molecules, FPALM uses repeated cycles of activation, localization, and photobleaching, combined with high-sensitivity fluorescence imaging, to identify and localize large numbers of molecules within a sample.  Procedures and    pitfalls for construction and use of such a microscope are discussed in detail. Representative images of cytosolic proteins, membrane proteins, and other structures, as well as examples of results during acquisition are shown. It is hoped that    these details can be used to perform FPALM on a variety of biological samples, to significantly advance the understanding of biological systems.</p>

	]]>
</description>

<author>S T. Hess et al.</author>


</item>


<item>
<title>Colocalization of somatic and meiotic double strand breaks near the Myc oncogene on mouse chromosome 15.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2026</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2026</guid>
<pubDate>Tue, 08 May 2012 23:42:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Both somatic and meiotic recombinations involve the repair of DNA double strand breaks (DSBs) that occur at preferred locations in the genome. Improper repair of DSBs during either mitosis or meiosis can lead to mutations,    chromosomal aberration such as translocations, cancer, and/or cell death. Currently, no model exists that explains the locations of either spontaneous somatic DSBs or programmed meiotic DSBs or relates them to each other. One common class of    tumorigenic translocations arising from DSBs is chromosomal rearrangements near the Myc oncogene. Myc translocations have been associated with Burkitt lymphoma in humans, plasmacytoma in mice, and immunocytoma in rats. Comparing the locations of    somatic and meiotic DSBs near the mouse Myc oncogene, we demonstrated that the placement of these DSBs is not random and that both events clustered in the same short discrete region of the genome. Our work shows that both somatic and meiotic DSBs    tend to occur in proximity to each other within the Myc region, suggesting that they share common originating features. It is likely that some regions of the genome are more susceptible to both somatic and meiotic DSBs, and the locations of    meiotic hotspots may be an indicator of genomic regions more susceptible to DNA damage.</p>

	]]>
</description>

<author>S H. Ng et al.</author>


</item>


<item>
<title>Encephalitogenic T cells that stably express both T-bet and ROR gamma t consistently produce IFNgamma but have a spectrum of IL-17 profiles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2025</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2025</guid>
<pubDate>Tue, 08 May 2012 23:42:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Th1/Th17 cells, secreting both IFNgamma and IL-17, are often associated with inflammatory pathology. We cloned and studied the cytokine phenotypes of MBP-specific, TCR-identical encephalitogenic CD4+ cells in relationship to Th1-    and Th17-associated transcription factors T-bet and RORgammat. IFNgamma-producing cells could be sub-divided into those that are T-bet(+)/RORgammat(-) and those that are T-bet(+)/RORgammat(+). The latter comprises a spectrum of phenotypes, as    defined by IL-17 production, and can be induced to up-regulate IL-23R with IL-12 or IL-23. The former, bona fide Th1 cells, lack IL-23R expression under all conditions. In vivo, T-bet(+)/RORgammat(-) and T-bet(+)/RORgammat(+) clones induce EAE    equally well.</p>

	]]>
</description>

<author>Leeman S. Abromson et al.</author>


</item>


<item>
<title>New Zealand Ginger mouse: novel model that associates the tyrp1b pigmentation gene locus with regulation of lean body mass.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2024</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2024</guid>
<pubDate>Tue, 08 May 2012 23:42:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The study of spontaneous mutations in mice over the last century has been fundamental to our understanding of normal physiology and mechanisms of disease.  Here we studied the phenotype and genotype of a novel mouse model we have    called the New Zealand Ginger (NZG/Kgm) mouse. NZG/Kgm mice are very large, rapidly growing, ginger-colored mice with pink eyes. Breeding NZG/Kgm mice with CAST/Ei or C57BL/6J mice showed that the ginger coat colour is a recessive trait, while    the excessive body weight and large body size exhibit a semidominant pattern of inheritance. Backcrossing F1 (NZG/Kgm x CAST/Ei) to NZG/Kgm mice to produce the N2 generation determined that the NZG/Kgm mouse has two recessive pigmentation variant    genes (oca2(p) and tyrp-1(b)) and that the tyrp-1(b) gene locus associates with large body size. Three coat colors appeared in the N2 generation; ginger, brown, and dark. Strikingly, N2 male coat colour associated with body weight; the    brown-colored mice weighed the most followed by ginger and then dark.  The male brown coat-colored offspring reached adult body weights indistinguishable from NZG/Kgm males. The large NZG/Kgm mouse body size is a result of excessive lean body    mass since these mice are not obese or diabetic.  NZG/Kgm mice exhibit an unusual pattern of fat distribution; compared with other mouse strains they have disproportionately higher amounts of subcutaneous and gonadal fat. These mice are    susceptible to high-fat diet-induced obesity but are resistant to high-fat diet-induced diabetes. We propose NZG/Kgm mice as a novel model to delineate gene(s) that regulate 1) growth and metabolism, 2) resistance to Type 2 diabetes, and 3)    preferential fat deposition in the subcutaneous and gonadal areas.</p>

	]]>
</description>

<author>C E. Duchesnes et al.</author>


</item>


<item>
<title>Szt2, a novel gene for seizure threshold in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2023</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2023</guid>
<pubDate>Tue, 08 May 2012 23:41:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>In a chemical mutagenesis screen we identified Szt2 (seizure threshold 2) as a gene that confers low seizure threshold to mice and may also enhance epileptogenesis. The semidominant phenotype was mapped to Chromosome 4 and narrowed    further to a critical interval of approximately 650 kb. A novel large (> 10 kb) transcript in the critical interval was found to have fourfold increased steady-state expression at the RNA level in Szt2 homozygous mutant brain. The corresponding    72 exon gene encodes a 378-kD protein with no significant or suggestive sequence similarities to any other protein. The mutant allele of Szt2 contains a splice donor mutation after exon 32, predicting transcriptional read-through, translational    frameshift and premature stop. A second Szt2 allele, containing a gene-trap mutation in exon 21, also conferred a low seizure threshold and increased RNA expression, but unlike the original allele, some gene-trap homozygotes died embryonically.    Szt2 is transcribed in many tissues, with the highest expression in brain, and it is also expressed during embryonic development. Szt2 is highly conserved in evolution, with a clear, single orthologue found in all land vertebrates and in many    invertebrates.  Interestingly, in mammals the Szt2 gene resides in a highly conserved head-to-head configuration with Med8 (which encodes a Mediator complex subunit), separated by only 91 nt. While the biological function of Szt2 remains unknown,    its high conservation, unique structure and effect on seizure threshold suggest that it serves an important role in the central nervous system.</p>

	]]>
</description>

<author>W N. Frankel et al.</author>


</item>


<item>
<title>Genetic analysis of blood pressure in 8 mouse intercross populations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2022</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2022</guid>
<pubDate>Tue, 08 May 2012 23:41:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genetic basis of hypertension is well established, yet very few genes that cause common forms of hypertension are known. Quantitative trait locus (QTL) analyses in rodent models can guide the search for human hypertension genes,    but the excellent genetic resources for mice have been underused in this regard. To address this issue, we surveyed blood pressure variation in mice from 37 inbred strains and generated 2577 mice in 8 intercross populations to perform QTL    analyses of blood pressure. We identified 14 blood pressure QTL in these populations, including > or =7 regions of the mouse genome not linked previously to blood pressure. Many QTL were detected in multiple crosses, either within our study or in    studies published previously, which facilitates the use of bioinformatics methods to narrow the QTL and focus the search for candidate genes. The regions of the human genome that correspond to all but 1 of the 14 blood pressure QTL in mice are    linked to blood pressure in humans, suggesting that these regions contain causal genes with a conserved role in blood pressure control. These results greatly expand our knowledge of the genomic regions underlying blood pressure regulation in mice    and support future studies to identify the causal genes within these QTL intervals.</p>

	]]>
</description>

<author>M Feng et al.</author>


</item>


<item>
<title>Adhesion molecules in establishing retinal circuitry.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2021</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2021</guid>
<pubDate>Tue, 08 May 2012 23:41:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The formation of neural circuits requires molecular mechanisms to confer cell identity, to establish appropriate dendritic arbors, and to space cell bodies within the groups of homotypic neurons. Recent work in a variety of    organisms has implicated cell adhesion molecules in these processes. The DSCAMs in particular have functions including cell identity and self-avoidance through repulsion in Drosophila, differential adhesion and synaptic pairing in chick retina,    and the masking of adhesion within specific cell types in the mouse retina. These differences in molecular function between different organisms, and potentially different cell types within a single tissue, emphasize how seemingly subtle    distinctions may be important for deciphering this molecular adhesion code.</p>

	]]>
</description>

<author>P G. Fuerst et al.</author>


</item>


<item>
<title>Isolation and short-term culture of mouse spermatocytes for analysis of meiosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2020</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2020</guid>
<pubDate>Tue, 08 May 2012 23:41:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Understanding meiosis is facilitated by in vitro experimental approaches, but this has not been easily applicable to mammalian meiocytes. Available methods for in vitro analysis of mammalian oocytes are generally limited to    experimental analysis of the late prophase period. Short-term cultures of male germ cells have been useful for analysis of earlier meiotic prophase pathways, as well as onset of the meiotic division phase, but no studies have achieved reliable    spermatogenesis in vitro. Here we describe a method for preparing highly enriched pachytene spermatocytes from mouse testicular cell suspensions using cell-size fractionation by sedimentation through a bovine serum albumin gradient at unit    gravity. We also provide a procedure for short-term culture of spermatocytes and the pharmacological induction of the prophase-to-division phase transition.</p>

	]]>
</description>

<author>Salle S. La et al.</author>


</item>


<item>
<title>A novel ENU-induced mutation, peewee, causes dwarfism in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2019</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2019</guid>
<pubDate>Tue, 08 May 2012 23:41:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>We identified a novel fertile autosomal recessive mutation called peewee that results in dwarfing, in a region-specific ENU-induced mutagenesis. These mice at litter size were smaller those of other strains. Histological analysis    revealed that the major organs appear normal, but abnormalities in cellular proliferation were observed in bone, liver, and testis. Haplotype analysis localized the peewee gene to a 3.3-Mb region between D5Mit83 and D5Mit356.3. There are 18 genes    in this linkage area. We also performed in silico mapping using the PosMed(SM) program, which searches for connections among keywords and genes in an interval, but no similar phenotype descriptions were found for these genes. In the peewee mutant    compared to the normal C57BL/6 J mouse, only Slc10a4 expression was lower.  Our preliminary mutation analysis examining the nucleotide sequence of three exons, two introns, and an untranslated region of Slc10a4 did not find any sequence    difference between the peewee mouse and the C57BL/6 J mouse. Detailed analysis of peewee mice might provide novel molecular insights into the complex mechanisms regulating body growth.</p>

	]]>
</description>

<author>B Lee et al.</author>


</item>


<item>
<title>The Gene Ontology&apos;s Reference Genome Project: a unified framework for functional annotation across species.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2018</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2018</guid>
<pubDate>Tue, 08 May 2012 23:41:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Gene Ontology (GO) is a collaborative effort that provides structured vocabularies for annotating the molecular function, biological role, and cellular location of gene products in a highly systematic way and in a    species-neutral manner with the aim of unifying the representation of gene function across different organisms. Each contributing member of the GO Consortium independently associates GO terms to gene products from the organism(s) they are    annotating.  Here we introduce the Reference Genome project, which brings together those independent efforts into a unified framework based on the evolutionary relationships between genes in these different organisms. The Reference Genome project    has two primary goals: to increase the depth and breadth of annotations for genes in each of the organisms in the project, and to create data sets and tools that enable other genome annotation efforts to infer GO annotations for homologous genes    in their organisms. In addition, the project has several important incidental benefits, such as increasing annotation consistency across genome databases, and providing important improvements to the GO's logical structure and biological    content.</p>

	]]>
</description>


</item>


<item>
<title>Aging in inbred strains of mice: study design and interim report on median lifespans and circulating IGF1 levels.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2017</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2017</guid>
<pubDate>Tue, 08 May 2012 23:41:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>To better characterize aging in mice, the Jackson Aging Center carried out a lifespan study of 31 genetically-diverse inbred mouse strains housed in a specific pathogen-free facility. Clinical assessments were carried out every 6    months, measuring multiple age-related phenotypes including neuromuscular, kidney and heart function, body composition, bone density, hematology, hormonal levels, and immune system parameters. In a concurrent cross-sectional study of the same 31    strains at 6, 12, and 20 months, more invasive measurements were carried out followed by necropsy to assess apoptosis, DNA repair, chromosome fragility, and histopathology. In this report, which is the initial paper of a series, the study design,    median lifespans, and circulating insulin-like growth factor 1 (IGF1) levels at 6, 12, and 18 months are described for the first cohort of 32 females and 32 males of each strain. Survival curves varied dramatically among strains with the median    lifespans ranging from 251 to 964 days. Plasma IGF1 levels, which also varied considerably at each time point, showed an inverse correlation with a median lifespan at 6 months (R = -0.33, P = 0.01). This correlation became stronger if the    short-lived strains with a median lifespan < 600 days were removed from the analysis (R = -0.53, P < 0.01). These results support the hypothesis that the IGF1 pathway plays a key role in regulating longevity in mice and indicates that common    genetic mechanisms may exist for regulating IGF1 levels and lifespan.</p>

	]]>
</description>

<author>R Tsaih S. Yuan et al.</author>


</item>


<item>
<title>Mutation discovery in the mouse using genetically guided array capture and resequencing.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2016</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2016</guid>
<pubDate>Tue, 08 May 2012 23:40:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Forward genetics (phenotype-driven approaches) remain the primary source for allelic variants in the mouse. Unfortunately, the gap between observable phenotype and causative genotype limits the widespread use of spontaneous and    induced mouse mutants. As alternatives to traditional positional cloning and mutation detection approaches, sequence capture and next-generation sequencing technologies can be used to rapidly sequence subsets of the genome. Application of these    technologies to mutation detection efforts in the mouse has the potential to significantly reduce the time and resources required for mutation identification by abrogating the need for high-resolution genetic mapping, long-range PCR, and    sequencing of individual PCR amplimers. As proof of principle, we used array-based sequence capture and pyrosequencing to sequence an allelic series from the classically defined Kit locus (approximately 200 kb) from each of five noncomplementing    Kit mutants (one known allele and four unknown alleles) and have successfully identified and validated a nonsynonymous coding mutation for each allele. These data represent the first documentation and validation that these new technologies can be    used to efficiently discover causative mutations. Importantly, these data also provide a specific methodological foundation for the development of large-scale mutation detection efforts in the laboratory mouse.</p>

	]]>
</description>

<author>M D&apos;Ascenzo et al.</author>


</item>


<item>
<title>Effects of sex, gonadal hormones, and augmented acoustic environments on sensorineural hearing loss and the central auditory system: insights from research on C57BL/6J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2015</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2015</guid>
<pubDate>Tue, 08 May 2012 23:40:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice of the C57BL/6J (B6) inbred strain exhibit genetic progressive sensorineural hearing loss and have been widely used as a model of adult-onset hearing loss and presbycusis. Males and females exhibit similar degrees of hearing    loss until about 3 months of age, after which, the loss accelerates in females. This paper reviews research on how the B6 auditory system is affected by sex, gonadectomy (i.e., a reduction of gonadal hormone levels), and nightly exposure to    moderately intense augmented acoustic environments (AAEs) - a low-frequency noise band (LAAE) or high-frequency band (HAAE). Several findings indicate a negative effect of ovarian hormones on the female B6 auditory system. Whereas the sex    difference in high-frequency hearing loss was not significantly affected by gondadectomies, the female disadvantage in ABR thresholds at lower frequencies was erased by ovariectomy. Moreover, exposure to the LAAE or HAAE caused losses of hair    cells that were more severe in intact females than in ovariectomized females or in males. Finally, intact females had more severe loss of neurons in the low-frequency region of the anterior ventral cochlear nucleus (AVCN) than other groups. In    contrast, the presence of androgens had beneficial effects. Loss of hair cells and AVCN neurons after AAE exposure were more severe in orchidectomized males than in intact males. Ideas, hypotheses, and potential mechanisms concerning the findings    are discussed.</p>

	]]>
</description>

<author>J F. Willott</author>


</item>


<item>
<title>Sepsis-induced human lymphocyte apoptosis and cytokine production in &quot;humanized&quot; mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2014</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2014</guid>
<pubDate>Tue, 08 May 2012 23:40:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sepsis is the leading cause of death in critically ill patients in the United States with over 210,000 deaths annually. One stumbling block to an effective therapy of sepsis has been the lack of a clinically relevant animal model.    There are important distinctions in the mouse versus human immune system regarding the host response to invading pathogens. These differences may explain the disappointing results in many sepsis clinical trials despite the clear efficacy of these    agents in mouse models of sepsis. The purpose of the present study was to develop a "humanized" mouse model of sepsis and to determine if the model recapitulated the major findings of lymphocyte apoptosis and cytokine response that exist in    patients with sepsis. Two-day-old NOD-scid IL2rgamma(null) mice received an adoptive transfer of hCD34(+) hematopoietic cord blood stem cells.  These mice acquired a functional human innate and adaptive immune system, as evidenced by the    development of all lineages of human immune cells as well as by mounting a DTH response. Eight weeks post-transfer, mice were made septic using the highly clinical relevant CLP model of sepsis, and sepsis induced marked elevations in human pro-    and anti-inflammatory cytokines as well as a dramatic increase in human T and B cell apoptosis. Collectively, these results show that the humanized mouse model recapitulates many of the classic findings in patients with sepsis. Therefore, it    represents an advanced, clinically relevant model for mechanistic studies of sepsis and testing of novel therapies.</p>

	]]>
</description>

<author>J Unsinger et al.</author>


</item>


<item>
<title>Single domain antibodies: promising experimental and therapeutic tools in infection and immunity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2013</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2013</guid>
<pubDate>Tue, 08 May 2012 23:40:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Antibodies are important tools for experimental research and medical applications. Most antibodies are composed of two heavy and two light chains.  Both chains contribute to the antigen-binding site which is usually flat or concave.    In addition to these conventional antibodies, llamas, other camelids, and sharks also produce antibodies composed only of heavy chains. The antigen-binding site of these unusual heavy chain antibodies (hcAbs) is formed only by a single domain,    designated VHH in camelid hcAbs and VNAR in shark hcAbs.  VHH and VNAR are easily produced as recombinant proteins, designated single domain antibodies (sdAbs) or nanobodies. The CDR3 region of these sdAbs possesses the extraordinary capacity to    form long fingerlike extensions that can extend into cavities on antigens, e.g., the active site crevice of enzymes. Other advantageous features of nanobodies include their small size, high solubility, thermal stability, refolding capacity, and    good tissue penetration in vivo. Here we review the results of several recent proof-of-principle studies that open the exciting perspective of using sdAbs for modulating immune functions and for targeting toxins and microbes.</p>

	]]>
</description>

<author>J Wesolowski et al.</author>


</item>


<item>
<title>Degradation of IRS1 leads to impaired glucose uptake in adipose tissue of the type 2 diabetes mouse model TALLYHO/Jng.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2012</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2012</guid>
<pubDate>Tue, 08 May 2012 23:40:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>The TALLYHO/Jng (TH) mouse strain is a polygenic model for type 2 diabetes (T2D) characterized by moderate obesity, impaired glucose tolerance and uptake, insulin resistance, and hyperinsulinemia. The goal of this study was to    elucidate the molecular mechanisms responsible for the reduced glucose uptake and insulin resistance in the adipose tissue of this model. The translocation and localization of glucose transporter 4 (GLUT4) to the adipocyte plasma membrane were    impaired in TH mice compared to control C57BL6/J (B6) mice. These defects were associated with decreased GLUT4 protein, reduced phosphatidylinositol 3-kinase activity, and alterations in the phosphorylation status of insulin receptor substrate 1    (IRS1). Activation of c-Jun N-terminal kinase 1/2, which can phosphorylate IRS1 on Ser307, was significantly higher in TH mice compared with B6 controls. IRS1 protein but not mRNA levels was found to be lower in TH mice than controls.    Immunoprecipitation with anti-ubiquitin and western blot analysis of IRS1 protein revealed increased total IRS1 ubiquitination in adipose tissue of TH mice. Suppressor of cytokine signaling 1, known to promote IRS1 ubiquitination and subsequent    degradation, was found at significantly higher levels in TH mice compared with B6. Immunohistochemistry showed that IRS1 colocalized with the 20S proteasome in proteasomal structures in TH adipocytes, supporting the notion that IRS1 is actively    degraded. Our findings suggest that increased IRS1 degradation and subsequent impaired GLUT4 mobilization play a role in the reduced glucose uptake in insulin resistant TH mice. Since low-IRS1 levels are often observed in human T2D, the TH mouse    is an attractive model to investigate mechanisms of insulin resistance and explore new treatments.</p>

	]]>
</description>

<author>Y Wang et al.</author>


</item>


<item>
<title>A customized and versatile high-density genotyping array for the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2011</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2011</guid>
<pubDate>Tue, 08 May 2012 23:40:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>We designed a high-density mouse genotyping array containing 623,124 single-nucleotide polymorphisms that captures the known genetic variation present in the laboratory mouse. The array also contains 916,269 invariant genomic probes    targeted to functional elements and regions known to harbor segmental duplications. The array opens the door to the characterization of genetic diversity, copy-number variation, allele-specific gene expression and DNA methylation, and will extend    the successes of human genome-wide association studies to the mouse.</p>

	]]>
</description>

<author>H Yang et al.</author>


</item>


<item>
<title>Inheritance patterns of progressive hearing loss in laboratory strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2010</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2010</guid>
<pubDate>Tue, 08 May 2012 23:39:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Positional cloning of mouse deafness mutations uncovered a plethora of proteins that have important functions in the peripheral auditory system in particular in the cochlear organ of Corti and stria vascularis. Most of these mutant    variants follow a monogenic form of inheritance and are rare, highly penetrant, and deleterious alleles. Inbred and heterogenous strains of mice, in contrast, present with non-syndromic hearing impairment due to the effects of multiple genes and    hypomorphic and less penetrant alleles that are often transmitted in a non-Mendelian manner. Here we review hearing loss inheritance patterns as they were discovered in different strains of mice and discuss the relevance of candidate genes to    late-onset progressive hearing impairment in mouse and human.</p>

	]]>
</description>

<author>Trauth K. Noben et al.</author>


</item>


<item>
<title>Skeletal consequences of deletion of steroid receptor coactivator-2/transcription intermediary factor-2.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2009</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2009</guid>
<pubDate>Tue, 08 May 2012 23:39:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Both estrogen receptor (ER) and peroxisome proliferator-activated receptor gamma (PPARgamma) regulate bone metabolism, and because steroid receptor coactivator (SRC)-2 (TIF-2) enhances ER and PPARgamma activity, we examined the    consequences of deletion of SRC-2 on bone using SRC-2 knock out (KO) mice. Loss of SRC-2 resulted in increased bone mass, with SRC-2 KO mice having 80% higher trabecular bone volume as compared with wild type mice. SRC-2 KO mice also had a marked    decrease (by 50%) in bone marrow adipocytes. These data suggested that marrow precursor cells in the SRC-2 KO mice may be resistant to the inhibitory effects of endogenous PPARgamma ligands on bone formation. Consistent with this, compared with    cultures from wild type mice, marrow stromal cultures from SRC-2 KO mice formed significantly more mineralized nodules (by 3-fold) in the presence of the PPARgamma agonist, rosiglitazone. Using chromatin immunoprecipitation analysis, we    demonstrated that in bone marrow stromal cells, loss of SRC-2 leads to destabilization of the transcription complex at the peroxisome proliferator response elements of a number of PPARgamma target genes, resulting in an overall decrease in the    expression of adipocyte-related genes and a marked decrease in adipocyte development. Using ovariectomy with or without estrogen replacement, we also demonstrated that SRC-2 KO mice were partially resistant to the skeletal actions of estrogen.    Collectively, these findings indicate that loss of SRC-2 leads to partial skeletal resistance to the ER and PPARgamma, but resistance to PPARgamma is dominant, leading to increased bone mass. Modulating SRC-2 action may, thus, represent a novel    therapeutic target for osteoporosis.</p>

	]]>
</description>

<author>U I. Modder et al.</author>


</item>


<item>
<title>Haploinsufficiency of AFG3L2, the gene responsible for spinocerebellar ataxia type 28, causes mitochondria-mediated Purkinje cell dark degeneration.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2008</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2008</guid>
<pubDate>Tue, 08 May 2012 23:39:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Paraplegin and AFG3L2 are ubiquitous nuclear-encoded mitochondrial proteins that form hetero-oligomeric paraplegin-AFG3L2 and homo-oligomeric AFG3L2 complexes in the inner mitochondrial membrane, named m-AAA proteases. These    complexes ensure protein quality control in the inner membrane, jointly with a chaperone-like activity on the respiratory chain complexes. Despite coassembling in the same complex, mutations of either paraplegin or AFG3L2 cause two different    neurodegenerative disorders. Indeed, mutations of paraplegin are responsible for a recessive form of hereditary spastic paraplegia, whereas mutations of AFG3L2 have been recently associated to a dominant form of spinocerebellar ataxia (SCA28). In    this work, we report that the mouse model haploinsufficient for Afg3l2 recapitulates important pathophysiological features of the human disease, thus representing the first SCA28 model. Furthermore, we propose a pathogenetic mechanism in which    respiratory chain dysfunction and increased reactive oxygen species production caused by Afg3l2 haploinsufficiency lead to dark degeneration of Purkinje cells and cerebellar dysfunction.</p>

	]]>
</description>

<author>F Maltecca et al.</author>


</item>


<item>
<title>Filaggrin deficiency confers a paracellular barrier abnormality that reduces inflammatory thresholds to irritants and haptens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2007</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2007</guid>
<pubDate>Tue, 08 May 2012 23:39:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Mutations in the human filaggrin gene (FLG) are associated with atopic dermatitis (AD) and are presumed to provoke a barrier abnormality. Yet additional acquired stressors might be necessary because the same mutations    can result in a noninflammatory disorder, ichthyosis vulgaris. OBJECTIVE: We examined here whether FLG deficiency alone suffices to produce a barrier abnormality, the basis for the putative abnormality, and its proinflammatory consequences.     METHODS: By using the flaky-tail mouse, which lacks processed murine filaggrin because of a frameshift mutation in the gene encoding profilaggrin that mimics some mutations in human AD, we assessed whether FLG deficiency provokes a barrier    abnormality, further localized the defect, identified its subcellular basis, and assessed thresholds to irritant- and hapten-induced dermatitis. RESULTS: Flaky-tail mice exhibit low-grade inflammation with increased bidirectional, paracellular    permeability of water-soluble xenobiotes caused by impaired lamellar body secretion and altered stratum corneum extracellular membranes. This barrier abnormality correlates with reduced inflammatory thresholds to both topical irritants and    haptens. Moreover, when exposed repeatedly to topical haptens at doses that produce no inflammation in wild-type mice, flaky-tail mice experience a severe AD-like dermatosis with a further deterioration in barrier function and features of a T(H)2    immunophenotype (increased CRTH levels plus inflammation, increased serum IgE levels, and reduced antimicrobial peptide [mBD3] expression).  CONCLUSIONS: FLG deficiency alone provokes a paracellular barrier abnormality in mice that reduces    inflammatory thresholds to topical irritants/haptens, likely accounting for enhanced antigen penetration in FLG-associated AD.</p>

	]]>
</description>

<author>T C. Scharschmidt et al.</author>


</item>


<item>
<title>Post-publication sharing of data and tools.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2006</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2006</guid>
<pubDate>Tue, 08 May 2012 23:39:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite existing guidelines on access to data and bioresources, good practice is not widespread. A meeting of mouse researchers in Rome proposes ways to promote a culture of sharing.</p>

	]]>
</description>

<author>P N. Schofield et al.</author>


</item>


<item>
<title>Gene therapy following subretinal AAV5 vector delivery is not affected by a previous intravitreal AAV5 vector administration in the partner eye.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2005</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2005</guid>
<pubDate>Tue, 08 May 2012 23:39:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: In an earlier study we found normal adeno-associated viral vector type 2 (AAV2)-mediated GFP expression after intravitreal injection to one eye of normal C57BL/6J mice. However, GFP expression was very poor in the partner    eye of the same mouse if this eye received an intravitreal injection of the same vector one month after the initial intravitreal injection. We also found both injections worked well if they were subretinal. In this study, we tested whether the    efficiency of subretinal AAV vector transduction is altered by a previous intravitreal injection in the partner eye and more importantly whether therapeutic efficiency is altered in the rd12 mouse (with a recessive RPE65 mutation) after the same    injection series. METHODS: One microl of scAAV5-smCBA-GFP (1 x 10(13) genome containing viral particles per ml) was intravitreally injected into the right eyes of four-week-old C57BL/6J mice and 1 microl of scAAV5-smCBA-hRPE65 (1 x 10(13) genome    containing viral particles per ml) was intravitreally injected into the right eyes of four-week-old rd12 mice Four weeks later, the same vectors were subretinally injected into the left eyes of the same C57BL/6J and rd12 mice. Left eyes of    another cohort of eight-week-old rd12 mice received a single subretinal injection of the same scAAV5-smCBA-hRPE65 vector as the positive control. Dark-adapted electroretinograms (ERGs) were recorded five months after the subretinal injections.    AAV-mediated GFP expression in C57BL/6J mice and RPE65 expression and ERG restoration in rd12 mice were evaluated five months after the second subretinal injection. Frozen section analysis was performed for GFP fluorescence in C57BL/6J mice and    immunostaining for RPE65 in rd12 eyes. RESULTS: In rd12 mice, dark-adapted ERGs were minimal following the first intravitreal injection of scAAV5-smCBA-RPE65. Following subsequent subretinal injection in the partner eye, dramatic ERG restoration    was recorded in that eye. In fact, ERG b-wave amplitudes were statistically similar to those from the eyes that received the initial subretinal injection at a similar age. In C57BL/6J mice, GFP positive cells were detected in eyes following the    first intravitreal injection around the injection site. Strong GFP expression in both the retinal pigment epithelium (RPE) and photoreceptor (PR) cells was detected in the partner eyes following the subsequent subretinal injection.     Immunostaining of retinal sections with anti-RPE65 antibody showed strong RPE65 expression mainly in the RPE cells of subretinally injected eyes but not in the intravitreally injected eyes except minimally around the injection site.  CONCLUSIONS:    These results show that an initial intravitreal injection of AAV vectors to one eye of a mouse does not influence AAV-mediated gene expression or related therapeutic effects in the other eye when vectors are administered to the subretinal space.    This suggests that the subretinal space possesses a unique immune privilege relative to the vitreous cavity.</p>

	]]>
</description>

<author>W Li et al.</author>


</item>


<item>
<title>Fat targets for skeletal health.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2004</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2004</guid>
<pubDate>Tue, 08 May 2012 23:38:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Emerging evidence points to a critical role for the skeleton in several homeostatic processes, including energy balance. The connection between fuel utilization and skeletal remodeling begins in the bone marrow with lineage    allocation of mesenchymal stem cells to adipocytes or osteoblasts. Mature bone cells secrete factors that influence insulin sensitivity, and fat cells synthesize cytokines that regulate osteoblast differentiation; thus, these two pathways are    closely linked. The emerging importance of the bone-fat interaction suggests that novel molecules could be used as targets to enhance bone formation and possibly prevent fractures. In this article, we discuss three pathways that could be    pharmacologically targeted for the ultimate goal of enhancing bone mass and reducing osteoporotic fracture risk: the leptin, peroxisome proliferator-activated receptor gamma and osteocalcin pathways. Not surprisingly, because of the complex    interactions across homeostatic networks, other pathways will probably be activated by this targeting, which could prove to be beneficial or detrimental for the organism. Hence, a more complete picture of energy utilization and skeletal    remodeling will be required to bring any potential agents into the future clinical armamentarium.</p>

	]]>
</description>

<author>M Kawai et al.</author>


</item>


<item>
<title>An ENU-induced mutation in mouse glycyl-tRNA synthetase (GARS) causes peripheral sensory and motor phenotypes creating a model of Charcot-Marie-Tooth type 2D peripheral neuropathy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2003</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2003</guid>
<pubDate>Tue, 08 May 2012 23:38:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the enzyme glycyl-tRNA synthetase (GARS) cause motor and sensory axon loss in the peripheral nervous system in humans, described clinically as Charcot-Marie-Tooth type 2D or distal spinal muscular atrophy type V. Here,    we characterise a new mouse mutant, Gars(C201R), with a point mutation that leads to a non-conservative substitution within GARS. Heterozygous mice with a C3H genetic background have loss of grip strength, decreased motor flexibility and    disruption of fine motor control; this relatively mild phenotype is more severe on a C57BL/6 background. Homozygous mutants have a highly deleterious set of features, including movement difficulties and death before weaning. Heterozygous animals    have a reduction in axon diameter in peripheral nerves, slowing of nerve conduction and an alteration in the recovery cycle of myelinated axons, as well as innervation defects. An assessment of GARS levels showed increased protein in 15-day-old    mice compared with controls; however, this increase was not observed in 3-month-old animals, indicating that GARS function may be more crucial in younger animals. We found that enzyme activity was not reduced detectably in heterozygotes at any    age, but was diminished greatly in homozygous mice compared with controls; thus, homozygous animals may suffer from a partial loss of function. The Gars(C201R) mutation described here is a contribution to our understanding of the mechanism by    which mutations in tRNA synthetases, which are fundamentally important, ubiquitously expressed enzymes, cause axonopathy in specific sets of neurons.</p>

	]]>
</description>

<author>F Achilli et al.</author>


</item>


<item>
<title>Using conventional fluorescent markers for far-field fluorescence localization nanoscopy allows resolution in the 10-nm range.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2002</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2002</guid>
<pubDate>Tue, 08 May 2012 23:38:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present a novel technique of far-field localization nanoscopy combining spectral precision distance microscopy with widely used fluorochromes like the Green Fluorescent Protein (GFP) derivatives eGFP, EmGFP, Yellow Fluorescent    Protein (YFP) and eYFP, synthetic dyes like Alexa 488 and Alexa 568, as well as fluoresceine derivates. Spectral precision distance microscopy allows the surpassing of conventional resolution limits in fluorescence far-field microscopy by precise    object localization after the optical isolation of single signals in time. Based on the principles of this technique, our novel nanoscopic method was realized for laser optical precision localization and image reconstruction with highly enhanced    optical resolution in intact cells. This allows for spatial assignment of individual fluorescent molecules with nanometre precision. The technique is based on excitation intensity dependent reversible photobleaching of the molecules used combined    with fast time sequential imaging under appropriate focusing conditions. A meaningful advantage of the technique is the simple applicability as a universal tool for imaging and investigations to the major part of already available preparations    according to standard protocols. Using the above mentioned fluorophores, the positions of single molecules within cellular structures were determined by visible light with an estimated localization precision down to 3 nm; hence distances in the    range of 10-30 nm were resolved between individual fluorescent molecules allowing to apply different quantitative structure analysis tools.</p>

	]]>
</description>

<author>P Lemmer et al.</author>


</item>


<item>
<title>MouseCyc: a curated biochemical pathways database for the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2001</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2001</guid>
<pubDate>Tue, 08 May 2012 23:38:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Linking biochemical genetic data to the reference genome for the laboratory mouse is important for comparative physiology and for developing mouse models of human biology and disease. We describe here a new database of curated    metabolic pathways for the laboratory mouse called MouseCyc http://mousecyc.jax.org.  MouseCyc has been integrated with genetic and genomic data for the laboratory mouse available from the Mouse Genome Informatics database and with pathway data    from other organisms, including human.</p>

	]]>
</description>

<author>A V. Evsikov et al.</author>


</item>


<item>
<title>Functional coding variation in recombinant inbred mouse lines reveals multiple serotonin transporter-associated phenotypes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2000</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2000</guid>
<pubDate>Tue, 08 May 2012 23:38:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The human serotonin (5-hydroxytryptamine, 5-HT) transporter (hSERT, SLC6A4) figures prominently in the etiology and treatment of many prevalent neurobehavioral disorders including anxiety, alcoholism, depression, autism, and    obsessive-compulsive disorder (OCD). Here, we use naturally occurring polymorphisms in recombinant inbred (RI) lines to identify multiple phenotypes associated with altered SERT function. The widely used mouse strain C57BL/6J, harbors a SERT    haplotype defined by 2 nonsynonymous coding variants [Gly-39 and Lys-152 (GK)]. At these positions, many other mouse lines, including DBA/2J, encode, respectively, Glu-39 and Arg-152 (ER haplotype), amino acids found also in hSERT. Ex vivo    synaptosomal 5-HT transport studies revealed reduced uptake associated with the GK variant, a finding confirmed by in vitro heterologous expression studies. Experimental and in silico approaches using RI lines (C57BL/6J x DBA/2J = BXD) identify    multiple anatomical, biochemical, and behavioral phenotypes specifically impacted by GK/ER variation. Among our findings are several traits associated with alcohol consumption and multiple traits associated with dopamine signaling. Further    bioinformatic analysis of BXD phenotypes, combined with biochemical evaluation of SERT knockout mice, nominates SERT-dependent 5-HT signaling as a major determinant of midbrain iron homeostasis that, in turn, dictates iron-regulated DA    phenotypes. Our studies provide an example of the power of coordinated in vitro, in vivo, and in silico approaches using mouse RI lines to elucidate and quantify the system-level impact of gene variation.</p>

	]]>
</description>

<author>A M. Carneiro et al.</author>


</item>


<item>
<title>Supplementing high-density SNP microarrays for additional coverage of disease-related genes: addiction as a paradigm.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1999</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1999</guid>
<pubDate>Tue, 08 May 2012 23:38:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Commercial SNP microarrays now provide comprehensive and affordable coverage of the human genome. However, some diseases have biologically relevant genomic regions that may require additional coverage. Addiction, for example, is    thought to be influenced by complex interactions among many relevant genes and pathways.  We have assembled a list of 486 biologically relevant genes nominated by a panel of experts on addiction. We then added 424 genes that showed evidence of    association with addiction phenotypes through mouse QTL mappings and gene co-expression analysis. We demonstrate that there are a substantial number of SNPs in these genes that are not well represented by commercial SNP platforms. We address this    problem by introducing a publicly available SNP database for addiction. The database is annotated using numeric prioritization scores indicating the extent of biological relevance. The scores incorporate a number of factors such as SNP/gene    functional properties (including synonymy and promoter regions), data from mouse systems genetics and measures of human/mouse evolutionary conservation. We then used HapMap genotyping data to determine if a SNP is tagged by a commercial    microarray through linkage disequilibrium. This combination of biological prioritization scores and LD tagging annotation will enable addiction researchers to supplement commercial SNP microarrays to ensure comprehensive coverage of biologically    relevant regions.</p>

	]]>
</description>

<author>S F. Saccone et al.</author>


</item>


<item>
<title>Insulin-like growth factor-I and bone: lessons from mice and men.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1998</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1998</guid>
<pubDate>Tue, 08 May 2012 23:38:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Studies of humans and animals have illustrated a strong association between insulin-like growth factor (IGF)-I and skeletal acquisition. However, the precise molecular and cellular mechanisms underlying this effect still largely    remain unknown. Recent advances in molecular and genetic techniques for in vivo studies provide excellent tools for us to explore how circulating and skeletal insulin-like growth factor-I (IGF-I) may affect not only peak bone mass but also bone    loss. This review highlights recent findings that shed new light on the interaction of the IGF-I signaling pathway with other skeletal networks, and the role of IGF-I in the bone marrow milieu.</p>

	]]>
</description>

<author>M Kawai et al.</author>


</item>


<item>
<title>Transforming growth factor-beta1 impairs neuropathic pain through pleiotropic effects.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1997</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1997</guid>
<pubDate>Tue, 08 May 2012 23:37:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Understanding the underlying mechanisms of neuropathic pain caused by damage to the peripheral nervous system remains challenging and could lead to significantly improved therapies. Disturbance of homeostasis not only    occurs at the site of injury but also extends to the spinal cord and brain involving various types of cells. Emerging data implicate neuroimmune interaction in the initiation and maintenance of chronic pain hypersensitivity. RESULTS: In this    study, we sought to investigate the effects of TGF-beta1, a potent anti-inflammatory cytokine, in alleviating nerve injury-induced neuropathic pain in rats. By using a well established neuropathic pain animal model (partial ligation of the    sciatic nerve), we demonstrated that intrathecal infusion of recombinant TGF-beta1 significantly attenuated nerve injury-induced neuropathic pain. TGF-beta1 treatment not only prevents development of neuropathic pain following nerve injury, but    also reverses previously established neuropathic pain conditions. The biological outcomes of TGF-beta1 in this context are attributed to its pleiotropic effects. It inhibits peripheral nerve injury-induced spinal microgliosis, spinal microglial    and astrocytic activation, and exhibits a powerful neuroprotective effect by preventing the induction of ATF3+ neurons following nerve ligation, consequently reducing the expression of chemokine MCP-1 in damaged neurons. TGF-beta1 treatment also    suppresses nerve injury-induced inflammatory response in the spinal cord, as revealed by a reduction in cytokine expression. CONCLUSION: Our findings revealed that TGF-beta1 is effective in the treatment of neuropathic by targeting both neurons    and glial cells. We suggest that therapeutic agents such as TGF-beta1 having multipotent effects on different types of cells could work in synergy to regain homeostasis in local spinal cord microenvironments, therefore contributing to attenuate    neuropathic pain.</p>

	]]>
</description>

<author>S Echeverry et al.</author>


</item>


<item>
<title>Hair interior defect in AKR/J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1996</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1996</guid>
<pubDate>Tue, 08 May 2012 23:37:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: All AKR/J mice have a subtle defect that involves malformation of the central portion of hair fibres that is best visualized under white and polarized light microscopy. AIMS: This study sought to characterize the    clinical and ultrastructural features of the hair interior defect (HID) phenotype and to determine the chromosomal localization of the hid mutant gene locus. METHODS: White and polarized light microscopy combined with scanning electron microscopy    (SEM) and transmission electron microscopy (TEM) were used to characterize the HID phenotype. Complementation testing and gene-linkage studies were performed to map the locus. RESULTS: Using SEM, the hair-fibre structure on the surface was found    to be similar to hairs obtained from normal BALB/cByJ+/+and C57BL/6 J+/+mice. There were also no differences in sulphur content. TEM revealed degenerative changes in the medulla similar to that seen by light microscopy.  This autosomal recessive    mutation is called HID (locus symbol: hid). We mapped the hid locus to the distal end of mouse chromosome 1. No genes reported to cause skin or hair abnormalities are known to be within this interval except for the lamin B receptor (Lbr), which    had been excluded previously as the cause of the hid phenotype in AKR/J mice. CONCLUSION: A potentially novel gene or known gene with a novel phenotype resides within this interval, which may shed light on human diseases with defects in the inner    structure of the hair fibre.</p>

	]]>
</description>

<author>K A. Giehl et al.</author>


</item>


<item>
<title>Rapamycin fed late in life extends lifespan in genetically heterogeneous mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1995</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1995</guid>
<pubDate>Tue, 08 May 2012 23:37:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inhibition of the TOR signalling pathway by genetic or pharmacological intervention extends lifespan in invertebrates, including yeast, nematodes and fruitflies; however, whether inhibition of mTOR signalling can extend lifespan in    a mammalian species was unknown. Here we report that rapamycin, an inhibitor of the mTOR pathway, extends median and maximal lifespan of both male and female mice when fed beginning at 600 days of age. On the basis of age at 90% mortality,    rapamycin led to an increase of 14% for females and 9% for males. The effect was seen at three independent test sites in genetically heterogeneous mice, chosen to avoid genotype-specific effects on disease susceptibility. Disease patterns of    rapamycin-treated mice did not differ from those of control mice. In a separate study, rapamycin fed to mice beginning at 270 days of age also increased survival in both males and females, based on an interim analysis conducted near the median    survival point. Rapamycin may extend lifespan by postponing death from cancer, by retarding mechanisms of ageing, or both. To our knowledge, these are the first results to demonstrate a role for mTOR signalling in the regulation of mammalian    lifespan, as well as pharmacological extension of lifespan in both genders. These findings have implications for further development of interventions targeting mTOR for the treatment and prevention of age-related diseases.</p>

	]]>
</description>

<author>D E. Harrison et al.</author>


</item>


<item>
<title>Human peripheral blood leucocyte non-obese diabetic-severe combined immunodeficiency interleukin-2 receptor gamma chain gene mouse model of xenogeneic graft-versus-host-like disease and the role of host major histocompatibility
   complex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1994</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1994</guid>
<pubDate>Tue, 08 May 2012 23:37:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Immunodeficient non-obese diabetic (NOD)-severe combined immune-deficient (scid) mice bearing a targeted mutation in the gene encoding the interleukin (IL)-2 receptor gamma chain gene (IL2rgamma(null)) engraft readily with human    peripheral blood mononuclear cells (PBMC). Here, we report a robust model of xenogeneic graft-versus-host-like disease (GVHD) based on intravenous injection of human PBMC into 2 Gy conditioned NOD-scid IL2rgamma(null) mice. These mice develop    xenogeneic GVHD consistently (100%) following injection of as few as 5 x 10(6) PBMC, regardless of the PBMC donor used. As in human disease, the development of xenogeneic GVHD is highly dependent on expression of host major histocompatibility    complex class I and class II molecules and is associated with severely depressed haematopoiesis. Interrupting the tumour necrosis factor-alpha signalling cascade with etanercept, a therapeutic drug in clinical trials for the treatment of human    GVHD, delays the onset and progression of disease. This model now provides the opportunity to investigate in vivo mechanisms of xenogeneic GVHD as well as to assess the efficacy of therapeutic agents rapidly.</p>

	]]>
</description>

<author>M A. King et al.</author>


</item>


<item>
<title>Gender- and compartment-specific bone loss in C57BL/6J mice: correlation to season?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1993</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1993</guid>
<pubDate>Tue, 08 May 2012 23:37:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Seasonal variation in bone mineral density (BMD) has been documented in humans, and has been attributed to changes in 25-hydroxyvitamin D [25(OH)D] synthesis. To test the hypothesis that seasonal changes in bone mass occur in    laboratory mice, we measured body composition, femoral bone phenotypes, and serum bone markers in 16-wk-old male and female C57BL/6 (B6) mice during the summer (June-August) and winter (December-February) months at The Jackson Laboratory in Bar    Harbor, Maine.  Both male and female B6 mice had higher volumetric BMD in the summer than winter.  Females showed reduced trabecular bone, whereas males showed changes in bone volume. Males, but not females, had higher insulin-like growth factor    1 in summer than in winter, and only males showed an increase in body weight during the winter. No seasonal differences in serum TRAP5b, osteocalcin, or 25(OH)D were noted for either sex. We conclude that seasonal variation in skeletal and body    composition parameters in B6 mice is significant and must be considered when performing longitudinal phenotyping of the skeleton. Further studies are needed to determine the environmental factors that cue seasonal changes in body composition and    the mechanisms that produce these changes.</p>

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</description>

<author>K M. Delahunty et al.</author>


</item>


<item>
<title>Immunofluorescence imaging of DNA damage response proteins: optimizing protocols for super-resolution microscopy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1992</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1992</guid>
<pubDate>Tue, 08 May 2012 23:37:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Immunofluorescence imaging has provided captivating visual evidence for numerous cellular events, from vesicular trafficking, organelle maturation and cell division to nuclear processes including the appearance of various proteins    and chromatin components in distinct foci in response to DNA damaging agents. With the advent of new super-resolution microscope technologies such as 4Pi microscopy, standard immunofluorescence protocols deserve some reevaluation in order to take    full advantage of these new technological accomplishments. Here we describe several methodological considerations that will help overcome some of the limitations that may result from the use of currently applied procedures, with particular    attention paid to the analysis of possible colocalization of fluorescent signals. We conclude with an example of how application of optimized methods led to a breakthrough in super-resolution imaging of nuclear events occurring in response to DNA    damage.</p>

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</description>

<author>B T. Bennett et al.</author>


</item>


<item>
<title>Zebrafish Hagoromo mutants up-regulate fgf8 postembryonically and develop neuroblastoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1991</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1991</guid>
<pubDate>Tue, 08 May 2012 23:36:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>We screened an existing collection of zebrafish insertional mutants for cancer susceptibility by histologic examination of heterozygotes at 2 years of age. As most mutants had no altered cancer predisposition, this provided the    first comprehensive description of spontaneous tumor spectrum and frequency in adult zebrafish. Moreover, the screen identified four lines, each carrying a different dominant mutant allele of Hagoromo previously linked to adult pigmentation    defects, which develop tumors with high penetrance and that histologically resemble neuroblastoma. These tumors are clearly neural in origin, although they do not express catecholaminergic neuronal markers characteristic of human neuroblastoma.    The zebrafish tumors result from inappropriate maintenance of a cell population within the cranial ganglia that are likely neural precursors.  These neoplasias typically remain small but they can become highly aggressive, initially traveling    along cranial nerves, and ultimately filling the head. The developmental origin of these tumors is highly reminiscent of human neuroblastoma. The four mutant Hagoromo alleles all contain viral insertions in the fbxw4 gene, which encodes an F-box    WD40 domain-containing protein. However, although one allele clearly reduced the levels of fbxw4 mRNA, the other three insertions had no detectable effect on fbw4 expression. Instead, we showed that all four mutations result in the postembryonic    up-regulation of the neighboring gene, fibroblast growth factor 8 (fgf8). Moreover, fgf8 is highly expressed in the tumorigenic lesions. Although fgf8 overexpression is known to be associated with breast and prostate cancer in mammals, this study    provides the first evidence that fgf8 misregulation can lead to neural tumors.</p>

	]]>
</description>

<author>A Amsterdam et al.</author>


</item>


<item>
<title>Foreword for special issue: mouse models for hearing research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1990</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1990</guid>
<pubDate>Tue, 08 May 2012 23:36:45 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K N. Alagramam et al.</author>


</item>


<item>
<title>Neuroendocrine inhibition of glucose production and resistance to cancer in dwarf mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1989</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1989</guid>
<pubDate>Tue, 08 May 2012 23:36:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pit1 null (Snell dwarf) and Proph1 null (Ames dwarf) mutant mice lack GH, PRL and TSH. Snell and Ames dwarf mice also exhibit reduced IGF-I, resistance to cancer and a longer lifespan than control mice. Endogenous glucose production    during fasting is reduced in Snell dwarf mice compared to fasting control mice. In view of cancer cell dependence on glucose for energy, low endogenous glucose production may provide Snell dwarf mice with resistance to cancer. We investigated    whether endogenous glucose production is lower in Snell dwarf mice during feeding. Inhibition of endogenous glucose production by glucose injection was enhanced in 12 to 14 month-old female Snell dwarf mice. Thus, we hypothesize that lower    endogenous glucose production during feeding and fasting reduces cancer cell glucose utilization providing Snell dwarf mice with resistance to cancer. The elevation of circulating adiponectin, a hormone produced by adipose tissue, may contribute    to the suppression of endogenous glucose production in 12 to 14 month-old Snell dwarf mice. We compared the incidence of cancer at time of death between old Snell dwarf and control mice. Only 18% of old Snell dwarf mice had malignant lesions at    the time of death compared to 82% of control mice. The median ages at death for old Snell dwarf and control mice were 33 and 26 months, respectively. By contrast, previous studies showed a high incidence of cancer in old Ames dwarf mice at the    time of death. Hence, resistance to cancer in old Snell dwarf mice may be mediated by neuroendocrine factors that reduce glucose utilization besides elevated adiponectin, reduced IGF-I and a lack of GH, PRL and TSH, seen in both Snell and Ames    dwarf mice. Proteomics analysis of pituitary secretions from Snell dwarf mice confirmed the absence of GH and PRL, the secretion of ACTH and elevated secretion of Chromogranin B and Secretogranin II.  Radioimmune assays confirmed that circulating    Chromogranin B and Secretogranin II were elevated in 12 to 14 month-old Snell dwarf mice. In summary, our results in Snell dwarf mice suggest that the pituitary gland and adipose tissue are part of a neuroendocrine loop that lowers the risk of    cancer during aging by reducing the availability of glucose.</p>

	]]>
</description>

<author>J M. Alderman et al.</author>


</item>


<item>
<title>Quantitative trait loci, genes, and polymorphisms that regulate bone mineral density in mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1988</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1988</guid>
<pubDate>Tue, 08 May 2012 23:36:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>This is an in silico analysis of data available from genome-wide scans. Through analysis of QTL, genes and polymorphisms that regulate BMD, we identified 82 BMD QTL, 191 BMD-associated (BMDA) genes, and 83 genes containing known    BMD-associated polymorphisms (BMDAP). The catalogue of all BMDA/BMDAP genes and relevant literatures are provided. In total, there are substantially more BMDA/BMDAP genes in regions of the genome where QTL have been identified than in non-QTL    regions. Among 191 BMDA genes and 83 BMDAP genes, 133 and 58 are localized in QTL regions, respectively. The difference was still noticeable for the chromosome distribution of these genes between QTL and non-QTL regions. These results have    allowed us to generate an integrative profile of QTL, genes, polymorphisms that determine BMD. These data could facilitate more rapid and comprehensive identification of causal genes underlying the determination of BMD in mouse and provide new    insights into how BMD is regulated in humans.</p>

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</description>

<author>Q Xiong et al.</author>


</item>


<item>
<title>The caBIG terminology review process.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1987</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1987</guid>
<pubDate>Tue, 08 May 2012 23:36:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>The National Cancer Institute (NCI) is developing an integrated biomedical informatics infrastructure, the cancer Biomedical Informatics Grid (caBIG), to support collaboration within the cancer research community. A key part of the    caBIG architecture is the establishment of terminology standards for representing data. In order to evaluate the suitability of existing controlled terminologies, the caBIG Vocabulary and Data Elements Workspace (VCDE WS) working group has    developed a set of criteria that serve to assess a terminology's structure, content, documentation, and editorial process. This paper describes the evolution of these criteria and the results of their use in evaluating four standard    terminologies: the Gene Ontology (GO), the NCI Thesaurus (NCIt), the Common Terminology for Adverse Events (known as CTCAE), and the laboratory portion of the Logical Objects, Identifiers, Names and Codes (LOINC). The resulting caBIG criteria are    presented as a matrix that may be applicable to any terminology standardization effort.</p>

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</description>

<author>J J. Cimino et al.</author>


</item>


<item>
<title>Genetic influence on electrocardiogram time intervals and heart rate in aging mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1986</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1986</guid>
<pubDate>Tue, 08 May 2012 23:36:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Understanding the genetic influence on ECG time intervals and heart rate (HR) is important for identifying the genes underlying susceptibility to cardiac arrhythmias. The objective of this study was to determine the genetic    influence on ECG parameters and their age-related changes in mice. ECGs were recorded in lead I on 8 males and 8 females from each of 28 inbred strains at the ages of 6, 12, and 18 mo. Significant interstrain differences in the P-R interval, QRS    complex duration, and HR were found. Age-related changes in the P-R interval, QRS complex duration, and HR differed among strains. The P-R interval increased with age in 129S1/SvlmJ females. The QRS complex duration decreased with age in C57BR/J    males and DBA2/J females but increased in NON/ShiLtJ females. HR decreased in C57L/J females and SM/J and P/J males but increased in BALB/cByJ males. Differences between males and females were found for HR in SJL/J mice and in the P-R interval in    129S1/SvlmJ mice. Broad-sense heritability estimates of ECG time intervals and HR ranged from 0.31 for the QRS complex duration to 0.52 for the P-R interval. Heritability estimates decreased with age for the P-R interval. Our study revealed that    genetic factors play a significant role on cardiac conduction activity and age-related changes in ECG time intervals and HR.</p>

	]]>
</description>

<author>S Xing et al.</author>


</item>


<item>
<title>Lineage-specific biology revealed by a finished genome assembly of the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1985</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1985</guid>
<pubDate>Tue, 08 May 2012 23:35:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse (Mus musculus) is the premier animal model for understanding human disease and development. Here we show that a comprehensive understanding of mouse biology is only possible with the availability of a finished,    high-quality genome assembly. The finished clone-based assembly of the mouse strain C57BL/6J reported here has over 175,000 fewer gaps and over 139 Mb more of novel sequence, compared with the earlier MGSCv3 draft genome assembly. In a    comprehensive analysis of this revised genome sequence, we are now able to define 20,210 protein-coding genes, over a thousand more than predicted in the human genome (19,042 genes). In addition, we identified 439 long, non-protein-coding RNAs    with evidence for transcribed orthologs in human. We analyzed the complex and repetitive landscape of 267 Mb of sequence that was missing or misassembled in the previously published assembly, and we provide insights into the reasons for its    resistance to sequencing and assembly by whole-genome shotgun approaches. Duplicated regions within newly assembled sequence tend to be of more recent ancestry than duplicates in the published draft, correcting our initial understanding of recent    evolution on the mouse lineage. These duplicates appear to be largely composed of sequence regions containing transposable elements and duplicated protein-coding genes; of these, some may be fixed in the mouse population, but at least 40% of    segmentally duplicated sequences are copy number variable even among laboratory mouse strains. Mouse lineage-specific regions contain 3,767 genes drawn mainly from rapidly-changing gene families associated with reproductive functions. The    finished mouse genome assembly, therefore, greatly improves our understanding of rodent-specific biology and allows the delineation of ancestral biological functions that are shared with human from derived functions that are not.</p>

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</description>

<author>D M. Church et al.</author>


</item>


<item>
<title>Androgen receptor in Sertoli cells is not required for testosterone-induced suppression of spermatogenesis, but contributes to Sertoli cell organization in Utp14b jsd mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1984</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1984</guid>
<pubDate>Tue, 08 May 2012 23:35:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Testosterone acting through the androgen receptor (AR) maintains the arrest of spermatogonial differentiation in juvenile spermatogonial depletion (jsd mutation in the Utp14b gene) mutant adult male mice. It is not known which of    the somatic cell types expressing AR mediates this inhibition. To determine whether Sertoli cells are responsible, we selectively eliminated AR in Sertoli cells in jsd mice containing a floxed-Ar gene and an anti-Mullerian hormone-Cre transgene.    In these Sertoli AR-knockout (SCARKO)-jsd mice, spermatogonial differentiation did not recover. However, the normal organization of Sertoli cell nuclei was drastically disrupted in SCARKO-jsd mice compared with SCARKO or jsd mice. In addition,    the extent of ectoplasmic specializations was reduced; tight junctions were not found; vinculin, an anchoring protein found in ectoplasmic specializations, became uniformly distributed in the cytoplasm; and the adult Sertoli cells showed excess    heterochromatin subjacent to their nuclear envelope. Despite the abnormalities in Sertoli cells in SCARKO-jsd mice, global suppression of testosterone action and levels was still effective in restoring the differentiated germ cells, and this was    accompanied by an improved arrangement of Sertoli cell nuclei. We conclude that Sertoli cells are not targets for the testosterone-mediated inhibition of spermatogonial differentiation in jsd mice, and that both AR in Sertoli cells and the    presence of differentiated germ cells contribute to maintaining the organization of Sertoli cells within the seminiferous tubules.</p>

	]]>
</description>

<author>G Wang et al.</author>


</item>


<item>
<title>Antagonism of the testis- and ovary-determining pathways during ovotestis development in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1983</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1983</guid>
<pubDate>Tue, 08 May 2012 23:35:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ovotestis development in B6-XY(POS) mice provides a rare opportunity to study the interaction of the testis- and ovary-determining pathways in the same tissue. We studied expression of several markers of mouse fetal testis (SRY,    SOX9) or ovary (FOXL2, Rspo1) development in B6-XY(POS) ovotestes by immunofluorescence, using normal testes and ovaries as controls. In ovotestes, SOX9 was expressed only in the central region where SRY is expressed earliest, resulting in testis    cord formation. Surprisingly, FOXL2-expressing cells also were found in this region, but individual cells expressed either FOXL2 or SOX9, not both. At the poles, even though SOX9 was not up-regulated, SRY expression was down-regulated normally as    in XY testes, and FOXL2 was expressed from an early stage, demonstrating ovarian differentiation in these areas. Our data (1) show that SRY must act within a specific developmental window to activate Sox9; (2) challenge the established view that    SOX9 is responsible for down-regulating Sry expression; (3) disprove the concept that testicular and ovarian cells occupy discrete domains in ovotestes; and (4) suggest that FOXL2 is actively suppressed in Sertoli cell precursors by the action of    SOX9. Together these findings provide important new insights into the molecular regulation of testis and ovary development.</p>

	]]>
</description>

<author>D Wilhelm et al.</author>


</item>


<item>
<title>NOD x 129.H2(g7) backcross delineates 129S1/SvImJ-derived genomic regions modulating type 1 diabetes development in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1982</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1982</guid>
<pubDate>Tue, 08 May 2012 23:35:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: Introduction of genes targeted in 129/Sv embryonic stem (ES) cells into NOD mice brings about linked genes that may modulate type 1 diabetes. Our objective was to identify 129S1/SvJ non-MHC regions contributing type 1    diabetes resistance or susceptibility in backcross to NOD/LtJ. RESEARCH DESIGN AND METHODS: After congenic transfer of the NOD H2(g7) haplotype onto 129S1/Sv, 310 females were produced by NOD x (NOD x 129.H2(g7))F1 backcross (N2). A genome scan    for quantitative trait locus (QTL) affecting clinical diabetes, age of diabetes onset, and insulitis severity was performed using subphenotype characteristics to improve power and resolution for detection of diabetes susceptibility loci.     RESULTS: Thirty-six of 310 (11.6%) N2 females developed type 1 diabetes between 14 and 40 weeks. Significant evidence of linkage for only a single previously reported Idd complex locus (Idd10/17/18, chromosome [Chr] 3) was indicated for clinical    diabetes. The quantitative traits of insulitis either alone or combined with age at type 1 diabetes onset were significantly linked to known Idd regions on Chr 1 (Idd5 region), Chr 4 (Idd9 region), Chr 8 (Idd22), Chr 11 (Idd4.3), and proximal Chr    17 (Idd16 region). Significant 129S1/Sv resistance contributions were identified on Chr 1, 15 (two loci), and 19, with suggestive evidence for additional novel 129/Sv resistance QTL on Chr 5 and 17 and susceptibility on Chr 2. CONCLUSIONS: The    129S1/SvJ genome harbors collections of both known and potentially novel non-MHC Idd loci. Investigators targeting 129/Sv genes mapping within chromosomal regions reported herein or elsewhere in the genome need to exclude potential contributions    from linked Idd loci by generating a NOD.129 control strain expressing the nontargeted allele.</p>

	]]>
</description>

<author>E H. Leiter et al.</author>


</item>


<item>
<title>Chromosome Y variants from different inbred mouse strains are linked to differences in the morphologic and molecular responses of cardiac cells to postpubertal testosterone.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1981</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1981</guid>
<pubDate>Tue, 08 May 2012 23:35:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: We have reported previously that when chromosome Y (chrY) from the mouse strain C57BL/6J (ChrYC57) was substituted for that of A/J mice (ChrYA), cardiomyocytes from the resulting "chromosome substitution" C57BL/6J-chrYA    strain were smaller than that of their C57BL/6J counterparts. In reverse, when chrYA from A/J mice was substituted for that of chrYC57, cardiomyocytes from the resulting A/J-chrYC57 strain were larger than in their A/J counterparts. We further    used these strains to test whether: 1) the origin of chrY could also be linked to differences in the profile of gene expression in the hearts of adult male mice, and 2) post-pubertal testosterone could play a role in the differential morphologic    and/or molecular effects of chrYC57 and chrYA. RESULTS: The increased size of cardiomyocytes from adult male C57BL/6J mice compared to C57BL/6J-chrYA resulted from the absence of hypertrophic effects of post-pubertal testosterone on cells from    the latter strain. However, gene profiling revealed that the latter effect could not be explained on the basis of an insensitivity of cells from C57BL/6J-chrYA to androgens, since even more cardiac genes were affected by post-pubertal    testosterone in C57BL/6J-chrYA hearts than in C57BL/6J.  By testing for interaction between the effects of surgery and strain, we identified 249 "interaction genes" whose expression was affected by post-pubertal testosterone differentially    according to the genetic origin of chrY. These interaction genes were found to be enriched within a limited number of signaling pathways, including: 1) p53 signaling, which comprises the interacting genes Ccnd1, Pten and Cdkn1a that are also    potential co-regulators of the androgen receptors, and 2) circadian rhythm, which comprises Arntl/Bmal1, which may in turn regulate cell growth via the control of Cdkn1a. CONCLUSION: Although post-pubertal testosterone increased the size of    cardiomyocytes from male C56BL/6J mice but not that from their C57BL/6J-chrYA counterparts, it affected gene expression in the hearts from both strains. However, several cardiac genes responded to post-pubertal testosterone in a strict    strain-selective manner, which provides possible mechanisms explaining how chrY may, in part via interference with androgen regulatory events, be linked to morphologic differences of cardiac cells of adult male mice.</p>

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</description>

<author>B Llamas et al.</author>


</item>


<item>
<title>Amino acid polymorphisms altering the glycosylation of IL-2 do not protect from type 1 diabetes in the NOD mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1980</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1980</guid>
<pubDate>Tue, 08 May 2012 23:35:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Idd3 is one of many gene regions that affect the development of type 1 diabetes (T1D) in the nonobese diabetic (NOD) mouse. Idd3 has been localized to a 650-kb region on chromosome 3 containing the IL-2 gene. Exon 1 of the IL-2 gene    is polymorphic between the susceptible NOD and the protective C57BL/6 (B6) alleles, causing multiple amino acid changes that have been proposed to be responsible for the differing glycosylation status. To address whether this coding polymorphism    recapitulates the disease suppression mediated by the B6 Idd3 allele, we generated knockin mice in which exon 1 of the B6 IL-2 allele replaces the homologous region in the NOD allele. We generated these mice by targeting the NOD allele of NOD/129    F(1) ES cells. IL-2 protein from the knockin mice showed the glycosylation pattern of the B6 IL-2 isoform, confirming that the amino acid differences encoded within exon 1 affect the glycosylation of the IL-2 protein.  However, unlike NOD.B6 Idd3    congenic mice, the knockin mice were not protected from T1D. Furthermore, the difference in amino acid sequence in the IL-2 protein did not affect the level of expression of IL-2. This approach provides a general method for the determination of a    functional role of a given genomic sequence in a disease process. Further, our result demonstrates that the variants in exon 1 of the IL-2 gene are not responsible for T1D suppression in NOD.B6 Idd3 mice, thereby supporting the hypothesis that    variants in the regulatory region affecting expression levels are causative.</p>

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</description>

<author>M Kamanaka et al.</author>


</item>


<item>
<title>Genetic complexity of absence seizures in substrains of C3H mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1979</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1979</guid>
<pubDate>Tue, 08 May 2012 23:34:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Absence epilepsy is a common form of idiopathic generalized epilepsy whose etiology is poorly understood because of genetic and phenotypic heterogeneity.  The inbred mouse strain C3H/He exhibits spontaneous absence seizures    characterized by spike and wave discharges (SWD) on the electroencephalogram concomitant with behavioral arrest. Previous studies using the C3H/HeJ (HeJ) substrain identified a mutation in the Gria4 gene as a major susceptibility locus. In the    present study, we found that two closely related substrains C3H/HeOuJ (OuJ) and C3H/HeSnJ, which have a similar SWD incidence as HeJ, do not contain the Gria4 mutation. Further analysis of backcross mice segregating OuJ and C57BL/6J alleles shows    that, unlike the HeJ substrain, OuJ does not have a major locus for SWD but has suggestive loci at best that would explain only a fraction of the phenotypic variance. These results illustrate how the genetic etiology of a common neurological    disorder can differ between substrains with similar phenotypes. We infer that all C3H strains are sensitized to SWD and that additional mutations affecting SWD arose or were fixed independently in the years since the substrains    diverged.</p>

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</description>

<author>S Tokuda et al.</author>


</item>


<item>
<title>Recombinant human hepatitis B vaccine initiating alopecia areata: testing the hypothesis using the C3H/HeJ mouse model.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1978</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1978</guid>
<pubDate>Tue, 08 May 2012 23:34:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Untoward effects of human vaccines suggest that recombinant hepatitis B vaccine may induce alopecia areata (AA) in some patients. Similar untoward immunological effects may also account for AA-like diseases in domestic species. In    this study, the C3H/HeJ spontaneous adult onset AA mouse model was used to test the role, if any, of recombinant hepatitis B vaccine on the initiation or activation of AA.  Initial experiments demonstrated no effect on induction of AA in young    adult female C3H/HeJ mice (P = 0.5689). By contrast, older females, those at the age when AA first begins to appear in this strain, had a significant increase (P = 0.0264) in the time of onset of AA, suggesting that the vaccine may initiate    disease in mice predisposed to AA. However, larger vaccine trials, which included diphtheria and tetanus toxoids as additional controls, did not support these initial result findings and suggest that AA associated with vaccination may be within    the normal background levels of the given population.</p>

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</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title>Heterozygous mutations of the voltage-gated sodium channel SCN8A are associated with spike-wave discharges and absence epilepsy in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1977</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1977</guid>
<pubDate>Tue, 08 May 2012 23:34:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>In a chemical mutagenesis screen, we identified the novel Scn8a(8J) allele of the gene encoding the neuronal voltage-gated sodium channel Na(v)1.6. The missense mutation V929F in this allele alters an evolutionarily conserved    residue in the pore loop of domain 2 of Na(v)1.6. Electroencephalography (EEG) revealed well-defined spike-wave discharges (SWD), the hallmark of absence epilepsy, in Scn8a(8J) heterozygotes and in heterozygotes for two classical Scn8a alleles,    Scn8a(med) (null) and Scn8a(med-jo) (missense). Mouse strain background had a significant effect on SWD, with mutants on the C3HeB/FeJ strain showing a higher incidence than on C57BL/6J. The abnormal EEG patterns in heterozygous mutant mice and    the influence of genetic background on SWD make SCN8A an attractive candidate gene for common human absence epilepsy, a genetically complex disorder.</p>

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</description>

<author>L A. Papale et al.</author>


</item>


<item>
<title>A new mouse model of metabolic syndrome and associated complications.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1976</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1976</guid>
<pubDate>Tue, 08 May 2012 23:34:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Metabolic syndrome (MS) encompasses a clustering of risk factors for cardiovascular disease, including obesity, insulin resistance, and dyslipidemia.  We characterized a new mouse model carrying a dominant mutation, C57BL/6J-Nmf15/+    (B6-Nmf15/+), which develops additional complications of MS such as adipose tissue inflammation and cardiomyopathy. A backcross was used to genetically map the Nmf15 locus. Mice were examined in the comprehensive laboratory animal monitoring    system, and dual energy X-ray absorptiometry and blood chemistry analyses were performed. Hypothalamic LEPR, SOCS1, and STAT3 phosphorylation were examined. Cardiac function was assessed by echo- and electrocardiography. Adipose tissue    inflammation was characterized by in situ hybridization and measurement of Jun kinase activity. The Nmf15 locus mapped to distal mouse chromosome 5 with an LOD (logarithm of odds) score of 13.8. Nmf15 mice developed obesity by 12 weeks of age.    Plasma leptin levels were significantly elevated in pre-obese Nmf15 mice at 8 weeks of age and an attenuated STAT3 phosphorylation in the hypothalamus suggests a primary leptin resistance. Adipose tissue from Nmf15 mice showed a remarkable degree    of inflammation and macrophage infiltration as indicated by expression of the F4/80 marker and increased phosphorylation of JUN N-terminal kinase 1/2. Lipidosis was observed in tubular epithelial cells and glomeruli of the kidney. Nmf15 mice    demonstrate both histological and pathophysiological evidence of cardiomyopathy. The Nmf15 mouse model provides a new entry point into pathways mediating leptin resistance and obesity. It is one of few models that combine many aspects of MS and    can be useful for testing new therapeutic approaches for combating obesity complications, particularly cardiomyopathy.</p>

	]]>
</description>

<author>Y Wang et al.</author>


</item>


<item>
<title>A mouse by any other name ...</title>
<link>http://mouseion.jax.org/stfb2000_2009/1975</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1975</guid>
<pubDate>Tue, 08 May 2012 23:34:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>A recurring motto from the Tony Blair government in the UK was "Education, Education, Education." An appropriate exhortation for the biomedical sciences would be "Standardization, Standardization, Standardization." Inevitably, the    two go hand in hand, and the challenge we face is how to encourage researchers to comply with existing or emerging standard terminologies and nomenclatures. This is both an educational and a regulatory task, one in which it is vital to succeed if    we are to efficiently and accurately share and use the huge volume of data emerging in the biosciences.</p>

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</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title>Macaca fascicularis papillomavirus type 1: a non-human primate betapapillomavirus causing rapidly progressive hand and foot papillomatosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1974</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1974</guid>
<pubDate>Tue, 08 May 2012 23:34:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Papillomaviruses (PVs) are a group of small, non-enveloped DNA viruses that cause mucosal or cutaneous neoplasia in a variety of animals. Whilst most papillomas will regress spontaneously, some may persist or undergo malignant    transformation.  In this study, aggressive, persistent and extensive warts were observed on the hands and feet of a cynomolgus macaque (Macaca fascicularis). The presence of PV in the wart biopsies was identified by immunohistochemistry and PCR    amplification of PV DNA. The genomic DNA of this PV was cloned and sequenced, and the PV was designated M. fascicularis papillomavirus type 1 (MfPV-1). Its genome was 7588 bp in length and the organization of its putative open reading frames (E1,    E2, E6, E7, L1, L2 and E4) was similar to that of other PVs. MfPV-1 had a short non-coding region (NCR) of 412 bp. Molecular analysis of MfPV-1 genomic DNA classified it into the genus Betapapillomavirus, to which all epidermodysplasia    verruciformis (EV)-type PVs belong. Diseases caused by PVs of the genus Betapapillomavirus are usually associated with natural or iatrogenic immunosuppression. The genomic characterization performed in this study showed that MfPV-1 clustered    within the genus Betapapillomavirus and also contained EV-type-specific motifs in its NCR. Further characterization of this virus and its host interactions may allow us to develop a non-human primate model for human betapapillomaviruses, a genus    populated by human PV types causing EV.</p>

	]]>
</description>

<author>J Joh et al.</author>


</item>


<item>
<title>Matrix metalloproteinase 9 plays a key role in lyme arthritis but not in dissemination of Borrelia burgdorferi.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1973</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1973</guid>
<pubDate>Tue, 08 May 2012 23:33:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Borrelia burgdorferi, the causative agent of Lyme arthritis, does not produce any exported proteases capable of degrading extracellular matrix despite the fact that it is able to disseminate from a skin insertion site to infect    multiple organs. Prior studies have shown that B. burgdorferi induces the host protease, matrix metalloproteinase 9 (MMP-9), and suggested that the induction of MMP-9 may allow the organism to disseminate and produce local tissue destruction. We    examined the role of MMP-9 in dissemination of B. burgdorferi and pathogenesis of Lyme arthritis. In a MMP-9(-/-) mouse model, MMP-9 was not required for the dissemination of the spirochete to distant sites. However, MMP-9(-/-) exhibited    significantly decreased arthritis compared to wild-type mice. The decrease in arthritis was not due to an inability to control infection since the spirochete numbers in the joints were identical. Levels of inflammatory chemokines and cytokines    were also similar in MMP-9(-/-) and wild-type mice. We examined whether decreased inflammation in MMP-9(-/-) mice may be the result of decreased production of neoattractants by MMP-9-dependent cleavage of collagen. MMP-9 cleavage of type I    collagen results in increased monocyte chemoattraction. MMP-9 plays an important role in regulating inflammation in Lyme arthritis, potentially through the cleavage of type I collagen.</p>

	]]>
</description>

<author>A J. Heilpern et al.</author>


</item>


<item>
<title>Parental origin of chromosomes influences crossover activity within the Kcnq1 transcriptionally imprinted domain of Mus musculus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1972</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1972</guid>
<pubDate>Tue, 08 May 2012 23:33:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Among the three functions of DNA, mammalian replication and transcription can be subject to epigenetic imprinting specified by the parental origin of chromosomes, and although there is suggestive indication that this is    also true for meiotic recombination, no definitive evidence has yet been reported. RESULTS: We have now obtained such evidence on mouse chromosome 7 by assaying meiotic recombination as it occurs in reciprocal F1 mice. A 166 kb region near the    Kcnq1 transcriptionally imprinted domain showed significantly higher recombination activity in the CAST x B6 parental direction (p < 0.03).  Characterizing hotspots within this domain revealed a cluster of three hotspots lying within a 100 kb    span, among these hotspots, Slc22a18 showed a definitive parent of origin effect on recombination frequency (p < 0.02). Comparing recombination activity in the mouse Kcnq1 and neighboring H19-Igf2 imprinted domains with their human counterparts,    we found that elevated recombination activity in these domains is a consequence of their chromosomal position relative to the telomere and not an intrinsic characteristic of transcriptionally imprinted domains as has been previously suggested.    CONCLUSION: Similar to replication and transcription, we demonstrate that meiotic recombination can be subjected to epigenetic imprinting and hotspot activity can be influenced by the parental origin of chromosomes. Furthermore, transcriptionally    imprinted regions exhibiting elevated recombination activity are likely a consequence of their chromosomal location rather than their transcriptional characteristic.</p>

	]]>
</description>

<author>S H. Ng et al.</author>


</item>


<item>
<title>One medicine, one pathology, and the one health concept.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1971</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1971</guid>
<pubDate>Tue, 08 May 2012 23:33:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title>Targeted suppression of Has2 mRNA in mouse cumulus cell-oocyte complexes by adenovirus-mediated short-hairpin RNA expression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1970</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1970</guid>
<pubDate>Tue, 08 May 2012 23:33:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>RNA interference (RNAi) is an effective tool for studying gene function in oocytes, but no studies have targeted somatic cells of primary cultured cumulus cell-oocyte complexes (COCs). This is probably due to difficulty in    introducing RNAi-inducing molecules, such as a short-hairpin RNA (shRNA) gene, into COCs by commonly used transfection reagents. We therefore tested whether a developmental process of intact COCs could be suppressed by adenovirus-mediated shRNA    expression. Has2, encoding hyaluronan synthase 2, was selected as the target transcript, because the process of cumulus expansion depends upon expression of Has2 mRNA and this process is easily evaluated in vitro. Intact COCs were infected with    replication-incompetent adenoviruses containing an expression sequence of shRNA targeting either Has2 (Has2 shRNA) or a control transcript not expressed in cumulus cells, and the effects on epidermal growth factor (EGF)-stimulated cumulus    expansion were determined. Has2 shRNA expression suppressed Has2 mRNA levels in COCs by more than 70%, without affecting expression levels of Ptgs2, Ptx3, Tnfaip6 mRNAs, which are also required for cumulus expansion, or other transcripts not    related to expansion. Interestingly, levels of Areg and Ereg mRNAs were decreased in COCs expressing Has2 shRNA when compared with those in controls, while Btc mRNA levels remained unaffected.  Furthermore, the degree of cumulus expansion by Has2    shRNA-expressing COCs was significantly less than that of controls. Thus adenovirus-mediated introduction of shRNA produces specific gene silencing and a phenotype in intact COCs, providing proof of principle that this method will be a helpful    tool for understanding mechanisms of COC development.</p>

	]]>
</description>

<author>K Sugiura et al.</author>


</item>


<item>
<title>Searching the Mouse Genome Informatics (MGI) resources for information on mouse biology from genotype to phenotype.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1969</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1969</guid>
<pubDate>Tue, 08 May 2012 23:33:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Informatics (MGI) resource provides the research community with access to information on the genetics, genomics, and biology of the laboratory mouse. Core data in MGI include gene characterization and function,    phenotype and disease model descriptions, DNA and protein sequence data, gene expression data, mammalian orthologies, SNPs and PCR polymorphisms, mapping data, and links to other bioinformatics databases. Data integration is supported through the    use of standardized nomenclature, and through the use of controlled vocabularies such as the mouse Anatomical Dictionary, the Mammalian Phenotype Ontology, and the Gene Ontologies. MGI extracts and organizes data from primary literature. MGI data    are shared with and widely displayed from other bioinformatics resources. The database is updated nightly with curated annotations, and regularly adds new datasets. This unit provides a guide to using the MGI bioinformatics    resource.</p>

	]]>
</description>

<author>D R. Shaw</author>


</item>


<item>
<title>Mouse H6 Homeobox 1 (Hmx1) mutations cause cranial abnormalities and reduced body mass.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1968</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1968</guid>
<pubDate>Tue, 08 May 2012 23:33:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The H6 homeobox genes Hmx1, Hmx2, and Hmx3 (also known as Nkx5-3; Nkx5-2 and Nkx5-1, respectively), compose a family within the NKL subclass of the ANTP class of homeobox genes. Hmx gene family expression is mostly    limited to sensory organs, branchial (pharyngeal) arches, and the rostral part of the central nervous system. Targeted mutation of either Hmx2 or Hmx3 in mice disrupts the vestibular system. These tandemly duplicated genes have functional overlap    as indicated by the loss of the entire vestibular system in double mutants. Mutants have not been described for Hmx1, the most divergent of the family. RESULTS: Dumbo (dmbo) is a semi-lethal mouse mutation that was recovered in a forward genetic    mutagenesis screen. Mutants exhibit enlarged ear pinnae with a distinctive ventrolateral shift. Here, we report on the basis of this phenotype and other abnormalities in the mutant, and identify the causative mutation as being an allele of Hmx1.    Examination of dumbo skulls revealed only subtle changes in cranial bone morphology, namely hyperplasia of the gonial bone and irregularities along the caudal border of the squamous temporal bone. Other nearby otic structures were unaffected. The    semilethality of dmbo/dmbo mice was found to be ~40%, occured perinatally, and was associated with exencephaly.  Surviving mutants of both sexes exhibited reduced body mass from ~3 days postpartum onwards. Most dumbo adults were microphthalmic.    Recombinant animals and specific deletion-bearing mice were used to map the dumbo mutation to a 1.8 Mb region on Chromosome 5. DNA sequencing of genes in this region revealed a nonsense mutation in the first exon of H6 Homeobox 1 (Hmx1; also    Nkx5-3). An independent spontaneous allele called misplaced ears (mpe) was also identified, confirming Hmx1 as the responsible mutant gene. CONCLUSION: The divergence of Hmx1 from its paralogs is reflected by different and diverse developmental    roles exclusive of vestibular involvement. Additionally, these mutant Hmx1 alleles represent the first mouse models of a recently-discovered Oculo-Auricular syndrome caused by mutation of the orthologous human gene.</p>

	]]>
</description>

<author>R J. Munroe et al.</author>


</item>


<item>
<title>Marrow fat and the bone microenvironment: developmental, functional, and pathological implications.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1967</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1967</guid>
<pubDate>Tue, 08 May 2012 23:33:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bone marrow adipogenesis is a normal physiologic process in all mammals. However, its function is unknown. The mesenchymal stem cell is the marrow precursor for adipocytes as well as osteoblasts, and PPARG is an essential    differentiation factor for entrance into the fat lineage. Mouse models have provided significant insight into the molecular cues that define stromal cell fate. In humans, accelerated marrow adipogenesis has been associated with aging and several    chronic conditions, including diabetes mellitus and osteoporosis. Newer imaging techniques have been used to determine the developmental time course of fat generation in bone marrow. However, more studies are needed to understand the    interrelationship among hematopoietic, osteoblastic, and adipogenic cells within the marrow niche.</p>

	]]>
</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title>Targeted deletion of the gamma-adducin gene (Add3) in mice reveals differences in alpha-adducin interactions in erythroid and nonerythroid cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1966</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1966</guid>
<pubDate>Tue, 08 May 2012 23:32:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>In red blood cells (RBCs) adducin heterotetramers localize to the spectrin-actin junction of the peripheral membrane skeleton. We previously reported that deletion of beta-adducin results in osmotically fragile, microcytic RBCs and    a phenotype of hereditary spherocytosis (HS). Notably, alpha-adducin was significantly reduced, while gamma-adducin, normally present in limited amounts, was increased approximately 5-fold, suggesting that alpha-adducin requires a heterologous    binding partner for stability and function, and that gamma-adducin can partially substitute for the absence of beta-adducin. To test these assumptions we generated gamma-adducin null mice. gamma-adducin null RBCs appear normal on Wright's stained    peripheral blood smears and by scanning electron microscopy. All membrane skeleton proteins examined are present in normal amounts, and all hematological parameters measured are normal. Despite a loss of approximately 70% of alpha-adducin in    gamma-adducin null platelets, no bleeding defect is observed and platelet structure appears normal. Moreover, systemic blood pressure and pulse are normal in gamma-adducin null mice. gamma- and beta-adducin null mice were intercrossed to generate    double null mice. Loss of gamma-adducin does not exacerbate the beta-adducin null HS phenotype although the amount alpha-adducin is reduced to barely detectable levels. The stability of alpha-adducin in the absence of a heterologous binding    partner varies considerably in various tissues. The amount of alpha-adducin is modestly reduced ( approximately 15%) in the kidney, while in the spleen and brain is reduced by approximately 50% with the loss of a heterologous beta- or    gamma-adducin binding partner. These results suggest that the structural properties of adducin differ significantly between erythroid and various nonerythroid cell types.</p>

	]]>
</description>

<author>K E. Sahr et al.</author>


</item>


<item>
<title>Caloric restriction in Alstrom syndrome prevents hyperinsulinemia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1965</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1965</guid>
<pubDate>Tue, 08 May 2012 23:32:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alstrom syndrome (AS; OMIM 203800) is an autosomal recessive disorder characterized by cone-rod dystrophy, dilated cardiomyopathy, sensorineural hearing impairment, developmental delay, and most case had both childhood-onset obesity    and hyperinsulinemia. Currently, the pathogenesis of this disease is not clear. Here we report on an 18-month-old boy with Alstrom syndrome. He had obesity but with normal insulin and glucose levels. Molecular analysis of the ALMS1 gene revealed    a 19 base pair homozygous deletion 11116_11134del in exon 16.  His body mass index decreased from 25.0 to 20.7 after calorie restriction for 9 months, and his insulin and glucose levels remained normal. Finding in this case suggests that    hyperinsulinemia is a secondary event in Alstrom syndrome, and early-commenced treatment prevents hyperinsulinemia.</p>

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</description>

<author>N C. Lee et al.</author>


</item>


<item>
<title>Directing experimental biology: a case study in mitochondrial biogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1964</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1964</guid>
<pubDate>Tue, 08 May 2012 23:32:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Computational approaches have promised to organize collections of functional genomics data into testable predictions of gene and protein involvement in biological processes and pathways. However, few such predictions have been    experimentally validated on a large scale, leaving many bioinformatic methods unproven and underutilized in the biology community. Further, it remains unclear what biological concerns should be taken into account when using computational methods    to drive real-world experimental efforts. To investigate these concerns and to establish the utility of computational predictions of gene function, we experimentally tested hundreds of predictions generated from an ensemble of three complementary    methods for the process of mitochondrial organization and biogenesis in Saccharomyces cerevisiae. The biological data with respect to the mitochondria are presented in a companion manuscript published in PLoS Genetics    (doi:10.1371/journal.pgen.1000407). Here we analyze and explore the results of this study that are broadly applicable for computationalists applying gene function prediction techniques, including a new experimental comparison with 48 genes    representing the genomic background. Our study leads to several conclusions that are important to consider when driving laboratory investigations using computational prediction approaches. While most genes in yeast are already known to    participate in at least one biological process, we confirm that genes with known functions can still be strong candidates for annotation of additional gene functions. We find that different analysis techniques and different underlying data can    both greatly affect the types of functional predictions produced by computational methods. This diversity allows an ensemble of techniques to substantially broaden the biological scope and breadth of predictions. We also find that performing    prediction and validation steps iteratively allows us to more completely characterize a biological area of interest. While this study focused on a specific functional area in yeast, many of these observations may be useful in the contexts of    other processes and organisms.</p>

	]]>
</description>

<author>M A. Hibbs et al.</author>


</item>


<item>
<title>Lung carcinogenesis induced by chronic tuberculosis infection: the experimental model and genetic control.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1963</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1963</guid>
<pubDate>Tue, 08 May 2012 23:32:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Coexistence of pulmonary tuberculosis (TB) and lung cancer in clinic poses significant challenges for the diagnostic and treatment of both diseases.  Although association of chronic inflammation and cancer is well-documented, causal    relationship between TB infection and lung cancer are not understood. We present experimental evidence that chronic TB infection induces cell dysplasia and squamous cell carcinoma (SCC) in a lung-specific manner. First, squamous cell aggregates    consistently appeared within the lung tissue associated with chronic TB lesions, and in some cases resembled SCCs. A transplantable tumor was established after the transfer of cells isolated from TB lung lesions into syngeneic recipients. Second,    the (Mycobacterium tuberculosis) MTB-infected macrophages play a pivotal role in TB-induced carcinogenesis by inducing DNA damage in their vicinity and by the production of a potent epidermal growth factor epiregulin, which may serve as a    paracrine survival and growth factor responsible for squamous metaplasia and tumorigenesis. Third, lung carcinogenesis during the course of chronic TB infection was more pronounced in animals with severe lung tissue damage mediated by    TB-susceptibility locus sst1. Together, our experimental findings showed a causal link between pulmonary TB and lung tumorigenesis and established a genetic model for further analysis of carcinogenic mechanisms activated by TB    infection.</p>

	]]>
</description>

<author>A Nalbandian et al.</author>


</item>


<item>
<title>TLR agonists prevent the establishment of allogeneic hematopoietic chimerism in mice treated with costimulation blockade.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1962</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1962</guid>
<pubDate>Tue, 08 May 2012 23:32:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Activation of TLR4 by administration of LPS shortens the survival of skin allografts in mice treated with costimulation blockade through a CD8 T cell-dependent, MyD88-dependent, and type I IFN receptor-dependent pathway. The effect    of TLR activation on the establishment of allogeneic hematopoietic chimerism in mice treated with costimulation blockade is not known. Using a costimulation blockade protocol based on a donor-specific transfusion (DST) and a short course of    anti-CD154 mAb, we show that LPS administration at the time of DST matures host alloantigen-presenting dendritic cells, prevents the establishment of mixed allogeneic hematopoietic chimerism, and shortens survival of donor-specific skin    allografts. LPS mediates its effects via a mechanism that involves both CD4(+) and CD8(+) T cells and results from signaling through either the MyD88 or the type I IFN receptor pathways. We also document that timing of LPS administration is    critical, as injection of LPS 24 h before treatment with DST and anti-CD154 mAb does not prevent hematopoietic engraftment but administration the day after bone marrow transplantation does. We conclude that TLR4 activation prevents the induction    of mixed allogeneic hematopoietic chimerism through type I IFN receptor and MyD88-dependent signaling, which leads to the up-regulation of costimulatory molecules on host APCs and the generation of alloreactive T cells. These data suggest that    distinct but overlapping cellular and molecular mechanisms control the ability of TLR agonists to block tolerance induction to hematopoietic and skin allografts in mice treated with costimulation blockade.</p>

	]]>
</description>

<author>D M. Miller et al.</author>


</item>


<item>
<title>Smooth muscle Notch1 mediates neointimal formation after vascular injury.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1961</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1961</guid>
<pubDate>Tue, 08 May 2012 23:31:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Notch1 regulates binary cell fate determination and is critical for angiogenesis and cardiovascular development. However, the pathophysiological role of Notch1 in the postnatal period is not known. We hypothesize that    Notch1 signaling in vascular smooth muscle cells (SMCs) may contribute to neointimal formation after vascular injury. METHODS AND RESULTS: We performed carotid artery ligation in wild-type, control (SMC-specific Cre recombinase transgenic    [smCre-Tg]), general Notch1 heterozygous deficient (N1+/-), SMC-specific Notch1 heterozygous deficient (smN1+/-), and general Notch3 homozygous deficient (N3-/-) mice. Compared with wild-type or control mice, N1+/- and smN1+/- mice showed a 70%    decrease in neointimal formation after carotid artery ligation. However, neointimal formation was similar between wild-type and N3-/- mice. Indeed, SMCs derived from explanted aortas of either N1(+/-)- or smN1+/- mice showed decreased chemotaxis    and proliferation and increased apoptosis compared with control or N3-/- mice. This correlated with decreased staining of proliferating cell nuclear antigen-positive cells and increased staining of cleaved caspase-3 in the intima of N1(+/-)- or    smN1+/- mice. In SMCs derived from CHF1/Hey2-/- mice, activation of Notch signaling did not lead to increased SMC proliferation or migration.  CONCLUSIONS: These findings indicate that Notch1, rather than Notch3, mediates SMC proliferation and    neointimal formation after vascular injury through CHF1/Hey2 and suggest that therapies that target Notch1/CHF1/Hey2 in SMCs may be beneficial in preventing vascular proliferative diseases.</p>

	]]>
</description>

<author>Y Li et al.</author>


</item>


<item>
<title>Effect of in vitro maturation of mouse oocytes on the health and lifespan of adult offspring.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1960</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1960</guid>
<pubDate>Tue, 08 May 2012 23:31:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: In vitro maturation of oocytes can, in some circumstances, provide an alternative approach to gonadotrophin-induced maturation in clinical settings.  However, the consequences of these protocols on the long-term health    of offspring are unknown. Here, the long-term health status and lifespans of offspring produced by in vitro maturation of mouse oocytes was compared with that of oocytes induced to mature in vivo using gonadotrophin treatment. METHODS: Mouse    oocytes were matured in vitro using both an established optimized system and in the absence of amino acids to produce a suboptimal condition for maturation.  Oocytes induced to mature in vivo with gonadotrophins constituted the control group. All    metaphase II oocytes were fertilized in vitro and transferred at the 2-cell stage to the oviducts of pseudo-pregnant foster mothers for development to term. Offspring were subjected to a wide variety of physiological and behavioral tests for the    first year of life and natural lifespan determined. RESULTS: There was no difference among the groups in lifespan or in most of the physiological and behavioral analyses. However, the pulse rate and cardiac output were slightly, but    significantly, reduced in the optimized in vitro matured group compared with the in vivo matured group (P = 0.0119 and P = 0.0197, respectively). Surprisingly, these decreases were largely abrogated in the in vitro group matured without amino    acids. CONCLUSIONS: Evidence presented here using a mouse model suggests that the in vitro maturation of oocytes has minimal effects on the long-term health of offspring. However, a finding of slight reductions in pulse rate and cardiac output    may focus future clinical attention.</p>

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</description>

<author>J J. Eppig et al.</author>


</item>


<item>
<title>Computationally driven, quantitative experiments discover genes required for mitochondrial biogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1959</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1959</guid>
<pubDate>Tue, 08 May 2012 23:31:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mitochondria are central to many cellular processes including respiration, ion homeostasis, and apoptosis. Using computational predictions combined with traditional quantitative experiments, we have identified 100 proteins whose    deficiency alters mitochondrial biogenesis and inheritance in Saccharomyces cerevisiae. In addition, we used computational predictions to perform targeted double-mutant analysis detecting another nine genes with synthetic defects in mitochondrial    biogenesis. This represents an increase of about 25% over previously known participants. Nearly half of these newly characterized proteins are conserved in mammals, including several orthologs known to be involved in human disease. Mutations in    many of these genes demonstrate statistically significant mitochondrial transmission phenotypes more subtle than could be detected by traditional genetic screens or high-throughput techniques, and 47 have not been previously localized to    mitochondria. We further characterized a subset of these genes using growth profiling and dual immunofluorescence, which identified genes specifically required for aerobic respiration and an uncharacterized cytoplasmic protein required for normal    mitochondrial motility.  Our results demonstrate that by leveraging computational analysis to direct quantitative experimental assays, we have characterized mutants with subtle mitochondrial defects whose phenotypes were undetected by    high-throughput methods.</p>

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</description>

<author>D C. Hess et al.</author>


</item>


<item>
<title>A missense mutation in the Capza3 gene and disruption of F-actin organization in spermatids of repro32 infertile male mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1958</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1958</guid>
<pubDate>Tue, 08 May 2012 23:31:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Males homozygous for the repro32 ENU-induced mutation produced by the Reproductive Genomics program at The Jackson Laboratory are infertile, have low epididymal sperm concentrations, and produce sperm with abnormally shaped heads    and poor motility. The purpose of the present study was to identify the mutated gene in repro32 mice and to define the structural and functional changes causing infertility and the aberrant sperm phenotype. In repro32/repro32 mice, we discovered    a failure to shed excess cytoplasm and disorganization of the middle piece of the flagellum at spermiation, resulting in the outer dense fibers being wrapped around the sperm head within a bag of cytoplasm. Using a candidate-gene approach, a    mutation was identified in the spermatid-specific "capping protein (actin filament) muscle Z-line, alpha 3" gene (Capza3). CAPZA3 protein localization was altered in spermatids concurrent with altered localization of a unique CAPZB variant    isoform and disruption of the filamentous actin (F-actin) network. These observations strongly suggest the missense mutation in Capza3 is responsible for the mutant phenotype of repro32/repro32 sperm and regulation of F-actin dynamics by a    spermatogenic cell-specific CAPZ heterodimer is essential for removal of the cytoplasm and maintenance of midpiece integrity during spermiation in the mouse.</p>

	]]>
</description>

<author>C B. Geyer et al.</author>


</item>


<item>
<title>A homozygous frameshift mutation in the mouse Flg gene facilitates enhanced percutaneous allergen priming.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1957</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1957</guid>
<pubDate>Tue, 08 May 2012 23:31:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Loss-of-function mutations in the FLG (filaggrin) gene cause the semidominant keratinizing disorder ichthyosis vulgaris and convey major genetic risk for atopic dermatitis (eczema), eczema-associated asthma and other allergic    phenotypes. Several low-frequency FLG null alleles occur in Europeans and Asians, with a cumulative frequency of approximately 9% in Europe. Here we report a 1-bp deletion mutation, 5303delA, analogous to common human FLG mutations, within the    murine Flg gene in the spontaneous mouse mutant flaky tail (ft). We demonstrate that topical application of allergen to mice homozygous for this mutation results in cutaneous inflammatory infiltrates and enhanced cutaneous allergen priming with    development of allergen-specific antibody responses. These data validate flaky tail as a useful model of filaggrin deficiency and provide experimental evidence for the hypothesis that antigen transfer through a defective epidermal barrier is a    key mechanism underlying elevated IgE sensitization and initiation of cutaneous inflammation in humans with filaggrin-related atopic disease.</p>

	]]>
</description>

<author>P G. Fallon et al.</author>


</item>


<item>
<title>Millisecond-timescale optical control of neural dynamics in the nonhuman primate brain.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1956</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1956</guid>
<pubDate>Tue, 08 May 2012 23:31:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>To understand how brain states and behaviors are generated by neural circuits, it would be useful to be able to perturb precisely the activity of specific cell types and pathways in the nonhuman primate nervous system. We used    lentivirus to target the light-activated cation channel channelrhodopsin-2 (ChR2) specifically to excitatory neurons of the macaque frontal cortex. Using a laser-coupled optical fiber in conjunction with a recording microelectrode, we showed that    activation of excitatory neurons resulted in well-timed excitatory and suppressive influences on neocortical neural networks. ChR2 was safely expressed, and could mediate optical neuromodulation, in primate neocortex over many months.  These    findings highlight a methodology for investigating the causal role of specific cell types in nonhuman primate neural computation, cognition, and behavior, and open up the possibility of a new generation of ultraprecise neurological and    psychiatric therapeutics via cell-type-specific optical neural control prosthetics.</p>

	]]>
</description>

<author>X Han et al.</author>


</item>


<item>
<title>A mouse model for Meckel syndrome type 3.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1955</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1955</guid>
<pubDate>Tue, 08 May 2012 23:30:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Meckel-Gruber syndrome type 3 (MKS3; OMIM 607361) is a severe autosomal recessive disorder characterized by bilateral polycystic kidney disease. Other malformations associated with MKS3 include cystic changes in the liver,    polydactyly, and brain abnormalities (occipital encephalocele, hydrocephalus, and Dandy Walker-type cerebellar anomalies). The disorder is hypothesized to be caused by defects in primary cilia. In humans, the underlying mutated gene, TMEM67,    encodes transmembrane protein 67, also called meckelin (OMIM 609884), which is an integral protein of the renal epithelial cell and membrane of the primary cilium. Here, we describe a spontaneous deletion of the mouse ortholog, Tmem67, which    results in polycystic kidney disease and death by 3 wk after birth.  Hydrocephalus also occurs in some mutants. We verified the mutated gene by transgenic rescue and characterized the phenotype with microcomputed tomography, histology, scanning    electron microscopy, and immunohistochemistry. This mutant provides a mouse model for MKS3 and adds to the growing set of mammalian models essential for studying the role of the primary cilium in kidney function.</p>

	]]>
</description>

<author>S A. Cook et al.</author>


</item>


<item>
<title>Biochemical and genetic evidence for a role of IGHMBP2 in the translational machinery.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1954</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1954</guid>
<pubDate>Tue, 08 May 2012 23:30:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>The human motor neuron degenerative disease spinal muscular atrophy with respiratory distress type 1 (SMARD1) is caused by loss of function mutations of immunoglobulin mu-binding protein 2 (IGHMBP2), a protein of unknown function    that contains DNA/RNA helicase and nucleic acid-binding domains. Reduced IGHMBP2 protein levels in neuromuscular degeneration (nmd) mice, the mouse model of SMARD1, lead to motor neuron degeneration. We report the biochemical characterization of    IGHMBP2 and the isolation of a modifier locus that rescues the phenotype and motor neuron degeneration of nmd mice. We find that a 166 kb BAC transgene derived from CAST/EiJ mice and containing tRNA genes and activator of basal transcription 1    (Abt1), a protein-coding gene that is required for ribosome biogenesis, contains the genetic modifier responsible for motor neuron rescue. Our biochemical investigations show that IGHMBP2 associates physically with tRNAs and in particular with    tRNA(Tyr), which are present in the modifier and with the ABT1 protein. We find that transcription factor IIIC-220 kDa (TFIIIC220), an essential factor required for tRNA transcription, and the helicases Reptin and Pontin, which function in    transcription and in ribosome biogenesis, are also part of IGHMBP2-containing complexes. Our findings strongly suggest that IGHMBP2 is a component of the translational machinery and that these components can be manipulated genetically to suppress    motor neuron degeneration.</p>

	]]>
</description>

<author>Saquer M. de Planell et al.</author>


</item>


<item>
<title>Increased bone marrow fat in anorexia nervosa.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1953</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1953</guid>
<pubDate>Tue, 08 May 2012 23:30:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>CONTEXT: Although women with anorexia nervosa (AN) have severe depletion of body fat, a paradoxical increase in bone marrow fat has been described. Recent data suggest that marrow fat measured by 1H-magnetic resonance spectroscopy    (MRS) in combination with bone mineral density (BMD) may be more valuable than either parameter alone in detecting bone weakness. OBJECTIVE: The objective of the study was to investigate the effect of AN on accumulation of marrow fat in spine and    femur using 1H-MRS and the relationship between marrow fat, BMD, and body composition in subjects with AN and normal-weight controls. DESIGN: This was a cross-sectional study. SETTING: The study was conducted at a referral center.  PATIENTS:    Patients included 10 women with AN (29.8 +/- 7.6 yr) and 10 normal-weight age-matched women (29.2 +/- 5.2 yr). INTERVENTIONS: There were no interventions. MAIN OUTCOMES MEASURE: Marrow fat content of the fourth lumbar vertebra and femur measured    by 1H-MRS. BMD of spine and hip measured by dual-energy x-ray absorptiometry. RESULTS: Subjects with AN had higher marrow fat at the fourth lumbar vertebra and femur compared with controls (P = 0.004-0.01).  There was an inverse correlation    between marrow fat of L4 and femur and BMD of the spine and hip (r = -0.56 to -0.71, P = 0.01-0.0002) and body mass index and sc adipose tissue of the thigh (r = -0.49 to -0.71, P = 0.03-0.0007). There was an inverse correlation between femur    marrow fat and sc and total abdominal adipose tissue (r = -0.53 to -0.67, P = 0.003-0.03). CONCLUSION: Women with AN have greater lumbar and femoral marrow fat than controls, and marrow fat correlates inversely with BMD. This paradoxical increase    in marrow fat at a time when sc and visceral fat are markedly reduced raises important questions about functional consequences of this process.</p>

	]]>
</description>

<author>M A. Bredella et al.</author>


</item>


<item>
<title>Failure of alpha-galactosylceramide to prevent diabetes in virus-inducible models of type 1 diabetes in the rat.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1952</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1952</guid>
<pubDate>Tue, 08 May 2012 23:30:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Alpha-galactosylceramide (alpha-GalCer) is an invariant natural killer T (iNKT) cell ligand that prevents type 1 diabetes in NOD mice. However, alpha-GalCer can activate or suppress immune responses, raising concern    about its potential use in human diabetes. MATERIALS AND METHODS: To evaluate this therapeutic issue further, BBDR and LEW.1WR1 rats were treated with Kilham rat virus (KRV) plus polyinosinic-polycytidylic acid, with or without alpha-GalCer, and    followed for onset of diabetes. RESULTS: alpha-GalCer did not prevent diabetes in inducible rat models. To investigate this discrepancy, we analyzed iNKT cell function. Splenocytes stimulated with alpha-GalCer produced similar levels of IFNgamma    in all rat strains, but less than mouse splenocytes. Rat splenocytes stimulated with alpha-GalCer preferentially produced IL-12, whereas mouse splenocytes preferentially produced IL-4. CONCLUSION: alpha-GalCer elicits species-specific cytokine    responses in iNKT cells. In humans with type 1 diabetes, differences in iNKT cell responses to stimulation with alpha-GalCer due to age, genetic variability and other factors may influence its therapeutic potential.</p>

	]]>
</description>

<author>P Chopra et al.</author>


</item>


<item>
<title>TGF-beta signaling proteins and the Protein Ontology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1951</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1951</guid>
<pubDate>Tue, 08 May 2012 23:30:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The Protein Ontology (PRO) is designed as a formal and principled Open Biomedical Ontologies (OBO) Foundry ontology for proteins. The components of PRO extend from a classification of proteins on the basis of    evolutionary relationships at the homeomorphic level to the representation of the multiple protein forms of a gene, including those resulting from alternative splicing, cleavage and/or post-translational modifications. Focusing specifically on    the TGF-beta signaling proteins, we describe the building, curation, usage and dissemination of PRO. RESULTS: PRO is manually curated on the basis of PrePRO, an automatically generated file with content derived from standard protein data sources.    Manual curation ensures that the treatment of the protein classes and the internal and external relationships conform to the PRO framework. The current release of PRO is based upon experimental data from mouse and human proteins wherein    equivalent protein forms are represented by single terms. In addition to the PRO ontology, the annotation of PRO terms is released as a separate PRO association file, which contains, for each given PRO term, an annotation from the experimentally    characterized sub-types as well as the corresponding database identifiers and sequence coordinates. The annotations are added in the form of relationship to other ontologies. Whenever possible, equivalent forms in other species are listed to    facilitate cross-species comparison. Splice and allelic variants, gene fusion products and modified protein forms are all represented as entities in the ontology. Therefore, PRO provides for the representation of protein entities and a resource    for describing the associated data. This makes PRO useful both for proteomics studies where isoforms and modified forms must be differentiated, and for studies of biological pathways, where representations need to take account of the different    ways in which the cascade of events may depend on specific protein modifications. CONCLUSION: PRO provides a framework for the formal representation of protein classes and protein forms in the OBO Foundry. It is designed to enable data retrieval    and integration and machine reasoning at the molecular level of proteins, thereby facilitating cross-species comparisons, pathway analysis, disease modeling and the generation of new hypotheses.</p>

	]]>
</description>

<author>C N. Arighi et al.</author>


</item>


<item>
<title>PhenoGO: an integrated resource for the multiscale mining of clinical and biological data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1950</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1950</guid>
<pubDate>Tue, 08 May 2012 23:30:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>The evolving complexity of genome-scale experiments has increasingly centralized the role of a highly computable, accurate, and comprehensive resource spanning multiple biological scales and viewpoints. To provide a resource to meet    this need, we have significantly extended the PhenoGO database with gene-disease specific annotations and included an additional ten species. This a computationally-derived resource is primarily intended to provide phenotypic context (cell type,    tissue, organ, and disease) for mining existing associations between gene products and GO terms specified in the Gene Ontology Databases Automated natural language processing (BioMedLEE) and computational ontology (PhenOS) methods were used to    derive these relationships from the literature, expanding the database with information from ten additional species to include over 600,000 phenotypic contexts spanning eleven species from five GO annotation databases. A comprehensive evaluation    evaluating the mappings (n = 300) found precision (positive predictive value) at 85%, and recall (sensitivity) at 76%.  Phenotypes are encoded in general purpose ontologies such as Cell Ontology, the Unified Medical Language System, and in    specialized ontologies such as the Mouse Anatomy and the Mammalian Phenotype Ontology. A web portal has also been developed, allowing for advanced filtering and querying of the database as well as download of the entire dataset    http://www.phenogo.org.</p>

	]]>
</description>

<author>L T. Sam et al.</author>


</item>


<item>
<title>Pathologic phenotyping of mutant mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1949</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1949</guid>
<pubDate>Tue, 08 May 2012 23:29:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>The easiest and cheapest way to analyze the phenotype of most knockout mice is to do a comprehensive necropsy and histopathologic examination of slides of all tissues. Once any lesion is found in a knockout mouse a vast contemporary    and traditional literature can be searched for occurrences of similar lesions in other species, including human beings. This may provide further insights into the molecular and cellular pathogenesis of the lesion. In this chapter we will focus on    the best way to turn a mouse into a set of slides which can thereafter be studied by investigators and pathologists. Some techniques suggested are not generally used in conventional histology laboratories. Most are decidedly old fashioned. They    have all been used successfully in many diverse studies of mice of all ages with all kinds of lesions.</p>

	]]>
</description>

<author>R T. Bronson</author>


</item>


<item>
<title>Jagged1 is the pathological link between Wnt and Notch pathways in colorectal cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1948</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1948</guid>
<pubDate>Tue, 08 May 2012 23:29:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Notch has been linked to beta-catenin-dependent tumorigenesis; however, the mechanisms leading to Notch activation and the contribution of the Notch pathway to colorectal cancer is not yet understood. By microarray analysis, we have    identified a group of genes downstream of Wnt/beta-catenin (down-regulated when blocking Wnt/beta-catenin) that are directly regulated by Notch (repressed by gamma-secretase inhibitors and up-regulated by active Notch1 in the absence of    beta-catenin signaling). We demonstrate that Notch is downstream of Wnt in colorectal cancer cells through beta-catenin-mediated transcriptional activation of the Notch-ligand Jagged1. Consistently, expression of activated Notch1 partially    reverts the effects of blocking Wnt/beta-catenin pathway in tumors implanted s.c. in nude mice. Crossing APC(Min/+) with Jagged1(+/Delta) mice is sufficient to significantly reduce the size of the polyps arising in the APC mutant background    indicating that Notch is an essential modulator of tumorigenesis induced by nuclear beta-catenin. We show that this mechanism is operating in human tumors from Familial Adenomatous Polyposis patients. We conclude that Notch activation,    accomplished by beta-catenin-mediated up-regulation of Jagged1, is required for tumorigenesis in the intestine. The Notch-specific genetic signature is sufficient to block differentiation and promote vasculogenesis in tumors whereas proliferation    depends on both pathways.</p>

	]]>
</description>

<author>V Rodilla et al.</author>


</item>


<item>
<title>Type 1 diabetes genes in rats: few or many?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1947</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1947</guid>
<pubDate>Tue, 08 May 2012 23:29:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E H. Leiter</author>


</item>


<item>
<title>SRp38 regulates alternative splicing and is required for Ca(2+) handling in the embryonic heart.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1946</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1946</guid>
<pubDate>Tue, 08 May 2012 23:29:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>SRp38 is an atypical SR protein splicing regulator. To define the functions of SRp38 in vivo, we generated SRp38 null mice. The majority of homozygous mutants survived only until E15.5 and displayed multiple cardiac defects.    Evaluation of gene expression profiles in the SRp38(-/-) embryonic heart revealed a defect in processing of the pre-mRNA encoding cardiac triadin, a protein that functions in regulation of Ca(2+) release from the sarcoplasmic reticulum during    excitation-contraction coupling. This defect resulted in significantly reduced levels of triadin, as well as those of the interacting protein calsequestrin 2.  Purified SRp38 was shown to bind specifically to the regulated exon and to modulate    triadin splicing in vitro. Extending these results, isolated SRp38(-/-) embryonic cardiomyocytes displayed defects in Ca(2+) handling compared with wild-type controls. Taken together, our results demonstrate that SRp38 regulates cardiac-specific    alternative splicing of triadin pre-mRNA and, reflecting this, is essential for proper Ca(2+) handling during embryonic heart development.</p>

	]]>
</description>

<author>Y Feng et al.</author>


</item>


<item>
<title>Genetic basis of HDL variation in 129/SvImJ and C57BL/6J mice: importance of testing candidate genes in targeted mutant mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1945</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1945</guid>
<pubDate>Tue, 08 May 2012 23:29:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>To evaluate the effect of genetic background on high-density lipoprotein cholesterol (HDL) levels in Soat1(-/-) mice, we backcrossed sterol O-acyltransferase 1 (Soat1)(-/-) mice, originally reported to have elevated HDL levels, to    C57BL/6 mice and constructed a congenic strain with only a small region (3.3Mb) of 129 alleles, specifically excluding the nearby apolipoprotein A-II (Apoa2) gene from 129. HDL levels in these Soat1(-/-) mice were no different from C57BL/6,    indicating that the passenger gene Apoa2 caused the previously reported elevation of HDL in these Soat1(-/-) mice. Because many knockouts are made in strain 129 and then subsequently backcrossed into C57BL/6, it is important to identify    quantitative trait loci (QTL) that differ between 129 and C57BL/6 so that one can guard against effects ascribed to a knockout but really caused by a passenger gene from 129. To provide such data, we generated 528 F(2) progeny from an intercross    of 129S1/SvImJ and C57BL/6 and measured HDL concentrations in F(2) animals first fed chow and then atherogenic diet. A genome wide scan using 508 single-nucleotide polymorphisms (SNPs) identified 19 QTL, 2 of which were male specific and 2 were    female specific. Using comparative genomics and haplotype analysis, we narrowed QTL on chromosomes 3, 5, 8, 17, and 18 to 0.5, 6.3, 2.6, 1.1, and 0.6 Mb, respectively. These data will serve as a reference for any effort to test the impact of    candidate genes on HDL using a knockout strategy.</p>

	]]>
</description>

<author>Z Su et al.</author>


</item>


<item>
<title>TRBP control of PACT-induced phosphorylation of protein kinase R is reversed by stress.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1944</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1944</guid>
<pubDate>Tue, 08 May 2012 23:29:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>The TAR RNA binding Protein, TRBP, inhibits the activity of the interferon-induced protein kinase R (PKR), whereas the PKR activator, PACT, activates its function. TRBP and PACT also bind to each other through their double-stranded    RNA binding domains (dsRBDs) and their Medipal domains, which may influence their activity on PKR. In a human immunodeficiency virus (HIV) long terminal repeat-luciferase assay, PACT unexpectedly reversed PKR-mediated inhibition of gene    expression. In a translation inhibition assay in HeLa cells, PACT lacking the 13 C-terminal amino acids (PACTDelta13), but not full-length PACT, activated PKR and enhanced interferon-mediated repression. In contrast, in the astrocytic U251MG    cells that express low TRBP levels, both proteins activate PKR, but PACTDelta13 is stronger. Immunoprecipitation assays and yeast two-hybrid assays show that TRBP and PACTDelta13 interact very weakly due to a loss of binding in the Medipal    domain. PACT-induced PKR phosphorylation was restored in Tarbp2(-/-) murine tail fibroblasts and in HEK293T or HeLa cells when TRBP expression was reduced by RNA interference. In HEK293T and HeLa cells, arsenite, peroxide, and serum    starvation-mediated stresses dissociated the TRBP-PACT interaction and increased PACT-induced PKR activation, demonstrating the relevance of this control in a physiological context. Our results demonstrate that in cells, TRBP controls PACT    activation of PKR, an activity that is reversed by stress.</p>

	]]>
</description>

<author>A Daher et al.</author>


</item>


<item>
<title>Protection from clinical peripheral sensory neuropathy in Alstrom syndrome in contrast to early-onset type 2 diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1943</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1943</guid>
<pubDate>Tue, 08 May 2012 23:28:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: Alstrom syndrome, with type 2 diabetes, and blindness could confer a high risk of foot ulceration. Clinical testing for neuropathy in Alstrom syndrome and matched young-onset type 2 diabetic subjects was therefore    undertaken.  RESEARCH DESIGN AND METHODS: Fifty-eight subjects with Alstrom syndrome (18 insulin-resistant nondiabetic and 40 diabetic; aged 8-43 years) and 30 young-onset diabetic subjects (aged 13-35 years) were studied. Neuropathy symptom    questionnaires were administered. Graded monofilament and 128-MHz tuning fork vibration perception were assessed in both feet. RESULTS: Neuropathic symptoms, loss of monofilament, and/or vibration perception were reported by 12 of the 30    young-onset type 2 diabetic subjects (6 had neuropathic ulceration) but none of the subjects with Alstrom syndrome. CONCLUSIONS: The striking preservation of protective foot sensation in Alstrom syndrome may provide a clue to the causes of    differential susceptibility to neuropathy in the wider diabetic population.</p>

	]]>
</description>

<author>R B. Paisey et al.</author>


</item>


<item>
<title>Many ribosomal protein mutations are associated with growth impairment and tumor predisposition in zebrafish.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1942</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1942</guid>
<pubDate>Tue, 08 May 2012 23:28:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have characterized 28 zebrafish lines with heterozygous mutations in ribosomal protein (rp) genes, and found that 17 of these are prone to develop zebrafish malignant peripheral nerve sheath tumors (zMPNST). Heterozygotes from    the vast majority of tumor-prone rp lines were found to be growth-impaired, though not all growth-impaired rp lines were tumor-prone. Significantly, however, the rp lines with the greatest incidence of zMPNSTs all displayed a growth impairment.     Furthermore, heterozygous cells from one tumor-prone rp line were out-competed by wild-type cells in chimeric embryos. The growth impairment resulting from heterozygosity for many rp genes suggests that a global defect in protein translation    exists in these lines, raising the possibility that a translation defect that precedes tumor development is predictive of tumorigenesis.</p>

	]]>
</description>

<author>K Lai et al.</author>


</item>


<item>
<title>PRIME importance of pathology expertise.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1941</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1941</guid>
<pubDate>Tue, 08 May 2012 23:28:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>P N. Schofield et al.</author>


</item>


<item>
<title>The aqueous humor outflow pathway of zebrafish.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1940</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1940</guid>
<pubDate>Tue, 08 May 2012 23:28:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: The structures of the ocular anterior segment responsible for aqueous humor secretion and absorption have been well characterized in mammals. However, the underlying molecular and cellular mechanisms that regulate aqueous    humor flow have remained elusive. Experimental analysis in Danio rerio, the zebrafish, is providing mechanistic insights into many cellular processes relevant to normal human physiology and disease. To facilitate studies on the molecular and    cellular mechanisms of aqueous humor dynamics using this species, the authors have characterized the anatomy of aqueous secretion and outflow in adult zebrafish eyes. METHODS: Analyses by light and transmission electron microscopy, coupled with    molecular tracers of fluid flow, were used to identify and study the sites of aqueous humor secretion and absorption in adult zebrafish eyes. RESULTS: Zebrafish eyes show aqueous humor secretion primarily from the dorsal ciliary region and    outflow through a ventral canalicular network that connects with an aqueous plexus and veins of the choroidal rete. CONCLUSIONS: Vectorial flow of zebrafish aqueous humor is in contrast to that in mammals in which secretion and absorption of    aqueous humor are circumferential around and through the iridocorneal angle. However, local anatomy and ultrastructure of the tissues and cells specialized for aqueous humor dynamics in zebrafish show conservation with that of mammals. These    observations suggest that zebrafish can serve as a useful genetic model to help understand the regulation and cellular basis of normal and abnormal aqueous humor dynamics in humans.</p>

	]]>
</description>

<author>M P. Gray et al.</author>


</item>


<item>
<title>Evolutionary origin and phylogenetic analysis of the novel oocyte-specific eukaryotic translation initiation factor 4E in Tetrapoda.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1939</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1939</guid>
<pubDate>Tue, 08 May 2012 23:28:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The transcriptionally active, growing oocyte accumulates mRNAs essential for early stages of development, the oocyte-to-embryo transition, in a stable, dormant form. Translational repression of mRNAs in eggs of various species is    conferred by interactions, either direct or via intermediate proteins, of repressive factors bound to the 3'-untranslated regions with the proteins of the eukaryotic translation initiation factor 4E (eIF4E) family bound to the 5'-cap of the    transcripts. Recently, a novel oocyte-specific eIF4E encoded by the Eif41b gene in mammals has been identified by our group. To further investigate this gene, the available cDNA libraries, as well as genome assemblies of nonmammalian vertebrates,    were surveyed. This analysis revealed that the Eif4e1b gene arose in Tetrapoda as a result of the ancestral Eif4e locus duplication. Unlike other known proteins of three subfamilies comprising eIF4E family (eIF4E1, eIF4E2, and eIF4E3), cDNA    library evidence suggests that Eif41b locus has an oocyte-restricted expression across all classes of Tetrapoda. To further understand the role of eIF4E1B during oocyte maturation, injections of antisense morpholino nucleotides in the X.    tropicalis fully-grown stage VI oocytes were performed. The resulted ablation of eIF4E1B protein led to significant acceleration of oocyte maturation after progesterone induction; morpholino-injected oocytes formed the metaphase plate 30 min    faster than the control groups. These results suggest that eIF4E1B protein acts as a repressor in translational regulation of maternal mRNAs activated during, and required for, oocyte maturation.</p>

	]]>
</description>

<author>A V. Evsikov et al.</author>


</item>


<item>
<title>Genetic mechanisms in Apc-mediated mammary tumorigenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1938</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1938</guid>
<pubDate>Tue, 08 May 2012 23:28:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many components of Wnt/beta-catenin signaling pathway also play critical roles in mammary tumor development, yet the role of the tumor suppressor gene APC (adenomatous polyposis coli) in breast oncongenesis is unclear. To better    understand the role of Apc in mammary tumorigenesis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-cre and WAP-cre transgenic mice that express Cre-recombinase in mammary    progenitor cells and lactating luminal cells, respectively. Only the K14-cre-mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological heterogeneity, suggesting the multilineage progenitor cell origin of these    tumors. These tumors harbored truncation mutation in a defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of beta-catenin signaling. Activating mutations at codons 12 and 61 of either H-Ras or    K-Ras were also found in a subset of these tumors. Expression profiles of acinar-type mammary tumors from K14-cre; Apc(CKO/+) mice showed luminal epithelial gene expression pattern, and clustering analysis demonstrated more correlation to    MMTV-neu model than to MMTV-Wnt1. In contrast, neither WAP-cre-induced Apc heterozygous nor homozygous mutations resulted in predisposition to mammary tumorigenesis, although WAP-cre-mediated Apc deficiency resulted in severe squamous metaplasia    of mammary glands.  Collectively, our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of beta-catenin signaling optimal for mammary tumor development and explain    partially the colon- but not mammary-specific tumor development in patients that carry germline mutations in APC.</p>

	]]>
</description>

<author>M Kuraguchi et al.</author>


</item>


<item>
<title>Noonan syndrome cardiac defects are caused by PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1937</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1937</guid>
<pubDate>Tue, 08 May 2012 23:28:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Noonan syndrome (NS), the most common single-gene cause of congenital heart disease, is an autosomal dominant disorder that also features proportionate short stature, facial abnormalities, and an increased risk of myeloproliferative    disease. Germline-activating mutations in PTPN11, which encodes the protein tyrosine phosphatase SHP2, cause about half of NS cases; other causative alleles include KRAS, SOS1, and RAF1 mutants. We showed previously that knock-in mice bearing the    NS mutant Ptpn11(D61G) on a mixed 129S4/SvJae X C57BL6/J background exhibit all major NS features, including a variety of cardiac defects, with variable penetrance. However, the cellular and molecular mechanisms underlying NS cardiac defects and    whether genetic background and/or the specific NS mutation contribute to the NS phenotype remained unclear. Here, using an inducible knock-in approach, we show that all cardiac defects in NS result from mutant Shp2 expression in the endocardium,    not in the myocardium or neural crest.  Furthermore, the penetrance of NS defects is affected by genetic background and the specific Ptpn11 allele. Finally, ex vivo assays and pharmacological approaches show that NS mutants cause cardiac valve    defects by increasing Erk MAPK activation, probably downstream of ErbB family receptor tyrosine kinases, extending the interval during which cardiac endocardial cells undergo endocardial-mesenchymal transformation. Our data provide a mechanistic    underpinning for the cardiac defects in this disorder.</p>

	]]>
</description>

<author>T Araki et al.</author>


</item>


<item>
<title>Kinetics of transmission, infectivity, and genome stability of two novel mouse norovirus isolates in breeding mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1936</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1936</guid>
<pubDate>Tue, 08 May 2012 23:27:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Murine noroviruses are a recently discovered group of viruses found within mouse research colonies in many animal facilities worldwide. In this study, we used 2 novel mouse norovirus (MNV) wildtype isolates to examine the kinetics    of transmission and tissue distribution in breeding units of NOD.CB17-Prkdc(scid)/J and backcrossed NOD.CB17-Prkdc(scid)/J x NOD/ShiLtJ (N1) mice. Viral shedding in feces and dissemination to tissues of infected offspring mice were monitored by    RT-PCR over a 6-wk period postpartum. Histologic sections of tissues from mice exposed to MNV were examined for lesions and their sera monitored for the presence of antibodies to MNV. Viruses shed in feces of parental and offspring mice were    compared for sequence homology of the Orf2 gene. Studies showed that the wildtype viruses MNV5 and MNV6 behaved differently in terms of the kinetics of transmission and distribution to tissues of offspring mice. For MNV5, virus transmission from    parents to offspring was not seen before 3 wk after birth, and neither isolate was transmitted between cages of infected and control mice.  Susceptibility to infection was statistically different between the 2 mouse strains used in the study.    Both immunodeficient NOD.CB17-Prkdc(scid)/J mice and NOD. CB17-Prkdc(scid)/J x NOD/ShiLtJ offspring capable of mounting an immune response shed virus in their feces throughout the 6-wk study period, but no gross or histologic lesions were present    in infected tissues. Progeny viruses isolated from the feces of infected offspring showed numerous mutations in the Orf2 gene for MNV5 but not MNV6. These results confirm previous studies demonstrating that the biology of MNV in mice varies    substantially with each virus isolate and mouse strain infected.</p>

	]]>
</description>

<author>J A. Kelmenson et al.</author>


</item>


<item>
<title>Mechanical stimulation of mesenchymal stem cell proliferation and differentiation promotes osteogenesis while preventing dietary-induced obesity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1935</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1935</guid>
<pubDate>Tue, 08 May 2012 23:27:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mesenchymal stem cells (MSCs) are defined by their ability to self-renew and differentiate into the cells that form mesodermal tissues such as bone and fat.  Low magnitude mechanical signals (LMMS) have been shown to be anabolic to    bone and have been recently reported to suppress the development of fat in normal animals fed a regular diet. Using male C57BL/6J mice, the ability of LMMS (0.2g, 90-Hz signal applied for 15 min/d, 5 d/wk) to simultaneously promote bone formation    and prevent diet-induced obesity was correlated to mechanical influences on the molecular environment of the bone marrow, as indicated by the population dynamics and lineage commitment of MSCs. Six weeks of LMMS increased the overall marrow-based    stem cell population by 37% and the number of MSCs by 46%. Concomitant with the increase in stem cell number, the differentiation potential of MSCs in the bone marrow was biased toward osteoblastic and against adipogenic differentiation, as    reflected by upregulation of the transcription factor Runx2 by 72% and downregulation of PPARgamma by 27%. The phenotypic impact of LMMS on MSC lineage determination was evident at 14 wk, where visceral adipose tissue formation was suppressed by    28%, whereas trabecular bone volume fraction in the tibia was increased by 11%. Translating this to the clinic, a 1-yr trial in young women (15-20 yr; n = 48) with osteopenia showed that LMMS increased trabecular bone in the spine and kept    visceral fat at baseline levels, whereas control subjects showed no change in BMD, yet an increase in visceral fat.  Mechanical modulation of stem cell proliferation and differentiation indicates a unique therapeutic target to aid in tissue    regeneration and repair and may represent the basis of a nonpharmacologic strategy to simultaneously prevent obesity and osteoporosis.</p>

	]]>
</description>

<author>E Capilla et al.</author>


</item>


<item>
<title>What are microarrays teaching us about sleep?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1934</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1934</guid>
<pubDate>Tue, 08 May 2012 23:27:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many fundamental questions about sleep remain unanswered. The presence of sleep across phyla suggests that it must serve a basic cellular and/or molecular function. Microarray studies, performed in several model systems, have    identified classes of genes that are sleep-state regulated. This has led to the following concepts: first, a function of sleep is to maintain synaptic homeostasis; second, sleep is a stage of macromolecule biosynthesis; third, extending    wakefulness leads to downregulation of several important metabolic pathways; and, fourth, extending wakefulness leads to endoplasmic reticulum stress. In human studies, microarrays are being applied to the identification of biomarkers for    sleepiness and for the common debilitating condition of obstructive sleep apnea.</p>

	]]>
</description>

<author>M Mackiewicz et al.</author>


</item>


<item>
<title>Oncogenic EGFR signaling cooperates with loss of tumor suppressor gene functions in gliomagenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1933</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1933</guid>
<pubDate>Tue, 08 May 2012 23:27:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Glioblastoma multiforme (GBM) is a highly lethal brain tumor for which little treatment is available. The epidermal growth factor receptor (EGFR) signaling pathway is thought to play a crucial role in GBM pathogenesis, initiating    the early stages of tumor development, sustaining tumor growth, promoting infiltration, and mediating resistance to therapy. The importance of this pathway is highlighted in the fact that EGFR is mutationally activated in over 50% of GBM tumors.    Consistent with this, we show here that concomitant activation of wild-type and/or mutant (vIII) EGFR and ablation of Ink4A/Arf and PTEN tumor suppressor gene function in the adult mouse central nervous system generates a fully penetrant,    rapid-onset high-grade malignant glioma phenotype with prominent pathological and molecular resemblance to GBM in humans. Studies of the activation of signaling events in these GBM tumor cells revealed notable differences between wild-type and    vIII EGFR-expressing cells. We show that wild-type EGF receptor signals through its canonical pathways, whereas tumors arising from expression of mutant EGFR(vIII) do not use these same pathways. Our findings provide critical insights into the    role of mutant EGFR signaling function in GBM tumor biology and set the stage for testing of targeted therapeutic agents in the preclinical models described herein.</p>

	]]>
</description>

<author>H Zhu et al.</author>


</item>


<item>
<title>Trans-regulation of mouse meiotic recombination hotspots by Rcr1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1932</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1932</guid>
<pubDate>Tue, 08 May 2012 23:27:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Meiotic recombination is required for the orderly segregation of chromosomes during meiosis and for providing genetic diversity among offspring. Among mammals, as well as yeast and higher plants, recombination preferentially occurs    at highly delimited chromosomal sites 1-2 kb long known as hotspots. Although considerable progress has been made in understanding the roles various proteins play in carrying out the molecular events of the recombination process, relatively    little is understood about the factors controlling the location and relative activity of mammalian recombination hotspots. To search for trans-acting factors controlling the positioning of recombination events, we compared the locations of    crossovers arising in an 8-Mb segment of a 100-Mb region of mouse Chromosome 1 (Chr 1) when the longer region was heterozygous C57BL/6J (B6) x CAST/EiJ (CAST) and the remainder of the genome was either similarly heterozygous or entirely    homozygous B6. The lack of CAST alleles in the remainder of the genome resulted in profound changes in hotspot activity in both females and males. Recombination activity was lost at several hotspots; new, previously undetected hotspots appeared;    and still other hotspots remained unaffected, indicating the presence of distant trans-acting gene(s) whose CAST allele(s) activate or suppress the activity of specific hotspots. Testing the activity of three activated hotspots in sperm samples    from individual male progeny of two genetic crosses, we identified a single trans-acting regulator of hotspot activity, designated Rcr1, that is located in a 5.30-Mb interval (11.74-17.04 Mb) on Chr 17. Using an Escherichia coli cloning assay to    characterize the molecular products of recombination at two of these hotspots, we found that Rcr1 controls the appearance of both crossover and noncrossover gene conversion events, indicating that it likely controls the sites of the double-strand    DNA breaks that initiate the recombination process.</p>

	]]>
</description>

<author>E D. Parvanov et al.</author>


</item>


<item>
<title>Bone, fat, and body composition: evolving concepts in the pathogenesis of osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1931</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1931</guid>
<pubDate>Tue, 08 May 2012 23:27:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Disorders of body composition, including obesity and osteoporosis, have reached record proportions. Coincidentally, our understanding of the mechanisms controlling body mass also has greatly improved. Shared regulation at the    hypothalamus and the bone marrow highlight major bone-fat interactions. The hypothalamus modulates fat and bone via the sympathetic nervous system by regulating appetite, insulin sensitivity, energy use, and skeletal remodeling. In the bone    marrow, fat and bone cells arise from the same stem cells. Insights from disorders such as anorexia nervosa provide a new rationale for examining the mechanisms that link bone to fat. This article explores these relationships in the context of a    new paradigm with implications for obesity and osteoporosis.</p>

	]]>
</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title>Strain-specific effects of rosiglitazone on bone mass, body composition, and serum insulin-like growth factor-I.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1930</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1930</guid>
<pubDate>Tue, 08 May 2012 23:26:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Activation of peroxisome proliferator activated receptor-gamma (PPARG) is required for the differentiation of marrow mesenchymal stem cell into adipocytes and is associated with the development of age-related marrow adiposity in    mice.  Thiazolidinediones are agonists for PPARG and have a heterogeneous effect on bone mineral density (BMD). We postulated that genetic determinants influence the skeletal response to thiazolidinediones. We examined the effects of    rosiglitazone (3 mg/kg . d for 8 wk) on BMD, body composition, and serum IGF-I in adult female mice from four inbred strains. C3H/HeJ mice showed the most significant response to treatment, exhibiting decreased femoral and vertebral BMD, reduced    distal femoral bone volume fraction and a decrease in serum IGF-I. In DBA/2J, there were no changes in femoral BMD or bone volume fraction, but there was a decrease in vertebral BMD. C57BL/6J mice showed increases in marrow adiposity, without    associated changes in trabecular bone volume; the skeletal effects from rosiglitazone in A/J mice were minimal. No association between trabecular bone volume and marrow adiposity was found. The effect of rosiglitazone on gene expression in the    femur was then examined in the C3H/HeJ and C57BL/6J strains by microarray. Increased gene expression was observed in the PPARG signaling pathway and fatty acid metabolism in both C3H/HeJ and C57BL/6J, but a significant down-regulation of genes    associated with cell cycle was noted only in the C3H/HeJ strain. The divergent skeletal responses to rosiglitazone in this study suggest the existence of a strong genetic background effect.</p>

	]]>
</description>

<author>Bicknell C. Ackert et al.</author>


</item>


<item>
<title>Mouse oocyte control of granulosa cell development and function: paracrine regulation of cumulus cell metabolism.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1929</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1929</guid>
<pubDate>Tue, 08 May 2012 23:26:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bidirectional communication between oocytes and the companion granulosa cells is essential for the development and functions of both compartments. Oocytes are deficient in their ability to transport certain amino acids and in    carrying out glycolysis and cholesterol biosynthesis. Cumulus cells must provide them with the specific amino acids and the products in these metabolic pathways. Oocytes control metabolic activities in cumulus cells by promoting the expression of    genes in cumulus cells encoding specific amino acid transporters and enzymes essential for the oocyte-deficient metabolic processes. Hence oocytes outsource metabolic functions to cumulus cells to compensate for oocyte metabolic deficiencies.    Oocyte control of granulosa cell metabolism may also participate in regulating the rate of follicular development in coordination with endocrine, paracrine, and autocrine signals. Oocytes influence granulosa cell development mainly by secretion    of paracrine factors, although juxtacrine signals probably also participate. Key oocyte-derived paracrine factors include growth differentiation factor 9, bone morphogenetic protein 15, and fibroblast growth factor 8B.</p>

	]]>
</description>

<author>Y Q. Su et al.</author>


</item>


<item>
<title>Notch signalling in the paraxial mesoderm is most sensitive to reduced Pofut1 levels during early mouse development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1928</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1928</guid>
<pubDate>Tue, 08 May 2012 23:26:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The evolutionarily conserved Notch signalling pathway regulates multiple developmental processes in a wide variety of organisms. One critical posttranslational modification of Notch for its function in vivo is the    addition of O-linked fucose residues by protein O-fucosyltransferase 1 (POFUT1). In addition, POFUT1 acts as a chaperone and is required for Notch trafficking. Mouse embryos lacking POFUT1 function die with a phenotype indicative of global    inactivation of Notch signalling. O-linked fucose residues on Notch can serve as substrates for further sugar modification by Fringe (FNG) proteins. Notch modification by Fringe differently affects the ability of ligands to activate Notch    receptors in a context-dependent manner indicating a complex modulation of Notch activity by differential glycosylation. Whether the context-dependent effects of Notch receptor glycosylation by FNG reflect different requirements of distinct    developmental processes for O-fucosylation by POFUT1 is unclear.  RESULTS: We have identified and characterized a spontaneous mutation in the mouse Pofut1 gene, referred to as "compact axial skeleton" (cax). Cax carries an insertion of an    intracisternal A particle retrotransposon into the fourth intron of the Pofut1 gene and represents a hypomorphic Pofut1 allele that reduces transcription and leads to reduced Notch signalling. Cax mutant embryos have somites of variable size,    showed partly abnormal Lfng expression and, consistently defective anterior-posterior somite patterning and axial skeleton development but had virtually no defects in several other Notch-regulated early developmental processes outside the    paraxial mesoderm that we analyzed.  CONCLUSION: Notch-dependent processes apparently differ with respect to their requirement for levels of POFUT1. Normal Lfng expression and anterior-posterior somite patterning is highly sensitive to reduced    POFUT1 levels in early mammalian embryos, whereas other early Notch-dependent processes such as establishment of left-right asymmetry or neurogenesis are not. Thus, it appears that in the presomitic mesoderm (PSM) Notch signalling is particularly    sensitive to POFUT1 levels. Reduced POFUT1 levels might affect Notch trafficking or overall O-fucosylation. Alternatively, reduced O-fucosylation might preferentially affect sites that are substrates for LFNG and thus important for somite    formation and patterning.</p>

	]]>
</description>

<author>Gossler K. Schuster et al.</author>


</item>


<item>
<title>Serotonin rising--the bone, brain, bowel connection.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1927</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1927</guid>
<pubDate>Tue, 08 May 2012 23:26:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title>Questioning the accuracy of a recent review of osteoporosis medications.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1926</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1926</guid>
<pubDate>Tue, 08 May 2012 23:26:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>L N. Kuhl et al.</author>


</item>


<item>
<title>Idd loci synergize to prolong islet allograft survival induced by costimulation blockade in NOD mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1925</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1925</guid>
<pubDate>Tue, 08 May 2012 23:26:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: NOD mice model human type 1 diabetes and are used to investigate tolerance induction protocols for islet transplantation in a setting of autoimmunity. However, costimulation blockade-based tolerance protocols have failed    in prolonging islet allograft survival in NOD mice. RESEARCH DESIGN AND METHODS: To investigate the underlying mechanisms, we studied the ability of costimulation blockade to prolong islet allograft survival in congenic NOD mice bearing    insulin-dependent diabetes (Idd) loci that reduce the frequency of diabetes. RESULTS: The frequency of diabetes is reduced in NOD.B6 Idd3 mice and is virtually absent in NOD.B6/B10 Idd3 Idd5 mice. Islet allograft survival in NOD.B6 Idd3 mice    treated with costimulation blockade is prolonged compared with NOD mice, and in NOD.B6/B10 Idd3 Idd5, mice islet allograft survival is similar to that achieved in C57BL/6 mice. Conversely, some Idd loci were not beneficial for the induction of    transplantation tolerance. Alloreactive CD8 T-cell depletion in (NOD x CBA)F1 mice treated with costimulation blockade was impaired compared with similarly treated (C57BL/6.H2(g7) x CBA)F1 mice. Injection of exogenous interleukin (IL)-2 into NOD    mice treated with costimulation prolonged islet allograft survival. NOD.B6 Idd3 mice treated with costimulation blockade deleted alloreactive CD8 T-cells and exhibited prolonged islet allograft survival.  CONCLUSIONS: Il2 is the Idd3 diabetes    susceptibility gene and can influence the outcome of T-cell deletion and islet allograft survival in mice treated with costimulation blockade. These data suggest that Idd loci can facilitate induction of transplantation tolerance by costimulation    blockade and that IL-2/Idd3 is a critical component in this process.</p>

	]]>
</description>

<author>J Mangada et al.</author>


</item>


<item>
<title>Age, experience and genetic background influence treadmill walking in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1924</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1924</guid>
<pubDate>Tue, 08 May 2012 23:26:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>The use of a treadmill to gather data for gait analysis in mice is a convenient, sensitive method to evaluate motor performance. However, evidence from several species, including mice, shows that treadmill locomotion is a novel task    that is not equivalent to over ground locomotion and that may be particularly sensitive to the test environment and protocol. We investigated the effects of age, genetic background and repeated trials on treadmill walking in mice and show that    these factors are important considerations in the interpretation of gait data.  Specifically we report that as C57BL/6J (B6) mice age, the animals use progressively longer, less frequent strides to maintain the same walking speed.  The increase    is most rapid between 1 and 6 months of age and is explained, in part, by changes in size and weight. We also extended previous findings showing that repeat trials cause mice to modify their treadmill gait pattern. In a second trial B6 mice    consistently walk with a shorter swing phase and greater duty factor. Also, with the shortest retest interval (3 min) mice use shorter more frequent steps but the response varies with the number and timing of trials.  Finally, we compared the    gait pattern of an additional seven inbred strains of mice and found significant variation in the length and frequency of strides used to maintain the same walking speed. The combined results offer the bases for further mechanistic studies and    can be used to guide optimal experimental design.</p>

	]]>
</description>

<author>C M. Wooley et al.</author>


</item>


<item>
<title>Surgical oocyte retrieval (SOR): a method for collecting mature mouse oocytes without euthanasia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1923</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1923</guid>
<pubDate>Tue, 08 May 2012 23:25:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>A novel surgical method for collecting oocytes from unique and irreplaceable mice is described. This method, surgical oocyte retrieval (SOR), facilitates the collection of ovulated oocytes, does not require euthanasia, and preserves    reproductive potential. The surgery involves a small incision in the ampulla region of the oviduct, through which the cumulus oocyte mass is removed with a gel-loading pipette. The incision then is closed by using a tissue adhesive, which is    required to ensure healing of the incision and containment of any oocytes ovulated after SOR. Two anesthetics, isoflurane and tribromoethanol, were compared for oocyte toxicity during SOR. More dead oocytes were recovered when tribromoethanol was    used than when isoflurane was used. Combining SOR and traditional oocyte collection methods yielded more oocytes per BALB/cByJ than did traditional methods alone (41 versus 28 oocytes, respectively). Oocytes collected by using SOR were fertilized    and subsequent embryos developed to term comparable to controls. This technique provides an alternative method for oocyte collection and will be valuable for maximizing the number of oocytes from irreplaceable mice.</p>

	]]>
</description>

<author>S L. Byers et al.</author>


</item>


<item>
<title>Ott1 (Rbm15) is essential for placental vascular branching morphogenesis and embryonic development of the heart and spleen.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1922</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1922</guid>
<pubDate>Tue, 08 May 2012 23:25:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The infant leukemia-associated gene Ott1 (Rbm15) has broad regulatory effects within murine hematopoiesis. However, germ line Ott1 deletion results in fetal demise prior to embryonic day 10.5, indicating additional developmental    requirements for Ott1. The spen gene family, to which Ott1 belongs, has a transcriptional activation/repression domain and RNA recognition motifs and has a significant role in the development of the head and thorax in Drosophila melanogaster.    Early Ott1-deficient embryos show growth retardation and incomplete closure of the notochord. Further analysis demonstrated placental defects in the spongiotrophoblast and syncytiotrophoblast layers, resulting in an arrest of vascular branching    morphogenesis. The rescue of the placental defect using a conditional allele with a trophoblast-sparing cre transgene allowed embryos to form a normal placenta and survive gestation. This outcome showed that the process of vascular branching    morphogenesis in Ott1-deficient animals was regulated by the trophoblast compartment rather than the fetal vasculature. Mice surviving to term manifested hyposplenia and abnormal cardiac development.  Analysis of global gene expression of    Ott1-deficient embryonic hearts showed an enrichment of hypoxia-related genes and a significant alteration of several candidate genes critical for cardiac development. Thus, Ott1-dependent pathways, in addition to being implicated in    leukemogenesis, may also be important for the pathogenesis of placental insufficiency and cardiac malformations.</p>

	]]>
</description>

<author>G D. Raffel et al.</author>


</item>


<item>
<title>Inhibition of pituitary tumors in Rb mutant chimeras through E2f4 loss reveals a key suppressive role for the pRB/E2F pathway in urothelium and ganglionic carcinogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1921</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1921</guid>
<pubDate>Tue, 08 May 2012 23:25:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The retinoblastoma protein pRB suppresses tumorigenesis largely through regulation of the E2F transcription factors. E2F4, the most abundant E2F protein, is thought to act in cooperation with pRB to restrain cell proliferation. In    this study, we analyse how loss of E2f4 affects the tumorigenicity of pRB-deficient tissues. As Rb(-/-);E2f4(-/-) germline mice die in utero, we generated Rb(-/-);E2f4(-/-) chimeric animals to allow examination of adult tumor phenotypes. We found    that loss of E2f4 had a differential effect on known Rb-associated neuroendocrine tumors. It did not affect thyroid and adrenal glands tumors but partially suppressed lung neuroendocrine hyperplasia. The most striking effect was in the pituitary    where E2F4 loss delayed the development, and reduced the incidence, of Rb mutant tumors. This tumor suppression increased the longevity of the Rb(-/-);E2f4(-/-) chimeric animals allowing us to identify novel tumor types. We observed ganglionic    neuroendocrine neoplasms, lesions not associated earlier with mutation of either Rb or E2f4. Moreover, a subset of the Rb(-/-);E2f4(-/-) chimeras developed either low- or high-grade carcinomas in the urothelium transitional epithelium supporting    a key role for Rb in bladder cancer.</p>

	]]>
</description>

<author>T Parisi et al.</author>


</item>


<item>
<title>MyD88 intrinsically regulates CD4 T-cell responses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1920</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1920</guid>
<pubDate>Tue, 08 May 2012 23:25:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Myeloid differentiation factor 88 (MyD88) is an essential adaptor protein in the Toll-like receptor-mediated innate signaling pathway, as well as in interleukin-1 receptor (IL-1R) and IL-18R signaling. The importance of MyD88 in the    regulation of innate immunity to microbial pathogens has been well demonstrated. However, its role in regulating acquired immunity to viral pathogens and neuropathogenesis is not entirely clear. In the present study, we examine the role of MyD88    in the CD4(+) T-cell response following lymphocytic choriomeningitis virus (LCMV) infection. We demonstrate that wild-type (WT) mice developed a CD4(+) T-cell-mediated wasting disease after intracranial infection with LCMV. In contrast, MyD88    knockout (KO) mice did not develop wasting disease in response to the same infection. This effect was not the result of MyD88 regulation of IL-1 or IL-18 responses since IL-1R1 KO and IL-18R KO mice were not protected from weight loss. In the    absence of MyD88, naive CD4(+) T cells failed to differentiate to LCMV-specific CD4 T cells. We demonstrated that MyD88 KO antigen-presenting cells are capable of activating WT CD4(+) T cells. Importantly, when MyD88 KO CD4(+) T cells were    reconstituted with an MyD88-expressing lentivirus, the rescued CD4(+) T cells were able to respond to LCMV infection and support IgG2a antibody production. Overall, these studies reveal a previously unknown role of MyD88-dependent signaling in    CD4(+) T cells in the regulation of the virus-specific CD4(+) T-cell response and in viral infection-induced immunopathology in the central nervous system.</p>

	]]>
</description>

<author>S Zhou et al.</author>


</item>


<item>
<title>HER2YVMA drives rapid development of adenosquamous lung tumors in mice that are sensitive to BIBW2992 and rapamycin combination therapy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1919</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1919</guid>
<pubDate>Tue, 08 May 2012 23:25:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the HER2 kinase domain have been identified in human clinical lung cancer specimens. Here we demonstrate that inducible expression of the most common HER2 mutant (HER2(YVMA)) in mouse lung epithelium causes invasive    adenosquamous carcinomas restricted to proximal and distal bronchioles.  Continuous expression of HER2(YVMA) is essential for tumor maintenance, suggesting a key role for HER2 in lung adenosquamous tumorigenesis. Preclinical studies assessing the    in vivo effect of erlotinib, trastuzumab, BIBW2992, and/or rapamycin on HER2(YVMA) transgenic mice or H1781 xenografts with documented tumor burden revealed that the combination of BIBW2992 and rapamycin is the most effective treatment paradigm    causing significant tumor shrinkage.  Immunohistochemical analysis of lung tumors treated with BIBW2992 and rapamycin combination revealed decreased phosphorylation levels for proteins in both upstream and downstream arms of MAPK and Akt/mTOR    signaling axes, indicating inhibition of these pathways. Based on these findings, clinical testing of the BIBW2992/rapamycin combination in non-small cell lung cancer patients with tumors expressing HER2 mutations is warranted.</p>

	]]>
</description>

<author>S A. Perera et al.</author>


</item>


<item>
<title>O6-methylguanine-induced cell death involves exonuclease 1 as well as DNA mismatch recognition in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1918</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1918</guid>
<pubDate>Tue, 08 May 2012 23:25:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alkylation-induced O(6)-methylguanine (O(6)MeG) DNA lesions can be mutagenic or cytotoxic if unrepaired by the O(6)MeG-DNA methyltransferase (Mgmt) protein.  O(6)MeG pairs with T during DNA replication, and if the O(6)MeG:T mismatch    persists, a G:C to A:T transition mutation is fixed at the next replication cycle. O(6)MeG:T mismatch detection by MutSalpha and MutLalpha leads to apoptotic cell death, but the mechanism by which this occurs has been elusive. To explore how    mismatch repair mediates O(6)MeG-dependent apoptosis, we used an Mgmt-null mouse model combined with either the Msh6-null mutant (defective in mismatch recognition) or the Exo1-null mutant (impaired in the excision step of mismatch repair). Mouse    embryonic fibroblasts and bone marrow cells derived from Mgmt-null mice were much more alkylation-sensitive than wild type, as expected. However, ablation of either Msh6 or Exo1 function rendered these Mgmt-null cells just as resistant to    alkylation-induced cytotoxicity as wild-type cells. Rapidly proliferating tissues in Mgmt-null mice (bone marrow, thymus, and spleen) are extremely sensitive to apoptosis induced by O(6)MeG-producing agents. Here, we show that ablation of either    Msh6 or Exo1 function in the Mgmt-null mouse renders these rapidly proliferating tissues alkylation-resistant. However, whereas the Msh6 defect confers total alkylation resistance, the Exo1 defect leads to a variable tissue-specific alkylation    resistance phenotype. Our results indicate that Exo1 plays an important role in the induction of apoptosis by unrepaired O(6)MeGs.</p>

	]]>
</description>

<author>J Klapacz et al.</author>


</item>


<item>
<title>Farp2 and Stk25 are candidate genes for the HDL cholesterol locus on mouse chromosome 1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1917</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1917</guid>
<pubDate>Tue, 08 May 2012 23:25:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: To identify the gene responsible for the quantitative trait locus (QTL) Hdlq14, a high-density lipoprotein cholesterol (HDL) QTL previously identified in a C57BL/6Jx129S1/SvImJ cross. METHODS AND RESULTS: Hdlq14 was first    confirmed as an independent QTL by detecting it in an intercross between NZB/B1NJ and NZW/LacJ, 2 strains that had identical genotypes at nearby QTL genes on chromosome 1. Using the bioinformatics tools of combined cross data and haplotype    analysis, we narrowed this QTL from a 45-Mb 225-gene region to 2 genes, Farp2 and Stk25. Sequencing and expression studies showed that Farp2 had an amino acid polymorphism in an important plekstrin domain and that Stk25 had a significant    expression difference between the parental strains. These 2 genes are immediately adjacent to each other and share the same haplotype over 45 inbred strains. The haplotype was associated with a significant difference in HDL levels among these    strains. CONCLUSIONS: We confirmed Hdlq14 as a separate independent QTL for HDL and narrowed the region to 2 genes, Farp2 and Stk25, with considerable evidence for both. Additional studies are needed to choose between these 2 genes or to show    that both are important in determining HDL levels.</p>

	]]>
</description>

<author>Z Su et al.</author>


</item>


<item>
<title>PPARgamma2 nuclear receptor controls multiple regulatory pathways of osteoblast differentiation from marrow mesenchymal stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1916</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1916</guid>
<pubDate>Tue, 08 May 2012 23:24:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rosiglitazone (Rosi), a member of the thiazolidinedione class of drugs used to treat type 2 diabetes, activates the adipocyte-specific transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma). This    activation causes bone loss in animals and humans, at least in part due to suppression of osteoblast differentiation from marrow mesenchymal stem cells (MSC). In order to identify mechanisms by which PPARgamma2 suppresses osteoblastogenesis and    promotes adipogenesis in MSC, we have analyzed the PPARgamma2 transcriptome in response to Rosi. A total of 4,252 transcriptional changes resulted when Rosi (1 microM) was applied to the U-33 marrow stromal cell line stably transfected with    PPARgamma2 (U-33/gamma2) as compared to non-induced U-33/gamma2 cells.  Differences between U-33/gamma2 and U-33 cells stably transfected with empty vector (U-33/c) comprised 7,928 transcriptional changes, independent of Rosi.  Cell type-, time-    and treatment-specific gene clustering uncovered distinct patterns of PPARgamma2 transcriptional control of MSC lineage commitment. The earliest changes accompanying Rosi activation of PPARgamma2 included effects on Wnt, TGFbeta/BMP and G-protein    signaling activities, as well as sustained induction of adipocyte-specific gene expression and lipid metabolism. While suppression of osteoblast phenotype is initiated by a diminished expression of osteoblast-specific signaling pathways,    induction of the adipocyte phenotype is initiated by adipocyte-specific transcriptional regulators. This indicates that distinct mechanisms govern the repression of osteogenesis and the stimulation of adipogenesis. The co-expression patterns    found here indicate that PPARgamma2 has a dominant role in controlling osteoblast differentiation and suggests numerous gene-gene interactions that could lead to the identification of a "master" regulatory scheme directing this    process.</p>

	]]>
</description>

<author>K R. Shockley et al.</author>


</item>


<item>
<title>New mouse models for recessive retinitis pigmentosa caused by mutations in the Pde6a gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1915</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1915</guid>
<pubDate>Tue, 08 May 2012 23:24:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>The heterotetrameric phosphodiesterase (PDE) 6 complex, made up of alpha, beta and two gamma subunits, regulates intracellular cGMP levels by hydrolyzing cGMP in response to light activation of G protein coupled receptors in cones    and rods, making it an essential component of the visual phototransduction cascade [Zhang, X. and Cote, R.H. (2005) cGMP signaling in vertebrate retinal photoreceptor cells. Front. Biosci., 10, 1191-1204.]. Using a genetic positional candidate    cloning strategy, we have identified missense mutations within the catalytic domain of the Pde6a gene in two mouse models from an ethyl nitrosourea chemical mutagenesis screen. In these first small rodent models of PDE6A, significantly different    biochemical outcomes and rates of degeneration of murine photoreceptor cells were observed, indicating allelic variation and previously unrecognized structure-function relationships. In addition, these new models reveal that the mutations not    only affect the function of the PDE6A protein itself, but also the level of PDE6B within the retina. Finally, we show that the variation of the disease phenotype by background modifier genes may be dependent upon the particular disease allele    present.</p>

	]]>
</description>

<author>K Sakamoto et al.</author>


</item>


<item>
<title>The deacetylase HDAC4 controls myocyte enhancing factor-2-dependent structural gene expression in response to neural activity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1914</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1914</guid>
<pubDate>Tue, 08 May 2012 23:24:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Histone deacetylase 4 (HDAC4) binds and inhibits activation of the critical muscle transcription factor myocyte enhancer factor-2 (MEF2). However, the physiological significance of the HDAC4-MEF2 complex in skeletal muscle has not    been established. Here we show that in skeletal muscle, HDAC4 is a critical modulator of MEF2-dependent structural and contractile gene expression in response to neural activity. We present evidence that loss of neural input leads to concomitant    nuclear accumulation of HDAC4 and transcriptional reduction of MEF2-regulated gene expression. Cell-based assays show that HDAC4 represses structural gene expression via direct binding to AT-rich MEF2 response elements.  Notably, using both    surgical denervation and the neuromuscular disease amyotrophic lateral sclerosis (ALS) model, we found that elevated levels of HDAC4 are required for efficient repression of MEF2-dependent structural gene expression, indicating a link between the    pathological induction of HDAC4 and subsequent MEF2 target gene suppression. Supporting this supposition, we show that ectopic expression of HDAC4 in muscle fibers is sufficient to induce muscle damage in mice. Our study identifies HDAC4 as an    activity-dependent regulator of MEF2 function and suggests that activation of HDAC4 in response to chronically reduced neural activity suppresses MEF2-dependent gene expression and contributes to progressive muscle dysfunction observed in    neuromuscular diseases.</p>

	]]>
</description>

<author>T J. Cohen et al.</author>


</item>


<item>
<title>Deletion of the G protein-coupled receptor 30 impairs glucose tolerance, reduces bone growth, increases blood pressure, and eliminates estradiol-stimulated insulin release in female mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1913</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1913</guid>
<pubDate>Tue, 08 May 2012 23:24:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>In vitro studies suggest that the G protein-coupled receptor (GPR) 30 is a functional estrogen receptor. However, the physiological role of GPR30 in vivo is unknown, and it remains to be determined whether GPR30 is an estrogen    receptor also in vivo. To this end, we studied the effects of disrupting the GPR30 gene in female and male mice. Female GPR30((-/-)) mice had hyperglycemia and impaired glucose tolerance, reduced body growth, increased blood pressure, and reduced    serum IGF-I levels. The reduced growth correlated with a proportional decrease in skeletal development. The elevated blood pressure was associated with an increased vascular resistance manifested as an increased media to lumen ratio of the    resistance arteries. The hyperglycemia and impaired glucose tolerance in vivo were associated with decreased insulin expression and release in vivo and in vitro in isolated pancreatic islets. GPR30 is expressed in islets, and GPR30 deletion    abolished estradiol-stimulated insulin release both in vivo in ovariectomized adult mice and in vitro in isolated islets. Our findings show that GPR30 is important for several metabolic functions in female mice, including estradiol-stimulated    insulin release.</p>

	]]>
</description>

<author>U E. Martensson et al.</author>


</item>


<item>
<title>Genetic factors contributing to obesity and body weight can act through mechanisms affecting muscle weight, fat weight, or both.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1912</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1912</guid>
<pubDate>Tue, 08 May 2012 23:24:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic loci for body weight and subphenotypes such as fat weight have been mapped repeatedly. However, the distinct effects of different loci and physiological interactions among different traits are often not accounted for in    mapping studies. Here we used the method of structural equation modeling to identify the specific relationships between genetic loci and different phenotypes influencing body weight. Using this technique, we were able to distinguish genetic loci    that affect adiposity from those that affect muscle growth. We examined the high body weight-selected mouse lines NMRI8 and DU6i and the intercross populations NMRI8 x DBA/2 and DU6i x DBA/2. Structural models help us understand whether genetic    factors affect lean mass and fat mass pleiotropically or nonpleiotropically. Sex has direct effects on both fat and muscle weight but also influences fat weight indirectly via muscle weight. Three genetic loci identified in these two crosses    showed exclusive effects on fat deposition, and five loci contributed exclusively to muscle weight. Two additional loci showed pleiotropic effects on fat and muscle weight, with one locus acting in both crosses. Fat weight and muscle weight were    influenced by epistatic effects. We provide evidence that significant fat loci in strains selected for body weight contribute to fat weight both directly and indirectly via the influence on lean weight. These results shed new light on the action    of genes in quantitative trait locus regions potentially influencing muscle and fat mass and thus controlling body weight as a composite trait.</p>

	]]>
</description>

<author>G A. Brockmann et al.</author>


</item>


<item>
<title>Aag-initiated base excision repair drives alkylation-induced retinal degeneration in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1911</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1911</guid>
<pubDate>Tue, 08 May 2012 23:24:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Vision loss affects >3 million Americans and many more people worldwide. Although predisposing genes have been identified their link to known environmental factors is unclear. In wild-type animals DNA alkylating agents induce    photoreceptor apoptosis and severe retinal degeneration. Alkylation-induced retinal degeneration is totally suppressed in the absence of the DNA repair protein alkyladenine DNA glycosylase (Aag) in both differentiating and postmitotic retinas.    Moreover, transgenic expression of Aag activity restores the alkylation sensitivity of photoreceptors in Aag null animals. Aag heterozygotes display an intermediate level of retinal degeneration, demonstrating haploinsufficiency and underscoring    that Aag expression confers a dominant retinal degeneration phenotype.</p>

	]]>
</description>

<author>L B. Meira et al.</author>


</item>


<item>
<title>A critical role for IL-21 receptor signaling in the pathogenesis of systemic lupus erythematosus in BXSB-Yaa mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1910</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1910</guid>
<pubDate>Tue, 08 May 2012 23:23:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Interleukin 21 (IL-21) is a pleiotropic cytokine produced by CD4 T cells that affects the differentiation and function of T, B, and NK cells by binding to a receptor consisting of the common cytokine receptor gamma chain and the    IL-21 receptor (IL-21R). IL-21, a product associated with IL-17-producing CD4 T cells (T(H)17) and follicular CD4 T helper cells (T(FH)), has been implicated in autoimmune disorders including the severe systemic lupus erythematosus (SLE)-like    disease characteristic of BXSB-Yaa mice. To determine whether IL-21 plays a significant role in this disease, we compared IL-21R-deficient and -competent BXSB-Yaa mice for multiple parameters of SLE. The deficient mice showed none of the    abnormalities characteristic of SLE in IL-21R-competent Yaa mice, including hypergammaglobulinemia, autoantibody production, reduced frequencies of marginal zone B cells and monocytosis, renal disease, and premature morbidity. IL-21 production    associated with this autoimmune disease was not a product of T(H)17 cells and was not limited to conventional CXCR5(+) T(FH) but instead was produced broadly by ICOS(+) CD4(+) splenic T cells. IL-21 arising from an abnormal population of CD4 T    cells is thus central to the development of this lethal disease, and, more generally, could play an important role in human SLE and related autoimmune disorders.</p>

	]]>
</description>

<author>J A. Bubier et al.</author>


</item>


<item>
<title>Breaking into bone biology: serotonin&apos;s secrets.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1909</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1909</guid>
<pubDate>Tue, 08 May 2012 23:23:49 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title>The Mouse Genome Database genotypes::phenotypes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1908</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1908</guid>
<pubDate>Tue, 08 May 2012 23:23:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Database (MGD, http://www.informatics.jax.org/), integrates genetic, genomic and phenotypic information about the laboratory mouse, a primary animal model for studying human biology and disease. Information in MGD    is obtained from diverse sources, including the scientific literature and external databases, such as EntrezGene, UniProt and GenBank. In addition to its extensive collection of phenotypic allele information for mouse genes that is curated from    the published biomedical literature and researcher submission, MGI includes a comprehensive representation of mouse genes including sequence, functional (GO) and comparative information. MGD provides a data mining platform that enables the    development of translational research hypotheses based on comparative genotype, phenotype and functional analyses. MGI can be accessed by a variety of methods including web-based search forms, a genome sequence browser and downloadable database    reports. Programmatic access is available using web services. Recent improvements in MGD described here include the unified mouse gene catalog for NCBI Build 37 of the reference genome assembly, and improved representation of mouse mutants and    phenotypes.</p>

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</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title>Mouse phenome database.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1907</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1907</guid>
<pubDate>Tue, 08 May 2012 23:23:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Phenome Database (MPD; http://www.jax.org/phenome) is an open source, web-based repository of phenotypic and genotypic data on commonly used and genetically diverse inbred strains of mice and their derivatives. MPD is also    a facility for query, analysis and in silico hypothesis testing. Currently MPD contains about 1400 phenotypic measurements contributed by research teams worldwide, including phenotypes relevant to human health such as cancer susceptibility,    aging, obesity, susceptibility to infectious diseases, atherosclerosis, blood disorders and neurosensory disorders. Electronic access to centralized strain data enables investigators to select optimal strains for many systems-based research    applications, including physiological studies, drug and toxicology testing, modeling disease processes and complex trait analysis. The ability to select strains for specific research applications by accessing existing phenotype data can bypass    the need to (re)characterize strains, precluding major investments of time and resources. This functionality, in turn, accelerates research and leverages existing community resources. Since our last NAR reporting in 2007, MPD has added more    community-contributed data covering more phenotypic domains and implemented several new tools and features, including a new interactive Tool Demo available through the MPD homepage (quick link:    http://phenome.jax.org/phenome/trytools).</p>

	]]>
</description>

<author>S C. Grubb et al.</author>


</item>


<item>
<title>The future of mouse genetics in osteoporosis research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1906</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1906</guid>
<pubDate>Tue, 08 May 2012 23:23:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bicknell C. Ackert</author>


</item>


<item>
<title>A critical window for experience-dependent plasticity at whisker sensory relay synapse in the thalamus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1905</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1905</guid>
<pubDate>Tue, 08 May 2012 23:23:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study investigated the role of sensory experience in the refinement of whisker sensory relay synapses in the ventral posterior medial nucleus (VPm) of the murine thalamus. Sensory deprivation was done by whisker plucking, and    synaptic connectivity was determined by whole-cell patch-clamp recording in acute slices. Sensory deprivation started at P12-P13, but not at P16, disrupted the elimination of VPm relay synapses. The majority of deprived neurons received multiple    relay inputs, whereas the majority of nondeprived neurons received a single relay input. Sensory deprivation started a few days earlier at P10, however, had no effect on synapse elimination. The disruption of synapse elimination was associated    with a delay in synapse maturation. The AMPA/NMDA ratio of EPSC was significantly smaller in deprived neurons. On the other hand, deprivation had no effect on the peak amplitude or decay time constant of the NMDA component, or the I-V    relationship of the AMPA component, nor does it affect the paired-pulse ratio of EPSCs. The reduction in the AMPA/NMDA ratio was already evident within 24 h of whisker plucking, and the effect is associated with a reduction in the amplitude of    quantal AMPA events. Thus, P12-P13 is a critical period for experience-dependent refinement at the whisker sensory relay synapse in the VPm.</p>

	]]>
</description>

<author>H Wang et al.</author>


</item>


<item>
<title>Genome Reshuffling for Advanced Intercross Permutation (GRAIP): simulation and permutation for advanced intercross population analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1904</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1904</guid>
<pubDate>Tue, 08 May 2012 23:23:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Advanced intercross lines (AIL) are segregating populations created using a multi-generation breeding protocol for fine mapping complex trait loci (QTL) in mice and other organisms. Applying QTL mapping methods for    intercross and backcross populations, often followed by naive permutation of individuals and phenotypes, does not account for the effect of AIL family structure in which final generations have been expanded and leads to inappropriately low    significance thresholds. The critical problem with naive mapping approaches in AIL populations is that the individual is not an exchangeable unit.  METHODOLOGY/PRINCIPAL FINDINGS: The effect of family structure has immediate implications for the    optimal AIL creation (many crosses, few animals per cross, and population expansion before the final generation) and we discuss these and the utility of AIL populations for QTL fine mapping. We also describe Genome Reshuffling for Advanced    Intercross Permutation, (GRAIP) a method for analyzing AIL data that accounts for family structure. GRAIP permutes a more interchangeable unit in the final generation crosses - the parental genome - and simulating regeneration of a permuted AIL    population based on exchanged parental identities. GRAIP determines appropriate genome-wide significance thresholds and locus-specific P-values for AILs and other populations with similar family structures. We contrast GRAIP with naive    permutation using a large densely genotyped mouse AIL population (1333 individuals from 32 crosses). A naive permutation using coat color as a model phenotype demonstrates high false-positive locus identification and uncertain significance    levels, which are corrected using GRAIP. GRAIP also detects an established hippocampus weight locus and a new locus, Hipp9a. CONCLUSIONS AND SIGNIFICANCE: GRAIP determines appropriate genome-wide significance thresholds and locus-specific    P-values for AILs and other populations with similar family structures. The effect of family structure has immediate implications for the optimal AIL creation and we discuss these and the utility of AIL populations.</p>

	]]>
</description>

<author>J L. Peirce et al.</author>


</item>


<item>
<title>Genetic mapping of vocalization to a series of increasing acute footshocks using B6.A consomic and B6.D2 congenic mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1903</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1903</guid>
<pubDate>Tue, 08 May 2012 23:22:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Footshock response is used to study a variety of biological functions in mammals including drug self-administration, learning and memory and nociception. However, the genetics underlying variability in footshock sensitivity are not    well understood. In the current studies, a panel of B6.A consomic mouse strains, two B6.D2 genome-tagged mouse lines, and the progenitor strains were screened for footshock sensitivity as measured by audible vocalization. It was found that A/J    (A) mice and C57BL/6J (B6) mice with an A Chromosome 1 (Chr 1) were less sensitive to footshock compared to B6 animals. Furthermore, the offspring of Chr 1 consomic mice crossed with B6 mice had vocalization levels that were intermediate to A/J    and B6 animals. A F2 mapping panel revealed two significant QTLs for footshock vocalization centered around D1Mit490 and D1Mit206 on Chr 1.  The role of these Chr 1 loci in footshock sensitivity was confirmed in B6.D2 genome-tagged mouse    lines.</p>

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</description>

<author>D B. Matthews et al.</author>


</item>


<item>
<title>Reprogramming and differentiation in mammals: motifs and mechanisms.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1902</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1902</guid>
<pubDate>Tue, 08 May 2012 23:22:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>The natural reprogramming of the mammalian egg and sperm genomes is an efficient process that takes place in less than 24 hours and gives rise to a totipotent zygote. Transfer of somatic nuclei to mammalian oocytes also leads to    their reprogramming and formation of totipotent embryos, albeit very inefficiently and requiring an activation step. Reprogramming of differentiated cells to induced pluripotent stem (iPS) cells takes place during a period of time substantially    longer than reprogramming of the egg and sperm nuclei and is significantly less efficient. The stochastic expression of endogenous proteins during this process would imply that controlled expression of specific proteins is crucial for    reprogramming to take place. The fact that OCT4, NANOG, and SOX2 form the core components of the pluripotency circuitry would imply that control at the transcriptional level is important for reprogramming to iPS cells. In contradistinction, the    much more efficient reprogramming of the mammalian egg and sperm genomes implies that other levels of control are necessary, such as chromatin remodeling, translational regulation, and efficient degradation of no longer needed proteins and    RNAs.</p>

	]]>
</description>

<author>Vries W. de et al.</author>


</item>


<item>
<title>Functional annotation of protein isoforms and modified forms.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1901</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1901</guid>
<pubDate>Tue, 08 May 2012 23:22:37 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H J. Drabkin et al.</author>


</item>


<item>
<title>PPAR signaling in placental development and function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1900</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1900</guid>
<pubDate>Tue, 08 May 2012 23:22:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Y Barak et al.</author>


</item>


<item>
<title>Modeling human leukemia using immune-compromised mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1899</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1899</guid>
<pubDate>Tue, 08 May 2012 23:22:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>F Ishikawa et al.</author>


</item>


<item>
<title>Identification of quantitative trait loci for locomotor activation and anxiety using closely-related inbred strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1898</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1898</guid>
<pubDate>Tue, 08 May 2012 23:22:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>We carried out a QTL mapping experiment in two phenotypically similar inbred mouse strains, C57BL/6J and C58/J, using the open field assay, a well-established model of anxiety-related behavior in rodents. This intercross was    initially carried out as a control cross for an ENU-mutagenesis mapping study.  Surprisingly, although open field behavior is similar in the two strains, we identified significant QTL in their F2 progeny. Marker regression identified a locus on    chromosome 8 having associations with multiple open field measures and a significant interaction between loci on chromosomes 13 and 17. Together, the chromosome 8 locus and the interaction effect form the core set of QTL controlling these    behaviors with additional loci on chromosomes 1 and 6 present in a subset of the behaviors.</p>

	]]>
</description>

<author>J S. Bailey et al.</author>


</item>


<item>
<title>An imputed genotype resource for the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1897</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1897</guid>
<pubDate>Tue, 08 May 2012 23:21:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have created a high-density SNP resource encompassing 7.87 million polymorphic loci across 49 inbred mouse strains of the laboratory mouse by combining data available from public databases and training a hidden Markov model to    impute missing genotypes in the combined data. The strong linkage disequilibrium found in dense sets of SNP markers in the laboratory mouse provides the basis for accurate imputation. Using genotypes from eight independent SNP resources, we    empirically validated the quality of the imputed genotypes and demonstrated that they are highly reliable for most inbred strains. The imputed SNP resource will be useful for studies of natural variation and complex traits. It will facilitate    association study designs by providing high-density SNP genotypes for large numbers of mouse strains. We anticipate that this resource will continue to evolve as new genotype data become available for laboratory mouse strains. The data are    available for bulk download or query at http://cgd.jax.org /.</p>

	]]>
</description>

<author>J P. Szatkiewicz et al.</author>


</item>


<item>
<title>Notch2 is required for the proliferation of cardiac neural crest-derived smooth muscle cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1896</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1896</guid>
<pubDate>Tue, 08 May 2012 23:21:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in Notch receptors and their ligands have been identified as the cause of human congenital heart diseases, indicating the importance of the Notch signaling pathway during heart development. In our study, we use Cre-Lox    technology to inactivate Notch2 in several cardiac cell lineages to determine the functional requirements for Notch2 during mammalian heart development.  Inactivation of Notch2 in cardiac neural crest cells resulted in abnormally narrow aortas    and pulmonary arteries due to a decrease in smooth muscle tissue.  The reduction in smooth muscle tissue was not due to cell migration defects but instead was found to be caused by less proliferation in smooth muscle cells during mid to late    gestation. Our findings demonstrate that Notch2 is required cell autonomously for proper formation of the heart outflow tract and provides insights into the role of Notch2 in vascular smooth muscle development and the cardiovascular defects    associated with Alagille syndrome.</p>

	]]>
</description>

<author>P Varadkar et al.</author>


</item>


<item>
<title>Humanized SCID mouse models for biomedical research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1895</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1895</guid>
<pubDate>Tue, 08 May 2012 23:21:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T Pearson et al.</author>


</item>


<item>
<title>Mechanisms of DNA double-strand break repair in hematopoietic homeostasis and oncogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1894</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1894</guid>
<pubDate>Tue, 08 May 2012 23:21:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>S A. Maas et al.</author>


</item>


<item>
<title>Genetic modeling of human blood cancers in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1893</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1893</guid>
<pubDate>Tue, 08 May 2012 23:21:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Y Hu et al.</author>


</item>


<item>
<title>Dietary restriction: a model system probing the cell fate decision between cancer and senescence.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1892</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1892</guid>
<pubDate>Tue, 08 May 2012 23:21:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R P. Ertl et al.</author>


</item>


<item>
<title>Modeling human Philadelphia chromosome-positive leukemia in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1891</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1891</guid>
<pubDate>Tue, 08 May 2012 23:21:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>S Li</author>


</item>


<item>
<title>Whole-body vibration slows the acquisition of fat in mature female rats.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1890</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1890</guid>
<pubDate>Tue, 08 May 2012 23:20:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: To evaluate the effects of whole-body vibration on fat, bone, leptin and muscle mass. METHODS/DESIGN: Thirty 7-month-old female 344 Fischer rats were randomized by weight into three groups (baseline, vibration or control;    n=8-10 per group). Rats in the vibration group were placed inside individual compartments attached to a Pneu-Vibe vibration platform (Pneumex, Sandpoint, ID, USA) and vibrated at 30-50 Hz (6 mm peak to peak) for 30 min per day, 5 days per week,    for 12 weeks. The vibration intervention consisted of six 5-min cycles with a 1-min break between cycles. RESULTS: There were significant body composition differences between the whole-body vibration and the control group. The whole-body    vibration group weighed approximately 10% less (mean+/-s.d.; 207+/-10 vs 222+/-15 g, P<0.03) and had less body fat (20.8+/-3.8 vs 26.8+/-5.9 g, P<0.05), a lower percentage of body fat (10.2+/-1.7 vs 12+/-2.0%, P<0.05), and lower serum leptin    levels (1.06+/-0.45 vs 2.27+/-0.57 ng ml(-1), P<0.01) than the age-matched controls. No differences were observed for total lean mass, bone mineral content (BMC), bone mineral density (BMD), insulin-like growth factor-I (IGF-I) or soleus (SOL)    and extensor digitorum longus (EDL) mass or function.  Regional high-resolution dual-energy X-ray absoptiometry scans of the lumbar spine (L1-4) revealed that the whole-body vibration group had significantly greater BMC (0.33+/-0.05 vs    0.26+/-0.03 g, P<0.01) and BMD (0.21+/-0.01 vs 0.19+/-0.01 g cm(-2), P<0.01) than the control group. No differences between the groups were observed in the amount of food consumed. CONCLUSION: These findings show that whole-body vibration reduced    body fat accumulation and serum leptin without affecting whole body BMC, BMD or lean mass. However, the increase in vertebral BMC and BMD suggests that vibration may have resulted in local increases in bone mass and density. Also, whole-body    vibration did not affect muscle function or food consumption.</p>

	]]>
</description>

<author>G F. Maddalozzo et al.</author>


</item>


<item>
<title>Practical applications of the bioinformatics toolbox for narrowing quantitative trait Loci.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1889</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1889</guid>
<pubDate>Tue, 08 May 2012 23:20:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dissecting the genes involved in complex traits can be confounded by multiple factors, including extensive epistatic interactions among genes, the involvement of epigenetic regulators, and the variable expressivity of traits.    Although quantitative trait locus (QTL) analysis has been a powerful tool for localizing the chromosomal regions underlying complex traits, systematically identifying the causal genes remains challenging. Here, through its application to plasma    levels of high-density lipoprotein cholesterol (HDL) in mice, we demonstrate a strategy for narrowing QTL that utilizes comparative genomics and bioinformatics techniques. We show how QTL detected in multiple crosses are subjected to both    combined cross analysis and haplotype block analysis; how QTL from one species are mapped to the concordant regions in another species; and how genomewide scans associating haplotype groups with their phenotypes can be used to prioritize the    narrowed regions. Then we illustrate how these individual methods for narrowing QTL can be systematically integrated for mouse chromosomes 12 and 15, resulting in a significantly reduced number of candidate genes, often from hundreds to <10.     Finally, we give an example of how additional bioinformatics resources can be combined with experiments to determine the most likely quantitative trait genes.</p>

	]]>
</description>

<author>Herbert S. Burgess et al.</author>


</item>


<item>
<title>Sugar and bone: a not-so sweet story.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1888</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1888</guid>
<pubDate>Tue, 08 May 2012 23:20:36 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title>Toward optimal health: advances in diagnosis and preventive strategies to promote bone health in women.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1887</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1887</guid>
<pubDate>Tue, 08 May 2012 23:20:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J R. Godfrey et al.</author>


</item>


<item>
<title>[Alstrom syndrome: clinical and genetic features, and a diagnostic guide to foresee complications.]</title>
<link>http://mouseion.jax.org/stfb2000_2009/1886</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1886</guid>
<pubDate>Tue, 08 May 2012 23:20:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND AND OBJECTIVE: Alstrom syndrome is a progressive autosomal recessive genetic disorder affecting multiple organ systems. It may be detected at birth or in early childhood. Clinically, patients with Alstrom syndrome develop    cone-rod dystrophy leading to eventual blindness, sensorineural deafness, and normal intelligence. Patients develop obesity, endocrine disturbances such as type 2 diabetes mellitus, dilated cardiomyopathy and progressive renal and hepatic    failure. Alstrom syndrome is caused by specific mutations in the ALMS1 gene, located at chromosome 2p13. PATIENTS AND METHOD: A case of a 23 year old patient with Alstrom syndrome, with a previous diagnosis of Laurence-Moon-Bardet-Biedl is    described. RESULTS: The subsequent molecular study revealed a mutation on the ALMS1 gene, confirming the diagnosis of Alstrom syndrome. CONCLUSIONS: The low frequency, the progressive multi-systemic disturbances, and the similarities with other    well-known syndromes may difficult the diagnosis of Alstrom syndrome. Thus, without a careful examination, it may be misdiagnosed and it would not be possible to perform any anticipatory therapeutic approach, with dramatic consequences for the    patients and their families. Moreover, as these patiens muts have a multidisciplinary approach, they may not receive the adequate treatment on time. therefore, it seems important to publish this case in our country, among with the clinical and    molecular characteristics of this syndrome, and to spread a diagnostic and anticipatory guidance for ist early detection.</p>

	]]>
</description>

<author>J Mendioroz et al.</author>


</item>


<item>
<title>Bone marrow expressing a diabetes resistance MHC class II allele: diabetes deviation by chronic immune stimulation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1885</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1885</guid>
<pubDate>Tue, 08 May 2012 23:20:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>The major histocompatibility complex (MHC) of the type 1 diabetes-prone NOD mouse lacks a functional class II H2-Ea gene such that antigen presenting cells (APCs) are I-E null. Transgenic expression of Ea in NOD mice both restores    I-E expression and confers complete protection from diabetes progression.  Non-myeloablative neonatal transplantation of bone marrow cells from such I-E+ transgenic donors into NOD recipients resulted in low-level but long-term haematopoietic    stem cell (HSC) engraftment. Despite low levels of I-E antigen expression in blood (averaging 0.4-3.8% of total MHC class II-positive population), chimeric recipients were protected from overt diabetes, although not insulitis development.    Adoptive transfer of diabetes into immunodeficient NOD-Rag recipients that received chimeric splenocytes from primary recipients confirmed the presence of an autoreactive T cell repertoire. The demonstration that purified T cells from these weak    chimeras were not tolerant to irradiated transgenic I-E+ splenocytes indicated that I-E+ donor cells provide a constant, low-level immune stimulation capable of up-regulating nominally deficient immunoregulatory networks. This study raises the    possibility that cord blood HSCs from infants with high risk HLA haplotypes and a family history of type 1 diabetes might be re-introduced without myoablative treatments following transfection with a single HLA class II allele associated with    diabetes resistance.</p>

	]]>
</description>

<author>P Reifsnyder et al.</author>


</item>


<item>
<title>Age-related retinal degeneration (arrd2) in a novel mouse model due to a nonsense mutation in the Mdm1 gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1884</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1884</guid>
<pubDate>Tue, 08 May 2012 23:19:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>We observed that a naturally occurring mouse strain developed age-related retinal degeneration (arrd2). These mice had normal fundi, electroretinograms (ERGs) and retinal histology at 6 months of age; vessel attenuation, RPE atrophy    and pigmentary abnormalities at 14 months, which progressed to complete loss of photoreceptors and extinguished ERG by 22 months. Genetic analysis revealed that the retinal degeneration in arrd2 segregates in an autosomal recessive manner and the    disease gene localizes to mouse chromosome 10. A positional candidate cloning approach detected a nonsense mutation in the mouse double minute-1 gene (Mdm1), which results in the truncation of the putative protein from 718 amino acids to 398. We    have identified a novel transcript of the Mdm1 gene, which is the predominant transcript in the retina. The Mdm1 transcript is localized to the nuclear layers of neural retina. Expression of Mdm1 in the retina increases steadily from post-natal    day 30 to 1 year, and a high level of Mdm1 are subsequently maintained. The Mdm1 transcript was found to be significantly depleted in the retina of arrd2 mice and the transcript was observed to degrade by nonsense-mediated decay. These results    indicate that the depletion of the Mdm1 transcript may underlie the mechanism leading to late-onset progressive retinal degeneration in arrd2 mice. Analysis of a cohort of patients with age-related macular degeneration (AMD) wherein the    susceptibility locus maps to chromosome 12q, a region bearing the human ortholog to MDM1, did not reveal association between human MDM1 and AMD.</p>

	]]>
</description>

<author>B Chang et al.</author>


</item>


<item>
<title>High precision size measurement of centromere 8 and the 8q24/c-myc gene region in metaphase and interphase human fibroblasts indicate differential condensation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1883</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1883</guid>
<pubDate>Tue, 08 May 2012 23:19:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>The hypothesis that distinct chromatin domains expand and are remodelled differently when they undergo transcription, replication or cell cycle processes is well accepted. The condensation changes by which chromosomes are    transformed at the metaphase-interphase transition are especially interesting and therefore extensively studied by light microscopy; however, quantitative information of the size on specific small chromatin domains during the cell cycle is    scarce. In this respect, a serious problem is the determination of structural features close to the resolution limit. In this report we use a novel approach to quantify the lateral extent of the 8q24/c-myc gene domain and the centromeric region    of chromosome 8 in doubly labelled normal human foreskin fibroblasts using confocal laser scanning microscopy (CLSM). The domains were analysed in both metaphase spreads and interphase nuclei. These high precision measurements revealed a somewhat    smaller (few 10s of nm) lateral extension of the centromere region in metaphase compared to interphase. Surprisingly, within the same cells the lateral extension of the 8q24/c-myc region was significantly smaller in interphase than in metaphase.    For comparison the centromere size was more condensed in metaphase than in interphase. This implies a different folding behaviour for specific chromatin domains with opposite condensation behaviour.</p>

	]]>
</description>

<author>C Batram et al.</author>


</item>


<item>
<title>Randomization in laboratory procedure is key to obtaining reproducible microarray results.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1882</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1882</guid>
<pubDate>Tue, 08 May 2012 23:19:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The quality of gene expression microarray data has improved dramatically since the first arrays were introduced in the late 1990s. However, the reproducibility of data generated at multiple laboratory sites remains a matter of    concern, especially for scientists who are attempting to combine and analyze data from public repositories. We have carried out a study in which a common set of RNA samples was assayed five times in four different laboratories using Affymetrix    GeneChip arrays. We observed dramatic differences in the results across laboratories and identified batch effects in array processing as one of the primary causes for these differences. When batch processing of samples is confounded with    experimental factors of interest it is not possible to separate their effects, and lists of differentially expressed genes may include many artifacts. This study demonstrates the substantial impact of sample processing on microarray analysis    results and underscores the need for randomization in the laboratory as a means to avoid confounding of biological factors with procedural effects.</p>

	]]>
</description>

<author>H Yang et al.</author>


</item>


<item>
<title>Cre recombinase activity specific to postnatal, premeiotic male germ cells in transgenic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1881</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1881</guid>
<pubDate>Tue, 08 May 2012 23:19:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have generated a transgenic mouse line,Tg(Stra8-cre)1Reb (Stra8-cre), which expresses improved Cre recombinase under the control of a 1.4 Kb promoter region of the germ cell-specific stimulated by retinoic acid gene 8 (Stra8).    cre is expressed only in males beginning at postnatal day (P)3 in early-stage spermatogonia and is detected through preleptotene-stage spermatocytes. To further define when cre becomes active, we crossed Stra8-cre males with    Tg(ACTB-Bgeo/GFP)21Lbe (Z/EG) reporter females and compared the expression of enhanced green fluorescent protein (EGFP) with the protein encoded by the zinc finger and BTB domain containing 16 (Zbtb16) gene, PLZF-a marker for undifferentiated    spermatogonia. Co-expression of EGFP is observed in the majority of PLZF+ cells. We also tested recombination efficiency by mating Stra8-cre;Z/EG males and females with wild-type mice and examining EGFP expression in the offspring. Recombination    is detected in >95% of Z/EG+ pups born to Stra8-cre;Z/EG fathers but in none of the offspring born to transgenic mothers, a verification that cre is not functional in females. The postnatal, premeiotic, male germ cell-specific activity of    Stra8-cre makes this mouse line a unique resource to study testicular germ cell development.</p>

	]]>
</description>

<author>Ngatchou P. Sadate et al.</author>


</item>


<item>
<title>Identification of mouse inbred strains through mitochondrial DNA single-nucleotide extension.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1880</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1880</guid>
<pubDate>Tue, 08 May 2012 23:19:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inbred mouse strains are used as model organisms for biomedical research in laboratories throughout the world. The most widely used of these strains had their genome sequenced recently, and phylogenetic studies have been performed,    namely, based on mitochondrial DNA (mtDNA). This has allowed determining that few polymorphisms distinguish the mtDNAs of the common inbred strains, but a high number of differences are observed among the wild-derived strains. Taking advantage of    these observations, we here present a single base extension typing strategy that, with only a pair of multiplex reactions, allows the distinction between common inbred and wild-derived mice strains, and provides the identification of ten    different common inbred and six wild-derived mice mtDNA haplotypes. Given that all the animals inside a strain present the same mtDNA, this strategy allows a rapid identification of the strains without the need for probability calculations. We    further test this approach in an island population of wild mice, which provides both an indication on its applicability in wild mice, and a comparison of evolutionary processes on inbred and wild mice that are restricted to a limited space. Rapid    genotyping methods that allow the distinction of the different strains are important for both the distinction of materials such as tissue and cell collections and to identify the origin of new strains. Moreover, it may also prove valuable in    forensic identification of materials collected in laboratory accidents, as well as in cases of scientific fraud.</p>

	]]>
</description>

<author>A Goios et al.</author>


</item>


<item>
<title>Cell adhesion to agrin presented as a nanopatterned substrate is consistent with an interaction with the extracellular matrix and not transmembrane adhesion molecules.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1879</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1879</guid>
<pubDate>Tue, 08 May 2012 23:19:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Molecular spacing is important for cell adhesion in a number of ways, ranging from the ordered arrangement of matrix polymers extracellularly, to steric hindrance of adhesion/signaling complexes intracellularly. This has    been demonstrated using nanopatterned RGD peptides, a canonical extracellular matrix ligand for integrin interactions. Cell adhesion was greatly reduced when the RGD-coated nanoparticles were separated by more than 60 nm, indicating a sharp    spacing-dependent threshold for this form of cell adhesion. RESULTS: Here we show a similar dependence of cell adhesion on the spacing of agrin, a protein that exists as both a secreted, matrix-bound form and a type-2 transmembrane form in vivo.    Agrin was presented as a substrate for cell adhesion assays by anchoring recombinant protein to gold nanoparticles that were arrayed at tunable distances onto glass coverslips. Cells adhered well to nanopatterned agrin, and when presented as    uniformly coated substrates, adhesion to agrin was comparable to other well-studied adhesion molecules, including N-Cadherin. Adhesion of both mouse primary cortical neurons and rat B35 neuroblastoma cells showed a spacing-dependent threshold,    with a sharp drop in adhesion when the space between agrin-coated nanoparticles increased from 60 to 90 nm. In contrast, adhesion to N-Cadherin decreased gradually over the entire range of distances tested (uniform, 30, 60, 90, and 160 nm). The    spacing of the agrin nanopattern also influenced cell motility, and peptide competition suggested adhesion was partially integrin dependent. Finally, differences in cell adhesion to C-terminal agrin fragments of different lengths were detected    using nanopatterned substrates, and these differences were not evident using uniformly coated substrates. CONCLUSION: These results suggest nanopatterned substrates may provide a physiological presentation of adhesive substrates, and are    consistent with cells adhering to agrin through a mechanism that more closely resembles an interaction with the extracellular matrix than a transmembrane adhesion molecule.</p>

	]]>
</description>

<author>T Wolfram et al.</author>


</item>


<item>
<title>Muscle development is disrupted in zebrafish embryos deficient for fibronectin.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1878</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1878</guid>
<pubDate>Tue, 08 May 2012 23:19:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>After somitogenesis, skeletal muscle precursors elongate into muscle fibers that anchor to the somite boundary, which becomes the myotome boundary. Fibronectin (Fn) is a major component of the extracellular matrix in both    boundaries.  Although Fn is required for somitogenesis, effects of Fn disruption on subsequent muscle development are unknown. We show that fn knockdown disrupts myogenesis.  Muscle morphogenesis is more disrupted in fn morphants than in a mutant    where initial somite boundaries did not form, aei/deltaD. We quantified this disruption using the two-dimensional Wavelet-Transform Modulus Maxima method, which uses the variation of intensity in an image with respect to the direction considered    to characterize the structure in a cell lattice. We show that fibers in fn morphants are less organized than in aei/deltaD mutant embryos. Fast- and slow-twitch muscle lengths are also more frequently uncoupled. These data suggest that fn may    function to regulate fiber organization and limit fast-twitch muscle fiber length.</p>

	]]>
</description>

<author>C J. Snow et al.</author>


</item>


<item>
<title>Differential effects of Usp14 and Uch-L1 on the ubiquitin proteasome system and synaptic activity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1877</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1877</guid>
<pubDate>Tue, 08 May 2012 23:18:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ubiquitin proteasome pathway has been implicated in the pathogenesis of many neurodegenerative diseases, and alterations in two different deubiquitinating enzymes, Uch-L1 and Usp14, result in neurological phenotypes in mice. We    identified a new mutation in Uch-L1 and compared the roles of Uch-L1 and Usp14 in the ubiquitin proteasome system. Deficiencies in either Uch-L1 or Usp14 result in decreased levels of ubiquitin, suggesting that they both regulate ubiquitin    stability in the nervous system. However, the effect of ubiquitin depletion on viability and onset of symptoms is more severe in the Usp14-deficient mice, and changes in hippocampal synaptic transmission were only observed in Usp14-deficient    mice. In addition, while Usp14 appears to function at the proteasome, Uch-L1 deficiency resulted in up-regulation of lysosomal components, indicating that Uch-L1 and Usp14 may differentially affect the ubiquitin proteasome system and synaptic    activity by regulating different pools of ubiquitin in the cell.</p>

	]]>
</description>

<author>B J. Walters et al.</author>


</item>


<item>
<title>Differences in DBA/1J and DBA/2J reveal lipid QTL genes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1876</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1876</guid>
<pubDate>Tue, 08 May 2012 23:18:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recent advances in mouse genomics have revealed considerable variation in the form of single-nucleotide polymorphisms (SNPs) among common inbred strains. This has made it possible to characterize closely related strains and to    identify genes that differ; such genes may be causal for quantitative phenotypes. The mouse strains DBA/1J and DBA/2J differ by just 5.6% at the SNP level. These strains exhibit differences in a number of metabolic and lipid phenotypes, such as    plasma levels of triglycerides (TGs) and HDL. A cross between these strains revealed multiple quantitative trait loci (QTLs) in 294 progeny. We identified significant TG QTLs on chromosomes (Chrs) 1, 2, 3, 4, 8, 9, 10, 11, 12, 13, 14, 16, and 19,    and significant HDL QTLs on Chrs 3, 9, and 16. Some QTLs mapped to chromosomes with limited variability between the two strains, thus facilitating the identification of candidate genes. We suggest that Tshr is the QTL gene for Chr 12 TG and HDL    levels and that Ihh may account for the TG QTL on Chr 1. This cross highlights the advantage of crossing closely related strains for subsequent identification of QTL genes.</p>

	]]>
</description>

<author>I M. Stylianou et al.</author>


</item>


<item>
<title>A new mouse mutant for the LDL receptor identified using ENU mutagenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1875</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1875</guid>
<pubDate>Tue, 08 May 2012 23:18:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>In an effort to discover new mouse models of cardiovascular disease using N-ethyl-N-nitrosourea (ENU) mutagenesis followed by high-throughput phenotyping, we have identified a new mouse mutation, C699Y, in the LDL receptor (Ldlr),    named wicked high cholesterol (WHC). When WHC was compared with the widely used Ldlr knockout (KO) mouse, notable phenotypic differences between strains were observed, such as accelerated atherosclerotic lesion formation and reduced    hepatosteatosis in the ENU mutant after a short exposure to an atherogenic diet.  This loss-of-function mouse model carries a single base mutation in the Ldlr gene on an otherwise pure C57BL/6J (B6) genetic background, making it a useful new tool    for understanding the pathophysiology of atherosclerosis and for evaluating additional genetic modifiers regulating hyperlipidemia and atherogenesis. Further investigation of genomic differences between the ENU mutant and KO strains may reveal    previously unappreciated sequence functionality.</p>

	]]>
</description>

<author>K L. Svenson et al.</author>


</item>


<item>
<title>Conditioned media from mouse osteosarcoma cells promote MC3T3-E1 cell proliferation using JAKs and PI3-K/Akt signal crosstalk.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1874</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1874</guid>
<pubDate>Tue, 08 May 2012 23:18:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>The maintenance of bone mass requires a strict balance between bone formation by osteoblasts and bone resorption by osteoclasts. In tumoral bone environment, tumor cells frequently disturb this balance by interaction with bone cells    to create a favorable site for tumor growth, and promote pathological bone changes.  Thus, elucidation of the mechanisms underlying interaction between tumor cells and bone cells might eventually lead to a more rational strategy for therapeutic    intervention for bone tumors and better understanding of bone biology. In the present study, the effects of mouse osteosarcoma cells on mouse preosteoblastic cells were determined by assessment of cell viability, osteoblastic differentiation and    signal transduction pathways. MOS-J/POS-1 conditioned media (CM) significantly induced MC3T3-E1 cell proliferation in a dose-dependent manner and reduced both alkaline phosphatase activity and mineralized nodule formation.  Piceatannol, AG490,    LY294002 and rapamycin significantly abrogated this up-regulated cell proliferation; however, UO126 and STAT3 inhibitor peptide did not affect this up-regulated cell proliferation. MOS-J/POS-1 CM activated ERK 1/2, STAT3 and Akt signal    transduction pathways; however, pro-proliferating signal induced by MOS-J/POS-1 CM was transmitted via Akt not ERK 1/2 and STAT3 pathways. Furthermore, Western blot analyses clearly revealed novel signal crosstalk between JAKs and PI3-K/Akt in    osteoblastic cells. The specific factor(s) involved in MOS-J/POS-1 CM-induced MC3T3-E1 cell proliferation that use JAKs/PI3-K/Akt/mTOR pathway remain(s) to be determined. Determination of the specific factor(s) responsible for JAKs and PI3-K/Akt    signal crosstalk that results in up-regulated preosteoblast proliferation will offer new insight into the pathology of osteosarcoma as well as other bone-related diseases.</p>

	]]>
</description>

<author>K Mori et al.</author>


</item>


<item>
<title>Humanized mice for the study of type 1 diabetes and beta cell function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1873</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1873</guid>
<pubDate>Tue, 08 May 2012 23:18:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Our understanding of the basic biology of diabetes has been guided by observations made using animal models, particularly rodents. However, humans are not mice, and outcomes predicted by murine studies are not always representative    of actual outcomes in the clinic. In particular, investigators studying diabetes have relied heavily on mouse and rat models of autoimmune type 1-like diabetes, and experimental results using these models have not been representative of many of    the clinical trials in type 1 diabetes. In this article, we describe the availability of new models of humanized mice for the study of three areas of diabetes. These include the use of humanized mice for the study of (1) human islet stem and    progenitor cells, (2) human islet allograft rejection, and (3) human immunity and autoimmunity. These humanized mouse models provide an important preclinical bridge between in vitro studies and rodent models and the translation of discoveries in    these model systems to the clinic.</p>

	]]>
</description>

<author>M King et al.</author>


</item>


<item>
<title>Regulation of the meiotic prophase I to metaphase I transition in mouse spermatocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1872</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1872</guid>
<pubDate>Tue, 08 May 2012 23:18:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>The meiotic prophase I to metaphase I transition (G2/MI) involves disassembly of synaptonemal complex (SC), chromatin condensation, and final compaction of morphologically distinct MI bivalent chromosomes. Control of these processes    is poorly understood. The G2/MI transition was experimentally induced in mouse pachytene spermatocytes by okadaic acid (OA), and kinetic analysis revealed that disassembly of the central element of the SC occurred very rapidly after OA treatment,    before histone H3 phosphorylation on Ser10. These events were followed by relocalization of SYCP3 and final condensation of bivalents. Enzymatic control of these G2/MI transition events was studied using small molecule inhibitors: butyrolactone I    (BLI), an inhibitor of cyclin-dependent kinases (CDKs) and ZM447439 (ZM), an inhibitor of aurora kinases (AURKs). The formation of highly condensed MI bivalents and disassembly of the SC are regulated by both CDKs and AURKs. AURKs also mediate    phosphorylation of histone H3 in meiosis. However, neither BLI nor ZM inhibited disassembly of the central element of the SC. Thus, despite evidence that the metaphase promoting factor is a universal regulator of the onset of cell division,    desynapsis, the first and key step of the G2/MI transition, occurs independently of BLI-sensitive CDKs and ZM-sensitive AURKs.</p>

	]]>
</description>

<author>F Sun et al.</author>


</item>


<item>
<title>Position-dependent motif characterization using non-negative matrix factorization.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1871</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1871</guid>
<pubDate>Tue, 08 May 2012 23:17:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>MOTIVATION: Cis-acting regulatory elements are frequently constrained by both sequence content and positioning relative to a functional site, such as a splice or polyadenylation site. We describe an approach to regulatory motif    analysis based on non-negative matrix factorization (NMF). Whereas existing pattern recognition algorithms commonly focus primarily on sequence content, our method simultaneously characterizes both positioning and sequence content of putative    motifs. RESULTS: Tests on artificially generated sequences show that NMF can faithfully reproduce both positioning and content of test motifs. We show how the variation of the residual sum of squares can be used to give a robust estimate of the    number of motifs or patterns in a sequence set. Our analysis distinguishes multiple motifs with significant overlap in sequence content and/or positioning.  Finally, we demonstrate the use of the NMF approach through characterization of    biologically interesting datasets. Specifically, an analysis of mRNA 3'-processing (cleavage and polyadenylation) sites from a broad range of higher eukaryotes reveals a conserved core pattern of three elements.</p>

	]]>
</description>

<author>L N. Hutchins et al.</author>


</item>


<item>
<title>A targeted deleterious allele of the splicing factor SCNM1 in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1870</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1870</guid>
<pubDate>Tue, 08 May 2012 23:17:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The auxiliary spliceosomal protein SCNM1 contributes to recognition of nonconsensus splice donor sites. SCNM1 was first identified as a modifier of the severity of a sodium channelopathy in the mouse. The most severely affected    strain, C57BL/6J, carries the variant allele SCNM1R187X, which is defective in splicing the mutated donor site in the Scn8a(medJ) transcript. To further probe the in vivo function of SCNM1, we constructed a floxed allele and generated a mouse    with constitutive deletion of exons 3-5. The SCNM1Delta3-5 protein is produced and correctly localized to the nucleus, but is more functionally impaired than the C57BL/6J allele. Deficiency of SCNM1 did not significantly alter other brain    transcripts. We characterized an ENU-induced allele of Scnm1 and evaluated the ability of wild-type SCNM1 to rescue lethal mutations of I-mfa and Brunol4. The phenotypes of the Scnm1Delta3-5 mutant confirm the role of this splice factor in    processing the Scn8a(medJ) transcript and provide a new allele of greater severity for future studies.</p>

	]]>
</description>

<author>V M. Howell et al.</author>


</item>


<item>
<title>Do-it-yourself (DIY) pathology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1869</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1869</guid>
<pubDate>Tue, 08 May 2012 23:17:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T A. Ince et al.</author>


</item>


<item>
<title>The Collaborative Cross, developing a resource for mammalian systems genetics: a status report of the Wellcome Trust cohort.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1868</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1868</guid>
<pubDate>Tue, 08 May 2012 23:17:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>We report on the progress of a project funded by the Wellcome Trust to produce over 100 recombinant inbred mouse lines as part of the Collaborative Cross (CC) genetic reference panel. These new strains of mice are being derived from    a set of eight genetically diverse founders. The genomes of the finished strains will be mosaics of the founder strains' genomes with a high density of independent recombination breakpoints. The CC mice will be available for distribution free of    any intellectual property constraints to serve as a community resource for systems genetics studies.</p>

	]]>
</description>

<author>F A. Iraqi et al.</author>


</item>


<item>
<title>The Collaborative Cross at Oak Ridge National Laboratory: developing a powerful resource for systems genetics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1867</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1867</guid>
<pubDate>Tue, 08 May 2012 23:17:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Complex traits and disease comorbidity in humans and in model organisms are the result of naturally occurring polymorphisms that interact with each other and with the environment. To ensure the availability of resources needed to    investigate biomolecular networks and systems-level phenotypes underlying complex traits, we have initiated breeding of a new genetic reference population of mice, the Collaborative Cross. This population has been designed to optimally support    systems genetics analysis. Its novel and important features include a high level of genetic diversity, a large population size to ensure sufficient power in high-dimensional studies, and high mapping precision through accumulation of independent    recombination events. Implementation of the Collaborative Cross has been ongoing at the Oak Ridge National Laboratory (ORNL) since May 2005.  Production has been systematically managed using a software-assisted breeding program with fully    traceable lineages, performed in a controlled environment.  Currently, there are 650 lines in production, and close to 200 lines are now beyond their seventh generation of inbreeding. Retired breeders enter a high-throughput phenotyping protocol    and DNA samples are banked for analyses of recombination history, allele drift and loss, and population structure. Herein we present a progress report of the Collaborative Cross breeding program at ORNL and a description of the kinds of    investigations that this resource will support.</p>

	]]>
</description>

<author>E J. Chesler et al.</author>


</item>


<item>
<title>Quantitative trait loci affecting phenotypic variation in the vacuolated lens mouse mutant, a multigenic mouse model of neural tube defects.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1866</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1866</guid>
<pubDate>Tue, 08 May 2012 23:17:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>The vacuolated lens (vl) mouse mutant arose spontaneously on the C3H/HeSn background and exhibits neural tube defects (NTDs), congenital cataract, and occasionally a white belly spot. We previously reported that 1) the vl phenotypes    are due to a mutation in an orphan G protein-coupled receptor (GPCR), Gpr161; 2) the penetrance of the vl NTD and cataract phenotypes are affected by genetic background, allowing three unlinked quantitative trait loci (QTL) to be mapped    (modifiers of vacuolated lens, Modvl1-3); and 3) phenotype-based bioinformatics followed by genetic and molecular analysis identified a lens-specific transcription factor that contributes to the cataract-modifying effect of Modvl3.  We now extend    this analysis in three ways. First, using the Gpr161 mutation to unequivocally identify mutant adults and embryos, we determined that approximately 50% of vl/vl NTD-affected embryos die during development. Second, the MOLF/Ei genetic background    suppresses this embryonic lethality but increases the incidence of the adult belly spot phenotype. Additional QTL analysis was performed, and two novel modifiers were mapped [Modvl4, logarithm of odds ratio (LOD) 4.4; Modvl5, LOD 5.0]. Third,    phenotype-based bioinformatics identified candidate genes for these modifiers including two GPCRs that cause NTD or skin/pigmentation defects (Modvl4: Frizzled homolog 6; Modvl5: Melanocortin 5 receptor). Because GPCRs form oligomeric complexes,    these genes were resequenced and nonsynonymous coding variants were identified. Bioinformatics and protein modeling suggest that these variants may be functional. Our studies further establish vl as a multigenic mouse model for NTDs and identify    additional QTL that interact with Gpr161 to regulate neurulation.</p>

	]]>
</description>

<author>R Korstanje et al.</author>


</item>


<item>
<title>Integrating mouse anatomy and pathology ontologies into a phenotyping database: tools for data capture and training.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1865</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1865</guid>
<pubDate>Tue, 08 May 2012 23:17:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Disease Information System (MoDIS) is a data capture system for pathology data from laboratory mice designed to support phenotyping studies. The system integrates the mouse anatomy (MA) and mouse pathology (MPATH)    ontologies into a Microsoft Access database facilitating the coding of organ, tissue, and disease process to recognized semantic standards. Grading of disease severity provides scores for all lesions that can then be used for quantitative trait    locus (QTL) analyses and haplotype association gene mapping. Direct linkage to the Pathbase online database provides reference definitions for disease terms and access to photomicrographic images of similar diagnoses in other mutant mice.  MoDIS    is an open source and freely available program (http://research.jax.org/faculty/sundberg/index.html). This provides a valuable tool for setting up a mouse pathology phenotyping program.</p>

	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title>The mouse hairy ears mutation exhibits an extended growth (anagen) phase in hair follicles and altered Hoxc gene expression in the ears.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1864</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1864</guid>
<pubDate>Tue, 08 May 2012 23:16:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse In(15)2Rl (hairy ears, Eh) mutation is a paracentric inversion of the distal half of chromosome 15 (Chr 15). Heterozygous Eh/+ mice display misshaped and hairy ears that have more and longer hair than the ears of their    wild-type littermates. We mapped, cloned and sequenced both inversion breakpoints. No protein-coding transcript was disrupted by either breakpoint. The proximal breakpoint is located between syntrophin basic 1 (Sntb1) and hyaluronan synthase 2    (Has2), and the distal breakpoint maps between homeobox C4 (Hoxc4) and single-strand selective monofunctional uracil DNA glycosylase (Smug1), near the middle and the telomere ends of Chr 15, respectively. The inversion spans ~47 megabases. Our    genetic analysis suggests that the hairy-ear phenotype is caused by the proximal breakpoint of the inversion-bearing Chr 15. Quantitative RNA analysis by real-time polymerase chain reaction for the genes flanking the breakpoint indicated no    changes in expression levels except for some homeobox C (Hoxc) genes whose expression was elevated in developing and mature skin of the ears but not of other body regions. The increased hair length on the ears of Eh/+ mice was due to an extension    of the anagen stage in the hair cycle, as determined by histological analysis. Our data indicate that the Eh phenotype arises from mis-expression of Hoxc genes.</p>

	]]>
</description>

<author>S E. Mentzer et al.</author>


</item>


<item>
<title>Allelic variance between GRM6 mutants, Grm6nob3 and Grm6nob4 results in differences in retinal ganglion cell visual responses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1863</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1863</guid>
<pubDate>Tue, 08 May 2012 23:16:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>An electroretinogram (ERG) screen identified a mouse with a normal a-wave but lacking a b-wave, and as such it was designated no b-wave3 (nob3). The nob3 phenotype mapped to chromosome 11 in a region containing the metabotropic    glutamate receptor 6 gene (Grm6). Sequence analyses of cDNA identified a splicing error in Grm6, introducing an insertion and an early stop codon into the mRNA of affected mice (designated Grm6(nob3)). Immunohistochemistry of the Grm6(nob3)    retina showed that GRM6 was absent. The ERG and visual behaviour abnormalities of Grm6(nob3) mice are similar to Grm6(nob4) animals, and similar deficits were seen in compound heterozygotes (Grm6(nob4/nob3)), indicating that Grm6(nob3) is allelic    to Grm6(nob4). Visual responses of Grm6(nob3) retinal ganglion cells (RGCs) to light onset were abnormal. Grm6(nob3) ON RGCs were rarely recorded, but when they were, had ill-defined receptive field (RF) centres and delayed onset latencies. When    Grm6(nob3) OFF-centre RGC responses were evoked by full-field stimulation, significantly fewer converted that response to OFF/ON compared to Grm6(nob4) RGCs. Grm6(nob4/nob3) RGC responses verified the conclusion that the two mutants are allelic.    We propose that Grm6(nob3) is a new model of human autosomal recessive congenital stationary night blindness. However, an allelic difference between Grm6(nob3) and Grm6(nob4) creates a disparity in inner retinal processing. Because the    localization of GRM6 is limited to bipolar cells in the On pathway, the observed difference between RGCs in these mutants is likely to arise from differences in their inputs.</p>

	]]>
</description>

<author>D M. Maddox et al.</author>


</item>


<item>
<title>Cancer stem cells are enriched in the side population cells in a mouse model of glioma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1862</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1862</guid>
<pubDate>Tue, 08 May 2012 23:16:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The recent identification of cancer stem cells (CSCs) in multiple human cancers provides a new inroad to understanding tumorigenesis at the cellular level. CSCs are defined by their characteristics of self-renewal,    multipotentiality, and tumor initiation upon transplantation. By testing for these defining characteristics, we provide evidence for the existence of CSCs in a transgenic mouse model of glioma, S100beta-verbB;Trp53. In this glioma model, CSCs are    enriched in the side population (SP) cells. These SP cells have enhanced tumor-initiating capacity, self-renewal, and multipotentiality compared with non-SP cells from the same tumors. Furthermore, gene expression analysis comparing    fluorescence-activated cell sorting-sorted cancer SP cells to non-SP cancer cells and normal neural SP cells identified 45 candidate genes that are differentially expressed in glioma stem cells. We validated the expression of two genes from this    list (S100a4 and S100a6) in primary mouse gliomas and human glioma samples. Analyses of xenografted human glioblastoma multiforme cell lines and primary human glioma tissues show that S100A4 and S100A6 are expressed in a small subset of cancer    cells and that their abundance is positively correlated to tumor grade. In conclusion, this study shows that CSCs exist in a mouse glioma model, suggesting that this model can be used to study the molecular and cellular characteristics of CSCs in    vivo and to further test the CSC hypothesis.</p>

	]]>
</description>

<author>M A. Harris et al.</author>


</item>


<item>
<title>Membrane frizzled-related protein is necessary for the normal development and maintenance of photoreceptor outer segments.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1861</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1861</guid>
<pubDate>Tue, 08 May 2012 23:16:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>A 4 base pair deletion in a splice donor site of the Mfrp (membrane-type frizzled-related protein) gene, herein referred to as Mfrprd6/rd6, is predicted to lead to the skipping of exon 4 and photoreceptor degeneration in retinal    degeneration 6 (rd6) mutant mice. Little, however, is known about the function of the protein or how the mutation causes the degenerative retinal phenotype. Here we examine ultrastructural changes in the retina of Mfrprd6/rd6 mice to determine    the earliest effects of the mutation. We also extend the reported observations of the expression pattern of the dicistronic Mfrp/C1qtnf5 message and the localization of these and other retinal pigment epithelium (RPE) and retinal proteins during    development and assess the ability of RPE cells to phagocytize outer segments (OSs) in mutant and wild-type (WT) mice. At the ultrastructural level, OSs do not develop normally in Mfrprd6/rd6 mutants. They are disorganized and become    progressively shorter as mutant mice age. Additionally, there are focal areas in which there is a reduction of apical RPE microvilli. At P25, the rod electroretinogram (ERG) a-wave of Mfrprd6/rd6 mice is reduced in amplitude by ~50% as are ERG    components generated by the RPE. Examination of beta-catenin localization and Fos and Tcf-1 expression, intermediates of the canonical Wnt pathway, showed that they were not different between mutant and WT mice, suggesting that MFRP may operate    through an alternative pathway. Finally, impaired OS phagocytosis was observed in Mfrprd6/rd6 mice both in standard ambient lighting conditions and with bright light exposure when compared to WT controls.</p>

	]]>
</description>

<author>J Won et al.</author>


</item>


<item>
<title>Human adult testis-derived pluripotent stem cells: revealing plasticity from the germline.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1860</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1860</guid>
<pubDate>Tue, 08 May 2012 23:16:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>A recent publication in Nature by Conrad et al. (2008) reports the generation of pluripotent stem cells from isolated human adult testicular germ cells. This work identifies a new source of stem cells for potential autologous    therapeutic applications in men.</p>

	]]>
</description>

<author>C J. Payne et al.</author>


</item>


<item>
<title>VAC14 nucleates a protein complex essential for the acute interconversion of PI3P and PI(3,5)P(2) in yeast and mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1859</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1859</guid>
<pubDate>Tue, 08 May 2012 23:16:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The signalling lipid PI(3,5)P(2) is generated on endosomes and regulates retrograde traffic to the trans-Golgi network. Physiological signals regulate rapid, transient changes in PI(3,5)P(2) levels. Mutations that lower PI(3,5)P(2)    cause neurodegeneration in human patients and mice. The function of Vac14 in the regulation of PI(3,5)P(2) was uncharacterized previously. Here, we predict that yeast and mammalian Vac14 are composed entirely of HEAT repeats and demonstrate that    Vac14 exerts an effect as a scaffold for the PI(3,5)P(2) regulatory complex by direct contact with the known regulators of PI(3,5)P(2): Fig4, Fab1, Vac7 and Atg18. We also report that the mouse mutant ingls (infantile gliosis) results from a    missense mutation in Vac14 that prevents the association of Vac14 with Fab1, generating a partial complex. Analysis of ingls and two additional mutants provides insight into the organization of the PI(3,5)P(2) regulatory complex and indicates    that Vac14 mediates three distinct mechanisms for the rapid interconversion of PI3P and PI(3,5)P(2). Moreover, these studies show that the association of Fab1 with the complex is essential for viability in the mouse.</p>

	]]>
</description>

<author>N Jin et al.</author>


</item>


<item>
<title>The C3H/HeJ mouse and DEBR rat models for alopecia areata: review of preclinical drug screening approaches and results.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1858</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1858</guid>
<pubDate>Tue, 08 May 2012 23:16:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>The C3H/HeJ inbred mouse strain and the Dundee Experimental Bald Rat (DEBR) strain spontaneously develop adult onset alopecia areata (AA), a cell-mediated disease directed against actively growing hair follicles. The low frequency    of AA and the inability to predict the stage of AA as it evolves in the naturally occuring C3H/HeJ model of AA can be converted into a highly predictable system by grafting full thickness skin from AA-affected mice to normal haired mice of the    same strain. The rat DEBR model develops spontaneous AA at a higher frequency than in the mouse model but they are more expensive to use in drug studies owing to their larger size. Regardless of the shortcomings of either model, these rodent    models can be used succesfully to screen novel or approved drugs for efficacy to treat human AA. As the pathogenesis of AA follows the canonical lymphocytic co-stimulatory cascade in the mouse AA model, it can be used to screen compounds    potentially useful to treat a variety of cell-mediated diseases.  Efficacy of various agents can easily be screened by simply observing the presence, rate, and cosmetic acceptability of hair regrowth. More sophisticated assays can refine how the    drugs induce hair regrowth and evaluate the underlying pathogenesis of AA. Some drugs commonly used to treat human AA patients work equally as well in both rodent models validating their usefulness as models for drug efficacy and safety for    humanAA.</p>

	]]>
</description>

<author>J Sun et al.</author>


</item>


<item>
<title>SIRT1 redistribution on chromatin promotes genomic stability but alters gene expression during aging.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1857</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1857</guid>
<pubDate>Tue, 08 May 2012 23:15:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genomic instability and alterations in gene expression are hallmarks of eukaryotic aging. The yeast histone deacetylase Sir2 silences transcription and stabilizes repetitive DNA, but during aging or in response to a DNA break, the    Sir complex relocalizes to sites of genomic instability, resulting in the desilencing of genes that cause sterility, a characteristic of yeast aging. Using embryonic stem cells, we show that mammalian Sir2, SIRT1, represses repetitive DNA and a    functionally diverse set of genes across the mouse genome. In response to DNA damage, SIRT1 dissociates from these loci and relocalizes to DNA breaks to promote repair, resulting in transcriptional changes that parallel those in the aging mouse    brain. Increased SIRT1 expression promotes survival in a mouse model of genomic instability and suppresses age-dependent transcriptional changes.  Thus, DNA damage-induced redistribution of SIRT1 and other chromatin-modifying proteins may be a    conserved mechanism of aging in eukaryotes.</p>

	]]>
</description>

<author>P Oberdoerffer et al.</author>


</item>


<item>
<title>A quantitative assay for crossover and noncrossover molecular events at individual recombination hotspots in both male and female gametes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1856</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1856</guid>
<pubDate>Tue, 08 May 2012 23:15:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Meiotic recombination is a fundamental process in all eukaryotes. Among organisms in which recombination initiates prior to synapsis, recombination preferentially occurs in short 1-to 2-kb regions, known as recombination hotspots.    Among mammals, genotyping sperm DNA has provided a means of monitoring recombination events at specific hotspots in male meiosis. To complement these current techniques, we developed an assay for amplifying all copies of a hotspot from the DNA of    male and female germ cells, cloning the products into Escherichia coli, and SNP genotyping the resulting colonies using fluorescence technology. This approach examines the molecular details of crossover and noncrossover events of individual    meioses directly at active hotspots while retaining the simplicity of using pooled DNA. Using this technique, we analyzed recombination events at the Hlx1 hotspot located on mouse chromosome 1, finding that the results agree well with a prior    genetic characterization of 3026 male and 3002 female meioses.</p>

	]]>
</description>

<author>S H. Ng et al.</author>


</item>


<item>
<title>A locus on distal chromosome 11 (ahl8) and its interaction with Cdh23 ahl underlie the early onset, age-related hearing loss of DBA/2J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1855</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1855</guid>
<pubDate>Tue, 08 May 2012 23:15:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The DBA/2J inbred strain of mice is used extensively in hearing research, yet little is known about the genetic basis for its early onset, progressive hearing loss. To map underlying genetic factors we analyzed recombinant inbred    strains and linkage backcrosses. Analysis of 213 mice from 31 BXD recombinant inbred strains detected linkage of auditory brain-stem response thresholds with a locus on distal chromosome 11, which we designate ahl8. Analysis of 225 N2 mice from a    backcross of (C57BL/6JxDBA/2J) F1 hybrids to DBA/2J mice confirmed this linkage (LOD>50) and refined the ahl8 candidate gene interval. Analysis of 214 mice from a backcross of (B6.CAST-Cdh23 Ahl+ xDBA/2J) F1 hybrids to DBA/2J mice demonstrated a    genetic interaction of Cdh23 with ahl8. We conclude that ahl8 is a major contributor to the hearing loss of DBA/2J mice and that its effects are dependent on the predisposing Cdh23 ahl genotype of this strain.</p>

	]]>
</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title>Targeted deletion of alpha-adducin results in absent beta- and gamma-adducin, compensated hemolytic anemia, and lethal hydrocephalus in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1854</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1854</guid>
<pubDate>Tue, 08 May 2012 23:15:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the red blood cell (RBC), adducin is present primarily as tetramers of alpha- and beta-subunits at spectrin-actin junctions, or junctional complexes. Mouse RBCs also contain small amounts of gamma-adducin. Platelets contain    alpha- and gamma-adducin only. Adducin functions as a barbed-end actin capping protein to regulate actin filament length and recruits spectrin to the ends of actin filaments. To further define adducin's role in vivo, we generated alpha-adducin    knockout mice. alpha-Adducin is absent in all tissues examined in homozygous null mice. In RBCs, beta- and gamma-adducin are also absent, indicating that alpha-adducin is the limiting subunit in tetramer formation at the spectrin-actin junction.    Similarly, gamma-adducin is absent in alpha-null platelets.  alpha-Adducin-null mice display compensated hemolytic anemia with features characteristic of RBCs in hereditary spherocytosis (HS), including spherocytes with significant loss of    surface area, decreased mean corpuscular volume (MCV), cell dehydration, and increased osmotic fragility. Platelets maintain their normal discoid shape, and bleeding times are normal. alpha-Adducin-null mice show growth retardation at birth and    throughout adulthood. Approximately 50% develop lethal communicating hydrocephalus with striking dilation of the lateral, third, and fourth ventricles. These data indicate that adducin plays a role in RBC membrane stability and in cerebrospinal    fluid homeostasis.</p>

	]]>
</description>

<author>R F. Robledo et al.</author>


</item>


<item>
<title>Early mechanical dysfunction of the diaphragm in the muscular dystrophy with myositis (Ttnmdm) model.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1853</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1853</guid>
<pubDate>Tue, 08 May 2012 23:15:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>A complex rearrangement mutation in the mouse titin gene leads to an in-frame 83-amino acid deletion in the N2A region of titin. Autosomal recessive inheritance of the titin muscular dystrophy with myositis (Ttn(mdm/mdm)) mutation    leads to a severe early-onset muscular dystrophy and premature death. We hypothesized that the N2A deletion would negatively impact the force-generating capacity and passive mechanical properties of the mdm diaphragm. We measured in vitro active    isometric contractile and passive length-tension properties to assess muscle function at 2 and 6 wk of age. Micro-CT, myosin heavy chain Western blotting, and histology were used to assess diaphragm structure. Marked chest wall distortions began    at 2 wk and progressively worsened until 5 wk. The percentage of myofibers with centrally located nuclei in mdm mice was significantly (P < 0.01) increased at 2 and 6 wk by 4% and 17%, respectively, compared with controls. At 6 wk, mdm diaphragm    twitch stress was significantly (P < 0.01) reduced by 71%, time to peak twitch was significantly (P < 0.05) reduced by 52%, and half-relaxation time was significantly (P < 0.05) reduced by 57%.  Isometric tetanic stress was significantly (P <    0.05) depressed in 2- and 6-wk mdm diaphragms by as much as 64%. Length-tension relationships of the 2- and 6-wk mdm diaphragms showed significantly (P < 0.05) decreased extensibility and increased stiffness. Slow myosin heavy chain expression    was aberrantly favored in the mdm diaphragm at 6 wk. Our data strongly support early contractile and passive mechanical aberrations of the respiratory pump in mdm mice.</p>

	]]>
</description>

<author>M A. Lopez et al.</author>


</item>


<item>
<title>Evidence for Hox-specified positional identities in adult vasculature.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1852</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1852</guid>
<pubDate>Tue, 08 May 2012 23:15:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The concept of specifying positional information in the adult cardiovascular system is largely unexplored. While the Hox transcriptional regulators have to be viewed as excellent candidates for assuming such a role,    little is known about their presumptive cardiovascular control functions and in vivo expression patterns. RESULTS: We demonstrate that conventional reporter gene analysis in transgenic mice is a useful approach for defining highly complex Hox    expression patterns in the adult vascular network as exemplified by our lacZ reporter gene models for Hoxa3 and Hoxc11. These mice revealed expression in subsets of vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) located in    distinct regions of the vasculature that roughly correspond to the embryonic expression domains of the two genes. These reporter gene patterns were validated as authentic indicators of endogenous gene expression by immunolabeling and PCR    analysis. Furthermore, we show that persistent reporter gene expression in cultured cells derived from vessel explants facilitates in vitro characterization of phenotypic properties as exemplified by the differential response of    Hoxc11-lacZ-positive versus-negative cells in migration assays and to serum. CONCLUSION: The data support a conceptual model of Hox-specified positional identities in adult blood vessels, which is of likely relevance for understanding the    mechanisms underlying regional physiological diversities in the cardiovascular system. The data also demonstrate that conventional Hox reporter gene mice are useful tools for visualizing complex Hox expression patterns in the vascular network    that might be unattainable otherwise. Finally, these mice are a resource for the isolation and phenotypic characterization of specific subpopulations of vascular cells marked by distinct Hox expression profiles.</p>

	]]>
</description>

<author>N D. Pruett et al.</author>


</item>


<item>
<title>NOTCH is part of the transcriptional network regulating cell growth and survival in mouse plasmacytomas.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1851</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1851</guid>
<pubDate>Tue, 08 May 2012 23:14:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Aside from Myc-activating translocations characteristic of plasmacytomas (PCT), little is known about genetic factors and signaling pathways responsible for the development of spontaneous B-cell lineage lymphomas of mice. Here, we    characterized the transcriptional profiles of PCT, centroblastic diffuse large B-cell lymphomas (CBL), and high-grade splenic marginal zone B-cell lymphoma (MZL++) using high-throughput quantitative reverse transcription-PCR. Expression profiles    of CBL and MZL++ were strikingly similar and quite unlike that of PCT.  Among the genes expressed at significantly higher levels by PCT were a number involved in NOTCH signaling, a finding supported by gene set enrichment analyses of microarray    data. To investigate the importance of this pathway, NOTCH signaling was blocked in PCT cell lines by treatment with a gamma-secretase inhibitor (GSI) or transduction of a dominant-negative mutant of MAML1. These treatments resulted in reduced    expression of NOTCH transcriptional targets in association with impaired proliferation and increased apoptosis. GSI treatment of transformed plasma cells in a primary PCT also induced apoptosis. These results integrate NOTCH activation with    oncogenic signaling pathways downstream of translocated Myc in the pathogenesis of mouse PCT, two signaling pathways also implicated in development of human multiple myeloma and T-cell lymphoblastic lymphoma.</p>

	]]>
</description>

<author>D M. Shin et al.</author>


</item>


<item>
<title>Members of the WNT signaling pathways are widely expressed in mouse ovaries, oocytes, and cleavage stage embryos.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1850</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1850</guid>
<pubDate>Tue, 08 May 2012 23:14:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mammalian oocyte-to-embryo transition, characterized by a period of transcriptional silence, is dependent on maternal RNAs and proteins produced during the growth phase of the oocyte. Signaling pathways control timely    transcription and translation of RNA, as well as post-translational modification of proteins. The WNT/beta-catenin pathway is clearly not active during preimplantation embryo development. However, alternative Wnt signaling pathways may play a    role during early embryo development. This study describes the extensive expression, at the transcript and protein level, of receptors, ligands, and intracellular molecules known to play a role in WNT signaling, as well as those known to    negatively regulate the canonical WNT/beta-catenin pathway in developing oocytes and preimplantation embryos. This expression of a wide array of molecules involved in WNT signaling suggests that the alternative WNT pathways may be active during    oogenesis and the oocyte-to-embryo transition.</p>

	]]>
</description>

<author>B N. Harwood et al.</author>


</item>


<item>
<title>E2f3a and E2f3b make overlapping but different contributions to total E2f3 activity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1849</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1849</guid>
<pubDate>Tue, 08 May 2012 23:14:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The E2f transcription factors are key downstream targets of the retinoblastoma protein tumor suppressor that control cell proliferation. E2F3 has garnered particular attention because it is amplified in various human tumors. E2f3    mutant mice typically die around birth and E2f3-deficient cells have a proliferation defect that correlates with impaired E2f target gene activation and also induction of p19(Arf) and p53. The E2f3 locus encodes two isoforms, E2f3a and E2f3b,    which differ in their N-termini. However, it is unclear how E2f3a versus E2f3b contributes to E2f3's requirement in either proliferation or development.  To address this, we use E2f3a- and E2f3b-specific knockouts. We show that inactivation of    E2f3a results in a low penetrance proliferation defect in vitro whereas loss of E2f3b has no effect. This proliferation defect appears insufficient to disrupt normal development as E2f3a and E2f3b mutant mice are both fully viable and have no    detectable defects. However, when combined with E2f1 mutation, inactivation of E2f3a, but not E2f3b, causes significant proliferation defects in vitro, neonatal lethality and also a striking cartilage defect. Thus, we conclude that E2f3a and    E2f3b have largely overlapping functions in vivo and that E2f3a can fully substitute for E2f1 and E2f3 in most murine tissues.</p>

	]]>
</description>

<author>P S. Danielian et al.</author>


</item>


<item>
<title>Complex genetic regulation of bone mineral density and insulin-like growth factor-I in C57BL/6J-Chr #A/J/NaJ chromosome substitution strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1848</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1848</guid>
<pubDate>Tue, 08 May 2012 23:14:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Low bone mineral density (BMD) is a phenotype associated with osteoporosis and increased risk of fracture. Since 60-80% of variation in BMD is associated with genetic factors, we used the novel approach of chromosome substitution    strains (CSS) to identify chromosomes that harbor genes that regulate BMD. Specifically, we evaluated 24 wk old C57BL/6J-Chr #(A/J)/NaJ CSS (n = 7 to 18) in which each chromosome in the host C57BL/6J strain is replaced by a corresponding    chromosome from the donor A/J strain (19 autosomes, X, Y). We determined several A/J chromosomes contribute to body weight (BW), percent body fat (BF), whole body areal BMD (aBMD), and serum insulin-like growth factor (IGF)-I in both a positive    and negative manner when compared with C57BL/6J. Specifically, C57BL/6J-Chr 5(A/J)/NaJ (B.A-5) (males) and B.A-13 (females) contributed to increased BW, whereas B.A-3, 4, 8, 9, 12, and 18 (males) and B.A-3, 4, and 11 (females) contributed to    reduced BW. B.A-5 (males) and B.A-13 (females) contributed to increased BF, whereas B.A-12 (males) and B.A-3, 4, 10, and 11 (females) contributed to reduced BF. B.A-14 (females) contributed to increased aBMD and B.A-1, 2, 6, 9, 10, and 18 (males)    and B.A-8, 9, and 10 (females) contributed to reduced aBMD. To determine if similar chromosomes regulate aBMD and IGF-I, we determined serum concentrations of IGF-I. B.A-14 and Y (males) and B.A-6 (females) contributed to increased IGF-I and male    B.A-3 and female B.A-8 contributed to reduced IGF-I. Overall, we identified several sex-dependent and -independent chromosomes that regulate aBMD and IGF-I in adult mice.</p>

	]]>
</description>

<author>K E. Govoni et al.</author>


</item>


<item>
<title>Commonalities of genetic resistance to spontaneous autoimmune and free radical--mediated diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1847</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1847</guid>
<pubDate>Tue, 08 May 2012 23:14:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>ALR/Lt, a NOD-related mouse strain, was selected for resistance to alloxan free radical-mediated diabetes (ALD). Despite extensive genomic identity with NOD (>70%), ALR mice display strong resistance to autoimmune type 1 diabetes    (T1D) due to both an unusual elevation in systemic antioxidant defenses and a reduction in cellular ROS production that extends to the beta cell level. Reciprocal backcross to NOD previously linked the ALR-derived T1D resistance to Chr. 3, 8, and    17 as well as to the ALR mt-Nd2(a) allele encoded by the mitochondrial genome (mtDNA). To determine whether any of the ALR-derived loci protecting against T1D also protected against ALD, 296 six-week-old F2 mice from reciprocal outcrosses were    alloxan-treated and assessed for diabetes onset, and a genome-wide scan (GWS) was conducted. GWS linked mt-Nd2 as well as three nuclear loci with alloxan-induced diabetes. A dominant ALR-derived ALD resistance locus on Chr. 8 colocalized with the    ALR-derived T1D resistance locus identified in the previous backcross analysis. In contrast, whereas ALR contributed a novel T1D resistance locus on Chr. 3 marked by Susp, a more proximal ALR-derived region marked by Il-2 contributed ALD    susceptibility, not resistance. In addition, a locus was mapped on Chr. 2, where heterozygosity provided heightened susceptibility. Tests for alloxan sensitivity in ALR conplastic mice encoding the NOD mt-Nd2(c) allele and NOD mice congenic for    the protective Chr. 8 locus supported our mapping results.  Alloxan sensitivity was increased in ALR.mt(NOD) mice, whereas it was decreased by congenic introduction of ALR genome on Chr. 8 into NOD. These data demonstrate both similarities and    differences in the genetic control of T1D versus ROS-induced diabetes.</p>

	]]>
</description>

<author>J Chen et al.</author>


</item>


<item>
<title>Idd9/11 genetic locus regulates diabetogenic activity of CD4 T-cells in nonobese diabetic (NOD) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1846</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1846</guid>
<pubDate>Tue, 08 May 2012 23:14:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: Although the H2(g7) major histocompatibility complex (MHC) provides the primary pathogenic component, the development of T-cell-mediated autoimmune type 1 diabetes in NOD mice also requires contributions from other    susceptibility (Idd) genes. Despite sharing the H2(g7) MHC, the closely NOD-related NOR strain remains type 1 diabetes resistant because of contributions of protective Idd5.2, Idd9/11, and Idd13 region alleles. To aid their eventual    identification, we evaluated cell types in which non-MHC Idd resistance genes in NOR mice exert disease-protective effects. RESEARCH DESIGN AND METHODS: Adoptive transfer and bone marrow chimerism approaches tested the diabetogenic activity of    CD4 and CD8 T-cells from NOR mice and NOD stocks congenic for NOR-derived Idd resistance loci. Tetramer staining and mimotope stimulation tested the frequency and proliferative capacity of CD4 BDC2.5-like cells. Regulatory T-cells (Tregs) were    identified by Foxp3 staining and functionally assessed by in vitro suppression assays. RESULTS: NOR CD4 T-cells were less diabetogenic than those from NOD mice.  The failure of NOR CD4 T-cells to induce type 1 diabetes was not due to decreased    proliferative capacity of BDC2.5 clonotypic-like cells. The frequency and function of Tregs in NOD and NOR mice were also equivalent. However, bone marrow chimerism experiments demonstrated that intrinsic factors inhibited the pathogenic activity    of NOR CD4 T-cells. The NOR Idd9/11 resistance region on chromosome 4 was found to diminish the diabetogenic activity of CD4 but not CD8 T-cells. CONCLUSIONS: In conclusion, we demonstrated that a gene(s) within the Idd9/11 region regulates the    diabetogenic activity of CD4 T-cells.</p>

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</description>

<author>Y G. Chen et al.</author>


</item>


<item>
<title>Effects of buprenorphine on body temperature, locomotor activity and cardiovascular function when assessed by telemetric monitoring in rats.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1845</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1845</guid>
<pubDate>Tue, 08 May 2012 23:14:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>N M. Gades et al.</author>


</item>


<item>
<title>Abnormal regulatory and effector T cell function predispose to autoimmunity following xenogeneic thymic transplantation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1844</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1844</guid>
<pubDate>Tue, 08 May 2012 23:13:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Porcine thymus grafts support robust murine and human thymopoiesis, generating a diverse T cell repertoire that is deleted of donor and host-reactive cells, achieving specific xenograft tolerance. Positive selection is mediated    exclusively by the xenogeneic thymic MHC. Although thymectomized, T cell-depleted normal mice usually remain healthy following xenogeneic thymic transplantation, thymus-grafted congenitally athymic mice frequently develop multiorgan autoimmunity.    We investigated the etiology of this syndrome by adoptively transferring lymphocyte populations from fetal pig thymus-grafted BALB/c nude mice to secondary BALB/c nude recipients. Fetal pig thymus-grafted nude mice generated normal numbers of    CD25(+)Foxp3(+)CD4 T cells, but these cells lacked the capacity to block autoimmunity. Moreover, thymocytes and peripheral CD4(+)CD25(-) cells from fetal pig thymus-grafted nude mice, but not those from normal mice, induced autoimmunity in nude    recipients. Injection of thymic epithelial cells from normal BALB/c mice into fetal pig thymus grafts reduced autoimmunity and enhanced regulatory function of splenocytes. Our data implicate abnormalities in postthymic maturation, expansion,    and/or survival of T cells positively selected by a xenogeneic MHC, as well as incomplete intrathymic deletion of thymocytes recognizing host tissue-specific Ags, in autoimmune pathogenesis. Regulatory cell function is enhanced and negative    selection of host-specific thymocytes may potentially also be improved by coimplantation of recipient thymic epithelial cells in the thymus xenograft.</p>

	]]>
</description>

<author>Y Fudaba et al.</author>


</item>


<item>
<title>Genetic influence on immune phenotype revealed strain-specific variations in peripheral blood lineages.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1843</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1843</guid>
<pubDate>Tue, 08 May 2012 23:13:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inbred mouse strains are routinely used as genetically defined animal models for studying a wide assortment of biological and pathological processes, including immune system function. However, no studies have presented large-scale    data on the immune cell populations among the inbred strains in physiological conditions.  Here we present a systematic, quantitative analysis of peripheral blood cell phenotypes of 30 mouse strains assessed by flow cytometry. This cohort of mice    represents a wide range of genetic origins and includes most of the strains used in genetic, physiological, and immunological studies. We evaluated the relative percentages of peripheral blood leukocyte subtypes (lymphocytes, granulocytes, and    monocytes) and lymphocyte subpopulations (CD4+ T, CD8+ T, B220+ B, and natural killer cells) of mature (6-mo-old) mice. Our comprehensive study demonstrated: 1) marked differences in the relative proportions of blood cell populations among the    strains at this age, 2) considerable variation of each immune trait with more than twofold difference between strains with the highest and the lowest trait values, and 3) haplotype analysis revealed a strong correlation between eosinophil    percentage and a single region on chromosome 14 containing two candidate genes. The strain differences described here provide important information for researchers applying immunophenotyping of peripheral blood in immunological and genetic    studies. The data from this study are available as part of the Mouse Phenome Database at http://www.jax.org/phenome.</p>

	]]>
</description>

<author>S B. Petkova et al.</author>


</item>


<item>
<title>Human BLyS facilitates engraftment of human PBL derived B cells in immunodeficient mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1842</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1842</guid>
<pubDate>Tue, 08 May 2012 23:13:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The production of fully immunologically competent humanized mice engrafted with peripheral lymphocyte populations provides a model for in vivo testing of new vaccines, the durability of immunological memory and cancer therapies.    This approach is limited, however, by the failure to efficiently engraft human B lymphocytes in immunodeficient mice. We hypothesized that this deficiency was due to the failure of the murine microenvironment to support human B cell survival.  We    report that while the human B lymphocyte survival factor, B lymphocyte stimulator (BLyS/BAFF) enhances the survival of human B cells ex vivo, murine BLyS has no such protective effect. Although human B cells bound both human and murine BLyS,    nuclear accumulation of NF-kappaB p52, an indication of the induction of a protective anti-apoptotic response, following stimulation with human BLyS was more robust than that induced with murine BLyS suggesting a fundamental disparity in BLyS    receptor signaling. Efficient engraftment of both human B and T lymphocytes in NOD rag1(-/-) Prf1(-/-) immunodeficient mice treated with recombinant human BLyS is observed after adoptive transfer of human PBL relative to PBS treated controls.    Human BLyS treated recipients had on average 40-fold higher levels of serum Ig than controls and mounted a de novo antibody response to the thymus-independent antigens in pneumovax vaccine. The data indicate that production of fully    immunologically competent humanized mice from PBL can be markedly facilitated by providing human BLyS.</p>

	]]>
</description>

<author>M R. Schmidt et al.</author>


</item>


<item>
<title>Non-obese diabetic-recombination activating gene-1 (NOD-Rag1 null) interleukin (IL)-2 receptor common gamma chain (IL2r gamma null) null mice: a radioresistant model for human lymphohaematopoietic engraftment.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1841</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1841</guid>
<pubDate>Tue, 08 May 2012 23:13:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Immunodeficient hosts engrafted with human lymphohaematopoietic cells hold great promise as a preclinical bridge for understanding human haematopoiesis and immunity. We now describe a new immunodeficient radioresistant non-obese    diabetic mice (NOD) stock based on targeted mutations in the recombination activating gene-1 (Rag1(null)) and interleukin (IL)-2 receptor common gamma chain (IL2rgamma(null)), and compare its ability to support lymphohaematopoietic cell    engraftment with that achieved in radiosensitive NOD.CB17-Prkdc(scid) (NOD-Prkdc(scid)) IL2rgamma(null) mice. We observed that immunodeficient NOD-Rag1(null) IL2rgamma(null) mice tolerated much higher levels of irradiation conditioning than did    NOD-Prkdc(scid) IL2rgamma(null) mice. High levels of human cord blood stem cell engraftment were observed in both stocks of irradiation-conditioned adult mice, leading to multi-lineage haematopoietic cell populations and a complete repertoire of    human immune cells, including human T cells. Human peripheral blood mononuclear cells also engrafted at high levels in unconditioned adult mice of each stock. These data document that Rag1(null) and scid stocks of immunodeficient NOD mice    harbouring the IL2rgamma(null) mutation support similar levels of human lymphohaematopoietic cell engraftment.  NOD-Rag1(null) IL2rgamma(null) mice will be an important new model for human lymphohaematopoietic cell engraftment studies that    require radioresistant hosts.</p>

	]]>
</description>

<author>T Pearson et al.</author>


</item>


<item>
<title>The Gene Ontology (GO) project: structured vocabularies for molecular biology and their application to genome and expression analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1840</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1840</guid>
<pubDate>Tue, 08 May 2012 23:13:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Scientists wishing to utilize genomic data have quickly come to realize the benefit of standardizing descriptions of experimental procedures and results for computer-driven information retrieval systems. The focus of the Gene    Ontology project is three-fold. First, the project goal is to compile the Gene Ontologies: structured vocabularies describing domains of molecular biology. Second, the project supports the use of these structured vocabularies in the annotation of    gene products. Third, the gene product-to-GO annotation sets are provided by participating groups to the public through open access to the GO database and Web resource. This unit describes the current ontologies and what is beyond the scope of    the Gene Ontology project. It addresses the issue of how GO vocabularies are constructed and related to genes and gene products. It concludes with a discussion of how researchers can access, browse, and utilize the GO project in the course of    their own research.</p>

	]]>
</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title>Loss of Rb1 in the gastrointestinal tract of Apc1638N mice promotes tumors of the cecum and proximal colon.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1839</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1839</guid>
<pubDate>Tue, 08 May 2012 23:13:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>To examine the role of Rb1 in gastrointestinal (GI) tumors, we generated mice with an Apc(1638N) allele, Rb(tm2brn) floxed alleles, and a villin-cre transgene (RBVCA). These animals had exon 19 deleted from Rb1 throughout the GI    tract. We have shown previously that Rb1 deficiency is insufficient for GI tumor initiation, with inactivation of an Apc allele capable of overcoming the insufficiency. In this study we demonstrate that RBVCA mice have reduced median survival    because of an increase in tumor incidence and multiplicity in the cecum and the proximal colon. Large intestinal tumors are predominantly adenomas, whereas the tumors of the small intestine are a mixture of adenomas and adenocarcinomas. We find    truncation mutations to the second Apc allele in tumors of both the large and small intestine. Expression profiles of duodenal and cecal tumors relative to each other show unique gene subsets up and down regulated.  Substantial expression    patterns compare to human colorectal cancer, including recapitulation of embryonic genes. Our results indicate that Rb1 has significant influence over tumor location in the GI tract, and that both cecal and duodenal tumors initiate through    inactivation of Apc. Expression profile analysis indicates the two tumor types differentially regulate distinct sets of genes that are over-expressed in a majority of human colorectal carcinomas.</p>

	]]>
</description>

<author>M H. Kucherlapati et al.</author>


</item>


<item>
<title>A new immunodeficient hyperglycaemic mouse model based on the Ins2Akita mutation for analyses of human islet and beta stem and progenitor cell function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1838</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1838</guid>
<pubDate>Tue, 08 May 2012 23:12:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>AIMS/HYPOTHESIS: To develop and validate a new immunodeficient mouse strain that spontaneously develops a non-autoimmune hyperglycaemia to serve as a diabetic host for human islets and human beta stem and progenitor cells without    the need for induction of hyperglycaemia by toxic chemicals with their associated side effects. METHODS: We generated and characterised a new strain of immunodeficient spontaneously hyperglycaemic mice, the NOD-Rag1null Prf1null Ins2Akita strain    and compared this strain with the NOD-scid Il2rgammanull (also known as Il2rg) immunodeficient strain rendered hyperglycaemic by administration of a single dose of streptozotocin. Hyperglycaemic mice were transplanted with human islets ranging    from 1,000 to 4,000 islet equivalents (IEQ) and were monitored for normalisation of blood glucose levels. RESULTS: NOD-Rag1null Prf1null Ins2Akita mice developed spontaneous hyperglycaemia, similar to Ins2Akita-harbouring strains of    immunocompetent mice. Histological examination of islets in the host pancreas validated the spontaneous loss of beta cell mass in the absence of mononuclear cell infiltration. Human islets transplanted into spontaneously diabetic NOD-Rag1null    Prf1null Ins2Akita and chemically diabetic NOD-scid Il2rgammanull mice resulted in a return to euglycaemia that occurred with transplantation of similar beta cell masses. CONCLUSIONS/INTERPRETATION: The NOD-Rag1null Prf1null Ins2Akita mouse is    the first immunodeficient, spontaneously hyperglycaemic mouse strain described that is based on the Ins2Akita mutation.  This strain is suitable as hosts for human islet and human beta stem and progenitor cell transplantation in the absence of    the need for pharmacological induction of diabetes. This strain of mice also has low levels of innate immunity and can be engrafted with a human immune system for the study of human islet allograft rejection.</p>

	]]>
</description>

<author>T Pearson et al.</author>


</item>


<item>
<title>Progressive morphological and functional defects in retinas from alpha1 integrin-null mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1837</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1837</guid>
<pubDate>Tue, 08 May 2012 23:12:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: The role of integrin/cell matrix interactions between the RPE and the basement membrane in retinal maintenance and function is not well characterized.  In this study the functional importance of alpha1beta1 integrin for    retinal pigment epithelial cell homeostasis and retinal health was assessed by comparing alpha1 integrin knockout mice with strain- and age-matched wild-type mice.  METHODS: Immunolocalization and Western blot analysis of retinas and ARPE19 cells    were performed to examine the expression of alpha1beta1 integrin in the RPE.  Retinal abnormality was assessed by funduscopy, histology, and transmission electron microscopy. Progressive retinal damage was quantified by direct counting of rod    photoreceptors. Light-induced translocation of arrestin and alpha-transducin was documented by immunohistochemical analysis of retinal cryosections. RESULTS: Integrin alpha1beta1 localizes to the basal aspect of retinal pigment epithelial cells    colocalizing with the basal lamina of the RPE.  Integrin alpha1-null mice have delayed-onset progressive retinal degeneration associated with thickening of the basement membrane, dysmorphology of basal processes, synaptic malformations, and    funduscopic abnormalities. Integrin alpha1-null mice display marked delays in transducin translocation compared with dark-adapted wild-type mice after exposure to light. CONCLUSIONS: Collectively, these data suggest an essential role for    alpha1beta1 integrin/basement membrane interactions in the RPE in basement membrane metabolism and translocation of transducin in photoreceptors. This is the first report describing evidence supporting an essential role for integrin/basement    membrane interaction in the RPE. Further, this report demonstrates a direct link between integrin alpha1beta1 function in retinal pigment epithelial and molecular defects in photoreceptor cell function before retinal abnormality is    apparent.</p>

	]]>
</description>

<author>Y W. Peng et al.</author>


</item>


<item>
<title>Nordihydroguaiaretic acid and aspirin increase lifespan of genetically heterogeneous male mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1836</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1836</guid>
<pubDate>Tue, 08 May 2012 23:12:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The National Institute on Aging's Interventions Testing Program was established to evaluate agents that are purported to increase lifespan and delay the appearance of age-related disease in genetically heterogeneous mice. Up to five    compounds are added to the study each year and each compound is tested at three test sites (The Jackson Laboratory, University of Michigan, and University of Texas Health Science Center at San Antonio). Mice in the first cohort were exposed to    one of four agents: aspirin, nitroflurbiprofen, 4-OH-alpha-phenyl-N-tert-butyl nitrone, or nordihydroguaiaretic acid (NDGA).  Sample size was sufficient to detect a 10% difference in lifespan in either sex,with 80% power, using data from two of    the three sites.Pooling data from all three sites, a log-rank test showed that both NDGA (p=0.0006) and aspirin (p=0.01) led to increased lifespan of male mice. Comparison of the proportion of live mice at the age of 90% mortality was used as a    surrogate for measurement of maximum lifespan;neither NDGA (p=0.12) nor aspirin (p=0.16) had a significant effect in this test. Measures of blood levels of NDGA or aspirin and its salicylic acid metabolite suggest that the observed lack of    effects of NDGA or aspirin on life span in females could be related to gender differences in drug disposition or metabolism. Further studies are warranted to find whether NDGA or aspirin, over a range of doses,might prove to postpone death and    various age-related outcomes reproducibly in mice.</p>

	]]>
</description>

<author>R Strong et al.</author>


</item>


<item>
<title>Promoting coherent minimum reporting guidelines for biological and biomedical investigations: the MIBBI project.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1835</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1835</guid>
<pubDate>Tue, 08 May 2012 23:12:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C F. Taylor et al.</author>


</item>


<item>
<title>Access to immunology through the Gene Ontology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1834</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1834</guid>
<pubDate>Tue, 08 May 2012 23:12:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Gene Ontology (GO) is widely recognized as the premier tool for the organization and functional annotation of molecular aspects of cellular systems.  However, for many immunologists the use of GO is a very foreign concept.    Indeed, as a controlled vocabulary, GO can almost be considered a new language, and it can be difficult to appreciate the use and value of this approach for understanding the immune system. This review reflects on the application of GO to the    field of immunology and explains the process of GO annotation. Finally, this review hopes to inspire immunologists to invest time and energy in improving both the content of the GO and the quality of GO annotations associated with genes of    immunological interest.</p>

	]]>
</description>

<author>R C. Lovering et al.</author>


</item>


<item>
<title>Interaction between Reelin and Notch signaling regulates neuronal migration in the cerebral cortex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1833</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1833</guid>
<pubDate>Tue, 08 May 2012 23:12:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Neuronal migration is a fundamental component of brain development whose failure is associated with various neurological and psychiatric disorders. Reelin is essential for the stereotypical inside-out sequential lamination of the    neocortex, but the molecular mechanisms of its action still remain unclear. Here we show that regulation of Notch activity plays an important part in Reelin-signal-dependent neuronal migration. We found that Reelin-deficient mice have reduced    levels of the cleaved form of Notch intracellular domain (Notch ICD) and that loss of Notch signaling in migrating neurons results in migration and morphology defects. Further, overexpression of Notch ICD mitigates the laminar and morphological    abnormalities of migrating neurons in Reeler. Finally, our in vitro biochemical studies show that Reelin signaling inhibits Notch ICD degradation via Dab1. Together, our results indicate that neuronal migration in the developing cerebral cortex    requires a Reelin-Notch interaction.</p>

	]]>
</description>

<author>Torii K. Hashimoto et al.</author>


</item>


<item>
<title>The chromosome 11 region from strain 129 provides protection from sex reversal in XYPOS mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1832</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1832</guid>
<pubDate>Tue, 08 May 2012 23:12:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>C57BL/6J (B6) mice containing the Mus domesticus poschiavinus Y chromosome, YPOS, develop ovarian tissue, whereas testicular tissue develops in DBA/2J or 129S1/SvImJ (129) mice containing the YPOS chromosome. To identify genes    involved in sex determination, we used a congenic strain approach to determine which chromosomal regions from 129Sl/SvImJ provide protection against sex reversal in XYPOS mice of the C57BL/6J.129-YPOS strain. Genome scans using microsatellite and    SNP markers identified a chromosome 11 region of 129 origin in C57BL/6J.129-YPOS mice. To determine if this region influenced testis development in XYPOS mice, two strains of C57BL/6J-YPOS mice were produced and used in genetic experiments.     XYPOS adults homozygous for the 129 region had a lower incidence of sex reversal than XYPOS adults homozygous for the B6 region. In addition, many homozygous 129 XYPOS fetuses developed normal-appearing testes, an occurrence never observed in    XYPOS mice of the C57BL/6J-YPOS strain. Finally, the amount of testicular tissue observed in ovotestes of heterozygous 129/B6 XYPOS fetuses was greater than the amount observed in ovotestes of homozygous B6 XYPOS fetuses. We conclude that a    chromosome 11 locus derived from 129Sl/SvImJ essentially protects against sex reversal in XYPOS mice. A number of genes located in this chromosome 11 region are discussed as potential candidates.</p>

	]]>
</description>

<author>G Nikolova et al.</author>


</item>


<item>
<title>AAV-mediated gene therapy for retinal degeneration in the rd10 mouse containing a recessive PDEbeta mutation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1831</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1831</guid>
<pubDate>Tue, 08 May 2012 23:11:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: To test AAV-mediated gene therapy in the rd10 mouse, a natural model of recessive RP caused by mutation of the beta-subunit of rod photoreceptor cGMP phosphodiesterase. METHODS: One eye of a cohort of rd10 mice kept in a    dark environment was subretinally injected at postnatal day (P) 14 with 1 microL AAV5-smCBA-PDEbeta. The contralateral eye was not injected. The animals were then maintained for 2 weeks in the dark before they were moved to a normal 12-hour    light/12-hour dark cycling light environment for visually guided behavioral training. Three weeks after injection, treated rd10 mice were examined by scotopic and photopic electroretinography and then killed for biochemical and morphologic    examination. RESULTS: Substantial scotopic ERG signals were maintained in treated rd10 eyes, whereas untreated eyes in the same animals showed minimal signals. Treated eyes showed photopic ERG b-wave amplitudes similar to those of the normal    eyes; in untreated partner eyes, only half the normal amplitudes remained. Strong PDEbeta expression was observed in photoreceptor outer segments only in treated eyes. Light microscopy showed a substantial preservation of the outer nuclear layer    in most parts of the treated retina only. Electron microscopy showed good outer segment preservation only in treated eyes. A visually guided water maze behavioral test under dim light showed significantly improved performance in one eye-treated    rd10 mice compared with untreated mice. CONCLUSIONS: These data demonstrate that P14 administration of AAV5-smCBA-PDEbeta can prevent retinal degeneration in rd10 mice, as reflected by significant structural, biochemical, electrophysiological,    and behavioral preservation/restoration. These results serve as a baseline for studying long-term retinal rescue in rd10 mice.</p>

	]]>
</description>

<author>J J. Pang et al.</author>


</item>


<item>
<title>Analysis of gene expression in a developmental context emphasizes distinct biological leitmotifs in human cancers.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1830</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1830</guid>
<pubDate>Tue, 08 May 2012 23:11:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: In recent years, the molecular underpinnings of the long-observed resemblance between neoplastic and immature tissue have begun to emerge.  Genome-wide transcriptional profiling has revealed similar gene expression    signatures in several tumor types and early developmental stages of their tissue of origin. However, it remains unclear whether such a relationship is a universal feature of malignancy, whether heterogeneities exist in the developmental component    of different tumor types and to which degree the resemblance between cancer and development is a tissue-specific phenomenon. RESULTS: We defined a developmental landscape by summarizing the main features of ten developmental time courses and    projected gene expression from a variety of human tumor types onto this landscape. This comparison demonstrates a clear imprint of developmental gene expression in a wide range of tumors and with respect to different, even non-cognate    developmental backgrounds. Our analysis reveals three classes of cancers with developmentally distinct transcriptional patterns. We characterize the biological processes dominating these classes and validate the class distinction with respect to    a new time series of murine embryonic lung development. Finally, we identify a set of genes that are upregulated in most cancers and we show that this signature is active in early development.  CONCLUSION: This systematic and quantitative    overview of the relationship between the neoplastic and developmental transcriptome spanning dozens of tissues provides a reliable outline of global trends in cancer gene expression, reveals potentially clinically relevant differences in the gene    expression of different cancer types and represents a reference framework for interpretation of smaller-scale functional studies.</p>

	]]>
</description>

<author>K Naxerova et al.</author>


</item>


<item>
<title>mTORC1 promotes survival through translational control of Mcl-1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1829</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1829</guid>
<pubDate>Tue, 08 May 2012 23:11:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Activation of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway is a frequent occurrence in human cancers and a major promoter of chemotherapeutic resistance. Inhibition of one downstream target in this pathway, mTORC1,    has shown potential to improve chemosensitivity. However, the mechanisms and genetic modifications that confer sensitivity to mTORC1 inhibitors remain unclear. Here, we demonstrate that loss of TSC2 in the E mu-myc murine lymphoma model leads to    mTORC1 activation and accelerated oncogenesis caused by a defective apoptotic program despite compromised AKT phosphorylation. Tumors from Tsc2(+/-)E mu-Myc mice underwent rapid apoptosis upon blockade of mTORC1 by rapamycin. We identified    myeloid cell leukemia sequence 1 (Mcl-1), a bcl-2 like family member, as a translationally regulated genetic determinant of mTORC1-dependent survival.  Our results indicate that the extent by which rapamycin can modulate expression of Mcl-1 is an    important feature of the rapamycin response.</p>

	]]>
</description>

<author>J R. Mills et al.</author>


</item>


<item>
<title>Conserving, distributing and managing genetically modified mouse lines by sperm cryopreservation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1828</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1828</guid>
<pubDate>Tue, 08 May 2012 23:11:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Sperm from C57BL/6 mice are difficult to cryopreserve and recover.  Yet, the majority of genetically modified (GM) lines are maintained on this genetic background. METHODOLOGY/PRINCIPAL FINDINGS: Reported here is the    development of an easily implemented method that consistently yields fertilization rates of 70+/-5% with this strain. This six-fold increase is achieved by collecting sperm from the vas deferens and epididymis into a cryoprotective medium of 18%    raffinose (w/v), 3% skim milk (w/v) and 477 microM monothioglycerol. The sperm suspension is loaded into 0.25 mL French straws and cooled at 37+/-1 degrees C/min before being plunged and then stored in LN(2).  Subsequent to storage, the sperm are    warmed at 2,232+/-162 degrees C/min and incubated in in vitro fertilization media for an hour prior to the addition of oocyte cumulus masses from superovulated females. Sperm from 735 GM mouse lines on 12 common genetic backgrounds including    C57BL/6J, BALB/cJ, 129S1/SvImJ, FVB/NJ and NOD/ShiLtJ were cryopreserved and recovered. C57BL/6J and BALB/cByJ fertilization rates, using frozen sperm, were slightly reduced compared to rates involving fresh sperm; fertilization rates using fresh    or frozen sperm were equivalent in all other lines. Developmental capacity of embryos produced using cryopreserved sperm was equivalent, or superior to, cryopreserved IVF-derived embryos. CONCLUSIONS/SIGNIFICANCE: Combined, these results    demonstrate the broad applicability of our approach as an economical and efficient option for archiving and distributing mice.</p>

	]]>
</description>

<author>G C. Ostermeier et al.</author>


</item>


<item>
<title>Two novel alleles of tottering with distinct Ca(v)2.1 calcium channel neuropathologies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1827</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1827</guid>
<pubDate>Tue, 08 May 2012 23:11:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The calcium channel CACNA1A gene encodes the pore-forming, voltage-sensitive subunit of the voltage-dependent calcium Ca(v)2.1 type channel. Mutations in this gene have been linked to several human disorders, including familial    hemiplegic migraine, episodic ataxia 2 and spinocerebellar ataxia type 6. The mouse homologue, Cacna1a, is associated with the tottering, Cacna1a(tg), mutant series.  Here we describe two new missense mutant alleles, Cacna1a(tg-4J) and    Cacna1a(Tg-5J). The Cacna1a(tg-4J) mutation is a valine to alanine mutation at amino acid 581, in segment S5 of domain II. The recessive Cacna1a(tg-4J) mutant exhibited the ataxia, paroxysmal dyskinesia and absence seizures reminiscent of the    original tottering mouse. The Cacna1a(tg-4J) mutant also showed altered activation and inactivation kinetics of the Ca(v)2.1 channel, not previously reported for other tottering alleles. The semi-dominant Cacna1a(Tg-5J) mutation changed a    conserved arginine residue to glutamine at amino acid 1252 within segment S4 of domain III. The heterozygous mouse was ataxic and homozygotes rarely survived. The Cacna1a(Tg-5J) mutation caused a shift in both voltage activation and inactivation    to lower voltages, showing that this arginine residue is critical for sensing Ca(v)2.1 voltage changes. These two tottering mouse models illustrate how novel allelic variants can contribute to functional studies of the Ca(v)2.1 calcium    channel.</p>

	]]>
</description>

<author>T Miki et al.</author>


</item>


<item>
<title>In childhood acute lymphoblastic leukemia, blasts at different stages of immunophenotypic maturation have stem cell properties.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1826</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1826</guid>
<pubDate>Tue, 08 May 2012 23:11:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>We examined the leukemic stem cell potential of blasts at different stages of maturation in childhood acute lymphoblastic leukemia (ALL). Human leukemic bone marrow was transplanted intrafemorally into NOD/scid mice. Cells sorted    using the B precursor differentiation markers CD19, CD20, and CD34 were isolated from patient samples and engrafted mice before serial transplantation into primary or subsequent (up to quaternary) recipients. Surprisingly, blasts representative    of all of the different maturational stages were able to reconstitute and reestablish the complete leukemic phenotype in vivo. Sorted blast populations mirrored normal B precursor cells with transcription of a number of stage-appropriate genes.    These observations inform a model for leukemia-propagating stem cells in childhood ALL.</p>

	]]>
</description>

<author>C le Viseur et al.</author>


</item>


<item>
<title>Big data: The future of biocuration.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1825</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1825</guid>
<pubDate>Tue, 08 May 2012 23:11:04 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D Howe et al.</author>


</item>


<item>
<title>A genomewide functional network for the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1824</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1824</guid>
<pubDate>Tue, 08 May 2012 23:10:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Establishing a functional network is invaluable to our understanding of gene function, pathways, and systems-level properties of an organism and can be a powerful resource in directing targeted experiments. In this study, we present    a functional network for the laboratory mouse based on a Bayesian integration of diverse genetic and functional genomic data. The resulting network includes probabilistic functional linkages among 20,581 protein-coding genes. We show that this    network can accurately predict novel functional assignments and network components and present experimental evidence for predictions related to Nanog homeobox (Nanog), a critical gene in mouse embryonic stem cell pluripotency. An analysis of the    global topology of the mouse functional network reveals multiple biologically relevant systems-level features of the mouse proteome. Specifically, we identify the clustering coefficient as a critical characteristic of central modulators that    affect diverse pathways as well as genes associated with different phenotype traits and diseases. In addition, a cross-species comparison of functional interactomes on a genomic scale revealed distinct functional characteristics of conserved    neighborhoods as compared to subnetworks specific to higher organisms. Thus, our global functional network for the laboratory mouse provides the community with a key resource for discovering protein functions and novel pathway components as well    as a tool for exploring systems-level topological and evolutionary features of cellular interactomes. To facilitate exploration of this network by the biomedical research community, we illustrate its application in function and disease gene    discovery through an interactive, Web-based, publicly available interface at http://mouseNET.princeton.edu.</p>

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</description>

<author>Y Guan et al.</author>


</item>


<item>
<title>Characterization of glycolytic enzyme interactions with murine erythrocyte membranes in wild-type and membrane protein knockout mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1823</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1823</guid>
<pubDate>Tue, 08 May 2012 23:10:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous research has shown that glycolytic enzymes (GEs) exist as multienzyme complexes on the inner surface of human erythrocyte membranes. Because GE binding sites have been mapped to sequences on the membrane protein, band 3,    that are not conserved in other mammalian homologs, the question arose whether GEs can organize into complexes on other mammalian erythrocyte membranes. To address this, murine erythrocytes were stained with antibodies to    glyceraldehyde-3-phosphate dehydrogenase, aldolase, phosphofructokinase, lactate dehydrogenase, and pyruvate kinase and analyzed by confocal microscopy. GEs were found to localize to the membrane in oxygenated erythrocytes but redistributed to    the cytoplasm upon deoxygenation, as seen in human erythrocytes. To identify membrane proteins involved in GE assembly, erythrocytes from mice lacking each of the major erythrocyte membrane proteins were examined for GE localization. GEs from    band 3 knockout mice were not membrane associated but distributed throughout the cytoplasm, regardless of erythrocyte oxygenation state. In contrast, erythrocytes from mice lacking alpha-spectrin, ankyrin, protein 4.2, protein 4.1, beta-adducin,    or dematin headpiece exhibited GEs bound to the membrane. These data suggest that oxygenation-dependent assembly of GEs on the membrane could be a general phenomenon of mammalian erythrocytes and that stability of these interactions depends    primarily on band 3.</p>

	]]>
</description>

<author>M E. Campanella et al.</author>


</item>


<item>
<title>A position effect on TRPS1 is associated with Ambras syndrome in humans and the Koala phenotype in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1822</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1822</guid>
<pubDate>Tue, 08 May 2012 23:10:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ambras syndrome (AS) is a rare form of congenital hypertrichosis with excessive hair on the shoulders, face and ears. Cytogenetic studies have previously implicated an association with rearrangements of chromosome 8. Here we define    an 11.5 Mb candidate interval for AS on chromosome 8q based on cytogenetic breakpoints in three patients. TRPS1, a gene within this interval, was deleted in a patient with an 8q23 chromosomal rearrangement, while its expression was significantly    downregulated in another patient with an inversion breakpoint 7.3 Mb downstream of TRPS1. Here, we describe the first potential long-range position effect on the expression of TRPS1. To gain insight into the mechanisms by which Trps1 affects the    hair follicle, we performed a detailed analysis of the hair abnormalities in Koa mice, a mouse model of hypertrichosis. We found that the proximal breakpoint of the Koa inversion is located 791 kb upstream of Trps1.  Quantitative real-time    polymerase chain reaction, in situ hybridization and immunofluorescence analysis revealed that Trps1 expression levels are reduced in Koa mutant mice at the sites of pathology for the phenotype. We determined that the Koa inversion creates a new    Sp1 binding site and translocates additional Sp1 binding sites within a highly conserved stretch spanning the proximal breakpoint, providing a potential mechanism for the position effect. Collectively, these results describe a position effect    that downregulates TRPS1 expression as the probable cause of hypertrichosis in AS in humans and the Koa phenotype in mice.</p>

	]]>
</description>

<author>K A. Fantauzzo et al.</author>


</item>


<item>
<title>Iris phenotypes and pigment dispersion caused by genes influencing pigmentation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1821</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1821</guid>
<pubDate>Tue, 08 May 2012 23:10:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Spontaneous mutations altering mouse coat colors have been a classic resource for discovery of numerous molecular pathways. Although often overlooked, the mouse iris is also densely pigmented and easily observed, thus representing a    similarly powerful opportunity for studying pigment cell biology. Here, we present an analysis of iris phenotypes among 16 mouse strains with mutations influencing melanosomes. Many of these strains exhibit biologically and medically relevant    phenotypes, including pigment dispersion, a common feature of several human ocular diseases. Pigment dispersion was identified in several strains with mutant alleles known to influence melanosomes, including beige, light, and vitiligo.  Pigment    dispersion was also detected in the recently arising spontaneous coat color variant, nm2798. We have identified the nm2798 mutation as a missense mutation in the Dct gene, an identical re-occurrence of the slaty light mutation.  These results    suggest that dysregulated events of melanosomes can be potent contributors to the pigment dispersion phenotype. Combined, these findings illustrate the utility of studying iris phenotypes as a means of discovering new pathways, and re-linking old    ones, to processes of pigmented cells in health and disease.</p>

	]]>
</description>

<author>M G. Anderson et al.</author>


</item>


<item>
<title>Cataracts in transgenic mice caused by a human papillomavirus type 18 E7 oncogene driven by KRT1-14.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1820</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1820</guid>
<pubDate>Tue, 08 May 2012 23:10:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human papillomavirus type 18 (HPV18) is a common cause of cervical cancer. To create a mouse model for this common neoplastic disease, we used a human keratin 14 promoter to drive the HPV18 E7 oncogene to create transgenic mice. No    mice up to a year of age developed cervical cancer. However, all transgenic mice and none of the controls developed progressive bilateral cortical cataracts. By 6 months of age, the cortex liquefied leaving the lens nucleus. Proliferation of lens    epithelium formed multifocal nodules and free floating lens epithelial cells within the liquefied cortex. These cells were hyperplastic not neoplastic. Other HPV transgenic stocks develop cataracts suggesting this virus may have a broad cellular    tropism.</p>

	]]>
</description>

<author>S Ghim et al.</author>


</item>


<item>
<title>Quantitative trait loci for BMD in an SM/J by NZB/BlNJ intercross population and identification of Trps1 as a probable candidate gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1819</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1819</guid>
<pubDate>Tue, 08 May 2012 23:10:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Identification of genes that regulate BMD will enhance our understanding of osteoporosis and could provide novel molecular targets for treatment or prevention. We generated a mouse intercross population and carried out a    quantitative trait locus (QTL) analysis of 143 female and 124 male F(2) progeny from progenitor strains SM/J and NZB/BlNJ using whole body and vertebral areal BMD (aBMD) as measured by DXA. We found that both whole body and vertebral aBMD was    affected by two loci on chromosome 9: one with a significant epistatic interaction on distal chromosome 8 and the other with a sex-specific effect. Two additional significant QTLs were identified on chromosome 12, and several suggestive ones were    identified on chromosomes 5, 8, 15, and 19. The chromosome 9, 12, and 15 loci have been previously identified in other crosses. SNP-based haplotype analysis of the progenitor strains identified blocks within the QTL region that distinguish the    low allele strains from the high allele strains, significantly narrowing the QTL region and reducing the possible candidate genes to 98 for chromosome 9, 31 for chromosome 12, and only 2 for chromosome 15. Trps1 is the most probable candidate    gene for the chromosome 15 QTL. The sex-specific effects may help to elucidate the BMD differences between males and females. This study shows the power of statistical modeling to resolve linked QTLs and the use of haplotype analysis in narrowing    the list of candidates.</p>

	]]>
</description>

<author>N Ishimori et al.</author>


</item>


<item>
<title>Developmental control of sumoylation pathway proteins in mouse male germ cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1818</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1818</guid>
<pubDate>Tue, 08 May 2012 23:10:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Protein sumoylation regulates a variety of nuclear functions and has been postulated to be involved in meiotic chromosome dynamics as well as other processes of spermatogenesis. Here, the expression and distribution of sumoylation    pathway genes and proteins were determined in mouse male germ cells, with a particular emphasis on prophase I of meiosis. Immunofluorescence microscopy revealed that SUMO1, SUMO2/3 and UBE2I (also known as UBC9) were localized to the XY body in    pachytene and diplotene spermatocytes, while only SUMO2/3 and UBE2I were detected near centromeres in metaphase I spermatocytes.  Quantitative RT-PCR and Western blotting were used to examine the expression of sumoylation pathway genes and    proteins in enriched preparations of leptotene/zygotene spermatocytes, prepubertal and adult pachytene spermatocytes, as well as round spermatids. Two general expression profiles emerged from these data. The first profile, where expression was    more prominent during meiosis, identified sumoylation pathway participants that could be involved in meiotic chromosome dynamics. The second profile, elevated expression in post-meiotic spermatids, suggested proteins that could be involved in    spermiogenesis-related sumoylation events. In addition to revealing differential expression of protein sumoylation mediators, which suggests differential functioning, these data demonstrate the dynamic nature of SUMO metabolism during    spermatogenesis.</p>

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</description>

<author>Salle S. La et al.</author>


</item>


<item>
<title>PPARG by dietary fat interaction influences bone mass in mice and humans.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1817</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1817</guid>
<pubDate>Tue, 08 May 2012 23:09:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adult BMD, an important risk factor for fracture, is the result of genetic and environmental interactions. A quantitative trait locus (QTL) for the phenotype of volumetric BMD (vBMD), named Bmd8, was found on mid-distal chromosome    (Chr) 6 in mice. This region is homologous to human Chr 3p25. The B6.C3H-6T (6T) congenic mouse was previously created to study this QTL. Using block haplotyping of the 6T congenic region, expression analysis in the mouse, and examination of    nonsynonymous SNPs, peroxisome proliferator activated receptor gamma (Pparg) was determined to be the most likely candidate gene for the Bmd8 QTL of the 630 genes located in the congenic region. Furthermore, in the C3H/HeJ (C3H) strain, which is    the donor strain for the 6T congenic, several polymorphisms were found in the Pparg gene. On challenge with a high-fat diet, we found that the 6T mouse has a lower areal BMD (aBMD) and volume fraction of trabecular bone (BV/TV%) of the distal    femur compared with B6 mice. Interactions between SNPs in the PPARG gene and dietary fat for the phenotype of BMD were examined in the Framingham Offspring Cohort. This analysis showed that there was a similar interaction of the PPARG gene and    diet (fat intake) on aBMD in both men and women. These findings suggest that dietary fat has a significant influence on BMD that is dependent on the alleles present for the PPARG gene.</p>

	]]>
</description>

<author>Bicknell C. Ackert et al.</author>


</item>


<item>
<title>Inflammation and autoimmunity caused by a SHP1 mutation depend on IL-1, MyD88, and a microbial trigger.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1816</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1816</guid>
<pubDate>Tue, 08 May 2012 23:09:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>A recessive phenotype called spin (spontaneous inflammation) was induced by N-ethyl-N-nitrosourea (ENU) mutagenesis in C57BL/6J mice. Homozygotes display chronic inflammatory lesions affecting the feet, salivary glands and lungs,    and antichromatin antibodies. They are immunocompetent and show enhanced resistance to infection by Listeria monocytogenes. TLR-induced TNF and IL-1 production are normal in macrophages derived from spin mice. The autoinflammatory phenotype of    spin mice is fully suppressed by compound homozygosity for Myd88(poc), Irak4(otiose), and Il1r1-null mutations, but not Ticam1(Lps2), Stat1(m1Btlr), or Tnf-null mutations. Both autoimmune and autoinflammatory phenotypes are suppressed when spin    homozygotes are derived into a germ-free environment. The spin phenotype was ascribed to a viable hypomorphic allele of Ptpn6, which encodes the tyrosine phosphatase SHP1, mutated in mice with the classical motheaten alleles me and me-v.    Inflammation and autoimmunity caused by SHP1 deficiency are thus conditional. The SHP1-deficient phenotype is driven by microbes, which activate TLR signaling pathways to elicit IL-1 production. IL-1 signaling via MyD88 elicits inflammatory    disease.</p>

	]]>
</description>

<author>B A. Croker et al.</author>


</item>


<item>
<title>A SNaPshot multiplex typing strategy for mtDNA identification of mouse inbred strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1815</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1815</guid>
<pubDate>Tue, 08 May 2012 23:09:36 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Goios A, Gusmao L, Rocha AM, Pereira L, Bogue M, Amorim A</author>


</item>


<item>
<title>A model for familial exudative vitreoretinopathy caused by LPR5 mutations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1814</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1814</guid>
<pubDate>Tue, 08 May 2012 23:09:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have identified a mouse recessive mutation that leads to attenuated and hyperpermeable retinal vessels, recapitulating some pathological features of familial exudative vitreoretinopathy (FEVR) in human patients. DNA sequencing    reveals a single nucleotide insertion in the gene encoding the low-density lipoprotein receptor-related protein 5 (LRP5), causing a frame shift and resulting in the replacement of the C-terminal 39 amino acid residues by 20 new amino acids. This    change eliminates the last three PPP(S/T)P repeats in the LRP5 cytoplasmic domain that are important for mediating Wnt/beta-catenin signaling.  Thus, mutant LRP5 protein is probably unable to mediate its downstream signaling.  Immunostaining and    three-dimensional reconstructions of retinal vasculature confirm attenuated retinal vessels. Ultrastructural data further reveal that some capillaries lack lumen structure in the mutant retina. We have also verified that LRP5 null mice develop    similar alterations in the retinal vasculature. This study provides direct evidence that LRP5 is essential for the development of retinal vasculature, and suggests a novel role played by LRP5 in capillary maturation.  LRP5 mutant mice can be a    useful model to explore the clinical manifestations of FEVR.</p>

	]]>
</description>

<author>C H. Xia et al.</author>


</item>


<item>
<title>Candidate genes for obesity revealed from a C57BL/6J x 129S1/SvImJ intercross.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1813</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1813</guid>
<pubDate>Tue, 08 May 2012 23:09:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: To identify the genes controlling body fat, we carried out a quantitative trait locus (QTL) analysis using C57BL/6J (B6) and 129S1/SvImJ (129) mice, which differ in obesity susceptibility after consuming an atherogenic    diet.  METHODS: Mice were fed chow until 8 weeks and an atherogenic diet from 8 to 16 weeks; body fatness was measured by X-ray absorptiometry in 528 (B6 x 129) F(2) at 8 and 16 weeks. A high-density genome scan was performed using 508    polymorphic markers. After identifying the genetic loci, we narrowed the QTL using comparative genomics and bioinformatics. RESULTS: The percentage of body fat was significantly linked to loci on chromosomes (Chr) 1 (22, 68 and 173 Mb), 4 (74    Mb), 5 (73 Mb), 7 (88 Mb), 8 (43 and 80 Mb), 9 (55 Mb), 11 (115 Mb) and 12 (32 Mb); three suggestive loci on Chrs 6 (76 Mb), 9 (30 Mb) and 16 (26 Mb) and two pairs of interacting loci (Chr 2 at 99.8 Mb with Chr 7; Chr 1 at 68 Mb with Chr 11).    Comparative genomics narrowed the QTL intervals by 20-57% depending on the chromosome; in most cases, haplotype analysis further narrowed them by about 90%.  CONCLUSIONS: Our analysis identified 15 QTL for percentage of body fat. We narrowed the    QTL using comparative genomics and haplotype analysis and suggest several candidate genes: Apcs on Chr 1, Ppargc1a on Chr 5, Ucp1 on Chr 8, Angptl6 on Chr 9 and Lpin1 on Chr 12.</p>

	]]>
</description>

<author>Z Su et al.</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 2 No 1</title>
<link>http://ro.uow.edu.au/uowgazette/9</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/9</guid>
<pubDate>Tue, 08 May 2012 23:09:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 2 No 2</title>
<link>http://ro.uow.edu.au/uowgazette/8</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/8</guid>
<pubDate>Tue, 08 May 2012 23:09:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 2 No 4</title>
<link>http://ro.uow.edu.au/uowgazette/6</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/6</guid>
<pubDate>Tue, 08 May 2012 23:09:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 2 No 3</title>
<link>http://ro.uow.edu.au/uowgazette/7</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/7</guid>
<pubDate>Tue, 08 May 2012 23:09:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 2 No 5</title>
<link>http://ro.uow.edu.au/uowgazette/5</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/5</guid>
<pubDate>Tue, 08 May 2012 23:09:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>University of Wollongong</author>


</item>


<item>
<title>A novel dwarfism with gonadal dysfunction due to loss-of-function allele of the collagen receptor gene, Ddr2, in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1812</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1812</guid>
<pubDate>Tue, 08 May 2012 23:09:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Smallie (slie), a spontaneous, autosomal-recessive mutation causes dwarfing and infertility in mice. The purpose of this study was to determine and characterize the underlying molecular genetic basis for its phenotype. The slie    locus was mapped to chromosome 1, and fine-structure mapping narrowed the slie allele within 2 Mb between genetic markers D1Mit36 and Mpz. To pinpoint the underlying mutation quantitative real-time PCR was used to measure the relative expression    levels for the genes residing within this region. Expression of one gene, Ddr2, which encodes discoidin domain receptor 2 (DDR2), was absent in slie homozygote mice. Genomic sequencing analysis detected a 150-kb deletion that extended into the    Ddr2 gene transcript. Detailed phenotype analysis revealed that gonadal dysregulation underlies infertility in slie mice because all females were anovulatory and most adult males lacked spermatogenesis. The pituitary gland of prepubertal slie    mice was smaller than in wild-type mice. The basal levels and gene expression for pituitary and hypothalamic hormones, and gene expression for hypothalamic-releasing hormones, were not significantly different between slie and wild-type mice.    Circulating levels of IGF-1 did not differ in slie mice despite lower Igf-1 mRNA expression in the liver. After exogenous gonadotropin administration, the levels of secreted steroid hormones in both male and female adult slie mice were blunted    compared to adult wild-type, but was similar to prepubertal wild-type mice. Taken together, our results indicate that the absence of DDR2 leads to growth retardation and gonadal dysfunction due to peripheral defects in hormonal-responsive    pathways in slie mice.</p>

	]]>
</description>

<author>K Kano et al.</author>


</item>


<item>
<title>The recombinational anatomy of a mouse chromosome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1811</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1811</guid>
<pubDate>Tue, 08 May 2012 23:09:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Among mammals, genetic recombination occurs at highly delimited sites known as recombination hotspots. They are typically 1-2 kb long and vary as much as a 1,000-fold or more in recombination activity. Although much is known about    the molecular details of the recombination process itself, the factors determining the location and relative activity of hotspots are poorly understood. To further our understanding, we have collected and mapped the locations of 5,472 crossover    events along mouse Chromosome 1 arising in 6,028 meioses of male and female reciprocal F1 hybrids of C57BL/6J and CAST/EiJ mice. Crossovers were mapped to a minimum resolution of 225 kb, and those in the telomere-proximal 24.7 Mb were further    mapped to resolve individual hotspots. Recombination rates were evolutionarily conserved on a regional scale, but not at the local level. There was a clear negative-exponential relationship between the relative activity and abundance of hotspot    activity classes, such that a small number of the most active hotspots account for the majority of recombination. Females had 1.2x higher overall recombination than males did, although the sex ratio showed considerable regional variation.    Locally, entirely sex-specific hotspots were rare. The initiation of recombination at the most active hotspot was regulated independently on the two parental chromatids, and analysis of reciprocal crosses indicated that parental imprinting has    subtle effects on recombination rates. It appears that the regulation of mammalian recombination is a complex, dynamic process involving multiple factors reflecting species, sex, individual variation within species, and the properties of    individual hotspots.</p>

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</description>

<author>K Paigen et al.</author>


</item>


<item>
<title>T cell-specific siRNA delivery suppresses HIV-1 infection in humanized mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1810</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1810</guid>
<pubDate>Tue, 08 May 2012 23:08:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Evaluation of the therapeutic potential of RNAi for HIV infection has been hampered by the challenges of siRNA delivery and lack of suitable animal models.  Using a delivery method for T cells, we show that siRNA treatment can    dramatically suppress HIV infection. A CD7-specific single-chain antibody was conjugated to oligo-9-arginine peptide (scFvCD7-9R) for T cell-specific siRNA delivery in NOD/SCIDIL2rgamma-/- mice reconstituted with human lymphocytes (Hu-PBL) or    CD34+ hematopoietic stem cells (Hu-HSC). In HIV-infected Hu-PBL mice, treatment with anti-CCR5 (viral coreceptor) and antiviral siRNAs complexed to scFvCD7-9R controlled viral replication and prevented the disease-associated CD4 T cell loss. This    treatment also suppressed endogenous virus and restored CD4 T cell counts in mice reconstituted with HIV+ peripheral blood mononuclear cells.  Moreover, scFvCD7-9R could deliver antiviral siRNAs to naive T cells in Hu-HSC mice and effectively    suppress viremia in infected mice. Thus, siRNA therapy for HIV infection appears to be feasible in a preclinical animal model.</p>

	]]>
</description>

<author>P Kumar et al.</author>


</item>


<item>
<title>Mouse genetic models: an ideal system for understanding glaucomatous neurodegeneration and neuroprotection.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1809</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1809</guid>
<pubDate>Tue, 08 May 2012 23:08:44 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Howell GR, Libby RT, John SWM</author>


</item>


<item>
<title>Anesthesia and Analgesia in Laboratory Animals.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1808</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1808</guid>
<pubDate>Tue, 08 May 2012 23:08:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>Anesthetic considerations for in vivo imaging studies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1807</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1807</guid>
<pubDate>Tue, 08 May 2012 23:08:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Nicholson A, Klaunberg B</author>


</item>


<item>
<title>Monitoring of anesthesia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1806</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1806</guid>
<pubDate>Tue, 08 May 2012 23:08:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Smith JC, Danneman PJ</author>


</item>


<item>
<title>Beyond positional cloning of single gene mutations: use of mouse models to examine allelic variance and to identify genetic modifiers.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1805</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1805</guid>
<pubDate>Tue, 08 May 2012 23:08:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Nishina PM, Naggert JK</author>


</item>


<item>
<title>Mouse models: a key system in revolutionizing the understanding of glaucoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1804</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1804</guid>
<pubDate>Tue, 08 May 2012 23:08:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Howell GR, Marchant JK, John SWM</author>


</item>


<item>
<title>The mouse A/HeJ Y chromosome: another good Y gone bad.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1803</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1803</guid>
<pubDate>Tue, 08 May 2012 23:07:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>In both humans and mice there are numerous reports of Y chromosome abnormalities that interfere with sex determination. Recent studies in the mouse of one such mutation have identified Y chromosome nondisjunction during    preimplantation development as the cause of abnormal testis determination that results in a high frequency of true hermaphroditism. We report here that the mouse Y chromosome from the A/HeJ inbred strain induces similar aberrations in sex    determination.  Our analyses provide evidence, however, that the mechanism underlying these aberrations is not Y chromosome nondisjunction. On the basis of our findings, we postulate that a mutation at or near the centromere affects both the    segregation and sex-determining properties of the A/HeJ Y chromosome. This Y chromosome adds to the growing list of Y chromosome aberrations in humans and mice. In both species, the centromere of the Y is structurally and morphologically distinct    from the centromeres of all other chromosomes. We conclude that these centromeric features make the human and mouse Y chromosomes extremely sensitive to minor structural alterations, and that our studies provide yet another example of a good Y    chromosome gone 'bad.'</p>

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</description>

<author>P A. Hunt et al.</author>


</item>


<item>
<title>Quantitative trait loci for urinary albumin in crosses between C57BL/6J and A/J inbred mice in the presence and absence of Apoe.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1802</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1802</guid>
<pubDate>Tue, 08 May 2012 23:07:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>We investigated the effect of apolipoprotein E (Apoe) on albuminuria in the males of two independent F2 intercrosses between C57BL/6J and A/J mice, using wild-type inbred strains in the first cross and B6-Apoe(-/-) animals in the    second cross.  In the first cross, we identified three quantitative trait loci (QTL): chromosome (Chr) 2 [LOD 3.5, peak at 70 cM, confidence interval (C.I.)  28-88 cM]; Chr 9 (LOD 2.0, peak 5 cM, C.I. 5-25 cM); and Chr 19 (LOD 1.9, peak 49 cM,    C.I. 23-54 cM).  The Chr 2 and Chr 19 QTL were concordant with previously found QTL for renal damage in rat and human. The Chr 9 QTL was concordant with a locus found in rat.  The second cross, testing only Apoe(-/-) progeny, did not identify any    of these loci, but detected two other loci on Chr 4 (LOD 3.2, peak 54 cM, C.I. 29-73 cM) and Chr 6 (LOD 2.6, peak 33 cM, C.I. 11-61 cM), one of which was concordant with a QTL found in rat. The dependence of QTL detection on the presence of Apoe    and the concordance of these QTL with rat and human kidney disease QTL suggest that Apoe plays a role in renal damage.</p>

	]]>
</description>

<author>C Doorenbos et al.</author>


</item>


<item>
<title>Mouse neutrophils lacking lamin B-receptor expression exhibit aberrant development and lack critical functional responses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1801</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1801</guid>
<pubDate>Tue, 08 May 2012 23:07:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: The capacity of neutrophils to eradicate bacterial infections is dependent on normal development and activation of functional responses, which include chemotaxis and generation of oxygen radicals during the respiratory    burst. A unique feature of the neutrophil is its highly lobulated nucleus, which is thought to facilitate chemotaxis, but may also play a role in other critical neutrophil functions. Nuclear lobulation is dependent on expression of the inner    nuclear envelope protein, the lamin B receptor (LBR), mutations of which cause hypolobulated neutrophil nuclei in human Pelger-Huet anomaly and the "ichthyosis" (ic) phenotype in mice. In this study, we have investigated roles for LBR in    mediating neutrophil development and activation of multiple neutrophil functions, including chemotaxis and the respiratory burst. MATERIALS AND METHODS: A progenitor EML cell line was generated from an ic/ic mouse, and derived cells that lacked    LBR expression were induced to mature neutrophils and then examined for abnormal morphology and functional responses. RESULTS: Neutrophils derived from EML-ic/ic cells exhibited nuclear hypolobulation identical to that observed in ichthyosis    mice. The ic/ic neutrophils also displayed abnormal chemotaxis, supporting the notion that nuclear segmentation augments neutrophil extravasation. Furthermore, promyelocytic forms of ic/ic cells displayed decreased proliferative responses and    produced a deficient respiratory burst upon terminal maturation. CONCLUSIONS: Our studies of promyelocytes that lack LBR expression have identified roles for LBR in regulating not only the morphologic maturation of the neutrophil nucleus, but    also proliferative and functional responses that are critical to innate immunity.</p>

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</description>

<author>P Gaines et al.</author>


</item>


<item>
<title>Klebsiella oxytoca: opportunistic infections in laboratory rodents.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1800</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1800</guid>
<pubDate>Tue, 08 May 2012 23:07:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Opportunistic pathogens have become increasingly relevant as the causative agents of clinical disease and pathological lesions in laboratory animals. This study was conducted to evaluate the role of Klebsiella oxytoca as an    opportunistic pathogen in laboratory rodents. Therefore, K. oxytoca-induced lesions were studied from 2004 to early 2006 in naturally infected rodent colonies maintained at The Jackson Laboratory (TJL), Bar Harbor, USA, the Animal Research Centre    (Tierforschungszentrum, TFZ) of the University of Ulm, Germany and the Central Animal Facility (ZTM) of the Hannover Medical School, Germany. K. oxytoca infections were observed in substrains of C3H/HeJ mice, which carry the Tlr4(Lps-d) allele;    in LEW.1AR1-iddm rats, the latter being prone to diabetes mellitus; in immunodeficient NMRI-Foxn1(nu) mice; and in mole voles, Ellobius lutescens. The main lesions observed were severe suppurative otitis media, urogenital tract infections and    pneumonia. Bacteriological examination revealed K. oxytoca as monocultures in all cases. Clonality analysis performed on strains isolated at the ZTM and TFZ (serotyping, pulse field gel electrophoresis [PFGE], enterobacterial repetitive    intergenic consensus (ERIC) polymerase chain reaction, sequencing of 16S rRNA and rpoB genes) revealed that the majority of bacteria belonged to two clones, one in each facility, expressing the capsule type K55 (ZTM) or K72 (TFZ). Two strains,    one isolated at the ZTM and one at the TFZ, showed different PFGE and ERIC pattern than all other isolates and both expressed capsule type K35. In conclusion, K. oxytoca is an opportunistic pathogen capable of inducing pathological lesions in    different rodent species.</p>

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</description>

<author>A Bleich et al.</author>


</item>


<item>
<title>PLoS Genetics turns three: looking back, looking ahead.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1799</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1799</guid>
<pubDate>Tue, 08 May 2012 23:07:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W N. Frankel et al.</author>


</item>


<item>
<title>Human acute leukemia cells injected in NOD/LtSz-scid/IL-2Rgamma null mice generate a faster and more efficient disease compared to other NOD/scid-related strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1798</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1798</guid>
<pubDate>Tue, 08 May 2012 23:07:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Transplantation of human acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) primary cells and cell lines in different strains of immunodeficient mice has led to preclinical models extensively used to investigate    acute leukemia stem cells, biology and drug sensitivity. We studied the engraftment kinetics of AML and ALL cell lines and primary cells in 3 strains of NOD.CB17-Prkdc(scid) (NOD/scid, NS)-related mice (NOD.Cg-Prkdc(scid)B2m(tm1Unc)/J,    abbreviated NOD/scid/beta2 null, NSB; and NOD.Cg-Prkdc(scid)Il2rg(tm1Wjll)/SzJ, abbreviated NOD/scid/IL-2Rgamma null, NSG).  The engraftment of human malignant cells was investigated by means of clinicopathological criteria, flow cytometry, PCR    and immunohistochemistry. In NSG mice, we observed a significantly faster development of leukemia-related symptoms and a higher percentage of leukemia cells in the blood, in the marrow and in the spleen. The leukemia-related angiogenic switch    (measured as the number of circulating endothelial cells and progenitors) was faster in NSG compared to NS and NSB mice. These models will be instrumental to studies on leukemia-initiating stem cells, leukemia biology, preclinical treatment    studies, and to obtain patient-specific preclinical models to design and investigate patient-tailored therapies.</p>

	]]>
</description>

<author>A Agliano et al.</author>


</item>


<item>
<title>Macrophage colony-stimulating factor is indispensable for repopulation and differentiation of Kupffer cells but not for splenic red pulp macrophages in osteopetrotic (op/op) mice after macrophage depletion.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1797</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1797</guid>
<pubDate>Tue, 08 May 2012 23:06:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>We previously reported that macrophage colony-stimulating factor (M-CSF, CSF-1) played important roles in the process of the repopulation of Kupffer cells after their elimination by administration of liposome-entrapped    dichloromethylene diphosphonate (lipo-MDP). In this study, we examined the repopulation of Kupffer cells and splenic red pulp macrophages in osteopetrotic (op/op) mice defective in the production of functional M-CSF and their littermate mice by    using the lipo-MDP model. In untreated op/op mice, numbers of F4/80-positive Kupffer cells in the liver and F4/80-positive splenic red pulp macrophages were reduced.  Repopulation of Kupffer cells and splenic macrophages was observed in    littermate (op/+) mice liver by 14 days after depletion. However, in op/op mice, repopulation of Kupffer cells was not observed in Kupffer-cell-depleted op/op mice until 56 days after depletion, whereas splenic red pulp macrophages repopulated    and recovered to the level of control op/op mice by 10 days after depletion. Single injection of M-CSF was effective for the induction of the repopulation of Kupffer cells, and daily administration of M-CSF induced remarkable repopulation and    maturation of Kupffer cells and proliferation of macrophage precursor cells in the liver of Kupffer-cell-depleted op/op mice.  These results suggest that Kupffer cells are completely M-CSF-dependent tissue macrophages, whereas splenic red pulp    macrophages are composed of M-CSF-dependent macrophages and M-CSF-independent macrophages. This mouse model provides a useful tool for the study of effects of growth factor on Kupffer cell differentiation in vivo.</p>

	]]>
</description>

<author>T Yamamoto et al.</author>


</item>


<item>
<title>Candidate genes for plasma triglyceride, FFA, and glucose revealed from an intercross between inbred mouse strains NZB/B1NJ and NZW/LacJ.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1796</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1796</guid>
<pubDate>Tue, 08 May 2012 23:06:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>To identify the genes controlling plasma concentrations of triglycerides (TGs), FFAs, and glucose, we carried out a quantitative trait loci (QTL) analysis of the closely related mouse strains New Zealand Black (NZB/B1NJ) and New    Zealand White (NZW/LacJ), which share 63% of their genomes. The NZB x NZW F(2) progeny were genotyped and phenotyped to detect QTL, and then comparative genomics, bioinformatics, and sequencing were used to narrow the QTL and reduce the number of    candidate genes. Triglyceride concentrations were linked to loci on chromosomes (Chr) 4, 7, 8, 10, and 18. FFA concentrations were affected by a significant locus on Chr 4, a suggestive locus on Chr 16, and two interacting loci on Chr 2 and 15.    Plasma glucose concentrations were affected by QTL on Chr 2, 4, 7, 8, 10, 15, 17, and 18. Comparative genomics narrowed the QTL by 31% to 86%; haplotype analysis was usually able to further narrow it by 80%. We suggest several candidate genes:    Gba2 on Chr 4, Irs2 on Chr 8, and Ppargc1b on Chr 18 for TG; A2bp1 on Chr 16 for FFA; and G6pc2 on Chr 2 and Timp3 on Chr 10 for glucose.</p>

	]]>
</description>

<author>Z Su et al.</author>


</item>


<item>
<title>A single point mutation in the LN domain of LAMA2 causes muscular dystrophy and peripheral amyelination.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1795</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1795</guid>
<pubDate>Tue, 08 May 2012 23:06:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the gene encoding the basal lamina (BL) component laminin alpha2 (LAMA2) cause merosin-deficient congenital muscular dystrophy 1A (MDC1A), a complex disorder that includes hypomyelination and myodegeneration. In    dystrophia muscularis (dy) mice bearing Lama2 mutations, myofibers and Schwann cells fail to assemble stable BLs, which are thought to be crucial for myofiber survival and Schwann cell differentiation. Here, we describe defects in a new allele of    Lama2 in mice, nmf417, in which a point mutation substitutes Arg for Cys79 at a universally conserved CxxC motif in the laminin N-terminal (LN) domain; this domain mediates laminin-laminin interactions. nmf417 homozygosity caused progressive    myodegeneration and severe peripheral amyelination in nerve roots, similar to previous Lama2 mutations, but without the pervasive BL thinning previously associated with the disorder. In direct contrast to the previously characterized dy and dy2J    alleles, nmf417 homozygous myofibers frequently had thickened BLs. Severe amyelination in nmf417-mutant nerve roots suggested complete laminin 2 inactivation for Schwann cells, although myelinated fibers had normal BLs. The results reveal crucial    roles for the LN domain CxxC motif in both nerve and muscle, but challenge expected relationships between LN-domain function, Ln2 activity and BL stability. The nmf417 mutation provides a defined animal model in which to investigate mechanisms    and treatments for moderate forms of MDC1A.</p>

	]]>
</description>

<author>B L. Patton et al.</author>


</item>


<item>
<title>Dependence of antibody-mediated presentation of antigen on FcRn.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1794</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1794</guid>
<pubDate>Tue, 08 May 2012 23:06:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The neonatal Fc receptor for IgG (FcRn) is a distant member of the MHC class I protein family. It binds IgG and albumin in a pH-dependent manner and protects these from catabolism by diverting them from a degradative fate in    lysosomes. In addition, FcRn-mediated IgG transport across epithelial barriers is responsible for the transmission of IgG from mother to infant and can also enhance IgG-mediated antigen uptake across mucosal epithelia. We now show a previously    undescribed role for FcRn in mediating the presentation of antigens by dendritic cells when antigens are present as a complex with antibody by uniquely directing multimeric immune complexes, but not monomeric IgG, to lysosomes.</p>

	]]>
</description>

<author>S W. Qiao et al.</author>


</item>


<item>
<title>A close examination of genes within quantitative trait loci of bone mineral density in whole mouse genome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1793</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1793</guid>
<pubDate>Tue, 08 May 2012 23:06:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bone mineral density (BMD) is one of the strongest determinants of osteoporotic fracture risk. Over the last decade, a large number of quantitative trait loci (QTL) that regulate BMD have been identified using the mouse model. In an    attempt to examine the relationship between those QTL and gene distribution in the mouse genome, we searched PubMed with keywords bone and QTL for every publication up to January 2007; we obtained a total of 75 QTL of BMD. We next obtained genes    within a QTL for measurements of BMD from the Ensembl database. We then evaluated the potential connection of every gene with bone biology with Online Mendelian Inheritance in Man (OMIM) and PubMed by using eight key words: bone mineral density,    BMD, bone strength, bone size, osteoporosis, osteoblast, osteoclast, and fracture. We obtained a total of 15,084 genes for 75 BMD QTL covering 1,211,376,097 base pairs of genomic sequence. Although this very large number of genes exists within    QTL regions, only 291 were identified as candidate genes according to our bioinformatics search. Importantly, the association between polymorphism of many candidate genes and BMD has been reported in human studies.  Thus, updated genome    information and resources should provide new insight for gene identification of QTL. Accordingly, the comprehensive search of candidate genes in the genome for known QTL may provide unexpected benefits for QTL studies.</p>

	]]>
</description>

<author>Q Xiong et al.</author>


</item>


<item>
<title>Expression of VLDLR in the retina and evolution of subretinal neovascularization in the knockout mouse model&apos;s retinal angiomatous proliferation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1792</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1792</guid>
<pubDate>Tue, 08 May 2012 23:06:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Very-low-density lipoprotein receptor (VLDLR) in knockout mice (vldlr(-/-)) has been reported to induce subretinal neovascularization.  Therefore, VLDLR expression in the wild-type mouse retina was investigated and the    retinal angiogenic process in vldlr(-/-) mice was characterized. METHODS: VLDLR expression in the retina and in purified retinal vascular endothelial cells (RECs) and retinal pigment epithelial (RPE) cells was determined by reverse    transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry.  Angiogenic evolution in vldlr(-/-) mice was examined by fundus fluorescein angiography, histology, double-staining of FITC-dextran perfusion and elastin    immunohistochemistry, isolectin staining, and confocal fluorescence microscopy.  RESULTS: VLDLR mRNA was detected in the wild-type mouse retina and in purified RECs and RPE cells. The VLDLR protein was localized in the RPE layer, vessels in the    ganglion cell layer, and around the outer limiting membrane of the retina.  The retinal pathogenic process in vldlr(-/-) mice recapitulates key features of retinal angiomatous proliferation (RAP) in humans, a subtype of neovascular age-related    macular degeneration (AMD). These include neovascular growth originating from retinal vessels and progressing to the subretinal space with intraretinal, subretinal, and choroidal angiogenic stages, RPE disruption and Bruch membrane exposure,    retinal-choroidal anastomosis, subsequent photoreceptor degeneration, RPE hyperplasia, and subretinal fibrosis at the end stage.  CONCLUSIONS: VLDLR is expressed in the wild-type mouse retina, especially in RECs and RPE cells. The vldlr(-/-)    mouse exhibits histologic and angiographic characteristics of RAP and is a reproducible animal model facilitating studies of the molecular mechanisms of RAP.</p>

	]]>
</description>

<author>W Hu et al.</author>


</item>


<item>
<title>Mapping of genetic modifiers of Nr2e3 rd7/rd7 that suppress retinal degeneration and restore blue cone cells to normal quantity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1791</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1791</guid>
<pubDate>Tue, 08 May 2012 23:06:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>The retinal degeneration 7 (rd7) mouse, lacking expression of the Nr2e3 gene, exhibits retinal dysplasia and a slow, progressive degeneration due to an abnormal production of blue opsin-expressing cone cells. In this study we    evaluated three strains of mice to identify alleles that would slow or ameliorate the retinal degeneration observed in Nr2e3 (rd7/rd7) mice. Our studies reveal that genetic background greatly influences the expression of the Nr2e3 (rd7/rd7)    phenotype and that the inbred mouse strains CAST/EiJ, AKR/J, and NOD.NON-H2 (nb1) carry alleles that confer resistance to Nr2e3 (rd7/rd7)-induced retinal degeneration. B6.Cg-Nr2e3 (rd7/rd7) mice were outcrossed to each strain and the F(1) progeny    were intercrossed to produce F(2) mice. In each intercross, 20-24% of the total F(2) progeny were homozygous for the Nr2e3 (rd7/rd7) mutation in a mixed genetic background; approximately 28-48% of the Nr2e3 (rd7/rd7) homozygotes were suppressed    for the degenerative retina phenotype in a mixed genetic background. The suppressed mice had no retinal spots and normal retinal morphology with a normal complement of blue opsin-expressing cone cells. An initial genome scan revealed a    significant association of the suppressed phenotype with loci on chromosomes 8 and 19 with the CAST/EiJ background, two marginal loci on chromosomes 7 and 11 with the AKR/J background, and no significant QTL with the NOD.NON-H2 (nb1) background.    We did not observe any significant epistatic effects in this study. Our results suggest that there are several genes that are likely to act in the same or parallel pathway as NR2E3 that can rescue the Nr2e3 (rd7/rd7) phenotype and may serve as    potential therapeutic targets.</p>

	]]>
</description>

<author>N B. Haider et al.</author>


</item>


<item>
<title>Gene Ontology annotations: what they mean and where they come from.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1790</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1790</guid>
<pubDate>Tue, 08 May 2012 23:05:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>To address the challenges of information integration and retrieval, the computational genomics community increasingly has come to rely on the methodology of creating annotations of scientific literature using terms from controlled    structured vocabularies such as the Gene Ontology (GO). Here we address the question of what such annotations signify and of how they are created by working biologists. Our goal is to promote a better understanding of how the results of    experiments are captured in annotations, in the hope that this will lead both to better representations of biological reality through annotation and ontology development and to more informed use of GO resources by experimental    scientists.</p>

	]]>
</description>

<author>D P. Hill et al.</author>


</item>


<item>
<title>Expanded CD34+ human umbilical cord blood cells generate multiple lymphohematopoietic lineages in NOD-scid IL2rgamma(null) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1789</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1789</guid>
<pubDate>Tue, 08 May 2012 23:05:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Umbilical cord blood (UCB) is increasingly being used for human hematopoietic stem cell (HSC) transplantation in children but often requires pooling multiple cords to obtain sufficient numbers for transplantation in adults. To    overcome this limitation, we have used an ex vivo two-week culture system to expand the number of hematopoietic CD34(+) cells in cord blood. To assess the in vivo function of these expanded CD34(+) cells, cultured human UCB containing 1 x 10(6)    CD34(+) cells were transplanted into conditioned NOD-scid IL2rgamma(null) mice.  The expanded CD34(+) cells displayed short- and long-term repopulating cell activity. The cultured human cells differentiated into myeloid, B-lymphoid, and erythroid    lineages, but not T lymphocytes. Administration of human recombinant TNFalpha to recipient mice immediately prior to transplantation promoted human thymocyte and T-cell development. These T cells proliferated vigorously in response to TCR    cross-linking by anti-CD3 antibody. Engrafted TNFalpha-treated mice generated antibodies in response to T-dependent and T-independent immunization, which was enhanced when mice were co-treated with the B cell cytokine BLyS. Ex vivo expanded    CD34(+) human UCB cells have the capacity to generate multiple hematopoietic lineages and a functional human immune system upon transplantation into TNFalpha-treated NOD-scid IL2rgamma(null) mice.</p>

	]]>
</description>

<author>L J. Giassi et al.</author>


</item>


<item>
<title>Genetic ablation of alphav integrins in epithelial cells of the eyelid skin and conjunctiva leads to squamous cell carcinoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1788</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1788</guid>
<pubDate>Tue, 08 May 2012 23:05:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Integrin-mediated cell adhesion and signaling events are essential for the proper development and homeostasis of most epithelial tissues. Dysregulation of integrin expression and function can cause abnormal epithelial cell    proliferation and/or differentiation, contributing to the pathogenesis of malignant epithelial cancers. Here we report on the use of a conditional knockout strategy exploiting the Cre/Lox technology to study the in vivo functions of alphav    integrins during epithelial cell proliferation and differentiation. We show that genetic ablation of alphav integrin expression in basal epithelial cells of the eyelid skin and conjunctiva causes the formation of tumors that are strikingly    similar to the malignant epithelial cancer, squamous cell carcinoma. These data suggest a mechanism whereby alphav integrins normally suppress epithelial cell proliferation, likely via adhesion to ECM ligands, as well as by the modulation of    intracellular signaling cascades. We propose that alphav gene deletion eliminates normal integrin-mediated growth suppression, ultimately leading to cellular transformation and tumorigenesis. Hence, these studies reveal a novel tumor    suppressor-like function of alphav integrins and provide a genetically tractable mouse model for studying the pathogenesis of squamous cell carcinoma and related cancers of epithelial origin, as well as to test and develop novel therapeutic    compounds to treat or prevent squamous cell carcinoma of the skin.</p>

	]]>
</description>

<author>J H. McCarty et al.</author>


</item>


<item>
<title>Regulation of Alstrom syndrome gene expression during adipogenesis and its relationship with fat cell insulin sensitivity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1787</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1787</guid>
<pubDate>Tue, 08 May 2012 23:05:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alstrom syndrome (ALMS) is an autosomal recessive genetic disease with characteristic phenotypical features including multi-organ fibrosis, insulin resistance, obesity and type 2 diabetes. ALMS1, a ubiquitously expressed gene    mutated in ALMS patients, gives rise to a protein of unknown function localized to basal bodies of ciliated cells and centrosomes. Together with Bardet-Biedl syndrome, ALMS is a member of genetic ciliopathies, but the link between    cilia/centrosome deficits and metabolic abnormalities remains to be determined.  In this study for the first time we quantified Alms1 expression in a cellular model of adipogenesis during the differentiation of 3T3-L1 cells. An early decrease in    Alms1 mRNA was observed during preadipocyte to adipocyte conversion.  However, acute treatment of preadipocytes with the adipogenic factors did not result in significant change of Alms1 expression. In addition, to study the possible relationship    between Alms1 and the degree of fat cell insulin sensitivity, as assessed with an insulin-dependent 2-[1-3H]-deoxyglucose uptake assay, we induced either a reduction or an increase in 3T3-L1 adipocytes insulin sensitivity by a chronic treatment    with insulin or rosiglitazone respectively. In all these conditions Alms1 expression remained unchanged. In conclusion, our results show that Alms1 is expressed at higher level in preadipocytes suggesting a role of the gene in the early phase of    adipogenesis. Moreover, changes in fat cell insulin sensitivity do not imply any effect on Alms1 expression.</p>

	]]>
</description>

<author>S Romano et al.</author>


</item>


<item>
<title>Impaired embryonic haematopoiesis yet normal arterial development in the absence of the Notch ligand Jagged1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1786</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1786</guid>
<pubDate>Tue, 08 May 2012 23:05:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Specific deletion of Notch1 and RBPjkappa in the mouse results in abrogation of definitive haematopoiesis concomitant with the loss of arterial identity at embryonic stage. As prior arterial determination is likely to be required    for the generation of embryonic haematopoiesis, it is difficult to establish the specific haematopoietic role of Notch in these mutants. By analysing different Notch-ligand-null embryos, we now show that Jagged1 is not required for the    establishment of the arterial fate but it is required for the correct execution of the definitive haematopoietic programme, including expression of GATA2 in the dorsal aorta. Moreover, successful haematopoietic rescue of the Jagged1-null AGM    cells was obtained by culturing them with Jagged1-expressing stromal cells or by lentiviral-mediated transduction of the GATA2 gene. Taken together, our results indicate that Jagged1-mediated activation of Notch1 is responsible for regulating    GATA2 expression in the AGM, which in turn is essential for definitive haematopoiesis in the mouse.</p>

	]]>
</description>

<author>Moreno A. Robert et al.</author>


</item>


<item>
<title>Utility of antiPax5 in the diagnosis of lymphoproliferative disorders and neoplasia in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1785</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1785</guid>
<pubDate>Tue, 08 May 2012 23:05:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>CD45R/B220 antigen (B220) is a common mouse panB-cell marker used for paraffin-embedded tissues. However, antiB220 has limited specificity in diagnostic pathology because the B220 antigen is expressed on subsets of cytotoxic T    lymphocytes and natural killer cells, on plasmacytic dendritic cells, and on T lymphocytes of mice with the lymphoproliferative disorder associated with Fas (lymphoproliferative mutant mouse, B6.MRL-Fas(lpr/J)) or Fas ligand (generalized    lymphoproliferative disease mutant mouse, C3H/ HeJ-Fasl(gld/J) or B6Smn.C3-Fasl(gld/J)). In addition, mouse B lymphocytes vary in the amount of B220 expressed, and some subsets of mouse B lymphocytes do not express B220 at all. In comparison,    Pax5 expression (detected by immunohistochemistry using antiPax5) offers greater specificity and sensitivity because of its earlier expression during B-cell differentiation, its ability to detect all committed B cells, and its restriction to the    B-cell lineage. Here we describe the use of an antibody to human Pax5 in diagnostic pathology with formalin-fixed, paraffin-embedded mouse tissue.</p>

	]]>
</description>

<author>J E. Rehg et al.</author>


</item>


<item>
<title>Synaptojanin 1-linked phosphoinositide dyshomeostasis and cognitive deficits in mouse models of Down&apos;s syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1784</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1784</guid>
<pubDate>Tue, 08 May 2012 23:05:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Phosphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P(2)] is a signaling phospholipid implicated in a wide variety of cellular functions. At synapses, where normal PtdIns(4,5)P(2) balance is required for proper neurotransmission, the    phosphoinositide phosphatase synaptojanin 1 is a key regulator of its metabolism. The underlying gene, SYNJ1, maps to human chromosome 21 and is thus a candidate for involvement in Down's syndrome (DS), a complex disorder resulting from the    overexpression of trisomic genes. Here, we show that PtdIns(4,5)P(2) metabolism is altered in the brain of Ts65Dn mice, the most commonly used model of DS. This defect is rescued by restoring Synj1 to disomy in Ts65Dn mice and is recapitulated in    transgenic mice overexpressing Synj1 from BAC constructs. These transgenic mice also exhibit deficits in performance of the Morris water maze task, suggesting that PtdIns(4,5)P(2) dyshomeostasis caused by gene dosage imbalance for Synj1 may    contribute to brain dysfunction and cognitive disabilities in DS.</p>

	]]>
</description>

<author>S V. Voronov et al.</author>


</item>


<item>
<title>Absence seizures in C3H/HeJ and knockout mice caused by mutation of the AMPA receptor subunit Gria4.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1783</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1783</guid>
<pubDate>Tue, 08 May 2012 23:04:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Absence epilepsy, characterized by spike-wave discharges (SWD) in the electroencephalogram, arises from aberrations within the circuitry of the cerebral cortex and thalamus that regulates awareness. The inbred mouse strain C3H/HeJ    is prone to absence seizures, with a major susceptibility locus, spkw1, accounting for most of the phenotype. Here we find that spkw1 is associated with a hypomorphic retroviral-like insertion mutation in the Gria4 gene, encoding one of the four    amino-3-hydroxy-5-methyl-4isoxazolepropionic acid (AMPA) receptor subunits in the brain. Consistent with this, Gria4 knockout mice also have frequent SWD and do not complement spkw1. In contrast, null mutants for the related gene Gria3 do not    have SWD, and Gria3 loss actually lowers SWD of spkw1 homozygotes. Gria3 and Gria4 encode the predominant AMPA receptor subunits in the reticular thalamus, which is thought to play a central role in seizure genesis by inhibiting thalamic relay    cells and promoting rebound burst firing responses. In Gria4 mutants, synaptic excitation of inhibitory reticular thalamic neurons is enhanced, with increased duration of synaptic responses-consistent with what might be expected from reduction of    the kinetically faster subunit of AMPA receptors encoded by Gria4. These results demonstrate for the first time an essential role for Gria4 in the brain, and suggest that abnormal AMPA receptor-dependent synaptic activity can be involved in the    network hypersynchrony that underlies absence seizures.</p>

	]]>
</description>

<author>B Beyer et al.</author>


</item>


<item>
<title>Minimum information specification for in situ hybridization and immunohistochemistry experiments (MISFISHIE).</title>
<link>http://mouseion.jax.org/stfb2000_2009/1782</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1782</guid>
<pubDate>Tue, 08 May 2012 23:04:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>One purpose of the biomedical literature is to report results in sufficient detail that the methods of data collection and analysis can be independently replicated and verified. Here we present reporting guidelines for gene    expression localization experiments: the minimum information specification for in situ hybridization and immunohistochemistry experiments (MISFISHIE). MISFISHIE is modeled after the Minimum Information About a Microarray Experiment (MIAME)    specification for microarray experiments. Both guidelines define what information should be reported without dictating a format for encoding that information.  MISFISHIE describes six types of information to be provided for each experiment:    experimental design, biomaterials and treatments, reporters, staining, imaging data and image characterizations. This specification has benefited the consortium within which it was developed and is expected to benefit the wider research    community. We welcome feedback from the scientific community to help improve our proposal.</p>

	]]>
</description>

<author>E W. Deutsch et al.</author>


</item>


<item>
<title>Randomized trial of once-weekly parathyroid hormone (1-84) on bone mineral density and remodeling.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1781</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1781</guid>
<pubDate>Tue, 08 May 2012 23:04:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>CONTEXT: Daily PTH administration increases bone mineral density (BMD) and reduces fracture risk. However, cost and compliance significantly limit clinical use. OBJECTIVE: Our objective was to determine whether less frequent PTH    administration increases lumbar spine BMD. PARTICIPANTS, DESIGN, AND SETTING: Fifty postmenopausal women ages 45-70 yr with femoral neck BMD T-score between -1.0 and -2.0 participated in a double-blind, randomized, placebo-controlled trial at St.    Joseph Hospital, Bangor, ME. INTERVENTION: Subjects received sc injections of daily PTH(1-84) (100 mug) or placebo for 1 month, followed by weekly injections (PTH or placebo) for 11 months. OUTCOMES: Change in lumbar spine dual-energy x-ray    absorptiometry areal BMD (primary) was assessed.  Secondary outcomes included volumetric BMD at spine and hip by quantitative computed tomography, trabecular bone microarchitecture by magnetic resonance imaging of distal radius, and biochemical    bone turnover markers. RESULTS: At 12 months, lumbar spine areal BMD increased 2.1% in PTH-treated women compared with placebo (P = 0.03). Vertebral trabecular volumetric BMD increased 3.8% in PTH-treated women compared with placebo group (P =    0.08). PTH-treated women also had higher distal radial trabecular bone volume, number, and thickness compared with placebo-treated women (P < 0.04). After 1 month of daily PTH, N-terminal propeptide of type I collagen (P1NP) was markedly    increased compared with placebo (P < 0 .0001), and a difference persisted, although lessened, throughout the study. Bone resorption indices were unchanged in PTH-treated women and were reduced in the placebo group. CONCLUSION: Once-weekly PTH    after 1 month of daily treatment increases spine BMD, radial trabecular bone, and bone formation markers in postmenopausal women. These results suggest that less frequent alternatives to daily PTH dosing for 2 yr could be effective. Additional    studies are required to define the optimal frequency of PTH administration.</p>

	]]>
</description>

<author>D M. Black et al.</author>


</item>


<item>
<title>Rapid identification of MHC class I-restricted antigens relevant to autoimmune diabetes using retrogenic T cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1780</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1780</guid>
<pubDate>Tue, 08 May 2012 23:04:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The method described herein provides a novel strategy for the rapid identification of CD8(+) T cell epitopes relevant to type 1 diabetes in the context of the nonobese diabetic (NOD) mouse model of disease. Obtaining the large    number of antigen-sensitive monospecific T cells required for conventional antigen discovery methods has historically been problematic due to (1) difficulties in culturing autoreactive CD8(+) T cells from NOD mice and (2) the large time and    resource investments required for the generation of transgenic NOD mice. We circumvented these problems by exploiting the rapid generation time of retrogenic (Rg) mice, relative to transgenic mice, as a novel source of sensitive monospecific    CD8(+) T cells, using the diabetogenic AI4 T cell receptor on NOD.SCID and NOD.Rag1(-/-) backgrounds as a model. Rg AI4 T cells are diabetogenic in vivo, demonstrating for the first time that Rg mice are a means for assessing the pathogenic    potential of CD8(+) T cell receptor specificities.  In order to obtain a sufficient number of Rg CD8(+) T cells for antigen screens, we optimized a method for their in vitro culture that resulted in a approximately 500 fold expansion. We    demonstrate the high sensitivity and specificity of expanded Rg AI4 T cells in the contexts of (1) specific peptide challenge, (2) islet cytotoxicity, and (3) their ability to resolve previously defined mimotope candidates from a positional    scanning peptide library. Our method is the first to combine the speed of Rg technology with an optimized in vitro Rg T cell expansion protocol to enable the rapid discovery of T cell antigens.</p>

	]]>
</description>

<author>R J. Chaparro et al.</author>


</item>


<item>
<title>From ER to Eph receptors: new roles for VAP fragments.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1779</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1779</guid>
<pubDate>Tue, 08 May 2012 23:04:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dominantly inherited mutations in an endoplasmic reticulum protein called VAPB have been found in a subset of patients with a rare familial form of amyotrophic lateral sclerosis (ALS). In this issue, Tsuda et al. (2008) identify a    secreted form of VAPB that binds directly to Eph receptors inducing their activation and signaling, providing fresh insights into ALS pathogenesis, including non-neuronal aspects of this disorder.</p>

	]]>
</description>

<author>S L. Ackerman et al.</author>


</item>


<item>
<title>Through regulation of TCR expression levels, an Idd7 region gene(s) interactively contributes to the impaired thymic deletion of autoreactive diabetogenic CD8+ T cells in nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1778</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1778</guid>
<pubDate>Tue, 08 May 2012 23:04:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>When expressed in NOD, but not C57BL/6 (B6) genetic background mice, the common class I variants encoded by the H2g7 MHC haplotype aberrantly lose the ability to mediate the thymic deletion of autoreactive CD8+ T cells contributing    to type 1 diabetes (T1D). This indicated some subset of the T1D susceptibility (Idd) genes located outside the MHC of NOD mice interactively impair the negative selection of diabetogenic CD8+ T cells. In this study, using both linkage and    congenic strain analyses, we demonstrate contributions from a polymorphic gene(s) in the previously described Idd7 locus on the proximal portion of Chromosome 7 predominantly, but not exclusively, determines the extent to which H2g7 class I    molecules can mediate the thymic deletion of diabetogenic CD8+ T cells as illustrated using the AI4 TCR transgenic system. The polymorphic Idd7 region gene(s) appears to control events that respectively result in high vs low expression of the AI4    clonotypic TCR alpha-chain on developing thymocytes in B6.H2g7 and NOD background mice. This expression difference likely lowers levels of the clonotypic AI4 TCR in NOD, but not B6.H2g7 thymocytes, below the threshold presumably necessary to    induce a signaling response sufficient to trigger negative selection upon Ag engagement. These findings provide further insight to how susceptibility genes, both within and outside the MHC, may interact to elicit autoreactive T cell responses    mediating T1D development in both NOD mice and human patients.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title>Mitochondrial oxidative phosphorylation and energetic status are reflected by morphology of mitochondrial network in INS-1E and HEP-G2 cells viewed by 4Pi microscopy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1777</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1777</guid>
<pubDate>Tue, 08 May 2012 23:04:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mitochondria in numerous cell types, especially in cultured cells, form a reticular network undergoing constant fusion and fission. The three dimensional (3D) morphology of these networks however has not been studied in detail to    our knowledge. We have investigated insulinoma INS-1E and hepatocellular carcinoma HEP-G2 cells transfected with mitochondria-addressed GFP. Using 4Pi microscopy, 3D morphology changes responding to decreased oxidative phosphorylation and/or    energetic status could be observed in these cells at an unprecedented 100 nm level of detail. In INS-1E cells cultivated at 11 mM glucose, the mitoreticulum appears predominantly as one interconnected mitochondrion with a nearly constant 262+/-26    nm tubule diameter. If cultured at 5 mM glucose, INS-1E cells show 311+/-36 nm tubules coexisting with numerous flat cisternae. Similar interconnected 284+/-38 nm and 417+/-110 nm tubules were found in HEP-G2 cells cultivated at 5 mM and    hyperglycaemic 25 mM glucose, respectively. With rotenone inhibiting respiration to approximately 10%, disintegration into several reticula and numerous approximately 300 nm spheres or short tubules was observed.  De-energization by uncoupling    additionally led to formation of rings and bulky cisternae of 1.4+/-0.4 microm diameter. Rotenone and uncoupler acted synergically in INS-1E cells and increased fusion (ongoing with fission) forming bowl-like shapes. In HEP-G2 cells fission    partially ceased with FCCP plus rotenone. Thus we have revealed previously undescribed details for shapes upon mitochondrial disintegration and clearly demonstrate that high resolution 3D microscopy is required for visualization of mitochondrial    network. We recommend 4Pi microscopy as a new standard.</p>

	]]>
</description>

<author>Hlavata L. Plecita et al.</author>


</item>


<item>
<title>Alopecia areata.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1776</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1776</guid>
<pubDate>Tue, 08 May 2012 23:03:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The pathogenesis of organ specific, cell mediated autoimmune alopecia areata (AA) has substantially progressed in the last decade. These advances are partly based upon advances in immunology and genetics, improved technological    methodology in RNA, DNA, proteomics, and computer analyses, as well as the development of the C3H/HeJ mouse model of AA. The discovery that full thickness skin grafts transfer AA from C3H/HeJ mice that spontaneously develop AA to multiple    non-affected C3H/HeJ mice greatly shortened the time of AA onset and provided many more affected mice in this highly reproducible model of AA. These methodological and genetic advances combine to form practical bases for identifying subtypes of    human and mouse AA, characterizing disease mechanisms, improving currently available treatments, and developing new, more effective therapies. In the next decade even more exciting new insights into the pathogenesis of subtypes of human AA, their    genetic bases, and therapy development will become available based on in-depth data on specific gene mutations and signaling pathways involved. Other organ specific autoimmune diseases will surely benefit from the rapid progress in understanding    AA.</p>

	]]>
</description>

<author>L E. King et al.</author>


</item>


<item>
<title>Seeing the world through a new set of glasses: emerging technologies for the study of cell nuclei and chromosomes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1775</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1775</guid>
<pubDate>Tue, 08 May 2012 23:03:48 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>L Shopland et al.</author>


</item>


<item>
<title>A critical assessment of Mus musculus gene function prediction using integrated genomic evidence.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1774</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1774</guid>
<pubDate>Tue, 08 May 2012 23:03:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Several years after sequencing the human genome and the mouse genome, much remains to be discovered about the functions of most human and mouse genes.  Computational prediction of gene function promises to help focus    limited experimental resources on the most likely hypotheses. Several algorithms using diverse genomic data have been applied to this task in model organisms; however, the performance of such approaches in mammals has not yet been evaluated.     RESULTS: In this study, a standardized collection of mouse functional genomic data was assembled; nine bioinformatics teams used this data set to independently train classifiers and generate predictions of function, as defined by Gene Ontology    (GO) terms, for 21,603 mouse genes; and the best performing submissions were combined in a single set of predictions. We identified strengths and weaknesses of current functional genomic data sets and compared the performance of function    prediction algorithms. This analysis inferred functions for 76% of mouse genes, including 5,000 currently uncharacterized genes. At a recall rate of 20%, a unified set of predictions averaged 41% precision, with 26% of GO terms achieving a    precision better than 90%. CONCLUSION: We performed a systematic evaluation of diverse, independently developed computational approaches for predicting gene function from heterogeneous data sources in mammals. The results show that currently    available data for mammals allows predictions with both breadth and accuracy. Importantly, many highly novel predictions emerge for the 38% of mouse genes that remain uncharacterized.</p>

	]]>
</description>

<author>Castillo L. Pena et al.</author>


</item>


<item>
<title>Reduced DIDS-sensitive chloride conductance in Ae1-/- mouse erythrocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1773</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1773</guid>
<pubDate>Tue, 08 May 2012 23:03:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The resting membrane potential of the human erythrocyte is largely determined by a constitutive Cl(-) conductance approximately 100-fold greater than the resting cation conductance. The 4,4'-diisothiocyanostilbene-2,2'-disulfonic    acid (DIDS)-sensitive electroneutral Cl(-) transport mediated by the human erythroid Cl(-)/HCO(3)(-) exchanger, AE1 (SLC4A1, band 3) is >10,000-fold greater than can be accounted for by the Cl(-) conductance of the red cell. The molecular    identities of conductive anion pathways across the red cell membrane remain poorly defined. We have examined red cell Cl(-) conductance in the Ae1(-/-) mouse as a genetic test of the hypothesis that Ae1 mediates DIDS-sensitive Cl(-) conductance    in mouse red cells. We report here that wildtype mouse red cell membrane potential resembles that of human red cells in the predominance of its Cl(-) conductance. We show with four technical approaches that the DIDS-sensitive component of    erythroid Cl(-) conductance is reduced or absent from Ae1(-/-) red cells. These results are consistent with the hypothesis that the Ae1 anion exchanger polypeptide can operate infrequently in a conductive mode. However, the fragile red cell    membrane of the Ae1(-/-) mouse red cell exhibits reduced abundance or loss of multiple polypeptides. Thus, loss of one or more distinct, DIDS-sensitive anion channel polypeptide(s) from the Ae1(-/-) red cell membrane cannot be ruled out as an    explanation for the reduced DIDS-sensitive anion conductance.</p>

	]]>
</description>

<author>S L. Alper et al.</author>


</item>


<item>
<title>Notch signaling regulates bile duct morphogenesis in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1772</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1772</guid>
<pubDate>Tue, 08 May 2012 23:03:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Alagille syndrome is a developmental disorder caused predominantly by mutations in the Jagged1 (JAG1) gene, which encodes a ligand for Notch family receptors. A characteristic feature of Alagille syndrome is intrahepatic    bile duct paucity. We described previously that mice doubly heterozygous for Jag1 and Notch2 mutations are an excellent model for Alagille syndrome. However, our previous study did not establish whether bile duct paucity in Jag1/Notch2 double    heterozygous mice resulted from impaired differentiation of bile duct precursor cells, or from defects in bile duct morphogenesis. METHODOLOGY/PRINCIPAL FINDINGS: Here we characterize embryonic biliary tract formation in our previously described    Jag1/Notch2 double heterozygous Alagille syndrome model, and describe another mouse model of bile duct paucity resulting from liver-specific deletion of the Notch2 gene. CONCLUSIONS/SIGNIFICANCE: Our data support a model in which bile duct    paucity in Notch pathway loss of function mutant mice results from defects in bile duct morphogenesis rather than cell fate specification.</p>

	]]>
</description>

<author>J Lozier et al.</author>


</item>


<item>
<title>High-precision structural analysis of subnuclear complexes in fixed and live cells via spatially modulated illumination (SMI) microscopy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1771</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1771</guid>
<pubDate>Tue, 08 May 2012 23:03:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Spatially modulated illumination (SMI) microscopy is a method of wide field fluorescence microscopy featuring interferometric illumination, which delivers structural information about nanoscale architecture in fluorescently labelled    cells. The first prototype of the SMI microscope proved its applicability to a wide range of biological questions. For the SMI live cell imaging this system was enhanced in terms of the development of a completely new upright configuration.  This    so called Vertico-SMI transfers the advantages of SMI nanoscaling to vital biological systems, and is shown to work consistently at different temperatures using both oil- and water-immersion objective lenses. Furthermore, we increased the speed    of data acquisition to minimize errors in the detection signal resulting from cellular or object movement. By performing accurate characterization, the present Vertico-SMI now offers a fully-fledged microscope enabling a complete    three-dimensional (3D) SMI data stack to be acquired in less than 2 seconds. We have performed live cell measurements of a tet-operator repeat insert in U2OS cells, which provided the first in vivo signatures of subnuclear complexes. Furthermore,    we have successfully implemented an optional optical configuration allowing the generation of high-resolution localization microscopy images of a nuclear pore complex distribution.</p>

	]]>
</description>

<author>J Reymann et al.</author>


</item>


<item>
<title>Spatial quantitative analysis of fluorescently labeled nuclear structures: problems, methods, pitfalls.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1770</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1770</guid>
<pubDate>Tue, 08 May 2012 23:03:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>The vast majority of microscopic data in biology of the cell nucleus is currently collected using fluorescence microscopy, and most of these data are subsequently subjected to quantitative analysis. The analysis process unites a    number of steps, from image acquisition to statistics, and at each of these steps decisions must be made that may crucially affect the conclusions of the whole study. This often presents a really serious problem because the researcher is    typically a biologist, while the decisions to be taken require expertise in the fields of physics, computer image analysis, and statistics. The researcher has to choose between multiple options for data collection, numerous programs for    preprocessing and processing of images, and a number of statistical approaches. Written for biologists, this article discusses some of the typical problems and errors that should be avoided. The article was prepared by a team uniting expertise in    biology, microscopy, image analysis, and statistics. It considers the options a researcher has at the stages of data acquisition (choice of the microscope and acquisition settings), preprocessing (filtering, intensity normalization,    deconvolution), image processing (radial distribution, clustering, co-localization, shape and orientation of objects), and statistical analysis.</p>

	]]>
</description>

<author>O Ronneberger et al.</author>


</item>


<item>
<title>An en masse phenotype and function prediction system for Mus musculus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1769</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1769</guid>
<pubDate>Tue, 08 May 2012 23:02:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Individual researchers are struggling to keep up with the accelerating emergence of high-throughput biological data, and to extract information that relates to their specific questions. Integration of accumulated    evidence should permit researchers to form fewer - and more accurate - hypotheses for further study through experimentation. RESULTS: Here a method previously used to predict Gene Ontology (GO) terms for Saccharomyces cerevisiae (Tian et al.:    Combining guilt-by-association and guilt-by-profiling to predict Saccharomyces cerevisiae gene function. Genome Biol 2008, 9(Suppl 1):S7) is applied to predict GO terms and phenotypes for 21,603 Mus musculus genes, using a diverse collection of    integrated data sources (including expression, interaction, and sequence-based data). This combined 'guilt-by-profiling' and 'guilt-by-association' approach optimizes the combination of two inference methodologies. Predictions at all levels of    confidence are evaluated by examining genes not used in training, and top predictions are examined manually using available literature and knowledge base resources. CONCLUSION: We assigned a confidence score to each gene/term combination. The    results provided high prediction performance, with nearly every GO term achieving greater than 40% precision at 1% recall. Among the 36 novel predictions for GO terms and 40 for phenotypes that were studied manually, >80% and >40%, respectively,    were identified as accurate. We also illustrate that a combination of 'guilt-by-profiling' and 'guilt-by-association' outperforms either approach alone in their application to M. musculus.</p>

	]]>
</description>

<author>M Tasan et al.</author>


</item>


<item>
<title>The Gene Ontology project in 2008.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1768</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1768</guid>
<pubDate>Tue, 08 May 2012 23:02:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Gene Ontology (GO) project (http://www.geneontology.org/) provides a set of structured, controlled vocabularies for community use in annotating genes, gene products and sequences (also see http://www.sequenceontology.org/). The    ontologies have been extended and refined for several biological areas, and improvements to the structure of the ontologies have been implemented. To improve the quantity and quality of gene product annotations available from its public    repository, the GO Consortium has launched a focused effort to provide comprehensive and detailed annotation of orthologous genes across a number of 'reference' genomes, including human and several key model organisms. Software developments    include two releases of the ontology-editing tool OBO-Edit, and improvements to the AmiGO browser interface.</p>

	]]>
</description>


</item>


<item>
<title>Retrotransposon target site selection by imitation of a cellular protein.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1767</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1767</guid>
<pubDate>Tue, 08 May 2012 23:02:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mobile elements rely on cellular processes to replicate, and therefore, mobile element proteins frequently interact with a variety of cellular factors. The integrase (IN) encoded by the retrotransposon Ty5 interacts with the    heterochromatin protein Sir4, and this interaction determines Ty5's preference to integrate into heterochromatin. We explored the hypothesis that Ty5's targeting mechanism arose by mimicking an interaction between Sir4 and another cellular    protein(s). Mutational analyses defined the requirements for the IN-Sir4 interaction, providing criteria to screen for cellular analogues. Esc1, a protein associated with the inner nuclear membrane, interacted with the same domain of Sir4 as IN,    and 75% of mutations that disrupted IN-Sir4 interactions also abrogated Esc1-Sir4 interactions. A small motif critical for recognizing Sir4 was identified in Esc1. The functional equivalency of this motif and the Sir4-interacting domain of IN was    demonstrated by swapping these motifs and showing that the chimeric IN and Esc1 proteins effectively target integration and partition DNA, respectively. We conclude that Ty5 targets integration by imitating the Esc1-Sir4 interaction and suggest    molecular mimicry as a general mechanism that enables mobile elements to interface with cellular processes.</p>

	]]>
</description>

<author>T L. Brady et al.</author>


</item>


<item>
<title>Dense nuclear cataract caused by the gammaB-crystallin S11R point mutation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1766</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1766</guid>
<pubDate>Tue, 08 May 2012 23:02:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: To identify the causative gene mutation for a new dominant cataract in mice and to investigate the molecular basis for how the mutated gene leads to a dense nuclear cataract. METHODS: Genomewide linkage analysis and DNA    sequencing were used to determine the gene mutation. Histology, immunohistochemistry, and Western blotting were used to characterize lens phenotypes. Ion concentrations were measured by an inductively coupled plasma-optical emission spectrometer    (ICP-OES). RESULTS: A point mutation (A to C) of the gammaB-crystallin gene, which results in the gammaB-S11R mutant protein, was identified in this cataractous mouse line. Homozygous mutant mice developed dense nuclear cataracts associated with    disrupted inner lens fiber cells. Immunohistochemistry data revealed gamma-crystallin aggregates at the cell boundaries of inner mature fibers that lose actin filaments. Western blotting showed an increased degradation of crystallin proteins    correlated with the nuclear cataract. ICP-OES confirmed a substantial elevation of calcium concentration in mutant lenses.  CONCLUSIONS: This dominant cataract was caused by the gammaB-S11R mutation.  Mutant gammaB-S11R proteins triggered the    gamma-crystallin aggregation that probably disrupted membrane-cytoskeleton structures of inner fiber cells, causing increased calcium influxes. Subsequent activation of calcium-dependent protein degradation and degeneration of inner mature fiber    cells led to the dense nuclear cataract.</p>

	]]>
</description>

<author>L Li et al.</author>


</item>


<item>
<title>Homologous recombination is necessary for normal lymphocyte development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1765</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1765</guid>
<pubDate>Tue, 08 May 2012 23:02:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Primary immunodeficiencies are rare but serious diseases with diverse genetic causes. Accumulating evidence suggests that defects in DNA double-strand break (DSB) repair can underlie many of these syndromes. In this context, the    nonhomologous end joining pathway of DSB repair is absolutely required for lymphoid development, but possible roles for the homologous recombination (HR) pathway have remained more controversial. While recent evidence suggests that HR may indeed    be important to suppress lymphoid transformation, the specific relationship of HR to normal lymphocyte development remains unclear. We have investigated roles of the X-ray cross-complementing 2 (Xrcc2) HR gene in lymphocyte development. We show    that HR is critical for normal B-cell development, with Xrcc2 nullizygosity leading to p53-dependent early S-phase arrest. In the absence of p53 (encoded by Trp53), Xrcc2-null B cells can fully develop but show high rates of chromosome and    chromatid fragmentation. We present a molecular model wherein Xrcc2 is important to preserve or restore replication forks during rapid clonal expansion of developing lymphocytes. Our findings demonstrate a key role for HR in lymphoid development    and suggest that Xrcc2 defects could underlie some human primary immunodeficiencies.</p>

	]]>
</description>

<author>L B. Caddle et al.</author>


</item>


<item>
<title>Plexin-A2 and its ligand, Sema6A, control nucleus-centrosome coupling in migrating granule cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1764</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1764</guid>
<pubDate>Tue, 08 May 2012 23:02:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>During their migration, cerebellar granule cells switch from a tangential to a radial mode of migration. We have previously demonstrated that this involves the transmembrane semaphorin Sema6A. We show here that plexin-A2 is the    receptor that controls Sema6A function in migrating granule cells. In plexin-A2-deficient (Plxna2(-/-)) mice, which were generated by homologous recombination, many granule cells remained in the molecular layer, as we saw in Sema6a mutants. A    similar phenotype was observed in mutant mice that were generated by mutagenesis with N-ethyl-N-nitrosourea and had a single amino-acid substitution in the semaphorin domain of plexin-A2. We found that this mutation abolished the ability of    Sema6A to bind to plexin-A2. Mouse chimera studies further suggested that plexin-A2 acts in a cell-autonomous manner. We also provide genetic evidence for a ligand-receptor relationship between Sema6A and plexin-A2 in this system. Using    time-lapse video microscopy, we found that centrosome-nucleus coupling and coordinated motility were strongly perturbed in Sema6a(-/-) and Plxna2(-/-) granule cells. This suggests that semaphorin-plexin signaling modulates cell migration by    controlling centrosome positioning.</p>

	]]>
</description>

<author>J Renaud et al.</author>


</item>


<item>
<title>Multiple signaling pathways promote B lymphocyte stimulator dependent B-cell growth and survival.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1763</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1763</guid>
<pubDate>Tue, 08 May 2012 23:02:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>We investigated the mechanism by which B lymphocyte stimulator (BLyS)/BAFF, a tumor necrosis factor superfamily ligand, promotes B-cell survival and resistance to atrophy. BLyS stimulation activates 2 independent signaling pathways,    Akt/mTOR and Pim 2, associated with cell growth and survival. BLyS blocks the cell volume loss (atrophy) that freshly isolated B cells normally undergo when maintained in vitro while concurrently increasing glycolytic activity and overall    metabolism.  This atrophy resistance requires Akt/mTOR. We used a genetic approach to resolve the contributions of Akt/mTOR and Pim kinase pathways to BLyS-mediated survival.  Pim 2-deficient B cells are readily protected from death by BLyS    stimulation, but this protection is completely abrogated by treatment with the mTOR inhibitor rapamycin. Furthermore, rapamycin treatment in vivo significantly reduces both follicular and marginal zone B cells in Pim-deficient but not healthy    hosts.  BLyS-dependent survival requires the antiapoptotic protein Mcl-1. Mcl-1 protein levels rise and fall in response to BLyS addition and withdrawal, respectively, and conditional deletion of the Mcl-1 gene renders B cells refractory to    BLyS-mediated protection. Because BlyS is required for the normal homeostasis of all B cells, these data suggest a therapeutic strategy simultaneously inhibiting mTOR and Pim 2 could target pathogenic B cells.</p>

	]]>
</description>

<author>R T. Woodland et al.</author>


</item>


<item>
<title>Analyses of the role of endogenous SPARC in mouse models of prostate and breast cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1762</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1762</guid>
<pubDate>Tue, 08 May 2012 23:01:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Secreted protein, acidic and rich in cysteine (SPARC, also known as osteonectin or BM-40) is a glycoprotein component of the extracellular matrix that has been reported to be involved with a variety of cellular processes. Although    SPARC expression levels are frequently altered in a variety of tumor types, the exact implications of deregulated SPARC expression--whether it promotes, inhibits or has no effect on tumor progression--have remained unclear. Our recent gene    expression analyses have shown that SPARC is significantly downregulated in highly metastatic human prostate cancer cells. To test the role of endogenous SPARC in tumorigenesis directly, we examined cancer progression and metastasis in SPARC(+/-)    and SPARC(-/-) mice using two separate transgenic mouse tumor models: transgenic adenocarcinoma of the mouse prostate (TRAMP) and murine mammary tumor virus-polyoma middle T (MMTV-PyMT). Surprisingly, in both instances, we found that loss of    SPARC had no significant effects on tumor initiation, progression or metastasis. Tumor angiogenesis and collagen deposition were also largely unaffected. Our results indicate that, although differential SPARC expression may be a useful marker of    aggressive, metastasis-prone tumors, loss of SPARC is not sufficient either to promote or to inhibit cancer progression in two spontaneous mouse tumor models.</p>

	]]>
</description>

<author>S Y. Wong et al.</author>


</item>


<item>
<title>Bone remodeling, energy metabolism, and the molecular clock.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1761</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1761</guid>
<pubDate>Tue, 08 May 2012 23:01:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The adult skeleton is constantly renewed through bone remodeling. Four recent papers (Baldock et al., 2007; Lee et al., 2007; Lundberg et al., 2007; Sato et al., 2007) provide new insights into central and peripheral control of this    remodeling sequence. Two of the studies add to our knowledge of the complex hypothalamic modulation of bone turnover mediated by NMU and NPY via the sympathetic nervous system, while the other two focus on the peripheral neural target, the    osteoblast, and its regulation by neuropeptides and osteocalcin.  These findings support a new paradigm concerning the regulation of bone remodeling and provide a foundation for novel approaches to preventing osteoporosis.</p>

	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title>The NLR gene family: a standard nomenclature.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1760</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1760</guid>
<pubDate>Tue, 08 May 2012 23:01:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J P. Ting et al.</author>


</item>


<item>
<title>Long-term engraftment and expansion of tumor-derived memory T cells following the implantation of non-disrupted pieces of human lung tumor into NOD-scid IL2Rgamma(null) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1759</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1759</guid>
<pubDate>Tue, 08 May 2012 23:01:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Non-disrupted pieces of primary human lung tumor implanted into NOD-scid IL2Rgamma(null) mice consistently result in successful xenografts in which tissue architecture, including tumor-associated leukocytes, stromal fibroblasts, and    tumor cells are preserved for prolonged periods with limited host-vs-graft interference. Human CD45(+) tumor-associated leukocytes within the xenograft are predominantly CD3(+) T cells with fewer CD138(+) plasma cells. The effector memory T cells    that had been shown to be quiescent in human lung tumor microenvironments can be activated in situ as determined by the production of human IFN-gamma in response to exogenous IL-12. Plasma cells remain functional as evidenced by production of    human Ig. Significant levels of human IFN-gamma and Ig were detected in sera from xenograft-bearing mice for up to 9 wk postengraftment.  Tumor-associated T cells were found to migrate from the microenvironment of the xenograft to the lung,    liver, and primarily the spleen. At 8 wk postengraftment, a significant portion of cells isolated from the mouse spleens were found to be human CD45(+) cells. The majority of CD45(+) cells were CD3(+) and expressed a phenotype consistent with an    effector memory T cell, consisting of CD4(+) or CD8(+) T cells that were CD45RO(+), CD44(+), CD62L(-), and CD25(-). Following adoptive transfer into non-tumor bearing NOD-scid IL2Rgamma(null) mice, these human T cells were found to expand in the    spleen, produce IFN-gamma, and maintain an effector memory phenotype. We conclude that the NOD-scid IL2Rgamma(null) tumor xenograft model provides an opportunity to study tumor and tumor-stromal cell interactions in situ for prolonged    periods.</p>

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</description>

<author>Abelson M. Simpson et al.</author>


</item>


<item>
<title>Applying gene expression, proteomics and single-nucleotide polymorphism analysis for complex trait gene identification.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1758</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1758</guid>
<pubDate>Tue, 08 May 2012 23:01:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous quantitative trait locus (QTL) analysis of an intercross involving the inbred mouse strains NZB/BlNJ and SM/J revealed QTL for a variety of complex traits. Many QTL have large intervals containing hundreds of genes, and    methods are needed to rapidly sort through these genes for probable candidates. We chose nine QTL: the three most significant for high-density lipoprotein (HDL) cholesterol, gallstone formation, and obesity. We searched for candidate genes using    three different approaches: mRNA microarray gene expression technology to assess >45,000 transcripts, publicly available SNPs to locate genes that are not identical by descent and that contain nonsynonymous coding differences, and a    mass-spectrometry-based proteomics technology to interrogate nearly 1000 proteins for differential expression in the liver of the two parental inbred strains. This systematic approach reduced the number of candidate genes within each QTL from    hundreds to a manageable list. Each of the three approaches selected candidates that the other two approaches missed. For example, candidate genes such as Apoa2 and Acads had differential protein levels although the mRNA levels were similar.  We    conclude that all three approaches are important and that focusing on a single approach such as mRNA expression may fail to identify a QTL gene.</p>

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</description>

<author>I M. Stylianou et al.</author>


</item>


<item>
<title>The dual bromodomain and WD repeat-containing mouse protein BRWD1 is required for normal spermiogenesis and the oocyte-embryo transition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1757</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1757</guid>
<pubDate>Tue, 08 May 2012 23:01:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>A novel mutation, repro5, was isolated in a forward genetic screen for infertility mutations induced by ENU mutagenesis. Homozygous mutant mice were phenotypically normal but were infertile. Oocytes from mutant females appeared    normal, but were severely maturation-defective in that they had reduced ability to progress to metaphase II (MII), and those reaching MII were unable to progress beyond the two pronuclei stage following in vitro fertilization (IVF). Mutant males    exhibited defective spermiogenesis, resulting in oligoasthenoteratospermia.  Genetic mapping, positional cloning, and complementation studies with a disruption allele led to the identification of a mutation in Brwd1 (Bromodomain and WD repeat    domain containing 1) as the causative lesion.  Bromodomain-containing proteins typically interact with regions of chromatin containing histones hyperacetylated at lysine residues, a characteristic of chromatin in early spermiogenesis before    eventual replacement of histones by the protamines. Previous data indicated that Brwd1 is broadly expressed, encoding a putative transcriptional regulator that is believed to act on chromatin through interactions with the Brg1-dependent SWI/SNF    chromatin-remodeling pathway. Brwd1 represents one of a small number of genes whose elimination disrupts gametogenesis in both sexes after the major events of meiotic prophase I have been completed.</p>

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</description>

<author>D L. Philipps et al.</author>


</item>


<item>
<title>Selective delivery of beta cell antigen to dendritic cells in vivo leads to deletion and tolerance of autoreactive CD8+ T cells in NOD mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1756</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1756</guid>
<pubDate>Tue, 08 May 2012 23:01:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Type 1 diabetes (T1D) is an autoimmune disease resulting from defects in central and peripheral tolerance and characterized by T cell-mediated destruction of islet beta cells. Cytotoxic CD8(+) T cells, reactive to beta cell    antigens, are required for T1D development in the NOD mouse model of the disease, and CD8(+) T cells specific for beta cell antigens can be detected in the peripheral blood of T1D patients. It has been evident that in nonautoimmune-prone mice,    dendritic cells (DCs) present model antigens in a tolerogenic manner in the steady state, e.g., in the absence of infection, and cause T cells to proliferate initially but then to be deleted or rendered unresponsive. However, this fundamental    concept has not been evaluated in the setting of a spontaneous autoimmune disease. To do so, we delivered a mimotope peptide, recognized by the diabetogenic CD8(+) T cell clone AI4, to DCs in NOD mice via the endocytic receptor DEC-205.    Proliferation of transferred antigen-specific T cells was initially observed, but this was followed by deletion. Tolerance was achieved because rechallenge of mice with the mimotope peptide in adjuvant did not induce an immune response. Thus,    targeting of DCs with beta cell antigens leads to deletion of autoreactive CD8(+) T cells even in the context of ongoing autoimmunity in NOD mice with known tolerance defects. Our results provide support for the development of DC targeting of    self antigens for treatment of chronic T cell-mediated autoimmune diseases.</p>

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</description>

<author>A Mukhopadhaya et al.</author>


</item>


<item>
<title>Humanized SCID mouse models for biomedical research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1755</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1755</guid>
<pubDate>Tue, 08 May 2012 23:00:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is a growing need for effective animal models to carry out experimental studies on human hematopoietic and immune systems without putting individuals at risk. Progress in development of small animal models for the in vivo    investigation of human hematopoiesis and immunity has seen three major breakthroughs over the last three decades. First, CB 17-Prkdc(scid) (abbreviated CB 17-scid) mice were discovered in 1983, and engraftment of these mice with human fetal    tissues (SCID-Hu model) and peripheral blood mononuclear cells (Hu-PBL-SCID model) was reported in 1988. Second, NOD-scid mice were developed and their enhanced ability to engraft with human hematolymphoid tissues as compared with CB17-scid mice    was reported in 1995. NOD-scid mice have been the "gold standard" for studies of human hematolymphoid engraftment in small animal models over the last 10 years. Third, immunodeficient mice bearing a targeted mutation in the IL-2 receptor common    gamma chain (IL2rgamma(null)) were developed independently by four groups between 2002 and 2005, and a major increase in the engraftment and function of human hematolymphoid cells as compared with NOD-scid mice has been reported. These new    strains of immunodeficient IL2rgamma(null) mice are now being used for studies in human hematopoiesis, innate and adaptive immunity, autoimmunity, infectious diseases, cancer biology, and regenerative medicine. In this chapter, we discuss the    current state of development of these strains of mice, the remaining deficiencies, and how approaches used to increase the engraftment and function of human hematolymphoid cells in CB 17-scid mice and in previous models based on NOD-scid mice may    enhance human hematolymphoid engraftment and function in NOD-scid IL2rgamma(null) mice.</p>

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</description>

<author>T Pearson et al.</author>


</item>


<item>
<title>Creation of &quot;humanized&quot; mice to study human immunity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1754</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1754</guid>
<pubDate>Tue, 08 May 2012 23:00:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>"Humanized" mice are a promising translational model for studying human hematopoiesis and immunity. Their utility has been enhanced by the development of new stocks of immunodeficient hosts, most notably mouse strains such as    NOD-scid IL2rgamma(null) mice that lack the IL-2 receptor common gamma chain. These stocks of mice lack adaptive immune function, display multiple defects in innate immunity, and support heightened levels of human hematolymphoid engraftment.     Humanized mice can support studies in many areas of immunology, including autoimmunity, transplantation, infectious diseases, and cancer. These models are particularly valuable in experimentation where there is no appropriate small animal model    of the human disease, as in the case of certain viral infections.  This unit details the creation of humanized mice by engraftment of immunodeficient mice with hematopoietic stem cells or peripheral blood mononuclear cells, provides methods for    evaluating engraftment, and discusses considerations for choosing the appropriate model system to meet specific goals.</p>

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</description>

<author>T Pearson et al.</author>


</item>


<item>
<title>Temporal migration of gonadotrophin-releasing hormone-1 neurones is modified in GAD67 knockout mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1753</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1753</guid>
<pubDate>Tue, 08 May 2012 23:00:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gonadotrophin-releasing hormone (GnRH-1) neurones reside in the forebrain and regulate gonadal function via the hypothalamic-pituitary-gonadal axis. Disruption of this axis results in reproductive dysfunction. During embryonic    development, GnRH-1 neurones migrate from the nasal pit through the nasal/forebrain junction (NFJ) into the developing brain. Prenatally gamma-aminobutyric acid (GABA) is excitatory and has been shown to play a role in nervous system development.    Both in vivo and in vitro experiments suggest that GABA inhibits migration of GnRH-1 neurones. The present study examines the migration of GnRH-1 neurones in GAD67 knockout (KO) mice to further elucidate the role of GABA on GnRH-1 neuronal    development. Three stages were examined, embryonic day (E)12.5, E14.5 and E17.5.  GnRH-1 cell number and location were analysed by immunocytochemistry and in situ hybridisation histochemistry. The total number of GnRH-1 immunopositive cells was    similar between wild-type (WT) and KO mice. However, significant differences were found in the overall distribution of GnRH-1 immunopositive cells in GAD67 KO compared to WT mice at all stages. Subsequent analysis by area revealed differences    occurred at the NFJ with an increase in GnRH-1 cells in GAD67 KO at E14.5 and a decrease in GnRH-1 cells in GAD67 KO at E17.5. Comparable counts for cells expressing GnRH-1 transcript and protein were obtained. These data indicate that attenuated    levels of GABA accelerate GnRH-1 cell migration in nasal areas as well as movement of GnRH-1 cells into the central nervous system at the NFJ.</p>

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</description>

<author>J M. Lee et al.</author>


</item>


<item>
<title>Src-family kinases in the development and therapy of Philadelphia chromosome-positive chronic myeloid leukemia and acute lymphoblastic leukemia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1752</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1752</guid>
<pubDate>Tue, 08 May 2012 23:00:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The BCR-ABL kinase inhibitor imatinib has shown significant efficacy in chronic myeloid leukemia (CML) and is the standard front-line therapy for patients in chronic phase. However, a substantial number of patients are either    primarily refractory or acquire resistance to imatinib. While a number of mechanisms are known to confer resistance to imatinib, increasing evidence has demonstrated a role for BCR-ABL-independent pathways. The Src-family kinases (SFKs) are one    such pathway and have been implicated in imatinib resistance. Additionally, these kinases are key to the progression of CML and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL). The dual SFK/BCR-ABL inhibitor dasatinib is    now clinically available and has markedly greater potency compared with imatinib against native BCR-ABL and the majority of imatinib-resistant BCR-ABL mutants. Therefore, this agent, as well as other dual SFK/BCR-ABL inhibitors under development,    could provide added therapeutic advantages by overcoming both BCR-ABL-dependent (i.e. BCR-ABL mutations) and -independent forms of imatinib resistance and delaying transition to advanced phase disease. In this review, we discuss the preclinical    and clinical evidence demonstrating the involvement of SFKs in imatinib resistance and the progression of CML and Ph+ ALL, as well as the potential role of dual SFK/BCR-ABL inhibition in the management of these diseases.</p>

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</description>

<author>S Li</author>


</item>


<item>
<title>CD34+CD38+CD19+ as well as CD34+CD38-CD19+ cells are leukemia-initiating cells with self-renewal capacity in human B-precursor ALL.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1751</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1751</guid>
<pubDate>Tue, 08 May 2012 23:00:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The presence of rare malignant stem cells supplying a hierarchy of malignant cells has recently been reported. In human acute myelogenous leukemia (AML), the leukemia stem cells (LSCs) have been phenotypically restricted within the    CD34+CD38- fraction. To understand the origin of malignant cells in primary human B-precursor acute lymphocytic leukemia (B-ALL), we established a novel in vivo xenotransplantation model. Purified CD34+CD38+CD19+, CD34+CD38-CD19+ and    CD34+CD38-CD19- bone marrow (BM) or peripheral blood (PB) cells from three pediatric B-ALL patients were intravenously injected into sublethally irradiated newborn NOD/SCID/IL2rgamma(null) mice. We found that both CD34+CD38+CD19+ and    CD34+CD38-CD19+ cells initiate B-ALL in primary recipients, whereas the recipients of CD34+CD38-CD10-CD19- cells showed normal human hematopoietic repopulation. The extent of leukemic infiltration into the spleen, liver and kidney was similar    between the recipients transplanted with CD34+CD38+CD19+ cells and those transplanted with CD34+CD38-CD19+ cells. In each of the three cases studied, transplantation of CD34+CD38+CD19+ cells resulted in the development of B-ALL in secondary    recipients, demonstrating self-renewal capacity. The identification of CD34+CD38+CD19+ self-renewing B-ALL cells proposes a hierarchy of leukemia-initiating cells (LICs) distinct from that of AML. Recapitulation of patient B-ALL in    NOD/SCID/IL2rgamma(null) recipients provides a powerful tool for directly studying leukemogenesis and for developing therapeutic strategies.</p>

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</description>

<author>Y Kong et al.</author>


</item>


<item>
<title>The Mouse Tumor Biology database.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1750</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1750</guid>
<pubDate>Tue, 08 May 2012 23:00:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The laboratory mouse has long been an important tool in the study of the biology and genetics of human cancer. With the advent of genetic engineering techniques, DNA microarray analyses, tissue arrays and other large-scale,    high-throughput data generating methods, the amount of data available for mouse models of cancer is growing exponentially. Tools to integrate, locate and visualize these data are crucial to aid researchers in their investigations. The Mouse Tumor    Biology database (http://tumor.informatics.jax.org) seeks to address that need.</p>

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</description>

<author>D M. Krupke et al.</author>


</item>


<item>
<title>Three-dimensional sub-100 nm resolution fluorescence microscopy of thick samples.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1749</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1749</guid>
<pubDate>Tue, 08 May 2012 22:59:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Imaging volumes as thick as whole cells at three-dimensional (3D) super-resolution is required to reveal unknown features of cellular organization.  We report a light microscope that generates images with translationally invariant    30 x 30 x 75 nm resolution over a depth of several micrometers. This method, named biplane (BP) FPALM, combines a double-plane detection scheme with fluorescence photoactivation localization microscopy (FPALM) enabling 3D sub-diffraction    resolution without compromising speed or sensitivity.</p>

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</description>

<author>M F. Juette et al.</author>


</item>


<item>
<title>The effects of a high-fruit and -vegetable, high-fiber, low-fat dietary intervention on serum concentrations of insulin, glucose, IGF-I and IGFBP-3.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1748</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1748</guid>
<pubDate>Tue, 08 May 2012 22:59:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: To determine the effects of dietary change on serum concentrations of insulin, glucose, IGF-I and IGFBP-3. SUBJECTS: From among participants in a randomized clinical trial of men and women without a history of diabetes    who were 35 years old or older and who had at least one histologically confirmed colorectal adenoma removed during a qualifying colonoscopy within the 6 months before randomization, 750 subjects were selected for this analysis. METHODS: The    authors analyzed fasting serum from 375 subjects with and 375 subjects without a recurrent polyp among participants in a randomized trial of a low-fat (20% of energy), high-fiber (18 g per 1000 kcals of energy intake) and high-fruit and    -vegetable (5-8 servings per day) dietary intervention. RESULTS: After 4 years of follow-up, IGF-I concentration in the intervention group (N=248) declined by 8.86 ng/ml (initial mean of 133 ng/ml) and 7.74 ng/ml (initial mean value of 139 ng/ml)    in the non-intervention group (N=502). Based on an unpaired t-test, these declines were both statistically significant, but the difference between groups for the decline in IGF-I (1.12 ng/ml ((95% confidence interval, -3.24 to 5.48)) was not.    After 4 years, concentrations of IGFBP-3, insulin and glucose were not statistically different from values at baseline, and there were no differences in these serum measures between the intervention and control groups. In analysis restricted to    lean (body mass index <25 kg>/m(2)) subjects only, however, glucose concentrations in the intervention group decreased by 0.28 mmol/l, while they increased in the control group by 0.01 mmol/l (t-test for mean differences P=0.0003) over 4 years.    CONCLUSIONS: A low-fat, high-fiber, high-fruit and -vegetable dietary intervention had minimal impact on serum concentrations of insulin, glucose, IGF-I and IGFBP-3 overall, but in lean subjects the intervention resulted in a significant    reduction in serum glucose concentration.</p>

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</description>

<author>A Flood et al.</author>


</item>


<item>
<title>Hormonal regulation of testicular steroid and cholesterol homeostasis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1747</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1747</guid>
<pubDate>Tue, 08 May 2012 22:59:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The male sex steroid, testosterone (T), is synthesized from cholesterol in the testicular Leydig cell under control of the pituitary gonadotropin LH. Unlike most cells that use cholesterol primarily for membrane synthesis,    steroidogenic cells have additional requirements for cholesterol, because it is the essential precursor for all steroid hormones. Little is known about how Leydig cells satisfy their specialized cholesterol requirements for steroid synthesis. We    show that in mice with a unique hypomorphic androgen mutation, which disrupts the feedback loop governing T synthesis, that genes involved in cholesterol biosynthesis/uptake and steroid biosynthesis are up-regulated. We identify LH as the central    regulatory molecule that controls both steroidogenesis and Leydig cell cholesterol homeostasis in vivo. In addition to the primary defect caused by high levels of LH, absence of T signaling exacerbates the lipid homeostasis defect in Leydig cells    by eliminating a short feedback loop. We show that T signaling can affect the synthesis of steroids and modulates the expression of genes involved in de novo cholesterol synthesis. Surprisingly, accumulation of active sterol response    element-binding protein 2 is not required for up-regulation of genes involved in cholesterol biosynthesis and uptake in Leydig cells.</p>

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</description>

<author>S M. Eacker et al.</author>


</item>


<item>
<title>Gender-specific changes in bone turnover and skeletal architecture in igfbp-2-null mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1746</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1746</guid>
<pubDate>Tue, 08 May 2012 22:59:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>IGF-binding protein-2 (IGFBP-2) is a 36-kDa protein that binds to the IGFs with high affinity. To determine its role in bone turnover, we compared Igfbp2(-/-) mice with Igfbp2(+/+) colony controls. Igfbp2(-/-) males had shorter    femurs and were heavier than controls but were not insulin resistant. Serum IGF-I levels in Igfbp2(-/-) mice were 10% higher than Igfbp2(+/+) controls at 8 wk of age; in males, this was accompanied by a 3-fold increase in hepatic Igfbp3 and    Igfbp5 mRNA transcripts compared with Igfbp2(+/+) controls. The skeletal phenotype of the Igfbp2(-/-) mice was gender and compartment specific; Igfbp2(-/-) females had increased cortical thickness with a greater periosteal circumference compared    with controls, whereas male Igfbp2(-/-) males had reduced cortical bone area and a 20% reduction in the trabecular bone volume fraction due to thinner trabeculae than Igfbp2(+/+) controls. Serum osteocalcin levels were reduced by nearly 40% in    Igfbp2(-/-) males, and in vitro, both CFU-ALP(+) preosteoblasts, and tartrate-resistant acid phosphatase-positive osteoclasts were significantly less abundant than in Igfbp2(+/+) male mice. Histomorphometry confirmed fewer osteoblasts and    osteoclasts per bone perimeter and reduced bone formation in the Igfbp2(-/-) males. Lysates from both osteoblasts and osteoclasts in the Igfbp2(-/-) males had phosphatase and tensin homolog (PTEN) levels that were significantly higher than    Igfbp2(+/+) controls and were suppressed by addition of exogenous IGFBP-2. In summary, there are gender- and compartment-specific changes in Igfbp2(-/-) mice. IGFBP-2 may regulate bone turnover in both an IGF-I-dependent and -independent    manner.</p>

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</description>

<author>V E. DeMambro et al.</author>


</item>


<item>
<title>Effects of low-dose parathyroid hormone on bone mass, turnover, and ectopic osteoinduction in a rat model for chronic alcohol abuse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1745</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1745</guid>
<pubDate>Tue, 08 May 2012 22:59:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Parathyroid hormone (PTH) is used clinically in osteoporotic patients to increase bone mass by enhancing bone formation. PTH therapy is not uniformly effective at all skeletal sites and "life-style" factors may modulate the skeletal    response to PTH. Alcohol may represent one of these factors. Chronic alcohol abuse is associated with osteoporosis and impaired fracture healing. Therefore, the present study investigated the effects of alcohol on the bone anabolic response to a    dose of PTH similar to a human therapeutic dose 1) during normal cancellous and cortical bone growth and turnover, and 2) in a model of demineralized allogeneic bone matrix (DABM)-induced osteoinduction. Three-month-old male Sprague Dawley rats    were fed a Lieber-DeCarli liquid diet with 35% of the calories derived from ethanol. The controls were pair-fed an alcohol-free isocaloric diet containing maltose-dextran. Following adaptation to the liquid diets, the rats were implanted    subcutaneously with DABM cylinders prepared from cortical bone of rats fed normal chow. The rats were subsequently treated daily with PTH (1 microg/kg/d sc, 5 d/week) or vehicle and measurements on bone and DABM implants performed 6 weeks later.    Total bone mass was evaluated on the day of necropsy using DXA. Tibiae were processed for histomorphometry. Bone mass and architecture in tibial diaphysis and DABM implants were evaluated by muCT. PTH treatment increased whole body bone mineral    content (BMC) and bone mineral density (BMD). The hormone also increased bone formation and bone area/tissue area in the proximal tibial metaphysis. In contrast, PTH treatment had no effect on periosteal bone formation and minimal effects on    DABM-induced osteoinduction.  Alcohol consumption decreased whole body BMC. Alcohol also decreased cancellous as well as cortical bone formation and bone mass in tibia and impaired DABM-mediated osteoinduction. There was no interaction between    PTH treatment and alcohol consumption for any of the endpoints evaluated. Our results indicate that the bone anabolic response to a therapeutic dose of PTH in the rat is largely confined to cancellous bone. In contrast, alcohol consumption    inhibits bone formation at all sites. Furthermore, alcohol inhibits osteoinduction and reduces periosteal and cancellous bone formation, irrespective of therapeutic PTH administration. Based on the animal model, our findings suggest that alcohol    consumption could impair the beneficial effects of PTH therapy in osteoporosis.</p>

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</description>

<author>U T. Iwaniec et al.</author>


</item>


<item>
<title>Editorial from the BOR Editors-in-Chief. The dreaded &quot;d&quot; word.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1744</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1744</guid>
<pubDate>Tue, 08 May 2012 22:59:16 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J Eppig et al.</author>


</item>


<item>
<title>Loss of apoptosis-inducing factor results in cell-type-specific neurogenesis defects.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1743</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1743</guid>
<pubDate>Tue, 08 May 2012 22:59:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mitochondrial dysfunction is commonly associated with neurodegeneration in the aging brain. In addition, the importance of mitochondrial function during brain development is illustrated by the neurological deficits observed in    infants with mitochondrial complex deficiencies. However, the extent to which abnormalities in mitochondrial function might impact neurogenesis during brain development is not well understood. Previously, we demonstrated that adult harlequin (Hq)    mutant mice, which have an 80% reduction in the mitochondrial protein apoptosis-inducing factor (AIF), exhibited signs of oxidative stress and progressive loss of adult cerebellar and retinal neurons. To assess whether in addition to its role in    postmitotic neuron survival Aif is also necessary for cerebellar development, we analyzed embryos in which Aif was deleted in the prospective midbrain and cerebellum at a very early stage of development using an En1 (engrailed 1) promoter-driven    cre recombinase gene. These mutant mice, which died at birth, had midbrain defects and dramatic deficits in cerebellar Purkinje and granule cell precursors. Additional analysis revealed that Aif-null Purkinje cell precursors prematurely entered    S-phase, but most failed to undergo mitosis and ultimately died via apoptosis. In contrast, proliferation of mutant granule cell precursors was blocked before S-phase. Mice in which Aif was deleted later in embryogenesis using a nestin    promoter-driven cre gene survive for several days after birth, and postnatal granule cell precursors in these mice also failed to enter S-phase. Our results indicate that the loss of Aif results in cell cycle abnormalities in a neuron-specific    manner during cerebellar development.</p>

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</description>

<author>R Ishimura et al.</author>


</item>


<item>
<title>The differentiative and regenerative properties of human hematopoietic stem/progenitor cells in NOD-SCID/IL2rgamma(null) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1742</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1742</guid>
<pubDate>Tue, 08 May 2012 22:58:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Biomedical research including immunology and stem cell biology has developed greatly because of the evolving technology of gene modification and conventional transplantation methods using the most common experimental laboratory    animal, the mouse. To translate promising research findings based on mouse research into clinical medicine, however, we need to clarify whether similar events take place in humans. In the study of hematology and immunology, humanized mice provide    a unique and efficient experimental system to evaluate differentiation, function, and interaction of human blood cells or immune components. Here we review the latest experimental findings in the fields of immunology, stem cell biology, and    regenerative medicine using humanized mice.</p>

	]]>
</description>

<author>F Ishikawa et al.</author>


</item>


<item>
<title>Notch2 is required for maintaining sustentacular cell function in the adult mouse main olfactory epithelium.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1741</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1741</guid>
<pubDate>Tue, 08 May 2012 22:58:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Notch receptors are expressed in neurons and glia in the adult nervous system, but why this expression persists is not well-understood. Here we examine the role of the Notch pathway in the postnatal mouse main olfactory system, and    show evidence consistent with a model where Notch2 is required for maintaining sustentacular cell function. In the absence of Notch2, the laminar nature of these glial-like cells is disrupted. Hes1, Hey1, and Six1, which are downstream effectors    of the Notch pathway, are down-regulated, and cytochrome P450 and Glutathione S-transferase (GST) expression by sustentacular cells is reduced.  Functional levels of GST activity are also reduced. These disruptions are associated with increased    olfactory sensory neuron degeneration. Surprisingly, expression of Notch3 is also down-regulated. This suggests the existence of a feedback loop where expression of Notch3 is initially independent of Notch2, but requires Notch2 for maintained    expression. While the Notch pathway has previously been shown to be important for promoting gliogenesis during development, this is the first demonstration that the persistent expression of Notch receptors is required for maintaining glial    function in adult.</p>

	]]>
</description>

<author>S Rodriguez et al.</author>


</item>


<item>
<title>Telomere dysfunction promotes genome instability and metastatic potential in a K-ras p53 mouse model of lung cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1740</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1740</guid>
<pubDate>Tue, 08 May 2012 22:58:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Current mouse models of lung cancer recapitulate signature genetic lesions and some phenotypic features of human lung cancer. However, because mice have long telomeres, models to date do not recapitulate the aspects of lung    carcinogenesis-telomere attrition and the genomic instability that ensues-believed to serve as key mechanisms driving lung tumor initiation and progression. To explore the contributions of telomere dysfunction to lung cancer progression, we    combined a telomerase catalytic subunit (mTerc) mutation with the well-characterized K-rasG12D mouse lung cancer model. K-ras(G12D) mTerc(-/-) mice with telomere dysfunction but intact p53 exhibited increased lung epithelial apoptosis, delayed    tumor formation and increased life span relative to K-ras(G12D) mTerc(+/-) mice with intact telomere function. This demonstrates that by itself, telomere dysfunction acts in a tumor-suppressive mechanism.  Introduction of a heterozygous p53    mutation exerted a marked histopathological, biological and genomic impact. K-ras(G12D) mTerc(-/-) p53(+/-) mice developed aggressive tumors with more chromosomal instabilities and high metastatic potential, leading to decreased overall survival.    Thus, we have generated a murine model that more faithfully recapitulates key aspects of the human disease.  Furthermore, these findings clearly demonstrate (in an in vivo model system) the dual nature of telomere shortening as both a    tumor-suppressive and tumor-promoting mechanism in lung cancer, dependent on p53 status.</p>

	]]>
</description>

<author>S A. Perera et al.</author>


</item>


<item>
<title>Targeted deletion reveals essential and overlapping functions of the miR-17 through 92 family of miRNA clusters.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1739</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1739</guid>
<pubDate>Tue, 08 May 2012 22:58:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>miR-17 approximately 92, miR-106b approximately 25, and miR-106a approximately 363 belong to a family of highly conserved miRNA clusters. Amplification and overexpression of miR-1792 is observed in human cancers, and its oncogenic    properties have been confirmed in a mouse model of B cell lymphoma. Here we show that mice deficient for miR-17 approximately 92 die shortly after birth with lung hypoplasia and a ventricular septal defect. The miR-17 approximately 92 cluster is    also essential for B cell development. Absence of miR-17 approximately 92 leads to increased levels of the proapoptotic protein Bim and inhibits B cell development at the pro-B to pre-B transition. Furthermore, while ablation of miR-106b    approximately 25 or miR-106a approximately 363 has no obvious phenotypic consequences, compound mutant embryos lacking both miR-106b approximately 25 and miR-17 approximately 92 die at midgestation. These results provide key insights into the    physiologic functions of this family of microRNAs and suggest a link between the oncogenic properties of miR-17 approximately 92 and its functions during B lymphopoiesis and lung development.</p>

	]]>
</description>

<author>A Ventura et al.</author>


</item>


<item>
<title>Somatic inactivation of the PHD2 prolyl hydroxylase causes polycythemia and congestive heart failure.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1738</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1738</guid>
<pubDate>Tue, 08 May 2012 22:58:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pharmacologic activation of the heterodimeric HIF transcription factor appears promising as a strategy to treat diseases, such as anemia, myocardial infarction, and stroke, in which tissue hypoxia is a prominent feature. HIF    accumulation is normally linked to oxygen availability because an oxygen-dependent posttranslational modification (prolyl hydroxylation) marks the HIFalpha subunit for polyubiquitination and destruction. Three enzymes (PHD1, PHD2, and PHD3)    capable of catalyzing this reaction have been identified, although PHD2 (also called Egln1) appears to be the primary HIF prolyl hydroxylase in cell culture experiments. We found that conditional inactivation of PHD2 in mice is sufficient to    activate a subset of HIF target genes, including erythropoietin, leading to striking increases in red blood cell production. Mice lacking PHD2 exhibit premature mortality associated with marked venous congestion and dilated cardiomyopathy. The    latter is likely the result of hyperviscosity syndrome and volume overload, although a direct effect of chronic, high-level HIF stimulation on cardiac myocytes cannot be excluded.</p>

	]]>
</description>

<author>Y A. Minamishima et al.</author>


</item>


<item>
<title>Analysis of the QTL for sleep homeostasis in mice: Homer1a is a likely candidate.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1737</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1737</guid>
<pubDate>Tue, 08 May 2012 22:58:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Electroencephalographic oscillations in the frequency range of 0.5-4 Hz, characteristic of slow-wave sleep (SWS), are often referred to as the delta oscillation or delta power. Delta power reflects sleep intensity and correlates    with the homeostatic response to sleep loss. A published survey of inbred strains of mice demonstrated that the time course of accumulation of delta power varied among inbred strains, and the segregation of the rebound of delta power in BxD    recombinant inbred strains identified a genomic region on chromosome 13 referred to as the delta power in SWS (or Dps1). The quantitative trait locus (QTL) contains genes that modify the accumulation of delta power after sleep deprivation. Here,    we narrow the QTL using interval-specific haplotype analysis and present a comprehensive annotation of the remaining genes in the Dps1 region with sequence comparisons to identify polymorphisms within the coding and regulatory regions. We    established the expression pattern of selected genes located in the Dps1 interval in sleep and wakefulness in B6 and D2 parental strains. Taken together, these steps reduced the number of potential candidate genes that may underlie the    accumulation of delta power after sleep deprivation and explain the Dps1 QTL. The strongest candidate gene is Homer1a, which is supported by expression differences between sleep and wakefulness and the SNP polymorphism in the upstream regulatory    regions.</p>

	]]>
</description>

<author>M Mackiewicz et al.</author>


</item>


<item>
<title>Relationships of dietary fat, body composition, and bone mineral density in inbred mouse strain panels.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1736</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1736</guid>
<pubDate>Tue, 08 May 2012 22:58:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Laboratory inbred mouse strains show a broad range of variation in phenotypes, such as body composition, bone mineral density (BMD), plasma leptin, and insulin-like growth factor I (IGF-I), and thus provide a basis for the study of    associations among them. We analyzed these phenotypes in male and female mice from 43 inbred strains fed on a high-fat (30% caloric content) diet and from 30 inbred strains fed on a low-fat (6%) diet. Structural equation modeling of these data    reveals that the relationship of body fat content and areal BMD is altered by dietary factors and genotypes. Sex has no net effect on areal BMD, but after accounting for body mass difference females have higher areal BMD. Leptin is affected by    relative fat mass and has no net effect on areal BMD. IGF-I has a direct effect on areal BMD.</p>

	]]>
</description>

<author>R Li et al.</author>


</item>


<item>
<title>Mutation of the Cyba gene encoding p22phox causes vestibular and immune defects in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1735</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1735</guid>
<pubDate>Tue, 08 May 2012 22:57:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>In humans, hereditary inactivation of either p22(phox) or gp91(phox) leads to chronic granulomatous disease (CGD), a severe immune disorder characterized by the inability of phagocytes to produce bacteria-destroying ROS.    Heterodimers of p22(phox) and gp91(phox) proteins constitute the superoxide-producing cytochrome core of the phagocyte NADPH oxidase. In this study, we identified the nmf333 mouse strain as what we believe to be the first animal model of    p22(phox) deficiency. Characterization of nmf333 mice revealed that deletion of p22(phox) inactivated not only the phagocyte NADPH oxidase, but also a second cytochrome in the inner ear epithelium. As a consequence, mice of the nmf333 strain    exhibit a compound phenotype consisting of both a CGD-like immune defect and a balance disorder caused by the aberrant development of gravity-sensing organs. Thus, in addition to identifying a model of p22(phox)-dependent immune deficiency, our    study indicates that a clinically identifiable patient population with an otherwise cryptic loss of gravity-sensor function may exist. Thus, p22(phox) represents a shared and essential component of at least 2 superoxide-producing cytochromes with    entirely different biological functions. The site of p22(phox) expression in the inner ear leads us to propose what we believe to be a novel mechanism for the control of vestibular organogenesis.</p>

	]]>
</description>

<author>Y Nakano et al.</author>


</item>


<item>
<title>The mitochondrial protease AFG3L2 is essential for axonal development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1734</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1734</guid>
<pubDate>Tue, 08 May 2012 22:57:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mitochondrial metalloprotease AFG3L2 assembles with the homologous protein paraplegin to form a supracomplex in charge of the essential protein quality control within mitochondria. Mutations of paraplegin cause a specific axonal    degeneration of the upper motoneuron and, therefore, hereditary spastic paraplegia. Here we present two Afg3l2 murine models: a newly developed null and a spontaneous mutant that we found carrier of a missense mutation. Contrasting with the mild    and late onset axonal degeneration of paraplegin-deficient mouse, Afg3l2 models display a marked impairment of axonal development with delayed myelination and poor axonal radial growth leading to lethality at P16. The increased severity of the    Afg3l2 mutants is explained by two main molecular features that differentiate AFG3L2 from paraplegin: its higher neuronal expression and its versatile ability to support both hetero-oligomerization and homo-oligomerization. Our data assign to    AFG3L2 a crucial role by linking mitochondrial metabolism and axonal development. Moreover, we propose AFG3L2 as an excellent candidate for motoneuron and cerebellar diseases with early onset unknown etiology.</p>

	]]>
</description>

<author>F Maltecca et al.</author>


</item>


<item>
<title>Sensitivity to Escherichia coli Nissle 1917 in mice is dependent on environment and genetic background.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1733</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1733</guid>
<pubDate>Tue, 08 May 2012 22:57:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Escherichia coli Nissle 1917 (EcN) is a well-characterized probiotic bacterium.  Although genomic comparisons of EcN with the uropathogenic E. coli strain CFT073 revealed high degrees of similarity, EcN is generally considered a    non-pathogenic organism. However, as recent evidence suggests that EcN is capable of inducing inflammatory responses in host intestinal epithelial cells, we aimed to investigate potential pathogenic properties of EcN in an in vivo model using    various germ-free (GF) mouse strains. With the exception of C3H/HeJZtm mice, which carry a defective toll-like receptor (TLR)4-allele, no lesions were obvious in mice of different strains orally inoculated with EcN for 1 week, although organ    cultures (blood, lung, mesenteric lymph node, pancreas, spleen, liver and kidney) tested positive to various degrees. C3H/HeJZtm mice inoculated with EcN became clinically ill and the majority died or had to be euthanized. Organs of all    gnotobiotic C3H/HeJZtm mice were positive for EcN by culture; major histological findings were moderate to severe pyogranulomatous serositis, typhlitis and pancreatitis. Histological findings were corroborated by highly elevated tumour necrosis    factor (TNF) serum levels. Lesions were not detected in specified pathogen free maintained C3H/HeJZtm mice, GF C3H/HeJ mice lacking the interleukin-10 gene, or GF C3H/HeJZtm mice that were inoculated with E. coli K12 strain MG1655 as a control.    In addition, mild histological lesions were detected in Ztm:NMRI mice 3 months after oral inoculation with EcN. This study shows that EcN is capable of displaying a virulent phenotype in GF C3H/HeJZtm mice. Whether this phenotype is linked to the    bacterium's probiotic nature should be the focus of further studies.</p>

	]]>
</description>

<author>A Bleich et al.</author>


</item>


<item>
<title>The RHOX5 homeodomain protein mediates transcriptional repression of the netrin-1 receptor gene Unc5c.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1732</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1732</guid>
<pubDate>Tue, 08 May 2012 22:57:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The X-linked mouse Rhox gene cluster contains more than 30 homeobox genes that are candidates to regulate multiple steps in male and female gametogenesis. The founding member of the Rhox gene cluster, Rhox5, is an androgen-dependent    gene expressed in Sertoli cells that promotes the survival and differentiation of the adjacent male germ cells. Here, we report the first identification and characterization of a Rhox5-regulated gene. This gene, Unc5c, encodes a pro-apoptotic    receptor with tumor suppressor activity that we found is negatively regulated by Rhox5 in the testis in vivo. Transfection analyses in cell lines of different origin indicated that Rhox5-dependent down-regulation of Unc5c requires another Sertoli    cell-specific cofactor. Examination of other mouse Rhox family members revealed that mouse RHOX2 and RHOX3 also have the ability to down-regulate Unc5c expression. The human RHOX protein PEPP2 (RHOXF2) also had this ability, indicating that Unc5c    repression is a conserved RHOX-dependent response. Deletion analysis identified a Rhox5-responsive element in the Unc5c 5'-untranslated region. Although 5'-untranslated regions typically house post-transcriptional elements, several lines of    evidence indicated that Rhox5 down-regulates Unc5c at the transcriptional level. The repression of Unc5c expression by Rhox5 may, in part, mediate the pro-survival function of Rhox5 in the testis, as we found that Unc5c mutant mice have decreased    germ cell apoptosis in the testis. Along with our other data, these findings led us to propose a model in which Rhox5 is a negative regulator upstream of Unc5c in a Sertoli-cell pathway that promotes germ-cell survival.</p>

	]]>
</description>

<author>Z Hu et al.</author>


</item>


<item>
<title>GpnmbR150X allele must be present in bone marrow derived cells to mediate DBA/2J glaucoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1731</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1731</guid>
<pubDate>Tue, 08 May 2012 22:57:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The Gpnmb gene encodes a transmembrane protein whose function(s) remain largely unknown. Here, we assess if a mutant allele of Gpnmb confers susceptibility to glaucoma by altering immune functions. DBA/2J mice have a    mutant Gpnmb gene and they develop a form of glaucoma preceded by a pigment dispersing iris disease and abnormalities of the immunosuppressive ocular microenvironment. RESULTS: We find that the Gpnmb genotype of bone-marrow derived cell lineages    significantly influences the iris disease and the elevation of intraocular pressure. GPNMB localizes to multiple cell types, including pigment producing cells, bone marrow derived F4/80 positive antigen-presenting cells (APCs) of the iris and    dendritic cells. We show that APCs of DBA/2J mice fail to induce antigen induced immune deviation (a form of tolerance) when treated with TGFbeta2. This demonstrates that some of the immune abnormalities previously identified in DBA/2J mice    result from intrinsic defects in APCs. However, the tested APC defects are not dependent on a mutant Gpnmb gene. Finally, we show that the Gpnmb mediated iris disease does not require elevated IL18 or mature B or T lymphocytes. CONCLUSION: These    results establish a role for Gpnmb in bone marrow derived lineages. They suggest that affects of Gpnmb on innate immunity influence susceptibility to glaucoma in DBA/2J mice.</p>

	]]>
</description>

<author>M G. Anderson et al.</author>


</item>


<item>
<title>A new Hu-PBL model for the study of human islet alloreactivity based on NOD-scid mice bearing a targeted mutation in the IL-2 receptor gamma chain gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1730</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1730</guid>
<pubDate>Tue, 08 May 2012 22:57:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Immunodeficient NOD-scid mice bearing a targeted mutation in the IL2 receptor common gamma chain (Il2rgamma(null)) readily engraft with human stem cells. Here we analyzed human peripheral blood mononuclear cells (PBMC) for their    ability to engraft NOD-scid Il2rgamma(null) mice and established engraftment kinetics, optimal cell dose, and the influence of injection route. Even at low PBMC input, NOD-scid Il2rgamma(null) mice reproducibly support high human PBMC engraftment    that plateaus within 3-4 weeks. In contrast to previous stocks of immunodeficient mice, we observed low intra- and inter-donor variability of engraftment. NOD-scid Il2rgamma(null) mice rendered hyperglycemic by streptozotocin treatment return to    normoglycemia following transplantation with human islets. Interestingly, these human islet grafts are rejected following injection of HLA-mismatched human PBMC as evidenced by return to hyperglycemia and loss of human C-peptide. These data    suggest that humanized NOD-scid Il2rgamma(null) mice may represent an important surrogate for investigating in vivo mechanisms of human islet allograft rejection.</p>

	]]>
</description>

<author>M King et al.</author>


</item>


<item>
<title>Mouse consomic strains: exploiting genetic divergence between Mus m. musculus and Mus m. domesticus subspecies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1729</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1729</guid>
<pubDate>Tue, 08 May 2012 22:57:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Consomic (chromosome substitution) strains (CSs) represent the most recent addition to the mouse genetic resources aimed to genetically analyze complex trait loci (QTLs). In this study, we report the development of a set of 28 mouse    intersubspecific CSs. In each CS, we replaced a single chromosome of the C57BL/6J (B6) inbred strain (mostly Mus m. domesticus) with its homolog from the PWD/Ph inbred strain of the Mus m. musculus subspecies. These two progenitor subspecies    diverged less than 1 million years ago and accumulated a large number of genetic differences that constitute a rich resource of genetic variation for QTL analyses. Altogether, the 18 consomic, nine subconsomic, and one conplastic strain covered    all 19 autosomes, X and Y sex chromosomes, and mitochondrial DNA.  Most CSs had significantly lower reproductive fitness compared with the progenitor strains. CSs homosomic for chromosomes 10 and 11, and the C57BL/6J-Chr X males, failed to    reproduce and were substituted by less affected subconsomics carrying either a proximal, central, or distal part of the respective chromosome.  A genome-wide scan of 965 DNA markers revealed 99.87% purity of the B6 genetic background.    Thirty-three nonsynonymous substitutions were uncovered in the protein-coding regions of the mitochondrial DNA of the B6.PWD-mt conplastic strain. A pilot-phenotyping experiment project revealed a high number of variations among B6.PWD    consomics.</p>

	]]>
</description>

<author>S Gregorova et al.</author>


</item>


<item>
<title>The mouse polyubiquitin gene Ubb is essential for meiotic progression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1728</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1728</guid>
<pubDate>Tue, 08 May 2012 22:56:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ubiquitin is encoded in mice by two polyubiquitin genes, Ubb and Ubc, that are considered to be stress inducible and two constitutively expressed monoubiquitin (Uba) genes. Here we report that targeted disruption of Ubb results in    male and female infertility due to failure of germ cells to progress through meiosis I and hypogonadism. In the absence of Ubb, spermatocytes and oocytes arrest during meiotic prophase, before metaphase of the first meiotic division. Although    cellular ubiquitin levels are believed to be maintained by a combination of functional redundancy among the four ubiquitin genes, stress inducibility of the two polyubiquitin genes, and ubiquitin recycling by proteasome-associated isopeptidases,    our results indicate that ubiquitin is required for and consumed during meiotic progression. The striking similarity of the meiotic phenotype in Ubb(-/-) germ cells to the sporulation defect in fission yeast (Schizosaccharomyces pombe) lacking a    polyubiquitin gene suggests that a meiotic role of the polyubiquitin gene has been conserved throughout eukaryotic evolution.</p>

	]]>
</description>

<author>K Y. Ryu et al.</author>


</item>


<item>
<title>Rapid conditional targeted ablation of cells expressing human CD59 in transgenic mice by intermedilysin.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1727</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1727</guid>
<pubDate>Tue, 08 May 2012 22:56:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Conditional targeted cell ablation is a powerful approach for investigating the pathogenesis of human diseases and in vivo cellular functions. Intermedilysin (ILY) is a cytolytic pore-forming toxin secreted by Streptococcus    intermedius that lyses human cells exclusively, owing to its receptor specificity for human CD59. We generated two transgenic mouse strains that express human CD59 either on erythrocytes (strain ThCD59(RBC)) or on endothelia (strain ThCD59(END)).     Intravenous injection of ILY in ThCD59(RBC) mice induced acute intravascular hemolysis, leading to reduced nitric oxide bioavailability, increased platelet activation and rapid death. In ThCD59(END) mice, ILY induced rapid endothelial damage,    leading to acute death and disseminated intravascular coagulation.  Additionally, we show that human serum contains ILY-specific neutralizing antibodies not found in any other animal species. Together, these results suggest that this new rapid    conditional targeted ILY-mediated cell ablation technique can be used in combination with any available transgenic expression system to study the physiologic role of specific cell populations.</p>

	]]>
</description>

<author>W Hu et al.</author>


</item>


<item>
<title>Repression of PTEN phosphatase by Snail1 transcriptional factor during gamma radiation-induced apoptosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1726</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1726</guid>
<pubDate>Tue, 08 May 2012 22:56:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The product of the Snail1 gene is a transcriptional repressor required for triggering the epithelial-to-mesenchymal transition. Furthermore, ectopic expression of Snail1 in epithelial cells promotes resistance to apoptosis. In this    study, we demonstrate that this resistance to gamma radiation-induced apoptosis caused by Snail1 is associated with the inhibition of PTEN phosphatase.  In MDCK cells, mRNA levels of the p53 target gene PTEN are induced after gamma radiation; the    transfection of Snail1 prevents this up-regulation. Decreased mRNA levels of PTEN were also detected in RWP-1 cells after the ectopic expression of this transcriptional factor. Snail1 represses and associates to the PTEN promoter as detected both    by the electrophoretic mobility shift assay and chromatin immunoprecipitation experiments performed with either endogenous or ectopic Snail1. The binding of Snail1 to the PTEN promoter increases after gamma radiation, correlating with the    stabilization of Snail1 protein, and prevents the association of p53 to the PTEN promoter. These results stress the critical role of Snail1 in the control of apoptosis and demonstrate the regulation of PTEN phosphatase by this transcriptional    repressor.</p>

	]]>
</description>

<author>M Escriva et al.</author>


</item>


<item>
<title>Neurite arborization and mosaic spacing in the mouse retina require DSCAM.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1725</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1725</guid>
<pubDate>Tue, 08 May 2012 22:56:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>To establish functional circuitry, retinal neurons occupy spatial domains by arborizing their processes, which requires the self-avoidance of neurites from an individual cell, and by spacing their cell bodies, which requires    positioning the soma and establishing a zone within which other cells of the same type are excluded. The mosaic patterns of distinct cell types form independently and overlap. The cues that direct these processes in the vertebrate retina are not    known. Here we show that some types of retinal amacrine cells from mice with a spontaneous mutation in Down syndrome cell adhesion molecule (Dscam), a gene encoding an immunoglobulin-superfamily member adhesion molecule, have defects in the    arborization of processes and in the spacing of cell bodies. In the mutant retina, cells that would normally express Dscam have hyperfasciculated processes, preventing them from creating an orderly arbor. Also, their cell bodies are randomly    distributed or pulled into clumps rather than being regularly spaced mosaics. Our results indicate that mouse DSCAM mediates isoneuronal self-avoidance for arborization and heteroneuronal self-avoidance within specific cell types to prevent    fasciculation and to preserve mosaic spacing. These functions are analogous to those of Drosophila DSCAM (ref. 6) and DSCAM2 (ref.  7). DSCAM may function similarly in other regions of the mammalian nervous system, and this role may extend to    other members of the mammalian Dscam gene family.</p>

	]]>
</description>

<author>P G. Fuerst et al.</author>


</item>


<item>
<title>The orphan G protein-coupled receptor, Gpr161, encodes the vacuolated lens locus and controls neurulation and lens development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1724</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1724</guid>
<pubDate>Tue, 08 May 2012 22:56:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The vacuolated lens (vl) mouse mutant causes congenital cataracts and neural tube defects (NTDs), with the NTDs being caused by abnormal neural fold apposition and fusion. Our positional cloning of vl indicates these phenotypes    result from a deletion mutation in an uncharacterized orphan G protein-coupled receptor (GPCR), Gpr161. Gpr161 displays restricted expression to the lateral neural folds, developing lens, retina, limb, and CNS. Characterization of the vl mutation    indicates that C-terminal tail of Gpr161 is truncated, leading to multiple effects on the protein, including reduced receptor-mediated endocytosis. We have also mapped three modifier quantitative trait loci (QTL) that affect the incidence of    either the vl cataract or NTD phenotypes. Bioinformatic, sequence, genetic, and functional data have determined that Foxe3, a key regulator of lens development, is a gene responsible for the vl cataract-modifying phenotype. These studies have    extended our understanding of the vl locus in three significant ways. One, the cloning of the vl locus has identified a previously uncharacterized GPCR-ligand pathway necessary for neural fold fusion and lens development, providing insight into    the molecular regulation of these developmental processes. Two, our QTL analysis has established vl as a mouse model for studying the multigenic basis of NTDs and cataracts. Three, we have identified Foxe3 as a genetic modifier that interacts    with Gpr161 to regulate lens development.</p>

	]]>
</description>

<author>P G. Matteson et al.</author>


</item>


<item>
<title>Deficiency of PPARbeta/delta in the epidermis results in defective cutaneous permeability barrier homeostasis and increased inflammation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1723</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1723</guid>
<pubDate>Tue, 08 May 2012 22:56:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>In cultured human keratinocytes or murine epidermis, peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) (NR1C2) activators (1) stimulate keratinocyte differentiation; (2) decrease keratinocyte proliferation; (3)    accelerate permeability barrier repair; (4) increase epidermal lipid synthesis; and (5) reduce cutaneous inflammation. Since these results suggest that PPARbeta/delta could play an important role in cutaneous homeostasis, we assessed here the    skin phenotype of mice deficient in PPARbeta/delta. Gross cutaneous abnormalities were not evident, and both stratum corneum (SC) skin hydration and surface pH were normal. However, the epidermis was thickened and proliferating cell nuclear    antigen (PCNA) staining was increased, indicating increased cell proliferation. No change in apoptosis was observed but the expression of differentiation markers, such as filaggrin, involucrin, and loricrin, was slightly increased in    PPARbeta/delta(-/-) mice.  Although basal permeability barrier function was normal, PPARbeta/delta knockout (KO) mice show a significant delay in barrier recovery rates following acute barrier disruption by either acetone treatment or    tape-stripping. Delayed barrier recovery correlated with decreased production and secretion of lamellar bodies (LBs), and with reduced numbers of extracellular lamellar membranes in the SC.  Finally, PPARbeta/delta KO mice displayed increased    inflammation in response to 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment. Together, these results further demonstrate that PPARbeta/delta in the epidermis: (1) is required for permeability barrier homeostasis; (2) regulates keratinocyte    proliferation; and (3) modulates cutaneous inflammation.</p>

	]]>
</description>

<author>M Q. Man et al.</author>


</item>


<item>
<title>Mice expressing a mutant Krt75 (K6hf) allele develop hair and nail defects resembling pachyonychia congenita.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1722</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1722</guid>
<pubDate>Tue, 08 May 2012 22:56:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>KRT75 (formerly known as K6hf) is one of the isoforms of the keratin 6 (KRT6) family located within the type II cytokeratin gene cluster on chromosome 12 of humans and chromosome 15 of mice. KRT75 is expressed in the companion layer    and upper germinative matrix region of the hair follicle, the medulla of the hair shaft, and in epithelia of the nail bed. Dominant mutations in members of the KRT6 family, such as in KRT6A and KRT6B cause pachyonychia congenita (PC) -1 and -2,    respectively. To determine the function of KRT75 in skin appendages, we introduced a dominant mutation into a highly conserved residue in the helix initiation peptide of Krt75. Mice expressing this mutant form of Krt75 developed hair and nail    defects resembling PC. This mouse model provides in vivo evidence for the critical roles played by Krt75 in maintaining hair shaft and nail integrity. Furthermore, the phenotypes observed in our mutant Krt75 mice suggest that KRT75 may be a    candidate gene for screening PC patients who do not exhibit obvious mutations in KRT6A, KRT6B, KRT16, or KRT17, especially those with extensive hair involvement.</p>

	]]>
</description>

<author>J Chen et al.</author>


</item>


<item>
<title>Replication of beta- and gammaretroviruses is restricted in I/LnJ mice via the same genetic mechanism.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1721</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1721</guid>
<pubDate>Tue, 08 May 2012 22:55:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice of the I/LnJ inbred strain are unique in their ability to mount a robust and sustained humoral immune response capable of neutralizing infection with a betaretrovirus, mouse mammary tumor virus (MMTV). Virus-neutralizing    antibodies (Abs) coat MMTV virions secreted by infected cells, preventing virus spread and hence the formation of mammary tumors. To investigate whether I/LnJ mice resist infection with other retroviruses besides MMTV, the animals were infected    with murine leukemia virus (MuLV), a gammaretrovirus. MuLV-infected I/LnJ mice produced virus-neutralizing Abs that block virus transmission and virally induced disease. Generation of virus-neutralizing Abs required gamma interferon but was    independent of interleukin-12. This unique mechanism of retrovirus resistance is governed by a single recessive gene, virus infectivity controller 1 (vic1), mapped to chromosome 17. In addition to controlling the antivirus humoral immune    response, vic1 is also required for an antiviral cytotoxic response. Both types of responses were maintained in mice of the susceptible genetic background but congenic for the I/LnJ vic1 locus. Although the vic1-mediated resistance to MuLV    resembles the mechanism of retroviral recovery controlled by the resistance to Friend virus 3 (rfv3) gene, the rfv3 gene has been mapped to chromosome 15 and confers resistance to MuLV but not to MMTV. Thus, we have identified a unique virus    resistance mechanism that controls immunity against two distinct retroviruses.</p>

	]]>
</description>

<author>L K. Case et al.</author>


</item>


<item>
<title>Effects of exposing C57BL/6J mice to high- and low-frequency augmented acoustic environments: auditory brainstem response thresholds, cytocochleograms, anterior cochlear nucleus morphology and the role of gonadal hormones.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1720</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1720</guid>
<pubDate>Tue, 08 May 2012 22:55:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gonadectomized and intact adult C57BL/6J (B6) mice of both sexes were exposed for 12h nightly to an augmented acoustic environment (AAE): repetitive bursts of a 70dB SPL noise band. The high-frequency AAE (HAAE) was a half-octave    band centered at 20kHz; the low-frequency AAE (LAAE) was a 2-8kHz band. The effects of sex, gonadectomy, and AAE treatment on genetic progressive hearing loss (a trait of B6 mice) were evaluated by obtaining auditory brainstem response (ABR)    thresholds at ages 3-, 6-, and 9-months. At 9-months of age, hair cell counts (cytocochleograms) were obtained, and morphometric measures of the anteroventral cochlear nucleus (AVCN) were obtained. LAAE treatment caused elevation in ABR    thresholds (8-24kHz), with the highest thresholds occurring in intact females.  LAAE treatment caused some loss of outer hair cells in the basal half of the cochlea (in addition to losses normally occurring in B6 mice), with intact females losing    more cells than intact males. The loss of AVCN neurons and shrinkage of tissue volume that typically occur in 9-month-old B6 mice was lessened by LAAE treatment in intact (but not gonadectomized) male mice, whereas the degenerative changes were    exacerbated in intact (but not gonadectomized) females. These LAAE effects were prominent in, but not restricted to, the tonotopic low-frequency (ventral) AVCN. HAAE treatment resulted in some loss of neurons in the high-frequency (dorsal) AVCN.    In general, LAAE treatment plus male gonadal hormones (intact males) had an ameliorative effect whereas HAAE or LAAE treatment plus ovarian hormones (intact females) had a negative effect on age-related changes in the B6 auditory    system.</p>

	]]>
</description>

<author>J F. Willott et al.</author>


</item>


<item>
<title>The Mouse Genome Database (MGD): mouse biology and model systems.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1719</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1719</guid>
<pubDate>Tue, 08 May 2012 22:55:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Database, (MGD, http://www.informatics.jax.org/), integrates genetic, genomic and phenotypic information about the laboratory mouse, a primary animal model for studying human biology and disease. MGD data content    includes comprehensive characterization of genes and their functions, standardized descriptions of mouse phenotypes, extensive integration of DNA and protein sequence data, normalized representation of genome and genome variant information    including comparative data on mammalian genes. Data within MGD are obtained from diverse sources including manual curation of the biomedical literature, direct contributions from individual investigator's laboratories and major informatics    resource centers such as Ensembl, UniProt and NCBI. MGD collaborates with the bioinformatics community on the development of data and semantic standards such as the Gene Ontology (GO) and the Mammalian Phenotype (MP) Ontology. MGD provides a    data-mining platform that enables the development of translational research hypotheses based on comparative genotype, phenotype and functional analyses. Both web-based querying and computational access to data are provided. Recent improvements in    MGD described here include the association of gene trap data with mouse genes and a new batch query capability for customized data access and retrieval.</p>

	]]>
</description>

<author>C J. Bult et al.</author>


</item>


<item>
<title>Regulation of Pcsk6 expression during the preantral to antral follicle transition in mice: opposing roles of FSH and oocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1718</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1718</guid>
<pubDate>Tue, 08 May 2012 22:55:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Several secreted products of the TGFbeta superfamily have important roles during follicular development and are produced by both oocytes and somatic cells (granulosa and theca) in the follicle. The proprotein convertases are a    family of seven known proteins that process TGFbeta ligands and other secreted products to their mature active form. The present study examined the regulation of steady-state levels of Pcsk6 mRNA, which encodes a convertase protein known to    process members of the TGFbeta superfamily, during mouse follicular development.  Pcsk6 mRNA and protein were expressed in preantral but not cumulus or mural granulosa cells. Pcsk6 mRNA levels in preantral granulosa cells were not regulated by    growing oocytes of preantral follicles, but were elevated by FSH.  Furthermore, Pcsk6 mRNA in preantral granulosa cells was potently suppressed by factor(s) secreted by fully grown oocytes from antral follicles, in part through SMAD2/3-mediated    pathways. Oocytes acquired the ability to suppress the steady-state levels of Pcsk6 mRNA in granulosa cells during the preantral to antral follicle transition. Suppression of Pcsk6 mRNA by oocytes could reflect a change in the mechanism(s)    regulating the activity of members of the TGFbeta superfamily.</p>

	]]>
</description>

<author>F J. Diaz et al.</author>


</item>


<item>
<title>Asymmetry and polymorphism of hybrid male sterility during the early stages of speciation in house mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1717</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1717</guid>
<pubDate>Tue, 08 May 2012 22:55:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>House mice offer a powerful system for dissecting the genetic basis of phenotypes that isolate species in the early stages of speciation. We used a series of reciprocal crosses between wild-derived strains of Mus musculus and M.    domesticus to examine F(1) hybrid male sterility, one of the primary phenotypes thought to isolate these species. We report four main results. First, we found significantly smaller testes and fewer sperm in hybrid male progeny of most crosses.    Second, in some crosses hybrid male sterility was asymmetric and depended on the species origin of the X chromosome. These observations confirm and extend previous findings, underscoring the central role that the M. musculus X chromosome plays in    reproductive isolation. Third, comparisons among reciprocal crosses revealed polymorphism at one or more hybrid incompatibilities within M. musculus. Fourth, the spermatogenic phenotype of this polymorphic interaction appears distinct from    previously described hybrid incompatibilities between these species. These data build on previous studies of speciation in house mice and show that the genetic basis of hybrid male sterility is fairly complex, even at this early stage of    divergence.</p>

	]]>
</description>

<author>J M. Good et al.</author>


</item>


<item>
<title>Naive application of permutation testing leads to inflated type I error rates.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1716</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1716</guid>
<pubDate>Tue, 08 May 2012 22:55:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Failure to account for family structure within populations or in complex mating designs via uninformed applications of permutation testing will lead to inflated type I error rates. Careful consideration of the design factors is    essential since some situations allow several valid permutation strategies, and the choice that maximizes statistical power will not always be intuitive.</p>

	]]>
</description>

<author>G A. Churchill et al.</author>


</item>


<item>
<title>Effects of dietary restriction on hematopoietic stem-cell aging are genetically regulated.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1715</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1715</guid>
<pubDate>Tue, 08 May 2012 22:55:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Diminished stem-cell functions with age may be a major cause of anemias and other defects. Unfortunately, treatments that increase stem-cell function can also increase the incidence of cancers. Lifelong dietary restriction (DR) is    known to decrease spontaneous cancers and lengthen lifespan. This study examines the effect of DR on the ability of bone marrow cells to repopulate irradiated recipients and produce erythrocytes and lymphocytes. In BALB/cByJ (BALB) mice,    repopulating abilities decline with age; DR ameliorates this trend. In C57BL/6J (B6) and (BALB x B6) F1 hybrid (F1) mice, repopulating abilities increase with age; DR maintains this increase. Hematopoietic stem cell (HSC) numbers are highly    variable in aged BALB mice; however, the observed loss of marrow function results from a major loss in repopulating ability per HSC. DR greatly ameliorates this loss of function with age. In contrast, function per HSC in B6 mice is affected    neither by age nor by DR. Thus, DR increases or maintains increased marrow repopulating ability with age in the 3 different genotypes tested, but effects on function per HSC depend on genotype. That DR increases or maintains stem-cell function    with age, while decreasing cancer, has far-reaching health implications.</p>

	]]>
</description>

<author>R P. Ertl et al.</author>


</item>


<item>
<title>Comparative therapeutic effects of orally administered 1,25-dihydroxyvitamin D(3) and 1alpha-hydroxyvitamin D(3) on type-1 diabetes in non-obese diabetic mice fed a normal-calcaemic diet.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1714</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1714</guid>
<pubDate>Tue, 08 May 2012 22:54:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Frequent injections of the hormonal form of vitamin D(3), 1,25 dihydroxyvitamin D(3) (1,25D3) reportedly inhibits autoimmune type 1 diabetes (T1D) in non-obese diabetic (NOD) mice by correcting some of the abnormalities in    antigen-presenting cells which contribute the development of pathogenic T cell responses. This route of administration greatly elevates the levels of these compounds in the bloodstream for hours after treatment, which requires mice to be fed    diets formulated to contain much reduced levels of Ca to avoid the toxic effects of hypercalcaemia. In the current work, we demonstrate that feeding 1,25D3 or its synthetic precursor, 1alpha(OH) vitamin D(3) (1alphaD3), as part of a T1D    supportive chow diet containing normal levels of Ca, is an effective means of reducing the incidence of disease in NOD mice, but the doses required for protection elicited hypercalcaemia. However, T1D protection elicited by D3 analogue feeding    appears, at least partially, to have an immunological basis, as splenic T cells from treated mice had a decreased capacity to adoptively transfer disease. Protection is associated with an increased proportion of T cells with CD4+ forkhead box P3+    regulatory phenotype within the islet infiltrate of treated animals. The 1alphaD3 precursor is converted rapidly to the active 1,25D3 isoform in vivo. However, feeding the 1alphaD3 analogue elicited stronger T1D protection than the 1,25D3    compound, but also induced more severe hypercalcaemia. In future, the dietary supplementation of novel low-calcaemic D3 analogues may enable their continuous delivery at levels that inhibit T1D development in susceptible humans consuming normal    levels of Ca.</p>

	]]>
</description>

<author>J P. Driver et al.</author>


</item>


<item>
<title>Light optical precision measurements of the active and inactive Prader-Willi syndrome imprinted regions in human cell nuclei.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1713</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1713</guid>
<pubDate>Tue, 08 May 2012 22:54:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite the major advancements during the last decade with respect to both knowledge of higher order chromatin organization in the cell nucleus and the elucidation of epigenetic mechanisms of gene control, the true three-dimensional    (3D) chromatin structure of endogenous active and inactive gene loci is not known. The present study was initiated as an attempt to close this gap. As a model case, we compared the chromatin architecture between the genetically active and    inactive domains of the imprinted Prader-Willi syndrome (PWS) locus in human fibroblast and lymphoblastoid cell nuclei by 3D fluorescence in situ hybridization and quantitative confocal laser scanning microscopy. The volumes and 3D compactions of    identified maternal and paternal PWS domains were determined in stacks of light optical serial sections using a novel threshold-independent approach. Our failure to detect volume and compaction differences indicates that possible differences are    below the limits of light optical resolution. To overcome this limitation, spectral precision distance microscopy, a method of localization microscopy at the nanometer scale, was used to measure 3D distances between differentially labeled probes    located both within the PWS region and in its neighborhood. This approach allows the detection of intranuclear differences between 3D distances down to about 70-90 nm, but again did not reveal clearly detectable differences between active and    inactive PWS domains. Despite this failure, a comparison of the experimental 3D distance measurements with computer simulations of chromatin folding strongly supports a non-random higher order chromatin configuration of the PWS locus and argues    against 3D configurations based on giant chromatin loops. Our results indicate that the search for differences between endogenous active and inactive PWS domains must be continued at still smaller scales than hitherto possible with conventional    light microscopic procedures. The possibilities to achieve this goal are discussed.</p>

	]]>
</description>

<author>J Rauch et al.</author>


</item>


<item>
<title>Oocyte regulation of metabolic cooperativity between mouse cumulus cells and oocytes: BMP15 and GDF9 control cholesterol biosynthesis in cumulus cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1712</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1712</guid>
<pubDate>Tue, 08 May 2012 22:54:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Oocyte-derived bone morphogenetic protein 15 (BMP15) and growth differentiation factor 9 (GDF9) are key regulators of follicular development. Here we show that these factors control cumulus cell metabolism, particularly glycolysis    and cholesterol biosynthesis before the preovulatory surge of luteinizing hormone.  Transcripts encoding enzymes for cholesterol biosynthesis were downregulated in both Bmp15(-/-) and Bmp15(-/-) Gdf9(+/-) double mutant cumulus cells, and in    wild-type cumulus cells after removal of oocytes from cumulus-cell-oocyte complexes. Similarly, cholesterol synthesized de novo was reduced in these cumulus cells. This indicates that oocytes regulate cumulus cell cholesterol biosynthesis by    promoting the expression of relevant transcripts. Furthermore, in wild-type mice, Mvk, Pmvk, Fdps, Sqle, Cyp51, Sc4mol and Ebp, which encode enzymes required for cholesterol synthesis, were highly expressed in cumulus cells compared with oocytes;    and oocytes, in the absence of the surrounding cumulus cells, synthesized barely detectable levels of cholesterol. Furthermore, coincident with reduced cholesterol synthesis in double mutant cumulus cells, lower levels were also detected in    cumulus-cell-enclosed double mutant oocytes compared with wild-type oocytes. Levels of cholesterol synthesis in double mutant cumulus cells and oocytes were partially restored by co-culturing with wild-type oocytes. Together, these results    indicate that mouse oocytes are deficient in synthesizing cholesterol and require cumulus cells to provide products of the cholesterol biosynthetic pathway. Therefore, oocyte-derived paracrine factors, particularly, BMP15 and GDF9, promote    cholesterol biosynthesis in cumulus cells, probably as compensation for oocyte deficiencies in cholesterol production.</p>

	]]>
</description>

<author>Y Q. Su et al.</author>


</item>


<item>
<title>Genetic variation in Glp1r expression influences the rate of gastric emptying in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1711</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1711</guid>
<pubDate>Tue, 08 May 2012 22:54:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>We demonstrated previously that food intake traits map to a quantitative trait locus (QTL) on proximal chromosome 17, which encompasses Glp1r (glucagon-like peptide 1 receptor), encoding an important modulator of gastric emptying.    We then confirmed this QTL in a B6.CAST-17 congenic strain that consumed 27% more carbohydrate and 17% more total calories, yet similar fat calories, per body weight compared with the recipient C57BL/6J. The congenic strain also consumed greater    food volume. The current aims were to 1) identify genetic linkage for total food volume in F(2) mice, 2) perform gene expression profiling in stomach of B6.CAST-17 congenic mice using oligonucleotide arrays, 3) test for allelic imbalance in Glp1r    expression, 4) evaluate gastric emptying rate in parental and congenic mice, and 5) investigate a possible effect of genetic variation in Glp1r on gastric emptying. A genome scan revealed a single QTL for total food volume (Tfv1) (log of the odds    ratio = 7.6), which was confirmed in B6.CAST-17 congenic mice. Glp1r exhibited allelic imbalance in stomach, which correlated with accelerated gastric emptying in parental CAST and congenic B6.CAST-17 mice.  Moreover, congenic mice displayed an    impaired gastric emptying response to exendin-(9-39). These results suggest that genetic variation in Glp1r contributes to the strain differences in gastric emptying rate.</p>

	]]>
</description>

<author>K G. Kumar et al.</author>


</item>


<item>
<title>Virtues and limitations of the preimplantation mouse embryo as a model system.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1710</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1710</guid>
<pubDate>Tue, 08 May 2012 22:54:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse is the most widely used model of preimplantation embryo development, but is it a good model? Its small size, prolificacy and ease of handling make the mouse a relatively low cost, readily available and attractive    alternative when embryos from other species are difficult or expensive to obtain. However, the real power of the mouse as a model lies in mouse genetics. The development of inbred mouse strains facilitated gene discovery as well as our    understanding of gene function and regulation while the development of tools to introduce precise genetic modifications uniquely positioned the mouse as a powerful model system for uncovering gene function. However, all models have limitations;    the small size of the mouse limits tissue availability and manipulations that can be performed and differences in physiology among species may make it inappropriate to extrapolate from the mouse to other species. Thus, rather than extrapolating    directly from the mouse to other species, it may be more useful to use the mouse as a model system for developing and refining hypotheses to be tested directly in species of interest. In this brief review, the value of the preimplantation mouse    embryo as a model is considered, both as a model for other species and as a model for the mouse, as understanding the virtues and limitations of the mouse as a model system is essential to its appropriate use.</p>

	]]>
</description>

<author>R A. Taft</author>


</item>


<item>
<title>Podocytes use FcRn to clear IgG from the glomerular basement membrane.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1709</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1709</guid>
<pubDate>Tue, 08 May 2012 22:54:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>The glomerular filtration barrier prevents large serum proteins from being lost into the urine. It is not known, however, why the filter does not routinely clog with large proteins that enter the glomerular basement membrane (GBM).    Here, we provide evidence that an active transport mechanism exists to remove immunoglobulins that accumulate at the filtration barrier. We found that FcRn, an IgG and albumin transport receptor, is expressed in podocytes and functions to    internalize IgG from the GBM. Mice lacking FcRn accumulated IgG in the GBM as they aged, and tracer studies showed delayed clearance of IgG from the kidneys of FcRn-deficient mice. Supporting a role for this pathway in disease, saturating the    clearance mechanism potentiated the pathogenicity of nephrotoxic sera. These studies support the idea that podocytes play an active role in removing proteins from the GBM and suggest that genetic or acquired impairment of the clearance machinery    is likely to be a common mechanism promoting glomerular diseases.</p>

	]]>
</description>

<author>S Akilesh et al.</author>


</item>


<item>
<title>Overexpression of innate immune response genes in a model of recessive polycystic kidney disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1708</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1708</guid>
<pubDate>Tue, 08 May 2012 22:54:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Defects in the primary cilium/basal body complex of renal tubular cells cause polycystic kidney disease (PKD). To uncover pathways associated with disease progression, we determined the kidney transcriptome of 10-day-old severely    and mildly affected cpk mice, a model of recessive PKD. In the severe phenotype, the most highly expressed genes were those associated with the innate immune response including many macrophage markers, particularly those associated with a    profibrotic alternative activation pathway. Additionally, gene expression of macrophage activators was dominated by the complement system factors including the central complement component 3. Additional studies confirmed increased complement    component 3 protein levels in both cystic and non-cystic epithelia in the kidneys of cpk compared to wild-type mice. We also found elevated complement component 3 activation in two other mouse-recessive models and human-recessive PKD. Our results    suggest that abnormal complement component 3 activation is a key element of progression in PKD.</p>

	]]>
</description>

<author>M Mrug et al.</author>


</item>


<item>
<title>Role of modulator recognition factor 2 in adipogenesis and leptin expression in 3T3-L1 cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1707</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1707</guid>
<pubDate>Tue, 08 May 2012 22:53:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>The complex network of adipogenic transcription factors regulates adipocyte differentiation, obesity, and insulin resistance. Modulator recognition factor (Mrf) 2 knockout mice exhibit defects in fat accumulation and are protected    from diet-induced obesity, suggesting that Mrf2 deficiency affects adipogenesis. Here, we report that the gene expressions of the 2 isoforms of the transcription factors Mrf2, Mrf2alpha, and Mrf2beta, were induced upon adipogenesis in 3T3-L1    cells. Mrf2 mRNA expression was sensitive to stimulation by insulin, dexamethasone, and TNF-alpha in 3T3-L1 preadipocytes and differentiated adipocytes. Down-regulation of Mrf2alpha and Mrf2beta gene expressions induced by small interfering RNAs    increased the mRNA expression of leptin. These results indicate that Mrf2 can be a potential regulator of adipocyte differentiation and a potential repressor of leptin.</p>

	]]>
</description>

<author>J Dong et al.</author>


</item>


<item>
<title>Full-field electroretinography and marked variability in clinical phenotype of Alstrom syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1706</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1706</guid>
<pubDate>Tue, 08 May 2012 22:53:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVES: To characterize the clinical phenotype and to study the course of disease in patients with Alstrom syndrome, with an emphasis on retinal function assessed with full-field electroretinography (ERG). METHODS: Three age-    and sex-matched patients with Alstrom syndrome were selected from our retinitis pigmentosa register for repeated ophthalmologic examinations that included tests for color vision and visual fields using Goldmann perimetry and for repeated    assessment of full-field ERGs. RESULTS: Electroretinography demonstrated cone-rod degeneration in all 3 patients. A concomitant impairment of color vision and visual fields was also observed as well as marked variation in retinal function and in    disease severity. CONCLUSIONS: Full-field ERGs confirmed that Alstrom syndrome is associated with a cone-rod type of retinal degeneration. In this study, we have shown a striking variability in retinal function and disease onset and severity,    which has, to our knowledge, not been described previously in Alstrom syndrome.</p>

	]]>
</description>

<author>E Malm et al.</author>


</item>


<item>
<title>Mouse Models of Human Blood Cancers</title>
<link>http://mouseion.jax.org/stfb2000_2009/1705</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1705</guid>
<pubDate>Tue, 08 May 2012 22:53:41 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>Strategies for assessing and minimizing pain.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1704</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1704</guid>
<pubDate>Tue, 08 May 2012 22:53:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Karas AZ, Danneman PJ, Cadillac JM</author>


</item>


<item>
<title>Age-related eye diseases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1703</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1703</guid>
<pubDate>Tue, 08 May 2012 22:53:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bo Chang</author>


</item>


<item>
<title>Prediction of phenotype and gene expression for combinations of mutations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1702</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1702</guid>
<pubDate>Tue, 08 May 2012 22:53:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Molecular interactions provide paths for information flows. Genetic interactions reveal active information flows and reflect their functional consequences. We integrated these complementary data types to model the transcription    network controlling cell differentiation in yeast. Genetic interactions were inferred from linear decomposition of gene expression data and were used to direct the construction of a molecular interaction network mediating these genetic effects.     This network included both known and novel regulatory influences, and predicted genetic interactions. For corresponding combinations of mutations, the network model predicted quantitative gene expression profiles and precise phenotypic effects.    Multiple predictions were tested and verified.</p>

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</description>

<author>G W. Carter et al.</author>


</item>


<item>
<title>Genome-level analysis of genetic regulation of liver gene expression networks.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1701</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1701</guid>
<pubDate>Tue, 08 May 2012 22:53:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The liver is the primary site for the metabolism of nutrients, drugs, and chemical agents. Although metabolic pathways are complex and tightly regulated, genetic variation among individuals, reflected in variations in gene    expression levels, introduces complexity into research on liver disease. This study dissected genetic networks that control liver gene expression through the combination of large-scale quantitative mRNA expression analysis with genetic mapping in    a reference population of BXD recombinant inbred mouse strains for which extensive single-nucleotide polymorphism, haplotype, and phenotypic data are publicly available. We profiled gene expression in livers of naive mice of both sexes from    C57BL/6J, DBA/2J, B6D2F1, and 37 BXD strains using Agilent oligonucleotide microarrays. These data were used to map quantitative trait loci (QTLs) responsible for variations in the expression of about 19,000 transcripts.  We identified    polymorphic local and distant QTLs, including several loci that control the expression of large numbers of genes in liver, by comparing the physical transcript position with the location of the controlling QTL.  CONCLUSION: The data are available    through a public web-based resource (www.genenetwork.org) that allows custom data mining, identification of coregulated transcripts and correlated phenotypes, cross-tissue, and cross-species comparisons, as well as testing of a broad array of    hypotheses.</p>

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</description>

<author>D Gatti et al.</author>


</item>


<item>
<title>Neurobehavioral mutants identified in an ENU-mutagenesis project.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1700</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1700</guid>
<pubDate>Tue, 08 May 2012 22:52:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>We report on a battery of behavioral screening tests that successfully identified several neurobehavioral mutants among a large-scale ENU-mutagenized mouse population. Large numbers of ENU-mutagenized mice were screened for    abnormalities in central nervous system function based on abnormal performance in a series of behavior tasks. We developed and used a high-throughput screen of behavioral tasks to detect behavioral outliers. Twelve mutant pedigrees, representing    a broad range of behavioral phenotypes, have been identified. Specifically, we have identified two open-field mutants (one displaying hyperlocomotion, the other hypolocomotion), four tail-suspension mutants (all displaying increased immobility),    one nociception mutant (displaying abnormal responsiveness to thermal pain), two prepulse inhibition mutants (displaying poor inhibition of the startle response), one anxiety-related mutant (displaying decreased anxiety in the light/dark test),    and one learning-and-memory mutant (displaying reduced response to the conditioned stimulus). These findings highlight the utility of a set of behavioral tasks used in a high-throughput screen to identify neurobehavioral mutants. Further analysis    (i.e., behavioral and genetic mapping studies) of mutants is in progress with the ultimate goal of identification of novel genes and mouse models relevant to human disorders as well as the identification of novel therapeutic    targets.</p>

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</description>

<author>M N. Cook et al.</author>


</item>


<item>
<title>An informatics approach to systems neurogenetics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1699</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1699</guid>
<pubDate>Tue, 08 May 2012 22:52:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>We outline the theory behind complex trait analysis and systems genetics and describe web-accessible resources including GeneNetwork (GN) that can be used for rapid exploratory analysis and hypothesis testing. GN, in particular, is    a tightly integrated suite of bioinformatics tools and data sets, which supports the investigation of complex networks of gene variants, molecules, and cellular processes that modulate complex traits, including behavior and disease    susceptibility. Using various statistical tools, users are able to analyze gene expression in various brain regions and tissues, map loci that modulate these traits, and explore genetic covariance among traits. Taken together, these tools enable    the user to begin to assess complex interactions of gene networks, and facilitate analysis of traits using a systems approach.</p>

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</description>

<author>G D. Rosen et al.</author>


</item>


<item>
<title>Mouse Phenotype Database Integration Consortium: integration [corrected] of mouse phenome data resources.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1698</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1698</guid>
<pubDate>Tue, 08 May 2012 22:52:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Understanding the functions encoded in the mouse genome will be central to an understanding of the genetic basis of human disease. To achieve this it will be essential to be able to characterize the phenotypic consequences of    variation and alterations in individual genes. Data on the phenotypes of mouse strains are currently held in a number of different forms (detailed descriptions of mouse lines, first-line phenotyping data on novel mutations, data on the normal    features of inbred lines) at many sites worldwide. For the most efficient use of these data sets, we have initiated a process to develop standards for the description of phenotypes (using ontologies) and file formats for the description of    phenotyping protocols and phenotype data sets. This process is ongoing and needs to be supported by the wider mouse genetics and phenotyping communities to succeed. We invite interested parties to contact us as we develop this process    further.</p>

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</description>

<author>J M. Hancock et al.</author>


</item>


<item>
<title>Modeling complex genetic interactions in a simple eukaryotic genome: actin displays a rich spectrum of complex haploinsufficiencies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1697</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1697</guid>
<pubDate>Tue, 08 May 2012 22:52:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Multigenic influences are major contributors to human genetic disorders. Since humans are highly polymorphic, there are a high number of possible detrimental, multiallelic gene pairs. The actin cytoskeleton of yeast was used to    determine the potential for deleterious bigenic interactions; approximately 4800 complex hemizygote strains were constructed between an actin-null allele and the nonessential gene deletion collection. We found 208 genes that have deleterious    complex haploinsufficient (CHI) interactions with actin. This set is enriched for genes with gene ontology terms shared with actin, including several actin-binding protein genes, and nearly half of the CHI genes have defects in actin organization    when deleted. Interactions were frequently seen with genes for multiple components of a complex or with genes involved in the same function. For example, many of the genes for the large ribosomal subunit (RPLs) were CHI with act1Delta and had    actin organization defects when deleted. This was generally true of only one RPL paralog of apparently duplicate genes, suggesting functional specialization between ribosomal genes. In many cases, CHI interactions could be attributed to localized    defects on the actin protein. Spatial congruence in these data suggest that the loss of binding to specific actin-binding proteins causes subsets of CHI interactions.</p>

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</description>

<author>B Haarer et al.</author>


</item>


<item>
<title>Nearest Neighbor Networks: clustering expression data based on gene neighborhoods.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1696</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1696</guid>
<pubDate>Tue, 08 May 2012 22:52:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The availability of microarrays measuring thousands of genes simultaneously across hundreds of biological conditions represents an opportunity to understand both individual biological pathways and the integrated workings    of the cell. However, translating this amount of data into biological insight remains a daunting task. An important initial step in the analysis of microarray data is clustering of genes with similar behavior. A number of classical techniques are    commonly used to perform this task, particularly hierarchical and K-means clustering, and many novel approaches have been suggested recently. While these approaches are useful, they are not without drawbacks; these methods can find clusters in    purely random data, and even clusters enriched for biological functions can be skewed towards a small number of processes (e.g. ribosomes).  RESULTS: We developed Nearest Neighbor Networks (NNN), a graph-based algorithm to generate clusters of    genes with similar expression profiles. This method produces clusters based on overlapping cliques within an interaction network generated from mutual nearest neighborhoods. This focus on nearest neighbors rather than on absolute distance    measures allows us to capture clusters with high connectivity even when they are spatially separated, and requiring mutual nearest neighbors allows genes with no sufficiently similar partners to remain unclustered. We compared the clusters    generated by NNN with those generated by eight other clustering methods. NNN was particularly successful at generating functionally coherent clusters with high precision, and these clusters generally represented a much broader selection of    biological processes than those recovered by other methods. CONCLUSION: The Nearest Neighbor Networks algorithm is a valuable clustering method that effectively groups genes that are likely to be functionally related. It is particularly    attractive due to its simplicity, its success in the analysis of large datasets, and its ability to span a wide range of biological functions with high precision.</p>

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</description>

<author>C Huttenhower et al.</author>


</item>


<item>
<title>Exploring the functional landscape of gene expression: directed search of large microarray compendia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1695</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1695</guid>
<pubDate>Tue, 08 May 2012 22:52:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>MOTIVATION: The increasing availability of gene expression microarray technology has resulted in the publication of thousands of microarray gene expression datasets investigating various biological conditions. This vast repository    is still underutilized due to the lack of methods for fast, accurate exploration of the entire compendium. RESULTS: We have collected Saccharomyces cerevisiae gene expression microarray data containing roughly 2400 experimental conditions. We    analyzed the functional coverage of this collection and we designed a context-sensitive search algorithm for rapid exploration of the compendium. A researcher using our system provides a small set of query genes to establish a biological search    context; based on this query, we weight each dataset's relevance to the context, and within these weighted datasets we identify additional genes that are co-expressed with the query set. Our method exhibits an average increase in accuracy of 273%    compared to previous mega-clustering approaches when recapitulating known biology. Further, we find that our search paradigm identifies novel biological predictions that can be verified through further experimentation. Our methodology provides    the ability for biological researchers to explore the totality of existing microarray data in a manner useful for drawing conclusions and formulating hypotheses, which we believe is invaluable for the research community. AVAILABILITY: Our    query-driven search engine, called SPELL, is available at http://function.princeton.edu/SPELL.  SUPPLEMENTARY INFORMATION: Several additional data files, figures and discussions are available at    http://function.princeton.edu/SPELL/supplement.</p>

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</description>

<author>M A. Hibbs et al.</author>


</item>


<item>
<title>Heat shock factor 1 is a powerful multifaceted modifier of carcinogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1694</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1694</guid>
<pubDate>Tue, 08 May 2012 22:52:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Heat shock factor 1 (HSF1) is the master regulator of the heat shock response in eukaryotes, a very highly conserved protective mechanism. HSF1 function increases survival under a great many pathophysiological conditions. How it    might be involved in malignancy remains largely unexplored. We report that eliminating HSF1 protects mice from tumors induced by mutations of the RAS oncogene or a hot spot mutation in the tumor suppressor p53. In cell culture, HSF1 supports    malignant transformation by orchestrating a network of core cellular functions including proliferation, survival, protein synthesis, and glucose metabolism. The striking effects of HSF1 on oncogenic transformation are not limited to mouse systems    or tumor initiation; human cancer lines of diverse origins show much greater dependence on HSF1 function to maintain proliferation and survival than their nontransformed counterparts. While it enhances organismal survival and longevity under most    circumstances, HSF1 has the opposite effect in supporting the lethal phenomenon of cancer.</p>

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</description>

<author>C Dai et al.</author>


</item>


<item>
<title>DNA-dependent protein kinase catalytic subunit is not required for dysfunctional telomere fusion and checkpoint response in the telomerase-deficient mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1693</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1693</guid>
<pubDate>Tue, 08 May 2012 22:51:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Telomeres are key structural elements for the protection and maintenance of linear chromosomes, and they function to prevent recognition of chromosomal ends as DNA double-stranded breaks. Loss of telomere capping function brought    about by telomerase deficiency and gradual erosion of telomere ends or by experimental disruption of higher-order telomere structure culminates in the fusion of defective telomeres and/or the activation of DNA damage checkpoints. Previous work    has implicated the nonhomologous end-joining (NHEJ) DNA repair pathway as a critical mediator of these biological processes. Here, employing the telomerase-deficient mouse model, we tested whether the NHEJ component DNA-dependent protein kinase    catalytic subunit (DNA-PKcs) was required for fusion of eroded/dysfunctional telomere ends and the telomere checkpoint responses. In late-generation mTerc(-/-) DNA-PKcs(-/-) cells and tissues, chromosomal end-to-end fusions and anaphase bridges    were readily evident. Notably, nullizygosity for DNA Ligase4 (Lig4)--an additional crucial NHEJ component--was also permissive for chromosome fusions in mTerc(-/-) cells, indicating that, in contrast to results seen with experimental disruption    of telomere structure, telomere dysfunction in the context of gradual telomere erosion can engage additional DNA repair pathways. Furthermore, we found that DNA-PKcs deficiency does not reduce apoptosis, tissue atrophy, or p53 activation in    late-generation mTerc(-/-) tissues but rather moderately exacerbates germ cell apoptosis and testicular degeneration. Thus, our studies indicate that the NHEJ components, DNA-PKcs and Lig4, are not required for fusion of critically shortened    telomeric ends and that DNA-PKcs is not required for sensing and executing the telomere checkpoint response, findings consistent with the consensus view of the limited role of DNA-PKcs in DNA damage signaling in general.</p>

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</description>

<author>R S. Maser et al.</author>


</item>


<item>
<title>Chromosomally unstable mouse tumours have genomic alterations similar to diverse human cancers.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1692</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1692</guid>
<pubDate>Tue, 08 May 2012 22:51:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Highly rearranged and mutated cancer genomes present major challenges in the identification of pathogenetic events driving the neoplastic transformation process. Here we engineered lymphoma-prone mice with chromosomal instability to    assess the usefulness of mouse models in cancer gene discovery and the extent of cross-species overlap in cancer-associated copy number aberrations. Along with targeted re-sequencing, our comparative oncogenomic studies identified FBXW7 and PTEN    to be commonly deleted both in murine lymphomas and in human T-cell acute lymphoblastic leukaemia/lymphoma (T-ALL). The murine cancers acquire widespread recurrent amplifications and deletions targeting loci syntenic to those not only in human    T-ALL but also in diverse human haematopoietic, mesenchymal and epithelial tumours. These results indicate that murine and human tumours experience common biological processes driven by orthologous genetic events in their malignant evolution. The    highly concordant nature of genomic events encourages the use of genomically unstable murine cancer models in the discovery of biological driver events in the human oncogenome.</p>

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</description>

<author>R S. Maser et al.</author>


</item>


<item>
<title>Alu elements mediate MYB gene tandem duplication in human T-ALL.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1691</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1691</guid>
<pubDate>Tue, 08 May 2012 22:51:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recent studies have demonstrated that the MYB oncogene is frequently duplicated in human T cell acute lymphoblastic leukemia (T-ALL). We find that the human MYB locus is flanked by 257-bp Alu repeats and that the duplication is    mediated somatically by homologous recombination between the flanking Alu elements on sister chromatids. Nested long-range PCR analysis indicated a low frequency of homologous recombination leading to MYB tandem duplication in the peripheral    blood mononuclear cells of approximately 50% of healthy individuals, none of whom had a MYB duplication in the germline. We conclude that Alu-mediated MYB tandem duplication occurs at low frequency during normal thymocyte development and is    clonally selected during the molecular pathogenesis of human T-ALL.</p>

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</description>

<author>J O&apos;Neil et al.</author>


</item>


<item>
<title>Models of signal transduction in cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1690</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1690</guid>
<pubDate>Tue, 08 May 2012 22:51:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Dongguang Li et al.</author>


</item>


<item>
<title>Cancer stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1689</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1689</guid>
<pubDate>Tue, 08 May 2012 22:51:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kyuson Yun et al.</author>


</item>


<item>
<title>Genetic and genomic insights into the molecular basis of atherosclerosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1688</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1688</guid>
<pubDate>Tue, 08 May 2012 22:51:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Atherosclerosis is a complex disease involving genetic and environmental risk factors, acting on their own or in synergy. Within the general population, polymorphisms within genes in lipid metabolism, inflammation, and    thrombogenesis are probably responsible for the wide range of susceptibility to myocardial infarction, a fatal consequence of atherosclerosis. Genetic linkage studies have been carried out in both humans and mouse models to identify these    polymorphisms.  Approximately 40 quantitative trait loci for atherosclerotic disease have been found in humans, and approximately 30 in mice. Recently, genome-wide association studies have been used to identify atherosclerosis-susceptibility    polymorphisms.  Although discovering new atherosclerosis genes through these approaches remains challenging, the pace at which these polymorphisms are being found is accelerating due to rapidly improving bioinformatics resources and    biotechnologies. The outcome of these efforts will not only unveil the molecular basis of atherosclerosis but also facilitate the discovery of drug targets and individualized medication against the disease.</p>

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</description>

<author>Y Chen et al.</author>


</item>


<item>
<title>Endocrinology: bone as a target tissue for hormonal regulation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1687</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1687</guid>
<pubDate>Tue, 08 May 2012 22:50:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K M. Delahunty et al.</author>


</item>


<item>
<title>Chemotherapy-resistant human AML stem cells home to and engraft within the bone-marrow endosteal region.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1686</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1686</guid>
<pubDate>Tue, 08 May 2012 22:50:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Acute myelogenous leukemia (AML) is the most common adult leukemia, characterized by the clonal expansion of immature myeloblasts initiating from rare leukemic stem (LS) cells. To understand the functional properties of human LS    cells, we developed a primary human AML xenotransplantation model using newborn nonobese diabetic/severe combined immunodeficient/interleukin (NOD/SCID/IL)2r gamma(null) mice carrying a complete null mutation of the cytokine gamma c upon the SCID    background. Using this model, we demonstrated that LS cells exclusively recapitulate AML and retain self-renewal capacity in vivo. They home to and engraft within the osteoblast-rich area of the bone marrow, where AML cells are protected from    chemotherapy-induced apoptosis. Quiescence of human LS cells may be a mechanism underlying resistance to cell cycle-dependent cytotoxic therapy.  Global transcriptional profiling identified LS cell-specific transcripts that are stable through    serial transplantation. These results indicate the potential utility of this AML xenograft model in the development of novel therapeutic strategies targeted at LS cells.</p>

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</description>

<author>F Ishikawa et al.</author>


</item>


<item>
<title>Mouse models in aging research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1685</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1685</guid>
<pubDate>Tue, 08 May 2012 22:50:40 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K Flurkey et al.</author>


</item>


<item>
<title>Genetic modifiers that affect phenotypic expression of retinal diseases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1684</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1684</guid>
<pubDate>Tue, 08 May 2012 22:50:31 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>M M. Edwards et al.</author>


</item>


<item>
<title>Impact of substrate glycoside linkage and elemental sulfur on bioenergetics of and hydrogen production by the hyperthermophilic archaeon Pyrococcus furiosus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1683</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1683</guid>
<pubDate>Tue, 08 May 2012 22:50:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Glycoside linkage (cellobiose versus maltose) dramatically influenced bioenergetics to different extents and by different mechanisms in the hyperthermophilic archaeon Pyrococcus furiosus when it was grown in continuous culture at a    dilution rate of 0.45 h(-1) at 90 degrees C. In the absence of S(0), cellobiose-grown cells generated twice as much protein and had 50%-higher specific H(2) generation rates than maltose-grown cultures. Addition of S(0) to maltose-grown cultures    boosted cell protein production fourfold and shifted gas production completely from H(2) to H(2)S. In contrast, the presence of S(0) in cellobiose-grown cells caused only a 1.3-fold increase in protein production and an incomplete shift from H(2)    to H(2)S production, with 2.5 times more H(2) than H(2)S formed. Transcriptional response analysis revealed that many genes and operons known to be involved in alpha- or beta-glucan uptake and processing were up-regulated in an S(0)-independent    manner. Most differentially transcribed open reading frames (ORFs) responding to S(0) in cellobiose-grown cells also responded to S(0) in maltose-grown cells; these ORFs included ORFs encoding a membrane-bound oxidoreductase complex (MBX) and two    hypothetical proteins (PF2025 and PF2026). However, additional genes (242 genes; 108 genes were up-regulated and 134 genes were down-regulated) were differentially transcribed when S(0) was present in the medium of maltose-grown cells, indicating    that there were different cellular responses to the two sugars. These results indicate that carbohydrate characteristics (e.g., glycoside linkage) have a major impact on S(0) metabolism and hydrogen production in P. furiosus. Furthermore, such    issues need to be considered in designing and implementing metabolic strategies for production of biofuel by fermentative anaerobes.</p>

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</description>

<author>C J. Chou et al.</author>


</item>


<item>
<title>Unexpected functional consequences of xenogeneic transgene expression in beta-cells of NOD mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1682</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1682</guid>
<pubDate>Tue, 08 May 2012 22:50:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>We describe unexpected alterations in the non-obese diabetic (NOD/Lt) mouse model of type 1 diabetes (T1D) following forced beta-cell expression of non-mammalian genes ligated to an insulin promoter sequence. These include the    jellyfish green fluorescent protein (GFP), useful for beta-cell identification, and the bacteriophage P1 Cre recombinase, necessary for beta cell-specific ablation of a gene using a Cre-loxP system. Homozygous expression of GFP, driven by the    mouse insulin 1 gene promoter (MIP-GFP) in a single transgenic line of NOD mice, produced T1D in postnatal mice that was not associated with insulitis, but rather beta cell-depleted islets. Hemizygous transgene expression suppressed spontaneous    autoimmune T1D in females, and produced a male glucose intolerance syndrome associated with age-dependent declines in plasma insulin content. Among lines of transgenic NOD/Lt mice expressing Cre recombinase driven by the rat insulin 2 promoter    (RIP-Cre), high, non-mosaic expression correlated with suppressed T1D development. These findings emphasize the need for careful characterization of genetically manipulated NOD mouse stocks to insure that model characteristics have not been    compromised.</p>

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</description>

<author>E H. Leiter et al.</author>


</item>


<item>
<title>Genetic Manipulations of PPARs: Effects on Obesity and Metabolic Disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1681</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1681</guid>
<pubDate>Tue, 08 May 2012 22:50:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The interest in genetic manipulations of PPARs is as old as their discovery as receptors of ligands with beneficial clinical activities. Considering the effects of PPAR ligands on critical aspects of systemic physiology, including    obesity, lipid metabolism, insulin resistance, and diabetes, gene knockout (KO) in mice is the ideal platform for both hypothesis testing and discovery of new PPAR functions in vivo. With the fervent pursuit of the magic bullet to eradicate the    obesity epidemic, special emphasis has been placed on the impacts of PPARs on obesity and its associated diseases. As detailed in this review, understanding how PPARs regulate gene expression and basic metabolic pathways is a necessary    intermediate en route to deciphering their effects on obesity. Over a decade and dozens of genetic modifications of PPARs into this effort, valuable lessons have been learned, but we are left with more questions to be answered. These lessons and    future prospects are the subject of this review.</p>

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</description>

<author>Y Barak et al.</author>


</item>


<item>
<title>Genetic control of lipids in the mouse cross DU6i x DBA/2.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1680</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1680</guid>
<pubDate>Tue, 08 May 2012 22:49:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>An F(2) pedigree based on the mouse lines DU6i and DBA/2 with extremely different growth and obesity characteristics was generated to search for QTLs affecting serum concentrations of triglycerides (TG), total cholesterol (CHOL),    HDL cholesterol (HDL-C), and LDL cholesterol (LDL-C). Compared with many other studies, we searched for spontaneous genetic variants contributing to high lipid levels under a standard breeding diet. Significant QTLs for CHOL were identified on    chromosomes 4 and 6, and a female-specific locus on chromosome 3. QTLs for HDL-C were detected on chromosome 11 for both sexes, and on chromosome 1 for females. These QTLs are located in syntenic human regions that have QTLs that have not been    previously confirmed in animal studies. LDL-C QTLs have been mapped for both sexes to chromosome 8 and in males on chromosome 13. Epistatic interactions that significantly accounted for the phenotypic variance of HDL-C, CHOL, and LDL-C serum    concentrations were also detected with one interaction between chromosomes 8 and 15, accounting for 22% of the observed variance in LDL-C levels. The identified loci coincide in part with regions controlling growth and obesity. Thus, multiple    genes or pleiotropic effects may be assumed.  The identified QTLs for cholesterol and its transport proteins as subcomponents of risk for coronary heart disease will further improve our understanding of the genetic net controlling plasma lipid    concentrations.</p>

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</description>

<author>G A. Brockmann et al.</author>


</item>


<item>
<title>Chromosome neighborhood composition determines translocation outcomes after exposure to high-dose radiation in primary cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1679</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1679</guid>
<pubDate>Tue, 08 May 2012 22:49:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Radiation exposure is an occupational hazard for military personnel, some health care professionals, airport security screeners, and medical patients, with some individuals at risk for acute, high-dose exposures. Therefore, the    biological effects of radiation, especially the potential for chromosome damage, are major occupational and health concerns. However, the biophysical mechanisms of chromosome instability subsequent to radiation-induced DNA damage are poorly    understood. It is clear that interphase chromosomes occupy discrete structural and functional subnuclear domains, termed chromosome territories (CT), which may be organized into 'neighborhoods' comprising groups of specific CTs. We directly    evaluated the relationship between chromosome positioning, neighborhood composition, and translocation partner choice in primary lymphocytes, using a cell-based system in which we could induce multiple, concentrated DNA breaks via high-dose    irradiation. We critically evaluated mis-rejoining profiles and tested whether breaks occurring nearby were more likely to fuse than breaks occurring at a distance. We show that CT neighborhoods comprise heterologous chromosomes, within which    inter-CT distances directly relate to translocation partner choice.  These findings demonstrate that interphase chromosome arrangement is a principal factor in genomic instability outcomes in primary lymphocytes, providing a structural context    for understanding the biological effects of radiation exposure, and the molecular etiology of tumor-specific translocation patterns.</p>

	]]>
</description>

<author>Caddle L. Brianna et al.</author>


</item>


<item>
<title>Mouse models for understanding the growth hormone insulin-like growth factor-I axis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1678</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1678</guid>
<pubDate>Tue, 08 May 2012 22:49:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Mouse models that include spontaneous mutations, as well as those carrying allelic differences, have been extremely useful in clarifying the role of skeletal and circulating insulin-like growth factor I (IGF-I) in peak    bone acquisition. The role of peroxisome proliferator-activated receptor gamma, a nuclear receptor and key differentiation factor for adipogenesis, has provided new insights into the relationship of marrow fat to skeletal mass. CONCLUSIONS: Mouse    models continue to deepen our understanding of IGF-I signaling and the role of IGF-I in determining marrow stromal cell fate.</p>

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</description>

<author>C J. Rosen</author>


</item>


<item>
<title>Notch1 expression and ligand interactions in progenitor cells of the mouse olfactory epithelium.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1677</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1677</guid>
<pubDate>Tue, 08 May 2012 22:49:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite the relatively simplified organization of the olfactory epithelium (OE), our understanding of the factors that regulate its cellular diversity is limited.  Genetic and localization studies suggest that Notch signaling may be    important in this process. We characterize here a population of Notch1 (+) olfactory basal cells in embryonic mice that coordinately express both the Notch effector Hes5 and the glycosyltransferase Lfng. These cells are distinct from Mash1(+)    neuronal precursors, but give rise to sensory neurons, suggesting that Notch1 signals may in part function to maintain a neurogenic progenitor pool. Furthermore, Lfng(+) cells also generate a population of cells in the migratory mass that appear    to be ensheathing glial precursors, indicating potential multipotency in these progenitors. The Notch ligand Dll4 is expressed by basal OE cells that are interspersed with Notch1(+) progenitors during later OE neurogenesis. In contrast, mice    deficient in Dll1 exhibit a smaller OE and a loss of Hes5 expression, indicating an earlier function in olfactory progenitor cell development. Taken together, these results further support a role for Notch signaling in the regulation of olfactory    neurogenesis and cell diversity.</p>

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</description>

<author>G A. Schwarting et al.</author>


</item>


<item>
<title>Crossover interference underlies sex differences in recombination rates.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1676</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1676</guid>
<pubDate>Tue, 08 May 2012 22:49:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>In many organisms, recombination rates differ between the two sexes. Here we show that in mice, this is because of a shorter genomic interference distance in females than in males, measured in Mb. However, the interference distance    is the same in terms of bivalent length. We propose a model in which the interference distance in the two sexes reflects the compaction of chromosomes at the pachytene stage of meiosis.</p>

	]]>
</description>

<author>P M. Petkov et al.</author>


</item>


<item>
<title>Gene expression profiling of leukemic cells and primary thymocytes predicts a signature for apoptotic sensitivity to glucocorticoids.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1675</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1675</guid>
<pubDate>Tue, 08 May 2012 22:49:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>ABSTRACT: BACKGROUND: Glucocorticoids (GC's) play an integral role in treatment strategies designed to combat various forms of hematological malignancies. GCs also are powerful inhibitors of the immune system, through regulation of    appropriate cytokines and by causing apoptosis of immature thymocytes. By activating the glucocorticoid receptor (GR), GCs evoke apoptosis through transcriptional regulation of a complex, interactive gene network over a period of time preceding    activation of the apoptotic enzymes. In this study we used microarray technology to determine whether several disparate types of hematologic cells, all sensitive to GC-evoked apoptosis, would identify a common set of regulated genes. We compared    gene expression signatures after treatment with two potent synthetic GCs, dexamethasone (Dex) and cortivazol (CVZ) using a panel of hematologic cells. Pediatric CD4+/CD8+ T-cell leukemia was represented by 3 CEM clones: two sensitive, CEM-C7-14    and CEM-C1-6, and one resistant, CEM-C1-15, to Dex. CEM-C1-15 was also tested when rendered GC-sensitive by several treatments.  GC-sensitive pediatric B-cell leukemia was represented by the SUP-B15 line and adult B-cell leukemia by RS4;11 cells.    Kasumi-1 cells gave an example of the rare Dex-sensitive acute myeloblastic leukemia (AML). To test the generality of the correlations in malignant cell gene sets, we compared with GC effects on mouse non-transformed thymocytes. RESULTS: We    identified a set of genes regulated by GCs in all GC-sensitive malignant cells. A portion of these were also regulated in the thymocytes. Because we knew that the highly Dex-resistant CEM-C1-15 cells could be killed by CVZ, we tested these cells    with the latter steroid and again found that many of the same genes were now regulated as in the inherently GC-sensitive cells. The same result was obtained when we converted the Dex-resistant clone to Dex-sensitive by treatment with forskolin    (FSK), to activate the adenyl cyclase/protein kinase A pathway (PKA). CONCLUSION: Our results have identified small sets of genes that correlate with GC-sensitivity in cells from several hematologic malignancies. Some of these are also regulated    in normal mouse thymocytes.</p>

	]]>
</description>

<author>A L. Miller et al.</author>


</item>


<item>
<title>Evaluation of gene expression profiling in a mouse model of L-gulonolactone oxidase gene deficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1674</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1674</guid>
<pubDate>Tue, 08 May 2012 22:49:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Humans and guinea pigs are species which are unable to synthesize ascorbic acid (vitamin C) because, unlike rodents, they lack the enzyme L-gulonolactone oxidase (Gulo). Although the phenotype of lacking vitamin C in humans, named    scurvy, has long been well known, information on the impact of lacking Gulo on the gene expression profiles of different tissues is still missing. This knowledge could improve our understanding of molecular pathways in which Gulo may be involved.     Recently, we discovered a deletion that includes all 12 exons in the gene for Gulo in the sfx mouse, characterized by spontaneous bone fractures. We report here the initial analysis of the impact of the Gulo gene deletion on the murine gene    expression profiles in the liver, femur and kidney.</p>

	]]>
</description>

<author>J Yan et al.</author>


</item>


<item>
<title>Role of novel protein kinase C isoforms in Lyme arthritis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1673</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1673</guid>
<pubDate>Tue, 08 May 2012 22:48:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inflammation caused by Borrelia burgdorferi infection occurs as a result of induction of pro-inflammatory cytokines from activation of multiple signalling pathways. It has previously been shown that mitogen-activated protein kinase    (MAPK) and Janus kinase/signal transducer and activator of transcription signalling pathways are activated by B. burgdorferi in cultured human chondrocytes. Protein kinase C (PKC) signalling pathways are potential candidates that may control    these downstream signalling pathways. Here we show that B. burgdorferi infection leads to phosphorylation and activation of novel PKC isoforms (PKC delta, epsilon, eta and theta) in a time-dependent manner. A specific inhibitor of novel PKC    isoforms blocked the induction of pro-inflammatory molecules in response to B. burgdorferi infection as did transient transfection of novel PKC dominant-negative plasmids into chondrocytes.  B. burgdorferi-induced p38 MAPK phosphorylation was    also significantly inhibited by an inhibitor of novel PKC isoforms, suggesting that PKC activation occurs upstream of p38 activation. In vivo, administration of an inhibitor of classical and novel PKC isoforms to C3H/HeN mice infected with B.    burgdorferi resulted in significantly reduced ankle inflammation and swelling. In conclusion, these data suggest that novel PKC isoforms are specifically activated by B. burgdorferi infection and this can contribute to the regulation of    inflammation in vitro and in vivo.</p>

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</description>

<author>O S. Shin et al.</author>


</item>


<item>
<title>Low utilization of circulating glucose after food withdrawal in Snell dwarf mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1672</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1672</guid>
<pubDate>Tue, 08 May 2012 22:48:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Glucose metabolism is altered in long-lived people and mice. Although it is clear that there is an association between altered glucose metabolism and longevity, it is not known whether this link is causal or not. Our current    hypothesis is that decreased fasting glucose utilization may increase longevity by reducing oxygen radical production, a potential cause of aging. We observed that whole body fasting glucose utilization was lower in the Snell dwarf, a long-lived    mutant mouse. Whole body fasting glucose utilization may be reduced by a decrease in the production of circulating glucose. Our isotope labeling analysis indicated both gluconeogenesis and glycogenolysis were suppressed in Snell dwarfs. Elevated    circulating adiponectin may contribute to the reduction of glucose production in Snell dwarfs. Adiponectin lowered the appearance of glucose in the media over hepatoma cells by suppressing gluconeogenesis and glycogenolysis. The suppression of    glucose production by adiponectin in vitro depended on AMP-activated protein kinase, a cell mediator of fatty acid oxidation. Elevated fatty acid oxidation was indicated in Snell dwarfs by increased utilization of circulating oleic acid, reduced    intracellular triglyceride content, and increased phosphorylation of acetyl-CoA carboxylase. Finally, protein carbonyl content, a marker of oxygen radical damage, was decreased in Snell dwarfs. The correlation between high glucose utilization and    elevated oxygen radical production was also observed in vitro by altering the concentrations of glucose and fatty acids in the media or pharmacologic inhibition of glucose and fatty acid oxidation with 4-hydroxycyanocinnamic acid and etomoxir,    respectively.</p>

	]]>
</description>

<author>N L. Brooks et al.</author>


</item>


<item>
<title>Alstrom syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1671</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1671</guid>
<pubDate>Tue, 08 May 2012 22:48:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alstrom Syndrome is an autosomal recessive, single gene disorder caused by mutations in ALMS1 (Chr 2p13), a novel gene of currently unknown molecular function. Alstrom Syndrome is multisystemic, with cone-rod retinal dystrophy    leading to juvenile blindness, sensorineural hearing loss, obesity, insulin resistance with hyperinsulinemia, and type 2 diabetes mellitus. Very high incidences of additional disease phenotypes that may severely affect prognosis and survival    include endocrine abnormalities, dilated cardiomyopathy, pulmonary fibrosis and restrictive lung disease, and progressive hepatic and renal failure.  Other clinical features in some patients are hypertension, hypothyroidism, hyperlipidemia,    hypogonadism, urological abnormalities, adult short stature, and bone-skeletal disturbances. Most patients demonstrate normal intelligence, although some reports indicate delayed psychomotor and intellectual development.  The life span of    patients with Alstrom Syndrome rarely exceeds 40 years. There is no specific therapy for Alstrom Syndrome, but early diagnosis and intervention can moderate the progression of the disease phenotypes and improve the longevity and quality of life    for patients.</p>

	]]>
</description>

<author>J D. Marshall et al.</author>


</item>


<item>
<title>PohnB6F1: a cross of wild and domestic mice that is a new model of extended female reproductive life span.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1670</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1670</guid>
<pubDate>Tue, 08 May 2012 22:48:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the search for novel genetic diversity that affects the timing of life history traits, we investigated a wild-derived stock of mice (Pohn). Early generations showed extended reproductive life span; however, this phenotype    diminished with propagation of the stock. Out-crossing latter generation Pohn mice to C57BL/6J (B6) mice produced PohnB6F1 hybrids with remarkably extended reproductive life spans-mean age at last litter of 647 +/- 32 days-longer than for the    parental strains (70% longer than Pohn, 88% longer than B6) and longer than for highly heterogeneous crosses of laboratory mice. Litter size among young PohnB6F1 adults was similar to parental stocks, but their age-related decline in litter size    was delayed by 150-200 days, resembling the earlier Pohn generations. Possibly, out-crossing Pohn mice unmasked cryptic alleles that promote extended female reproduction. This work establishes the PohnB6F1 hybrid as a new model for delayed    reproductive aging.</p>

	]]>
</description>

<author>K Flurkey et al.</author>


</item>


<item>
<title>ETV6-NTRK3 fusion oncogene initiates breast cancer from committed mammary progenitors via activation of AP1 complex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1669</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1669</guid>
<pubDate>Tue, 08 May 2012 22:48:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>To better understand the cellular origin of breast cancer, we developed a mouse model that recapitulates expression of the ETV6-NTRK3 (EN) fusion oncoprotein, the product of the t(12;15)(p13;q25) translocation characteristic of    human secretory breast carcinoma. Activation of EN expression in mammary tissues by Wap-Cre leads to fully penetrant, multifocal malignant breast cancer with short latency. We provide genetic evidence that, in nulliparous Wap-Cre;EN females,    committed alveolar bipotent or CD61(+) luminal progenitors are targets of tumorigenesis. Furthermore, EN transforms these otherwise transient progenitors through activation of the AP1 complex. Given the increasing relevance of chromosomal    translocations in epithelial cancers, such mice serve as a paradigm for the study of their genetic pathogenesis and cellular origins, and generation of preclinical models.</p>

	]]>
</description>

<author>Z Li et al.</author>


</item>


<item>
<title>The classical complement cascade mediates CNS synapse elimination.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1668</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1668</guid>
<pubDate>Tue, 08 May 2012 22:48:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>During development, the formation of mature neural circuits requires the selective elimination of inappropriate synaptic connections. Here we show that C1q, the initiating protein in the classical complement cascade, is expressed by    postnatal neurons in response to immature astrocytes and is localized to synapses throughout the postnatal CNS and retina. Mice deficient in complement protein C1q or the downstream complement protein C3 exhibit large sustained defects in CNS    synapse elimination, as shown by the failure of anatomical refinement of retinogeniculate connections and the retention of excess retinal innervation by lateral geniculate neurons. Neuronal C1q is normally downregulated in the adult CNS; however,    in a mouse model of glaucoma, C1q becomes upregulated and synaptically relocalized in the adult retina early in the disease. These findings support a model in which unwanted synapses are tagged by complement for elimination and suggest that    complement-mediated synapse elimination may become aberrantly reactivated in neurodegenerative disease.</p>

	]]>
</description>

<author>B Stevens et al.</author>


</item>


<item>
<title>Inducible nitric oxide synthase, Nos2, does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1667</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1667</guid>
<pubDate>Tue, 08 May 2012 22:47:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Nitric oxide synthase 2 (NOS2) contributes to neural death in some settings, but its role in glaucoma remains controversial. NOS2 is implicated in retinal ganglion cell degeneration in a rat glaucoma model in which    intraocular pressure (IOP) is experimentally elevated by blood vessel cauterization, but not in a rat glaucoma model where IOP was elevated by injection of hypertonic saline.  To test the importance of NOS2 for an inherited glaucoma, in this    study we both genetically and pharmacologically decreased NOS2 activity in the DBA/2J mouse glaucoma model. METHODS: The expression of Nos2 in the optic nerve head was analyzed at both the RNA and protein levels at different stages of disease    pathogenesis. To test the involvement of Nos2 in glaucomatous neurodegeneration, a null allele of Nos2 was backcrossed into DBA/2J mice and the incidence and severity of glaucoma was assessed in mice of each Nos2 genotype. Additionally, DBA/2J    mice were treated with the NOS2 inhibitor aminoguanidine and the disease compared to untreated mice. RESULTS: Optic nerve head Nos2 RNA levels varied and increased during moderate but decreased at early and severe stages of disease.  Despite the    presence of a few NOS2 positive cells in the optic nerve head, NOS2 protein was not substantially increased during the glaucoma. Genetic deficiency of Nos2 or aminoguanidine treatment did not alter the IOP profile of DBA/2J mice.  Additionally,    neither Nos2 deficiency nor aminoguanidine had any detectable affect on the glaucomatous optic nerve damage. CONCLUSION: Glaucomatous neurodegeneration in DBA/2J mice does not require NOS2 activity. Further experiments involving various models    are needed to assess the general importance of Nos2 in glaucoma.</p>

	]]>
</description>

<author>R T. Libby et al.</author>


</item>


<item>
<title>Axons of retinal ganglion cells are insulted in the optic nerve early in DBA/2J glaucoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1666</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1666</guid>
<pubDate>Tue, 08 May 2012 22:47:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Here, we use a mouse model (DBA/2J) to readdress the location of insult(s) to retinal ganglion cells (RGCs) in glaucoma. We localize an early sign of axon damage to an astrocyte-rich region of the optic nerve just posterior to the    retina, analogous to the lamina cribrosa. In this region, a network of astrocytes associates intimately with RGC axons. Using BAX-deficient DBA/2J mice, which retain all of their RGCs, we provide experimental evidence for an insult within or very    close to the lamina in the optic nerve. We show that proximal axon segments attached to their cell bodies survive to the proximity of the lamina. In contrast, axon segments in the lamina and behind the eye degenerate. Finally, the Wld(s) allele,    which is known to protect against insults to axons, strongly protects against DBA/2J glaucoma and preserves RGC activity as measured by pattern electroretinography. These experiments provide strong evidence for a local insult to axons in the    optic nerve.</p>

	]]>
</description>

<author>G R. Howell et al.</author>


</item>


<item>
<title>Integrated coastal zone management and sustainable development of coastal area: a short overview of International legal framework</title>
<link>http://epubs.scu.edu.au/law_pubs/212</link>
<guid isPermaLink="true">http://epubs.scu.edu.au/law_pubs/212</guid>
<pubDate>Tue, 08 May 2012 22:47:49 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Einar Dahl et al.</author>


</item>


<item>
<title>Macromolecule biosynthesis: a key function of sleep.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1665</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1665</guid>
<pubDate>Tue, 08 May 2012 22:47:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The function(s) of sleep remains a major unanswered question in biology. We assessed changes in gene expression in the mouse cerebral cortex and hypothalamus following different durations of sleep and periods of sleep deprivation.    There were significant differences in gene expression between behavioral states; we identified 3,988 genes in the cerebral cortex and 823 genes in the hypothalamus with altered expression patterns between sleep and sleep deprivation. Changes in    the steady-state level of transcripts for various genes are remarkably common during sleep, as 2,090 genes in the cerebral cortex and 409 genes in the hypothalamus were defined as sleep specific and changed (increased or decreased) their    expression during sleep. The largest categories of overrepresented genes increasing expression with sleep were those involved in biosynthesis and transport. In both the cerebral cortex and hypothalamus, during sleep there was upregulation of    multiple genes encoding various enzymes involved in cholesterol synthesis, as well as proteins for lipid transport. There was also upregulation during sleep of genes involved in synthesis of proteins, heme, and maintenance of vesicle pools, as    well as antioxidant enzymes and genes encoding proteins of energy-regulating pathways. We postulate that during sleep there is a rebuilding of multiple key cellular components in preparation for subsequent wakefulness.</p>

	]]>
</description>

<author>M Mackiewicz et al.</author>


</item>


<item>
<title>Nanostructure analysis using spatially modulated illumination microscopy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1664</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1664</guid>
<pubDate>Tue, 08 May 2012 22:47:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>We describe the usage of the spatially modulated illumination (SMI) microscope to estimate the sizes (and/or positions) of fluorescently labeled cellular nanostructures, including a brief introduction to the instrument and its    handling. The principle setup of the SMI microscope will be introduced to explain the measures necessary for a successful nanostructure analysis, before the steps for sample preparation, data acquisition and evaluation are given. The protocol    starts with cells already attached to the cover glass. The protocol and duration outlined here are typical for fixed specimens; however, considerably faster data acquisition and in vivo measurements are possible.</p>

	]]>
</description>

<author>D Baddeley et al.</author>


</item>


<item>
<title>Adipogenesis is inhibited by brief, daily exposure to high-frequency, extremely low-magnitude mechanical signals.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1663</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1663</guid>
<pubDate>Tue, 08 May 2012 22:47:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Obesity, a global pandemic that debilitates millions of people and burdens society with tens of billions of dollars in health care costs, is deterred by exercise. Although it is presumed that the more strenuous a physical challenge    the more effective it will be in the suppression of adiposity, here it is shown that 15 weeks of brief, daily exposure to high-frequency mechanical signals, induced at a magnitude well below that which would arise during walking, inhibited    adipogenesis by 27% in C57BL/6J mice. The mechanical signal also reduced key risk factors in the onset of type II diabetes, nonesterified free fatty acid and triglyceride content in the liver, by 43% and 39%, respectively.  Over 9 weeks, these    same signals suppressed fat production by 22% in the C3H.B6-6T congenic mouse strain that exhibits accelerated age-related changes in body composition. In an effort to understand the means by which fat production was inhibited, irradiated mice    receiving bone marrow transplants from heterozygous GFP+ mice revealed that 6 weeks of these low-magnitude mechanical signals reduced the commitment of mesenchymal stem cell differentiation into adipocytes by 19%, indicating that formation of    adipose tissue in these models was deterred by a marked reduction in stem cell adipogenesis. Translated to the human, this may represent the basis for the nonpharmacologic prevention of obesity and its sequelae, achieved through developmental,    rather than metabolic, pathways.</p>

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</description>

<author>C T. Rubin et al.</author>


</item>


<item>
<title>Large-scale genome-wide linkage analysis for loci linked to BMD at different skeletal sites in extreme selected sibships.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1662</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1662</guid>
<pubDate>Tue, 08 May 2012 22:47:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Few genome-wide linkage studies of osteoporosis have been conducted in the Asian population. We performed a genome-wide scan involving 3093 adult siblings with at least one sib-pair extremely concordant or discordant for hip BMD.    Our results indicated four genome-wide significant QTLs for BMD. In comparison with 12 previous reported linkage studies, we reveal novel linkage regions that have reaching global significance. INTRODUCTION: The genetic basis for osteoporosis has    been firmly established, but efforts to identify genes associated with this complex trait have been incomplete, especially in Asian populations. The purpose of this study was to identify quantitative trait loci (QTLs) for BMD in a Chinese    population. MATERIALS AND METHODS: We performed a genome-wide scan involving 3093 siblings 25-64 years of age from 941 families, with at least one sib-pair extreme concordant or discordant for total hip BMD from a large community-based cohort (n    = 23,327) in Anhui, China. Linkage analysis was performed on BMD residuals adjusted for age, height, weight, occupation, cigarette smoking, physical activity, and alcohol consumption using the revised Haseman-Elston regression-based linkage    model. RESULTS: Our results revealed significant QTLs on chromosome 7p21.2 for femoral neck BMD (LOD = 3.68) and on chromosome 2q24.3 for total hip BMD (LOD = 3.65). Suggestive linkage regions were found to overlap among different skeletal sites    on chromosomes 2q, 7p, and 16q. Sex-specific linkage analysis further revealed a significant QTL for lumbar spine BMD on chromosome 13q21.1 (LOD = 3.62) in women only. When performing multivariate linkage analysis by combining BMDs at four    skeletal sites (i.e., whole body, total hip, femoral neck, and lumbar spine BMD), an additional significant QTL was found at chromosome 5q21.2 (LOD = 4.56). None of these significant QTLs found in our study overlapped with major QTLs reported by    other studies. CONCLUSIONS: This study reveals four novel QTLs in a Chinese population and suggests that BMD at different skeletal sites may also share common genetic determinants.</p>

	]]>
</description>

<author>Y H. Hsu et al.</author>


</item>


<item>
<title>The nonhomologous end joining factor Artemis suppresses multi-tissue tumor formation and prevents loss of heterozygosity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1661</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1661</guid>
<pubDate>Tue, 08 May 2012 22:47:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nonhomologous end joining (NHEJ) is a critical DNA repair pathway, with proposed tumor suppression functions in many tissues. Mutations in the NHEJ factor ARTEMIS cause radiation-sensitive severe combined immunodeficiency in humans    and may increase susceptibility to lymphoma in some settings. We now report that deficiency for Artemis (encoded by Dclre1c/Art in mouse) accelerates tumorigenesis in several tissues in a Trp53 heterozygous setting, revealing tumor suppression    roles for NHEJ in lymphoid and non-lymphoid cells. We also show that B-lineage lymphomas in these mice undergo loss of Trp53 heterozygosity by allele replacement, but arise by mechanisms distinct from those in Art Trp53 double null mice. These    findings demonstrate a general tumor suppression function for NHEJ, and reveal that interplay between NHEJ and Trp53 loss of heterozygosity influences the sequence of multi-hit oncogenesis. We present a model where p53 status at the time of tumor    initiation is a key determinant of subsequent oncogenic mechanisms. Because Art deficient mice represent a model for radiation-sensitive severe combined immunodeficiency, our findings suggest that these patients may be at risk for both lymphoid    and non-lymphoid cancers.</p>

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</description>

<author>Y Woo et al.</author>


</item>


<item>
<title>The presynaptic CaV2.2 channel-transmitter release site core complex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1660</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1660</guid>
<pubDate>Tue, 08 May 2012 22:46:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>CaV2.2 channels play a key role in the gating of transmitter release sites (TRS) at presynaptic terminals. Physiological studies predict that the channels are linked directly to the TRS but the molecular composition of this complex    remains poorly understood. We have used a high-affinity anti-CaV2.2 antibody, Ab571, to test a range of proteins known to contribute to TRS function for both an association in situ and a link in vitro. CaV2.2 clusters were isolated intact on    immunoprecipitation beads and coprecipitated with a number of these proteins.  Quantitative staining covariance analysis (ICA/ICQ method) was applied to the transmitter release face of the giant calyx terminal in the chick ciliary ganglion to    test for TRS proteins with staining intensities that covary in situ with CaV2.2, resulting in a covariance sequence of NSF>RIM>spectrin>Munc18>VAMP>alpha-catenin, CASK>SV2>Na+-K+ approximately 0. A high-NaCl dissociation challenge applied to the    immunoprecipitated complex, using the fractional recovery (FR) method [Khanna, R., Li, Q. & Stanley, E.F. (2006) PLoS.ONE., 1, e67], was used to test which proteins were most intimately associated with the channel, generating an FR sequence for    CaV2.2 of: VAMP>or=actin>tubulin, NSF, Munc18, syntaxin 1>spectrin>CASK, SNAP25>RIM, Na+-K+ pump, v-ATPase, beta-catenin approximately 0. Proteins associated with endocytosis are considered in a companion paper [Khanna et al. (2007)Eur. J.    Neurosci., 26, 560-574]. With the exception of VAMP and RIM, the ICQ and FR sequences were consistent, suggesting that proteins that covary the most strongly with CaV2.2 in situ are also the most intimately attached. Our findings suggest that the    CaV2.2 cluster is an integral element of a multimolecular vesicle-fusion module that forms the core of a multifunctional TRS.</p>

	]]>
</description>

<author>R Khanna et al.</author>


</item>


<item>
<title>A missense mutation in the conserved C2B domain of otoferlin causes deafness in a new mouse model of DFNB9.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1659</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1659</guid>
<pubDate>Tue, 08 May 2012 22:46:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations of the otoferlin gene have been shown to underlie deafness disorders in humans and mice. Analyses of genetically engineered mice lacking otoferlin have demonstrated an essential role for this protein in vesicle exocytosis    at the inner hair cell afferent synapse. Here, we report on the molecular and phenotypic characterization of a new ENU-induced missense mutation of the mouse otoferlin gene designated Otof(deaf5Jcs). The mutation is a single T to A base    substitution in exon 10 of Otof that causes a non-conservative amino acid change of isoleucine to asparagine in the C2B domain of the protein. Although strong immunoreactivity with an otoferlin-specific antibody was detected in cochlear hair    cells of wildtype mice, no expression was detected in mutant mice, indicating that the missense mutation has a severe effect on the stability of the protein and potentially its localization. Auditory brainstem response (ABR) analysis demonstrated    that mice homozygous for the missense mutation are profoundly deaf, consistent with an essential role for otoferlin in inner hair cell neurotransmission. Vestibular-evoked potentials (VsEPs) of mutant mice, however, were equivalent to those of    wildtype mice, indicating that otoferlin is unnecessary for vestibular function even though it is highly expressed in both vestibular and cochlear hair cells.</p>

	]]>
</description>

<author>Guess C. Longo et al.</author>


</item>


<item>
<title>Ancient papillomavirus-host co-speciation in Felidae.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1658</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1658</guid>
<pubDate>Tue, 08 May 2012 22:46:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Estimating evolutionary rates for slowly evolving viruses such as papillomaviruses (PVs) is not possible using fossil calibrations directly or sequences sampled over a time-scale of decades. An ability to correlate their    divergence with a host species, however, can provide a means to estimate evolutionary rates for these viruses accurately. To determine whether such an approach is feasible, we sequenced complete feline PV genomes, previously available only for    the domestic cat (Felis domesticus, FdPV1), from four additional, globally distributed feline species: Lynx rufus PV type 1, Puma concolor PV type 1, Panthera leo persica PV type 1, and Uncia uncia PV type 1.  RESULTS: The feline PVs all belong    to the Lambdapapillomavirus genus, and contain an unusual second noncoding region between the early and late protein region, which is only present in members of this genus. Our maximum likelihood and Bayesian phylogenetic analyses demonstrate    that the evolutionary relationships between feline PVs perfectly mirror those of their feline hosts, despite a complex and dynamic phylogeographic history. By applying host species divergence times, we provide the first precise estimates for the    rate of evolution for each PV gene, with an overall evolutionary rate of 1.95 x 10(-8) (95% confidence interval 1.32 x 10(-8) to 2.47 x 10(-8)) nucleotide substitutions per site per year for the viral coding genome. CONCLUSION: Our work provides    evidence for long-term virus-host co-speciation of feline PVs, indicating that viral diversity in slowly evolving viruses can be used to investigate host species evolution.  These findings, however, should not be extrapolated to other viral    lineages without prior confirmation of virus-host co-divergence.</p>

	]]>
</description>

<author>A Rector et al.</author>


</item>


<item>
<title>A revised nomenclature for the human and rodent alpha-tubulin gene family.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1657</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1657</guid>
<pubDate>Tue, 08 May 2012 22:46:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>An essential component of microtubules, alpha-tubulin is also a multigene family in many species. An orthology-based nomenclature for this gene family has previously been difficult to assign due to incomplete genome builds and the    high degree of sequence similarity between members of this family. Using the current genome builds, sequence analysis of human, mouse, and rat alpha-tubulin genes has enabled an updated nomenclature to be generated. This revised nomenclature    provides a unified language for the discussion of these genes in mammalian species; it has been approved by the gene nomenclature committees of the three species and is supported by researchers in the field.</p>

	]]>
</description>

<author>V K. Khodiyar et al.</author>


</item>


<item>
<title>Bone quality and bone strength in BXH recombinant inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1656</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1656</guid>
<pubDate>Tue, 08 May 2012 22:46:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>The relationship between bone quality and strength was studied in 11 BXH recombinant inbred (RI) strains of mice. The bone quality parameters studied were bone mineralization, microhardness, architecture, and connectivity. Previous    studies have demonstrated considerable variability in bone density, biomechanical properties, and microstructure among inbred strains of mice. In particular, C3H/HeJ (C3H) mice exhibit thicker femoral and vertebral cortices and fewer trabeculae    in the vertebral body compared with C57BL/6J (B6) mice, despite having similar vertebral bone strength. A set of RI mouse strains has been generated from B6 and C3H (denoted BXH) in an attempt to isolate genetic regulation of numerous traits,    including bone. The objective of this study was to investigate relationships among bone quality and bone strength in femurs and vertebrae among BXH RI mice. The study involved 11 BXH RI strains of female mice (n = 5-7) as well as the B6 and C3H    progenitor strains. Parameters contributing to bone quality were evaluated, including BMD, bone mineralization, microhardness, architecture, and connectivity. There was a strong correlation between femoral and vertebral BMD in all strains (P <    0.001) except in BXH-9 and -10 (P < 0.001).  Within the vertebrae, cortical bone was more mineralized than trabecular bone, and a strong correlation existed between the two (P < 0.001). However, cortical microhardness did not differ from    trabecular microhardness. Cortical bone was more mineralized in the femur than in the vertebrae and significantly harder, by 30%. There was a wide range in trabecular connectivity, architecture, and femur geometry among BXH RI strains. BMD    explained 43% of vertebral bone strength but only 11% of femoral bone strength. Trabecular connectivity explained an additional 8% of vertebral strength, while mineralization and femur geometry explained 7% and 50% of femoral strength,    respectively. Different bone quality parameters had varying influences on bone mechanical properties, depending on bone site. BMD may play a larger role in explaining bone strength in the vertebrae than in the femur. Moreover, cortical bone in    the femur is harder than in vertebrae. The control of cortical bone material properties may be site-dependent.</p>

	]]>
</description>

<author>A H. Ng et al.</author>


</item>


<item>
<title>Ulcerative colitis and autoimmunity induced by loss of myeloid alphav integrins.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1655</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1655</guid>
<pubDate>Tue, 08 May 2012 22:46:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>The gastrointestinal tract is constantly challenged by foreign antigens and commensal bacteria but nonetheless is able to maintain a state of immunological quiescence. Recent advances have highlighted the importance of active    suppression by regulatory lymphocytes and immunosuppressive cytokines in controlling mucosal immunity. Failures of these mechanisms contribute to the development of inflammatory bowel disease, but how these regulatory networks are established    remains unclear. Here, we demonstrate key roles for alphav integrins in regulation of mucosal immunity. We report that deletion of alphav in the immune system causes severe colitis, autoimmunity, and cancer. Mice lacking immune cell alphav have    fewer regulatory T (Treg) cells in the colon and corresponding increases in activated T cells and T cell cytokine production, leading to colitis. Using conditional gene targeting, we demonstrate that this is specifically attributable to loss of    alphav from myeloid cells. Furthermore, we show that gut-associated macrophages and dendritic cells fail both to remove apoptotic cells efficiently and to induce Treg cells. Our results identify a vital role for myeloid alphav integrins in    generating mucosal Treg cells and emphasize the importance of antigen-presenting cells in establishing immune tolerance.</p>

	]]>
</description>

<author>Hulbert A. Lacy et al.</author>


</item>


<item>
<title>A dominant, recombination-defective allele of Dmc1 causing male-specific sterility.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1654</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1654</guid>
<pubDate>Tue, 08 May 2012 22:46:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>DMC1 is a meiosis-specific homolog of bacterial RecA and eukaryotic RAD51 that can catalyze homologous DNA strand invasion and D-loop formation in vitro.  DMC1-deficient mice and yeast are sterile due to defective meiotic    recombination and chromosome synapsis. The authors identified a male dominant sterile allele of Dmc1, Dmc1(Mei11), encoding a missense mutation in the L2 DNA binding domain that abolishes strand invasion activity. Meiosis in male heterozygotes    arrests in pachynema, characterized by incomplete chromosome synapsis and no crossing-over.  Young heterozygous females have normal litter sizes despite having a decreased oocyte pool, a high incidence of meiosis I abnormalities, and    susceptibility to premature ovarian failure. Dmc1(Mei11) exposes a sex difference in recombination in that a significant portion of female oocytes can compensate for DMC1 deficiency to undergo crossing-over and complete gametogenesis.    Importantly, these data demonstrate that dominant alleles of meiosis genes can arise and propagate in populations, causing infertility and other reproductive consequences due to meiotic prophase I defects.</p>

	]]>
</description>

<author>L A. Bannister et al.</author>


</item>


<item>
<title>Developmental biology. Home for the precious few.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1653</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1653</guid>
<pubDate>Tue, 08 May 2012 22:45:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>S DiNardo et al.</author>


</item>


<item>
<title>Determinants of memory in experimental filarial infections in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1652</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1652</guid>
<pubDate>Tue, 08 May 2012 22:45:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this communication, we examine the determinants and duration of memory responses against filarial parasites using an intraperitoneal mouse model of Brugia pahangi infection. We assessed the role of T cells in the memory response    against B. pahangi larvae by transferring splenic T cells from wild-type mice primed with L3 into T-cell-deficient mice. We found that mice reconstituted with primed T cells cleared intraperitoneal infections with infective larvae in an    accelerated manner. To determine the components that may be responsible for the memory response, we transferred unfractionated T cells or purified CD4+ T cells or CD8+ T cells from BALB/cByJ mice primed a month earlier with L3 into    T-cell-deficient BALB/c TCRbeta-/- mice. Recipients were challenged 10 days after adoptive transfer. Our data demonstrated that while either CD4+ or CD8+ T cells are able to confer some level of protection, both are required for an optimal recall    response. To evaluate the longevity of the memory response, we primed several groups of wild-type mice at different times over a year. These mice were then challenged with a single injection of B. pahangi L3. The gap between the priming and    second injections of larvae ranged between 4 and 60 weeks. We found that the memory responses in BALB/cByJ mice lasted over a year whereas those in C57BL/6 mice waned more rapidly.</p>

	]]>
</description>

<author>Y Dash et al.</author>


</item>


<item>
<title>Dynamic clustered distribution of hemagglutinin resolved at 40 nm in living cell membranes discriminates between raft theories.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1651</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1651</guid>
<pubDate>Tue, 08 May 2012 22:45:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Organization in biological membranes spans many orders of magnitude in length scale, but limited resolution in far-field light microscopy has impeded distinction between numerous biomembrane models. One canonical example of a    heterogeneously distributed membrane protein is hemagglutinin (HA) from influenza virus, which is associated with controversial cholesterol-rich lipid rafts. Using fluorescence photoactivation localization microscopy, we are able to image    distributions of tens of thousands of HA molecules with subdiffraction resolution ( approximately 40 nm) in live and fixed fibroblasts. HA molecules form irregular clusters on length scales from approximately 40 nm up to many micrometers,    consistent with results from electron microscopy. In live cells, the dynamics of HA molecules within clusters is observed and quantified to determine an effective diffusion coefficient. The results are interpreted in terms of several established    models of biological membranes.</p>

	]]>
</description>

<author>S T. Hess et al.</author>


</item>


<item>
<title>Enhanced thymic selection of FoxP3+ regulatory T cells in the NOD mouse model of autoimmune diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1650</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1650</guid>
<pubDate>Tue, 08 May 2012 22:45:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>FoxP3(+)CD4(+) regulatory T cells (Tregs) play a key role in the maintenance of peripheral self-tolerance, and it has been suggested that diabetes-susceptible nonobese diabetic (NOD) mice are defective in the generation and numbers    of Tregs. We found thymic selection of Tregs to be under genetic control. Fetal thymic organ cultures on the NOD background required 3- to 10-fold more antigen than corresponding cultures on the B6 background for optimal induction of Tregs, but    once the threshold for induction was reached the NOD background yielded close to 10-fold more Tregs. This increased selection of Tregs was also found in nontransgenic NOD mice in fetal through adult stages. This trait did not map to the MHC,    idd3, or the chromosome 3 (Chr3) regions that control clonal deletion, but mainly to two regions on Chr1 and Chr11. Thus, NOD mice do not have a global defect in the generation or maintenance of Tregs; if anything, they show the    opposite.</p>

	]]>
</description>

<author>M Feuerer et al.</author>


</item>


<item>
<title>Invasion of the killer B&apos;s in type 1 diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1649</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1649</guid>
<pubDate>Tue, 08 May 2012 22:45:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Type 1 Diabetes (T1D) is an autoimmune disease requiring contributions from effectors in both CD4+ and CD8+ T cell compartments in order to destroy insulin producing pancreatic beta cells. Autoantibodies specific for islet cell    proteins are also often generated during the prodromal stages of T1D development. While providing excellent prognostic markers of future disease risk, it has generally been believed that the induction of autoantibody secretion by B cells was a    secondary consequence of the ongoing autoreactive T cell response. However, studies in the NOD mouse model of disease have demonstrated that B cells play a key function during T1D development by serving as a subpopulation of antigen presenting    cell (APC) which can most efficiently support the expansion of diabetogenic CD4+ T cells. Furthermore, studies utilizing this model have indicated that autoantibodies may play an important role in initiating an early phase of pancreatic beta cell    destruction ultimately leading to overt T1D. This review will focus on the under appreciated role B cells play in T1D development not only in NOD mice, but also potentially in humans.</p>

	]]>
</description>

<author>P A. Silveira et al.</author>


</item>


<item>
<title>The Fas pathway is involved in pancreatic beta cell secretory function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1648</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1648</guid>
<pubDate>Tue, 08 May 2012 22:45:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pancreatic beta cell mass and function increase in conditions of enhanced insulin demand such as obesity. Failure to adapt leads to diabetes. The molecular mechanisms controlling this adaptive process are unclear. Fas is a death    receptor involved in beta cell apoptosis or proliferation, depending on the activity of the caspase-8 inhibitor FLIP. Here we show that the Fas pathway also regulates beta cell secretory function. We observed impaired glucose tolerance in    Fas-deficient mice due to a delayed and decreased insulin secretory pattern.  Expression of PDX-1, a beta cell-specific transcription factor regulating insulin gene expression and mitochondrial metabolism, was decreased in Fas-deficient beta    cells. As a consequence, insulin and ATP production were severely reduced and only partly compensated for by increased beta cell mass. Up-regulation of FLIP enhanced NF-kappaB activity via NF-kappaB-inducing kinase and RelB. This led to increased    PDX-1 and insulin production independent of changes in cell turnover.  The results support a previously undescribed role for the Fas pathway in regulating insulin production and release.</p>

	]]>
</description>

<author>D M. Schumann et al.</author>


</item>


<item>
<title>The near-naked hairless (Hr(N)) mutation disrupts hair formation but is not due to a mutation in the Hairless coding region.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1647</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1647</guid>
<pubDate>Tue, 08 May 2012 22:45:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Near-naked hairless (Hr(N)) is a semi-dominant, spontaneous mutation that was suggested by allelism testing to be allelic with mouse Hairless (Hr). Hr(N) mice differ from other Hr mutants in that hair loss appears as the postnatal    coat begins to emerge, rather than as an inability to regrow hair after the first catagen and that the mutation displays semi-dominant inheritance. We sequenced the Hr cDNA in Hr(N)/Hr(N) mice and characterized the pathological and molecular    phenotypes to identify the basis for hair loss in this model. Hr(N)/Hr(N) mice exhibit dystrophic hairs that are unable to emerge consistently from the hair follicle, whereas Hr(N)/+ mice display a sparse coat of hair and a milder degree of    follicular dystrophy than their homozygous littermates. DNA microarray analysis of cutaneous gene expression demonstrates that numerous genes are downregulated in Hr(N)/Hr(N) mice, primarily genes important for hair structure.  By contrast, Hr    expression is significantly increased. Sequencing the Hr-coding region, intron-exon boundaries, 5'- and 3'-untranslated region, and immediate upstream region did not reveal the underlying mutation. Therefore, Hr(N) does not appear to be an allele    of Hr but may result from a mutation in a closely linked gene or from a regulatory mutation in Hr.</p>

	]]>
</description>

<author>Y Liu et al.</author>


</item>


<item>
<title>Immunolocalization of enzymes, binding proteins, and receptors sufficient for retinoic acid synthesis and signaling during the hair cycle.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1646</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1646</guid>
<pubDate>Tue, 08 May 2012 22:44:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Retinoic acid (RA) is essential for maintenance of most epithelial tissues. One RA biosynthesis pathway consists of cellular retinol-binding protein (Crbp), retinol dehydrogenase (Dhrs9/eRoldh), retinal dehydrogenase 1-3    (Aldh1a1-3), and cellular RA-binding protein 2 (Crabp2). Previously, we localized Aldh1a2 and Aldh1a3 to both epithelial and mesenchymal cells within the hair follicle throughout the hair cycle. This study expands that observation by examining    the complete pathway of RA biosynthesis and signaling via RA receptors alpha, beta, and gamma by immunohistochemistry in C57BL/6J mice wax-stripped to initiate and synchronize the cycle. This pathway of RA biosynthesis and signaling localized to    the majority of layers of the hair follicle, sebaceous gland, and interfollicular epidermis in a hair cycle-dependent manner, suggesting that RA biosynthesis within the hair follicle is regulated in both a spatial and temporal manner. This    localization pattern also revealed insights into epithelial-mesenchymal interactions and differentiation state differences within the RA biosynthesis and signaling pathway, as well as novel observations on nuclear versus cytoplasmic localization    of Crabp2 and RA receptors. This complex pattern of RA biosynthesis and signaling identified by immunolocalization suggests that endogenous RA regulates specific aspects of hair follicle growth, differentiation, and cycling.</p>

	]]>
</description>

<author>H B. Everts et al.</author>


</item>


<item>
<title>Heat shock protein 90: a potential therapeutic target in leukemic progenitor and stem cells harboring mutant BCR-ABL resistant to kinase inhibitors.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1645</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1645</guid>
<pubDate>Tue, 08 May 2012 22:44:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Development of drug resistance has become a major obstacle for tyrosine kinase inhibitors (TKIs) in the treatment of Philadelphia chromosome-positive (Ph(+)) chronic myelogenous leukemia (CML) and other cancers. The BCR-ABL-T315I    mutant does not respond to clinically available TKIs, although some newly developed anti-BCR-ABL-T315I TKIs are now being tested in patients. TKIs transiently inhibit kinase activity of BCR-ABL, but do not reduce the level of the BCR-ABL protein.    Elimination of mutant BCR-ABL protein would provide a new therapeutic strategy for treating Ph(+) leukemia. We recently showed that inhibition of heat shock protein 90 (Hsp90) by a novel Hsp90 inhibitor, IPI- 504, causes BCR-ABL protein    degradation, decreased numbers of leukemia stem cells, and prolonged survival of mice with CML induced by BCR-ABL-T315I. Here we discuss further the mechanisms and effectiveness of Hsp90 inhibition in suppression of survival and proliferation of    leukemic progenitor and stem cells in CML mice, and the potential of this anti-Hsp90 strategy in treating CML patients, including those who have developed resistance to TKIs.</p>

	]]>
</description>

<author>C Peng et al.</author>


</item>


<item>
<title>Substance P as an immunomodulatory neuropeptide in a mouse model for autoimmune hair loss (alopecia areata).</title>
<link>http://mouseion.jax.org/stfb2000_2009/1644</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1644</guid>
<pubDate>Tue, 08 May 2012 22:44:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata (AA) is an autoimmune disorder of the hair follicle characterized by inflammatory cell infiltrates around actively growing (anagen) hair follicles.  Substance P (SP) plays a critical role in the cutaneous neuroimmune    network and influences immune cell functions through the neurokinin-1 receptor (NK-1R). To better understand the role of SP as an immunomodulatory neuropeptide in AA, we studied its expression and effects on immune cells in a C3H/HeJ mouse model    for AA. During early stages of AA development, the number of SP-immunoreactive nerve fibers in skin is increased, compared to non-affected mice. However, during advanced stages of AA, the number of SP-immunoreactive nerves and SP protein levels    in skin are decreased, whereas the expression of the SP-degrading enzyme neutral endopeptidase (NEP) is increased, compared to control skin. In AA, NK-1R is expressed on CD8+ lymphocytes and macrophages accumulating around affected hair    follicles. Additional SP supply to the skin of AA-affected mice leads to a significant increase of mast cell degranulation and to accelerated hair follicle regression (catagen), accompanied by an increase of CD8+ cells-expressing granzyme B.    These data suggest that SP, NEP, and NK-1R serve as important regulators in the molecular signaling network modulating inflammatory response in autoimmune hair loss.</p>

	]]>
</description>

<author>F Siebenhaar et al.</author>


</item>


<item>
<title>Src kinase signaling in leukaemia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1643</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1643</guid>
<pubDate>Tue, 08 May 2012 22:44:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Role of Src kinases in acute lymphoblastic leukaemia has been recently demonstrated in leukaemia mouse model. Retained activation of Src kinases by the BCR-ABL oncoprotein in leukaemic cells following inhibition of BCR-ABL kinase    activity by imatinib indicates that Src activation by BCR-ABL is independent of BCR-ABL kinase activity and provides an explanation for reduced effectiveness of the BCR-ABL kinase activity inhibitors in Philadelphia chromosome-positive acute    lymphoblastic leukaemia. Simultaneous inhibition of kinase activity of both BCR-ABL and Src kinases results in long-term survival of mice with acute lymphoblastic leukaemia. Leukaemic stem cells exist in acute lymphoblastic leukaemia, and    complete eradication of this group of cells would provide a curative therapy for this disease.</p>

	]]>
</description>

<author>S Li</author>


</item>


<item>
<title>The developmental program of human dendritic cells is operated independently of conventional myeloid and lymphoid pathways.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1642</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1642</guid>
<pubDate>Tue, 08 May 2012 22:44:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Two distinct dendritic cell (DC) subsets, conventional DCs (cDCs) and plasmacytoid DCs (pDCs), have been shown to develop via either the myeloid or the lymphoid pathway in murine hematopoiesis. Lineage-specific phenotypes or    functions of "myeloid" and "lymphoid" DCs, however, still remain elusive.  Furthermore, such analysis has been particularly difficult in humans, due to lack of an assay system appropriate for the analysis of human stem and progenitor cell    differentiation. Here, using a highly efficient xenotransplantation model, we extensively analyze the origin and the molecular signature of human DCs. Purified human common myeloid progenitors (CMPs) and common lymphoid progenitors (CLPs) were    intravenously transplanted into nonobese diabetic-severe combined immunodeficiency (NOD-scid)/IL2rgamma(null) newborn mice. CMPs and CLPs displayed significant expansion in the xenogeneic host, and human cDC and pDC progeny were isolatable.    Strikingly, each human DC subset possessed indistinguishable expression patterns of surface phenotype and gene transcripts regardless of their CMP or CLP origin, even at the genome-wide level. Thus, cDC and pDC normally develop after cells have    committed to the myeloid or the lymphoid lineage in human hematopoiesis, while their transcriptional signatures are well preserved irrespective of their lineage origin. We propose that human DCs use unique and flexible developmental programs that    cannot be categorized into the conventional myeloid or lymphoid pathway.</p>

	]]>
</description>

<author>F Ishikawa et al.</author>


</item>


<item>
<title>Cardiac manifestations of Alstrom syndrome: echocardiographic findings.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1641</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1641</guid>
<pubDate>Tue, 08 May 2012 22:44:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Alstrom syndrome is an extremely rare autosomal recessive genetic disorder characterized by infantile-onset cardiomyopathy (CMP), blindness, hearing impairment/loss, and obesity. Prior reports have demonstrated that the    dilated CMP of Alstrom syndrome occurs in about 62% of patients with this syndrome. To date, there have been no reports examining the echocardiographic features of Alstrom-related heart disease. METHODS: Eleven patients diagnosed with Alstrom    syndrome who underwent one or more transthoracic echocardiograms from 1994 to 2003 were retrospectively evaluated. A total of 16 transthoracic echocardiograms were comprehensively reviewed with an emphasis on chamber sizes, wall thickness, left    ventricular (LV) and right ventricular (RV) systolic function, and valve function. RESULTS: Four of 11 patients (36%) had evidence of global LV systolic dysfunction (quantitative ejection fraction [EF] range 9%-29%). Three of these 4 patients    also had severe generalized RV systolic dysfunction, whereas one had normal RV systolic function. LV and RV dilation was present in 3 of 4. All patients with low EF had an apically tethered mitral valve closure pattern although only one of 4 had    more than mild mitral regurgitation.  Although 3 of 4 patients with low EF had an apically tethered tricuspid valve closure pattern, none had more than mild tricuspid regurgitation. Reduced EF was not associated with regional wall-motion    abnormalities. Three of 11 patients (27%) overall and two of 4 of the patients with low EF (50%) had pericardial effusions. CONCLUSIONS: The Alstrom CMP in this cohort of patients was typically dilated and nonsegmental with predominantly    biventricular involvement. It was infrequently associated with myocardial hypertrophy. Apically tethered mitral and tricuspid valve closure patterns were visualized, although severe functional valvular insufficiency was not present. LV and left    atrial dilation was observed in a number of patients without reduced EF, and may be an early stage in the development of the CMP.</p>

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</description>

<author>A N. Makaryus et al.</author>


</item>


<item>
<title>Genetic ablation of NMDA receptor subunit NR3B in mouse reveals motoneuronal and nonmotoneuronal phenotypes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1640</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1640</guid>
<pubDate>Tue, 08 May 2012 22:44:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>NR3B is a modulatory subunit of the NMDA receptor, abundantly expressed in both cranial and spinal somatic motoneurons and at lower levels in other regions of the brain as well. Recently, we found the human NR3B gene (GRIN3B) to be    highly genetically heterogeneous, and that approximately 10% of the normal European-American population lacks NR3B due to homozygous occurrence of a null allele in the gene. Therefore, it is especially important to understand the phenotypic    consequences of the genetic loss of NR3B in both humans and animal models. We here provide results of behavioral analysis of mice genetically lacking NR3B, which is an ideal animal model due to homogeneity in genetic and environmental background.    The NR3B(-/-) mice are viable and fertile. Consistent with the expression of NR3B in somatic motoneurons, the NR3B(-/-) mice showed a moderate but significant impairment in motor learning or coordination, and decreased activity in their home    cages. Remarkably, the NR3B(-/-) mice showed a highly increased social interaction with their familiar cage mates in their home cage but moderately increased anxiety-like behaviour and decreased social interaction in a novel environment,    consistent with the inhibitory role of NR3B on the functions of NMDA receptors. This work is the first reporting of the functional significance of NR3B in vivo and may give insight into the contribution of genetic variability of NR3B in the    phenotypic heterogeneity among human population.</p>

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</description>

<author>S Niemann et al.</author>


</item>


<item>
<title>Lipolytic and ligand-binding functions of hepatic lipase protect against atherosclerosis in LDL receptor-deficient mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1639</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1639</guid>
<pubDate>Tue, 08 May 2012 22:43:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>To elucidate the separate contributions of the lipolytic versus ligand-binding functions of hepatic lipase (HL) to lipoprotein metabolism and atherosclerosis, and to investigate the role of the low density lipoprotein receptor    (LDLr) in these processes, we compared mice expressing catalytically active HL (HL-WT) with mice expressing inactive HL (HL-S145G) in a background lacking endogenous HL and the LDLr (LDLr-KOxHL-KO). HL-WT and HL-S145G reduced (P < 0.05 for all)    cholesterol (55% vs. 20%), non-HDL-cholesterol (63% vs. 22%), and apolipoprotein B (apoB; 34% vs. 16%) by enhancing the catabolism of autologous (125)I-apoB-intermediate density lipoprotein (IDL)/LDL (fractional catabolic rate in day(-1): 6.07    +/- 0.25, LDLr-KOxHL-WT; 4.76 +/- 0.30, LDLr-KOxHL-S145G; 3.70 +/- 0.13, LDLr-KOxHL-KO); HL-WT had a greater impact on the concentration, composition, particle size, and catabolism of apoB-containing lipoproteins (apoB-Lps) and HDL. Importantly,    consistent with the changes in apoB-Lps, atherosclerosis in LDLr-KOxHL-KO mice fed a regular chow diet (RCD) was reduced by both HL-WT and HL-S145G (by 71% and 51% in cross-sectional analysis, and by 85% and 67% in en face analysis; P < 0.05 for    all). These data identify physiologically relevant but distinct roles for the lipolytic versus ligand-binding functions of HL in apoB-Lp metabolism and atherosclerosis and demonstrate that their differential effects on these processes are    mediated by changes in catabolism via non-LDLr pathways. These changes, evident even in the presence of apoE, establish an antiatherogenic role of the ligand-binding function of HL in LDLr-deficient mice.</p>

	]]>
</description>

<author>L Freeman et al.</author>


</item>


<item>
<title>Heterozygous kit mutants with little or no apparent anemia exhibit large defects in overall hematopoietic stem cell function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1638</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1638</guid>
<pubDate>Tue, 08 May 2012 22:43:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: The evolutionarily conserved Kit receptor is vital for function of hematopoietic stem cells (HSC). Kit(W-41) (W-41) and Kit(W-42) (W-42) are single residue changes in the KIT intracellular phosphotransferase domain, while    Kit(W-v) (W-v) is a single residue change in the ATP binding domain. This study tests how each mutation affects HSC function. METHODS: Cells in mutant and C57BL/6J(+/+) blood and marrow were compared. Overall HSC function was measured by    competitive repopulation. Functions of specific progenitor populations were tested with stage-specific competitive repopulation and standard colony-forming unit assays. RESULTS: Bone marrow cells from these Kit mutants are severely defective at    reconstituting peripheral blood lineages and bone marrow of irradiated recipients, when compared to +/+ control marrow. These defects increased with time. Marrow from W-41/+ and W-v/+ functions similarly but better than marrow from W-41/W-41 and    W-42/+, to repopulate the erythroid and lymphoid lineages. Long-term (LT) and short-term (ST) HSC from W-v/+, W-41/W-41, and W-42/+ are more defective at reconstituting bone marrow than LT- and ST-HSC from W-41/+ and +/+. Common myeloid    progenitor (CMP) cells from W-42/+ and W-41/W-41 are more defective at producing spleen colonies than CMP from W-v/+ and W-41/+.  CONCLUSION: Heterozygous Kit mutants with little or no apparent anemia exhibit surprisingly large defects in overall    HSC function. Multiplying the fractional defects in LT-HSC, ST-HSC, and CMP can account for overall effects of W-v/+, but does not completely account for the defects observed with W-41/+, W-42/+, and W-41/W-41.</p>

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</description>

<author>Y Sharma et al.</author>


</item>


<item>
<title>Rodent Lce gene clusters; new nomenclature, gene organization, and divergence of human and rodent genes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1637</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1637</guid>
<pubDate>Tue, 08 May 2012 22:43:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>S J. Brown et al.</author>


</item>


<item>
<title>Integration of mouse phenome data resources. The Mouse Phenotype Database Integration Consortium.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1636</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1636</guid>
<pubDate>Tue, 08 May 2012 22:43:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Understanding the functions encoded in the mouse genome will be central to an understanding of the genetic basis of human disease. To achieve this it will be essential to be able to characterize the phenotypic consequences of    variation and alterations in individual genes. Data on the phenotypes of mouse strains are currently held in a number of different forms (detailed descriptions of mouse lines, first-line phenotyping data on novel mutations, data on the normal    features of inbred lines) at many sites worldwide. For the most efficient use of these data sets, we have initiated a process to develop standards for the description of phenotypes (using ontologies) and file formats for the description of    phenotyping protocols and phenotype data sets. This process is ongoing and needs to be supported by the wider mouse genetics and phenotyping communities to succeed. We invite interested parties to contact us as we develop this process    further.</p>

	]]>
</description>


</item>


<item>
<title>A standardized nomenclature for the mouse and rat prolactin superfamilies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1635</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1635</guid>
<pubDate>Tue, 08 May 2012 22:43:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M J. Soares et al.</author>


</item>


<item>
<title>Ena/VASP Is Required for neuritogenesis in the developing cortex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1634</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1634</guid>
<pubDate>Tue, 08 May 2012 22:43:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mammalian cortical development involves neuronal migration and neuritogenesis; this latter process forms the structural precursors to axons and dendrites.  Elucidating the pathways that regulate the cytoskeleton to drive these    processes is fundamental to our understanding of cortical development. Here we show that loss of all three murine Ena/VASP proteins, a family of actin regulatory proteins, causes neuronal ectopias, alters intralayer positioning in the cortical    plate, and, surprisingly, blocks axon fiber tract formation during corticogenesis. Cortical fiber tract defects in the absence of Ena/VASP arise from a failure in neurite initiation, a prerequisite for axon formation. Neurite initiation defects    in Ena/VASP-deficient neurons are preceded by a failure to form bundled actin filaments and filopodia. These findings provide insight into the regulation of neurite formation and the role of the actin cytoskeleton during cortical    development.</p>

	]]>
</description>

<author>A V. Kwiatkowski et al.</author>


</item>


<item>
<title>Col4a1 mutation causes endoplasmic reticulum stress and genetically modifiable ocular dysgenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1633</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1633</guid>
<pubDate>Tue, 08 May 2012 22:43:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ocular anterior segment dysgenesis (ASD) is a complex and poorly understood group of conditions. A large proportion of individuals with ASD develop glaucoma, a leading cause of blindness resulting from retinal ganglion cell death.    Optic nerve hypoplasia is thought to have distinct causes and is a leading cause of blindness in children. Here, we show that a mutation in the type IV collagen alpha 1 (Col4a1) gene can cause both ASD and optic nerve hypoplasia. COL4A1 is a    major component of almost all basement membranes. The mutation results in non-secretion of the mutant COL4A1 proteins, which instead accumulate within cells. Basement membrane abnormalities may, therefore, contribute to the phenotype. The    mutation also induces endoplasmic reticulum stress and so intracellular stress may contribute to pathogenesis. The overall consequence of the Col4a1 mutation depends on genetic context. In one genetic context, the mutation causes severe ASD with    intraocular pressure abnormalities and optic nerve hypoplasia. In a different genetic context, both the ASD and optic nerve hypoplasia are rescued, and we have identified a single dominant locus that confers the phenotypic    modification.</p>

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</description>

<author>D B. Gould et al.</author>


</item>


<item>
<title>LH analog and dietary isoflavones support ovarian granulosa cell tumor development in a spontaneous mouse model.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1632</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1632</guid>
<pubDate>Tue, 08 May 2012 22:42:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>The reproductive hormone environment is an important influence upon spontaneous ovarian granulosa cell (GC) tumor development in genetically susceptible (SWR x SWXJ-9) F1 female mice: androgenic support during puberty stimulates    tumorigenesis, while exposure to 17beta-estradiol (E(2)) suppresses tumor initiation. We sought to determine whether gonadotropic stimulation was sufficient to initiate GC tumors in a grafted model system, and to determine the potential for    dietary isoflavones (genistein and daidzein) as alternatives to E(2) for tumor chemoprevention in vivo. Isolated ovaries from pre-pubertal (SWR x SWXJ-9) F1 females were transferred to the kidney capsule of host mice homozygous for the    hypogonadal (hpg/hpg) and severe combined immunodeficiency (scid/scid) mutations. CB17; HPG-Prkdc(scid) Gnrh1(hpg)/Bm host mice received either follicle-stimulating hormone (FSH), or a functional analog for LH human chorionic gonadotropin for 2    consecutive weeks, at which time the ovary grafts were examined for evidence of tumor initiation. LH analog administration, but not FSH, initiated GC tumorigenesis in the graft system, suggesting that the LH surge at puberty initiates GC tumor    development in genetically susceptible female mice. To assess the chemopreventive potential of phytoestrogens, GC tumor frequency was compared between (SWR x SWXJ-9) F1 females reared on an isoflavone-free diet versus a diet supplemented with 125    mug/g each of the isoflavones daidzein and genistein. It was observed that (SWR x SWXJ-9) F1 females reared on isoflavone-supplemented diet maintained significantly higher GC tumor frequency (22%) than females reared on isoflavone-free diet    (11%), and that non-tumor-bearing siblings reared on the isoflavones had significantly increased ovarian weight, indicative of an overall stimulation of the reproductive hormone axis. The stimulation of GC tumorigenesis by isoflavones, which    contrasts with the chemopreventive action of E(2) (2.5 mg/kg) administration during pubertal maturation, may result from general stimulation of ovarian growth, and the inability of the genistein and daidzein supplements to suppress LH    secretion.</p>

	]]>
</description>

<author>A M. Dorward et al.</author>


</item>


<item>
<title>Effect of metformin and rosiglitazone in a prepubertal boy with Alstrom syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1631</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1631</guid>
<pubDate>Tue, 08 May 2012 22:42:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alstrom syndrome (AS) is an autosomal recessive disorder characterized by progressive pigmentary retinopathy, sensorineural hearing loss, fatty liver infiltration, obesity, insulin resistance and early-onset type 2 diabetes mellitus    (DM2). Early onset of insulin resistance and DM2 are key components of this syndrome. AIM: To study the effect of early initiation of the insulin sensitizer metformin combined with rosiglitazone in a patient with AS with impaired glucose    tolerance. PATIENT: An 8 year-old boy with AS presented with acanthosis nigricans and insulin resistance at the age of 6 years. He had progressive excessive weight gain from 9 months of age. By the age of 1 year he developed photosensitivity,    blindness and nystagmus. At the age of 5.5 years, his body mass index (BMI) was above the 95th percentile. He developed impaired glucose tolerance at 6 years of age and treatment with metformin was initiated.  After 8 months of treatment with    metformin he developed DM2. The dose of metformin was increased, and rosiglitazone added. METHODS: A 2-hour oral glucose tolerance test (OGTT) and a rapid intravenous glucose tolerance test (IVGTT) were performed before treatment was initiated,    after treatment with metformin and at the end of 1 year of combination therapy with metformin and rosiglitazone to calculate quantitative insulin sensitivity check index (QUICKI) and acute insulin response (AIR). For mutation analysis, all exons    and splice site sequences of the ALMS1 gene were amplified and sequenced. RESULTS: Metformin treatment alone at the stage of impaired glucose tolerance did not prevent progression to DM2.  However, metformin at a higher dose and in combination    with rosiglitazone resulted in improvement of pancreatic beta-cell function, shown by markedly improved first-phase insulin response to glucose measured by AIR. The patient was found to have two heterozygous nonsense mutations in ALMS1, 8008    C-->T Ter, R2670X, and 11449 C-->T Ter, Q3817X. These alterations cause premature stops and result in a truncated ALMS1 protein. CONCLUSION: We suggest that early initiation of combined therapy comprising a high dose of metformin plus    rosiglitazone may be valuable in managing insulin resistance and DM2 in children with AS.</p>

	]]>
</description>

<author>S K. Sinha et al.</author>


</item>


<item>
<title>Inhibition of heat shock protein 90 prolongs survival of mice with BCR-ABL-T315I-induced leukemia and suppresses leukemic stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1630</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1630</guid>
<pubDate>Tue, 08 May 2012 22:42:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Development of kinase domain mutations is a major drug-resistance mechanism for tyrosine kinase inhibitors (TKIs) in cancer therapy. A particularly challenging example is found in Philadelphia chromosome-positive chronic myelogenous    leukemia (CML) where all available kinase inhibitors in clinic are ineffective against the BCR-ABL mutant, T315I. As an alternative approach to kinase inhibition, an orally administered heat shock protein 90 (Hsp90) inhibitor, IPI-504, was    evaluated in a murine model of CML. Treatment with IPI-504 resulted in BCR-ABL protein degradation, decreased numbers of leukemia stem cells, and prolonged survival of leukemic mice bearing the T315I mutation. Hsp90 inhibition more potently    suppressed T315I-expressing leukemia clones relative to the wild-type (WT) clones in mice. Combination treatment with IPI-504 and imatinib was more effective than either treatment alone in prolonging survival of mice simultaneously bearing both    WT and T315I leukemic cells. These results provide a rationale for use of an Hsp90 inhibitor as a first-line treatment in CML by inhibiting leukemia stem cells and preventing the emergence of imatinib-resistant clones in patients.  Rather than    inhibiting kinase activity, elimination of mutant kinases provides a new therapeutic strategy for treating BCR-ABL-induced leukemia as well as other cancers resistant to treatment with tyrosine kinase inhibitors.</p>

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</description>

<author>C Peng et al.</author>


</item>


<item>
<title>Neural logic molecular, counter-intuitive.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1629</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1629</guid>
<pubDate>Tue, 08 May 2012 22:42:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>A hypothesis is proposed that multiple "LOGIC" genes control Boolean logic in a neuron. Each hypothetical LOGIC gene encodes a transcription factor that regulates another LOGIC gene(s). Through transcription regulation, LOGIC genes    connect into a complex circuit, such as a XOR logic gate or a two-input flip-flop logic circuit capable of retaining information. LOGIC gene duplication, mutation and recombination may result in the diversification of Boolean logic gates.     Creative thinking may sometimes require counter-intuitive reasoning, rather than common sense. Such reasoning is likely to engage novel logic circuits produced by LOGIC somatic mutations. An individual's logic maturates by a mechanism of somatic    hypermutation, gene conversion and recombination of LOGIC genes in precursor cells followed by selection of neurons in the brain for functional competence. In this model, a single neuron among billions in the brain may contain a unique logic    circuit being the key to a hard intellectual problem. The output of a logic neuron is likely to be a neurotransmitter. This neuron is connected to other neurons in the spiking neural network. The LOGIC gene hypothesis is testable by molecular    techniques. Understanding mechanisms of authentic human ingenuity may help to invent digital systems capable of creative thinking.</p>

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</description>

<author>I K. Egorov</author>


</item>


<item>
<title>Restoration of cone vision in a mouse model of achromatopsia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1628</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1628</guid>
<pubDate>Tue, 08 May 2012 22:42:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Loss of cone function in the central retina is a pivotal event in the development of severe vision impairment for many prevalent blinding diseases. Complete achromatopsia is a genetic defect resulting in cone vision loss in 1 in    30,000 individuals. Using adeno-associated virus (AAV) gene therapy, we show that it is possible to target cones and rescue both the cone-mediated electroretinogram response and visual acuity in the Gnat2 ( cpfl3 ) mouse model of    achromatopsia.</p>

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</description>

<author>J J. Alexander et al.</author>


</item>


<item>
<title>Mitochondria, redox signaling and axis specification in metazoan embryos.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1627</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1627</guid>
<pubDate>Tue, 08 May 2012 22:42:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mitochondria are not only the major energy generators of the eukaryotic cell but they are also sources of signals that control gene expression and cell fate.  While mitochondria are often asymmetrically distributed in early embryos,    little is known about how they contribute to axial patterning. Here we review studies of mitochondrial distribution in metazoan eggs and embryos and the mechanisms of redox signaling, and speculate on the role that mitochondrial anisotropies    might play in the developmental specification of cell fate during embryogenesis of sea urchins and other animals.</p>

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</description>

<author>J A. Coffman et al.</author>


</item>


<item>
<title>The genetics of Alzheimer&apos;s disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1626</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1626</guid>
<pubDate>Tue, 08 May 2012 22:42:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genetics of Alzheimer's disease is produced by 3 essentially interactive gene groups: (1) APP and presenilin 1 and 2; (2) APOE E2, E3, and E4; (3) genes on chromosomes 9, 10, 12, etc. If any gene in (1) mutates, beta amyloid    (Abeta) increases sharply beyond what the genes of (3) can remove, with early-onset Alzheimer's disease the result. With retention of Abeta by E4 in (2), Alzheimer's disease might result even though (1) and (3) are normal. If any gene in (3)    mutates, the level of Abeta will rise, but because many genes are involved in Abeta removal, late-onset Alzheimer's disease would be detected only eventually.</p>

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</description>

<author>C K. Chai</author>


</item>


<item>
<title>Characterization of human embryonic stem cell lines by the International Stem Cell Initiative.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1625</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1625</guid>
<pubDate>Tue, 08 May 2012 22:41:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>The International Stem Cell Initiative characterized 59 human embryonic stem cell lines from 17 laboratories worldwide. Despite diverse genotypes and different techniques used for derivation and maintenance, all lines exhibited    similar expression patterns for several markers of human embryonic stem cells. They expressed the glycolipid antigens SSEA3 and SSEA4, the keratan sulfate antigens TRA-1-60, TRA-1-81, GCTM2 and GCT343, and the protein antigens CD9, Thy1 (also    known as CD90), tissue-nonspecific alkaline phosphatase and class 1 HLA, as well as the strongly developmentally regulated genes NANOG, POU5F1 (formerly known as OCT4), TDGF1, DNMT3B, GABRB3 and GDF3. Nevertheless, the lines were not identical:    differences in expression of several lineage markers were evident, and several imprinted genes showed generally similar allele-specific expression patterns, but some gene-dependent variation was observed. Also, some female lines expressed readily    detectable levels of XIST whereas others did not. No significant contamination of the lines with mycoplasma, bacteria or cytopathic viruses was detected.</p>

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</description>

<author>The International Stem Cell Initiative et al.</author>


</item>


<item>
<title>Tympanometry assessment of 61 inbred strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1624</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1624</guid>
<pubDate>Tue, 08 May 2012 22:41:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Otitis media (OM) accounts for more than 20 million clinic visits in the United States every year. Resistance to antibiotics has hampered current management of the disease. Identification of genetic factors underlying susceptibility    to OM is greatly needed in order to develop alternative treatment strategies. Genetically defined inbred mouse strains offer a powerful tool for dissecting genetic and environmental factors that may lead to OM in mice. Here, we report a study of    middle ear function of 61 genetically diverse inbred strains of mice using tympanometry. Of the 61 inbred strains tested, the 129P1/ReJ, 129P3/J, 129S1/SvImJ, 129X1/SvJ, A/HeJ, BALB/cJ, BUB/BnJ, C57L/J, EL/SuzSeyFrkJ, FVB/NJ, I/LnJ, LP/J,    NZB/BlNJ, PL/J and YBR/Ei strains exhibited tympanograms that were statistically different from other healthy strains according to parameters including middle ear pressure, volume and compliance. These differences are most likely the result of    genetic factors that, when understood, will facilitate prevention and treatment of otitis media in humans. In addition, a negative correlation between age and compliance of the tympanic membrane was discovered.  This is the first report to    successfully use tympanometry to measure mouse middle ear function, which has been a challenge for the hearing research field because of the mouse's tiny ear size.</p>

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</description>

<author>Q Y. Zheng et al.</author>


</item>


<item>
<title>Failure to induce alopecia areata in C3H/HeJ mice with exogenous interferon gamma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1623</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1623</guid>
<pubDate>Tue, 08 May 2012 22:41:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title>Type 1 IFN mediates cross-talk between innate and adaptive immunity that abrogates transplantation tolerance.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1622</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1622</guid>
<pubDate>Tue, 08 May 2012 22:41:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>TLR activation of innate immunity prevents the induction of transplantation tolerance and shortens skin allograft survival in mice treated with costimulation blockade. The mechanism by which TLR signaling mediates this effect has    not been clear. We now report that administration of the TLR agonists LPS (TLR4) or polyinosinic:polycytidylic acid (TLR3) to mice treated with costimulation blockade prevents alloreactive CD8(+) T cell deletion, primes alloreactive CTLs, and    shortens allograft survival. The TLR4- and MyD88-dependent pathways are required for LPS to shorten allograft survival, whereas polyinosinic:polycytidylic acid mediates its effects through a TLR3-independent pathway. These effects are all    mediated by signaling through the type 1 IFN (IFN-alphabeta) receptor. Administration of IFN-beta recapitulates the detrimental effects of TLR agonists on transplantation tolerance. We conclude that the type 1 IFN generated as part of an innate    immune response to TLR activation can in turn activate adaptive immune responses that abrogate transplantation tolerance. Blocking of type 1 IFN-dependent pathways in patients may improve allograft survival in the presence of exogenous TLR    ligands.</p>

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</description>

<author>T B. Thornley et al.</author>


</item>


<item>
<title>The rosiglitazone story--lessons from an FDA Advisory Committee meeting.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1621</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1621</guid>
<pubDate>Tue, 08 May 2012 22:41:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title>FcRn: the neonatal Fc receptor comes of age.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1620</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1620</guid>
<pubDate>Tue, 08 May 2012 22:41:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>The neonatal Fc receptor for IgG (FcRn) has been well characterized in the transfer of passive humoral immunity from a mother to her fetus. In addition, throughout life, FcRn protects IgG from degradation, thereby explaining the    long half-life of this class of antibody in the serum. In recent years, it has become clear that FcRn is expressed in various sites in adults, where its potential function is now beginning to emerge. In addition, recent studies have examined the    interaction between FcRn and the Fc portion of IgG with the aim of either improving the serum half-life of therapeutic monoclonal antibodies or reducing the half-life of pathogenic antibodies. This Review summarizes these two areas of FcRn    biology.</p>

	]]>
</description>

<author>D C. Roopenian et al.</author>


</item>


<item>
<title>NF-kappaB signaling regulates functional expression of the MHC class I-related neonatal Fc receptor for IgG via intronic binding sequences.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1619</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1619</guid>
<pubDate>Tue, 08 May 2012 22:40:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>The neonatal Fc receptor for IgG (FcRn) functions to transport maternal IgG to a fetus or newborn and to protect IgG from degradation. Although FcRn is expressed in a variety of tissues and cell types, the extent to which FcRn    expression is regulated by immunological and inflammatory events remains unknown. Stimulation of intestinal epithelial cell lines, macrophage-like THP-1, and freshly isolated human monocytes with the cytokine TNF-alpha rapidly up-regulated FcRn    gene expression. In addition, the TLR ligands LPS and CpG oligodeoxynucleotide enhanced the level of FcRn expression in THP-1 and monocytes. Treatment of TNF-stimulated THP-1 cells with the NF-kappaB-specific inhibitor or overexpression of a    dominant negative mutant inhibitory NF-kappaB (IkappaBalpha; S32A/S36A) resulted in down-regulation of FcRn expression. By using chromatin immunoprecipitation we identified three NF-kappaB binding sequences within introns 2 and 4 of the human    FcRn gene. An EMSA confirmed the p50/p50 and/or p65/p50 complex (s) bound to intron 2- or 4-derived oligonucleotides containing putative NF-kappaB binding sequences, respectively. The intronic NF-kappaB sequences in combination with the promoter    or alone regulated the expression of a luciferase reporter gene in response to TNF-alpha stimulation or overexpression of NF-kappaB p65 and p50. DNA looping interactions potentially occurred after the stimulation between intronic NF-kappaB    sequences and the FcRn promoter as shown by a chromosome conformation capture assay. Finally, TNF-alpha stimulations enhanced IgG transport across an intestinal Caco-2 epithelial monolayer.  Together, these data provide the first evidence that    NF-kappaB signaling via intronic sequences regulates FcRn expression and function.</p>

	]]>
</description>

<author>X Liu et al.</author>


</item>


<item>
<title>Neonatal FcR expression in bone marrow-derived cells functions to protect serum IgG from catabolism.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1618</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1618</guid>
<pubDate>Tue, 08 May 2012 22:40:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>The neonatal FcR (FcRn) is a receptor that protects IgG from catabolism and is important in maintaining high serum Ab levels. A major site of expression of FcRn is vascular endothelial cells where FcRn functions to extend the serum    persistence of IgG by recycling internalized IgG back to the surface. Because FcRn is expressed in other tissues, it is unclear whether endothelial cells are the only site of IgG protection. In this study, we used FcRn-deficient mice and specific    antiserum to determine the tissue distribution of FcRn in the adult mouse. In addition to its expression in the vascular endothelium of several organs, we found FcRn to be highly expressed in bone marrow-derived cells and professional APCs in    different tissues. Experiments using bone marrow chimeras showed that FcRn expression in these cells acted to significantly extend the half-life of serum IgG indicating that in addition to the vascular endothelium, bone marrow-derived phagocytic    cells are a major site of IgG homeostasis.</p>

	]]>
</description>

<author>S Akilesh et al.</author>


</item>


<item>
<title>Multiple trait measurements in 43 inbred mouse strains capture the phenotypic diversity characteristic of human populations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1617</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1617</guid>
<pubDate>Tue, 08 May 2012 22:40:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The breadth of genetic and phenotypic variation among inbred strains is often underappreciated because assessments include only a limited number of strains.  Evaluation of a larger collection of inbred strains provides not only a    greater understanding of this variation but collectively mimics much of the variation observed in human populations. We used a high-throughput phenotyping protocol to measure females and males of 43 inbred strains for body composition (weight,    fat, lean tissue mass, and bone mineral density), plasma triglycerides, high-density lipoprotein and total cholesterol, glucose, insulin, and leptin levels while mice consumed a high-fat, high-cholesterol diet. Mice were fed a chow diet until    they were 6-8 wk old and then fed the high-fat diet for an additional 18 wk. As expected, broad phenotypic diversity was observed among these strains.  Significant variation between the sexes was also observed for most traits measured.    Additionally, the response to the high-fat diet differed considerably among many strains. By the testing of such a large set of inbred strains for many traits, multiple phenotypes can be considered simultaneously and thereby aid in the selection    of certain inbred strains as models for complex human diseases.  These data are publicly available in the web-accessible Mouse Phenome Database (http://www.jax.org/phenome), an effort established to promote systematic characterization of    biochemical and behavioral phenotypes of commonly used and genetically diverse inbred mouse strains. Data generated by this effort builds on the value of inbred mouse strains as a powerful tool for biomedical research.</p>

	]]>
</description>

<author>K L. Svenson et al.</author>


</item>


<item>
<title>Carbonic anhydrase related protein 8 mutation results in aberrant synaptic morphology and excitatory synaptic function in the cerebellum.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1616</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1616</guid>
<pubDate>Tue, 08 May 2012 22:40:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Carbonic anhydrase related protein 8 (Car8) is known to be abundantly expressed in Purkinje cells (PCs), and its genetic mutation causes a motor coordination defect. To determine the underlying mechanism, we analyzed the mouse    cerebellum carrying a Car8 mutation. Electrophysiological analysis showed that spontaneous excitatory transmission was largely diminished while paired pulse ratio at parallel fiber-PC synapses was comparable to wild-type, suggesting functional    synapses have normal release probability but the number of functional synapses may be lower in mutants. Light microscopic study revealed an abnormal extension of climbing fibers to the distal PC dendrites. At the ultrastructural level, we found    numerous PC spines not forming synapses primarily in distal dendrites and occasionally multiple spines contacting a single varicosity. These abnormalities of parallel fiber-PC synapses may underlie the functional defect in excitatory    transmission. Thus, Car8 plays a critical role in synaptogenesis and/or maintenance of proper synaptic morphology and function in the cerebellum.</p>

	]]>
</description>

<author>M Hirasawa et al.</author>


</item>


<item>
<title>Identification of conserved gene expression features between murine mammary carcinoma models and human breast tumors.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1615</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1615</guid>
<pubDate>Tue, 08 May 2012 22:40:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Although numerous mouse models of breast carcinomas have been developed, we do not know the extent to which any faithfully represent clinically significant human phenotypes. To address this need, we characterized mammary    tumor gene expression profiles from 13 different murine models using DNA microarrays and compared the resulting data to those from human breast tumors.  RESULTS: Unsupervised hierarchical clustering analysis showed that six models (TgWAP-Myc,    TgMMTV-Neu, TgMMTV-PyMT, TgWAP-Int3, TgWAP-Tag, and TgC3(1)-Tag) yielded tumors with distinctive and homogeneous expression patterns within each strain. However, in each of four other models (TgWAP-T121, TgMMTV-Wnt1, Brca1Co/Co;TgMMTV-Cre;p53+/-    and DMBA-induced), tumors with a variety of histologies and expression profiles developed. In many models, similarities to human breast tumors were recognized, including proliferation and human breast tumor subtype signatures. Significantly,    tumors of several models displayed characteristics of human basal-like breast tumors, including two models with induced Brca1 deficiencies. Tumors of other murine models shared features and trended towards significance of gene enrichment with    human luminal tumors; however, these murine tumors lacked expression of estrogen receptor (ER) and ER-regulated genes. TgMMTV-Neu tumors did not have a significant gene overlap with the human HER2+/ER- subtype and were more similar to human    luminal tumors.  CONCLUSION: Many of the defining characteristics of human subtypes were conserved among the mouse models. Although no single mouse model recapitulated all the expression features of a given human subtype, these shared expression    features provide a common framework for an improved integration of murine mammary tumor models with human breast tumors.</p>

	]]>
</description>

<author>J I. Herschkowitz et al.</author>


</item>


<item>
<title>Spectrum of ALMS1 variants and evaluation of genotype-phenotype correlations in Alstrom syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1614</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1614</guid>
<pubDate>Tue, 08 May 2012 22:40:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alstrom syndrome is a monogenic recessive disorder featuring an array of clinical manifestations, with systemic fibrosis and multiple organ involvement, including retinal degeneration, hearing loss, childhood obesity, diabetes    mellitus, dilated cardiomyopathy (DCM), urological dysfunction, and pulmonary, hepatic, and renal failure. We evaluated a large cohort of patients with Alstrom syndrome for mutations in the ALMS1 gene. In total, 79 disease-causing variants were    identified, of which 55 are novel mutations. The variants are primarily clustered in exons 8, 10, and 16, although we also identified novel mutations in exons 12 and 18. Most alleles were identified only once (45/79), but several were found    recurrently. Founder effects are likely in families of English and Turkish descent. We also identified 66 SNPs and assessed the functional significance of these variants based on the conserved identity of the protein and the severity of the    resulting amino acid substitution. A genotype-phenotype association study examining 18 phenotypic parameters in a subset of 58 patients found suggestive associations between disease-causing variants in exon 16 and the onset of retinal    degeneration before the age of 1 year (P = 0.02), the occurrence of urological dysfunction (P = 0.02), of DCM (P = 0.03), and of diabetes (P = 0.03). A significant association was found between alterations in exon 8 and absent, mild, or delayed    renal disease (P = 0.0007). This data may have implications for the understanding of the molecular mechanisms of ALMS1 and provides the basis for further investigation of how alternative splicing of ALMS1 contributes to the severity of the    disease.</p>

	]]>
</description>

<author>J D. Marshall et al.</author>


</item>


<item>
<title>Molecular analysis and long-term clinical evaluation of three siblings with Alstrom syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1613</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1613</guid>
<pubDate>Tue, 08 May 2012 22:40:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alstrom syndrome is a rare, autosomal recessive disorder characterized by a wide spectrum of clinical features including early-onset retinal degeneration leading to blindness, sensorineural hearing loss, short stature, obesity, type    2 diabetes, hyperlipidemia and dilated cardiomyopathy. Renal, hepatic and pulmonary dysfunction may occur in the later phases of the disease. The three affected sisters, from a consanguineous Turkish family, with the characteristic features of    Alstrom syndrome, were clinically diagnosed in 1987 and followed for 20 years.  DNA sequence analysis of ALMS1, the causative gene in Alstrom syndrome, identified a novel homozygous disease-causing mutation, c.8164C>T, resulting in a premature    termination codon in exon 10 in each of the three affected sisters.  Furthermore, we describe the longitudinal disease progression in this family and report new clinical findings likely associated with Alstrom syndrome, such as pes planus and    hyperthyroidism.</p>

	]]>
</description>

<author>R K. Ozgul et al.</author>


</item>


<item>
<title>Hyperglycemia, maturity-onset obesity, and insulin resistance in NONcNZO10/LtJ males, a new mouse model of type 2 diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1612</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1612</guid>
<pubDate>Tue, 08 May 2012 22:39:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>As a new mouse model of obesity-induced diabetes generated by combining quantitative trait loci from New Zealand Obese (NZO/HlLt) and Nonobese Nondiabetic (NON/LtJ) mice, NONcNZO10/LtJ (RCS10) male mice developed type 2 diabetes    characterized by maturity onset obesity, hyperglycemia, and insulin resistance. To metabolically profile the progression to diabetes in preobese and obese states, a 2-h hyperinsulinemic euglycemic clamp was performed and organ-specific changes in    insulin action were assessed in awake RCS10 and NON/LtJ (control) males at 8 and 13 wk of age. Prior to development of obesity and attendant increases in hepatic lipid content, 8-wk-old RCS10 mice developed insulin resistance in liver and    skeletal muscle due to significant decreases in insulin-stimulated glucose uptake and GLUT4 expression in muscle. Transition to an obese and hyperglycemic state by 13 wk of age exacerbated insulin resistance in skeletal muscle, liver, and heart    associated with organ-specific increases in lipid content. Thus, this polygenic mouse model of type 2 diabetes, wherein plasma insulin is only modestly elevated and obesity develops with maturity yet insulin action and glucose metabolism in    skeletal muscle and liver are reduced at an early prediabetic age, should provide new insights into the etiology of type 2 diabetes.</p>

	]]>
</description>

<author>Y R. Cho et al.</author>


</item>


<item>
<title>Leptin in autoimmunity: many questions, some answers.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1611</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1611</guid>
<pubDate>Tue, 08 May 2012 22:39:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>It has recently become apparent that several molecules involved in the control of metabolism also play an important function in the regulation of immune responses.  Among those molecules, the adipocyte-derived cytokine leptin has    been shown to significantly influence innate and adaptive immune responses both in normal and in pathological conditions. For example, levels of leptin are typically low in infection and high in autoimmunity, both systemically and at the site of    inflammation. Moreover, in addition to its long-known effects on the promotion of T helper 1 immune responses and cell-mediated immunity, leptin has more recently been found capable to constrain proliferation of regulatory T cells. As such,    leptin represents not only a link between metabolism and immune responses in general but also a pivotal modulator of the magnitude of selected mechanisms of peripheral immunity in relation to body fat mass. We review here the most recent advances    on the role of leptin in the control of immune tolerance and critically discuss how strategies aimed at neutralizing the leptin axis could represent innovative tools for the therapy of autoimmune disorders.</p>

	]]>
</description>

<author>G Matarese et al.</author>


</item>


<item>
<title>Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1610</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1610</guid>
<pubDate>Tue, 08 May 2012 22:39:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The glaucomas are a common but incompletely understood group of diseases. DBA/2J mice develop a pigment liberating iris disease that ultimately causes elevated intraocular pressure (IOP) and glaucoma. We have shown    previously that mutations in two genes, Gpnmb and Tyrp1, initiate the iris disease. However, mechanisms involved in the subsequent IOP elevation and optic nerve degeneration remain unclear. RESULTS: Here we present new mouse strains with Gpnmb    and/or Tyrp1 genes of normal function and with a DBA/2J genetic background. These strains do not develop elevated IOP or glaucoma with age. CONCLUSION: These strains provide much needed controls for studying pathogenic mechanisms of glaucoma    using DBA/2J mice. Given the involvement of Gpnmb and/or Tyrp1 in areas such as immunology and tumor development and progression, these strains are also important in other research fields.</p>

	]]>
</description>

<author>G R. Howell et al.</author>


</item>


<item>
<title>Anti-CD40 conditioning enhances the T(CD8) response to a highly tolerogenic epitope and subsequent immunotherapy of simian virus 40 T antigen-induced pancreatic tumors.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1609</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1609</guid>
<pubDate>Tue, 08 May 2012 22:39:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rapid loss of adoptively transferred tumor-specific CD8(+) T cells (T(CD8)) following Ag recognition in the periphery and their limited accumulation within the tumor stroma reduces the effectiveness of T cell-based immunotherapy. To    better understand the role of T(CD8) in the control of autochthonous tumors, we have used mice of the RIP1-Tag4 lineage that develop pancreatic beta cell tumors due to expression of the SV40 large T Ag from the rat insulin promoter. We previously    showed that the kinetics of functional T(CD8) tolerance varies toward two distinct epitopes derived from T Ag. Epitope I ((206)SAINNYAQKL(215))-specific T(CD8) are rapidly deleted whereas T(CD8) targeting epitope IV ((404)VVYDFLKC(411)) persist    over the lifetime of tumor-bearing animals. In this report, we show that the conditioning of tumor-bearing RIP1-Tag4 mice with agonistic anti-CD40 Ab induces extensive expansion of naive epitope I-specific TCR transgenic (TCR-I) T cells in this    tolerogenic environment and delays their loss from the host. In addition, functional TCR-I T cells intensively infiltrate pancreatic tumors, resulting in increased survival of RIP1-Tag4 mice. These results suggest that a similar approach could    effectively enhance T cell-based immunotherapies to cancer when targeting other highly tolerogenic epitopes.</p>

	]]>
</description>

<author>P Otahal et al.</author>


</item>


<item>
<title>Ovalbumin serves as a neo-transplantation antigen in retinal pigment epithelial cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1608</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1608</guid>
<pubDate>Tue, 08 May 2012 22:39:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Our long-term goal is to determine the optimal methods for inducing allograft tolerance to facilitate transplantation of retinal pigment epithelial cells or stem cells for the treatment of retinal degenerative diseases.    These goals have been hampered by the extreme complexity of allograft rejection and the heterogeneity of responding T cells. The current studies were undertaken to develop a simplified transplant model for studying rejection and tolerance in the    unique environment of the eye. METHODS: To provide a defined transplantation antigen, transgenic C57BL/6 (B6) mice were produced, which express the exogenous chicken egg ovalbumin (OVA) gene under the regulation of the mouse tyrosinase related    protein-1 (TRP-1) promoter that is transcriptionally active in retinal pigmented epithelial (RPE) cells. To determine whether the transgene was expressed as a neo-transplantation antigen, RPE from TRP-1-OVA mice were injected into the subretinal    space of B6 mice or B6 mice expressing the OVA-specific (OT1) TCR transgenes and examined for inflammatory cell infiltration. RESULTS: The TRP-1-OVA transgenic mice expressed OVA mRNA in the brain and eye but not the heart or kidney. RPE cells    from TRP-1-OVA transgenic mice expressed mRNA and protein encoded by the OVA gene and RPE expressing TRP-1-OVA induced an inflammatory response within the subretinal space of OT1 mice but not in B6 mice.  CONCLUSIONS: OVA serves as a defined,    neo-transplantation antigen in RPE that is recognized by mice whose CD8+ T cells recognize OVA peptide. These observations provide new tools for future studies of the mechanisms of rejection and prolongation of RPE transplants in the    eye.</p>

	]]>
</description>

<author>J R. Wajchman et al.</author>


</item>


<item>
<title>Treatment of BXSB-Yaa mice with IL-21R-Fc fusion protein minimally attenuates systemic lupus erythematosus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1607</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1607</guid>
<pubDate>Tue, 08 May 2012 22:39:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Interleukin-21 (IL-21) is a pleiotropic cytokine whose function is only now being unraveled. Abundant evidence indicates that activated CD4 T cells are the primary, if not the only, source of IL-21. While it is clear that IL-21 is    actively transcribed by naive activated T cells, recent studies have shown that IL-21 potentially promotes a developmental shift of naive T cells toward the Th2 phenotype. BXSB-Yaa mice develop an autoimmune syndrome similar to systemic lupus    erythematosus (SLE), affecting males earlier than females on account of the presence of the Yaa (Y-linked autoimmune acceleration) locus. Previous results indicate the elevation of IL-21 expression by BXSB-Yaa mice at an age when the early    characteristics of autoimmune processes first become evident. We set out to determine whether IL-21 was necessary for disease progression in BXSB-Yaa mice.  Mice were treated for 24 weeks with soluble IL-21R-Fc in order to therapeutically    neutralize the IL-21 present. The results overall suggest a biphasic effect of IL-21, negatively influencing survival early on and positively influencing survival at later stages. We propose that IL-21 exerts a pleiotropic effect in which it    promotes the protective effects of CD8+ suppressor cells in the early disease phase and then promotes the humoral components of SLE in the later disease stages. This experiment provides preliminary evidence for a role of IL-21 in modulating the    severity of SLE in BXSB-Yaa mice.</p>

	]]>
</description>

<author>J A. Bubier et al.</author>


</item>


<item>
<title>Dietary thyroid hormone replacement ameliorates hearing deficits in hypothyroid mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1606</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1606</guid>
<pubDate>Tue, 08 May 2012 22:39:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Thyroid hormone (TH) insufficiency causes variable hearing impairment and mental deficiency in humans. Rodents lacking TH have congenital hearing deficiency that has been attributed to physiologic, morphologic, and developmental    abnormalities of the auditory system. We examined four genetically defined strains of hypothyroid mice for development of hearing and response to TH replacement initiated during late gestation and continued through six weeks of age. Auditory    brain stem response studies showed variable hearing impairment in homozygous mutants of each strain at three weeks of age relative to normal littermates.  Mutants from three of the strains still had hearing deficiencies at six weeks of age.    TH-enriched diet significantly improved hearing in three-week-old mutants of each strain relative to untreated mutants. Differences in the level of hearing impairment between the Prop1df and Pit1dw mutants, which have defects in the same    developmental pathway, were determined to be due to genetic background modifier genes. Further physiologic and morphologic studies in the Cgatm1Sac strain indicated that poor hearing was due to cochlear defects. We conclude that TH supplement    administered during the critical period of hearing development in mice can prevent deafness associated with congenital hypothyroidism of heterogeneous genetic etiology.</p>

	]]>
</description>

<author>I J. Karolyi et al.</author>


</item>


<item>
<title>Targeted knockout and lacZ reporter expression of the mouse Tmhs deafness gene and characterization of the hscy-2J mutation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1605</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1605</guid>
<pubDate>Tue, 08 May 2012 22:38:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Tmhs gene codes for a tetraspan transmembrane protein that is expressed in hair cell stereocilia. We previously showed that a spontaneous missense mutation of Tmhs underlies deafness and vestibular dysfunction in the    hurry-scurry (hscy) mouse. Subsequently, mutations in the human TMHS gene were shown to be responsible for DFNB67, an autosomal recessive nonsyndromic deafness locus. Here we describe a genetically engineered null mutation of the mouse Tmhs gene    (Tmhs ( tm1Kjn )) and show that its phenotype is identical to that of the hscy missense mutation, confirming the deleterious nature of the hscy cysteine-to-phenylalanine substitution. In the targeted null allele, the Tmhs promoter drives    expression of a lacZ reporter gene. Visualization of beta-galactosidase activity in Tmhs ( tm1Kjn ) heterozygous mice indicates that Tmhs is highly expressed in the cochlear and vestibular hair cells of the inner ear. Expression is first    detectable at E15.5, peaks around P0, decreases slightly at P6, and is absent by P15, a duration that supports the involvement of Tmhs in stereocilia development.  Tmhs reporter gene expression also was detected in several cranial and cervical    sensory ganglia, but not in the vestibular or spiral ganglia. We also describe a new nontargeted mutation of the Tmhs gene, hscy-2J, that causes abnormal splicing from a cryptic splice site within exon 2 and is predicted to produce a functionally    null protein lacking 51 amino acids of the wild-type sequence.</p>

	]]>
</description>

<author>Guess C. Longo et al.</author>


</item>


<item>
<title>Analysis of ocular hypopigmentation in Rab38cht/cht mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1604</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1604</guid>
<pubDate>Tue, 08 May 2012 22:38:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: To characterize the ocular phenotype resulting from mutation of Rab38, a candidate gene for Hermansky-Pudlak syndrome. METHODS: Chocolate mice (cht, Rab38(cht/cht)) and control heterozygous (Rab38(cht/)(+)) and wild-type    mice were examined clinically, histologically, ultrastructurally, and electrophysiologically. Mice homozygous for both the Rab38(cht) and the Tyrp1(b) alleles were similarly examined. RESULTS: Rab38(cht/cht) mice showed variable peripheral iris    transillumination defects at 2 months of age. Patches of RPE hypopigmentation were noted clinically in 57% of Rab38(cht/cht) eyes and 6% of Rab38(cht/)(+) eyes. Rab38(cht/cht) mice exhibited thinning of the iris and RPE and larger b-wave    amplitudes in the scotopic range when compared with the control animals. Compared with wild-type mice, Rab38(cht/cht) melanosomes were smaller and there were fewer in neuroectodermally derived retinal pigment epithelium; in neural crest-derived    choroid melanocytes, they were smaller in size only.  Mutation of both Rab38 and Tyrp1 produced mice with ocular and coat color pigment dilution greater than that seen with either mutation alone. Comprehensive clinical and pathologic analyses    showed no other organ system or blood defects in Rab38(cht/cht) mice. CONCLUSIONS: Rab38(cht/cht) mice show ocular characteristics reminiscent of human oculocutaneous albinism, as well as iris and RPE thinning.  The synergistic effects of the    Rab38(cht) and Tyrp1(b) alleles suggest that TYRP1 is not the only target of RAB38 trafficking. This mouse line provides a useful model for studying melanosome biology and its role in human ocular diseases.</p>

	]]>
</description>

<author>B P. Brooks et al.</author>


</item>


<item>
<title>Adipokine and insulin profiles distinguish diabetogenic and non-diabetogenic obesities in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1603</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1603</guid>
<pubDate>Tue, 08 May 2012 22:38:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: To use longitudinal profiling of plasma adipokines to distinguish diabetogenic vs. non-diabetogenic obesity syndrome in two new mouse models of polygenic obesity. RESEARCH METHODS AND PROCEDURES: Male mice of the NONcNZO5    strain develop a polygenic obesity syndrome uncomplicated by diabetes, whereas NONcNZO10 males develop a comparable polygenic obesity that precipitates type 2 diabetes. A multiplex immunoassay for simultaneous measurement of insulin and a panel    of mouse adipokines (leptin, resistin, adiponectin, interleukin-6, tumor necrosis factor alpha, macrophage chemoattractant protein-1, plasminogen activator inhibitor-1) were used to profile longitudinal changes in these strains between 4 and 16    weeks of age that might distinguish the non-diabetogenic vs.  diabetogenic obesity (diabesity). RESULTS: Both strains became adipose, with NONcNZO5 males attaining a higher mean body weight with a higher percentage fat content. Weight gain in    NONcNZO5 was accompanied by a transient peak in plasma insulin (PI) at 8 weeks followed by a decline into normal range, with normoglycemia maintained throughout. In contrast, NONcNZO10 showed no early PI secretory response because both body    weight and plasma glucose increased between 4 and 8 weeks. Only after 12 weeks, with hyperglycemia established, was a delayed PI secretory response observed. Neither plasma leptin nor adiponectin concentrations significantly differentiated the    two syndromes over time. However, repeated measures ANOVA showed that NONcNZO10 males maintained significantly higher plasma concentrations of two adipokines, resistin and plasminogen activator inhibitor-1, and the pro-inflammatory    cytokine/adipokine macrophage chemoattractant protein-1. DISCUSSION: Longitudinal profiling of PI and adipokines in two new mouse models developing moderate obesity demonstrated that specific marker signatures differentiated a non-diabetogenic    obesity from a diabetogenic obesity.</p>

	]]>
</description>

<author>E H. Leiter et al.</author>


</item>


<item>
<title>Direct regulation of Gata3 expression determines the T helper differentiation potential of Notch.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1602</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1602</guid>
<pubDate>Tue, 08 May 2012 22:38:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>CD4(+) T helper cells differentiate into T helper 1 (Th1) or Th2 effector lineages, which orchestrate immunity to different types of microbes. Both Th1 and Th2 differentiation can be induced by Notch, but what dictates which of    these programs is activated in response to Notch is not known. By using T cell-specific gene ablation of the Notch effector RBP-J or the Notch1 and 2 receptors, we showed here that Notch was required on CD4(+) T cells for physiological Th2    responses to parasite antigens. GATA-3 was necessary for Notch-induced Th2 differentiation, and we identified an upstream Gata3 promoter as a direct target for Notch signaling. Moreover, absence of GATA-3 turned Notch from a Th2 inducer into a    powerful inducer of Th1 differentiation. Therefore, Gata3 is a critical element determining inductive Th2 differentiation and limiting Th1 differentiation by Notch.</p>

	]]>
</description>

<author>D Amsen et al.</author>


</item>


<item>
<title>C. elegans sequences that control trans-splicing and operon pre-mRNA processing.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1601</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1601</guid>
<pubDate>Tue, 08 May 2012 22:38:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many mRNAs in Caenorhabditis elegans are generated through a trans-splicing reaction that adds one of two classes of spliced leader RNA to an independently transcribed pre-mRNA. SL1 leaders are spliced mostly to pre-mRNAs from genes    with outrons, intron-like sequences at the 5'-ends of the pre-mRNAs. In contrast, SL2 leaders are nearly exclusively trans-spliced to genes that occur downstream in polycistronic pre-mRNAs produced from operons. Operon pre-mRNA processing    requires separation into individual transcripts, which is accomplished by 3'-processing of upstream genes and spliced leader trans-splicing to the downstream genes. We used a novel computational analysis, based on nonnegative matrix    factorization, to identify and characterize significant differences in the cis-acting sequence elements that differentiate various types of functional site, including internal versus terminal 3'-processing sites, and SL1 versus SL2 trans-splicing    sites. We describe several key elements, including the U-rich (Ur) element that couples 3'-processing with SL2 trans-splicing, and a novel outron (Ou) element that occurs upstream of SL1 trans-splicing sites. Finally, we present models of the    distinct classes of trans-splicing reaction, including SL1 trans-splicing at the outron, SL2 trans-splicing in standard operons, competitive SL1-SL2 trans-splicing in operons with large intergenic separation, and SL1 trans-splicing in SL1-type    operons, which have no intergenic separation.</p>

	]]>
</description>

<author>J H. Graber et al.</author>


</item>


<item>
<title>Notch signaling in vascular development and physiology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1600</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1600</guid>
<pubDate>Tue, 08 May 2012 22:38:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Notch signaling is an ancient intercellular signaling mechanism that plays myriad roles during vascular development and physiology in vertebrates. These roles include regulation of artery/vein differentiation in endothelial and    vascular smooth muscle cells, regulation of blood vessel sprouting and branching during both normal development and tumor angiogenesis, and the differentiation and physiological responses of vascular smooth muscle cells. Defects in Notch    signaling also cause inherited vascular and cardiovascular diseases. In this review, I summarize recent findings and discuss the growing relevance of Notch pathway modulation for therapeutic applications in disease.</p>

	]]>
</description>

<author>T Gridley</author>


</item>


<item>
<title>Correct dosage of Fog2 and Gata4 transcription factors is critical for fetal testis development in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1599</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1599</guid>
<pubDate>Tue, 08 May 2012 22:37:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous reports suggested that humans and mice differ in their sensitivity to the genetic dosage of transcription factors that play a role in early testicular development. This difference implies that testis determination might be    somewhat different in these two species. We report that the Fog2 and Gata4 transcription factors are haploinsufficient for testis determination in mice. Whether gonadal sex reversal occurs depends on genetic background (i.e., modifier genes). For    example, C57BL/6J (B6) XY mice develop testes if they are heterozygous for a mutant Fog2 (Fog2-) or Gata4 (Gata4(ki)) allele. However, if the B6 Y chromosome (Y(B6)) is replaced by the AKR Y chromosome (Y(AKR)), B6 Fog2-/+ XY(AKR) mice develop    ovaries, and B6 Gata4(ki)/+ XY(AKR) mice develop ovaries and ovotestes (gonads containing both ovarian and testicular tissue). Furthermore, DBA/2J (D2) Fog2-/+ XY(AKR) mice and (B6 x D2)F1 hybrid Gata4(ki)/+ XY(AKR) mice develop testes. Sry is    expressed in the mutant XY gonads, indicating that the lack of Sry expression is not the cause of ovarian tissue development in B6 Fog2-/+ or Gata4(ki)/+ XY(AKR) mice. However, up-regulation of Sox9 expression, which is critical for normal    testicular development, does not occur in mutant XY gonads that develop as ovaries. We conclude that under certain genetic conditions, Sox9 up-regulation depends on the proper dosage of Fog2 and Gata4. We propose that in humans the FOG2 and/or    GATA4 genes might be haploinsufficient for normal testis determination and thus could be the cause of some previously unassigned cases of XY gonadal sex reversal.</p>

	]]>
</description>

<author>G J. Bouma et al.</author>


</item>


<item>
<title>An Aging Interventions Testing Program: study design and interim report.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1598</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1598</guid>
<pubDate>Tue, 08 May 2012 22:37:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>The National Institute on Aging's Interventions Testing Program (ITP) has developed a plan to evaluate agents that are considered plausible candidates for delaying rates of aging. Key features include: (i) use of genetically    heterogeneous mice (a standardized four-way cross), (ii) replication at three test sites (the Jackson Laboratory, TJL; University of Michigan, UM; and University of Texas, UT), (iii) sufficient statistical power to detect 10% changes in lifespan,    (iv) tests for age-dependent changes in T cell subsets and physical activity, and (v) an annual solicitation for collaborators who wish to suggest new interventions for evaluation. Mice in the first cohort were exposed to one of four agents:    aspirin, nitroflurbiprofen (NFP), 4-OH-alpha-phenyl-N-tert-butyl nitrone (4-OH-PBN), or nordihydroguiaretic acid (NDGA). An interim analysis was conducted using survival data available on the date at which at least 50% of the male control mice    had died at each test site.  Survival of control males was significantly higher, at the interim time-point, at UM than at UT or TJL; all three sites had similar survival of control females.  Males in the NDGA group had significantly improved    survival (P = 0.0004), with significant effects noted at TJL (P < 0.01) and UT (P < 0.04). None of the other agents altered survival, although there was a suggestion (P = 0.07) of a beneficial effect of aspirin in males. More data will be needed    to determine if any of these compounds can extend maximal lifespan, but the current data show that NDGA reduces early life mortality risks in genetically heterogeneous mice at multiple test sites.</p>

	]]>
</description>

<author>R A. Miller et al.</author>


</item>


<item>
<title>Oocyte-derived BMP15 and FGFs cooperate to promote glycolysis in cumulus cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1597</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1597</guid>
<pubDate>Tue, 08 May 2012 22:37:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mammalian oocytes are deficient in their ability to carry out glycolysis.  Therefore, the products of glycolysis that are necessary for oocyte development are provided to oocytes by companion cumulus cells. Mouse oocytes secrete    paracrine factors that promote glycolysis in cumulus cells. The objective of this study was to identify paracrine factors secreted by oocytes that promote glycolysis and expression of mRNA encoding the glycolytic enzymes PFKP and LDHA.     Candidates included growth differentiation factor 9 (GDF9), bone morphogenetic protein 15 (BMP15) and fibroblast growth factors (FGFs). Bmp15-/- and Gdf9+/- Bmp15-/- (double mutant, DM) cumulus cells exhibited reduced levels of both glycolysis    and Pfkp and Ldha mRNA, and mutant oocytes were deficient in promoting glycolysis and expression of Pfkp and Ldha mRNA in cumulus cells of wild-type (WT) mice. Alone, neither recombinant BMP15, GDF9 nor FGF8 promoted glycolysis and expression of    Pfkp and Ldha mRNA in WT cumulus cells. Co-treatment with BMP15 and FGF8 promoted glycolysis and increased expression of Pfkp and Ldha mRNA in WT cumulus cells to the same levels as WT oocytes; however, the combinations of BMP15/GDF9 or GDF9/FGF8    did not. Furthermore, SU5402, an FGF receptor-dependent protein kinase inhibitor, inhibited Pfkp and Ldha expression in cumulus cells promoted by paracrine oocyte factors. Therefore, oocyte-derived BMP15 and FGFs cooperate to promote glycolysis    in cumulus cells.</p>

	]]>
</description>

<author>K Sugiura et al.</author>


</item>


<item>
<title>Oocytes are required for the preantral granulosa cell to cumulus cell transition in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1596</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1596</guid>
<pubDate>Tue, 08 May 2012 22:37:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Preantral granulosa cells (PAGCs) differentiate into cumulus cells following antrum formation. Cumulus cells, but not PAGCs, are competent to undergo expansion. Experiments reported here tested the respective roles of both oocytes    and FSH in the transition of preantral granulosa cells to cumulus cells competent to undergo expansion. PAGC-oocyte complexes were cultured with or without a low dose of FSH (0.005 IU/ml) and isolated PAGCs were cultured with or without oocytes.    At the end of culture, complexes or isolated PAGCs were tested for their ability to undergo cumulus expansion and upregulate expansion transcripts in response to EGF or FSH (0.5 IU/ml). The ability to undergo expansion in response to EGF required    the presence of oocytes but not FSH during the culture period.  Likewise, complexes isolated from the ovaries of hypogonadal mice, which lack circulating gonadotropins, underwent expansion in response to EGF, but not FSH.  In contrast, the    ability to activate MAPK3/1 and MAPK14 and undergo expansion in response to FSH required prior exposure to low doses of FSH. However, these low levels (0.005 or 0.025 IU FSH/ml) suppressed expression of Slc38a3 and Amh, two transcripts highly    expressed in cumulus cells, suggesting opposing effects of FSH on cumulus cell differentiation. In conclusion, the ability to undergo expansion in response to FSH requires prior exposure to FSH during development, while oocyte-derived factors    alone are sufficient to promote the ability to undergo expansion in response to EGF. These results highlight the crucial role of oocytes in driving the differentiation of PAGCs into cumulus cells during the preantral to antral follicle    transition.</p>

	]]>
</description>

<author>F J. Diaz et al.</author>


</item>


<item>
<title>Genetic background modifies inner ear and eye phenotypes of jag1 heterozygous mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1595</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1595</guid>
<pubDate>Tue, 08 May 2012 22:37:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice heterozygous for missense mutations of the Notch ligand Jagged1 (Jag1) exhibit head-shaking behavior indicative of an inner ear vestibular defect. In contrast, mice heterozygous for a targeted deletion of the Jag1 gene    (Jag1del1) do not demonstrate obvious head-shaking behavior. To determine whether the differences in inner ear phenotypes were due to the types of Jag1 mutations or to differences in genetic background, we crossed Jag1del1 heterozygous mice onto    the same genetic background as the missense mutants. This analysis revealed that variation of the Jag1 mutant inner ear phenotype is caused by genetic background differences and is not due to the type of Jag1 mutation. Genome scans of N2    backcross mice identified a significant modifier locus on chromosome 7, as well as a suggestive locus on chromosome 14. We also analyzed modifiers of an eye defect in Jag1del1 heterozygous mice from this same cross.</p>

	]]>
</description>

<author>A E. Kiernan et al.</author>


</item>


<item>
<title>The histone deacetylase HDAC4 connects neural activity to muscle transcriptional reprogramming.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1594</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1594</guid>
<pubDate>Tue, 08 May 2012 22:37:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Neural activity actively regulates muscle gene expression. This regulation is crucial for specifying muscle functionality and synaptic protein expression. How neural activity is relayed into nuclei and connected to the muscle    transcriptional machinery, however, is not known. Here we identify the histone deacetylase HDAC4 as the critical linker connecting neural activity to muscle transcription. We found that HDAC4 is normally concentrated at the neuromuscular junction    (NMJ), where nerve innervates muscle. Remarkably, reduced neural input by surgical denervation or neuromuscular diseases dissociates HDAC4 from the NMJ and dramatically induces its expression, leading to robust HDAC4 nuclear accumulation. We    present evidence that nuclear accumulated HDAC4 is responsible for the coordinated induction of synaptic genes upon denervation. Inactivation of HDAC4 prevents denervation-induced synaptic acetyl-choline receptor (nAChR) and MUSK transcription    whereas forced expression of HDAC4 mimics denervation and activates ectopic nAChR transcription throughout myofibers. We determined that HDAC4 executes activity-dependent transcription by regulating the Dach2-myogenin transcriptional cascade    where inhibition of the repressor Dach2 by HDAC4 permits the induction of the transcription factor myogenin, which in turn activates synaptic gene expression. Our findings establish HDAC4 as a neural activity-regulated deacetylase and a key    signaling component that relays neural activity to the muscle transcriptional machinery.</p>

	]]>
</description>

<author>T J. Cohen et al.</author>


</item>


<item>
<title>Genetic analysis of albuminuria in a cross between C57BL/6J and DBA/2J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1593</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1593</guid>
<pubDate>Tue, 08 May 2012 22:37:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chronic kidney disease (CKD) is a growing medical problem and a significant risk factor for the development of end-stage renal disease, cardiovascular disease, and cardiovascular mortality. The genetic basis of CKD is recognized,    but knowledge of the specific genes that contribute to the onset and progression of kidney disease is limited, mainly because of the difficulty and expense of identifying genes underlying CKD in humans. Results from genetic studies of CKD in    rodents often correspond to findings in humans; therefore, we used quantitative trait locus (QTL) analysis to detect genomic regions affecting albuminuria in a cross between C57BL/6J and DBA/2J mice, strains resistant and susceptible to CKD,    respectively. We identified several independent and interacting loci affecting albuminuria, including one QTL on mouse chromosome (Chr) 2 that is concordant with QTL influencing urinary albumin excretion on rat Chr 3 and diabetic nephropathy on    human Chr 20p. Because this QTL was identified in multiple mouse crosses, as well as in rats and in humans, we used comparative genomics, haplotype analysis, and expression profiling to narrow the initial QTL interval from 386 genes to 10 genes    with known coding sequence polymorphisms or expression differences between the strains. These results support the continued use of multiple cross-mapping and cross-species comparisons to further our understanding of the genetic basis of kidney    disease.</p>

	]]>
</description>

<author>S Sheehan et al.</author>


</item>


<item>
<title>Recombinant inbred strain panels: a tool for systems genetics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1592</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1592</guid>
<pubDate>Tue, 08 May 2012 22:36:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>G A. Churchill</author>


</item>


<item>
<title>Automated compartmental analysis for high-throughput skeletal phenotyping in femora of genetic mouse models.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1591</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1591</guid>
<pubDate>Tue, 08 May 2012 22:36:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mouse models are widely used in genomic studies for quantitative trait loci (QTL) analyses. In the field of skeletal micro-structure, microCT has proven to be an invaluable imaging tool for the characterization of structural bone    traits.  However, the definition of analysis compartments requires a lot of user interaction, and therefore is not applicable as a standard way to analyze genetic linkage studies with several hundreds of animals. Here, we developed an automated    three-dimensional based algorithm for a high-throughput regional analysis of three compartments in murine femora, including whole bone, cortical bone in the diaphysis and trabecular bone in the metaphysis. The algorithm relies on basic image    processing concepts using morphological operators as well as a new approach of separating cortical from trabecular bone. Reproducibility of the automatic approach was investigated with respect to precision errors (PE(%CV)) of micro-structural    indices analyzed in these automatically defined compartments.  The developed algorithm was then used to perform a high-throughput analysis of over 2000 femora in a genetic linkage study for further examination of stability and performance.    Precision errors were 3.5% or less for all micro-structural indices. The analysis of one femur (mask generation and parameter evaluation) took 7 min on an AlphaServer DS25. The algorithm showed a very high reliability and worked successfully for    99.64% of all femora. Investigations of correlations amongst the assessed micro-structural indices together with heritability and polygene estimates revealed apparent volume density (AVD), trabecular thickness (Tb.Th), trabecular separation    (Tb.Sp) and cortical thickness (Ct.Th) as candidates for a successful QTL analysis. The presented automatic analysis allows for standardized high-throughput phenotypic screening in mice femora for large genetic linkage studies with very high    reliability and good precision.</p>

	]]>
</description>

<author>T Kohler et al.</author>


</item>


<item>
<title>On the subspecific origin of the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1590</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1590</guid>
<pubDate>Tue, 08 May 2012 22:36:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genome of the laboratory mouse is thought to be a mosaic of regions with distinct subspecific origins. We have developed a high-resolution map of the origin of the laboratory mouse by generating 25,400 phylogenetic trees at    100-kb intervals spanning the genome. On average, 92% of the genome is of Mus musculus domesticus origin, and the distribution of diversity is markedly nonrandom among the chromosomes. There are large regions of extremely low diversity, which    represent blind spots for studies of natural variation and complex traits, and hot spots of diversity. In contrast with the mosaic model, we found that most of the genome has intermediate levels of variation of intrasubspecific origin.  Finally,    mouse strains derived from the wild that are supposed to represent different mouse subspecies show substantial intersubspecific introgression, which has strong implications for evolutionary studies that assume these are pure representatives of a    given subspecies.</p>

	]]>
</description>

<author>H Yang et al.</author>


</item>


<item>
<title>Quantitative trait loci associated with blood pressure of metabolic syndrome in the progeny of NZO/HILtJxC3H/HeJ intercrosses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1589</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1589</guid>
<pubDate>Tue, 08 May 2012 22:36:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>In a previous study in 15 inbred mouse strains, we found highest and lowest systolic blood pressures in NZO/HILtJ mice (metabolic syndrome) and C3H/HeJ mice (common lean strain), respectively. To identify the loci involved in    hypertension in metabolic syndrome, we performed quantitative trait locus (QTL) analysis for blood pressure with direction of cross as a covariate in segregating F2 males derived from NZO/HILtJ and C3H/HeJ mice. We detected three suggestive    main-effect QTLs affecting systolic and diastolic blood pressures (SBP and DBP). We analyzed the first principle component (PC1) generated from SBP and DBP to investigate blood pressure. In addition to all the suggestive QTLs (Chrs 1, 3, and 8)    in SBP and DBP, one suggestive QTL on Chr 4 was found in PC1 in the main scan.  Simultaneous search identified two significant epistatic locus pairs (Chrs 1 and 4, Chrs 4 and 8) for PC1. Multiple regression analysis revealed three blood pressure    QTLs (Bpq10, 100 cM on Chr 1; Bpq11, 6 cM on Chr 4; Bpq12, 29 cM on Chr 8) accounting for 29.4% of blood pressure variance. These were epistatic interaction QTLs constructing a small network centered on Chr 4, suggesting the importance of genetic    interaction for development of hypertension. The blood pressure QTLs on Chrs 1, 4, and 8 were detected repeatedly in multiple studies using common inbred nonobese mouse strains, implying substantial QTL independent of development of obesity and    insulin resistance. These results enhance our understanding of complicated genetic factors of hypertension in metabolic diseases.</p>

	]]>
</description>

<author>E Nishihara et al.</author>


</item>


<item>
<title>Modifier locus for exencephaly in Cecr2 mutant mice is syntenic to the 10q25.3 region associated with neural tube defects in humans.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1588</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1588</guid>
<pubDate>Tue, 08 May 2012 22:36:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Neural tube defects (NTDs), the second most common birth defect in humans, are multifactorial with complex genetic and environmental causes, although the genetic factors are almost completely unknown. In mice, >100 single gene    mutations cause NTDs; however, the penetrance in many of these single gene mutant lines is highly dependent on the genetic background. We previously reported that a homozygous Cecr2 mutation on a BALB/c background causes exencephaly at a    frequency of 74% compared with 0% on an FVB/N background. We now report that a major genetic modifier on chromosome 19, mapped using whole genome linkage analysis, increases the relative risk of exencephaly by 3.74 times in homozygous BALB    embryos vs. BALB/FVB heterozygotes. Scanning electron microscopy revealed that the modifier does not affect the location of neural tube closure site 2, a known murine susceptibility factor for exencephaly. Crossing the Sp (Splotch) mutation in    the Pax3 gene onto the FVB/N background for two generations indicated that this resistant strain also decreases the penetrance of spina bifida. The chromosome 19 modifier region corresponds to a linkage region on human chromosome 10q25.3 mapped    in a whole genome scan of human NTD families. Since the FVB/N genetic background affects susceptibility to both exencephaly and spina bifida, the human homolog of the chromosome 19 modifier locus may be a better candidate for human NTD    susceptibility factors than genes that when mutated actually cause NTDs in mice.</p>

	]]>
</description>

<author>C E. Davidson et al.</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 1 No 2</title>
<link>http://ro.uow.edu.au/uowgazette/4</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/4</guid>
<pubDate>Tue, 08 May 2012 22:36:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>The University of Wollongong</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 1 No 3</title>
<link>http://ro.uow.edu.au/uowgazette/3</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/3</guid>
<pubDate>Tue, 08 May 2012 22:36:13 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>The University of Wollongong</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 1 No 4</title>
<link>http://ro.uow.edu.au/uowgazette/2</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/2</guid>
<pubDate>Tue, 08 May 2012 22:36:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>The University of Wollongong</author>


</item>


<item>
<title>Over 60% of NIH extramural funding involves animal-related research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1587</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1587</guid>
<pubDate>Tue, 08 May 2012 22:36:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T Valli et al.</author>


</item>


<item>
<title>Ena/VASP is required for endothelial barrier function in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1586</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1586</guid>
<pubDate>Tue, 08 May 2012 22:35:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Enabled/vasodilator-stimulated phosphoprotein (Ena/VASP) proteins are key actin regulators that localize at regions of dynamic actin remodeling, including cellular protrusions and cell-cell and cell-matrix junctions. Several studies    have suggested that Ena/VASP proteins are involved in the formation and function of cellular junctions. Here, we establish the importance of Ena/VASP in endothelial junctions in vivo by analysis of Ena/VASP-deficient animals. In the absence of    Ena/VASP, the vasculature exhibits patterning defects and lacks structural integrity, leading to edema, hemorrhaging, and late stage embryonic lethality. In endothelial cells, we find that Ena/VASP activity is required for normal F-actin content,    actomyosin contractility, and proper response to shear stress. These findings demonstrate that Ena/VASP is critical for actin cytoskeleton remodeling events involved in the maintenance of functional endothelia.</p>

	]]>
</description>

<author>C Furman et al.</author>


</item>


<item>
<title>Inactivation of the UNC5C Netrin-1 receptor is associated with tumor progression in colorectal malignancies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1585</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1585</guid>
<pubDate>Tue, 08 May 2012 22:35:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND & AIMS: The UNC5H netrin-1 receptors (UNC5H1-3 also called UNC5A-C) belong to the functional dependence receptors family, which share the ability to induce apoptosis in the absence of their ligands. Such a trait has been    hypothesized to confer a tumor-suppressor activity. Indeed, cells harboring these receptors are thought to be dependent on ligand availability for their survival, thereby inhibiting uncontrolled tumor cell proliferation. We investigate here    whether UNC5C acts as a tumor suppressor in colorectal malignancies. METHODS: The level of UNC5C was analyzed in a panel of 86 primary sporadic colorectal carcinomas. Loss of heterozygosity in the UNC5C locus and epigenetic alterations in the    UNC5C promoter were also analyzed. Intestinal tumor progression was monitored in mice bearing both UNC5C and APC1638N mutations, and apoptosis was measured in intestinal tumors developed in UNC5C/APC1638N mutant mice. RESULTS: We show here that    UNC5C expression is down-regulated in a large fraction of human colorectal cancers, mainly through promoter methylation. Moreover, in mice, inactivation of UNC5C is associated with increased intestinal tumor progression and a decrease in tumor    cell apoptosis. CONCLUSIONS: The loss of UNC5C expression observed in human colorectal cancer is a selective advantage for tumor progression, in agreement with the dependence receptor hypothesis. Thus, the UNC5C dependence receptor is a tumor    suppressor that regulates sporadic colorectal cancer.</p>

	]]>
</description>

<author>A Bernet et al.</author>


</item>


<item>
<title>Mammalian Sir2 homolog SIRT3 regulates global mitochondrial lysine acetylation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1584</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1584</guid>
<pubDate>Tue, 08 May 2012 22:35:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Homologs of the Saccharomyces cerevisiae Sir2 protein, sirtuins, promote longevity in many organisms. Studies of the sirtuin SIRT3 have so far been limited to cell culture systems. Here, we investigate the localization and function    of SIRT3 in vivo. We show that endogenous mouse SIRT3 is a soluble mitochondrial protein. To address the function and relevance of SIRT3 in the regulation of energy metabolism, we generated and phenotypically characterized SIRT3 knockout mice.    SIRT3-deficient animals exhibit striking mitochondrial protein hyperacetylation, suggesting that SIRT3 is a major mitochondrial deacetylase. In contrast, no mitochondrial hyperacetylation was detectable in mice lacking the two other mitochondrial    sirtuins, SIRT4 and SIRT5. Surprisingly, despite this biochemical phenotype, SIRT3-deficient mice are metabolically unremarkable under basal conditions and show normal adaptive thermogenesis, a process previously suggested to involve SIRT3.    Overall, our results extend the recent finding of lysine acetylation of mitochondrial proteins and demonstrate that SIRT3 has evolved to control reversible lysine acetylation in this organelle.</p>

	]]>
</description>

<author>D B. Lombard et al.</author>


</item>


<item>
<title>A mouse model of conditional lipodystrophy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1583</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1583</guid>
<pubDate>Tue, 08 May 2012 22:35:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lipodystrophies are syndromes of adipose tissue degeneration associated with severe defects in lipid and glucose homeostasis. We report here the generation and analysis of Pparg(ldi), a targeted allele that confers conditional    dominant lipodystrophy in mice. The Pparg(ldi) allele was generated by insertion of the Tet activator (tTA) and a tTA-regulated Flag-Pparg1 transgene into the Pparg gene. Unexpectedly, tTA elicits mild lipodystrophy, insulin resistance, and    dyslipidemia, and the Flag-PPARgamma1 transgene surprisingly exacerbates these traits. Doxycycline can both completely prevent and reverse these phenotypes, providing a mouse model of inducible lipodystrophy. Embryonic fibroblasts from either    Pparg(ldi/+) or the phenotypically similar aP2-nSrebp1c (Sr) transgenic mice undergo robust adipogenesis, suggesting that neither strain develops lipodystrophy because of defective adipocyte differentiation. In addition, Pparg(ldi/+) adipose    tissue shares extensive gene expression aberrations with that of Sr mice, authenticating the phenotype at the molecular level and revealing a common expression signature of lipodystrophic fat. Thus, the Pparg(ldi/+) mouse provides a conditional    animal model for studying lipodystrophy and its associated physiology and gene expression.</p>

	]]>
</description>

<author>S Kim et al.</author>


</item>


<item>
<title>Acute but not chronic macrophage recruitment in filarial infections in mice is dependent on C-C chemokine ligand 2.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1582</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1582</guid>
<pubDate>Tue, 08 May 2012 22:35:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Macrophages play an important role in the formation of granulomas and the clearance of Brugia pahangi infections in mice. However, the factors responsible for the recruitment of these cells to the site of infection are not known. In    this study we examined the role of the C-C chemokine ligand 2 (CCL2; also known as macrophage chemotactic factor - MCP1) in macrophage recruitment in intraperitoneal infections with B. pahangi. We observed that CCL2 was expressed by peritoneal    exudate cells and was present in the sera of wild-type mice. Serum levels of CCL2 peaked twice during the immune response, once during the early, acute phase and again during the late, chronic phase. To further elucidate the role of this    chemokine in the anti-filarial immune response, we compared CCL2 deficient (CCL2(-/-)) mice to wild-type mice. We observed that macrophage recruitment was impaired only during the acute phase in the former. While macrophage recruitment was    unaffected during the chronic phase, increased accumulation of B and T lymphocytes was seen in these mice. We further report that larval clearance and the in vitro adhesion of PECs to larvae were unimpaired in these mice.</p>

	]]>
</description>

<author>M Ramesh et al.</author>


</item>


<item>
<title>In vivo cytotoxicity of insulin-specific CD8+ T-cells in HLA-A*0201 transgenic NOD mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1581</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1581</guid>
<pubDate>Tue, 08 May 2012 22:35:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: CD8(+) T-cells specific for islet antigens are essential for the development of type 1 diabetes in the NOD mouse model of the disease. Such T-cells can also be detected in the blood of type 1 diabetic patients, suggesting    their importance in the pathogenesis of the human disease as well. The development of peptide-based therapeutic reagents that target islet-reactive CD8(+) T-cells will require the identification of disease-relevant epitopes.  RESEARCH DESIGN AND    METHODS: We used islet-infiltrating CD8(+) T-cells from HLA-A*0201 transgenic NOD mice in an interferon-gamma enzyme-linked immunospot assay to identify autoantigenic peptides targeted during the spontaneous development of disease. We    concentrated on insulin (Ins), which is a key target of the autoimmune response in NOD mice and patients alike. RESULTS: We found that HLA-A*0201-restricted T-cells isolated from the islets of the transgenic mice were specific for Ins1 L3-11,    Ins1 B5-14, and Ins1/2 A2-10. Insulin-reactive T-cells were present in the islets of mice as young as 5 weeks of age, suggesting an important function for these specificities early in the pathogenic process.  Although there was individual    variation in peptide reactivity, Ins1 B5-14 and Ins1/2 A2-10 were the immunodominant epitopes. Notably, in vivo cytotoxicity to cells bearing these peptides was observed, further confirming them as important targets of the pathogenic process.    CONCLUSIONS: The human versions of B5-14 and A2-10, differing from the murine peptides by only a single residue, represent excellent candidates to explore as CD8(+) T-cell targets in HLA-A*0201-positive type 1 diabetic patients.</p>

	]]>
</description>

<author>I Jarchum et al.</author>


</item>


<item>
<title>Subcongenic analysis of genetic basis for impaired development of invariant NKT cells in NOD mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1580</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1580</guid>
<pubDate>Tue, 08 May 2012 22:35:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Reduced numbers and function of invariant NKT (iNKT) cells partially contribute to type 1 diabetes (T1D) development in NOD mice. Previous linkage analysis identified a genetic locus on chromosome 2 controlling numbers of thymic    iNKT cells. Interestingly, this locus resides within the Idd13 region that distinguishes NOD mice from the closely genetically related, but strongly T1D-resistant NOR strain. Thus, we tested if a genetic variant that confers T1D resistance in NOR    mice may do so by enhancing iNKT cell numbers. iNKT cells were enumerated by an alpha-GalCer analog loaded CD1d tetramer in NOD and NOR mice as well as in NOD stocks carrying NOR-derived congenic regions on chromosome 1, 2, or 4. Significantly,    more thymic and splenic iNKT cells were present in NOR than NOD mice. The NOR-derived Idd13 region on chromosome 2 contributed the most significant effect on increasing iNKT cell numbers. Subcongenic analyses indicated that at least two genes    within the Idd13 region regulate iNKT cell numbers. These results further define the genetic basis for numerical iNKT cell defects contributing to T1D development in NOD mice.</p>

	]]>
</description>

<author>Y G. Chen et al.</author>


</item>


<item>
<title>From whence will they come? - A perspective on the acute shortage of pathologists in biomedical research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1579</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1579</guid>
<pubDate>Tue, 08 May 2012 22:34:57 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>S W. Barthold et al.</author>


</item>


<item>
<title>Genetic regulation of femoral bone mineral density: complexity of sex effect in chromosome 1 revealed by congenic sublines of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1578</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1578</guid>
<pubDate>Tue, 08 May 2012 22:34:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The findings that sex-specific effects on femoral structure and peak bone mineral density (BMD) are linked to quantitative trait loci (QTL) provide evidence for the involvement of specific genes that contribute to gender variation    in skeletal phenotype. Based on previous findings that the BMD QTL in chromosome 1 (Chr 1) exerts a sex-specific effect on femoral structure, we predicted that congenic sublines of mice that carry one or more of the Chr 1 BMD loci would exhibit    gender difference in the volumetric BMD (vBMD) phenotype. To test this hypothesis, we compared skeletal parameters of male and female of five C57BL/6J (B6).CAST/EiJ (CAST)-1 congenic sublines of mice that carry overlapping CAST chromosomal    segments from the vBMD loci in Chr 1. Femur vBMD measurements were performed by the peripheral quantitative computed tomography in male and female mice at 16 weeks of age. The skeletal phenotype of the C175-185 and C178-185 congenic sublines of    mice provided evidence for the presence of the BMD1-4 locus at 178-180 Mb from the centromere. This QTL affects femur vBMD only in female mice. In contrast, CAST chromosomal region carrying BMD1-1 locus increased femur vBMD both in male and    female mice. Furthermore, a gender specific effect on BMD of femur mid-shaft region (mid-BMD) was identified at 168-176 Mb in Chr 1 (F=16.49, P=0.0002), while no significant effect was found on total femur BMD (F=2.67, P=0.11). Moreover, this    study allowed us to locate a body weight QTL at 168-172 Mb of Chr 1, the effect of this locus was altered in female mice that carry CAST chromosomal segment 168-176 Mb of Chr 1. Based on this study, we conclude that Chr 1 carries at least two    vBMD gender-dependent loci; one genetic locus at 178-180 Mb (BMD1-4 locus) which affects both mid-shaft and total femur vBMD in female mice only, and another gender-dependent locus at 168-176 Mb (BMD1-2 locus) which affects femur mid-shaft vBMD    in female but not male mice.</p>

	]]>
</description>

<author>B Edderkaoui et al.</author>


</item>


<item>
<title>Imaging axonal transport of mitochondria in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1577</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1577</guid>
<pubDate>Tue, 08 May 2012 22:34:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Neuronal mitochondria regulate synaptic physiology and cellular survival, and disruption of their function or transport causes neurological disease. We present a fluorescence method to selectively image mitochondrial dynamics in the    mouse nervous system, in both live mice and acute explants. We show that axon damage and recovery lead to early and sustained changes in anterograde and retrograde transport. In vivo imaging of mitochondria will be a useful tool to analyze this    essential organelle.</p>

	]]>
</description>

<author>T Misgeld et al.</author>


</item>


<item>
<title>Quantitative trait loci that determine mouse tibial nanoindentation properties in an F2 population derived from C57BL/6J x C3H/HeJ.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1576</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1576</guid>
<pubDate>Tue, 08 May 2012 22:34:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Use of nanoindentation technology to identify quantitative trait loci (QTL) that regulate bone properties represents a novel approach to improving our understanding of molecular mechanisms that control bone matrix properties. Tibiae    for QTL mapping were from an F2 population derived from C57BL/6J and C3H/HeJ. A nanoindenter (Triboindenter; Hysitron, Minneapolis, MN) was used to conduct indentation tests on transverse sections. Genotyping was performed in The Jackson    Laboratory. QTL mapping was conducted using software. We found that (1) tibiae from mice at 16 weeks of age were mature and suitable for measurement by a nanoindentor; (2) both stiffness modulus and hardness modulus in the F2 population appeared    to have normal distributions, which suggested that multiple genetic factors control the bone properties; and (3) QTL for hardness were identified from five chromosomes (Chr 8, 12, 13, 17, and 19) and for stiffness, from four chromosomes (Chr 3,    8, 12, and 13). Among all detected QTL, one at the same location on Chr 12 was detected for both hardness and stiffness data. It explained the highest percentage of phenotypic variation in bone properties.  Using nanoindentation technology to    identify QTL that regulate bone properties yielded as many as six different chromosomal regions. Although the actual genes remain to be identified, nanoindentation will contribute to our understanding of molecular mechanisms and normal    development processes that control the matrix properties of bone.</p>

	]]>
</description>

<author>Y Jiao et al.</author>


</item>


<item>
<title>UNC5C is required for spinal accessory motor neuron development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1575</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1575</guid>
<pubDate>Tue, 08 May 2012 22:34:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>In both invertebrates and vertebrates, UNC5 receptors facilitate chemorepulsion away from a Netrin source. Unlike most motor neurons in the embryonic vertebrate spinal cord, spinal accessory motor neuron (SACMN) cell bodies and    their axons translocate along a dorsally directed trajectory away from the floor plate/ventral midline and toward the lateral exit point (LEP). We have recently shown that Netrin-1 and DCC are required for the migration of SACMN cell bodies, in    vivo. These observations raised the possibility that vertebrate UNC5 proteins mediate the presumed repulsion of SACMN away from the Netrin-rich ventral midline. Here, we show that SACMN are likely to express UNC5A and UNC5C. Whereas SACMN    development proceeds normally in UNC5A null mice, many SACMN cell bodies fail to migrate away from the ventral midline and inappropriately cluster in the ventrolateral spinal cord of mouse embryos lacking UNC5C. These results support an important    role for UNC5C in SACMN development.</p>

	]]>
</description>

<author>A K. Dillon et al.</author>


</item>


<item>
<title>Mutations in BRAF and KRAS converge on activation of the mitogen-activated protein kinase pathway in lung cancer mouse models.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1574</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1574</guid>
<pubDate>Tue, 08 May 2012 22:34:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the BRAF and KRAS genes occur in approximately 1% to 2% and 20% to 30% of non-small-cell lung cancer patients, respectively, suggesting that the mitogen-activated protein kinase (MAPK) pathway is preferentially    activated in lung cancers. Here, we show that lung-specific expression of the BRAF V600E mutant induces the activation of extracellular signal-regulated kinase (ERK)-1/2 (MAPK) pathway and the development of lung adenocarcinoma with    bronchioloalveolar carcinoma features in vivo. Deinduction of transgene expression led to dramatic tumor regression, paralleled by dramatic dephosphorylation of ERK1/2, implying a dependency of BRAF-mutant lung tumors on the MAPK pathway.    Accordingly, in vivo pharmacologic inhibition of MAPK/ERK kinase (MEK; MAPKK) using a specific MEK inhibitor, CI-1040, induced tumor regression associated with inhibition of cell proliferation and induction of apoptosis in these de novo lung    tumors. CI-1040 treatment also led to dramatic tumor shrinkage in murine lung tumors driven by a mutant KRas allele. Thus, somatic mutations in different signaling intermediates of the same pathway induce exquisite dependency on a shared    downstream effector.  These results unveil a potential common vulnerability of BRAF and KRas mutant lung tumors that potentially affects rational deployment of MEK targeted therapies to non-small-cell lung cancer patients.</p>

	]]>
</description>

<author>H Ji et al.</author>


</item>


<item>
<title>Mapping genetic loci that regulate lipid levels in a NZB/B1NJxRF/J intercross and a combined intercross involving NZB/B1NJ, RF/J, MRL/MpJ, and SJL/J mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1573</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1573</guid>
<pubDate>Tue, 08 May 2012 22:34:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>The NZB/B1NJ (NZB) mouse strain exhibits high cholesterol and HDL levels in blood compared with several other strains of mice. To study the genetic regulation of blood lipid levels, we performed a genome-wide linkage analysis in 542    chow-fed F2 female mice from an NZBxRF/J (RF) intercross and in a combined data set that included NZBxRF and MRL/MpJxSJL/J intercrosses. In the NZBxRF F2 mice, the cholesterol and HDL concentrations were influenced by quantitative trait loci    (QTL) on chromosome (Chr) 5 [logarithm of odds (LOD) 17-19; D5Mit10] that was in the region identified earlier in crosses involving NZB mice, but two QTLs on Chr 12 (LOD 4.7; D12Mit182) and Chr 19 (LOD 5.7; D19Mit1) were specific to the NZBxRF    intercross. Triglyceride levels were affected by two novel QTLs at D12Mit182 (LOD 8.7) and D15Mit13 (LOD 3.5). The combined-cross linkage analysis (1,054 mice, 231 markers) 1) identified four shared QTLs (Chrs 5, 7, 14, and 17) that were not    detected in one of the parental crosses and 2) improved the resolution of two shared QTLs. In summary, we report additional loci regulating lipid levels in NZB mice that had not been identified earlier in crosses involving the NZB strain of mice.    The identification of shared loci from multiple crosses increases confidence toward finding the QTL gene.</p>

	]]>
</description>

<author>J E. Wergedal et al.</author>


</item>


<item>
<title>Ligand-activated peroxisome proliferator activated receptor gamma alters placental morphology and placental fatty acid uptake in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1572</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1572</guid>
<pubDate>Tue, 08 May 2012 22:33:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The nuclear receptor peroxisome proliferator activated receptor gamma (PPARgamma) is essential for murine placental development. We previously showed that activation of PPARgamma in primary human trophoblasts enhances the uptake of    fatty acids and alters the expression of several proteins associated with fatty acid trafficking. In this study we examined the effect of ligand-activated PPARgamma on placental development and transplacental fatty acid transport in wild-type    (wt) and PPARgamma(+/-) embryos. We found that exposure of pregnant mice to the PPARgamma agonist rosiglitazone for 8 d (embryonic d 10.5-18.5) reduced the weights of wt, but not PPARgamma(+/-) placentas and embryos. Exposure to rosiglitazone    reduced the thickness of the spongiotrophoblast layer and the surface area of labyrinthine vasculature, and altered expression of proteins implicated in placental development. The expression of fatty acid transport protein 1 (FATP1), FATP4,    adipose differentiation related protein, S3-12, and myocardial lipid droplet protein was enhanced in placentas of rosiglitazone-treated wt embryos, whereas the expression of FATP-2, -3, and -6 was decreased. Additionally, rosiglitazone treatment    was associated with enhanced accumulation of the fatty acid analog 15-(p-iodophenyl)-3-(R, S)-methyl pentadecanoic acid in the placenta, but not in the embryos. These results demonstrate that in vivo activation of PPARgamma modulates placental    morphology and fatty acid accumulation.</p>

	]]>
</description>

<author>W T. Schaiff et al.</author>


</item>


<item>
<title>Identification of mouse Duffy antigen receptor for chemokines (Darc) as a BMD QTL gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1571</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1571</guid>
<pubDate>Tue, 08 May 2012 22:33:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>It is now well known that bone mineral density (BMD) variance is determined by both genetic and environmental factors. Accordingly, studies in human and animal models have revealed evidence for the presence of several quantitative    trait loci (QTL) that contribute to BMD variations. However, the identification of BMD QTL genes remains a big challenge. In the current study, we focused our efforts to identify the BMD candidate gene in chromosome 1 (Chr 1) QTL that was    detected from a cross involving high BMD CAST/EiJ (CAST) and low BMD C57BL/6J (B6) mice.  To this end, we have combined several approaches including: (1) fine mapping the BMD QTL in Chr 1 of the B6.CAST F2 female mice using a large number of    polymorphic markers; (2) the generation of congenic sublines of mice by repeated backcrossing of CAST with B6 mice and phenotype characterization; (3) expression profiling genes in the QTL region; and (4) SNP analyses to identify the mouse Duffy    Antigen Receptor for Chemokines (Darc) as a candidate gene for Chr 1 BMD QTL2. We verified the involvement of the Darc protein in BMD variation by evaluating the skeletal phenotype of Darc-knockout mice and congenic sublines of mice carrying    small chromosomal segments from CAST BMD QTL. Based on the findings that Darc-antibody blocked formation of multinucleated osteoclasts in vitro and that Darc from CAST binds chemokines, known to regulate osteoclast formation, with reduced    affinity compared with Darc from B6 mice, we conclude that Darc regulates BMD negatively by increasing osteoclast formation, and that the genetic association between Darc gene polymorphism and BMD variations in humans merits    investigation.</p>

	]]>
</description>

<author>B Edderkaoui et al.</author>


</item>


<item>
<title>Complex seizure disorder caused by Brunol4 deficiency in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1570</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1570</guid>
<pubDate>Tue, 08 May 2012 22:33:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Idiopathic epilepsy is a common human disorder with a strong genetic component, usually exhibiting complex inheritance. We describe a new mouse mutation in C57BL/6J mice, called frequent-flyer (Ff), in which disruption of the gene    encoding RNA-binding protein Bruno-like 4 (Brunol4) leads to limbic and severe tonic-clonic seizures in heterozygous mutants beginning in their third month.  Younger heterozygous adults have a reduced seizure threshold. Although homozygotes do    not survive well on the C57BL/6J background, on mixed backgrounds homozygotes and some heterozygotes also display spike-wave discharges, the electroencephalographic manifestation of absence epilepsy. Brunol4 is widely expressed in the brain with    enrichment in the hippocampus. Gene expression profiling and subsequent analysis revealed the down-regulation of at least four RNA molecules encoding proteins known to be involved in neuroexcitability, particularly in mutant hippocampus. Genetic    and phenotypic assessment suggests that Brunol4 deficiency in mice results in a complex seizure phenotype, likely due to the coordinate dysregulation of several molecules, providing a unique new animal model of epilepsy that mimics the complex    genetic architecture of common disease.</p>

	]]>
</description>

<author>Y Yang et al.</author>


</item>


<item>
<title>Spontaneous mutations in the mouse Sharpin gene result in multiorgan inflammation, immune system dysregulation and dermatitis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1569</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1569</guid>
<pubDate>Tue, 08 May 2012 22:33:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Homologues of the SHARPIN (SHANK-associated RH domain-interacting protein) gene have been identified in the human, rat and mouse genomes. SHARPIN and its homologues are expressed in many tissues. SHARPIN protein forms homodimers and    associates with SHANK in the post-synaptic density of excitatory neurotransmitters in the brain. SHARPIN is hypothesized to have roles in the crosslinking of SHANK proteins and in enteric nervous system function. We demonstrate that two    independently arising spontaneous mutations in the mouse Sharpin gene, cpdm and cpdm(Dem), cause a chronic proliferative dermatitis phenotype, which is characterized histologically by severe inflammation, eosinophilic dermatitis and defects in    secondary lymphoid organ development.  These are the first examples of disease-causing mutations in the Sharpin gene and demonstrate the importance of SHARPIN protein in normal immune development and control of inflammation.</p>

	]]>
</description>

<author>R E. Seymour et al.</author>


</item>


<item>
<title>Evidence of a large-scale functional organization of Mammalian chromosomes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1568</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1568</guid>
<pubDate>Tue, 08 May 2012 22:33:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>P M. Petkov et al.</author>


</item>


<item>
<title>Genetic dissection of mouse distal chromosome 1 reveals three linked BMD QTLs with sex-dependent regulation of bone phenotypes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1567</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1567</guid>
<pubDate>Tue, 08 May 2012 22:33:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic analyses with mouse congenic strains for distal Chr1 have identified three closely linked QTLs regulating femoral vBMD, mid-diaphyseal cortical thickness, and trabecular microstructure in a sex-dependent fashion. The    homologous relationship between distal mouse Chr 1 and human 1q21-24 offers the possibility of finding common regulatory genes for cortical and trabecular bone.  INTRODUCTION: The distal third of mouse chromosome 1 (Chr 1) has been shown to carry    a major quantitative trait locus (QTL) for BMD from several inbred mouse strain crosses. Genetic and functional analyses are essential to identify genes and cellular mechanisms for acquisition of peak bone mass. MATERIALS AND METHODS: Nested    congenic sublines of mice were developed with a C57BL/6J (B6) background carrying <1- to 9-Mbp-sized segments donated from C3H/HeJ (C3H). Isolated femurs from 16-wk-old female and male mice were measured by pQCT and microCT40 for volumetric    (v)BMD, mid-diaphyseal cortical thickness, and distal trabecular phenotypes. Static and dynamic histomorphologic data were obtained on selected females and males at 16 wk. RESULTS AND CONCLUSIONS: We found that the original BMD QTL, Bmd5, mapped    to distal Chr 1 consists of three QTLs with different effects on vBMD and trabecular bone in both sexes. Compared with B6 controls, femoral vBMD, BMD, and cortical thickness (p < 0.0001) were significantly increased in congenic subline females,    but not in males, carrying C3H alleles at QTL-1. Both females and males carrying C3H alleles at QTL-1 showed marked increases in BV/TV by microCT compared with B6 mice (p < 0.0001). Females increased BV/TV by increasing trabecular thickness,    whereas males increased trabecular number. In addition, the microCT40 data showed two unique QTLs for male trabecular bone, QTL-2 and QTL-3, which may interact to regulate trabecular thickness and number. These QTLs are closely linked with and    proximal to QTL-1.  The histomorphometric data revealed sex-specific differences in cellular and bone formation parameters. Mice and humans share genetic homology between distal mouse Chr 1 and human Chr 1q20-24 that is associated with adult    human skeletal regulation. Sex- and compartment-specific regulatory QTLs in the mouse suggest the need to partition human data by sex to improve accuracy of mapping and genetic loci identification.</p>

	]]>
</description>

<author>W G. Beamer et al.</author>


</item>


<item>
<title>Congenital hypothyroidism, dwarfism, and hearing impairment caused by a missense mutation in the mouse dual oxidase 2 gene, Duox2.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1566</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1566</guid>
<pubDate>Tue, 08 May 2012 22:33:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dual oxidases generate the hydrogen peroxide needed by thyroid peroxidase for the incorporation of iodine into thyroglobulin, an essential step in thyroid hormone synthesis. Mutations in the human dual oxidase 2 gene, DUOX2, have    been shown to underlie several cases of congenital hypothyroidism. We report here the first mouse Duox2 mutation, which provides a new genetic model for studying the specific function of DUOX2 in the thyroid gland and in other organ systems where    it is hypothesized to play a role. We mapped the new spontaneous mouse mutation to chromosome 2 and identified it as a T>G base pair change in exon 16 of Duox2.  The mutation changes a highly conserved valine to glycine at amino acid position 674    (V674G) and was named "thyroid dyshormonogenesis" (symbol thyd) to signify a defect in thyroid hormone synthesis. Thyroid glands of mutant mice are goitrous and contain few normal follicles, and anterior pituitaries are dysplastic. Serum T(4) in    homozygotes is about one-tenth the level of controls and is accompanied by a more than 100-fold increase in TSH. The weight of adult mutant mice is approximately half that of littermate controls, and serum IGF-I is reduced. The cochleae of mutant    mice exhibit abnormalities characteristic of hypothyroidism, including a delayed formation of the inner sulcus and tunnel of Corti and an abnormally thickened tectorial membrane. Hearing thresholds of adult mutant mice are on average 50-60    decibels (dB) above those of controls.</p>

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</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title>R/qtlDesign: inbred line cross experimental design.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1565</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1565</guid>
<pubDate>Tue, 08 May 2012 22:32:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>An investigator planning a QTL (quantitative trait locus) experiment has to choose which strains to cross, the type of cross, genotyping strategies, and the number of progeny to raise and phenotype. To help make such choices, we    have developed an interactive program for power and sample size calculations for QTL experiments, R/qtlDesign. Our software includes support for selective genotyping strategies, variable marker spacing, and tools to optimize information content    subject to cost constraints for backcross, intercross, and recombinant inbred lines from two parental strains. We review the impact of experimental design choices on the variance attributable to a segregating locus, the residual error variance,    and the effective sample size. We give examples of software usage in real-life settings. The software is available at http://www.biostat.ucsf.edu/sen/software.html .</p>

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</description>

<author>S Sen et al.</author>


</item>


<item>
<title>Low-level accelerations applied in the absence of weight bearing can enhance trabecular bone formation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1564</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1564</guid>
<pubDate>Tue, 08 May 2012 22:32:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>High-frequency whole body vibrations can be osteogenic, but their efficacy appears limited to skeletal segments that are weight bearing and thus subject to the induced load. To determine the anabolic component of this signal, we    investigated whether low-level oscillatory displacements, in the absence of weight bearing, are anabolic to skeletal tissue. A loading apparatus, developed to shake specific segments of the murine skeleton without the direct application of    deformations to the tissue, was used to subject the left tibia of eight anesthesized adult female C57BL/6J mice to small (0.3 g or 0.6 g) 45 Hz sinusoidal accelerations for 10 min/day, while the right tibia served as an internal control. Video    and strain analysis revealed that motions of the apparatus and tibia were well coupled, inducing dynamic cortical deformations of less than three microstrain. After 3 weeks, trabecular metaphyseal bone formation rates and the percentage of    mineralizing surfaces (MS/BS) were 88% and 64% greater (p < 0.05) in tibiae accelerated at 0.3 g than in their contralateral controls. At 0.6 g, bone formation rates and mineral apposition rates were 66% and 22% greater (p < 0.05) in accelerated    tibiae. Changes in bone morphology were evident only in the epiphysis, where stimulated tibiae displayed significantly greater cortical area (+8%) and thickness (+8%). These results suggest that tiny acceleratory motions--independent of direct    loading of the matrix--can influence bone formation and bone morphology. If confirmed by clinical studies, the unique nature of the signal may ultimately facilitate the stimulation of skeletal regions that are prone to osteoporosis even in    patients that are suffering from confinement to wheelchairs, bed rest, or space travel.</p>

	]]>
</description>

<author>R Garman et al.</author>


</item>


<item>
<title>A spatially and temporally restricted mouse model of soft tissue sarcoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1563</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1563</guid>
<pubDate>Tue, 08 May 2012 22:32:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Soft tissue sarcomas are mesenchymal tumors that are fatal in approximately one-third of patients. To explore mechanisms of sarcoma pathogenesis, we have generated a mouse model of soft tissue sarcoma. Intramuscular delivery of an    adenovirus expressing Cre recombinase in mice with conditional mutations in Kras and Trp53 was sufficient to initiate high-grade sarcomas with myofibroblastic differentiation. Like human sarcomas, these tumors show a predilection for lung rather    than lymph node metastasis. Using this model, we showed that a prototype handheld imaging device can identify residual tumor during intraoperative molecular imaging. Deletion of the Ink4a-Arf locus (Cdkn2a), but not Bak1 and Bax, could substitute    for mutation of Trp53 in this model. Deletion of Bak1 and Bax, however, was able to substitute for mutation of Trp53 in the development of sinonasal adenocarcinoma. Therefore, the intrinsic pathway of apoptosis seems sufficient to mediate p53    tumor suppression in an epithelial cancer, but not in this model of soft tissue sarcoma.</p>

	]]>
</description>

<author>D G. Kirsch et al.</author>


</item>


<item>
<title>LKB1 modulates lung cancer differentiation and metastasis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1562</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1562</guid>
<pubDate>Tue, 08 May 2012 22:32:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Germline mutation in serine/threonine kinase 11 (STK11, also called LKB1) results in Peutz-Jeghers syndrome, characterized by intestinal hamartomas and increased incidence of epithelial cancers. Although uncommon in most sporadic    cancers, inactivating somatic mutations of LKB1 have been reported in primary human lung adenocarcinomas and derivative cell lines. Here we used a somatically activatable mutant Kras-driven model of mouse lung cancer to compare the role of Lkb1    to other tumour suppressors in lung cancer. Although Kras mutation cooperated with loss of p53 or Ink4a/Arf (also known as Cdkn2a) in this system, the strongest cooperation was seen with homozygous inactivation of Lkb1. Lkb1-deficient tumours    demonstrated shorter latency, an expanded histological spectrum (adeno-, squamous and large-cell carcinoma) and more frequent metastasis compared to tumours lacking p53 or Ink4a/Arf. Pulmonary tumorigenesis was also accelerated by hemizygous    inactivation of Lkb1. Consistent with these findings, inactivation of LKB1 was found in 34% and 19% of 144 analysed human lung adenocarcinomas and squamous cell carcinomas, respectively. Expression profiling in human lung cancer cell lines and    mouse lung tumours identified a variety of metastasis-promoting genes, such as NEDD9, VEGFC and CD24, as targets of LKB1 repression in lung cancer. These studies establish LKB1 as a critical barrier to pulmonary tumorigenesis, controlling    initiation, differentiation and metastasis.</p>

	]]>
</description>

<author>H Ji et al.</author>


</item>


<item>
<title>A sequence-based variation map of 8.27 million SNPs in inbred mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1561</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1561</guid>
<pubDate>Tue, 08 May 2012 22:32:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>A dense map of genetic variation in the laboratory mouse genome will provide insights into the evolutionary history of the species and lead to an improved understanding of the relationship between inter-strain genotypic and    phenotypic differences. Here we resequence the genomes of four wild-derived and eleven classical strains. We identify 8.27 million high-quality single nucleotide polymorphisms (SNPs) densely distributed across the genome, and determine the    locations of the high (divergent subspecies ancestry) and low (common subspecies ancestry) SNP-rate intervals for every pairwise combination of classical strains.  Using these data, we generate a genome-wide haplotype map containing 40,898    segments, each with an average of three distinct ancestral haplotypes. For the haplotypes in the classical strains that are unequivocally assigned ancestry, the genetic contributions of the Mus musculus subspecies--M. m. domesticus, M. m.    musculus, M. m. castaneus and the hybrid M. m. molossinus--are 68%, 6%, 3% and 10%, respectively; the remaining 13% of haplotypes are of unknown ancestral origin. The considerable regional redundancy of the SNP data will facilitate imputation of    the majority of these genotypes in less-densely typed classical inbred strains to provide a complete view of variation in additional strains.</p>

	]]>
</description>

<author>K A. Frazer et al.</author>


</item>


<item>
<title>Protein 4.1B suppresses prostate cancer progression and metastasis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1560</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1560</guid>
<pubDate>Tue, 08 May 2012 22:32:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Protein 4.1B is a 4.1/ezrin/radixin/moesin domain-containing protein whose expression is frequently lost in a variety of human tumors, including meningiomas, non-small-cell lung cancers, and breast carcinomas. However, its potential    tumor-suppressive function under in vivo conditions remains to be validated. In a screen for genes involved with prostate cancer metastasis, we found that 4.1B expression is reduced in highly metastatic tumors.  Down-regulation of 4.1B increased    the metastatic propensity of poorly metastatic cells in an orthotopic model of prostate cancer. Furthermore, 4.1B-deficient mice displayed increased susceptibility for developing aggressive, spontaneous prostate carcinomas. In both cases,    enhanced tumor malignancy was associated with reduced apoptosis. Because expression of Protein 4.1B is frequently down-regulated in human clinical prostate cancer, as well as in a spectrum of other tumor types, these results suggest a more    general role for Protein 4.1B as a negative regulator of cancer progression to metastatic disease.</p>

	]]>
</description>

<author>S Y. Wong et al.</author>


</item>


<item>
<title>The archetypal R90C CADASIL-NOTCH3 mutation retains NOTCH3 function in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1559</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1559</guid>
<pubDate>Tue, 08 May 2012 22:32:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cerebral Autosomal Dominant Arteriopathy with Subcortical infarcts and Leukoencephalopathy (CADASIL) is the most prominent known cause of inherited stroke and vascular dementia in human adult. The disease gene, NOTCH3, encodes a    transmembrane receptor primarily expressed in arterial smooth muscle cells (SMC).  Pathogenic mutations lead to an odd number of cysteine residues within the NOTCH3 extracellular domain (NOTCH3(ECD)), and are associated with progressive    accumulation of NOTCH3(ECD) at the SMC plasma membrane. The murine homolog, Notch3, is dispensable for viability but required post-natally for the elaboration and maintenance of arteries. How CADASIL-associated mutations impact NOTCH3 function    remains a fundamental, yet unresolved issue. Particularly, whether NOTCH3(ECD) accumulation may titrate the ligand and inhibit the normal pathway is unknown. Herein, using genetic analyses in the mouse, we assessed the functional significance of    an archetypal CADASIL-associated mutation (R90C), in vivo, in brain arteries. We show that transgenic mouse lines expressing either the wild-type human NOTCH3 or the mutant R90C human NOTCH3, at comparable and physiological levels, can rescue the    arterial defects of Notch3-/- mice to similar degrees. In vivo assessment of NOTCH3/RBP-Jk activity provides evidence that the mutant NOTCH3 protein exhibits normal level of activity in brain arteries. Remarkably, the mutant NOTCH3 protein    remains functional and does not exhibit dominant negative interfering activity, even when NOTCH3(ECD) accumulates. Collectively, these data suggest a model that invokes novel pathogenic roles for the mutant NOTCH3 protein rather than compromised    NOTCH3 function as the primary determinant of the CADASIL arteriopathy.</p>

	]]>
</description>

<author>M Monet et al.</author>


</item>


<item>
<title>E2f4 is required for normal development of the airway epithelium.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1558</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1558</guid>
<pubDate>Tue, 08 May 2012 22:31:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The airway epithelium is comprised of specialized cell types that play key roles in protecting the lungs from environmental insults. The cellular composition of the murine respiratory epithelium is established during development and    different cell types populate specific regions along the airway. Here we show that E2f4-deficiency leads to an absence of ciliated cells from the entire airway epithelium and the epithelium of the submucosal glands in the paranasal sinuses.  This    defect is particularly striking in the nasal epithelium of E2f4-/- mice where ciliated cells are replaced by columnar secretory cells that produce mucin-like substances. In addition, in the proximal lung, E2f4 loss causes a reduction in Clara    cell marker expression indicating that Clara cell development is also affected. These defects arise during embryogenesis and, in the nasal epithelium, appear to be independent of any changes in cell proliferation, the principal process regulated    by members of the E2f family of transcription factors. We therefore conclude that E2f4 is required to determine the appropriate development of the airway epithelium. Importantly, the combination of no ciliated cells and excess mucous cells can    account for the chronic rhinitis and increased susceptibility to opportunistic infections that causes the postnatal lethality of E2f4 mutant mice.</p>

	]]>
</description>

<author>P S. Danielian et al.</author>


</item>


<item>
<title>Oocytes determine cumulus cell lineage in mouse ovarian follicles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1557</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1557</guid>
<pubDate>Tue, 08 May 2012 22:31:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>The two principal functions of ovarian follicles are developmental and endocrine.  The cumulus cells surrounding the oocyte are specialized to serve the development of the oocyte and steroidogenesis is a principal role of mural    granulosa cells that line the follicle wall. The findings in this report demonstrate that oocytectomy or treatment with an inhibitor of SMAD2/3 activation results in decreased cumulus marker mRNA transcript levels and allows FSH to induce mural    marker transcripts in cumulus cells. In addition, SMAD2/3 signaling is involved in enabling cumulus expansion and EGF-induced increases in Ptx3, Ptgs2 and Has2 mRNA levels. By contrast, follicle-stimulating hormone (FSH) stimulated expression of    mural transcripts, but suppressed levels of cumulus transcripts.  Thus, FSH and oocyte-stimulated SMAD2/3 signaling establish opposing gradients of influence in the follicle. These specify the mural and cumulus granulosa cell phenotypes that are    pivotal for appropriate endocrine function and oocyte development.</p>

	]]>
</description>

<author>F J. Diaz et al.</author>


</item>


<item>
<title>Distal renal tubular acidosis in mice lacking the AE1 (band3) Cl-/HCO3- exchanger (slc4a1).</title>
<link>http://mouseion.jax.org/stfb2000_2009/1556</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1556</guid>
<pubDate>Tue, 08 May 2012 22:31:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the human gene that encodes the AE1 Cl(-)/HCO(3)(-) exchanger (SLC4A1) cause autosomal recessive and dominant forms of distal renal tubular acidosis (dRTA). A mouse model that lacks AE1/slc4a1 (slc4a1-/-) exhibited dRTA    characterized by spontaneous hyperchloremic metabolic acidosis with low net acid excretion and, inappropriately, alkaline urine without bicarbonaturia.  Basolateral Cl(-)/HCO(3)(-) exchange activity in acid-secretory intercalated cells of    isolated superfused slc4a1-/- medullary collecting duct was reduced, but alternate bicarbonate transport pathways were upregulated. Homozygous mice had nephrocalcinosis associated with hypercalciuria, hyperphosphaturia, and hypocitraturia. A    severe urinary concentration defect in slc4a1-/- mice was accompanied by dysregulated expression and localization of the aquaporin-2 water channel. Mice that were heterozygous for the AE1-deficient allele had no apparent defect. Thus, the    slc4a1-/- mouse is the first genetic model of complete dRTA and demonstrates that the AE1/slc4a1 Cl(-)/HCO(3)(-) exchanger is required for maintenance of normal acid-base homeostasis by distal renal regeneration of bicarbonate in the mouse as    well as in humans.</p>

	]]>
</description>

<author>P A. Stehberger et al.</author>


</item>


<item>
<title>Complete genomic characterization of a murine papillomavirus isolated from papillomatous lesions of a European harvest mouse (Micromys minutus).</title>
<link>http://mouseion.jax.org/stfb2000_2009/1555</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1555</guid>
<pubDate>Tue, 08 May 2012 22:31:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>The papillomaviruses form a large group of species-specific pathogens that cause epithelial proliferations in a wide spectrum of animal hosts. Previous reports demonstrated a relatively high frequency of a variety of skin lesions in    captive European harvest mice. The Micromys minutus papillomavirus (MmPV) was isolated from one of these lesions found on a captive European harvest mouse in a regional zoo in Chicago. In this study we present the entire genomic sequence of MmPV.    The MmPV genome is organized into the seven classical papillomaviral open reading frames. Phylogenetic analysis places MmPV together with a papillomavirus (PV) isolated from a Syrian golden Hamster (HaOPV) in the genus Pipapillomavirus. The    similar clustering pattern of the MmPV-HaOPV pair and their rodent hosts support the hypothesis of papillomaviral and host co-phylogenetic descent. The availability of the complete genomic sequence of a mouse PV should allow researchers to use    MmPV as a model for PV carcinogenesis.</p>

	]]>
</description>

<author>Doorslaer K. Van et al.</author>


</item>


<item>
<title>Characterization of the IGF system in 15 patients with Alstrom syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1554</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1554</guid>
<pubDate>Tue, 08 May 2012 22:31:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Alstrom syndrome (ALMS) is a rare recessively inherited progressive disease (OMIM 203800). Among its diverse spectrum of clinical features are phenotypes associated with deficiencies of the GH/IGF-I axis, including short    stature, obesity, insulin resistance, hypertriglyceridaemia and heart failure.  PATIENTS AND MEASUREMENTS: To characterize the IGF system in ALMS, we evaluated a subset of 15 young adults with ALMS for hepatic, renal and thyroid function.     Glycaemic and hormone measurements such as insulin, GH, FSH, LH, testosterone and 17-beta-oestradiol were clinically assessed. In addition, we measured IGF-I, IGF-II, IGF binding-protein-3 (IGFBP-3) and acid labile subunit (ALS - the subunits    that constitute the main somatomedin complex in the circulation), and IGFBP-1 and IGFBP-2 (known to influence the bioavailability of the IGFs).  RESULTS: A significantly lower height was observed in ALMS patients compared to age-matched controls.    ALMS patients were clinically obese (by weight and body mass index (BMI) standards) and leptin levels correlated with BMI. Renal and hepatic dysfunction was implicated in some patients by increased values of blood urea nitrogen (BUN) and    creatinine, and transaminases, respectively. One-third of the patients presented with fasting hyperglycaemia and 80% were hyperinsulinaemic. TSH was slightly increased in 20% of patients. Baseline FSH and LH in females were within the normal    range, while half of the males had abnormally low testosterone values. Male patients with hypogonadism showed significantly lower testosterone, oestrogen and ALS levels. Baseline GH values were not found to be increased. ALS and IGFBP-1 were    significantly reduced and IGFBP-2 was markedly increased in ALMS patients compared to age-matched controls.  The IGFs and IGFBPs were not significantly different between males and females affected with ALMS. No significant association was    observed between IGFs or IGFBPs levels and weight, height, BMI, glycaemia, hyperinsulinaemia and testosterone levels. However, we found a significant association of gamma-glutamyltransferase (GGT) with IGFBP-2. IGF-I levels were significantly    associated with LH in female patients. CONCLUSIONS: In summary, the reduction of ALS and the increase of IGFBP-2 points to a growth hormone deficiency (GHD) condition in ALMS. However, further tests, including GH dynamics, are needed to determine    whether, or to what degree disturbances in the GH/IGF axis contribute to the relatively short stature.</p>

	]]>
</description>

<author>P Maffei et al.</author>


</item>


<item>
<title>Euthanasia</title>
<link>http://mouseion.jax.org/stfb2000_2009/1553</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1553</guid>
<pubDate>Tue, 08 May 2012 22:31:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>P J. Danneman</author>


</item>


<item>
<title>Genome plasticity in the mouse oocyte and early embryo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1552</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1552</guid>
<pubDate>Tue, 08 May 2012 22:31:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>In dissecting the molecules and molecular mechanisms that control mammalian oocyte-to-embryo transition, we found abundant transcripts representing developmentally regulated ERVs (endogenous retroviruses) in mouse oocyte and    two-cell stage embryo cDNA libraries. These retrotransposons can act as alternative promoters and first exons for diverse genes, synchronizing their expression. Heritable genetic change due to replication of these retrotransposons probably occurs    specifically in oocytes and early embryos. ERVs are usually epigenetically silenced, through DNA methylation and chromatin-based mechanisms.  Their activation and silencing indicates a change in the epigenetic state of the genome. The thousands    of endogenous retro-elements in the mouse genome provides potential scope for large-scale co-ordinated epigenetic fluctuations and leads to the hypothesis that differential transposable element expression triggers sequential reprogramming of the    embryonic genome during the oocyte-to-embryo transition.</p>

	]]>
</description>

<author>A E. Peaston et al.</author>


</item>


<item>
<title>Different mechanisms control peripheral and central tolerance in hematopoietic chimeric mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1551</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1551</guid>
<pubDate>Tue, 08 May 2012 22:30:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Regulatory T cells (Treg) are important in peripheral tolerance, but their role in establishing and maintaining hematopoietic mixed chimerism and generating central tolerance is unclear. We now show that costimulation blockade using    a donor-specific transfusion and anti-CD154 antibody applied to mice given bone marrow and simultaneously transplanted with skin allografts leads to hematopoietic chimerism and permanent skin allograft survival. Chimeric mice bearing intact skin    allografts fail to generate effector/memory T cells against allogeneic targets as shown by the absence of IFNgamma-producing CD44(high)CD8+ T cells and in vivo cytotoxicity. Depletion of Tregs by injection of anti-CD4 or anti-CD25 antibody prior    to costimulation blockade prevents chimerism, shortens skin allograft survival and leads to generation of effector/memory cytotoxic T cells. Depletion of Tregs by injection of anti-CD4 or anti-CD25 antibody two months after transplantation leads    to loss of skin allografts even though mice remain chimeric and exhibit little in vivo cytotoxicity. In contrast, chimerism is lost, but skin allografts survive following naive T-cell injection. We conclude that hematopoietic chimerism and    peripheral tolerance may be maintained by different mechanisms in mixed hematopoietic chimeras.</p>

	]]>
</description>

<author>M Yamazaki et al.</author>


</item>


<item>
<title>Disruption of glomerular basement membrane charge through podocyte-specific mutation of agrin does not alter glomerular permselectivity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1550</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1550</guid>
<pubDate>Tue, 08 May 2012 22:30:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Glomerular charge selectivity has been attributed to anionic heparan sulfate proteoglycans (HSPGs) in the glomerular basement membrane (GBM). Agrin is the predominant GBM-HSPG, but evidence that it contributes to the charge barrier    is lacking, because newborn agrin-deficient mice die from neuromuscular defects. To study agrin in adult kidney, a new conditional allele was used to generate podocyte-specific knockouts. Mutants were viable and displayed no renal histopathology    up to 9 months of age. Perlecan, a HSPG normally confined to the mesangium in mature glomeruli, did not appear in the mutant GBM, which lacked heparan sulfate. Moreover, GBM agrin was found to be derived primarily from podocytes.    Polyethyleneimine labeling of fetal kidneys revealed anionic sites along both laminae rarae of the GBM that became most prominent along the subepithelial aspect at maturity; labeling was greatly reduced along the subepithelial aspect in    agrin-deficient and conditional knockout mice. Despite this severe charge disruption, the glomerular filtration barrier was not compromised, even when challenged with bovine serum albumin overload. We conclude that agrin is not required for    establishment or maintenance of GBM architecture.  Although agrin contributes significantly to the anionic charge to the GBM, both it and its charge are not needed for glomerular permselectivity. This calls into question whether charge    selectivity is a feature of the GBM.</p>

	]]>
</description>

<author>S J. Harvey et al.</author>


</item>


<item>
<title>Hepatic ABCG5/G8 overexpression reduces apoB-lipoproteins and atherosclerosis when cholesterol absorption is inhibited.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1549</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1549</guid>
<pubDate>Tue, 08 May 2012 22:30:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>We previously reported that liver-specific overexpression of ABCG5/G8 in mice is not atheroprotective, suggesting that increased biliary cholesterol secretion must be coupled with decreased intestinal cholesterol absorption to    increase net sterol loss from the body and reduce atherosclerosis. To evaluate this hypothesis, we fed low density lipoprotein receptor-knockout (LDLr-KO) control and ABCG5/G8-transgenic (ABCG5/G8-Tg)xLDLr-KO mice, which overexpress ABCG5/G8 only    in liver, a Western diet containing ezetimibe to reduce intestinal cholesterol absorption. On this dietary regimen, liver-specific ABCG5/G8 overexpression increased hepatobiliary cholesterol concentration and secretion rates (1.5-fold and    1.9-fold, respectively), resulting in 1.6-fold increased fecal cholesterol excretion, decreased hepatic cholesterol, and increased (4.4-fold) de novo hepatic cholesterol synthesis versus LDLr-KO mice. Plasma lipids decreased (total cholesterol,    32%; cholesteryl ester, 32%; free cholesterol, 30%), mostly as a result of reduced non-high density lipoprotein-cholesterol and apolipoprotein B (apoB; 36% and 25%, respectively).  ApoB-containing lipoproteins were smaller and lipid-depleted in    ABCG5/G8-TgxLDLr-KO mice. Kinetic studies revealed similar 125I-apoB intermediate density lipoprotein/LDL fractional catabolic rates, but apoB production rates were decreased 37% in ABCG5/G8-TgxLDLr-KO mice. Proximal aortic atherosclerosis    decreased by 52% (male) and 59% (female) in ABCG5/G8-TgxLDLr-KO versus LDLr-KO mice fed the Western/ezetimibe diet. Thus, increased biliary secretion, resulting from hepatic ABCG5/G8 overexpression, reduces atherogenic risk in LDLr-KO mice fed a    Western diet containing ezetimibe. These findings identify distinct roles for liver and intestinal ABCG5/G8 in modulating sterol metabolism and atherosclerosis.</p>

	]]>
</description>

<author>F Basso et al.</author>


</item>


<item>
<title>Characterization of HKE2: an ancient antigen encoded in the major histocompatibility complex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1548</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1548</guid>
<pubDate>Tue, 08 May 2012 22:30:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genes at the centromeric end of the human leukocyte antigen region influence adaptive autoimmune diseases and cancer. In this study, we characterized protein expression of HKE2, a gene located in the centromeric portion of the class    II region of the major histocompatibility complex encoding subunit 6 of prefoldin.  Immunohistochemical analysis using an anti-HKE2 antibody indicated that HKE2 protein expression is dramatically upregulated as a consequence of activation. In a    tissue microarray and in several tumors, HKE2 was overexpressed in certain cancers compared with normal counterparts. The localization of the HKE2 gene to the class II region, its cytoplasmic expression and putative protein-binding domain suggest    that HKE2 may function in adaptive immunity and cancer.</p>

	]]>
</description>

<author>D A. Ostrov et al.</author>


</item>


<item>
<title>Two mouse retinal degenerations caused by missense mutations in the beta-subunit of rod cGMP phosphodiesterase gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1547</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1547</guid>
<pubDate>Tue, 08 May 2012 22:30:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>We report the chromosomal localization, mutant gene identification, ophthalmic appearance, histology, and functional analysis of two new hereditary mouse models of retinal degeneration not having the Pde6brd1("r", "rd", or    "rodless") mutation. One strain harbors an autosomal recessive mutation that maps to mouse chromosome 5. Sequence analysis showed that the retinal degeneration is caused by a missense point mutation in exon 13 of the beta-subunit of the rod cGMP    phosphodiesterase (beta-PDE) gene (Pde6b). The gene symbol for this strain was set as Pde6brd10, abbreviated rd10 hereafter. Mice homozygous for the rd10 mutation showed histological changes at postnatal day 16 (P16) of age and sclerotic retinal    vessels at four weeks of age, consistent with retinal degeneration. Retinal sections were highly positive for TUNEL and activated caspase-3 immunoreactivity, specifically in the outer nuclear layer (ONL). ERGs were never normal, but rod and cone    ERG a- and b-waves were easily measured at P18 and steadily declined over 90% by two months of age. Protein extracts from rd10 retinas were positive for beta-PDE immunoreactivity starting at about the same time as wild-type (P10), though signal    averaged less than 40% of wild-type.  Interestingly, rearing rd10 mice in total darkness delayed degeneration for at least a week, after which morphological and functional loss progressed irregularly. With the second strain, a complementation    test with rd1 mice revealed that the retinal degeneration phenotype observed represents a possible new allele of Pde6b. Sequencing demonstrated a missense point mutation in exon 16 of the beta-subunit of rod phosphodiesterase gene, different from    the point mutations in rd1 and rd10. The gene symbol for this strain was set as Pde6bnmf137, abbreviated nmf137 hereafter. Mice homozygous for this mutation showed retinal degeneration with a mottled retina and white retinal vessels at three    weeks of age. The exon 13 missense mutation (rd10) is the first known occurrence of a second mutant allele spontaneously arising in the Pde6b gene in mice and may provide a model for studying the pathogenesis of autosomal recessive retinitis    pigmentosa (arRP) in humans. It may also provide a better model for experimental pharmaceutical-based therapy for RP because of its later onset and milder retinal degeneration than rd1 and nmf137.</p>

	]]>
</description>

<author>B Chang et al.</author>


</item>


<item>
<title>Ontology development for biological systems: immunology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1546</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1546</guid>
<pubDate>Tue, 08 May 2012 22:30:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>We recently implemented improvements to the representation of immunology content of the biological process branch of the Gene Ontology (GO). The aims of the revision were to provide a comprehensive representation of immunological    processes and to improve the organization of immunology related terms in the GO to match current concepts in the field of immunology. With these improvements, the GO will better reflect current understanding in the field of immunology and thus    prove to be a more valuable resource for knowledge representation in gene annotation and analysis in the areas of immunology related to genomics and bioinformatics. AVAILABILITY: http://www.geneontology.org.</p>

	]]>
</description>

<author>A D. Diehl et al.</author>


</item>


<item>
<title>Editing of the serotonin 2C receptor pre-mRNA: Effects of the Morris Water Maze.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1545</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1545</guid>
<pubDate>Tue, 08 May 2012 22:29:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The pre-mRNA encoding the serotonin 2C receptor, HTR2C (official mouse gene symbol, Htr2c), is subject to adenosine deamination that produces inosine at five sites within the coding region. Combinations of this site-specific A-to-I    editing can produce 32 different mRNA sequences encoding 24 different protein isoforms with differing biochemical and pharmacological properties. Studies in humans have reported abnormalities in patterns of HTR2C editing in psychiatric disorders,    and studies in rodents show altered patterns of editing in response to drug treatments and stressful situations. To further explore the biological significance of editing of the Htr2c mRNA and its regulation, we have examined patterns of Htr2c    editing in C57BL/6J mice after exposure to the hidden platform version of the Morris Water Maze, a test of spatial learning that, in mice, is also associated with stress. In brains of both swimming controls and mice trained to find the platform,    subtle time dependent changes in editing patterns are seen as soon as 1 h after a probe trial and typically last less than 24 h. Changes in whole brain with cerebellum removed differ from those seen in isolated hippocampus and cortex.    Unexpectedly, in hippocampi from subsets of mice, abnormally low levels of editing were seen that were not correlated with behavior or with editing levels in cortex. These data implicate responses to spatial learning and stress, in addition to    stochastic processes, in the generation of subtle changes in editing patterns of Htr2c.</p>

	]]>
</description>

<author>Y Du et al.</author>


</item>


<item>
<title>Humanized NOD/LtSz-scid IL2 receptor common gamma chain knockout mice in diabetes research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1544</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1544</guid>
<pubDate>Tue, 08 May 2012 22:29:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>There are many rodent models of autoimmune diabetes that have been used to study the pathogenesis of human type 1 diabetes (T1D), including the non-obese diabetic (NOD) mouse, the biobreeding (BB) rat, and the transgenic mouse    models. However, mice and rats are not humans, and these rodent models do not completely recapitulate the autoimmune pathogenesis of the human disease. In addition, many of the reagents, tools, and therapeutics proposed for use in humans may be    species specific and cannot be investigated in rodents. Researchers have used nonhuman primates to more closely mimic the human immune system and, to study species-specific therapeutics, but these studies are associated with additional ethical    and economic constraints and, to date, no model of autoimmune diabetes in this species has been described. New animal models are needed that will permit the in vivo investigation of human immune systems and analyses of the pathogenesis of human    T1D without putting individuals at risk. To fill this need, we are developing humanized mouse models for the in vivo study of T1D. These models are based on our newly generated stock of NOD-scid IL2rgamma(null) mice, which engraft at higher    levels with human hematolymphoid cells and exhibit enhanced function of the engrafted human immune systems compared with previous humanized mouse models. Overall, development of these new generations of humanized mice should facilitate in vivo    studies of the human immune system as well as permit the investigation of the pathogenesis and effector phases of human T1D.</p>

	]]>
</description>

<author>L D. Shultz et al.</author>


</item>


<item>
<title>&quot;Humanized&quot; HLA transgenic NOD mice to identify pancreatic beta cell autoantigens of potential clinical relevance to type 1 diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1543</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1543</guid>
<pubDate>Tue, 08 May 2012 22:29:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mechanistic basis by which the H2(g7) major histocompatibility complex (MHC) provides the primary risk factor for the development of T cell-mediated autoimmune type 1 diabetes (T1D) in non-obese diabetic (NOD) mice involves    contributions not only from the unusual A(g7) class II molecule, but also from the more common K(d) and/or D(b) class I variants it encodes. Similarly, transgenic studies in NOD mice have confirmed the possibility first suggested in association    studies that in the proper genetic context the common human HLA-A2.1 class I variant can mediate diabetogenic CD8 T cell responses. T1D continues to develop in a further refined NOD stock that expresses human HLA-A2.1, but no murine class I    molecules (designated NOD.beta2m-.HHD). Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) is an important antigenic target of diabetogenic CD8 cells in standard NOD mice. Three IGRP-derived peptides have also been    identified that are presented by human HLA-A2.1 molecules to diabetogenic CD8 T cells in NOD.beta2m-.HHD mice. At least one of these IGRP peptides (265-273) can also be the target of autoreactive CD8 T cells in HLA-A2.1-expressing human T1D    patients. Studies are currently under way to determine whether HLA-A2.1-restricted IGRP peptides can be used in a tolerance-inducing protocol that inhibits T1D development in NOD. beta2m-.HHD mice. If so, this knowledge could ultimately lead to    the development of a similar T1D prevention protocol in humans.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title>Development of new-generation HU-PBMC-NOD/SCID mice to study human islet alloreactivity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1542</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1542</guid>
<pubDate>Tue, 08 May 2012 22:29:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The use of "humanized" mice represents an appealing translational model for studies of the pathogenesis of immune-mediated diseases and for the evaluation of potential therapeutics. The utility of humanized mice depends on their    ability to model the human immune system with high fidelity, and, in this respect, previous models have fallen short. The recently developed NOD-scid Il2rgamma(null) mouse, however, exhibits greatly enhanced ability to support the engraftment of    human peripheral blood mononuclear cells. Herein, we describe the challenges of recapitulating human immunity in humanized mice and features of NOD-scid Il2rgamma(null) mice that help overcome them.</p>

	]]>
</description>

<author>M King et al.</author>


</item>


<item>
<title>Human clonal CD8 autoreactivity to an IGRP islet epitope shared between mice and men.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1541</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1541</guid>
<pubDate>Tue, 08 May 2012 22:29:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Type 1 diabetes (T1D) is a multifactorial disease characterized by the infiltration and subsequent destruction of the pancreatic insulin-producing beta cells by autoreactive T cells. CD8(+) T cells play an essential role in this    beta cell destruction. However, little is known about the target antigens of CD8(+) T cells in human T1D patients. The aim of this study was to assess whether an epitope derived from the islet-specific glucose-6-phosphatase catalytic    subunit-related protein (IGRP), IGRP(265-273,) which has recently been identified as a target in non-obese diabetic (NOD) mice and is fully homologous to the human epitope, is a target of human diabetogenic CD8(+) T cells. We isolated a human CD8    T cell clone against this epitope, which confirms that this IGRP epitope is shared across species.</p>

	]]>
</description>

<author>W W. Unger et al.</author>


</item>


<item>
<title>Elimination of antigen-presenting cells and autoreactive T cells by Fas contributes to prevention of autoimmunity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1540</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1540</guid>
<pubDate>Tue, 08 May 2012 22:29:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fas (also known as Apo-1 and CD95) receptor has been suggested to control T cell expansion by triggering T cell-autonomous apoptosis. This paradigm is based on the extensive lymphoproliferation and systemic autoimmunity in mice and    humans lacking Fas or its ligand. However, with systemic loss of Fas, it is unclear whether T cell-extrinsic mechanisms contribute to autoimmunity. We found that tissue-specific deletion of Fas in mouse antigen-presenting cells (APCs) was    sufficient to cause systemic autoimmunity, implying that normally APCs are destroyed during immune responses via a Fas-mediated mechanism. Fas expression by APCs was increased by exposure to microbial stimuli. Analysis of mice with Fas loss    restricted to T cells revealed that Fas indeed controls autoimmune T cells, but not T cells responding to strong antigenic stimulation. Thus, Fas-dependent elimination of APCs is a major regulatory mechanism curbing autoimmune responses and acts    in concert with Fas-mediated regulation of chronically activated autoimmune T cells.</p>

	]]>
</description>

<author>P B. Stranges et al.</author>


</item>


<item>
<title>Diminished lifespan and acute stress-induced death in DNA-PKcs-deficient mice with limiting telomeres.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1539</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1539</guid>
<pubDate>Tue, 08 May 2012 22:29:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>An adequate and appropriate response to physiological and pathophysiological stresses is critical for long-term homeostasis and viability of the aging organism. Previous work has pointed to the immune system, telomeres and DNA    repair pathways as important and distinct determinants of a normal healthy lifespan. In this study, we explored the genetic interactions of telomeres and DNA-PKcs, a protein involved in non-homologous end-joining (NHEJ) and immune responses, in    the context of a key aspect of aging and lifespan--the capacity to mount an acute and appropriate immune-mediated stress response. We observed that the combination of DNA-PKcs deficiency and telomere dysfunction resulted in a shortened lifespan    that was reduced further following viral infection or experimental activation of the innate immune response. Analysis of the innate immune response in the DNA-PKcs-deficient mice with short dysfunctional telomeres revealed high basal serum levels    of tumor necrosis factor alpha (TNFalpha) and hyper-active cytokine responses upon challenge with polyinosinic-polycytidylic acid (poly-IC). We further show that serum cytokine levels become elevated in telomere dysfunctional mice as a function    of age. These results raise speculation that these genetic factors may contribute to misdirected immune responses of the aged under conditions of acute and chronic stress.</p>

	]]>
</description>

<author>K K. Wong et al.</author>


</item>


<item>
<title>Interleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1538</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1538</guid>
<pubDate>Tue, 08 May 2012 22:28:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Autoimmune diseases are thought to result from imbalances in normal immune physiology and regulation. Here, we show that autoimmune disease susceptibility and resistance alleles on mouse chromosome 3 (Idd3) correlate with    differential expression of the key immunoregulatory cytokine interleukin-2 (IL-2). In order to test directly that an approximately twofold reduction in IL-2 underpins the Idd3-linked destabilization of immune homeostasis, we show that engineered    haplodeficiency of Il2 gene expression not only reduces T cell IL-2 production by twofold but also mimics the autoimmune dysregulatory effects of the naturally occurring susceptibility alleles of Il2. Reduced IL-2 production achieved by either    genetic mechanism correlates with reduced function of CD4(+) CD25(+) regulatory T cells, which are critical for maintaining immune homeostasis.</p>

	]]>
</description>

<author>J Yamanouchi et al.</author>


</item>


<item>
<title>Survival and function of MiHA epitope-specific host CD8 TM cells following ablative conditioning and HCT.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1537</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1537</guid>
<pubDate>Tue, 08 May 2012 22:28:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Memory T cell (TM) populations specific for transplantation Ags may arise from sensitization due to blood transfusions, tissue transplants, or in multiparous females. In each of these scenarios, TM cells are likely generated, and    have been shown to persist in such individuals for extended time periods. Heightened resistance to allogeneic marrow engraftment in certain individuals is therefore consistent with the presence of antidonor TM. CD8 TM were generated against a    single minor H Ag (MiHA) epitope to determine if such cells could inhibit allogeneic marrow engraftment. The present results demonstrate that B6 mice sensitized to a single immunodominant (H60) epitope efficiently reject donor marrow allografts    expressing this MiHA alone or together with multiple minor transplantation antigens, even following ablative TBI conditioning. To further address the survival and function of these CD8 TM, sensitized mice were ablatively conditioned and    administered a syngeneic HCT. CD8(+)H60(TCR+) TM were clearly detected up to 2 weeks later in such recipients. Additionally, the memory cells present were capable of mediating effector responses as evidenced by their ability to resist a second,    allogeneic HCT. In summary, these observations highlight the increased risk of resistance in the presence of antidonor antigen-specific CD8 TM due to their ability to survive and function even following rigorous conditioning and    HCT.</p>

	]]>
</description>

<author>A M. Shatry et al.</author>


</item>


<item>
<title>A single nucleotide mutation in Nppc is associated with a long bone abnormality in lbab mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1536</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1536</guid>
<pubDate>Tue, 08 May 2012 22:28:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The long bone abnormality (lbab) mouse is a new autosomal recessive mutant characterized by overall smaller body size with proportionate dwarfing of all organs and shorter long bones. Previous linkage analysis has    located the lbab mutation on chromosome 1 between the markers D1Mit9 and D1Mit488. RESULTS: A genome-based positional approach was used to identify a mutation associated with lbab disease. A total of 122 genes and expressed sequence tags at the    lbab region were screened for possible mutation by using genomic DNA from lbabl/lbab, lbab/+, and +/+ B6 mice and high throughput temperature gradient capillary electrophoresis. A sequence difference was identified in one of the amplicons of gene    Nppc between lbab/lbab and +/+ mice. One-step reverse transcriptase polymerase chain reaction was performed to validate the difference of Nppc in different types of mice at the mRNA level. The mutation of Nppc was unique in lbab/lbab mice among    multiple mouse inbred strains. The mutation of Nppc is co-segregated with lbab disease in 200 progenies produced from heterozygous lbab/+ parents. CONCLUSION: A single nucleotide mutation of Nppc is associated with dwarfism in lbab/lbab mice.    Current genome information and technology allow us to efficiently identify single nucleotide mutations from roughly mapped disease loci. The lbab mouse is a useful model for hereditary human achondroplasia.</p>

	]]>
</description>

<author>Y Jiao et al.</author>


</item>


<item>
<title>Elevated neuronal expression of CD200 protects Wlds mice from inflammation-mediated neurodegeneration.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1535</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1535</guid>
<pubDate>Tue, 08 May 2012 22:28:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Axonal damage secondary to inflammation is likely the substrate of chronic disability in multiple sclerosis and is found in the animal model of experimental autoimmune encephalomyelitis (EAE). Wld(s) mice have a triplication of the    fusion gene Ube4b/Nmnat and a phenotype of axon protection. Wld(s) mice develop an attenuated disease course of EAE, with decreased demyelination, reduced axonal pathology, and decreased central nervous system (CNS) macrophage and microglial    accumulation. We show that attenuated disease in Wld(s) mice was associated with robust constitutive expression of the nonsignaling CD200 molecule on neurons in the CNS compared with control mice. CD200 interacts with its signaling receptor    CD200R, which we found to be expressed on microglia, astrocytes, and oligodendrocytes at similar levels in control and Wld(s) mice.  Administration of blocking anti-CD200 antibody to Wld(s) mice abrogated disease attenuation and was associated    with increased CNS inflammation and neurodegeneration. In vitro, Wld(s) neuronal cultures were protected from microglial-induced neurotoxicity compared with control cultures, but protection was abrogated by anti-CD200 antibody. The CD200-CD200R    pathway plays a critical role in attenuating EAE and reducing inflammation-mediated damage in the CNS. Strategies that up-regulate the expression of CD200 in the CNS or molecules that ligate the CD200R may be relevant as neuroprotective    strategies in multiple sclerosis.</p>

	]]>
</description>

<author>T Chitnis et al.</author>


</item>


<item>
<title>In vivo distribution of human adipose-derived mesenchymal stem cells in novel xenotransplantation models.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1534</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1534</guid>
<pubDate>Tue, 08 May 2012 22:28:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>The potential for human adipose-derived mesenchymal stem cells (AMSC) to traffic into various tissue compartments was examined using three murine xenotransplantation models: nonobese diabetic/severe combined immunodeficient    (NOD/SCID), nude/NOD/SCID, and NOD/SCID/MPSVII mice.  Enhanced green fluorescent protein was introduced into purified AMSC via retroviral vectors to assist in identification of cells after transplantation. Transduced cells were administered to    sublethally irradiated immune-deficient mice through i.v., intraperitoneal, or subcutaneous injection. Up to 75 days after transplantation, tissues were harvested and DNA polymerase chain reaction (PCR) was performed for specific vector sequences    as well as for human Alu repeat sequences.  Duplex quantitative PCR using human beta-globin and murine rapsyn primers assessed the contribution of human cells to each tissue. The use of the novel NOD/SCID/MPSVII mouse as a recipient allowed rapid    identification of human cells in the murine tissues, using an enzyme reaction that was independent of surface protein expression or transduction with an exogenous transgene. For up to 75 days after transplantation, donor-derived cells were    observed in multiple tissues, consistently across the various administration routes and independent of transduction parameters. Tissue localization studies showed that the primary MSC did not proliferate extensively at the sites of lodgement. We    conclude that human AMSC represent a population of stem cells with a ubiquitous pattern of tissue distribution after administration. AMSC are easily obtained and highly amenable to current transduction protocols for retroviral transduction,    making them an excellent avenue for cell-based therapies that involve a wide range of end tissue targets.</p>

	]]>
</description>

<author>T E. Meyerrose et al.</author>


</item>


<item>
<title>Mutation of a ubiquitously expressed mouse transmembrane protein (Tapt1) causes specific skeletal homeotic transformations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1533</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1533</guid>
<pubDate>Tue, 08 May 2012 22:28:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>L5Jcs1 is a perinatal lethal mutation uncovered in a screen for ENU-induced mutations on mouse chromosome 5. L5Jcs1 homozygotes exhibit posterior-to-anterior transformations of the vertebral column midsection, similar to mice    deficient for Hoxc8 and Hoxc9. Positional cloning efforts identified a mutation in a novel, evolutionarily conserved, and ubiquitously expressed gene dubbed Tapt1 (Transmembrane anterior posterior transformation 1). TAPT1 is predicted to contain    several transmembrane domains, and part of the gene is orthologous to an unusual alternatively spliced human transcript encoding the cytomegalovirus gH receptor. We speculate that TAPT1 is a downstream effector of HOXC8 that may act by    transducing or transmitting extracellular information required for axial skeletal patterning during development.</p>

	]]>
</description>

<author>G R. Howell et al.</author>


</item>


<item>
<title>Herpesvirus saimiri terminal membrane proteins modulate HIV-1 replication by altering Nef and Tat functions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1532</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1532</guid>
<pubDate>Tue, 08 May 2012 22:28:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Herpesvirus saimiri (HVS)-transformed human T cells expressing terminal membrane proteins (TMPs) tyrosine kinase interacting protein (Tip) and saimiri transformation associated protein strain C (StpC) are highly permissive for R5    and X4 strains of HIV-1. StpC expression enhances replication of R5 and X4 strains of HIV-1 and induces latent reservoirs of replication competent HIV-1 in cell lines derived from T cells or monocytes. Paradoxically Tip expression restricts    replication and cytopathic effects of R5 and X4 strains of HIV-1 in T cells and monocytes post-retrotransposition. Understanding the canonical pathways whereby Tip and StpC alter HIV-1 replication may uncover novel therapeutic approaches to HIV-1    infection. Here we show Tip inhibits Tat-mediated transcriptional activation of the long terminal repeat (LTR). Tip mediated inhibition of Tat transactivation is reversed by Nef. Tip also mediates restriction of late-stage replication of HIV-1 by    disrupting Nef interaction with lymphocyte-specific protein-tyrosine kinase (Lck) in lipid rafts.  Specifically, in the presence of Tip, Lck does not localize to lipid rafts reducing Nef interaction with Lck within the lipid rafts. Finally, the    permissive phenotype conferred by StpC is the result of synergy with Tat during transcriptional activation of the HIV-1 LTR. This transcriptional synergy between StpC and Tat requires Lck and NF-kappaB consensus binding sequences. These findings    demonstrate that the HVS TMPs influence transcriptional and post-transcriptional stages in HIV-1 replication. We propose that HVS-encoded TMPs associated with T cell transformation have evolved ability to modulate the replication of competing    retroviruses.  Gene based approaches utilizing Tip and StpC may provide therapeutic models for treating acute and latent HIV-1 infections, respectively.</p>

	]]>
</description>

<author>A D. Raymond et al.</author>


</item>


<item>
<title>Bile duct proliferation in liver-specific Jag1 conditional knockout mice: effects of gene dosage.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1531</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1531</guid>
<pubDate>Tue, 08 May 2012 22:27:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Notch signaling pathway is involved in determination of cell fate and control of cell proliferation in multiple organ systems. Jag1 encodes a ligand in the Notch pathway and has been identified as the disease-causing gene for    the developmental disorder Alagille syndrome. Evidence from the study of human disease and mouse models has implicated Jag1 as having an important role in the development of bile ducts. We have derived a conditional knockout allele (Jag1(loxP))    to study the role of Jag1 and Notch signaling in liver and bile duct development. We crossed Jag1(loxP) mice with a transgenic line carrying Cre recombinase under the control of the albumin promoter and alpha-fetoprotein enhancer to ablate Jag1    in hepatoblasts. The liver-specific Jag1 conditional knockout mice showed normal bile duct development. To further decrease Notch pathway function, we crossed the Jag1 conditional knockout mice with mice carrying the hypomorphic Notch2 allele,    and bile duct anatomy remained normal. When Jag1 conditional mice were crossed with mice carrying the Jag1 null allele, the adult progeny exhibited striking bile duct proliferation.  Conclusion: These results indicate that Notch signaling in the    liver is sensitive to Jag1 gene dosage and suggest a role for the Notch pathway in postnatal growth and morphogenesis of bile ducts.</p>

	]]>
</description>

<author>K M. Loomes et al.</author>


</item>


<item>
<title>Sequential quantitative trait locus mapping in experimental crosses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1530</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1530</guid>
<pubDate>Tue, 08 May 2012 22:27:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>The etiology of complex diseases is heterogeneous. The presence of risk alleles in one or more genetic loci affects the function of a variety of intermediate biological pathways, resulting in the overt expression of disease. Hence,    there is an increasing focus on identifying the genetic basis of disease by systematically studying phenotypic traits pertaining to the underlying biological functions. In this paper we focus on identifying genetic loci linked to quantitative    phenotypic traits in experimental crosses. Such genetic mapping methods often use a one stage design by genotyping all the markers of interest on the available subjects. A genome scan based on single locus or multi-locus models is used to    identify the putative loci. Since the number of quantitative trait loci (QTLs) is very likely to be small relative to the number of markers genotyped, a one-stage selective genotyping approach is commonly used to reduce the genotyping burden,    whereby markers are genotyped solely on individuals with extreme trait values. This approach is powerful in the presence of a single quantitative trait locus (QTL) but may result in substantial loss of information in the presence of multiple    QTLs. Here we investigate the efficiency of sequential two stage designs to identify QTLs in experimental populations. Our investigations for backcross and F2 crosses suggest that genotyping all the markers on 60% of the subjects in Stage 1 and    genotyping the chromosomes significant at 20% level using additional subjects in Stage 2 and testing using all the subjects provides an efficient approach to identify the QTLs and utilizes only 70% of the genotyping burden relative to a one stage    design, regardless of the heritability and genotyping density. Complex traits are a consequence of multiple QTLs conferring main effects as well as epistatic interactions.  We propose a two-stage analytic approach where a single-locus genome scan    is conducted in Stage 1 to identify promising chromosomes, and interactions are examined using the loci on these chromosomes in Stage 2.  We examine settings under which the two-stage analytic approach provides sufficient power to detect the    putative QTLs.</p>

	]]>
</description>

<author>J M. Satagopan et al.</author>


</item>


<item>
<title>Effects of parathyroid hormone (1-34) on tibia in an adult rat model for chronic alcohol abuse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1529</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1529</guid>
<pubDate>Tue, 08 May 2012 22:27:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chronic alcohol abuse is a risk factor for osteoporosis in men. Human recombinant parathyroid hormone (1-34) (PTH) therapy increases bone mass in patients with osteoporosis. The purpose of the present study was to determine whether    PTH is effective in increasing bone formation and bone mass in a rat model for established osteopenia caused by chronic alcohol abuse. Eight-month-old male Sprague Dawley rats were fed the Lieber-DeCarli liquid diet in which 35% of the calories    were derived from either maltose-dextran or ethanol. Measurements were performed 16 weeks later to establish the magnitude of bone changes in the rats fed alcohol.  High dose PTH (80 microg/kg/day) was administered 5 days/week for 6 weeks to    establish the differential efficacy of hormone therapy on bone formation in alcohol consuming and alcohol withdrawn rats. The effects of alcohol and PTH on cancellous and cortical bone mass, architecture and turnover were determined by    densitometry and histomorphometry. Rats fed alcohol had reduced bone mineral contents and densities, cancellous and cortical bone areas and cancellous bone formation rates compared to pair-fed controls. Following the withdrawal of alcohol,    indices of bone formation increased compared to baseline values. PTH treatment increased bone mineral content and density, bone formation rates, cortical bone area, cancellous bone area and trabecular number and thickness, but several indices of    bone formation were reduced in the presence of continued alcohol consumption. These results suggest that alcohol consumption, in addition to inducing bone loss, may reduce the efficacy of PTH therapy to reverse osteoporosis.</p>

	]]>
</description>

<author>J D. Sibonga et al.</author>


</item>


<item>
<title>Mutation in mouse hei10, an e3 ubiquitin ligase, disrupts meiotic crossing over.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1528</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1528</guid>
<pubDate>Tue, 08 May 2012 22:27:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J O. Ward et al.</author>


</item>


<item>
<title>Detecting novel bone density and bone size quantitative trait loci using a cross of MRL/MpJ and CAST/EiJ inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1527</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1527</guid>
<pubDate>Tue, 08 May 2012 22:27:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Most previous studies to identify loci involved in bone mineral density (BMD) regulation have used inbred strains with high and low BMD in generating F(2) mice. However, differences in BMD may not be a requirement in selecting    parental strains for BMD quantitative trait loci (QTL) studies. In this study, we intended to identify novel QTL using a cross of two strains, MRL/MpJ (MRL) and CAST/EiJ (CAST), both of which exhibit relatively high BMD when compared to    previously used strains. In addition, CAST was genetically distinct. We generated 328 MRL x CAST F(2) mice of both sexes and measured femur BMD and periosteal circumference (PC) using peripheral quantitative computed tomography. Whole-genome    genotyping was performed with 86 microsatellite markers. A new BMD QTL on chromosome 10 and another suggestive one on chromosome 15 were identified. A significant femur PC QTL identified on chromosome 9 and a suggestive one on chromosome 2 were    similar to those detected in MRL x SJL. QTL were also identified for other femur and forearm bone density and bone size phenotypes, some of which were colocalized within the same chromosomal positions as those for femur BMD and femur PC. This    study demonstrates the utility of crosses involving inbred strains of mice which exhibit a similar phenotype in QTL identification.</p>

	]]>
</description>

<author>H Yu et al.</author>


</item>


<item>
<title>Distinct target-derived signals organize formation, maturation, and maintenance of motor nerve terminals.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1526</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1526</guid>
<pubDate>Tue, 08 May 2012 22:27:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Target-derived factors organize synaptogenesis by promoting differentiation of nerve terminals at synaptic sites. Several candidate organizing molecules have been identified based on their bioactivities in vitro, but little is known    about their roles in vivo. Here, we show that three sets of organizers act sequentially to pattern motor nerve terminals: FGFs, beta2 laminins, and collagen alpha(IV) chains. FGFs of the 7/10/22 subfamily and broadly distributed collagen IV    chains (alpha1/2) promote clustering of synaptic vesicles as nerve terminals form. beta2 laminins concentrated at synaptic sites are dispensable for embryonic development of nerve terminals but are required for their postnatal maturation.    Synapse-specific collagen IV chains (alpha3-6) accumulate only after synapses are mature and are required for synaptic maintenance. Thus, multiple target-derived signals permit discrete control of the formation, maturation, and maintenance of    presynaptic specializations.</p>

	]]>
</description>

<author>M A. Fox et al.</author>


</item>


<item>
<title>Multiple functions of Snail family genes during palate development in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1525</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1525</guid>
<pubDate>Tue, 08 May 2012 22:27:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Palate development requires precise regulation of gene expression changes, morphogenetic movements and alterations in cell physiology. Defects in any of these processes can result in cleft palate, a common human birth defect. The    Snail gene family encodes transcriptional repressors that play essential roles in the growth and patterning of vertebrate embryos. Here we report the functions of Snail (Snai1) and Slug (Snai2) genes during palate development in mice. Snai2(-/-)    mice exhibit cleft palate, which is completely penetrant on a Snai1 heterozygous genetic background. Cleft palate in Snai1(+/-) Snai2(-/-) embryos is due to a failure of the elevated palatal shelves to fuse. Furthermore, while tissue-specific    deletion of the Snai1 gene in neural crest cells does not cause any obvious defects, neural-crest-specific Snai1 deletion on a Snai2(-/-) genetic background results in multiple craniofacial defects, including a cleft palate phenotype distinct    from that observed in Snai1(+/-) Snai2(-/-) embryos. In embryos with neural-crest-specific Snai1 deletion on a Snai2(-/-) background, palatal clefting results from a failure of Meckel's cartilage to extend the mandible and thereby allow the    palatal shelves to elevate, defects similar to those seen in the Pierre Robin Sequence in humans.</p>

	]]>
</description>

<author>S A. Murray et al.</author>


</item>


<item>
<title>The University of Wollongong Gazette Vol 1 No 1</title>
<link>http://ro.uow.edu.au/uowgazette/1</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowgazette/1</guid>
<pubDate>Tue, 08 May 2012 22:27:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>The University of Wollongong</author>


</item>


<item>
<title>Different evolutionary histories of the two classical class I genes BF1 and BF2 illustrate drift and selection within the stable MHC haplotypes of chickens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1524</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1524</guid>
<pubDate>Tue, 08 May 2012 22:26:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Compared with the MHC of typical mammals, the chicken MHC (BF/BL region) of the B12 haplotype is smaller, simpler, and rearranged, with two classical class I genes of which only one is highly expressed. In this study, we describe    the development of long-distance PCR to amplify some or all of each class I gene separately, allowing us to make the following points. First, six other haplotypes have the same genomic organization as B12, with a poorly expressed (minor) BF1 gene    between DMB2 and TAP2 and a well-expressed (major) BF2 gene between TAP2 and C4. Second, the expression of the BF1 gene is crippled in three different ways in these haplotypes: enhancer A deletion (B12, B19), enhancer A divergence and    transcription start site deletion (B2, B4, B21), and insertion/rearrangement leading to pseudogenes (B14, B15). Third, the three kinds of alterations in the BF1 gene correspond to dendrograms of the BF1 and poorly expressed class II B (BLB1)    genes reflecting mostly neutral changes, while the dendrograms of the BF2 and well-expressed class II (BLB2) genes each have completely different topologies reflecting selection. The common pattern for the poorly expressed genes reflects the fact    the BF/BL region undergoes little recombination and allows us to propose a pattern of descent for these chicken MHC haplotypes from a common ancestor. Taken together, these data explain how stable MHC haplotypes predominantly express a single    class I molecule, which in turn leads to striking associations of the chicken MHC with resistance to infectious pathogens and response to vaccines.</p>

	]]>
</description>

<author>I Shaw et al.</author>


</item>


<item>
<title>Training mouse pathologists: five years of pathology of mouse models of human disease workshops.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1523</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1523</guid>
<pubDate>Tue, 08 May 2012 22:26:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title>Mouse genome informatics (MGI) resources for pathology and toxicology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1522</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1522</guid>
<pubDate>Tue, 08 May 2012 22:26:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J T. Eppig et al.</author>


</item>


<item>
<title>Transcriptional profiling of androgen receptor (AR) mutants suggests instructive and permissive roles of AR signaling in germ cell development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1521</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1521</guid>
<pubDate>Tue, 08 May 2012 22:26:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The androgen receptor (AR) is a transcription factor that plays a critical role in male sexual development, spermatogenesis, and maintenance of hormonal homeostasis. Despite the extensive knowledge of the phenotypic consequences of    mutations in Ar, very little is known about the transcriptional targets of AR within the testis. To identify potential targets of androgen signaling in the testis, we have analyzed the transcriptional profile of adult testes from Ar hypomorphs    alone or in combination with Sertoli cell-specific Ar ablation. Using Affymetrix MOE430A mouse genome arrays we interrogated more than 22,000 transcripts.  We found the expression level of 62 transcripts in the Ar mutants differed by greater than    2-fold compared with wild type. We also found that more transcripts were up-regulated than down-regulated, highlighting AR's role as a transcriptional repressor in the testis. Twelve transcripts were uniquely affected, and 16 transcripts were    more severely affected in Sertoli cell-specific Ar ablation compared with hypomorphic Ar mutants.  Using a comparative genomic approach, we analyzed the 6 kb around the transcriptional start sites of affected transcripts for conserved AREs    (androgen response elements). We identified at least one conserved ARE in 65% of the genes misregulated in our microarray analysis where clear mouse-human orthologs were available. We used a reporter assay in cell culture to functionally verify    the AREs for the kallikrein 27 gene. This suggests that the majority of the misregulated transcripts have a high probability of being direct AR targets. The transcripts affected by these Ar mutations encode a diverse array of proteins whose    molecular functions support the contention that AR supports spermatogenesis in both a permissive and instructive fashion.</p>

	]]>
</description>

<author>S M. Eacker et al.</author>


</item>


<item>
<title>Utp14b: A unique retrogene within a gene that has acquired multiple promoters and a specific function in spermatogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1520</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1520</guid>
<pubDate>Tue, 08 May 2012 22:26:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse retrogene Utp14b is essential for male fertility, and a mutation in its sequence results in the sterile juvenile spermatogonial depletion (jsd) phenotype. It is a retrotransposed copy of the Utp14a gene, which is located    on the X chromosome, and is inserted within an intron of the autosomal acyl-CoA synthetase long-chain family member 3 (Acsl3) gene. To elucidate the roles of the Utp14 genes in normal spermatogenic cell development as a basis for understanding    the defects that result in the jsd phenotype, we analyzed the various mRNAs produced from the Utp14b retrogene and their expression in different cell types. Two classes of transcripts were identified: variant 1, a transcript driven by the host    gene promoter, that is predominantly found in germ cells but is ubiquitously expressed at low levels; and variants 2-5, a group of alternatively spliced transcripts containing some unique untranslated exons that are transcribed from a novel    promoter that is germ-cell-specific. Utp14b (predominantly variant 1) is expressed at moderately high levels in pachytene spermatocytes, the developmental stage at which the expression of the X-linked Utp14a is suppressed. The levels of both    classes of Utp14b transcripts were highest in round spermatids despite the transcription of Utp14a in these cells. We propose that when Utp14b initially inserted into Acsl3, it utilized the Acsl3 promoter to drive expression in pachytene    spermatocytes to compensate for inactivation of Utp14a expression. The novel cell-type-specific promoter for Utp14b likely evolved later, as the protein may have acquired a germ cell-specific function in spermatid development.</p>

	]]>
</description>

<author>M Zhao et al.</author>


</item>


<item>
<title>Defects in eye development in transgenic mice overexpressing the heparan sulfate proteoglycan agrin.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1519</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1519</guid>
<pubDate>Tue, 08 May 2012 22:26:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>The importance of heparan sulfate proteoglycans (HSPGs) in neurodevelopment is becoming increasingly clear. However, studies on HSPGs are hampered by pleiotropic effects when synthesis or modification of heparan sulfate itself is    targeted, and by redundancy when the core proteins are altered. Gain-of-function experiments can sometimes circumvent these issues. Here we establish that transgenic mice overexpressing the HSPG agrin have severe ocular dysgenesis. The defects    occur through a gain-of-function mechanism and penetrance is dependent on agrin dosage. The agrin-induced developmental defects are highly variable, and include anophthalmia, persistence of vitreous vessels, and fusion of anterior chamber    structures. A frequently observed defect is an optic stalk coloboma leading to the misdifferentiation of the optic stalk as retina, which becomes continuous with the forebrain. The defects in optic-stalk differentiation correlate with reduced    sonic hedgehog immunoreactivity and overexpansion of the PAX6 domain from the retina into the optic stalk. The ocular phenotypes associated with agrin overexpression are dependent on genetic background, occurring with high penetrance in inbred    C57BL/6J mice. Distinct loci sensitizing C57BL/6J mice to agrin-induced dysgenesis were identified. These results indicate that agrin overexpression will provide a tool to explore the molecular interactions of the extracellular matrix and cell    surface in eye development, and provide a means for identifying modifier loci that sensitize mice to developmental eye defects.</p>

	]]>
</description>

<author>P G. Fuerst et al.</author>


</item>


<item>
<title>Cellular expression requirements for inhibition of type 1 diabetes by a dominantly protective major histocompatibility complex haplotype.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1518</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1518</guid>
<pubDate>Tue, 08 May 2012 22:26:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>The H2(g7) (K(d), A(g7), E(null), and D(b)) major histocompatibility complex (MHC) is the primary genetic contributor to type 1 diabetes in NOD mice. NOD stocks congenically expressing other MHC haplotypes such as H2(nb1) (K(b),    A(nb1), E(k), and D(b)) in a heterozygous state are type 1 diabetes resistant. Hematopoietically derived antigen-presenting cells (APCs) expressing H2(nb1) MHC molecules delete or inactivate autoreactive diabetogenic T-cells. Thus, provided a    relatively benign preconditioning protocol is ultimately developed, hematopoietic chimerization by APCs expressing dominantly protective MHC molecules could conceivably provide a means for type 1 diabetes prevention in humans. Before    hematopoietic chimerization can be considered for type 1 diabetes prevention, it must be determined what subtype(s) of APCs (B-cells, macrophages, and/or dendritic cells) expressing protective MHC molecules most efficiently inhibit disease, as    well as the engraftment level they must achieve to accomplish this. These issues were addressed through analyses of NOD background bone marrow chimeras in which H2(nb1) molecules were selectively expressed on variable proportions of different APC    subtypes. While a modest B-cell effect was observed, the strongest type 1 diabetes protection resulted from at least 50% of dendritic cells and macrophages expressing H2(nb1) molecules. At this engraftment level, H2(nb1)-expressing dendritic    cells and macrophages mediated virtually complete deletion of a highly pathogenic CD8 T-cell population.</p>

	]]>
</description>

<author>Y G. Chen et al.</author>


</item>


<item>
<title>mtDNA phylogeny and evolution of laboratory mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1517</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1517</guid>
<pubDate>Tue, 08 May 2012 22:25:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inbred mouse strains have been maintained for more than 100 years, and they are thought to be a mixture of four different mouse subspecies.  Although genealogies have been established, female inbred mouse phylogenies remain    unexplored. By a phylogenetic analysis of newly generated complete mitochondrial DNA sequence data in 16 strains, we show here that all common inbred strains descend from the same Mus musculus domesticus female wild ancestor, and suggest that    they present a different mitochondrial evolutionary process than their wild relatives with a faster accumulation of replacement substitutions. Our data complement forthcoming results on resequencing of a group of priority strains, and they follow    recent efforts of the Mouse Phenome Project to collect and make publicly available information on various strains.</p>

	]]>
</description>

<author>A Goios et al.</author>


</item>


<item>
<title>Vascular biology: vessel guidance.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1516</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1516</guid>
<pubDate>Tue, 08 May 2012 22:25:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T Gridley</author>


</item>


<item>
<title>Novel method for high-throughput phenotyping of sleep in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1515</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1515</guid>
<pubDate>Tue, 08 May 2012 22:25:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Assessment of sleep in mice currently requires initial implantation of chronic electrodes for assessment of electroencephalogram (EEG) and electromyogram (EMG) followed by time to recover from surgery. Hence, it is not ideal for    high-throughput screening. To address this deficiency, a method of assessment of sleep and wakefulness in mice has been developed based on assessment of activity/inactivity either by digital video analysis or by breaking infrared beams in the    mouse cage. It is based on the algorithm that any episode of continuous inactivity of > or =40 s is predicted to be sleep. The method gives excellent agreement in C57BL/6J male mice with simultaneous assessment of sleep by EEG/EMG recording. The    average agreement over 8,640 10-s epochs in 24 h is 92% (n = 7 mice) with agreement in individual mice being 88-94%. Average EEG/EMG determined sleep per 2-h interval across the day was 59.4 min. The estimated mean difference (bias) per 2-h    interval between inactivity-defined sleep and EEG/EMG-defined sleep was only 1.0 min (95% confidence interval for mean bias -0.06 to +2.6 min). The standard deviation of differences (precision) was 7.5 min per 2-h interval with 95% limits of    agreement ranging from -13.7 to +15.7 min. Although bias significantly varied by time of day (P = 0.0007), the magnitude of time-of-day differences was not large (average bias during lights on and lights off was +5.0 and -3.0 min per 2-h    interval, respectively). This method has applications in chemical mutagenesis and for studies of molecular changes in brain with sleep/wakefulness.</p>

	]]>
</description>

<author>A I. Pack et al.</author>


</item>


<item>
<title>Selective degradation of transcripts during meiotic maturation of mouse oocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1514</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1514</guid>
<pubDate>Tue, 08 May 2012 22:25:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is massive destruction of transcripts during the maturation of mouse oocytes. The objective of this project was to identify and characterize the transcripts that are degraded versus those that are stable during the    transcriptionally silent germinal vesicle (GV)-stage to metaphase II (MII)-stage transition using a microarray approach. A system for oocyte transcript amplification using both internal and 3'-poly(A) priming was utilized to minimize the impact    of complex variations in transcript polyadenylation prevalent during this transition. Transcripts were identified and quantified using the Affymetrix Mouse Genome 430 v2.0 GeneChip. The significantly changed and stable transcripts were analyzed    using Ingenuity Pathways Analysis and GenMAPP/MAPPFinder to characterize the biological themes underlying global changes in oocyte transcripts during maturation. It was concluded that the destruction of transcripts during the GV to MII transition    is a selective rather than promiscuous process in mouse oocytes. In general, transcripts involved in processes that are associated with meiotic arrest at the GV-stage and the progression of oocyte maturation, such as oxidative phosphorylation,    energy production, and protein synthesis and metabolism, were dramatically degraded. In contrast, transcripts encoding participants in signaling pathways essential for maintaining the unique characteristics of the MII-arrested oocyte, such as    those involved in protein kinase pathways, were the most prominent among the stable transcripts.</p>

	]]>
</description>

<author>Y Q. Su et al.</author>


</item>


<item>
<title>The mouse Gene Expression Database (GXD): 2007 update.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1513</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1513</guid>
<pubDate>Tue, 08 May 2012 22:25:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Gene Expression Database (GXD) provides the scientific community with an extensive and easily searchable database of gene expression information about the mouse. Its primary emphasis is on developmental studies. By integrating    different types of expression data, GXD aims to provide comprehensive information about expression patterns of transcripts and proteins in wild-type and mutant mice. Integration with the other Mouse Genome Informatics (MGI) databases places the    gene expression information in the context of genetic, sequence, functional and phenotypic information, enabling valuable insights into the molecular biology that underlies developmental and disease processes. In recent years the utility of GXD    has been greatly enhanced by a large increase in data content, obtained from the literature and provided by researchers doing large-scale in situ and cDNA screens. In addition, we have continued to refine our query and display features to make it    easier for users to interrogate the data. GXD is available through the MGI web site at http://www.informatics.jax.org/ or directly at http://www.informatics.jax.org/menus/expression_menu.shtml.</p>

	]]>
</description>

<author>C M. Smith et al.</author>


</item>


<item>
<title>Assessing human germ-cell mutagenesis in the Postgenome Era: a celebration of the legacy of William Lawson (Bill) Russell.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1512</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1512</guid>
<pubDate>Tue, 08 May 2012 22:25:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Birth defects, de novo genetic diseases, and chromosomal abnormality syndromes occur in approximately 5% of all live births, and affected children suffer from a broad range of lifelong health consequences.  Despite the social and    medical impact of these defects, and the 8 decades of research in animal systems that have identified numerous germ-cell mutagens, no human germ-cell mutagen has been confirmed to date. There is now a growing consensus that the inability to    detect human germ-cell mutagens is due to technological limitations in the detection of random mutations rather than biological differences between animal and human susceptibility. A multidisciplinary workshop responding to this challenge    convened at The Jackson Laboratory in Bar Harbor, Maine. The purpose of the workshop was to assess the applicability of an emerging repertoire of genomic technologies to studies of human germ-cell mutagenesis. Workshop participants recommended    large-scale human germ-cell mutation studies be conducted using samples from donors with high-dose exposures, such as cancer survivors. Within this high-risk cohort, parents and children could be evaluated for heritable changes in (a) DNA    sequence and chromosomal structure, (b) repeat sequences and minisatellites, and (c) global gene expression profiles and pathways. Participants also advocated the establishment of a bio-bank of human tissue samples from donors with    well-characterized exposure, including medical and reproductive histories.  This mutational resource could support large-scale, multiple-endpoint studies. Additional studies could involve the examination of transgenerational effects associated    with changes in imprinting and methylation patterns, nucleotide repeats, and mitochondrial DNA mutations.  The further development of animal models and the integration of these with human studies are necessary to provide molecular insights into    the mechanisms of germ-cell mutations and to identify prevention strategies.  Furthermore, scientific specialty groups should be convened to review and prioritize the evidence for germ-cell mutagenicity from common environmental, occupational,    medical, and lifestyle exposures. Workshop attendees agreed on the need for a full-scale assault to address key fundamental questions in human germ-cell environmental mutagenesis. These include, but are not limited to, the following: Do human    germ-cell mutagens exist? What are the risks to future generations? Are some parents at higher risk than others for acquiring and transmitting germ-cell mutations? Obtaining answers to these, and other critical questions, will require strong    support from relevant funding agencies, in addition to the engagement of scientists outside the fields of genomics and germ-cell mutagenesis.</p>

	]]>
</description>

<author>A J. Wyrobek et al.</author>


</item>


<item>
<title>Effects of carbonic anhydrase VIII deficiency on cerebellar gene expression profiles in the wdl mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1511</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1511</guid>
<pubDate>Tue, 08 May 2012 22:25:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recently, the waddles (wdl) mouse was identified as a carbonic anhydrase VIII (Car8) mutant. The mutation is associated with marked deficiency of Car8, an inositol triphosphate receptor 1-binding protein expressed at high levels in    cerebellar Purkinje cells. To help unravel the molecular aberrations contributing to motor dysfunction in wdl mice, cerebellar gene expression profiles were examined in the mutants and their wild-type littermates. Genes involved in signaling,    cell division, zinc ion-binding, synapse integrity and plasticity were downregulated in wdl mice. Several of the upregulated genes encode proteins that function in the Golgi apparatus which suggests that Car8 deficiency has important effects on    synaptic vesicle formation and transport.</p>

	]]>
</description>

<author>J Yan et al.</author>


</item>


<item>
<title>Anaplastic, plasmablastic, and plasmacytic plasmacytomas of mice: relationships to human plasma cell neoplasms and late-stage differentiation of normal B cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1510</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1510</guid>
<pubDate>Tue, 08 May 2012 22:24:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have compared histologic features and gene expression profiles of newly identified plasmacytomas from NFS.V(+) congenic mice with plasmacytomas of IL6 transgenic, Fasl mutant, and SJL-beta2M(-/-) mice. NFS.V(+) tumors comprised    an overlapping morphologic spectrum of high-grade/anaplastic, intermediate-grade/plasmablastic, and low-grade/plasmacytic cases with similarities to subsets of human multiple myeloma and plasmacytoma.  Microarray and immunohistochemical analyses    of genes expressed by the most prevalent tumors, plasmablastic plasmacytomas, showed them to be most closely related to immunoblastic lymphomas, less so to plasmacytomas of Fasl mutant and SJL mice, and least to plasmacytic plasmacytomas of IL6    transgenic mice. Plasmablastic tumors seemed to develop in an inflammatory environment associated with gene signatures of T cells, natural killer cells, and macrophages not seen with plasmacytic plasmacytomas.  Plasmablastic plasmacytomas from    NFS.V(+) and SJL-beta2M(-/-) mice did not have structural alterations in Myc or T(12;15) translocations and did not express Myc at high levels, regular features of transgenic and pristane-induced plasmacytomas. These findings imply that, as for    human multiple myeloma, Myc-independent routes of transformation contribute to the pathogenesis of these tumors. These findings suggest that plasma cell neoplasms of mice and humans exhibit similar degrees of complexity. Mouse plasmacytomas,    previously considered to be homogeneous, may thus be as diverse as their human counterparts with respect to oncogenic mechanisms of plasma cell transformation. Selecting specific types of mouse plasmacytomas that relate most closely to subtypes    of human multiple myeloma may provide new opportunities for preclinical testing of drugs for treatment of the human disease.</p>

	]]>
</description>

<author>C F. Qi et al.</author>


</item>


<item>
<title>Sprouty-2 regulates oncogenic K-ras in lung development and tumorigenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1509</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1509</guid>
<pubDate>Tue, 08 May 2012 22:24:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Somatic activation of Ras occurs frequently in human cancers, including one-third of lung cancers. Activating Ras mutations also occur in the germline, leading to complex developmental syndromes. The precise mechanism by which Ras    activation results in human disease is uncertain.  Here we describe the phenotype of a mouse engineered to harbor a germline oncogenic K-rasG12D mutation. This mouse exhibits early embryonic lethality due to a placental trophoblast defect.    Reconstitution with a wild-type placenta rescues the early lethality, but mutant embryos still succumb to cardiovascular and hematopoietic defects. In addition, mutant embryos demonstrate a profound defect in lung branching morphogenesis    associated with striking up-regulation of the Ras/mitogen-activated protein kinase (MAPK) antagonist Sprouty-2 and abnormal localization of MAPK activity within the lung epithelium. This defect can be significantly suppressed by lentiviral short    hairpin RNA (shRNA)-mediated knockdown of Sprouty-2 in vivo. Furthermore, in the context of K-rasG12D-mediated lung tumorigenesis, Sprouty-2 is also up-regulated and functions as a tumor suppressor to limit tumor number and overall tumor burden.    These findings indicate that in the lung, Sprouty-2 plays a critical role in the regulation of oncogenic K-ras, and implicate counter-regulatory mechanisms in the pathogenesis of Ras-based disease.</p>

	]]>
</description>

<author>A T. Shaw et al.</author>


</item>


<item>
<title>Effects of loss of classical estrogen response element signaling on bone in male mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1508</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1508</guid>
<pubDate>Tue, 08 May 2012 22:24:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>The role of estrogen signaling in the male skeleton via estrogen receptor (ER)-alpha is now well established. ERalpha can elicit responses through either classical estrogen response elements (ERE) pathways or nonclassical, non-ERE    pathways. In the present study, we examined the effects of either the attenuation or loss of classical ERalpha signaling on the murine male skeleton. To accomplish this, we crossed male mice heterozygous for a knock-in mutation [nonclassical    ERalpha knock-in (NERKI)], which abolishes the ERE-mediated pathway with female heterozygous ERalpha knockout mice (ERalpha+/-) and studied the F1 generation ERalpha+/+, ERalpha+/-, ERalpha+/NERKI, and ERalpha-/NERKI male progeny longitudinally    using bone density and histomorphometry. The only ERalpha allele present in ERalpha-/NERKI mice is incapable of classical ERE-mediated signaling, whereas the heterozygous ERalpha+/NERKI mice have both one intact ERalpha and one NERKI allele. As    compared with ERalpha+/+ littermates (n=10/genotype), male ERalpha+/NERKI and ERalpha-/NERKI mice displayed axial and appendicular skeletal osteopenia at 6, 12, 20, and 25 wk of age, as demonstrated by significant reductions in total bone mineral    density (BMD) at representative sites (areal BMD by dual-energy x-ray absorptiometry at the lumbar vertebrae and femur and volumetric BMD by peripheral quantitative computed tomography at the tibia; P<0.05-0.001 vs.  ERalpha+/+). The observed    osteopenia in these mice was evident in both trabecular and cortical bone compartments. However, these decreases were more severe in mice lacking classical ERalpha signaling (ERalpha-/NERKI mice), compared with mice in which one wild-type ERalpha    allele was present (ERalpha+/NERKI mice). Collectively, these data demonstrate that classical ERalpha signaling is crucial for the development of the murine male skeleton.</p>

	]]>
</description>

<author>F A. Syed et al.</author>


</item>


<item>
<title>Impact of trisomy on fertility and meiosis in male mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1507</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1507</guid>
<pubDate>Tue, 08 May 2012 22:24:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Chromosomal abnormalities frequently are associated with impairment or arrest of spermatogenesis in mammals but are compatible with fertility in female carriers of the same anomaly. In the case of trisomy, mice have    extra genomic DNA as well as the chromosomal abnormality, usually present as an extra, unpaired chromosome. Thus, impairment of spermatogenesis in trisomic males could be due to the presence of extra genomic material (i.e. triplicated genes) or    due to the chromosomal abnormality and presence of an unpaired chromosome in meiosis. METHODS: In this study, fertility and chromosomal pairing configurations during meiotic prophase were analysed in male mice trisomic for different segments of    the genome. Four have an extra segmental or tertiary trisomic chromosome--Ts(17(16))65Dn, Ts(10(16))232Dn, Ts(12(17))4Rk and Ts(4(17))2Lws--and one has the triplicated segment attached to another chromosome--Ts(16C-tel)1Cje. Ts(17(16))65Dn and    Ts(16C-tel)1Cje have similar gene content triplication and differ primarily in whether the extra DNA is in an extra chromosome or not. RESULTS: The presence of an intact extra chromosome, rather than trisomy per se, is associated with male    sterility. Additionally, sterility is correlated with a high frequency of association of the unpaired chromosome with the XY body, which contains the largely unpaired X and Y chromosomes. CONCLUSIONS: Intact extra chromosomes disrupt    spermatogenesis, and unpaired chromosomes establish a unique chromatin territory within meiotic nuclei.</p>

	]]>
</description>

<author>M Davisson et al.</author>


</item>


<item>
<title>Combined deletion of mouse dematin-headpiece and beta-adducin exerts a novel effect on the spectrin-actin junctions leading to erythrocyte fragility and hemolytic anemia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1506</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1506</guid>
<pubDate>Tue, 08 May 2012 22:24:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dematin and adducin are actin-binding proteins of the erythrocyte "junctional complex." Individually, they exert modest effects on erythrocyte shape and membrane stability, and their homologues are expressed widely in non-erythroid    cells. Here we report generation and characterization of double knock-out mice lacking beta-adducin and the headpiece domain of dematin. The combined mutations result in altered erythrocyte morphology, increased membrane instability, and severe    hemolysis. Peripheral blood analysis shows evidence of severe hemolytic anemia with reduced number of erythrocytes/hematocrit/hemoglobin and an approximately 12-fold increase in the number of circulating reticulocytes.  The presence of a variety    of misshapen and fragmented erythrocytes correlates with increased osmotic fragility and reduced in vivo life span.  Despite the apparently normal protein composition of the mutant erythrocyte membrane, the retention of the spectrin-actin complex    in the membrane under low ionic strength conditions is significantly reduced by the double mutation. Atomic force microscopy reveals an increase in grain size and a decrease in filament number of the mutant membrane cytoskeleton, although the    volume parameter is similar to wild type erythrocytes. Aggregated, disassembled, and irregular features are visualized in the mutant membrane, consistent with the presence of large protein aggregates. Importantly, purified dematin binds to the    stripped inside-out vesicles in a saturable manner, and dematin-membrane binding is abolished upon pretreatment of membrane vesicles with trypsin. Together, these results reveal an essential role of dematin and adducin in the maintenance of    erythrocyte shape and membrane stability, and they suggest that the dematin-membrane interaction could link the junctional complex to the plasma membrane in erythroid cells.</p>

	]]>
</description>

<author>H Chen et al.</author>


</item>


<item>
<title>A closer look: secondary glaucoma more likely.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1505</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1505</guid>
<pubDate>Tue, 08 May 2012 22:24:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K Boyd et al.</author>


</item>


<item>
<title>Humanized mice in translational biomedical research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1504</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1504</guid>
<pubDate>Tue, 08 May 2012 22:24:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>The culmination of decades of research on humanized mice is leading to advances in our understanding of human haematopoiesis, innate and adaptive immunity, autoimmunity, infectious diseases, cancer biology and regenerative medicine.    In this Review, we discuss the development of these new generations of humanized mice, how they will facilitate translational research in several biomedical disciplines and approaches to overcome the remaining limitations of these    models.</p>

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</description>

<author>L D. Shultz et al.</author>


</item>


<item>
<title>Mutagenesis-generated mouse models of human infertility with abnormal sperm.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1503</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1503</guid>
<pubDate>Tue, 08 May 2012 22:23:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The aetiology of human male fertility, with impairment of sperm number, motility and morphology (oligoasthenoteratozoospermia), has been difficult to understand, partly for lack of animal models. METHODS: An    ethylnitrosourea (ENU) mutagenesis strategy has been successful in producing heritable gene mutations with phenotypes similar to human male infertility, and here, we describe three independent ENU-induced mutations that cause a phenotype of    oligoasthenoteratozoospermia in mice. RESULTS: The loci identified by these three mutations are designated swm2, repro2 and repro3. All mutant males were characterized by low sperm concentration, poor sperm morphology and negligible motility, but    the infertile males were apparently normal in other respects. Sperm from mutant males failed to fertilize oocytes in vitro. Ultrastructural analyses revealed varied abnormalities apparent in both testicular spermatids and epididymal sperm.    Genetic mapping placed the swm2 gene on chromosome 7, the repro2 gene on chromosome 5 and the repro3 gene on chromosome 10. CONCLUSION: The single-gene mutations caused complex and non-specific sperm pathologies, a point with important    implications for managing cases of human male infertility. The ultimate identification of the loci for the mutations causing these phenotypes will clarify aetiology of complex syndromes of infertility with sperm abnormalities consistent with    oligoasthenoteratozoospermia.</p>

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</description>

<author>C Lessard et al.</author>


</item>


<item>
<title>Mouse Tumor Biology Database (MTB): status update and future directions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1502</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1502</guid>
<pubDate>Tue, 08 May 2012 22:23:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Tumor Biology (MTB) database provides access to data about endogenously arising tumors (both spontaneous and induced) in genetically defined mice (inbred, hybrid, mutant and genetically engineered mice).  Data include    information on the frequency and latency of mouse tumors, pathology reports and images, genomic changes occurring in the tumors, genetic (strain) background and literature or contributor citations. Data are curated from the primary literature or    submitted directly from researchers. MTB is accessed via the Mouse Genome Informatics web site (http://www.informatics.jax.org). Integrated searches of MTB are enabled through use of multiple controlled vocabularies and by adherence to    standardized nomenclature, when available. Recently MTB has been redesigned and its database infrastructure replaced with a robust relational database management system (RDMS). Web interface improvements include a new advanced query form and    enhancements to already existing search capabilities. The Tumor Frequency Grid has been revised to enhance interactivity, providing an overview of reported tumor incidence across mouse strains and an entree into the database. A new pathology data    submission tool allows users to submit, edit and release data to the MTB system.</p>

	]]>
</description>

<author>D A. Begley et al.</author>


</item>


<item>
<title>The mouse genome database (MGD): new features facilitating a model system.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1501</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1501</guid>
<pubDate>Tue, 08 May 2012 22:23:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse genome database (MGD, http://www.informatics.jax.org/), the international community database for mouse, provides access to extensive integrated data on the genetics, genomics and biology of the laboratory mouse. The mouse    is an excellent and unique animal surrogate for studying normal development and disease processes in humans. Thus, MGD's primary goals are to facilitate the use of mouse models for studying human disease and enable the development of    translational research hypotheses based on comparative genotype, phenotype and functional analyses. Core MGD data content includes gene characterization and functions, phenotype and disease model descriptions, DNA and protein sequence data,    polymorphisms, gene mapping data and genome coordinates, and comparative gene data focused on mammals. Data are integrated from diverse sources, ranging from major resource centers to individual investigator laboratories and the scientific    literature, using a combination of automated processes and expert human curation. MGD collaborates with the bioinformatics community on the development of data and semantic standards, and it incorporates key ontologies into the MGD annotation    system, including the Gene Ontology (GO), the Mammalian Phenotype Ontology, and the Anatomical Dictionary for Mouse Development and the Adult Anatomy. MGD is the authoritative source for mouse nomenclature for genes, alleles, and mouse strains,    and for GO annotations to mouse genes. MGD provides a unique platform for data mining and hypothesis generation where one can express complex queries simultaneously addressing phenotypic effects, biochemical function and process, sub-cellular    location, expression, sequence, polymorphism and mapping data. Both web-based querying and computational access to data are provided. Recent improvements in MGD described here include the incorporation of single nucleotide polymorphism data and    search tools, the addition of PIR gene superfamily classifications, phenotype data for NIH-acquired knockout mice, images for mouse phenotypic genotypes, new functional graph displays of GO annotations, and new orthology displays including    sequence information and graphic displays.</p>

	]]>
</description>

<author>J T. Eppig et al.</author>


</item>


<item>
<title>Gene replacement reveals a specific role for E-cadherin in the formation of a functional trophectoderm.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1500</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1500</guid>
<pubDate>Tue, 08 May 2012 22:23:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>During mammalian embryogenesis the trophectoderm represents the first epithelial structure formed. The cell adhesion molecule E-cadherin is ultimately necessary for the transition from compacted morula to the formation of the    blastocyst to ensure correct establishment of adhesion junctions in the trophectoderm. Here, we analyzed to what extent E-cadherin confers unique adhesion and signaling properties in trophectoderm formation in vivo. Using a gene replacement    approach, we introduced N-cadherin cDNA into the E-cadherin genomic locus. We show that the expression of N-cadherin driven from the E-cadherin locus reflects the expression pattern of endogenous E-cadherin. Heterozygous mice co-expressing E- and    N-cadherin are vital and show normal embryonic development. Interestingly, N-cadherin homozygous mutant embryos phenocopy E-cadherin-null mutant embryos. Upon removal of the maternal E-cadherin, we demonstrate that N-cadherin is able to provide    sufficient cellular adhesion to mediate morula compaction, but is insufficient for the subsequent formation of a fully polarized functional trophectoderm. When ES cells were isolated from N-cadherin homozygous mutant embryos and teratomas were    produced, these ES cells differentiated into a large variety of tissue-like structures. Importantly, different epithelial-like structures expressing N-cadherin were formed, including respiratory epithelia, squamous epithelia with signs of    keratinization and secretory epithelia with goblet cells. Thus, N-cadherin can maintain epithelia in differentiating ES cells, but not during the formation of the trophectoderm. Our results point to a specific and unique function for E-cadherin    during mouse preimplantation development.</p>

	]]>
</description>

<author>N G. Kan et al.</author>


</item>


<item>
<title>Mouse Phenome Database (MPD).</title>
<link>http://mouseion.jax.org/stfb2000_2009/1499</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1499</guid>
<pubDate>Tue, 08 May 2012 22:23:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Phenome Database (MPD; http://www.jax.org/phenome) is a repository of phenotypic and genotypic data on commonly used and genetically diverse inbred strains of mice. Strain characteristics data are contributed by members of    the scientific community. Electronic access to centralized strain data enables biomedical researchers to choose appropriate strains for many systems-based research applications, including physiological studies, drug and toxicology testing and    modeling disease processes. MPD provides a community data repository and a platform for data analysis and in silico hypothesis testing. The laboratory mouse is a premier genetic model for understanding human biology and pathology; MPD facilitates    research that uses the mouse to identify and determine the function of genes participating in normal and disease pathways.</p>

	]]>
</description>

<author>M A. Bogue et al.</author>


</item>


<item>
<title>Factors affecting hearing in mice, rats, and other laboratory animals.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1498</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1498</guid>
<pubDate>Tue, 08 May 2012 22:23:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>The auditory system of rodents and other animals is affected by numerous genetic and environmental variables. These include genes that cause hearing loss, exposure to noise that induces hearing loss, ameliorative effects of an    augmented acoustic environment on hearing loss, and effects of background noise on arousal. An understanding of genetic and environmental influences on hearing and auditory behavior is important for those who provide, use, and care for laboratory    animals.</p>

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</description>

<author>J F. Willott</author>


</item>


<item>
<title>Impact of seafood and fruit consumption on bone mineral density.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1497</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1497</guid>
<pubDate>Tue, 08 May 2012 22:22:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVES: Over the past decade, dietary choices and nutrition have proven to be major modulators of bone mineral density (BMD) in men and women. We investigated environmental determinants, specifically dietary habits, of BMD by    using multiple regression models in a rural Chinese population. METHODS: BMDs were measured at the hip and total body in 5848 men and 6207 women, aged 25-64. Dietary and supplemental intakes were assessed by a simple, one-page questionnaire    tailored to collect nutritional information from large rural populations. Another questionnaire was used to collect information on the subjects' age, disease history, smoking, alcohol consumption, physical activity as well as women's menstrual    status and reproductive history. Multiple regression models were used to assess the relationships among dietary variables and BMD, after adjusting for age, BMI (body mass index), weight, occupation, smoking status, and alcohol consumption.    RESULTS: Increasing seafood consumption was significantly associated with greater BMD in women (p<0.001), especially those consuming more than 250 g per week of seafood.  One thousand and three hundred and twenty-four men and 1479 women    consumed</p>

	]]>
</description>

<author>P A. Zalloua et al.</author>


</item>


<item>
<title>Transcriptional profile of mouse pre-granulosa and Sertoli cells isolated from early-differentiated fetal gonads.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1496</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1496</guid>
<pubDate>Tue, 08 May 2012 22:22:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gonadal sex determining (GSD) genes that initiate fetal ovarian and testicular development and differentiation are expressed in the cells of the urogenital ridge that differentiate as somatic support cells (SSCs), i.e., granulosa    cells of the ovary and Sertoli cells of the testis. To identify potential new mammalian GSD genes, we used the Mouse Genome 430v2.0 GeneChip to analyze gene expression differences between XX and XY SSCs cells isolated from the gonads of embryonic    day (E) 13 C57BL/6J fetuses carrying an EGFP reporter transgene expressed specifically in SSCs. In addition, genome wide expression differences between XX and XY E13 whole gonads were examined. Analysis revealed that XX and XY E13 SSCs    differentially express 647 transcripts (False Discovery Rate cutoff 1%), including transcripts not previously reported to exhibit a sexually dimorphic expression pattern in this unique cell population. Enrichment for genes controlling cell    proliferation was noted in XY SSCs, whereas enrichment for genes controlling cell morphology and metabolic status was identified in XX SSCs. Among the newly identified differentially expressed transcripts are potential GSD genes involved in    unexplained human sex reversal cases.</p>

	]]>
</description>

<author>G J. Bouma et al.</author>


</item>


<item>
<title>Role of the beta1 subunit in the function and stability of the 20S proteasome in the hyperthermophilic archaeon Pyrococcus furiosus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1495</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1495</guid>
<pubDate>Tue, 08 May 2012 22:22:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The hyperthermophilic archaeon Pyrococcus furiosus genome encodes three proteasome component proteins: one alpha protein (PF1571) and two beta proteins (beta1-PF1404 and beta2-PF0159), as well as an ATPase (PF0115), referred to as    proteasome-activating nucleotidase. Transcriptional analysis of the P. furiosus dynamic heat shock response (shift from 90 to 105 degrees C) showed that the beta1 gene was up-regulated over twofold within 5 minutes, suggesting a specific role    during thermal stress.  Consistent with transcriptional data, two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that incorporation of the beta1 protein relative to beta2 into the 20S proteasome (core particle    [CP]) increased with increasing temperature for both native and recombinant versions. For the recombinant enzyme, the beta2/beta1 ratio varied linearly with temperature from 3.8, when assembled at 80 degrees C, to 0.9 at 105 degrees C. The    recombinant alpha+beta1+beta2 CP assembled at 105 degrees C was more thermostable than either the alpha+beta1+beta2 version assembled at 90 degrees C or the alpha+beta2 version assembled at either 90 degrees C or 105 degrees C, based on melting    temperature and the biocatalytic inactivation rate at 115 degrees C. The recombinant CP assembled at 105 degrees C was also found to have different catalytic rates and specificity for peptide hydrolysis, compared to the 90 degrees C assembly    (measured at 95 degrees C). Combination of the alpha and beta1 proteins neither yielded a large proteasome complex nor demonstrated any significant activity. These results indicate that the beta1 subunit in the P. furiosus 20S proteasome plays a    thermostabilizing role and influences biocatalytic properties, suggesting that beta subunit composition is a factor in archaeal proteasome function during thermal stress, when polypeptide turnover is essential to cell survival.</p>

	]]>
</description>

<author>L S. Madding et al.</author>


</item>


<item>
<title>Activation of peroxisome proliferator-activated receptor gamma (PPARgamma) by rosiglitazone suppresses components of the insulin-like growth factor regulatory system in vitro and in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1494</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1494</guid>
<pubDate>Tue, 08 May 2012 22:22:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rosiglitazone (Rosi) belongs to the class of thiazolidinediones (TZDs) that are ligands for peroxisome proliferator-activated receptor gamma (PPARgamma). Stimulation of PPARgamma suppresses bone formation and enhances marrow    adipogenesis. We hypothesized that activation of PPARgamma down-regulates components of the IGF regulatory system, leading to impaired osteoblast function. Rosi treatment (1 microm) of a marrow stromal cell line (UAMS-33) transfected with empty    vector (U-33/c) or with PPARgamma2 (U-33/gamma2) were analyzed by microarray. Rosi reduced IGF-I, IGF-II, IGFBP-4, and the type I and II IGF receptor (IGF1R and IGF2R) expression at 72 h in U-33/gamma2 compared with U-33/c cells (P < 0.01); these    findings were confirmed by RT-PCR. Rosi reduced secreted IGF-I from U-33/gamma2 cells by 75% (P < 0.05). Primary marrow stromal cells (MSCs) extracted from adult (8 months) and old (24 months) C57BL/6J (B6) mice were treated with Rosi (1 microm)    for 48 h. IGF-I, IGFBP-4, and IGF1R transcripts were reduced in Rosi-treated MSCs compared with vehicle (P < 0.01) and secreted IGF-I was also suppressed (P < 0.05). B6 mice treated with Rosi (20 mg/kg.d) for short duration (i.e. 4 d), and long    term (i.e.  7 wk) had reduced serum IGF-I; this was accompanied by markedly suppressed IGF-I transcripts in the liver and peripheral fat of treated animals. To determine whether Rosi affected circulating IGF-I in humans, we measured serum IGF-I,    IGFBP-2, and IGFBP-3 at four time points in 50 postmenopausal women randomized to either Rosi (8 mg/d) or placebo. Rosi-treated subjects had significantly lower IGF-I at 8 wk than baseline (-25%, P < 0.05), and at 16 wk their levels were reduced    14% vs. placebo (P = 0.15). We conclude that Rosi suppresses IGF-I expression in bone and liver; these changes could affect skeletal acquisition through endocrine and paracrine pathways.</p>

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</description>

<author>Czernik B. Lecka et al.</author>


</item>


<item>
<title>Laser surgery for mouse geneticists.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1493</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1493</guid>
<pubDate>Tue, 08 May 2012 22:22:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T Gridley et al.</author>


</item>


<item>
<title>Ability of herpes simplex virus vectors to boost immune responses to DNA vectors and to protect against challenge by simian immunodeficiency virus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1492</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1492</guid>
<pubDate>Tue, 08 May 2012 22:22:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>The immunogenicity and protective capacity of replication-defective herpes simplex virus (HSV) vector-based vaccines were examined in rhesus macaques. Three macaques were inoculated with recombinant HSV vectors expressing Gag, Env,    and a Tat-Rev-Nef fusion protein of simian immunodeficiency virus (SIV). Three other macaques were primed with recombinant DNA vectors expressing Gag, Env, and a Pol-Tat-Nef-Vif fusion protein prior to boosting with the HSV vectors. Robust    anti-Gag and anti-Env cellular responses were detected in all six macaques. Following intravenous challenge with wild-type, cloned SIV239, peak and 12-week plasma viremia levels were significantly lower in vaccinated compared to control macaques.    Plasma SIV RNA in vaccinated macaques was inversely correlated with anti-Rev ELISPOT responses on the day of challenge (P value<0.05), anti-Tat ELISPOT responses at 2 weeks post challenge (P value <0.05) and peak neutralizing antibody titers    pre-challenge (P value 0.06).  These findings support continued study of recombinant herpesviruses as a vaccine approach for AIDS.</p>

	]]>
</description>

<author>A Kaur et al.</author>


</item>


<item>
<title>A viable allele of Mcm4 causes chromosome instability and mammary adenocarcinomas in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1491</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1491</guid>
<pubDate>Tue, 08 May 2012 22:22:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mcm4 (minichromosome maintenance-deficient 4 homolog) encodes a subunit of the MCM2-7 complex (also known as MCM2-MCM7), the replication licensing factor and presumptive replicative helicase. Here, we report that the mouse    chromosome instability mutation Chaos3 (chromosome aberrations occurring spontaneously 3), isolated in a forward genetic screen, is a viable allele of Mcm4. Mcm4(Chaos3) encodes a change in an evolutionarily invariant amino acid (F345I),    producing an apparently destabilized MCM4.  Saccharomyces cerevisiae strains that we engineered to contain a corresponding allele (resulting in an F391I change) showed a classical minichromosome loss phenotype. Whereas homozygosity for a    disrupted Mcm4 allele (Mcm4(-)) caused preimplantation lethality, Mcm(Chaos3/-) embryos died late in gestation, indicating that Mcm4(Chaos3) is hypomorphic.  Mutant embryonic fibroblasts were highly susceptible to chromosome breaks induced by the    DNA replication inhibitor aphidicolin. Most notably, >80% of Mcm4(Chaos3/Chaos3) females succumbed to mammary adenocarcinomas with a mean latency of 12 months. These findings suggest that hypomorphic alleles of the genes encoding the subunits of    the MCM2-7 complex may increase breast cancer risk.</p>

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</description>

<author>N Shima et al.</author>


</item>


<item>
<title>Evidence that MIG-6 is a tumor-suppressor gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1490</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1490</guid>
<pubDate>Tue, 08 May 2012 22:21:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mitogen-inducible gene 6 (MIG-6) is located in human chromosome 1p36, a locus frequently associated with human lung cancer. MIG-6 is a negative regulator of epidermal growth factor (EGF) signaling, and we show that Mig-6 - like EGF    - is induced by hepatocyte growth factor/scatter factor (HGF/SF) in human lung cancer cell lines. Frequently, the receptors for both factors, EGFR and Met, are expressed in same lung cancer cell line, and MIG-6 is induced by both factors in a    mitogen-activated protein kinase-dependent fashion. However, not all tumor lines express MIG-6 in response to either EGF or HGF/SF. In these cases, we find missense and nonsense mutations in the MIG-6 coding region, as well as evidence for MIG-6    transcriptional silencing. Moreover, germline disruption of Mig-6 in mice leads to the development of animals with epithelial hyperplasia, adenoma, and adenocarcinoma in organs like the lung, gallbladder, and bile duct. These data suggests that    MIG-6 is a tumor-suppressor gene and is therefore a candidate gene for the frequent 1p36 genetic alterations found in lung cancer.</p>

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</description>

<author>Y W. Zhang et al.</author>


</item>


<item>
<title>Estimating p-values in small microarray experiments.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1489</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1489</guid>
<pubDate>Tue, 08 May 2012 22:21:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>MOTIVATION: Microarray data typically have small numbers of observations per gene, which can result in low power for statistical tests. Test statistics that borrow information from data across all of the genes can improve power, but    these statistics have non-standard distributions, and their significance must be assessed using permutation analysis. When sample sizes are small, the number of distinct permutations can be severely limited, and pooling the permutation-derived    test statistics across all genes has been proposed. However, the null distribution of the test statistics under permutation is not the same for equally and differentially expressed genes. This can have a negative impact on both p-value estimation    and the power of information borrowing statistics.  RESULTS: We investigate permutation based methods for estimating p-values.  One of methods that uses pooling from a selected subset of the data are shown to have the correct type I error rate    and to provide accurate estimates of the false discovery rate (FDR). We provide guidelines to select an appropriate subset. We also demonstrate that information borrowing statistics have substantially increased power compared to the t-test in    small experiments.</p>

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</description>

<author>H Yang et al.</author>


</item>


<item>
<title>Critical role of endothelial Notch1 signaling in postnatal angiogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1488</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1488</guid>
<pubDate>Tue, 08 May 2012 22:21:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Notch receptors are important mediators of cell fate during embryogenesis, but their role in adult physiology, particularly in postnatal angiogenesis, remains unknown. Of the Notch receptors, only Notch1 and Notch4 are expressed in    vascular endothelial cells. Here we show that blood flow recovery and postnatal neovascularization in response to hindlimb ischemia in haploinsufficient global or endothelial-specific Notch1(+/-) mice, but not Notch4(-/-) mice, were impaired    compared with wild-type mice. The expression of vascular endothelial growth factor (VEGF) in response to ischemia was comparable between wild-type and Notch mutant mice, suggesting that Notch1 is downstream of VEGF signaling.  Treatment of    endothelial cells with VEGF increases presenilin proteolytic processing, gamma-secretase activity, Notch1 cleavage, and Hes-1 (hairy enhancer of split homolog-1) expression, all of which were blocked by treating endothelial cells with inhibitors    of phosphatidylinositol 3-kinase/protein kinase Akt or infecting endothelial cells with a dominant-negative Akt mutant. Indeed, inhibition of gamma-secretase activity leads to decreased angiogenesis and inhibits VEGF-induced endothelial cell    proliferation, migration, and survival. Overexpression of the active Notch1 intercellular domain rescued the inhibitory effects of gamma-secretase inhibitors on VEGF-induced angiogenesis. These findings indicate that the phosphatidylinositol    3-kinase/Akt pathway mediates gamma-secretase and Notch1 activation by VEGF and that Notch1 is critical for VEGF-induced postnatal angiogenesis. These results suggest that Notch1 may be a novel therapeutic target for improving angiogenic response    and blood flow recovery in ischemic limbs.</p>

	]]>
</description>

<author>K Takeshita et al.</author>


</item>


<item>
<title>Systematic variation in mRNA 3&apos;-processing signals during mouse spermatogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1487</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1487</guid>
<pubDate>Tue, 08 May 2012 22:21:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gene expression and processing during mouse male germ cell maturation (spermatogenesis) is highly specialized. Previous reports have suggested that there is a high incidence of alternative 3'-processing in male germ cell mRNAs,    including reduced usage of the canonical polyadenylation signal, AAUAAA. We used EST libraries generated from mouse testicular cells to identify 3'-processing sites used at various stages of spermatogenesis (spermatogonia, spermatocytes and round    spermatids) and testicular somatic Sertoli cells. We assessed differences in 3'-processing characteristics in the testicular samples, compared to control sets of widely used 3'-processing sites. Using a new method for comparison of degenerate    regulatory elements between sequence samples, we identified significant changes in the use of putative 3'-processing regulatory sequence elements in all spermatogenic cell types. In addition, we observed a trend towards truncated 3'-untranslated    regions (3'-UTRs), with the most significant differences apparent in round spermatids. In contrast, Sertoli cells displayed a much smaller trend towards 3'-UTR truncation and no significant difference in 3'-processing regulatory sequences.    Finally, we identified a number of genes encoding mRNAs that were specifically subject to alternative 3'-processing during meiosis and postmeiotic development. Our results highlight developmental differences in polyadenylation site choice and in    the elements that likely control them during spermatogenesis.</p>

	]]>
</description>

<author>D Liu et al.</author>


</item>


<item>
<title>The mouse as a model for human biology: a resource guide for complex trait analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1486</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1486</guid>
<pubDate>Tue, 08 May 2012 22:21:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse has been a powerful force in elucidating the genetic basis of human physiology and pathophysiology. From its beginnings as the model organism for cancer research and transplantation biology to the present, when dissection    of the genetic basis of complex disease is at the forefront of genomics research, an enormous and remarkable mouse resource infrastructure has accumulated. This review summarizes those resources and provides practical guidelines for their use,    particularly in the analysis of quantitative traits.</p>

	]]>
</description>

<author>L L. Peters et al.</author>


</item>


<item>
<title>Effects of loss of classical estrogen response element signaling on bone in male mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1485</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1485</guid>
<pubDate>Tue, 08 May 2012 22:21:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Syed FA Fraser DG Spelsberg TC Rosen CJ Krust A Chambon P Jameson JL Khosia S</author>


</item>


<item>
<title>Mouse models of RP.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1484</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1484</guid>
<pubDate>Tue, 08 May 2012 22:20:59 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>B Chang et al.</author>


</item>


<item>
<title>Eye research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1483</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1483</guid>
<pubDate>Tue, 08 May 2012 22:20:50 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R S. Smith et al.</author>


</item>


<item>
<title>Genetic monitoring.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1482</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1482</guid>
<pubDate>Tue, 08 May 2012 22:20:42 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R R. Fox et al.</author>


</item>


<item>
<title>Reproductive bology of the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1481</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1481</guid>
<pubDate>Tue, 08 May 2012 22:20:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K R. Pritchett et al.</author>


</item>


<item>
<title>Cytogenetics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1480</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1480</guid>
<pubDate>Tue, 08 May 2012 22:20:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M T, Handel Davisson</author>


</item>


<item>
<title>Gene mapping.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1479</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1479</guid>
<pubDate>Tue, 08 May 2012 22:20:16 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M T. Davisson</author>


</item>


<item>
<title>Mouse strain and genetic nomenclature: an abbreviated guide.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1478</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1478</guid>
<pubDate>Tue, 08 May 2012 22:20:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J T. Eppig</author>


</item>


<item>
<title>Breeding systems: considerations, genetic fundamentals, genetic background, and strain types.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1477</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1477</guid>
<pubDate>Tue, 08 May 2012 22:19:57 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M L. Berry et al.</author>


</item>


<item>
<title>Disentangling information flow in the Ras-cAMP signaling network.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1476</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1476</guid>
<pubDate>Tue, 08 May 2012 22:19:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The perturbation of signal-transduction molecules elicits genomic-expression effects that are typically neither restricted to a small set of genes nor uniform. Instead there are broad, varied, and complex changes in expression    across the genome. These observations suggest that signal transduction is not mediated by isolated pathways of information flow to distinct groups of genes in the genome. Rather, multiple entangled paths of information flow influence overlapping    sets of genes. Using the Ras-cAMP pathway in Saccharomyces cerevisiae as a model system, we perturbed key pathway elements and collected genomic-expression data. Singular value decomposition was applied to separate the genome-wide transcriptional    response into weighted expression components exhibited by overlapping groups of genes. Molecular interaction data were integrated to connect gene groups to perturbed signaling elements. The resulting series of linked subnetworks maps multiple    putative pathways of information flow through a dense signaling network, and provides a set of testable hypotheses for complex gene-expression effects across the genome.</p>

	]]>
</description>

<author>G W. Carter et al.</author>


</item>


<item>
<title>Canadian Association of Neurosciences review: postnatal development of the mammalian neocortex: role of activity revisited.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1475</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1475</guid>
<pubDate>Tue, 08 May 2012 22:19:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mammalian neocortex is the largest structure in the brain, and plays a key role in brain function. A critical period for the development of the neocortex is the early postnatal life, when the majority of synapses are formed and    when much of synaptic remodeling takes place. Early studies suggest that initial synaptic connections lack precision, and this rudimentary wiring pattern is refined by experience-related activity through selective elimination and consolidation.    This view has been challenged by recent studies revealing the presence of a relatively precise pattern of connections before the onset of sensory experience. The recent data support a model in which specificity of neuronal connections is largely    determined by genetic factors. Spontaneous activity is required for the formation of neural circuits, but whether it plays an instructive role is still controversial. Neurotransmitters including acetylcholine, serotonin, and gamma-Aminobutyric    acid (GABA) may have key roles in the regulation of spontaneous activity, and in the maturation of synapses in the developing brain.</p>

	]]>
</description>

<author>Z W. Zhang</author>


</item>


<item>
<title>Developmental refinement in the mammalian thalamus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1474</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1474</guid>
<pubDate>Tue, 08 May 2012 22:19:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The sensory relay synapses in the thalamus undergo extensive refinement during early life. Disruptions of spontaneous activity, but not sensory deprivation, can induce large-scale re-organization of neuronal connections in the    thalamus.  Recent studies also reveal an extended period of synaptic refinement in the visual and somatosensory relay synapses, where sensory deprivation produces some unexpected effects on synaptic remodeling. This article aims to provide a    brief overview of recent findings and current ideas about the refinement of relay synapses in the thalamus.</p>

	]]>
</description>

<author>Z W. Zhang</author>


</item>


<item>
<title>Integrative genetic analysis of transcription modules: towards filling the gap between genetic loci and inherited traits.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1473</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1473</guid>
<pubDate>Tue, 08 May 2012 22:19:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic loci that regulate inherited traits are routinely identified using quantitative trait locus (QTL) mapping methods. However, the genotype-phenotype associations do not provide information on the gene expression program    through which the genetic loci regulate the traits. Transcription modules are 'self-consistent regulatory units' and are closely related to the modular components of gene regulatory network [Ihmels, J., Friedlander, G., Bergmann, S., Sarig, O.,    Ziv, Y. and Barkai, N. (2002) Revealing modular organization in the yeast transcriptional network. Nat. Genet., 31, 370-377; Segal, E., Shapira, M., Regev, A., Pe'er, D., Botstein, D., Koller, D. and Friedman, N. (2003) Module networks:    identifying regulatory modules and their condition-specific regulators from gene expression data. Nat. Genet., 34, 166-176]. We used genome-wide genotype and gene expression data of a genetic reference population that consists of mice of 32    recombinant inbred strains to identify the transcription modules and the genetic loci regulating them. Twenty-nine transcription modules defined by genetic variations were identified. Statistically significant associations between the    transcription modules and 18 classical physiological and behavioral traits were found. Genome-wide interval mapping showed that major QTLs regulating the transcription modules are often co-localized with the QTLs regulating the associated    classical traits. The association and the possible co-regulation of the classical trait and transcription module indicate that the transcription module may be involved in the gene pathways connecting the QTL and the classical trait. Our results    show that a transcription module may associate with multiple seemingly unrelated classical traits and a classical trait may associate with different modules. Literature mining results provided strong independent evidences for the relations among    genes of the transcription modules, genes in the regions of the QTLs regulating the transcription modules and the keywords representing the classical traits.</p>

	]]>
</description>

<author>H Li et al.</author>


</item>


<item>
<title>Natural variation and genetic covariance in adult hippocampal neurogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1472</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1472</guid>
<pubDate>Tue, 08 May 2012 22:19:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adult hippocampal neurogenesis is highly variable and heritable among laboratory strains of mice. Adult neurogenesis is also remarkably plastic and can be modulated by environment and activity. Here, we provide a systematic    quantitative analysis of adult hippocampal neurogenesis in two large genetic reference panels of recombinant inbred strains (BXD and AXB/BXA, n = 52 strains). We combined data on variation in neurogenesis with a new transcriptome database to    extract a set of 190 genes with expression patterns that are also highly variable and that covary with rates of (i) cell proliferation, (ii) cell survival, or the numbers of surviving (iii) new neurons, and (iv) astrocytes. Expression of a subset    of these neurogenesis-associated transcripts was controlled in cis across the BXD set. These self-modulating genes are particularly interesting candidates to control neurogenesis. Among these were musashi (Msi1h) and prominin1/CD133 (Prom1), both    of which are linked to stem-cell maintenance and division. Twelve neurogenesis-associated transcripts had significant cis-acting quantitative trait loci, and, of these, six had plausible biological association with adult neurogenesis (Prom1,    Ssbp2, Kcnq2, Ndufs2, Camk4, and Kcnj9). Only one cis-acting candidate was linked to both neurogenesis and gliogenesis, Rapgef6, a downstream target of ras signaling. The use of genetic reference panels coupled with phenotyping and global    transcriptome profiling thus allowed insight into the complexity of the genetic control of adult neurogenesis.</p>

	]]>
</description>

<author>G Kempermann et al.</author>


</item>


<item>
<title>Progress in using mouse inbred strains, consomics, and mutants to identify genes related to stress, anxiety, and alcohol phenotypes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1471</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1471</guid>
<pubDate>Tue, 08 May 2012 22:19:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>This article summarizes the proceedings of a symposium that took place at the 2005 meeting of the Research Society on Alcoholism. The organizers/chairs were Daniel Goldowitz and Katheen A. Grant. The presentations were as follows:    (1) High-Throughput Screening for Ethanol Phenotypes, by Douglas B. Matthews and Kristin M. Hamre; (2) Genetic Basis of Schedule-Induced Polydipsia in Mice, by Guy Mittleman and Elissa J. Chesler; (3) Effects of Stress and Ethanol Dependence on    Ethanol Self-administration in Inbred and Mutant Mice, by Howard C. Becker and Marcelo F. Lopez; (4) Changes in Dopaminergic Mechanisms Associated With Ethanol Dependence, by Sara R. Jones and Tiffany A. Mathews; and (5) Defining Brain    Region-Specific Gene Networks Relevant to Ethanol Behaviors, by Michael F. Miles and Robnet Kerns.</p>

	]]>
</description>

<author>D Goldowitz et al.</author>


</item>


<item>
<title>Extracting gene networks for low-dose radiation using graph theoretical algorithms.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1470</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1470</guid>
<pubDate>Tue, 08 May 2012 22:18:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genes with common functions often exhibit correlated expression levels, which can be used to identify sets of interacting genes from microarray data. Microarrays typically measure expression across genomic space, creating a massive    matrix of co-expression that must be mined to extract only the most relevant gene interactions. We describe a graph theoretical approach to extracting co-expressed sets of genes, based on the computation of cliques. Unlike the results of    traditional clustering algorithms, cliques are not disjoint and allow genes to be assigned to multiple sets of interacting partners, consistent with biological reality. A graph is created by thresholding the correlation matrix to include only the    correlations most likely to signify functional relationships. Cliques computed from the graph correspond to sets of genes for which significant edges are present between all members of the set, representing potential members of common or    interacting pathways. Clique membership can be used to infer function about poorly annotated genes, based on the known functions of better-annotated genes with which they share clique membership (i.e., "guilt-by-association"). We illustrate our    method by applying it to microarray data collected from the spleens of mice exposed to low-dose ionizing radiation. Differential analysis is used to identify sets of genes whose interactions are impacted by radiation exposure. The correlation    graph is also queried independently of clique to extract edges that are impacted by radiation. We present several examples of multiple gene interactions that are altered by radiation exposure and thus represent potential molecular pathways that    mediate the radiation response.</p>

	]]>
</description>

<author>B H. Voy et al.</author>


</item>


<item>
<title>A scalable method for integration and functional analysis of multiple microarray datasets.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1469</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1469</guid>
<pubDate>Tue, 08 May 2012 22:18:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>MOTIVATION: The diverse microarray datasets that have become available over the past several years represent a rich opportunity and challenge for biological data mining. Many supervised and unsupervised methods have been developed    for the analysis of individual microarray datasets. However, integrated analysis of multiple datasets can provide a broader insight into genetic regulation of specific biological pathways under a variety of conditions. RESULTS: To aid in the    analysis of such large compendia of microarray experiments, we present Microarray Experiment Functional Integration Technology (MEFIT), a scalable Bayesian framework for predicting functional relationships from integrated microarray datasets.    Furthermore, MEFIT predicts these functional relationships within the context of specific biological processes. All results are provided in the context of one or more specific biological functions, which can be provided by a biologist or drawn    automatically from catalogs such as the Gene Ontology (GO). Using MEFIT, we integrated 40 Saccharomyces cerevisiae microarray datasets spanning 712 unique conditions. In tests based on 110 biological functions drawn from the GO biological process    ontology, MEFIT provided a 5% or greater performance increase for 54 functions, with a 5% or more decrease in performance in only two functions.</p>

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</description>

<author>C Huttenhower et al.</author>


</item>


<item>
<title>Finding function: evaluation methods for functional genomic data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1468</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1468</guid>
<pubDate>Tue, 08 May 2012 22:18:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Accurate evaluation of the quality of genomic or proteomic data and computational methods is vital to our ability to use them for formulating novel biological hypotheses and directing further experiments. There is    currently no standard approach to evaluation in functional genomics. Our analysis of existing approaches shows that they are inconsistent and contain substantial functional biases that render the resulting evaluations misleading both    quantitatively and qualitatively. These problems make it essentially impossible to compare computational methods or large-scale experimental datasets and also result in conclusions that generalize poorly in most biological applications. RESULTS:    We reveal issues with current evaluation methods here and suggest new approaches to evaluation that facilitate accurate and representative characterization of genomic methods and data. Specifically, we describe a functional genomics gold standard    based on curation by expert biologists and demonstrate its use as an effective means of evaluation of genomic approaches. Our evaluation framework and gold standard are freely available to the community through our website.  CONCLUSION: Proper    methods for evaluating genomic data and computational approaches will determine how much we, as a community, are able to learn from the wealth of available data. We propose one possible solution to this problem here but emphasize that this topic    warrants broader community discussion.</p>

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</description>

<author>C L. Myers et al.</author>


</item>


<item>
<title>GOLEM: an interactive graph-based gene-ontology navigation and analysis tool.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1467</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1467</guid>
<pubDate>Tue, 08 May 2012 22:18:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The Gene Ontology has become an extremely useful tool for the analysis of genomic data and structuring of biological knowledge. Several excellent software tools for navigating the gene ontology have been developed.     However, no existing system provides an interactively expandable graph-based view of the gene ontology hierarchy. Furthermore, most existing tools are web-based or require an Internet connection, will not load local annotations files, and provide    either analysis or visualization functionality, but not both. RESULTS: To address the above limitations, we have developed GOLEM (Gene Ontology Local Exploration Map), a visualization and analysis tool for focused exploration of the gene ontology    graph. GOLEM allows the user to dynamically expand and focus the local graph structure of the gene ontology hierarchy in the neighborhood of any chosen term. It also supports rapid analysis of an input list of genes to find enriched gene ontology    terms. The GOLEM application permits the user either to utilize local gene ontology and annotations files in the absence of an Internet connection, or to access the most recent ontology and annotation information from the gene ontology webpage.    GOLEM supports global and organism-specific searches by gene ontology term name, gene ontology id and gene name. CONCLUSION: GOLEM is a useful software tool for biologists interested in visualizing the local directed acyclic graph structure of    the gene ontology hierarchy and searching for gene ontology terms enriched in genes of interest. It is freely available both as an application and as an applet at http://function.princeton.edu/GOLEM.</p>

	]]>
</description>

<author>R S. Sealfon et al.</author>


</item>


<item>
<title>Telomere shortening and mood disorders: preliminary support for a chronic stress model of accelerated aging.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1466</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1466</guid>
<pubDate>Tue, 08 May 2012 22:18:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Little is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial evidence supports abnormalities in stress-related biological systems in    depression. Accelerated telomere shortening may reflect stress-related oxidative damage to cells and accelerated aging, and severe psychosocial stress has been linked to telomere shortening. We propose that chronic stress associated with mood    disorders may contribute to excess vulnerability for diseases of aging such as cardiovascular disease and possibly some cancers through accelerated organismal aging. METHODS: Telomere length was measured by Southern Analysis in 44 individuals    with chronic mood disorders and 44 nonpsychiatrically ill age-matched control subjects. RESULTS: Telomere length was significantly shorter in those with mood disorders, representing as much as 10 years of accelerated aging. CONCLUSIONS: These    results provide preliminary evidence that mood disorders are associated with accelerated aging and may suggest a novel mechanism for mood disorder-associated morbidity and mortality.</p>

	]]>
</description>

<author>N M. Simon et al.</author>


</item>


<item>
<title>A natural language processing (NLP) tool to assist in the curation of the laboratory Mouse Tumor Biology Database.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1465</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1465</guid>
<pubDate>Tue, 08 May 2012 22:18:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>A substantial effort of the biological community involves the development of model organism databases containing key genomic information concerning specific organisms. This paper describes a developing natural language processing    (NLP) tool, which is aimed at assisting curators of the Mouse Tumor Biology (MTB) Database of the Mouse Genome Informatics (MGI) group by helping them quickly find key information in the articles.</p>

	]]>
</description>

<author>H Xu et al.</author>


</item>


<item>
<title>Discrimination of Non-Protein-Coding Transcripts from Protein-Coding mRNA.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1464</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1464</guid>
<pubDate>Tue, 08 May 2012 22:18:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Several recent studies indicate that mammals and other organisms produce large numbers of RNA transcripts that do not correspond to known genes. It has been suggested that these transcripts do not encode proteins, but may instead    function as RNAs. However, discrimination of coding and non-coding transcripts is not straightforward, and different laboratories have used different methods, whose ability to perform this discrimination is unclear. In this study, we examine ten    bioinformatic methods that assess protein-coding potential and compare their ability and congruency in the discrimination of non-coding from coding sequences, based on four underlying principles: open reading frame size, sequence similarity to    known proteins or protein domains, statistical models of protein-coding sequence, and synonymous versus non-synonymous substitution rates. Despite these different approaches, the methods show broad concordance, suggesting that coding and    non-coding transcripts can, in general, be reliably discriminated, and that many of the recently discovered extra-genic transcripts are indeed non-coding. Comparison of the methods indicates reasons for unreliable predictions, and approaches to    increase confidence further. Conversely and surprisingly, our analyses also provide evidence that as much as approximately 10% of entries in the manually curated protein database Swiss-Prot are erroneous translations of actually non-coding    transcripts.</p>

	]]>
</description>

<author>M C. Frith et al.</author>


</item>


<item>
<title>Histone lysine trimethylation exhibits a distinct perinuclear distribution in Plzf-expressing spermatogonia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1463</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1463</guid>
<pubDate>Tue, 08 May 2012 22:17:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chromatin structure plays an important role in the regulation of gene expression. Methylation of lysine residues on histone tails is an epigenetic mark that influences chromatin repression when specifically imparted on lysines 9 and    27 of histone H3, and on lysine 20 of H4.  Histone lysines can be mono-, di-, and trimethylated, and all three modification states have been identified in different nuclear domains.  Correlation of these methylated histone states to different    stages of cell differentiation, however, is not extensive. Mammalian spermatogenesis is a developmental process ideal for studying the epigenetic control of differentiation. Maintenance of spermatogonial stem cells requires the transcriptional    repressor Plzf, but a role for histone methylation has not been established. Here we show that Plzf-expressing spermatogonia completely lack monomethyl-H3-K27 and monomethyl-H4-K20, and contain very little monomethyl-H3-K9. Dimethylated H3-K27    and H4-K20 are detected as punctate foci in Plzf-positive cells, but dimethyl-H3-K9 is absent.  Trimethylated H3-K9 and H4-K20 exhibit a unique perinuclear distribution that coincides with Plzf expression, localizing to punctate foci in more    differentiated spermatogonia. Loss of Plzf correlates with increased punctate distribution of trimethylated H3-K9 and H4-K20 at the expense of perinuclear localization. These data signify the possible importance of different histone lysine    methylation states in the epigenetic control of spermatogenesis.</p>

	]]>
</description>

<author>C Payne et al.</author>


</item>


<item>
<title>TEX14 is essential for intercellular bridges and fertility in male mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1462</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1462</guid>
<pubDate>Tue, 08 May 2012 22:17:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cytokinesis in somatic cells concludes with the formation of a midbody, which is abscised to form individual daughter cells. In contrast, germ cell cytokinesis results in a permanent intercellular bridge connecting the daughter    cells through a large cytoplasmic channel. During spermatogenesis, proposed roles for the intercellular bridge include germ cell communication, synchronization, and chromosome dosage compensation in haploid cells. Although several essential    components of the midbody have recently been identified, essential components of the vertebrate germ cell intercellular bridge have until now not been described. Herein, we show that testis-expressed gene 14 (TEX14) is a novel protein that    localizes to germ cell intercellular bridges. In the absence of TEX14, intercellular bridges are not observed by using electron microscopy and other markers.  Spermatogenesis in Tex14(-/-) mice progresses through the transit amplification of    diploid spermatogonia and the expression of early meiotic markers but halts before the completion of the first meiotic division.  Thus, TEX14 is required for intercellular bridges in vertebrate germ cells, and these studies provide evidence that    the intercellular bridge is essential for spermatogenesis and fertility.</p>

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</description>

<author>M P. Greenbaum et al.</author>


</item>


<item>
<title>Glial cell line-derived neurotrophic factor maintains a POZ-itive influence on stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1461</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1461</guid>
<pubDate>Tue, 08 May 2012 22:17:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C Payne et al.</author>


</item>


<item>
<title>Pathway to totipotency: lessons from germ cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1460</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1460</guid>
<pubDate>Tue, 08 May 2012 22:17:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Oocytes and sperm are some of the most differentiated cells in our bodies, yet they generate all cell types after fertilization. Accumulating evidence suggests that this extraordinary potential is conferred to germ cells from the    time of their formation during embryogenesis. In this Review, we describe common themes emerging from the study of germ cells in vertebrates and invertebrates. Transcriptional repression, chromatin remodeling, and an emphasis on    posttranscriptional gene regulation preserve the totipotent genome of germ cells through generations.</p>

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</description>

<author>G Seydoux et al.</author>


</item>


<item>
<title>Multiple genetic loci from CAST/EiJ chromosome 1 affect vBMD either positively or negatively in a C57BL/6J background.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1459</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1459</guid>
<pubDate>Tue, 08 May 2012 22:17:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Skeletal phenotype analyses of 10 B6.CAST-1 congenic sublines of mice have revealed evidence for the presence of three closely linked QTLs in Chr 1 that influence femoral vBMD both positively and negatively. INTRODUCTION: BMD is an    important component of bone strength and a recognized predictor of risk for osteoporotic fracture. Our goal in this study was to fine map the chromosomal location of volumetric BMD (vBMD) quantitative trait loci (QTLs) in mouse distal chromosome    1 (Chr 1). MATERIALS AND METHODS: After several backcrosses of the B6.CAST-1T congenic strain, which carried the initial BMD QTL in Chr 1 with B6 mice, the N10F1 generation mice were intercrossed to obtain recombinations that yielded different    regions of the QTL. Thirty-eight polymorphic markers were used to fine map the initial 1T QTL region (100-192 Mb). Different skeletal parameters were compared between the 10 sublines and B6 female mice at 16 weeks of age. A t-test was used to    determine the significant difference between sublines and B6 control mice, whereas one-way ANOVA and posthoc (Newman-Keuls) tests were performed to compare the phenotype between the sublines.  RESULTS: Significantly higher femur vBMD was found in    sublines that carried cast alleles from 100 to 169 and 172 to 185 Mb of the centromere compared with the B6 control mice (10-12%, p < 0.001). However, sublines that carried cast alleles from 185 to 192 Mb showed significantly lower femur vBMD    compared with the control mice (-6%, p < 0.05). Furthermore, femur vBMD phenotype showed a negative correlation with endosteal circumference (r = -0.8, p = 0.003), and a strong correlation with cortical thickness for combined data from the 10    sublines (r = 0.97, p < 0.001). Moreover, a high correlation was found between body weight and both periosteal and endosteal circumferences for sublines carrying cast alleles from 167 to 175, 168 to 185, and 169 to 185 Mb, whereas no significant    correlation was found between these parameters for sublines carrying cast alleles from 172 to 185 Mb. CONCLUSIONS: Genetic analysis using congenic sublines revealed that the initial BMD QTL on Chr 1 is a complex site with multiple loci affecting    bone phenotypes, showing the value of the congenic approach in clearly identifying loci that control specific traits.</p>

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</description>

<author>B Edderkaoui et al.</author>


</item>


<item>
<title>Dlx5 and Dlx6 homeobox genes are required for specification of the mammalian vestibular apparatus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1458</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1458</guid>
<pubDate>Tue, 08 May 2012 22:17:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mammalian inner ear is a complex organ that develops from a surface ectoderm into distinct auditory and vestibular components. Congenital malformation of these two components resulting from single or multiple gene defects is a    common clinical occurrence and is observed in patients with split hand/split foot malformation, a malformation which is phenocopied by Dlx5/6 null mice. Analysis of mice lacking Dlx5 and Dlx6 homeobox genes identified their restricted and    combined expression in the otic epithelium as a crucial regulator of vestibular cell fates. Otic induction initiates without incident in Dlx5/6(-/-) embryos, but dorsal otic derivatives including the semicircular ducts, utricle, saccule, and    endolymphatic duct fail to form. Dlx5 and Dlx6 seem to influence vestibular cell fates by restricting Pax2 and activating Gbx2 and Bmp4 expression domains. Given their proximity to the disease locus and the observed phenotype in Dlx5/6 null mice,    Dlx5/6 are likely candidates to mediate the inner ear defects observed in patients with split hand/split foot malformation.</p>

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</description>

<author>R F. Robledo et al.</author>


</item>


<item>
<title>Cone photoreceptor function loss-3, a novel mouse model of achromatopsia due to a mutation in Gnat2.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1457</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1457</guid>
<pubDate>Tue, 08 May 2012 22:17:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: To report a novel mouse model of achromatopsia with a cpfl3 mutation found in the ALS/LtJ strain. METHODS: The effects of a cpfl3 mutation were documented using fundus photography, electroretinography (ERG), and    histopathology. Genetic analysis was performed using linkage studies and PCR gene identification. RESULTS: Homozygous cpfl3 mice had poor cone-mediated responses on ERG at 3 weeks that became undetectable by 9 months. Rod-mediated waveforms were    initially normal, but declined with age. Microscopy of the retinas revealed progressive vacuolization of the photoreceptor outer segments. Immunocytochemistry with cone-specific markers showed progressive loss of labeling for alpha-transducin,    but the cone outer segments in the oldest mice examined remained intact and positive with peanut agglutinin (PNA). The cpfl3 mapped to mouse chromosome 3 at the same location as human GNAT2, known to cause achromatopsia. Sequence analysis    revealed a missense mutation due to a single base pair substitution in exon 6 in cpfl3. CONCLUSIONS: The Gnat2(cpfl3) mutation leads to cone dysfunction and the progressive loss of cone alpha-transducin immunolabeling. Despite a poor cone ERG    signal and loss of cone alpha-transducin label, the cones survive at 14 weeks as demonstrated by PNA staining. This mouse model of achromatopsia will be useful in the study of the development, pathophysiology, and treatment of achromatopsia and    other cone degenerations. The gene symbol for the cpfl3 mutation has been changed to Gnat2(cpfl3).</p>

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</description>

<author>B Chang et al.</author>


</item>


<item>
<title>From vivarium to bedside: lessons learned from animal models.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1456</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1456</guid>
<pubDate>Tue, 08 May 2012 22:16:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this review, we focus primarily on information obtained by studying mouse models of heritable ocular diseases. These models have proven to be important in advancing our understanding of disease etiology and of pathological    consequences of heritable disorders. Careful phenotypic analyses of these models have lead to hypotheses regarding the function of various molecules as well as the mechanisms underlying the observed pathologies. Specific examples of the utility    of mouse models in vision research are discussed.</p>

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</description>

<author>E Budzynski et al.</author>


</item>


<item>
<title>Relationship between insulin-like growth factor I, dehydroepiandrosterone sulfate and proresorptive cytokines and bone density in cystic fibrosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1455</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1455</guid>
<pubDate>Tue, 08 May 2012 22:16:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>INTRODUCTION: Patients with cystic fibrosis (CF) are known to be at risk for early osteoporosis, and the mechanisms that mediate bone loss are still being delineated. The aim of the present investigation was to investigate if a    correlation exists in these patients between skeletal measurements by dual-energy x-ray absorptiometry (DXA) and two anabolic factors, dehydroepiandrosterone (DHEA) and insulin-like growth factor I (IGF-I), and proresorptive factors such as the    cytokines interleukin-1beta, tumor necrosis factor alpha, and interleukin-6.  METHODS: We studied 32 outpatients (18 females; mean age: 26.2+/-7.9 years) at a tertiary care medical center. The subjects had venous samples obtained, underwent    anthropometric and bone mineral density (BMD) measurements, and completed a health survey. Serum IGF-I concentrations were below the age-adjusted mean in 78% of the participants, and DHEA sulfate (DHEAS) concentrations were low in 72%. Serum    concentrations of all cytokines were on the low side of normal; nonetheless, there was a modest inverse correlation between IL-1beta and BMD at all sites. RESULTS: In univariate analyses, IGF-I and DHEAS were significant correlates of BMD or bone    mineral content. In final multivariate models controlling for anthropometric and other variables of relevance to bone density, only IGF-I was identified as a significant independent skeletal predictor.  While alterations in DHEAS, IGF-I, and    specific cytokines may contribute to skeletal deficits in patients with CF, of these factors a low IGF-I concentration appears to be most strongly correlated with BMD.  CONCLUSIONS: These findings may have therapeutic implications for enhancing    bone density in these patients.</p>

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</description>

<author>C M. Gordon et al.</author>


</item>


<item>
<title>Treatment and transfer of emphysema by a new bone marrow transplantation method from normal mice to Tsk mice and vice versa.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1454</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1454</guid>
<pubDate>Tue, 08 May 2012 22:16:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have recently established a new bone marrow transplantation (BMT) method in which bone marrow cells are injected into the intrabone marrow (IBM). In the present study, we used an animal model for emphysema (tight-skin [Tsk]    mouse) to examine whether IBM-BMT could be used to treat emphysema in Tsk mice. IBM-BMT was carried out from C3H mice into Tsk mice (8-10 weeks old) that had already shown emphysema. Six months after transplantation, the lungs of all the Tsk mice    treated with IBM-BMT [C3H-->Tsk] showed similar structures to those of normal mice, whereas the [Tsk-->Tsk] mice showed emphysema, as seen in age-matched Tsk mice. Next, we attempted to transfer emphysema from Tsk mice to C3H mice by IBM-BMT.     Six months after IBM-BMT, the [Tsk-->C3H] mice showed emphysema. These results strongly suggest that emphysema in Tsk mice originates from defects of stem cells in the bone marrow.</p>

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</description>

<author>Y Adachi et al.</author>


</item>


<item>
<title>4Pi microscopy of quantum dot-labeled cellular structures.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1453</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1453</guid>
<pubDate>Tue, 08 May 2012 22:16:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The most prominent restrictions of fluorescence microscopy are the limited resolution and the finite signal. Established conventional, confocal, and multiphoton microscopes resolve at best approximately 200nm in the focal plane and    only 500nm in depth. Additionally, organic fluorophores and fluorescent proteins are bleached after 10(4)-10(5) excitation cycles. To overcome these restrictions, we synergistically combine the 3- to 7-fold improved axial resolution of 4Pi    microscopy with the greatly enhanced photostability of semiconductor quantum dots. Co-localization studies of immunolabeled microtubules and mitochondria demonstrate the feasibility of this approach for routine biological measurements. In    particular, we visualize the three-dimensional entanglement of the two networks with unprecedented detail.</p>

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</description>

<author>R Medda et al.</author>


</item>


<item>
<title>Validation of high-throughput methods for measuring blood urea nitrogen and urinary albumin concentrations in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1452</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1452</guid>
<pubDate>Tue, 08 May 2012 22:16:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chronic kidney disease is a substantial medical and economic burden.  Animal models, including mice, are a crucial component of kidney disease research; however, recent studies disprove the ability of autoanalyzer methods to    accurately quantify plasma creatinine levels, an established marker of kidney disease, in mice. Therefore, we validated autoanalyzer methods for measuring blood urea nitrogen (BUN) and urinary albumin concentrations, 2 common markers of kidney    disease, in samples from mice.  We used high-performance liquid chromatography to validate BUN concentrations measured using an autoanalyzer, and we utilized mouse albumin standards to determine the accuracy of the autoanalyzer over a wide range    of albumin concentrations. We observed a significant, linear correlation between BUN concentrations measured by autoanalyzer and high-performance liquid chromatography. We also found a linear relationship between known and measured albumin    concentrations, although the autoanalyzer method underestimated the known amount of albumin by 3.5- to 4-fold. We confirmed that plasma and urine constituents do not interfere with the autoanalyzer methods for measuring BUN and urinary albumin    concentrations. In addition, we verified BUN and albuminuria as useful markers to detect kidney disease in aged mice and mice with 5/6-nephrectomy. We conclude that autoanalyzer methods are suitable for high-throughput analysis of BUN and albumin    concentrations in mice. The autoanalyzer accurately quantifies BUN concentrations in mouse plasma samples and is useful for measuring urinary albumin concentrations when used with mouse albumin standards.</p>

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</description>

<author>S Grindle et al.</author>


</item>


<item>
<title>A rostrocaudal muscular dystrophy caused by a defect in choline kinase beta, the first enzyme in phosphatidylcholine biosynthesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1451</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1451</guid>
<pubDate>Tue, 08 May 2012 22:16:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Muscular dystrophies include a diverse group of genetically heterogeneous disorders that together affect 1 in 2000 births worldwide. The diseases are characterized by progressive muscle weakness and wasting that lead to severe    disability and often premature death. Rostrocaudal muscular dystrophy (rmd) is a new recessive mouse mutation that causes a rapidly progressive muscular dystrophy and a neonatal forelimb bone deformity. The rmd mutation is a 1.6-kb intragenic    deletion within the choline kinase beta (Chkb) gene, resulting in a complete loss of CHKB protein and enzymatic activity. CHKB is one of two mammalian choline kinase (CHK) enzymes (alpha and beta) that catalyze the phosphorylation of choline to    phosphocholine in the biosynthesis of the major membrane phospholipid phosphatidylcholine. While mutant rmd mice show a dramatic decrease of CHK activity in all tissues, the dystrophy is only evident in skeletal muscle tissues in an unusual    rostral-to-caudal gradient. Minor membrane disruption similar to dysferlinopathies suggest that membrane fusion defects may underlie this dystrophy, because severe membrane disruptions are not evident as determined by creatine kinase levels,    Evans Blue infiltration, and unaltered levels of proteins in the dystrophin-glycoprotein complex. The rmd mutant mouse offers the first demonstration of a defect in a phospholipid biosynthetic enzyme causing muscular dystrophy, representing a    unique model for understanding mechanisms of muscle degeneration.</p>

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</description>

<author>R B. Sher et al.</author>


</item>


<item>
<title>Effects of exposing DBA/2J mice to a high-frequency augmented acoustic environment on the cochlea and anteroventral cochlear nucleus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1450</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1450</guid>
<pubDate>Tue, 08 May 2012 22:15:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>DBA/2J (D2) mice, which exhibit very early progressive sensorineural hearing loss, were treated for 12h nightly with an augmented acoustic environment (AAE) initiated before the onset of hearing. The AAE consisted of repetitive    bursts of a 70 dB sound pressure level, half-octave noise band centered at 20 kHz (i.e. low frequencies were excluded). At 55 days of age, AAE-treated mice, compared to control mice, exhibited less elevation of auditory brainstem response    thresholds for tone frequencies from 16 to 32 kHz and fewer missing outer hair cells in the high-frequency tonotopic region of the cochlea. The dorsal region of their anteroventral cochlear nucleus (most strongly stimulated by the AAE) was    larger, had more surviving neurons, and larger neurons than those of untreated control mice. These and previous findings using an AAE band containing lower frequencies indicate that AAE treatment effects are frequency-related. The findings    provide support for the hypothesis that the beneficial effects of AAE treatment on the cochlea are associated with increased physiological activity evoked by the AAE, and the central AAE effects result from increased AAE-evoked neural activity    and a healthier cochlea providing the auditory input.</p>

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</description>

<author>J F. Willott et al.</author>


</item>


<item>
<title>A new spontaneous mutation in the mouse protocadherin 15 gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1449</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1449</guid>
<pubDate>Tue, 08 May 2012 22:15:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have characterized a new allele of the protocadherin 15 gene (designatedPcdh15(av-6J)) that arose as a spontaneous, recessive mutation in the C57BL/6J inbred strain at Jackson Laboratory. Analysis revealed an inframe deletion in    Pcdh15, which is predicted to result in partial deletion of cadherin domain (domain 9) in Pcdh15. Morphologic study revealed normal to moderately defective cochlear hair cell stereocilia in Pcdh15(av-6J) mutants at postnatal day 2 (P2).    Stereocilia abnormalities were consistently present at P5 and P10. Degenerative changes including loss of inner and outer hair cells were seen at P20, with severe sensory cell loss in all cochlear turns occurring by P40. The hair cell phenotype    observed in the 6J allele between P0 and P20 is the least severe phenotype yet observed in Pcdh15 alleles. However, young Pcdh15(av-6J) mice are unresponsive to auditory stimulation and show circling behavior indicative of vestibular dysfunction.    Since these animals show severe functional deficits but have relatively mild stereocilia defects at a young age they may provide an appropriate model to test for a direct role of Pcdh15 in mechanotransduction.</p>

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</description>

<author>Q Y. Zheng et al.</author>


</item>


<item>
<title>Development of the Minimum Information Specification for In Situ Hybridization and Immunohistochemistry Experiments (MISFISHIE).</title>
<link>http://mouseion.jax.org/stfb2000_2009/1448</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1448</guid>
<pubDate>Tue, 08 May 2012 22:15:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>We describe the creation process of the Minimum Information Specification for In Situ Hybridization and Immunohistochemistry Experiments (MISFISHIE). Modeled after the existing minimum information specification for microarray data,    we created a new specification for gene expression localization experiments, initially to facilitate data sharing within a consortium. After successful use within the consortium, the specification was circulated to members of the wider biomedical    research community for comment and refinement. After a period of acquiring many new suggested requirements, it was necessary to enter a final phase of excluding those requirements that were deemed inappropriate as a minimum requirement for all    experiments. The full specification will soon be published as a version 1.0 proposal to the community, upon which a more full discussion must take place so that the final specification may be achieved with the involvement of the whole    community.</p>

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</description>

<author>E W. Deutsch et al.</author>


</item>


<item>
<title>In search of new targets for plasma high-density lipoprotein cholesterol levels: promise of human-mouse comparative genomics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1447</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1447</guid>
<pubDate>Tue, 08 May 2012 22:15:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many lines of evidence suggest that raising plasma high-density lipoprotein cholesterol (HDL-C) levels may inhibit, perhaps even reverse, atherosclerosis. Quantitative trait locus (QTL) analysis has been performed in both humans and    mice. So far, approximately 40 high-density lipoprotein (HDL)-regulating QTLs have been identified in each species. To compare human and mouse HDL-C QTLs, we generate human-mouse comparative chromosome maps based on homologous genes in humans and    mice. The comparative maps reveal that most human and mouse HDL-C QTLs are concordant, which suggests that identifying the underlying QTL genes in mice will facilitate identifying their homologs in humans. The maps also help to narrow QTLs by    mouse-human homologous QTL comparison. By using a combination of classic genetic approaches and newer bioinformatics tools (including comparative genomics as highlighted in this study), identifying new drug targets for plasma HDL-C levels holds    more promise than ever.</p>

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</description>

<author>J Rollins et al.</author>


</item>


<item>
<title>The transcription factor Nr2e3 functions in retinal progenitors to suppress cone cell generation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1446</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1446</guid>
<pubDate>Tue, 08 May 2012 22:15:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>The transcription factor Nr2e3 is an essential component for development and specification of rod and cone photoreceptors; however, the mechanism through which it acts is not well understood. In this study, we use Nr2e3(rd7/rd7)    mice that harbor a mutation in Nr2e3, to serve as a model for the human retinal disease Enhanced S Cone Syndrome. Our studies reveal that NR2E3 is expressed in late retinal progenitors and differentiating photoreceptors of the developing retina    and localized to the cell bodies of mature rods and cones. In particular, we demonstrate that the abnormal increase in cone photoreceptors observed in Nr2e3(rd7/rd7) mice arise from ectopic mitotic progenitor cells that are present in the outer    nuclear layer of the mature Nr2e3(rd7/rd7) retina. A prolonged phase of proliferation is observed followed by abnormal retinal lamination with fragmented and disorganized photoreceptor synapses that result in a progressive loss of rod and cone    function. An extended and pronounced wave of apoptosis is also detected at P30 and temporally correlates with the phase of prolonged proliferation. Approximately twice as many apoptotic cells were detected compared to proliferating cells. This    wave of apoptosis appears to affect both rod and cone cells and thus may account for the concurrent loss of rod and cone function. We further show that Nr2e3(rd7/rd7) cones do not express rod specific genes and Nr2e3(rd7/rd7) rods do not express    cone specific genes. Our studies suggest that, based on its temporal and spatial expression, NR2E3 acts simultaneously in different cell types: in late mitotic progenitors, newly differentiating post mitotic cells, and mature rods and cones. In    particular, this study reveals the function of NR2E3 in mitotic progenitors is to repress the cone generation program. NR2E3 is thus one of the few genes known to influence the competency of retinal progenitors while simultaneously directing the    rod and cone differentiation.</p>

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</description>

<author>N B. Haider et al.</author>


</item>


<item>
<title>Response rate of bone mineral density to teriparatide in postmenopausal women with osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1445</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1445</guid>
<pubDate>Tue, 08 May 2012 22:15:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: It is desirable for clinicians to know what bone mineral density (BMD) response they can expect in women treated with osteoporosis therapies. The focus of this analysis was to determine what percentage of women attained a    lumbar spine BMD response to teriparatide that equaled or exceeded the least significant change (LSC) value of 3%. METHODS: Data from three clinical trials involving postmenopausal women with osteoporosis were examined. The Fracture Prevention    Trial was a double-blinded, placebo-controlled clinical trial examining the safety and efficacy of teriparatide 20 and 40 microg/day. The other two trials were double-blinded, head-to-head comparisons of alendronate 10 mg/day and teriparatide 20    or 40 microg/day, respectively. Only treatment-compliant women who had lumbar spine BMD measurements at all specified time points in these trials were included. For reference, we also examined the percentage of women with lumbar spine BMD    responses to alendronate. Hip BMD responses that equaled or exceeded 3% were also examined. RESULTS: According to the LSC criteria, 91% of the teriparatide 20 microg/day group and 94% of the teriparatide 40 microg/day group were lumbar spine BMD    responders at 18 months in the Fracture Prevention Trial. In the teriparatide 20 microg/alendronate head-to-head trial, 94% of women receiving teriparatide had a lumbar spine BMD response that equaled or exceeded the 3% criterion at 18 months    compared to 75% of those receiving alendronate 10 mg/day (p < 0.01). In the teriparatide 40 microg/day group of the other head-to-head trial, 92% of women achieved the 3% criterion for the lumbar spine at 12 months compared to 69% of those    receiving alendronate 10 mg/day (p < 0.01). The median 3-month change in amino-terminal extension peptide of procollagen type 1 [PINP] in women who had a lumbar spine BMD response to teriparatide at 18 months was larger than in women who did not    have a lumbar spine BMD response. However, the median 3-month PINP change in lumbar spine BMD nonresponders still exceeded the LSC value of 10 microg/L. Although the percentage of teriparatide-treated women with a hip BMD response that met the 3%    criterion was significantly greater than for placebo, there was no significant difference between the percentage of teriparatide 20 microg/day and alendronate 10 mg/day responders  in the comparison trial.  The baseline characteristics of    teriparatide lumbar spine responders and nonresponders were similar. CONCLUSION: This analysis demonstrates that the vast majority of treatment-compliant postmenopausal women with osteoporosis and minimal prior bisphosphonate exposure have a    lumbar spine BMD response to teriparatide that meets or exceeds the LSC. The characteristics of teriparatide responders and nonresponders were not significantly different; thus, we were unable to discern any characteristics that could be used to    identify potential nonresponders.</p>

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</description>

<author>J C. Gallagher et al.</author>


</item>


<item>
<title>Cochlear developmental defect and background-dependent hearing thresholds in the Jackson circler (jc) mutant mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1444</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1444</guid>
<pubDate>Tue, 08 May 2012 22:14:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Jackson circler (jc) is a spontaneous, recessive mouse mutation that results in circling behavior and an impaired acoustic startle response. In this study, we refined the phenotypic and genetic parameters of the original jc mutation    and characterized a new mutant allele, jc(2J). In open-field behavior tests, homozygous jc mutants exhibited abnormal circling and ambulatory behavior that was indistinguishable from that of phenotypically similar mutants with defects in the    vestibule of the inner ear. The jc/jc and jc(2J)/jc(2J) mice had stable elevated auditory-evoked brainstem response (ABR) thresholds at the 16kHz stimulus of 88+/-9dB sound pressure levels (SPL) and 43+/-11dB SPL, respectively. Peak latencies and    peak time intervals were normal in jc mutants. The jc mice showed no measurable distortion-product otoacoustic emissions (DPOAEs) above the system noise floor. In the mutant cochlea, the apical turn failed to form due to the developmental growth    arrest of the cochlear duct at the level of the first turn at gestational day 13.5. In a large intrasubspecific intercross, jc localized to a 0.2cM interval at position 25cM on chromosome 10, which is homologous to the human 6q21 region. On    CZECHII/Ei and CAST/Ei backgrounds jc/jc mutant hearing thresholds at the 16kHz stimulus were significantly lower than those observed on the C57BL/6J background, with means of 62+/-22dB SPL and 55+/-18dB SPL, respectively. Genome-wide linkage    scans of backcross, intercross, and congenic progeny revealed a complex pattern of genetic and stochastic effects.</p>

	]]>
</description>

<author>A Calderon et al.</author>


</item>


<item>
<title>Effects of exposing gonadectomized and intact C57BL/6J mice to a high-frequency augmented acoustic environment: Auditory brainstem response thresholds and cytocochleograms.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1443</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1443</guid>
<pubDate>Tue, 08 May 2012 22:14:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gonadectomized and surgically intact adult C57BL/6J (B6) mice of both sexes were exposed for 12h nightly to a high-frequency augmented acoustic environment (AAE): repetitive bursts of a half-octave noise band centered at 20 kHz, 70    dB SPL. The effects of sex, gonadectomy, and AAE treatment on genetic progressive hearing loss (exhibited by B6 mice) were evaluated by obtaining auditory brainstem response thresholds at ages 3-, 6-, and 9-months; hair cell counts    (cytocochleograms) were obtained at 9 months. A sex difference in the rate of genetic progressive hearing loss in B6 mice (observed by earlier studies) was confirmed, with females exhibiting a faster rate of threshold elevations and more severe    loss of hair cells at age 9 months. Gonadectomy had no consistent effects on the rate or severity of hearing loss in non-exposed mice of either sex. An unexpected finding was that the high-frequency AAE treatment caused additional ABR threshold    elevations and hair cell loss. In an earlier study, the same high-frequency AAE treatment on DBA/2J mice ameliorated hearing loss. The most severe AAE-induced losses occurred in surgically intact females, suggesting a potentiating effect of    ovarian hormone(s).</p>

	]]>
</description>

<author>J F. Willott et al.</author>


</item>


<item>
<title>The X chromosome in quantitative trait locus mapping.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1442</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1442</guid>
<pubDate>Tue, 08 May 2012 22:14:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The X chromosome requires special treatment in the mapping of quantitative trait loci (QTL). However, most QTL mapping methods, and most computer programs for QTL mapping, have focused exclusively on autosomal loci. We describe a    method for appropriate treatment of the X chromosome for QTL mapping in experimental crosses. We address the important issue of formulating the null hypothesis of no linkage appropriately. If the X chromosome is treated like an autosome, a sex    difference in the phenotype can lead to spurious linkage on the X chromosome. Further, the number of degrees of freedom for the linkage test may be different for the X chromosome than for autosomes, and so an X chromosome-specific significance    threshold is required. To address this issue, we propose a general procedure to obtain chromosome-specific significance thresholds that controls the genomewide false positive rate at the desired level. We apply our methods to data on gut length    in a large intercross of mice carrying the Sox10Dom mutation, a model of Hirschsprung disease. We identified QTL contributing to variation in gut length on chromosomes 5 and 18. We found suggestive evidence of linkage to the X chromosome, which    would be viewed as strong evidence of linkage if the X chromosome was treated as an autosome. Our methods have been implemented in the package R/qtl.</p>

	]]>
</description>

<author>K W. Broman et al.</author>


</item>


<item>
<title>Phenotypic characterization of polygenic type 2 diabetes in TALLYHO/JngJ mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1441</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1441</guid>
<pubDate>Tue, 08 May 2012 22:14:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>The TALLYHO/JngJ (TH) strain is a newly established, polygenic mouse model for type 2 diabetes (T2D) and obesity, and we have previously reported some key physiological features of this model after the overt onset of diabetes. In    the present work, we conducted a comprehensive phenotypic characterization of TH in order to completely characterize this new and relevant model for human T2D and obesity. We monitored the development of obesity and diabetes starting at 4 weeks    of age by measuring body weight, glucose tolerance, and plasma levels of insulin, glucose, and triglyceride. Additionally, histological alterations in the pancreas and glucose uptake and glucose transporter 4 (GLUT4) content in soleus muscle were    also examined. Compared with age- and sex-matched C57BL/6J (B6) mice, both male and female TH mice were significantly heavier, hyperleptinemic, and hyperinsulinemic at 4 weeks of age, without glucose intolerance or hyperglycemia. TH mice    maintained higher body weights throughout the study period of 16 weeks. The hyperinsulinemia in TH mice worsened with age, but to a lesser degree in females than in males. Both the male and the female TH mice had enlarged pancreatic islets. Male    TH mice showed impaired glucose tolerance at 8 weeks that became more prominent at 16 weeks.  Plasma glucose levels continuously increased with age in male TH mice resulting in frank diabetes, while female TH mice remained normoglycemic    throughout the study. Impaired glucose tolerance and hyperglycemia in male TH mice were accompanied by impaired 2-deoxyglucose uptake in the soleus muscle at basal and insulin-stimulated states, but without any reduction in GLUT4 content.    Interestingly, male TH mice exhibited a drastic elevation in plasma triglyceride levels in the pre-diabetic stage that was maintained throughout the study. These findings suggest that obesity and insulin resistance are an inherent part of the TH    phenotype and glucose intolerance is evident preceding progression to overt diabetes in male TH mice.</p>

	]]>
</description>

<author>J H. Kim et al.</author>


</item>


<item>
<title>Snail1 gene function during early embryo patterning in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1440</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1440</guid>
<pubDate>Tue, 08 May 2012 22:14:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Originally identified as one of two zygotically expressed genes required for gastrulation in Drosophila, the Snail gene and other family members play critical roles in vertebrate development. Functionally, these genes are thought to    drive epithelial-mesenchymal transitions at several points during development, and also during the metastatic progression of cancer.  Although the Snai2-null mouse is viable and fertile, the early embryonic lethality of Snai1-null mice has    precluded the detailed analysis of Snai1 function after gastrulation. We have recently generated a conditional allele of the Snai1 gene and examined its function during the formation of the neural crest and establishment of the left-right axis.    We uncovered new details regarding Snai1 function during gastrulation and left-right asymmetry determination, while surprisingly showing that neither the Snai1 nor Snai2 genes are essential for neural crest cell delamination. These results shed    new light on the role of Snail family genes in early mouse development, and raise interesting questions concerning the diversity of gene function among vertebrate species.</p>

	]]>
</description>

<author>S A. Murray et al.</author>


</item>


<item>
<title>Postnatal growth and bone mass in mice with IGF-I haploinsufficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1439</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1439</guid>
<pubDate>Tue, 08 May 2012 22:14:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>We examined the influence of IGF-I haploinsufficiency on growth, bone mass and osteoblast differentiation in Igf1 heterozygous knockout (HET) mice.  Cohorts of male and female wild type (WT) and HET mice in the outbred CD-1    background were analyzed at 1, 2, 4, 8, 12, 15 and 18 months of age for body weight, serum IGF-I and bone morphometry. Compared to WT mice, HET mice had 20-30% lower serum IGF-I levels in both genders and in all age groups. Female HET mice showed    significant reductions in body weight (10-20%), femur length (4-6%) and femoral bone mineral density (BMD) (7-12%) before 15 months of age. Male HET mice showed significant differences in all parameters at 2 months and thereafter. At 8 and 12    months, WT mice also showed a significant gender effect: despite their lower body weight, female mice had higher femoral BMD and femur length compared to males. Microcomputed tomography showed a significant reduction in cortical bone area (7-20%)    and periosteal circumference (5-13%) with no consistent pattern of change in trabecular bone measurements in 2- and 8-month old HET mice in both genders. HET primary osteoblast cultures showed a 40% reduction in IGF-I protein expression and a 50%    decrease in IGF-I mRNA expression. Cell growth and proliferation were decreased in HET cultures. Thus, IGF-I haploinsufficiency in outbred male and female mice resulted in reduced body weight, femur length and areal BMD at most ages.  Serum IGF-I    levels showed a high level of positive correlation with body weight and skeletal morphometry. These studies show that IGF-I is a determinant of bone size and mass in postnatal life. We speculate that impaired osteoblast proliferation may    contribute to the skeletal phenotype of mice with IGF-I haploinsufficiency.</p>

	]]>
</description>

<author>J He et al.</author>


</item>


<item>
<title>Constant rate of steady-state self-antigen trafficking from skin to regional lymph nodes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1438</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1438</guid>
<pubDate>Tue, 08 May 2012 22:14:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>It is suggested that dendritic cells (DCs) capture and present both foreign antigens such as components of pathogens as well as endogenous self-antigens. However, the magnitude of self-antigen trafficking to secondary lymphoid    organs is still unclear. Here we show constitutive trafficking of self-antigens from skin to regional lymph nodes (LNs) quantitatively using a KRT14-Kitl transgenic mouse. This mouse model expresses the Kit ligand in keratinocytes, shows    hyperpigmentation of the epidermis and exhibits constitutive accumulation of melanin granules (MGs) in skin regional LNs transported by Langerhans cells. Using an MG-solubilization technique, we revealed that 128 microg per week of MGs, a marker    of self-antigens, accumulated in skin regional LNs and that the rate of accumulation was constant from 3 to 50 weeks. Activation markers such as CD40, CD54 and CD86 did not increase in the LNs, and abrogation of CD40 signaling did not affect the    accumulation. Additionally, the total amount of MGs did not increase significantly following stimulation with intravenous LPS injections. These results suggest that the accumulation is not caused by inflammatory stimuli, and the steady-state    trafficking of self-antigens is intrinsically maintained at a constant rate. Because the levels of self-antigens as well as the phenotype of these DCs are thought to be important in the strength of immune responses, the results may imply that the    constant rate of trafficking of self-antigens is required for maintaining homeostatic conditions, such as self-tolerance.</p>

	]]>
</description>

<author>M Yoshino et al.</author>


</item>


<item>
<title>fjoin: simple and efficient computation of feature overlaps.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1437</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1437</guid>
<pubDate>Tue, 08 May 2012 22:13:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sets of biological features with genome coordinates (e.g., genes and promoters) are a particularly common form of data in bioinformatics today.  Accordingly, an increasingly important processing step involves comparing coordinates    from large sets of features to find overlapping feature pairs.  This paper presents fjoin, an efficient, robust, and simple algorithm for finding these pairs, and a downloadable implementation. For typical bioinformatics feature sets, fjoin    requires O(n log(n)) time (O(n) if the inputs are sorted) and uses O(1) space. The reference implementation is a stand-alone Python program; it implements the basic algorithm and a number of useful extensions, which are also discussed in this    paper.</p>

	]]>
</description>

<author>J E. Richardson</author>


</item>


<item>
<title>Effects of FXR in foam-cell formation and atherosclerosis development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1436</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1436</guid>
<pubDate>Tue, 08 May 2012 22:13:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Farnesoid X receptor (FXR), a bile-acid-activated member of the nuclear receptor superfamily, is essential in regulating bile-acid, cholesterol, and triglyceride homeostasis. Disruption of the FXR gene in mice results in a    proatherosclerotic lipid profile with increased serum cholesterols and triglycerides. However, the role of FXR in foam-cell formation and atherosclerosis development remains unclear. The current study showed that the peritoneal macrophages    isolated from FXR-null mice took up less oxidized LDL-cholesterol (oxLDL-C), which was accompanied by a marked reduction in CD36 expression in these cells. This result appears to be FXR-independent, as FXR was not detected in the peritoneal    macrophages. To assess to what extent FXR modulates atherosclerosis development, FXR/ApoE double-null mice were generated. Female mice were used for atherosclerosis analysis. Compared to ApoE-null mice, the FXR/ApoE double-null mice were found to    have less atherosclerotic lesion area in the aorta, despite a further increase in the serum cholesterols and triglycerides. Our results indicate that disruption of the FXR gene could attenuate atherosclerosis development, most likely resulting    from reduced oxLDL-C uptake by macrophages. Our study cautions the use of serum lipid levels as a surrogate marker to determine the efficiency of FXR modulators in treating hyperlipidemia.</p>

	]]>
</description>

<author>G L. Guo et al.</author>


</item>


<item>
<title>Low-level mechanical vibrations can influence bone resorption and bone formation in the growing skeleton.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1435</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1435</guid>
<pubDate>Tue, 08 May 2012 22:13:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Short durations of extremely small magnitude, high-frequency, mechanical stimuli can promote anabolic activity in the adult skeleton. Here, it is determined if such signals can influence trabecular and cortical formative and    resorptive activity in the growing skeleton, if the newly formed bone is of high quality, and if the insertion of rest periods during the loading phase would enhance the efficacy of the mechanical regimen.  Eight-week-old female BALB/cByJ mice    were divided into four groups, baseline control (n = 8), age-matched control (n = 10), whole-body vibration (WBV) at 45 Hz (0.3 g) for 15 min day(-1) (n = 10), and WBV that were interrupted every second by 10 of rest (WBV-R, n = 10). In vivo    strain gaging of two additional mice indicated that the mechanical signal induced strain oscillations of approximately 10 microstrain on the periosteal surface of the proximal tibia. After 3 weeks of WBV, applied for 15 min each day, osteoclastic    activity in the trabecular metaphysis and epiphysis of the tibia was 33% and 31% lower (P <0.05) than in age-matched controls. Bone formation rates (BFR.BS(-1)) on the endocortical surface of the metaphysis were 30% greater (P <0.05) in WBV than    in age-matched control mice but trabecular and middiaphyseal BFR were not significantly altered. The insertion of rest periods (WBV-R) failed to potentiate the cellular effects. Three weeks of either WBV or WBV-R did not negatively influence body    mass, bone length, or chemical bone matrix properties of the tibia. These data indicate that in the growing skeleton, short daily periods of extremely small, high-frequency mechanical signals can inhibit trabecular bone resorption, site    specifically attenuate the declining levels of bone formation, and maintain a high level of matrix quality. If WBV prove to be efficacious in the growing human skeleton, they may be able to provide the basis for a non-pharmacological and safe    means to increase peak bone mass and, ultimately, reduce the incidence of osteoporosis or stress fractures later in life.</p>

	]]>
</description>

<author>L Xie et al.</author>


</item>


<item>
<title>Enhanced ABCG1 expression increases atherosclerosis in LDLr-KO mice on a western diet.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1434</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1434</guid>
<pubDate>Tue, 08 May 2012 22:13:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>ABCG1 promotes cholesterol efflux from cells, but ABCG1(-/-) bone marrow transplant into ApoE(-/-) and LDLr(-/-) mice reduces atherosclerosis. To further investigate the role of ABCG1 in atherosclerosis, ABCG1 transgenic mice were    crossed with LDLr-KO mice and placed on a high-fat western diet.  Increased expression of ABCG1 mRNA was detected in liver (1.8-fold) and macrophages (2.7-fold), and cholesterol efflux from macrophages to HDL was also increased (1.4-fold) in    ABCG1xLDLr-KO vs. LDLr-KO mice. No major differences were observed in total plasma lipids. However, cholesterol in the IDL-LDL size range was increased by approximately 50% in ABCG1xLDLr-KO mice compared to LDLr-KO mice. Atherosclerosis increased    by 39% (10.1+/-0.8 vs 6.1+/-0.9% lesion area, p=0.02), as measured by en face analysis, and by 53% (221+/-98 vs 104+/-58x10(3)microm(2), p =0.01), as measured by cross-sectional analysis in ABCG1xLDLr-KO mice. Plasma levels for MCP-1 (1.5-fold)    and TNF-alpha (1.2-fold) were also increased in ABCG1xLDLr-KO mice. In summary, these findings suggest that enhanced expression of ABCG1 increases atherosclerosis in LDLr-KO mice, despite its role in promoting cholesterol efflux from    cells.</p>

	]]>
</description>

<author>F Basso et al.</author>


</item>


<item>
<title>Enhanced half-life of genetically engineered human IgG1 antibodies in a humanized FcRn mouse model: potential application in humorally mediated autoimmune disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1433</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1433</guid>
<pubDate>Tue, 08 May 2012 22:13:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>The MHC class I-like Fc receptor FcRn plays an essential role in extending the half-life (t(1/2)) of IgG antibodies and IgG-Fc-based therapeutics in the circulation. The goal of this study was to analyze the effect of human IgG1    (hIgG1) antibodies with enhanced in vitro binding to FcRn on their in vivo t(1/2) in mice expressing human FcRn (hFcRn). Mutants of the humanized monoclonal Herceptin antibody (Hu4D5-IgG1), directed against human epidermal growth factor receptor    2 (p185 (HER2)), show altered pH-dependent binding to hFcRn in vitro. Two engineered IgG1 mutants (N434A and T307A/E380A/N434A) showed a considerably extended t(1/2) in vivo compared with wild-type antibody in mice expressing an hFcRn transgene    (Tg) but not in mice expressing the endogenous mouse FcRn. The efficiency of hFcRn-mediated protection was dependent on hFcRn Tg copy number.  Moreover, when injected into FcRn-humanized mice at a concentration sufficient to partially saturate    hFcRn, the engineered IgG1 mutants with an extended serum t(1/2) were most effective in reducing the t(1/2) of a tracer hIgG1 antibody. Finally, administration of mutant with high binding to hFcRn ameliorated arthritis induced by passive transfer    with human pathogenic plasma. These results indicate that Fc regions modified for high binding affinity to hFcRn increases serum persistence of therapeutic antibodies, that the same approach can be exploited as an anti-autoimmune therapy to    promote the clearance of endogenous pathogenic IgG and that FcRn-humanized mice are a promising surrogate for hIgG therapeutic development.</p>

	]]>
</description>

<author>S B. Petkova et al.</author>


</item>


<item>
<title>H2AX chromatin structures and their response to DNA damage revealed by 4Pi microscopy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1432</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1432</guid>
<pubDate>Tue, 08 May 2012 22:13:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>DNA double-strand breaks (DSBs) caused by cellular exposure to genotoxic agents or produced by inherent metabolic processes initiate a rapid and highly coordinated series of molecular events resulting in DNA damage signaling and    repair. Phosphorylation of histone H2AX to form gamma-H2AX is one of the earliest of these events and is important for coordination of signaling and repair activities. An intriguing aspect of H2AX phosphorylation is that gamma-H2AX spreads a    limited distance up to 1-2 Mbp from the site of a DNA break in mammalian cells. However, neither the distribution of H2AX throughout the genome nor the mechanism that defines the boundary of gamma-H2AX spreading have yet been described. Here, we    report the identification of previously undescribed H2AX chromatin structures by successfully applying 4Pi microscopy to visualize endogenous nuclear proteins. Our observations suggest that H2AX is not distributed randomly throughout bulk    chromatin, rather it exists in distinct clusters that themselves are uniformly distributed within the nuclear volume. These data support a model in which the size and distribution of H2AX clusters define the boundaries of gamma-H2AX spreading and    also may provide a platform for the immediate and robust response observed after DNA damage.</p>

	]]>
</description>

<author>J Bewersdorf et al.</author>


</item>


<item>
<title>TRPV1+ sensory neurons control beta cell stress and islet inflammation in autoimmune diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1431</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1431</guid>
<pubDate>Tue, 08 May 2012 22:12:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>In type 1 diabetes, T cell-mediated death of pancreatic beta cells produces insulin deficiency. However, what attracts or restricts broadly autoreactive lymphocyte pools to the pancreas remains unclear. We report that TRPV1(+)    pancreatic sensory neurons control islet inflammation and insulin resistance. Eliminating these neurons in diabetes-prone NOD mice prevents insulitis and diabetes, despite systemic persistence of pathogenic T cell pools. Insulin resistance and    beta cell stress of prediabetic NOD mice are prevented when TRPV1(+) neurons are eliminated.  TRPV1(NOD), localized to the Idd4.1 diabetes-risk locus, is a hypofunctional mutant, mediating depressed neurogenic inflammation.  Delivering the    neuropeptide substance P by intra-arterial injection into the NOD pancreas reverses abnormal insulin resistance, insulitis, and diabetes for weeks. Concordantly, insulin sensitivity is enhanced in trpv1(-/-) mice, whereas    insulitis/diabetes-resistant NODxB6Idd4-congenic mice, carrying wild-type TRPV1, show restored TRPV1 function and insulin sensitivity. Our data uncover a fundamental role for insulin-responsive TRPV1(+) sensory neurons in beta cell function and    diabetes pathoetiology.</p>

	]]>
</description>

<author>R Razavi et al.</author>


</item>


<item>
<title>Targeting PIM kinases impairs survival of hematopoietic cells transformed by kinase inhibitor-sensitive and kinase inhibitor-resistant forms of Fms-like tyrosine kinase 3 and BCR/ABL.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1430</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1430</guid>
<pubDate>Tue, 08 May 2012 22:12:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous studies have shown that activation of the signal transducer and activator of transcription 5 (STAT5) plays an essential role in leukemogenesis mediated through constitutive activated protein tyrosine kinases (PTK). Because    PIM-1 is a STAT5 target gene, we analyzed the role of the family of PIM serine/threonine kinases (PIM-1 to PIM-3) in PTK-mediated transformation of hematopoietic cells. Ba/F3 cells transformed to growth factor independence by various oncogenic    PTKs (TEL/JAK2, TEL/TRKC, TEL/ABL, BCR/ABL, FLT3-ITD, and H4/PDGFbetaR) show abundant expression of PIM-1 and PIM-2. Suppression of PIM-1 activity had a negligible effect on transformation. In contrast, expression of kinase-dead PIM-2 mutant    (PIM-2KD) led to a rapid decline of survival in Ba/F3 cells transformed by FLT3-ITD but not by other oncogenic PTKs tested. Coexpression of PIM-1KD and PIM-2KD abrogated growth factor-independent growth of Ba/F3 transformed by several PTKs,    including BCR/ABL. Targeted down-regulation of PIM-2 by RNA interference (RNAi) selectively abrogated survival of Ba/F3 cells transformed by various Fms-like tyrosine kinase 3 (FLT3)-activating mutants [internal tandem duplication (ITD) and    kinase domain] and attenuated growth of human cell lines containing FLT3 mutations. Interestingly, cells transformed by FLT3 and BCR/ABL mutations that confer resistance to small-molecule tyrosine kinase inhibitors were still sensitive to    knockdown of PIM-2, or PIM-1 and PIM-2 by RNAi. Our observations indicate that combined inactivation of PIM-1 and PIM-2 interferes with oncogenic PTKs and suggest that PIMs are alternative therapeutic targets in PTK-mediated leukemia. Targeting    the PIM kinase family could provide a new avenue to overcome resistance against small-molecule tyrosine kinase inhibitors.</p>

	]]>
</description>

<author>M Adam et al.</author>


</item>


<item>
<title>Interferon-gamma-deficient mice are resistant to the development of alopecia areata.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1429</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1429</guid>
<pubDate>Tue, 08 May 2012 22:12:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Alopecia areata (AA) is a T-cell mediated putative autoimmune disease of hair follicles, which can be transferred by CD4(+) T cells.  However, whether T-helper (Th) 1 or Th2 cytokines are predominant has not yet been    defined. OBJECTIVES: To elucidate the importance of Th1 cells in the pathogenesis of AA we investigated the functional role of interferon (IFN)-gamma in the experimental induction of AA. METHODS: AA was experimentally induced by grafting    full-thickness skin from AA-affected C3H/HeJ mice on to C3H/HeJ mice with a targeted deletion of the Th1 cytokine IFN-gamma gene (IFNgamma(-/-)) and on to wild-type mice (IFNgamma(+/+)). RESULTS: While 90% of wild-type mice developed AA, none of    the IFNgamma(-/-) mice exhibited hair loss. Immunohistochemistry of skin sections revealed a dense perifollicular and intrafollicular infiltrate of CD4(+) and CD8(+) T cells in controls, while in IFNgamma(-/-) mice skin-infiltrating CD8(+) T    cells were absent and the number of CD4(+) cells was significantly reduced. Aberrant expression of major histocompatibility complex class I and II molecules in the putative immune-privileged infrainfundibular site of the hair follicle was found    to be weaker in AA-resistant IFNgamma(-/-) mice than in control mice with AA.  Flow cytometry revealed that leucocytes of IFNgamma(-/-) mice did not respond to the transfer of AA-affected skin. As distinct from IFNgamma(+/+) mice, neither T-cell    activation markers nor Th1 cytokines were upregulated in draining lymph node cells or skin-infiltrating leucocytes of AA-resistant IFNgamma(-/-) mice. However, there was no evidence for a shift towards a Th2 cytokine profile, nor for upregulation    of regulatory T cells in IFNgamma(-/-) mice. CONCLUSIONS: IFNgamma(-/-) mice fail to activate Th1 cells in response to the transplanted (auto)antigens, which suggests an essential requirement for IFN-gamma-mediated Th1 activation in the induction    of AA.</p>

	]]>
</description>

<author>Paul P. Freyschmidt et al.</author>


</item>


<item>
<title>Mutant myocilin nonsecretion in vivo is not sufficient to cause glaucoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1428</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1428</guid>
<pubDate>Tue, 08 May 2012 22:12:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Glaucoma is a leading cause of blindness, affecting over 70 million people worldwide. Vision loss is the result of death of the retinal ganglion cells. The best-known risk factor for glaucoma is an elevated intraocular pressure    (IOP); however, factors leading to IOP elevation are poorly understood. Mutations in the MYOC gene are an important cause of open-angle glaucoma. Over 70 MYOC mutations have been identified, and they lead to approximately 5% of all primary    open-angle glaucoma cases.  Nevertheless, the pathogenic mechanisms by which these mutations elevate IOP are presently unclear. Data suggest that a dominant interfering effect of misfolded mutant MYOC molecules may be pathogenic. To test this    hypothesis, we have generated mice carrying a mutant allele of Myoc that is analogous to a human mutation that leads to aggressive glaucoma in patients. We show that mutant MYOC is not secreted into the aqueous humor.  Instead of being secreted,    mutant MYOC accumulates within the iridocorneal angle of the eye, consistent with the behavior of abnormally folded protein. Surprisingly, the accumulated mutant protein does not activate the unfolded protein response and lead to elevated    intraocular pressure or glaucoma in aged mice of different strains. These data suggest that production, apparent misfolding, and nonsecretion of mutant MYOC are not, by themselves, sufficient to cause glaucoma in vivo.</p>

	]]>
</description>

<author>D B. Gould et al.</author>


</item>


<item>
<title>Multiple mechanisms limit the duration of wakefulness in Drosophila brain.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1427</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1427</guid>
<pubDate>Tue, 08 May 2012 22:12:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>The functions of sleep and what controls it remain unanswered biological questions. According to the two-process model, a circadian process and a homeostatic process interact to regulate sleep. While progress has been made in    understanding the molecular and cellular functions of the circadian process, the mechanisms of the homeostatic process remain undiscovered. We use the recently established sleep model system organism Drosophila melanogaster to examine dynamic    changes in gene expression during sleep and during prolonged wakefulness in the brain. Our experimental design controls for circadian processes by killing animals at three matched time points from the beginning of the consolidated rest period    [Zeitgeber time (ZT) 14)] under two conditions, sleep deprived and spontaneously sleeping. Using ANOVA at a false discovery rate of 5%, we have identified 252 genes that were differentially expressed between sleep-deprived and control groups in    the Drosophila brain. Using linear trends analysis, we have separated the significant differentially expressed genes into nine temporal expression patterns relative to a common anchor point (ZT 14). The most common expression pattern is a    decrease during extended wakefulness but no change during spontaneous sleep (n = 114). Genes in this category were involved in protein production (n = 47), calcium homeostasis, and membrane excitability (n = 5). Multiple mechanisms, therefore,    act to limit wakefulness. In addition, by studying the effects of the mechanical stimulus used in our deprivation studies during the period when the animals are predominantly active, we provide evidence for a previously unappreciated role for the    Drosophila immune system in the brain response to stress.</p>

	]]>
</description>

<author>J E. Zimmerman et al.</author>


</item>


<item>
<title>Know thy mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1426</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1426</guid>
<pubDate>Tue, 08 May 2012 22:12:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>In science it is imperative that the basic reagents and materials are defined and uniform. Unlike chemical reagents, which are uniform over time, mice, like all living creatures, have an intrinsic genetic drive to change, with    mutations accumulating over time leading to increasing genetic variation and phenotypic change. Such changes compromise the reproducibility of experimental data over time and place. The use of the mouse has expanded rapidly in recent years and    many scientists who have turned to the mouse as a research model might be unaware of the profound impact of changes in genetic background. Here we discuss the sources of genetic change and strategies to reduce them with the idea of strengthening    international genetic standards for inbred mice.</p>

	]]>
</description>

<author>R A. Taft et al.</author>


</item>


<item>
<title>The genetics of gene expression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1425</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1425</guid>
<pubDate>Tue, 08 May 2012 22:11:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>G A. Churchill</author>


</item>


<item>
<title>Gene expression analysis of mouse chromosome substitution strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1424</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1424</guid>
<pubDate>Tue, 08 May 2012 22:11:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>An analysis of transcriptional variation in the liver using a panel of B.A chromosome substitution strains identified 4209 transcripts that are differentially expressed relative to the C57BL/6J background and 1010 transcripts that    are differentially expressed between C57BL/6J and A/J strains. A subset of these strains (substituting Chromosomes 1, 6, and 15) was used to identify 386 additional differentially expressed transcripts in the kidney. Approximately 15% of    differentially expressed transcripts are located on the substituted chromosome. These cis-QTL are codirectionally expressed with the donor strain A/J. By comparison, trans-regulated loci comprise 85% of differentially expressed transcripts, often    show opposite direction of change compared with A/J, and can be regulated by multiple chromosome substitutions. Gene expression differences in this study provide evidence for transgressive segregation: Only 438 of 4209 QTL in liver were inside    the parental range. By combining QTL data with known biological functions, we were able to identify physiologic pathways altered in multiple strains. In many cases the same pathways were altered by multiple distinct chromosome substitutions.    Taken together, these results suggest that widespread epistatic background effects may result in complex and overlapping transcriptional relationships among different chromosome substitution strains.  Transcriptional profiling of chromosome    substitution strains reveals a complex genetic architecture of transcriptional regulation.</p>

	]]>
</description>

<author>K R. Shockley et al.</author>


</item>


<item>
<title>Genetic analysis of the stress-responsive adrenocortical axis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1423</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1423</guid>
<pubDate>Tue, 08 May 2012 22:11:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The underlying genetic components contributing to individual variability in functions of the stress-responsive hypothalamic-pituitary-adrenal (HPA) axis are poorly understood. To determine genetic loci mediating three aspects of the    adrenocortical function, we conducted a quantitative trait locus (QTL) analysis in the segregating F2 generation of a Wistar Kyoto (WKY) x Fischer 344 (F344) cross, two inbred rat strains that differ in several HPA axis measures. The following    three components of adrenocortical function are known to be regulated by different mechanisms that are mediated via suprahypothalamic, hypothalamic, pituitary, and intra-adrenal influences: basal plasma corticosterone (Cort) levels, plasma Cort    response to a 10-min restraint stress, and adrenal weight.  Genome scans identified a complex genetic architecture for the basal Cort phenotype, including sex and maternal lineage effects. Pairwise interactions were also identified for this    trait. We identified three significant and two suggestive QTLs for stress Cort, along with two pairs of interacting loci for this trait. Four highly significant and two suggestive loci were identified for adrenal weight, with no interacting loci.    In contrast to basal Cort, no sex- or lineage-dependent QTL were identified for stress Cort or adrenal weight, despite the large sex differences in these phenotypes. We identified three nucleotide alterations in an obvious candidate gene mapped    to the most significant QTL for stress Cort, Cort-binding globulin (CBG), one of which is known to alter CBG binding. This analysis confirms that three separate traits regulated by the HPA axis are controlled by multiple, but mainly    nonoverlapping, QTLs.</p>

	]]>
</description>

<author>L C. Solberg et al.</author>


</item>


<item>
<title>Nmf11 is a novel ENU-induced mutation in the mouse glycine receptor alpha 1 subunit.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1422</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1422</guid>
<pubDate>Tue, 08 May 2012 22:11:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nmf11 is an N-ethyl-N-nitrosourea-induced recessive mouse mutation. In this article we show that the mutation is in the gene that encodes the glycine receptor alpha 1 subunit (Glra1). The new Glra1 mutation appears to affect    glycine's inhibitory neurotransmission in the central nervous system (CNS) of the nmf11 homozygotes, which suffer from a severe startle disease-related phenotype and die by postnatal day 21. The nmf11 mutation involves a C-to-A transition of    nucleotide 518, which results in the N46K substitution in the long extracellular NH(2) terminal or ligand-binding domain of the GLRA1 mature protein. The mutation does not result in reduced expression of GLRA1 at the mRNA or protein levels and    the mutant glycine receptor localizes properly in synaptic sites of nmf11 homozygotes.</p>

	]]>
</description>

<author>M Traka et al.</author>


</item>


<item>
<title>p63 protects the female germ line during meiotic arrest.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1421</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1421</guid>
<pubDate>Tue, 08 May 2012 22:10:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Meiosis in the female germ line of mammals is distinguished by a prolonged arrest in prophase of meiosis I between homologous chromosome recombination and ovulation. How DNA damage is detected in these arrested oocytes is poorly    understood, but it is variably thought to involve p53, a central tumour suppressor in mammals. While the function of p53 in monitoring the genome of somatic cells is clear, a consensus for the importance of p53 for germ line integrity has yet to    emerge. Here we show that the p53 homologue p63 (refs 5, 6), and specifically the TAp63 isoform, is constitutively expressed in female germ cells during meiotic arrest and is essential in a process of DNA damage-induced oocyte death not involving    p53. We also show that DNA damage induces both the phosphorylation of p63 and its binding to p53 cognate DNA sites and that these events are linked to oocyte death. Our data support a model whereby p63 is the primordial member of the p53 family    and acts in a conserved process of monitoring the integrity of the female germ line, whereas the functions of p53 are restricted to vertebrate somatic cells for tumour suppression. These findings have implications for understanding female germ    line fidelity, the regulation of fertility and the evolution of tumour suppressor mechanisms.</p>

	]]>
</description>

<author>E K. Suh et al.</author>


</item>


<item>
<title>A-to-I pre-mRNA editing of the serotonin 2C receptor: comparisons among inbred mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1420</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1420</guid>
<pubDate>Tue, 08 May 2012 22:10:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>The serotonin receptor 5HT2CR pre-mRNA is subject to adenosine deamination (RNA editing) at five residues located within a 15 nucleotide stretch of the coding region. Such changes of adenosine to inosine (A-to-I) can produce 32 mRNA    variants, encoding 24 different protein isoforms, some of which vary in biochemical and pharmacological properties. Because serotonin mediates diverse neurological processes relevant to behavior and because inbred mouse strains vary in their    responses to tests of learning and behavior, we have examined the A-to-I editing patterns of the 5HT2CR mRNA in whole brains from eight mouse strains. By sequencing approximately 100 clones from individual mice, we generated detailed information    on levels of editing at each site and patterns of editing that identify a total of 28 mRNA and 20 protein isoforms. Significant differences between individuals from different strains were found in total editing frequency, in the proportion of    transcripts with 1 and 4 edited sites, in editing frequency at the A, B, E and D sites, in amino acid frequencies at positions 157 and 161, and in subsets of major protein isoforms. Primer extension assays were used to show that individuals    within strains (six C3H.B-+rd1 and four 129SvImrJ) displayed no significant differences in any feature. These findings suggest that genetic background contributes to subtle variation in 5HT2CR mRNA editing patterns which may have consequences for    pharmacological treatments and behavioral testing.</p>

	]]>
</description>

<author>Y Du et al.</author>


</item>


<item>
<title>Adenomatous polyposis coli (APC) is required for normal development of skin and thymus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1419</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1419</guid>
<pubDate>Tue, 08 May 2012 22:10:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The tumor suppressor gene Apc (adenomatous polyposis coli) is a member of the Wnt signaling pathway that is involved in development and tumorigenesis. Heterozygous knockout mice for Apc have a tumor predisposition phenotype and    homozygosity leads to embryonic lethality. To understand the role of Apc in development we generated a floxed allele.  These mice were mated with a strain carrying Cre recombinase under the control of the human Keratin 14 (K14) promoter, which is    active in basal cells of epidermis and other stratified epithelia. Mice homozygous for the floxed allele that also carry the K14-cre transgene were viable but had stunted growth and died before weaning. Histological and immunochemical    examinations revealed that K14-cre-mediated Apc loss resulted in aberrant growth in many ectodermally derived squamous epithelia, including hair follicles, teeth, and oral and corneal epithelia. In addition, squamous metaplasia was observed in    various epithelial-derived tissues, including the thymus. The aberrant growth of hair follicles and other appendages as well as the thymic abnormalities in K14-cre; Apc(CKO/CKO) mice suggest the Apc gene is crucial in embryonic cells to specify    epithelial cell fates in organs that require epithelial-mesenchymal interactions for their development.</p>

	]]>
</description>

<author>M Kuraguchi et al.</author>


</item>


<item>
<title>Cracking the egg: molecular dynamics and evolutionary aspects of the transition from the fully grown oocyte to embryo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1418</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1418</guid>
<pubDate>Tue, 08 May 2012 22:10:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fully grown oocytes (FGOs) contain all the necessary transcripts to activate molecular pathways underlying the oocyte-to-embryo transition (OET). To elucidate this critical period of development, an extensive survey of the FGO    transcriptome was performed by analyzing 19,000 expressed sequence tags of the Mus musculus FGO cDNA library. Expression of 5400 genes and transposable elements is reported. For a majority of genes expressed in mouse FGOs, homologs transcribed in    eggs of Xenopus laevis or Ciona intestinalis were found, pinpointing evolutionary conservation of most regulatory cascades underlying the OET in chordates.  A large proportion of identified genes belongs to several gene families with    oocyte-restricted expression, a likely result of lineage-specific genomic duplications. Gene loss by mutation and expression in female germline of retrotransposed genes specific to M. musculus is documented.  These findings indicate rapid    diversification of genes involved in female reproduction. Comparison of the FGO and two-cell embryo transcriptomes demarcated the processes important for oogenesis from those involved in OET and identified novel motifs in maternal mRNAs    associated with transcript stability. Discovery of oocyte-specific eukaryotic translation initiation factor 4E distinguishes a novel system of translational regulation. These results implicate conserved pathways underlying transition from    oogenesis to initiation of development and illustrate how genes acquire and lose reproductive functions during evolution, a potential mechanism for reproductive isolation.</p>

	]]>
</description>

<author>A V. Evsikov et al.</author>


</item>


<item>
<title>Partial versus full allogeneic hemopoietic chimerization is a preferential means to inhibit type 1 diabetes as the latter induces generalized immunosuppression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1417</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1417</guid>
<pubDate>Tue, 08 May 2012 22:10:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>In both humans and NOD mice, particular combinations of MHC genes provide the primary risk factor for development of the autoreactive T cell responses causing type 1 diabetes (T1D). Conversely, other MHC variants can confer dominant    T1D resistance, and previous studies in NOD mice have shown their expression on hemopoietically derived APC is sufficient to induce disease protection. Although allogeneic hemopoietic chimerization can clearly provide a means for blocking T1D    development, its clinical use for this purpose has been obviated by a requirement to precondition the host with what would be a lethal irradiation dose if bone marrow engraftment is not successful. There have been reports in which T1D-protective    allogeneic hemopoietic chimerization was established in NOD mice that were preconditioned by protocols not including a lethal dose of irradiation. In most of these studies, virtually all the hemopoietic cells in the NOD recipients eventually    converted to donor type. We now report that a concern about such full allogeneic chimeras is that they are severely immunocompromised potentially because their T cells are positively selected in the thymus by MHC molecules differing from those    expressed by the APC available in the periphery to activate T cell effector functions. However, this undesirable side effect of generalized immunosuppression is obviated by a new protocol that establishes without a lethal preconditioning    component, a stable state of mixed allogeneic hemopoietic chimerism sufficient to inhibit T1D development and also induce donor-specific tolerance in NOD recipients.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title>Genes within the Idd5 and Idd9/11 diabetes susceptibility loci affect the pathogenic activity of B cells in nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1416</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1416</guid>
<pubDate>Tue, 08 May 2012 22:10:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Autoreactive T cells clearly mediate the pancreatic beta cell destruction causing type 1 diabetes (T1D). However, studies in NOD mice indicate that B cells also contribute to pathogenesis because their ablation by introduction of an    Igmunull mutation elicits T1D resistance. T1D susceptibility is restored in NOD.Igmunull mice that are irradiated and reconstituted with syngeneic bone marrow plus NOD B cells, but not syngeneic bone marrow alone. Thus, we hypothesized some    non-MHC T1D susceptibility (Idd) genes contribute to disease by allowing development of pathogenic B cells. Supporting this hypothesis was the finding that unlike those from NOD donors, engraftment with B cells from H2g7 MHC-matched, but    T1D-resistant, nonobese-resistant (NOR) mice failed to restore full disease susceptibility in NOD.Igmunull recipients. T1D resistance in NOR mice is mainly encoded within the Idd13, Idd5.2, and Idd9/11 loci. B cells from NOD congenic stocks    containing Idd9/11 or Idd5.1/5.2-resistance loci, respectively, derived from the NOR or C57BL/10 strains were characterized by suppressed diabetogenic activity. Immature autoreactive B cells in NOD mice have an impaired ability to be rendered    anergic upon Ag engagement. Interestingly, both Idd5.1/5.2 and Idd9/11-resistance loci were found to normalize this B cell tolerogenic process, which may represent a mechanism contributing to the inhibition of T1D.</p>

	]]>
</description>

<author>P A. Silveira et al.</author>


</item>


<item>
<title>Inheritance patterns of transcript levels in F1 hybrid mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1415</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1415</guid>
<pubDate>Tue, 08 May 2012 22:09:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic analysis of transcriptional regulation is a rapidly emerging field of investigation that promises to shed light on the regulatory networks that control gene expression. Although a number of such studies have been carried    out, the nature and extent of the heritability of gene expression traits have not been well established. We describe the inheritance of transcript levels in liver tissue in the first filial (F1) generation of mice obtained from reciprocal crosses    between the common inbred strains A/J and C57BL/6J. We obtain estimates of genetic and technical variance components from these data and demonstrate that shrinkage estimators can increase detectable heritability. Estimates of heritability vary    widely from transcript to transcript, with one-third of transcripts showing essentially no heritability (<0.01) and one-quarter showing very high heritability (>0.50). Roughly half of all transcripts are differentially expressed between the two    parental strains. Most transcripts show an additive pattern of inheritance. Dominance effects were observed for 20% of transcripts and a small number of transcripts were identified as showing an overdominance mode of inheritance. In addition, we    identified 314 transcripts with expression levels that differ between the reciprocal F1 animals. These genes may be related to maternal effect.</p>

	]]>
</description>

<author>X Cui et al.</author>


</item>


<item>
<title>Complex genetic architecture revealed by analysis of high-density lipoprotein cholesterol in chromosome substitution strains and F2 crosses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1414</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1414</guid>
<pubDate>Tue, 08 May 2012 22:09:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Intercrosses between inbred lines provide a traditional approach to analysis of polygenic inheritance in model organisms. Chromosome substitution strains (CSSs) have been developed as an alternative to accelerate the pace of gene    identification in quantitative trait mapping.  We compared a classical intercross and three CSS intercrosses to examine the genetic architecture underlying plasma high-density lipoprotein cholesterol (HDL) levels in the C57BL/6J (B) and A/J (A)    mouse strains.  The B x A intercross revealed significant quantitative trait loci (QTL) for HDL on chromosomes 1, 4, 8, 15, 17, 18, and 19. A CSS survey revealed that many have significantly different HDL levels compared to the background strain    B, including chromosomes with no significant QTL in the intercross and, in some cases (CSS-1, CSS-17), effects that are opposite to those observed in the B x A intercross population. Intercrosses between B and three CSSs (CSS-3, CSS-11, and    CSS-8) revealed significant QTL but with some unexpected differences from the B x A intercross. Our inability to predict the results of CSS intercrosses suggests that additional complexity will be revealed by further crosses and that the CSS    mapping strategy should be viewed as a complement to, rather than a replacement for, classical intercross mapping.</p>

	]]>
</description>

<author>I M. Stylianou et al.</author>


</item>


<item>
<title>Ribosomal protein S6 gene haploinsufficiency is associated with activation of a p53-dependent checkpoint during gastrulation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1413</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1413</guid>
<pubDate>Tue, 08 May 2012 22:09:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nascent ribosome biogenesis is required during cell growth. To gain insight into the importance of this process during mouse oogenesis and embryonic development, we deleted one allele of the ribosomal protein S6 gene in growing    oocytes and generated S6-heterozygous embryos. Oogenesis and embryonic development until embryonic day 5.5 (E5.5) were normal.  However, inhibition of entry into M phase of the cell cycle and apoptosis became evident post-E5.5 and led to    perigastrulation lethality. Genetic inactivation of p53 bypassed this checkpoint and prolonged development until E12.5, when the embryos died, showing decreased expression of D-type cyclins, diminished fetal liver erythropoiesis, and placental    defects.  Thus, a p53-dependent checkpoint is activated during gastrulation in response to ribosome insufficiency to prevent improper execution of the developmental program.</p>

	]]>
</description>

<author>L Panic et al.</author>


</item>


<item>
<title>Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1412</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1412</guid>
<pubDate>Tue, 08 May 2012 22:09:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>It is generally believed that shutting down the kinase activity of BCR-ABL by imatinib will completely inhibit its functions, leading to inactivation of its downstream signaling pathways and cure of the disease. Imatinib is highly    effective at treating human Philadelphia chromosome-positive (Ph(+)) chronic myeloid leukemia (CML) in chronic phase but not Ph(+) B cell acute lymphoblastic leukemia (B-ALL) and CML blast crisis. We find that SRC kinases activated by BCR-ABL    remain fully active in imatinib-treated mouse leukemic cells, suggesting that imatinib does not inactivate all BCR-ABL-activated signaling pathways. This SRC pathway is essential for leukemic cells to survive imatinib treatment and for CML    transition to lymphoid blast crisis. Inhibition of both SRC and BCR-ABL kinase activities by dasatinib affords complete B-ALL remission. However, curing B-ALL and CML mice requires killing leukemic stem cells insensitive to both imatinib and    dasatinib. Besides BCR-ABL and SRC kinases, stem cell pathways must be targeted for curative therapy of Ph(+) leukemia.</p>

	]]>
</description>

<author>Y Hu et al.</author>


</item>


<item>
<title>Quantitative comparison of EST libraries requires compensation for systematic biases in cDNA generation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1411</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1411</guid>
<pubDate>Tue, 08 May 2012 22:09:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Publicly accessible EST libraries contain valuable information that can be utilized for studies of tissue-specific gene expression and processing of individual genes. This information is, however, confounded by multiple    systematic effects arising from the procedures used to generate these libraries. RESULTS: We used alignment of ESTs against a reference set of transcripts to estimate the size distributions of the cDNA inserts and sampled mRNA transcripts in    individual EST libraries and show how these measurements can be used to inform quantitative comparisons of libraries. While significant attention has been paid to the effects of normalization and substraction, we also find significant biases in    transcript sampling introduced by the combined procedures of reverse transcription and selection of cDNA clones for sequencing. Using examples drawn from studies of mRNA 3'-processing (cleavage and polyadenylation), we demonstrate effects of the    transcript sampling bias, and provide a method for identifying libraries that can be safely compared without bias.  All data sets, supplemental data, and software are available at our supplemental web site. CONCLUSION: The biases we characterize    in the transcript sampling of EST libraries represent a significant and heretofore under-appreciated source of false positive candidates for tissue-, cell type-, or developmental stage-specific activity or processing of genes. Uncorrected,    quantitative comparison of dissimilar EST libraries will likely result in the identification of statistically significant, but biologically meaningless changes.</p>

	]]>
</description>

<author>D Liu et al.</author>


</item>


<item>
<title>Inactivation of conditional Rb by Villin-Cre leads to aggressive tumors outside the gastrointestinal tract.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1410</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1410</guid>
<pubDate>Tue, 08 May 2012 22:09:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have crossed mice carrying the conditional Rb(tm2Brn) allele with a constitutive Villin-Cre transgenic mouse. The Villin promoter in these animals is highly expressed in adult intestine and kidney proximal tubules and is    expressed in the gut and nephros anlagen during embryogenesis. We report here that these mice develop tumors between 12 and 17 months old outside the gastrointestinal (GI) tract. A high penetrance of pituitary tumors and medullar carcinoma of the    thyroid is observed with a lower incidence of hyperplasia of pulmonary neuroendocrine cells and aggressive liver, bile duct, stomach, oral cavity tumors, and lipomas. Rb rearrangement due to ectopic Villin promoter activity in neural crest or    neural crest stem cells during embryogenesis is most likely responsible for the medullar carcinoma of the thyroid phenotype. The aggressive nature of the medullar carcinoma of the thyroid and its ability to metastasize to unusual sites make the    model suitable for the study of tumor progression and mechanism of metastasis. Observed sites of metastasis include the stomach, small intestine, liver, lung, kidney, pancreas, spleen, bone marrow, salivary gland, fat, lymph nodes, and dorsal    root ganglion.  Because the Villin promoter is highly active throughout the GI and in the nephros anlagen during development, we find that Rb inactivation is not sufficient to initiate tumorigenesis in the GI or kidneys in mice.</p>

	]]>
</description>

<author>M H. Kucherlapati et al.</author>


</item>


<item>
<title>The preantral granulosa cell to cumulus cell transition in the mouse ovary: development of competence to undergo expansion.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1409</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1409</guid>
<pubDate>Tue, 08 May 2012 22:09:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>The transition of preantral to antral follicles is one of the major steps in follicular development, yet little is known about the molecular and functional changes that occur as preantral granulosa cells differentiate into cumulus    cells. The cumulus oophorus of large antral follicles undergoes expansion in response to the preovulatory surge of gonadotropins, but preantral granulosa cells do not. The objective of this project was to determine the molecular mechanisms    underlying this differential response. Cumulus expansion in vitro requires secretion of cumulus-expansion enabling factors (CEEFs) by the oocyte and stimulation by a ligand, epidermal growth factor (EGF) or follicle-stimulating hormone (FSH).    This combined stimulation results in activation of MAPKs (MAPK3/1 (formerly ERK1/2) and MAPK14 (formerly p38)) and increased Has2, Ptgs2, Tnfaip6 and Ptx3 mRNA levels, all of which are required for cumulus expansion. Only fully-grown oocytes from    antral follicles were competent to enable expansion and increases in expansion-related transcripts in cumulus cells, whereas growing oocytes of preantral follicles did not. To assess the competence of preantral granulosa cells to generate    responses associated with expansion, they were treated with FSH or EGF and co-cultured with fully-grown oocytes secreting CEEFs. MAPKs were activated by EGF in preantral granulosa cells to essentially the same levels as in cumulus cells.    Preantral granulosa cells treated with EGF, but not those treated with FSH increased Has2, Ptgs2 and Ptx3 mRNAs to 17-96% of the levels observed in cumulus cells. In contrast, the level of Tnfaip6 mRNA was minimally stimulated in preantral    granulosa cells. Therefore, preantral granulosa cells do not undergo expansion for two fundamental reasons. First, the growing oocytes of preantral follicles do not secrete active CEEFs. Second, activation of MAPKs alone in preantral granulosa    cells, even in the presence of CEEFs, is not sufficient to increase the expression of essential transcripts, particularly Tnfaip6 mRNA. Thus, preantral granulosa cells differ from cumulus cells in CEEF-dependent processes downstream of the    activation of MAPKs.</p>

	]]>
</description>

<author>F J. Diaz et al.</author>


</item>


<item>
<title>ABCA1 overexpression in the liver of LDLr-KO mice leads to accumulation of pro-atherogenic lipoproteins and enhanced atherosclerosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1408</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1408</guid>
<pubDate>Tue, 08 May 2012 22:08:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The identification of ABCA1 as a key transporter responsible for cellular lipid efflux has led to considerable interest in defining its role in cholesterol metabolism and atherosclerosis. In this study, the effect of overexpressing    ABCA1 in the liver of LDLr-KO mice was investigated.  Compared with LDLr-KO mice, ABCA1-Tg x LDLr-KO (ABCA1-Tg) mice had significantly increased plasma cholesterol levels, mostly because of a 2.8-fold increase in cholesterol associated with a    large pool of apoB-lipoproteins. ApoB synthesis was unchanged but the catabolism of (125)I-apoB-VLDL and -LDL were significantly delayed, accounting for the 1.35-fold increase in plasma apoB levels in ABCA1-Tg mice. We also found rapid in vivo    transfer of free cholesterol from HDL to apoB-lipoproteins in ABCA1-Tg mice, associated with a significant 2.7-fold increase in the LCAT-derived cholesteryl linoleate content found primarily in apoB-lipoproteins. ABCA1-Tg mice had 1.4-fold    increased hepatic cholesterol concentrations, leading to a compensatory 71% decrease in de novo hepatic cholesterol synthesis, as well as enhanced biliary cholesterol, and bile acid secretion. CAV-1, CYP2b10, and ABCG1 were significantly induced    in ABCA1-overexpressing livers; however, no differences were observed in the hepatic expression of CYP7alpha1, CYP27alpha1, or ABCG5/G8 between ABCA1-Tg and control mice. As expected from the pro-atherogenic plasma lipid profile, aortic    atherosclerosis was increased 10-fold in ABCA1-Tg mice. In summary, hepatic overexpression of ABCA1 in LDLr-KO mice leads to: 1) expansion of the pro-atherogenic apoB-lipoprotein cholesterol pool size via enhanced transfer of HDL-cholesterol to    apoB-lipoproteins and delayed catabolism of cholesterol-enriched apoB-lipoproteins; 2) increased cholesterol concentration in the liver, resulting in up-regulated hepatobiliary sterol secretion; and 3) significantly enhanced aortic    atherosclerotic lesions.</p>

	]]>
</description>

<author>C W. Joyce et al.</author>


</item>


<item>
<title>Genomes as geography: using GIS technology to build interactive genome feature maps.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1407</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1407</guid>
<pubDate>Tue, 08 May 2012 22:08:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Many commonly used genome browsers display sequence annotations and related attributes as horizontal data tracks that can be toggled on and off according to user preferences. Most genome browsers use only simple keyword    searches and limit the display of detailed annotations to one chromosomal region of the genome at a time. We have employed concepts, methodologies, and tools that were developed for the display of geographic data to develop a Genome Spatial    Information System (GenoSIS) for displaying genomes spatially, and interacting with genome annotations and related attribute data. In contrast to the paradigm of horizontally stacked data tracks used by most genome browsers, GenoSIS uses the    concept of registered spatial layers composed of spatial objects for integrated display of diverse data. In addition to basic keyword searches, GenoSIS supports complex queries, including spatial queries, and dynamically generates genome maps.    Our adaptation of the geographic information system (GIS) model in a genome context supports spatial representation of genome features at multiple scales with a versatile and expressive query capability beyond that supported by existing genome    browsers. RESULTS: We implemented an interactive genome sequence feature map for the mouse genome in GenoSIS, an application that uses ArcGIS, a commercially available GIS software system. The genome features and their attributes are represented    as spatial objects and data layers that can be toggled on and off according to user preferences or displayed selectively in response to user queries. GenoSIS supports the generation of custom genome maps in response to complex queries about    genome features based on both their attributes and locations. Our example application of GenoSIS to the mouse genome demonstrates the powerful visualization and query capability of mature GIS technology applied in a novel domain. CONCLUSION:    Mapping tools developed specifically for geographic data can be exploited to display, explore and interact with genome data. The approach we describe here is organism independent and is equally useful for linear and circular chromosomes. One of    the unique capabilities of GenoSIS compared to existing genome browsers is the capacity to generate genome feature maps dynamically in response to complex attribute and spatial queries.</p>

	]]>
</description>

<author>M E. Dolan et al.</author>


</item>


<item>
<title>Defective carbohydrate metabolism in mice homozygous for the tubby mutation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1406</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1406</guid>
<pubDate>Tue, 08 May 2012 22:08:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Tub is a member of a small gene family, the tubby-like proteins (TULPs), with predominant expression in neurons. Mice carrying a mutation in Tub develop retinal and cochlear degeneration as well as late-onset obesity with insulin    resistance. During behavioral and metabolic testing, we found that homozygous C57BL/6J-Tub(tub) mice have a lower respiratory quotient than C57BL/6J controls before the onset of obesity, indicating that tubby homozygotes fail to activate    carbohydrate metabolism and instead rely on fat metabolism for energy needs. In concordance with this, tubby mice show higher excretion of ketone bodies and accumulation of glycogen in the liver. Quantitation of liver mRNA levels shows that,    during the transition from light to dark period, tubby mice fail to induce glucose-6-phosphate dehydrogenase (G6pdh), the rate-limiting enzyme in the pentose phosphate pathway that normally supplies NADPH for de novo fatty acid synthesis and    glutathione reduction. Reduced G6PDH protein levels and enzymatic activity in tubby mice lead accordingly to lower levels of NADPH and reduced glutathione (GSH), respectively. mRNA levels for the lipolytic enzymes acetyl-CoA synthetase and    carnitine palmitoyltransferase are increased during the dark cycle and decreased during the light period, and several citric acid cycle genes are dysregulated in tubby mice. Examination of hypothalamic gene expression showed high levels of    preproorexin mRNA leading to accumulation of orexin peptide in the lateral hypothalamus. We hypothesize that abnormal hypothalamic orexin expression leads to changes in liver carbohydrate metabolism and may contribute to the moderate obesity    observed in tubby mice.</p>

	]]>
</description>

<author>Y Wang et al.</author>


</item>


<item>
<title>Patterns and mechanisms of genome organization in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1405</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1405</guid>
<pubDate>Tue, 08 May 2012 22:08:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>The physical and functional organizations of a genome are correlated outcomes of evolution. Inbred strains of mice provide a unique opportunity for exploring these relationships, representing as they do, diverse genomes originally    separated by millions of generations that were then scrambled in the laboratory and subjected to intense selection during inbreeding to homozygosity. Here we show that the resulting pattern of chromosome organization includes regional domains of    functionally related elements that promote the co-inheritance and survival of compatible sets of alleles. There are also patterns of linkage disequilibrium between domains on separate chromosomes; these are distinctly non-random and form networks    with scale-free architecture. The strong conservation of gene order among mammals suggests that the domains and networks we find likely characterize all mammals, and possibly beyond.</p>

	]]>
</description>

<author>J H. Graber et al.</author>


</item>


<item>
<title>p25/cyclin-dependent kinase 5 induces production and intraneuronal accumulation of amyloid beta in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1404</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1404</guid>
<pubDate>Tue, 08 May 2012 22:08:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Aberrant processing of the amyloid precursor protein (APP) and the subsequent accumulation of amyloid beta (Abeta) peptide has been widely established as a central event in Alzheimer's disease (AD) pathogenesis.  The sequential    cleavage steps required for the generation of Abeta are well outlined; however, there is a relative dearth of knowledge pertaining to signaling pathways and molecular mechanisms that can modulate this process. Here, we demonstrate a novel role    for p25/cyclin-dependent kinase 5 (Cdk5) in regulating APP processing, Abeta peptide generation, and intraneuronal Abeta accumulation in inducible p25 transgenic and compound PD-APP transgenic mouse models that demonstrate deregulated Cdk5    activity and a neurodegenerative phenotype. Induction of p25 resulted in enhanced forebrain Abeta levels before any evidence of neuropathology in these mice. Intracellular Abeta accumulated in perinuclear regions and distended axons within the    forebrains of these mice. Evidence for modulations in axonal transport or beta-site APP cleaving enzyme 1 protein levels and activity are presented as mechanisms that may account for the Abeta accumulation caused by p25/Cdk5 deregulation.    Collectively, these findings delineate a novel pathological mechanism involving aberrant APP processing by p25/Cdk5 and have important implications in AD pathogenesis.</p>

	]]>
</description>

<author>J C. Cruz et al.</author>


</item>


<item>
<title>A polymorphism in New Zealand inbred mouse strains that inactivates phosphatidylcholine transfer protein.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1403</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1403</guid>
<pubDate>Tue, 08 May 2012 22:08:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>New Zealand obese (NZO/HlLt) male mice develop polygenic diabetes and altered phosphatidylcholine metabolism. The gene encoding phosphatidylcholine transfer protein (PC-TP) is sited within the support interval for Nidd3, a recessive    NZO-derived locus on Chromosome 11 identified by prior segregation analysis between NZO/HlLt and NON/Lt.  Sequence analysis revealed that the NZO-derived PC-TP contained a non-synonymous point mutation that resulted in an Arg120His substitution,    which was shared by the related NZB/BlNJ and NZW/LacJ mouse strains.  Consistent with the structure-based predictions, functional studies demonstrated that Arg120His PC-TP was inactive, suggesting that this mutation contributes to the    deficiencies in phosphatidylcholine metabolism observed in NZO mice.</p>

	]]>
</description>

<author>H J. Pan et al.</author>


</item>


<item>
<title>A novel somatic mouse model to survey tumorigenic potential applied to the Hedgehog pathway.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1402</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1402</guid>
<pubDate>Tue, 08 May 2012 22:07:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>We report a novel mouse model for the generation of sporadic tumors and show the efficiency of this approach by surveying Hedgehog (Hh)-related tumors. Up-regulation of the Hh pathway is achieved by conditionally regulated    expression of an activated allele of Smoothened (R26-SmoM2) using either sporadic leakage or global postnatal induction of a ubiquitously expressed inducible Cre transgene (CAGGS-CreER). Following postnatal tamoxifen induction, CAGGS-CreER;    R26-SmoM2 mice developed tumors with short latency and high penetrance. All mice exhibited rhabdomyosarcoma and basal cell carcinoma; 40% also developed medulloblastoma. In addition, mice showed a novel pancreatic lesion resembling low-grade    mucinous cystic neoplasms in humans. In contrast, widespread activation of SmoM2 in the postnatal prostate epithelium results in no detectable morphologic outcome in 12-month-old mice.  Comparison of gene expression profiles among diverse tumors    identified several signature genes, including components of platelet-derived growth factor and insulin-like growth factor pathways, which may provide a common mechanistic link to the Hh-related malignancies. This experimental model provides a    robust tool for exploring the process of Hh-dependent tumorigenesis and the treatment of such tumors. More generally, this approach provides a genetic platform for identifying tumorigenic potential in putative oncogenes and tumor suppressors and    for more effective modeling of sporadic cancers in mice.</p>

	]]>
</description>

<author>J Mao et al.</author>


</item>


<item>
<title>Effect of complete protein 4.1R deficiency on ion transport properties of murine erythrocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1401</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1401</guid>
<pubDate>Tue, 08 May 2012 22:07:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Moderate hemolytic anemia, abnormal erythrocyte morphology (spherocytosis), and decreased membrane stability are observed in mice with complete deficiency of all erythroid protein 4.1 protein isoforms (4.1(-/-); Shi TS et al. J Clin    Invest 103: 331, 1999). We have examined the effects of erythroid protein 4.1 (4.1R) deficiency on erythrocyte cation transport and volume regulation. 4.1(-/-) mice exhibited erythrocyte dehydration that was associated with reduced cellular K and    increased Na content. Increased Na permeability was observed in these mice, mostly mediated by Na/H exchange with normal Na-K pump and Na-K-2Cl cotransport activities. The Na/H exchange of 4.1(-/-) erythrocytes was markedly activated by exposure    to hypertonic conditions (18.2 +/- 3.2 in 4.1(-/-) vs. 9.8 +/- 1.3 mmol/10(13) cell x h in control mice), with an abnormal dependence on osmolality (EC(50) = 417 +/- 42 in 4.1(-/-) vs. 460 +/- 35 mosmol/kgH(2)O in control mice), suggestive of an    upregulated functional state. While the affinity for internal protons was not altered (K(0.5) = 489.7 +/- 0.7 vs. 537.0 +/- 0.56 nM in control mice), the V(max) of the H-induced Na/H exchange activity was markedly elevated in 4.1(-/-)    erythrocytes (V(max) 91.47 +/- 7.2 compared with 46.52 +/- 5.4 mmol/10(13) cell x h in control mice). Na/H exchange activation by okadaic acid was absent in 4.1(-/-) erythrocytes. Altogether, these results suggest that erythroid protein 4.1 plays    a major role in volume regulation and physiologically downregulates Na/H exchange in mouse erythrocytes.  Upregulation of the Na/H exchange is an important contributor to the elevated cell Na content of 4.1(-/-) erythrocytes.</p>

	]]>
</description>

<author>A Rivera et al.</author>


</item>


<item>
<title>Evidence that the satin hair mutant gene Foxq1 is among multiple and functionally diverse regulatory targets for Hoxc13 during hair follicle differentiation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1400</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1400</guid>
<pubDate>Tue, 08 May 2012 22:07:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>It is increasingly evident that the molecular mechanisms underlying hair follicle differentiation and cycling recapitulate principles of embryonic patterning and organ regeneration. Here we used Hoxc13-overexpressing transgenic mice    (also known as GC13 mice), known to develop severe hair growth defects and alopecia, as a tool for defining pathways of hair follicle differentiation. Gene array analysis performed with RNA from postnatal skin revealed differential expression of    distinct subsets of genes specific for cells of the three major hair shaft compartments (cuticle, cortex, and medulla) and their precursors. This finding correlates well with the structural defects observed in each of these compartments and    implicates Hoxc13 in diverse pathways of hair follicle differentiation. The group of medulla-specific genes was particularly intriguing because this included the developmentally regulated transcription factor-encoding gene Foxq1 that is altered    in the medulladefective satin mouse hair mutant. We provide evidence that Foxq1 is a downstream target for Hoxc13 based on DNA binding studies as well as co-transfection and chromatin immunoprecipitation assays. Expression of additional    medulla-specific genes down-regulated upon overexpression of Hoxc13 requires functional Foxq1 as their expression is ablated in hair follicles of satin mice. Combined, these results demonstrate that Hoxc13 and Foxq1 control medulla    differentiation through a common regulatory pathway. The apparent regulatory interactions between members of the mammalian Hox and Fox gene families shown here may establish a paradigm for "cross-talk" between these two conserved regulatory gene    families in different developmental contexts including embryonic patterning as well as organ development and renewal.</p>

	]]>
</description>

<author>C S. Potter et al.</author>


</item>


<item>
<title>Intestinal-specific PPARgamma deficiency enhances tumorigenesis in ApcMin/+ mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1399</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1399</guid>
<pubDate>Tue, 08 May 2012 22:07:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Multiple investigations of the effects of peroxisome proliferator-activated receptor gamma (PPARgamma) ligands on colon cancer have produced contradictory results. While some studies demonstrated increased numbers of colonic polyps    in Apc(Min/+) mice treated with various thiazolidinedione (TZD) PPARgamma ligands, others reported amelioration of tumor multiplicity and progression in both Apc(Min/+) mice and in mice with chemically-induced colon cancer. Here, we addressed the    role of PPARgamma in murine intestinal tumorigenesis using gene knockout methodology. We found that either heterozygous or homozygous intestinal-specific PPARgamma deficiency enhanced the number of Apc(Min/+) tumors in both the small intestine    and colon, especially in the colon, where PPARgamma deficiency also modulated tumor incidence. Gender significantly affected tumor multiplicity independent of PPARgamma genotype. Female Apc(Min/+) mice developed more tumors in the small intestine    and more tumors overall, whereas male Apc(Min/+) mice developed more tumors in the colon. Nevertheless, intestinal PPARgamma deficiency enhanced tumorigenesis irrespective of gender. Our results suggest that PPARgamma functions as a tumor    resistance factor in the mouse intestine and warrant further investigation of the PPARgamma-dependent and independent actions of TZDs in cancer.</p>

	]]>
</description>

<author>C A. McAlpine et al.</author>


</item>


<item>
<title>Mechanisms of disease: is osteoporosis the obesity of bone?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1398</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1398</guid>
<pubDate>Tue, 08 May 2012 22:07:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Osteoporosis and obesity, two disorders of body composition, are growing in prevalence. Interestingly, these diseases share several features including a genetic predisposition and a common progenitor cell. With aging, the    composition of bone marrow shifts to favor the presence of adipocytes, osteoclast activity increases, and osteoblast function declines, resulting in osteoporosis. Secondary causes of osteoporosis, including diabetes mellitus, glucocorticoids and    immobility, are associated with bone-marrow adiposity. In this review, we ask a provocative question: does fat infiltration in the bone marrow cause low bone mass or is it a result of bone loss? Unraveling the interface between bone and fat at a    molecular and cellular level is likely to lead to a better understanding of several diseases, and to the development of drugs for both osteoporosis and obesity.</p>

	]]>
</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title>The chloride intracellular channel protein CLIC5 is expressed at high levels in hair cell stereocilia and is essential for normal inner ear function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1397</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1397</guid>
<pubDate>Tue, 08 May 2012 22:07:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although CLIC5 is a member of the chloride intracellular channel protein family, its association with actin-based cytoskeletal structures suggests that it may play an important role in their assembly or maintenance. Mice homozygous    for a new spontaneous recessive mutation of the Clic5 gene, named jitterbug (jbg), exhibit impaired hearing and vestibular dysfunction. The jbg mutation is a 97 bp intragenic deletion that causes skipping of exon 5, which creates a translational    frame shift and premature stop codon. Western blot and immunohistochemistry results confirmed the predicted absence of CLIC5 protein in tissues of jbg/jbg mutant mice. Histological analysis of mutant inner ears revealed dysmorphic stereocilia and    progressive hair cell degeneration. In wild-type mice, CLIC5-specific immunofluorescence was detected in stereocilia of both cochlear and vestibular hair cells and also along the apical surface of Kolliker's organ during cochlear development.    Refined immunolocalization in rat and chicken vestibular hair cells showed that CLIC5 is limited to the basal region of the hair bundle, similar to the known location of radixin. Radixin immunostaining appeared reduced in hair bundles of jbg    mutant mice. By mass spectrometry and immunoblotting, CLIC5 was shown to be expressed at high levels in stereocilia of the chicken utricle, in an approximate 1:1 molar ratio with radixin. These results suggest that CLIC5 associates with radixin    in hair cell stereocilia and may help form or stabilize connections between the plasma membrane and the filamentous actin core.</p>

	]]>
</description>

<author>L H. Gagnon et al.</author>


</item>


<item>
<title>Epithelial-specific and stage-specific functions of insulin-like growth factor-I during postnatal mammary development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1396</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1396</guid>
<pubDate>Tue, 08 May 2012 22:06:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Postnatal development of the mammary gland requires interactions between the epithelial and stromal compartments, which regulate actions of hormones and growth factors. IGF-I is expressed in both epithelial and stromal compartments    during postnatal development of the mammary gland.  However, little is known about how local expression of IGF-I in epithelium or stroma regulates mammary growth and differentiation during puberty and pregnancy-induced alveolar development. The    goal of this study was to investigate the mechanisms of IGF-I actions in the postnatal mammary gland and test the hypothesis that IGF-I expressed in stromal and epithelial compartments has distinct functions. We established mouse lines with    inactivation of the igf1 gene in mammary epithelium by crossing igf1/loxP mice with mouse lines expressing Cre recombinase under the control of either the mouse mammary tumor virus long-terminal repeat or the whey acidic protein gene promoter.    Epithelial-specific loss of IGF-I during pubertal growth resulted in deficits in ductal branching. In contrast, heterozygous reduction of IGF-I throughout the gland decreased expression of cyclins A2 and B1 during pubertal growth and resulted in    alterations in proliferation of the alveolar epithelium and milk protein levels during pregnancy-induced differentiation. Reduction in epithelial IGF-I at either of these stages had no effect on these indices. Taken together, our results support    distinct roles for IGF-I expressed in epithelial and stromal compartments in mediating growth of the postnatal mammary gland.</p>

	]]>
</description>

<author>A V. Loladze et al.</author>


</item>


<item>
<title>Femur mechanical properties in the F2 progeny of an NZB/B1NJ x RF/J cross are regulated predominantly by genetic loci that regulate bone geometry.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1395</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1395</guid>
<pubDate>Tue, 08 May 2012 22:06:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic analysis of an NZB/B1NJ x RF/J cross has identified QTLs for femur mechanical, geometric, and densitometric phenotypes. Most mechanical QTLs were associated with geometric QTLs, strongly suggesting common genetic regulation.    INTRODUCTION: Previous studies have shown that bone architecture and BMD are important factors affecting bone strength, and both are genetically regulated. We conducted genetic analyses for loci regulating femur mechanical properties, geometric    properties, and BMD in a cohort of F2 mice derived from intercross matings of (NZB/B1NJ x RF/J)F1 parents. MATERIALS AND METHODS: Femurs were isolated from 662 10-week-old females. Mechanical properties were determined for a femur from each    animal by three-point bending. Geometric properties and volumetric BMD (vBMD) were determined by pQCT. Genotype data were obtained by PCR assays for polymorphic markers carried in the genomic DNA of each mouse.  Genome-wide scans were carried out    for co-segregation of genetic marker data with values from 23 different phenotypes. Quantitative trait loci (QTLs) were identified for mechanical, geometric, and mineral density phenotypes. RESULTS: QTLs for many phenotypes were significantly    refined by covariate analyses using body weight and femur length. Major QTLs for mechanical and geometric phenotypes were found on chromosomes 5, 7, 9, 11, and 12. Nine chromosomal locations were identified with mechanical QTLs and 17 locations    with one or more geometric QTLs. The significance of five mechanical and nine geometric QTLs was affected by the inclusion of covariates. These changes included both decreases and increases in significance. The QTLs on chromosomes 5 and 12 were    decreased by inclusion of the covariates in the analysis, but QTLs on 7 and 11 were unaffected.  Mechanical QTLs were almost always associated with geometric QTLs and less commonly (two of six) with vBMD QTLs. CONCLUSIONS: Genetic regulation of    mechanical properties in the F(2) mice of this NZB/B1NJ x RF/J cross seems to be caused by genes regulating femur geometry.</p>

	]]>
</description>

<author>J E. Wergedal et al.</author>


</item>


<item>
<title>Editing-defective tRNA synthetase causes protein misfolding and neurodegeneration.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1394</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1394</guid>
<pubDate>Tue, 08 May 2012 22:06:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Misfolded proteins are associated with several pathological conditions including neurodegeneration. Although some of these abnormally folded proteins result from mutations in genes encoding disease-associated proteins (for example,    repeat-expansion diseases), more general mechanisms that lead to misfolded proteins in neurons remain largely unknown. Here we demonstrate that low levels of mischarged transfer RNAs (tRNAs) can lead to an intracellular accumulation of misfolded    proteins in neurons. These accumulations are accompanied by upregulation of cytoplasmic protein chaperones and by induction of the unfolded protein response. We report that the mouse sticky mutation, which causes cerebellar Purkinje cell loss and    ataxia, is a missense mutation in the editing domain of the alanyl-tRNA synthetase gene that compromises the proofreading activity of this enzyme during aminoacylation of tRNAs. These findings demonstrate that disruption of translational fidelity    in terminally differentiated neurons leads to the accumulation of misfolded proteins and cell death, and provide a novel mechanism underlying neurodegeneration.</p>

	]]>
</description>

<author>J W. Lee et al.</author>


</item>


<item>
<title>An active dominant mutation of glycyl-tRNA synthetase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1393</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1393</guid>
<pubDate>Tue, 08 May 2012 22:06:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Of the many inherited Charcot-Marie-Tooth peripheral neuropathies, type 2D (CMT2D) is caused by dominant point mutations in the gene GARS, encoding glycyl tRNA synthetase (GlyRS). Here we report a dominant mutation in Gars that    causes neuropathy in the mouse. Importantly, both sensory and motor axons are affected, and the dominant phenotype is not caused by a loss of the GlyRS aminoacylation function. Mutant mice have abnormal neuromuscular junction morphology and    impaired transmission, reduced nerve conduction velocities, and a loss of large-diameter peripheral axons, without defects in myelination. The mutant GlyRS enzyme retains aminoacylation activity, and a loss-of-function allele, generated by a    gene-trap insertion, shows no dominant phenotype in mice. These results indicate that the CMT2D phenotype is caused not by reduction of the canonical GlyRS activity and insufficiencies in protein synthesis, but instead by novel pathogenic roles    for the mutant GlyRS that specifically affect peripheral neurons.</p>

	]]>
</description>

<author>K L. Seburn et al.</author>


</item>


<item>
<title>Expression of chitinase-like proteins in the skin of chronic proliferative dermatitis (cpdm/cpdm) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1392</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1392</guid>
<pubDate>Tue, 08 May 2012 22:06:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mammalian chitinase-like proteins belong to a family of proteins structurally related to chitinases but devoid of enzymatic activity. They have a postulated role in remodeling of extracellular matrix and defense mechanisms against    chitin-containing pathogens. The expression of these proteins is increased in parasitic infections and allergic airway disease, but their expression in dermatitis has not been examined. The mRNA expression of two chitinase 3-like (Chi3L)    proteins, Chi3L3 (Ym1) and Chi3L4 (Ym2), was determined in the skin of normal mice, chronic proliferative dermatitis (cpdm/cpdm) mutant mice and mice with experimentally induced contact hypersensitivity reaction. The localization of Chi3L3 and    Chi3L4 proteins in cells was determined by fluorescence microscopy of double-labeled frozen sections of skin, and confirmed in vitro by stimulation of macrophages and mast cells with cytokines.  Quantitative RT-PCR demonstrated a 976-fold    increase of Chi3l4 mRNA expression and a 24-fold increase of Chi3l3 mRNA expression in the skin of cpdm/cpdm mice. Their expression was also increased in the ears of mice with 2,4-dinitrofluorobenzene-induced contact hypersensitivity, but the    increase was greater for Chi3l3 mRNA (51-fold) than Chi3l4 mRNA (32-fold).  Western blot analysis with an antibody against Chi3L3 and Chi3L4 confirmed the increased amount of these proteins in the skin of cpdm/cpdm mice.  Two-color    immunofluorescence identified macrophages, dendritic cells and mast cells as cellular sources of Chi3L3 and Chi3L4 proteins. Eosinophils and neutrophils did not contain detectable concentrations of these proteins. Treatment of macrophages and    mast cells in vitro with interleukin-4 induced expression of Chi3l3 and Chi3l4 mRNA.</p>

	]]>
</description>

<author>H HogenEsch et al.</author>


</item>


<item>
<title>Pituitary removal in adult mice increases life span.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1391</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1391</guid>
<pubDate>Tue, 08 May 2012 22:06:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dwarf mutations reduce levels of pituitary hormones and increase life span in mice. But because these dwarf mutations confer life-long hormone deficits that alter development and dramatically reduce fecundity, the relevance of these    models to normal aging has been questioned. We examined effects of pituitary hormone withdrawal at different ages using hypophysectomy (surgical removal of the pituitary). Hypophysectomy at 1 month of age extended life span significantly (15%),    but hypophysectomy at 9 months of age extended life span to the greatest magnitude (21%) of any age we tested. These results demonstrate pituitary hormone withdrawal can extend life span even if these hormones are removed relatively late in    life.</p>

	]]>
</description>

<author>R W. Powers et al.</author>


</item>


<item>
<title>Adverse hepatic and cardiac responses to rosiglitazone in a new mouse model of type 2 diabetes: relation to dysregulated phosphatidylcholine metabolism.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1390</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1390</guid>
<pubDate>Tue, 08 May 2012 22:06:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Given the heterogeneous nature of metabolic dysfunctions associated with insulin resistance and type 2 diabetes (T2D), a single pharmaceutical cannot be expected to provide complication-free therapy in all patients.     Thiazolidinediones (TZD) increase insulin sensitivity, reduce blood glucose and improve cardiovascular parameters. However, in addition to increasing fat mass, TZD have the potential in certain individuals to exacerbate underlying hepatosteatosis    and diabetic cardiomyopathy.  Pharmacogenetics should allow patient selection to maximize therapy and minimize risk. To this end, we have combined two genetically diverse inbred strains, NON/Lt and NZO/Lt, to produce a "negative heterosis"    increasing the frequency of T2D in F1 males. As in humans with T2D, treatment of diabetic and hyperlipemic F1 males with rosiglitazone (Rosi), an agonist of peroxisome proliferator-activated gamma receptor (PPARgamma), reverses these disease    phenotypes. However, the hybrid genome perturbed both major pathways for phosphatidylcholine (PC) biosynthesis in the liver, and effected remarkable alterations in the composition of cardiolipin in heart mitochondria. These metabolic defects    severely exacerbated an underlying hepatosteatosis and increased levels of the adipokine, plasminogen activator inhibitor-1 (PAI-1), a risk factor for cardiovascular events. This model system demonstrates how the power of mouse genetics can be    used to identify the metabolic signatures of individuals who may be prone to drug side effects.</p>

	]]>
</description>

<author>H J. Pan et al.</author>


</item>


<item>
<title>The diabetes-prone NZO/Hl strain. Proliferation capacity of beta cells in hyperinsulinemia and hyperglycemia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1389</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1389</guid>
<pubDate>Tue, 08 May 2012 22:05:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>New Zealand Obese (NZO) male mice develop a polygenic juvenile-onset obesity and maturity onset hyperinsulinemia. Approximately 50% transit to chronic hyperglycemia. Here we report on the proliferation of beta cells in relation to    both the individual's metabolic status and structural parameters of the endocrine pancreas. Proliferating beta cells were quantified in pancreas sections by immunoenzymatic double staining of Ki-67 protein, as a marker for proliferating cells,    and endocrine non-beta cells in order to distinguish them from beta cells. In normoglycemic NZO/Hl males Ki-67 labelling indices (IKi-67) of beta cells varied between 0.14 and 1.5%, and correlated significantly with both serum insulin levels and    beta cell size. There was no correlation with the glycemic status. In diabetic males, beta cell size was increased. IKi-67 varied between 1 and 3%. The data suggest that the secretory activity of beta cells triggered by glucose, entailed changes    in both beta cell hypertrophy and proliferation. As shown by morphometric measurements, beta cell expansion in diabetic mice was limited, in spite of high IKi-67 values. This suggested increased death rates of beta cells.</p>

	]]>
</description>

<author>C Lange et al.</author>


</item>


<item>
<title>Folding and organization of a contiguous chromosome region according to the gene distribution pattern in primary genomic sequence.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1388</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1388</guid>
<pubDate>Tue, 08 May 2012 22:05:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Specific mammalian genes functionally and dynamically associate together within the nucleus. Yet, how an array of many genes along the chromosome sequence can be spatially organized and folded together is unknown. We investigated    the 3D structure of a well-annotated, highly conserved 4.3-Mb region on mouse chromosome 14 that contains four clusters of genes separated by gene "deserts." In nuclei, this region forms multiple, nonrandom "higher order" structures. These    structures are based on the gene distribution pattern in primary sequence and are marked by preferential associations among multiple gene clusters. Associating gene clusters represent expressed chromatin, but their aggregation is not simply    dependent on ongoing transcription. In chromosomes with aggregated gene clusters, gene deserts preferentially align with the nuclear periphery, providing evidence for chromosomal region architecture by specific associations with functional    nuclear domains. Together, these data suggest dynamic, probabilistic 3D folding states for a contiguous megabase-scale chromosomal region, supporting the diverse activities of multiple genes and their conserved primary sequence    organization.</p>

	]]>
</description>

<author>L S. Shopland et al.</author>


</item>


<item>
<title>Altered growth characteristics of skin fibroblasts from wild-derived mice, and genetic loci regulating fibroblast clone size.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1387</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1387</guid>
<pubDate>Tue, 08 May 2012 22:05:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mouse fibroblast senescence in vitro is an important model for the study of aging at cellular level. However, common laboratory mouse strains may have lost some important allele variations related to aging processes. In this study,    growth in vitro of tail skin fibroblasts (TSFs) derived from a wild-derived stock, Pohnpei (Pohn) mice, differed from growth of control C57BL/6 J (B6) TSFs. Pohn TSFs exhibited higher proliferative ability, fewer apoptotic cells, decreased    expression of Cip1, smaller surface areas, fewer cells positive for senescence associated-beta-galactosidase (SA-beta-gal) and greater resistance to H(2)O(2)-induced SA-beta-gal staining and Cip1 expression. These data suggest that TSFs from Pohn    mice resist cellular senescence-like changes. Using large clone ratio (LCR) as the phenotype, a quantitative trait locus (QTL) analysis in a Pohn/B6 backcross population found four QTLs for LCR: Fcs1 on Chr 3 at 55 CM; Fcs2 on Chr X at 50 CM;    Fcs3 on Chr 4 at 51 CM and Fcs4 on Chr 10 at 25 CM.  Together, these four QTLs explain 26.1% of the variations in LCRs in the N2 population. These are the first QTLs reported that regulate fibroblast growth. Glutathione S transferase mu (GST-mu)    genes are overrepresented in the 95% confidence interval of Fcs1, and Pohn TSFs have higher H(2)O(2)-induced GST-mu 4, 5 and 7 mRNA levels than B6 TSFs. These enzymes may protect Pohn TSFs from oxidation.</p>

	]]>
</description>

<author>R Yuan et al.</author>


</item>


<item>
<title>Strategies for managing an ever increasing mutant mouse repository.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1386</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1386</guid>
<pubDate>Tue, 08 May 2012 22:05:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Over 10,000 mouse strains and more than 20,000 mouse ES cells containing gene-trapped or targeted mutations are available to researchers. The mouse strains and stocks include those with spontaneous, genetically engineered and    induced mutations, as well as 100s of inbred strains and strain panels, valuable for quantitative trait locus (QTL) and modifier gene identification. Current worldwide initiatives are expected to result in multiple mutations in every mouse gene    in the first 10 years of the 21st century. Managing the rapid and cost effective distribution of these burgeoning resources to scientists around the world will be challenging for scientists and mouse repositories. Here we describe new strategies    for managing and distributing mice.</p>

	]]>
</description>

<author>M T. Davisson et al.</author>


</item>


<item>
<title>Inner ear proteomics of mouse models for deafness, a discovery strategy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1385</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1385</guid>
<pubDate>Tue, 08 May 2012 22:05:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inner ear dysfunction is often associated with defective hair cells.  Therefore, hair cells are the focus of study in many of the mouse mutants showing auditory and vestibular deficits. However, harvesting sufficient numbers of hair    cells from the tiny bony mouse inner ear for proteomic analysis is challenging. New approaches that would take advantage of mouse mutants and avoid processing steps, such as decalcification or microdissetion, would be more suitable for proteomic    analysis. Here, we propose a novel approach called SSUMM-Subtractive Strategy Using Mouse Mutants. SSUMM takes advantage of the differences between control and affected or mutant samples. We predict that SSUMM would be a useful method in    proteomics, especially in those cases in which the investigator must work with small numbers of diverse cell types from a tiny organ. Here, we discuss the potential utility of SSUMM to unravel the protein expression profiles of hair cells using    the Pou4f3 mouse mutant as an example. Pou4f3 mutant mice exhibit a total loss of inner and outer hair cells, but supporting cells remain relatively intact in the cochlea, thus providing an excellent model for identifying proteins and transcripts    that are specific to the hair cell at all life stages. SSUMM would maximize the sensitivity of the analyses while obviating the need for tedious sessions of microdissection and collection of hair cells. By comparing the mutant to control ears at    specific time points, it is possible to identify direct targets of a gene product of interest. Further, SSUMM could be used to identify and analyze inner ear development markers and other known genes/proteins that are coexpressed in the ear. In    this short technical report, we also discuss protein-profiling approaches suitable for SSUMM and briefly discuss other approaches used in the field of proteomics.</p>

	]]>
</description>

<author>Q Y. Zheng et al.</author>


</item>


<item>
<title>Snail family genes are required for left-right asymmetry determination, but not neural crest formation, in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1384</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1384</guid>
<pubDate>Tue, 08 May 2012 22:05:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Snail family genes encode zinc finger transcriptional repressors that are key regulators of epithelial-mesenchymal transitions in vertebrates, including the transitions that generate the mesoderm and neural crest.  Here, we show    that, contrary to observations in frog and avian embryos, the Snail family genes Snail (Snai1) and Slug (Snai2) are not required for formation and delamination of the neural crest in mice. However, embryos with conditional inactivation of Snai1    function exhibit defects in left-right asymmetry determination. This work demonstrates that although some aspects of Snail family gene function, such as a role in left-right asymmetry determination, appear to be evolutionarily conserved, their    role in neural crest cell formation and delamination is not.</p>

	]]>
</description>

<author>S A. Murray et al.</author>


</item>


<item>
<title>Resistance of C57BL/6 mice to amoebiasis is mediated by nonhemopoietic cells but requires hemopoietic IL-10 production.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1383</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1383</guid>
<pubDate>Tue, 08 May 2012 22:04:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Resistance to intestinal amoebiasis is mouse strain dependent. C57BL/6 (B6) mice clear Entamoeba histolytica within hours of challenge, whereas C3H and CBA strains are susceptible to infection and disease. In this study, we show    using bone marrow (BM) chimeric mice that mouse strain-dependent resistance is mediated by nonhemopoietic cells; specifically, B6 BM --> CBA recipients remained susceptible as measured by amoeba score and culture, whereas CBA BM --> B6 recipients    remained resistant. Interestingly, hemopoietic IL-10 was required for maintaining the resistance of B6 mice, in that B6 IL-10-deficient mice and IL-10(-/-) BM --> wild-type recipients, but not IL-10(+/+) BM --> IL-10(-/-) recipients, exhibited    higher amoeba scores than their wild-type controls.  Additionally, C57BL/10 IL-10(-/-)Rag2(-/-) mice exhibited diminished amoeba scores and culture rates vs IL-10(-/-) mice, indicating that lymphocytes potentiated the susceptibility of    IL-10-deficient mice. We conclude that nonhemopoietic cells mediate the natural resistance to intestinal amoebiasis of B6 mice, yet this resistance depends on hemopoietic IL-10 activity.</p>

	]]>
</description>

<author>S Hamano et al.</author>


</item>


<item>
<title>Mouse models as a tool to unravel the genetic basis for human otitis media.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1382</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1382</guid>
<pubDate>Tue, 08 May 2012 22:04:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>The pathogenesis of otitis media (OM) is multifactorial and includes infection, anatomical factors, immunologic status, genetic predisposition, and environmental factors. OM remains the most common cause of hearing impairment in    childhood. Genetic predisposition is increasingly recognized as an important factor. The completion of the mouse genome sequence has offered a powerful basket of tools for investigating gene function and can expect to generate a rich resource of    mouse mutants for the elucidation of genetic factors underlying OM. We review the literature and discuss recent progresses in developing mouse models and using mouse models to uncover the genetic basis for human OM.</p>

	]]>
</description>

<author>Q Y. Zheng et al.</author>


</item>


<item>
<title>Transgenic mice with osteoblast-targeted insulin-like growth factor-I show increased bone remodeling.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1381</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1381</guid>
<pubDate>Tue, 08 May 2012 22:04:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>To determine the effects of locally-expressed insulin-like growth factor (IGF-I) on bone remodeling, a transgene was produced in which murine IGF-I cDNA was cloned downstream of a gene fragment comprising 3.6 kb of 5' upstream    regulatory sequence and most of the first intron of the rat Col1a1 gene. The construct was expressed at the mRNA and protein level in transfected osteoblasts. Five lines of transgenic mice were generated by embryo microinjection. Transgene mRNA    levels were highest in calvaria, long bone and tendon, and lower in skin. Serum IGF-I and body weight were increased in males and females only in the highest expressing line.  Histomorphometry showed that transgenic calvaria were wider and had    greater marrow area and bone area. Transgenic calvaria had increased osteoclast number per bone surface. Percent collagen synthesis and cell replication were increased in transgenic calvaria. Femur length, cortical width and cross-sectional area    were increased in transgenic femurs of the highest expressing line, while femoral trabecular bone volume was little affected. Thus, broad overexpression of IGF-I in cells of the osteoblast lineage increased indices of bone formation and    resorption.</p>

	]]>
</description>

<author>J Jiang et al.</author>


</item>


<item>
<title>Congenic mice provide in vivo evidence for a genetic locus that modulates serum insulin-like growth factor-I and bone acquisition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1380</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1380</guid>
<pubDate>Tue, 08 May 2012 22:04:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>We identified quantitative trait loci (QTL) that determined the genetic variance in serum IGF-I through genome-wide scanning of mice derived from C57BL/6J(B6) x C3H/HeJ(C3H) intercrosses. One QTL (Igf1s2), on mouse chromosome 10    (Chr10), produces a 15% increase in serum IGF-I in B6C3 F2 mice carrying c3 alleles at that position. We constructed a congenic mouse, B6.C3H-10 (10T), by backcrossing c3 alleles from this 57-Mb region into B6 for 10 generations. 10T mice have    higher serum and skeletal IGF-I, greater trabecular bone volume fraction, more trabeculae, and a higher number of osteoclasts at 16 wk, compared with B6 (P < 0.05). Nested congenic sublines generated from further backcrossing of 10T allowed for    recombination and produced four smaller sublines with significantly increased serum IGF-I at 16 wk (i.e. 10-4, 10-7, 10-10, and 10-13), compared with B6 (P < 0.0003), and three smaller sublines that showed no differences in IGF-I vs. age- and    gender-matched B6 mice. Like 10T, the 10-4 nested sublines at 16 wk had higher femoral mineral (P < 0.0001) and greater trabecular connectivity density with significantly more trabeculae than B6 (P < 0.01). Thus, by comprehensive phenotyping, we    were able to narrow the QTL to an 18.3-Mb region containing approximately 148 genes, including Igf1 and Elk-3(ETS domain protein). Allelic differences in the Igf1s2 QTL produce a phenotype characterized by increased serum IGF-I and greater peak    bone density. Congenic mice establish proof of concept of shared genetic determinants for both circulating IGF-I and bone acquisition.</p>

	]]>
</description>

<author>K M. Delahunty et al.</author>


</item>


<item>
<title>A mouse TRAPP-related protein is involved in pigmentation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1379</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1379</guid>
<pubDate>Tue, 08 May 2012 22:04:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>We identified a new spontaneous recessive mutation in the mouse, mhyp (mosaic hypopigmentation), in a screen for novel proviral integration sites in a multiple ecotropic provirus mapping stock. Integration of an 8.4-kb retrovirus    results in mosaic loss of coat pigment in mhyp homozygotes. Patchy loss of pigmentation in the retinal pigmented epithelial layer of the eye with abnormal melanosomes is also evident. We mapped mhyp to mouse chromosome 7 and cloned the underlying    gene. mhyp is a defect in the Trappc6a gene. Expression of Trappc6a is markedly diminished in mhyp homozygotes. The normal protein, TRAPPC6A, is a subunit of the TRAPP (transport protein particle) I and II complexes. While TRAPP complexes are    essential for ER-to-Golgi and intra-Golgi vesicle trafficking in yeast, TRAPP subunits participate in additional, including post-Golgi, transport events in mammals. The data implicate mammalian TRAPPC6A in vesicle trafficking during melanosome    biogenesis.</p>

	]]>
</description>

<author>B Gwynn et al.</author>


</item>


<item>
<title>Endoplasmic reticulum stress in health and disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1378</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1378</guid>
<pubDate>Tue, 08 May 2012 22:03:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Unfolded proteins and other conditions affecting endoplasmic reticulum (ER) homeostasis cause ER stress. The cell reacts to ER stress by activation of the unfolded protein response (UPR), which induces profound changes in cellular    metabolism including general translation attenuation, transcriptional upregulation of molecular chaperone genes, and activation of ER-associated degradation. However, prolonged or acute ER stress results in cell death. Recent progress suggests    that ER stress and UPR play key roles in the immune response, diabetes, tumor growth under hypoxic conditions, and in some neurodegenerative diseases. Further research on ER stress and UPR will greatly enhance the understanding of these    physiological and pathological processes, and provide novel avenues to potential therapies.</p>

	]]>
</description>

<author>L Zhao et al.</author>


</item>


<item>
<title>Embryology: does prepatterning occur in the mouse egg?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1377</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1377</guid>
<pubDate>Tue, 08 May 2012 22:03:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>A recurring question in developmental biology has been whether localized determinants play any role in mammalian preimplantation development. This is a controversial issue that brings back the idea of prepatterning and is explored    further by Plusa et al., who claim it is the first cleavage of the mouse zygote that predicts the blastocyst axis, rather than the animal pole or sperm entry point, as previously suggested. However, other evidence indicates that the blasotcyst    axis is not predetermined and there is no prepatterning in the mouse egg. Here we investigate the origin of these different views and conclude that they arise from differences in the data themselves and in their interpretation.</p>

	]]>
</description>

<author>T Hiiragi et al.</author>


</item>


<item>
<title>A multispecies comparison of the metazoan 3&apos;-processing downstream elements and the CstF-64 RNA recognition motif.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1376</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1376</guid>
<pubDate>Tue, 08 May 2012 22:03:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The Cleavage Stimulation Factor (CstF) is a required protein complex for eukaryotic mRNA 3'-processing. CstF interacts with 3'-processing downstream elements (DSEs) through its 64-kDa subunit, CstF-64; however, the exact    nature of this interaction has remained unclear. We used EST-to-genome alignments to identify and extract large sets of putative 3'-processing sites for mRNA from ten metazoan species, including Homo sapiens, Canis familiaris, Rattus norvegicus,    Mus musculus, Gallus gallus, Danio rerio, Takifugu rubripes, Drosophila melanogaster, Anopheles gambiae, and Caenorhabditis elegans. In order to further delineate the details of the mRNA-protein interaction, we obtained and multiply aligned    CstF-64 protein sequences from the same species. RESULTS: We characterized the sequence content and specific positioning of putative DSEs across the range of organisms studied. Our analysis characterized the downstream element (DSE) as two    distinct parts - a proximal UG-rich element and a distal U-rich element. We find that while the U-rich element is largely conserved in all of the organisms studied, the UG-rich element is not. Multiple alignment of the CstF-64 RNA recognition    motif revealed that, while it is highly conserved throughout metazoans, we can identify amino acid changes that correlate with observed variation in the sequence content and positioning of the DSEs. CONCLUSION: Our analysis confirms the early    reports of separate U- and UG-rich DSEs. The correlated variations in protein sequence and mRNA binding sequences provide novel insights into the interactions between the precursor mRNA and the 3'-processing machinery.</p>

	]]>
</description>

<author>J Salisbury et al.</author>


</item>


<item>
<title>The long and short of it: somite formation in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1375</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1375</guid>
<pubDate>Tue, 08 May 2012 22:03:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>A fundamental characteristic of the vertebrate body plan is its segmentation along the anterior-posterior axis. This segmental pattern is established during embryogenesis by the formation of somites, the transient epithelial blocks    of cells that derive from the unsegmented presomitic mesoderm. Somite formation involves a molecular oscillator, termed the segmentation clock, in combination with gradients of signaling molecules such as fibroblast growth factor 8, WNT3A, and    retinoic acid.  Disruption of somitogenesis in humans can result in disorders such as spondylocostal dysostosis, which is characterized by vertebral malformations. This review summarizes recent findings concerning the role of Notch signaling in    the segmentation clock, the complex regulatory network that governs somitogenesis, the genes that cause inherited spondylocostal dysostosis, and the mechanisms that regulate bilaterally symmetric somite formation.</p>

	]]>
</description>

<author>T Gridley</author>


</item>


<item>
<title>The mouse gcd2 mutation causes primordial germ cell depletion.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1374</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1374</guid>
<pubDate>Tue, 08 May 2012 22:03:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Germ cell depletion 2 (gcd2) is a chemically induced recessive mutation that causes infertility in male and female mice. The infertility is caused by germ cell depletion as early as 11.5 days post-coitum, when primordial germ cells    have completed their migration to the embryonic gonads. Thus, the gcd2 mutation affects the proliferation and/or survival of germ cells after they arrive in the embryonic gonad, a developmental time when little is known about the requirements for    germ cell proliferation and survival.  The sterility phenotype is incompletely penetrant, has variable expressivity, and is modulated by strain background. The penetrance ranges from 37% in strain C57BL/6J to nearly 100% in CAST/EiJ. Genetic    mapping localized gcd2 to a approximately 1Mb region on Chr 2. This interval contains a small number of annotated genes, of which none are known to have a role in germ cell development. Sequencing the coding regions of these genes failed to    reveal a mutation, and BACs containing two of the candidate genes failed to rescue the phenotype. This raises the possibilities that the gcd2 mutation resides in non-coding sequences, and regulates genes outside the genetically defined critical    region.</p>

	]]>
</description>

<author>L G. Reinholdt et al.</author>


</item>


<item>
<title>Genetic context determines susceptibility to intraocular pressure elevation in a mouse pigmentary glaucoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1373</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1373</guid>
<pubDate>Tue, 08 May 2012 22:03:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: DBA/2J (D2) mice develop an age-related form of glaucoma.  Their eyes progressively develop iris pigment dispersion and iris atrophy followed by increased intraocular pressure (IOP) and glaucomatous optic nerve damage.    Mutant alleles of the Gpnmb and Tyrp1 genes are necessary for the iris disease, but it is unknown whether alleles of other D2 gene(s) are necessary for the distinct later stages of disease. We initiated a study of congenic strains to further    define the genetic requirements and disease mechanisms of the D2 glaucoma. RESULTS: To further understand D2 glaucoma, we created congenic strains of mice on the C57BL/6J (B6) genetic background. B6 double-congenic mice carrying D2-derived Gpnmb    and Tyrp1 mutations develop a D2-like iris disease. B6 single-congenics with only the Gpnmb and Tyrp1 mutations develop milder forms of iris disease. Genetic epistasis experiments introducing a B6 tyrosinase mutation into the congenic strains    demonstrated that both the single and double-congenic iris diseases are rescued by interruption of melanin synthesis. Importantly, our experiments analyzing mice at ages up to 27 months indicate that the B6 double-congenic mice are much less    prone to IOP elevation and glaucoma than are D2 mice. CONCLUSION: As demonstrated here, the Gpnmb and Tyrp1 iris phenotypes are both individually dependent on tyrosinase function. These results support involvement of abnormal melanosomal events    in the diseases caused by each gene. In the context of the inbred D2 mouse strain, the glaucoma phenotype is clearly influenced by more genes than just Gpnmb and Tyrp1. Despite the outward similarity of pigment-dispersing iris disease between D2    and the B6 double-congenic mice, the congenic mice are much less susceptible to developing high IOP and glaucoma. These new congenic strains provide a valuable new resource for further studying the genetic and mechanistic complexity of this form    of glaucoma.</p>

	]]>
</description>

<author>M G. Anderson et al.</author>


</item>


<item>
<title>Where do we stand now? Mouse early embryo patterning meeting in Freiburg, Germany (2005).</title>
<link>http://mouseion.jax.org/stfb2000_2009/1372</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1372</guid>
<pubDate>Tue, 08 May 2012 22:02:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mechanism underlying mammalian preimplantation development has long been a subject of controversy and the central question has been if any "determinants" play a key role in a manner comparable to the non-mammalian "model" system.    During the last decade, this issue has been revived (Pearson, 2002; Rossant and Tam, 2004) by claims that the axes of the mouse blastocyst are anticipated at the egg ("prepatterning model"; Gardner, 1997; Gardner, 2001; Piotrowska et al., 2001;    Piotrowska and Zernicka-Goetz, 2001; Zernicka-Goetz, 2005), suggesting that a mechanism comparable to that operating in non-mammals may be at work. However, recent studies by other laboratories do not support these claims ("regulative model";    Alarcon and Marikawa, 2003; Chroscicka et al., 2004; Hiiragi and Solter, 2004; Alarcon and Marikawa, 2005; Louvet-Vallee et al., 2005; Motosugi et al., 2005) and the issue is currently under hot debate (Vogel, 2005). Deepening our knowledge of    this issue will not only provide an essential basis for understanding mammalian development, but also directly apply to ongoing clinical practices such as intracytoplasmic sperm injection (ICSI) and preimplantation genetic diagnosis (PGD). These    practices were originally supported by a classical premise that mammalian preimplantation embryos are highly regulative (Tarkowski, 1959; Tarkowski, 1961; Tarkowski and Wroblewska, 1967; Rossant, 1976), in keeping with the "regulative model".    However, if the "prepatterning model" is correct, the latter will require critical reassessment.</p>

	]]>
</description>

<author>T Hiiragi et al.</author>


</item>


<item>
<title>Auditory brainstem responses in 10 inbred strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1371</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1371</guid>
<pubDate>Tue, 08 May 2012 22:02:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>The auditory brainstem response (ABR) is an evoked potential response of auditory activity in the auditory nerve and subsequent fiber tracts and nuclei within the auditory brainstem pathways.</p>

	]]>
</description>

<author>X Zhou et al.</author>


</item>


<item>
<title>Scanning transmission X-ray microscopic analysis of purified melanosomes of the mouse iris.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1370</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1370</guid>
<pubDate>Tue, 08 May 2012 22:02:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Melanosomes are specialized intracellular membrane bound organelles that produce and store melanin pigment.</p>

	]]>
</description>

<author>M G. Anderson et al.</author>


</item>


<item>
<title>Interaction between fidgetin and protein kinase A-anchoring protein AKAP95 is critical for palatogenesis in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1369</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1369</guid>
<pubDate>Tue, 08 May 2012 22:02:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The gene defective in fidget mice encodes fidgetin, a member of the AAA (ATPases associated with diverse cellular activities) family of ATPases.  Using a yeast two-hybrid screen, we identified cAMP-dependent protein kinase A    anchoring protein 95 kDa (AKAP95) as a potential fidgetin-binding protein.</p>

	]]>
</description>

<author>Y Yang et al.</author>


</item>


<item>
<title>EUK-8, a superoxide dismutase and catalase mimetic, reduces cardiac oxidative stress and ameliorates pressure overload-induced heart failure in the harlequin mouse mutant.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1368</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1368</guid>
<pubDate>Tue, 08 May 2012 22:02:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVES: The purpose of this study was to identify apoptosis-inducing factor (AIF) as a cardiac mitochondrial antioxidant and assess the efficacy of EUK-8, a salen-manganese catalytic free radical scavenger, to protect the    AIF-deficient myocardium against pressure overload.  BACKGROUND: Oxidative stress has been postulated to provoke cell death and pathologic remodeling in heart failure.</p>

	]]>
</description>

<author>Empel V. van et al.</author>


</item>


<item>
<title>Adult mice lacking the p53/p63 target gene Perp are not predisposed to spontaneous tumorigenesis but display features of ectodermal dysplasia syndromes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1367</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1367</guid>
<pubDate>Tue, 08 May 2012 22:02:06 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R A. Ihrie et al.</author>


</item>


<item>
<title>Adherence to bisphosphonate therapy and fracture rates in osteoporotic women: relationship to vertebral and nonvertebral fractures from 2 US claims databases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1366</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1366</guid>
<pubDate>Tue, 08 May 2012 22:01:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: To characterize the relationships between adherence (complance and persistence) to bisphosphonate therapy and risk of specific fracture types in postmenopausal women. PATIENTS AND METHODS: Data were collected from 45    employers and 100 health plans in the continental United States from 2 claims databases during a 5-year period (January 1, 1999, through December 31, 2003). Claims from patients receiving a bisphosphonate prescription (alendronate or risedronate)    were evaluated for 6 months before the Index prescription and during 24 months of follow-up to determine total, vertebral, and nonvertebral osteoporotic fractures, persistence (no gap in refills for >30 days during 24 months), and refill    compliance (medication possession ratio > or = 0.80). RESULTS: The eligible cohort included 35,537 women (age, > or = 45 years) who received a bisphosphonate prescription. A subgroup with a specified diagnosis of postmenopausal osteoporosis was    also evaluated. Forty-three percent were refill compliant, and 20% persisted with bisphosphonate therapy during the 24-month study period. Total, vertebral, nonvertebral, and hip fractures were significantly lower in refill-compliant and    persistent patients, with relative risk reductions of 20% to 45%. The relationship between adherence and fracture risk remained significant after adjustment for baseline age, concomitant medications, and fracture history. There was a progressive    relationship between refill compliance and fracture risk reduction, commencing at refill compliance rates of approximately 50% and becoming more pronounced at compliance rates of 75% and higher. CONCLUSIONS: Adherence to bisphosphonate therapy    was associated with significantly fewer fractures at 24 months. Increasing refill compliance levels were associated with progressively lower fracture rates. These findings suggest that incremental changes in medication-taking habits could improve    clinical outcomes of osteoporosis treatment.</p>

	]]>
</description>

<author>E S. Siris et al.</author>


</item>


<item>
<title>CD38 is required for the peripheral survival of immunotolerogenic CD4+ invariant NK T cells in nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1365</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1365</guid>
<pubDate>Tue, 08 May 2012 22:01:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>T cell-mediated autoimmune type-1 diabetes (T1D) in NOD mice partly results from this strain's numerical and functional defects in invariant NK T (iNKT) cells. T1D is inhibited in NOD mice treated with the iNKT cell superagonist    alpha-galactosylceramide through a process involving enhanced accumulation of immunotolerogenic dendritic cells in pancreatic lymph nodes. Conversely, T1D is accelerated in NOD mice lacking CD38 molecules that play a role in dendritic cell    migration to inflamed tissues. Unlike in standard NOD mice, alpha-galactosylceramide pretreatment did not protect the CD38-deficient stock from T1D induced by an adoptively transferred pancreatic beta cell-autoreactive CD8 T cell clone (AI4). We    found that in the absence of CD38, ADP-ribosyltransferase 2 preferentially activates apoptotic deletion of peripheral iNKT cells, especially the CD4+ subset. Therefore, this study documents a previously unrecognized role for CD38 in maintaining    survival of an iNKT cell subset that preferentially contributes to the maintenance of immunological tolerance.</p>

	]]>
</description>

<author>Y G. Chen et al.</author>


</item>


<item>
<title>Early immunization induces persistent tumor-infiltrating CD8+ T cells against an immunodominant epitope and promotes lifelong control of pancreatic tumor progression in SV40 tumor antigen transgenic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1364</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1364</guid>
<pubDate>Tue, 08 May 2012 22:01:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ability to recruit the host's CD8+ T lymphocytes (T(CD8)) against cancer is often limited by the development of peripheral tolerance toward the dominant tumor-associated Ags. Because multiple epitopes derived from a given tumor    Ag (T Ag) can be targeted by T(CD8), vaccine approaches should be directed toward those T(CD8) that are more likely to survive under conditions of persistent Ag expression. In this study, we investigated the effect of peripheral tolerance on the    endogenous T(CD8) response toward two epitopes, designated epitopes I and IV, from the SV40 large T Ag. Using rat insulin promoter (RIP) 1-Tag4 transgenic mice that express T Ag from the RIP and develop pancreatic insulinomas, we demonstrate that    epitope IV- but not epitope I-specific T(CD8) are maintained long term in tumor-bearing RIP1-Tag4 mice. Even large numbers of TCR-transgenic T cells specific for epitope I were rapidly eliminated from RIP1-Tag4 mice after adoptive transfer and    recognition of the endogenous T Ag. Importantly, immunization of RIP1-Tag4 mice at 5 wk of age against epitope IV resulted in complete protection from tumor progression over a 2-year period despite continued expression of T Ag in the pancreas.    This extensive control of tumor progression was associated with the persistence of functional epitope IV-specific T(CD8) within the pancreas for the lifetime of the mice without the development of diabetes.  This study indicates that an    equilibrium is reached in which immune surveillance for spontaneous cancer can be achieved for the lifespan of the host while maintaining normal organ function.</p>

	]]>
</description>

<author>P Otahal et al.</author>


</item>


<item>
<title>A comparison of vestibular and auditory phenotypes in inbred mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1363</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1363</guid>
<pubDate>Tue, 08 May 2012 22:01:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purposes of this research were to quantify gravity receptor function in inbred mouse strains and compare vestibular and auditory function for strain- and age-matched animals. Vestibular evoked potentials (VsEPs) were collected    for 19 inbred strains at ages from 35 to 389 days old. On average, C57BL/6J (35 to 190 days), BALB/cByJ, C3H/HeSnJ, CBA/J, and young LP/J mice had VsEP thresholds comparable to normal. Elevated VsEP thresholds were found for elderly C57BL/6J,    NOD.NONH2(kb), BUB/BnJ, A/J, DBA/2J, NOD/LtJ, A/WySnJ, MRL/MpJ, A/HeJ, CAST/Ei, SJL/J, elderly LP/J, and CE/J. These results suggest that otolithic function varies among inbred strains and several strains displayed gravity receptor deficits by 90    days old. Auditory brainstem response (ABR) thresholds were compared to VsEP thresholds for 14 age-matched strains. C57BL/6J mice (up to 190 days) showed normal VsEPs with normal to mildly elevated ABR thresholds. Four strains (BUB/BnJ, NOD/LtJ,    A/J, elderly LP/J) had significant hearing loss and elevated VsEP thresholds. Four strains (DBA/2J, A/WySnJ, NOD.NONH2(kb), A/HeJ) had elevated VsEP thresholds (including absent VsEPs) with mild to moderate elevations in ABR thresholds. Three    strains (MRL/MpJ, Ce/J, SJL/J) had significant vestibular loss with no concomitant hearing loss. These results suggest that functional change in one sensory system does not obligate change in the other. We hypothesize that genes responsible for    early onset hearing loss may affect otolithic function, yet the time course of functional change may vary. In addition, some genetic mutations may produce primarily gravity receptor deficits.  Potential genes responsible for selective gravity    receptor impairment demonstrated herein remain to be identified.</p>

	]]>
</description>

<author>S M. Jones et al.</author>


</item>


<item>
<title>Strain background effects and genetic modifiers of hearing in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1362</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1362</guid>
<pubDate>Tue, 08 May 2012 22:01:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic modifiers can be detected in mice by looking for strain background differences in inheritance or phenotype of a mutation. They can be mapped by analyses of appropriate linkage crosses and congenic lines, and modifier genes    of large effect can be identified by positional-candidate gene testing. Inbred strains of mice vary widely in onset and severity of age-related hearing loss (AHL), an important consideration when assessing hearing in mutant mice. At least 8    mapped loci and a mitochondrial variant (mt-Tr) are known to contribute to AHL in mouse strains; one locus (ahl) has been identified as a variant of the cadherin 23 gene (Cdh23(753A/G)).  This variant also was shown to modify hearing loss    associated with the Atp2b2(dfw-2J) and Mass1(frings) mutations. The hearing modifier (Moth1) of tubby (Tub(tub)) mutant mice was shown to be a strain variant of the Mtap1a gene. Human hearing modifiers include DFNM1, which suppresses recessive    deafness DFNB26, and a nuclear gene that modulates the severity of hearing loss associated with a mitochondrial mutation. Recently, a variant of the human ATP2B2 gene was shown to exacerbate hearing loss in individuals homozygous for a CDH23    mutation, similar to the Atp2b2(dfw-2J)-Cdh23(753A/G) interaction affecting hearing in mice.  Because modifier genes and digenic inheritance are not always distinguishable, we also include in this review several examples of digenic inheritance of    hearing loss that have been reported in both mice and humans.</p>

	]]>
</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title>QTL mapping for genetic determinants of lipoprotein cholesterol levels in combined crosses of inbred mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1361</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1361</guid>
<pubDate>Tue, 08 May 2012 22:01:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>To identify additional loci that influence lipoprotein cholesterol levels, we performed quantitative trait locus (QTL) mapping in offspring of PERA/EiJxI/LnJ and PERA/EiJxDBA/2J intercrosses and in a combined data set from both    crosses after 8 weeks of consumption of a high fat-diet. Most QTLs identified were concordant with homologous chromosomal regions that were associated with lipoprotein levels in human studies. We detected significant new loci for HDL cholesterol    levels on chromosome (Chr) 5 (Hdlq34) and for non-HDL cholesterol levels on Chrs 15 (Nhdlq9) and 16 (Nhdlq10). In addition, the analysis of combined data sets identified a QTL for HDL cholesterol on Chr 17 that was shared between both crosses;    lower HDL cholesterol levels were conferred by strain PERA. This QTL colocalized with a shared QTL for cholesterol gallstone formation detected in the same crosses. Haplotype analysis narrowed this QTL, and sequencing of the candidate genes Abcg5    and Abcg8 confirmed shared alleles in strains I/LnJ and DBA/2J that differed from the alleles in strain PERA/EiJ. In conclusion, our analysis furthers the knowledge of genetic determinants of lipoprotein cholesterol levels in inbred mice and    substantiates the hypothesis that polymorphisms of Abcg5/Abcg8 contribute to individual variation in both plasma HDL cholesterol levels and susceptibility to cholesterol gallstone formation.</p>

	]]>
</description>

<author>H Wittenburg et al.</author>


</item>


<item>
<title>Neonatal Fc receptor for IgG regulates mucosal immune responses to luminal bacteria.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1360</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1360</guid>
<pubDate>Tue, 08 May 2012 22:00:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The neonatal Fc receptor for IgG (FcRn) plays a major role in regulating host IgG levels and transporting IgG and associated antigens across polarized epithelial barriers. Selective expression of FcRn in the epithelium is shown here    to be associated with secretion of IgG into the lumen that allows for defense against an epithelium-associated pathogen (Citrobacter rodentium). This pathway of host resistance to a bacterial pathogen as mediated by FcRn involves retrieval of    bacterial antigens from the lumen and initiation of adaptive immune responses in regional lymphoid structures. Epithelial-associated FcRn, through its ability to secrete and absorb IgG, may thus integrate luminal antigen encounters with systemic    immune compartments and as such provide essential host defense and immunoregulatory functions at the mucosal surfaces.</p>

	]]>
</description>

<author>M Yoshida et al.</author>


</item>


<item>
<title>From information to understanding: the role of model organism databases in comparative and functional genomics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1359</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1359</guid>
<pubDate>Tue, 08 May 2012 22:00:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Data integration is key to functional and comparative genomics because integration allows diverse data types to be evaluated in new contexts. To achieve data integration in a scalable and sensible way, semantic standards are needed,    both for naming things (standardized nomenclatures, use of key words) and also for knowledge representation. The Mouse Genome Informatics database and other model organism databases help to close the gap between information and understanding of    biological processes because these resources enforce well-defined nomenclature and knowledge representation standards. Model organism databases have a critical role to play in ensuring that diverse kinds of data, especially genome-scale data sets    and information, remain useful to the biological community in the long-term. The efforts of model organism database groups ensure not only that organism-specific data are integrated, curated and accessible but also that the information is    structured in such a way that comparison of biological knowledge across model organisms is facilitated.</p>

	]]>
</description>

<author>C J. Bult</author>


</item>


<item>
<title>Absence of erythroblast macrophage protein (Emp) leads to failure of erythroblast nuclear extrusion.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1358</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1358</guid>
<pubDate>Tue, 08 May 2012 22:00:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>In mammals, the functional unit for definitive erythropoiesis is the erythroblastic island, a multicellular structure composed of a central macrophage surrounded by developing erythroblasts. Erythroblast-macrophage interactions play    a central role in the terminal maturation of erythroblasts, including enucleation. One possible mediator of this cell-cell interaction is the protein Emp (erythroblast macrophage protein). We used targeted gene inactivation to define the function    of Emp during hematopoiesis. Emp null embryos die perinatally and show profound alterations in the hematopoietic system. A dramatic increase in the number of nucleated, immature erythrocytes is seen in the peripheral blood of Emp null fetuses. In    the fetal liver virtually no erythroblastic islands are observed, and the number of F4/80-positive macrophages is substantially reduced. Those present lack cytoplasmic projections and are unable to interact with erythroblasts. Interestingly, wild    type macrophages can bind Emp-deficient erythroblasts, but these erythroblasts do not extrude their nuclei, suggesting that Emp impacts enucleation in a cell autonomous fashion. Previous studies have implicated the actin cytoskeleton and its    reorganization in both erythroblast enucleation as well as in macrophage development. We demonstrate that Emp associates with F-actin and that this interaction is important in the normal distribution of F-actin in both erythroblasts and    macrophages. Thus, Emp appears to be required for erythroblast enucleation and in the development of the mature macrophages.  The availability of an Emp null model provides a unique experimental system to study the enucleation process and to    evaluate the function of macrophages in definitive erythropoiesis.</p>

	]]>
</description>

<author>S Soni et al.</author>


</item>


<item>
<title>Abnormal lymphoid organ development in immunodeficient mutant mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1357</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1357</guid>
<pubDate>Tue, 08 May 2012 22:00:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Development of the primary and secondary lymphoid organs is a tightly controlled process. These tissues are highly organized to maximize efficiency of the immune response. Spontaneous and targeted mutations in laboratory mice have    led to better understanding of the molecular interactions and signaling pathways essential to the development and organization of lymphoid tissues, and the functional consequences of loss or disruption of the normal structures. On the basis of    studies of mutations in mice and other species, it has been determined that a wild-type allele of the Foxn1 gene is required for normal thymic development and function. The Tlx1, Bapx1, Tcf21, Wt1 and Dh genes are essential for development of the    spleen, while mutations of Nkx2-3, Lta, Ltb, Ltbr, Map3k14, Relb, Tnf, Tnfrsf1a, Cxcl13, Blr1 (Cxcr5), or cpdm genes result in disruption of normal splenic microarchitecture. The requirements for organized lymph nodes vary according to anatomic    location, but most rely on Id2 (Idb2) and Rorc, in addition to lymphotoxins and Tnfrsf11a, Tnfsf11, Relb, Map3k14, Cxcl13, and Blr1 genes. Development of Peyer's patches is dependent on Id2 and Rorc genes, lymphotoxins, and Relb, Map3k14, Il7r,    and cpdm genes. Less is known about the requirements for nasal-associated lymphoid tissues (NALT), but Id2 is a requirement. Here we review abnormalities of lymphoid organ development in immunodeficient mutant mice, including spontaneous and    targeted mutations of Id2, Rorc, Tnf, Tnfrsf1a, Lta, Ltb, Ltbr, Tnfrsf11a, Tnfsf11, Relb, Map3k14, IL7r, Blr1, and Cxcl13 genes.</p>

	]]>
</description>

<author>R Seymour et al.</author>


</item>


<item>
<title>Structural model analysis of multiple quantitative traits.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1356</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1356</guid>
<pubDate>Tue, 08 May 2012 22:00:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>We introduce a method for the analysis of multilocus, multitrait genetic data that provides an intuitive and precise characterization of genetic architecture. We show that it is possible to infer the magnitude and direction of    causal relationships among multiple correlated phenotypes and illustrate the technique using body composition and bone density data from mouse intercross populations. Using these techniques we are able to distinguish genetic loci that affect    adiposity from those that affect overall body size and thus reveal a shortcoming of standardized measures such as body mass index that are widely used in obesity research. The identification of causal networks sheds light on the nature of genetic    heterogeneity and pleiotropy in complex genetic systems.</p>

	]]>
</description>

<author>R Li et al.</author>


</item>


<item>
<title>Albumin turnover: FcRn-mediated recycling saves as much albumin from degradation as the liver produces.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1355</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1355</guid>
<pubDate>Tue, 08 May 2012 21:59:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>It is now understood that the nonclassical major histocompatibility complex-I molecule FcRn binds albumin and retrieves it from an intracellular degradative fate. Whether FcRn in the liver modulates albumin turnover through effects    on biosynthesis and production is not known. Thus we quantified the appearance of biosynthetically labeled albumin in plasma after an intravenous bolus injection of [(3)H]leucine in FcRn-deficient mice. The production rates for both albumin (FcRn    substrate) and transferrin (nonsubstrate) are increased by approximately 20% in FcRn-deficient mice compared with normal mice, likely compensating for the lowered plasma oncotic pressure caused by hypoalbuminemia in FcRn-deficient mice.    Determining the magnitude of FcRn-mediated effects on albumin turnover, we then measured the steady-state plasma concentrations of biosynthetically labeled albumin and transferrin during [(3)H]leucine infusion. The concentration of albumin was    approximately 40% lower in FcRn-deficient mice compared with normal mice. Furthermore, the approximately 40% lower plasma albumin concentration in FcRn-deficient mice along with the approximately 20% increase in albumin production indicate, by    the mass-balance equation, that albumin degradation in FcRn-deficient mice is twice that of normal mice. These studies of biosynthetically labeled, and thus native, albumin support our previous finding that FcRn protects albumin from degradation.    Permitting quantification of the magnitude of FcRn-mediated recycling, they further indicate that FcRn has extraordinary capacity: the amount of albumin saved from degradation by FcRn-mediated recycling is the same as that produced by the    liver.</p>

	]]>
</description>

<author>J Kim et al.</author>


</item>


<item>
<title>The Mouse Genome Database (MGD): updates and enhancements.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1354</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1354</guid>
<pubDate>Tue, 08 May 2012 21:59:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Database (MGD) integrates genetic and genomic data for the mouse in order to facilitate the use of the mouse as a model system for understanding human biology and disease processes. A core component of the MGD    effort is the acquisition and integration of genomic, genetic, functional and phenotypic information about mouse genes and gene products.  MGD works within the broader bioinformatics community to define referential and semantic standards to    facilitate data exchange between resources including the incorporation of information from the biomedical literature. MGD is also a platform for computational assessment of integrated biological data with the goal of identifying candidate genes    associated with complex phenotypes. MGD is web accessible at http://www.informatics.jax.org. Recent improvements in MGD described here include the incorporation of an interactive genome browser, the enhancement of phenotype resources and the    further development of functional annotation resources.</p>

	]]>
</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title>Effects of GH and/or sex steroids on circulating IGF-I and IGFBPs in healthy, aged women and men.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1353</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1353</guid>
<pubDate>Tue, 08 May 2012 21:59:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Circulating GH, IGF-I, IGFBP-3, and sex steroid concentrations decrease with age. GH or sex steroid treatment increases IGFBP-3, but little is known regarding the effects of these hormones on other IGFBPs. We assessed the effects of    26 wk of administration of GH, sex steroids, or GH + sex steroids on AM levels of IGF-I, IGFBPs 1-5, insulin, glucose, and osteocalcin and 2-h urinary excretion of deoxypyridinolline (DPD) cross-links in 53 women and 71 men aged 65-88 yr. Before    treatment, in women and men, IGF-I was directly related to IGFBP-3 (P < 0.001 and P < 0.0001) and IGFBP-1 to IGFBP-2 (P = 0.0001). In women, IGFBP-1 was inversely related to insulin (P < 0.0005) and glucose (P < 0.005) and IGFBP-4 to osteocalcin    (P < 0.01). IGFBP-4 and IGFBP-5 were not significantly related to DPD cross-links. GH and/or sex steroid increased IGF-I levels in both sexes, with higher concentrations in men (P < 0.001).  In women, the IGF-I increment after GH was attenuated    by hormone replacement therapy (HRT) coadministration (P < 0.05). Hormone administration also increased IGFBP-3. IGFBP-1 was unaffected by GH + sex steroids, whereas GH decreased IGFBP-2 by 15% in men (P < 0.05). Hormone administration did not    change IGFBP-4, whereas in men IGFBP-5 increased by 20% after GH (P < 0.05) and 56% after GH + testosterone (P = 0.0003).  These data demonstrate sexually dimorphic IGFBP responses to GH.  Additionally, HRT attenuated or prevented GH-mediated    increases in IGF-I and IGFBP-3. Whether GH and/or sex steroid administration alters local tissue production of IGFBPs and whether the latter influence autocrine or paracrine actions of IGF-I remain to be determined.</p>

	]]>
</description>

<author>T Munzer et al.</author>


</item>


<item>
<title>The Notch ligand JAG1 is required for sensory progenitor development in the mammalian inner ear.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1352</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1352</guid>
<pubDate>Tue, 08 May 2012 21:59:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>In mammals, six separate sensory regions in the inner ear are essential for hearing and balance function. Each sensory region is made up of hair cells, which are the sensory cells, and their associated supporting cells, both arising    from a common progenitor. Little is known about the molecular mechanisms that govern the development of these sensory organs. Notch signaling plays a pivotal role in the differentiation of hair cells and supporting cells by mediating lateral    inhibition via the ligands Delta-like 1 and Jagged (JAG) 2. However, another Notch ligand, JAG1, is expressed early in the sensory patches prior to cell differentiation, indicating that there may be an earlier role for Notch signaling in sensory    development in the ear. Here, using conditional gene targeting, we show that the Jag1 gene is required for the normal development of all six sensory organs within the inner ear. Cristae are completely lacking in Jag1-conditional knockout (cko)    mutant inner ears, whereas the cochlea and utricle show partial sensory development. The saccular macula is present but malformed. Using SOX2 and p27kip1 as molecular markers of the prosensory domain, we show that JAG1 is initially expressed in    all the prosensory regions of the ear, but becomes down-regulated in the nascent organ of Corti by embryonic day 14.5, when the cells exit the cell cycle and differentiate. We also show that both SOX2 and p27kip1 are down-regulated in Jag1-cko    inner ears. Taken together, these data demonstrate that JAG1 is expressed early in the prosensory domains of both the cochlear and vestibular regions, and is required to maintain the normal expression levels of both SOX2 and p27kip1. These data    demonstrate that JAG1-mediated Notch signaling is essential during early development for establishing the prosensory regions of the inner ear.</p>

	]]>
</description>

<author>A E. Kiernan et al.</author>


</item>


<item>
<title>The fibrinolytic system facilitates tumor cell migration across the blood-brain barrier in experimental melanoma brain metastasis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1351</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1351</guid>
<pubDate>Tue, 08 May 2012 21:59:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Patients with metastatic tumors to the brain have a very poor prognosis. Increased metastatic potential has been associated with the fibrinolytic system. We investigated the role of the fibrinolytic enzyme plasmin in    tumor cell migration across brain endothelial cells and growth of brain metastases in an experimental metastatic melanoma model. METHODS: Metastatic tumors to the brain were established by direct injection into the striatum or by intracarotid    injection of B16F10 mouse melanoma cells in C57Bl mice. The role of plasminogen in the ability of human melanoma cells to cross a human blood-brain barrier model was studied on a transwell system. RESULTS : Wild type mice treated with the plasmin    inhibitor epsilon-aminocaproic acid (EACA) and plg-/- mice developed smaller tumors and survived longer than untreated wild type mice. Tumors metastasized to the brain of wild type mice treated with EACA and plg-/- less efficiently than in    untreated wild type mice. No difference was observed in the tumor growth in any of the three groups of mice. Human melanoma cells were able to cross the human blood-brain barrier model in a plasmin dependent manner. CONCLUSION: Plasmin    facilitates the development of tumor metastasis to the brain. Inhibition of the fibrinolytic system could be considered as means to prevent tumor metastasis to the brain.</p>

	]]>
</description>

<author>G Perides et al.</author>


</item>


<item>
<title>Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1350</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1350</guid>
<pubDate>Tue, 08 May 2012 21:59:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate. CD38 exerts pleiotropic actions in hemopoietic and nonhemopoietic compartments via effects on calcium    mobilization. ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells. ART2-catalyzed ADP-ribosylation of the P2X7 purinoreceptor elicits apoptosis. Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone    NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect. However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by    combining both ART2 and CD38 deficiencies. Reciprocal bone marrow reconstitution studies demonstrated accelerated diabetes only when CD38-deficient bone marrow was transferred into CD38-deficient recipients.  Neither decreases in beta cell    function nor viability were indicated.  Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice. In these mice, significant reductions in total viable CD8+ T cells were observed.    This was accompanied by an age-dependent increase in a diabetogenic CD8 clonotype. This in turn correlated with impaired T-regulatory development (10-fold reduction in Foxp3 mRNA expression). These changes were corrected when CD38 deficiency was    combined with ART2 deficiency. Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+    subset.  Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome    7.</p>

	]]>
</description>

<author>J Chen et al.</author>


</item>


<item>
<title>Jag2-Notch1 signaling regulates oral epithelial differentiation and palate development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1349</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1349</guid>
<pubDate>Tue, 08 May 2012 21:59:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>During mammalian palatogenesis, palatal shelves initially grow vertically from the medial sides of the paired maxillary processes flanking the developing tongue and subsequently elevate and fuse with each other above the tongue to    form the intact secondary palate. Pathological palate-mandible or palate-tongue fusions have been reported in humans and other mammals, but the molecular and cellular mechanisms that prevent such aberrant adhesions during normal palate    development are unknown. We previously reported that mice deficient in Jag2, which encodes a cell surface ligand for the Notch family receptors, have cleft palate associated with palate-tongue fusions. In this report, we show that Jag2 is    expressed throughout the oral epithelium and is required for Notch1 activation during oral epithelial differentiation. We show that Notch1 is normally highly activated in the differentiating oral periderm cells covering the developing tongue and    the lateral oral surfaces of the mandibular and maxillary processes during palate development. Oral periderm activation of Notch1 is significantly attenuated during palate development in the Jag2 mutants. Further molecular and ultrastructural    analyses indicate that oral epithelial organization and periderm differentiation are disrupted in the Jag2 mutants. Moreover, we show that the Jag2 mutant tongue fused to wild-type palatal shelves in recombinant explant cultures. These data    indicate that Jag2-Notch1 signaling is spatiotemporally regulated in the oral epithelia during palate development to prevent premature palatal shelf adhesion to other oral tissues and to facilitate normal adhesion between the elevated palatal    shelves.</p>

	]]>
</description>

<author>L M. Casey et al.</author>


</item>


<item>
<title>In-frame deletion in a novel centrosomal/ciliary protein CEP290/NPHP6 perturbs its interaction with RPGR and results in early-onset retinal degeneration in the rd16 mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1348</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1348</guid>
<pubDate>Tue, 08 May 2012 21:58:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Centrosome- and cilia-associated proteins play crucial roles in establishing polarity and regulating intracellular transport in post-mitotic cells. Using genetic mapping and positional candidate strategy, we have identified an    in-frame deletion in a novel centrosomal protein CEP290 (also called NPHP6), leading to early-onset retinal degeneration in a newly identified mouse mutant, rd16. We demonstrate that CEP290 localizes primarily to centrosomes of dividing cells and    to the connecting cilium of retinal photoreceptors. We show that, in the retina, CEP290 associates with several microtubule-based transport proteins including RPGR, which is mutated in approximately 15% of patients with retinitis pigmentosa. A    truncated CEP290 protein (DeltaCEP290) is detected in the rd16 retina, but in considerably reduced amounts; however, the mutant protein exhibits stronger association with specific RPGR isoform(s). Immunogold labeling studies demonstrate the    redistribution of RPGR and of phototransduction proteins in the photoreceptors of rd16 retina. Our findings suggest a critical function for CEP290 in ciliary transport and provide insights into the mechanism of early-onset photoreceptor    degeneration.</p>

	]]>
</description>

<author>B Chang et al.</author>


</item>


<item>
<title>Transcript annotation in FANTOM3: mouse gene catalog based on physical cDNAs.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1347</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1347</guid>
<pubDate>Tue, 08 May 2012 21:58:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The international FANTOM consortium aims to produce a comprehensive picture of the mammalian transcriptome, based upon an extensive cDNA collection and functional annotation of full-length enriched cDNAs. The previous dataset,    FANTOM2, comprised 60,770 full-length enriched cDNAs.  Functional annotation revealed that this cDNA dataset contained only about half of the estimated number of mouse protein-coding genes, indicating that a number of cDNAs still remained to be    collected and identified. To pursue the complete gene catalog that covers all predicted mouse genes, cloning and sequencing of full-length enriched cDNAs has been continued since FANTOM2. In FANTOM3, 42,031 newly isolated cDNAs were subjected to    functional annotation, and the annotation of 4,347 FANTOM2 cDNAs was updated. To accomplish accurate functional annotation, we improved our automated annotation pipeline by introducing new coding sequence prediction programs and developed a    Web-based annotation interface for simplifying the annotation procedures to reduce manual annotation errors.  Automated coding sequence and function prediction was followed with manual curation and review by expert curators. A total of 102,801    full-length enriched mouse cDNAs were annotated. Out of 102,801 transcripts, 56,722 were functionally annotated as protein coding (including partial or truncated transcripts), providing to our knowledge the greatest current coverage of the mouse    proteome by full-length cDNAs. The total number of distinct non-protein-coding transcripts increased to 34,030. The FANTOM3 annotation system, consisting of automated computational prediction, manual curation, and final expert curation,    facilitated the comprehensive characterization of the mouse transcriptome, and could be applied to the transcriptomes of other species.</p>

	]]>
</description>

<author>N Maeda et al.</author>


</item>


<item>
<title>Spermatocyte responses in vitro to induced DNA damage.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1346</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1346</guid>
<pubDate>Tue, 08 May 2012 21:58:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Spermatocytes normally sustain many meiotically induced double-strand DNA breaks (DSBs) early in meiotic prophase; in autosomal chromatin, these are repaired by initiation of meiotic homologous-recombination processes.  Little is    known about how spermatocytes respond to environmentally induced DNA damage after recombination-related DSBs have been repaired. The experiments described here tested the hypothesis that, even though actively completing meiotic recombination,    pachytene spermatocytes cultured in the absence of testicular somatic cells initiate appropriate chromatin remodeling and cell-cycle responses to environmentally induced DNA damage. Two DNA-damaging agents were employed for in vitro treatment of    pachytene spermatocytes: gamma-irradiation and etoposide, a topoisomerase II (TOP2) inhibitor that results in persistent unligated DSBs. Chromatin modifications associated with DSBs were monitored after exposure by labeling surface-spread    chromatin with antibodies against RAD51 (which recognizes DSBs) and the phosphorylated variant of histone H2AFX (herein designated by its commonly used symbol, H2AX), gammaH2AX (which modifies chromatin associated with DSBs). Both gammaH2AX and    RAD51 were rapidly recruited to irradiation- or etoposide-damaged chromatin.  These chromatin modifications imply that spermatocytes recruit active DNA damage responses, even after recombination is substantially completed.  Furthermore,    irradiation-induced DNA damage inhibited okadaic acid-induced progression of spermatocytes from meiotic prophase to metaphase I (MI), implying efficacy of DNA damage checkpoint mechanisms. Apoptotic responses of spermatocytes with DNA damage    differed, with an increase in frequency of early apoptotic spermatocytes after etoposide treatment, but not following irradiation. Taken together, these results demonstrate modification of pachytene spermatocyte chromatin and inhibition of    meiotic progress after DNA damage by mechanisms that may ensure gametic genetic integrity.</p>

	]]>
</description>

<author>S Matulis et al.</author>


</item>


<item>
<title>Genomic instability and aging-like phenotype in the absence of mammalian SIRT6.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1345</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1345</guid>
<pubDate>Tue, 08 May 2012 21:58:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Sir2 histone deacetylase functions as a chromatin silencer to regulate recombination, genomic stability, and aging in budding yeast. Seven mammalian Sir2 homologs have been identified (SIRT1-SIRT7), and it has been speculated    that some may have similar functions to Sir2. Here, we demonstrate that SIRT6 is a nuclear, chromatin-associated protein that promotes resistance to DNA damage and suppresses genomic instability in mouse cells, in association with a role in base    excision repair (BER).  SIRT6-deficient mice are small and at 2-3 weeks of age develop abnormalities that include profound lymphopenia, loss of subcutaneous fat, lordokyphosis, and severe metabolic defects, eventually dying at about 4 weeks. We    conclude that one function of SIRT6 is to promote normal DNA repair, and that SIRT6 loss leads to abnormalities in mice that overlap with aging-associated degenerative processes.</p>

	]]>
</description>

<author>R Mostoslavsky et al.</author>


</item>


<item>
<title>Targeted disruption of tyrosylprotein sulfotransferase-2, an enzyme that catalyzes post-translational protein tyrosine O-sulfation, causes male infertility.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1344</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1344</guid>
<pubDate>Tue, 08 May 2012 21:58:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Tyrosine O-sulfation is a post-translational modification mediated by one of two Golgi tyrosylprotein sulfotransferases (TPST-1 and -2) expressed in all mammalian cells. Tyrosine sulfation plays an important role in the function of    some known TPST substrates by enhancing protein-protein interactions. To explore the role of these enzymes in vivo and gain insight into other potential TPST substrates, TPST-2-deficient mice were generated by targeted disruption of the Tpst2    gene. Tpst2(+/-) mice appear normal and, when interbred, yield litters of normal size with a Mendelian distribution of the targeted mutation. Tpst2(-/-) mice have moderately delayed growth but appear healthy and attain normal body weight by 10    weeks of age. In contrast to Tpst1(-/-) males that have normal fertility, Tpst2(-/-) males are infertile. Tpst2(-/-) sperm are normal in number, morphology, and motility in normal media and appear to capacitate and undergo acrosomal exocytosis    normally. However, they are severely defective in their motility in viscous media and in their ability to fertilize zona pellucida-intact eggs. Adhesion of Tpst2(-/-) sperm to the egg plasma membrane is reduced compared with wild type sperm, but    sperm-egg fusion is similar or even increased. These data strongly suggest that tyrosine sulfation of unidentified substrate(s) play a crucial role in these processes and document for the first time the critical importance of post-translational    tyrosine sulfation in male fertility.</p>

	]]>
</description>

<author>A Borghei et al.</author>


</item>


<item>
<title>Beyond the data deluge: data integration and bio-ontologies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1343</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1343</guid>
<pubDate>Tue, 08 May 2012 21:58:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Biomedical research is increasingly a data-driven science. New technologies support the generation of genome-scale data sets of sequences, sequence variants, transcripts, and proteins; genetic elements underpinning understanding of    biomedicine and disease. Information systems designed to manage these data, and the functional insights (biological knowledge) that come from the analysis of these data, are critical to mining large, heterogeneous data sets for new biologically    relevant patterns, to generating hypotheses for experimental validation, and ultimately, to building models of how biological systems work.  Bio-ontologies have an essential role in supporting two key approaches to effective interpretation of    genome-scale data sets: data integration and comparative genomics. To date, bio-ontologies such as the Gene Ontology have been used primarily in community genome databases as structured controlled terminologies and as data aggregators. In this    paper we use the Gene Ontology (GO) and the Mouse Genome Informatics (MGI) database as use cases to illustrate the impact of bio-ontologies on data integration and for comparative genomics. Despite the profound impact ontologies are having on the    digital categorization of biological knowledge, new biomedical research and the expanding and changing nature of biological information have limited the development of bio-ontologies to support dynamic reasoning for knowledge    discovery.</p>

	]]>
</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title>Epidermal growth factor receptor variant III mutations in lung tumorigenesis and sensitivity to tyrosine kinase inhibitors.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1342</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1342</guid>
<pubDate>Tue, 08 May 2012 21:57:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The tyrosine kinase inhibitors gefitinib (Iressa) and erlotinib (Tarceva) have shown anti-tumor activity in the treatment of non-small cell lung cancer (NSCLC). Dramatic and durable responses have occurred in NSCLC tumors with    mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR). In contrast, these inhibitors have shown limited efficacy in glioblastoma, where a distinct EGFR mutation, the variant III (vIII) in-frame deletion of exons    2-7, is commonly found. In this study, we determined that EGFRvIII mutation was present in 5% (3/56) of analyzed human lung squamous cell carcinoma (SCC) but was not present in human lung adenocarcinoma (0/123). We analyzed the role of the    EGFRvIII mutation in lung tumorigenesis and its response to tyrosine kinase inhibition. Tissue-specific expression of EGFRvIII in the murine lung led to the development of NSCLC. Most importantly, these lung tumors depend on EGFRvIII expression    for maintenance. Treatment with an irreversible EGFR inhibitor, HKI-272, dramatically reduced the size of these EGFRvIII-driven murine tumors in 1 week. Similarly, Ba/F3 cells transformed with the EGFRvIII mutant were relatively resistant to    gefitinib and erlotinib in vitro but proved sensitive to HKI-272. These findings suggest a therapeutic strategy for cancers harboring the EGFRvIII mutation.</p>

	]]>
</description>

<author>H Ji et al.</author>


</item>


<item>
<title>FIMRe: Federation of International Mouse Resources: global networking of resource centers.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1341</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1341</guid>
<pubDate>Tue, 08 May 2012 21:57:47 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M Davisson</author>


</item>


<item>
<title>Novel mutations in three families confirm a major role of COL4A1 in hereditary porencephaly.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1340</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1340</guid>
<pubDate>Tue, 08 May 2012 21:57:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Porencephaly (cystic cavities of the brain) is caused by perinatal vascular accidents from various causes. Several familial cases have been described and autosomal dominant inheritance linked to chromosome 13q has been    suggested. COL4A1 is an essential component in basal membrane stability. Mouse mutants bearing an in-frame deletion of exon 40 of Col4a1 either die from haemorrhage in the perinatal period or have porencephaly in survivors. A report of inherited    mutations in COL4A1 in two families has shown that familial porencephaly may have the same cause in humans. OBJECTIVE: To describe three novel COL4A1 mutations.  RESULTS: The three mutations occurred in three unrelated Dutch families.  There were    two missense mutations of glycine residues predicted to result in abnormal collagen IV assembly, and one mutation predicted to abolish the traditional COL4A1 start codon. The last mutation was also present in an asymptomatic obligate carrier with    white matter abnormalities on brain magnetic resonance imaging. CONCLUSIONS: This observation confirms COL4A1 as a major locus for genetic predisposition to perinatal cerebral haemorrhage and porencephaly and suggests variable expression of    COL4A1 mutations.</p>

	]]>
</description>

<author>G Breedveld et al.</author>


</item>


<item>
<title>Expression and localization of PCSK9 in rat hepatic cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1339</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1339</guid>
<pubDate>Tue, 08 May 2012 21:57:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Proprotein convertase subtilisin/kexin type 9 (PCSK9), recently cloned in several laboratories, including ours, causes a third form of autosomal dominant hypercholesterolemia. Its mechanism of action remains unclear. We studied the    expression and subcellular localization of PCSK9 in fetal and adult rat tissues associated with cholesterol homeostasis using quantitative reverse transcriptase--PCR, Western blot analysis, subcellular fractionation, and confocal    immunofluorescent microscopy.  PCSK9 mRNA is most abundant in yolk sac and fetal liver, but the highest expression of the protein was found in differentiated hepatoma FAO-1 cell line, which also shows the highest expression of LDLR. In FAO-1    cells PCSK9 expression is downregulated by cholesterol and 25-hydroxycholesterol and upregulated in the absence of sterols following the same pattern of expression as HMG-CoA reductase, synthase, and LDLR. Subcellular fractionation, combined with    Western blotting, showed that PCSK9 is localized in the ER and intermediate vesicular compartment of the cell but not in Golgi cisternae. The mature enzyme is secreted from the liver and hepatoma cells. Double labeling with antibodies to PCSK9    and LDLR or clathrin revealed some colocalization of PCSK9 with clathrin-coated vesicles and LDLR. In conclusion, our results show that PCSK9 is processed in the ER, and the mature convertase is secreted in the plasma.</p>

	]]>
</description>

<author>P N. Grozdanov et al.</author>


</item>


<item>
<title>Developmental remodelling of the lemniscal synapse in the ventral basal thalamus of the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1338</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1338</guid>
<pubDate>Tue, 08 May 2012 21:57:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Synapse elimination occurs throughout the nervous system during development, and is essential for the formation of neural circuits. The mechanisms underlying synapse elimination in the brain, however, remain largely unknown. Using    whole-cell patch-clamp recording in a slice preparation, we examined synaptic refinement at the somatosensory relay synapse (lemniscal synapse) in the ventral basal thalamus of the mouse during postnatal development. At 1 week old, each neuron in    the ventral basal thalamus is innervated by multiple lemniscal fibres, as revealed by multiple increments of the synaptic response. By 16 days after birth (P16), the majority of neurons showed an all-or-none response, suggesting a single fibre    innervation. In addition to synapse elimination, extensive modifications in synaptic properties occur during the second week after birth. The ratio of AMPA to NMDA component of the synaptic current tripled between P7 and P17. The decay constant    of the NMDA component decreased by about 70% between P7 and P17; ifenprodil (3 microm) reduced the NMDA component by about 40% in neurons at P7-9, but was much less effective at P20-24. On the other hand, there was little change in the inward    rectification of AMPA component between P11 and P24. Paired-pulse ratios, measured at -70 and +40 mV, were stable between P7 and P24. Whisker deprivation from P5 through P19 had no effect on the elimination or the maturation of the lemniscal    synapse. These results suggest that the lemniscal synapse in the ventral basal thalamus undergoes extensive refinement during the second week, and that sensory experience has a rather limited role in this process.</p>

	]]>
</description>

<author>D Arsenault et al.</author>


</item>


<item>
<title>The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1337</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1337</guid>
<pubDate>Tue, 08 May 2012 21:57:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>To understand the role of human epidermal growth factor receptor (hEGFR) kinase domain mutations in lung tumorigenesis and response to EGFR-targeted therapies, we generated bitransgenic mice with inducible expression in type II    pneumocytes of two common hEGFR mutants seen in human lung cancer. Both bitransgenic lines developed lung adenocarcinoma after sustained hEGFR mutant expression, confirming their oncogenic potential. Maintenance of these lung tumors was dependent    on continued expression of the EGFR mutants. Treatment with small molecule inhibitors (erlotinib or HKI-272) as well as prolonged treatment with a humanized anti-hEGFR antibody (cetuximab) led to dramatic tumor regression. These data suggest that    persistent EGFR signaling is required for tumor maintenance in human lung adenocarcinomas expressing EGFR mutants.</p>

	]]>
</description>

<author>H Ji et al.</author>


</item>


<item>
<title>Visualization of Vapor Formation Regimes during Capillary-Fed Boiling</title>
<link>http://docs.lib.purdue.edu/coolingpubs/175</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/coolingpubs/175</guid>
<pubDate>Tue, 08 May 2012 21:57:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The current study investigates capillary-fed boiling of water from porous sintered powder wicks used in emerging high-effective-conductivity vapor chamber heat spreaders intended for management of hot spots with heat fluxes exceeding 500Wcm-2. Characterization of 1 mm thick wicks composed of 100 lm sintered copper particles is performed in a test facility which replicates the capillary feeding conditions that occur in such devices. Boiling curves are obtained for a 5 mm x 5 mm heated input area, along with high-speed in-situ visualization of the evaporation/boiling processes. Understanding the vapor formation regimes is essential to predictive modeling of the observed characteristics. Schematic representations of such regimes along the boiling curves are presented for homogeneous and modified wick structures. In general, incipience of boiling in sintered-powder wicks reduces the effective thermal resistance and, for small heat input areas, does not cause liquid starvation due to a capillary limitation. The thermal performance enhancement provided by two different augmentation methods is quantified and explained in terms of the observed vapor formation characteristics. Patterns fabricated within the sintered powder create multi-scale wicks with regions of different pore size. These patterns reduce thermal resistance throughout the boiling regime by increasing the permeability to vapor exiting the wick, as confirmed by visualization of the preferential vapor venting from the surface. At the highest heat fluxes investigated prior to dryout, a thin liquid film is observed to form in the recessed patterned areas at the base of the wick. Integration of copper-coated carbon nanotubes on to the sintered powder reduces the required superheat for boiling incipience, thus reducing the overall thermal resistance at low heat fluxes. Evaporation and boiling regime heat transfer predictions from several available correlations are compared to the current results, and are shown to corroborate the conclusions regarding vapor permeability.</p>

	]]>
</description>

<author>J. A. Weibel et al.</author>


</item>


<item>
<title>Anti-mouse CD154 antibody treatment facilitates generation of mixed xenogeneic rat hematopoietic chimerism, prevents wasting disease and prolongs xenograft survival in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1336</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1336</guid>
<pubDate>Tue, 08 May 2012 21:56:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The induction of xenogeneic hematopoietic chimerism is an attractive approach for overcoming the host response to xenografts, but establishing xenogeneic chimerism requires severe myeloablative conditioning of the    recipient. The goal of this study was to determine if co-stimulation blockade would facilitate chimerism and xenograft tolerance in irradiation-conditioned concordant recipients. METHODS: Wistar Furth rat bone marrow (BM) cells were injected into    irradiation-conditioned C57BL/6 mice with or without co-administration of anti-mouse CD154 monoclonal antibody (mAb). Chimerism was quantified by flow cytometry, and mice were transplanted with WF rat skin and islet xenografts. RESULTS: Blockade    of CD40-CD154 interaction facilitated establishment of xenogeneic chimerism in mice conditioned with 600 cGy irradiation. Anti-CD154 mAb was not required for establishment of chimerism in mice treated with 700 cGy.  However, mice irradiated with    700 cGy but not treated with anti-CD154 mAb developed a "graft-versus-host disease (GVHD)-like" wasting syndrome and died, irrespective of their development of chimerism. Xenogeneic chimeras established with irradiation and anti-CD154 mAb    treatment exhibited prolonged skin and, in many cases, permanent islet xenograft survival.  Chimerism was unstable and eventually lost in most recipients. Skin xenografts were rejected even in mice that remained chimeric, whereas most islet    xenografts survived to the end of the observation period.  CONCLUSIONS: Blockade of host CD40-CD154 interaction facilitates the establishment of xenogeneic chimerism and prevents wasting disease and death. Chimerism permits prolonged xenograft    survival, but chimerism generated in this way is unstable over time. Skin xenografts are eventually rejected, whereas most islet xenografts survive long term and perhaps permanently.</p>

	]]>
</description>

<author>H Masaki et al.</author>


</item>


<item>
<title>DCC-dependent phospholipase C signaling in netrin-1-induced neurite elongation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1335</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1335</guid>
<pubDate>Tue, 08 May 2012 21:56:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Netrins, a family of secreted molecules, play important roles in axon pathfinding during nervous system development. Although phosphatidylinositol signaling has been implicated in this event, how netrin-1 regulates    phosphatidylinositol signaling remains poorly understood. Here we provide evidence that netrin-1 stimulates phosphatidylinositol bisphosphate hydrolysis in cortical neurons. This event appears to be mediated by DCC (deleted in colorectal cancer),    but not neogenin or Unc5h2. Netrin-1 induces phospholipase Cgamma (PLCgamma) tyrosine phosphorylation. Inhibition of PLC activity attenuates netrin-1-induced cortical neurite outgrowth. These results suggest that netrin-1 regulates    phosphatidylinositol turnover and demonstrate a crucial role of PLC signaling in netrin-1-induced neurite elongation.</p>

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</description>

<author>Y Xie et al.</author>


</item>


<item>
<title>Epigenetics and phenotypic variation in mammals.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1334</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1334</guid>
<pubDate>Tue, 08 May 2012 21:56:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>What causes phenotypic variation? By now it is clear that phenotype is a result of the interaction between genotype and environment, in addition to variation not readily attributable to either. Epigenetic phenomena associated with    phenotypic variation at the biochemical, cellular, tissue, and organism level are now well recognized and are likely to contribute to the "intangible variation" alluded to. While it is clear that epigenetic modifications are mitotically    heritable, the fidelity of this process is not well understood. Inheritance through more than one generation of meioses is even less well studied. So it remains unclear to what extent epigenetic changes contribute to phenotypic variation in    natural populations. How might such evidence be obtained? What are the features of phenotypes that might suggest an epigenetic component? How much of the epigenetic component is truly independent of genetic changes? The answers to such questions    must come from studies designed specifically to detect subtle, stochastically determined phenotypic variation in suitable animal models.</p>

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</description>

<author>A E. Peaston et al.</author>


</item>


<item>
<title>Safety and efficacy of teriparatide in elderly women with established osteoporosis: bone anabolic therapy from a geriatric perspective.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1333</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1333</guid>
<pubDate>Tue, 08 May 2012 21:56:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVES: To assess the safety and efficacy of teriparatide in patients aged 75 and older and compare these findings with those of women younger than 75 using data from the Fracture Prevention Trial (FPT). DESIGN: The FPT was a    randomized, multicenter, double-blind, placebo-controlled study.  SETTING: The FPT multicenter international study. PARTICIPANTS: Postmenopausal women aged 42 to 86 were randomized to placebo (N=544) or teriparatide 20 mug (N=541) by daily    self-injection for a median of 19 months. Patients received daily oral supplements of 1,000 mg calcium and 400 to 1,200 IU vitamin D. For this analysis, subgroups were defined according to patient age younger than 75 (N=841) and 75 and older    (N=244).  MEASUREMENTS: The effects of teriparatide on bone mineral density (BMD) of the lumbar spine and femoral neck; the incidence of new vertebral and new nonvertebral fragility fractures; bone turnover markers, including bone-specific    alkaline phosphatase; and urinary deoxypyridinoline corrected for creatinine clearance, as well as the safety of teriparatide, were investigated. RESULTS: There were no significant treatment-by-age interactions for the bone turnover markers,    femoral neck BMD, vertebral fractures, nonvertebral fragility fractures, height loss, hyperuricemia, or hypercalcemia. A significant treatment-by-age interaction for lumbar spine BMD (P=.08) was due to an increase in BMD observed in the placebo    group aged 75 and older. There were no treatment-by-age interactions for important treatment-emergent adverse events (TEAEs), including back pain, nausea, leg cramps, and dizziness. The most important TEAEs in women aged 80 and older (23 patients    from the placebo group and 25 patients from the teriparatide group) were also reviewed; no unexpected TEAEs were found in the patients treated with teriparatide. These results indicate that the clinical effects of teriparatide were consistent in    the older and younger women. CONCLUSION: Age does not affect the safety and efficacy of teriparatide in postmenopausal women with osteoporosis.</p>

	]]>
</description>

<author>S Boonen et al.</author>


</item>


<item>
<title>Identification of candidate alkylator-induced cancer susceptibility genes by whole genome scanning in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1332</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1332</guid>
<pubDate>Tue, 08 May 2012 21:56:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Secondary malignancies are a serious adverse consequence of alkylator chemotherapy. The risk of developing an alkylator-associated malignancy is influenced by genetic background, although the relevant genetic factors are poorly    understood. To screen for novel susceptibility factors, we established a mouse model of alkylator-induced malignancy. We exposed mice from 20 inbred strains to the prototypical alkylating agent, N-nitroso-N-ethylurea (ENU). ENU was a potent    carcinogen in many of the strains tested, inducing 140 tumors in 240 ENU-treated mice (66% incidence of at least one tumor in evaluable mice), compared with a background incidence of 8% spontaneous tumors in 240 strain-, age-, and sex-matched    control mice (relative risk, 8.4; P < 0.0001). A wide variety of tumor histologies were noted, including epithelial carcinomas, soft tissue sarcomas, and hematopoietic tumors. Cancer susceptibility was a heritable trait for the most common tumor    types, lung adenocarcinoma (H(2) = 0.25), T cell lymphoma (H(2) = 0.19), and myeloid malignancies (H(2) = 0.10).  Quantitative trait locus mapping identified regions on chromosomes 3, 6, 9, and 15 containing candidate genes associated with lung    adenoma, lung carcinoma, and lymphoma susceptibility. This novel mouse model recapitulates many features of human alkylator-associated cancer and supports the hypothesis that susceptibility to this syndrome is influenced by inherited    polymorphisms that could be used to make informed clinical treatment decisions.</p>

	]]>
</description>

<author>T S. Fenske et al.</author>


</item>


<item>
<title>Motor axon guidance of the mammalian trochlear and phrenic nerves: dependence on the netrin receptor Unc5c and modifier loci.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1331</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1331</guid>
<pubDate>Tue, 08 May 2012 21:56:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Netrin signaling is important to guide migrating neurons and axons in many systems. Experiments with vertebrate CNS explants suggested netrin is bifunctional, attracting some axons and repelling others.  Netrin1-expressing cells    attracted spinal commissural axons and repelled trochlear cranial nerve axons in these experiments. Subsequent genetic studies demonstrated that multiple axon types, including those of the spinal commissural neurons, are attracted to netrin in    vivo; however, an in vivo role for netrin signaling in trochlear nerve repulsion has not been observed. Here, we demonstrate that mice with a null mutation in the netrin receptor Unc5c on the inbred C57BL/6J (B6) genetic background have    ventral/ipsilateral trochlear nerve misprojections. These misprojections are attenuated on a hybrid B6 x SJL background. In addition, B6.Unc5c(-/-) mice die as neonates of apparent respiratory distress and have incomplete phrenic nerve    innervation of the diaphragm muscle. Neither the trochlear nerve misprojections nor the phrenic nerve phenotype was observed in B6 embryos lacking the netrin receptors DCC or Neogenin1, or the ligand netrin1, indicating these signaling molecules    are dispensable for guidance of these axons. Like the trochlear nerve, the phrenic nerve phenotype is modified in a B6 x SJL hybrid background. To identify these modifier loci, we performed genome scans of the hybrid Unc5c(-/-) mice and found a    major SJL-derived suppressor locus on Chromosome 17. Our results provide the first evidence that genes involved in netrin signaling are necessary for proper mammalian spinal motor axon development and trochlear axon guidance. In addition, they    demonstrate the importance of modifier genes in vertebrate axonal guidance.</p>

	]]>
</description>

<author>R W. Burgess et al.</author>


</item>


<item>
<title>Performance of ten inbred mouse strains following assisted reproductive technologies (ARTs).</title>
<link>http://mouseion.jax.org/stfb2000_2009/1330</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1330</guid>
<pubDate>Tue, 08 May 2012 21:55:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Superovulation, in vitro fertilization, embryo cryopreservation, and embryo transfer are assisted reproductive technologies (ARTs) widely used in laboratory mice. Inbred strains of mice have inherent genetic differences that cause    them to respond differently to these technologies.  Knowing how common inbred strains will perform when used for ARTs will ensure the most efficient use of mice, time, and resources. In this study, we characterized the ability of 10 inbred    strains: 129S1/SvImJ, A/J, BALB/cJ, BALB/cByJ, C3H/HeJ, C57BL/6J, DBA/2J, FVB/NJ, NOD/LtJ, and SJL/J to superovulate, fertilize in vitro, and produce live pups subsequent to embryo transfer. Three-week-old female mice were superovulated using eCG    (5.0 IU) and hCG (5.0 IU). The resulting oocytes were fertilized in vitro in human tubal fluid medium with spermatozoa of the same strain. The following day, two-cell embryos were either transferred into pseudopregnant recipient females or    cryopreserved. The cryopreserved embryos were later thawed and transferred into pseudopregnant recipient females. Differences in response to superovulation, fertilization, and number of live born produced after embryo transfer were observed    between strains, substantiating the influence of genetic variability on ARTs. The response to the superovulation treatment varied among strains and ranged from 5+/-1(A/J) to 40+/-3 (129S1/SvImJ) normal oocytes per female. The average proportion    of oocytes that fertilized ranged among strains from 24% (129S1/SvImJ) to 93% (DBA/2J and A/J). The average proportion of two-cell embryos that were transferred into recipient females and subsequently developed into live pups varied from 5% (A/J)    to 53% (C57BL/6J) for fresh embryos and from 18% (BALB/cByJ) to 45% (129S1/SvImJ) for thawed embryos.</p>

	]]>
</description>

<author>S L. Byers et al.</author>


</item>


<item>
<title>Genetic increase in serum insulin-like growth factor-I (IGF-I) in C3H/HeJ compared with C57BL/6J mice is associated with increased transcription from the IGF-I exon 2 promoter.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1329</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1329</guid>
<pubDate>Tue, 08 May 2012 21:55:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>C3H/HeJ (C3H) mice exhibit 30-40% higher serum IGF-I than do C57BL/6J (B6) mice, in association with increased bone mineral density and strength.  These differences are inherited and thus provide a model for determining molecular    mechanisms for genetic variation of serum IGF-I and downstream actions. We now report that increased serum IGF-I in C3H mice is associated with increased transcription from the minor exon 2 promoter in liver from female and male mice. The    increase in hepatic IGF-I gene expression caused by increased abundance of IGF-I mRNA transcribed from the exon 2 promoter can quantitatively account for the increased serum IGF-I in C3H mice. Also, levels of both Ea and Eb IGF-I mRNAs are    increased in livers of male C3H mice. Fasting lowered serum IGF-I and liver IGF-I mRNA levels in female mice of both strains. However, serum IGF-I and liver IGF-I mRNA levels remained higher in fasted C3H mice compared with fasted B6 mice. Levels    of IGF-I transcripts initiated from exon 2 are also significantly increased in skeletal muscle, fat, ovaries, and kidneys of C3H mice. IGF binding protein (IGFBP)-5 mRNA levels are significantly higher in muscle and fat of C3H mice than in B6    mice. Levels of exon 1-containing transcripts are increased in whole femurs of male and female C3H mice. We conclude that increased transcription of the IGF-I gene occurs in a promoter- and tissue-specific manner in C3H mice. The increased IGF    binding protein-5 mRNA levels in fat and muscle suggest that IGF-I signaling is increased in these tissues in C3H mice.</p>

	]]>
</description>

<author>M L. Adamo et al.</author>


</item>


<item>
<title>Mutations in the gene encoding the low-density lipoprotein receptor LRP4 cause abnormal limb development in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1328</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1328</guid>
<pubDate>Tue, 08 May 2012 21:55:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Positional cloning of two recessive mutations of the mouse that cause polysyndactyly (dan and mdig-Chr 2) confirmed that the gene encoding MEGF7/LRP4, a member of the low-density lipoprotein receptor family, plays an essential role    in the process of digit differentiation. Pathologies observed in the mutant mice provide insight into understanding the function(s) of LRP4 as a negative regulator of the Wnt-beta-catenin signaling pathway and may help identify the genetic basis    for common human disorders with similar phenotypes.</p>

	]]>
</description>

<author>Chazottes D. Simon et al.</author>


</item>


<item>
<title>Purified human hematopoietic stem cells contribute to the generation of cardiomyocytes through cell fusion.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1327</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1327</guid>
<pubDate>Tue, 08 May 2012 21:55:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>To obtain insights into the cardiomyogenic potential of hematopoietic tissue, we intravenously (i.v.)  injected purified hematopoietic stem/progenitor cells into newborn recipients that may fully potentiate the developmental    plasticity of stem cells. Transplantation of mouse bone marrow (BM) lineage antigen-negative (Lin-) cells resulted in the generation of the cells that displayed cardiomyocyte-specific antigenic profiles and contractile function when transplanted    into syngeneic newborn recipients. To clarify the mechanism underlying the cardiomyogenic potential, green fluorescent protein (GFP)-labeled BM Lin-ScaI+ hematopoietic progenitors were transplanted into neonatal mice constitutively expressing    cyan fluorescence protein (CFP). Lambda image acquisition and linear unmixing analysis using confocal microscopy successfully separated GFP and CFP, and revealed that donor GFP+ cardiomyocytes coexpressed host-derived CFP. We further    reconstituted human hemopoietic- and immune systems in mice by injecting human cord blood (CB)-derived Lin-CD34+CD38- hematopoietic stem cells (HSCs) into neonatal T cell(-)B cell(-)NK cell- immune-deficient NOD/SCID/IL2rgamma(null) mice.    Fluoroescence in situ hybridization analysis of recipient cardiac tissues demonstrated that human and murine chromosomes were colocalized in the same cardiomyocytes, indicating that cell fusion occurred between human hematopoietic progeny and    mouse cardiomyocytes. These syngeneic- and xenogeneic neonatal transplantations provide compelling evidence that hematopoietic stem/progenitor cells contribute to the postnatal generation of cardiomyocytes through cell fusion, not through    transdifferentiation.</p>

	]]>
</description>

<author>F Ishikawa et al.</author>


</item>


<item>
<title>In vivo magnetic resonance imaging and semiautomated image analysis extend the brain phenotype for cdf/cdf mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1326</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1326</guid>
<pubDate>Tue, 08 May 2012 21:55:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Magnetic resonance imaging and computer image analysis in human clinical studies effectively identify abnormal neuroanatomy in disease populations.  As more mouse models of neurological disorders are discovered, such an approach may    prove useful for translational studies. Here, we demonstrate the effectiveness of a similar strategy for mouse neuroscience studies by phenotyping mice with the cerebellar deficient folia (cdf) mutation. Using in vivo multiple-mouse magnetic    resonance imaging for increased throughput, we imaged groups of cdf mutant, heterozygous, and wild-type mice and made an atlas-based segmentation of the structures in 15 individual brains. We then performed computer automated volume measurements    on the structures. We found a reduced cerebellar volume in the cdf mutants, which was expected, but we also found a new phenotype in the inferior colliculus and the olfactory bulbs. Subsequent local histology revealed additional cytoarchitectural    abnormalities in the olfactory bulbs. This demonstrates the utility of anatomical magnetic resonance imaging and semiautomated image analysis for detecting abnormal neuroarchitecture in mutant mice.</p>

	]]>
</description>

<author>N A. Bock et al.</author>


</item>


<item>
<title>The ternary IGF complex influences postnatal bone acquisition and the skeletal response to intermittent parathyroid hormone.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1325</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1325</guid>
<pubDate>Tue, 08 May 2012 21:55:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>The role of circulating IGF-I in skeletal acquisition and the anabolic response to PTH is not well understood. We generated IGF-I-deficient mice by gene deletions of IGF ternary complex components including: (1) liver-specific    deletion of the IGF-I gene (LID), (2) global deletion of the acid-labile (ALS) gene (ALSKO), and (3) both liver IGF-I and ALS inactivated genes (LA). Twelve-week-old male control (CTL), LID, ALSKO, and LA mice were treated with vehicle (VEH) or    human PTH(1-34) for 4 weeks. VEH-treated IGF-I-deficient mice (i.e. LID, ALSKO and LA mice) exhibited reduced cortical cross-sectional area (P = 0.001) compared with CTL mice; in contrast, femoral trabecular bone volume fractions (BV/TV) of the    IGF-I-deficient mice were consistently greater than CTL (P < 0.01).  ALSKO mice exhibited markedly reduced osteoblast number and surface (P < 0.05), as well as mineral apposition rate compared with other IGF-I-deficient and CTL mice. Adherent    bone marrow stromal cells, cultured in beta-glycerol phosphate and ascorbic acid, showed no strain differences in secreted IGF-I. In response to PTH, there were both compartment- and strain-specific effects. Cortical bone area was increased by    PTH in CTL and ALSKO mice, but not in LID or LA mice. In the trabecular compartment, PTH increased femoral and vertebral BV/TV in LID, but not in ALSKO or LA mice. In conclusion, we demonstrated that the presentation of IGF-I as a circulating    complex is essential for skeletal remodeling and the anabolic response to PTH. We postulate that the ternary complex itself, rather than IGF-I alone, influences bone acquisition in a compartment-specific manner (i.e. cortical vs trabecular    bone).</p>

	]]>
</description>

<author>S Yakar et al.</author>


</item>


<item>
<title>Clusters of internally primed transcripts reveal novel long noncoding RNAs.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1324</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1324</guid>
<pubDate>Tue, 08 May 2012 21:54:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Non-protein-coding RNAs (ncRNAs) are increasingly being recognized as having important regulatory roles. Although much recent attention has focused on tiny 22- to 25-nucleotide microRNAs, several functional ncRNAs are orders of    magnitude larger in size. Examples of such macro ncRNAs include Xist and Air, which in mouse are 18 and 108 kilobases (Kb), respectively. We surveyed the 102,801 FANTOM3 mouse cDNA clones and found that Air and Xist were present not as single,    full-length transcripts but as a cluster of multiple, shorter cDNAs, which were unspliced, had little coding potential, and were most likely primed from internal adenine-rich regions within longer parental transcripts. We therefore conducted a    genome-wide search for regional clusters of such cDNAs to find novel macro ncRNA candidates. Sixty-six regions were identified, each of which mapped outside known protein-coding loci and which had a mean length of 92 Kb. We detected several known    long ncRNAs within these regions, supporting the basic rationale of our approach. In silico analysis showed that many regions had evidence of imprinting and/or antisense transcription. These regions were significantly associated with microRNAs    and transcripts from the central nervous system. We selected eight novel regions for experimental validation by northern blot and RT-PCR and found that the majority represent previously unrecognized noncoding transcripts that are at least 10 Kb    in size and predominantly localized in the nucleus. Taken together, the data not only identify multiple new ncRNAs but also suggest the existence of many more macro ncRNAs like Xist and Air.</p>

	]]>
</description>

<author>M Furuno et al.</author>


</item>


<item>
<title>Role of hepatocyte nuclear factor 4alpha in control of blood coagulation factor gene expression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1323</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1323</guid>
<pubDate>Tue, 08 May 2012 21:54:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hepatocyte nuclear factor 4alpha (HNF4alpha) plays an important role in the maintenance of many liver-specific functions. Liver-specific HNF4alpha-null mice were used to determine whether hepatic HNF4alpha regulates blood    coagulation in vivo. These mice exhibited reduced expression of hepatic coagulation factors V, IX, XI, XII, and XIIIB and a prolonged activated partial thromboplastin time but not prothrombin time.  Promoter analysis of the mouse FXII and FXIIIB    genes was performed to determine whether HNF4alpha directly regulates the genes encoding these coagulation factors. Sequence analysis revealed the presence of one and two HNF4alpha binding sites in the mouse FXII and FXIIIB genes, respectively.    Using transient transfection and electrophoretic mobility shift analyses with the mouse FXII and FXIIIB promoters, it was established that the high levels of promoter activity were dependent on HNF4alpha binding sites and the expression of    HNF4alpha. In conclusion, HNF4alpha has a critical role in blood coagulation homeostasis by directing transcription of the FXII and XIIIB genes.</p>

	]]>
</description>

<author>Y Inoue et al.</author>


</item>


<item>
<title>Mutagenesis as an unbiased approach to identify novel contraceptive targets.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1322</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1322</guid>
<pubDate>Tue, 08 May 2012 21:54:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>To accommodate diverse personal needs in family planning, diverse contraceptive approaches are desirable. This goal requires identification of new contraceptive targets. Phenotype-driven mutagenesis is an unbiased approach to    identify novel genes and functions in reproductive processes.  The ReproGenomics Program at The Jackson Laboratory is a United States National Institutes of Health resource for production, identification and distribution of mutant mouse models of    infertility that can be used for identification of potential targets for contraception. The strategy of this program is whole genome, random ENU mutagenesis, coupled with a phenotype screen for breeding failure as the only phenotype. A    three-generation breeding scheme selects recessive mutations affecting reproductive functions. G3 males and females that fail to reproduce by natural mating to wild-type animals undergo secondary phenotype screens to assess gonad and accessory    organ histology, hormone production, gamete production and gamete function in fertilization. The genetic transmission of the infertility trait in each family is confirmed and each mutation is genetically mapped to a defined chromosome region,    facilitating identification of candidate genes from sequence and expression databases.  Genes essential for fertility in both males and females and acting both meiotically and post-meiotically have been identified by this strategy.  Phenotypes    include male infertility with normal sperm count, but failure in fertilization of oocytes. Phenotype descriptions of each mutation are posted on the program website, . These unique reproductive mutant mouse resources will lead to new discoveries    in andrology (and gynecology) research, as well as reproductive medicine. Dissection of gene function in known and newly discovered reproductive pathways will expand our focus to reveal novel targets for contraception.</p>

	]]>
</description>

<author>M A. Handel et al.</author>


</item>


<item>
<title>Influence of caloric restriction on motor behavior, longevity, and brain lipid composition in Sandhoff disease mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1321</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1321</guid>
<pubDate>Tue, 08 May 2012 21:54:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Caloric restriction (CR), which improves health and increases longevity, was studied as a therapy in a hexosaminidase beta knockout mouse model of Sandhoff disease (SD), an incurable neurodegenerative disease involving accumulation    of brain ganglioside GM2 and asialo-GM2 (GA2). Adult mice were fed a rodent chow diet either ad libitum (AL) or restricted to reduce body weight by 15-18% (CR). Although GM2 and GA2 were elevated, no significant differences were seen between the    Hexb-/- and the Hexb+/- mice for most brain phospholipids and cholesterol. Cerebrosides and sulfatides were reduced in the Hexb-/- mice. In addition, rotorod performance was significantly worse in the Hexb-/- mice than in the Hexb+/- mice. CR,    which decreased circulating glucose and elevated ketone bodies, significantly improved rotorod performance and extended longevity in the Hexb-/- mice but had no significant effect on brain lipid composition or on cytoplasmic neuronal vacuoles.    The expression of CD68 and F4/80 was significantly less in the CR-fed than in the AL-fed Hexb-/- mice. We suggest that the CR delays disease progression in SD and possibly in other ganglioside storage diseases through anti-inflammatory    mechanisms.</p>

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</description>

<author>C A. Denny et al.</author>


</item>


<item>
<title>Space asymmetry directs preferential sperm entry in the absence of polarity in the mouse oocyte.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1320</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1320</guid>
<pubDate>Tue, 08 May 2012 21:54:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Knowledge about the mechanism that establishes embryonic polarity is fundamental in understanding mammalian development. In re-addressing several controversial claims, we recently proposed a model in which mouse embryonic polarity    is not specified until the blastocyst stage. Before fertilization, the fully differentiated oocyte has been characterized as "polarized," and we indeed observed that the sperm preferentially enters the polar body half. Here we show that    preferential sperm entry is not due to an intrinsic polarity of the oocyte, since fertilization takes place uniformly when the zona pellucida is removed. We suggest that the term "asymmetry" denotes morphological differences, whereas "polarity"    in addition implies developmental consequences. Thus, the mouse oocyte can be considered "asymmetric" but "non-polarized." The penetration through the zona pellucida is also random, and a significant proportion of sperm binds to the oocyte    membrane at a point distant from the zona penetration site.  Time-lapse recordings confirmed that sperm swim around the perivitelline space before fertilization. Experimental enlargement of the perivitelline space in the non-polar body half    increased the regional probability of fertilization. Based on these experiments, we propose a model in which the space asymmetry exerted by the first polar body and the zona pellucida directs sperm entry preferentially to the polar body half,    with no need for oocyte polarity.</p>

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</description>

<author>N Motosugi et al.</author>


</item>


<item>
<title>Gradual elimination of retroviruses in YBR/Ei mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1319</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1319</guid>
<pubDate>Tue, 08 May 2012 21:53:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mouse mammary tumor virus (MMTV), a well-characterized retrovirus that causes mammary tumors in susceptible mice, is commonly used to investigate virus-host interactions. We have shown that YBR/Ei mice demonstrate a novel, dominant    mechanism of resistance to MMTV infection and MMTV-induced mammary tumors. MMTV can both establish infection in YBR/Ei mice and be transmitted by YBR/Ei mice as an infectious virus. However, virus production is severely attenuated, resulting in    gradual clearance of infection in successive generations. Our transfer experiments showed that T cells generated in MMTV-infected resistant mice were required to restrict MMTV replication in susceptible mice. These results emphasize the    importance of inducing T-cell responses for effective protection against retroviral infections.</p>

	]]>
</description>

<author>C C. MacDearmid et al.</author>


</item>


<item>
<title>The leukotriene B4 receptor (BLT1) is required for effector CD8+ T cell-mediated, mast cell-dependent airway hyperresponsiveness.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1318</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1318</guid>
<pubDate>Tue, 08 May 2012 21:53:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Studies in both humans and rodents have suggested that CD8+ T cells contribute to the development of airway hyperresponsiveness (AHR) and that leukotriene B4 (LTB4) is involved in the chemotaxis of effector CD8+ T cells (T(EFF)) to    the lung by virtue of their expression of BLT1, the receptor for LTB4. In the present study, we used a mast cell-CD8-dependent model of AHR to further define the role of BLT1 in CD8+ T cell-mediated AHR. C57BL/6+/+ and CD8-deficient (CD8-/-) mice    were passively sensitized with anti-OVA IgE and exposed to OVA via the airways. Following passive sensitization and allergen exposure, C57BL/6+/+ mice developed altered airway function, whereas passively sensitized and allergen-exposed CD8-/-    mice failed to do so. CD8-/- mice reconstituted with CD8+ T(EFF) developed AHR in response to challenge. In contrast, CD8-/- mice reconstituted with BLT1-deficient effector CD8+ T cells did not develop AHR. The induction of increased airway    responsiveness following transfer of CD8+ T(EFF) or in wild-type mice could be blocked by administration of an LTB4 receptor antagonist confirming the role of BLT1 in CD8+ T cell-mediated AHR.  Together, these data define the important role for    mast cells and the LTB4-BLT1 pathway in the development of CD8+ T cell-mediated allergic responses in the lung.</p>

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</description>

<author>C Taube et al.</author>


</item>


<item>
<title>HLA-A*0201-restricted T cells from humanized NOD mice recognize autoantigens of potential clinical relevance to type 1 diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1317</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1317</guid>
<pubDate>Tue, 08 May 2012 21:53:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>In both humans and NOD mice, particular MHC genes are primary contributors to development of the autoreactive CD4+ and CD8+ T cell responses against pancreatic beta cells that cause type 1 diabetes (T1D). Association studies have    suggested, but not proved, that the HLA-A*0201 MHC class I variant is an important contributor to T1D in humans. In this study, we show that transgenic expression in NOD mice of HLA-A*0201, in the absence of murine class I MHC molecules, is    sufficient to mediate autoreactive CD8+ T cell responses contributing to T1D development. CD8+ T cells from the transgenic mice are cytotoxic to murine and human HLA-A*0201-positive islet cells. Hence, the murine and human islets must present one    or more peptides in common. Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) is one of several important T1D autoantigens in standard NOD mice. Three IGRP-derived peptides were identified as targets of diabetogenic    HLA-A*0201-restricted T cells in our NOD transgenic stock. Collectively, these results indicate the utility of humanized HLA-A*0201-expressing NOD mice in the identification of T cells and autoantigens of potential relevance to human T1D. In    particular, the identified antigenic peptides represent promising tools to explore the potential importance of IGRP in the development of human T1D.</p>

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</description>

<author>T Takaki et al.</author>


</item>


<item>
<title>Sequences within the gag gene of mouse mammary tumor virus needed for mammary gland cell transformation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1316</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1316</guid>
<pubDate>Tue, 08 May 2012 21:53:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previously, we identified a group of replication-competent exogenous mouse mammary tumor viruses that failed to induce mammary tumors in susceptible mice. Sequence comparison of tumorigenic and tumor-attenuated virus variants has    linked the ability of virus to cause high-frequency mammary tumors to the gag gene. To determine the specific sequences within the gag gene that contribute to tumor induction, we constructed five distinct chimeric viruses that have various amino    acid coding sequences of gag derived from a tumor-attenuated virus replaced by those of highly tumorigenic virus and tested these viruses for tumorigenic capacities in virus-susceptible C3H/HeN mice. Comparing the tumorigenic potentials of these    viruses has allowed us to map the region responsible for tumorigenesis to a 253-amino-acid region within the CA and NC regions of the Gag protein. Unlike C3H/HeN mice, BALB/cJ mice develop tumors when infected with all viral variants,    irrespective of the gag gene sequences.  Using genetic crosses between BALB/cJ and C3H/HeN mice, we were able to determine that the mechanism that confers susceptibility to Gag-independent mammary tumors in BALB/cJ mice is inherited as a dominant    trait and is controlled by a single gene, called mammary tumor susceptibility (mts), that maps to chromosome 14.</p>

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</description>

<author>I Swanson et al.</author>


</item>


<item>
<title>Targeting gastrin-releasing peptide receptors on small cell lung cancer cells with a bispecific molecule that activates polyclonal T lymphocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1315</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1315</guid>
<pubDate>Tue, 08 May 2012 21:53:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Gastrin-releasing peptide (GRP) is a growth factor for small cell lung cancer (SCLC). GRP belongs to the bombesin peptide family and has significant homology to bombesin. We constructed a bispecific molecule, OKT3xAntag2,    by conjugating a monoclonal antibody OKT3 (anti-CD3) with a bombesin/GRP antagonist (Antag2) and evaluated cytotoxicity against SCLC cells. EXPERIMENTAL DESIGN: We tested binding of the bispecific molecule to SCLC cell lines and T cells by flow    cytometry, antibody-dependent cellular cytotoxicity (ADCC) of SCLC cells in vitro and in a murine SCLC xenograft model. We studied SCLC apoptosis and necrosis during ADCC and the activity and cleavage of caspase-3, caspase-9, and poly(ADP-ribose)    polymerase (PARP). RESULTS: The bispecific molecule functions as a cross-linker between T cells and SCLC cells, induces T cell activation, and mediates ADCC of SCLC cells; 40% to 80% growth inhibition of SCLC cells mediated by the bispecific    molecule at low effector to target cell ratios was achieved. Activation of T cells by the bispecific molecule resulted in significant increases in IFNgamma production and apoptosis and necrosis of SCLC cells associated with cleavage of PARP and    caspase-3.  Targeted immunotherapy with the bispecific molecule-armed human T cells significantly reduced SCLC tumor burdens in a mouse model. CONCLUSION: The bispecific molecule OKT3xAntag2 mediates growth inhibition and apoptosis of SCLC cells    by activated T cells through activation and cleavage of caspase-3 and PARP in vitro and in vivo. Clinical trials of this bispecific molecule through adoptive transfer of ex vivo activated T cells in GRP receptor-positive tumors, such as SCLC, are    warranted.</p>

	]]>
</description>

<author>J Zhou et al.</author>


</item>


<item>
<title>K-ras activation generates an inflammatory response in lung tumors.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1314</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1314</guid>
<pubDate>Tue, 08 May 2012 21:53:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Activating mutations in K-ras are one of the most common genetic alterations in human lung cancer. To dissect the role of K-ras activation in bronchial epithelial cells during lung tumorigenesis, we created a model of lung    adenocarcinoma by generating a conditional mutant mouse with both Clara cell secretory protein (CC10)-Cre recombinase and the Lox-Stop-Lox K-ras(G12D) alleles. The activation of K-ras mutant allele in CC10 positive cells resulted in a progressive    phenotype characterized by cellular atypia, adenoma and ultimately adenocarcinoma. Surprisingly, K-ras activation in the bronchiolar epithelium is associated with a robust inflammatory response characterized by an abundant infiltration of    alveolar macrophages and neutrophils. These mice displayed early mortality in the setting of this pulmonary inflammatory response with a median survival of 8 weeks. Bronchoalveolar lavage fluid from these mutant mice contained the MIP-2, KC,    MCP-1 and LIX chemokines that increased significantly with age. Cell lines derived from these tumors directly produced MIP-2, LIX and KC. This model demonstrates that K-ras activation in the lung induces the elaboration of inflammatory chemokines    and provides an excellent means to further study the complex interactions between inflammatory cells, chemokines and tumor progression.</p>

	]]>
</description>

<author>H Ji et al.</author>


</item>


<item>
<title>A spontaneous mutation involving Kcnq2 (Kv7.2) reduces M-current density and spike frequency adaptation in mouse CA1 neurons.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1313</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1313</guid>
<pubDate>Tue, 08 May 2012 21:52:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The M-type K+ current [IK(M)] activates in response to membrane depolarization and regulates neuronal excitability. Mutations in two subunits (KCNQ2 and KCNQ3; Kv7.2 and Kv7.3) that underlie the M-channel cause the human seizure    disorder benign familial neonatal convulsions (BFNC), presumably by reducing IK(M) function. In mice, the Szt1 mutation, which deletes the genomic DNA encoding the KCNQ2 C terminus and all of CHRNA4 (nicotinic acetylcholine receptor alpha4    subunit) and ARFGAP-1 (GTPase-activating protein that inactivates ADP-ribosylation factor 1), reduces seizure threshold, and alters M-channel pharmacosensitivity.  Genomic deletions affecting the C terminus of KCNQ2 have been identified in human    families with BFNC, and truncation of the C terminus prevents proper KCNQ2/KCNQ3 channel assembly in Xenopus oocytes. We showed previously that Szt1 mice have a reduced baseline seizure threshold and altered sensitivity to drugs that act at the    M-channel. Specifically, the proconvulsant M-channel blocker linopirdine and anticonvulsant enhancer retigabine display increased and decreased potency, respectively, in Szt1 mice. To investigate the effects of the Szt1 mutation on IK(M) function    explicitly, perforated-patch electrophysiology was performed in CA1 pyramidal neurons of the hippocampus in brain slices prepared from C57BL/6J-Szt1/+ and control C57BL/6J+/+ mice. Our results show that Szt1 reduces both IK(M) amplitude and    current density, inhibits spike frequency adaptation, and alters many aspects of M-channel pharmacology. This is the first evidence that a naturally occurring Kcnq2 mutation diminishes the amplitude and function of the native neuronal IK(M),    resulting in significantly increased neuronal excitability. Finally, the changes in single-cell biophysical properties likely underlie the altered seizure threshold and pharmacosensitivity reported previously in Szt1 mice.</p>

	]]>
</description>

<author>J F. Otto et al.</author>


</item>


<item>
<title>Pten deficiency activates distinct downstream signaling pathways in a tissue-specific manner.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1312</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1312</guid>
<pubDate>Tue, 08 May 2012 21:52:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>PTEN deficiency predisposes to a subset of human cancers, but the mechanism that underlies such selectivity is unknown. We have generated a mouse line that conditionally deletes Pten in urogenital epithelium. These mice develop    carcinomas at high frequency in the prostate but at relatively low frequency in the bladder, despite early and complete penetrance of hyperplasia in both organs. Cell proliferation is initially high in the bladder of newborn Pten-deficient mice    but within days is inhibited by p21 induction. In contrast, proliferation remains elevated in Pten-deficient prostate, where p21 is never induced, suggesting that p21 induction is a bladder-specific compensatory mechanism to inhibit proliferation    caused by Pten deletion. Furthermore, the AKT/mammalian target of rapamycin growth pathway, which is highly activated in Pten-deficient prostate, is not activated in bladder epithelium. Our results reveal alternative downstream signaling pathways    activated by Pten deficiency that lead to tissue-specific susceptibilities to tumorigenesis.</p>

	]]>
</description>

<author>L I. Yoo et al.</author>


</item>


<item>
<title>MyD88 deficiency results in tissue-specific changes in cytokine induction and inflammation in interleukin-18-independent mice infected with Borrelia burgdorferi.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1311</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1311</guid>
<pubDate>Tue, 08 May 2012 21:52:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Toll-like receptors (TLRs) play an important role in the control of infection with Borrelia burgdorferi. Deficiencies in TLR-2 or the shared TLR adapter molecule MyD88 have been shown to result in greatly increased bacterial burdens    in mice. However, although in vitro studies have shown that the activation of TLR pathways by B. burgdorferi results in the release of inflammatory cytokines, studies in deficient mice have shown either no change or increased rather than    decreased inflammation in infected animals. In this study, we looked at mechanisms to explain the increase in inflammation in the absence of MyD88. We found that MyD88-deficient mice infected with B. burgdorferi did not show increased    inflammation at sites typically associated with Lyme disease (joints and heart). However, there was markedly increased inflammation in the muscles, kidneys, pancreas, and lungs of deficient animals. Muscle inflammation was typically seen    perivascularly and perineuronally similar to that seen in infected humans. Chemotactic chemokines and cytokines were greatly increased in the muscle and kidneys of MyD88-deficient animals but not in the joints or heart tissue, suggesting that    MyD88-independent pathways for recognizing B. burgdorferi and inducing these chemokines are present in the muscle and kidneys. Interleukin-18 signaling through MyD88 does not appear to play a role in either control of infection or    inflammation.</p>

	]]>
</description>

<author>A K. Behera et al.</author>


</item>


<item>
<title>Visualization of Vapor Formation Regimes during Capillary-Fed Boiling</title>
<link>http://docs.lib.purdue.edu/coolingpubs/174</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/coolingpubs/174</guid>
<pubDate>Tue, 08 May 2012 21:52:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The current study investigates capillary-fed boiling of water from porous sintered powder wicks used in emerging high-effective-conductivity vapor chamber heat spreaders intended for management of hot spots with heat fluxes exceeding 500Wcm-2. Characterization of 1 mm thick wicks composed of 100 lm sintered copper particles is performed in a test facility which replicates the capillary feeding conditions that occur in such devices. Boiling curves are obtained for a 5 mm x 5 mm heated input area, along with high-speed in-situ visualization of the evaporation/boiling processes. Understanding the vapor formation regimes is essential to predictive modeling of the observed characteristics. Schematic representations of such regimes along the boiling curves are presented for homogeneous and modified wick structures. In general, incipience of boiling in sintered-powder wicks reduces the effective thermal resistance and, for small heat input areas, does not cause liquid starvation due to a capillary limitation. The thermal performance enhancement provided by two different augmentation methods is quantified and explained in terms of the observed vapor formation characteristics. Patterns fabricated within the sintered powder create multi-scale wicks with regions of different pore size. These patterns reduce thermal resistance throughout the boiling regime by increasing the permeability to vapor exiting the wick, as confirmed by visualization of the preferential vapor venting from the surface. At the highest heat fluxes investigated prior to dryout, a thin liquid film is observed to form in the recessed patterned areas at the base of the wick. Integration of copper-coated carbon nanotubes on to the sintered powder reduces the required superheat for boiling incipience, thus reducing the overall thermal resistance at low heat fluxes. Evaporation and boiling regime heat transfer predictions from several available correlations are compared to the current results, and are shown to corroborate the conclusions regarding vapor permeability.</p>

	]]>
</description>

<author>J. A. Weibel et al.</author>


</item>


<item>
<title>Role of COL4A1 in small-vessel disease and hemorrhagic stroke.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1310</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1310</guid>
<pubDate>Tue, 08 May 2012 21:52:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Small-vessel diseases of the brain underlie 20 to 30 percent of ischemic strokes and a larger proportion of intracerebral hemorrhages. In this report, we show that a mutation in the mouse Col4a1 gene, encoding procollagen type IV    alpha1, predisposes both newborn and adult mice to intracerebral hemorrhage. Surgical delivery of mutant mice alleviated birth-associated trauma and hemorrhage. We identified a COL4A1 mutation in a human family with small-vessel disease. We    concluded that mutation of COL4A1 may cause a spectrum of cerebrovascular phenotypes and that persons with COL4A1 mutations may be predisposed to hemorrhage, especially after environmental stress.</p>

	]]>
</description>

<author>D B. Gould et al.</author>


</item>


<item>
<title>Short-term changes in bone turnover markers and bone mineral density response to parathyroid hormone in postmenopausal women with osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1309</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1309</guid>
<pubDate>Tue, 08 May 2012 21:52:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>CONTEXT: Treatment of osteoporotic women with PTH increases biochemical markers of bone turnover, increases axial bone mineral density (BMD), and reduces fracture risk. OBJECTIVE: Our objective was to determine the relationship    between levels of baseline turnover before PTH therapy and short-term changes in turnover during PTH therapy and subsequent changes in areal and volumetric BMD. DESIGN AND SETTING: We conducted a randomized, placebo-controlled trial at four    academic centers. PATIENTS: Patients included 238 postmenopausal women with low hip or spine BMD.  INTERVENTION: Subjects were randomized to sc PTH (1-84), 100 mug/d (119 women), for 1 yr. MAIN OUTCOME MEASURE: Bone turnover markers were measured    in fasting blood samples collected before therapy and after 1 and 3 months. Areal and volumetric BMD at the spine and hip were assessed by dual-energy x-ray absorptiometry and quantitative computed tomography (QCT) after 1 yr of therapy. RESULTS:    Among women treated with PTH alone, the relationships between baseline turnover and 1-yr changes in dual-energy x-ray absorptiometry and QCT BMD were inconsistent. Greater 1- and 3-month increases in turnover, particularly the formation marker    N-propeptide of type I collagen, were associated with greater increases in areal BMD. When volumetric hip and spine BMD were assessed by QCT, greater short-term increases in turnover were even more positively associated with 1-yr increases in    BMD. Each sd increase in the 3-month change of N-propeptide of type I collagen was associated with an a 21% greater increase in QCT spine trabecular BMD. CONCLUSIONS: Greater short-term changes in turnover with PTH therapy are associated with    greater 1-yr increases in spine and hip BMD among postmenopausal osteoporotic women.</p>

	]]>
</description>

<author>D C. Bauer et al.</author>


</item>


<item>
<title>Impaired bone anabolic response to parathyroid hormone in Fgf2-/- and Fgf2+/- mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1308</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1308</guid>
<pubDate>Tue, 08 May 2012 21:52:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Since parathyroid hormone (PTH) increased FGF2 mRNA and protein expression in osteoblasts, and serum FGF-2 was increased in osteoporotic patients treated with PTH, we assessed whether the anabolic effect of PTH was impaired in    Fgf2-/- mice. Eight-week-old Fgf2+/+ and Fgf2-/- male mice were treated with rhPTH 1-34 (80mug/kg) for 4 weeks. Micro-CT and histomorphometry demonstrated that PTH significantly increased parameters of bone formation in femurs from Fgf2+/+ mice    but the changes were smaller and not significant in Fgf2-/- mice. IGF-1 was significantly reduced in serum from PTH-treated Fgf2-/- mice. DEXA analysis of femurs from Fgf2+/+, Fgf2+/-, and Fgf2-/- mice treated with rhPTH (160mug/kg) for 10 days    showed that PTH significantly increased femoral BMD in Fgf2+/+ by 18%; by only 3% in Fgf2+/- mice and reduced by 3% in Fgf2-/- mice. We conclude that endogenous Fgf2 is important for maximum bone anabolic effect of PTH in mice.</p>

	]]>
</description>

<author>M M. Hurley et al.</author>


</item>


<item>
<title>Severe epilepsy resulting from genetic interaction between Scn2a and Kcnq2.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1307</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1307</guid>
<pubDate>Tue, 08 May 2012 21:52:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>A mutation in the voltage-gated sodium-channel Scn2a results in moderate epilepsy in transgenic Scn2a(Q54) mice maintained on a C57BL/6J strain background. The onset of progressive epilepsy begins in adults with short-duration    partial seizures that originate in the hippocampus. The underlying abnormality is an increase in persistent sodium current in hippocampal neurons. The voltage-gated potassium channel Kcnq2 is responsible for generating M current (I(KM)) that is    thought to control excitability and limit repetitive firing of hippocampal neurons. To determine whether impaired M current would exacerbate the seizure phenotype of Scn2a(Q54) mice, we carried out genetic crosses with two mutant alleles of    Kcnq2. Szt1 mice carry a spontaneous deletion that removes the C-terminal domain of Kcnq2. A novel Kcnq2 missense mutation V182M was identified by screening the offspring of ENU-treated males for reduced threshold to electrically evoked minimal    clonic seizures. Double mutant mice carrying the Scn2a(Q54) transgene together with either of the Kcnq2 mutations exhibited severe epilepsy with early onset, generalized tonic-clonic seizures and juvenile lethality by 3 weeks of age. This    dramatic exacerbation of the sodium-channel mutant phenotype indicates that M current plays a critical role in preventing seizure initiation and spreading in this animal model. The genetic interaction between Scn2a and Kcnq2 demonstrates that    combinations of mild alleles of monogenic epilepsy genes can result in severe disease and provides a model for complex inheritance of human epilepsy. The data suggest that interaction between these genes might contribute to the variable    expressivity observed in human families with sodium-channel mutations. In a screen of 23 SMEI patients with missense mutations of SCN1A, no second-site mutations in KCNQ2 were identified.</p>

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</description>

<author>J A. Kearney et al.</author>


</item>


<item>
<title>Deficiency of SHP-1 protein-tyrosine phosphatase in &quot;viable motheaten&quot; mice results in retinal degeneration.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1306</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1306</guid>
<pubDate>Tue, 08 May 2012 21:51:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Viable motheaten mutant mice (abbreviated allele symbol me(v)) are deficient in Src-homology 2-domain phosphatase (SHP)-1, a critical negative regulator of signal transduction in hematopoietic cells. These mice exhibit    immune dysfunction, hyperproliferation of myeloid cells, and regenerative anemia. This study focused on the role of SHP-1 in retinal homeostasis. METHODS: Ophthalmoscopy, histology, transmission electron microscopy (TEM), electroretinography    (ERG), immunohistochemistry, Western blot, bone marrow transplantation, and genetic crosses were performed for phenotypic characterization and functional studies of retinal degeneration (RD) in me(v)/me(v) mice. RESULTS: Fundus examinations of    me(v)/me(v) mice revealed numerous, small white spots. Histologic examination demonstrated photoreceptor loss beginning at 3 weeks of age, and TEM revealed disorganization and reduction in the number of outer segments, as well as the presence of    phagocytic cells in the subretinal space. Rod- and cone-mediated ERGs were abnormal. SHP-1 protein was expressed in mouse and human retinal lysates and was localized to the outer nuclear layer of the retina in me(v)/me(v) and control mice.    Autoantibodies are not necessary for RD, as B-cell-deficient me(v)/me(v) Igh-6(tm1Cgn) mice had no attenuation of photoreceptor cell loss compared with age-matched me(v)/me(v) mice. Histologic examination of lungs and retinas from normal    recipients of me(v)/me(v) marrow revealed the classic acidophilic macrophage pneumonia of me(v)/me(v) mice, but no retinal degeneration.  CONCLUSIONS: me(v)/me(v) mice exhibit normal retinal development with the onset of RD at 3 weeks of age and    a rapidly progressive loss of photoreceptors. These findings support the hypothesis that SHP-1 plays a critical role in retinal homeostasis.</p>

	]]>
</description>

<author>B L. Lyons et al.</author>


</item>


<item>
<title>Dorsally derived netrin 1 provides an inhibitory cue and elaborates the ;waiting period&apos; for primary sensory axons in the developing spinal cord.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1305</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1305</guid>
<pubDate>Tue, 08 May 2012 21:51:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dorsal root ganglion (DRG) neurons extend axons to specific targets in the gray matter of the spinal cord. During development, DRG axons grow into the dorsolateral margin of the spinal cord and projection into the dorsal mantle    layer occurs after a ;waiting period' of a few days. Netrin 1 is a long-range diffusible factor expressed in the ventral midline of the developing neural tube, and has chemoattractive and chemorepulsive effects on growing axons. Netrin 1 is also    expressed in the dorsal spinal cord.  However, the roles of dorsally derived netrin 1 remain totally unknown.  Here, we show that dorsal netrin 1 controls the correct guidance of primary sensory axons. During the waiting period, netrin 1 is    transiently expressed or upregulated in the dorsal spinal cord, and the absence of netrin 1 results in the aberrant projection of sensory axons, including both cutaneous and proprioceptive afferents, into the dorsal mantle layer.  Netrin 1    derived from the dorsal spinal cord, but not the floor plate, is involved in the correct projection of DRG axons. Furthermore, netrin 1 suppresses axon outgrowth from DRG in vitro. Unc5c(rcm) mutant shows abnormal invasion of DRG axons as    observed in netrin 1 mutants. These results are the first direct evidence that netrin 1 in the dorsal spinal cord acts as an inhibitory cue for primary sensory axons and is a crucial signal for the formation of sensory afferent neural    networks.</p>

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</description>

<author>K Watanabe et al.</author>


</item>


<item>
<title>Differential endocrine responses to rosiglitazone therapy in new mouse models of type 2 diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1304</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1304</guid>
<pubDate>Tue, 08 May 2012 21:51:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Polygenic mouse models for obesity-induced type 2 diabetes (T2D) more accurately reflect the most common manifestations of the human disease.  Two inbred mouse strains (NON/Lt and NZO/HlLt) separately contributed T2D susceptibility-    conferring quantitative trait loci to F1 males. Although chronic administration of rosiglitazone (Rosi) in diet (50 mg/kg) effectively suppressed F1 diabetes, hepatosteatosis was an undesired side effect. Three recombinant congenic strains    (designated RCS1, -2, and -10) developed on the NON/Lt background carry variable numbers of these quantitative trait loci that elicit differential weight gain and male glucose intolerance syndromes of variable severity. We previously showed that    RCS1 and -2 mice responded to chronic Rosi therapy without severe steatosis, whereas RCS10 males were moderately sensitive. In contrast, another recombinant congenic strain, RCS8, responded to Rosi therapy with the extreme hepatosteatosis    observed in the F1. Longitudinal changes in multiple plasma analytes, including insulin, the adipokines leptin, resistin, and adiponectin, and plasminogen activator inhibitor-1 (PAI-1) allowed profiling of the differential Rosi responses in    steatosis-exacerbated F1 and RCS8 males vs. the resistant RCS1 and RCS2 or moderately sensitive RCS10. Of these biomarkers, PAI-1 most effectively predicted adverse drug responses. Unexpectedly, mean resistin concentrations were higher in    Rosi-treated RCS8 and RCS10. In summary, longitudinal profiling of multiple plasma analytes identified PAI-1 as a useful biomarker to monitor for differential pharmacogenetic responses to Rosi in these new mouse models of T2D.</p>

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</description>

<author>E H. Leiter et al.</author>


</item>


<item>
<title>Not all lunatic fringe null female mice are infertile.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1303</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1303</guid>
<pubDate>Tue, 08 May 2012 21:51:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J Xu et al.</author>


</item>


<item>
<title>IGF-I secretion by prostate carcinoma cells does not alter tumor-bone cell interactions in vitro or in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1302</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1302</guid>
<pubDate>Tue, 08 May 2012 21:51:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: IGF-I is an important growth and differentiative factor for osteoblasts and may have a role in defining prostate cancer risk and skeletal metastases. METHODS: Conditioned media (CM) from human prostate cancer (PC), C4-2    and C4-2B, which produce osteoblastic lesions, and PC-3, which causes osteolysis, was added to MC3T3-E1 bone cultures. SCID mice were injected intratibially with these engineered cells. Tumor bearing tibiae were analyzed by microCT and pQCT.    RESULTS: CM from PC cells increased osteoblast proliferation and differentiation and was unaltered by the type of PC cell, IGF-I antibodies, or exogenous IGF-I and IGFBP2.  Study of intratibial PC tumors in SCID mice showed that C4-2 cells grew    slowly preserving bone structure, while PC-3 tumors caused rapid osteolysis. Overexpression of IGF-I did not change either tumor progression or skeletal response. CONCLUSIONS: IGF-I is neither necessary nor sufficient for the osteoblastic    response to PC metastases. Prostate (c) 2006 Wiley-Liss, Inc.</p>

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</description>

<author>J Rubin et al.</author>


</item>


<item>
<title>In vivo role of ER-associated peptidase activity in tailoring peptides for presentation by MHC class Ia and class Ib molecules.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1301</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1301</guid>
<pubDate>Tue, 08 May 2012 21:51:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Endoplasmic reticulum (ER)-associated aminopeptidase (ERAP)1 has been implicated in the final proteolytic processing of peptides presented by major histocompatibility complex (MHC) class I molecules. To evaluate the in vivo role of    ERAP1, we have generated ERAP1-deficient mice. Cell surface expression of the class Ia molecules H-2Kb and H-2Db and of the class Ib molecule Qa-2 was significantly reduced in these animals.  Although cells from mutant animals exhibited reduced    capacity to present several self- and foreign antigens to Kb-, Db-, or Qa-1b-restricted CD8+ cytotoxic T cells, presentation of some antigens was unaffected or significantly enhanced. Consistent with these findings, mice generated defective CD8+    T cell responses against class I-presented antigens. These findings reveal an important in vivo role of ER-associated peptidase activity in tailoring peptides for presentation by MHC class Ia and class Ib molecules.</p>

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</description>

<author>J Yan et al.</author>


</item>


<item>
<title>Generation and characterization of a novel tetravalent anti-CD22 antibody with improved antitumor activity and pharmacokinetics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1300</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1300</guid>
<pubDate>Tue, 08 May 2012 21:50:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to prepare a tetravalent anti-human CD22 recombinant antibody with improved antitumor activity and a half life longer than that of its divalent counterpart. We compared the ability of tetravalent vs.    divalent antibody to associate/dissociate to/from CD22-positive Daudi cells, to interact with murine and human Fcgamma receptors (FcgammaR), to bind human complement component C1q, to inhibit the growth of tumor cells, to diffuse into various    tissues, to be internalized by Daudi cells, to react with human neonatal Fc receptors (FcRn), and to persist in the circulation of normal mice. As compared to the murine or chimeric divalent antibodies, the chimeric tetravalent counterpart has a    longer half life in mice. It also has an affinity for FcRns that is identical to that of human IgG. The tetravalent antibody has increased antitumor activity in vitro and completely conserved effector functions (binding to FcgammaR-positive cells    and to C1q) in vitro.  Despite its 33% higher molecular weight, it penetrates mouse tissues as well as its divalent antibody counterpart. Based on the improved in vitro performance and pharmacokinetics of the tetravalent antibody it will now be    tested for its antitumor activity in vivo.</p>

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</description>

<author>X Y. Liu et al.</author>


</item>


<item>
<title>Chromosomal inversion discovered in C3H/HeJ mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1299</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1299</guid>
<pubDate>Tue, 08 May 2012 21:50:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice of the inbred mouse strain C3H/HeJ have been shown to be homozygous for a chromosomal inversion on Chromosome (Chr) 6. The inversion encompasses about 20% of the chromosome from approximately 73 Mb to approximately 116 Mb. The    importance of this finding is that linkage crosses using C3H/HeJ will show no recombination in this region of Chr 6.  The inversion has no apparent effect on the phenotype of C3H/HeJ mice and its presence should not affect biological studies;    however, use of C3H/HeJ mice for genetic analysis of Chr 6 should be avoided or the results interpreted with the inversion in mind. The inversion has been named In(6)1J (inversion Chr 6, Jackson 1).</p>

	]]>
</description>

<author>E C. Akeson et al.</author>


</item>


<item>
<title>The MHC class I-related FcRn ameliorates murine Lyme arthritis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1298</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1298</guid>
<pubDate>Tue, 08 May 2012 21:50:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The identification of the neonatal FcR (FcRn) as an IgG homeostasis regulator has led to research aimed at delineating a role for FcRn in humorally mediated disease. FcRn is a class I-related molecule that prolongs the half-life of    serum IgG by preferentially binding IgG at low pH and inhibiting its degradation. Its role in protective immunity to infectious organisms is unknown. We investigated the function of FcRn in the murine model of Lyme arthritis, caused by infection    with Borrelia burgdorferi. We infected FcRn(-/-) and wild-type mice with B. burgdorferi and monitored the development of arthritis. Infected FcRn(-/-) mice demonstrated decreased serum levels of anti-B. burgdorferi antibodies and borreliacidal    activity. Moreover, these mutant mice developed increased ankle swelling and joint histopathology following infection. Our data suggest that FcRn ameliorates murine Lyme arthritis by preventing the degradation of protective borreliacidal    antibodies.</p>

	]]>
</description>

<author>H Crowley et al.</author>


</item>


<item>
<title>Development and progression of alopecia in the vitamin D receptor null mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1297</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1297</guid>
<pubDate>Tue, 08 May 2012 21:50:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Humans with selected mutations in the vitamin D receptor (VDR) and mouse models lacking VDR develop alopecia. Mice null for the Vdr gene are born with a normal coat of hair, but fail to initiate normal hair follicle cycling. In this    study, we examined the morphology of the hair follicle of the Vdr null mouse during days 13-22 when the hair follicle normally initiates and completes the first catagen. We then explored the possibility that the abnormality in hair follicle    cycling was associated with abnormal expression of hairless (Hr), a putative transcriptional regulator known to regulate hair follicle cycling and recently shown to regulate VDR transcriptional activity. Our results demonstrate the progressive    deterioration of the hair follicle through catagen. Comparable to VDR, Hr was found in the basal cells of the epidermis and ORS of the hair follicle. However, Hr was also found in the IRS and matrix of the follicle, regions with little or no VDR.    Hr levels increased during catagen, reaching a peak by day 19. Levels of Hr were greater in the Vdr null mice compared to wildtype controls, results confirmed by quantitative RT-PCR. We conclude that lack of VDR causes disruption of hair follicle    structure during the first catagen resulting in failure of subsequent hair follicle cycling. These changes are associated with increased expression of Hr, suggesting a role for VDR in regulating Hr expression. Both Hr and VDR are required for    normal hair follicle cycling. J. Cell. Physiol. 207: 340-353, 2006. (c) 2006 Wiley-Liss, Inc.</p>

	]]>
</description>

<author>D D. Bikle et al.</author>


</item>


<item>
<title>Helicobacter pylori infection in the pharynx of patients with chronic pharyngitis detected with TDI-FP and modified Giemsa stain.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1296</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1296</guid>
<pubDate>Tue, 08 May 2012 21:50:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>AIM: To detect whether there is Helicobacter pylori (H pylori) colonization in the pharynx mucous membrane of healthy people and whether chronic pharyngitis is related to H pylori infection. METHODS: Fifty cases of chronic    pharyngitis refractory over three months were prospectively studied from March 2004 to August 2004 in the otolaryngology outpatient department of the Second Hospital of Xi'an Jiaotong University.  Template-directed dye-terminator incorporated    with fluorescence polarization detection (TDI-FP) and modified Giemsa stain were used to examine pharynx mucous membrane tissue for H pylori colonization in the patients with chronic pharyngitis and the healthy people as a control group. RESULTS:    In the control group, no people were detected to have H pylori in the pharynx. In contrast, in 50 cases with chronic pharyngitis, 19 (38.0%) cases were H pylori positive with a TDI-FP assay and 4 (8%) cases were TDI-FP positive with Giemsa    staining in the pharynx. Sixteen of the 50 pharyngitis cases had stomach ailment history, 11 cases (68.8%) of these 16 patients were determined to be H pylori positive in the pharynx with the TDI-FP assay. c2 test showed that this infection rate    was remarkably higher (P=0.0007) than that in the cases without stomach ailment history. Giemsa staining showed that 3 cases (18.8%) of the patients with stomach ailment history were infected with H pylori in the pharynx, which was remarkably    higher (P=0.042) than that in the patients without stomach ailment history (1 case, which was 2.9%). CONCLUSION: H pylori may not be detected in the pharynx of healthy people. Chronic pharyngitis may be related to H pylori infection. The    infection rate with H pylori in the pharynx is higher in patients with stomach ailment histories than in patients without stomach ailment histories, suggesting that chronic pharyngitis may be related to stomach ailment history.</p>

	]]>
</description>

<author>J P. Zhang et al.</author>


</item>


<item>
<title>From teratocarcinomas to embryonic stem cells and beyond: a history of embryonic stem cell research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1295</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1295</guid>
<pubDate>Tue, 08 May 2012 21:50:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>We are currently facing an unprecedented level of public interest in research on embryonic stem cells, an area of biomedical research that until recently was small, highly specialized and of limited interest to anyone but experts in    the field. Real and imagined possibilities for the treatment of degenerative and other diseases are of special interest to our rapidly ageing population; real and imagined associations of stem cells to cloning, embryos and reproduction stir    deeply held beliefs and prejudices. The conjunction of these factors could explain the recent sudden interest in embryonic stem cells but we ought to remember that this research has a long and convoluted history, and that the findings described    today in the scientific and popular press are firmly grounded in research that has been going on for several decades. Here I briefly recapitulate this fascinating history.</p>

	]]>
</description>

<author>D Solter</author>


</item>


<item>
<title>Mice deficient in the Rab5 guanine nucleotide exchange factor ALS2/alsin exhibit age-dependent neurological deficits and altered endosome trafficking.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1294</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1294</guid>
<pubDate>Tue, 08 May 2012 21:49:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>ALS2/alsin is a member of guanine nucleotide exchange factors for the small GTPase Rab5 (Rab5GEFs), which act as modulators in endocytic pathway. Loss-of-function mutations in human ALS2 account for a number of juvenile recessive    motor neuron diseases (MNDs). However, the normal physiological role of ALS2 in vivo and the molecular mechanisms underlying motor dysfunction are still unknown. To address these issues, we have generated mice homozygous for disruption of the    Als2 gene. The Als2-null mice observed through 21 months of age demonstrated no obvious developmental, reproductive or motor abnormalities. However, immunohistochemical and electrophysiological analyses identified an age-dependent, slowly    progressive loss of cerebellar Purkinje cells and disturbance of spinal motor neurons associated with astrocytosis and microglial cell activation, indicating a subclinical dysfunction of motor system in Als2-null mice. Further, quantitative    epidermal growth factor (EGF)-uptake analysis identified significantly smaller-sized EGF-positive endosomes in Als2-null fibroblasts, suggesting an alteration of endosome/vesicle trafficking in the cells. Collectively, while loss of ALS2 does not    produce a severe disease phenotype in mice, these Als2-null animals should provide a useful model with which to understand the interplay between endosomal dynamics and the long-term viability of large neurons such as Purkinje cells and spinal    motor neurons.</p>

	]]>
</description>

<author>S Hadano et al.</author>


</item>


<item>
<title>Trak1 mutation disrupts GABA(A) receptor homeostasis in hypertonic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1293</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1293</guid>
<pubDate>Tue, 08 May 2012 21:49:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hypertonia, which results from motor pathway defects in the central nervous system (CNS), is observed in numerous neurological conditions, including cerebral palsy, stroke, spinal cord injury, stiff-person syndrome, spastic    paraplegia, dystonia and Parkinson disease. Mice with mutation in the hypertonic (hyrt) gene exhibit severe hypertonia as their primary symptom. Here we show that hyrt mutant mice have much lower levels of gamma-aminobutyric acid type A (GABA(A))    receptors in their CNS, particularly the lower motor neurons, than do wild-type mice, indicating that the hypertonicity of the mutants is likely to be caused by deficits in GABA-mediated motor neuron inhibition. We cloned the responsible gene,    trafficking protein, kinesin binding 1 (Trak1), and showed that its protein product interacts with GABA(A) receptors. Our data implicate Trak1 as a crucial regulator of GABA(A) receptor homeostasis and underscore the importance of hyrt mice as a    model for studying the molecular etiology of hypertonia associated with human neurological diseases.</p>

	]]>
</description>

<author>S L. Gilbert et al.</author>


</item>


<item>
<title>Human antibodies induce arthritis in mice deficient in the low-affinity inhibitory IgG receptor Fc gamma RIIB.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1292</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1292</guid>
<pubDate>Tue, 08 May 2012 21:49:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rheumatoid arthritis (RA) is a complex autoimmune disease with a poorly understood pathogenesis. The disease is associated with polyclonal B cell activation and the production of autoantibodies (autoAbs), but there is a longstanding    controversy as to whether such Abs contribute to, or are secondary to, the pathogenesis of RA. To address the potential pathogenicity of human RA-associated Abs, we developed a passive transfer model involving mice deficient in the low-affinity    inhibitory Fc receptor, FcgammaRIIB. We report that plasma or serum from patients with active RA can induce inflammation and histological lesions in FcgammaRIIB-/- mice consistent with arthritis, and that this pathogenic activity is caused by the    immunoglobulin G-rich fraction. Our results suggest that humoral autoimmunity can contribute directly to autoimmune arthritis, and that FcgammaRIIB-/- mice are a promising model to evaluate the arthritogenic potential of human    autoAbs.</p>

	]]>
</description>

<author>S B. Petkova et al.</author>


</item>


<item>
<title>Test- and behavior-specific genetic factors affect WKY hypoactivity in tests of emotionality.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1291</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1291</guid>
<pubDate>Tue, 08 May 2012 21:49:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inbred Wistar-Kyoto rats consistently display hypoactivity in tests of emotional behavior. We used them to test the hypothesis that the genetic factors underlying the behavioral decision-making process will vary in different    environmental contexts. The contexts used were the open-field test (OFT), a novel environment with no explicit threats present, and the defensive-burying test (DB), a habituated environment into which a threat has been introduced. Rearing, a    voluntary behavior was measured in both tests, and our study was the first to look for genetic loci affecting grooming, a relatively automatic, stress-responsive stereotyped behavior.  Quantitative trait locus analysis was performed on a    population of 486 F2 animals bred from reciprocal inter-crosses. The genetic architectures of DB and OFT rearing, and of DB and OFT grooming, were compared. There were no common loci affecting grooming behavior in both tests. These different    contexts produced the stereotyped behavior via different pathways, and genetic factors seem to influence the decision-making pathways and not the expression of the behavior. Three loci were found that affected rearing behavior in both tests.    However, in both contexts, other loci had greater effects on the behavior. Our results imply that environmental context's effects on decision-making vary depending on the category of behavior.</p>

	]]>
</description>

<author>A E. Baum et al.</author>


</item>


<item>
<title>Quantitative trait loci for baseline erythroid traits.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1290</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1290</guid>
<pubDate>Tue, 08 May 2012 21:49:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>A substantial genetic contribution underlies variation in baseline peripheral blood counts. We performed quantitative trait locus/loci (QTL) analyses to identify chromosome (Chr) regions harboring genes influencing the baseline    erythroid parameters in F2 intercrosses between NZW/LacJ, SM/J, and C57BLKS/J inbred mice. We identified multiple significant QTL for red blood cell (RBC) count, hemoglobin (Hgb) and hematocrit (Hct) levels, mean corpuscular volume (MCV), mean    corpuscular hemoglobin (MCH), and mean cell hemoglobin concentration (CHCM). We identified four RBC count QTL: Rbcq1 (Chr 1, peak LOD score at 62 cM,), Rbcq2 (Chr 4, 60 cM), Rbcq3 (Chr 11, 34 cM), and Rbcq4 (Chr 10, 60 cM). Three MCV QTL were    identified: Mcvq1 (Chr 7, 30 cM), Mvcq2 (Chr 11, 6 cM), and Mcvq3 (Chr 10, 60 cM). Single significant loci for Hgb (Hgbq1, Chr 16, 32 cM), Hct (Hctq1, Chr 3, 42 cM), and MCH (Mchq1, Chr 10, 60 cM) were identified. The data support the existence    of a common RBC/MCH/MCV locus on Chr 10. Two QTL for CHCM (Chcmq1, Chr 2, 48 cM; Chcmq2, Chr 9, 44 cM) and an interaction between Chcmq2 with a locus on Chr 19 were identified. These analyses emphasize the genetic complexity underlying the    regulation of erythroid peripheral blood traits in normal populations and suggest that genes not previously recognized as significantly impacting normal erythropoiesis exist.</p>

	]]>
</description>

<author>L L. Peters et al.</author>


</item>


<item>
<title>Nras loss induces metastatic conversion of Rb1-deficient neuroendocrine thyroid tumor.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1289</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1289</guid>
<pubDate>Tue, 08 May 2012 21:49:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the gene encoding the retinoblastoma tumor suppressor predispose humans and mice to tumor development. Here we have assessed the effect of Nras loss on tumor development in Rb1 heterozygous mice. Loss of one or two Nras    alleles is shown to significantly reduce the severity of pituitary tumors arising in Rb1(+/-) animals by enhancing their differentiation. By contrast, C-cell thyroid adenomas occurring in Rb1(+/-) mice progress to metastatic medullary carcinomas    after loss of Nras. In Rb1(+/-)Nras(+/-) animals, distant medullary thyroid carcinoma metastases are associated with loss of the remaining wild-type Nras allele. Loss of Nras in Rb1-deficient C cells results in elevated Ras homolog family A    (RhoA) activity, and this is causally linked to the invasiveness and metastatic behavior of these cells. These findings suggest that the loss of the proto-oncogene Nras in certain cellular contexts can promote malignant tumor    progression.</p>

	]]>
</description>

<author>C Takahashi et al.</author>


</item>


<item>
<title>Fatal flaws in the case for prepatterning in the mouse egg.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1288</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1288</guid>
<pubDate>Tue, 08 May 2012 21:48:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The presence or absence of predetermination and polarity in the mouse preimplantation embryo is still controversial. The question is if the mechanisms underlying early mammalian development is comparable to those operating in    non-mammalian 'model' organisms. In a recent article by Gardner in this journal, the author criticizes two of our recent publications. However, in order to resolve this controversy it is essential to read relevant reports carefully without bias    and to provide data on which a particular claim is based.</p>

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</description>

<author>T Hiiragi et al.</author>


</item>


<item>
<title>Attenuation of murine lysosomal storage disease by allogeneic neonatal bone marrow transplantation using costimulatory blockade and donor lymphocyte infusion without myeloablation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1287</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1287</guid>
<pubDate>Tue, 08 May 2012 21:48:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Treatment of nonmalignant childhood disorders by bone marrow transplantation (BMT) is limited by toxicity from preparatory regimens and immune consequences associated with engraftment of allogeneic donor cells.  Using costimulatory    blockade (anti-CD40L mAb and CTLA-4Ig) combined with high-dose BMT in nonablated neonates, we obtained engraftment and established tolerance using both partially MHC mismatched (H2(g7) into H2(b)) and fully mismatched BM (H2(s) into H2(b)).    Recipients were mucopolysaccharidosis type VII (MPS VII) mice with lysosomal storage disease in order to assess therapeutic outcome. Recipients treated with donor lymphocyte infusion (DLI) amplified microchimerism to full donor.  Recipients    without DLI maintained long-term engraftment, tolerance, and had extended life spans. DLI increased donor cell mediated replacement of beta-glucuronidase (GUSB) activity in all tissues and maintained clearance of lysosomes better than in    non-DLI-treated mice. DLI amplification of partially mismatched BM and fully mismatched BM caused late onset chronic GvHD in 56% and 100% of recipients, respectively.</p>

	]]>
</description>

<author>M D. Lessard et al.</author>


</item>


<item>
<title>Mitoferrin is essential for erythroid iron assimilation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1286</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1286</guid>
<pubDate>Tue, 08 May 2012 21:48:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Iron has a fundamental role in many metabolic processes, including electron transport, deoxyribonucleotide synthesis, oxygen transport and many essential redox reactions involving haemoproteins and Fe-S cluster proteins. Defective    iron homeostasis results in either iron deficiency or iron overload. Precise regulation of iron transport in mitochondria is essential for haem biosynthesis, haemoglobin production and Fe-S cluster protein assembly during red cell development.    Here we describe a zebrafish mutant, frascati (frs), that shows profound hypochromic anaemia and erythroid maturation arrest owing to defects in mitochondrial iron uptake.  Through positional cloning, we show that the gene mutated in the frs    mutant is a member of the vertebrate mitochondrial solute carrier family (SLC25) that we call mitoferrin (mfrn). mfrn is highly expressed in fetal and adult haematopoietic tissues of zebrafish and mouse. Erythroblasts generated from murine    embryonic stem cells null for Mfrn (also known as Slc25a37) show maturation arrest with severely impaired incorporation of 55Fe into haem. Disruption of the yeast mfrn orthologues, MRS3 and MRS4, causes defects in iron metabolism and    mitochondrial Fe-S cluster biogenesis. Murine Mfrn rescues the defects in frs zebrafish, and zebrafish mfrn complements the yeast mutant, indicating that the function of the gene may be highly conserved. Our data show that mfrn functions as the    principal mitochondrial iron importer essential for haem biosynthesis in vertebrate erythroblasts.</p>

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</description>

<author>G C. Shaw et al.</author>


</item>


<item>
<title>Grey, a novel mutation in the murine Lyst gene, causes the beige phenotype by skipping of exon 25.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1285</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1285</guid>
<pubDate>Tue, 08 May 2012 21:48:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>The murine beige mutant phenotype and the human Chediak-Higashi syndrome are caused by mutations in the murine Lyst (lysosomal trafficking regulator) gene and the human CHS gene, respectively. In this report we have analyzed a novel    murine mutant Lyst allele, called Lyst(bg-grey), that had been found in an ENU mutation screen and named grey because of the grey coat color of affected mice. The phenotype caused by the Lyst(bg-grey) mutation was inherited in a recessive    fashion. Melanosomes of melanocytes associated with hair follicles and the choroid layer of the eye, as well as melanosomes in the neural tube-derived pigment epithelium of the retina, were larger and irregularly shaped in homozygous mutants    compared with those of wild-type controls. Secretory vesicles in dermal mast cells of the mutant skin were enlarged as well. Test crosses with beige homozygous mutant mice (Lyst(bg)) showed that double heterozygotes (Lyst(bg)/Lyst(bg-grey)) were    phenotypically indistinguishable from either homozygous parent, demonstrating that the ENU mutation was an allele of the murine Lyst gene. RT-PCR analyses revealed the skipping of exon 25 in Lyst(bg-grey) mutants, which is predicted to cause a    missense D2399E mutation and the loss of the following 77 amino acids encoded by exon 25 but leave the C-terminal end of the protein intact. Analysis of the genomic Lyst locus around exon 25 showed that the splice donor at the end of exon 25    showed a T-to-C transition point mutation. Western blot analysis suggests that the Lyst(bg-grey) mutation causes instability of the LYST protein. Because the phenotype of Lyst(bg) and Lyst(bg-grey) mutants is indistinguishable, at least with    respect to melanosomes and secretory granules in mast cells, the Lyst(bg-grey) mutation defines a critical region for the stability of the murine LYST protein.</p>

	]]>
</description>

<author>F Runkel et al.</author>


</item>


<item>
<title>An siRNA-based microbicide protects mice from lethal herpes simplex virus 2 infection.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1284</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1284</guid>
<pubDate>Tue, 08 May 2012 21:47:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Herpes simplex virus 2 (HSV-2) infection causes significant morbidity and is an important cofactor for the transmission of HIV infection. A microbicide to prevent sexual transmission of HSV-2 would contribute substantially to    controlling the spread of HIV and other infections.  Because RNA interference (RNAi) provides effective antiviral defence in plants and other organisms, several studies have focused on harnessing RNAi to inhibit viral infection. Here we show that    vaginal instillation of small interfering RNAs (siRNAs) targeting HSV-2 protects mice from lethal infection. siRNAs mixed with lipid are efficiently taken up by epithelial and lamina propria cells and silence gene expression in the mouse vagina    and ectocervix for at least nine days. Intravaginal application of siRNAs targeting the HSV-2 UL27 and UL29 genes (which encode an envelope glycoprotein and a DNA binding protein, respectively) was well tolerated, did not induce    interferon-responsive genes or cause inflammation, and protected mice when administered before and/or after lethal HSV-2 challenge. These results suggest that siRNAs are attractive candidates for the active component of a microbicide designed to    prevent viral infection or transmission.</p>

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</description>

<author>D Palliser et al.</author>


</item>


<item>
<title>An imprinted locus epistatically influences Nstr1 and Nstr2 to control resistance to nerve sheath tumors in a neurofibromatosis type 1 mouse model.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1283</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1283</guid>
<pubDate>Tue, 08 May 2012 21:47:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cancer is a complex disease in which cells acquire many genetic and epigenetic alterations. We have examined how three types of alterations, mutations in tumor suppressor genes, changes in an imprinted locus, and polymorphic loci,    interact to affect tumor susceptibility in a mouse model of neurofibromatosis type 1 (NF1). Mutations in tumor suppressor genes such as TP53 and in oncogenes such as KRAS have major effects on tumorigenesis due to the central roles of these genes    in cell proliferation and cell survival. Imprinted genes expressed from only one parental chromosome affect tumorigenesis if their monoallelic expression is lost or duplicated. Because imprinted loci are within regions deleted or amplified in    cancer, the parental origin of genomic rearrangements could affect tumorigenesis. Gene polymorphisms can vary tumor incidence by affecting rate-limiting steps in tumorigenesis within tumor cells or surrounding stroma. In our mouse model of NF1,    the incidence of tumors mutant for the tumor suppressor genes Nf1 and Trp53 is strongly modified by a linked imprinted locus acting epistatically on two unlinked polymorphic loci, Nstr1 and Nstr2. This interaction of an imprinted locus and    polymorphic susceptibility loci has profound implications for human mapping studies where the parental contribution of alleles is often unknown.</p>

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</description>

<author>K M. Reilly et al.</author>


</item>


<item>
<title>Generation of new Notch2 mutant alleles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1282</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1282</guid>
<pubDate>Tue, 08 May 2012 21:47:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Notch signaling pathway is an evolutionarily conserved intercellular signaling mechanism, and mutations in its components disrupt embryonic development in many organisms and cause inherited diseases in humans. We previously    described construction and analysis of a hypomorphic allele of the Notch2 gene. Homozygosity for this allele leads to embryonic and perinatal lethality due to cardiovascular and kidney defects. We report here novel Notch2 mutant alleles generated    by gene targeting in embryonic stem cells, including a conditional null allele in which exon 3 of the Notch2 gene is flanked by loxP sequences. These new Notch2 mutant alleles expand the set of tools available for studying the myriad roles of the    Notch pathway during mammalian development and will enable analysis of Notch2 function at additional stages of embryogenesis and in adult mice.</p>

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</description>

<author>B McCright et al.</author>


</item>


<item>
<title>Expression of terminal differentiation proteins defines stages of mouse mammary gland development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1281</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1281</guid>
<pubDate>Tue, 08 May 2012 21:47:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Immunohistochemical analysis using paraffin-embedded specimens is the method of choice to evaluate protein expression at a cellular level while preserving tissue architecture in normal and neoplastic tissues. Current knowledge of    the expression of terminal differentiation markers in the mouse mammary gland relies on the evaluation of frozen tissues by use of immunofluorescence. We assessed changes in patterns of expression of terminal differentiation markers throughout    the development of the mouse mammary gland in paraffin-embedded tissues. The expression of alpha-smooth muscle actin (SMA) and keratins (K) 5, 8/18, and 14 was influenced by the development stage of the mammary gland. Expression of K5 and SMA was    restricted to basal cells. Keratin 14 was consistently expressed by mammary basal cells, and was detected in scattered luminal cells from 13.5 days after conception through puberty. Labeling for K8/18 of luminal cells was heterogeneous at all    times. Heterogeneous expression patterns in luminal cells suggest this layer has cells with a variety of biological functions. The absence of K6 expression at any stage of the development of the mammary gland was confirmed by use of reverse    transcriptase-polymerase chain reaction analysis, which indicates that this intermediate filament is not a marker of the mammary gland stem cell. Finally, consistent with results of earlier studies, keratins 1, 10, 13, and 15, and filaggrin,    involucrin, and loricrin were not detected at any stage of mammary gland development.</p>

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</description>

<author>I Mikaelian et al.</author>


</item>


<item>
<title>Quantitative trait locus analysis for obesity reveals multiple networks of interacting loci.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1280</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1280</guid>
<pubDate>Tue, 08 May 2012 21:46:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Obesity is a highly heritable and genetically complex trait with hundreds of potential loci identified. An intercross of 513 F(2) progeny between the SM/J x NZB/BINJ inbred mouse strains was generated to identify quantitative trait    loci (QTL) that are involved in the weight of four fat pads: mesenteric, inguinal, gonadal, and retroperitoneal. Sex and lean body weight were treated as covariates in the analysis of these fat pads.  This analysis uncoupled genetic effects    related to overall body size from those influencing the adiposity of a mouse. We identified multiple significant QTL. QTL alleles associated with increased lean body weight and individual fat pad weights are contributed by the NZB background.     Adiposity loci are distinct from these body size QTLs and high-adiposity alleles are contributed by the SM background. An extended network of epistatic QTL is also observed. A QTL on Chr 19 is the center of a network of eight interacting QTL, Chr    4 is the center of six, and Chr 17 the center of four interacting QTL. We conclude that interacting networks of multiple genes characterize the regulation of fat pad depots and body weight. Haplotype patterns and a literature-driven approach were    used to generate hypotheses regarding the identity of the genes and pathways underlying the QTL.</p>

	]]>
</description>

<author>I M. Stylianou et al.</author>


</item>


<item>
<title>Loss of notch activity in the developing central nervous system leads to increased cell death.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1279</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1279</guid>
<pubDate>Tue, 08 May 2012 21:46:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many cells in the mammalian brain undergo apoptosis as a normal and critical part of development but the signals that regulate the survival and death of neural progenitor cells and the neurons they produce are not well understood.    The Notch signaling pathway is involved in multiple decision points during development and has been proposed to regulate the survival and apoptosis of neural progenitor cells in the developing brain; however, previous experiments have not    resolved whether Notch activity is pro- or anti-apoptotic. To elucidate the function of Notch signaling in the survival and death of cells in the nervous system, we have produced single and compound Notch conditional mutants in which Notch1 and    Notch3 are removed at different times during brain development and in different populations of cells. We show here that a large number of neural progenitor cells, as well as differentiating neurons, undergo apoptosis in the absence of Notch1 and    Notch3, suggesting that Notch activity promotes the survival of both progenitors and newly differentiating cells in the developing nervous system. Finally, we show that postmitotic neurons do not require Notch activity indefinitely to regulate    their survival since elevated levels of cell death are observed only during embryogenesis in the Notch mutants and are not detected in neonates.</p>

	]]>
</description>

<author>H A. Mason et al.</author>


</item>


<item>
<title>The nob2 mouse, a null mutation in Cacna1f: anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1278</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1278</guid>
<pubDate>Tue, 08 May 2012 21:46:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Glutamate release from photoreceptor terminals is controlled by voltage-dependent calcium channels (VDCCs). In humans, mutations in the Cacna1f gene, encoding the alpha1F subunit of VDCCs, underlie the incomplete form of X-linked    congenital stationary night blindness (CSNB2).  These mutations impair synaptic transmission from rod and cone photoreceptors to bipolar cells. Here, we report anatomical and functional characterizations of the retina in the nob2 (no b-wave 2)    mouse, a naturally occurring mutant caused by a null mutation in Cacna1f. Not surprisingly, the b-waves of both the light- and dark-adapted electroretinogram are abnormal in nob2 mice. The outer plexiform layer (OPL) is disorganized, with    extension of ectopic neurites through the outer nuclear layer that originate from rod bipolar and horizontal cells, but not from hyperpolarizing bipolar cells. These ectopic neurites continue to express mGluR6, which is frequently associated with    profiles that label with the presynaptic marker Ribeye, indicating potential points of ectopic synapse formation. However, the morphology of the presynaptic Ribeye-positive profiles is abnormal. While cone pedicles are present their morphology    also appears compromised. Characterizations of visual responses in retinal ganglion cells in vivo, under photopic conditions, demonstrate that ON-center cells have a reduced dynamic range, although their basic center-surround organization is    retained; no alteration in the responses of OFF-center cells was evident. These results indicate that nob2 mice are a valuable model in which to explore the pathophysiological mechanisms associated with Cacna1f mutations causing CSNB2, and the    subsequent effects on visual information processing. Further, the nob2 mouse represents a model system in which to define the signals that guide synapse formation and/or maintenance in the OPL.</p>

	]]>
</description>

<author>B Chang et al.</author>


</item>


<item>
<title>The benefits of strain donation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1277</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1277</guid>
<pubDate>Tue, 08 May 2012 21:46:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M Davisson et al.</author>


</item>


<item>
<title>Generation of a Snail1 (Snai1) conditional null allele.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1276</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1276</guid>
<pubDate>Tue, 08 May 2012 21:46:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Members of the Snail gene superfamily, which encode zinc finger transcriptional repressors, play critical roles in the establishment of the vertebrate body plan. The Snail1 (Snai1) gene promotes epithelial-mesenchymal transitions    during development and disease progression, and Snai1 null mouse embryos exhibit defects in gastrulation.  However, the early embryonic lethality of Snai1 null embryos precludes the study of Snai1 function in other developmental contexts or    diseases. To overcome this restriction, we generated a Snai1 conditional null allele by flanking the promoter and first two exons of the Snai1 gene with loxP sites. Cre-mediated deletion of the Snai1(flox) allele generates the Snai1(del2) allele,    which behaves genetically as a Snai1 null allele. This conditional null allele will enable investigation of Snai1 function in a variety of developmental and pathological contexts.</p>

	]]>
</description>

<author>S A. Murray et al.</author>


</item>


<item>
<title>Imprinting today: end of the beginning or beginning of the end?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1275</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1275</guid>
<pubDate>Tue, 08 May 2012 21:45:56 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D Solter</author>


</item>


<item>
<title>Mouse models of efficient and inefficient anti-tumor immunity, with emphasis on minimal residual disease and tumor escape.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1274</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1274</guid>
<pubDate>Tue, 08 May 2012 21:45:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Tumor escape from the host immune response remains the major problem holding the development of immunotherapies for cancer. In this review, congenic mouse lines are discussed that differ dramatically in their ability to respond to    tumors tested and, thereby, to survive or to succumb to the tumor and/or its metastases. This ability is under the control of either MHC class I or nontrivial MHC class II beta genes expressed in a small subpopulation of antigen-presenting cells.    Two hypotheses can explain the results obtained so far: (1) emergence of tumor cell variants that escape the host immune response in morbid mice but are eliminated in survivors, and (2) tumor-induced immunosuppression, which is either efficient    or not, depending on the congenic line used. It is argued that further experimentation on these congenics will allow to choose the correct hypothesis, and to characterize the mechanism(s) of elimination of minimal residual disease and prevention    of tumor escape by the immune system of survivors as well as the reason(s) for its failure in morbid mice. It is also argued that the use of these models will substantially increase the chance to resolve the controversy of poor correlation of    immunotherapy testing in mice with clinical results.</p>

	]]>
</description>

<author>I K. Egorov</author>


</item>


<item>
<title>The pleiotropic function of PPARgamma in the placenta.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1273</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1273</guid>
<pubDate>Tue, 08 May 2012 21:45:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>At different stages of placental development the cytotrophoblasts differentiate into specialized cells that are vital for specific placental tasks. These types include the invasive trophoblasts, which are responsible for invasion of    the placenta into the uterine wall, and syncytiotrophoblasts, which form a barrier between the maternal and fetal circulations, govern trans-placental transport of gas, nutrient and waste, and produce placental hormones. Recent research    illuminated the role of the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARgamma) in the areas of adipocyte and macrophage biology, insulin action, bioenergetics and inflammation. It was somewhat surprising that PPARgamma    was also found to play a pivotal role in placental biology. In this review we summarize recent data, which show that PPARgamma is expressed in the placenta, particularly in trophoblasts, and is essential for placental development, trophoblast    invasion, differentiation of cytotrophoblasts into syncytium, and regulation of fat accumulation in trophoblasts. PPARgamma may also play a role in modulating fetal membrane signals toward parturition. The data presented here underscore the need    for a focused investigation of the unique aspects of PPARgamma function in trophoblasts, which may have direct implications for the use of PPARgamma ligands during pregnancy.</p>

	]]>
</description>

<author>W T. Schaiff et al.</author>


</item>


<item>
<title>Variation in genes involved in the RANKL/RANK/OPG bone remodeling pathway are associated with bone mineral density at different skeletal sites in men.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1272</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1272</guid>
<pubDate>Tue, 08 May 2012 21:45:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>In order to assess the contribution of polymorphisms in the RANKL (TNFSF11), RANK (TNFRSF11A) and OPG (TNFRSF11B) genes to variations in bone mineral density (BMD), a population-based cohort with 1,120 extreme low hip BMD cases or    extreme high hip BMD controls was genotyped on five SNPs. We further explored the associations between these genetic variations and forearm BMDs by genotyping 266 offspring and 309 available parents from 160 nuclear families. A family-based    association test was used. Significantly positive associations were found for A163G polymorphisms in the promoter regions of the OPG gene, a missense substitution in exon 7 (Ala192Val) of the RANK gene and rs9594782 SNP in the 5' UTR of the RANKL    gene with BMD in men only. Men with TC/CC genotypes of the rs9594782 SNP had a 2.1 times higher risk of extremely low hip BMD (P=0.004), and lower whole body BMD (P<0.001). Subjects with the TC genotype of the Ala192Val polymorphism had a 40%    reduced risk of having extremely low hip BMD (P<0.01), and higher whole body BMD (P<0.01).  Subjects with the GG genotype of the A163G polymorphism had a 70% reduced risk of having extremely low hip BMD (P<0.05), and higher whole body BMD    (P<0.01). Significant gene-gene interactions were also observed among the OPG, RANK and RANKL genes. Our findings suggest that genetic variation in genes involved in the RANKL/RANK/OPG bone remodeling pathway are strongly associated with BMD at    different skeletal sites in adult men, but not in women.</p>

	]]>
</description>

<author>Y H. Hsu et al.</author>


</item>


<item>
<title>Nuclear receptor coactivator-3 alleles are associated with serum bioavailable testosterone, insulin-like growth factor-1, and vertebral bone mass in men.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1271</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1271</guid>
<pubDate>Tue, 08 May 2012 21:45:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>CONTEXT: Nuclear receptor coactivator-3 (NCOA3) is a member of the steroid receptor coactivator family that interacts with nuclear hormone receptors to enhance their transcriptional activation function and may play a role in somatic    growth. OBJECTIVE: The aim of this study was to examine the relationships between the CAG/CAA (glutamine) length variation at the NCOA3 locus, sex steroid hormone, and IGF-I levels and bone mineral density (BMD) in a cohort of older Caucasian    men. DESIGN AND METHODS: We analyzed the association between potentially functional alleles at this locus, serum sex steroid hormone, and IGF-I levels and lumbar spine and proximal femur BMD (Hologic QDR) in 263 community-dwelling Caucasian men    (age 66 +/- 7 yr, mean +/- sd; range 51-84 yr). Men were genotyped for a CAG/CAA repeat polymorphism in NCOA3, which encodes a polyglutamine tract of variable length in the C-terminal transcriptional activation domain of the protein. RESULTS: We    found a significant monotonic decrease in lumbar spine, but not hip, BMD with increasing copies of the most common allele (29 repeats, 53%). For example, men with the 29/29 genotype had 6% or nearly 0.5 sd lower spine BMD than men without this    genotype, and NCOA3 genotype explained 3.2% of the phenotypic variation in this trait. Serum levels of bioavailable testosterone and IGF-I paralleled genotype-related differences in lumbar spine BMD. CONCLUSION: Allelic variation at the NCOA3    locus may contribute to the genetic control of androgenic hormone and IGF levels and vertebral bone mass among older men.</p>

	]]>
</description>

<author>Y T. Sheu et al.</author>


</item>


<item>
<title>Flow Regime-Based Modeling of Heat Transfer and Pressure Drop in Microchannel Flow Boiling</title>
<link>http://docs.lib.purdue.edu/coolingpubs/173</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/coolingpubs/173</guid>
<pubDate>Tue, 08 May 2012 21:45:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Local heat transfer coefficients and pressure drops during boiling of the dielectric liquid fluorinert FC-77 in parallel microchannels were experimentally investigated in recent work by the authors. Detailed visu- alizations of the corresponding two-phase flow regimes were performed as a function of a wide range of operational and geometric parameters. A new transition criterion was developed for the delineation of a regime where microscale effects become important to the boiling process and a conventional, macroscale treatment becomes inadequate. A comprehensive flow regime map was developed for a wide range of channel dimensions and experimental conditions, and consisted of four distinct regions – bubbly, slug, confined annular, and alternating churn/annular/wispy-annular flow regimes. In the present work, phys- ics-based analyses of local heat transfer in each of the four regimes of the comprehensive map are formu- lated. Flow regime-based models for prediction of heat transfer coefficient in slug flow and annular/ wispy-annular flow are developed and compared to the experimental data. Also, a regime-based predic- tion of pressure drop in microchannels is presented by computing the pressure drop during each flow regime that occurs along the microchannel length. The results of this study reveal the promise of flow regime-based modeling efforts for predicting heat transfer and pressure drop in microchannel boiling.</p>

	]]>
</description>

<author>T. Harirchian et al.</author>


</item>


<item>
<title>Novel leptin receptor mutation in NOD/LtJ mice suppresses type 1 diabetes progression: II. Immunologic analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1270</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1270</guid>
<pubDate>Tue, 08 May 2012 21:45:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recently, we identified in normally type 1 diabetes-prone NOD/LtJ mice a spontaneous new leptin receptor (LEPR) mutation (designated Lepr(db-5J)) producing juvenile obesity, hyperglycemia, hyperinsulinemia, and hyperleptinemia. This    early type 2 diabetes syndrome suppressed intra-islet insulitis and permitted spontaneous diabetes remission. No significant differences in plasma corticosterone, splenic CD4(+) or CD8(+) T-cell percentages, or functions of CD3(+) T-cells in    vitro distinguished NOD wild-type from mutant mice. Yet splenocytes from hyperglycemic mutant donors failed to transfer type 1 diabetes into NOD.Rag1(-/-) recipients over a 13-week period, whereas wild-type donor cells did so. This correlated    with significantly reduced (P < 0.01) frequencies of insulin and islet-specific glucose-6-phosphatase catalytic subunit-related protein-reactive CD8(+) T-effector clonotypes in mutant mice. Intra-islet insulitis was also significantly suppressed    in lethally irradiated NOD-Lepr(db-5J)/Lt recipients reconstituted with wild-type bone marrow (P < 0.001). In contrast, type 1 diabetes eventually developed when mutant marrow was transplanted into irradiated wild-type recipients.     Mitogen-induced T-cell blastogenesis was significantly suppressed when splenic T-cells from both NOD/Lt and NOD-Lepr(db-5J)/Lt donors were incubated with irradiated mutant peritoneal exudate cells (P < 0.005). In conclusion, metabolic    disturbances elicited by a type 2 diabetes syndrome (insulin and/or leptin resistance, but not hypercorticism) appear to suppress type 1 diabetes development in NOD-Lepr(db-5J)/Lt by inhibiting activation of T-effector cells.</p>

	]]>
</description>

<author>C H. Lee et al.</author>


</item>


<item>
<title>TLR agonists abrogate costimulation blockade-induced prolongation of skin allografts.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1269</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1269</guid>
<pubDate>Tue, 08 May 2012 21:44:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Costimulation blockade protocols are effective in prolonging allograft survival in animal models and are entering clinical trials, but how environmental perturbants affect graft survival remains largely unstudied.  We used a    costimulation blockade protocol consisting of a donor-specific transfusion and anti-CD154 mAb to address this question. We observed that lymphocytic choriomeningitis virus infection at the time of donor-specific transfusion and anti-CD154 mAb    shortens allograft survival. Lymphocytic choriomeningitis virus 1) activates innate immunity, 2) induces allo-cross-reactive T cells, and 3) generates virus-specific responses, all of which may adversely affect allograft survival. To investigate    the role of innate immunity, mice given costimulation blockade and skin allografts were coinjected with TLR2 (Pam3Cys), TLR3 (polyinosinic:polycytidylic acid), TLR4 (LPS), or TLR9 (CpG) agonists.  Costimulation blockade prolonged skin allograft    survival that was shortened after coinjection by TLR agonists. To investigate underlying mechanisms, we used "synchimeric" mice which circulate trace populations of anti-H2b transgenic alloreactive CD8+ T cells. In synchimeric mice treated with    costimulation blockade, coadministration of all four TLR agonists prevented deletion of alloreactive CD8+ T cells and shortened skin allograft survival. These alloreactive CD8+ T cells 1) expressed the proliferation marker Ki-67, 2) up-regulated    CD44, and 3) failed to undergo apoptosis. B6.TNFR2-/- and B6.IL-12R-/- mice treated with costimulation blockade plus LPS also exhibited short skin allograft survival whereas similarly treated B6.CD8alpha-/- and TLR4-/- mice exhibited prolonged    allograft survival. We conclude that TLR signaling abrogates the effects of costimulation blockade by preventing alloreactive CD8+ T cell apoptosis through a mechanism not dependent on TNFR2 or IL-12R signaling.</p>

	]]>
</description>

<author>T B. Thornley et al.</author>


</item>


<item>
<title>Increased susceptibility to UV-induced skin carcinogenesis in polymerase eta-deficient mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1268</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1268</guid>
<pubDate>Tue, 08 May 2012 21:44:44 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Q Lin et al.</author>


</item>


<item>
<title>Quantitative Trait Loci That Determine BMD in C57BL/6J and 129S1/SvImJ Inbred Mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1267</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1267</guid>
<pubDate>Tue, 08 May 2012 21:44:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>BMD is highly heritable; however, little is known about the genes. To identify loci controlling BMD, we conducted a QTL analysis in a (B6 x 129) F(2) population of mice. We report on additional QTLs and also narrow one QTL by    combining the data from multiple crosses and through haplotype analysis. INTRODUCTION: Previous studies have identified quantitative trait loci (QTL) that determine BMD in mice; however, identification of genes underlying QTLs is impeded by the    large size of QTL regions.  MATERIALS AND METHODS: To identify loci controlling BMD, we performed a QTL analysis of 291 (B6 x 129) F(2) females. Total body and vertebral areal BMD (aBMD) were determined by peripheral DXA when mice were 20 weeks    old and had consumed a high-fat diet for 14 weeks. RESULTS AND CONCLUSIONS: Two QTLs were common for both total body and vertebral aBMD: Bmd20 on chromosome (Chr) 6 (total aBMD; peak cM 26, logarithm of odds [LOD] 3.8, and vertebral aBMD; cM 32,    LOD 3.6) and Bmd22 on Chr 1 (total aBMD; cM 104, LOD 2.5, and vertebral aBMD; cM 98, LOD 2.6). A QTL on Chr 10 (Bmd21, cM 68, LOD 3.0) affected total body aBMD and a QTL on Chr 7 (Bmd9, cM 44, LOD 2.7) affected vertebral aBMD. A pairwise    genome-wide search did not reveal significant gene-gene interactions. Collectively, the QTLs accounted for 21.6% of total aBMD and 17.3% of vertebral aBMD of the F(2) population variances. Bmd9 was previously identified in a cross between    C57BL/6J and C3H/HeJ mice, and we narrowed this QTL from 34 to 22 cM by combining the data from these crosses. By examining the Bmd9 region for conservation of ancestral alleles among the low allele strains (129S1/SvImJ and C3H/HeJ) that differed    from the high allele strain (C57BL/6J), we further narrowed the region to approximately 9.9 cM, where the low allele strains share a common haplotype. Identifying the genes for these QTLs will enhance our understanding of skeletal    biology.</p>

	]]>
</description>

<author>N Ishimori et al.</author>


</item>


<item>
<title>Comparative genomics of asthma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1266</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1266</guid>
<pubDate>Tue, 08 May 2012 21:44:23 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>I M. Stylianou et al.</author>


</item>


<item>
<title>The mouse tumour biology database: an online resource for mouse models of human cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1265</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1265</guid>
<pubDate>Tue, 08 May 2012 21:44:13 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Bult et al.</author>


</item>


<item>
<title>Using ontology visualization to coordinate cross-species functional annotation for human disease genes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1264</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1264</guid>
<pubDate>Tue, 08 May 2012 21:44:03 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M E. Dolan et al.</author>


</item>


<item>
<title>Pooling and PCR as a method to combat low frequency gene targeting in mouse embryonic stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1263</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1263</guid>
<pubDate>Tue, 08 May 2012 21:43:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>A C. Brown et al.</author>


</item>


<item>
<title>T-cell co-stimulators as anti-inflammatory targets for atherosclerotic disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1262</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1262</guid>
<pubDate>Tue, 08 May 2012 21:43:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>X Wang</author>


</item>


<item>
<title>Common diseases found in inbred strains of laboratory mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1261</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1261</guid>
<pubDate>Tue, 08 May 2012 21:43:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Sundberg JP, Ichiki T</author>


</item>


<item>
<title>Phenotyping postpartum mutant laboratorymice and determining their value for human diseases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1260</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1260</guid>
<pubDate>Tue, 08 May 2012 21:43:12 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Sundberg JP, Ichiki T</author>


</item>


<item>
<title>Professional use of mutant laboratory mice in research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1259</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1259</guid>
<pubDate>Tue, 08 May 2012 21:43:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Sundberg JP, Bult CJ</author>


</item>


<item>
<title>Controlling the differentiation of mouse ES cells in vitro.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1258</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1258</guid>
<pubDate>Tue, 08 May 2012 21:42:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Wiles MV, Proetzel G</author>


</item>


<item>
<title>Microbiological monitoring of laboratory mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1257</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1257</guid>
<pubDate>Tue, 08 May 2012 21:42:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Fahey JR</author>


</item>


<item>
<title>Biological methods for archiving and maintaining mutant laboratory mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1256</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1256</guid>
<pubDate>Tue, 08 May 2012 21:42:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Fray MD, Glenister PH, Rockwood S, Kaneko T, Nakagata N</author>


</item>


<item>
<title>Computational pathology: challenges in the informatics of phenotype description in mutant mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1255</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1255</guid>
<pubDate>Tue, 08 May 2012 21:42:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Schofield PN, Bard JBL, Rozell B, Sundberg JP</author>


</item>


<item>
<title>Mouse genome informatics: database access to integrated phenotype data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1254</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1254</guid>
<pubDate>Tue, 08 May 2012 21:41:55 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>A W, Ringwald M, Sundberg JP, Bult CJ, Eppig JT Goldsmith C</author>


</item>


<item>
<title>Managing success: mutant mouse repositories.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1253</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1253</guid>
<pubDate>Tue, 08 May 2012 21:41:44 PDT</pubDate>
<description>
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</description>

<author>Rockwood SF, Fray MD, Nakagata N</author>


</item>


<item>
<title>Sharing research tools: the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1252</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1252</guid>
<pubDate>Tue, 08 May 2012 21:41:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Einhorn D</author>


</item>


<item>
<title>Genetically engineered mice: past, present and future</title>
<link>http://mouseion.jax.org/stfb2000_2009/1251</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1251</guid>
<pubDate>Tue, 08 May 2012 21:41:18 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sundberg JP, Ichiki T, Ward JM, Rozell B</author>


</item>


<item>
<title>Special issue: mouse models for hearing research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1250</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1250</guid>
<pubDate>Tue, 08 May 2012 21:41:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K R. Johnson</author>


</item>


<item>
<title>Genetically Engineered Mice Handbook</title>
<link>http://mouseion.jax.org/stfb2000_2009/1249</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1249</guid>
<pubDate>Tue, 08 May 2012 21:40:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>


</item>


<item>
<title>Derivation of genetic interaction networks from quantitative phenotype data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1248</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1248</guid>
<pubDate>Tue, 08 May 2012 21:40:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have generalized the derivation of genetic-interaction networks from quantitative phenotype data. Familiar and unfamiliar modes of genetic interaction were identified and defined. A network was derived from agar-invasion    phenotypes of mutant yeast. Mutations showed specific modes of genetic interaction with specific biological processes. Mutations formed cliques of significant mutual information in their large-scale patterns of genetic interaction. These local    and global interaction patterns reflect the effects of gene perturbations on biological processes and pathways.</p>

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</description>

<author>B L. Drees et al.</author>


</item>


<item>
<title>Inferring network interactions within a cell.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1247</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1247</guid>
<pubDate>Tue, 08 May 2012 21:40:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>The continuing growth in high-throughput data acquisition has led to a proliferation of network models to represent and analyse biological systems.  These networks involve distinct interaction types detected by a combination of    methods, ranging from directly observed physical interactions based in biochemistry to interactions inferred from phenotype measurements, genomic expression and comparative genomics. The discovery of interactions increasingly requires a blend of    experimental and computational methods. Considering yeast as a model system, recent analytical methods are reviewed here and specific aims are proposed to improve network interaction inference and facilitate predictive biological    modelling.</p>

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</description>

<author>G W. Carter</author>


</item>


<item>
<title>Gain modulation by serotonin in pyramidal neurones of the rat prefrontal cortex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1246</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1246</guid>
<pubDate>Tue, 08 May 2012 21:40:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Serotonin (5-HT) is widely implicated in brain functions and diseases. The vertebrate brain is extensively innervated by 5-HT fibres originating from the brain stem, and 5-HT axon terminals interact with other neurones in complex    ways.  The cellular mechanisms underlying 5-HT function in the brain are not well understood. The present study examined the effect of 5-HT on the responsiveness of neurones in the neocortex. Using patch-clamp recording in acute slices, we showed    that 5-HT substantially increased the slope (gain) of the firing rate-current curve in layer 5 pyramidal neurones of the rat prefrontal cortex.  The effect of 5-HT on gain is confined to the range of firing rate (0-10 Hz) that is known to be    behaviourally relevant. 5-HT also changed current threshold for spike train generation, but this effect was inconsistent, and was independent of the effect on gain. The gain modulation by 5-HT was mediated by 5-HT2 receptors, and involved    postsynaptic mechanisms. 5-HT2-mediated gain increase could not be attributed to changes in the membrane potential, the input resistance or the properties of action potentials, but was associated with a reduction of the afterhyperpolarization and    an induction of the slow afterdepolarization. Blocking Ca2+ entry with Cd2+ increased the gain by itself and blocked 5-HT2- mediated gain increase. Buffering [Ca2+](i) with 25 mM EGTA also substantially reduced 5-HT2- mediated gain increase.    Noradrenaline, which blocked the afterhyperpolarization, also induced a moderate increase in gain. Together, our results suggest that 5-HT may regulate the dynamics of cortical circuits through multiplicative scaling.</p>

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</description>

<author>Z W. Zhang et al.</author>


</item>


<item>
<title>Cholinergic modulation of vibrissal receptive fields in trigeminal nuclei.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1245</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1245</guid>
<pubDate>Tue, 08 May 2012 21:39:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>In sensory systems, it is usually considered that mesopontine cholinergic neurons exert their modulatory action in the thalamus by enhancing the relay of sensory messages during states of neural network desynchronization. Here, we    report a projection heretofore unknown of these cholinergic cells to the interpolar division of the brainstem trigeminal complex in rats. After FluoroGold injection in the interpolar nucleus, a number of retrogradely labeled cells were found    bilaterally in the pedunculopontine tegmental nucleus, and immunostaining revealed that the vast majority of these cells were also positive for choline acetyltransferase. Immunostaining for the acetylcholine vesicular transporter confirmed the    presence of cholinergic terminals in the interpolar nucleus, where electron microscopy showed that they make symmetric and asymmetric synaptic contacts with dendrites and axon terminals. In agreement with these anatomical data, recordings in    slices showed that the cholinergic agonist carbachol depolarizes large-sized interpolaris cells and increases their excitability.  Local application of carbachol in vivo enhances responses to adjacent whiskers, whereas systemic administration of    the cholinergic antagonist scopolamine produces an opposite effect. Together, these results show that mesopontine cholinergic neurons exert a direct, effective control over receptive field size at the very first relay stations of the vibrissal    system in rodents. As far as receptive field synthesis in the lemniscal pathway relies on intersubnuclear projections from the spinal complex, it follows that cholinergic modulation of sensory transmission in the interpolar nucleus will have a    direct bearing on the type of messages that is forwarded to the thalamus and cerebral cortex.</p>

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</description>

<author>E Timofeeva et al.</author>


</item>


<item>
<title>Uncovering regulatory pathways that affect hematopoietic stem cell function using &apos;genetical genomics&apos;.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1244</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1244</guid>
<pubDate>Tue, 08 May 2012 21:39:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>We combined large-scale mRNA expression analysis and gene mapping to identify genes and loci that control hematopoietic stem cell (HSC) function. We measured mRNA expression levels in purified HSCs isolated from a panel of densely    genotyped recombinant inbred mouse strains. We mapped quantitative trait loci (QTLs) associated with variation in expression of thousands of transcripts. By comparing the physical transcript position with the location of the controlling QTL, we    identified polymorphic cis-acting stem cell genes. We also identified multiple trans-acting control loci that modify expression of large numbers of genes. These groups of coregulated transcripts identify pathways that specify variation in stem    cells. We illustrate this concept with the identification of candidate genes involved with HSC turnover. We compared expression QTLs in HSCs and brain from the same mice and identified both shared and tissue-specific QTLs.  Our data are    accessible through WebQTL, a web-based interface that allows custom genetic linkage analysis and identification of coregulated transcripts.</p>

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</description>

<author>L Bystrykh et al.</author>


</item>


<item>
<title>Complex trait analysis of gene expression uncovers polygenic and pleiotropic networks that modulate nervous system function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1243</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1243</guid>
<pubDate>Tue, 08 May 2012 21:39:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Patterns of gene expression in the central nervous system are highly variable and heritable. This genetic variation among normal individuals leads to considerable structural, functional and behavioral differences. We devised a    general approach to dissect genetic networks systematically across biological scale, from base pairs to behavior, using a reference population of recombinant inbred strains. We profiled gene expression using Affymetrix oligonucleotide arrays in    the BXD recombinant inbred strains, for which we have extensive SNP and haplotype data.  We integrated a complementary database comprising 25 years of legacy phenotypic data on these strains. Covariance among gene expression and pharmacological    and behavioral traits is often highly significant, corroborates known functional relations and is often generated by common quantitative trait loci. We found that a small number of major-effect quantitative trait loci jointly modulated large sets    of transcripts and classical neural phenotypes in patterns specific to each tissue. We developed new analytic and graph theoretical approaches to study shared genetic modulation of networks of traits using gene sets involved in neural synapse    function as an example. We built these tools into an open web resource called WebQTL that can be used to test a broad array of hypotheses.</p>

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</description>

<author>E J. Chesler et al.</author>


</item>


<item>
<title>P2P-R expression is genetically coregulated with components of the translation machinery and with PUM2, a translational repressor that associates with the P2P-R mRNA.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1242</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1242</guid>
<pubDate>Tue, 08 May 2012 21:39:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>P2P-R is a nuclear protein with potential functional roles in the control of gene expression and mitosis. The P2P-R protein also interacts with the p53 and Rb1 tumor suppressor proteins. To search for additional functional    associations of P2P-R, we employed the WebQTL database that contains the results of cDNA microarray analysis on forebrain, cerebellum, and hematopoietic stem cell (HSC) specimens of multiple BXD recombinant inbred strains of mice. Using WebQTL,    gene products were identified that show genetically based coexpression with P2P-R.  Initial studies identified general groups of mRNAs that share common functional roles and high covariation in expression with P2P-R. These functional groups    involved the regulation of transcription, nucleotide binding, translation control, and ion transport. The findings related to translational mechanisms were further evaluated. In HSCs, expression of P2P-R mRNA demonstrates an impressive expression    correlation with a group of gene products associated with translation; high expression of P2P-R specifically was associated with decreased expression of 29 ribosomal protein mRNAs. In all three tissues that were screened using the WebQTL    database, a strong positive expression covariance between P2P-R and the Pum2 gene product also was observed. PUM2 is a member of the highly conserved Puf family of RNA binding proteins that often function as gene-specific translation regulators.    The ability of Puf proteins to repress translation is mediated by their binding to specific elements located in the 3' untranslated region (UTR) of their target mRNAs. To assess the functional significance of the strong genetic correlation in    expression of P2P-R and PUM2, the 3' UTR of the P2P-R mRNA was analyzed and found to contain one perfect consensus and two near-perfect consensus PUM2 binding sequences. PUM2 pull-down methods combined with reverse transcription and RT-PCR    confirmed that PUM2 does indeed bind P2P-R mRNA. These results suggest that P2P-R expression may be translationally regulated by PUM2 and that P2P-R may modulate translation by influencing ribosomal protein gene expression. This study represents    the first description of a RNA target for mammalian Puf proteins and the first molecular confirmation of information obtained using the WebQTL database.</p>

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</description>

<author>R E. Scott et al.</author>


</item>


<item>
<title>Inferring gene transcriptional modulatory relations: a genetical genomics approach.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1241</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1241</guid>
<pubDate>Tue, 08 May 2012 21:39:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bayesian network modeling is a promising approach to define and evaluate gene expression circuits in diverse tissues and cell types under different experimental conditions. The power and practicality of this approach can be improved    by restricting the number of potential interactions among genes and by defining causal relations before evaluating posterior probabilities for billions of networks. A newly developed genetical genomics method that combines transcriptome profiling    with complex trait analysis now provides strong constraints on network architecture. This method detects those chromosomal intervals responsible for differences in mRNA expression using quantitative trait locus (QTL) mapping. We have developed an    efficient Bayesian approach that exploits the genetical genomics method to focus computational effort on the most plausible gene modulatory networks. We exploit a dense marker map for a genetic reference population (GRP) that consists of 32 BXD    strains of mice made by intercrossing two progenitor strains--C57BL/6J and DBA/2J. These progenitors differ at approximately 1.3 million known single nucleotide polymorphisms (SNPs), all of which can be exploited to estimate the probability that    a gene contains functional polymorphisms that segregate within the GRP. We constructed 66 candidate networks that include all the candidate modulator genes located in the 209 statistically significant trans-acting QTL regions. SNPs that    distinguish between the two progenitor strains were used to further winnow the list of candidate modulators. Bayesian network was then used to identify the genetic modulatory relations that best explain the microarray data.</p>

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</description>

<author>H Li et al.</author>


</item>


<item>
<title>Heritability, correlations and in silico mapping of locomotor behavior and neurochemistry in inbred strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1240</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1240</guid>
<pubDate>Tue, 08 May 2012 21:38:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>The midbrain dopamine system mediates normal and pathologic behaviors related to motor activity, attention, motivation/reward and cognition. These are complex, quantitative traits whose variation among individuals is modulated by    genetic, epigenetic and environmental factors. Conventional genetic methods have identified several genes important to this system, but the majority of factors contributing to the variation remain unknown. To understand these genetic and    environmental factors, we initiated a study measuring 21 behavioral and neurochemical traits in 15 common inbred mouse strains. We report trait data, heritabilities and genetic and non-genetic correlations between pheno-types. In general, the    behavioral traits were more heritable than neurochemical traits, and both genetic and non-genetic correlations within these trait sets were high.  Surprisingly, there were few significant correlations between the behavioral and the individual    neurochemical traits. However, striatal serotonin and one measure of dopamine turnover (DOPAC/DA) were highly correlated with most behavioral measures. The variable accounting for the most variation in behavior was mouse strain and not a specific    neurochemical measure, suggesting that additional genetic factors remain to be determined to account for these behavioral differences. We also report the prospective use of the in silico method of quantitative trait loci (QTL) analysis and    demonstrate difficulties in the use of this method, which failed to detect significant QTLs for the majority of these traits. These data serve as a framework for further studies of correlations between different midbrain dopamine traits and as a    guide for experimental cross designs to identify QTLs and genes that contribute to these traits.</p>

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</description>

<author>T R. Mhyre et al.</author>


</item>


<item>
<title>Correlations between edema and the immediate and prolonged painful consequences of inflammation: therapeutic implications?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1239</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1239</guid>
<pubDate>Tue, 08 May 2012 21:38:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The precise relationship between the degree of pain and the degree of inflammation in the individual remains debated. A quantitative analysis simultaneously applied to the immediate and prolonged painful consequences of inflammation    has not yet been done. Thus, the correlations between edema, nociception and hypersensitivity following an inflammatory insult were assessed in rodents. To better understand the therapeutic value of modifying specific aspects of inflammation, the    effects of an anti-inflammatory drug were compared to the results. Inbred strains of mice and outbred rats received an intraplantar injection of honeybee venom and the between-group and within-group correlations were calculated for spontaneous    nociceptive measures, thermal and mechanical hypersensitivity, and edema and temperature. The effect of indomethacin on the pain and inflammation measures was examined. Edema correlated with spontaneous flinching, licking and lifting of the    injected paw (P< or =0.003), and not with thermal or mechanical hypersensitivity. Indomethacin affected edema and spontaneous nociception dose-dependently, and affected hypersensitivity only at the highest dose tested (P< 0.05). These results    suggest that edema may contribute only to immediate spontaneous nociceptive responses to an inflammatory insult, and not to the more clinically relevant prolonged hypersensitivity. This analysis represents a method for determining which    inflammatory processes are the most promising therapeutic targets against the multiple painful consequences of inflammation.</p>

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</description>

<author>W R. Lariviere et al.</author>


</item>


<item>
<title>Computational, integrative, and comparative methods for the elucidation of genetic coexpression networks.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1238</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1238</guid>
<pubDate>Tue, 08 May 2012 21:38:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gene expression microarray data can be used for the assembly of genetic coexpression network graphs. Using mRNA samples obtained from recombinant inbred Mus musculus strains, it is possible to integrate allelic variation with    molecular and higher-order phenotypes. The depth of quantitative genetic analysis of microarray data can be vastly enhanced utilizing this mouse resource in combination with powerful computational algorithms, platforms, and data repositories. The    resulting network graphs transect many levels of biological scale. This approach is illustrated with the extraction of cliques of putatively co-regulated genes and their annotation using gene ontology analysis and cis-regulatory element    discovery. The causal basis for co-regulation is detected through the use of quantitative trait locus mapping.</p>

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</description>

<author>N E. Baldwin et al.</author>


</item>


<item>
<title>Identification of quantitative trait loci for susceptibility to mouse adenovirus type 1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1237</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1237</guid>
<pubDate>Tue, 08 May 2012 21:38:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adult SJL/J mice are highly susceptible to mouse adenovirus type 1 (MAV-1) infections, whereas other inbred strains, including BALB/cJ, are resistant (K. R. Spindler, L. Fang, M. L. Moore, C. C. Brown, G. N. Hirsch, and A. K. Kajon,    J. Virol. 75:12039-12046, 2001). Using congenic mouse strains, we showed that the H-2(s) haplotype of SJL/J mice is not associated with susceptibility to MAV-1.  Susceptibility of MAV-1-infected (BALB/cJ x SJL/J)F(1) mice was intermediate between    that of SJL/J mice and that of BALB/cJ mice, indicating that susceptibility is a genetically controlled quantitative trait. We mapped genetic loci involved in mouse susceptibility to MAV-1 by analysis of 192 backcross progeny in a genome scan    with 65 simple sequence length polymorphic markers. A major quantitative trait locus (QTL) was detected on chromosome 15 (Chr 15) with a highly significant logarithm of odds score of 21. The locus on Chr 15 alone accounts for 40% of the total    trait variance between susceptible and resistant strains. QTL modeling of the data indicated that there are a number of other QTLs with small effects that together with the major QTL on Chr 15 account for 54% of the trait variance. Identification    of the major QTL is the first step in characterizing host genes involved in susceptibility to MAV-1.</p>

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</description>

<author>A R. Welton et al.</author>


</item>


<item>
<title>Variable sensitivity to noxious heat is mediated by differential expression of the CGRP gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1236</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1236</guid>
<pubDate>Tue, 08 May 2012 21:37:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Heat sensitivity shows considerable functional variability in humans and laboratory animals, and is fundamental to inflammatory and possibly neuropathic pain. In the mouse, at least, much of this variability is genetic because    inbred strains differ robustly in their behavioral sensitivity to noxious heat. These strain differences are shown here to reflect differential responsiveness of primary afferent thermal nociceptors to heat stimuli. We further present convergent    behavioral and electrophysiological evidence that the variable responses to noxious heat are due to strain-dependence of CGRP expression and sensitivity. Strain differences in behavioral response to noxious heat could be abolished by peripheral    injection of CGRP, blockade of cutaneous and spinal CGRP receptors, or long-term inactivation of CGRP with a CGRP-binding Spiegelmer.  Linkage mapping supports the contention that the genetic variant determining variable heat pain sensitivity    across mouse strains affects the expression of the Calca gene that codes for CGRPalpha.</p>

	]]>
</description>

<author>J S. Mogil et al.</author>


</item>


<item>
<title>Complex genetics of interactions of alcohol and CNS function and behavior.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1235</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1235</guid>
<pubDate>Tue, 08 May 2012 21:37:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>This work summarizes the proceedings of a symposium at the 2004 RSA Meeting in Vancouver, Canada. The organizers were R. W. Williams and D. B. Matthews; the Chair was M. F. Miles. The presentations were (1) WebQTL: A resource for    analysis of gene expression variation and the genetic dissection of alcohol related phenotypes, by E. J. Chesler, (2) The marriage of microarray and qtl analyses: what's to gain, by J. K. Belknap, (3) Use of WebQTL to identify QTLs associated    with footshock stress and ethanol related behaviors, by D. B. Matthews, (4) A high throughput strategy for the detection of quantitative trait genes, by R. J. Hitzemann, and (5) The use of gene arrays in conjunction with transgenic and selected    animals to understand anxiety in alcoholism, by. B. Tabakoff.</p>

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</description>

<author>D B. Matthews et al.</author>


</item>


<item>
<title>Genetics of body weight in the LXS recombinant inbred mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1234</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1234</guid>
<pubDate>Tue, 08 May 2012 21:37:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>This is the first phenotypic analysis of 75 new recombinant inbred (RI) strains derived from ILS and ISS progenitors. We analyzed body weight in two independent cohorts of female mice at various ages and in males at 60 days. Body    weight is a complex trait which has been mapped in numerous crosses in rodents. The LXS RI strains displayed a large range of weights, transgressing those of the inbred progenitors, supporting the utility of this large panel for mapping traits    not selected in the progenitors. Numerous QTLs for body weight mapped in single- and multilocus scans. We assessed replication between these and previously reported QTLs based on overlapping confidence intervals of published QTLs for body weight    at 60 days and used meta-analyses to determine combined p values for three QTL regions located on Chromosomes 4, 5, and 11. Strain distribution patterns of microsatellite marker genotypes, weight, and other phenotypes are available on WebQTL    (http://www.webqtl.org/search.html ) and allow genetic mapping of any heritable quantitative phenotype measured in these strains. We report one such analysis, correlating brain and body weights. Large reference panels of RI strains, such as the    LXS, are invaluable for identifying genetic correlations, GXE (Gene X Environment) interactions, and replicating previously identified QTLs.</p>

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</description>

<author>B Bennett et al.</author>


</item>


<item>
<title>Genetic networks controlling retinal injury.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1233</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1233</guid>
<pubDate>Tue, 08 May 2012 21:37:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: The present study defines genomic loci underlying coordinate changes in gene expression following retinal injury. METHODS: A group of acute phase genes expressed in diverse nervous system tissues was defined by combining    microarray results from injury studies from rat retina, brain, and spinal cord. Genomic loci regulating the brain expression of acute phase genes were identified using a panel of BXD recombinant inbred (RI) mouse strains. Candidate upstream    regulators within a locus were defined using single nucleotide polymorphism databases and promoter motif databases. RESULTS: The acute phase response of rat retina, brain, and spinal cord was dominated by transcription factors. Three genomic loci    control transcript expression of acute phase genes in brains of BXD RI mouse strains. One locus was identified on chromosome 12 and was highly correlated with the expression of classic acute phase genes. Within the locus we identified the    inhibitor of DNA binding 2 (Id2) as a candidate upstream regulator. Id2 was upregulated as an acute phase transcript in injury models of rat retina, brain, and spinal cord. CONCLUSIONS: We defined a group of transcriptional changes associated    with the retinal acute injury response. Using genetic linkage analysis of natural transcript variation, we identified regulatory loci and candidate regulators that control transcript levels of acute phase genes.</p>

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</description>

<author>Chona F. Vazquez et al.</author>


</item>


<item>
<title>Tools and applications for large-scale display walls.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1232</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1232</guid>
<pubDate>Tue, 08 May 2012 21:37:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>G Wallace et al.</author>


</item>


<item>
<title>Visualization methods for statistical analysis of microarray clusters.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1231</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1231</guid>
<pubDate>Tue, 08 May 2012 21:36:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The most common method of identifying groups of functionally related genes in microarray data is to apply a clustering algorithm. However, it is impossible to determine which clustering algorithm is most appropriate to    apply, and it is difficult to verify the results of any algorithm due to the lack of a gold-standard. Appropriate data visualization tools can aid this analysis process, but existing visualization methods do not specifically address this issue.    RESULTS: We present several visualization techniques that incorporate meaningful statistics that are noise-robust for the purpose of analyzing the results of clustering algorithms on microarray data. This includes a rank-based visualization    method that is more robust to noise, a difference display method to aid assessments of cluster quality and detection of outliers, and a projection of high dimensional data into a three dimensional space in order to examine relationships between    clusters. Our methods are interactive and are dynamically linked together for comprehensive analysis. Further, our approach applies to both protein and gene expression microarrays, and our architecture is scalable for use on both desktop/laptop    screens and large-scale display devices. This methodology is implemented in GeneVAnD (Genomic Visual ANalysis of Datasets) and is available at http://function.princeton.edu/GeneVAnD. CONCLUSION: Incorporating relevant statistical information into    data visualizations is key for analysis of large biological datasets, particularly because of high levels of noise and the lack of a gold-standard for comparisons. We developed several new visualization techniques and demonstrated their    effectiveness for evaluating cluster quality and relationships between clusters.</p>

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</description>

<author>M A. Hibbs et al.</author>


</item>


<item>
<title>Discovery of biological networks from diverse functional genomic data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1230</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1230</guid>
<pubDate>Tue, 08 May 2012 21:36:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have developed a general probabilistic system for query-based discovery of pathway-specific networks through integration of diverse genome-wide data. This framework was validated by accurately recovering known networks for 31    biological processes in Saccharomyces cerevisiae and experimentally verifying predictions for the process of chromosomal segregation. Our system, bioPIXIE, a public, comprehensive system for integration, analysis, and visualization of biological    network predictions for S. cerevisiae, is freely accessible over the worldwide web.</p>

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</description>

<author>C L. Myers et al.</author>


</item>


<item>
<title>HSP90: a rising star on the horizon of anticancer targets.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1229</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1229</guid>
<pubDate>Tue, 08 May 2012 21:36:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Over the past decade, heat-shock protein (HSP)90 has begun to draw increasing attention as a novel anticancer target with unique features. As a molecular chaperone, HSP90 promotes the maturation and maintains the stability of a    large number of conformationally labile client proteins, most of which are involved in biologic processes that are often deranged within tumor cells, such as signal transduction, cell-cycle progression and apoptosis. As a result, and in contrast    to other molecular targeted therapeutics, inhibitors of HSP90 achieve their promising anticancer activity through simultaneous disruption of many oncogenic substrates within cancer cells. This review provides a brief summary of HSP90 biology and    its association with cancer. It describes the discovery and development of HSP90 inhibitors as anticancer agents and their current status in the clinic. Finally, it closes with a discussion of the unique challenges confronting the further    development of these agents and their prospects for the future.</p>

	]]>
</description>

<author>C Dai et al.</author>


</item>


<item>
<title>The characteristics of astrocytomas and oligodendrogliomas are caused by two distinct and interchangeable signaling formats.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1228</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1228</guid>
<pubDate>Tue, 08 May 2012 21:36:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chronic platelet-derived growth factor (PDGF) signaling in glial progenitors leads to the formation of oligodendrogliomas in mice, whereas chronic combined Ras and Akt signaling leads to astrocytomas. Different histologies of these    tumors imply that the pathways activated by these two oncogenic stimulations are different, and that the apparent lineage of the tumor cells may result from specific signaling activity. Therefore, we have investigated the signaling effects of    PDGF in culture and in gliomas in vivo. In culture, PDGF transiently activates ERK1/2 and Akt, and subsequently elevates p21 and PCNA expression similar to chronic PDGF autocrine signaling in cultured astrocytes and PDGF-induced    oligodendrogliomas in vivo. Culture experiments show that autocrine PDGF stimulation, and combined active Ras and Akt generate signaling patterns that are in some ways mutually exclusive. Furthermore, forced Akt activity in the context of chronic    PDGF stimulation results in cells with an astrocytic differentiation pattern both in culture and in vivo. These data imply that these two interconvertible signaling motifs are distinct in mice and lead to gliomas resembling the two major glioma    histologies found in humans. The ability of signaling activity to convert tumor cells from one lineage to another presents a mechanism for the development of tumors apparently comprised of cells from multiple lineages.</p>

	]]>
</description>

<author>C Dai et al.</author>


</item>


<item>
<title>Mouse oocytes control metabolic co-operativity between oocytes and cumulus cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1227</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1227</guid>
<pubDate>Tue, 08 May 2012 21:35:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J J. Eppig</author>


</item>


<item>
<title>Diminished gallbladder motility in rotund leptin-resistant obese mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1226</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1226</guid>
<pubDate>Tue, 08 May 2012 21:35:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Background. Obesity is a risk factor for cholesterol gallstone formation, but the pathogenesis of this phenomenon remains unclear. Most human obesity is associated with diabetes and leptin-resistance. Previous studies from this    laboratory have demonstrated that diabetic leptin-resistant (Lep(db)) obese mice have low biliary cholesterol saturation indices, enlarged gallbladders and diminished gallbladder response to neurotransmitters. Recently, a novel leptin-resistant    mouse strain Lepr(db-rtnd) (Rotund) has been discovered. Rotund mice are also obese, diabetic, and have an abnormal leptin receptor. Therefore, we tested the hypothesis that leptin-resistant obese Rotund mice would have large gallbladders and    reduced biliary motility.Methods. Eight-week-old control (C57BL/6J, N=12) and Rotund leptin-resistant (Lepr(db-rnd), N=9) mice were fed a non- lithogenic diet for four weeks. Animals were fasted and underwent cholecystectomy. Gallbladder volumes    were recorded, and contractile responses (N/cm(2)) to acetylcholine (10(-5) M), Neuropeptide Y (10(-8,-7,-6) M), and cholecystokinin (10(-10,-9,-8,-7) M) were measured. Results were analyzed using the Mann-Whitney Rank Sum Test.Results. Compared    to control mice, Rotund mice had larger body weights, higher serum glucose levels, and greater gallbladder volumes (p<0.05).  Rotund gallbladders had less contractility (p<0.05)) to acetylcholine and cholecystokinin than control mice. Responses    to Neuropeptide Y were also less, but not statistically significant, in the Rotund mice.Conclusions. These data suggest that leptin-resistant Rotund mice have (1) enlarged gallbladders with (2) diminished contractility compared to lean control    mice. Therefore, this study confirms that leptin-resistance is associated with abnormal biliary motility and may lead to gallstone formation in leptin-resistant obesity.</p>

	]]>
</description>

<author>S J. Graewin et al.</author>


</item>


<item>
<title>Glaucoma: thinking in new ways-a role for autonomous axonal self-destruction and other compartmentalised processes?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1225</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1225</guid>
<pubDate>Tue, 08 May 2012 21:35:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Glaucoma is a common neurodegenerative disease that affects retinal ganglion cells (RGCs). Substantial effort is being expended to determine how RGCs die in glaucoma. As in other neurodegenerative diseases, the majority of effort    focuses on characterising apoptotic self-destruct pathways. However, apoptosis is not the only self-destruct mechanism that may be activated in neurons. It is now known that neurons have distinct classes of self-destruct programme that are    spatially compartmentalised. In addition to the well-described intracellular suicide machinery in the neuronal soma, responsible for apoptosis, there is another, molecularly distinct, self-destruct programme localised in the axon. Evidence also    supports the existence of compartmentalised degeneration programmes in synapses and dendrites. RGCs are no exception to this. Recent data, from in vitro studies and from an inherited mouse model of glaucoma, suggest that molecularly distinct    degenerative pathways underlie the destruction of RGC somata and RGC axons. In various neurodegenerative diseases, axons, dendrites and synapses often degenerate well before the cells die, and there is increasing evidence that this is important    for the production of clinical symptoms and signs. We hypothesise that such compartmentalised and autonomous programmes are of critical importance in the pathophysiology of glaucoma, and we suggest that studies of these processes are essential    for a complete understanding of this complex disease.</p>

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</description>

<author>A V. Whitmore et al.</author>


</item>


<item>
<title>The transcriptional landscape of the mammalian genome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1224</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1224</guid>
<pubDate>Tue, 08 May 2012 21:35:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study describes comprehensive polling of transcription start and termination sites and analysis of previously unidentified full-length complementary DNAs derived from the mouse genome. We identify the 5' and 3' boundaries of    181,047 transcripts with extensive variation in transcripts arising from alternative promoter usage, splicing, and polyadenylation. There are 16,247 new mouse protein-coding transcripts, including 5154 encoding previously unidentified proteins.    Genomic mapping of the transcriptome reveals transcriptional forests, with overlapping transcription on both strands, separated by deserts in which few transcripts are observed. The data provide a comprehensive platform for the comparative    analysis of mammalian transcriptional regulation in differentiation and development.</p>

	]]>
</description>


</item>


<item>
<title>The Tetratricopeptide repeat domain 7 gene is mutated in flaky skin mice: a model for psoriasis, autoimmunity, and anemia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1223</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1223</guid>
<pubDate>Tue, 08 May 2012 21:35:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The flaky skin (fsn) mutation in mice causes pleiotropic abnormalities including psoriasiform dermatitis, anemia, hyper-IgE, and anti-dsDNA autoantibodies resembling those detected in systemic lupus erythematosus. The fsn mutation    was mapped to an interval of 3.9 kb on chromosome 17 between D17Mit130 and D17Mit162.  Resequencing of known and predicted exons and regulatory sequences from this region in fsn/fsn and wild-type mice indicated that the mutation is due to the    insertion of an endogenous retrovirus (early transposon class) into intron 14 of the Tetratricopeptide repeat (TPR) domain 7 (Ttc7) gene. The insertion leads to reduced levels of wild-type Ttc7 transcripts in fsn mice and the insertion of an    additional exon derived from the retrovirus into the majority of Ttc7 mRNAs. This disrupts one of the TPRs within TTC7 and may affect its interaction with an as-yet unidentified protein partner. The Ttc7 is expressed in multiple types of tissue    including skin, kidney, spleen, and thymus, but is most abundant in germinal center B cells and hematopoietic stem cells, suggesting an important role in the development of immune system cells. Its role in immunologic and hematologic disorders    should be further investigated.</p>

	]]>
</description>

<author>C Helms et al.</author>


</item>


<item>
<title>Disruption of murine Tenr results in teratospermia and male infertility.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1222</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1222</guid>
<pubDate>Tue, 08 May 2012 21:34:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gametes rely heavily on posttranscriptional control for their differentiation. Translational control, alternative splicing, and alternative processing of the 3' end of mRNAs are all common during spermatogenesis. Tenr, which encodes    a highly conserved 72-kDa protein, is expressed solely in germ cells of the testis from the mid-pachytene stage until the elongating spermatid stage. TENR contains a double-stranded RNA binding domain, is localized to the nucleus, and is    phylogenetically related to a family of adenosine deaminases involved in RNA editing. We show here that targeted mutation of the Tenr gene causes male sterility.  Tenr mutant males have a reduced sperm count, and Tenr-/- sperm show a decrease in    motility and an increase in malformed heads. Despite their sterility, some epididymal sperm from Tenr mutants have normal morphology.  The ability of Tenr mutant sperm to fertilize zona pellucida-free oocytes and to bind to, but not fertilize,    zona pellucida-intact oocytes suggests that the normal-appearing sperm are not able to penetrate the zona pellucida. These data suggest that TENR plays an essential function in spermatid morphogenesis.</p>

	]]>
</description>

<author>C M. Connolly et al.</author>


</item>


<item>
<title>Differential regulation of KiSS-1 mRNA expression by sex steroids in the brain of the male mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1221</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1221</guid>
<pubDate>Tue, 08 May 2012 21:34:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Kisspeptins are products of the Kiss1 gene, which bind to GPR54, a G protein-coupled receptor. Kisspeptins and GPR54 have been implicated in the neuroendocrine regulation of GnRH secretion. To test the hypothesis that testosterone    regulates Kiss1 gene expression, we compared the expression of KiSS-1 mRNA among groups of intact, castrated, and castrated/testosterone (T)-treated male mice. In the arcuate nucleus (Arc), castration resulted in a significant increase in KiSS-1    mRNA, which was completely reversed with T replacement, whereas in the anteroventral periventricular nucleus, the results were the opposite, i.e. castration decreased and T increased KiSS-1 mRNA expression. In the Arc, the effects of T on KiSS-1    mRNA were completely mimicked by estrogen but only partially mimicked by dihydrotestosterone, a nonaromatizable androgen, suggesting that both estrogen receptor (ER) and androgen receptor (AR) play a role in T-mediated regulation of KiSS-1.    Studies of the effects of T on KiSS-1 expression in mice with either a deletion of the ERalpha or a hypomorphic allele to the AR revealed that the effects of T are mediated by both ERalpha and AR pathways, which was confirmed by the presence of    either ERalpha or AR coexpression in most KiSS-1 neurons in the Arc. These observations suggest that KiSS-1 neurons in the Arc, whose transcriptional activity is inhibited by T, are targets for the negative feedback regulation of GnRH secretion,    whereas KiSS-1 neurons in the anteroventral periventricular nucleus, whose activity is stimulated by T, may mediate other T-dependent processes.</p>

	]]>
</description>

<author>J T. Smith et al.</author>


</item>


<item>
<title>Androgens regulate the permeability of the blood-testis barrier.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1220</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1220</guid>
<pubDate>Tue, 08 May 2012 21:34:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Within the mammalian testis, specialized tight junctions between somatic Sertoli cells create basal and apical polarity within the cells, restrict movement of molecules between cells, and separate the seminiferous epithelium into    basal and adluminal compartments. These tight junctions form the basis of the blood-testis barrier, a structure whose function and dynamic regulation is poorly understood. In this study, we used microarray gene expression profiling to identify    genes with altered transcript levels in a mouse model for conditional androgen insensitivity. We show that testosterone, acting through its receptor expressed in Sertoli cells, regulates the expression of claudin 3, which encodes a transient    component of newly formed tight junctions. Sertoli cell-specific ablation of androgen receptor results in increased permeability of the blood-testis barrier to biotin, suggesting claudin 3 regulates the movement of small molecules across the    Sertoli cell tight junctions. These results suggest that androgen action in Sertoli cells regulates germ cell differentiation, in part by controlling the microenvironment of the seminiferous epithelium. Our studies also indicate that hormonal    strategies for male contraception may interfere with the blood-testis barrier.</p>

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</description>

<author>J Meng et al.</author>


</item>


<item>
<title>The Pim kinases control rapamycin-resistant T cell survival and activation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1219</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1219</guid>
<pubDate>Tue, 08 May 2012 21:34:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although Pim-1 or Pim-2 can contribute to lymphoid transformation when overexpressed, the physiologic role of these kinases in the immune response is uncertain. We now report that T cells from Pim-1(-/-)Pim-2(-/-) animals display an    unexpected sensitivity to the immunosuppressant rapamycin. Cytokine-induced Pim-1 and Pim-2 promote the rapamycin-resistant survival of lymphocytes. The endogenous function of the Pim kinases was not restricted to the regulation of cell survival.     Like the rapamycin target TOR, the Pim kinases also contribute to the regulation of lymphocyte growth and proliferation. Although rapamycin has a minimal effect on wild-type T cell expansion in vitro and in vivo, it completely suppresses the    response of Pim-1(-/-)Pim-2(-/-) cells. Thus, endogenous levels of the Pim kinases are required for T cells to mount an immune response in the presence of rapamycin. The existence of a rapamycin-insensitive pathway that regulates T cell growth    and survival has important implications for understanding how rapamycin functions as an immunomodulatory drug and for the development of complementary immunotherapeutics.</p>

	]]>
</description>

<author>C J. Fox et al.</author>


</item>


<item>
<title>Pim and Akt oncogenes are independent regulators of hematopoietic cell growth and survival.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1218</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1218</guid>
<pubDate>Tue, 08 May 2012 21:33:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Akt kinases promote hematopoietic cell growth and accumulation through phosphorylation of apoptotic effectors and stimulation of mTOR-dependent translation. In Akt-transformed leukemic cells, tumor growth can be inhibited by the    mTOR inhibitor rapamycin, and clinical trials of rapamycin analogs for the treatment of leukemia are under way.  Surprisingly, nontransformed hematopoietic cells can grow and proliferate in the presence of rapamycin. Here, we show that Pim-2 is    required to confer rapamycin resistance. Primary hematopoietic cells from Pim-2- and Pim-1/Pim-2-deficient animals failed to accumulate and underwent apoptosis in the presence of rapamycin. Although animals deficient in Akt-1 or Pim-1/Pim-2 are    viable, few animals with a compound deletion survived development, and those that were born had severe anemia. Primary hematopoietic cells from Akt-1/Pim-1/Pim-2-deficient animals displayed marked impairments in cell growth and survival.    Conversely, ectopic expression of either Pim-2 or Akt-1 induced increased cell size and apoptotic resistance. However, though the effects of ectopic Akt-1 were reversed by rapamycin or a nonphosphorylatable form of 4EBP-1, those of Pim-2 were    not. Coexpression of the transgenes in mice led to additive increases in cell size and survival and predisposed animals to rapid tumor formation. Together, these data indicate that Pim-2 and Akt-1 are critical components of overlapping but    independent pathways, either of which is sufficient to promote the growth and survival of nontransformed hematopoietic cells.</p>

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</description>

<author>P S. Hammerman et al.</author>


</item>


<item>
<title>Mechanical modulation of molecular signals which regulate anabolic and catabolic activity in bone tissue.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1217</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1217</guid>
<pubDate>Tue, 08 May 2012 21:33:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Identifying the molecular mechanisms that regulate bone's adaptive response to alterations in load bearing may potentiate the discovery of interventions to curb osteoporosis. Adult female mice (BALB/cByJ) were subjected to catabolic    (disuse) and anabolic (45 Hz, 0.3g vibration for 10 min/day) signals, and changes in the mRNA levels of thirteen genes were compared to altered indices of bone formation. Age-matched mice served as controls. Following 4 days of disuse,    significant (P = 0.05) decreases in mRNA levels were measured for several genes, including collagen type I (-55%), osteonectin (-44%), osterix (-36%), and MMP-2 (-36%) all of which, after 21 days, had normalized to control levels. In contrast,    expression of several genes in the vibrated group, which failed to show significant changes at 4 days, demonstrated significant increases after 21 days, including inducible nitric oxide synthase (iNOS) (39%, P = 0.07), MMP-2 (54%), and receptor    activator of the nuclear factor kB ligand (RANKL) (32%). Correlations of gene expression patterns across experimental conditions and time points allowed the functional clustering of responsive genes into two distinct groups. Each cluster's    specific regulatory role (formation vs. resorption) was reinforced by the 60% suppression of formation rates caused by disuse, and the 55% increase in formation rates stimulated by mechanical signals (P < 0.05). These data confirm the complexity    of the bone remodeling process, both in terms of the number of genes involved, their interaction and coordination of resorptive and formative activity, and the temporal sensitivity of the processes. More detailed spatial and temporal correlations    between altered mRNA levels and tissue plasticity may further delineate the molecules responsible for the control of bone mass and morphology.</p>

	]]>
</description>

<author>S Judex et al.</author>


</item>


<item>
<title>Spontaneous fractures in the mouse mutant sfx are caused by deletion of the gulonolactone oxidase gene, causing vitamin C deficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1216</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1216</guid>
<pubDate>Tue, 08 May 2012 21:33:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Using a mouse mutant that fractures spontaneously and dies at a very young age, we identified that a deletion of the GULO gene, which is involved in the synthesis of vitamin C, is the cause of impaired osteoblast differentiation,    reduced bone formation, and development of spontaneous fractures. INTRODUCTION: A major public health problem worldwide, osteoporosis is a disease characterized by inadequate bone mass necessary for mechanical support, resulting in bone fracture.    To identify the genetic basis for osteoporotic fractures, we used a mouse model that develops spontaneous fractures (sfx) at a very early age. MATERIALS AND METHODS: Skeletal phenotype of the sfx phenotype was evaluated by DXA using PIXImus    instrumentation and by dynamic histomorphometry. The sfx gene was identified using various molecular genetic approaches, including fine mapping and sequencing of candidate genes, whole genome microarray, and PCR amplification of candidate genes    using cDNA and genomic DNA as templates. Gene expression of selected candidate genes was performed using real-time PCR analysis. Osteoblast differentiation was measured by bone marrow stromal cell nodule assay. RESULTS: Femur and tibial BMD were    reduced by 27% and 36%, respectively, in sfx mice at 5 weeks of age.  Histomorphometric analyses of bones from sfx mice revealed that bone formation rate is reduced by >90% and is caused by impairment of differentiated functions of osteoblasts.    The sfx gene was fine mapped to a 2 MB region containing approximately 30 genes in chromosome 14. By using various molecular genetic approaches, we identified that deletion of the gulonolactone oxidase (GULO) gene, which is involved in the    synthesis of ascorbic acid, is responsible for the sfx phenotype. We established that ascorbic acid deficiency caused by deletion of the GULO gene (38,146-bp region) contributes to fractures and premature death because the sfx phenotype can be    corrected in vivo by treating sfx mice with ascorbic acid and because osteoblasts derived from sfx mice are only able to form mineralized nodules when treated with ascorbic acid. Treatment of bone marrow stromal cells derived from sfx/sfx mice in    vitro with ascorbic acid increased expression levels of type I collagen, alkaline phosphatase, and osteocalcin several-fold. CONCLUSION: The sfx is a mutation of the GULO gene, which leads to ascorbic acid deficiency, impaired osteoblast cell    function, and fractures in affected mice. Based on these and other findings, we propose that ascorbic acid is essential for the maintenance of differentiated functions of osteoblasts and other cell types.</p>

	]]>
</description>

<author>S Mohan et al.</author>


</item>


<item>
<title>High-dose radiation with bone marrow transfer prevents neurodegeneration in an inherited glaucoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1215</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1215</guid>
<pubDate>Tue, 08 May 2012 21:33:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Here, we show that high-dose gamma-irradiation accompanied with syngeneic bone marrow transfer can confer complete protection against glaucoma in a mouse model. Because bone marrow genotype was unaltered by this procedure, it was    not the causative agent. The neuroprotection is robust and highly reproducible. Glaucoma-prone DBA/2J mice received a single treatment at 5-8 weeks of age and were protected from glaucomatous retinal ganglion cell degeneration out to 14 months of    age (oldest assessed). By 12-14 months, retinal ganglion cell degeneration is usually very severe and essentially complete in the majority of untreated DBA/2J mice. To assess reproducibility, three groups of mice were treated at different times,    and the results were essentially the same each time. Considering all experiments, the vast majority of treated mice had no detectable glaucomatous neurodegeneration. A beneficial effect of treatment including high-dose radiation is unprecedented,    and we are not aware of any other neuroprotective effects this substantial. Because of the robust protective effect, this treatment offers another tool for studying mechanisms of neuroprotection.</p>

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</description>

<author>M G. Anderson et al.</author>


</item>


<item>
<title>Human lymphoid and myeloid cell development in NOD/LtSz-scid IL2R gamma null mice engrafted with mobilized human hemopoietic stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1214</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1214</guid>
<pubDate>Tue, 08 May 2012 21:33:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ethical considerations constrain the in vivo study of human hemopoietic stem cells (HSC). To overcome this limitation, small animal models of human HSC engraftment have been used. We report the development and characterization of a    new genetic stock of IL-2R common gamma-chain deficient NOD/LtSz-scid (NOD-scid IL2Rgamma(null)) mice and document their ability to support human mobilized blood HSC engraftment and multilineage differentiation. NOD-scid IL2Rgamma(null) mice are    deficient in mature lymphocytes and NK cells, survive beyond 16 mo of age, and even after sublethal irradiation resist lymphoma development. Engraftment of NOD-scid IL2Rgamma(null) mice with human HSC generate 6-fold higher percentages of human    CD45(+) cells in host bone marrow than with similarly treated NOD-scid mice. These human cells include B cells, NK cells, myeloid cells, plasmacytoid dendritic cells, and HSC. Spleens from engrafted NOD-scid IL2Rgamma(null) mice contain human    Ig(+) B cells and lower numbers of human CD3(+) T cells. Coadministration of human Fc-IL7 fusion protein results in high percentages of human CD4(+)CD8(+) thymocytes as well human CD4(+)CD8(-) and CD4(-)CD8(+) peripheral blood and splenic T    cells. De novo human T cell development in NOD-scid IL2Rgamma(null) mice was validated by 1) high levels of TCR excision circles, 2) complex TCRbeta repertoire diversity, and 3) proliferative responses to PHA and streptococcal superantigen,    streptococcal pyrogenic exotoxin. Thus, NOD-scid IL2Rgamma(null) mice engrafted with human mobilized blood stem cells provide a new in vivo long-lived model of robust multilineage human HSC engraftment.</p>

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</description>

<author>L D. Shultz et al.</author>


</item>


<item>
<title>Targeted disruption of Mig-6 in the mouse genome leads to early onset degenerative joint disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1213</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1213</guid>
<pubDate>Tue, 08 May 2012 21:32:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Degenerative joint disease, also known as osteoarthritis, is the most common joint disorder in human beings. The molecular mechanism underlying this disease is not fully understood. Here, we report that disruption of    mitogen-inducible gene 6 (Mig-6) in mice by homologous recombination leads to early onset degenerative joint disease, which is revealed by simultaneous enlargement and deformity of multiple joints, degradation of articular cartilage, and the    development of bony outgrowths or osteophyte formation within joint space. The osteophyte formation appears to be derived from proliferation of mesenchymal progenitor cells followed by differentiation into chondrocytes. Absence of the Rag2 gene    does not rescue the joint phenotype, excluding a role for the acquired immune system in the development of this disease. Our results provide insight into the mechanism of osteoarthritis by showing that loss of Mig-6 leads to early onset of this    disease, implying that this gene or its pathway is important in normal joint maintenance. Because of the striking similarity of osteoarthritis in humans and mice, the Mig-6 mutant mouse should provide a useful animal model for studying the    mechanism of this disease and for testing drugs or therapies for treating osteoarthritis.</p>

	]]>
</description>

<author>Y W. Zhang et al.</author>


</item>


<item>
<title>Mdm muscular dystrophy: interactions with calpain 3 and a novel functional role for titin&apos;s N2A domain.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1212</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1212</guid>
<pubDate>Tue, 08 May 2012 21:32:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human tibial muscular dystrophy and limb-girdle muscular dystrophy 2J are caused by mutations in the giant sarcomeric protein titin (TTN) adjacent to a binding site for the muscle-specific protease calpain 3 (CAPN3).  Muscular    dystrophy with myositis (mdm) is a recessive mouse mutation with severe and progressive muscular degeneration caused by a deletion in the N2A domain of titin (TTN-N2ADelta83), disrupting a putative binding site for CAPN3. To determine whether the    muscular dystrophy in mutant mdm mice is caused by misregulation of CAPN3 activity, genetic crosses with CAPN3 overexpressing transgenic (C3Tg) and CAPN3 knockout (C3KO) mice were generated. Here, we report that overexpression of CAPN3    exacerbates the mdm disease, leading to a shorter life span and more severe muscular dystrophy. However, in a direct genetic test of CAPN3's role as a mediator of mdm pathology, C3KO;mdm double mutant mice showed no change in the progression or    severity of disease indicating that aberrant CAPN3 activity is not a primary mechanism in this disease. To determine whether we could detect a functional deficit in titin in a non-disease state, we examined the treadmill locomotion of    heterozygous +/mdm mice and detected a significant increase in stride time with a concomitant increase in stance time. Interestingly, these altered gait parameters were completely corrected by CAPN3 overexpression in transgenic C3Tg;+/mdm mice,    supporting a CAPN3-dependent role for the N2A domain of TTN in the dynamics of muscle contraction.</p>

	]]>
</description>

<author>K A. Huebsch et al.</author>


</item>


<item>
<title>TGF-beta1 inhibits T-bet induction by IFN-gamma in murine CD4+ T cells through the protein tyrosine phosphatase Src homology region 2 domain-containing phosphatase-1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1211</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1211</guid>
<pubDate>Tue, 08 May 2012 21:32:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>TGF-beta1 prevents the development of autoimmune disease by restraining the development of autoreactive Th1 cells. TGF-beta1 inhibits Th1 development in part by suppressing the expression of T-bet, an IFN-gamma-induced transcription    factor that promotes Th1 differentiation, but how TGF-beta1 suppresses T-bet is not known. In this study we show that TGF-beta1 suppresses IFN-gamma-induced T-bet expression through the hemopoietic protein tyrosine phosphatase (PTP) Src homology    region 2 domain-containing phosphatase-1 (Shp-1). In murine CD4+ T cells, IFN-gamma rapidly induced the expression of T-bet as well as of IFN regulatory factor-1, another transcription factor important for Th1 development.  TGF-beta1 antagonized    the effects of IFN-gamma, inhibiting IFN-gamma's induction of both Th1 transcription factors. In the presence of IFN-gamma, TGF-beta1 rapidly induced in Th cells the synthesis of the PTP Shp-1, but did not induce Shp-2 or several members of the    suppressor of cytokine signaling family of Jak-Stat inhibitors. We tested the requirement for Shp-1 by using T cells from the Shp-1-deficient me(v)/me(v) mouse strain.  Shp-1 was required for TGF-beta1's suppressive effects, because its    suppression of T-bet and IFN regulatory factor-1 was completely abrogated in me(v)/me(v) CD4+ T cells. Receptor-proximal responses to IFN-gamma, such as the induction of Jak-Stat phosphorylation, were inhibited by TGF-beta1 in wild-type T cells,    but not in me(v)/me(v) T cells. Consistent with a direct role for Shp-1, TGF-beta1's inhibition of IFN-gamma-induced Stat1 phosphorylation was sensitive to the general PTP inhibitor pervanadate. Together, these data show that TGF-beta1 suppresses    IFN-gamma signaling and transcriptional responses in CD4+ T cells through the PTP Shp-1.</p>

	]]>
</description>

<author>I K. Park et al.</author>


</item>


<item>
<title>Mutations in Col4a1 cause perinatal cerebral hemorrhage and porencephaly.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1210</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1210</guid>
<pubDate>Tue, 08 May 2012 21:31:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Porencephaly is a rare neurological disease, typically manifest in infants, which is characterized by the existence of degenerative cavities in the brain. To investigate the molecular pathogenesis of porencephaly, we studied a mouse    mutant that develops porencephaly secondary to focal disruptions of vascular basement membranes. Half of the mutant mice died with cerebral hemorrhage within a day of birth, and approximately 18% of survivors had porencephaly. We show that    vascular defects are caused by a semidominant mutation in the procollagen type IV alpha 1 gene (Col4a1) in mice, which inhibits the secretion of mutant and normal type IV collagen.  We also show that COL4A1 mutations segregate with porencephaly    in human families. Because not all mutant mice develop porencephaly, we propose that Col4a1 mutations conspire with environmental trauma in causing the disease.</p>

	]]>
</description>

<author>D B. Gould et al.</author>


</item>


<item>
<title>The Importance of Turbulence during Condensation in a Horizontal Circular Minichannel</title>
<link>http://docs.lib.purdue.edu/coolingpubs/172</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/coolingpubs/172</guid>
<pubDate>Tue, 08 May 2012 21:31:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Three-dimensional simulations of condensation of refrigerant R134a in a horizontal minichannel are presented. Mass fluxes ranging from 50kgm-2 s-1 up to 1000kgm-2 s-1 are considered in a circular minichannel of 1mm diameter, and uniform wall and vapour–liquid interface temperatures are imposed as boundary conditions. The Volume of Fluid (VOF) method is used to track the vapour–liquid interface; the effects of interfacial shear stress, gravity and surface tension are taken into account. The influence of turbulence in the condensate film is analysed and compared against the assumption of laminar condensate flow by employing different computational approaches and validating the results against experimental data. Under the assumption of laminar condensate flow, experimental heat transfer coefficient values at low mass fluxes can be predicted, but the computed heat transfer coefficient is found to be almost independent of mass flux and vapour quality. Only when turbulence in the condensate film is taken into account does the numerical model capture the influence of mass flux that is observed in the experimental measurements.</p>

	]]>
</description>

<author>E. da Riva et al.</author>


</item>


<item>
<title>Effects of growth hormone transgene expression on vertebrae in a mouse model of osteogenesis imperfecta.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1209</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1209</guid>
<pubDate>Tue, 08 May 2012 21:31:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>STUDY DESIGN: A human growth hormone transgene was bred into mice of the Cola2oim (oim) lineage. Caudal (tail) vertebrae from male and female mice at early skeletal maturity and at midlife were evaluated for physical and    biomechanical properties. OBJECTIVE: To test whether constant low-level growth hormone expression within the marrow could improve structural or material properties of caudal vertebrae in oim mice. SUMMARY OF BACKGROUND DATA: A spontaneous genetic    defect in a type I procollagen gene created the oim mouse model for osteogenesis imperfecta. Bones of heterozygous oim mice are biomechanically inferior to wild-type controls. Bone marrow expression of human growth hormone was demonstrated    previously to enhance bone deposition and structural biomechanical properties in caudal vertebrae of transgenic mice. METHODS: Compression tests were performed individually on three caudal vertebrae (Ca4, 5, and 6) from each mouse to determine    their structural biomechanical properties. Volumetric and mineral content measurements were also made. In a subset of vertebrae, the ashing measurements were confirmed and extended by peripheral quantitative tomographic scanning, which also    allowed calculation of the failure stress. RESULTS: Heterozygous oim mouse vertebrae had structural and material properties inferior to the wild-type controls. Growth hormone transgene expression increased the size and mineral content of the    vertebrae from mutant mice, and increased biomechanical structural values for maximum load and energy to failure. Failure stress was not improved.  CONCLUSIONS: Growth hormone stimulation of size and bone mineral content of osteogenesis    imperfecta mutant mouse caudal vertebrae contributed to their improved performance in axial compression. There was no evidence for improved material properties, however.</p>

	]]>
</description>

<author>D King et al.</author>


</item>


<item>
<title>Dilated cardiomyopathy in the nmd mouse: transgenic rescue and QTLs that improve cardiac function and survival.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1208</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1208</guid>
<pubDate>Tue, 08 May 2012 21:31:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the immunoglobulin mu binding protein-2 (Ighmbp2) gene cause motor neuron disease and dilated cardiomyopathy (DCM) in the neuromuscular degeneration (nmd) mouse and spinal muscular atrophy with respiratory distress    (SMARD1) in humans. To investigate the role of IGHMBP2 in the pathogenesis of DCM, we generated transgenic mice expressing the full-length Ighmbp2 cDNA specifically in myocytes under the control of the mouse titin promoter. This tissue-specific    transgene increased the lifespan of nmd mice up to 8-fold by preventing primary DCM and showed complete functional correction as measured by ECG, echocardiography and plasma creatine kinase-MB. Double-transgenic nmd mice expressing Ighmbp2 both    in myocytes and in neurons display correction of both DCM and motor neuron disease, resulting in an essentially wild-type appearance.  Additionally, quantitative trait locus (QTL) analysis was undertaken to identify genetic modifier loci    responsible for the preservation of cardiac function and a marked delay in the onset of cardiomyopathy in a CAST/EiJ backcross population. Three major CAST-derived cardiac modifiers of nmd were identified on chromosomes 9, 10 and 16, which    account for over 26% of the genetic variance and that continue to suppress the exacerbation of cardiomyopathy, otherwise resulting in early death, as incipient B6.CAST congenics. Overall, our results verify the tissue-specific requirement for    IGHMBP2 in cardiomyocyte maintenance and survival and describe genetic modifiers that can alter the course of DCM through cardiac functional adaptation and physical remodeling in response to changes in load and respiratory demand.</p>

	]]>
</description>

<author>T P. Maddatu et al.</author>


</item>


<item>
<title>Identification of a ferrireductase required for efficient transferrin-dependent iron uptake in erythroid cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1207</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1207</guid>
<pubDate>Tue, 08 May 2012 21:31:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The reduction of iron is an essential step in the transferrin (Tf) cycle, which is the dominant pathway for iron uptake by red blood cell precursors. A deficiency in iron acquisition by red blood cells leads to hypochromic,    microcytic anemia. Using a positional cloning strategy, we identified a gene, six-transmembrane epithelial antigen of the prostate 3 (Steap3), responsible for the iron deficiency anemia in the mouse mutant nm1054. Steap3 is expressed highly in    hematopoietic tissues, colocalizes with the Tf cycle endosome and facilitates Tf-bound iron uptake. Steap3 shares homology with F(420)H(2):NADP(+) oxidoreductases found in archaea and bacteria, as well as with the yeast FRE family of    metalloreductases.  Overexpression of Steap3 stimulates the reduction of iron, and mice lacking Steap3 are deficient in erythroid ferrireductase activity. Taken together, these findings indicate that Steap3 is an endosomal ferrireductase required    for efficient Tf-dependent iron uptake in erythroid cells.</p>

	]]>
</description>

<author>R S. Ohgami et al.</author>


</item>


<item>
<title>Phosphatidylinositol transfer protein-alpha in netrin-1-induced PLC signalling and neurite outgrowth.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1206</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1206</guid>
<pubDate>Tue, 08 May 2012 21:30:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Neurite extension is essential for wiring the nervous system during development. Although several factors are known to regulate neurite outgrowth, the underlying mechanisms remain unclear. Here, we provide evidence for a role of    phosphatidylinositol transfer protein-alpha (PlTPalpha) in neurite extension in response to netrin-1, an extracellular guidance cue. PlTPalpha interacts with the netrin receptor DCC (deleted in colorectal cancer) and neogenin. Netrin-1 stimulates    PlTPalpha binding to DCC and to phosphatidylinositol (5) phosphate [Pl(5)P], increases its lipid-transfer activity and elevates hydrolysis of phosphatidylinositol bisphosphate (PlP2). In addition, the stimulated PIP2 hydrolysis requires    PlTPalpha. Furthermore, cortical explants of PlTPalpha mutant mice are defective in extending neurites in response to netrin-1. Commissural neurons from chicken embryos expressing a dominant-negative PlTPalpha mutant show reduced axon outgrowth.    Morpholino-mediated knockdown of PlTPalpha expression in zebrafish embryos leads to dose-dependent defects in motor-neuron axons and reduced numbers of spinal-cord neurons. Taken together, these results identify a crucial role for PlTPalpha in    netrin-1-induced neurite outgrowth, revealing a signalling mechanism for DCC/neogenin and PlTPalpha regulation.</p>

	]]>
</description>

<author>Y Xie et al.</author>


</item>


<item>
<title>Accelerated wound healing of alkali-burned corneas in MRL mice is associated with a reduced inflammatory signature.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1205</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1205</guid>
<pubDate>Tue, 08 May 2012 21:30:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: The present study was conducted to investigate healing of alkali-burned corneas in MRL/MpJ (MRL) mice. METHODS: Gross, clinical, and histologic criteria were used to compare healing of alkali-burned corneas in MRL and    control C57BL/6J (B6) mice. Effects of neutrophil depletion of B6 mice and allogeneic reconstitution of B6 mice with MRL bone marrow on wound healing were evaluated. Gene expression patterns in normal and wounded corneas were surveyed with    array-based quantitative real-time RT-PCR (AQPCR). RESULTS: MRL mice showed accelerated reepithelialization and decreased corneal opacity compared with B6 mice after alkali wounding.  Marked inflammatory cell infiltration and fibrosis were    evident in the corneas and anterior chambers of B6 mice. MRL mice showed less severe lesions, except for stromal edema. Rapid reepithelialization and reduced keratitis/iritis were also observed in neutrophil-depleted B6 mice, but not in B6 mice    reconstituted with MRL bone marrow. AQPCR showed transcriptional changes of fewer genes associated with inflammation and corneal tissue homeostasis in alkali-burned corneas from MRL mice.  Increased expression of an anti-inflammatory gene, Socs1,    and a gene associated with healing, Mmp1a, were evident in MRL corneas. CONCLUSIONS: Alkali-burned corneas heal faster and more completely in MRL mice than in B6 mice, by means of rapid reepithelialization, reduced inflammation, and reduced    fibrosis. Reduced inflammation, including decreased neutrophil infiltrates and the lack of a robust proinflammatory gene expression signature correlates with the rapid healing. However, the rapid-healing phenotype is not intrinsic to MRL    hematopoietic progenitor cells.</p>

	]]>
</description>

<author>M Ueno et al.</author>


</item>


<item>
<title>Loss of the putative tumor suppressor band 4.1B/Dal1 gene is dispensable for normal development and does not predispose to cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1204</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1204</guid>
<pubDate>Tue, 08 May 2012 21:30:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The band 4.1 proteins are cytoskeletal proteins, harboring a conserved FERM domain highly homologous to the N-terminal FERM domain of ezrin, radixin, moesin, and merlin. Recently, a truncated form of the 4.1B protein, termed Dal-1,    was identified in a screen as down regulated in adenocarcinoma of the lung and was mapped to chromosome 18p11.3, which is lost in 38% of primary non-small cell lung carcinoma tumors. Analysis of several meningiomas has shown that Dal-1 expression    was lost in 76% of the tumors. To further elucidate the function of the 4.1B/Dal-1 gene in development and tumorigenesis we generated mice deficient for this allele.  The 4.1B/Dal-1 null mice develop normally and are fertile. Rates of cellular    proliferation and apoptosis in brain, mammary, and lung tissues from the 4.1B/Dal-1 null mice were indistinguishable from those seen with wild-type mice. Aging studies indicate that these mice do not have a propensity to develop tumors. Analysis    of fibroblasts from these mice demonstrated that the growth characteristics and kinetics of these cells were not different from those of cells from the wild-type mice. These findings indicate that the 4.1B gene is not required for normal    development and that 4.1B/Dal-1 does not function as a tumor suppressor gene.</p>

	]]>
</description>

<author>C Yi et al.</author>


</item>


<item>
<title>Further characterization of reproductive abnormalities in mCd59b knockout mice: a potential new function of mCd59 in male reproduction.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1203</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1203</guid>
<pubDate>Tue, 08 May 2012 21:29:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>CD59 is a GPI-linked membrane protein that inhibits formation of the membrane attack complex of complement. We reported recently that mice have two CD59 genes (termed mCd59a and mCd59b), and that the targeted deletion of mCd59b    (mCd59b-/-) results in spontaneous hemolytic anemia and progressive loss of male fertility. Further studies of the reproductive abnormalities in mCd59b-/- mice reported in this study revealed the presence of abnormal multinucleated cells and    increased apoptotic cells within the walls of the seminiferous tubules, and a decrease in the number, motility, and viability of sperm associated with a significant increase in abnormal sperm morphologies. Both the capacitation-associated    tyrosine phosphorylation and the ionophore-induced acrosome reaction as well as luteinizing hormone, follicle-stimulating hormone, and testosterone serum levels were similar in mCd59b-/- and mCd59b+/+.  Surprisingly, the functional deficiency of    the complement protein C3 did not rescue the abnormal reproductive phenotype of mCd59b-/-, although it was efficient in rescuing their hemolytic anemia. These results indicate that the male reproductive abnormalities in mCd59b-/- are    complement-independent, and that mCd59 may have a novel function in spermatogenesis that is most likely unrelated to its function as an inhibitor of membrane attack complex formation.</p>

	]]>
</description>

<author>X Qin et al.</author>


</item>


<item>
<title>Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1202</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1202</guid>
<pubDate>Tue, 08 May 2012 21:29:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND & AIMS: The absence of interleukin 10, a key cytokine in gut homeostasis, causes severe colitis in C3H/HeJBir but not C57BL/6J mice.  The major modifier for colitis was mapped on chromosome 3 and designated cytokine    deficiency-induced colitis susceptibility 1 (Cdcs1). We developed reciprocal Cdcs1 congenic stocks on both interleukin 10-deficient backgrounds to identify the susceptibility gene and its function. METHODS: C3H/HeJBir congenic for the    C57BL/6J-derived Cdcs1 allele and reciprocal C57BL/6J congenic for the C3H/HeJBir allele were analyzed for colitis development. Parental strains were compared by electrophoretic mobility shift assay to assess the candidacy of nuclear    factor-kappaB p50 in the Cdcs1 interval. Functional differences were observed in innate and adaptive immune responses of parental and congenic stocks after bacterial ligand exposure in vitro (cytokine release from bone marrow-derived macrophage    and dendritic cells) and in vivo (serum cytokines and primed CD4+ T cell proliferation). RESULTS: Cdcs1 was positioned within a minimum 7-megabase interval containing nuclear factor-kappaB p50. C3H/HeJBir colitis was significantly diminished by    the C57BL/6J genome in this interval. Conversely, colitis in C57BL/6J was significantly exacerbated by the reciprocal C3H/HeJBir genome. C3H/HeJBir macrophages constitutively expressed higher nuclear factor-kappaB p50. Functional assays showed    that C3H/HeJBir showed reduced innate responsiveness both in vivo and in vitro to bacterial ligands but showed increased CD4 T-cell responses compared with C57BL/6J. This differential responsiveness was controlled by the respective allele at    Cdcs1. CONCLUSIONS: The colitogenic Cdcs1 allele impairs innate immunity to bacterial products and in turn skews the adaptive immune response toward compensatory hyperresponsiveness and chronic intestinal inflammation.</p>

	]]>
</description>

<author>J Beckwith et al.</author>


</item>


<item>
<title>Molecular and cellular basis of the retrovirus resistance in I/LnJ mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1201</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1201</guid>
<pubDate>Tue, 08 May 2012 21:29:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previously, we showed that IFN-gamma elicited by mouse mammary tumor virus (MMTV) infection in I/LnJ mice stimulated production of virus-neutralizing Abs, mostly of the IgG2a isotype. These Abs coated virions secreted by infected    I/LnJ cells, and thus completely prevented virus transmission to offspring. However, the mechanism of virus neutralization by isotype-specific Abs remained unknown. Ab coating is capable of blocking virus infection by interfering with    receptor-virus binding, by virus opsonization, by complement activation, and via FcgammaR-mediated effector mechanisms. The aim of the studies described in this work was to uncover the cellular basis of anti-virus Ab production, to evaluate the    importance of the IgG2a subclass of IgGs in virus neutralization, and to investigate which of the blocking mechanisms plays a role in virus neutralization. We showed that I/LnJ-derived bone marrow cells, specifically IFN-gamma-producing CD4+ T    cells, were key cells conferring resistance to MMTV infection in susceptible mice upon transfer. We also established that a unique bias in the subclass selection toward the IgG2a isotype in infected I/LnJ mice was not due to their potent    neutralizing ability, as anti-virus Abs of other isotypes were also able to neutralize the virus, but were a product of virally induced IFN-gamma. Finally, we demonstrated that F(ab')2 of anti-MMTV IgGs neutralized the virus as efficiently as    total IgGs, suggesting that Ab-mediated interference with viral entry is the sole factor inhibiting virus replication in I/LnJ mice. We propose and discuss possible mechanisms by which infected I/LnJ mice eradicate retrovirus.</p>

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</description>

<author>L K. Case et al.</author>


</item>


<item>
<title>Bayesian model selection for genome-wide epistatic quantitative trait loci analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1200</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1200</guid>
<pubDate>Tue, 08 May 2012 21:29:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The problem of identifying complex epistatic quantitative trait loci (QTL) across the entire genome continues to be a formidable challenge for geneticists. The complexity of genome-wide epistatic analysis results mainly from the    number of QTL being unknown and the number of possible epistatic effects being huge. In this article, we use a composite model space approach to develop a Bayesian model selection framework for identifying epistatic QTL for complex traits in    experimental crosses from two inbred lines. By placing a liberal constraint on the upper bound of the number of detectable QTL we restrict attention to models of fixed dimension, greatly simplifying calculations. Indicators specify which main and    epistatic effects of putative QTL are included. We detail how to use prior knowledge to bound the number of detectable QTL and to specify prior distributions for indicators of genetic effects. We develop a computationally efficient Markov chain    Monte Carlo (MCMC) algorithm using the Gibbs sampler and Metropolis-Hastings algorithm to explore the posterior distribution. We illustrate the proposed method by detecting new epistatic QTL for obesity in a backcross of CAST/Ei mice onto    M16i.</p>

	]]>
</description>

<author>N Yi et al.</author>


</item>


<item>
<title>Isolation and cloning of the raccoon (Procyon lotor) papillomavirus type 1 by using degenerate papillomavirus-specific primers.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1199</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1199</guid>
<pubDate>Tue, 08 May 2012 21:28:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Partial sequences of a novel papillomavirus were amplified from a cutaneous lesion biopsy of a raccoon (Procyon lotor), by using PCR with degenerate papillomavirus-specific primers. The Procyon lotor papillomavirus type 1 (PlPV-1)    DNA was amplified with long template PCR in two overlapping fragments, together encompassing the entire genome, and the complete PlPV-1 genomic sequence was determined. The PlPV-1 genome consists of 8170 bp, and contains the typical    papillomaviral open reading frames, encoding five early proteins and two late capsid proteins. Besides the classical non-coding region (NCR1) between the end of L1 and the start of E6, PlPV-1 contains an additional non-coding region (NCR2) of    1065 bp between the early and late protein region, which has previously also been described for the canine oral papillomavirus (COPV) and the Felis domesticus papillomavirus (FdPV-1). Phylogenetic analysis places PlPV-1 together with COPV and    FdPV-1 in a monophyletic branch which encompasses the Lambda papillomavirus genus.</p>

	]]>
</description>

<author>A Rector et al.</author>


</item>


<item>
<title>Efficient engraftment of primary adult T-cell leukemia cells in newborn NOD/SCID/beta2-microglobulin(null) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1198</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1198</guid>
<pubDate>Tue, 08 May 2012 21:28:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adult T-cell leukemia (ATL) develops via multiple oncogenic steps in human T-cell leukemia virus type I (HTLV-I) carriers. To better understand pathogenesis of ATL, we developed a novel xenogeneic engraftment model in which primary    ATL cells are intravenously transplanted into neonatal nonobese diabetic (NOD)/severe-combined immunodeficiency (SCID)/beta2-microglobulin(null) (NOD/SCID/beta2m(null)) mice. Acute-type ATL cells engrafted in the peripheral blood and in the lymph    nodes of recipients at a high efficiency. Engrafted ATL cells were dually positive for human CD4 and CD25, and displayed patterns of HTLV-I integration identical to those of donors by Southern blot analysis. These cells infiltrated into    recipients' liver, and formed nodular lesions, recapitulating the clinical feature of each patient. In contrast, in smoldering-type ATL cases, multiple clones of ATL cells engrafted efficiently in NOD/SCID/beta2m(null) mice. When smoldering-type    ATL cells were retransplanted into secondary NOD/SCID/beta2m(null) recipients, single HTLV-I-infected clones became predominant, suggesting that clones with dominant proliferative activity can be competitively selected in this xenogeneic system.    Taken together, the NOD/SCID/beta2m(null) newborn system is useful to understand kinetics, metastasis, and disease progression of ATL in vivo.</p>

	]]>
</description>

<author>N Kawano et al.</author>


</item>


<item>
<title>Alms1-disrupted mice recapitulate human Alstrom syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1197</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1197</guid>
<pubDate>Tue, 08 May 2012 21:28:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the human ALMS1 gene cause Alstrom syndrome (AS), a progressive disease characterized by neurosensory deficits and by metabolic defects including childhood obesity, hyperinsulinemia and Type 2 diabetes. Other features    that are more variable in expressivity include dilated cardiomyopathy, hypertriglyceridemia, hypercholesterolemia, scoliosis, developmental delay and pulmonary and urological dysfunctions.  ALMS1 encodes a ubiquitously expressed protein of    unknown function. To obtain an animal model in which the etiology of the observed pathologies could be further studied, we generated a mouse model using an Alms1 gene-trapped ES cell line. Alms1-/- mice develop features similar to patients with    AS, including obesity, hypogonadism, hyperinsulinemia, retinal dysfunction and late-onset hearing loss. Insulin resistance and increased body weight are apparent between 8 and 12 weeks of age, with hyperglycemia manifesting at approximately 16    weeks of age. In addition, Alms1-/- mice have normal hearing until 8 months of age, after which they display abnormal auditory brainstem responses. Diminished cone ERG b-wave response is observed early, followed by the degeneration of    photoreceptor cells. Electron microscopy revealed accumulation of intracellular vesicles in the inner segments of photoreceptors, whereas immunohistochemical analysis showed mislocalization of rhodopsin to the outer nuclear layer.  These findings    suggest that ALMS1 has a role in intracellular trafficking.</p>

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</description>

<author>G B. Collin et al.</author>


</item>


<item>
<title>Direct regulatory role of NKT cells in allogeneic graft survival is dependent on the quantitative strength of antigenicity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1196</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1196</guid>
<pubDate>Tue, 08 May 2012 21:27:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The role of NKT cells during immune responses is diverse, ranging from antiviral and antitumor activity to the regulation of autoimmune diseases; however, the regulatory function of CD1d-dependent NKT cells in rejection responses    against allogeneic graft is uncertain. In this study, we demonstrated the direct regulatory effects of CD1d-dependent NKT cells using an allogeneic skin transplantation model. H-Y-mismatched skin graft survival was shortened in CD1d-/- recipients    compared with wild-type recipients. Adoptive transfer of syngeneic NKT cells via splenocytes or hepatic mononuclear cells into CD1d-/- recipients restored graft survival times to those of wild-type recipients. alpha-Galactosylceramide, a specific    activator of NKT cells, further prolonged graft survival.  Although CD1d-dependent NKT cells did not extend skin graft survival in either major or complete minor histocompatibility-mismatched models, these cells affected graft survival in minor    Ag mismatch models according to the magnitude of the antigenic difference. The afferent arm of NKT cell activation during transplantation required CD1d molecules expressed on host APCs and the migration of CD1d-dependent NKT cells into grafts.     Moreover, the regulatory effects of CD1d-dependent NKT cells against alloantigen were primarily IL-10 dependent. Taken together, we concluded that CD1d-dependent NKT cells may directly affect the outcome of allogeneic skin graft through an    IL-10-dependent regulatory mechanism.</p>

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</description>

<author>K Oh et al.</author>


</item>


<item>
<title>Disruption of the Jnk2 (Mapk9) gene reduces destructive insulitis and diabetes in a mouse model of type I diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1195</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1195</guid>
<pubDate>Tue, 08 May 2012 21:27:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The c-Jun NH(2)-terminal kinase isoform (JNK) 1 is implicated in type 2 diabetes. However, a potential role for the JNK2 protein kinase in diabetes has not been established. Here, we demonstrate that JNK2 may play an important role    in type 1 (insulin-dependent) diabetes that is caused by autoimmune destruction of beta cells. Studies of nonobese diabetic mice demonstrated that disruption of the Mapk9 gene (which encodes the JNK2 protein kinase) decreased destructive    insulitis and reduced disease progression to diabetes. CD4(+) T cells from JNK2-deficient nonobese diabetic mice produced less IFN-gamma but significantly increased amounts of IL-4 and IL-5, indicating polarization toward the Th2 phenotype. This    role of JNK2 to control the Th1/Th2 balance of the immune response represents a mechanism of protection against autoimmune diabetes. We conclude that JNK protein kinases may have important roles in diabetes, including functions of JNK1 in type 2    diabetes and JNK2 in type 1 diabetes.</p>

	]]>
</description>

<author>A Jaeschke et al.</author>


</item>


<item>
<title>Gonadal sex reversal in mutant Dax1 XY mice: a failure to upregulate Sox9 in pre-Sertoli cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1194</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1194</guid>
<pubDate>Tue, 08 May 2012 21:27:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The nuclear receptor transcription factor Dax1 is hypothesized to play a role in testicular development, although the mechanism of its action is unknown. Here, we present evidence that Dax1 plays an early essential role in fetal    testis development. We hypothesize that upregulation of Sox9 expression in precursor somatic cells, a process required for their differentiation as Sertoli cells, depends on the coordinated expression of Dax1, Sry and another gene, Tda1. Our    conclusion and model are based on the following experimental findings: (1) presence of a mutant Dax1 allele (Dax1-) results in complete gonadal sex reversal in C57BL/6JEi (B6) XY mice, whereas testes develop in DBA/2J (D2) and (B6xD2)F1 XY mice;    (2) B6-DAX1 sex reversal is inherited as a complex trait that includes the chromosome 4 gene Tda1; (3) B6 Dax1-/Y fetal gonads initiate development as ovaries, even though Sry expression is activated at the correct time and at appropriate levels;    (4) upregulation of Sox9 does not occur in B6 Dax1-/Y fetal gonads in spite of apparently normal Sry expression; and (5) overexpression of Sry in B6 Dax1-/Y fetal gonads upregulates Sox9 and corrects testis development.</p>

	]]>
</description>

<author>G J. Bouma et al.</author>


</item>


<item>
<title>Mechanistic insights into glaucoma provided by experimental genetics the cogan lecture.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1193</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1193</guid>
<pubDate>Tue, 08 May 2012 21:27:05 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>S W. John</author>


</item>


<item>
<title>Susceptibility to neurodegeneration in a glaucoma is modified by Bax gene dosage.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1192</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1192</guid>
<pubDate>Tue, 08 May 2012 21:26:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>In glaucoma, harmful intraocular pressure often contributes to retinal ganglion cell death. It is not clear, however, if intraocular pressure directly insults the retinal ganglion cell axon, the soma, or both. The pathways that    mediate pressure-induced retinal ganglion cell death are poorly defined, and no molecules are known to be required. DBA/2J mice deficient in the proapoptotic molecule BCL2-associated X protein (BAX) were used to investigate the roles of    BAX-mediated cell death pathways in glaucoma. Both Bax+/- and Bax-/- mice were protected from retinal ganglion cell death. In contrast, axonal degeneration was not prevented in either Bax+/- or Bax-/- mice. While BAX deficiency did not prevent    axonal degeneration, it did slow axonal loss. Additionally, we compared the effects of BAX deficiency on the glaucoma to its effects on retinal ganglion cell death due to two insults that are proposed to participate in glaucoma. As in the    glaucoma, BAX deficiency protected retinal ganglion cells after axon injury by optic nerve crush. However, it did not protect retinal ganglion cells from N-methyl-D-aspartate (NMDA)-induced excitotoxicity. BAX is required for retinal ganglion    cell death in an inherited glaucoma; however, it is not required for retinal ganglion cell axon degeneration. This indicates that distinct somal and axonal degeneration pathways are active in this glaucoma. Finally, our data support a role for    optic nerve injury but not for NMDA receptor-mediated excitotoxicity in this glaucoma. These findings indicate a need to understand axon-specific degeneration pathways in glaucoma, and they suggest that distinct somal and axonal degeneration    pathways may need to be targeted to save vision.</p>

	]]>
</description>

<author>R T. Libby et al.</author>


</item>


<item>
<title>A missense mutation in the previously undescribed gene Tmhs underlies deafness in hurry-scurry (hscy) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1191</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1191</guid>
<pubDate>Tue, 08 May 2012 21:26:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mouse deafness mutations provide valuable models of human hearing disorders and entry points into molecular pathways important to the hearing process. A newly discovered mouse mutation named hurry-scurry (hscy) causes deafness and    vestibular dysfunction. Scanning electron microscopy of cochleae from 8-day-old mutants revealed disorganized hair bundles, and by 50 days of age, many hair cells are missing. To positionally clone hscy, 1,160 F(2) mice were produced from an    intercross of (C57BL/6-hscy x CAST/EiJ) F(1) hybrids, and the mutation was localized to a 182-kb region of chromosome 17. A missense mutation causing a critical cysteine to phenylalanine codon change was discovered in a previously undescribed    gene within this candidate interval. The gene is predicted to encode an integral membrane protein with four transmembrane helices. A synthetic peptide designed from the predicted protein was used to produce specific polyclonal antibodies, and    strong immunoreactivity was observed on hair bundles of both inner and outer hair cells in cochleae of newborn +/+ controls and +/hscy heterozygotes but was absent in hscy/hscy mutants. Accordingly, the gene was given the name "tetraspan membrane    protein of hair cell stereocilia," symbol Tmhs. Two related proteins (>60% amino acid identity) are encoded by genes on mouse chromosomes 5 and 6 and, together with the Tmhs-encoded protein (TMHS), comprise a distinct tetraspan subfamily. Our    localization of TMHS to the apical membrane of inner ear hair cells during the period of stereocilia formation suggests a function in hair bundle morphogenesis.</p>

	]]>
</description>

<author>Guess C. Longo et al.</author>


</item>


<item>
<title>The Importance of Turbulence during Condensation in a Horizontal Circular Minichannel</title>
<link>http://docs.lib.purdue.edu/coolingpubs/171</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/coolingpubs/171</guid>
<pubDate>Tue, 08 May 2012 21:26:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Three-dimensional simulations of condensation of refrigerant R134a in a horizontal minichannel are presented. Mass fluxes ranging from 50kgm-2 s-1 up to 1000kgm-2 s-1 are considered in a circular minichannel of 1mm diameter, and uniform wall and vapour–liquid interface temperatures are imposed as boundary conditions. The Volume of Fluid (VOF) method is used to track the vapour–liquid interface; the effects of interfacial shear stress, gravity and surface tension are taken into account. The influence of turbulence in the condensate film is analysed and compared against the assumption of laminar condensate flow by employing different computational approaches and validating the results against experimental data. Under the assumption of laminar condensate flow, experimental heat transfer coefficient values at low mass fluxes can be predicted, but the computed heat transfer coefficient is found to be almost independent of mass flux and vapour quality. Only when turbulence in the condensate film is taken into account does the numerical model capture the influence of mass flux that is observed in the experimental measurements.</p>

	]]>
</description>

<author>E. da Riva et al.</author>


</item>


<item>
<title>Variation in IL-1beta gene expression is a major determinant of genetic differences in arthritis aggressivity in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1190</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1190</guid>
<pubDate>Tue, 08 May 2012 21:26:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>In humans and in animal models, susceptibility to arthritis is under complex genetic control, reflecting influences on the immunological processes that initiate autoimmunity and on subsequent inflammatory mechanisms in the joints.    The effector phases are conveniently modeled by the K/BxN serum transfer system, a robust model well suited for genetic analysis where arthritis is initiated by pathogenic Ig. Here, we mapped the genetic loci distinguishing the high-responder    BALB/c vs.  low-responder SJL strains. After computational modeling of potential breeding schemes, we adapted a stepwise selective breeding strategy, with a whole-genome scan performed on a limited number of animals. Several genomic regions    proved significantly associated with high sensitivity to arthritis. One of these regions, on distal chr2, was centered on the interleukin 1 gene family. Quantitation of transcripts of the Il1a and Il1b candidate genes revealed a 10-fold greater    induction of Il1b mRNA in BALB/c than in SJL splenocytes after injection of LPS, whereas Il1a showed much less difference. The differential activity of the Il1b gene was associated with a particular sequence haplotype of noncoding polymorphisms.    The BALB/c haplotype was found in 75% of wild-derived strains but was rare among conventional inbred strains (4/33 tested, one of which is DBA/1, the prototype arthritis-susceptible strain) and was associated with vigorous Il1b responses in a    panel of inbred strains.  Inbred strains carrying this allele were far more responsive to serum-transferred arthritis, confirming its broad importance in controlling arthritis severity.</p>

	]]>
</description>

<author>K Ohmura et al.</author>


</item>


<item>
<title>Notch signaling coordinates the patterning of striatal compartments.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1189</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1189</guid>
<pubDate>Tue, 08 May 2012 21:26:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Numerous lines of evidence suggest that Notch signaling plays a pivotal role in controlling the production of neurons from progenitor cells.  However, most experiments have relied on gain-of-function approaches because perturbation    of Notch signaling results in death prior to the onset of neurogenesis. Here, we examine the requirement for Notch signaling in the development of the striatum through the analysis of different single and compound Notch1 conditional and Notch3    null mutants.  We find that normal development of the striatum depends on the presence of appropriate Notch signals in progenitors during a critical window of embryonic development. Early removal of Notch1 prior to neurogenesis alters early-born    patch neurons but not late-born matrix neurons in the striatum. We further show that the late-born striatal neurons in these mutants are spared as a result of functional compensation by Notch3.  Notably, however, the removal of Notch signaling    subsequent to cells leaving the germinal zone has no obvious effect on striatal organization and patterning. These results indicate that Notch signaling is required in neural progenitor cells to control cell fate in the striatum, but is    dispensable during subsequent phases of neuronal migration and differentiation.</p>

	]]>
</description>

<author>H A. Mason et al.</author>


</item>


<item>
<title>Novel leptin receptor mutation in NOD/LtJ mice suppresses type 1 diabetes progression: I. Pathophysiological analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1188</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1188</guid>
<pubDate>Tue, 08 May 2012 21:25:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>A spontaneous single-base mutation in the leptin receptor of type 1 diabetes-prone NOD/LtJ mice (designated as Lepr(db-5J)) produced a glycine640valine transversion in the extracellular domain. All mutant mice became obese and    hyperinsulinemic at weaning, with 70-80% developing early-onset hyperglycemia. However, these obese diabetic mice continued to gain weight without insulin therapy. Spontaneous diabetes remission was observed in all obese females and a subset of    obese males. Insulitis was largely limited to islet perimeters, with intraislet insulitis infrequently observed. In 17 obese males (age 39 weeks), we observed phenotypic heterogeneity, including full remission from hyperglycemia (24%),    intermediate hyperglycemia with elevated body weight (41%), and severe hyperglycemia and weight loss (35%). The remitting normoglycemic and intermediate hyperglycemic phenotypes were associated with extensive beta-cell hyperplasia. Unlike the    extensive intraislet insulitis present in diabetic lean NOD/Lt mice, the severe obese diabetic phenotype was associated with islet atrophy without extensive intraislet insulitis.  These results indicated that the manipulation of the leptin/leptin    receptor axis may provide a novel means of downregulating autoimmunity in type 1 diabetes and confirmed a role for leptin as a mediator in the development of this disease in NOD mice.</p>

	]]>
</description>

<author>C H. Lee et al.</author>


</item>


<item>
<title>Targeted ablation of the abcc6 gene results in ectopic mineralization of connective tissues.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1187</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1187</guid>
<pubDate>Tue, 08 May 2012 21:25:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pseudoxanthoma elasticum (PXE), characterized by connective tissue mineralization of the skin, eyes, and cardiovascular system, is caused by mutations in the ABCC6 gene. ABCC6 encodes multidrug resistance-associated protein 6    (MRP6), which is expressed primarily in the liver and kidneys.  Mechanisms producing ectopic mineralization as a result of these mutations remain unclear. To elucidate this complex disease, a transgenic mouse was generated by targeted ablation of    the mouse Abcc6 gene. Abcc6 null mice were negative for Mrp6 expression in the liver, and complete necropsies revealed profound mineralization of several tissues, including skin, arterial blood vessels, and retina, while heterozygous animals were    indistinguishable from the wild-type mice. Particularly striking was the mineralization of vibrissae, as confirmed by von Kossa and alizarin red stains. Electron microscopy revealed mineralization affecting both elastic structures and collagen    fibers. Mineralization of vibrissae was noted as early as 5 weeks of age and was progressive with age in Abcc6(-/-) mice but was not observed in Abcc6(+/-) or Abcc6(+/+) mice up to 2 years of age. A total body computerized tomography scan of    Abcc6(-/-) mice revealed mineralization in skin and subcutaneous tissue as well as in the kidneys.  These data demonstrate aberrant mineralization of soft tissues in PXE-affected organs, and, consequently, these mice recapitulate features of this    complex disease.</p>

	]]>
</description>

<author>J F. Klement et al.</author>


</item>


<item>
<title>The Notch ligands DLL1 and JAG2 act synergistically to regulate hair cell development in the mammalian inner ear.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1186</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1186</guid>
<pubDate>Tue, 08 May 2012 21:25:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mammalian auditory sensory epithelium, the organ of Corti, contains sensory hair cells and nonsensory supporting cells arranged in a highly patterned mosaic. Notch-mediated lateral inhibition is the proposed mechanism for    creating this sensory mosaic. Previous work has shown that mice lacking the Notch ligand JAG2 differentiate supernumerary hair cells in the cochlea, consistent with the lateral inhibitory model. However, it was not clear why only relatively    modest increases in hair cell production were observed in Jag2 mutant mice. Here, we show that another Notch ligand, DLL1, functions synergistically with JAG2 in regulating hair cell differentiation in the cochlea. We also show by conditional    inactivation that these ligands probably signal through the NOTCH1 receptor.  Supernumerary hair cells in Dll1/Jag2 double mutants arise primarily through a switch in cell fate, rather than through excess proliferation.  Although these results    demonstrate an important role for Notch-mediated lateral inhibition during cochlear hair cell patterning, we also detected abnormally prolonged cellular proliferation that preferentially affected supporting cells in the organ of Corti. Our    results demonstrate that the Notch pathway plays a dual role in regulating cellular differentiation and patterning in the cochlea, acting both through lateral inhibition and the control of cellular proliferation.</p>

	]]>
</description>

<author>A E. Kiernan et al.</author>


</item>


<item>
<title>Evidence of a large-scale functional organization of mammalian chromosomes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1185</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1185</guid>
<pubDate>Tue, 08 May 2012 21:25:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Evidence from inbred strains of mice indicates that a quarter or more of the mammalian genome consists of chromosome regions containing clusters of functionally related genes. The intense selection pressures during inbreeding favor    the coinheritance of optimal sets of alleles among these genetically linked, functionally related genes, resulting in extensive domains of linkage disequilibrium (LD) among a set of 60 genetically diverse inbred strains. Recombination that    disrupts the preferred combinations of alleles reduces the ability of offspring to survive further inbreeding. LD is also seen between markers on separate chromosomes, forming networks with scale-free architecture. Combining LD data with pathway    and genome annotation databases, we have been able to identify the biological functions underlying several domains and networks.  Given the strong conservation of gene order among mammals, the domains and networks we find in mice probably    characterize all mammals, including humans.</p>

	]]>
</description>

<author>P M. Petkov et al.</author>


</item>


<item>
<title>A quantitative survey of gravity receptor function in mutant mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1184</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1184</guid>
<pubDate>Tue, 08 May 2012 21:24:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this research was to identify vestibular deficits in mice using linear vestibular evoked potentials (VsEPs). VsEP thresholds, peak latencies, and peak amplitudes from 24 strains with known genetic mutations and 6    inbred background strains were analyzed and descriptive statistics generated for each strain. Response parameters from mutant homozygotes were compared with heterozygote and/or background controls and all strain averages were contrasted to    normative ranges. Homozygotes of the following recessive mutations had absent VsEPs at the ages tested: Espn(je), Atp2b2dfw-2J, Spnb4qv-lnd2J, Spnb4qv-3J, Myo7ash1, Tmie(sr), Myo6sv, jc, Pcdh15av-J, Pcdh15av-2J, Pcdh15av-3J, Cdh23v-2J, Sans(js),    hr, Kcne1pkr and Pou3f4del. These results suggest profound gravity receptor deficits for these homozygotes, which is consistent with the structural deficits that have been documented for many of these strains. Homozygotes of Catna2cdf, Grid2ho4J,    Wnt1sw, qk, and Mbpshi strains and heterozygotes of Grid2lc had measurable VsEPs but one or more response parameters differed from the respective control group (heterozygote or background strain) or were outside normal ranges. For example, qk and    Mbpshi homozygotes showed significantly prolonged latencies consistent with the abnormal myelin that has been described for these strains. Prolonged latencies may suggest deficits in neural conduction; elevated thresholds suggest reduced    sensitivity, and reduced amplitudes may be suggestive for reduced neural synchrony. One mutation, Otx1jv, had all VsEP response parameters within normal limits--an expected finding because the abnormality in Otxljv is presumably restricted to the    lateral semicircular canal. Interestingly, some heterozygote groups also showed abnormalities in one or more VsEP response parameters, suggesting that vestibular dysfunction, although less severe, may be present in some heterozygous    animals.</p>

	]]>
</description>

<author>S M. Jones et al.</author>


</item>


<item>
<title>Humanized mice: are we there yet?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1183</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1183</guid>
<pubDate>Tue, 08 May 2012 21:24:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Animal models have been instrumental in increasing the understanding of human physiology, particularly immunity. However, these animal models have been limited by practical considerations and genetic diversity. The creation of    humanized mice that carry partial or complete human physiological systems may help overcome these obstacles. The National Institute of Allergy and Infectious Diseases convened a workshop on humanized mouse models for immunity in Bethesda, MD, on    June 13-14, 2005, during which researchers discussed the benefits and limitations of existing animal models and offered insights into the development of future humanized mouse models.</p>

	]]>
</description>

<author>F Macchiarini et al.</author>


</item>


<item>
<title>Mouse models and the genetics of diabetes: is there evidence for genetic overlap between type 1 and type 2 diabetes?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1182</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1182</guid>
<pubDate>Tue, 08 May 2012 21:24:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>In humans, both type 1 and type 2 diabetes exemplify genetically heterogeneous complex diseases in which epigenetic factors contribute to underlying genetic susceptibility. Extended human pedigrees often show inheritance of both    diabetes types. A common pathophysiological denominator in both disease forms is pancreatic beta-cell exposure to proinflammatory cytokines. Hence, it is intuitive that systemically expressed genes regulating beta-cell ability to withstand    chronic diabetogenic stress may represent a component of shared susceptibility to both major disease forms. In this review, the authors assemble evidence from genetic experiments using animal models developing clearly distinct diabetes syndromes    to inquire whether some degree of overlap in genes contributing susceptibility can be demonstrated. The conclusion is that although overlap exists in the pathophysiological insults leading to beta-cell destruction in the currently studied rodent    models, the genetic bases seem quite distinct.</p>

	]]>
</description>

<author>E H. Leiter et al.</author>


</item>


<item>
<title>Carbonic anhydrase-related protein VIII deficiency is associated with a distinctive lifelong gait disorder in waddles mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1181</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1181</guid>
<pubDate>Tue, 08 May 2012 21:24:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>The waddles (wdl) mouse is a unique animal model that exhibits ataxia and appendicular dystonia without pathological abnormalities of either the central or the peripheral nervous systems. A 19-bp deletion in exon 8 of the carbonic    anhydrase-related protein VIII gene (Car8) was detected by high-throughput temperature-gradient capillary electrophoresis heteroduplex analysis of PCR amplicons of genes and ESTs within the wdl locus on mouse chromosome 4. Although regarded as a    member of the carbonic anhydrase gene family, the encoded protein (CAR8) has no reported enzymatic activity. In normal mice, CAR8 is abundantly expressed in cerebellar Purkinje cells as well as in several other cell groups.  Compatible with    nonsense-mediated decay of mutant transcripts, CAR8 is virtually absent in mice homozygous for the wdl mutation. These data indicate that the wdl mouse is a Car8 null mutant and that CAR8 plays a central role in motor control.</p>

	]]>
</description>

<author>Y Jiao et al.</author>


</item>


<item>
<title>Human cord blood--derived cells generate insulin-producing cells in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1180</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1180</guid>
<pubDate>Tue, 08 May 2012 21:24:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Here we report the capacity of human cord blood (CB)-derived cells to generate insulin-producing cells. To investigate in vivo capacity of human CB-derived cells, T cell-depleted mononuclear cells were intravenously transplanted    into nonobese diabetic/severe combined immunodeficient/beta2-microglobulinnull mice within 48 hours of birth. At 1-2 months post-transplantation, immunofluorescence staining for insulin and fluorescence in situ hybridization (FISH) analysis using    a human chromosome probe indicated that human CB-derived cells generated insulin-producing cells at a frequency of 0.65%+/-0.64% in xenogeneic hosts. Reverse transcription-polymerase chain reaction analysis confirmed the transcription of human    insulin in the pancreatic tissue of the recipient mice. To clarify the mechanism underlying CB-derived insulin-producing cells, double FISH analysis using species-specific probes was performed. Almost equal proportions of human chromosome+ murine    chromosome- insulin+ cells and human chromosome+ murine chromosome+ insulin+ cells were present in recipient pancreatic islets. Taken together, human CB contains progenitor cells, which can generate insulin-producing cells in recipient pancreatic    tissues across a xenogeneic histocompatibility barrier by fusion-dependent and -independent mechanisms.</p>

	]]>
</description>

<author>S Yoshida et al.</author>


</item>


<item>
<title>Disruption and recovery of patterned retinal activity in the absence of acetylcholine.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1179</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1179</guid>
<pubDate>Tue, 08 May 2012 21:23:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many developing neural circuits generate synchronized bursting activity among neighboring neurons, a pattern thought to be important for sculpting precise neural connectivity. Network output remains relatively constant as the    cellular and synaptic components of these immature circuits change during development, suggesting the presence of homeostatic mechanisms. In the retina, spontaneous waves of activity are present even before chemical synapse formation, needing gap    junctions to propagate. However, as synaptogenesis proceeds, retinal waves become dependent on cholinergic neurotransmission, no longer requiring gap junctions. Later still in development, waves are driven by glutamatergic rather than cholinergic    synapses. Here, we asked how retinal activity evolves in the absence of cholinergic transmission by using a conditional mutant in which the gene encoding choline acetyltransferase (ChAT), the sole synthetic enzyme for acetylcholine (ACh), was    deleted from large retinal regions. ChAT-negative regions lacked retinal waves for the first few days after birth, but by postnatal day 5 (P5), ACh-independent waves propagated across these regions. Pharmacological analysis of the waves in ChAT    knock-out regions revealed a requirement for gap junctions but not glutamate, suggesting that patterned activity may have emerged via restoration of previous gap-junctional networks. Similarly, in P5 wild-type retinas, spontaneous activity    recovered after a few hours in nicotinic receptor antagonists, often as local patches of coactive cells but not waves. The rapid recovery of rhythmic spontaneous activity in the presence of cholinergic antagonists and the eventual emergence of    waves in ChAT knock-out regions suggest that homeostatic mechanisms regulate retinal output during development.</p>

	]]>
</description>

<author>R C. Stacy et al.</author>


</item>


<item>
<title>Politically correct human embryonic stem cells?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1178</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1178</guid>
<pubDate>Tue, 08 May 2012 21:23:41 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D Solter</author>


</item>


<item>
<title>HoxD cluster scanning deletions identify multiple defects leading to paralysis in the mouse mutant Ironside.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1177</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1177</guid>
<pubDate>Tue, 08 May 2012 21:23:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>A spontaneous semidominant mutation (Ironside, Irn) was isolated in mice, leading to severe hindlimb paralysis following multiple deletions in cis at the HoxD locus. To understand its cellular and molecular etiology, we embarked on    a comparative analysis using systematic HoxD cluster deletions, produced via targeted meiotic recombination (TAMERE). Different lines of mice were classified according to the severity of their paralyses, and subsequent analyses revealed that    multiple causative factors were involved, alone or in combination, in the occurrence of this pathology. Among them are the loss of Hoxd10 function, the sum of remaining Hoxd gene activity, and the ectopic gain of function of the neighboring gene    Evx2, all contributing to the mispositioning, the absence, or misidentification of specific lumbo-sacral pools of motoneurons, nerve root homeosis, and hindlimb innervation defects. These results highlight the importance of a systematic approach    when studying such clustered gene families, and give insights into the function and regulation of Hox and Evx2 genes during early spinal cord development.</p>

	]]>
</description>

<author>B Tarchini et al.</author>


</item>


<item>
<title>Evidence for a protective role of the Gardos channel against hemolysis in murine spherocytosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1176</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1176</guid>
<pubDate>Tue, 08 May 2012 21:23:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>It has been shown that mice with complete deficiency of all 4.1R protein isoforms (4.1-/-) exhibit moderate hemolytic anemia, with abnormal erythrocyte morphology (spherocytosis) and decreased membrane stability.  Here, we    characterized the Gardos channel function in vitro and in vivo in erythrocytes of 4.1-/- mice. Compared with wild-type, the Gardos channel of 4.1-/- erythrocytes showed an increase in Vmax (9.75 +/- 1.06 vs 6.08 +/- 0.09 mM cell x minute; P <    .04) and a decrease in Km (1.01 +/- 0.06 vs 1.47 +/- 1.02 microM; P < .03), indicating an increased sensitivity to activation by intracellular calcium. In vivo function of the Gardos channel was assessed by the oral administration of    clotrimazole, a well-characterized Gardos channel blocker. Clotrimazole treatment resulted in worsening of anemia and hemolysis, with decreased red cell survival and increased numbers of circulating hyperchromic spherocytes and microspherocytes.    Clotrimazole induced similar changes in 4.2-/- and band 3+/- mice, indicating that these effects of the Gardos channel are shared in different models of murine spherocytosis. Thus, potassium and water loss through the Gardos channel may play an    important protective role in compensating for the reduced surface-membrane area of hereditary spherocytosis (HS) erythrocytes and reducing hemolysis in erythrocytes with cytoskeletal impairments.</p>

	]]>
</description>

<author>Franceschi L. De et al.</author>


</item>


<item>
<title>Spontaneous corneal hem- and lymphangiogenesis in mice with destrin-mutation depend on VEGFR3 signaling.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1175</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1175</guid>
<pubDate>Tue, 08 May 2012 21:23:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lymphangiogenesis, the formation of new lymphatic vessels, is important for tumor metastasis and induction of immunity to peripheral antigens including organ transplants. We herein describe a novel mouse model of spontaneous,    secondary lymphangiogenesis in the normally avascular cornea.  corn1 mice, which suffer from a deletion in the gene encoding the cytoskeletal protein destrin, develop hemangiogenesis as well as spontaneous outgrowth of LYVE-1+++/CD31+ lymphatic    vessels into the cornea starting at age 4 weeks. Corneal lymphangiogenesis is delayed in onset, is less intense, and regresses earlier compared with hemangiogenesis.  Moreover, the lymphangiogenesis is preceded only by a mild recruitment of CD45+    inflammatory cells into the cornea. In contrast to mice with inflammation-induced hem- and lymphangiogenesis, corn1 mice do not develop breakdown of the blood-aqueous barrier. Finally, in this novel mouse model, a blocking anti-VEGFR3 antibody    significantly inhibited not only lymph- but also hemangiogenesis. In summary, destrin deletion has differential effects on spontaneous hem- and lymphangiogenesis in the normally avascular cornea and represents a novel mouse model to study the    mechanisms of lymphangiogenesis and to test the antihem- and antilymphangiogenic properties of known or new antiangiogenic agents.</p>

	]]>
</description>

<author>C Cursiefen et al.</author>


</item>


<item>
<title>Development of functional human blood and immune systems in NOD/SCID/IL2 receptor {gamma} chain(null) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1174</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1174</guid>
<pubDate>Tue, 08 May 2012 21:22:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Here we report that a new nonobese diabetic/severe combined immunodeficient (NOD/SCID) mouse line harboring a complete null mutation of the common cytokine receptor gamma chain (NOD/SCID/interleukin 2 receptor [IL2r] gamma(null))    efficiently supports development of functional human hemato-lymphopoiesis. Purified human (h) CD34(+) or hCD34(+)hCD38(-) cord blood (CB) cells were transplanted into NOD/SCID/IL2rgamma(null) newborns via a facial vein. In all recipients injected    with 10(5) hCD34(+) or 2 x 10(4) hCD34(+)hCD38(-) CB cells, human hematopoietic cells were reconstituted at approximately 70% of chimerisms.  A high percentage of the human hematopoietic cell chimerism persisted for more than 24 weeks after    transplantation, and hCD34(+) bone marrow grafts of primary recipients could reconstitute hematopoiesis in secondary NOD/SCID/IL2rgamma(null) recipients, suggesting that this system can support self-renewal of human hematopoietic stem cells.    hCD34(+)hCD38(-) CB cells differentiated into mature blood cells, including myelomonocytes, dendritic cells, erythrocytes, platelets, and lymphocytes. Differentiation into each lineage occurred via developmental intermediates such as common    lymphoid progenitors and common myeloid progenitors, recapitulating the steady-state human hematopoiesis. B cells underwent normal class switching, and produced antigen-specific immunoglobulins (Igs). T cells displayed the human leukocyte antigen    (HLA)-dependent cytotoxic function.  Furthermore, human IgA-secreting B cells were found in the intestinal mucosa, suggesting reconstitution of human mucosal immunity. Thus, the NOD/SCID/IL2rgamma(null) newborn system might be an important    experimental model to study the human hemato-lymphoid system.</p>

	]]>
</description>

<author>F Ishikawa et al.</author>


</item>


<item>
<title>Downregulation of apoptosis-inducing factor in harlequin mutant mice sensitizes the myocardium to oxidative stress-related cell death and pressure overload-induced decompensation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1173</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1173</guid>
<pubDate>Tue, 08 May 2012 21:22:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Apoptosis-inducing factor (AIF), or programmed cell death 8 (Pdcd8), is a highly conserved, ubiquitous flavoprotein localized in the mitochondrial intermembrane space. In vivo, AIF provides protection against neuronal apoptosis    induced by oxidative stress. Conversely, in vitro, AIF has been demonstrated to have a proapoptotic role when, on induction of the mitochondrial death pathway, AIF translocates to the nucleus where it facilitates chromatin condensation and large    scale DNA fragmentation. To determine the role of AIF in myocardial apoptotic processes, we examined cardiomyocytes from an AIF-deficient mouse mutant, Harlequin (Hq). Hq mutant cardiomyocytes demonstrated increased sensitivity to H2O2-induced    cell death. Further, Hq hearts subjected to ischemia/reperfusion revealed more cardiac damage and, unlike wild-type mice, the amount of damage increased with the age of the animal. Aortic banding caused enhanced hypertrophy, increased    cardiomyocyte apoptotic and necrotic cell death, and accelerated progression toward maladaptive left ventricular remodeling in Hq mutant mice compared with wild-type counterparts. These findings correlated with a reduced capacity of    subsarcolemmal mitochondria from Hq mutant hearts to scavenge free radicals. Together, these data demonstrate a critical role for AIF as a cardiac antioxidant in the protection against oxidative stress-induced cell death and development of heart    failure induced by pressure overload.</p>

	]]>
</description>

<author>Empel VPM van et al.</author>


</item>


<item>
<title>A procedure for assessing GO annotation consistency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1172</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1172</guid>
<pubDate>Tue, 08 May 2012 21:22:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>MOTIVATION: The Gene Ontology (GO) is widely used to annotate molecular attributes of genes and gene products. Multiple groups undertaking functional annotations of genomes contribute their annotation sets to the GO database    resource and these data are subsequently used in comparative functional analysis research. Although GO curators adhere to the same protocols and standards while assigning GO annotations, the specific procedure followed by each annotation group    can vary. Since differences in application of annotation standards would dilute the effectiveness of comparative analysis, methods for assessing annotation consistency are essential. The development of methodologies that are broadly applicable    for the assessment of GO annotation consistency is an important issue for the comparative genomics community. RESULTS: We have developed a methodology for assessing the consistency of GO annotations provided by different annotation groups. The    method is completely general and can be applied to compare any two sets of GO annotations. This is the first attempt to assess cross-species GO annotation consistency. Our method compares annotation sets utilizing the hierarchical structure of    the GO to compare GO annotations between orthologous gene pairs. The method produces a report on the annotation consistency and inconsistency for each orthologous pair. We present results obtained by comparing GO annotations for mouse and human    gene sets. AVAILABILITY: The complete current MGI_GOA GO annotation consistency report is available online at http://www.spatial.maine.edu/~mdolan/ CONTACT: mdolan@informatics.jax.org.</p>

	]]>
</description>

<author>M E. Dolan et al.</author>


</item>


<item>
<title>nm1054: a spontaneous, recessive, hypochromic, microcytic anemia mutation in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1171</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1171</guid>
<pubDate>Tue, 08 May 2012 21:22:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hypochromic, microcytic anemias are typically the result of inadequate hemoglobin production because of globin defects or iron deficiency. Here, we describe the phenotypic characteristics and pathogenesis of a new recessive,    hypochromic, microcytic anemia mouse mutant, nm1054. Although the mutation nm1054 is pleiotropic, also resulting in sparse hair, male infertility, failure to thrive, and hydrocephaly, the anemia is the focus of this study. Hematologic analysis    reveals a moderately severe, congenital, hypochromic, microcytic anemia, with an elevated red cell zinc protoporphyrin, consistent with functional erythroid iron deficiency.  However, serum and tissue iron analyses show that nm1054 animals are    not systemically iron deficient. From hematopoietic stem cell transplantation and iron uptake studies in nm1054 reticulocytes, we provide evidence that the nm1054 anemia is due to an intrinsic hematopoietic defect resulting in inefficient    transferrin-dependent iron uptake by erythroid precursors.  Linkage studies demonstrate that nm1054 maps to a genetic locus not previously implicated in microcytic anemia or iron phenotypes.</p>

	]]>
</description>

<author>R S. Ohgami et al.</author>


</item>


<item>
<title>PACdb: PolyA Cleavage Site and 3&apos;-UTR Database.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1170</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1170</guid>
<pubDate>Tue, 08 May 2012 21:21:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>SUMMARY: The PolyA Cleavage Site and 3'-UTR Database (PACdb) is a web-accessible database that catalogs putative 3'-processing sites and 3'-UTR sequences for multiple organisms. Sites have been identified primarily via expressed    sequence tag-genome alignments, enabling delineation of both the specificities and heterogeneity of 3'-processing events. AVAILABILITY: By web browser or CGI: PACdb: http://harlequin.jax.org/pacdb/; AtPACdb: http://harlequin.jax.org/atpacdb/.    SUPPLEMENTARY INFORMATION: Available online at http://harlequin.jax.org/pacdb/supplemental.php.</p>

	]]>
</description>

<author>J M. Brockman et al.</author>


</item>


<item>
<title>Mice lacking the p53/p63 target gene Perp are resistant to papilloma development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1169</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1169</guid>
<pubDate>Tue, 08 May 2012 21:21:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Perp is a target of the p53 tumor suppressor involved in the DNA damage-induced apoptosis pathway. In addition, Perp is a target of the p53-related transcription factor p63 during skin development, where it participates in cell-cell    adhesion mediated through desmosomes. Here we test the role of Perp in tumorigenesis in a two-step skin carcinogenesis model system. We find that mice lacking Perp in the skin are resistant to papilloma development, displaying fewer and smaller    papillomas than wild-type mice. Proliferation levels, apoptotic indices and differentiation patterns are similar in the skin of treated Perp-deficient and wild-type mice. Instead, impaired adhesion through aberrant desmosome assembly may explain    the diminished tumor development in the absence of Perp. These studies indicate that in certain contexts, Perp is required for efficient carcinogenesis and suggest a role for intact cell-cell adhesion in supporting tumor development in these    settings.</p>

	]]>
</description>

<author>M R. Marques et al.</author>


</item>


<item>
<title>Early neoplastic and metastatic mammary tumours of transgenic mice detected by 5-aminolevulinic acid-stimulated protoporphyrin IX accumulation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1168</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1168</guid>
<pubDate>Tue, 08 May 2012 21:21:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>A photodynamic technique for human breast cancer detection founded upon the ability of tumour cells to rapidly accumulate the fluorescent product protoporphyrin IX (PpIX) has been applied to transgenic mouse models of mammary    tumorigenesis. A major goal of this investigation was to determine whether mouse mammary tumours are reliable models of human disease in terms of PpIX accumulation, for future mechanistic and therapeutic studies. The haeme substrate    5-aminolevulinic acid (5-ALA) (200 mg kg(-1)) was administered to mouse strains that develop mammary tumours of various histological subtypes upon expression of the transgenic oncogenes HRAS, Polyoma Virus middle T antigen, or Simian Virus 40    large T antigen in the mammary gland. Early neoplastic lesions, primary tumours and metastases showed consistent and rapid PpIX accumulation compared to the normal surrounding tissues, as evidenced by red fluorescence (635 nm) when the tumours    were directly illuminated with blue light (380-440 nm). Detection of mouse mammary tumours at the stage of ductal carcinoma in situ by red fluorescence emissions suggests that enhanced PpIX synthesis is a good marker for early tumorigenic    processes in the mammary gland. We propose the mouse models provide an ideal experimental system for further investigation of the early diagnostic and therapeutic potential of 5-ALA-stimulated PpIX accumulation in human breast cancer    patients.</p>

	]]>
</description>

<author>A M. Dorward et al.</author>


</item>


<item>
<title>Tumor-secreted vascular endothelial growth factor-C is necessary for prostate cancer lymphangiogenesis, but lymphangiogenesis is unnecessary for lymph node metastasis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1167</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1167</guid>
<pubDate>Tue, 08 May 2012 21:21:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dissemination to draining lymph nodes is a frequent first step in prostate cancer metastasis. Although tumors metastasize to lymph nodes via the lymphatics, the importance of lymphangiogenesis in mediating the process remains    controversial. Here, we inhibit intratumoral lymphangiogenesis in s.c. and surgical orthotopic implantation mouse models of human prostate cancer using several strategies. Stable expression of small interfering RNAs (siRNA) targeted against human    vascular endothelial growth factor-C (VEGF-C) in PC-3 cells reduced intratumoral lymphatics by 99% in s.c.  tumors, indicating that tumor-secreted VEGF-C is necessary for lymphangiogenesis. Expression of siRNAs against human VEGF-A somewhat    reduced tumor lymphangiogenesis. Secretion of a soluble VEGF receptor-3/Flt4 fusion protein by PC-3 cells reduced intratumoral lymphatics by 100% in s.c. tumors. Combination of soluble Flt4 and VEGF-C siRNA yielded >92% reduction of intratumoral    lymphatics in orthotopic prostate tumors. However, metastasis to lymph nodes was not significantly affected regardless of intratumoral lymphatic vessel density. The abundance of marginal lymphatics at the tumor-stromal interface was unchanged in    orthotopic tumors whose intratumoral lymphatics were inhibited, suggesting that these marginal vessels could be sufficient for lymph node metastasis. Hematogenous metastasis (blood tumor burden, lung metastasis) correlated with degree of lymph    node invasion. We also analyzed the lymphatics in spontaneous transgenic adenocarcinomas of the mouse prostate which metastasize to lymph nodes. Progression from well-differentiated prostate intraepithelial neoplasia to metastatic,    undifferentiated adenocarcinoma was accompanied by loss of lymphatics.  These results suggest that tumor-secreted VEGF-C and, to a lesser extent, VEGF-A, are important for inducing prostate cancer intratumoral lymphangiogenesis but are    unnecessary for lymph node metastasis.</p>

	]]>
</description>

<author>S Y. Wong et al.</author>


</item>


<item>
<title>A direct test of potential roles for beta3 and beta5 integrins in growth and metastasis of murine mammary carcinomas.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1166</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1166</guid>
<pubDate>Tue, 08 May 2012 21:20:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>alphavbeta3 or alphavbeta5 integrins are widely expressed on blood and endothelial cells. Inhibition of the functions of these integrins has been reported to suppress neovascularization and tumor growth, suggesting that they may be    critical modulators of angiogenesis. However, mice lacking these integrins exhibit extensive angiogenesis. Tumors arising from s.c.  injections of tumor cells into mice lacking one or both integrins show enhanced tumor growth compared with growth    in control mice due to both increased angiogenesis and to altered innate immune response. Other data suggest additional roles for these integrins, on either platelets or the tumor cells themselves, in enhancing tumor progression and metastasis.     Here, we investigate the involvement of beta3 and beta5 integrins in the development and progression of mammary carcinomas. We intercrossed mouse mammary tumor virus (MMTV)-c-neu transgenic mice with beta3 or beta5 or beta3beta5    integrin-deficient mice and observed that multiple, large mammary tumors developed in 100% of mice on all genetic backgrounds. A statistically significant earlier onset of tumor growth was observed in the MMTV-c-neu/beta3beta5 integrin-null    females compared with control mice. No major differences were observed in tumor size or number, vessel number or vessel structure and lung metastases were observed with similar frequency and size in all strains. MMTV-c-neu/beta3beta5    integrin-null mice had higher numbers of mammary acini, which may account for the earlier onset of tumors in this strain. These data indicate that alphavbeta3 or alphavbeta5 integrins are not essential for tumor growth and progression, although    they might play some role in mammary gland development.</p>

	]]>
</description>

<author>D Taverna et al.</author>


</item>


<item>
<title>An improved technique for tail-cuff blood pressure measurements with dark-tailed mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1165</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1165</guid>
<pubDate>Tue, 08 May 2012 21:20:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Study of the genetics of hypertension has been facilitated greatly by the use of mice with modified genes that affect blood pressure. A current successful method for measuring blood pressure in mice relies on detection of light    passing through the tail to determine the pressure in a tail-cuff necessary to stop pulsed flow. Success in obtaining reliable blood pressure measurements in light-tailed strains of mice (e.g., C57BL/6J) has been excellent. However, in our and    others' experience, mice having highly pigmented tails (e.g., 129S6/SvEvTac) have yielded less consistent measurements. We report here that simple modifications to the channel containing the pulse detection sensor can greatly improve the pulse    detection of dark-tailed mice. The first modification--lining the sensor channel with four layers of clear plastic wrap--increased the frequency of successful blood pressure measurements of 129S6/SvEvTac mice twofold and reduced variability by    one-third. The second modification--lining the sides of the channel with reflective foil--also improved the success rate with dark-tailed mice. Mean blood pressures were unaffected by these modifications, which enhance detection of the pulse wave    and likely will be helpful in diverse applications in which blood pressure is measured in rodent strains with pigmented tails.</p>

	]]>
</description>

<author>J R. Hagaman et al.</author>


</item>


<item>
<title>&quot;Agouti NOD&quot;: identification of a CBA-derived Idd locus on Chromosome 7 and its use for chimera production with NOD embryonic stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1164</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1164</guid>
<pubDate>Tue, 08 May 2012 21:20:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Penetrance of the complex of genes predisposing the nonobese diabetic (NOD) mouse to autoimmune diabetes is affected by the maternal environment. NOD.CBALs-Tyr(+)/Lt is an agouti-pigmented Chromosome 7 congenic stock of NOD/Lt mice    produced as a resource for embryo transfer experiments to provide the necessary maternal factors and allow the easy identification of NOD (albino) embryo donor phenotype. CBcNO6/Lt, a recombinant congenic agouti stock already containing    approximately 50% NOD genome, was used as the donor source of a wild-type CBA tyrosinase allele.  When the incidence of diabetes was assessed after nine generations of backcrossing and one generation of sib-sib mating, significant reduction in    diabetes development was observed. No difference in diabetes development was observed in Tyr/Tyr(c) heterozygotes, showing that protection was recessive. Analysis of diabetes progression in another NOD stock congenic for C57BL/6 alleles on    Chromosome 7 linked to the glucose phosphate isomerase (Gpi1(b)) locus provided no protection, indicating that the diabetes resistance (Idd) gene was distal to 34 cM (D7Mit346).  Approximately 5 cM of the distal congenic region overlaps a region    from C57L previously associated with protection when homozygous. The delayed onset and reduced frequency of diabetes in the NOD.CBALs-Tyr(+)/Lt stock is an advantage when females of this stock are used as surrogate mothers in studies involving    hysterectomy or embryo transfers. Indeed, a newly developed NOD embryonic stem (ES) cell line injected into NOD.CBALs- Tyr(+)/Lt blastocysts produced approximately 50% live-born mice, of which approximately 11% were chimeric. Presumably because    of high genomic instability, no germline transmission was observed.</p>

	]]>
</description>

<author>J Chen et al.</author>


</item>


<item>
<title>Inherited glaucoma in DBA/2J mice: pertinent disease features for studying the neurodegeneration.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1163</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1163</guid>
<pubDate>Tue, 08 May 2012 21:20:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>The glaucomas are neurodegenerative diseases involving death of retinal ganglion cells and optic nerve head excavation. A major risk factor for this neurodegeneration is a harmfully elevated intraocular pressure (IOP).  Human    glaucomas are typically complex, progressive diseases that are prevalent in the elderly. Family history and genetic factors are clearly important in human glaucoma. Mouse studies have proven helpful for investigating the genetic and mechanistic    basis of complex diseases. We previously reported inherited, age-related progressive glaucoma in DBA/2J mice. Here, we report our updated findings from studying the disease in a large number of DBA/2J mice. The period when mice have elevated IOP    extends from 6 months to 16 months, with 8-9 months representing an important transition to high IOP for many mice. Optic nerve degeneration follows IOP elevation, with the majority of optic nerves being severely damaged by 12 months of age. This    information should help with the design of experiments, and we present the data in a manner that will be useful for future studies of retinal ganglion cell degeneration and optic neuropathy.</p>

	]]>
</description>

<author>R T. Libby et al.</author>


</item>


<item>
<title>Society for Reproductive Biology Founders&apos; Lecture 2005. Control of metabolic cooperativity between oocytes and their companion granulosa cells by mouse oocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1162</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1162</guid>
<pubDate>Tue, 08 May 2012 21:20:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Oocytes orchestrate the rate of follicular development and expression of genes in the surrounding granulosa cells. Oocytes are deficient in their ability to carry out some metabolic processes, such as glycolysis and amino acid    uptake, and depend on the cooperation of granulosa cells to carry out these processes. In this dependency, the oocyte was previously considered a passive recipient of the nutritional support from granulosa cells. However, recent studies indicate    an active role for the oocyte in controlling metabolic activity in granulosa cells. The ability of oocytes to control granulosa cell metabolism is achieved, at least in part, by regulating granulosa cell expression of genes encoding proteins    involved in the metabolic processes. This review summarises current knowledge of intercellular communication between oocytes and granulosa cells from the perspective of oocyte control of gene expression in granulosa cells and metabolic    cooperativity between the two cell types. The oocyte probably controls metabolism in granulosa cells to provide metabolites for its own development. In addition, we hypothesise that oocytes use their ability to regulate metabolic pathways in    granulosa cells to orchestrate the rate of follicular development.</p>

	]]>
</description>

<author>K Sugiura et al.</author>


</item>


<item>
<title>Analysis of hair follicles in mutant laboratory mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1161</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1161</guid>
<pubDate>Tue, 08 May 2012 21:19:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hair follicles, or pilosebacous units, are complicated anatomic structures. Analysis of abnormalities of these structures can be difficult without adequate knowledge of normal changes associated with embryonic and postnatal    development as well as regular cycling. A variety of systematic approaches to analysis of the pilosebacous unit are provided here.</p>

	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title>The functional relevance of the type 1 cytokines IFN-gamma and IL-2 in alopecia areata of C3H/HeJ mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1160</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1160</guid>
<pubDate>Tue, 08 May 2012 21:19:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Paul P. Freyschmidt et al.</author>


</item>


<item>
<title>Complete FcRn dependence for intravenous Ig therapy in autoimmune skin blistering diseases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1159</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1159</guid>
<pubDate>Tue, 08 May 2012 21:19:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Numerous mechanisms of action have been proposed for intravenous Ig (IVIG). In this study, we used IgG passive transfer murine models of bullous pemphigoid (BP), pemphigus foliaceus (PF), and pemphigus vulgaris (PV) to test the    hypothesis that the effect of IVIG in autoantibody-mediated cutaneous bullous diseases is to accelerate the degradation of pathogenic IgG by saturation of the MHC-like Fc receptor neonatal Fc receptor (FcRn). BP, PF, and PV are organ-specific    antibody-mediated diseases in which autoantibodies target the hemidesmosomal antigen BP180 and desmosomal antigens Dsg1 and Dsg3, respectively. Antibodies against BP180, Dsg1, and Dsg3, when injected into neonatal mice, induce the BP, PF, and PV    disease phenotypes, respectively.  We found that FcRn-deficient mice were resistant to experimental BP, PF, and PV. Circulating levels of pathogenic IgG in FcRn-deficient mice were significantly reduced compared with those in WT mice.    Administration of high-dose human IgG (HDIG) to WT mice also drastically reduced circulating pathogenic IgG levels and prevented blistering. In FcRn-deficient mice, no additional protective effect with HDIG was realized. These data demonstrate    that the therapeutic efficacy of HDIG treatment in the pemphigus and pemphigoid models is dependent on FcRn. Thus, FcRn is a promising therapeutic target for treating such IgG-mediated autoimmune diseases.</p>

	]]>
</description>

<author>N Li et al.</author>


</item>


<item>
<title>The role of parathyroid hormone in the management of osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1158</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1158</guid>
<pubDate>Tue, 08 May 2012 21:19:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>It has been over 2 years since parathyroid hormone (PTH 1-34) was approved in the US and Europe for the treatment of osteoporosis in postmenopausal women and men. Clinical experience with this peptide has enhanced confidence in its    use and its application in specific clinical scenarios.  There is no doubt that PTH 1-34 is safe and effective in reducing spine and non-vertebral fractures in men and women. However, the lack of several randomized placebo-controlled trials and    their relatively short duration raise several questions that still need to be answered. This paper reviews three major areas of uncertainty: (1) Is there significant heterogeneity in the bone density response of individuals to PTH? If so, what    factors are important predictors? (2) What other regimens are available for PTH use? (3) What, if anything, should the clinician do after PTH is discontinued? Answers to these questions will undoubtedly lead to even greater utilization of this    drug and some of its future derivatives.</p>

	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title>p53 is a suppressor of inflammatory response in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1157</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1157</guid>
<pubDate>Tue, 08 May 2012 21:18:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chronic inflammation is known to promote cancer, suggesting that negative regulation of inflammation is likely to be tumor suppressive. We found that p53 is a general inhibitor of inflammation that acts as an antagonist of nuclear    factor kappaB (NFkappaB). We first observed striking similarities in global gene expression profiles in human prostate cancer cells LNCaP transduced with p53 inhibitory genetic element or treated with TNF, suggesting that p53 inhibits    transcription of TNF-inducible genes that are largely regulated by NFkappaB. Consistently, ectopically expressed p53 acts as an inhibitor of transcription of NFkappaB-dependent promoters. Furthermore, suppression of inflammatory response by p53    was observed in vivo in mice by comparing wild-type and p53 null animals at molecular (inhibition of transcription of genes encoding cytokines and chemokines, reducing accumulation of reactive oxygen species and protein oxidation products),    cellular (activation of macrophages and neutrophil clearance) and organismal (high levels of metabolic markers of inflammation in tissues of p53-deficient mice and their hypersensitivity to LPS) levels. These observations indicate that p53,    acting through suppression of NFkappaB, plays the role of a general "buffer" of innate immune response in vivo that is well consistent with its tumor suppressor function and frequent constitutive activation of NFkappaB in tumors.</p>

	]]>
</description>

<author>E A. Komarova et al.</author>


</item>


<item>
<title>Brain lipid-binding protein is a direct target of Notch signaling in radial glial cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1156</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1156</guid>
<pubDate>Tue, 08 May 2012 21:18:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Radial glia function during CNS development both as neural progenitors and as a scaffolding supporting neuronal migration. To elucidate pathways involved in these functions, we mapped in vivo the promoter for Blbp, a radial glial    gene. We show here that a binding site for the Notch effector CBF1 is essential for all Blbp transcription in radial glia, and that BLBP expression is significantly reduced in the forebrains of mice lacking the Notch1 and Notch3 receptors. These    results identify Blbp as the first predominantly CNS-specific Notch target gene and suggest that it mediates some aspects of Notch signaling in radial glia.</p>

	]]>
</description>

<author>T E. Anthony et al.</author>


</item>


<item>
<title>Polarity of the mouse embryo is established at blastocyst and is not prepatterned.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1155</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1155</guid>
<pubDate>Tue, 08 May 2012 21:18:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Polarity formation in mammalian preimplantation embryos has long been a subject of controversy. Mammalian embryos are highly regulative, which has led to the conclusion that polarity specification does not exist until the blastocyst    stage; however, some recent reports have now suggested polarity predetermination in the egg. Our recent time-lapse recordings have demonstrated that the first cleavage plane is not predetermined in the mouse egg. Here we show that, in contrast to    previous claims, two-cell blastomeres do not differ and their precise future contribution to the inner cell mass and/or the trophectoderm cannot be anticipated. Thus, all evidence so far strongly suggests the absence of predetermined axes in the    mouse egg. We observe that the ellipsoidal zona pellucida exerts mechanical pressure and space constraints as the coalescing multiple cavities are restricted to one end of the long axis of the blastocyst. We propose that these mechanical cues, in    conjunction with the epithelial seal in the outer cell layer, lead to specification of the embryonic-abembryonic axis, thus establishing first polarity in the mouse embryo.</p>

	]]>
</description>

<author>N Motosugi et al.</author>


</item>


<item>
<title>Random mutagenesis of proximal mouse chromosome 5 uncovers predominantly embryonic lethal mutations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1154</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1154</guid>
<pubDate>Tue, 08 May 2012 21:18:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>A region-specific ENU mutagenesis screen was conducted to elucidate the functional content of proximal mouse Chr 5. We used the visibly marked, recessive, lethal inversion Rump White (Rw) as a balancer in a three-generation breeding    scheme to identify recessive mutations within the approximately 50 megabases spanned by Rw. A total of 1003 pedigrees were produced, representing the largest inversion screen performed in mice. Test-class animals, homozygous for the    ENU-mutagenized proximal Chr 5 and visibly distinguishable from nonhomozygous littermates, were screened for fertility, hearing, vestibular function, DNA repair, behavior, and dysmorphology. Lethals were identifiable by failure to derive    test-class animals within a pedigree. Embryonic lethal mutations (total of 34) were overwhelmingly the largest class of mutants recovered.  We characterized them with respect to the time of embryonic death, revealing that most act at midgestation    (8.5-10.5) or sooner. To position the mutations within the Rw region and to guide allelism tests, we performed complementation analyses with a set of new and existing chromosomal deletions, as well as standard recombinational mapping on a subset    of the mutations. By pooling the data from this and other region-specific mutagenesis projects, we calculate that the mouse genome contains approximately 3479-4825 embryonic lethal genes, or about 13.7%-19% of all genes.</p>

	]]>
</description>

<author>L Wilson et al.</author>


</item>


<item>
<title>High incidence, early onset of histiocytic sarcomas in mice with Hertwig&apos;s anemia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1153</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1153</guid>
<pubDate>Tue, 08 May 2012 21:18:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: Histiocytic sarcoma (HS) is a rare, rapidly disseminated, usually lethal tumor in humans. Treatment specific for HS has not been developed primarily due to deficiencies of appropriate animal models with high    incidence/early onset. Mice with Hertwig's anemia (an/an) provide a potential model. METHODS: Here, we compare HS susceptibility in an/an and unaffected control mice maintained on three genetic backgrounds. As a potential therapeutic measure,    genetically marked bone marrow is transplanted between high and low susceptibility animals. RESULTS: HS is detected earlier and the overall incidence is 15-fold higher in WBB6F1(F1)-an/an than in F1-+/?, B6-an/an and -+/? mice. Neither WB-an/an    nor their normal WB-+/? littermates present with HS. Liver myelopoiesis and aneuploidy coexist with HS but the former is also rampant (33.7% incidence) in HS-free +/? and an/an mice. Marrow transplantation experiments provide evidence that (1)    myelopoiesis is associated with HS and (2) early-onset/high-incidence HS is blocked by using late-onset F1-+/+ mice, as either donor or recipient. CONCLUSIONS: Homozygosity for an on an F1 genetic background is essential for    high-incidence/early-onset HS; myelopoiesis and HS coexist; and therapeutic transplantation may be feasible.</p>

	]]>
</description>

<author>J E. Barker et al.</author>


</item>


<item>
<title>Cytokinesis failure generating tetraploids promotes tumorigenesis in p53-null cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1152</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1152</guid>
<pubDate>Tue, 08 May 2012 21:17:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>A long-standing hypothesis on tumorigenesis is that cell division failure, generating genetically unstable tetraploid cells, facilitates the development of aneuploid malignancies. Here we test this idea by transiently blocking    cytokinesis in p53-null (p53-/-) mouse mammary epithelial cells (MMECs), enabling the isolation of diploid and tetraploid cultures. The tetraploid cells had an increase in the frequency of whole-chromosome mis-segregation and chromosomal    rearrangements. Only the tetraploid cells were transformed in vitro after exposure to a carcinogen.  Furthermore, in the absence of carcinogen, only the tetraploid cells gave rise to malignant mammary epithelial cancers when transplanted    subcutaneously into nude mice. These tumours all contained numerous non-reciprocal translocations and an 8-30-fold amplification of a chromosomal region containing a cluster of matrix metalloproteinase (MMP) genes. MMP overexpression is linked to    mammary tumours in humans and animal models. Thus, tetraploidy enhances the frequency of chromosomal alterations and promotes tumour development in p53-/- MMECs.</p>

	]]>
</description>

<author>T Fujiwara et al.</author>


</item>


<item>
<title>Science fact and the SENS agenda. What can we reasonably expect from ageing research?</title>
<link>http://mouseion.jax.org/stfb2000_2009/1151</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1151</guid>
<pubDate>Tue, 08 May 2012 21:17:32 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H Warner et al.</author>


</item>


<item>
<title>Developmental transcription factor slug is required for effective re-epithelialization by adult keratinocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1150</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1150</guid>
<pubDate>Tue, 08 May 2012 21:17:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>During re-epithelialization of cutaneous wounds, keratinocytes recapitulate several aspects of the embryonic process of epithelial-mesenchymal transition (EMT), including migratory activity and reduced intercellular adhesion. The    transcription factor Slug modulates EMT in the embryo and controls desmosome number in adult epithelial cells, therefore, we investigated Slug expression and function during cutaneous wound re-epithelialization. Slug expression was elevated in    keratinocytes bordering cutaneous wounds in mice in vivo, in keratinocytes migrating from mouse skin explants ex vivo, and in human keratinocytes at wound margins in vitro. Expression of the related transcription factor Snail was not    significantly modulated in keratinocytes during re-epithelialization in vitro. Epithelial cell outgrowth from skin explants of Slug knockout mice was severely compromised, indicating a critical role for Slug in epithelial keratinocyte migration.    Overexpression of Slug in cultured human keratinocytes caused increased cell spreading and desmosomal disruption, both of which were most pronounced at wound margins.  Furthermore, in vitro wound healing was markedly accelerated in keratinocytes    that ectopically expressed Slug. Taken together, these findings suggest that Slug plays an important role during wound re-epithelialization in adult skin and indicate that Slug controls some aspects of epithleial cell behavior in adult tissues as    well as during embryonic development.</p>

	]]>
</description>

<author>P Savagner et al.</author>


</item>


<item>
<title>Mutations in snail family genes enhance craniosynostosis of Twist1 haplo-insufficient mice: implications for Saethre-Chotzen Syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1149</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1149</guid>
<pubDate>Tue, 08 May 2012 21:17:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>In Drosophila, mutations in the Twist gene interact with mutations in the Snail gene. We show that the mouse Twist1 mutation interacts with Snai1 and Snai2 mutations to enhance aberrant cranial suture fusion, demonstrating that    genetic interactions between genes of the Twist and Snail families have been conserved during evolution.</p>

	]]>
</description>

<author>K F. Oram et al.</author>


</item>


<item>
<title>Meiotic messenger RNA and noncoding RNA targets of the RNA-binding protein Translin (TSN) in mouse testis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1148</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1148</guid>
<pubDate>Tue, 08 May 2012 21:16:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>In postmeiotic male germ cells, TSN, formerly known as testis brain-RNA binding protein, is found in the cytoplasm and functions as a posttranscriptional regulator of a group of genes transcribed by the transcription factor    CREM-tau. In contrast, in pachytene spermatocytes, TSN is found predominantly in nuclei. Tsn-null males show a reduced sperm count and high levels of apoptosis in meiotic cells, suggesting a critical function for TSN during meiosis. To identify    meiotic target RNAs that associate in vivo with TSN, we reversibly cross-linked TSN to RNA in testis extracts from 17-day-old and adult mice and immunoprecipitated the complexes with an affinity-purified TSN antibody. Extracts from Tsn-null mice    were used as controls. Cloning and sequencing the immunoprecipitated RNAs, we identified four new TSN target mRNAs, encoding diazepam-binding inhibitor-like 5, arylsulfatase A, a tetratricopeptide repeat structure-containing protein, and ring    finger protein 139. In contrast to the population of postmeiotic translationally delayed mRNAs that bind TSN, these four mRNAs are initially expressed in pachytene spermatocytes. In addition, anti-TSN also precipitated a nonprotein-coding RNA    (ncRNA), which is abundant in nuclei of pachytene spermatocytes and has a putative polyadenylation signal, but no open reading frame. A second similar ncRNA is adjacent to a GGA repeat, a motif frequently associated with recombination hot spots.    RNA gel-shift assays confirm that the four new target mRNAs and the ncRNA specifically bind to TSN in testis extracts.  These studies have, for the first time, identified both mRNAs and a ncRNA as TSN targets expressed during    meiosis.</p>

	]]>
</description>

<author>Y S. Cho et al.</author>


</item>


<item>
<title>Protein accumulation and neurodegeneration in the woozy mutant mouse is caused by disruption of SIL1, a cochaperone of BiP.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1147</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1147</guid>
<pubDate>Tue, 08 May 2012 21:16:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Endoplasmic reticulum (ER) chaperones and ER stress have been implicated in the pathogenesis of neurodegenerative disorders, such as Alzheimer and Parkinson diseases, but their contribution to neuron death remains uncertain. In this    study, we establish a direct in vivo link between ER dysfunction and neurodegeneration. Mice homozygous with respect to the woozy (wz) mutation develop adult-onset ataxia with cerebellar Purkinje cell loss. Affected cells have intracellular    protein accumulations reminiscent of protein inclusions in both the ER and the nucleus. In addition, upregulation of the unfolded protein response, suggestive of ER stress, occurs in mutant Purkinje cells. We report that the wz mutation disrupts    the gene Sil1 that encodes an adenine nucleotide exchange factor of BiP, a crucial ER chaperone. These findings provide evidence that perturbation of ER chaperone function in terminally differentiated neurons leads to protein accumulation, ER    stress and subsequent neurodegeneration.</p>

	]]>
</description>

<author>L Zhao et al.</author>


</item>


<item>
<title>Biodistribution of (225)Ra citrate in mice: retention of daughter radioisotopes in bone.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1146</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1146</guid>
<pubDate>Tue, 08 May 2012 21:16:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alpha-particle-emitting radionuclides have potential for therapy of localized disease due to their high linear energy transformation and short pathlengths. Radiometals that home naturally to bone can be exploited for this purpose,    and (223)Ra (t(1/2)=11.4 days) recently has been studied for therapy of bone tumors in mice and rats. Actinium-225 (t(1/2)=10 days) is also an attractive radioisotope for endoradiotherapy. In a single decay of a (225)Ac nucleus and its subsequent    decay daughters, over 27 MeV ( approximately 90% of total energy) is released by sequential emission of four alpha particles, ranging in energy from 5.7 to 8.4 MeV. Although Ac(3+) does not home naturally to bone, its parent radioisotope (225)Ra    (beta(-), t(1/2)=15 days) can be used as an in vivo source for (225)Ac.  Thus, injection of (225)Ra takes advantage of the bone-homing properties of radium coupled with the significant amount of energy released from the (225)Ac decay chain. Our    data confirm that a large fraction of radium citrate injected intravenously into mice localizes rapidly in bone.  Injected doses per gram (ID/g) for (225)Ra range from 25% in skull to about 10% in sternum. Once deposited, the (225)Ra remains in    the bone with a biological half life of >40 days. Furthermore, >95% of the daughter radioisotope, (225)Ac, is retained in the bone. However, a significant fraction of one of the daughter radioisotopes, (213)Bi, is found in kidney. The    biodistribution data indicate that (225)Ra injection should be a powerful agent for killing cells associated with bone; however, the toxicity of this radioisotope which is similar to that of other alpha emitters limits the dose that can be    tolerated.</p>

	]]>
</description>

<author>S J. Kennel et al.</author>


</item>


<item>
<title>Increased expression of chemokines in the skin of chronic proliferative dermatitis mutant mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1145</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1145</guid>
<pubDate>Tue, 08 May 2012 21:15:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chemokines direct the migration of leukocytes to sites of inflammation and are potential targets for anti-inflammatory therapy. Chronic proliferative dermatitis (cpdm/cpdm) mutant mice develop a persistent eosinophilic dermatitis    associated with increased T(H)2 cytokines in the skin.  Expression patterns of chemokines in the skin of cpdm/cpdm mice were evaluated to define the mechanisms driving cutaneous infiltration by leukocytes. RNA isolated from the skin of mutant and    littermate control mice revealed a significant increase in Ccl1 (TCA-3), Ccl2 (MCP-1), Ccl11 (eotaxin), Ccl17 (TARC), Cxcl10 (IP-10), and the chemokine receptor Ccr3.  The concentration of CCL11 protein was increased two- to threefold in the skin    of cpdm/cpdm mice by enzyme-linked immunosorbent assay. In vitro culture of primary dermal fibroblasts from cpdm/cpdm and control mice with tumor necrosis factor, IL-4, and IL-13 stimulation did not reveal differences in their ability to secrete    CCL11, suggesting that the increased chemokine expression observed in the skin of cpdm/cpdm mice is most likely caused by the increased T(H)2 cytokines in the dermis of this mouse model. Treatment of cpdm/cpdm mice with CCL11-neutralizing    polyclonal antibodies did not affect the number of eosinophils in the skin or the severity of the dermatitis. Neutralizing multiple chemokines or chemokine receptors may be necessary to decrease eosinophil accumulation.  The cpdm/cpdm mutant    mouse is a potentially useful model to determine the role of various chemokines in eosinophil accumulation in chronic inflammation.</p>

	]]>
</description>

<author>M L. Renninger et al.</author>


</item>


<item>
<title>Reduced expression of interleukin-2 decreases the frequency of alopecia areata onset in C3H/HeJ mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1144</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1144</guid>
<pubDate>Tue, 08 May 2012 21:15:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata (AA) is an autoimmune hair loss disease, that can be transferred between C3H/HeJ mice by skin grafting. We explored whether AA susceptibility is influenced by the availability of interleukin (IL)-2, a cytokine with    leukocyte activating and regulatory properties. Mice heterozygous for a targeted deletion of IL-2 from the histocompatible C3.129P2(B6)-Il2(tm1Hor) substrain, that produce reduced levels of IL-2, were examined for AA development after grafting    skin from AA-affected C3H/HeJ mice. After grafting, nine of 19 (47%) heterozygous IL-2+/-versus 16 of 18 (88%) IL-2+/+ wild-type littermates developed AA. Although dense follicular leukocyte infiltrates were apparent in AA affected wild-type    mice, AA-developing IL-2+/- littermates had a reduced leukocyte infiltration, and AA-resistant IL-2+/- mice had no inflammation. Lymph node cell analysis revealed a reduction in leukocyte activation markers in AA-developing IL-2+/- mice. IL-2+/-    mice presented with low level expression of cytokines (IL-4, IL-10, interferon-gamma, transforming growth factor-beta), upregulation of tumor necrosis factor receptors, and increased leukocyte apoptosis susceptibility independent of AA    expression.  In the skin, CD4+ cells and monocytes were reduced; activation markers were not upregulated and very few CD44v3+ or CD44v10+ leukocytes were recovered. Taken together, our data suggest that AA resistance of IL-2+/- mice is because of    the failure of activated leukocyte recruitment, thus pointing toward an involvement of IL-2 in AA pathogenesis.</p>

	]]>
</description>

<author>Paul P. Freyschmidt et al.</author>


</item>


<item>
<title>Hepatic gene and protein expression of primary components of the IGF-I axis in long lived Snell dwarf mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1143</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1143</guid>
<pubDate>Tue, 08 May 2012 21:15:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recent evidence indicates that the GH/IGF-I axis plays a key role in the control of aging and longevity. To better understand this biological relationship we examined the mRNA and corresponding protein levels of primary IGF-I axis    genes in the livers of young and aged long-lived Snell dwarf mice relative to their age-matched controls. We demonstrated that the level of IGF-I and ALS mRNAs is dramatically decreased in both young and aged dwarf livers, transcripts encoding    IGF-IR and IGFBP-I are elevated in young dwarfs, but normalize to control levels in aged dwarf livers while transcripts encoding IGFBP-3 are elevated only in aged controls. Interestingly, regulation at the protein level of several IGF-I axis    components in the Snell dwarf appears to involve both altered gene expression and post-translational regulation. In this study, we reveal both concordant and discordant relationships between mRNA and protein levels for particular components of    the IGF-I axis, illustrating that some of these gene products are not solely regulated by transcriptional mechanisms. These results are consistent with a delay in the molecular maturation of the IGF-I axis in dwarf livers, suggesting the    preservation of some neonatal characteristics in young adult and aged dwarf livers. Our studies provide gene expression and protein abundance profiles for components of IGF-I axis that are distinguishing characteristics of both young and aged    dwarf mice, and suggest that delayed development of the IGF-I axis in the young adult Pit1(dw/dwJ) dwarf liver may play an important role in the endocrine regulation of mammalian longevity.</p>

	]]>
</description>

<author>J Papaconstantinou et al.</author>


</item>


<item>
<title>Identification of bronchioalveolar stem cells in normal lung and lung cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1142</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1142</guid>
<pubDate>Tue, 08 May 2012 21:15:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Injury models have suggested that the lung contains anatomically and functionally distinct epithelial stem cell populations. We have isolated such a regional pulmonary stem cell population, termed bronchioalveolar stem cells    (BASCs). Identified at the bronchioalveolar duct junction, BASCs were resistant to bronchiolar and alveolar damage and proliferated during epithelial cell renewal in vivo. BASCs exhibited self-renewal and were multipotent in clonal assays,    highlighting their stem cell properties. Furthermore, BASCs expanded in response to oncogenic K-ras in culture and in precursors of lung tumors in vivo. These data support the hypothesis that BASCs are a stem cell population that maintains the    bronchiolar Clara cells and alveolar cells of the distal lung and that their transformed counterparts give rise to adenocarcinoma. Although bronchiolar cells and alveolar cells are proposed to be the precursor cells of adenocarcinoma, this work    points to BASCs as the putative cells of origin for this subtype of lung cancer.</p>

	]]>
</description>

<author>C F. Kim et al.</author>


</item>


<item>
<title>Mice severely deficient in growth hormone have normal hematopoiesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1141</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1141</guid>
<pubDate>Tue, 08 May 2012 21:14:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: Many studies suggest that growth hormone (GH) is important for hematopoietic stem cell (HSC) function. The objective of this study is to determine if the genetic absence of GH reduces hematopoietic function and recovery,    by testing various points in hematopoiesis, from numbers and functional abilities of primitive stem cells to the maintenance of normal numbers of differentiated cells. MATERIALS AND METHODS: Analyses were conducted on blood and bone marrow to    compare GH-deficient C57BL/6J-Ghrhr(lit) / Ghrhr(lit) (lit/lit) mice with their normal (lit/+) littermates. Flow cytometric analysis was used to measure numbers of HSC and progenitor cells based on antigenic markers. Spleen colony-forming units    (CFU-S) were examined to determine function of common myeloid progenitor (CMP) cells. Competitive repopulation assays were conducted to test whether normally functional HSCs are produced and supported in the lit/lit hematopoietic environment.    RESULTS: The lit/lit mutant mice produced HSC and progenitor cells at least as well as their lit/+ control littermates. In CFU-S assays, the CMP from the lit/lit mice functioned as well as those from the lit/+ controls. Marrow cells from lit/lit    mice repopulated irradiated recipients long-term better than did marrow cells from C57BL/6J(+/+) controls; thus, HSC produced in the absence of GH can replenish irradiated recipients. When lit/lit mice were used as irradiated recipients, they    supported HSC function as well as lit/+ control recipients did; thus, the lit/lit hematopoietic environment can support normal hematopoiesis.</p>

	]]>
</description>

<author>Y Sharma et al.</author>


</item>


<item>
<title>Bioinformatics toolbox for narrowing rodent quantitative trait loci.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1140</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1140</guid>
<pubDate>Tue, 08 May 2012 21:14:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Quantitative trait locus (QTL) analysis is a powerful method for localizing disease genes, but identifying the causal gene remains difficult. Rodent models of disease facilitate QTL gene identification, and causal genes underlying    rodent QTL are often associated with the corresponding human diseases. Recently developed bioinformatics methods, including comparative genomics, combined cross analysis, interval-specific and genome-wide haplotype analysis, followed by sequence    and expression analysis, each facilitated by public databases, provide new tools for narrowing rodent QTLs. Here we discuss each tool, illustrate its application and generate a bioinformatics strategy for narrowing QTLs.  Combining these    bioinformatics tools with classical experimental methods should accelerate QTL gene identification.</p>

	]]>
</description>

<author>K DiPetrillo et al.</author>


</item>


<item>
<title>Quantitative trait loci for baseline white blood cell count, platelet count, and mean platelet volume.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1139</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1139</guid>
<pubDate>Tue, 08 May 2012 21:14:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>A substantial genetic contribution to baseline peripheral blood counts has been established. We performed quantitative trait locus/loci (QTL) analyses to identify chromosome (Chr) regions harboring genes influencing the baseline    white blood cell (WBC) count, platelet (Plt) count, and mean platelet volume (MPV) in F(2) intercrosses between NZW/LacJ, SM/J, and C57BLKS/J inbred mice. We identified six significant WBC QTL: Wbcq1 (peak LOD score at 38 cM, Chr 1), Wbcq2 (42    cM, Chr 3), Wbcq3 (0 cM, Chr 15), Wbcq4 (58 cM, Chr 1), Wbcq5 (82 cM, Chr 1), and Wbcq6 (8 cM, Chr 14).  Three significant Plt QTL were identified: Pltq1 (24 cM, Chr 2), Pltq2 (36 cM, Chr 7), and Pltq3 (10 cM, Chr 12). Two significant MPV QTL    were identified, Mpvq1 (62 cM, Chr 15) and Mpvq2 (44 cM, Chr 8). In total, the WBC QTL accounted for up to 31% of the total variance in baseline WBC count, while the Plt and MPV QTL accounted for up to 30% and 49% of the total variance,    respectively. These analyses underscore the genetic complexity underlying these traits in normal populations and provide the basis for future studies to identify novel genes involved in the regulation of mammalian hematopoiesis.</p>

	]]>
</description>

<author>L L. Peters et al.</author>


</item>


<item>
<title>Supplementary data need to be kept in public repositories.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1138</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1138</guid>
<pubDate>Tue, 08 May 2012 21:13:53 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C Santos et al.</author>


</item>


<item>
<title>Gene expression patterns in bone after 4 days of hind-limb unloading in two inbred strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1137</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1137</guid>
<pubDate>Tue, 08 May 2012 21:13:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>INTRODUCTION: An improved understanding of the interdependence of transcriptional and genomic control of bone loss is critical for the design of effective and safe countermeasures for osteoporosis in space and on Earth. In an effort    to test whether molecular pathways modulating the loss of functional weight bearing are dependent on genetic makeup, we quantified the differential expression of genes critical to the early stages of bone remodeling in two different strains of    mice. METHODS: Adult (4-mo-old) female BALB/cByJ (BALB) and C3H/HeJ (C3H) mice, strains with different sensitivities to unloading, were subjected to hind-limb unloading (HLU) or normal cage activities. RNA was extracted from the tibia following 4    d of HLU and expression levels were determined. RESULTS: In the BALB mice, HLU significantly altered transcriptional levels of osterix (-36%), alkaline phosphatase (-36%), osteonectin (-44%), collagen type 1 (-55%), MMP2 (-36%), osteocalcin    (-68%), and osteopontin (+28%).  This expression pattern was highly correlated (R2 = 0.75) with altered expression levels in the C3H mice, but the magnitude of altered mRNA levels was less than half of those in the BALB mice. These    strain-specific changes in gene expression were consistent with the differential changes in bone formation, as determined in a second group of BALB and C3H mice.  Discussion and CONCLUSIONS: These data indicate that genetics may influence the    absolute changes in gene expression of genes during spaceflight, but that the molecular pathways targeted by countermeasures of bone loss may not need to be specific to an individual's genetic makeup.</p>

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</description>

<author>N Zhong et al.</author>


</item>


<item>
<title>One year of alendronate after one year of parathyroid hormone (1-84) for osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1136</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1136</guid>
<pubDate>Tue, 08 May 2012 21:13:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Since the use of parathyroid hormone as a treatment for osteoporosis is limited to two years or less, the question of whether antiresorptive therapy should follow parathyroid hormone therapy is important. We previously    reported results after the first year of this randomized trial comparing the use of full-length parathyroid hormone (1-84) alone, alendronate alone, or both combined. In the continuation of this trial, we asked whether antiresorptive therapy is    required to maintain gains in bone mineral density after one year of therapy with parathyroid hormone (1-84). METHODS: In the data reported here, women who had received parathyroid hormone (1-84) monotherapy (100 microg daily) in year 1 were    randomly reassigned to one additional year with either placebo (60 subjects) or alendronate (59 subjects). Subjects who had received combination therapy in year 1 received alendronate in year 2; those who had received alendronate monotherapy in    year 1 continued with alendronate in year 2. Bone mineral density at the spine and hip was assessed with the use of dual-energy x-ray absorptiometry and quantitative computed tomography (CT). RESULTS: Over two years, alendronate therapy after    parathyroid hormone therapy led to significant increases in bone mineral density in comparison with the results for placebo after parathyroid hormone therapy, a difference particularly evident for bone mineral density in trabecular bone at the    spine on quantitative CT (an increase of 31 percent in the parathyroid hormone-alendronate group as compared with 14 percent in the parathyroid hormone-placebo group). During year 2, subjects receiving placebo lost substantial bone mineral    density.  CONCLUSIONS: After one year of parathyroid hormone (1-84), densitometric gains appear to be maintained or increased with alendronate but lost if parathyroid hormone is not followed by an antiresorptive agent. These results have clinical    implications for therapeutic choices after the discontinuation of parathyroid hormone.</p>

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</description>

<author>D M. Black et al.</author>


</item>


<item>
<title>An enzymatic cascade of Rab5 effectors regulates phosphoinositide turnover in the endocytic pathway.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1135</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1135</guid>
<pubDate>Tue, 08 May 2012 21:13:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Generation and turnover of phosphoinositides (PIs) must be coordinated in a spatial- and temporal-restricted manner. The small GTPase Rab5 interacts with two PI 3-kinases, Vps34 and PI3Kbeta, suggesting that it regulates the    production of 3-PIs at various stages of the early endocytic pathway.  Here, we discovered that Rab5 also interacts directly with PI 5- and PI 4-phosphatases and stimulates their activity. Rab5 regulates the production of phosphatidylinositol    3-phosphate (PtdIns[3]P) through a dual mechanism, by directly phosphorylating phosphatidylinositol via Vps34 and by a hierarchical enzymatic cascade of phosphoinositide-3-kinasebeta (PI3Kbeta), PI 5-, and PI 4-phosphatases. The functional    importance of such an enzymatic pathway is demonstrated by the inhibition of transferrin uptake upon silencing of PI 4-phosphatase and studies in weeble mutant mice, where deficiency of PI 4-phosphatase causes an increase of PtdIns(3,4)P2 and a    reduction in PtdIns(3)P. Activation of PI 3-kinase at the plasma membrane is accompanied by the recruitment of Rab5, PI 4-, and PI 5-phosphatases to the cell cortex. Our data provide the first evidence for a dual role of a Rab GTPase in    regulating both generation and turnover of PIs via PI kinases and phosphatases to coordinate signaling functions with organelle homeostasis.</p>

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</description>

<author>H W. Shin et al.</author>


</item>


<item>
<title>Of mice and men: use of animal models to identify possible interventions for the prevention of autoimmune type 1 diabetes in humans.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1134</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1134</guid>
<pubDate>Tue, 08 May 2012 21:12:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Animal model and clinical studies indicate that type 1 diabetes (T1D) results from T cell-mediated autoimmune destruction of insulin-producing pancreatic beta-cells. This review discusses the knowledge gained from animal models    about the nature of the autoreactive T cells that cause T1D and the possible basis for their development. Based on this information, the possible positive and negative aspects of various antigen-specific and non-specific immunotherapies, which    could potentially prevent the onset of T1D in at risk individuals, are discussed.</p>

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</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title>Conditioning the genome identifies additional diabetes resistance loci in Type I diabetes resistant NOR/Lt mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1133</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1133</guid>
<pubDate>Tue, 08 May 2012 21:12:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>While sharing the H2g7 MHC and many other important Type I diabetes susceptibility (Idd) genes with NOD mice, the NOR strain remains disease free due to resistance alleles within the approximately 12% portion of their genome that is    of C57BLKS/J origin. Previous F2 segregation analyses indicated multiple genes within the 'Idd13' locus on Chromosome 2 provide the primary component of NOR diabetes resistance. However, it was clear other genes also contribute to NOR diabetes    resistance, but were difficult to detect in the original segregation analyses because they were relatively weak compared to the strong Idd13 protection component. To identify these further genetic components of diabetes resistance, we performed a    new F2 segregation analyses in which NOD mice were outcrossed to a 'genome-conditioned' NOR stock in which a large component of Idd13-mediated resistance was replaced with NOD alleles. These F2 segregation studies combined with subsequent    congenic analyses confirmed the presence of additional NOR resistance genes on Chr. 1 and Chr. 4, and also potentially on Chr. 11. These findings emphasize the value for diabetes gene discovery of stratifying not only MHC loci conferring the    highest relative risk but also as many as possible of the non-MHC loci presumed to contribute significantly.</p>

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</description>

<author>P C. Reifsnyder et al.</author>


</item>


<item>
<title>Regulation of meiotic cell divisions and determination of gamete quality: impact of reproductive toxins.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1132</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1132</guid>
<pubDate>Tue, 08 May 2012 21:12:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>The events and tempo of mammalian meiosis show sexual dimorphism with gametogenic context having a significant influence on both chromosome dynamics and cell cycle transitions. However, although some regulators of the meiotic cell    cycle may differ between males and females, there appears to be extraordinary conservation of key components in common with the mitotic cell cycle and between sexes in meiosis. Evidence is presented for the existence of meiotic checkpoints that    might modify or ameliorate cellular error or damage by reproductive toxins. Although these checkpoints seem relatively inefficient, they may be more so in female meiosis than in male meiosis. Insight into mechanisms of meiotically acting    reproductive toxins coupled with genetic models will ultimately bring about understanding of the basic mechanisms of meiotic cell divisions and chemically induced meiotic error.</p>

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</description>

<author>M A. Handel et al.</author>


</item>


<item>
<title>Euthanasia of neonatal mice with carbon dioxide.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1131</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1131</guid>
<pubDate>Tue, 08 May 2012 21:11:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Exposure to carbon dioxide (CO2) is the most prevalent method used to euthanize rodents in biomedical research. The purpose of this study was to determine the time of CO2 exposure required to euthanize neonatal mice (0 to 10 days    old). Multiple groups of mice were exposed to 100% CO2 for time periods between 5 and 60 min. Mice were placed in room air for 10 or 20 min after CO2 exposure, to allow for the chance of recovery. If mice recovered at one time point, a longer    exposure was examined. Inbred and outbred mice were compared. Results of the study indicated that time to death varied with the age of the animals and could be as long as 50 min on the day of birth and differed between inbred and outbred mice.     Institutions euthanizing neonatal mice with CO2 may wish to adjust their CO2 exposure time periods according to the age of the mice and their genetic background.</p>

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</description>

<author>K Pritchett et al.</author>


</item>


<item>
<title>Skeletal effects of estrogen are mediated by opposing actions of classical and nonclassical estrogen receptor pathways.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1130</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1130</guid>
<pubDate>Tue, 08 May 2012 21:11:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>ER alpha acts either through classical (ERE-mediated) or nonclassical (non-ERE) pathways. The generation of mice carrying a mutation that eliminates classical ER alpha signaling presents a unique opportunity to study the relative    roles of these pathways in bone. This study defines the skeletal phenotype and responses to ovariectomy and estrogen replacement in these mice. INTRODUCTION: Estrogen receptor alpha (ER alpha) can act either through classical estrogen response    elements (EREs) or through non-ERE (nonclassical) pathways. To unravel these in bone, we crossed mice heterozygous for a knock-in mutation abolishing ERE binding (nonclassical ER alpha knock-in [NERKI]) with heterozygote ER alpha knockout mice    and studied the resulting female ER alpha(+/+), ER alpha(+/NERKI), and ER alpha(-/NERKI) mice. The only ER alpha present in ER alpha(-/NERKI) mice is incapable of activating EREs but can signal through nonclassical pathways, whereas ER    alpha(+/NERKI) mice may have a less drastic alteration in the balance between classical and nonclassical estrogen signaling pathways. MATERIALS AND METHODS: BMD was measured using DXA and pQCT at 3 months of age (n = 46-48/genotype). The mice    were randomly assigned to sham surgery, ovariectomy, ovariectomy + estradiol (0.25 microg/day), or ovariectomy + estradiol (1.0 microg/day; n = 10-12/group) and restudied 60 days later. RESULTS AND CONCLUSIONS: At 3 months of age, both the ER    alpha(+/NERKI) and ER alpha(-/NERKI) mice had deficits in cortical, but not in trabecular, bone. Remarkably, changes in cortical bone after ovariectomy and estrogen replacement in ER alpha(-/NERKI) mice were the opposite of those in ER alpha(+/+)    mice. Relative to sham mice, ovariectomized ER alpha(-/NERKI) mice gained more bone (not less, as in ER alpha(+/+) mice), and estrogen suppressed this increase (whereas augmenting it in ER alpha(+/+) mice). Estrogen also had opposite effects on    bone formation and resorption parameters on endocortical surfaces in ER alpha(-/NERKI) versus ER alpha(+/+) mice. Collectively, these data show that alteration of the balance between classical and nonclassical ER alpha signaling pathways leads to    deficits in cortical bone and also represent the first demonstration, in any tissue, that complete loss of classical ERE signaling can lead to paradoxical responses to estrogen. Our findings strongly  support the hypothesis that there exists a    balance between classical and nonclassical ER alpha signaling pathways, which, when altered, can result in a markedly aberrant response to estrogen.</p>

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</description>

<author>F A. Syed et al.</author>


</item>


<item>
<title>Mouse models of ocular diseases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1129</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1129</guid>
<pubDate>Tue, 08 May 2012 21:11:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Jackson Laboratory, having the world's largest collection of mouse mutant stocks and genetically diverse inbred strains, is an ideal place to discover genetically determined eye variations and disorders. In this paper, we list    and describe mouse models for ocular research available from Mouse Eye Mutant Resource at The Jackson Laboratory. While screening mouse strains and stocks at The Jackson Laboratory (TJL) for genetic mouse models of human ocular disorders, we have    identified numerous spontaneous or naturally occurring mutants. We characterized these mutants using serial indirect ophthalmoscopy, fundus photography, electroretinography (ERG) and histology, and performed genetic analysis including linkage    studies and gene identification. Utilizing ophthalmoscopy, electroretinography, and histology, to date we have discovered 109 new disorders affecting all aspects of the eye including the lid, cornea, iris, lens, and retina, resulting in corneal    disorders, glaucoma, cataracts, and retinal degenerations. The number of known serious or disabling eye diseases in humans is large and affects millions of people each year. Yet research on these diseases frequently is limited by the obvious    restrictions on studying pathophysiologic processes in the human eye. Likewise, many human ocular diseases are genetic in origin, but appropriate families often are not readily available for genetic studies.  Mouse models of inherited ocular    disease provide powerful tools for rapid genetic analysis, characterization, and gene identification. Because of the great similarity among mammalian genomes, these findings in mice have direct relevance to the homologous human    conditions.</p>

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</description>

<author>B Chang et al.</author>


</item>


<item>
<title>Carbon Nanotube Coatings for Enhanced Capillary-Fed Boiling from Porous Microstructures</title>
<link>http://docs.lib.purdue.edu/coolingpubs/170</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/coolingpubs/170</guid>
<pubDate>Tue, 08 May 2012 21:11:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Due to their high intrinsic thermal conductivity, carbon nanotubes (CNTs) have previously been incorporated into a variety of thermal management applications to improve cooling performance. Implementation of controlled CNT growth techniques and functionalization methods are applied herein to enhance boiling heat transfer from the porous capillary wicking surfaces widely used in high heat flux thermal management devices. A microwave plasma-enhanced chemical vapor deposition (MPCVD) synthesis process resulted in growth of a permeable CNT coating, and physical vapor deposition of copper over these nanotubes yielded the requisite hydrophilic wicking surface. An array of test samples was fabricated and then evaluated using an experimental test facility to determine the reduction in surface temperature resulting from CNT coating and micropatterning of the porous surfaces under two-phase heat transfer conditions with water as the working fluid. Both CNT coating and micropatterning techniques were able to provide significant performance enhancements, reducing the surface superheat up to 72% compared to baseline tests and eliminating disad- vantageous temperature overshoot corresponding to boiling incipience. Such performance gains are attributable to the formation of nanoporous cavities that increase nucleation site density and high permeability vents through which vapor can readily depart the surface under vigorous boiling conditions. The synthesis procedures developed that result in the observed enhancement can be readily incorporated into currently employed devices.</p>

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</description>

<author>J. A. Weibel et al.</author>


</item>


<item>
<title>Rapid destruction of encapsulated islet xenografts by NOD mice is CD4-dependent and facilitated by B-cells: innate immunity and autoimmunity do not play significant roles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1128</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1128</guid>
<pubDate>Tue, 08 May 2012 21:10:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Spontaneously diabetic NOD mice rapidly reject microencapsulated islet xenografts via an intense pericapsular inflammatory response. METHODS: Tilapia (fish) islets were encapsulated in 1.5% alginate gel microspheres.    Recipients in series 1 were spontaneously diabetic NOD mice and streptozotocin-diabetic nude, euthymic Balb/c, prediabetic NOD, and NOR (a recombinant congenic strain not prone to autoimmune diabetes) mice. Recipients in Series 2 were    STZ-diabetic NOD, NOD-scid, NOD CD4 T-cell KO, NOD CD8 T-cell KO, and NOD B-cell KO mice.  RESULTS: In Series 1, encapsulated fish islet grafts uniformly survived long-term in nude mice but were rejected in Balb/c and, at a markedly accelerated    rate, in spontaneously diabetic NOD, streptozotocin-diabetic NOD and NOR recipients. Histologically, intense inflammation (macrophages and eosinophils) surrounding the microcapsules was seen only in NOD and NOR recipients. In Series 2,    encapsulated fish islets uniformly survived long-term in NOD-scid and NOD CD4 KO mice; graft survival was markedly prolonged in B-cell KO (P<0.001) but not CD8 KO mice. CONCLUSIONS: The rapid rejection of alginate encapsulated islet xenografts by    NOD mice is not solely a consequence of beta-cell directed autoimmunity nor is it merely a vigorous innate immune response. Graft rejection requires CD4 T-cells, is facilitated by B-cells, and does not require CD8 T-cells.</p>

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</description>

<author>B Y. Xu et al.</author>


</item>


<item>
<title>Quantitative trait mapping in a diallel cross of recombinant inbred lines.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1127</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1127</guid>
<pubDate>Tue, 08 May 2012 21:10:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>A recombinant inbred intercross (RIX) is created by generating diallel F1 progeny from one or more panels of recombinant inbred (RI) strains. This design was originally introduced to extend the power of small RI panels for the    confirmation of quantitative trait loci (QTL) provisionally detected in a parental RI set. For example, the set of 13 C x B (C57BL/6ByJ x BALB/cByJ) RI strains can, in principle, be supplemented with 156 isogenic F1s. We describe and test a    method of analysis, based on a linear mixed model, that accounts for the correlation structure of RIX populations. This model suggests a novel permutation algorithm that is needed to obtain appropriate threshold values for genome-wide scans of an    RIX population. Despite the combinational multiplication of unique genotypes that can be generated using an RIX design, the effective sample size of the RIX population is limited by the number of progenitor RI genomes that are combined. When    using small RI panels such as the C x B there appears to be only modest advantage of the RIX design when compared with the original RI panel for detecting QTLs with additive effects. The RIX, however, does have an inherent ability to detect    dominance effects, and, unlike RI strains, the RIX progeny are genetically reproducible but are not fully inbred, providing somewhat more natural genetic context. We suggest a breeding strategy, the balanced partial RIX, that balances the    advantage of RI and RIX designs. This involves the use of a partial RIX population derived from a large RI panel in which the available information is maximized by minimizing correlations among RIX progeny.</p>

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</description>

<author>S W. Tsaih et al.</author>


</item>


<item>
<title>Genetic differences in the IGF-I gene among inbred strains of mice with different serum IGF-I levels.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1126</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1126</guid>
<pubDate>Tue, 08 May 2012 21:10:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is significant heterogeneity in serum IGF-I concentrations among normal healthy individuals across all ages and among inbred strains of mice. C3H/HeJ (C3H) mice have 30% higher serum IGF-I concentrations over a lifetime than    C57BL/6J (B6), even though body size and length are identical. The underlying mechanism for this disparity remains unknown although several possibilities exist including altered GH secretion, resistance to GH action, or impaired IGF-I secretion    from the liver or peripheral tissues. To study this further, we evaluated mRNA levels of pituitary GH, and of IGF-I, GH receptor (GHR) and acid-labile subunit (ALS) in liver and skeletal muscle of male C3H and B6 strains. mRNA levels of hepatic    IGF-I paralleled serum IGF-I levels, whereas pituitary GH mRNA expression was significantly lower in C3H than B6. In addition, reduced hepatic mRNA levels of ALS and GHR in B6 suggests hepatic GH resistance in B6. In contrast, mRNA levels of    IGF-I and GHR in skeletal muscle were not different between B6 and C3H. There was a single sequence repeat polymorphism (SSR) in the promoter region of both GHR and IGF-I genes in mice; the SSR in the IGF-I gene was significantly different    between the two strains. The SSR in the IGF-I gene corresponds to the E2F binding site, which is critical for regulating IGF-I gene expression. These results suggest that the SSR in the promoter region of the IGF-I gene may be partially    responsible for differences in serum IGF-I levels between B6 and C3H strains.</p>

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</description>

<author>K Iida et al.</author>


</item>


<item>
<title>Association of a lithogenic Abcg5/Abcg8 allele on Chromosome 17 (Lith9) with cholesterol gallstone formation in PERA/EiJ mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1125</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1125</guid>
<pubDate>Tue, 08 May 2012 21:09:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>To examine further the genetic determinants of cholesterol gallstone susceptibility in inbred mice, we performed quantitative trait locus (QTL) analysis of an intercross of gallstone-susceptible PERA/EiJ and gallstone-resistant    DBA/2J inbred mice. Three hundred twenty-four F2 offspring were phenotyped for cholelithiasis during consumption of a lithogenic diet and genotyped using microsatellite markers. Linkage analysis was performed by interval mapping. In addition, we    analyzed the combined datasets from this cross and from an independent cross of strain PERA and gallstone-resistant I/Ln mice. QTL mapping detected one significant new gallstone susceptibility (Lith) locus on Chromosome 13 (Lith15). A second    significant QTL on Chr 6 (Lith16) confirmed a previous QTL. Furthermore, suggestive QTLs confirmed Lith loci from previous crosses on Chromosomes 1, 2, 5, 16 and X. QTL analysis of the dataset derived from the combined crosses increased the    detection power and narrowed confidence intervals of Lith loci on Chromosomes 2, 6, 13, and 16. Moreover, the analysis of combined datasets revealed a shared QTL between both crosses on Chromosome 17 (Lith9). Significantly higher mRNA expression    of Abcg5 and Abcg8 in strain PERA compared with strains I/Ln and DBA/2 further substantiated that the PERA allele of Abcg5/Abcg8 was responsible for lithogenicity underlying Lith9.</p>

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</description>

<author>H Wittenburg et al.</author>


</item>


<item>
<title>Transcript profiling during mouse oocyte development and the effect of gonadotropin priming and development in vitro.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1124</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1124</guid>
<pubDate>Tue, 08 May 2012 21:09:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The molecular basis for acquisition of meiotic and developmental competence, the two main outcomes of oocyte development and essential for producing an egg capable of being fertilized and supporting development to term, is largely    unknown. Using microarrays, we characterized global changes in gene expression in oocytes derived from primordial, primary, secondary, small antral, and large antral follicles and used Expression Analysis Systematic Explorer (EASE) to identify    biological and molecular processes that accompany these transitions and likely underpin acquisition of meiotic and developmental competence. The greatest degree of change in gene expression occurs during the primordial to primary follicle    transition. Of particular interest is that specific chromosomes display significant changes in their overall transcriptional activity and that in some cases these changes are largely confined to specific regions on these chromosomes. We also    examined the transcript profile of oocytes that developed in vitro, as well as following eCG priming. Remarkably, the expression profiles only differed by 4% and 2% from oocytes that developed in vivo when compared to oocytes that developed in    vitro from either primordial or secondary follicles, respectively. About 1% of the genes were commonly mis-expressed, and EASE analysis revealed there is an over-representation of genes involved in transcription. Developmental competence of    oocytes obtained from eCG-primed mice was substantially improved when compared to oocytes obtained from unprimed mice, and this correlated with decreased expression of genes implicated in basal transcription.</p>

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</description>

<author>H Pan et al.</author>


</item>


<item>
<title>Discovery genetics: serendipity in basic research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1123</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1123</guid>
<pubDate>Tue, 08 May 2012 21:09:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>The role of serendipity in science has no better example than the discovery of spontaneous mutations that leads to new mouse models for research. The approach of finding phenotypes and then carrying out genetic analysis is called    forward genetics. Serendipity is a key component of discovering and developing mice with spontaneous mutations into animal models of human disease. In this article, the role of serendipity in discovering and developing mouse models is described    within a program at The Jackson Laboratory that capitalizes on serendipitous discoveries in large breeding colonies. Also described is how any scientists working with mice can take advantage of serendipitous discoveries as a research strategy to    develop new models. Spontaneous mutations cannot be planned but happen in all research mouse colonies and are discovered as unexpected phenotypes. The alert scientist or technician can rationally exploit such chance observations to create new    research opportunities.</p>

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</description>

<author>M T. Davisson</author>


</item>


<item>
<title>Retinal ganglion cell degeneration is topological but not cell type specific in DBA/2J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1122</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1122</guid>
<pubDate>Tue, 08 May 2012 21:09:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Using a variety of double and triple labeling techniques, we have reevaluated the death of retinal neurons in a mouse model of hereditary glaucoma. Cell-specific markers and total neuron counts revealed no cell loss in any retinal    neurons other than the ganglion cells. Within the limits of our ability to define cell types, no group of ganglion cells was especially vulnerable or resistant to degeneration. Retrograde labeling and neurofilament staining showed that axonal    atrophy, dendritic remodeling, and somal shrinkage (at least of the largest cell types) precedes ganglion cell death in this glaucoma model. Regions of cell death or survival radiated from the optic nerve head in fan-shaped sectors.     Collectively, the data suggest axon damage at the optic nerve head as an early lesion, and damage to axon bundles would cause this pattern of degeneration. However, the architecture of the mouse eye seems to preclude a commonly postulated source    of mechanical damage within the nerve head.</p>

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</description>

<author>T C. Jakobs et al.</author>


</item>


<item>
<title>Modifications to husbandry and housing conditions of laboratory rodents for improved well-being.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1121</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1121</guid>
<pubDate>Tue, 08 May 2012 21:08:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>For a change to be considered enriching, the change must enhance animal welfare and improve biological functioning of the animals. A review of the literature shows that a consensus on the definition of changes constituting    "environmental enrichment" has yet to be reached. For this reason, the results of studies on the effects of rodent enrichment are inconsistent. In many cases, changes have not been shown to be real improvements. However, enrichment is    increasingly appreciated as a way to improve the well-being of rodents, providing them with opportunities for species-specific behaviors that might be available to them in the wild.  Frequently defined as "change to the environment," enrichment    can be as complex as devices (frequently termed "toys") or as simple as the provision of tissues from which mice readily construct nests. Nest making is a learned behavior in rats, and laboratory rats do show preferences for chewable objects in    their environment. Rather than attempting a comprehensive review of the entire literature on environmental enrichment and its effects on rodent physiology and behavior, this paper focuses on husbandry and housing alterations that may improve the    welfare of laboratory rodents. The effects of beneficial changes in housing and husbandry on rodent well-being and on experimental variability--and thus cost--are discussed. Areas that require more research are suggested. Also suggested are    possible inexpensive and effective enrichment schemes for laboratory mice that might include reducing the cage floor space per mouse combined with providing nesting material.</p>

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</description>

<author>A L. Smith et al.</author>


</item>


<item>
<title>Igf-I and postnatal growth of weaver mutant mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1120</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1120</guid>
<pubDate>Tue, 08 May 2012 21:08:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>IGF-I is an anabolic growth factor essential for growth and development, both as a mediator of growth hormone (GH) action and as a local stimulator of cell proliferation and differentiation. Although the importance of IGF-I in    postnatal growth has been studied for several decades, its functions in pathological states are not fully understood. The weaver (wv) mutant mouse is a commonly used model for studying hereditary cerebellar ataxia and provides us with an    opportunity to study the function of IGF-I in postnatal growth during neurodegeneration. In prepubertal wv mice, we found a parallel decrease in body weight and serum IGF-I. This parallel relationship was maintained in females, but not in males,    as wv mice entered puberty. Interestingly, we found an increase in the levels of circulating IGF-I and hepatic mRNA preceded the catch-up of body weight of pubertal male wv mice. The increase in IGF-I levels coincided with a surge of circulating    androgen at the onset of male puberty, suggesting that androgen might trigger the increase in IGF-I production in the pubertal and adult male wv mice. Overall, our results support the concept that IGF-I plays an important role in postnatal growth    during and after neurodegeneration of wv mice. In addition, IGF-I's regulation of systemic growth during and after puberty is likely modulated by androgen in male wv mice.</p>

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</description>

<author>W Yao et al.</author>


</item>


<item>
<title>Behavioral, cognitive and biochemical responses to different environmental conditions in male Ts65Dn mice, a model of Down syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1119</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1119</guid>
<pubDate>Tue, 08 May 2012 21:08:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ts65Dn mouse is the most widely accepted model for Down syndrome. We previously showed that environmental enrichment improved spatial learning in female but deteriorated it in male Ts65Dn mice. This study analyzed the factors    contributing to the disturbed cognition of male Ts65Dn mice after enriched housing, by allocating male control and Ts65Dn mice in four conditions after weaning: small (n = 2-3) and large group (n = 8-10) housing, and enriched housing in small    (2-3) and large groups (8-10).  Learning, aggressive behavior, anxiety-like behavior and biochemical correlates of stress were evaluated when Ts65Dn and control mice were 4-5 months old. Environmental enrichment in large mixed colonies of Ts65Dn    and diploid littermates disturbed behavioral and learning skills of Ts65Dn mice in the Morris water maze. ACTH and testosterone levels were not modified in any group of mice. Ts65Dn and control mice subjected to enriched housing in large groups    and Ts65Dn mice housed in large groups showed higher corticosterone levels. Aggressive behavior was evaluated by measuring the number of attacks performed in the presence of an intruder.  Ts65Dn mice performed less attacks than controls in all    conditions, especially after enriched housing, indicating subordination. In the plus maze, cognitive aspects (i.e. risk assessment) and motor components (open arm avoidance) of anxiety behavior were evaluated; no difference in any condition was    found. It is suggested that an excess of social and/or physical stimulation in Ts65Dn mice may affect cognition by disturbing the emotional and behavioral components of the learning process.</p>

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</description>

<author>Cue C. Martinez et al.</author>


</item>


<item>
<title>Cu/Zn superoxide dismutase and age-related hearing loss.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1118</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1118</guid>
<pubDate>Tue, 08 May 2012 21:07:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice, in which the genetics can be manipulated and the life span is relatively short, enable evaluation of the effects of specific gene expression on cochlear degeneration over time. Antioxidant enzymes such as Cu/Zn superoxide    dismutase (SOD1) protect cells from toxic, reactive oxygen species and may be involved in age-related degeneration. The effects of SOD1 deletion and over-expression on the cochlea were examined in Sod1-null mice, Sod1 transgenic mice and in age-    and genetics-matched controls. Auditory brainstem responses (ABR) were measured and cochleae were histologically examined. The absence of SOD1 resulted in hearing loss at an earlier age than in wildtype or heterozygous mice. The cochleae of the    null mice had severe spiral ganglion cell degeneration at 7-9 months of age. The stria vascularis in the aged, null mice was thinner than in the heterozygous or wildtype mice. Over-expression of SOD1 did not protect against hearing loss except at    24 months of age. In conclusion, SOD1 seems important for survival of cochlear neurons and the stria vascularis, however even half the amount is sufficient and an over abundance does not provide much protection from age-related hearing    loss.</p>

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</description>

<author>E M. Keithley et al.</author>


</item>


<item>
<title>Ocular abnormalities in Large(myd) and Large(vls) mice, spontaneous models for muscle, eye, and brain diseases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1117</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1117</guid>
<pubDate>Tue, 08 May 2012 21:07:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Here we demonstrate previously unreported ocular defects in mice homozygous for a new allele of the Large gene, veils, and for Large(myd) mice. Clinically, vitreal fibroplasia and retinal vessel tortuosity and fluorescein leakage    are observed. These vascular defects may be due to the extreme disorganization of the astrocytic template on which endothelial cells migrate in the retina. Abnormal electroretinograms recorded from Large(vls) or Large(myd) mice are accompanied by    disorganization of the outer plexiform layer (OPL) with a dramatic reduction in the number of synaptic complexes. In both mutants, the internal limiting membrane (ILM) is disrupted with ectopic cells in the vitreous. Interestingly, while all    components of the dystrophin glycoprotein complex are present at reduced levels in the OPL, they were absent in the ILM of affected mice. Finally, hypoglycosylation of alpha-dystroglycan previously implicated in muscle and brain defects is also    observed in the retina and may contribute to the ocular abnormalities.</p>

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</description>

<author>Y Lee et al.</author>


</item>


<item>
<title>Complex genetics of glaucoma susceptibility.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1116</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1116</guid>
<pubDate>Tue, 08 May 2012 21:07:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Glaucoma describes a group of diseases that kill retinal ganglion cells.  There are different types of glaucoma, and each appears to be genetically heterogeneous. Different glaucoma genes have been identified, but these genes    account for only a small proportion of glaucoma. Most glaucoma cases appear to be multifactorial, and are likely affected by multiple interacting loci. A number of genetic susceptibility factors have been suggested to contribute to glaucoma.    These factors fit into two broad groups, those affecting intraocular pressure and those important in modulating retinal ganglion cell viability. Defining the complex genetics of glaucoma will require significant further study of the human disease    and animal models. Genetic approaches are essential and will be enhanced by recently developed genomic and proteomic technologies. These technologies will provide valuable clues about pathogenesis for subsequent testing. In this review, we focus    on endogenous genetic susceptibility factors and on how experimental studies will be valuable for dissecting the multifactorial complexity of their interactions.</p>

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</description>

<author>R T. Libby et al.</author>


</item>


<item>
<title>Stargazer-a mouse to seize!</title>
<link>http://mouseion.jax.org/stfb2000_2009/1115</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1115</guid>
<pubDate>Tue, 08 May 2012 21:07:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>The goals of this short review are to familiarize readers with the stargazer mouse and to outline the major functional defects associated with this mutant. The roles of the stargazin protein in calcium channel function and    alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-receptor trafficking are discussed; focus is placed on studies regarding the thalamus, whence absence seizures potentially originate, and the cerebellum, which is associated with the    ataxic phenotype. Finally, two additional alleles of stargazer, waggler and stargazer 3Jackson (3J), illustrate the value of an allelic series for understanding stargazin function.</p>

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</description>

<author>V A. Letts</author>


</item>


<item>
<title>The insulin-like growth factor-I gene and osteoporosis: A critical appraisal.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1114</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1114</guid>
<pubDate>Tue, 08 May 2012 21:07:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Osteoporosis, a disorder of skeletal fragility, is common in the elderly, and its prevalence is increasing as more individuals with low bone mineral density (BMD), the strongest predictor of fracture risk, are detected.  Previous    basic and clinical studies imply there is a significant role for insulin-like growth factor-I (IGF-I) in determining BMD. Recently, polymorphisms upstream of the P1 promoter region of the human IGF-I gene have been found to be associated with    serum levels of IGF-I, BMD and fracture risk in various ethnic groups. Multiple quantitative trait loci (QTLs) have been identified that underlie serum IGF-I in a mouse intercross between two inbred strains. The most promising QTL on mouse    chromosome 6 has provided clues for unraveling the molecular mechanisms that regulate osteoblast differentiation. Genomic engineering resulting in IGF-I deficient mice, and mice with targeted over-expression of IGF-I reinforce the essential role    of IGF-I in bone development at both the embryonic and postnatal stages. Thus, it is apparent that significant new insights into the role of the IGF-I gene in bone remodeling occur through several distinct mechanisms: (1) the skeletal IGF    regulatory system; (2) the systemic growth hormone/IGF-I axis; (3) parathyroid hormone signaling; (4) sex steroids; and (5) the OPG/RANKL/RANK cytokine system. Molecular dissection of the IGF regulatory system and its signaling pathway in bone    may reveal novel therapeutic targets for the treatment of osteoporosis.</p>

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</description>

<author>T Niu et al.</author>


</item>


<item>
<title>Simultaneous serodetection of 10 highly prevalent mouse infectious pathogens in a single reaction by multiplex analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1113</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1113</guid>
<pubDate>Tue, 08 May 2012 21:06:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Under current practices of mouse colony maintenance, sera from mice are analyzed for antibodies against several widespread infectious pathogens by conventional immunoassays, generally enzyme-linked immunosorbent assay (ELISA). To    test for multiple agents, these methods consume large volumes of mouse serum and are laborious and time-consuming. More efficient immunoassays, using small amounts of sample, are therefore needed.  Accordingly, we have developed a novel multiplex    diagnostic system that employs fluorescent microbeads, coated with purified antigens, for simultaneous serodetection of 10 mouse infectious agents. Individually identifiable, fluorescent microbeads were coated with antigens from Sendai virus,    mouse hepatitis virus, Theiler's mouse encephalomyelitis virus/GDVII strain, mouse minute virus, mouse cytomegalovirus, respiratory enteric orphan virus (Reo-3 virus), mouse parvovirus, calf rotavirus for epizootic diarrhea virus of infant mice,    vaccinia virus for ectromelia virus, and Mycoplasma pulmonis. Standard sera, singly positive for antibodies to individual infectious agents, were generated by inoculation of BALB/cj and C57BL/6j mice. Sera from these experimentally infected mice,    as well as sera from naturally infected mice, were analyzed using a mixture of microbeads coated with antigens of the 10 infectious agents listed above. Results demonstrated that the multiplex assay was at least as sensitive and specific as ELISA    for serodetection. Importantly, the multiplex assay required only 1 microliter of serum for simultaneous serodetection of the 10 mouse infectious agents in one reaction vessel.  Thus, this multiplex microbead assay is a reliable, efficient, and    cost-effective diagnostic modality that will impact serosurveillance of mice used in research.</p>

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</description>

<author>I H. Khan et al.</author>


</item>


<item>
<title>An assay for human hematopoietic stem cells based on transplantation into nonobese diabetic recombination activating gene-null perforin-null mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1112</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1112</guid>
<pubDate>Tue, 08 May 2012 21:06:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract Nonobese diabetic recombination activating gene-null perforin-null (NOD- Rag1 null Prf1 null ) mice, which totally lack mature T and B cells and natural killer cell cytotoxic function, survive longer and are easier to breed    than NOD-severe combined immunodeficiency ( scid ) or NOD- scid /beta 2 -microglobulin null mice. We have tested the use of NOD- Rag1 null Prf1 null mice as recipients in a long-term xenograft assay for human hematopoietic stem cells (HSCs) by    adopting Yoder and colleagues' method of conditioned newborn mice, with minor modifications.  Pregnant NOD- Rag1 null Prf1 null dams were treated with busulfan 22.5 mg/kg. On the day of delivery, the busulfan-exposed pups underwent    transplantation with 4 to 5 million T cell--depleted human cord blood mononuclear cells via the facial vein. At 2 months after transplantation, all 11 transplanted mice showed human hematopoietic engraftment in the peripheral blood. At 6 months    after transplantation, human cells were detected in 5 mice, which showed higher than 0.9% human cell engraftment at 2 months. The mean percentage of human CD45 + cells in the bone marrow of engrafted mice was 43.9% +/- 36.5% (range, 2.0%-79.9%).    Next, we tested the usefulness of conditioned newborn NOD- Rag1 null Prf1 null mice for applications to characterize the dye efflux capability and phenotypic features of human HSCs. Given that cord blood HSCs have the ability to efflux rhodamine    123 (Rho), we attempted transplantations of sorted cells that retained a low level (Rho low ) or high level (Rho high ) of Rho.  Six-month engraftment was found only with the Rho low cells, which contained high percentages of CD34 + CD38 - cells    and side population cells with Hoechst 33324 efflux activity. These observations suggest that Rho low cells are highly enriched for primitive hematopoietic cells.  Accordingly, conditioned newborn NOD- Rag1 null Prf1 null mice provide a desirable    model for an assay of long-term transplantable human HSCs.</p>

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</description>

<author>H Minamiguchi et al.</author>


</item>


<item>
<title>Insulin-like growth factor-I and insulin are associated with the presence and advancement of adenomatous polyps.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1111</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1111</guid>
<pubDate>Tue, 08 May 2012 21:06:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND & AIMS: Insulin and insulin-like growth factor-I (IGF-I) affect proliferation, differentiation, and apoptosis and are potential risk factors for colorectal cancer (CRC). Visceral obesity, possibly via hyperinsulinemia,    has also been linked to CRC risk. We evaluated the relationship of insulin, IGF-I, insulin-like growth factor binding protein (IGFBP) 3, and visceral adipose tissue (VAT) in subjects with adenomatous polyps, the precursor lesion of colorectal    cancer. METHODS: Participants were asymptomatic subjects who underwent screening flexible sigmoidoscopy (FSG) within the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Subjects underwent single-slice, computerized    tomography scanning to measure VAT and serum fasting insulin, IGF-I, and IGFBP-3 measurements. RESULTS: Four hundred fifty-eight subjects were enrolled, of which 202 subjects had an adenoma, 70 of which were an advanced adenoma.  IGF-I (P = .02),    IGF-I/IGFBP-3 ratio (P = .003), and insulin (P = .02) were significantly increased in subjects with adenomas compared with controls. In an unadjusted logistic regression analysis using sex-specific quartile cut points, subjects in quartile 4 in    comparison with quartile 1 of IGF-I (odds ratio [OR] = 1.7; [95% CI: 1.0-2.9], Ptrend = .03), IGF-I/IGFBP-3 ratio (OR = 1.9 [95% CI: 1.1-3.3], Ptrend = .01), and insulin (OR = 2.1 [95% CI: 1.2-3.6], Ptrend = .04) were at increased risk of    adenoma. When limiting the case group to advanced adenomas, the effect was more pronounced: IGF-I (OR = 2.8 [95% CI: 1.3-6.2], Ptrend = .006), IGF-I/IGFBP-3 ratio (OR = 2.3, [95% CI: 1.0-5.2], Ptrend = .04), and insulin (OR = 2.3 [95% CI:    1.1-4.9], Ptrend = .14). Visceral adipose tissue was not associated with adenoma risk. CONCLUSIONS: Levels of IGF-I, ratio of IGF-I/IGFBP-3, and insulin are associated with adenomas and even more so with advanced adenomas. These data support the    hypothesis that insulin and IGF-I may contribute to the development and advancement of adenomatous polyps.</p>

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</description>

<author>R E. Schoen et al.</author>


</item>


<item>
<title>Clinical practice. Postmenopausal osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1110</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1110</guid>
<pubDate>Tue, 08 May 2012 21:06:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title>Quantitative trait locus study design from an information perspective.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1109</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1109</guid>
<pubDate>Tue, 08 May 2012 21:05:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>We examine the efficiency of different genotyping and phenotyping strategies in inbred line crosses from an information perspective. This provides a mathematical framework for the statistical aspects of QTL experimental design,    while guiding our intuition. Our central result is a simple formula that quantifies the fraction of missing information of any genotyping strategy in a backcross. It includes the special case of selectively genotyping only the phenotypic extreme    individuals. The formula is a function of the square of the phenotype and the uncertainty in our knowledge of the genotypes at a locus. This result is used to answer a variety of questions. First, we examine the cost-information trade-off varying    the density of markers and the proportion of extreme phenotypic individuals genotyped. Then we evaluate the information content of selective phenotyping designs and the impact of measurement error in phenotyping. A simple formula quantifies the    information content of any combined phenotyping and genotyping design. We extend our results to cover multigenotype crosses, such as the F(2) intercross, and multiple QTL models. We find that when the QTL effect is small, any contrast in a    multigenotype cross benefits from selective genotyping in the same manner as in a backcross. The benefit remains in the presence of a second unlinked QTL with small effect (explaining <20% of the variance), but diminishes if the second QTL has a    large effect. Software for performing power calculations for backcross and F(2) intercross incorporating selective genotyping and marker spacing is available from http://www.biostat.ucsf.edu/sen.</p>

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</description>

<author>S Sen et al.</author>


</item>


<item>
<title>Mouse oocytes regulate metabolic cooperativity between granulosa cells and oocytes: amino Acid transport.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1108</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1108</guid>
<pubDate>Tue, 08 May 2012 21:05:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>A search for genes expressed more highly in mouse cumulus cells than mural granulosa cells by subtraction hybridization yielded Slc38a3. SLC38A3 is a sodium-coupled neutral amino acid transporter having substrate preference for    l-glutamate, l-histidine, and l-alanine. Detectable levels of Slc38a3 mRNA were found by in situ hybridization in granulosa cells of large preantral follicles, but levels were higher in all granulosa cells of small antral follicles; expression    became limited to cumulus cells of large antral follicles. Expression of Slc38a3 mRNA in granulosa cells was promoted by fully grown oocytes from antral follicles but not by growing oocytes from preantral follicles. Fully grown oocytes were    dependent on cumulus cells for uptake of l-alanine and l-histidine but not l-leucine.  Fully grown but not growing oocytes secreted one or more paracrine factors that promoted cumulus cell uptake of all three amino acids but of l-alanine and    l-histidine to a much greater extent than l-leucine. Uptake of l-leucine appeared dependent primarily on contact-mediated signals from fully grown oocytes. Fully grown oocytes also promoted elevated levels of Slc38a3 mRNA and l-alanine transport    by preantral granulosa cells, but growing oocytes did not. Therefore, fully grown oocytes secrete one or more paracrine factors that promote cumulus cell uptake of amino acids that oocytes themselves transport poorly. These amino acids are likely    transferred to oocytes via gap junctions. Thus, oocytes use paracrine signals to promote their own development via metabolic cooperativity with cumulus cells. The ability of oocytes to mediate this cooperativity is developmentally regulated and    acquired only in later stages of oocyte development.</p>

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</description>

<author>J J. Eppig et al.</author>


</item>


<item>
<title>Src kinases as targets for B cell acute lymphoblastic leukaemia therapy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1107</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1107</guid>
<pubDate>Tue, 08 May 2012 21:05:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>The participation of Src kinases in the induction of BCR-ABL-induced B cell acute lymphoblastic leukaemia (B-ALL), but not chronic myeloid leukaemia (CML), demonstrates cell type-specific signalling in Philadelphia    chromosome-positive (Ph+) leukaemias. Different therapeutic strategies are therefore needed for B-ALL and CML. Activation of Src kinases is independent of BCR-ABL kinase activity for activation. Thus, Src kinases provide a mechanism for    resistance to the BCR-ABL kinase inhibitors and potential targets for B-ALL therapy. Simultaneous targeting of both BCR-ABL and Src kinases may benefit human B-ALL patients.  Leukaemic stem cells may exist in Ph+ B-ALL, and eradication of this    group of cells would provide a curative method for this disease.</p>

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</description>

<author>S Li</author>


</item>


<item>
<title>Ethics: Moral issues of human-non-human primate neural grafting.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1106</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1106</guid>
<pubDate>Tue, 08 May 2012 21:05:01 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M Greene et al.</author>


</item>


<item>
<title>Immunolocalization of retinoic acid biosynthesis systems in selected sites in rat.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1105</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1105</guid>
<pubDate>Tue, 08 May 2012 21:04:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Vitamin A deficiency leads to focal metaplasia of numerous epithelial tissues with altered differentiation from columnar (in general) to stratified squamous cells. This process can be reversed with vitamin A repletion. Previously,    we described a system of retinoic acid (RA) synthesis in the cycling rat uterus consisting of cellular retinol binding protein (Crbp), epithelial retinol dehydrogenase (eRoldh), retinal dehydrogenase 2 (Aldh1a2), and cellular retinoic acid    binding protein type II (Crabp2). Western blot analysis, RT-PCR, and immunohistochemistry were performed to test whether this retinoic acid synthesis system was also present in other vitamin A sensitive tissues. We found that combinations of    Crbp, eRoldh, Aldh1a2 or Aldh1a3, and Crabp2 were present in all vitamin A sensitive tissues examined. In the ureter, while eRoldh was present, another short chain alcohol dehydrogenase reductase (possibly Roldh 1, 2, or 3) was in higher    concentration in the transitional epithelia. In several tissues, Crbp, Aldh1a2, and/or Aldh1a3 localized to mesenchyme and/or epithelial cells, while eRoldh and Crabp2 were expressed only in epithelial cells. This suggests that    mesenchymal-epithelial interactions may be as important in the adult as they are during development and that local synthesis of RA is important in maintenance of these tissues.</p>

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</description>

<author>H B. Everts et al.</author>


</item>


<item>
<title>Adipose tissue transplantation protects ob/ob mice from obesity, normalizes insulin sensitivity and restores fertility.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1104</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1104</guid>
<pubDate>Tue, 08 May 2012 21:04:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adipose tissue affects metabolism by secreting various adipokines.  Lipodystropic mice benefit both from leptin replacement therapy and from transplantation of normal fat. Leptin-deficient Lep(ob)/Lep(ob) (ob/ob) mice can also be    treated with leptin. Surprisingly, there have been no reports of successful treatment of obese ob/ob mice by transplantation of normal white adipose tissue (WAT). If WAT transplantation is ineffective in treating insulin resistance and diabetes    in obese individuals, its applicability may be limited in humans as such abnormalities are usually associated with obesity. In the current study, we tested whether WAT transplantation might prevent, and even reverse, abnormalities characteristic    of ob/ob mice. To assess the preventive potential, 6-week-old ob/ob mice were transplanted, subcutaneously, with gonadal fat pads from normal mice. Profound effects on multiple physiological phenotypes were achieved despite leptin levels below    25% of those in control mice. WAT from one donor reduced body weight gain, and WAT from 4 or 8 donors prevented obesity in ob/ob mice. Nonfasting insulin levels and insulin tolerance test were normalized. Corticosterone elevation was also    prevented. Finally, WAT from 4 donors restored fertility in ob/ob females.  The effects of WAT transplantation were long-lasting, with body weight gain suppressed for at least 40 weeks. To assess the therapeutic potential, obese 13-month-old    ob/ob mice with a long history of leptin deficiency were used. Their body weight decreased by approximately 50% when transplanted with WAT from 8 donors. As in young recipients, transplantation greatly reduced nonfasting insulin, suggesting    normalized insulin sensitivity. Thus, WAT transplantation was effective for both prevention and therapy. In the future, WAT transplantation may become a useful alternative to hormone replacement in treating not only lipodystropy, but also certain    types of obesity.</p>

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</description>

<author>S Klebanov et al.</author>


</item>


<item>
<title>Targeted deletion of the sciellin gene resulted in normal development and maturation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1103</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1103</guid>
<pubDate>Tue, 08 May 2012 21:04:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sciellin, together with other precursor proteins, was cross-linked by transglutaminase 1 to form the cornified envelope, an essential component of the physical barrier of the epidermis and stratified squamous epithelia. To more    fully understand the function of sciellin in cornified envelope formation, we generated sciellin null mice. The mice appeared normal in their development and maturation and there were no structural features that distinguished them from littermate    controls. Isolated cornified envelopes appeared normal in structure and were not more fragile to mechanical stress. There was no evidence of decreased barrier function or altered expression of other cornified envelope components. Transgenic mice    expressing the repeat domain appeared to have a normal phenotype, like the null, and did not alter endogenous sciellin expression. We conclude that sciellin null mice had no structural anomalies and the transgenic mice did not act as a    dominant-negative mutation. genesis 42:219-228, 2005. (c) 2005 Wiley-Liss, Inc.</p>

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</description>

<author>H P. Baden et al.</author>


</item>


<item>
<title>H1FOO is coupled to the initiation of oocytic growth.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1102</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1102</guid>
<pubDate>Tue, 08 May 2012 21:03:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>We previously reported the discovery of a novel mammalian H1 linker histone termed H1FOO (formerly H1OO), a replacement H1, the expression of which is restricted to the growing/ maturing oocyte and to the zygote. The significance of    this pre-embryonic H1 draws on its substantial orthologous conservation, singular structural attributes, selectivity for the germ cell lineage, prolonged nucleosomal residence, and apparent predominance among germ cell H1s. Herein, we report that    the intronic, single-copy, five-exon (> or =5301 base pair) H1foo gene maps to chromosome 6 and that the corresponding primary H1foo transcript gives rise to two distinct, alternatively spliced mRNA species (H1foo(alpha) and H1foo(beta)). The    expression of the oocytic H1FOO transcript and protein proved temporally coupled to the recruitment of resting primordial follicles into a developing primary follicular cohort and thus to the critical transition marking the onset of oocytic    growth. The corresponding potential protein isoforms (H1FOO(alpha) and H1FOO(beta)), both nuclear localization sequence-endowed but export consensus sequence-free and possessing a significant net positive charge, localized primarily to    perinucleolar heterochromatin in the oocytic germinal vesicle. Further investigation will be required to define the functional role of the H1FOO protein in the ordering of the chromatin of early mammalian development as well as its potential role    in defining the primordial-to-primary follicle transition.</p>

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</description>

<author>M Tanaka et al.</author>


</item>


<item>
<title>Coxsackievirus and adenovirus receptor is essential for cardiomyocyte development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1101</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1101</guid>
<pubDate>Tue, 08 May 2012 21:03:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The coxsackievirus and adenovirus receptor (CAR) is a transmembrane protein that is known to be a site of viral attachment and entry, but its physiologic functions are undefined. CAR expression is maximal in neonates and wanes    rapidly after birth in organs such as heart, muscle, and brain, suggesting that CAR plays a role in the development of these tissues.  Here, we show that CAR deficiency resulted in an embryonic lethal condition associated with cardiac defects.    Specifically, commencing approximately 10.5 days postconception (dpc), CAR-/- cardiomyocytes exhibited regional apoptosis evidenced by both histopathologic features of cell death and positive staining for the apoptotic marker cleaved caspase 3.    CAR-/- fetuses invariably suffered from degeneration of the myocardial wall and thoracic hemorrhaging, leading to death by 11.5 dpc. These findings are consistent with the view that CAR provides positive survival signals to cardiomyocytes that    are essential for normal heart development.</p>

	]]>
</description>

<author>D R. Asher et al.</author>


</item>


<item>
<title>Genetic modifiers interact with Cpefat to affect body weight, adiposity, and hyperglycemia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1100</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1100</guid>
<pubDate>Tue, 08 May 2012 21:03:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Obesity and Type II diabetes are complex diseases in the human population.  The existence of a large number of contributing loci and gene-gene as well as gene-environment interactions make it difficult to identify the disease genes    underlying these complex traits. In mouse models of obesity and Type II diabetes such as the murine fat mutation, genetic crosses can be used to dissect the genetic complexity influencing the observed phenotypes. The underlying defect in the fat    mutant is a Ser202Pro change in carboxypeptidase E (CPE), an enzyme responsible for the final proteolytic processing step of prohormone intermediates. On the HRS/J (HRS) inbred strain background, mice homozygous for the fat mutation exhibit early    onset hyperinsulinemia followed by postpubertal moderate obesity without hyperglycemia. In contrast, on the C57BLKS/J (BKS) genetic background, fat/fat mice become severely obese, hyperinsulinemic, and hyperglycemic.  Therefore, in the Cpe(fat)    genetic model, the fat mutation is necessary but not sufficient for the development of obesity, Type II diabetes, and related metabolic disorders. To dissect the susceptibility loci responsible for modifying obesity- and diabetes-associated    traits, we characterized, both genetically and phenotypically, fat/fat male progeny from a large intercross between BKS. HRS-fat/fat and HRS-+/+ mice. Four major loci were mapped, including a locus for body weight (body weight 1) on chromosome    14; a locus for hyperglycemia (fat-induced diabetes 1) on chromosome 19; a locus for hyperglycemia, hyperinsulinemia, and hypercholesterolemia (fat-induced diabetes 2) on chromosome 5; and a locus for adiposity and body weight (fat-induced    adiposity 1) on chromosome 11.  The identification of these interacting genetic determinants for obesity and Type II diabetes may allow better definition of the obesity/diabetes-related hormone signaling pathways and ultimately may provide new    insights into the pathogenesis of these complex diseases.</p>

	]]>
</description>

<author>G B. Collin et al.</author>


</item>


<item>
<title>Type 2 diabetes mouse model TallyHo carries an obesity gene on chromosome 6 that exaggerates dietary obesity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1099</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1099</guid>
<pubDate>Tue, 08 May 2012 21:03:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>The TallyHo (TH) mouse strain is a polygenic model for Type 2 diabetes with obesity. Genetic analysis in backcross progeny from a cross between F1 [C57BL/6J (B6) x TH] and TH mice mapped a quantitative trait locus (QTL) named    TH-associated body weight 2 (tabw2) to chromosome 6. The TH-derived allele is associated with increased body weight. As a first step to identify the molecular basis of this obesity QTL, we constructed a congenic line of mice on the B6 genetic    background that carries a genomic region from TH mice containing tabw2. Congenic mice homozygous for tabw2 (B6.TH-tabw2/tabw2) fed a chow diet exhibited slightly, but significantly, higher body weight and body fat and plasma leptin levels    compared with controls (B6.TH-+/+). This difference was exacerbated when the animals were maintained on a high-fat and high-sucrose (HFS) diet. The diet-induced obesity in tabw2 congenic mice is accompanied by hyperleptinemia, mild    hyperinsulinemia, impaired glucose tolerance, and reduced glucose uptake in adipose tissue in response to insulin administration. Using F2 progeny fed a HFS diet from an intercross of B6.TH-tabw2/+ mice, we were able to refine the map position of    the tabw2 obesity susceptibility locus to a 15-cM region (95% confidence interval) extending distally from the marker D6Mit102. In summary, tabw2 congenic mice are a new animal model for diet-induced obesity that will be valuable for the study of    gene-diet interactions.</p>

	]]>
</description>

<author>J H. Kim et al.</author>


</item>


<item>
<title>Mei1 is epistatic to Dmc1 during mouse meiosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1098</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1098</guid>
<pubDate>Tue, 08 May 2012 21:02:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mei1(m1Jcs) allele contains a point mutation in a novel gene required for normal meiosis in male and female mice. We previously hypothesized that Mei1 is likely required for the formation of genetically programmed double-strand    breaks (DSBs), the initiating event of meiotic recombination because in mutant spermatocytes (1) RAD51 foci are greatly reduced at zygonema; (2) RAD51 foci can be restored by cisplatin-induced DNA damage; and (3) phosphorylated H2AX is greatly    reduced at leptonema. If this hypothesis is correct, Mei1 would act upstream of genes required for repair of DSBs by homologous recombination. To test this, we examined meiosis in Mei(m1Jcs)/Mei1(m1Jcs) (Mei1(-/-)) and Dmc1(tm1Jcs)/Dmc1(tm1Jcs)    (Dmc1(-/-)) mice and mice homozygous at both loci (Dmc1(-/-) Mei1(-/-)), exploiting the fact that oogenesis is much more severely affected by the absence of DMC1 than by the absence of MEI1.  The phenotypes of both male and female double mutants    were identical to that of Mei1(-/-) animals. Therefore, Mei1 can be positioned upstream of Dmc1 in the genetic pathway that operates during mammalian meiosis.  Furthermore, this epistatic interaction provides additional evidence in support of the    hypothesis that Mei1 is required for the initiating events of meiotic recombination.</p>

	]]>
</description>

<author>L G. Reinholdt et al.</author>


</item>


<item>
<title>Identifying novel genes for atherosclerosis through mouse-human comparative genetics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1097</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1097</guid>
<pubDate>Tue, 08 May 2012 21:02:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Susceptibility to atherosclerosis is determined by both environmental and genetic factors. Its genetic determinants have been studied by use of quantitative-trait-locus (QTL) analysis. So far, 21 atherosclerosis QTLs have been    identified in the mouse: 7 in a high-fat-diet model only, 9 in a sensitized model (apolipoprotein E- or LDL [low-density lipoprotein] receptor-deficient mice) only, and 5 in both models, suggesting that different gene sets operate in each model    and that a subset operates in both. Among the 27 human atherosclerosis QTLs reported, 17 (63%) are located in regions homologous (concordant) to mouse QTLs, suggesting that these mouse and human atherosclerosis QTLs have the same underlying    genes.  Therefore, genes regulating human atherosclerosis will be found most efficiently by first finding their orthologs in concordant mouse QTLs.  Novel mouse QTL genes will be found most efficiently by using a combination of the following    strategies: identifying QTLs in new crosses performed with previously unused parental strains; inducing mutations in large-scale, high-throughput mutagenesis screens; and using new genomic and bioinformatics tools. Once QTL genes are identified    in mice, they can be tested in human association studies for their relevance in human atherosclerotic disease.</p>

	]]>
</description>

<author>X Wang et al.</author>


</item>


<item>
<title>Restricted MHC-peptide repertoire predisposes to autoimmunity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1096</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1096</guid>
<pubDate>Tue, 08 May 2012 21:02:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>MHC molecules associated with autoimmunity possess known structural features that limit the repertoire of peptides that they can present. Such limitation gives a selective advantage to TCRs that rely on interaction with the MHC    itself, rather than with the peptide residues. At the same time, negative selection is impaired because of the lack of negatively selecting peptide ligands. The combination of these factors may predispose to autoimmunity. We found that mice with    an MHC class II-peptide repertoire reduced to a single complex demonstrated various autoimmune reactions. Transgenic mice bearing a TCR (MM14.4) cloned from such a mouse developed severe autoimmune dermatitis. Although MM14.4 originated from a    CD4(+) T cell, dermatitis was mediated by CD8(+) T cells. It was established that MM14.4(+) is a highly promiscuous TCR with dual MHC class I/MHC class II restriction. Furthermore, mice with a limited MHC-peptide repertoire selected elevated    numbers of TCRs with dual MHC class I/MHC class II restriction, a likely source of autoreactivity. Our findings may help to explain the link between MHC class I responses that are involved in major autoimmune diseases and the well-established    genetic linkage of these diseases with MHC class II.</p>

	]]>
</description>

<author>N N. Logunova et al.</author>


</item>


<item>
<title>Development of intestinal M cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1095</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1095</guid>
<pubDate>Tue, 08 May 2012 21:01:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Summary: Intestinal epithelium contains several specialized cell types including M cells, which can be found in the follicle-associated epithelium (FAE) or occasionally on the villi. M cells are critical for sampling of intestinal    flora and for transferring pathogens across the epithelial barrier for recognition by the immune system. Development of M cells on the villi (M(v)) is independent of the presence of lymphocytes, while development of the FAE and M cells within the    FAE (M(f)) is dependent on B lymphocytes. Here, the concept is discussed that B cells are not required for induction of M(f) differentiation but are required for transition to and maintenance of the mature M(f) phenotype. Signaling pathways    possibly involved in the B-cell-independent stages of M-cell development are also discussed.</p>

	]]>
</description>

<author>J Mach et al.</author>


</item>


<item>
<title>Gait analysis detects early changes in transgenic SOD1(G93A) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1094</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1094</guid>
<pubDate>Tue, 08 May 2012 21:01:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The effective treatment or cure of motoneuron disease will require understanding the disease processes that precede irreversible cell loss.  To study these early stages, and to evaluate potential treatments in relevant animal    models, requires a sensitive functional assay. To this end, we sought to determine whether the gait pattern of SOD1 transgenic mice changed prior to overt symptoms. Using a simplified video-based approach we compared the treadmill gait of    C57BL/6J and B6.SOD1 transgenic mice at 8 and 10 weeks of age. B6.SOD1 mice had significantly longer stride and stance times than controls by 8 weeks. Consistent with disease progression, hindpaw measures of B6.SOD1 mice showed larger changes    than front paws. Differences between control and B6.SOD1 mice increased at 10 weeks, but only because repeat testing caused habituation in control mice to a greater extent than in B6.SOD1 mice. Together the results demonstrate that simplified    gait analysis is sensitive to early processes of motor system disease in mice.</p>

	]]>
</description>

<author>C M. Wooley et al.</author>


</item>


<item>
<title>Mutations in Serac1 or Synj2 cause proximal t haplotype-mediated male mouse sterility but not transmission ratio distortion.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1093</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1093</guid>
<pubDate>Tue, 08 May 2012 21:01:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Transmission ratio distortion (TRD) and sterility are male-specific quantitative trait phenomena associated with the mouse t haplotype. TRD occurs in t haplotype-heterozygous males and is caused by the deleterious action of    distorter products on sperm bearing a wild-type responder locus.  It has been proposed that t-mediated male sterility is a severe manifestation of TRD caused by homozygosity for distorter loci; thus, the distorter and sterility loci would be    identical. In this, study a transgenic approach was used to identify the proximal sterility locus, tcs1 (S1), and test its role in TRD. Mice transgenic for a wild-type bacterial artificial chromosome (BAC) derived from the S1-critical region were    bred onto t haplotype backgrounds. Mating results conclusively showed that the BAC is sufficient to restore fertility in otherwise sterile males. Multiple mutations were identified in the t alleles of Synj2 and Serac1, two genes in the BAC; thus,    they are candidates for S1. In addition, whereas the BAC transgene rescued sterility, it had no effect on TRD. These results uncouple the proximal t haplotype sterility locus, S1, from TRD, demonstrating that S1 and the proximal distorter locus,    D1, are not the same gene.</p>

	]]>
</description>

<author>J C. Schimenti et al.</author>


</item>


<item>
<title>The Mass1(frings) mutation underlies early onset hearing impairment in BUB/BnJ mice, a model for the auditory pathology of Usher syndrome IIC.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1092</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1092</guid>
<pubDate>Tue, 08 May 2012 21:01:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>The human ortholog of the gene responsible for audiogenic seizure susceptibility in Frings and BUB/BnJ mice (mouse gene symbol Mass1) recently was shown to underlie Usher syndrome type IIC (USH2C). Here we report that the    Mass1(frings) mutation is responsible for the early onset hearing impairment of BUB/BnJ mice. We found highly significant linkage of Mass1 with ABR threshold variation among mice from two backcrosses involving BUB/BnJ mice with mice of strains    CAST/EiJ and MOLD/RkJ. We also show an additive effect of the Cdh23 locus in modulating the progression of hearing loss in backcross mice. Together, these two loci account for more than 70% of the total ABR threshold variation among the backcross    mice at all ages. The modifying effect of the strain-specific Cdh23(ahl) variant may account for the hearing and audiogenic seizure differences observed between Frings and BUB/BnJ mice, which share the Mass1(frings) mutation. During postnatal    cochlear development in BUB/BnJ mice, stereocilia bundles develop abnormally and remain immature and splayed into adulthood, corresponding with the early onset hearing impairment associated with Mass1(frings). Progressive base-apex hair cell    degeneration occurs at older ages, corresponding with the age-related hearing loss associated with Cdh23(ahl). The molecular basis and pathophysiology of hearing loss suggest BUB/BnJ and Frings mice as models to study cellular and molecular    mechanisms underlying USH2C auditory pathology.</p>

	]]>
</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title>Familial variable expression of dilated cardiomyopathy in Alstrom syndrome: A report of four sibs.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1091</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1091</guid>
<pubDate>Tue, 08 May 2012 21:00:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alstrom syndrome is an autosomal recessive disorder comprised of progressive vision loss (nystagmus, photophobia, and pigmentary retinopathy), progressive sensorineural hearing loss, morbid obesity, male hypogonadism, insulin    resistant diabetes, renal failure, and dilated cardiomyopathy. We report on four sibs with Alstrom syndrome with intra-familial variability in onset, severity, and spectrum of manifestations; the most serious manifestation being dilated    cardiomyopathy. This report emphasizes the difficulty of recognizing this constellation of symptoms as Alstrom syndrome at an early age, the seriousness of cardiac involvement, and the intra-familial variability of phenotypic expression. (c) 2005    Wiley-Liss, Inc.</p>

	]]>
</description>

<author>J D. Hoffman et al.</author>


</item>


<item>
<title>Archiving mouse strains by cryopreservation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1090</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1090</guid>
<pubDate>Tue, 08 May 2012 21:00:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>A great deal of time and energy goes into the creation of each new line of transgenic mice; established lines are expensive and labor-intensive to maintain. Archiving of mice by cryopreservation of germ cells or embryos represents a    means to free up facility space, while protecting the line from loss due to environmental disasters, genetic drift, or infectious disease. The author reviews the available cryopreservation techniques and presents considerations for setting up a    cryopreservation facility.</p>

	]]>
</description>

<author>C P. Landel</author>


</item>


<item>
<title>The Adult Mouse Anatomical Dictionary: a tool for annotating and integrating data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1089</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1089</guid>
<pubDate>Tue, 08 May 2012 20:59:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have developed an ontology to provide standardized nomenclature for anatomical terms in the postnatal mouse. The Adult Mouse Anatomical Dictionary is structured as a directed acyclic graph, and is organized hierarchically both    spatially and functionally. The ontology will be used to annotate and integrate different types of data pertinent to anatomy, such as gene expression patterns and phenotype information, which will contribute to an integrated description of    biological phenomena in the mouse.</p>

	]]>
</description>

<author>T F. Hayamizu et al.</author>


</item>


<item>
<title>Improved statistical tests for differential gene expression by shrinking variance components estimates.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1088</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1088</guid>
<pubDate>Tue, 08 May 2012 20:59:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Combining information across genes in the statistical analysis of microarray data is desirable because of the relatively small number of data points obtained for each individual gene. Here we develop an estimator of the error    variance that can borrow information across genes using the James-Stein shrinkage concept. A new test statistic (FS) is constructed using this estimator. The new statistic is compared with other statistics used to test for differential    expression: the gene-specific F test (F1), the pooled-variance F statistic (F3), a hybrid statistic (F2) that uses the average of the individual and pooled variances, the regularized t-statistic, the posterior odds statistic B, and the SAM    t-test. The FS-test shows best or nearly best power for detecting differentially expressed genes over a wide range of simulated data in which the variance components associated with individual genes are either homogeneous or heterogeneous. Thus    FS provides a powerful and robust approach to test differential expression of genes that utilizes information not available in individual gene testing approaches and does not suffer from biases of the pooled variance approach.</p>

	]]>
</description>

<author>X Cui et al.</author>


</item>


<item>
<title>Searching QTL by gene expression: analysis of diabesity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1087</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1087</guid>
<pubDate>Tue, 08 May 2012 20:59:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Recent developments in sequence databases provide the opportunity to relate the expression pattern of genes to their genomic position, thus creating a transcriptome map. Quantitative trait loci (QTL) are    phenotypically-defined chromosomal regions that contribute to allelically variant biological traits, and by overlaying QTL on the transcriptome, the search for candidate genes becomes extremely focused.  RESULTS: We used our novel data mining    tool, ExQuest, to select genes within known diabesity QTL showing enriched expression in primary diabesity affected tissues. We then quantified transcripts in adipose, pancreas, and liver tissue from Tally Ho mice, a multigenic model for Type II    diabetes (T2D), and from diabesity-resistant C57BL/6J controls.  Analysis of the resulting quantitative PCR data using the Global Pattern Recognition analytical algorithm identified a number of genes whose expression is altered, and thus are    novel candidates for diabesity QTL and/or pathways associated with diabesity. CONCLUSION: Transcription-based data mining of genes in QTL-limited intervals followed by efficient quantitative PCR methods is an effective strategy for identifying    genes that may contribute to complex pathophysiological processes.</p>

	]]>
</description>

<author>A C. Brown et al.</author>


</item>


<item>
<title>Kinesin family member 12 is a candidate polycystic kidney disease modifier in the cpk mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1086</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1086</guid>
<pubDate>Tue, 08 May 2012 20:58:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>The cpk mouse is the most extensively characterized model of autosomal recessive polycystic kidney disease (ARPKD). The major ARPKD-related renal and biliary phenotypes are modulated in F2 mutants by genetic background, suggesting    that quantitative trait loci (QTL) modulate disease severity.  In 461 F2 cpk mice, kidney length, weight, and volume were scored as quantitative traits (QT), and a semiquantitative method to assess biliary duct number, area (BDA), portal vein    area, and total area of each portal field, as well as the severity of cholangitis, was developed. QTL mapping was performed with Pseudomarker v1.02. Candidate genes were identified within the QTL intervals on the basis of expression profiling,    reverse transcriptase-PCR, haplotypes, and sequence analysis. The renal QT were normally distributed in the F2 cohort and strongly correlated (P < 0.001).  Among the biliary QT, only BDA correlated with the renal QT (P < 0.01).  Genome-wide scan    identified a major effect QTL on chromosome (Chr) 4 for the renal traits, adjusted BDA, and cholangitis with logarithm of odds scores of 18, 8, and 5, respectively. Regression modeling refined the Chr 4 main effect into an approximately 50-cM    region with three distinct QTL peaks at 16, 34, and 54 cM. Kif12, a gene encoding a novel kinesin, mapped beneath the 34 cM QTL peak and has expression level variants and strain-specific sequences that were associated with renal disease severity    in affected mice. Therefore, the positional candidate gene, Kif12, fulfills the major criteria for QTL gene discovery established by the Complex Trait Consortium, and, thus, it is proposed that Kif12 is a cpk modifier gene.</p>

	]]>
</description>

<author>M Mrug et al.</author>


</item>


<item>
<title>Lineage is an epigenetic modifier of QTL influencing behavioral coping with stress.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1085</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1085</guid>
<pubDate>Tue, 08 May 2012 20:58:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>A genome-wide scan was carried out on a segregating F2 population of rats derived from reciprocal intercrosses between two inbred strains of rats, Fisher 344 (F344) and Wistar Kyoto (WKY) that differ significantly in their    behavioral coping responses to stress measured by the defensive burying (DB) test. The DB test measures differences in coping strategies by assaying an animal's behavioral response to an immediate threat. We have previously identified three    X-linked loci contributing to the phenotypic variance in behavioral coping. Here we report on six significant autosomal quantitative trait loci (QTL) related to different behaviors in the DB test:one for the number of shocks received, three for    number of prod approaches, one for latency to bury, and one pleiotropic locus affecting both approach and latency. These QTL contributing to different aspects of coping behaviors show that the effect of genotype on phenotype is highly dependent    on lineage. The WKY lineage was particularly influential, with five out of the six QTL affecting coping behavior only in rats of the WKY lineage, and one locus affecting only those in the F344 lineage. Thus, epigenetic factors, primarily of WKY    origin, may significantly modulate the genetic contribution to variance in behavioral responses to stress in the DB test.</p>

	]]>
</description>

<author>N Ahmadiyeh et al.</author>


</item>


<item>
<title>Interacting genetic loci cause airway hyperresponsiveness.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1084</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1084</guid>
<pubDate>Tue, 08 May 2012 20:58:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Airway hyperresponsiveness (AHR) is a key physiological component of asthma, and the genetic basis of this complex trait has remained elusive.  We created recombinant congenic mice with increased naive AHR by serially backcrossing    A/J mice (which have elevated naive AHR) with C57BL/6J mice and selecting for mice with an elevated naive AHR phenotype. The seventh backcross-generation hyperresponsive mice retained A/J loci in three regions. Quantitative trait linkage (QTL)    analysis of 123 unselected N8 progeny demonstrated that the AHR phenotype was not associated with any single locus but was significantly associated with an interaction of loci on chromosomes 2 and 6. These findings were confirmed in an    independent analysis of chromosome substitution strain mice. The identification of genomic regions containing loci causally associated with AHR and the demonstration that this trait requires their interaction have important implications for the    dissection of the genetic etiology of asthma in humans.</p>

	]]>
</description>

<author>K G. Ackerman et al.</author>


</item>


<item>
<title>Genetics of variation in HDL cholesterol in humans and mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1083</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1083</guid>
<pubDate>Tue, 08 May 2012 20:57:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Plasma high-density lipoprotein cholesterol (HDL-C) concentrations are genetically determined to a great extent, and quantitative trait locus (QTL) analysis has been used to identify chromosomal regions containing genes regulating    HDL-C levels. We discuss new genes found to participate in HDL metabolism. We also summarize 37 mouse and 30 human QTLs for plasma HDL-C levels, finding that all but three of the mouse QTLs have been confirmed by a second cross or a homologous    human QTL, that the mouse QTL map is almost saturated because 92% of recently reported QTLs are repeats of those already found, and that 28 of the 30 human QTLs are located in regions homologous to mouse QTLs. This high degree of concordance    between mouse and human QTLs suggests that the underlying genes may be the same.  Strategies to more rapidly identify genes underlying mouse and human QTLs for HDL-C include focusing on the mouse and using mouse-human homologies, combining    crosses, and haplotyping to narrow the region. Sequence analysis and expression studies can distinguish candidate genes consistent across multiple mouse crosses, and testing the candidate genes in human association studies can provide additional    evidence for the candidacy of a gene. Together these strategies can accelerate the pace of finding genes that regulate HDL.</p>

	]]>
</description>

<author>X Wang et al.</author>


</item>


<item>
<title>Positional identification of TNFSF4, encoding OX40 ligand, as a gene that influences atherosclerosis susceptibility.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1082</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1082</guid>
<pubDate>Tue, 08 May 2012 20:57:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ath1 is a quantitative trait locus on mouse chromosome 1 that renders C57BL/6 mice susceptible and C3H/He mice resistant to diet-induced atherosclerosis. The quantitative trait locus region encompasses 11 known genes, including    Tnfsf4 (also called Ox40l or Cd134l), which encodes OX40 ligand. Here we report that mice with targeted mutations of Tnfsf4 had significantly (P</p>

	]]>
</description>

<author>X Wang et al.</author>


</item>


<item>
<title>Unity: University of Wollongong Quarterly Vol 1 No 3</title>
<link>http://ro.uow.edu.au/uowunity/3</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowunity/3</guid>
<pubDate>Tue, 08 May 2012 20:57:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>Unity: University of Wollongong Quarterly Vol 1 No 2</title>
<link>http://ro.uow.edu.au/uowunity/2</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowunity/2</guid>
<pubDate>Tue, 08 May 2012 20:57:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>University of Wollongong</author>


</item>


<item>
<title>Unity: University of Wollongong Quarterly Vol 1 No 1</title>
<link>http://ro.uow.edu.au/uowunity/1</link>
<guid isPermaLink="true">http://ro.uow.edu.au/uowunity/1</guid>
<pubDate>Tue, 08 May 2012 20:57:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>University of Wollongong</author>


</item>


<item>
<title>Genome-wide search for new genes controlling plasma lipid concentrations in mice and humans.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1081</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1081</guid>
<pubDate>Tue, 08 May 2012 20:57:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE OF REVIEW: Quantitative trait locus analysis has been used in both humans and mice for the purpose of finding new genes regulating plasma lipid levels. We review these methods and discuss new approaches that can help find    quantitative trait locus genes. RECENT FINDINGS: Many quantitative trait loci have been found that regulate plasma levels for HDL cholesterol (37 in mice and 30 in humans), LDL cholesterol (25 in mice and 20 in humans) and triglycerides (19 in    mice and 30 in humans). Most of the human quantitative trait loci have concordant mouse quantitative trait loci mapping to homologous regions (93% for HDL cholesterol, 100% for LDL cholesterol and 80% for triglycerides), suggesting that many    genes identified in mice may also regulate the same traits in humans. New approaches based on recently developed genomic and bioinformatic technologies and resources should greatly facilitate finding these genes.  SUMMARY: New genes regulating    plasma lipid levels can be found in mice and then tested in humans. Some of these genes could be potential therapeutic targets for human atherosclerosis.</p>

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</description>

<author>X Wang et al.</author>


</item>


<item>
<title>Impaired synaptic plasticity and learning in mice lacking beta-adducin, an actin-regulating protein.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1080</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1080</guid>
<pubDate>Tue, 08 May 2012 20:56:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The adducin family of proteins interacts with the actin cytoskeleton and the plasma membrane in a calcium- and cAMP-dependent manner. Thus, adducins may be involved in changes in cytoskeletal organization resulting from synaptic    stimulation. beta-Adducin knock-out mice were examined in physiological and behavioral paradigms related to synaptic plasticity to elucidate the role the adducin family plays in processes underlying learning and memory. In situ hybridization for    alpha- and beta-adducin demonstrates that these mRNAs are found throughout the brain, with high levels of expression in the hippocampus. Schaffer collateral-CA1 tetanic long-term potentiation decayed rapidly in acute hippocampal slices from    beta-adducin knock-out mice, although baseline spine morphology and postsynaptic density were normal. Interestingly, the input-output relationship was significantly increased in hippocampal slices from beta-adducin knock-out mice. Furthermore,    beta-adducin knock-out mice were impaired in performance of fear conditioning and the water maze paradigm.  The current results indicate that beta-adducin may play an important role in the cellular mechanisms underlying activity-dependent    synaptic plasticity associated with learning and memory.</p>

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</description>

<author>R L. Rabenstein et al.</author>


</item>


<item>
<title>Single and interacting QTLs for cholesterol gallstones revealed in an intercross between mouse strains NZB and SM.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1079</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1079</guid>
<pubDate>Tue, 08 May 2012 20:56:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Quantitative trait locus (QTL) mapping was employed to investigate the genetic determinants of cholesterol gallstone formation in a large intercross between mouse strains SM/J (resistant) and NZB/B1NJ (susceptible). Animals consumed    a gallstone-promoting diet for 18 weeks.  QTL analyses were performed using gallstone weight and gallstone absence/presence as phenotypes; various models were explored for genome scans. We detected seven single QTLs: three new, significant QTLs    were named Lith17 [chromosome (Chr) 5, peak=60 cM, LOD=5.4], Lith18 (Chr 5, 76 cM, LOD=4.3), and Lith19 (Chr 8, 0 cM, LOD=5.3); two confirmed QTLs identified previously and were named Lith20 (Chr 9, 44 cM, LOD=2.7) and Lith21 (Chr 10, 24 cM,    LOD=2.9); one new, suggestive QTL (Chr 17) remains unnamed. Upon searching for epistatic interactions that contributed to gallstone susceptibility, the final suggestive QTL on Chr 7 was determined to interact significantly with Lith18 and,    therefore, was named Lith22 (65 cM). A second interaction was identified between Lith19 and a locus on Chr 11; this QTL was named Lith23 (13 cM). mRNA expression analyses and amino acid haplotype analyses likely eliminated Slc10a2 as a candidate    gene for Lith19. The QTLs identified herein largely contributed to gallstone formation rather than gallstone severity. Cloning the genes underlying these murine QTLs should facilitate prediction and cloning of the orthologous human    genes.</p>

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</description>

<author>M A. Lyons et al.</author>


</item>


<item>
<title>Combining data from multiple inbred line crosses improves the power and resolution of quantitative trait Loci mapping.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1078</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1078</guid>
<pubDate>Tue, 08 May 2012 20:55:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rodent inbred line crosses are widely used to map genetic loci associated with complex traits. This approach has proven to be powerful for detecting quantitative trait loci (QTL); however, the resolution of QTL locations, typically    approximately 20 cM, means that hundreds of genes are implicated as potential candidates. We describe analytical methods based on linear models to combine information available in two or more inbred line crosses. Our strategy is motivated by the    hypothesis that common inbred strains of the laboratory mouse are derived from a limited ancestral gene pool and thus QTL detected in multiple crosses are likely to represent shared ancestral polymorphisms. We demonstrate that the combined-cross    analysis can improve the power to detect weak QTL, can narrow support intervals for QTL regions, and can be used to separate multiple QTL that colocalize by chance. Moreover, combined-cross analysis can establish the allelic states of a QTL among    a set of parental lines, thus providing critical information for narrowing QTL regions by haplotype analysis.</p>

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</description>

<author>R Li et al.</author>


</item>


<item>
<title>A torrid zone on mouse chromosome 1 containing a cluster of recombinational hotspots.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1077</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1077</guid>
<pubDate>Tue, 08 May 2012 20:55:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Within the 2.38-Mb Ath1 region of mouse chromosome 1, 42 of 45 genetic crossovers from crosses between C57BL/6J (B6) and either C3H/HeJ (H) or Mus spretus (SPRET) occurred in four zones (A-D); zone A, 100 kb long, contained a    cluster of at least four recombination hotspots. F1 sperm assays indicate that within this "torrid zone" the most active hotspot (A3) can initiate recombination on H and SPRET but not B6 chromosomes. The A3 DNA sequence contains a (G/C)TTT    repeat, long stretches of A or T, and a cyclic variation in AT content. Recombination was drastically reduced in a cross between B6 and a B6.SPRET Ath1 congenic strain, but was unaffected in a B6 x B6.H Ath1 congenic cross. Similar nonrandom    clustering of hotspots has been observed in yeast and the major histocompatibility complexes of human and mouse. To the extent that torrid zones are a general feature of mammalian genomes, they have considerable implications for genetic mapping    strategies in both human populations and mouse crosses.</p>

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</description>

<author>P M. Kelmenson et al.</author>


</item>


<item>
<title>Ontological visualization of protein-protein interactions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1076</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1076</guid>
<pubDate>Tue, 08 May 2012 20:55:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Cellular processes require the interaction of many proteins across several cellular compartments. Determining the collective network of such interactions is an important aspect of understanding the role and regulation of    individual proteins. The Gene Ontology (GO) is used by model organism databases and other bioinformatics resources to provide functional annotation of proteins. The annotation process provides a mechanism to document the binding of one protein    with another. We have constructed protein interaction networks for mouse proteins utilizing the information encoded in the GO annotations. The work reported here presents a methodology for integrating and visualizing information on    protein-protein interactions. RESULTS: GO annotation at Mouse Genome Informatics (MGI) captures 1318 curated, documented interactions. These include 129 binary interactions and 125 interaction involving three or more gene products. Three networks    involve over 30 partners, the largest involving 109 proteins. Several tools are available at MGI to visualize and analyze these data. CONCLUSIONS: Curators at the MGI database annotate protein-protein interaction data from experimental reports    from the literature. Integration of these data with the other types of data curated at MGI places protein binding data into the larger context of mouse biology and facilitates the generation of new biological hypotheses based on physical    interactions among gene products.</p>

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</description>

<author>H J. Drabkin et al.</author>


</item>


<item>
<title>Functional characterization of fidgetin, an AAA-family protein mutated in fidget mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1075</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1075</guid>
<pubDate>Tue, 08 May 2012 20:54:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse fidget mutation is an autosomal recessive mutation that renders reduced or absent semicircular canals, microphthalmia, and various skeletal abnormalities to affected mice. We previously identified the defective gene which    encodes fidgetin, a new member of the ATPases associated with diverse cellular activities (AAA proteins). Here, we report on the subcellular localization of fidgetin as well as that of two closely related proteins, fidgetin-like 1 and    fidgetin-like 2.  Epitope-tagging and immunostaining revealed that both fidgetin and fidgetin-like 2 were predominantly localized to the nucleus, whereas fidgetin-like 1 was both nuclear and cytoplasmic. Furthermore, deletion studies identified a    putative bipartite nuclear localization signal in the middle portion of the fidgetin protein. Since AAA proteins are known to form functional hetero- or homo-hexamers, we used reciprocal immunoprecipitation to examine the potential interaction    among these proteins. We found that fidgetin interacted with itself and this specific interaction was abolished when either the N- or C-terminus of the protein was truncated. Taken together, our results suggest that fidgetin is a nuclear    AAA-family protein with the potential to form homo-oligomers, thus representing the first step towards the elucidation of fidgetin's cellular function and the disease mechanism in fidget mutant mice.</p>

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</description>

<author>Y Yang et al.</author>


</item>


<item>
<title>A targeted mutation in Cacng4 exacerbates spike-wave seizures in stargazer (Cacng2) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1074</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1074</guid>
<pubDate>Tue, 08 May 2012 20:54:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>The voltage-dependent calcium channel gamma4 subunit protein, CACNG4, is closely related to the gamma2 subunit, CACNG2. Both are expressed primarily in the brain and share 53% amino acid identity. The Cacng2 gene is disrupted in the    stargazer mouse, with its distinctive phenotype including ataxia, frequent absence seizure episodes, and head elevation. A disruption within Cacng4 was engineered to assess its particular function.  The homozygous Cacng4-targeted mutant mouse    appeared normal with no ataxic gait or absence seizures, suggesting that other members of the gamma subunit family might functionally compensate for the absence of CACNG4. To test this hypothesis, the targeted Cacng4 mutation was combined with    alleles of Cacng2. Absence seizures were observed in combination with the stargazer 3J mutation, which itself does not have seizures, and increased seizure activity was observed in combination with the waggler allele.  Furthermore, within the    corticothalamic loop, where absence seizures arise, CACNG4 expression is restricted to the thalamus. Our studies show that the CACNG4 protein has seizure suppressing activity, but this effect is revealed only when CACNG2 expression is also    compromised, suggesting that CACNG subunits have in vivo overlapping functions.</p>

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</description>

<author>V A. Letts et al.</author>


</item>


<item>
<title>Development of a new genetic model for absence epilepsy: spike-wave seizures in C3H/He and backcross mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1073</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1073</guid>
<pubDate>Tue, 08 May 2012 20:53:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>To characterize the genetic basis of spike-wave discharges (SWDs) detected by electroencephalography (EEG) in C3H/He mice, substrains of C3H mice were evaluated by EEG and sensitivity to ethosuximide. Crosses with the SWD-negative    strain C57BL/6J were performed to map the underlying gene(s).  C3H/He substrains exhibited a modest incidence (average of 19 SWDs per hour) of 7-8 Hz SWDs when at rest, compared with the C3HeB/Fe subline (four SWDs per hour). In the mapping    backcross, however, many mice showed a very high incidence (50-220 SWDs per hour) throughout the recording period. SWDs were first detected at 3.5 weeks of age, were associated with behavioral arrest, were suppressed by ethosuximide, and were    strongest in the cerebral cortex and thalamus. The major C3H determinant of SWDs, spkw1 (spike-wave 1), mapped to chromosome (Chr 9), and together with a C57BL/6J determinant on Chr 8, spkw2, accounted for more than one-half of the phenotypic    variation in the backcross mice. The modest SWD incidence in C3H/He mice and the high incidence in backcrosses implies that SWD could be a confounding variable for other behaviors. Because C3H/He mice have no other brain abnormalities, they are    an attractive alternative for studying idiopathic absence epilepsy.</p>

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</description>

<author>W N. Frankel et al.</author>


</item>


<item>
<title>Genetic regulation of hematopoietic stem cell exhaustion during development and growth.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1072</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1072</guid>
<pubDate>Tue, 08 May 2012 20:53:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: During aging, hematopoietic stem cell (HSC) exhaustion is more severe in BALB/cByJ (BALB) mice than in C57BL/6J (B6) mice. Our objective is to determine whether HSC exhaustion during development from fetus to adult also    is more severe for BALB than for B6 mice. MATERIALS AND METHODS: Hematopoietic stem cells from fetal liver cells (FLCs) and from young adult bone marrow cells (BMCs) were compared using the competitive repopulation assay to measure long-term    repopulating ability (LTRA) and HSC expansion after serial transplantation. LTRAs were measured in repopulating units (RU), as the ability to produce donor-type erythrocytes and lymphocytes in lethally irradiated recipients relative to the    congenic fresh marrow competitor. To test expansion, FLCs or BMCs were serially transplanted into lethally irradiated carriers whose marrow cells were compared using fluorescence-activated cell staining (FACS), and subsequently tested for LTRA.    RESULTS: BALB and B6 FLCs, respectively, repopulated 2.6 and 13.5 times as well as BMCs. LTRAs correlated with HSC expansion for BALB, but not B6. Per million donor cells, CD34(-) HSC-enriched fractions (HEFs) and total RU values were 6.8 and 4.6    times higher for FLCs than for BMCs in BALB carriers, while these ratios were only 1.2 and 0.97 higher in B6 carriers. CONCLUSION: In B6 HSC development, LTRA is dissociated from expansion. Although 1 x 10(6) BMCs have much lower LTRA, they    expand HSCs as well as 1 x 10(6) FLCs. HSC expansion is partly exhausted in BALB, but not B6, during development.</p>

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</description>

<author>R Yuan et al.</author>


</item>


<item>
<title>Major Histocompatibility Complex-Linked Diabetes Susceptibility in NOD/Lt Mice: Subcongenic Analysis Localizes a Component of Idd16 at the H2-D End of the Diabetogenic H2g7 Complex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1071</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1071</guid>
<pubDate>Tue, 08 May 2012 20:53:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>The diabetogenic major histocompatibility complex (MHC) (H2(g7)) of NOD mice comprises contributions from several class II loci collectively designated as Idd1. Introduction of the H2(gx) haplotype from the related but    diabetes-resistant cataract Shionogi (CTS) strain demonstrated an additional MHC-linked locus designated Idd16. The NOD-related alloxan resistant (ALR)/Lt strain is also characterized by the H2(gx) haplotype, which does not differ from H2(g7)    from the class I H2-K(d) gene distally through the class II and into the class III region. Polymorphisms distal to the heat shock protein 70 locus (Hspa1b) include a rare H2-D(dx) rather than the H2(g7) encoded D(b) allele. Two    differential-length NOD.ALR-H2(gx) congenic stocks (D.R1 and D.R2), both containing H2-D(dx), significantly suppressed diabetogenesis. This protection was lost when ALR alleles between the class III region and H2-D were removed in a shorter    interval congenic (D.R3). Because no differences were observed in the ALR-derived interval extending 0.41 mB proximal to H2-K in any of these congenic stocks, a component of what was originally designated "Idd16" was sited to an interval shorter    than 7.33 mB, distinguishing D.R2 from D.R3.  Evidence supporting the candidacy of the ALR/CTS-shared H2-D(dx) MHC class I variant present in both diabetes-resistant stocks, but not the susceptible stock, is discussed.</p>

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</description>

<author>D P. Pomerleau et al.</author>


</item>


<item>
<title>mt-Nd2 Allele of the ALR/Lt mouse confers resistance against both chemically induced and autoimmune diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1070</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1070</guid>
<pubDate>Tue, 08 May 2012 20:53:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>AIMS/HYPOTHESIS: ALR/Lt, a mouse strain with strong resistance to type 1 diabetes, is closely related to autoimmune type 1 diabetes-prone NOD/Lt mice. ALR pancreatic beta cells are resistant to the beta cell toxin alloxan,    combinations of cytotoxic cytokines, and diabetogenic NOD T-cell lines. Reciprocal F1 hybrids between either ALR and NOD or ALR and NON/Lt, showed that alloxan resistance was transmitted to F1 progeny only when ALR was the maternal parent. Here    we show that the mitochondrial genome (mtDNA) of ALR mice contributes resistance to diabetes. METHODS: When F1 progeny from reciprocal outcrosses between ALR and NOD were backcrossed to NOD, a four-fold lower frequency of spontaneous type 1    diabetes development occurred when ALR contributed the mtDNA. Because of the apparent interaction between nuclear and mtDNA, the mitochondrial genomes were sequenced. RESULTS: An ALR-specific sequence variation in the mt-Nd2 gene producing a    leucine to methionine substitution at amino acid residue 276 in the NADH dehydrogenase 2 was discovered. An isoleucine to valine mutation in the mt-Co3 gene encoding COX3 distinguished ALR and NOD from NON and ALS. All four strains were    distinguished by variation in a mt-encoded arginyl tRNA polyadenine tract. Shared alleles of mt-Co3 and mt-Tr comparing NOD and ALR allowed for exclusion of these two genes as candidates, implicating the mt-Nd2 variation as a potential    ALR-derived type 1 diabetes protective gene. CONCLUSIONS/INTERPRETATION: The unusual resistance of ALR mice to both ROS-mediated and autoimmune type 1 diabete stresses reflects an interaction between the nuclear and mt genomes. The latter    contribution is most likely via a single nucleotide polymorphism in mt-Nd2.</p>

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</description>

<author>C E. Mathews et al.</author>


</item>


<item>
<title>Nonobese diabetic mice and the genetics of diabetes susceptibility.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1069</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1069</guid>
<pubDate>Tue, 08 May 2012 20:52:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The nonobese diabetic mouse spontaneously develops an autoimmune, T-cell-mediated type 1 diabetes (T1D). Common and rare alleles both within a diabetogenic major histocompatibility complex (MHC) and multiple non-MHC genes combine to    impair normal communication between the innate and acquired immune system, leading to loss of immune tolerance. An understanding of how variable collections of genes interact with each other and with environmental cues offers important insights    as to the complexities of T1D inheritance in humans.</p>

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</description>

<author>E H. Leiter</author>


</item>


<item>
<title>CD38 controls ADP-ribosyltransferase-2-catalyzed ADP-ribosylation of T cell surface proteins.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1068</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1068</guid>
<pubDate>Tue, 08 May 2012 20:52:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>ADP-ribosyltransferase-2 (ART2), a GPI-anchored, toxin-related ADP-ribosylating ectoenzyme, is prominently expressed by murine T cells but not by B cells. Upon exposure of T cells to NAD, the substrate for ADP-ribosylation, ART2    catalyzes ADP-ribosylation of the P2X7 purinoceptor and other functionally important cell surface proteins. This in turn activates P2X7 and induces exposure of phosphatidylserine and shedding of CD62L. CD38, a potent ecto-NAD-glycohydrolase, is    strongly expressed by most B cells but only weakly by T cells. Following incubation with NAD, CD38-deficient splenocytes exhibited lower NAD-glycohydrolase activity and stronger ADP-ribosylation of cell surface proteins than their wild-type    counterparts. Depletion of CD38(high) cells from wild-type splenocytes resulted in stronger ADP-ribosylation on the remaining cells. Similarly, treatment of total splenocytes with the CD38 inhibitor nicotinamide 2'-deoxy-2'-fluoroarabinoside    adenine dinucleotide increased the level of cell surface ADP-ribosylation. Furthermore, the majority of T cells isolated from CD38-deficient mice "spontaneously" exposed phosphatidylserine and lacked CD62L, most likely reflecting previous    encounter with ecto-NAD. Our findings support the notion that ecto-NAD functions as a signaling molecule following its release from cells by lytic or nonlytic mechanisms. ART2 can sense and translate the local concentration of ecto-NAD into    corresponding levels of ADP-ribosylated cell surface proteins, whereas CD38 controls the level of cell surface protein ADP-ribosylation by limiting the substrate availability for ART2.</p>

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</description>

<author>C Krebs et al.</author>


</item>


<item>
<title>Proteasome Inhibition Alters Glucose-stimulated (Pro)insulin Secretion and Turnover in Pancreatic {beta}-Cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1067</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1067</guid>
<pubDate>Tue, 08 May 2012 20:52:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Metabolic labeling studies were conducted in freshly isolated mouse islets and a beta-cell line (MIN6) to examine the effects of proteasome inhibition on glucose-stimulated (pro)insulin synthesis and secretion.  Glucose-stimulated    (pro)insulin synthesis, as determined by the incorporation of [(3)H]tyrosine, decreased significantly by 90% in islets and 71% in MIN6 cells pretreated with the proteasome inhibitor lactacystin (10 mum) for 2 h. To follow the fate of newly    synthesized (pro)insulin, islets were pulse-labeled with [(3)H]tyrosine (40 muCi) for 20 min and chased +/- lactacystin (10 mum) for up to 4 h. The release of newly synthesized (pro)insulin ([(3)H]tyrosine-labeled) was similar between    lactacystin-treated and control islets despite a 51% decrease (p <0.05) in total immunoreactive (pro)insulin secretion by lactacystin-treated islets.  The specific radioactivity of [(3)H]tyrosine-labeled (pro)insulin in the extracellular medium    of lactacystin-treated islets (0.52 +/- 0.16 cpm/microunits) was 2-fold greater relative to control islets (0.25 +/- 0.06 cpm/microunits). Induction of the unfolded protein response by lactacystin, as evidenced by the up-regulation of endoplasmic    reticulum (ER) chaperones (GRP78/BiP, GRP94, protein disulfide isomerase) and induction of the stress-inducible transcription factor C/EBP-homologous protein/GADD153 (CHOP/GADD153), likely contributed to the release of newly synthesized    (pro)insulin to relieve ER stress. The present data indicate proteasome inhibition did not prevent, but increased (p <0.05), the intracellular degradation of [(3)H]tyrosine-labeled (pro-)insulin from 8 to 24% in islets. Collectively, these data    indicate beta-cells may balance glucose-stimulated (pro)insulin synthesis and secretion with the activity of the proteasome to regulate protein concentrations in the ER.</p>

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</description>

<author>K Kitiphongspattana et al.</author>


</item>


<item>
<title>P2X7 receptor-dependent and -independent T cell death is induced by nicotinamide adenine dinucleotide.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1066</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1066</guid>
<pubDate>Tue, 08 May 2012 20:51:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adding NAD to murine T lymphocytes inhibits their functions and induces annexin V binding. This report shows that NAD induces cell death in a subset of T cells within seconds whereas others do not die until many hours later. Low NAD    concentrations (<10 >microM) suffice to trigger rapid cell death, which is associated with annexin V binding and membrane pore formation, is not blocked by the caspase inhibitor Z-VADfmk, and requires functional P2X7 receptors. The slower    induction of death requires higher NAD concentrations (>100 microM), is blocked by caspase inhibitor Z-VADfmk, is associated with DNA fragmentation, and does not require P2X7 receptors. T cells degrade NAD to ADP-ribose (ADPR), and adding ADPR to    T cells leads to slow but not rapid cell death. NAD but not ADPR provides the substrate for ADP-ribosyltransferase (ART-2)-mediated attachment of ADP-ribosyl groups to cell surface proteins; expression of ART-2 is required for NAD to trigger    rapid but not slow cell death. These results support the hypothesis that cell surface ART-2 uses NAD but not ADPR to attach ADP-ribosyl groups to the cell surface, and that these groups act as ligands for P2X7 receptors that then induce rapid    cell death. Adding either NAD or ADPR also triggers a different set of mechanisms, not requiring ART-2 or P2X7 receptors that more slowly induce cell death.</p>

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</description>

<author>H Kawamura et al.</author>


</item>


<item>
<title>Reprogramming is essential in nuclear transfer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1065</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1065</guid>
<pubDate>Tue, 08 May 2012 20:51:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fertile offspring have been produced by nuclear transfer from adult somatic cells in several mammalian species (Wilmut et al., 1997; Kato et al., 1998; Wakayama et al., 1998; Polejaeva et al., 2000; Chesne et al., 2002; Shin et al.,    2002; Zhou et al., 2003). Various possible causes have been suggested for the overall low efficiency (Perry and Wakayama, 2002).  Notably, however, it has not yet been clearly demonstrated whether reprogramming after nuclear transfer is necessary    for successful cloning.  Here we show that reprogramming is essential in nuclear transfer, by comparing the developmental efficiency after the transfer of cumulus cell nuclei with that for zygote nuclei. Nuclear transfers from blastomeres of a    series of pre-implantation stages showed further that, as development proceeds, the nuclei progressively lose their potency and become more difficult to reprogram upon their transfer into enucleated MII oocytes. We also found that naturally    ovulated oocytes are much better recipients of a nucleus than are superovulated oocytes, which have been used in all the nuclear transfer experiments reported so far. This indicates that cloning efficiency can also be increased to some extent by    technical improvements.  All these results enable us to distinguish more clearly between the inherent problem of reprogramming and technical problems associated with materials, manipulation, and in vitro culture.</p>

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</description>

<author>T Hiiragi et al.</author>


</item>


<item>
<title>Genetic variation in femur extrinsic strength in 29 different inbred strains of mice is dependent on variations in femur cross-sectional geometry and bone density.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1064</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1064</guid>
<pubDate>Tue, 08 May 2012 20:51:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>The femurs from groups of mice from 29 different inbred strains were characterized to study the genetic variations in bone parameters. For these analyses, we used peripheral quantitative computed tomography to assess bone size and    density in addition to three-point bend testing to assess bone mechanical properties. Highly significant differences between inbred strains were found for all size, density, and mechanical parameters measured (P < 0.0001). Correcting femoral    cross-sectional geometry values or bone mechanical properties values for body weight or femur length reduced but did not eliminate the variations in bone geometry or bone mechanical properties. Mice of similar body size had as much as a 40%    difference in the midshaft total area of the femur. Regression analysis suggested that 50.9% of the variation in maximum load among strains was related to variations in section modulus, i.e., cross-sectional geometry, 21.5% was related to    variations in material bone density, and 27.7% to variations in quality. These components were further analyzed to show that 3.9-27.8% of the variation in maximum load was related to adaptation to mechanical stress. These findings indicate that    there is a significant genetic variation in the femur cross-sectional area, density, and mechanical properties between inbred mouse strains. These studies identify inbred mouse strains suitable for future studies identifying genes regulating bone    geometry and mechanical properties.</p>

	]]>
</description>

<author>J E. Wergedal et al.</author>


</item>


<item>
<title>Allelic differences in a quantitative trait locus affecting insulin-like growth factor-I impact skeletal acquisition and body composition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1063</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1063</guid>
<pubDate>Tue, 08 May 2012 20:50:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Insulin-like growth factor-I (IGF-I) is critical for optimal skeletal growth and maintenance. Knockout and transgenic models have provided significant insights into the role of IGF-I in bone modeling and remodeling. Congenic mice    demonstrate allelic differences in particular quantitative trait loci (QTL). One such model is congenic 6T, which contains a QTL for reduced serum IGF-I donated from C3H/HeJ on a pure C57Bl/6 J (B6) background. In this study we found a 30%-50%    reduction in IGF-I expression in bone, liver, and fat of the congenic 6T mouse, as well as lower circulating IGF-I compared with control B6. 6T mice also had a greater percentage body fat, but reduced serum leptin. These changes were associated    with reduced cortical and trabecular bone mineral density, impaired bone formation but no change in bone resorption. Moreover, the anabolic skeletal response to intermittent parathyroid hormone (PTH) therapy was blunted in 6T compared with B6,    potentially in response to greater programmed cell death in osteocytes and osteoblasts of 6T. In summary, allelic differences in IGF-I expression impact peak bone acquisition and body composition, as well as the skeletal response to PTH.     Lifelong changes in circulating and skeletal IGF-I may be relevant for the pathophysiology of several diseases, including chronic renal failure.</p>

	]]>
</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title>Isolation and cloning of a papillomavirus from a North American porcupine by using multiply primed rolling-circle amplification: the Erethizon dorsatum papillomavirus type 1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1062</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1062</guid>
<pubDate>Tue, 08 May 2012 20:50:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The complete genome of a novel papillomavirus was isolated from a cutaneous papillomatous lesion of a North American porcupine (Erethizon dorsatum) using multiply primed rolling-circle amplification (RCA). The nucleotide sequence,    genome organization, and phylogenetic position of the Erethizon dorsatum papillomavirus type 1 (EdPV-1) were determined. EdPV-1 is only distantly related to other benign cutaneous papillomavirus sequences and is the first member of the novel    Sigma papillomavirus genus.</p>

	]]>
</description>

<author>A Rector et al.</author>


</item>


<item>
<title>Urogenital and caudal dysgenesis in adrenocortical dysplasia (acd) mice is caused by a splicing mutation in a novel telomeric regulator.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1061</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1061</guid>
<pubDate>Tue, 08 May 2012 20:50:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adrenocortical dysplasia (acd) is a spontaneous autosomal recessive mouse mutant with developmental defects in organs derived from the urogenital ridge. In surviving adult mutants, adrenocortical dysplasia and hypofunction are    predominant features. Adults are infertile due to lack of mature germ cells, and 50% develop hydronephrosis due to ureteral hyperplasia. We report the identification of a splice donor mutation in a novel gene, which is the mouse ortholog of a    newly discovered telomeric regulator. This gene (Acd) has recently been characterized as a novel component of the TRF1 protein complex that controls telomere elongation by telomerase. Characterization of Acd transcripts in mutant animals reveals    two abnormal transcripts, consistent with a splicing defect. Expression of a wild-type Acd transgene in acd mutants rescues the observed phenotype.  Most mutants die within 1-2 days of life on the original genetic background. Analysis of these    mutant embryos reveals variable, yet striking defects in caudal specification, limb patterning and axial skeleton formation. In the tail bud, reduced expression of Wnt3a and Dll1 correlates with phenotypic severity of caudal regression. In the    limbs, expression of Fgf8 is expanded in the dorsal-ventral axis of the apical ectodermal ridge and shortened in the anterior-posterior axis, consistent with the observed loss of anterior digits in older embryos. The axial skeleton of mutant    embryos shows abnormal vertebral fusions in cervical, lumbar and caudal regions. This is the first report to show that a telomeric regulator is required for proper urogenital ridge differentiation, axial skeleton specification and limb patterning    in mice.</p>

	]]>
</description>

<author>C E. Keegan et al.</author>


</item>


<item>
<title>A deletion causing spontaneous fracture identified from a candidate region of mouse Chromosome 14.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1060</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1060</guid>
<pubDate>Tue, 08 May 2012 20:49:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Map-based cloning is an iterative approach that identifies the underlying genetic cause of a mutant phenotype. However, the classic protocol of positional cloning is time-consuming and labor-intensive. We now describe a genome    sequence-based cloning approach that has led to localizing the underlying genetic cause of spontaneous fractures (sfx) in a mouse model.  The sfx/sfx mouse is characterized by a spontaneous femoral fracture seen around 6 weeks of age, which    represents a new mouse model for bone fragility. Genetic studies indicate that the phenotype of sfx/sfx mice is caused by an alteration at a single locus that is roughly mapped onto the central region of mouse Chromosome 14. Using our strategy of    combining mouse genome resources and high-throughput technology, we discovered a deletion of all 12 exons in the gene for L-gulonolactone oxidase (LGO), a key enzyme in the synthesis of ascorbic acid. We have also examined the expression of LGO    and found no expression of LGO in sfx mice while the LGO expresses in several tissues of normal mice. Our data demonstrated the feasibility to positionally clone the mutated gene from a non-fine-mapped locus, which has applicability to the    positional cloning of genes from many other animal models, as their genome sequences are sequenced or will be sequenced soon.</p>

	]]>
</description>

<author>Y Jiao et al.</author>


</item>


<item>
<title>Report on the &apos;Expert Workshop on the Biology of Chromosome 21: towards gene-phenotype correlations in Down syndrome&apos;, held June 11-14, 2004, Washington D.C.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1059</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1059</guid>
<pubDate>Tue, 08 May 2012 20:49:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K Gardiner et al.</author>


</item>


<item>
<title>Digenic inheritance of deafness caused by mutations in genes encoding cadherin 23 and protocadherin 15 in mice and humans.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1058</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1058</guid>
<pubDate>Tue, 08 May 2012 20:49:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in genes coding for cadherin 23 and protocadherin 15 cause deafness in both mice and humans. Here, we provide evidence that mutations at these two cadherin loci can interact to cause hearing loss in digenic heterozygotes    of both species. Using a classical genetic approach, we generated mice that were heterozygous for both Cdh23 and Pcdh15 mutations on a uniform C57BL/6J background. Significant levels of hearing loss were detected in these mice when compared to    age-matched single heterozygous animals or normal controls. Cytoarchitectural defects in the cochlea of digenic heterozygotes, including degeneration of the stereocilia and a base-apex loss of hair cells and spiral ganglion cells, were consistent    with the observed age-related hearing loss of these mice beginning with the high frequencies. In humans, we also have obtained evidence for a digenic inheritance of a USH1 phenotype in three unrelated families with mutations in CDH23 and PCDH15.    Altogether, our data indicate that CDH23 and PCDH15 play an essential long-term role in maintaining the normal organization of the stereocilia bundle.</p>

	]]>
</description>

<author>Q Y. Zheng et al.</author>


</item>


<item>
<title>Retinal degeneration 12 (rd12): a new, spontaneously arising mouse model for human Leber congenital amaurosis (LCA).</title>
<link>http://mouseion.jax.org/stfb2000_2009/1057</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1057</guid>
<pubDate>Tue, 08 May 2012 20:48:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: To report the phenotype and characterization of a new, naturally occurring mouse model of hereditary retinal degeneration (rd12). METHODS: The retinal phenotype of rd12 mice were studied using serial indirect    ophthalmoscopy, fundus photography, electroretinography (ERG), genetic analysis including linkage studies and gene identification, immunohistochemistry, and biochemical analysis. RESULTS: Mice homozygous for the rd12 mutation showed small    punctate white spots on fundus examination at 5 months of age. The retina in the rd12 homozygote had a normal appearance at the light microscopic level until 6 weeks of age when occasional voids appeared in the outer segments (OS) of the    photoreceptor (PR) cells. The outer nuclear layer (ONL) appeared normal until 3 months of age though more obvious voids were detected in the OS. By 7 months of age, 6 to 8 layers of ONL remained in the mutant retina, and the OS were obviously    shorter. The first sign of retinal degeneration was detected at the electron microscopic level around 3 weeks of age when occasional small lipid-like droplets were detected in the retinal pigment epithelium (RPE).  By 3 months of age, much    larger, lipid-like droplets accumulated in RPE cells accompanied by some OS degeneration. While the histology indicated a relatively slow retinal degeneration in the rd12 homozygous mutant mice, the rod ERG response was profoundly diminished even    at 3 weeks of age.  Genetic analysis showed that rd12 was an autosomal recessive mutation and mapped to mouse chromosome 3 closely linked to D3Mit19, a location known to be near the mouse Rpe65 gene. Sequence analysis showed that the mouse    retinal degeneration is caused by a nonsense mutation in exon 3 of the Rpe65 gene, and the gene symbol for the rd12 mutation has been updated to Rpe65rd12 to reflect this. No RPE65 expression, 11-cis retinal, or rhodopsin could be detected in    retinas from rd12 homozygotes, while retinyl esters were found to accumulate in the retinal pigment epithelium (RPE). CONCLUSIONS: Mutations in the retinal pigment epithelium gene encoding RPE65 cause an early onset autosomal recessive form of    human retinitis pigmentosa, known as Leber congenital amaurosis (LCA), which results in blindness or severely impaired vision in children. A naturally arising mouse Rpe65 mutation provides a good model for studying the pathology of human RPE65    mutations and the effects of retinyl ester accumulation.</p>

	]]>
</description>

<author>J J. Pang et al.</author>


</item>


<item>
<title>SHP-1 regulates STAT6 phosphorylation and IL-4-mediated function in a cell type-specific manner.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1056</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1056</guid>
<pubDate>Tue, 08 May 2012 20:48:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>SHP-1 has been shown to play positive and negative regulatory roles in IL-4-induced STAT6 phosphorylation and in IL-4-mediated functions. To determine whether SHP-1 can regulate STAT6 phosphorylation and IL-4-mediated functions in a    cell type-specific manner in the immune system, we examined the IL-4 receptor (IL-4R) expression, STAT6 phosphorylation, and IL-4-mediated functions in CD4+ and CD8+ T cells of viable motheaten (me(v)/me(v)) and littermate control (+/-) mice.    CD4+ T cells as well as CD8+ T cells from the lymph node of me(v)/me(v) and +/- mice expressed comparable levels of IL-4R. In CD4+ T cells, the loss of SHP-1 activity did not affect IL-4-induced STAT6 phosphorylation or IL-4-mediated function. In    contrast, SHP-1-deficient CD8+ T cells from me(v)/me(v) mice failed to develop into IL-4-producing type-2 cytotoxic T cells (Tc2) in the presence of IL-4 despite that they showed comparable levels of STAT6 phosphorylation to that of +/- CD8+ T    cells. Loss of SHP-1 activity also abolished IL-4-mediated inhibition of c-kit expression in bone marrow-derived mast cell (BMMC). Thus, our data suggest that SHP-1 may regulate IL-4-induced STAT6 phosphorylation and IL-4-mediated functions in a    cell type-specific manner.</p>

	]]>
</description>

<author>Z Huang et al.</author>


</item>


<item>
<title>Oocyte control of metabolic cooperativity between oocytes and companion granulosa cells: energy metabolism.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1055</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1055</guid>
<pubDate>Tue, 08 May 2012 20:48:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Intercellular communication between oocytes and granulosa cells is essential for normal follicular differentiation and oocyte development.  Subtraction hybridization was used to identify genes more highly expressed in cumulus cells    than in mural granulosa cells of mouse antral follicles.  This screen identified six genes involved in glycolysis: Eno1, Pkm2, Tpi, Aldoa, Ldh1, and Pfkp. When oocytes were microsurgically removed from cumulus cell-oocyte complexes, the isolated    cumulus cells exhibited decreased expression levels of genes encoding glycolytic enzymes, glycolysis and activity of the tricarboxylic acid (TCA) cycle. These decreases were prevented by culturing the cumulus cells with paracrine factors secreted    by fully grown oocytes. Paracrine factors from fully grown oocytes exhibited greater ability than those from growing oocytes to promote expression of genes encoding glycolytic enzymes and glycolysis in the granulosa cells of preantral follicles.    However, neither fully grown nor growing oocytes secreted paracrine factors affecting activity of the TCA cycle. These results indicate that oocytes regulate glycolysis and the TCA cycle in granulosa cells in a manner specific to the population    of granulosa cells and to the stage of growth and development of the oocyte.  Oocytes control glycolysis in granulosa cells by regulating expression levels of genes encoding glycolytic enzymes. Therefore, mouse oocytes control the intercellular    metabolic cooperativity between cumulus cells and oocytes needed for energy production by granulosa cells and required for oocyte and follicular development.</p>

	]]>
</description>

<author>K Sugiura et al.</author>


</item>


<item>
<title>The Mammalian Phenotype Ontology as a tool for annotating, analyzing and comparing phenotypic information.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1054</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1054</guid>
<pubDate>Tue, 08 May 2012 20:48:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mammalian Phenotype (MP) Ontology enables robust annotation of mammalian phenotypes in the context of mutations, quantitative trait loci and strains that are used as models of human biology and disease. The MP Ontology supports    different levels and richness of phenotypic knowledge and flexible annotations to individual genotypes. It continues to develop dynamically via collaborative input from research groups, mutagenesis consortia, and biological domain experts. The MP    Ontology is currently used by the Mouse Genome Database and Rat Genome Database to represent phenotypic data.</p>

	]]>
</description>

<author>C L. Smith et al.</author>


</item>


<item>
<title>The Mouse Tumor Biology Database: integrated access to mouse cancer biology data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1053</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1053</guid>
<pubDate>Tue, 08 May 2012 20:47:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice have long been used as models for the study of human cancer. The National Cancer Institute has included among its research areas of extraordinary opportunity the development of new mouse genetic models of human cancer and the    exploration of cancer imaging as a research tool.  Because of the volume and interconnectedness of relevant data, the creation and maintenance of bioinformatics resources of mouse tumor biology is necessary to facilitate current and future cancer    research. The Mouse Tumor Biology (MTB) Database provides electronic access to data generated through the study of spontaneous and induced tumors in genetically defined mice (inbred, hybrid, spontaneous and induced mutant, and genetically    engineered strains of mice).</p>

	]]>
</description>

<author>D Krupke et al.</author>


</item>


<item>
<title>The Mouse Genome Database (MGD): from genes to mice--a community resource for mouse biology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1052</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1052</guid>
<pubDate>Tue, 08 May 2012 20:47:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Database (MGD) forms the core of the Mouse Genome Informatics (MGI) system (http://www.informatics.jax.org), a model organism database resource for the laboratory mouse. MGD provides essential integration of    experimental knowledge for the mouse system with information annotated from both literature and online sources. MGD curates and presents consensus and experimental data representations of genotype (sequence) through phenotype information,    including highly detailed reports about genes and gene products. Primary foci of integration are through representations of relationships among genes, sequences and phenotypes. MGD collaborates with other bioinformatics groups to curate a    definitive set of information about the laboratory mouse and to build and implement the data and semantic standards that are essential for comparative genome analysis. Recent improvements in MGD discussed here include the enhancement of phenotype    resources, the re-development of the International Mouse Strain Resource, IMSR, the update of mammalian orthology datasets and the electronic publication of classic books in mouse genetics.</p>

	]]>
</description>

<author>J T. Eppig et al.</author>


</item>


<item>
<title>Diabetes acceleration or prevention by a coxsackievirus B4 infection: critical requirements for both interleukin-4 and gamma interferon.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1051</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1051</guid>
<pubDate>Tue, 08 May 2012 20:47:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Type 1 diabetes acceleration in nonobese diabetic (NOD) mice through coxsackievirus B4 (CVB4) infection requires a preexisting critical mass of autoreactive T cells in pancreatic islets, and in the absence of this insulitic    threshold, CVB4 infection leads to long-term disease protection.  To understand this acceleration and protection process, we challenged 8- and 12-week-old NOD mice containing a disruption in interleukin-4 (IL-4) or gamma interferon (IFN-gamma)    genes (NOD IL-4-/- and NOD IFN-gamma-/-, respectively) with a diabetogenic, pancreatropic Edwards strain of CVB4.  The elimination of IL-4 did not alter the rate of insulitis or diabetes development in NOD mice, while the elimination of IFN-gamma    delayed these events several weeks. CVB4 infection in 8-week-old mice only significantly accelerated the onset of diabetes in a subset of standard, but not IL-4- or IFN-gamma-deficient, NOD mice. Long-term diabetes protection was established in    standard NOD mice as well as in the NOD IFN-gamma-/- mice that did not rapidly develop disease following CVB4 infection at 8 weeks of age. When mice were infected at 12 weeks of age, the onset of diabetes was accelerated in NOD IL-4-/- mice,    while neither acceleration nor long-term protection was elicited in NOD IFN-gamma-/- mice. No differences were observed in the kinetics of CVB4 clearance in pancreases from NOD, NOD IL-4-/-, and NOD IFN-gamma-/- mice. Collectively, these results    suggest that at the insulitis threshold at which CVB4 infection can first accelerate the onset of diabetes in NOD mice, IL-4 as well as IFN-gamma contributes to this pathogenic process. The protective mechanism against diabetes elicited in NOD    mice infected with CVB4 prior to the development of a critical threshold level of insulitis requires neither IL-4 nor IFN-gamma.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title>Adenovirus early region 3 transgenes expressed in beta cells prevent autoimmune diabetes in nonobese diabetic mice: effects of deleting the adenovirus death protein 11.6K.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1050</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1050</guid>
<pubDate>Tue, 08 May 2012 20:46:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The incidence of type 1 diabetes (T1D) is decreased in nonobese diabetic mice expressing the complete cassette of adenovirus early region 3 (E3) immunomodulating genes in pancreatic beta cells. Embedded among the antiapoptotic E3    genes is one encoding an adenovirus death protein (ADP), which contributes to release of virion particles by promoting cell lysis.  Because removal of this proapoptotic protein might have further enhanced the ability of E3 proteins to prevent    T1D, an ADP-inactivated E3 construct was tested. Significantly, deletion of ADP did not improve the diabetes-protective effect of an E3 gene cassette.</p>

	]]>
</description>

<author>M A. Pierce et al.</author>


</item>


<item>
<title>Autoimmune diabetes and resistance to xenograft transplantation tolerance in NOD mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1049</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1049</guid>
<pubDate>Tue, 08 May 2012 20:46:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Costimulation blockade induces prolonged rat islet and skin xenograft survival in C57BL/6 mice. Nonobese diabetic (NOD) mice, which are used to model human autoimmune diabetes, are resistant to costimulation blockade-induced    allograft tolerance. We tested the hypothesis that NOD mice would also be resistant to costimulation blockade-induced rat xenograft tolerance. We report that rat islet xenograft survival is short in spontaneously diabetic NOD mice treated with a    tolerizing regimen of donor-specific transfusion and anti-CD154 antibody. Rat islet xenograft survival is only marginally longer in chemically diabetic NOD mice treated with costimulation blockade but is prolonged further in NOD Idd congenic mice    bearing C57-derived chromosome 3 loci. Reciprocally, the presence of NOD-derived chromosome 3 loci shortens islet xenograft survival in tolerized C57BL/6 mice. Islet xenograft survival is longer in tolerized NOD.CD4a(-/-) and (NOD x C57BL/6)F1    mice than in NOD mice but still much shorter than in C57BL/6 mice. Skin xenograft survival in (NOD x C57BL/6)F1 mice treated with costimulation blockade is short, suggesting a strong genetic resistance to skin xenograft tolerance induction. We    conclude that the resistance of NOD mice to xenograft tolerance induction involves some mechanisms that also participate in the expression of autoimmunity and other mechanisms that are distinct.</p>

	]]>
</description>

<author>E J. Gordon et al.</author>


</item>


<item>
<title>The good turned ugly: immunopathogenic basis for diabetogenic CD8+ T cells in NOD mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1048</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1048</guid>
<pubDate>Tue, 08 May 2012 20:46:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Type 1 diabetes (T1D) in both humans and nonobese diabetic (NOD) mice is a T-cell-mediated autoimmune disease in which the insulin-producing pancreatic islet beta-cells are selectively eliminated. As a result, glucose metabolism    cannot be regulated unless exogenous insulin is administered. Both the CD4(+) and the CD8(+) T-cell subsets are required for T1D development. Approximately 20 years ago, an association between certain class II major histocompatibility complex    (MHC) alleles and susceptibility to T1D was reported. This finding led to enormous interest in the CD4(+) T cells participating in the development of T1D, while the CD8(+) subset was relatively ignored. However, the isolation of    beta-cell-autoreactive CD8(+) T-cell clones from the islets of NOD mice helped to generate interest in the pathogenic role of this subset, as has accumulating evidence that certain class I MHC alleles are additional risk factors for T1D    development in humans. Three distinct diabetogenic CD8(+) T-cell populations have now been characterized in NOD mice. Here, we review recent investigations exploring their selection, activation, trafficking, and antigenic specificities. As CD8(+)    T cells are suspected contributors to beta-cell demise in humans, continued exploration of these critical areas could very possibly lead to tangible benefits for T1D patients and at-risk individuals.</p>

	]]>
</description>

<author>T P. DiLorenzo et al.</author>


</item>


<item>
<title>Activated NKT cells inhibit autoimmune diabetes through tolerogenic recruitment of dendritic cells to pancreatic lymph nodes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1047</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1047</guid>
<pubDate>Tue, 08 May 2012 20:46:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>NKT cell activation by alpha-galactosylceramide (alpha-GalCer) inhibits autoimmune diabetes in NOD mice, in part by inducing recruitment to pancreatic lymph nodes (PLNs) of mature dendritic cells (DCs) with disease-protective    effects. However, how activated NKT cells promote DC maturation, and what downstream effect this has on diabetogenic T cells was unknown. Activated NKT cells were found to produce a soluble factor(s) inducing DC maturation. Initially, there was a    preferential accumulation of mature DCs in the PLNs of alpha-GalCer-treated NOD mice, followed by a substantial increase in T cells. Adoptive transfer of a diabetogenic CD8 T cell population (AI4) induced a high rate of disease (75%) in    PBS-treated NOD recipients, but not in those pretreated with alpha-GalCer (8%).  Significantly, more AI4 T cells accumulated in PLNs of alpha-GalCer than PBS-treated recipients, while no differences were found in mesenteric lymph nodes from each    group. Compared with those in mesenteric lymph nodes, AI4 T cells entering PLNs underwent greater levels of apoptosis, and the survivors became functionally anergic. NKT cell activation enhanced this process. Hence, activated NKT cells elicit    diabetes protection in NOD mice by producing a soluble factor(s) that induces DC maturation and accumulation in PLNs, where they subsequently recruit and tolerize pathogenic T cells.</p>

	]]>
</description>

<author>Y G. Chen et al.</author>


</item>


<item>
<title>Selective ablation of alphav integrins in the central nervous system leads to cerebral hemorrhage, seizures, axonal degeneration and premature death.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1046</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1046</guid>
<pubDate>Tue, 08 May 2012 20:45:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mouse embryos genetically null for all alphav integrins develop intracerebral hemorrhage owing to defective interactions between blood vessels and brain parenchymal cells. Here, we have used conditional knockout technology to    address whether the cerebral hemorrhage is due to primary defects in vascular or neural cell types. We show that ablating alphav expression in the vascular endothelium has no detectable effect on cerebral blood vessel development, whereas    deletion of alphav expression in central nervous system glial cells leads to embryonic and neonatal cerebral hemorrhage. Conditional deletion of alphav integrin in both central nervous system glia and neurons also leads to cerebral hemorrhage,    but additionally to severe neurological defects. Approximately 30% of these mutants develop seizures and die by 4 weeks of age. The remaining mutants survive for several months, but develop axonal deterioration in the spinal cord and cerebellum,    leading to ataxia and loss of hindlimb coordination. Collectively, these data provide evidence that alphav integrins on embryonic central nervous system neural cells, particularly glia, are necessary for proper cerebral blood vessel development,    and also reveal a novel function for alphav integrins expressed on axons in the postnatal central nervous system.</p>

	]]>
</description>

<author>J H. McCarty et al.</author>


</item>


<item>
<title>New Alstrom syndrome phenotypes based on the evaluation of 182 cases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1045</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1045</guid>
<pubDate>Tue, 08 May 2012 20:45:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Alstrom syndrome is a recessively inherited genetic disorder characterized by congenital retinal dystrophy that leads to blindness, hearing impairment, childhood obesity, insulin resistance, and type 2 diabetes mellitus.    We provide new details on cardiologic, hepatic, gastrointestinal, urologic, pulmonary, and neurobehavioral phenotypes in Alstrom syndrome and describe the histopathologic findings in 5 individuals. METHODS: We obtained data on 182 patients from    clinical examinations, medical record reviews, standardized questionnaires, and personal interviews with physicians and parents. RESULTS: Dilated cardiomyopathy occurred in 60% of patients. Age at onset was either during infancy, often before    vision disturbances were noted, or in adolescence or adulthood. There is a risk of recurrence of infantile cardiomyopathy.  Hyperinsulinemia (92%) developed in early childhood and progressed to type 2 diabetes mellitus in 82% of those older than    16 years.  Hypertriglyceridemia (54%) precipitated pancreatitis in 8 patients.  Urologic dysfunction and gastrointestinal disturbances occurred in 48% and 35% of patients, respectively. Fifty-three percent of patients had persistent pulmonary    symptoms. Neurologic symptoms in 20% of patients included clonic tic and absence seizures. Developmental motor or language delays were observed in 46% of patients. Fibrotic infiltrations of multiple organs, that is, kidney, heart, liver, lung,    urinary bladder, gonads, and pancreas, were observed. CONCLUSIONS: The wide-ranging and complex spectrum of phenotypes reported herein broadens those previously described for Alstrom syndrome. These findings will aid physicians in making an early    and accurate diagnosis and will help effect appropriate monitoring and treatment.</p>

	]]>
</description>

<author>J D. Marshall et al.</author>


</item>


<item>
<title>Essential role of endothelial Notch1 in angiogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1044</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1044</guid>
<pubDate>Tue, 08 May 2012 20:45:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Notch signaling influences binary cell fate decisions in a variety of tissues. The Notch1 receptor is widely expressed during embryogenesis and is essential for embryonic development. Loss of global Notch1 function    results in early embryonic lethality, but the cell type responsible for this defect is not known. Here, we identify the endothelium as the primary target tissue affected by Notch1 signaling.  METHODS AND RESULTS: We generated an    endothelium-specific deletion of Notch1 using Tie2Cre and conditional Notch1(flox/flox) mice. Mutant embryos lacking endothelial Notch1 died at approximately embryonic day 10.5 with profound vascular defects in placenta, yolk sac, and embryo    proper, whereas heterozygous deletion had no effect. In yolk sacs of mutant embryos, endothelial cells formed a primary vascular plexus indicative of intact vasculogenesis but failed to induce the secondary vascular remodeling required to form a    mature network of well-organized large and small blood vessels, which demonstrates a defect in angiogenesis. These vascular defects were also evident in the placenta, where blood vessels failed to invade the placental labyrinth, and in the embryo    proper, where defective blood vessel maturation led to pericardial and intersomitic hemorrhage. Enhanced activation of caspase-3 was detected in endothelial and neural cells of mutant mice, which resulted in enhanced apoptotic degeneration of    somites and the neural tube. CONCLUSIONS: These findings recapitulate the vascular phenotype of global Notch1-/- mutants and indicate an essential cell-autonomous role of Notch1 signaling in the endothelium during vascular development. These    results may have important clinical implications with regard to Notch1 signaling in adult angiogenesis.</p>

	]]>
</description>

<author>F P. Limbourg et al.</author>


</item>


<item>
<title>Perp is a p63-regulated gene essential for epithelial integrity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1043</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1043</guid>
<pubDate>Tue, 08 May 2012 20:44:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>p63 is a master regulator of stratified epithelial development that is both necessary and sufficient for specifying this multifaceted program. We show here that Perp, a tetraspan membrane protein originally identified as an    apoptosis-associated target of the p53 tumor suppressor, is the first direct target of p63 clearly involved in mediating this developmental program in vivo. During embryogenesis, Perp is expressed in an epithelial pattern, and its expression    depends on p63. Perp-/- mice die postnatally, with dramatic blistering in stratified epithelia symptomatic of compromised adhesion. Perp localizes specifically to desmosomes, adhesion junctions important for tissue integrity, and numerous    structural defects in desmosomes are observed in Perp-deficient skin, suggesting a role for Perp in promoting the stable assembly of desmosomal adhesive complexes.  These findings demonstrate that Perp is a key effector in the p63 developmental    program, playing an essential role in an adhesion subprogram central to epithelial integrity and homeostasis.</p>

	]]>
</description>

<author>R A. Ihrie et al.</author>


</item>


<item>
<title>Distal Chr 4 harbors a genetic locus (Gct1) fundamental for spontaneous ovarian granulosa cell tumorigenesis in a mouse model.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1042</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1042</guid>
<pubDate>Tue, 08 May 2012 20:44:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The spontaneous development of juvenile-onset ovarian granulosa cell tumors in mice of the SWXJ-9 recombinant inbred strain is a model for juvenile-type granulosa cell tumors that appear in very young girls. To expedite gene    discovery in this mouse model of childhood cancer, we did a gene mapping study with the SWXJ-9 recombinant inbred strain and the evolutionarily divergent Mus musculus castaneus (CAST/Ei) strain as a mapping partner. Our mapping strategy focused    on autosomal determinants of susceptibility with a backcross scheme that exploited a paternal, parent-of-origin effect for a X-linked gene (Gct4) that strongly supports granulosa cell tumor development. Of 1,968 backcross females examined, we    detected 81 granulosa cell tumor-bearing animals and compared their allelic inheritance patterns to non-tumor-bearing siblings in a case-control analysis. The results of our study have confirmed an important locus on mouse chromosome (Chr) 4    (Gct1) and have revealed new loci for granulosa cell tumor susceptibility (Gct7-Gct9) on Chrs 1, 2, and 13 with susceptibility alleles contributed by the SWXJ-9 progenitor. Two novel gene-gene interactions supportive for granulosa cell tumor    development were also observed between loci on Chrs 17 and 18 and loci on Chrs 2 and 10. Our data substantiate the evidence that Gct1 on Chr 4 is a fundamental oncogene for granulosa cell tumorigenesis in mice and has identified additional    interacting autosomal loci that support tumor development.</p>

	]]>
</description>

<author>A M. Dorward et al.</author>


</item>


<item>
<title>Mouse models of Down syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1041</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1041</guid>
<pubDate>Tue, 08 May 2012 20:44:14 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M T. Davisson</author>


</item>


<item>
<title>Introducing PLoS Genetics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1040</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1040</guid>
<pubDate>Tue, 08 May 2012 20:43:56 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W N. Frankel</author>


</item>


<item>
<title>Maturation of layer V pyramidal neurons in the rat prefrontal cortex: intrinsic properties and synaptic function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1039</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1039</guid>
<pubDate>Tue, 08 May 2012 20:43:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Layer V pyramidal neurons in the rat medial prefrontal cortex (PFC) were examined with whole cell patch-clamp recording in acute slices from postnatal day 1 (P1) to P36. In the first few days after birth, layer V pyramidal neurons    had low resting potentials, high-input resistance, and long membrane time constant.  During the next 2 wk, the resting potential shifted by -14 mV, while the input resistance and time constant decreased by 15- and 4-fold, respectively. Between P3    and P21, the surface area of the cell body doubled, while the total lengths of apical and basal dendrites increased by 5- and 13-fold, respectively. Action potentials (APs) were observed at all aged tested. The peak amplitude of APs increased by    30 mV during the first 3 wk, while AP rise time and half-maximum duration shortened significantly. Compared with neurons at P21 or older, neurons in the first week required much smaller currents to reach their maximum firing frequencies, but the    maximum frequencies were lower than those at older ages.  Stimulation of layer II/III induced monosynaptic responses in neurons older than P5. Paired-pulse responses showed a short-term depression at P7, which shifted progressive to facilitation    at older ages. These results demonstrate that, similar to other neurons in the brain, layer V pyramidal neurons in the PFC undergo a period of rapid development during the first 3 wk after birth. These findings suggest that the intrinsic    properties of neurons and the properties of synaptic inputs develop concomitantly during early life.</p>

	]]>
</description>

<author>Z W. Zhang</author>


</item>


<item>
<title>WebQTL: rapid exploratory analysis of gene expression and genetic networks for brain and behavior.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1038</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1038</guid>
<pubDate>Tue, 08 May 2012 20:43:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E J. Chesler et al.</author>


</item>


<item>
<title>The ldis1 lens mutation in RIIIS/J mice maps to chromosome 8 near cadherin 1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1037</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1037</guid>
<pubDate>Tue, 08 May 2012 20:43:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: We have discovered a spontaneous and severe mutation that leads to partial or complete disruption of the lens and cataract in the RIIIS/J inbred strain of mice. The purpose of this study was to determine the mode of    inheritance, specificity, and range of phenotypes using histological, ophthalmic, quantitative electron microscopic, and microarray-based methods. We also have fine-mapped the mutation, ldis1 (lens disrupter 1), and have evaluated positional    candidate genes. METHODS: Eyes from mutant RIIIS/J animals and from an F2 intercross between RIIIS/J and DBA/2J were examined and scored to map the ldis1 mutation. Axons in the optic nerve were counted. Messenger RNA from mutant eyes was    hybridized to Affymetrix short oligomer microarrays and compared to five control strains. Expression differences were used to evaluate molecular sequellae of the mutation. RESULTS: Mice that are homozygous for ldis1 have small eyes.  Lenses are    without exception opaque, deformed, dislocated, fragmented, and small.  In contrast, retinal architecture and ganglion cell numbers are within normal range. We have not detected any other ldis1-associated ocular or systemic abnormalities. ldis1    is recessive and maps to chromosome 8 at about 106.5 Mb between D8Mit242 and D8Mit199 with a peak LOD score near cadherin 1. The homologous human chromosomal interval is 16q22.1. The expression of several downstream crystallin transcripts are    severely affected in the mutant, as are the expression levels of multiple members of the transforming growth factor superfamily and the glutathione S-transferases. CONCLUSIONS: We have discovered and mapped a recessive mutation to mouse    chromosome 8 between 105 and 109 Mb.  Homozygous mutant mice have a selective and severe effect on lens integrity. On the basis of the phenotype and the locus position, several candidate genes have been identified.</p>

	]]>
</description>

<author>M M. Jablonski et al.</author>


</item>


<item>
<title>Mapping of a quantitative trait locus for morphine withdrawal severity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1036</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1036</guid>
<pubDate>Tue, 08 May 2012 20:42:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chronic morphine exposure results in physical dependence, manifested by physical symptoms during naloxone-precipitated withdrawal. Jumping frequency is widely considered the most sensitive and reliable index of withdrawal intensity    in mice.  Inbred mouse strains surveyed for naloxone-precipitated withdrawal display large and significant strain differences in jumping frequency, including an approximately tenfold difference between C57BL/6 and 129P3 mice. In the present    study, (B6 x 129)F2 hybrid mice were given daily morphine injections for four days using an escalating dosing schedule, and naloxone-precipitated withdrawal on day 5 was measured. A full-genome scan for linkage to phenotypic data was performed    using polymorphic microsatellite markers. Significant linkage was observed between withdrawal jumping frequencies and a 28 cM-wide region of Chromosome 1 (32-60 cM; peak at 51 cM), accounting for 20% of the overall phenotypic variance. Two other    suggestive QTLs were found, on Chromosomes 5 and 10, and an additive model fitting all three loci accounted for 43% of the total variance. F2 mice were also assessed for changes in morphine analgesic potency using the tail-withdrawal test in    dose-response studies on days 1 and 4. No linkage was observed between Chromosomes 1, 5, and 10 and morphine analgesic tolerance, suggestive of genetic dissociation of naloxone-precipitated withdrawal from morphine and chronic morphine intake per    se. The significant quantitative trait locus for naloxone-precipitated withdrawal severity in morphine-dependent mice, which we name Depmq1, may prove to be of considerable heuristic value once the underlying gene or genes are    identified.</p>

	]]>
</description>

<author>B Kest et al.</author>


</item>


<item>
<title>Acute progesterone can recruit sex-specific neurochemical mechanisms mediating swim stress-induced and kappa-opioid analgesia in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1035</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1035</guid>
<pubDate>Tue, 08 May 2012 20:42:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is a qualitative sex difference in the neurochemical mediation of stress-induced and kappa-opioid analgesia; these phenomena are dependent on N-methyl-d-aspartic acid (NMDA) receptors in males but not females. Progesterone    modulation of this sex difference was examined in mice. Analgesia against thermal nociception was produced by forced cold water swim or by systemic administration of the kappa-opioid agonist, U50,488. As seen previously, the NMDA receptor    antagonist MK-801 blocked both forms of analgesia in male but not female mice.  Also as in previous studies, this sex difference was found to be dependent on ovarian hormones such that ovariectomy induced female mice to "switch" to the male-like,    NMDAergic system. We now demonstrate that a single injection of progesterone (50 microg), systemically administered 30 min before analgesia assessment, is sufficient to restore female-specific mediation of analgesia (i.e., insensitivity to MK-801    blockade) in ovariectomized female mice. The rapidity of this neurochemical "switching" action of progesterone suggests mediation via cell surface receptors or the action of neuroactive steroid metabolites of progesterone.</p>

	]]>
</description>

<author>W F. Sternberg et al.</author>


</item>


<item>
<title>Brain gene expression: genomics and genetics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1034</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1034</guid>
<pubDate>Tue, 08 May 2012 20:42:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E J. Chesler et al.</author>


</item>


<item>
<title>Overexpression of c-MYC promotes an undifferentiated phenotype in cultured astrocytes and allows elevated Ras and Akt signaling to induce gliomas from GFAP-expressing cells in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1033</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1033</guid>
<pubDate>Tue, 08 May 2012 20:41:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The c-MYC protooncogene is overexpressed in the most malignant primary brain tumor, glioblastoma multiforme (GBM), and has been correlated with the undifferentiated character of several cell types. However, the role of Myc activity    in the generation of GBMs is not known. In this report, we show that gene transfer of c-MYC to GFAP-expressing astrocytes in vitro promotes the outgrowth of GFAP-negative, nestin-expressing cells with progenitor-like morphology, growth    characteristics and gene-expression pattern. In addition, gene transfer of c-MYC to GFAP-expressing astrocytes in vivo induces GBMs when co-expressed with activated Ras and Akt. Without c-MYC, Ras+Akt induces GBMs from nestin-expressing CNS    progenitors but is insufficient in GFAP-expressing differentiated astrocytes. The ability of Myc activity to enhance the oncogenic effects of Ras+Akt appears to be limited to GFAP-expressing astrocytes because nestin-expressing progenitors show    no increase in GBM formation with the addition of MYC to Ras+Akt. These studies indicate that one role of MYC activity in the formation of gliomas might be to either promote or reinforce an undifferentiated phenotype required for glioma cells to    respond to the oncogenic effects of elevated Ras and Akt activity.</p>

	]]>
</description>

<author>A B. Lassman et al.</author>


</item>


<item>
<title>Dose-dependent effects of platelet-derived growth factor-B on glial tumorigenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1032</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1032</guid>
<pubDate>Tue, 08 May 2012 20:41:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Platelet-derived growth factor (PDGF) is expressed in many different tumors, but its precise roles in tumorigenesis remain to be fully defined. Here, we report on a mouse model that demonstrates dose-dependent effects of PDGF-B on    glial tumorigenesis. By removing inhibitory regulatory elements in the PDGFB mRNA, we are able to substantially elevate its expression in tumor cells using a retroviral delivery system. This elevation in PDGF-B production results in tumors with    shortened latency, increased cellularity, regions of necrosis, and general high-grade character. In addition, elevated PDGF-B in these tumors also mediates vascular smooth muscle cell recruitment that supports tumor angiogenesis. PDGF receptor    (PDGFR) signaling appears to be required for the maintenance of these high-grade characteristics, because treatment of high-grade tumors with a small molecule inhibitor of PDGFR results in reversion to a lower grade tumor histology. Our data show    that PDGFR signaling quantitatively regulates tumor grade and is required to sustain high-grade oligodendrogliomas.</p>

	]]>
</description>

<author>A H. Shih et al.</author>


</item>


<item>
<title>Telomeres and the DNA damage response: why the fox is guarding the henhouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1031</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1031</guid>
<pubDate>Tue, 08 May 2012 20:41:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>DNA double strand breaks (DSBs) are repaired by an extensive network of proteins that recognize damaged DNA and catalyze its repair. By virtue of their similarity, the normal ends of linear chromosomes and internal DNA DSBs are both    potential substrates for DSB repair enzymes. Thus, telomeres, specialized nucleo-protein complexes that cap chromosomal ends, serve a critical function to differentiate themselves from internal DNA strand breaks, and as a result prevent genomic    instability that can result from their inappropriate involvement in repair reactions. Telomeres that become critically short due to failure of telomere maintenance mechanisms, or which become dysfunctional by loss of telomere binding proteins,    elicit extensive checkpoint responses that in normal cells blocks proliferation. In this situation, the DNA DSB repair machinery plays a major role in responding to these "damaged" telomeres - creating chromosome fusions or capturing telomeres    from other chromosomes in an effort to rid the cell of the perceived damage. However, a surprising aspect of telomere maintenance is that many of the same proteins that facilitate this repair of damaged telomeres are also necessary for their    proper integrity. Here, we review recent work defining the roles for DSB repair machinery in telomere maintenance and in response to telomere dysfunction.</p>

	]]>
</description>

<author>R S. Maser et al.</author>


</item>


<item>
<title>The SOFG Anatomy Entry List (SAEL): An Annotation Tool for Functional Genomics Data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1030</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1030</guid>
<pubDate>Tue, 08 May 2012 20:41:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>A great deal of data in functional genomics studies needs to be annotated with low-resolution anatomical terms. For example, gene expression assays based on manually dissected samples (microarray, SAGE, etc.)  need high-level    anatomical terms to describe sample origin. First-pass annotation in high-throughput assays (e.g. large-scale in situ gene expression screens or phenotype screens) and bibliographic applications, such as selection of keywords, would also benefit    from a minimum set of standard anatomical terms. Although only simple terms are required, the researcher faces serious practical problems of inconsistency and confusion, given the different aims and the range of complexity of existing anatomy    ontologies. A Standards and Ontologies for Functional Genomics (SOFG) group therefore initiated discussions between several of the major anatomical ontologies for higher vertebrates. As we report here, one result of these discussions is a simple,    accessible, controlled vocabulary of gross anatomical terms, the SOFG Anatomy Entry List (SAEL). The SAEL is available from http://www.sofg.org and is intended as a resource for biologists, curators, bioinformaticians and developers of software    supporting functional genomics. It can be used directly for annotation in the contexts described above. Importantly, each term is linked to the corresponding term in each of the major anatomy ontologies. Where the simple list does not provide    enough detail or sophistication, therefore, the researcher can use the SAEL to choose the appropriate ontology and move directly to the relevant term as an entry point.  The SAEL links will also be used to support computational access to the    respective ontologies.</p>

	]]>
</description>

<author>H Parkinson et al.</author>


</item>


<item>
<title>Androgen receptor function is required in Sertoli cells for the terminal differentiation of haploid spermatids.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1029</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1029</guid>
<pubDate>Tue, 08 May 2012 20:40:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Androgen receptor function is required for male embryonic sexual differentiation, pubertal development and the regulation of spermatogenesis in mammals. During spermatogenesis, this requirement is thought to be mediated by Sertoli    cells and its genetic and pharmacological disruption is manifested in spermatocytes as meiotic arrest. Through studies of a hypomorphic and conditional allele of the androgen receptor (Ar) gene, we have uncovered a dual post-meiotic requirement    for androgen receptor activity during male germ cell differentiation. Observations in Ar hypomorphic animals demonstrate that terminal differentiation of spermatids and their release from the seminiferous epithelium is AR dependent and maximally    sensitive to AR depletion within the testis. Cell-specific disruption of Ar in Sertoli cells of hypomorphic animals further shows that progression of late-round spermatids to elongating steps is sensitive to loss of Sertoli cell AR function, but    that progression through meiosis and early-round spermatid differentiation are surprisingly unaffected.</p>

	]]>
</description>

<author>R W. Holdcraft et al.</author>


</item>


<item>
<title>Plzf is required in adult male germ cells for stem cell self-renewal.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1028</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1028</guid>
<pubDate>Tue, 08 May 2012 20:40:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adult germline stem cells are capable of self-renewal, tissue regeneration and production of large numbers of differentiated progeny. We show here that the classical mouse mutant luxoid affects adult germline stem cell self-renewal.    Young homozygous luxoid mutant mice produce limited numbers of normal spermatozoa and then progressively lose their germ line after birth. Transplantation studies showed that germ cells from mutant mice did not colonize recipient testes,    suggesting that the defect is intrinsic to the stem cells. We determined that the luxoid mutant contains a nonsense mutation in the gene encoding Plzf, a transcriptional repressor that regulates the epigenetic state of undifferentiated cells, and    showed that Plzf is coexpressed with Oct4 in undifferentiated spermatogonia. This is the first gene shown to be required in germ cells for stem cell self-renewal in mammals.</p>

	]]>
</description>

<author>F W. Buaas et al.</author>


</item>


<item>
<title>Hormonal regulation of spermatogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1027</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1027</guid>
<pubDate>Tue, 08 May 2012 20:40:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Proper functioning of the mammalian testis is dependent upon an array of hormonal messengers acting through endocrine, paracrine, and autocrine pathways. Within the testis, the primary messengers are the gonadotrophins, follicle    stimulating hormone and luteinizing hormone, and the androgens. Abundant evidence indicates that the role of the gonadotrophins is to maintain proper functioning of testicular somatic cells. It is the androgens, primarily testosterone, which act    through the somatic cells to regulate germ cell differentiation. Despite extensive research in this area, little is known about the cell-specific requirements for androgens and even less is understood about the downstream effectors of androgen    signalling. However, recent work using cell-specific ablation of androgen receptor function has demonstrated a clear requirement for androgen signalling at multiple, discrete time points during spermatogenesis. These models also provide useful    tools for identifying the targets of androgen receptor activity. The purpose of this review is to provide a brief overview of recent advances in our understanding of hormonal regulation of spermatogenesis, with an emphasis on the role of    testosterone within the testis, and to pose important questions for future research in this field.</p>

	]]>
</description>

<author>R W. Holdcraft et al.</author>


</item>


<item>
<title>Id4 regulates neural progenitor proliferation and differentiation in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1026</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1026</guid>
<pubDate>Tue, 08 May 2012 20:39:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mechanisms that determine whether a precursor cell re-enters the cell cycle or exits and differentiates are crucial in determining the types and numbers of cells that constitute a particular organ. Here, we report that Id4 is    required for normal brain size, and regulates lateral expansion of the proliferative zone in the developing cortex and hippocampus. In its absence, proliferation of stem cells in the ventricular zone (VZ) is compromised. In early cortical    progenitors, Id4 is required for the normal G1-S transition. By contrast, at later ages, ectopically positioned proliferating cells are found in the mantle zone of the Id4-/- cortex.  These observations, together with evidence for the premature    differentiation of early cortical stem cells, indicate that Id4 has a unique and complex function in regulating neural stem cell proliferation and differentiation.</p>

	]]>
</description>

<author>K Yun et al.</author>


</item>


<item>
<title>Epigenetic mechanisms in early mammalian development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1025</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1025</guid>
<pubDate>Tue, 08 May 2012 20:39:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D Solter et al.</author>


</item>


<item>
<title>Cross-priming of CD8+ T cells by viral and tumor antigens is a robust phenomenon.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1024</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1024</guid>
<pubDate>Tue, 08 May 2012 20:39:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>"Cross-priming" refers to the activation of naive CD8+ T cells by antigen-presenting cells that have acquired nominal antigens from another cell. The biological relevance of cross-priming of CD8+ T cells has recently been challenged    (Zinkernagel, R. M., Eur. J. Immunol. 2002. 32: 2385-2392), on the basis that responses are weak or poorly quantitated, and the determinants recognized are undefined. Here we show that cross-priming is a robust process that elicits vigorous    primary responses to multiple peptides in two well-defined systems. Our findings support the relevance of cross-priming in CD8+ T cell responses to viruses and tumor cells, and demonstrate that cross-priming elicits CD8+ T cells to determinants    generated by the endogenous processing pathway.</p>

	]]>
</description>

<author>W Chen et al.</author>


</item>


<item>
<title>Exploration of low-dose estrogen effects: identification of No Observed Transcriptional Effect Level (NOTEL).</title>
<link>http://mouseion.jax.org/stfb2000_2009/1023</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1023</guid>
<pubDate>Tue, 08 May 2012 20:38:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Identifying a minimal dose capable of eliciting a biological response is a fundamental issue in a number of scientific fields, including: drug development, signal transduction research, and environmental toxicology.  Frequently,    proliferation, viability, and other assays based on the cellular response to a treatment are used to assess the threshold dose for minimal activity. Here we propose a novel approach for identifying the effects of low dose treatments and    pinpointing the threshold dose. Using microarrays, we examined the transcriptional response of a hormone responsive breast cancer cell line (MCF-7) stimulated with various concentrations of estrogen. Previous studies have focused on    transcriptional responses to physiologically relevant concentrations of estrogen. However, relatively few studies have examined the transcriptional effects of concentrations below normal physiologic levels.  These doses may not stimulate the    expression of any genes or, alternatively, may regulate a different subset of genes that had not been previously characterized as estrogen responsive. We used gene expression profiling, coupled with a detailed analysis of replicates, to measure    estrogen effects on many transcriptional targets and found that only physiologically relevant doses of estrogen (1 x 10(-10) M and higher) were capable of inducing a transcriptional response. This study demonstrates the utility of gene expression    profiling as a means to identify concentrations that do not elicit a change in gene expression, or simply a No Observed Transcriptional Effect Level (NOTEL). The identification of a NOTEL for a given compound may be beneficial in several    different scientific disciplines. For example, in the development of therapeutic drugs, a NOTEL could be used to identify doses of pharmaceutical compounds that are no longer effective at modulating the expression of biomarkers of    efficacy.</p>

	]]>
</description>

<author>E K. Lobenhofer et al.</author>


</item>


<item>
<title>Unraveling the genetics of chronic kidney disease using animal models.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1022</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1022</guid>
<pubDate>Tue, 08 May 2012 20:38:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Identifying genes underlying common forms of kidney disease in humans has proven difficult, expensive, and time consuming. Quantitative trait loci (QTL) for several complex traits are concordant among mice, rats, and humans,    suggesting that genetic findings from these animal models are relevant to human disease. Therefore, we reviewed the literature on genetic studies of kidney disease in rat and mouse and examined the concordance between kidney disease QTL across    species. Fifteen genomic regions contribute to kidney disease in the rat, with 12 replicated either in a separate rat cross or in another species. Five loci found in humans were concordant to QTL found in the rat. Two of these were found by    homology to a previously identified rat QTL on chromosome 1, demonstrating that kidney disease loci in animal models can predict the location of kidney disease loci in humans. In contrast to the rat, the mouse has been underutilized in the    genetic analysis of polygenic kidney disease, although mutagenesis and QTL analysis in the mouse are likely to contribute new findings in the near future. Knowledge of kidney disease loci conserved between the mouse and rat will identify prime    candidate loci to test for association with chronic kidney disease in humans.</p>

	]]>
</description>

<author>R Korstanje et al.</author>


</item>


<item>
<title>Untying the gordian knot of autoimmunity and b cell lineage lymphomas.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1021</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1021</guid>
<pubDate>Tue, 08 May 2012 20:38:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H C. Morse et al.</author>


</item>


<item>
<title>Divide and die: cell cycle events as triggers of nerve cell death.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1020</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1020</guid>
<pubDate>Tue, 08 May 2012 20:38:03 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K Herrup et al.</author>


</item>


<item>
<title>Evidence for selective transformation of autoreactive immature plasma cells in mice deficient in Fasl.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1019</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1019</guid>
<pubDate>Tue, 08 May 2012 20:37:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Germline mutations in Fas and Fasl induce nonmalignant T cell hyperplasia and systemic autoimmunity and also greatly increase the risk of B cell neoplasms. B lymphomas occurring in Fasl mutant (gld) mice usually are immunoglobulin    (Ig) isotype switched, secrete Ig, and are plasmacytoid in appearance but lack Myc translocations characteristic of other plasma cell (PC) neoplasms. Here, we explore the relationship between B cell autoreactivity and transformation and use gene    expression profiling to further classify gld plasmacytoid lymphomas (PLs) and to identify genes of potential importance in transformation. We found that the majority of PLs derive from antigen-experienced autoreactive B cells producing    antinuclear antibody or rheumatoid factor and exhibit the skewed Ig V gene repertoire and Ig gene rearrangement patterns associated with these specificities.  Gene expression profiling revealed that both primary and transplanted PLs share a    transcriptional profile that places them at an early stage in PC differentiation and distinguishes them from other B cell neoplasms. In addition, genes were identified whose altered expression might be relevant in lymphomagenesis. Our findings    provide a strong case for targeted transformation of autoreactive B cells in gld mice and establish a valuable model for understanding the relationship between systemic autoimmunity and B cell neoplasia.</p>

	]]>
</description>

<author>J Q. Zhang et al.</author>


</item>


<item>
<title>Effects of housing density and cage floor space on C57BL/6J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1018</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1018</guid>
<pubDate>Tue, 08 May 2012 20:37:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Guide for the Care and Use of Laboratory Animals (the Guide) is widely accepted as the housing standard by most Institutional Animal Care and Use Committees. The recommendations are based on best professional judgment rather    than experimental data. Current efforts are directed toward replacing these guidelines with data-driven, species-appropriate standards. Our studies were undertaken to determine the optimum housing density for C57BL/6J mice, the most commonly used    inbred mouse strain.  Four-week-old mice were housed for 8 weeks at four densities (the recommended approximately 12 in2 [ca. 77.4 cm2]/mouse down to 5.6 in2 [ca.  36.1 cm2]/mouse) in three cage types with various amounts of floor space.  Housing    density did not affect a variety of physiologic parameters but did affect certain micro-environmental parameters, although these remained within accepted ranges. A second study was undertaken housing C57BL/6J mice with as little as 3.2 in2/mouse    (ca. 20.6 cm2). The major effect was elevated ammonia concentrations that exceeded limits acceptable in the workplace at increased housing densities; however, the nasal passages and eyeballs of the mice remained microscopically normal. On the    basis of these results, we conclude that C57BL/6J mice as large as 29 g may be housed with 5.6 in2 of floor space per mouse. This area is approximately half the floor space recommended in the Guide. The role of the Guide is to ensure that    laboratory animals are well treated and housed in a species-appropriate manner. Our data suggest that current policies could be altered in order to provide the optimal habitation conditions matched to this species' social needs.</p>

	]]>
</description>

<author>A L. Smith et al.</author>


</item>


<item>
<title>Lack of the adhesion molecules P-selectin and intercellular adhesion molecule-1 accelerate the development of BCR/ABL-induced chronic myeloid leukemia-like myeloproliferative disease in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1017</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1017</guid>
<pubDate>Tue, 08 May 2012 20:37:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>In vitro studies show that BCR/ABL-expressing hematopoietic cells exhibit altered adhesion properties. No in vivo studies show whether the altered adhesion properties affect BCR/ABL leukemogenesis. Using mice with homozygous    inactivation of genes encoding the 2 adhesion molecules P-selectin and intercellular adhesion molecule-1 (ICAM1), we show that the mutant mice develop BCR/ABL-induced chronic myeloid leukemia (CML)-like leukemia at a significantly faster rate    than do wild-type (WT) mice. Lack of P-selectin and ICAM1 did not have a significant effect on the development of B-cell acute lymphoblastic leukemia (BALL) induced by BCR/ABL. Using mice deficient for P-selectin or ICAM1 alone, we show that    P-selectin plays a major role in the acceleration of CML-like leukemia.  Lack of P-selectin resulted in early release of BCR/ABL-expressing myeloid progenitors from bone marrow, appearing to alter the biologic properties of leukemic cells rather    than their growth rate by increasing their homing to the lungs, causing fatal lung hemorrhages. These results indicate that adhesion of BCR/ABL-expressing myeloid progenitors to marrow stroma through P-selectin and ICAM1 play an inhibitory role    in the development of CML-like disease, suggesting that improvement of adhesion between BCR/ABL-expressing myeloid progenitor cells and bone marrow stroma may be of therapeutic value for human CML.</p>

	]]>
</description>

<author>S D. Pelletier et al.</author>


</item>


<item>
<title>Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1016</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1016</guid>
<pubDate>Tue, 08 May 2012 20:36:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>The p53 tumor suppressor gene is commonly altered in human tumors, predominantly through missense mutations that result in accumulation of mutant p53 protein. These mutations may confer dominant-negative or gain-of-function    properties to p53. To ascertain the physiological effects of p53 point mutation, the structural mutant p53R172H and the contact mutant p53R270H (codons 175 and 273 in humans) were engineered into the endogenous p53 locus in mice. p53R270H/+ and    p53R172H/+ mice are models of Li-Fraumeni Syndrome; they developed allele-specific tumor spectra distinct from p53+/- mice. In addition, p53R270H/- and p53R172H/- mice developed novel tumors compared to p53-/- mice, including a variety of    carcinomas and more frequent endothelial tumors. Dominant effects that varied by allele and function were observed in primary cells derived from p53R270H/+ and p53R172H/+ mice. These results demonstrate that point mutant p53 alleles expressed    under physiological control have enhanced oncogenic potential beyond the simple loss of p53 function.</p>

	]]>
</description>

<author>K P. Olive et al.</author>


</item>


<item>
<title>Developing a comprehensive mouse pathology program.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1015</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1015</guid>
<pubDate>Tue, 08 May 2012 20:36:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title>The mouse genomic instability mutation chaos1 is an allele of Polq that exhibits genetic interaction with Atm.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1014</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1014</guid>
<pubDate>Tue, 08 May 2012 20:36:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>chaos1 (for chromosome aberrations occurring spontaneously 1) is a recessive mutation that was originally identified in a phenotype-based screen for chromosome instability mutants in mice. Mutant animals exhibit significantly higher    frequencies of spontaneous and radiation- or mitomycin C-induced micronucleated erythrocytes, indicating a potential defect in homologous recombination or interstrand cross-link repair. The chaos1 allele was genetically associated with a missense    mutation in Polq, which encodes DNA polymerase theta;. We demonstrate here that chaos1 is a mutant allele of Polq by using two genetic approaches: chaos1 mutant phenotype correction by a bacterial artificial chromosome carrying wild-type Polq and    a failed complementation test between chaos1 and a Polq-disrupted allele generated by gene targeting. To investigate the potential involvement of Polq in DNA double-strand break repair, we introduced chaos1 into an Atm (for ataxia telangiectasia    mutated)-deficient background. The majority ( approximately 90%) of double-homozygous mice died during the neonatal period. Surviving double mutants exhibited synergistic phenotypes such as severe growth retardation and enhanced chromosome    instability. However, remarkably, double mutants had delayed onset of thymic lymphoma, significantly increasing life span.  These data suggest a unique role of Polq in maintaining genomic integrity, which is probably distinctive from the major    homologous recombination pathway regulated by ATM.</p>

	]]>
</description>

<author>N Shima et al.</author>


</item>


<item>
<title>Pathbase: a new reference resource and database for laboratory mouse pathology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1013</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1013</guid>
<pubDate>Tue, 08 May 2012 20:35:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pathbase (http://www.pathbase.net) is a web accessible database of histopathological images of laboratory mice, developed as a resource for the coding and archiving of data derived from the analysis of mutant or genetically    engineered mice and their background strains. The metadata for the images, which allows retrieval and interoperability with other databases, is derived from a series of orthogonal ontologies and controlled vocabularies. One of these controlled    vocabularies, MPATH, was developed by the Pathbase Consortium as a formal description of the content of mouse histopathological images. The database currently has over 1000 images on-line with 2000 more under curation and presents a paradigm for    the development of future databases dedicated to aspects of experimental biology.</p>

	]]>
</description>

<author>P N. Schofield et al.</author>


</item>


<item>
<title>Characterization of a novel close-to-root papillomavirus from a Florida manatee by using multiply primed rolling-circle amplification: Trichechus manatus latirostris papillomavirus type 1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1012</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1012</guid>
<pubDate>Tue, 08 May 2012 20:35:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>By using an isothermal multiply primed rolling-circle amplification protocol, the complete genomic DNA of a novel papillomavirus was amplified from a skin lesion biopsy of a Florida manatee (Trichechus manatus latirostris), one of    the most endangered marine mammals in United States coastal waters. The nucleotide sequence, genome organization, and phylogenetic position of the Trichechus manatus latirostris papillomavirus type 1 (TmPV-1) were determined. TmPV-1 is the first    virus isolated from the order of Sirenia. A phylogenetic analysis shows that TmPV-1 is only distantly related to other papillomavirus sequences, and it appears in our phylogenetic tree as a novel close-to-root papillomavirus genus.</p>

	]]>
</description>

<author>A Rector et al.</author>


</item>


<item>
<title>Repositioning of muscle-specific genes relative to the periphery of SC-35 domains during skeletal myogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1011</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1011</guid>
<pubDate>Tue, 08 May 2012 20:35:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous studies have shown that in a given cell type, certain active genes associate with SC-35 domains, nuclear regions rich in RNA metabolic factors and excluded from heterochromatin. This organization is not seen for all active    genes; therefore, it is important to determine whether and when this locus-specific organization arises during development and differentiation of specific cell types. Here, we investigate whether gene organization relative to SC-35 domains is    cell type specific by following several muscle and nonmuscle genes in human fibroblasts, committed but proliferative myoblasts, and terminally differentiated muscle. Although no change was seen for other loci, two muscle genes (Human beta-cardiac    myosin heavy chain and myogenin) became localized to the periphery of an SC-35 domain in terminally differentiated muscle nuclei, but not in proliferative myoblasts or in fibroblasts. There was no apparent change in gene localization relative to    either the chromosome territory or the heterochromatic compartment; thus, the gene repositioning seemed to occur specifically with respect to SC-35 domains. This gene relocation adjacent to a prominent SC-35 domain was recapitulated in mouse 3T3    cells induced into myogenesis by introduction of MyoD. Results demonstrate a cell type-specific reorganization of specific developmentally regulated loci relative to large domains of RNA metabolic factors, which may facilitate developmental    regulation of genome expression.</p>

	]]>
</description>

<author>P T. Moen et al.</author>


</item>


<item>
<title>FOXN1 is critical for onycholemmal terminal differentiation in nude (Foxn1) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1010</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1010</guid>
<pubDate>Tue, 08 May 2012 20:35:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nude mice have a mutation in the transcription factor Foxn1(nu), resulting in downregulation of hair keratins. Although hair follicles develop normally, the hair fibers become structurally weak, curl, and break off at the surface.    Nails in nude mice are deformed, based on alterations of the onychocyte differentiation process. Elemental microanalysis of the nail plate reveals marked decreases in sulfur concentrations in the nude mouse nail plates. Immunohistochemistry shows    a lack of keratin 1 expression in terminally differentiating keratinocytes of the nail matrix. Instead, the typical differentiation process of the matrix is altered toward an epidermis-like differentiation pattern, comprising the production of    filaggrin-containing keratohyalin granules in cells resembling those of the stratum granulosum, which are never observed in normally haired mice.  The nail plate has diffuse basophilic stippling. It is thinner than normal, weak, and in most    Foxn1(nu)/Foxn1(nu) mice breaks where it separates from the hyponychium. These studies indicate that the Foxn1(nu) mutated gene has effects beyond downregulating keratin expression, including changes in filaggrin expression, and is critical for    normal onycholemmal differentiation. The nails of nude mice provide new insights into the molecular controls of onychocyte differentiation, and they offer a useful model to investigate the pathogenesis of nail hypergranulosis, a common feature in    human nail diseases.</p>

	]]>
</description>

<author>L Mecklenburg et al.</author>


</item>


<item>
<title>Evaluation of donor-specific transfusion sources: unique failure of bone marrow cells to induce prolonged skin allograft survival with anti-CD154 monoclonal antibody.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1009</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1009</guid>
<pubDate>Tue, 08 May 2012 20:34:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Treatment with anti-CD154 monoclonal antibody (mAb) plus a donor-specific transfusion (DST) of spleen cells prolongs skin allograft survival in mice through a mechanism involving deletion of host alloreactive CD8(+) T    cells. It is unknown if other lymphohematopoietic cell populations can be used as a DST. METHODS: Murine recipients of allogeneic skin grafts on day 0 were either untreated or given a DST on day -7 plus 4 doses of anti-CD154 mAb on days -7, -4,    0, and +4. Deletion of CD8(+) alloreactive cells was measured using "synchimeric" CBA recipients, which circulate trace populations of TCR transgenic alloreactive CD8(+) T cells. RESULTS: Transfusion of splenocytes, thymocytes, lymph node cells,    or buffy coat cells led to prolonged skin allograft survival in recipients treated with anti-CD154 mAb. In contrast, bone marrow DST failed to delete host alloreactive CD8(+) T cells and was associated with brief skin allograft survival.    Transfusions consisting of bone marrow-derived dendritic cells or a mixture of splenocytes and bone marrow cells were also ineffective. CONCLUSIONS: Donor-specific transfusions of splenocytes, thymocytes, lymph node cells, or buffy coat cells can    prolong skin allograft survival in recipients treated with costimulation blockade. Bone marrow cells fail to serve this function, in part by failing to delete host alloreactive CD8(+) T cells, and they may actively interfere with the function of    a spleen cell DST. The data suggest that transplantation tolerance induction protocols that incorporate bone marrow cells to serve as a DST may not be effective.</p>

	]]>
</description>

<author>T G. Markees et al.</author>


</item>


<item>
<title>Scd1ab-Xyk: a new asebia allele characterized by a CCC trinucleotide insertion in exon 5 of the stearoyl-CoA desaturase 1 gene in mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1008</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1008</guid>
<pubDate>Tue, 08 May 2012 20:34:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>We describe here a spontaneous, autosomal recessive mutant mouse suffering from skin and hair defects, which arose in the outbred Kunming strain. By haplotype analysis and direct sequencing of PCR products, we show that this    mutation is a new allele of the asebia locus with a naturally occurring mutation in the Scd1 gene (a CCC insertion at nucleotide position 835 in exon 5), which codes for stearoyl-CoA desaturase 1. This mutation introduces an extra proline residue    at position 279 in the Scd1 protein. The mutant mice, originally designated km/km but now assigned the name Scd1ab-Xyk (hereafter abbreviated as abXyk/abXyk), have a similar gross and histological phenotype to that reported for previously    characterized allelic asebia mutations (Scd1ab, Scd1abJ, Scd1ab2J, and Scd1tm1Ntam). Histological analysis showed they were also characterized by hypoplasic sebaceous glands and abnormal hair follicles. In a cross between Kunming- abXyk/abXyk and    ABJ/Le-abJ/abJ mice, all the progeny showed the same phenotype, indicating that the two mutations were non-complementing and therefore allelic. Comparisons with the other four allelic mutants indicate that the Scd1ab-Xyk mutation causes the    mildest change in Scd1 function. This new mouse mutant is a good model not only for the study of scarring alopecias in humans, which are characterized by hypoplasic sebaceous glands, but also for studying the structure and function of the Scd1    protein.</p>

	]]>
</description>

<author>Y Lu et al.</author>


</item>


<item>
<title>Individual nonobese diabetic mice exhibit unique patterns of CD8+ T cell reactivity to three islet antigens, including the newly identified widely expressed dystrophia myotonica kinase.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1007</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1007</guid>
<pubDate>Tue, 08 May 2012 20:34:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Spontaneous autoimmune diabetes development in NOD mice requires both CD8(+) and CD4(+) T cells. Three pathogenic CD8(+) T cell populations (represented by the G9C8, 8.3, and AI4 clones) have been described.  Although the Ags for    G9C8 and 8.3 are known to be insulin and islet-specific glucose-6-phosphatase catalytic subunit-related protein, respectively, only mimotope peptides had previously been identified for AI4. In this study, we used peptide/MHC tetramers to detect    and quantify these three pathogenic populations among beta cell-reactive T cells cultured from islets of individual NOD mice. Even within age-matched groups, each individual mouse exhibited a unique distribution of beta cell-reactive CD8(+) T    cells, both in terms of the number of tetramer-staining populations and the relative proportion of each population in the islet infiltrate. Thus, the inflammatory process in each individual follows its own distinctive course. Screening of a    combinatorial peptide library in positional scanning format led to the identification of a peptide derived from dystrophia myotonica kinase (DMK) that is recognized by AI4-like T cells. Importantly, the antigenic peptide is naturally processed    and presented by DMK-transfected cells. DMK is a widely expressed protein that is nonetheless the target of a beta cell-specific autoimmune response.</p>

	]]>
</description>

<author>S M. Lieberman et al.</author>


</item>


<item>
<title>Human cord blood- and bone marrow-derived CD34+ cells regenerate gastrointestinal epithelial cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1006</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1006</guid>
<pubDate>Tue, 08 May 2012 20:34:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the present study, we aimed to clarify the capacity of human cord blood- and bone marrow-derived progenitor cells to generate gastrointestinal epithelial cells in clinical and experimental transplantation settings. First, in a    clinical transplantation setting, gastrointestinal tissues derived from female pediatric or juvenile recipients of allogeneic sex-mismatched bone marrow and cord blood transplantation were examined for the presence of donor-derived epithelial    cells. Gastrointestinal specimens of allogeneic recipients included Y chromosome+ cytokeratin+ epithelial cells at a frequency of 0.4-1.9%. To further determine the capacity of purified human progenitor cells, human cord blood- or bone    marrow-derived CD34+ cells were transplanted into newborn NOD/SCID/beta2-microglobulin(null) mice as an experimental transplantation assay. When gastrointestinal tissues derived from recipient mice were subjected to FISH and immunofluorescence    analyses, human epithelial cells were identified at a frequency of 0.24-0.58% at 3 months posttransplantation. Finally, double FISH analyses using species-specific probes revealed that human chromosome+ epithelial cells did not possess any murine    chromosomes, indicating that donor-derived epithelial cells were not generated only by cell fusion. On the basis of these findings, it is concluded that purified human cord blood and bone marrow CD34+ progenitor cells can generate    gastrointestinal epithelial cells across allogeneic and xenogeneic histocompatibility barriers.</p>

	]]>
</description>

<author>F Ishikawa et al.</author>


</item>


<item>
<title>Identification of a cryptic lethal mutation in the mouse t(w73) haplotype.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1005</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1005</guid>
<pubDate>Tue, 08 May 2012 20:33:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>t haplotypes are naturally occurring, variant forms of the t complex on mouse chromosome 17, characterized by the presence of four inversions with respect to wild-type. They harbour mutations causing male sterility, male    transmission ratio distortion (TRD) and embryonic lethality. Mice carrying t haplotypes have been found throughout the world, and genetic studies of the lethal mutations have identified at least 16 complementation groups.  The embryonic lethal    phenotypes of many t haplotypes have been characterized in detail, and are thought to be the consequence of homozygosity for single gene mutations. However, the existence of additional mutations in genes that function at later stages of    development would be obscured. Here we investigated the possibility of multiple mutations in t haplotypes by screening the t(w73) haplotype for the presence of novel mutations. Since genetic analysis of t haplotype mutations is hindered by    recombination suppression due to the inversions, deletion complexes covering the proximal two-thirds of the t complex were used to uncover the presence of any new lethal alleles. This analysis revealed a novel mutation between D17Jcs41 and    D17Mit100, causing mice carrying both t(w73) and selected deletions to die at birth, prior to feeding. The finding of a new, cryptic lethal mutation in t haplotypes is an indication that these recombinationally isolated chromosomes, which already    contain at least one lethal mutation that prevents homozygosity, may serve as sinks for the accumulation of additional recessive mutations.</p>

	]]>
</description>

<author>G R. Howell et al.</author>


</item>


<item>
<title>Lipopolysaccharide-induced osteoclastogenesis in Src homology 2-domain phosphatase-1-deficient viable motheaten mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1004</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1004</guid>
<pubDate>Tue, 08 May 2012 20:33:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Osteoclasts are hemopoietic cells that participate in bone resorption and remodeling. Receptor activator of nuclear factor-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) are critical for development of    osteoclasts. The Toll-like receptor (TLR) family shares some of the downstream signaling with RANK. The TLR4 ligand, lipopolysaccharide (LPS), is reported to accelerate bone lysis; however, signaling via TLRs has never been reported to induce    osteoclastogenesis without RANKL. In this study we showed that significant numbers of mature osteoclasts were generated from protein tyrosine phosphatase Src homology 2-domain phosphatase-1-defective Hcph(me-v)/Hcph(me-v) (me(v)/me(v)) bone    marrow cells in the presence of M-CSF and LPS without addition of RANKL in culture. This M-CSF plus LPS-induced osteoclastogenesis was not inhibited by an anti-TNFalpha antagonistic antibody or by osteoprotegerin, a decoy receptor for RANKL. The    replacement of RANKL by TLR ligands only occurred with LPS. Other ligands, a peptidoglycan for TLR2 or an unmethylated CpG oligonucleotide for TLR9, did not support osteoclast generation. The osteoclast precursors as well as RANKL-responsive    osteoclast precursors were present in the Kit-positive cell-enriched fraction of bone marrow cells. Although me(v)/me(v) bone marrow cells required a comparable concentration of RANKL or TNFalpha as wild-type cells for the initiation of    osteoclastogenesis, the numbers of multinucleated osteoclasts in me(v)/me(v) bone marrow cultures were significantly increased by the equivalent dose of RANKL or TNFalpha in the presence of M-CSF. These results indicate that a defect of Src    homology 2-domain phosphatase-1 function not only accelerates physiological osteoclast development by RANKL/RANK, but also acquires a novel pathway for osteoclastogenesis by LPS.</p>

	]]>
</description>

<author>S Hayashi et al.</author>


</item>


<item>
<title>Equine papillomavirus type 1: complete nucleotide sequence and characterization of recombinant virus-like particles composed of the EcPV-1 L1 major capsid protein.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1003</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1003</guid>
<pubDate>Tue, 08 May 2012 20:33:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Equus caballus papillomavirus type 1 (EcPV-1) was isolated from a cutaneous papilloma, the most common neoplasm in horses. The complete EcPV-1 nucleotide sequence and genomic organization were determined.  Phylogenetic analysis    showed that EcPV-1 is a close-to-root papillomavirus, with only distant relationships to the fibropapillomaviruses and the benign cutaneous papillomaviruses. To produce EcPV-1 virus-like particles (VLPs), the EcPV-1 L1 major capsid protein was    expressed in insect cells using a recombinant baculovirus vector. The self-assembled EcPV-1 VLPs were morphologically indistinguishable from wild type papillomavirus virions. Monoclonal antibodies were developed against intact and denatured    EcPV-1 VLPs. When tested by ELISA, all monoclonal antibodies produced against intact (#18) and some against denatured EcPV-1 VLPs (#16) reacted with intact EcPV-1 VLPs only, demonstrating that the VLPs carry type-specific conformational as well    as linear epitopes on their surface. Recombinant EcPV-1 VLPs offer the potential of a noninfectious vaccine to prevent and eradicate equine cutaneous papillomatosis.</p>

	]]>
</description>

<author>S J. Ghim et al.</author>


</item>


<item>
<title>CTLA-4-Ig activates forkhead transcription factors and protects dendritic cells from oxidative stress in nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1002</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1002</guid>
<pubDate>Tue, 08 May 2012 20:33:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Prediabetes and diabetes in nonobese diabetic (NOD) mice have been targeted by a variety of immunotherapies, including the use of a soluble form of cytotoxic T lymphocyte antigen 4 (CTLA-4) and interferon (IFN)-gamma. The cytokine,    however, fails to activate tolerogenic properties in dendritic cells (DCs) from highly susceptible female mice early in prediabetes. The defect is characterized by impaired induction of immunosuppressive tryptophan catabolism, is related to    transient blockade of the signal transducer and activator of transcription (STAT)1 pathway of intracellular signaling by IFN-gamma, and is caused by peroxynitrite production. Here, we show that soluble CTLA-4 imparts suppressive properties to DCs    from early prediabetic NOD female mice through mechanisms that rely on autocrine signaling by IFN-gamma. Although phosphorylation of STAT1 in response to IFN-gamma is compromised in those mice, CTLA-4 obviates the defect. IFN-gamma-driven    expression of tryptophan catabolism by CTLA-4-immunoglobulin is made possible through the concomitant activation of the Forkhead Box class O (FOXO) transcription factor FOXO3a, induction of the superoxide dismutase gene, and prevention of    peroxynitrite formation.</p>

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</description>

<author>F Fallarino et al.</author>


</item>


<item>
<title>Positional cloning and characterization of mouse mei8, a disrupted allelle of the meiotic cohesin Rec8.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1001</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1001</guid>
<pubDate>Tue, 08 May 2012 20:32:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>A novel mutation, mei8, was isolated in a forward genetic screen for infertility mutations induced by chemical mutagenesis of ES cells.  Homozygous mutant mice are sterile. Mutant females exhibit ovarian dysgenesis and lack ovarian    follicles at reproductive maturity. Affected males have small testes due to arrest of spermatogenesis during meiotic prophase I. Genetic mapping and positional cloning of mei8 led to the identification of a mutation in Rec8, a homolog of the    yeast meiosis-specific cohesin gene REC8. Analysis of meiosis in Rec8(mei8)/Rec8(mei8) spermatocytes showed that, while initiation of recombination and synapsis occurs, REC8 is required for the completion and/or maintenance of synapsis, cohesion    of sister chromatids, and the formation of chiasmata, as it is in other organisms. However, unlike yeast and Caenorhabditis elegans, localization of REC8 on meiotic chromosomes is not required for the assembly of axial elements.</p>

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</description>

<author>L A. Bannister et al.</author>


</item>


<item>
<title>Peroxiredoxin 6 deficiency and atherosclerosis susceptibility in mice: significance of genetic background for assessing atherosclerosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1000</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1000</guid>
<pubDate>Tue, 08 May 2012 20:32:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Peroxiredoxin 6 (Prdx6; also called antioxidant protein 2, or Aop2) is a candidate gene for Ath1, a locus responsible for the respective susceptibility and resistance of mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) to diet-induced    atherosclerosis. To evaluate if Prdx6 underlies Ath1, we compared the diet-induced atherosclerotic lesions in Prdx6 targeted mutant (Prdx6-/-) mice of different genetic backgrounds: B6, 129, and B6;129. PRDX6 protein and mRNA were expressed in    normal and atherosclerotic aortas. B6;129 Prdx6-/- macrophages oxidized LDL significantly more than did controls. Plasma lipid hydroperoxide levels were higher in atherogenic diet-fed Prdx6-/- mice with B6;129 and B6 backgrounds than in controls.    Prdx6-/- and controls in a 129 genetic background were equally lesion-resistant, and Prdx6-/- and controls in a B6 background were equally lesion-susceptible. In contrast, Prdx6-/- mice in a B6;129 background had significantly larger aortic root    lesions than did littermate wild type controls. Therefore, although PRDX6 protein did not affect atherosclerosis susceptibility in either the resistant 129 background or the susceptible B6 background, it may inhibit atherosclerosis in backgrounds    with mixed pro- and anti-atherogenic genes.  Thus, genetic background plays an important role in modulating atherogenesis in targeted mutant mice. However, we think it is unlikely that Prdx6 underlies Ath1.</p>

	]]>
</description>

<author>X Wang et al.</author>


</item>


<item>
<title>Blood pressure in 15 inbred mouse strains and its lack of relation with obesity and insulin resistance in the progeny of an NZO/HILtJ x C3H/HeJ intercross.</title>
<link>http://mouseion.jax.org/stfb2000_2009/999</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/999</guid>
<pubDate>Tue, 08 May 2012 20:32:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>We characterized the systolic and diastolic blood pressures of 10-week-old males from 15 inbred mouse strains and found that blood pressures among strains were continuously distributed and that strain C3H/HeJ had the lowest mean    systolic and diastolic pressure (100.5 +/- 3.2 and 66.8 +/- 3.5 mmHg), and a strain with obesity and diabetes, NZO/HILtJ, had the highest (132.4 +/- 3.1 and 86.6 +/- 6.9 mmHg). To understand the relationship of blood pressure with insulin    resistance and obesity, we produced F1 and F2 progeny from reciprocal crosses of NZO, the strain with obesity, diabetes, and high blood pressure, and the strain with the lowest blood pressures, C3H/HeJ. Mean systolic pressures of 10-week-old (NZO    x C3H)F1 and (C3H x NZO)F1 males were similar to each other (114.9 +/- 3.8 and 117.2 +/- 5.0 mmHg) and were intermediate to those of the parental strains. Systolic pressure of F2 males (n = 223) was distributed normally about the mean, suggesting    that blood pressure is a polygenic trait. The body mass index (BMI) and plasma insulin levels of F2 progeny correlated significantly and positively with plasma leptin levels, suggesting that obesity is associated with insulin resistance. In    contrast, systolic pressure did not correlate with BMI, plasma leptin levels, and plasma insulin levels, suggesting that genes underlying the development of hypertension in this intercross are not associated with the development of obesity and    insulin resistance. Our results demonstrate that the progeny of NZO and C3H intercrosses are a practical and powerful tool for identifying blood pressure genes and for understanding human polygenic hypertension.</p>

	]]>
</description>

<author>C Tsukahara et al.</author>


</item>


<item>
<title>Was there type 1 diabetes in the Olduvai Gorge?</title>
<link>http://mouseion.jax.org/stfb2000_2009/998</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/998</guid>
<pubDate>Tue, 08 May 2012 20:32:05 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title>Prostate carcinoma cells that have resided in bone have an upregulated IGF-I axis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/997</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/997</guid>
<pubDate>Tue, 08 May 2012 20:31:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Prostate cancer (PC) has a propensity to metastasize to the skeleton, inducing an osteoblastic response in the host. Recent epidemiological studies have suggested that circulating IGF-I may be important for both the    pathogenesis and dissemination of PC. We have postulated that tumor secreted IGF-I in conjunction with endogenous IGF-I contributes to the osteoblastic phenotype characteristic of metastatic PC.  METHODS: To test this thesis we studied the    established LNCaP PC progression model consisting of three genetically related human PC cell lines. RESULTS: Using RIA, we found serum-free conditioned media (CM) of LNCaP and C4-2 had no measurable IGF-I, whereas IGF-I was easily detected in CM    from C4-2B cells at 24 hr (i.e., 1.8 +/- 0.53 ng/mg cell protein).  Real-time PCR of IGF-I mRNA showed that C4-2B expressed 100-fold more IGF-I mRNA than LNCaP cells. In addition, C4-2B expression of IGF-I mRNA was substantially increased in the    presence of exogenous IGF-I to nearly twofold. While IGFBP-3 and IGFBP-1 were not detectable in the CM of any PC line, all cells secreted IGFBP-2. C4-2B cells produced 40% more IGFBP-2 than LNCaP or C4-2 cells (C4-2B at 167 +/- 43 ng/mg cell    protein). RANKL, a product of bone stromal cells, was also differentially expressed: LNCaP had threefold higher RANKL mRNA compared to C4-2 and C4-2B and at least equivalent protein expression. CONCLUSIONS: Our results suggest that PC cells that    have metastasized to bone have an upregulated IGF-I regulatory system. This suggests an activated IGF-I axis contributes to the host-PC interaction in promoting osteoblastic metastases.</p>

	]]>
</description>

<author>J Rubin et al.</author>


</item>


<item>
<title>Vignettes in osteoporosis: a road map to successful therapeutics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/996</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/996</guid>
<pubDate>Tue, 08 May 2012 20:31:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The diagnosis and management of osteoporosis have become increasingly more complex as new drugs enter the marketplace and meta-analyses of randomized trials with "other" agents become more prolific. We describe five common clinical    scenarios encountered in the practice of osteoporosis medicine and various road maps that could lead to successful therapy. INTRODUCTION: The diagnosis and treatment of osteoporosis have changed dramatically in the last decade. Advances in    diagnostic technologies and a range of newer treatment options have provided the clinician with a wide array of choices for treating this chronic disease. Despite the issuance of several "guidelines" and practice recommendations, there still    remains confusion among clinicians about basic approaches to the management of osteoporosis.  This paper should be used as a case-based approach to define optimal therapeutic choices. MATERIALS AND METHODS: Five representative cases were selected    from two very large clinical practices (Bangor, ME; Pittsburgh, PA). Diagnostic modalities and treatment options used in these cases were selected on an evidence-based analysis of respective clinical trials.  Subsequent to narrative choices by    two metabolic bone disease specialists (SG and CR), calculation of future fracture risk and selection of potential alternative therapeutic regimens were reviewed and critiqued by an epidemiologist (DB). RESULTS: A narrative about each case and    possible management choices for each of the five cases are presented with references to justify selection of the various therapeutic options.  Alternatives are considered and discussed based on literature and references through July 2003. The    disposition of the individual patient is noted at the end of each case. CONCLUSIONS: A case-based approach to the management of osteoporosis provides a useful interface between guidelines, evidence-based meta-analyses, and clinical practice    dilemmas.</p>

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</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title>What&apos;s new with PTH in osteoporosis: where are we and where are we headed?</title>
<link>http://mouseion.jax.org/stfb2000_2009/995</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/995</guid>
<pubDate>Tue, 08 May 2012 20:31:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>A new era in osteoporosis management began with the recent approval of parathyroid hormone (PTH) for postmenopausal and idiopathic osteoporosis treatment. Intermittent PTH dramatically increases spine bone mineral density and    significantly reduces fragility fractures. However, the skeletal response to PTH varies greatly and there are few large scale, randomized, placebo-controlled trials in conditions such as glucocorticoid-induced osteoporosis. Moreover, the    mechanisms of PTH action are complex, involving multiple pathways linked to common signaling peptides regulating osteoblast gene transcription. In addition, important interactions between osteoclasts and osteoblasts are activated by PTH.  This    review presents recent findings on PTH signaling in bone and discusses how they could be used to design randomized trials and establish clinical practice guidelines for this novel anabolic peptide.</p>

	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title>Arsenic availability from chromated copper arsenate (CCA)-treated wood.</title>
<link>http://mouseion.jax.org/stfb2000_2009/994</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/994</guid>
<pubDate>Tue, 08 May 2012 20:30:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lumber used to construct raised garden beds is often treated with chromated copper arsenate (CCA). This project aimed to determine (i) how far As, Cu, and Cr had diffused away from CCA-treated wood surfaces in raised garden beds    under realistic conditions, (ii) the uptake of these elements by crops, and (iii) the effect of CCA solution on soil bacteria.  This study showed that As, Cu, and Cr diffuse into soil from CCA-treated wood used to construct raised garden beds. To    determine crop uptake of these elements, contaminated soil 0 to 2 cm from the treated wood was obtained from two different beds (40-50 mg kg(-1) As); control soil was collected 1.5 m away from the treated wood (<3-10 mg kg(-1) As). Four    replicates of carrot (Daucus carota var. sativus Hoffm. cv. Thumbelina), spinach (Spinacia oleracea L. cv. Indian Summer), bush bean (Phaseolus vulgaris L. cv. Provider), and buckwheat (Fagopyrum esculentum Moench cv.  Common) were grown in pots    containing these soils in a greenhouse. After harvest, plant materials were dried, ground, digested, and analyzed for As by inductively coupled plasma-hydride generation (ICP-HG). Concentrations of As in all crops grown in contaminated soils were    higher than those from control soils. The levels of As in the crops remained well below the recommended limit for As set by the United States Public Health Service (2.6 mg kg(-1) fresh wt.). To determine if bacteria in soils 0 to 2 cm from the    treated wood had higher resistance to Type C chromated copper arsenate (CCA-C) solution than those from reference soils, dilution plates were set up using quarter-strength tryptic soy agar (TSA) media and 0 to 22.94 g L(-1) (0-1.25% v/v) CCA-C    working solution. The microorganisms from soils adjacent to treated wood had greater growth on the CCA-amended media than those from reference soils outside the bed.</p>

	]]>
</description>

<author>F A. Rahman et al.</author>


</item>


<item>
<title>Gene expression pattern in hepatic stem/progenitor cells during rat fetal development using complementary DNA microarrays.</title>
<link>http://mouseion.jax.org/stfb2000_2009/993</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/993</guid>
<pubDate>Tue, 08 May 2012 20:30:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>To identify new and differentially expressed genes in rat fetal liver epithelial stem/progenitor cells during their proliferation, lineage commitment, and differentiation, we used a high throughput method-mouse complementary DNA    (cDNA) microarrays-for analysis of gene expression. The gene expression pattern of rat hepatic cells was studied during their differentiation in vivo: from embryonic day (ED) 13 until adulthood. The differentially regulated genes were grouped    into two clusters: a cluster of up-regulated genes comprised of 281 clones and a cluster of down-regulated genes comprised of 230 members. The expression of the latter increased abruptly between ED 16 and ED 17. Many of the overexpressed genes    from the first cluster fall into distinct, differentially expressed functional groups: genes related to development, morphogenesis, and differentiation; calcium- and phospholipid-binding proteins and signal transducers; and cell adhesion,    migration, and matrix proteins. Several other functional groups of genes that are initially down-regulated, then increase during development, also emerged: genes related to inflammation, blood coagulation, detoxification, serum proteins, amino    acids, lipids, and carbohydrate metabolism. Twenty-eight genes overexpressed in fetal liver that were not detected in adult liver are suggested as potential markers for identification of liver progenitor cells. In conclusion, our data show that    the gene expression program of fetal hepatoblasts differs profoundly from that of adult hepatocytes and that it is regulated in a specific manner with a major switch at ED 16 to 17, marking a dramatic change in the gene expression program during    the transition of fetal liver progenitor cells from an undifferentiated to a differentiated state. Supplementary material for this article can be found on the HEPATOLOGY website    (http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html).</p>

	]]>
</description>

<author>P M. Petkov et al.</author>


</item>


<item>
<title>Regulation of B cell differentiation and plasma cell generation by IL-21, a novel inducer of Blimp-1 and Bcl-6.</title>
<link>http://mouseion.jax.org/stfb2000_2009/992</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/992</guid>
<pubDate>Tue, 08 May 2012 20:30:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>IL-21 is a type I cytokine whose receptor is expressed on T, B, and NK cells. Within the B cell lineage, IL-21 regulates IgG1 production and cooperates with IL-4 for the production of multiple Ab classes in vivo.  Using    IL-21-transgenic mice and hydrodynamics-based gene delivery of IL-21 plasmid DNA into wild-type mice as well as in vitro studies, we demonstrate that although IL-21 induces death of resting B cells, it promotes differentiation of B cells into    postswitch and plasma cells.  Thus, IL-21 differentially influences B cell fate depending on the signaling context, explaining how IL-21 can be proapoptotic for B cells in vitro yet critical for Ag-specific Ig production in vivo. Moreover, we    demonstrate that IL-21 unexpectedly induces expression of both Blimp-1 and Bcl-6, indicating mechanisms as to how IL-21 can serve as a complex regulator of B cell maturation and terminal differentiation. Finally, BXSB-Yaa mice, which develop a    systemic lupus erythematosus-like disease, have greatly elevated IL-21, suggesting a role for IL-21 in the development of autoimmune disease.</p>

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</description>

<author>K Ozaki et al.</author>


</item>


<item>
<title>Spontaneous cholecysto- and hepatolithiasis in Mdr2-/- mice: a model for low phospholipid-associated cholelithiasis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/991</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/991</guid>
<pubDate>Tue, 08 May 2012 20:30:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previously, we identified needle-like and filamentous, putatively "anhydrous" cholesterol crystallization in vitro at very low phospholipid concentrations in model and native biles. Our aim now was to address whether spontaneous    gallstone formation occurs in Mdr2 (Abcb4) knockout mice that are characterized by phospholipid-deficient bile. Biliary phenotypes and cholesterol crystallization sequences in fresh gallbladder biles and non-fixed liver sections were determined    by direct and polarizing light microscopy. The physical chemical nature and composition of crystals and stones were determined by sucrose density centrifugation and before mass and infrared spectroscopy. Gallbladder biles of Mdr2(-/-) mice    precipitate needle-like cholesterol crystals at 12 weeks of age on chow. After 15 weeks, more than 50% of Mdr2(-/-) mice develop gallbladder stones, with female mice displaying a markedly higher gallstone-susceptibility. Although gallbladder    biles of Mdr2(-/-) mice contain only traces (</p>

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</description>

<author>F Lammert et al.</author>


</item>


<item>
<title>Reduced pigmentation (rp), a mouse model of Hermansky-Pudlak syndrome, encodes a novel component of the BLOC-1 complex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/990</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/990</guid>
<pubDate>Tue, 08 May 2012 20:29:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hermansky-Pudlak syndrome (HPS), a disorder of organelle biogenesis, affects lysosomes, melanosomes, and platelet dense bodies. Seven genes cause HPS in humans (HPS1-HPS7) and at least 15 nonallelic mutations cause HPS in mice.    Where their function is known, the HPS proteins participate in protein trafficking and vesicle docking/fusion events during organelle biogenesis. HPS-associated genes participate in at least 4 distinct protein complexes: the adaptor complex AP-3;    biogenesis of lysosome-related organelles complex 1 (BLOC-1), consisting of 4 HPS proteins (pallidin, muted, cappuccino, HPS7/sandy); BLOC-2, consisting of HPS6/ruby-eye, HPS5/ruby-eye-2, and HPS3/cocoa; and BLOC-3, consisting of HPS1/pale ear    and HPS4/light ear. Here, we report the cloning of the mouse HPS mutation reduced pigmentation (rp). We show that the wild-type rp gene encodes a novel, widely expressed 195-amino acid protein that shares 87% amino acid identity with its human    orthologue and localizes to punctate cytoplasmic structures. Further, we show that phosphorylated RP is part of the BLOC-1 complex. In mutant rp/rp mice, a premature stop codon truncates the protein after 79 amino acids. Defects in all the 5    known components of BLOC-1, including RP, cause severe HPS in mice, suggesting that the subunits are nonredundant and that BLOC-1 plays a key role in organelle biogenesis.</p>

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</description>

<author>B Gwynn et al.</author>


</item>


<item>
<title>The ligand-binding function of hepatic lipase modulates the development of atherosclerosis in transgenic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/989</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/989</guid>
<pubDate>Tue, 08 May 2012 20:29:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>To investigate the separate contributions of the lipolytic versus ligand-binding function of hepatic lipase (HL) to plasma lipoprotein metabolism and atherosclerosis, we compared mice expressing catalytically active wild-type HL    (HL-WT) and inactive HL (HL-S145G) with no endogenous expression of mouse apoE or HL (E-KO x HL-KO, where KO is knockout). HL-WT and HL-S145G reduced plasma cholesterol (by 40 and 57%, respectively), non-high density lipoprotein cholesterol (by    48 and 61%, respectively), and apoB (by 36 and 44%, respectively) (p < 0.01), but only HL-WT decreased high density lipoprotein cholesterol (by 67%) and apoA-I (by 54%). Compared with E-KO x HL-KO mice, both active and inactive HL lowered the    pro-atherogenic lipoproteins by enhancing the catabolism of autologous (125)I-apoB very low density/intermediate density lipoprotein (VLDL/IDL) (fractional catabolic rates of 2.87 +/- 0.04/day for E-KO x HL-KO, 3.77 +/- 0.03/day for E-KO x HL-WT,    and 3.63 +/- 0.09/day for E-KO x HL-S145G mice) and (125)I-apoB-48 low density lipoprotein (LDL) (fractional catabolic rates of 5.67 +/- 0.34/day for E-KO x HL-KO, 18.88 +/- 1.72/day for E-KO x HL-WT, and 9.01 +/- 0.14/day for E-KO x HL-S145G    mice). In contrast, the catabolism of apoE-free, (131)I-apoB-100 LDL was not increased by either HL-WT or HL-S145G. Infusion of the receptor-associated protein (RAP), which blocks LDL receptor-related protein function, decreased plasma clearance    and hepatic uptake of (131)I-apoB-48 LDL induced by HL-S145G. Despite their similar effects on lowering pro-atherogenic apoB-containing lipoproteins, HL-WT enhanced atherosclerosis by up to 50%, whereas HL-S145G markedly reduced aortic    atherosclerosis by up to 96% (p < 0.02) in both male and female E-KO x HL-KO mice. These data identify a major receptor pathway (LDL receptor-related protein) by which the ligand-binding function of HL alters remnant lipoprotein uptake in vivo    and delineate the separate contributions of the lipolytic versus ligand-binding function of HL to plasma lipoprotein size and metabolism, identifying an anti-atherogenic role of the ligand-binding function of HL in vivo.</p>

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</description>

<author>Navarro H. Gonzalez et al.</author>


</item>


<item>
<title>Hybrid poplar and forest soil response to municipal and industrial by-products: a greenhouse study.</title>
<link>http://mouseion.jax.org/stfb2000_2009/988</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/988</guid>
<pubDate>Tue, 08 May 2012 20:29:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Little research has been conducted in the Lake States (Minnesota, Wisconsin, and Michigan) to evaluate the effects of municipal and industrial by-product applications on the early growth of short rotation woody crops such as hybrid    poplar. Anticipated shortages of harvestable-age aspen in the next decade can be alleviated and rural development can be enhanced through the application of by-products to forest soils. This study was conducted to evaluate the effects of    inorganic fertilizer, boiler ash, biosolids, and the co-application of ash and biosolids application on tree growth and soil properties by measuring hybrid poplar clone NM-6 (Populus nigra L. x P. maximowiczii A. Henry) yield, nutrient uptake,    and select post-harvest soil properties after 15 wk of greenhouse growth. Treatments included a control of no amendment; agricultural lime; inorganic N, P, and K; three types of boiler ash; biosolids application rates equivalent to 70, 140, 210,    and 280 kg available N ha(-1); and boiler ash co-applied with biosolids. All of the by-products treatments showed biomass production that was equal to or greater than inorganic fertilizer and lime treatments. A trend of increased biomass with    increasing rates of biosolids was observed. Soil P concentration increased with increasing rates of biosolids application.  None of the by-products treatments resulted in plant tissue metal concentrations greater than metal concentrations of    plant tissue amended with inorganic amendments. Biosolids, boiler ash, and the co-application of biosolids and boiler ash together on forest soils were as beneficial to plant growth as inorganic fertilizers.</p>

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</description>

<author>M A. Cavaleri et al.</author>


</item>


<item>
<title>An open letter on microarray data from the MGED Society.</title>
<link>http://mouseion.jax.org/stfb2000_2009/987</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/987</guid>
<pubDate>Tue, 08 May 2012 20:29:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C Ball et al.</author>


</item>


<item>
<title>Intraocular pressure in zebrafish: comparison of inbred strains and identification of a reduced melanin mutant with raised IOP.</title>
<link>http://mouseion.jax.org/stfb2000_2009/986</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/986</guid>
<pubDate>Tue, 08 May 2012 20:28:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: The goal was to establish an accurate method for measuring intraocular pressure (IOP) in living adult zebrafish and to determine the average IOPs of genetically different strains and mutants. The overall purpose was to    develop the zebrafish system for studies of IOP and glaucoma. Elevated IOP and anterior segment dysgenesis are two known risk factors for glaucoma. Because albino mammals have increased IOP and are prone to anterior segment anomalies, the study    was focused on a reduced melanin zebrafish mutant, brass. METHODS: Servo-null electrophysiology was used to measure IOP in anesthetized adult zebrafish. A pulled-glass microelectrode was used to penetrate the cornea into the anterior chamber, and    pressure transduction was recorded. IOP, histology, and visual behavioral assays were used to assess the brass mutant. RESULTS: Significant differences in IOP were detected between genetically distinct zebrafish strains. IOP averages were highest    in the long fin (LF) strain (20.5 +/- 1.2 mm Hg) and lowest in the Oregon AB (AB) strain (10.8 +/- 0.3 mm Hg). In brass mutants, which show a reduced melanin phenotype, IOPs were elevated and mild iris hypoplasia was noted. No defects were    observed within the retina or in visual function. CONCLUSIONS: In the present study, an accurate method was developed for measuring IOP in adult zebrafish. Both the ability to measure IOP in the genetically powerful zebrafish model and the    conservation of elevated IOP and anterior segment anomalies between albino mammals and hypopigmented fish are important.  They strongly support the use of zebrafish for studying the complex genetics of elevated IOP and glaucoma.</p>

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</description>

<author>B A. Link et al.</author>


</item>


<item>
<title>Animal models have little to teach us about type 1 diabetes: 2. In opposition to this proposal.</title>
<link>http://mouseion.jax.org/stfb2000_2009/985</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/985</guid>
<pubDate>Tue, 08 May 2012 20:28:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E H. Leiter et al.</author>


</item>


<item>
<title>Anterior segment development relevant to glaucoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/984</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/984</guid>
<pubDate>Tue, 08 May 2012 20:28:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Development of the ocular anterior segment involves a series of inductive interactions between neural ectoderm, surface ectoderm and periocular mesenchyme. The timing of these events is well established but less is known about the    molecular mechanisms involved. Various genes that participate in these processes have been identified. As the roles of more genes are determined, developmental pathways and networks will emerge.  Here, we focus on recent advances made using mouse    models. We summarize key morphological events in formation of anterior chamber structures, including the aqueous humor drainage structures that are involved in intraocular pressure (IOP) regulation and glaucoma. We discuss the developmental roles    of genes that associate with abnormal anterior segment development and elevated IOP or glaucoma (including Bmp4, Cyp1b1, Foxc1, Foxc2, Pitx2, Lmx1b and Tyr ) and how some of these genes may fit into developmental networks.</p>

	]]>
</description>

<author>D B. Gould et al.</author>


</item>


<item>
<title>Refined histopathologic scoring system improves power to detect colitis QTL in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/983</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/983</guid>
<pubDate>Tue, 08 May 2012 20:27:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Induction of colitis in mice by a targeted mutation in the I110 gene is inbred strain dependent. C3H/ HeJBir (C3H) mice are colitis susceptible while C57BL/6J (B6) mice are resistant. Identification of quantitative trait loci (QTL)    determining the differential strain responsiveness requires histopathologic scoring of multiple lesion subphenotypes in both cecum and colon. Here we show that ability to detect a major C3H-derived QTL on Chr 3 (cytokine deficiency-induced    colitis susceptibility 1, Cdcs1) was critically dependent upon the degree of refinement of the histopathologic scoring system. QTL mapping was performed using a first-back-cross population of interleukin-10-deficient mice and applying two    different grading systems to assess lesion subphenotypes. The same histological specimens were scored by two independent pathologists using either a very detailed scoring system for four subphenotypes developed at The Jackson Laboratory (TJL) or    a simpler scoring system developed at the Hannover Medical School (MHH). The more detailed TJL subphenotyping protocol increased power to identify Cdcs1 (a maximum LOD score of 4.28 versus a LOD score of 1.77 when using the abbreviated MHH    subphenotyping scoring system). This study shows that for QTL mapping in a mouse model of colitis, in which histology represents the gold standard for phenotyping, ability to detect linkage is critically dependent upon the degree of refinement    adopted for separately scoring the multiple histopathologic lesions comprising this complex phenotype.</p>

	]]>
</description>

<author>A Bleich et al.</author>


</item>


<item>
<title>A comparison of cDNA, oligonucleotide, and Affymetrix GeneChip gene expression microarray platforms.</title>
<link>http://mouseion.jax.org/stfb2000_2009/982</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/982</guid>
<pubDate>Tue, 08 May 2012 20:27:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have conducted a study to compare the variability in measured gene expression levels associated with three types of microarray platforms.  Total RNA samples were obtained from liver tissue of four male mice, two each from inbred    strains A/J and C57BL/6J. The same four samples were assayed on Affymetrix Mouse Genome Expression Set 430 GeneChips (MOE430A and MOE430B), spotted cDNA microarrays, and spotted oligonucleotide microarrays using eight arrays of each type.    Variances associated with measurement error were observed to be comparable across all microarray platforms. The MOE430A GeneChips and cDNA arrays had higher precision across technical replicates than the MOE430B GeneChips and oligonucleotide    arrays. The Affymetrix platform showed the greatest range in the magnitude of expression levels followed by the oligonucleotide arrays. We observed good concordance in both estimated expression level and statistical significance of common genes    between the Affymetrix MOE430A GeneChip and the oligonucleotide arrays. Despite their apparently high precision, cDNA arrays showed poor concordance with other platforms.</p>

	]]>
</description>

<author>Y Woo et al.</author>


</item>


<item>
<title>&quot;Follicular stem cell carcinoma: histologic, immunohistochemical, ultrastructural, and clinical characterization in 30 days&quot;.</title>
<link>http://mouseion.jax.org/stfb2000_2009/981</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/981</guid>
<pubDate>Tue, 08 May 2012 20:27:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>I Mikaelian et al.</author>


</item>


<item>
<title>Spontaneous proliferative lesions and tumors of the uterus of captive African hedgehogs (Atelerix albiventris).</title>
<link>http://mouseion.jax.org/stfb2000_2009/980</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/980</guid>
<pubDate>Tue, 08 May 2012 20:27:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fifteen captive female African hedgehogs (Atelerix albiventris), 3- to 5-yr-old, were diagnosed with proliferative uterine lesions (n = 28).  Lesions were associated with vaginal bleeding in all cases, hematuria in 11 of 13 cases,    and weight loss in 7 of 12 cases. Lesions were multiple in eight cases and single in seven cases. The lesions identified were 13 adenosarcomas, 7 endometrial stromal sarcomas, 6 endometrial polyps, 1 adenoleiomyosarcoma, and 1 adenoleiomyoma. In    one animal with adenosarcoma, peritoneal seeding was detected at the time of hysterectomy.  Mean survival time was 303 days (n = 10). Ovariohysterectomy allows prolonged survival of hedgehogs with uterine tumors.</p>

	]]>
</description>

<author>I Mikaelian et al.</author>


</item>


<item>
<title>Snail regulates p21(WAF/CIP1) expression in cooperation with E2A and Twist.</title>
<link>http://mouseion.jax.org/stfb2000_2009/979</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/979</guid>
<pubDate>Tue, 08 May 2012 20:26:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Snail, a zinc-finger transcriptional repressor, is essential for mesoderm and neural crest cell formation and epithelial-mesenchymal transition. The basic helix-loop-helix transcription factors E2A and Twist have been linked with    Snail during embryonic development. In this study, we examined the role of Snail in cellular differentiation through regulation of p21(WAF/CIP1) expression. A reporter assay with the p21 promoter demonstrated that Snail inhibited expression of    p21 induced by E2A.  Co-expression of Snail with Twist showed additive inhibitory effects.  Deletion mutants of the p21 promoter revealed that sequences between -270 and -264, which formed a complex with unidentified nuclear factor(s), were    critical for E2A and Snail function. The E2A-dependent expression of the endogenous p21 gene was also inhibited by Snail.</p>

	]]>
</description>

<author>E Takahashi et al.</author>


</item>


<item>
<title>SUMO modified proteins localize to the XY body of pachytene spermatocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/978</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/978</guid>
<pubDate>Tue, 08 May 2012 20:26:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The XY body is a specialized chromatin territory that forms during meiotic prophase of spermatogenesis and comprises the transcriptionally repressed sex chromosomes. Remodeling of the XY chromatin is brought about by recruitment of    specific proteins to the X and Y chromosomes during meiosis, and also by post-translational modifications of histones and other chromatin-associated proteins. Here, we demonstrate that SUMO, a small ubiquitin-related modifier protein that    regulates a wide variety of nuclear functions in somatic cells, dramatically localizes to the XY body.  SUMO was first detected in the XY body of early pachytene spermatocytes and gradually accumulated, reaching maximal levels there during the    mid to late pachytene stages. Several known SUMO substrates, including PML and DAXX, were also found to accumulate in the XY body of mid to late stage pachytene spermatocytes. These same proteins localize to PML nuclear bodies of somatic    interphase nuclei. Together, these findings indicate a role for SUMO modification in regulating the structure and function of the XY body and reveal molecular similarities between the XY body and PML nuclear bodies.</p>

	]]>
</description>

<author>R S. Rogers et al.</author>


</item>


<item>
<title>gamma-secretase functions through Notch signaling to maintain skin appendages but is not required for their patterning or initial morphogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/977</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/977</guid>
<pubDate>Tue, 08 May 2012 20:26:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The role of Notch signaling during skin development was analyzed using Msx2-Cre to create mosaic loss-of-function alleles with precise temporal and spatial resolution. We find that gamma-secretase is not involved in skin patterning    or cell fate acquisition within the hair follicle. In its absence, however, inner root sheath cells fail to maintain their fates and by the end of the first growth phase, the epidermal differentiation program is activated in outer root sheath    cells. This results in complete conversion of hair follicles to epidermal cysts that bears a striking resemblance to Nevus Comedonicus. Sebaceous glands also fail to form in gamma-secretase-deficient mice. Importantly, mice with compound loss of    Notch genes in their skin phenocopy loss of gamma-secretase in all three lineages, demonstrating that Notch proteolysis accounts for the major signaling function of this enzyme in this organ and that both autonomous and nonautonomous    Notch-dependent signals are involved.</p>

	]]>
</description>

<author>Y Pan et al.</author>


</item>


<item>
<title>Haploinsufficient lethality and formation of arteriovenous malformations in Notch pathway mutants.</title>
<link>http://mouseion.jax.org/stfb2000_2009/976</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/976</guid>
<pubDate>Tue, 08 May 2012 20:26:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Notch signaling pathway is essential for embryonic vascular development in vertebrates. Here we show that mouse embryos heterozygous for a targeted mutation in the gene encoding the DLL4 ligand exhibit haploinsufficient    lethality because of defects in vascular remodeling. We also describe vascular defects in embryos homozygous for a mutation in the Rbpsuh gene, which encodes the primary transcriptional mediator of Notch signaling. Conditional inactivation of    Rpbsuh function demonstrates that Notch activation is essential in the endothelial cell lineage. Notch pathway mutant embryos exhibit defects in arterial specification of nascent blood vessels and develop arteriovenous malformations. These    results demonstrate that vascular remodeling in the mouse embryo is sensitive to Dll4 gene dosage and that Notch activation in endothelial cells is essential for embryonic vascular remodeling.</p>

	]]>
</description>

<author>L T. Krebs et al.</author>


</item>


<item>
<title>A requirement for Notch1 distinguishes 2 phases of definitive hematopoiesis during development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/975</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/975</guid>
<pubDate>Tue, 08 May 2012 20:25:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Notch1 is known to play a critical role in regulating fates in numerous cell types, including those of the hematopoietic lineage. Multiple defects exhibited by Notch1-deficient embryos confound the determination of Notch1 function    in early hematopoietic development in vivo. To overcome this limitation, we examined the developmental potential of Notch1(-/-) embryonic stem (ES) cells by in vitro differentiation and by in vivo chimera analysis. Notch1 was found to affect    primitive erythropoiesis differentially during ES cell differentiation and in vivo, and this result reflected an important difference in the regulation of Notch1 expression during ES cell differentiation relative to the developing mouse embryo.     Notch1 was dispensable for the onset of definitive hematopoiesis both in vitro and in vivo in that Notch1(-/-) definitive progenitors could be detected in differentiating ES cells as well as in the yolk sac and early fetal liver of chimeric mice.    Despite the fact that Notch1(-/-) cells can give rise to multiple types of definitive progenitors in early development, Notch1(-/-) cells failed to contribute to long-term definitive hematopoiesis past the early fetal liver stage in the context    of a wild-type environment in chimeric mice. Thus, Notch1 is required, in a cell-autonomous manner, for the establishment of long-term, definitive hematopoietic stem cells (HSCs).</p>

	]]>
</description>

<author>B K. Hadland et al.</author>


</item>


<item>
<title>Kick it up a Notch: NOTCH1 activation in T-ALL.</title>
<link>http://mouseion.jax.org/stfb2000_2009/974</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/974</guid>
<pubDate>Tue, 08 May 2012 20:25:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>While the human NOTCH1 gene initially was cloned as part of a translocation breakpoint in T cell acute lymphoblastic leukemia (T-ALL) tumors, this translocation is present in only a small percentage of T-ALL patients. A recent paper    by Weng et al. (2004) demonstrates that novel types of activating mutations in the NOTCH1 gene occur in more than half of all T-ALL cases, implicating NOTCH1 as a major player in the etiology of T-ALL.</p>

	]]>
</description>

<author>T Gridley</author>


</item>


<item>
<title>Notch3 is required for arterial identity and maturation of vascular smooth muscle cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/973</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/973</guid>
<pubDate>Tue, 08 May 2012 20:25:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Formation of a fully functional artery proceeds through a multistep process. Here we show that Notch3 is required to generate functional arteries in mice by regulating arterial differentiation and maturation of vascular smooth    muscle cells (vSMC). In adult Notch3-/- mice distal arteries exhibit structural defects and arterial myogenic responses are defective. The postnatal maturation stage of vSMC is deficient in Notch3-/- mice. We further show that Notch3 is required    for arterial specification of vSMC but not of endothelial cells. Our data reveal Notch3 to be the first cell-autonomous regulator of arterial differentiation and maturation of vSMC.</p>

	]]>
</description>

<author>V Domenga et al.</author>


</item>


<item>
<title>Genetic approaches to studying mouse models of human seizure disorders.</title>
<link>http://mouseion.jax.org/stfb2000_2009/972</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/972</guid>
<pubDate>Tue, 08 May 2012 20:25:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>In conclusion, we have discussed a reverse genetics approach to studying seizure disorders in mice (Fig. 1), employing a targeted mutagenesis method to exploit the genetic defects identified in human epilepsy families. After    detailed characterization of the nature of the human mutation and the mouse counterpart gene, a targeting vector containing the human disease allele is created. The endogenous mouse gene is replaced by the human disease allele through homologous    recombination in ES cells, leading to the generation of chimeric animals. Mice carrying one copy or both copies of the human mutation can be bred to study the phenotypic effect of heterozygous and homozygous mutations. At this stage, one may want    to split the newly created mice into two groups. One group will go through seizure phenotyping tests, while the other group will be used to generate disease allele-carrying mice on a different genetic background.  Phenotypic characterization of    mice on different inbred strains includes behavioral monitoring and EEG analysis looking for the occurrence of spontaneous seizures, as well as routine cage examination looking for handling-provoked seizure and ECT- and PTZ- induced seizure    paradigms looking for sensitivity to these stimuli. A complete evaluation of the seizure phenotype at the whole-animal level establishes the relevance of the mouse model to the human condition. Further investigation including imaging,    electrophysiology and AED response in these mouse models will shed light on the mechanistic basis of the convulsive disorder. Current epilepsy research in mouse genetics offers promise for understanding the molecular mechanisms that underlie    epileptogenesis in humans. A large-scale forward genetic effort to create novel mouse mutants with seizure phenotypes by in vivo chemical mutagenesis with ethyl-nitroso urea (ENU) is underway at the Jackson Laboratory (http://www.jax.org/nmf/).     Genetic mapping and isolation of the affected genes in these seizure-prone models will provide additional molecular pathways involved in seizures.  The mutant mice generated through both forward and reverse genetic approaches will be a valuable    resource for the biomedical community to study epilepsy at the molecular level and to characterize the pathological consequences of seizures in the whole organism.</p>

	]]>
</description>

<author>Y Yang et al.</author>


</item>


<item>
<title>Protein kinase C activity regulates the onset of anaphase I in mouse oocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/971</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/971</guid>
<pubDate>Tue, 08 May 2012 20:24:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>The metaphase-to-anaphase I transition is a key step in the completion of meiosis I. In mouse oocytes, competence to exit metaphase I (MI) is developmentally regulated and typically not acquired until the preovulatory stage. The    possible role of protein kinase C (PKC) in regulating this critical transition was assessed in both normal oocytes isolated from small antral follicles (18-day-old B6SJLF1 mice), which have not yet developed the capacity to progress to metaphase    II (MII), and also oocytes defective in their ability to exit MI despite development to the preovulatory stage (24-day-old CX8 recombinant inbred strains). In both systems, transient suppression of endogenous PKC activity by treatment with a    PKC-specific inhibitor, bisindolylmaleimide I (BIM), promoted the onset of anaphase I in a dose-dependent manner, while activation of PKC with the phorbol ester TPA blocked progression to MII. Following a 2-h incubation with BIM, the majority of    oocytes progressed to, and arrested at, MII. The resulting MII oocytes were fertilizable in vitro, showing similar cleavage and blastocyst development rates between BIM treated and untreated controls. Transferred embryos resulted in the    development of pups to term in both groups. These data demonstrate that PKC plays an important role in regulating the onset of anaphase I in mouse oocytes.  Moreover, it is concluded that oocytes isolated from small antral follicles become    blocked at MI due to a PKC-mediated signal, suggesting that acquisition of competence to complete meiosis I involves, in part, the control of PKC activity. Similarly, failure to regulate PKC activity at the preovulatory stage likely promotes    arrest at MI.</p>

	]]>
</description>

<author>M M. Viveiros et al.</author>


</item>


<item>
<title>Synergistic roles of BMP15 and GDF9 in the development and function of the oocyte-cumulus cell complex in mice: genetic evidence for an oocyte-granulosa cell regulatory loop.</title>
<link>http://mouseion.jax.org/stfb2000_2009/970</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/970</guid>
<pubDate>Tue, 08 May 2012 20:24:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bone morphogenetic protein 15 (BMP15) and growth differentiation factor 9 (GDF9) are oocyte-specific growth factors that appear to play key roles in granulosa cell development and fertility in most mammalian species. We have    evaluated the role(s) of these paracrine factors in the development and function of both the cumulus cells and oocytes by assessing cumulus expansion, oocyte maturation, fertilization, and preimplantation embryogenesis in Gdf9+/-Bmp15-/-    [hereafter, double mutant (DM)] mice. We found that cumulus expansion, as well as the expression of hyaluronon synthase 2 (Has2) mRNA was impaired in DM oocyte-cumulus cell complexes.  This aberrant cumulus expansion was not remedied by coculture    with normal wild-type (WT) oocytes, indicating that the development and/or differentiation of cumulus cells in the DM, up to the stage of the preovulatory luteinizing hormone (LH) surge, is impaired. In addition, DM oocytes failed to enable FSH    to induce cumulus expansion in WT oocytectomized (OOX) cumulus. Moreover, LH-induced oocyte meiotic resumption was significantly delayed in vivo, and this delayed resumption of meiosis was correlated with the reduced activation of    mitogen-activated protein kinase (MAPK) in the cumulus cells, thus suggesting that GDF9 and BMP15 also regulate the function of cumulus cells after the preovulatory LH surge. Although spontaneous in vitro oocyte maturation occurred normally,    oocyte fertilization and preimplantation embryogenesis were significantly altered in the DM, suggesting that the full complement of both GDF9 and BMP15 are essential for the development and function of oocytes. Because receptors for GDF9 and    BMP15 have not yet been identified in mouse oocytes, the effects of the mutations in the Bmp15 and Gdf9 genes on oocyte development and functions must be produced indirectly by first affecting the granulosa cells and then the oocyte. Therefore,    this study provides further evidence for the existence and functioning of an oocyte-granulosa cell regulatory loop.</p>

	]]>
</description>

<author>Y Q. Su et al.</author>


</item>


<item>
<title>Visualizing the laboratory mouse: capturing phenotype information.</title>
<link>http://mouseion.jax.org/stfb2000_2009/969</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/969</guid>
<pubDate>Tue, 08 May 2012 20:24:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>A concerted effort to develop myriad new phenotypic alleles through mutagenesis programs presents new challenges for the biomedical community and for the informatics infrastructure needed to support this work. To handle and    co-ordinate large programs of treatment, breeding, and sequential or longitudinal testing for a variety of obvious and subtle traits requires sophisticated data management software. Further, trait analyses, heritability testing, and animal    availability and status must be captured and disseminated to the wider community. The Mouse Genome Database (MGD) will serve as the central integration point for the various mutagenesis programs, registering new alleles, providing accession    identifiers, and capturing phenotypic descriptions. In addition, MGD will provide public access to unified searches over all alleles with links to the centres of origin for detailed testing data.</p>

	]]>
</description>

<author>M Strivens et al.</author>


</item>


<item>
<title>Mice carrying the szt1 mutation exhibit increased seizure susceptibility and altered sensitivity to compounds acting at the m-channel.</title>
<link>http://mouseion.jax.org/stfb2000_2009/968</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/968</guid>
<pubDate>Tue, 08 May 2012 20:24:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Mutations in the genes that encode subunits of the M-type K+ channel (KCNQ2/KCNQ3) and nicotinic acetylcholine receptor (CHRNA4) cause epilepsy in humans. The purpose of this study was to examine the effects of the Szt1    mutation, which not only deletes most of the C-terminus of mouse Kcnq2, but also renders the Chnra4 and Arfgap-1 genes hemizygous, on seizure susceptibility and sensitivity to drugs that target the M-type K+ channel. METHODS: The proconvulsant    effects of the M-channel blocker linopirdine (LPD) and anticonvulsant effects of the M-channel enhancer retigabine (RGB) were assessed by electroconvulsive threshold (ECT) testing in C57BL/6J-Szt1/+ (Szt1) and littermate control C57BL/6J+/+ (B6)    mice. The effects of the Szt1 mutation on minimal clonic, minimal tonic hindlimb extension, and partial psychomotor seizures were evaluated by varying stimulation intensity and frequency. RESULTS: Szt1 mouse seizure thresholds were significantly    reduced relative to B6 littermates in the minimal clonic, minimal tonic hindlimb extension, and partial psychomotor seizure models. Mice were injected with LPD and RGB and subjected to ECT testing. In the minimal clonic seizure model, Szt1 mice    were significantly more sensitive to LPD than were B6 mice [median effective dose (ED50) = 3.4 +/- 1.1 mg/kg and 7.6 +/- 1.0 mg/kg, respectively]; in the partial psychomotor seizure model, Szt1 mice were significantly less sensitive to RGB than    were B6 mice (ED50 = 11.6 +/- 1.4 mg/kg and 3.4 +/- 1.3 mg/kg, respectively). CONCLUSIONS: These results suggest that the Szt1 mutation alters baseline seizure susceptibility and pharmacosensitivity in a naturally occurring mouse    model.</p>

	]]>
</description>

<author>J F. Otto et al.</author>


</item>


<item>
<title>Anti-insulin receptor autoantibodies are not required for type 2 diabetes pathogenesis in NZL/Lt mice, a New Zealand obese (NZO)-derived mouse strain.</title>
<link>http://mouseion.jax.org/stfb2000_2009/967</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/967</guid>
<pubDate>Tue, 08 May 2012 20:23:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The New Zealand obese (NZO) mouse strain shares with the related New Zealand black (NZB) strain a number of immunophenotypic traits. Among these is a high proportion of B-1 B lymphocytes, a subset associated with autoantibody    production. Approximately 50% of NZO/HlLt males develop a chronic insulin-resistant type 2 diabetes syndrome associated with 2 unusual features: the presence of B lymphocyte-enriched peri-insular infiltrates and the development of anti-insulin    receptor autoantibodies (AIRAs). To establish the potential pathogenic contributions of B lymphocytes and AIRAs in this model, a disrupted immunoglobulin heavy chain gene (Igh-6) congenic on the NZB/BlJ background was backcrossed 4 generations    into the NZO/HlLt background and was then intercrossed to produce mice that initially segregated for wild-type versus the mutant Igh-6 allele and thus permitted comparison of syndrome development. A new flow cytometric assay (AIRA binding to    transfected Chinese hamster ovary cells stably expressing mouse insulin receptor) showed IgM and IgG subclass AIRAs in serum from Igh-6 intact males, but not in Igh-6null male serum. However, the absence of B lymphocytes and antibodies    distinguishing mutant from wild-type males failed to significantly affect diabetes-free survival. The Igh-6null males gained weight less rapidly than wild-type males, probably accounting for a retardation, but not prevention, of hyperglycemia.    Thus, AIRA and the B-lymphocyte component of the peri-insulitis in chronic diabetics were not essential either to development of insulin resistance or to eventual pancreatic beta cell failure and loss. A new substrain, designated NZL, was    generated by inbreeding Igh-6 wild-type segregants. Currently at the F10 generation, NZL mice exhibit the same juvenile-onset obesity as NZO/HlLt males, but develop type 2 diabetes at a higher frequency (> 80%). Also, unlike NZO/HlLt mice that    are difficult to breed, the NZL/Lt strain breeds well and thus offers clear advantages to obesity/diabetes researchers.</p>

	]]>
</description>

<author>M F. McInerney et al.</author>


</item>


<item>
<title>A synthetic analogue of meiosis-activating sterol (FF-MAS) is a potent agonist promoting meiotic maturation and preimplantation development of mouse oocytes maturing in vitro.</title>
<link>http://mouseion.jax.org/stfb2000_2009/966</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/966</guid>
<pubDate>Tue, 08 May 2012 20:23:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Follicular fluid-meiosis-activating sterol (FF-MAS) is a factor present in the pre-ovulatory follicle during the time of oocyte maturation. In mouse oocytes maturing in vitro, FF-MAS promotes the completion of meiotic    maturation to metaphase II (MII) and improves competence to complete the 2-cell stage to blastocyst transition. We produced analogues of FF-MAS and selected three on the basis of potency to promote the resumption of meiosis by mouse oocytes    maintained in meiotic arrest by hypoxanthine. The objective of this study was to determine whether these FF-MAS analogues also affect the quality of oocytes maturing in vitro with respect to the completion of meiotic maturation and augmenting the    frequency of development to the blastocyst stage after fertilization in vitro. METHODS: Cumulus cell-enclosed oocytes were isolated from the small antral follicles of 18 or 20 day post-natal mice.  These oocytes normally have a reduced competence    to complete meiotic maturation and preimplantation embryo development. Oocytes were isolated at the germinal vesicle stage and matured in vitro using media supplemented with 0.1% ethanol, 1 micromol/l FF-MAS, or 0.1-10 micromol/l FF-MAS analogues    ZK255884 (884), ZK255933 (933) and ZK255991 (991).  Oocytes that progressed to MII were fertilized in vitro and the percentage developing to the 2-cell and blastocyst stages was determined. RESULTS: At 1 micromol/l, 991 and 933 increased the    portion of oocytes progressing to MII, whereas the lowest dose of 991 and 884 was ineffective. Treatment of maturing oocytes with either 0.1 or 1 micromol/l 933 dramatically increased oocyte competence to complete preimplantation development.     CONCLUSIONS: The synthetic analogue of FF-MAS, ZK255933, is a potent agonist that improves the quality of mouse oocytes matured in vitro. This compound may therefore have therapeutic value for treatment of oocytes from women undergoing therapy    for infertility owing to poor oocyte quality.</p>

	]]>
</description>

<author>Bivens C. Marin et al.</author>


</item>


<item>
<title>Major chromatin remodeling in the germinal vesicle (GV) of mammalian oocytes is dispensable for global transcriptional silencing but required for centromeric heterochromatin function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/965</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/965</guid>
<pubDate>Tue, 08 May 2012 20:23:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Global silencing of transcriptional activity in the oocyte genome occurs just before the resumption of meiosis and is a crucial developmental transition at the culmination of oogenesis. Transcriptionally quiescent oocytes rely on    stored maternal transcripts to sustain the completion of meiosis, fertilization, and early embryonic cleavage stages. Thus, the timing of silencing is key for successful embryo development. Yet, the cellular and molecular pathways coordinating    dynamic changes in large-scale chromatin structure with the onset of transcriptional repression are poorly understood. Here, oocytes obtained from nucleoplasmin 2 knockout (Npm2-/-) mice were used to investigate the relationship between    transcriptional repression and chromatin remodeling in the germinal vesicle (GV) of mammalian oocytes. Although temporally linked, global silencing of transcription and chromatin remodeling in the oocyte genome can be experimentally dissociated    and therefore must be regulated through distinct pathways. Detection of centromeric heterochromatin DNA sequences with a mouse pan-centromeric chromosome paint revealed that most centromeres are found in close apposition with the nucleolus in    transcriptionally quiescent oocytes and therefore constitute an important component of the perinucleolar heterochromatin rim or karyosphere. Pharmacological inhibition of histone deacetylases (HDACs) with trichostatin A (TSA) revealed that HDACs    are essential for large-scale chromatin remodeling in the GV. Importantly, the specialized nuclear architecture acquired upon transcriptional repression is essential for meiotic progression as interference with global deacetylation and partial    disruption of the karyosphere resulted in a dramatic increase in the proportion of oocytes exhibiting abnormal meiotic chromosome and spindle configuration. These results indicate that the unique chromatin remodeling mechanism in oocytes may be    specifically related to meiotic cell division in female mammals.</p>

	]]>
</description>

<author>La Fuente De et al.</author>


</item>


<item>
<title>Mutation rate and predicted phenotypic target sizes in ethylnitrosourea-treated mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/964</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/964</guid>
<pubDate>Tue, 08 May 2012 20:23:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chemical mutagenesis of the mouse is ongoing in several centers around the world, with varying estimates of mutation rate and number of sites mutable to phenotype. To address these questions, we sequenced approximately 9.6 Mb of DNA    from G1 progeny of ethylnitrosourea-treated mice in a large, broad-spectrum screen. We identified 10 mutations at eight unique sites, including six nonsynonymous coding substitutions. This calibrates the nucleotide mutation rate for two    mutagenesis centers, implies significance criteria for positional cloning efforts, and provides working estimates of effective genetic target sizes for selected phenotypes.</p>

	]]>
</description>

<author>D Concepcion et al.</author>


</item>


<item>
<title>Implementing large-scale ENU mutagenesis screens in North America.</title>
<link>http://mouseion.jax.org/stfb2000_2009/963</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/963</guid>
<pubDate>Tue, 08 May 2012 20:22:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>A step towards annotating the mouse genome is to use forward genetics in phenotype-driven screens to saturate the genome with mutations. The purpose of this article is to highlight the new projects in North America that are focused    on isolating mouse mutations after ENU mutagenesis and phenotype screening.</p>

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</description>

<author>A T. Clark et al.</author>


</item>


<item>
<title>Altered cholesterologenic and lipogenic transcriptional profile in livers of aging Snell dwarf (Pit1dw/dwJ) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/962</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/962</guid>
<pubDate>Tue, 08 May 2012 20:22:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Several murine models demonstrate that mammalian longevity can be increased by single gene mutations affecting endocrine signalling, particularly via the GH/IGF-1 axis. In this study, we identify age-independent patterns of hepatic    gene expression characteristic of long-lived Snell (Pit1(dw/dwJ)) dwarf mice. Comparative microarray analysis of young and aged male livers was performed to discover specific genes differentially expressed between Pit1(dw/dwJ) and control mice.     Further examination by real-time RT-PCR confirmed that transcripts encoding HMG-CoA synthase-1, HMG-CoA reductase, farnesyl diphosphate synthase, isopentenyl pyrophosphate isomerase, mevalonate decarboxylase, squalene epoxidase, lanosterol    demethylase, malic enzyme and apolipoprotein A-IV were significantly decreased in both male and female Pit1(dw/dwJ) livers at 3-5 and 24-28 months of age. In contrast, transcripts encoding the beta(3)-adrenergic receptor, lipoprotein lipase, PPAR    gamma and a very low-density lipoprotein receptor homologue were increased significantly in dwarf livers relative to age-matched controls.  These studies reveal enduring transcriptional changes characteristic of Pit1(dw/dwJ) dwarf mice that    involve genes regulating cholesterol biosynthesis, fatty acid metabolism and lipoprotein homeostasis. Linked to global energy metabolism, this stable shift in hepatic gene expression may contribute to longevity determination by influencing    particular metabolic functions often compartmentalized within the mitochondrion and peroxisome; further this metabolic shift may also parallel many transcriptional changes induced by caloric restriction.</p>

	]]>
</description>

<author>W H. Boylston et al.</author>


</item>


<item>
<title>Using real time RT-PCR analysis to determine multiple gene expression patterns during XX and XY mouse fetal gonad development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/961</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/961</guid>
<pubDate>Tue, 08 May 2012 20:22:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>New techniques are being applied to identify all the genes involved in mammalian gonad development and differentiation. As this list of genes increases, understanding the potential interactions between these genes will become    increasingly difficult. We used a real time reverse transcription PCR (real time RTPCR) protocol to examine and compare the relative expression levels of 55 genes in individual mouse fetal gonads.  Real time PCR analysis demonstrated that except    for Sry, no differences in relative gene expression were detectable between XX and XY gonad/mesonephroi complexes at embryonic day (E)11.5. Following Sry peak expression at E11.5, a number of genes were expressed at significantly higher relative    levels in E12-14 XY than XX gonads. Of six genes expressed at higher levels in E12.5-14 XX than XY gonads, three, Bmp2, Emx2, and Fgfr2, had not been reported previously. Our results caution that differential localization patterns observed with    whole mount in situ hybridization techniques may not accurately reflect changes in transcript levels. We conclude that real time PCR is an efficient and powerful tool for studying multiple gene expression patterns during gonad development and    differentiation, and can provide insight into gene interactions.</p>

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</description>

<author>G J. Bouma et al.</author>


</item>


<item>
<title>Genetic variations that regulate bone morphology in the male mouse skeleton do not define its susceptibility to mechanical unloading.</title>
<link>http://mouseion.jax.org/stfb2000_2009/960</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/960</guid>
<pubDate>Tue, 08 May 2012 20:22:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetics can substantially influence bone morphology and may define the skeleton's response to mechanical unloading. Recent data indicated that disuse produces different site-specific responses in the skeleton of genetically    distinct adult female C3H/HeJ (C3H) and BALB/cByJ (BALB) mice; while disuse BALB mice had significantly less bone than age-matched controls in the distal and diaphyseal femur, the removal of weight bearing had a much smaller influence in C3H.    Using adult male mice from these two inbred strains, the hypothesis was tested that interactions between genetic variations and anatomic location define bone morphology and its susceptibility to unloading. Four-month-old male BALB and C3H mice    were either subjected to 21 days of hindlimb unloading or served as controls.  Multiple cortical and trabecular regions within the distal and diaphyseal femur were analyzed by micro-computed tomography. C3H controls had significantly greater    diaphyseal and metaphyseal cortical bone area (45% and 32%) and greater metaphyseal trabecular bone volume fraction (67%) than BALB controls, but epiphyseal trabecular bone volume fraction was similar between the two strains. Despite these    substantial, site-specific differences in bone morphology, disuse induced similar changes in bone morphology in these two strains. Compared to controls, disuse BALB and C3H had significantly less metaphyseal (17% and 19%) and epiphyseal (10% and    13%) trabecular bone, while diaphyseal and metaphyseal cortical bone geometry was unaffected. These data indicate that the genetic variations that caused spatially nonuniform differences in trabecular and cortical bone morphology between the two    strains had little influence on the susceptibility of a specific site to unloading. Cross-gender comparisons with previous data from female BALB and C3H mice further suggest strong interactions by which gender, genotype, and anatomical location    define the response of the skeleton to the removal of weight bearing.</p>

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</description>

<author>M Squire et al.</author>


</item>


<item>
<title>Congenic mice with low serum IGF-I have increased body fat, reduced bone mineral density, and an altered osteoblast differentiation program.</title>
<link>http://mouseion.jax.org/stfb2000_2009/959</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/959</guid>
<pubDate>Tue, 08 May 2012 20:21:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Targeted gene studies have demonstrated the importance of insulin-like growth factor-I (IGF-I) for osteoblast (OB) differentiation and the acquisition of peak bone mineral density (BMD). The skeletal response to allelic differences    in IGF-I expression can also be measured in vivo, using congenic mice. We created a congenic strain with reduced (approximately 20%) circulating IGF-I (C3H.B6-6T [6T]) by backcrossing a small genomic region (30 cM) of Chromosome 6 (Chr6) from    C3H/HeJ (C3H) onto a C57Bl/6J (B6) background. 6T female mice have lower serum IGF-I (P<0.001 vs. B6) but similar growth hormone (GH) and serum IGF binding protein (IGFBP) concentrations as B6. At 16 weeks of age, congenics have greater body fat    (P<0.02 vs. B6) despite less total body weight, and exhibit smaller femoral cross-sectional size (P=0.001), reduced cortical thickness (P<0.001) and lower trabecular BV/TV (P<0.05) than B6. 6T mice also have suppressed serum leptin (P<0.01), but    compared to B6 have similar markers of bone resorption (i.e., urine CTx and serum TRAP 5B). At 8 weeks of age, skeletal IGF-I mRNA from long bones was reduced by 40% (P<0.05) as were liver mRNA transcripts (i.e., 50%, P<0.01). Osteoblast    progenitors from the bone marrow of 6T mice formed less colony forming unit fibroblasts by crystal violet staining than B6 (P<0.007) and had significantly reduced alkaline phosphatase-positive colonies than B6(P<0.0001). In addition, staining of    bone marrow with oil red O revealed greater numbers of adipocytes in 6T than B6. Several candidate genes in the Chr6 QTL were excluded by lack of strain-related expression differences in bone, but genes positively regulating adipocyte    differentiation including Alox 5 and PPAR-gamma require further study as either "pathway" or candidate genes. In summary, allelic differences in a QTL on Chr6 result in altered IGF-I gene expression, changes in OB lineage allocation, and reduced    peak bone mass. Congenic mice are useful models not only for mapping genes related to bone mass but also for elucidating the biology underlying various skeletal phenotypes associated with more subtle manipulation  of the mouse    genome.</p>

	]]>
</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title>Proteotypic classification of spontaneous and transgenic mammary neoplasms.</title>
<link>http://mouseion.jax.org/stfb2000_2009/958</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/958</guid>
<pubDate>Tue, 08 May 2012 20:21:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>INTRODUCTION: Mammary tumors in mice are categorized by using morphologic and architectural criteria. Immunolabeling for terminal differentiation markers was compared among a variety of mouse mammary neoplasms because expression of    terminal differentiation markers, and especially of keratins, provides important information on the origin of neoplastic cells and their degree of differentiation. METHODS: Expression patterns for terminal differentiation markers were used to    characterize tumor types and to study tumor progression in transgenic mouse models of mammary neoplasia (mice overexpressing Neu (Erbb2), Hras, Myc, Notch4, SV40-TAg, Tgfa, and Wnt1), in spontaneous mammary carcinomas, and in mammary neoplasms    associated with infection by the mouse mammary tumor virus (MMTV).  RESULTS: On the basis of the expression of terminal differentiation markers, three types of neoplasm were identified: first, simple carcinomas composed exclusively of cells with    a luminal phenotype are characteristic of neoplasms arising in mice transgenic for Neu, Hras, Myc, Notch4, and SV40-TAg; second, 'complex carcinomas' displaying luminal and myoepithelial differentiation are characteristic of type P tumors arising    in mice transgenic for Wnt1, neoplasms arising in mice infected by the MMTV, and spontaneous adenosquamous carcinomas; and third, 'carcinomas with epithelial to mesenchymal transition (EMT)' are a characteristic feature of tumor progression in    Hras-, Myc-, and SV40-TAg-induced mammary neoplasms and PL/J and SJL/J mouse strains, and display de novo expression of myoepithelial and mesenchymal cell markers. In sharp contrast, EMT was not detected in papillary adenocarcinomas arising in    BALB/cJ mice, spontaneous adenoacanthomas, neoplasms associated with MMTV-infection, or in neoplasms arising in mice transgenic for Neu and Wnt1. CONCLUSIONS: Immunohistochemical profiles of complex neoplasms are consistent with a stem cell    origin, whereas simple carcinomas might originate from a cell committed to the luminal lineage. In addition, these results suggest that the initiating oncogenic events determine the morphologic features associated with cancer progression because    EMT is observed only in certain types of neoplasm.</p>

	]]>
</description>

<author>I Mikaelian et al.</author>


</item>


<item>
<title>Locating Ath8, a locus for murine atherosclerosis susceptibility and testing several of its candidate genes in mice and humans.</title>
<link>http://mouseion.jax.org/stfb2000_2009/957</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/957</guid>
<pubDate>Tue, 08 May 2012 20:21:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>A previous study revealed that the difference in susceptibility to atherosclerotic lesions between inbred mouse strains SM/J and NZB/BlNJ was determined by one major locus (Ath8). In this study a (SM/J x NZB/BlNJ) F(1) x SM/J    backcross localized Ath8 by quantitative trait locus mapping to chromosome 4 with a suggestive LOD score of 2.7. This quantitative trait locus (QTL) was confirmed using an (SM/J x NZB/BlNJ) intercross; Ath8 mapped to a 23cM region with a    significant LOD score of 3.6. The genes for toll-like receptor 4 (T1r4), arachidonic acid epoxygenase (Cyp2j5), and angiopoietin-like protein 3 (Angptl3) map to this region.  These candidate genes were analyzed for expression and sequence    differences in the mouse and for associations with cardiovascular traits in human. Sequence analysis of Angptl3 shows a base pair substitution in SM, the susceptible strain, giving rise to an amino acid change in the fibrinogen homology domain of    the protein. We found a significant association between ANGPTL3 and atherosclerotic lesions (P < 0.05) in human. These results suggest that Angptl3 is involved in atherosclerosis susceptibility in both mouse and human.</p>

	]]>
</description>

<author>R Korstanje et al.</author>


</item>


<item>
<title>Stabilization of beta-catenin in the mouse zygote leads to premature epithelial-mesenchymal transition in the epiblast.</title>
<link>http://mouseion.jax.org/stfb2000_2009/956</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/956</guid>
<pubDate>Tue, 08 May 2012 20:20:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many components of the Wnt/beta-catenin signaling pathway are expressed during mouse pre-implantation embryo development, suggesting that this pathway may control cell proliferation and differentiation at this time.  We find no    evidence for a functional activity of this pathway in cleavage-stage embryos using the Wnt-reporter line, BAT-gal. To further probe the activity of this pathway, we activated beta-catenin signaling by mating a zona pellucida3-cre (Zp3-cre)    transgenic mouse line with a mouse line containing an exon3-floxed beta-catenin allele. The result is expression of a stabilized form of beta-catenin, resistant to degradation by the GSK3beta-mediated proteasome pathway, expressed in the    developing oocyte and in each cell of the resulting embryos. Nuclear localization and signaling function of beta-catenin were not observed in cleavage-stage embryos derived from these oocytes. These results indicate that in pre-implantation    embryos, molecular mechanisms independent of the GSK3beta-mediated ubiquitination and proteasome degradation pathway inhibit the nuclear function of beta-catenin. Although the mutant blastocysts initially developed normally, they then exhibited a    specific phenotype in the embryonic ectoderm layer of early post-implantation embryos. We show a nuclear function of beta-catenin in the mutant epiblast that leads to activation of Wnt/beta-catenin target genes. As a consequence, cells of the    embryonic ectoderm change their fate, resulting in a premature epithelial-mesenchymal transition.</p>

	]]>
</description>

<author>R Kemler et al.</author>


</item>


<item>
<title>Selective phenotyping for increased efficiency in genetic mapping studies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/955</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/955</guid>
<pubDate>Tue, 08 May 2012 20:20:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The power of a genetic mapping study depends on the heritability of the trait, the number of individuals included in the analysis, and the genetic dissimilarity among them. In experiments that involve microarrays or other complex    physiological assays, phenotyping can be expensive and time-consuming and may impose limits on the sample size. A random selection of individuals may not provide sufficient power to detect linkage until a large sample size is reached. We present    an algorithm for selecting a subset of individuals solely on the basis of genotype data that can achieve substantial improvements in sensitivity compared to a random sample of the same size. The selective phenotyping method involves    preferentially selecting individuals to maximize their genotypic dissimilarity. Selective phenotyping is most effective when prior knowledge of genetic architecture allows us to focus on specific genetic regions. However, it can also provide    modest improvements in efficiency when applied on a whole-genome basis. Importantly, selective phenotyping does not reduce the efficiency of mapping as compared to a random sample in regions that are not considered in the selection process. In    contrast to selective genotyping, inferences based solely on a selectively phenotyped population of individuals are representative of the whole population. The substantial improvement introduced by selective phenotyping is particularly useful    when phenotyping is difficult or costly and thus limits the sample size in a genetic mapping study.</p>

	]]>
</description>

<author>C Jin et al.</author>


</item>


<item>
<title>Building protein interaction maps for Down&apos;s syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/954</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/954</guid>
<pubDate>Tue, 08 May 2012 20:20:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Now that the complete sequences for human chromosome 21 and the orthologous mouse genomic regions are known, reasonably complete, conserved, protein-coding gene catalogues are also available. The central issue now facing Down's    syndrome researchers is the correlation of increased expression of specific, normal, chromosome 21 genes with the development of specific deficits in learning and memory. Because of the number of candidate genes involved, the number of    alternative splice variants of individual genes and the number of pathways in which these genes function, a pathway analysis approach will be critical to success.  Here, three examples, both gene specific and pathway related, that would benefit    from pathway analysis are discussed: (1) the potential roles of eight chromosome 21 proteins in RNA processing pathways; (2) the chromosome 21 protein intersectin 1 and its domain composition, alternative splicing, protein interactions and    functions; and (3) the interactions of ten chromosome 21 proteins with components of the mitogen-activated protein kinase and the calcineurin signalling pathways.  A productive approach to developing gene-phenotype correlations in Down's syndrome    will make use of known and predicted functions and interactions of chromosome 21 genes to predict pathways that may be perturbed by their increased levels of expression. Investigations may then be targeted in animal models to specific    interactions, intermediate steps or end-points of such pathways and the downstream - perhaps amplified - consequences of gene dosage directly assessed. Once pathway perturbations have been identified, the potential for rational design of    therapeutics becomes practical.</p>

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</description>

<author>K Gardiner et al.</author>


</item>


<item>
<title>Genetic interaction between Rb and K-ras in the control of differentiation and tumor suppression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/953</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/953</guid>
<pubDate>Tue, 08 May 2012 20:20:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although the retinoblastoma protein (pRb) has been implicated in the processes of cellular differentiation, there is no compelling genetic or in vivo evidence that such activities contribute to pRb-mediated tumor suppression.    Motivated by cell culture studies suggesting that Ras is a downstream effector of pRb in the control of differentiation, we have examined the tumor and developmental phenotypes of Rb and K-ras double-knockout mice. We find that heterozygosity for    K-ras (i) rescued a unique subset of developmental defects that characterize Rb-deficient embryos by affecting differentiation but not proliferation and (ii) significantly enhanced the degree of differentiation of pituitary adenocarcinomas    arising in Rb heterozygotes, leading to their prolonged survival. These observations suggest that Rb and K-ras function together in vivo, in the contexts of both embryonic and tumor development, and that the ability to affect differentiation is a    major facet of the tumor suppressor function of pRb.</p>

	]]>
</description>

<author>C Takahashi et al.</author>


</item>


<item>
<title>Peroxisome proliferator-activated receptor gamma controls Muc1 transcription in trophoblasts.</title>
<link>http://mouseion.jax.org/stfb2000_2009/952</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/952</guid>
<pubDate>Tue, 08 May 2012 20:19:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma) is essential for placental development. Here, we show that the mucin gene Muc1 is a PPARgamma target, whose expression is lost in PPARgamma null    placentas. During differentiation of trophoblast stem cells, PPARgamma is strongly induced, and Muc1 expression is upregulated by the PPARgamma agonist rosiglitazone. Muc1 promoter is activated strongly and specifically by liganded PPARgamma but    not PPARalpha or PPARdelta. A PPAR binding site (DR1) in the proximal Muc1 promoter acts as a basal silencer in the absence of PPARgamma, and its cooperation with a composite upstream enhancer element is both necessary and sufficient for    PPARgamma-dependent induction of Muc1. In the placenta, MUC1 protein is localized exclusively to the apical surface of the labyrinthine trophoblast around maternal blood sinuses, resembling its luminal localization on secretory epithelia. Last,    variably penetrant maternal blood sinus dilation in Muc1-deficient placentas suggests that Muc1 regulation by PPARgamma contributes to normal placental development but also that the essential functions of PPARgamma in the organ are mediated by    other targets.</p>

	]]>
</description>

<author>Barak T. Shalom et al.</author>


</item>


<item>
<title>Susceptibility to astrocytoma in mice mutant for Nf1 and Trp53 is linked to chromosome 11 and subject to epigenetic effects.</title>
<link>http://mouseion.jax.org/stfb2000_2009/951</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/951</guid>
<pubDate>Tue, 08 May 2012 20:19:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common during tumor progression. We have shown previously that mice mutant for    Trp53 and Nf1 develop astrocytoma, progressing to glioblastoma, on a C57BL/6J strain background. In contrast, here we present data that mice mutant for Trp53 and Nf1 on a 129S4/SvJae background are highly resistant to developing astrocytoma.    Through analysis of F1 progeny, we demonstrate that susceptibility to astrocytoma is linked to chromosome 11, and that the modifier gene(s) responsible for differences in susceptibility is closely linked to Nf1 and Trp53. Furthermore, this    modifier of astrocytoma susceptibility is itself epigenetically modified.  These data demonstrate that epigenetic effects can have a strong effect on whether cancer develops in the context of mutant ras signaling and mutant p53, and that this    mouse model of astrocytoma can be used to identify modifier phenotypes with complex inheritance patterns that would be unidentifiable in humans. Because analysis of gene function in the mouse is often performed on a mixed C57BL/6,129 strain    background, these data also provide a powerful example of the potential of these strains to mask interesting gene functions.</p>

	]]>
</description>

<author>K M. Reilly et al.</author>


</item>


<item>
<title>Use of a dense single nucleotide polymorphism map for in silico mapping in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/950</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/950</guid>
<pubDate>Tue, 08 May 2012 20:19:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rapid expansion of available data, both phenotypic and genotypic, for multiple strains of mice has enabled the development of new methods to interrogate the mouse genome for functional genetic perturbations. In silico mapping    provides an expedient way to associate the natural diversity of phenotypic traits with ancestrally inherited polymorphisms for the purpose of dissecting genetic traits. In mouse, the current single nucleotide polymorphism (SNP) data have lacked    the density across the genome and coverage of enough strains to properly achieve this goal. To remedy this, 470,407 allele calls were produced for 10,990 evenly spaced SNP loci across 48 inbred mouse strains. Use of the SNP set with statistical    models that considered unique patterns within blocks of three SNPs as an inferred haplotype could successfully map known single gene traits and a cloned quantitative trait gene. Application of this method to high-density lipoprotein and gallstone    phenotypes reproduced previously characterized quantitative trait loci (QTL). The inferred haplotype data also facilitates the refinement of QTL regions such that candidate genes can be more easily identified and characterized as shown    foradenylate cyclase 7.</p>

	]]>
</description>

<author>M T. Pletcher et al.</author>


</item>


<item>
<title>Genomewide two-generation screens for recessive mutations by ES cell mutagenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/949</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/949</guid>
<pubDate>Tue, 08 May 2012 20:18:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Forward genetic mutation screens in mice are typically begun by mutagenizing the germline of male mice with N-ethyl-N-nitrosourea (ENU).  Genomewide recessive mutations transmitted by these males can be rendered homozygous after    three generations of breeding, at which time phenotype screens can be performed. An alternative strategy for randomly mutagenizing the mouse genome is by chemical treatment of embryonic stem (ES) cells. Here we demonstrate the feasibility of    performing genome-wide mutation screens with only two generations of breeding. Mice potentially homozygous for mutations were obtained by crossing chimeras derived from ethylmethane sulfonate (EMS)-mutagenized ES cells to their daughters, or by    intercrossing offspring of chimeras. This strategy was possible because chimeras transmit variations of the same mutagenized diploid genome, whereas ENU-treated males transmit numerous unrelated genomes. This also results in a doubling of    screenable mutations in a pedigree compared to germline ENU mutagenesis. Coupled with the flexibility to treat ES cells with a variety of potent mutagens and the ease of producing distributable, quality-controlled, long-term supplies of cells in    a single experiment, this strategy offers a number of advantages for conducting forward genetic screens in mice.</p>

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</description>

<author>R J. Munroe et al.</author>


</item>


<item>
<title>A collaborative database of inbred mouse strain characteristics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/948</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/948</guid>
<pubDate>Tue, 08 May 2012 20:18:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>A database and website (MPD: Mouse Phenome Database) have been developed to serve as a consolidated home for mouse strain characterization data being generated by the scientific community. Physiological, anatomical and behavioral    data are being collected and integrated into a common framework for tabulation by strain and sex. Genotypic data are being collected as well. The current focus is on a set of 40 inbred strains. The MPD as of February 2004 contains approximately    500 phenotypic parameters relevant to human health, voluntarily contributed by several dozen investigators and laboratories. AVAILABILITY: www.jax.org/phenome</p>

	]]>
</description>

<author>S C. Grubb et al.</author>


</item>


<item>
<title>Large-scale mutagenesis of the mouse to understand the genetic bases of nervous system structure and function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/947</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/947</guid>
<pubDate>Tue, 08 May 2012 20:17:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>N-ethyl-N-nitrosourea (ENU) mutagenesis is presented as a powerful approach to developing models for human disease. The efforts of three NIH Mutagenesis Centers established for the detection of neuroscience-related phenotypes are    described. Each center has developed an extensive panel of phenotype screens that assess nervous system structure and function. In particular, these screens focus on complex behavioral traits from drug and alcohol responses to circadian rhythms    to epilepsy. Each of these centers has developed a bioinformatics infrastructure to track the extensive number of transactions that are inherent in these large-scale projects.  Over 100 new mouse mutant lines have been defined through the efforts    of these three mutagenesis centers and are presented to the research community via the centralized Web presence of the Neuromice.org consortium (http://www.neuromice.org). This community resource provides visitors with the ability to search for    specific mutant phenotypes, to view the genetic and phenotypic details of mutant mouse lines, and to order these mice for use in their own research program.</p>

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</description>

<author>D Goldowitz et al.</author>


</item>


<item>
<title>The Collaborative Cross, a community resource for the genetic analysis of complex traits.</title>
<link>http://mouseion.jax.org/stfb2000_2009/946</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/946</guid>
<pubDate>Tue, 08 May 2012 20:17:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>The goal of the Complex Trait Consortium is to promote the development of resources that can be used to understand, treat and ultimately prevent pervasive human diseases. Existing and proposed mouse resources that are optimized to    study the actions of isolated genetic loci on a fixed background are less effective for studying intact polygenic networks and interactions among genes, environments, pathogens and other factors. The Collaborative Cross will provide a common    reference panel specifically designed for the integrative analysis of complex systems and will change the way we approach human health and disease.</p>

	]]>
</description>

<author>G A. Churchill et al.</author>


</item>


<item>
<title>The Mouse Phenome Project.</title>
<link>http://mouseion.jax.org/stfb2000_2009/945</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/945</guid>
<pubDate>Tue, 08 May 2012 20:17:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>The laboratory mouse is the organism of choice for many studies in biology and medicine. Reliable phenotypic data are essential for the full utility of genotypic information emerging from efforts to sequence human and mouse genomes.    The Mouse Phenome Project has been organized to help accomplish this task by establishing a collection of baseline phenotypic data on commonly used and genetically diverse inbred mouse strains and making this information publicly available    through a web-accessible database. The Mouse Phenome Database (MPD) is being developed to manage these data and to provide researchers with tools for exploring both raw phenotypic data and comparative summary analyses. The MPD serves as a    repository for detailed protocols and raw data. This resource enables investigators to identify appropriate strains for (1) physiological testing, (2) drug discovery, (3) toxicology studies, (4) mutagenesis, (5) modeling human diseases, (6) QTL    analyses and identification of new genes and (7) unraveling the influence of environment on genotype.</p>

	]]>
</description>

<author>M A. Bogue et al.</author>


</item>


<item>
<title>Hereditary haemolytic anaemias: unexpected sequelae of mutations in the genes for erythroid membrane skeletal proteins.</title>
<link>http://mouseion.jax.org/stfb2000_2009/944</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/944</guid>
<pubDate>Tue, 08 May 2012 20:16:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although the haemolytic anaemia may be the primary concern for hereditary spherocytosis and elliptocytosis patients, it is clear that their situation can be compromised by primary and secondary defects in erythroid and non-erythroid    systems of the body. All seven of the red cell membrane skeletal proteins discussed in this review are also expressed in non-erythroid tissues, and mutations in their genes have the potential to cause non-erythroid defects. In some instances,    such as the protein 4.1R and ANK1 neurological deficits, the diagnosis is clear. In other instances, because of the complex expression patterns involved, the non-erythroid effects may be difficult to assess. An example is the large multidomain,    multifunctional band 3 protein. In this case, the location of the mutation can cause defects in one functional domain or isoform and not the other. In other cases, such as the beta-adducin null mutation, other isoforms may partially compensate    for the primary deficiency. In such cases, it may be that the effects of the deficit are subtle but could increase under stress or with age. To be completely successful, treatment strategies must address both primary and secondary effects of the    anaemia.  If gene replacement therapy is to be used, the more that is known about the underlying genetic mechanisms producing the multiple isoforms the better we will be able to design the best replacement gene. The various animal models that are    now available should be invaluable in this regard.  They continue to contribute to our understanding of both the primary and the secondary effects and their treatment.</p>

	]]>
</description>

<author>C S. Birkenmeier et al.</author>


</item>


<item>
<title>Mouse model of Noonan syndrome reveals cell type- and gene dosage-dependent effects of Ptpn11 mutation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/943</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/943</guid>
<pubDate>Tue, 08 May 2012 20:16:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Noonan syndrome is a common human autosomal dominant birth defect, characterized by short stature, facial abnormalities, heart defects and possibly increased risk of leukemia. Mutations of Ptpn11 (also known as Shp2), which encodes    the protein-tyrosine phosphatase Shp2, occur in approximately 50% of individuals with Noonan syndrome, but their molecular, cellular and developmental effects, and the relationship between Noonan syndrome and leukemia, are unclear. We generated    mice expressing the Noonan syndrome-associated mutant D61G. When homozygous, the D61G mutant is embryonic lethal, whereas heterozygotes have decreased viability. Surviving Ptpn11(D61G/+) embryos ( approximately 50%) have short stature,    craniofacial abnormalities similar to those in Noonan syndrome, and myeloproliferative disease. Severely affected Ptpn11(D61G/+) embryos ( approximately 50%) have multiple cardiac defects similar to those in mice lacking the Ras-GAP protein    neurofibromin. Their endocardial cushions have increased Erk activation, but Erk hyperactivation is cell and pathway specific. Our results clarify the relationship between Noonan syndrome and leukemia and show that a single Ptpn11    gain-of-function mutation evokes all major features of Noonan syndrome by acting on multiple developmental lineages in a gene dosage-dependent and pathway-selective manner.</p>

	]]>
</description>

<author>T Araki et al.</author>


</item>


<item>
<title>The Gs-linked receptor GPR3 maintains meiotic arrest in mammalian oocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/942</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/942</guid>
<pubDate>Tue, 08 May 2012 20:15:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mammalian oocytes are held in prophase arrest by an unknown signal from the surrounding somatic cells. Here we show that the orphan Gs-linked receptor GPR3, which is localized in the oocyte, maintains this arrest.  Oocytes from Gpr3    knockout mice resume meiosis within antral follicles, independently of an increase in luteinizing hormone, and this phenotype can be reversed by injection of Gpr3 RNA into the oocytes. Thus, the GPR3 receptor is a link in communication between    the somatic cells and oocyte of the ovarian follicle and is crucial for the regulation of meiosis.</p>

	]]>
</description>

<author>L M. Mehlmann et al.</author>


</item>


<item>
<title>Serotonin induces tonic firing in layer V pyramidal neurons of rat prefrontal cortex during postnatal development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/941</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/941</guid>
<pubDate>Tue, 08 May 2012 20:15:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The effects of serotonin (5-HT) on neuronal activity were examined during postnatal development in layer V pyramidal neurons of the rat prefrontal cortex (PFC) in vitro. Whole-cell patch-clamp recordings were made in slices obtained    from rats aged between postnatal day (P) 6 and P31. In P14 or younger neurons, bath application of 5-HT (10 microM) induced a large depolarization followed by tonic firing at 2-5 Hz. The excitatory effects of 5-HT decreased rapidly after P14, so    that by P21, 5-HT produced a small depolarization or hyperpolarization without cell firing. The excitatory effects of 5-HT at younger ages were attributed to 5-HT2A receptors because the effects were mimicked by the 5-HT2 agonist    alpha-methyl-5-HT but not by the 5-HT3 agonist 1-(m-chlorophenyl)-biguanide, nor by the 5-HT2B/2C agonist 1-(3-chlorophenyl)piperazine, and were blocked by the 5-HT2A antagonists ketanserin and alpha-phenyl-1-(2-phenylethyl)-4-piperidinemethanol.    The excitatory responses persisted in 0 [Ca2+]o and high [Mg2+]o in the presence of TTX or blockers of ionotropic glutamate receptors, suggesting that the effects were mediated essentially by postsynaptic mechanisms. The responses to 5-HT involve    a reduction of K+ conductance and an enhancement of the hyperpolarization-activated Na+/K+ current. The developmental decline of 5-HT-induced excitatory effects was associated with a downregulation of 5-HT2A receptor function and a decrease in    the input resistance during early life. These results suggest that 5-HT is an important regulator of neuronal activity in the neonatal PFC and may play a role in activity-dependent developmental processes.</p>

	]]>
</description>

<author>Z W. Zhang</author>


</item>


<item>
<title>The heritability of antinociception: common pharmacogenetic mediation of five neurochemically distinct analgesics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/940</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/940</guid>
<pubDate>Tue, 08 May 2012 20:15:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>The heritability of nociception and antinociception has been well established in the mouse. The pharmacogenetics of morphine analgesia are fairly well characterized, but far less is known about other analgesics. The purpose of this    work was to begin the systematic genetic study of non-mu-opioid analgesics. We tested mice of 12 inbred mouse strains for baseline nociceptive sensitivity (49 degrees C tail-withdrawal assay) and subsequent antinociceptive sensitivity to systemic    administration of (trans)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]benzeneacetamide methane-sulfonate hydrate (U50,488; 10-150 mg/kg), a kappa-opioid receptor agonist;    (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzox azin-6-yl]-1-naphthalenylmethanone (WIN55,212-2; 0.5-480 mg/kg), a synthetic cannabinoid receptor agonist; epibatidine (7.5-150 microg/kg), a nicotinic receptor    agonist; clonidine (0.1-5 mg/kg), an alpha(2)-adrenergic receptor agonist; and, for purposes of comparison, the prototypic mu-opioid receptor agonist, morphine (5-200 mg/kg). Robust interstrain variability was observed in nociceptive sensitivity    and in the antinociceptive effects of each of the drugs, with extreme-responding strains exhibiting antinociceptive potencies differing up to 37-fold. Unexpectedly, we observed moderate-to-high genetic correlations of strain sensitivities to the    five drugs (r = 0.39-0.77). We also found moderate-to-high correlations between baseline nociceptive sensitivity and subsequent analgesic response to each drug (r = 0.33-0.68). The generalizability of these findings was established in follow-up    experiments investigating morphine and clonidine inhibition of formalin test nociception. Despite the fact that each drug activates a unique receptor, our results suggest that the potency of each drug is affected by a common set of genes.    However, the genes in question may affect antinociception indirectly, via a primary action on baseline nociceptive sensitivity.</p>

	]]>
</description>

<author>S G. Wilson et al.</author>


</item>


<item>
<title>The heritability of antinociception II: pharmacogenetic mediation of three over-the-counter analgesics in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/939</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/939</guid>
<pubDate>Tue, 08 May 2012 20:14:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chromosomal loci containing genes affecting antinociceptive sensitivity to morphine have been identified, but virtually nothing is known about the genetic mediation of sensitivity to over-the-counter analgesics. Such knowledge would    be of great clinical interest, as prodigious interindividual variability has been noted in the efficacy of these ubiquitously used drugs. In the present study, we assessed heritability and genetic correlations among three over-the-counter    analgesics in mice of 12 inbred mouse strains on the 0.9% acetic acid (i.p.)  writhing test. Analgesics included the centrally acting analgesic, acetaminophen (150 mg/kg, s.c.), and the nonsteroidal anti-inflammatory drugs (NSAIDs), indomethacin    (40 mg/kg, s.c.)  and lysine-acetylsalicylic acid (800 mg/kg, s.c.).  Significant strain differences in sensitivity to each of the drugs were observed, with narrow-sense heritability estimates ranging from 23 to 45%. Similar strains were    sensitive and resistant, respectively, to the two NSAIDs (r(s) = 0.64). In contrast, a completely different pattern of sensitivities was observed for acetaminophen, implying genetic dissociation (r(s) = 0.29 and 0.02) compared with the NSAIDs.    Additional experiments were performed on two strains, C57BL/6 and DBA/2, with extreme sensitivities to acetaminophen. Plasma acetaminophen levels in these strains were not significantly different during the time of antinociception assessment,    suggesting the existence of genetic factors affecting acetaminophen pharmacodynamics rather than pharmacokinetics.</p>

	]]>
</description>

<author>S G. Wilson et al.</author>


</item>


<item>
<title>The melanocortin-1 receptor gene mediates female-specific mechanisms of analgesia in mice and humans.</title>
<link>http://mouseion.jax.org/stfb2000_2009/938</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/938</guid>
<pubDate>Tue, 08 May 2012 20:14:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sex specificity of neural mechanisms modulating nociceptive information has been demonstrated in rodents, and these qualitative sex differences appear to be relevant to analgesia from kappa-opioid receptor agonists, a drug class    reported to be clinically effective only in women. Via quantitative trait locus mapping followed by a candidate gene strategy using both mutant mice and pharmacological tools, we now demonstrate that the melanocortin-1 receptor (Mc1r) gene    mediates kappa-opioid analgesia in female mice only. This finding suggested that individuals with variants of the human MC1R gene, associated in our species with red hair and fair skin, might also display altered kappa-opioid analgesia. We found    that women with two variant MC1R alleles displayed significantly greater analgesia from the kappa-opioid, pentazocine, than all other groups. This study demonstrates an unexpected role for the MC1R gene, verifies that pain modulation in the two    sexes involves neurochemically distinct substrates, and represents an example of a direct translation of a pharmacogenetic finding from mouse to human.</p>

	]]>
</description>

<author>J S. Mogil et al.</author>


</item>


<item>
<title>Genetic architecture of the mouse hippocampus: identification of gene loci with selective regional effects.</title>
<link>http://mouseion.jax.org/stfb2000_2009/937</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/937</guid>
<pubDate>Tue, 08 May 2012 20:13:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>We recently mapped two quantitative trait loci that have widespread effects on hippocampal architecture in mouse: Hipp1a and Hipp5a. We also noted remarkable strain differences in the relative sizes of different hippocampal regions.     Estimated heritable variation for these differences was 42% in hippocampus proper, 40% in dentate gyrus, 31% in granule cell layer and 18% in pyramidal cell layer. Region size varied at least 50% from largest to smallest measurement. Here we have    utilized these differences to identify loci with effects on the dentate gyrus, granule cell layer, hippocampus proper and pyramidal cell layer. Our sample consists of C57BL/6J and DBA/2J and 32 BXD recombinant inbred strains.  Volumetric data    were corrected for shrinkage and for differences in brain weight.  We identified significant loci on chromosomes (Chr) 6, 13 and 15, and a significant interaction locus on proximal Chr 11. A suggestive distal Chr 1 locus overlaps with Hipp1a.    HipV13a (Chr 13, 42-78Mb) has an additive effect of 0.56 mm3 (12.1%) on dentate gyrus volume, while GrV6a (Chr 6, 29-65 Mb) has additive effects of 0.14 mm3 (16.0%) on the volume of the granule cell layer. HipV13a also interacts with DGVi11a, a    locus on proximal Chr 11 that operates exclusively through its epistatic effect on HipV13a and has no independent main effect HipV15a (Chr 15, 0-51 Mb) has an additive effect of 1.76 mm3 (9.0%) on the volume of the hippocampus proper. We used    WebOTL, a recently described web-based tool, to examine genetic correlation of gene expression with hippocampal volume. We identified a number of genes that map within the OTL intervals and have highly correlated expression patterns. Using    WebQTL's extensive database of published BXD phenotypes, we also detected a strong and potentially biologically meaningful correlation between hippocampal volume and the acoustic startle response.</p>

	]]>
</description>

<author>J L. Peirce et al.</author>


</item>


<item>
<title>Genotype-dependence of gabapentin and pregabalin sensitivity: the pharmacogenetic mediation of analgesia is specific to the type of pain being inhibited.</title>
<link>http://mouseion.jax.org/stfb2000_2009/936</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/936</guid>
<pubDate>Tue, 08 May 2012 20:13:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>The antiepileptic drug, gabapentin, and another structurally related compound, pregabalin, are increasingly employed in the pharmacotherapy of chronic pain states, although their primary mechanism of action remains a topic of active    study. A genomic approach to the study of these drugs may elucidate their potentially novel mechanisms. We examined the heritability of sensitivity to analgesia from gabapentin and pregabalin as a precursor to linkage mapping efforts.    Accordingly, 11 inbred mouse strains were tested for inhibition of nociception by gabapentin or pregabalin (50-300 mg/kg, i.p.)  in two different preclinical assays of inflammatory pain, the formalin test (5% formalin; 20 microl) and zymosan    thermal hyperalgesia on the paw-withdrawal test (3 mg/ml zymosan; 20 microl). Significant strain-dependence of drug action was noted in each case, indicating that sensitivity to these analgesics is heritable.  Furthermore, the pattern of strain    sensitivities to gabapentin and pregabalin were mostly similar, supporting the notion that they act via similar genetic and physiological mechanisms. However, there was virtually no correlation between strain sensitivities to pregabalin    inhibition of formalin nociception and zymosan thermal hyperalgesia. In light of previous data from our laboratory and others regarding morphine analgesia, we now establish and empirically demonstrate the general principle that pharmacogenetic    mechanisms underlying analgesic sensitivity are specific to the type of pain being inhibited. This has considerable implications for ongoing pharmacogenetic investigations and, more generally, for the choices of preclinical models of pain used in    drug development.</p>

	]]>
</description>

<author>E J. Chesler et al.</author>


</item>


<item>
<title>Genetic correlates of gene expression in recombinant inbred strains: a relational model system to explore neurobehavioral phenotypes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/935</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/935</guid>
<pubDate>Tue, 08 May 2012 20:13:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Full genome sequencing, high-density genotyping, expanding sets of microarray assays, and systematic phenotyping of neuroanatomical and behavioral traits are producing a wealth of data on the mouse central nervous system (CNS).    These disparate resources are still poorly integrated. One solution is to acquire these data using a common reference population of isogenic lines of mice, providing a point of integration between the data types. Recombinant inbred (RI) mice,    derived through inbreeding of progeny from an inbred cross, are a powerful tool for complex trait mapping and analysis of the challenging phenotypes of neuroscientific interest. These isogenic RI lines are a retrievable genetic resource that can    be repeatedly studied using a wide variety of assays. Diverse data sets can be related through fixed and known genomes, using tools such as the interactive web-based system for complex trait analysis, www.WebQTL.org. In this report, we    demonstrate the use of WebQTL to explore complex interactions among a wide variety of traits--from mRNA transcripts to the impressive behavioral and pharmacological variation among RI strains. The relational approach exploiting a common set of    strains facilitates study of multiple effects of single genes (pleiotropy) without a priori hypotheses required. Here we demonstrate the power of this technique through genetic correlation of gene expression with a database of neurobehavioral    phenotypes collected in these strains of mice through more than 20 years of experimentation. By repeatedly studying the same panel of mice, early data can be re-examined in light of technological advances unforeseen at the time of their initial    collection.</p>

	]]>
</description>

<author>E J. Chesler et al.</author>


</item>


<item>
<title>p190RhoGAP can act to inhibit PDGF-induced gliomas in mice: a putative tumor suppressor encoded on human chromosome 19q13.3.</title>
<link>http://mouseion.jax.org/stfb2000_2009/934</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/934</guid>
<pubDate>Tue, 08 May 2012 20:12:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>p190RhoGAP and Rho are key regulators of oligodendrocyte differentiation. The gene encoding p190RhoGAP is located at 19q13.3 of the human chromosome, a locus that is deleted in 50%-80% of oligodendrogliomas. Here we provide evidence    that p190RhoGAP may suppress gliomagenesis by inducing a differentiated glial phenotype. Using a cell culture model of autocrine loop PDGF stimulation, we show that reduced Rho activity via p190RhoGAP overexpression or Rho kinase inhibition    induced cellular process extension, a block in proliferation, and reduced expression of the neural precursor marker nestin. In vivo infection of mice with retrovirus expressing PDGF and the p190 GAP domain caused a decreased incidence of    oligodendrogliomas compared with that observed with PDGF alone. Independent experiments revealed that the retroviral vector insertion site in 3 of 50 PDGF-induced gliomas was within the p190RhoGAP gene. This evidence strongly suggests that p190    regulates critical components of PDGF oncogenesis and can act as a tumor suppressor in PDGF-induced gliomas by down-regulating Rho activity.</p>

	]]>
</description>

<author>R M. Wolf et al.</author>


</item>


<item>
<title>Astrocyte differentiation states and glioma formation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/933</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/933</guid>
<pubDate>Tue, 08 May 2012 20:12:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gliomas are the most common primary malignancy in human central nervous system.  Many similarities in cell morphology and expression of markers exist between cancerous cells and normal undifferentiated progenitor cells. At the    molecular level, many important gene products are causally implicated in both the glial differentiation process and glial neoplasm formation. These observations raise the question of to what degree cell differentiation state influences glioma    formation. In this review, we discuss new insights into the parallels between glial differentiation and glioma formation as well as the potential application of differentiation-inducing therapy.</p>

	]]>
</description>

<author>C Dai et al.</author>


</item>


<item>
<title>Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing.</title>
<link>http://mouseion.jax.org/stfb2000_2009/932</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/932</guid>
<pubDate>Tue, 08 May 2012 20:12:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ataxia-telangiectasia (A-T) results from the loss of ataxia-telangiectasia mutated (Atm) function and is characterized by accelerated telomere loss, genomic instability, progressive neurological degeneration, premature ageing and    increased neoplasia incidence. Here we evaluate the functional interaction of Atm and telomeres in vivo. We examined the impact of Atm deficiency as a function of progressive telomere attrition at both the cellular and whole-organism level in    mice doubly null for Atm and the telomerase RNA component (Terc). These compound mutants showed increased telomere erosion and genomic instability, yet they experienced a substantial elimination of T-cell lymphomas associated with Atm deficiency.    A generalized proliferation defect was evident in all cell types and tissues examined, and this defect extended to tissue stem/progenitor cell compartments, thereby providing a basis for progressive multi-organ system compromise, accelerated    ageing and premature death. We show that Atm deficiency and telomere dysfunction act together to impair cellular and whole-organism viability, thus supporting the view that aspects of A-T pathophysiology are linked to the functional state of    telomeres and its adverse effects on stem/progenitor cell reserves.</p>

	]]>
</description>

<author>K K. Wong et al.</author>


</item>


<item>
<title>Patterning of the lateral ganglionic eminence by the Gsh1 and Gsh2 homeobox genes regulates striatal and olfactory bulb histogenesis and the growth of axons through the basal ganglia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/931</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/931</guid>
<pubDate>Tue, 08 May 2012 20:11:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>The function of the Gsh1 and Gsh2 homeobox transcription factors during development of the mouse telencephalon was studied using loss of function mutations. No telencephalic phenotype was observed in Gsh1 mutants, whereas Gsh2 and    Gsh1/2 mutants showed progressively more severe defects in development of neurons derived from the lateral ganglionic eminence (LGE). These defects arise from abnormal dorsoventral specification of LGE progenitor cells. Mice lacking both Gsh1 and    Gsh2 have severe hypoplasia of the striatum, olfactory tubercle, and interneurons that migrate from the dorsal LGE to the olfactory bulb. In addition, Gsh function is linked to the development of telencephalic dopaminergic neurons. These    observations show that Gsh1 and Gsh2 have early roles in defining the identity of LGE progenitor cells. As a result of the basal ganglia defects in the Gsh1/2 mutants, there are pallial heterotopia near the cortical/subcortical limit and defects    in the pathfinding of corticofugal and thalamocortical fibers. These findings highlight the developmental interdependence of adjacent telencephalic structures.</p>

	]]>
</description>

<author>K Yun et al.</author>


</item>


<item>
<title>Dlx transcription factors regulate differentiation of dopaminergic neurons of the ventral thalamus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/930</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/930</guid>
<pubDate>Tue, 08 May 2012 20:11:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recent studies have provided many lines of evidence that specific homeodomain factors act to regulate differentiation into specific neuron types. However, these studies have mainly focused on the caudal CNS, while in the forebrain,    the regulation of neuron specification remains relatively unknown. To investigate the genetic regulatory networks that control neuron differentiation in the forebrain, we have analyzed the expression patterns and functions of DLX homeodomain    factors in the ventral thalamus of early mouse embryos. During initial neurogenesis (E9.5-E10.5), DLX(+) cells are the first progenitors to make terminal divisions and differentiate as neurons. We have defined a set of regulatory genes    coexpressed with DLX, in both progenitors (PAX6 and MASH1) and in the differentiating neurons (PAX6, along with a combination of LIM-type homeodomain factors, including ISL1, Lhx1/Lim1, and Lhx5/Lim2). These initial neurons express tyrosine    hydroxylase (TH), and become the PAX6-expressing A13 dopaminergic neurons of the zona incerta.  To test for DLX function, the initial differentiation of the ventral thalamic neurons was examined in embryos mutant for Dlx1 and Dlx2. Dlx1/2 double    homozygous mutants formed ventral thalamic neurons, but these neurons lacked PAX6, ISL1, and TH expression. These data suggest that DLX genes act as forebrain-specific factors linking general neuron-inducing signals to region-specific neuron    differentiation programs.</p>

	]]>
</description>

<author>G L. Andrews et al.</author>


</item>


<item>
<title>Molecular control of the oocyte to embryo transition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/929</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/929</guid>
<pubDate>Tue, 08 May 2012 20:11:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>The elucidation of the molecular control of the initiation of mammalian embryogenesis is possible now that the transcriptomes of the full-grown oocyte and two-cell stage embryo have been prepared and analysed.  Functional annotation    of the transcriptomes using gene ontology vocabularies, allows comparison of the oocyte and two-cell stage embryo between themselves, and with all known mouse genes in the Mouse Genome Database. Using this methodology one can outline the general    distinguishing features of the oocyte and the two-cell stage embryo. This, when combined with oocyte-specific targeted deletion of genes, allows us to dissect the molecular networks at play as the differentiated oocyte and sperm transit into    blastomeres with unlimited developmental potential.</p>

	]]>
</description>

<author>B B. Knowles et al.</author>


</item>


<item>
<title>Genetic analysis of resistance to Type-1 Diabetes in ALR/Lt mice, a NOD-related strain with defenses against autoimmune-mediated diabetogenic stress.</title>
<link>http://mouseion.jax.org/stfb2000_2009/928</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/928</guid>
<pubDate>Tue, 08 May 2012 20:10:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>ALR mice are closely related to type-1 diabetes mellitus (T1DM)-prone NOD mice. The ALR genome confers systemically elevated free radical defenses, dominantly protecting their pancreatic islets from free radical generating toxins,    cytotoxic cytokines, and diabetogenic T cells. The ALR major histocompatibility complex (MHC) ( H2(gx) haplotype) is largely, but not completely identical with the NOD H2(g7) haplotype, sharing alleles from H2-K through the class II and distally    into the class III region. This same H2(gx) haplotype in the related CTS strain was linked to the Idd16 resistance locus. In the present study, ALR was outcrossed to NOD to fine map the Idd16 locus and establish chromosomal regions carrying other    ALR non-MHC-linked resistance loci. To this end, 120 (NODxALR)xNOD backcross progeny females were monitored for T1DM and genetic linkage analysis was performed on all progeny using 88 markers covering all chromosomes.  Glucosuria or end-stage    insulitis developed in 32 females, while 88 remained both aglucosuria and insulitis free. Three ALR-derived resistance loci segregated. As expected, one mapped to Chromosome 17, with peak linkage mapping just proximal to H2-K. A novel resistance    locus mapped to Chr 8. A pairwise scan for interactions detected a significant interaction between the loci on Chr 8 and Chr 17. On Chr 3, resistance segregated with a marker between previously described Idd loci and coinciding with an    independently mapped locus conferring a suppressed superoxide burst by ALR neutrophils (Susp). These results indicate that the Idd16 resistance allele, defined originally by linkage to the H2(gx) haplotype of CTS, is immediately proximal to H2-K.    Two additional ALR-contributed resistance loci may be ALR-specific and contribute to this strain's ability to dissipate free-radical stress.</p>

	]]>
</description>

<author>C E. Mathews et al.</author>


</item>


<item>
<title>Identification of quantitative trait loci for chemical/inflammatory nociception in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/927</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/927</guid>
<pubDate>Tue, 08 May 2012 20:10:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sensitivity to pain is widely variable, and much of this variability is genetic in origin. The specific genes responsible have begun to be identified, but only for thermal nociception. In order to facilitate the identification of    polymorphic, pain-related genes with more clinical relevance, we performed quantitative trait locus (QTL) mapping studies of the most common assay of inflammatory nociception, the formalin test. QTL mapping is a technique that exploits naturally    occurring variability among inbred strains for the identification of genomic locations containing genes contributing to that variability. An F2 intercross was constructed using inbred A/J and C57BL/6J mice as progenitors, strains previously shown    to display resistance and sensitivity, respectively, to formalin-induced nociception. Following phenotypic testing (5% formalin, 25 microl intraplantar injection), mice were genotyped at 90 microsatellite markers spanning the genome. We provide    evidence for two statistically significant formalin test QTLs - chromosomal regions whose inheritance is associated with trait variability - on distal mouse chromosomes 9 and 10. Identification of the genes underlying these QTLs may illuminate    the basis of individual differences in inflammatory pain, and lead to novel analgesic treatment strategies.</p>

	]]>
</description>

<author>S G. Wilson et al.</author>


</item>


<item>
<title>Influences of laboratory environment on behavior.</title>
<link>http://mouseion.jax.org/stfb2000_2009/926</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/926</guid>
<pubDate>Tue, 08 May 2012 20:09:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E J. Chesler et al.</author>


</item>


<item>
<title>Identification and ranking of genetic and laboratory environment factors influencing a behavioral trait, thermal nociception, via computational analysis of a large data archive.</title>
<link>http://mouseion.jax.org/stfb2000_2009/925</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/925</guid>
<pubDate>Tue, 08 May 2012 20:09:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Laboratory conditions in biobehavioral experiments are commonly assumed to be 'controlled', having little impact on the outcome. However, recent studies have illustrated that the laboratory environment has a robust effect on    behavioral traits. Given that environmental factors can interact with trait-relevant genes, some have questioned the reliability and generalizability of behavior genetic research designed to identify those genes. This problem might be alleviated    by the identification of the most relevant environmental factors, but the task is hindered by the large number of factors that typically vary between and within laboratories. We used a computational approach to retrospectively identify and rank    sources of variability in nociceptive responses as they occurred in a typical research laboratory over several years. A machine-learning algorithm was applied to an archival data set of 8034 independent observations of baseline thermal    nociceptive sensitivity. This analysis revealed that a factor even more important than mouse genotype was the experimenter performing the test, and that nociception can be affected by many additional laboratory factors including season/humidity,    cage density, time of day, sex and within-cage order of testing.  The results were confirmed by linear modeling in a subset of the data, and in confirmatory experiments, in which we were able to partition the variance of this complex trait among    genetic (27%), environmental (42%) and genetic x environmental (18%) sources.</p>

	]]>
</description>

<author>E J. Chesler et al.</author>


</item>


<item>
<title>Slug is a novel downstream target of MyoD. Temporal profiling in muscle regeneration.</title>
<link>http://mouseion.jax.org/stfb2000_2009/924</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/924</guid>
<pubDate>Tue, 08 May 2012 20:09:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Temporal expression profiling was utilized to define transcriptional regulatory pathways in vivo in a mouse muscle regeneration model. Potential downstream targets of MyoD were identified by temporal expression, promoter data base    mining, and gel shift assays; Slug and calpain 6 were identified as novel MyoD targets. Slug, a member of the snail/slug family of zinc finger transcriptional repressors critical for mesoderm/ectoderm development, was further shown to be a    downstream target by using promoter/reporter constructs and demonstration of defective muscle regeneration in Slug null mice.</p>

	]]>
</description>

<author>P Zhao et al.</author>


</item>


<item>
<title>Lack of association between adipose tissue distribution and IGF-1 and IGFBP-3 in men and women.</title>
<link>http://mouseion.jax.org/stfb2000_2009/923</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/923</guid>
<pubDate>Tue, 08 May 2012 20:08:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Insulin, insulin-like growth factor-1 (IGF-1), IGF binding protein-3 (IGFBP-3), and obesity, and in particular visceral obesity, are putative cancer risk factors. Little is known, however, about the relationship between IGFs and    obesity. We investigated the relationship between adipose tissue distribution and IGF-1 and IGFBP-3. Single-slice abdominal computed tomography scanning through the L4-L5 interspace was used to measure visceral adipose tissue (VAT) and    subcutaneous adipose tissue (SQAT) in 432 community-based subjects (267 men, 165 women; ages, 55-77), participating in a cancer screening trial. Insulin, IGF-1, IGFBP-3, and the ratio of IGF-1:IGFBP-3, measured by radioimmunoassay, were compared    with age, body mass index, absolute and relative VAT and SQAT, and total abdominal fat. We found that men had a higher mean IGF-1 (129.5 versus 108.9 ng/ml; P < 0.0001) and more VAT (201.5 cm(3) versus 166.6 cm(3); P < 0.0001) than women. In men    and women, there was no correlation between IGF-1, IGFBP-3, or the ratio of IGF-1:IGFBP-3 with body mass index, total fat, VAT or SQAT, or fasting insulin. In contrast, fasting insulin was highly correlated to all measures of obesity (P =    0.0001). We conclude that obesity, adipose tissue distribution, and in particular VAT are not correlated with IGF-1, IGFBP-3, or the molar ratio of IGF-1:IGFBP-3. The lack of association between obesity and the IGF-1 axis suggests that the IGF-1    axis is not a likely mediator between VAT and disease.</p>

	]]>
</description>

<author>R E. Schoen et al.</author>


</item>


<item>
<title>A p21-activated kinase-controlled metabolic switch up-regulates phagocyte NADPH oxidase.</title>
<link>http://mouseion.jax.org/stfb2000_2009/922</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/922</guid>
<pubDate>Tue, 08 May 2012 20:08:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chemoattractant-stimulated phagocytes increase their glucose uptake and divert energy production from glycolysis to the pentose phosphate pathway to generate NADPH. NADPH is a required cofactor for the NADPH oxidase to produce    reactive oxygen metabolites, an important microbicidal tool in host defense. p21-Activated kinases (Paks) are regulated by the GTPases Rac and Cdc42 and control actin dynamics and phosphorylation of the oxidase component p47(phox). Here we report    the interaction of Pak with phosphoglycerate mutase (PGAM)-B, an enzyme of the glycolytic pathway. Activated Pak1 inhibits glycolysis by association of its catalytic domain with PGAM-B and subsequent phosphorylation of the enzyme on serine    residues 23 and 118, thereby abolishing PGAM activity. Leukocyte activation through chemoattractant receptors leads to Pak activation and transient inhibition of endogenous PGAM-B activity. Consistent with these observations, treatment of    neutrophils with phosphoglycolic acid, a competitive PGAM-B inhibitor, increases upstream intermediates, thereby amplifying the respiratory burst. These results demonstrate that Rho GTPases regulate the glycolytic pathway through Pak and suggest    a link between chemoattractant signaling and metabolic responses to enhance host defense.</p>

	]]>
</description>

<author>Barak T. Shalom et al.</author>


</item>


<item>
<title>The subventricular zone: new molecular and cellular developments.</title>
<link>http://mouseion.jax.org/stfb2000_2009/921</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/921</guid>
<pubDate>Tue, 08 May 2012 20:08:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>The subventricular zone (SVZ), which lines the lateral walls of the lateral ventricle, persists as a neurogenic zone into adulthood and functions as the largest site of neurogenesis in the adult brain. In recent years, with the    acceptance of the concept of postembryonic mammalian neurogenesis, neurogenesis in the adult SVZ has been an area of active research. With the rapid accumulation of new information on the SVZ, some of which is contradictory, summarizing existing    knowledge on the SVZ and outlining future research directions in this area become important. In this review, we will cover recent molecular and cellular investigations that characterize the SVZ niche, SVZ neurogenesis, and SVZ cell migration    within the adult brain.</p>

	]]>
</description>

<author>J C. Conover et al.</author>


</item>


<item>
<title>Electronic tools to manage gene expression data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/920</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/920</guid>
<pubDate>Tue, 08 May 2012 20:07:55 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Begley DA, Ringwald M</author>


</item>


<item>
<title>MYC expression promotes the proliferation of neural progenitor cells in culture and in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/919</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/919</guid>
<pubDate>Tue, 08 May 2012 20:07:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Primitive neuroectodermal tumors (PNETs) are pediatric brain tumors that result from defects in signaling molecules governing the growth and differentiation of neural progenitor cells. We used the RCAS-TVA system to study the growth    effects of three genetic alterations implicated in human PNETs on a subset of neural progenitor cells that express the intermediate filament protein, nestin. The genetic alterations tested were: 1) overexpression of the cellular oncoprotein, MYC;    2) activation of transcription factor, beta-catenin; and 3) haploinsufficiency of Ptc, the hedgehog receptor gene. The RCAS-TVA system uses an avian retroviral vector, RCAS, to target gene expression to specific cell types in transgenic mice. To    express exogenous genes in neural progenitor cells, we used Ntv-a mice. In these mice, the Nestin gene promoter drives expression of TVA, the cell surface receptor for the virus. Ectopic expression of MYC, but not activated beta-catenin, promoted    the proliferation of neural progenitor cells in culture and in the cerebral leptomeninges in vivo. These effects were equally penetrant in mice with Ptc+/- and Ptc+/+ genetic backgrounds. Although overexpression of MYC is not sufficient to cause    intraparenchymal tumors, it may facilitate PNET formation by sustaining the growth of undifferentiated progenitor cells.</p>

	]]>
</description>

<author>D Fults et al.</author>


</item>


<item>
<title>Ink4a-Arf loss cooperates with KRas activation in astrocytes and neural progenitors to generate glioblastomas of various morphologies depending on activated Akt.</title>
<link>http://mouseion.jax.org/stfb2000_2009/918</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/918</guid>
<pubDate>Tue, 08 May 2012 20:07:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Deletion of the INK4a-ARF locus is found in the majority of human malignant gliomas. However, the role of INK4a-ARF loss in gliomagenesis is unclear. Animal modeling has shown that mice with targeted deletions in the Ink4a-Arf gene    do not develop spontaneous gliomas. We have previously reported that combined KRas and Akt signaling could induce glioblastoma (GBM) formation from neural progenitor cells but had no effect in differentiated astrocytes. In this investigation, we    have studied the effects of Ink4a-Arf loss on the formation of GBM induced by KRas and Akt gene transfer into neural progenitor cells and astrocytes. We show here that Ink4a-Arf deficiency allows for GBM formation from astrocytes and that it    enhances tumor incidence in neural progenitor cells. Furthermore, KRas alone can cooperate with deletion of the Ink4a-Arf locus in tumor formation from both neural progenitor cells and astrocytes. The resulting tumors were nestin positive and    resembled a spectrum of glioma morphologies ranging in astrocytic character depending on cell-of-origin and presence of activated Akt. Our data strongly supports the view that one role of loss of Ink4a-Arf in gliomagenesis could be to sensitize    astrocytes to transformation through dedifferentiation in response to the appropriate oncogenic stimuli.</p>

	]]>
</description>

<author>L Uhrbom et al.</author>


</item>


<item>
<title>The Gene Ontology (GO) project: structured vocabularies for molecular biology and their application to genome and expression analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/917</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/917</guid>
<pubDate>Tue, 08 May 2012 20:06:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Scientists wishing to utilize genomic data have quickly come to realize the benefit of standardizing descriptions of experimental procedures and results for computer-driven information retrieval systems. The focus of the Gene    Ontology project is three-fold. First, the project goal is to compile the Gene Ontologies; structured vocabularies describing domains of molecular biology. Second, the project supports the use of these structured vocabularies in the annotation of    gene products. Third, the gene product-to-GO annotation sets are provided by participating groups to the public through open access to the GO database and Web resource. This unit describes the current ontologies and what is beyond the scope of    the Gene Ontology project. It addresses the issue of how GO vocabularies are constructed and related to genes and gene products. It concludes with a discussion of how researchers can access, browse, and utilize the GO project in the course of    their own research.</p>

	]]>
</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title>Meiotic chromosome missegregation during apyrene meiosis in the gypsy moth, Lymantria dispar, is preceded by an aberrant prophase I.</title>
<link>http://mouseion.jax.org/stfb2000_2009/916</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/916</guid>
<pubDate>Tue, 08 May 2012 20:06:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The gypsy moth, Lymantria dispar, produces two structurally and genetically distinct types of spermatozoa. The eupyrene spermatozoa are genetically haploid and structurally typical. The apyrene spermatozoa are anucleate and    structurally different from eupyrene spermatozoa. To understand further the events contributing to meiotic chromosome missegregation in apyrene spermatocytes, we examined the progression of meiosis in these cells with respect to their eupyrene    counterparts. Chromosomal bouquet formation and fusion of nucleolar organizing regions are disrupted in apyrene nuclei. In addition, the chromatin of apyrene nuclei is prematurely and extremely condensed compared with that of eupyrene nuclei. An    antibody to the conserved synaptonemal complex protein 3 (SCP3) labeled eupyrene pachytene chromosomes, but not apyrene pachytene chromosomes. In addition, apyrene meiotic spindles are missing a subset of microtubules, which likely include    kinetochore microtubules. Because the condensation behavior of meiotic chromatin in apyrene spermatocytes deviates from that of eupyrene spermatocytes, we examined the appearance and distribution of the phosphorylated form of histone H3, but no    significant differences in histone H3 phosphorylation were found between apyrene and eupyrene spermatocytes. We argue that because a pachytene checkpoint is not initiated in apyrene spermatocytes, this system may provide a way to understand    better the underlying biochemical connections between pairing, recombination, synapsis, kinetochore assembly and segregation of chromosomes during meiosis in a higher eukaryote.</p>

	]]>
</description>

<author>L G. Reinholdt et al.</author>


</item>


<item>
<title>Female Characters as Role Models in Young Adult Literature</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1526</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1526</guid>
<pubDate>Tue, 08 May 2012 20:06:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Julia S. Stamper</author>


</item>


<item>
<title>Reduced growth of human sarcoma xenografts in hosts homozygous for the lit mutation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/915</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/915</guid>
<pubDate>Tue, 08 May 2012 20:06:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND AND OBJECTIVES: Prior studies have shown that sarcoma growth can be stimulated by insulin-like growth factor-I (IGF-I). To extend this line of research, we carried out in vivo growth studies of primary human sarcoma in    immunosuppressed control and IGF-I-deficient mice. METHODS: Human sarcoma specimens (one osteosarcoma and seven soft tissue sarcomas) were harvested in the operating room and implanted in immunosuppressed mice. Second-generation sarcomas were    transplanted to control (GH replete lit/+ mice) and to experimental (GH/IGF-I-deficient lit/lit) animals. When tumors reached 1,000 mm(3) in one group, average tumor size was compared in the two groups. IGF-I receptor expression was measured by    RT-PCR and IGF-I receptor binding sites were assayed by radiolabeled IGF-I. RESULTS: Five of eight sarcomas demonstrated reduced growth in the GH/IGF-I-deficient lit/lit animals. In four of the five sarcomas that demonstrated growth inhibition,    IGF-R was elevated relative to placenta or a positive control cell line (MCF-7, which is known to be responsive to IGF-I in vitro and in vivo). In three of the five sarcomas that demonstrated growth suppression, IGF-R was elevated twofold after    implantation in the experimental IGF-I-deficient animals. CONCLUSIONS: The GH-IGF axis may be an important stimulator of tumor growth in sarcomas. These experiments suggest that IGF suppression may inhibit sarcoma growth in vivo.</p>

	]]>
</description>

<author>K Deitel et al.</author>


</item>


<item>
<title>Effect of social status on social defeat-induced neural activation in the dorsal raphe nucleus</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1525</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1525</guid>
<pubDate>Tue, 08 May 2012 20:06:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Danielle M. Gerhard et al.</author>


</item>


<item>
<title>Lith genes control mucin accumulation, cholesterol crystallization, and gallstone formation in A/J and AKR/J inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/914</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/914</guid>
<pubDate>Tue, 08 May 2012 20:05:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>We recently identified 2 Lith genes that determine cholesterol gallstone formation in C57L/J inbred mice, which show a gallstone prevalence of approximately 80% on feeding 1.0% cholesterol and 0.5% cholic acid. The aim of this study    was to explore if the same Lith loci contribute to the variation in gallstone susceptibility in a new experimental cross. After 12 weeks of feeding the lithogenic diet to inbred mice of strains A/J and AKR/J as well as their F(1) progeny, we used    microscopy of bile to assess mucin accumulation, crystallization pathways, and stone formation. Backcross progeny (n = 225) were phenotyped and genotyped selectively for microsatellite markers spanning the genome.  Quantitative trait loci (QTL)    affecting gallstone phenotypes were identified by linkage analysis. Both inbred strains showed accumulation of mucin gel and cholesterol supersaturation. However, only strain AKR developed gallstones (prevalence of 20%), whereas strain A showed a    stable liquid crystalline state and no stones. QTL analysis identified a gallstone locus on chromosome 17 (Lith3). A second gene locus on chromosome 15 that controls mucin accumulation harbors the mucin gene Glycam1, which was shown to be    expressed in gallbladder epithelia by immunohistochemistry. Gallstone and mucin loci colocalized with potential QTLs affecting the formation of cholesterol crystals. In conclusion, QTL analysis identified specific gene loci determining mucin    accumulation, cholesterol crystallization, and gallstone formation. Characterization of the pathophysiologic roles of Lith3 and the new biliary mucin gene Glycam1 might provide insights into primary defects of human cholelithiasis and lead to new    therapeutic strategies for prestone intervention.</p>

	]]>
</description>

<author>F Lammert et al.</author>


</item>


<item>
<title>Mountain Dew&apos;s Brand Personality</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1524</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1524</guid>
<pubDate>Tue, 08 May 2012 20:05:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Cara Nicole Hollenbeck</author>


</item>


<item>
<title>Exploring Moroccan Identities: The Tension between Traditional and Modern Cuisine in an Urban Context</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1523</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1523</guid>
<pubDate>Tue, 08 May 2012 20:05:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Miriam R. Dike</author>


</item>


<item>
<title>Lipid metabolome-wide effects of the PPARgamma agonist rosiglitazone.</title>
<link>http://mouseion.jax.org/stfb2000_2009/913</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/913</guid>
<pubDate>Tue, 08 May 2012 20:05:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Successful therapy for chronic diseases must normalize a targeted aspect of metabolism without disrupting the regulation of other metabolic pathways essential for maintaining health. Use of a limited number of single molecule    surrogates for disease, or biomarkers, to monitor the efficacy of a therapy may fail to predict undesirable side effects. In this study, a comprehensive metabolomic assessment of lipid metabolites was employed to determine the specific effects of    the peroxisome proliferator-activated receptor gamma (PPARgamma) agonist rosiglitazone on structural lipid metabolism in a new mouse model of Type 2 diabetes. Dietary supplementation with rosiglitazone (200 mg/kg diet) suppressed Type 2 diabetes    in obese (NZO x NON)F1 male mice, but chronic treatment markedly exacerbated hepatic steatosis. The metabolomic data revealed that rosiglitazone i) induced hypolipidemia (by dysregulating liver-plasma lipid exchange), ii) induced de novo fatty    acid synthesis, iii) decreased the biosynthesis of lipids within the peroxisome, iv) substantially altered free fatty acid and cardiolipin metabolism in heart, and v) elicited an unusual accumulation of polyunsaturated fatty acids within adipose    tissue. These observations suggest that the phenotypes induced by rosiglitazone are mediated by multiple tissue-specific metabolic variables. Because many of the effects of rosiglitazone on tissue metabolism were reflected in the plasma lipid    metabolome, metabolomics has excellent potential for developing clinical assessments of metabolic response to drug therapy.</p>

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</description>

<author>S M. Watkins et al.</author>


</item>


<item>
<title>Africa: The Next Frontier</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1522</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1522</guid>
<pubDate>Tue, 08 May 2012 20:05:06 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Jack A. Parker</author>


</item>


<item>
<title>Ahl2, a second locus affecting age-related hearing loss in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/912</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/912</guid>
<pubDate>Tue, 08 May 2012 20:04:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inbred mouse strains with age-related hearing loss (AHL) provide valuable models for studying the genetic basis of human presbycusis. Here we report the genetic mapping of a second AHL locus in mice (designated Ahl2) that is a major    contributor to the 8- to 10-month difference in hearing loss onset times between NOD/LtJ and C57BL/6J mice. A whole-genome linkage scan of 110 progeny from a (C57BL/6JxNOD/LtJ)xNOD/LtJ backcross revealed statistically significant associations of    ABR thresholds with markers on chromosome 5, with a peak lod score of 5.5 for D5Mit309. At 6 months of age, backcross progeny that inherited two copies of the recessive NOD/LtJ-derived allele at this locus (genotype ahl2/ahl2) exhibited ABR    thresholds that were on average 26 decibels above those of heterozygous mice. Analysis of a (CAST/EixNOD/LtJ)xNOD/LtJ backcross, which segregates strain-specific alleles at both Ahl2 and the Ahl locus on chromosome 10, showed that the hearing    loss attributable to Ahl2 is dependent on a predisposing Ahl genotype. The statistically significant effect of Ahl2 observed in crosses with NOD/LtJ was not seen in crosses involving three other strains with early onset AHL: A/J, BUB/BnJ, and    SKH2/J.</p>

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</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title>The Impact of the Patient Protection and Affordable Care Act on Middle-sized Businesses</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1521</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1521</guid>
<pubDate>Tue, 08 May 2012 20:04:47 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Charles R. Edwards</author>


</item>


<item>
<title>The human and mouse replication-dependent histone genes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/911</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/911</guid>
<pubDate>Tue, 08 May 2012 20:04:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The multigene family encoding the five classes of replication-dependent histones has been identified from the human and mouse genome sequence. The large cluster of histone genes, HIST1, on human chromosome 6 (6p21-p22) contains 55    histone genes, and Hist1 on mouse chromosome 13 contains 51 histone genes. There are two smaller clusters on human chromosome 1: HIST2 (at 1q21), which contains six genes, and HIST3 (at 1q42), which contains three histone genes. Orthologous Hist2    and Hist3 clusters are present on mouse chromosomes 3 and 11, respectively. The organization of the human and mouse histone genes in the HIST1 cluster is essentially identical. All of the histone H1 genes are in HIST1, which is spread over about    2 Mb. There are two large gaps (>250 kb each) within this cluster where there are no histone genes, but many other genes. Each of the histone genes encodes an mRNA that ends in a stemloop followed by a purine-rich region that is complementary to    the 5' end of U7 snRNA. In addition to the histone genes on these clusters, only two other genes containing the stem-loop sequence were identified, a histone H4 gene on human chromosome 12 (mouse chromosome 6) and the previously described H2a.X    gene located on human chromosome 11. Each of the 14 histone H4 genes encodes the same protein, and there are only three histone H3 proteins encoded by the 12 histone H3 genes in each species. In contrast, both the mouse and human H2a and H2b    proteins consist of at least 10 non-allelic variants, making the complexity of the histone protein complement significantly greater than previously thought.</p>

	]]>
</description>

<author>W F. Marzluff et al.</author>


</item>


<item>
<title>A Historical Analysis of the Portrayal of Teens in Popular Literature:  The Chronicles of Narnia and Harry Potter</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1520</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1520</guid>
<pubDate>Tue, 08 May 2012 20:04:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Susan F. Gregory</author>


</item>


<item>
<title>Spent Nuclear Fuel Storage in a Molten Salt Pool</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1519</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1519</guid>
<pubDate>Tue, 08 May 2012 20:04:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Chelsea Burnham et al.</author>


</item>


<item>
<title>Comparative genetics of atherosclerosis and restenosis: exploration with mouse models.</title>
<link>http://mouseion.jax.org/stfb2000_2009/910</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/910</guid>
<pubDate>Tue, 08 May 2012 20:04:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>X Wang et al.</author>


</item>


<item>
<title>Perceived Interpersonal Support as Protective Factors for Adolescent Depressive Symptoms</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1518</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1518</guid>
<pubDate>Tue, 08 May 2012 20:03:50 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Richard D. Gibson</author>


</item>


<item>
<title>Cell movements during gastrulation: snail dependent and independent pathways.</title>
<link>http://mouseion.jax.org/stfb2000_2009/909</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/909</guid>
<pubDate>Tue, 08 May 2012 20:03:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The morphogenetic process of gastrulation requires multiple inputs and intricate coordination. Genetic analyses demonstrate critical roles of vertebrate and invertebrate Snail proteins in this process. Together with other regulatory    molecules including Wnt and BMP, the Snail pathways specify cell fate and reorganize cellular machineries to coordinate morphological changes and cell movements during gastrulation.</p>

	]]>
</description>

<author>Y T. Ip et al.</author>


</item>


<item>
<title>Reclaiming Identity: White Street Pier, Key West</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1517</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1517</guid>
<pubDate>Tue, 08 May 2012 20:03:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Adam H. Richards</author>


</item>


<item>
<title>Ahl2, a second locus affecting age-related hearing loss in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/908</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/908</guid>
<pubDate>Tue, 08 May 2012 20:03:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inbred mouse strains with age-related hearing loss (AHL) provide valuable models for studying the genetic basis of human presbycusis. Here we report the genetic mapping of a second AHL locus in mice (designated Ahl2) that is a major    contributor to the 8- to 10-month difference in hearing loss onset times between NOD/LtJ and C57BL/6J mice. A whole-genome linkage scan of 110 progeny from a (C57BL/6JxNOD/LtJ)xNOD/LtJ backcross revealed statistically significant associations of    ABR thresholds with markers on chromosome 5, with a peak lod score of 5.5 for D5Mit309. At 6 months of age, backcross progeny that inherited two copies of the recessive NOD/LtJ-derived allele at this locus (genotype ahl2/ahl2) exhibited ABR    thresholds that were on average 26 decibels above those of heterozygous mice. Analysis of a (CAST/EixNOD/LtJ)xNOD/LtJ backcross, which segregates strain-specific alleles at both Ahl2 and the Ahl locus on chromosome 10, showed that the hearing    loss attributable to Ahl2 is dependent on a predisposing Ahl genotype. The statistically significant effect of Ahl2 observed in crosses with NOD/LtJ was not seen in crosses involving three other strains with early onset AHL: A/J, BUB/BnJ, and    SKH2/J.</p>

	]]>
</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title>Powerful Hermeneutics: British Readings of Hindu Texts and Concepts in Late Eighteenth-Century Bengal</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1516</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1516</guid>
<pubDate>Tue, 08 May 2012 20:03:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>David Fredrickson Burman</author>


</item>


<item>
<title>Computational Studies of the N2-H2 Interaction-Induced Dipole Moment</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1515</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1515</guid>
<pubDate>Tue, 08 May 2012 20:02:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Hailey R. Bureau</author>


</item>


<item>
<title>Functional and comparative genomic analysis of the piebald deletion region of mouse chromosome 14.</title>
<link>http://mouseion.jax.org/stfb2000_2009/907</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/907</guid>
<pubDate>Tue, 08 May 2012 20:02:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Several developmentally important genomic regions map within the piebald deletion complex on distal mouse chromosome 14. We have combined computational gene prediction and comparative sequence analysis to characterize an    approximately 4.3-Mb segment of the piebald region to identify candidate genes for the phenotypes presented by homozygous deletion mice. As a result we have ordered 13 deletion breakpoints, integrated the sequence with markers from a bacterial    artificial chromosome (BAC) physical map, and identified 16 known or predicted genes and >1500 conserved sequence elements (CSEs) across the region. The candidate genes identified include Phr1 (formerly Pam) and Spry2, which are mouse homologs of    genes required for development in Drosophila melanogaster. Gene content, order, and position are highly conserved between mouse chromosome 14 and the orthologous region of human chromosome 13. Our studies combining computational gene prediction    with genetic and comparative genomic analyses provide insight regarding the functional composition and organization of this defined chromosomal region.</p>

	]]>
</description>

<author>K A. Peterson et al.</author>


</item>


<item>
<title>Orderly ε-Homotopies of Discrete Chains</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1514</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1514</guid>
<pubDate>Tue, 08 May 2012 20:02:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alexander Thomas Happ</author>


</item>


<item>
<title>Gonadal differentiation, sex determination and normal Sry expression in mice require direct interaction between transcription partners GATA4 and FOG2.</title>
<link>http://mouseion.jax.org/stfb2000_2009/906</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/906</guid>
<pubDate>Tue, 08 May 2012 20:02:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>In mammals, Sry expression in the bipotential, undifferentiated gonad directs the support cell precursors to differentiate as Sertoli cells, thus initiating the testis differentiation pathway. In the absence of Sry, or if Sry is    expressed at insufficient levels, the support cell precursors differentiate as granulosa cells, thus initiating the ovarian pathway. The molecular mechanisms upstream and downstream of Sry are not well understood. We demonstrate that the    transcription factor GATA4 and its co-factor FOG2 are required for gonadal differentiation. Mouse fetuses homozygous for a null allele of Fog2 or homozygous for a targeted mutation in Gata4 (Gata4(ki)) that abrogates the interaction of GATA4 with    FOG co-factors exhibit abnormalities in gonadogenesis. We found that Sry transcript levels were significantly reduced in XY Fog2(-/-) gonads at E11.5, which is the time when Sry expression normally reaches its peak. In addition, three genes    crucial for normal Sertoli cell function (Sox9, Mis and Dhh) and three Leydig cell steroid biosynthetic enzymes (p450scc, 3betaHSD and p450c17) were not expressed in XY Fog2(-/-) and Gata(ki/ki) gonads, whereas Wnt4, a gene required for normal    ovarian development, was expressed ectopically. By contrast, Wt1 and Sf1, which are expressed prior to Sry and necessary for gonad development in both sexes, were expressed normally in both types of mutant XY gonads. These results indicate that    GATA4 and FOG2 and their physical interaction are required for normal gonadal development.</p>

	]]>
</description>

<author>S G. Tevosian et al.</author>


</item>


<item>
<title>The Physiological and Psychological Connection: The Body’s Response to Ceased Exercise from Athletic Injury</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1513</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1513</guid>
<pubDate>Tue, 08 May 2012 20:02:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Patricia Rotella Ligon</author>


</item>


<item>
<title>Quantitative trait loci and candidate genes regulating HDL cholesterol: a murine chromosome map.</title>
<link>http://mouseion.jax.org/stfb2000_2009/905</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/905</guid>
<pubDate>Tue, 08 May 2012 20:02:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: Summarizing the many discovered mouse and human quantitative trait loci (QTL) for high density lipoprotein (HDL) cholesterol (HDL-C) levels is important for guiding future research on the genetic regulation of HDL    concentrations and for finding gene targets for upregulating HDL levels in mice and humans. METHODS AND RESULTS: We summarized the 27 QTL and candidate genes associated with HDL-C concentrations in mice and plotted them on a mouse chromosome map.    We also summarized the 22 human QTL for HDL-C levels and compared them with those of the mouse by comparative genomics. At least part of the mouse homologies for 18 of the 22 human HDL-C QTL were within the murine HDL-C QTL. CONCLUSIONS: Murine    QTL for HDL-C levels may predict their homologous location in humans, and their underlying genes may be appropriate genes to test in humans.</p>

	]]>
</description>

<author>X Wang et al.</author>


</item>


<item>
<title>Viral Online Content and the College Market Using RateMyProfessors.com and HowsTheLiving.com as Case Studies</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1512</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1512</guid>
<pubDate>Tue, 08 May 2012 20:01:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Aeron L. Glover</author>


</item>


<item>
<title>Exploring Nutrition in the Community: The Effects of Nutrition Education</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1511</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1511</guid>
<pubDate>Tue, 08 May 2012 20:01:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Andrew Brendan Harrison</author>


</item>


<item>
<title>Genetic and environmental context determines the course of colitis developing in IL-10-deficient mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/904</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/904</guid>
<pubDate>Tue, 08 May 2012 20:01:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>This review summarizes how interleukin-10 (IL-10)-deficient mice have permitted new insight into the complex interaction between genes and environment underlying pathogenesis of inflammatory bowel disease (IBD).  The C57BL/6J strain    develops only mild typhlocolitis in response to IL-10 deficiency. In contrast, C3H/HeJBir represents an unrelated inbred strain with high IBD susceptibility. Ability to identify quantitative trait loci segregating for susceptibility when the two    IL-10-deficient stocks were intercrossed depended both on genome "context" (F2 versus reciprocal backcrosses) and on the physical environment. These findings are discussed in the context of recent advances in understanding the complex genetic    basis for IBD in humans.</p>

	]]>
</description>

<author>M Mahler et al.</author>


</item>


<item>
<title>Vowel Perception in Normal and Hearing Impaired Listeners</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1510</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1510</guid>
<pubDate>Tue, 08 May 2012 20:01:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Lauren Charles</author>


</item>


<item>
<title>The immunogenomics of minor histocompatibility antigens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/903</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/903</guid>
<pubDate>Tue, 08 May 2012 20:01:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Minor histocompatibility (H) antigens are a diverse assemblage of major histocompatibility complex (MHC)-bound peptides with the unifying property of acting as alloantigens that induce allogeneic tissue rejection. They are a    consequence of any form of accumulated genetic variation that translates to differential MHC-presented peptide epitopes, the most common form of which is simple sequence polymorphisms. The universe of potential minor H antigens is large when    transplantation is performed between genetically unrelated, MHC-matched individuals, especially considering the remarkable discriminative sensitivity of T cells. However, the phenomenon of immunodominance greatly simplifies immune responses that    ensue. One mouse minor H antigen, H60, stands out in that the preponderance of the CD8 T cell response elicited in a complex alloantigenic setting is directed against this single minor H antigen epitope. Its immunodominance is because mice    lacking H60 develop an unusually robust T cell repertoire dedicated to this single minor H antigen. The now well-characterized mouse minor H antigen system should provide a vehicle to assess the degree to which immunodominant alloantigens    contribute to transplant rejection.</p>

	]]>
</description>

<author>D Roopenian et al.</author>


</item>


<item>
<title>Investigating the Flexibility of Intrinsically Disordered Proteins in Folding and Binding</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1509</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1509</guid>
<pubDate>Tue, 08 May 2012 20:00:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Amanda Leilah Debuhr</author>


</item>


<item>
<title>Optimizing detection of QTLs retarding aging: choice of statistical model and animal requirements.</title>
<link>http://mouseion.jax.org/stfb2000_2009/902</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/902</guid>
<pubDate>Tue, 08 May 2012 20:00:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Quantitative trait locus (QTL) analysis makes no assumptions about the identity of genes involved in regulating aging. Moreover, it may be used as the first step in identifying such genes and, thus QTL analysis may be instrumental    in formulating new hypotheses about aging. Genetic experiments, however, require hundreds to thousands of animals and are very expensive in mammals. Statistical power to detect longevity genes could be improved by excluding accidental, unrelated    to aging mortality.  While many early deaths are probably accidental, excluding early mortality altogether eliminates the age-related component, too. We used computer simulations to assess the effect of excluding early age-related, mortality on    the statistical power of several common tests, such as t-test, Mann-Whitney and chi(2). Surprisingly, even the age-related, Gompertz component of early mortality reduces the statistical power of the t- and Mann-Whitney tests. For example, in a    backcross design, to detect a gene slowing down the rate of aging and increasing mouse life span by 10% (P=0.0001; power=0.8), a regular t-test will require 640 mice, all kept for the entire life span and genotyped. If life spans of only 25% of    the longest-lived animals from each of the two groups, carrying a putative longevity allele and not carrying it, are compared, population size can be reduced by two-fold, to about 300, and genotyping by seven-fold, to 90.  Confirming simulation    results, the significance of the effect of caloric restriction on life span increased from P=3.4x10(-5) to 1.1x10(-7), when life spans of only 40% of the longest-lived mice from each of the two groups, ad libitum fed and calorie restricted, were    compared. Finally, finding the optimal combination of statistical test, the number of phenotyped and the number of genotyped animals, which would minimize experimental costs was addressed.</p>

	]]>
</description>

<author>S Klebanov et al.</author>


</item>


<item>
<title>Reported Experience of Maltreatment in Adolescents Whose Mothers Have Borderline Personality Disorder</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1508</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1508</guid>
<pubDate>Tue, 08 May 2012 20:00:42 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Chelsea R. Ennis</author>


</item>


<item>
<title>A System for Cooling Nuclear Spent Fuel using Fluidized Bed Technology</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1507</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1507</guid>
<pubDate>Tue, 08 May 2012 20:00:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ian J. Miller</author>


</item>


<item>
<title>Intercellular communication in the mammalian ovary: oocytes carry the conversation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/901</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/901</guid>
<pubDate>Tue, 08 May 2012 20:00:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>The production of functional female gametes is essential for the propagation of all vertebrate species. The growth of oocytes within ovarian follicles and their development to mature eggs have fascinated biologists for centuries,    and scientists have long realized the importance of the ovarian follicle's somatic cells in nurturing oogenesis and delivering the oocyte to the oviduct by ovulation. Recent studies have revealed key roles of the oocyte in folliculogenesis and    established that bidirectional communication between the oocyte and companion somatic cells is essential for development of an egg competent to undergo fertilization and embryogenesis. The challenge for the future is to identify the factors that    participate in this communication and their mechanisms of action.</p>

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</description>

<author>M M. Matzuk et al.</author>


</item>


<item>
<title>Untapped Revenue:  Smartphones, A Smart Move for the Music Industry</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1506</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1506</guid>
<pubDate>Tue, 08 May 2012 20:00:01 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Hunter David Ripley</author>


</item>


<item>
<title>Lunatic fringe, FGF, and BMP regulate the Notch pathway during epithelial morphogenesis of teeth.</title>
<link>http://mouseion.jax.org/stfb2000_2009/900</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/900</guid>
<pubDate>Tue, 08 May 2012 19:59:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Teeth develop as epithelial appendages, and their morphogenesis is regulated by epithelial-mesenchymal interactions and conserved signaling pathways common to many developmental processes. A key event during tooth morphogenesis is    the transition from bud to cap stage when the epithelial bud is divided into specific compartments distinguished by morphology as well as gene expression patterns. The enamel knot, a signaling center, forms and regulates the shape and size of the    tooth. Mesenchymal signals are necessary for epithelial patterning and for the formation and maintenance of the epithelial compartments. We studied the expression of Notch pathway molecules during the bud-to-cap stage transition of the developing    mouse tooth. Lunatic fringe expression was restricted to the epithelium, where it formed a boundary flanking the enamel knot. The Lunatic fringe expression domains overlapped only partly with the expression of Notch1 and Notch2, which were    coexpressed with Hes1. We examined the regulation of Lunatic fringe and Hes1 in cultured explants of dental epithelium. The expression of Lunatic fringe and Hes1 depended on mesenchymal signals and both were positively regulated by FGF-10. BMP-4    antagonized the stimulatory effect of FGF-10 on Lunatic fringe expression but had a synergistic effect with FGF-10 on Hes1 expression. Recombinant Lunatic fringe protein induced Hes1 expression in the dental epithelium, suggesting that Lunatic    fringe can act also extracellularly. Lunatic fringe mutant mice did not reveal tooth abnormalities, and no changes were observed in the expression patterns of other Fringe genes. We conclude that Lunatic fringe may play a role in boundary    formation of the enamel knot and that Notch-signaling in the dental epithelium is regulated by mesenchymal FGFs and BMP.</p>

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</description>

<author>T Mustonen et al.</author>


</item>


<item>
<title>The Role of Nonprofit Microfinance Institutions in Alleviating Poverty: From Theory to Practice</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1505</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1505</guid>
<pubDate>Tue, 08 May 2012 19:59:44 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Leah Rebecca Oldham</author>


</item>


<item>
<title>The Impact of Cultural Distances on the Country Selection Process</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1504</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1504</guid>
<pubDate>Tue, 08 May 2012 19:59:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan M. Blizzard</author>


</item>


<item>
<title>The human and mouse replication-dependent histone genes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/899</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/899</guid>
<pubDate>Tue, 08 May 2012 19:59:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The multigene family encoding the five classes of replication-dependent histones has been identified from the human and mouse genome sequence. The large cluster of histone genes, HIST1, on human chromosome 6 (6p21-p22) contains 55    histone genes, and Hist1 on mouse chromosome 13 contains 51 histone genes. There are two smaller clusters on human chromosome 1: HIST2 (at 1q21), which contains six genes, and HIST3 (at 1q42), which contains three histone genes. Orthologous Hist2    and Hist3 clusters are present on mouse chromosomes 3 and 11, respectively. The organization of the human and mouse histone genes in the HIST1 cluster is essentially identical. All of the histone H1 genes are in HIST1, which is spread over about    2 Mb.  There are two large gaps (>250 kb each) within this cluster where there are no histone genes, but many other genes. Each of the histone genes encodes an mRNA that ends in a stemloop followed by a purine-rich region that is complementary to    the 5' end of U7 snRNA. In addition to the histone genes on these clusters, only two other genes containing the stem-loop sequence were identified, a histone H4 gene on human chromosome 12 (mouse chromosome 6) and the previously described H2a.X    gene located on human chromosome 11. Each of the 14 histone H4 genes encodes the same protein, and there are only three histone H3 proteins encoded by the 12 histone H3 genes in each species. In contrast, both the mouse and human H2a and H2b    proteins consist of at least 10 non-allelic variants, making the complexity of the histone protein complement significantly greater than previously thought.</p>

	]]>
</description>

<author>W F. Marzluff et al.</author>


</item>


<item>
<title>Modeling insertional mutagenesis using gene length and expression in murine embryonic stem cells</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1036</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1036</guid>
<pubDate>Tue, 08 May 2012 19:59:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alex S. Nord et al.</author>


</item>


<item>
<title>A Survey of Mission Opportunities to Trans-Neptunian Objects – Part II</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1503</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1503</guid>
<pubDate>Tue, 08 May 2012 19:59:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ashley M. Gleaves</author>


</item>


<item>
<title>Mammalian septins nomenclature.</title>
<link>http://mouseion.jax.org/stfb2000_2009/898</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/898</guid>
<pubDate>Tue, 08 May 2012 19:59:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>There are 10 known mammalian septin genes, some of which produce multiple splice variants. The current nomenclature for the genes and gene products is very confusing, with several different names having been given to the same gene    product and distinct names given to splice variants of the same gene. Moreover, some names are based on those of yeast or Drosophila septins that are not the closest homologues. Therefore, we suggest that the mammalian septin field adopt a common    nomenclature system, based on that adopted by the Mouse Genomic Nomenclature Committee and accepted by the Human Genome Organization Gene Nomenclature Committee. The human and mouse septin genes will be named SEPT1-SEPT10 and Sept1-Sept10,    respectively. Splice variants will be designated by an underscore followed by a lowercase "v" and a number, e.g., SEPT4_v1.</p>

	]]>
</description>

<author>I G. Macara et al.</author>


</item>


<item>
<title>Stabilization of beta-catenin induces lesions reminiscent of prostatic intraepithelial neoplasia, but terminal squamous transdifferentiation of other secretory epithelia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/897</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/897</guid>
<pubDate>Tue, 08 May 2012 19:58:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The present study documents that stabilization of beta-catenin is sufficient to induce lesions reminiscent of prostate intraepithelial neoplasia (PIN). Such lesions were present in all compound mutant mice and all prostate acini    expressing stabilized beta-catenin. High grade PIN-like lesions resembling early human prostate cancer were detected as early as 10 weeks of age. Surprisingly, stabilization of beta-catenin in other secretory epithelia including salivary,    preputial, harderian, and mammary glands induced extensive squamous metaplasia and keratinization associated with terminal differentiation of the target cells, but failed to cause neoplastic transformation. Epidermal hyperplasia, hair follicle    cysts, and odontomas were also observed. The prostatic lesions exhibited upregulation of c-myc, increased rate of cellular proliferation, loss of the Na-K-Cl co-transporter NKCC1, and expression of androgen receptor. Basal cell markers such as    p63 and keratin 5 were not expressed by the masses of PIN-like lesions, but were present in small foci of proliferating beta-catenin expressing basal cells. Our observations indicate that beta-catenin stabilization is a crucial event for the    initiation of PIN-like lesions, but induces squamous metaplasia rather than tumorigenesis in secretory epithelia other than the prostate.</p>

	]]>
</description>

<author>F Gounari et al.</author>


</item>


<item>
<title>Genetic modification of retinal degeneration in tubby mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/896</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/896</guid>
<pubDate>Tue, 08 May 2012 19:58:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice that carry the recessive mutation tub develop neurosensory defects including retinal and cochlear degeneration, as well as maturity-onset obesity associated with insulin resistance. The biological function of the gene and the    mechanism by which it induces its phenotypes are still unclear. In order to elucidate the pathways through which tub functions, in the current study, QTL modifiers were identified in an F2 intercross between (C57BL/6J- tub/tub and AKR/J-+/+) F1    hybrids (AKR intercross). The thickness of the outer nuclear layer of the retina and the number of photoreceptor nuclei were assessed in F2 mice homozygous for the tub mutation. A genome-wide scan revealed a significant linkage on chromosome 11    (named motr1) and two suggestive linkages on chromosomes 2 and 8.  Interestingly, the same chromosome 2 region identified for the hearing modifier of tubby, the moth1 locus, showed a peak lod score of 2.3 for protection from retinal degeneration.    This result suggests that the gene responsible for the QTL on chromosome 2 might be involved in a common pathway through which retinal and cochlear degeneration are induced in tubby mice.</p>

	]]>
</description>

<author>A Ikeda et al.</author>


</item>


<item>
<title>Leptin promotes biliary cholesterol elimination during weight loss in ob/ob mice by regulating the enterohepatic circulation of bile salts.</title>
<link>http://mouseion.jax.org/stfb2000_2009/895</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/895</guid>
<pubDate>Tue, 08 May 2012 19:57:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Leptin administration to obese C57BL/6J (ob/ob) mice results in weight loss by reducing body fat. Because adipose tissue is an important storage depot for cholesterol, we explored evidence that leptin-induced weight loss in ob/ob    mice was accompanied by transport of cholesterol to the liver and its elimination via bile. Consistent with mobilization of stored cholesterol, cholesterol concentrations in adipose tissue remained unchanged during weight loss. Plasma cholesterol    levels fell sharply, and microscopic analyses of gallbladder bile revealed cholesterol crystals as well as cholesterol gallstones. Surprisingly, leptin reduced biliary cholesterol secretion rates without affecting secretion rates of bile salts or    phospholipids. Instead, cholesterol supersaturation of gallbladder bile was due to marked decreases in bile salt hydrophobicity and not to hypersecretion of biliary cholesterol per se, such as occurs in humans during weight loss. In addition to    regulating bile salt composition, leptin treatment decreased bile salt pool size. The smaller, more hydrophilic bile salt pool was associated with substantial decreases in intestinal cholesterol absorption. Within the liver, leptin treatment    reduced the activity of 3-hydroxy-3-methylglutaryl-CoA reductase, but it did not change activities of cholesterol 7alpha-hydroxylase or acyl-CoA:cholesterol acyltransferase. These data suggest that leptin regulates biliary lipid metabolism to    promote efficient elimination of excess cholesterol stored in adipose tissue. Cholesterol gallstone formation during weight loss in ob/ob mice appears to represent a pathologic consequence of an adaptive response that prevents absorption of    biliary and dietary cholesterol.</p>

	]]>
</description>

<author>H Hyogo et al.</author>


</item>


<item>
<title>The diabetes-prone NZO/HlLt strain. I. Immunophenotypic comparison to the related NZB/BlNJ and NZW/LacJ strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/894</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/894</guid>
<pubDate>Tue, 08 May 2012 19:57:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>New Zealand Obese (NZO)/HlLt male mice exhibit a polygenic obesity and approximately 50% develop type 2 diabetes. This strain is known to produce a variety of autoantibodies, including autoantibodies to the insulin receptor. Because    of their relatedness to the autoimmune-predisposed New Zealand Black (NZB) and New Zealand White (NZW) inbred strains, we compared NZO to its two related strains for shared hematologic and immunologic characteristics. Comparison of the three    strains by serotyping and genotyping methods indicated that NZO shared with NZW the rare (recombinant) H2(z) haplotype at the major histocompatibility complex.  Similar to the NZB and NZW strains, spleens from NZO mice contained increased numbers    of CD19(+)CD43(+) IgM(+) B-1 B cells, a phenotype associated with natural autoantibody production. NZO mice developed a progressive microcytic anemia that was distinguished from NZB hemolytic anemia by absence of demonstrable antierythrocyte    antibodies in the former. Outcross of NZO females with NZB males accelerated development of obesity and diabetes in F1 males. NZO males made B-lymphocyte-deficient by a disrupted immunoglobulin heavy chain gene did not become diabetic. These    results suggest that NZO mice should be useful to investigators interested in studying the genetic contributions to autoimmunity made by the related NZW and NZB strains. Further, these results, combined with the pancreatic histopathology    contained in the companion manuscript, suggest that B lymphocytes may be important contributors to diabetes pathogenesis in the NZO mouse.</p>

	]]>
</description>

<author>B D. Haskell et al.</author>


</item>


<item>
<title>The diabetes-prone NZO/Hl strain. II. Pancreatic immunopathology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/893</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/893</guid>
<pubDate>Tue, 08 May 2012 19:57:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>We report the first combined light and electron microscopic analysis of the pancreas during the development of type 2 diabetes in the New Zealand Obese (NZO) mouse. As in most other polygenic rodent models of type 2 diabetes,    hyperglycemia associated with beta cell destruction is male sex-limited. Increasing degrees of hyperinsulinemia and transition to diabetes were clearly reflected by the islet volume fraction, by the beta cell granulation state, and by    ultrastructural changes, primarily of the endoplasmic reticulum. One of the unusual histopathologic features of NZO mice of both sexes was the presence of B-lymphocyte enriched leukocytic aggregates in the pancreas. Immunocytochemical analysis of    the pancreas of 52-week-old diabetic males indicated enrichment for CD19(+) B lymphocytes.  Staining of adjacent sections for CD3 and CD5 indicated CD5 coexpression on some of the CD19(+) cells, suggesting the presence of the B1-B subset    associated with generation of natural autoantibodies in other autoimmune-prone New Zealand mouse strains. In addition, plasma cells in peri-insular leukocytic infiltrates were identified by electron microscopy. Hence, although autoimmunity has    previously proven to be a secondary manifestation of beta cell destruction in most rodent models of type 2 diabetes, the present observations suggest that B lymphocyte function, in association with male gender, may contribute to the development    of insulin resistance and chronic hyperglycemia in the NZO model.</p>

	]]>
</description>

<author>E Junger et al.</author>


</item>


<item>
<title>Novel vertebrate genes and putative regulatory elements identified at kidney disease and NR2E1/fierce loci.</title>
<link>http://mouseion.jax.org/stfb2000_2009/892</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/892</guid>
<pubDate>Tue, 08 May 2012 19:56:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fierce (frc) mice are deleted for nuclear receptor 2e1 (Nr2e1), and exhibit cerebral hypoplasia, blindness, and extreme aggression. To characterize the Nr2e1 locus, which may also contain the mouse kidney disease (kd) allele, we    compared sequence from human, mouse, and the puffer fish Fugu rubripes. We identified a novel gene, c222389, containing conserved elements in noncoding regions. We also discovered a novel vertebrate gene conserved across its length in prokaryotes    and invertebrates. Based on a dramatic upregulation in lactating breast, we named this gene lactation elevated-1 (LACE1). Two separate 100-bp elements within the first NR2E1 intron were virtually identical between the three species, despite an    estimated 450 million years of divergent evolution.  These elements represent strong candidates for functional NR2E1 regulatory elements in vertebrates. A high degree of conservation across NR2E1 combined with a lack of interspersed repeats    suggests that an array of regulatory elements embedded within the gene is required for proper gene expression.</p>

	]]>
</description>

<author>B S. Abrahams et al.</author>


</item>


<item>
<title>Cholesterol gallstone formation in overweight mice establishes that obesity per se is not linked directly to cholelithiasis risk.</title>
<link>http://mouseion.jax.org/stfb2000_2009/891</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/891</guid>
<pubDate>Tue, 08 May 2012 19:56:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>The relationship between obesity and cholesterol cholelithiasis is not well understood at physiologic or genetic levels. To clarify whether obesity per se leads to increased prevalence of cholelithiasis, we examined cholesterol    gallstone susceptibility in three polygenic (KK/H1J, NON/LtJ, NOD/LtJ) and five monogenic [carboxypeptidase E (Cpe (fat)), agouti yellow (A(y)), tubby (tub), leptin (Lep(ob)), leptin receptor (Lepr (db))] murine models of obesity during ingestion    of a lithogenic diet containing dairy fat, cholesterol, and cholic acid. At 8 weeks on the diet, one strain of polygenic obese mice was resistant whereas the others revealed low or intermediate prevalence rates of cholelithiasis. Monogenic obese    mice showed distinct patterns with either high or low gallstone prevalence rates depending upon the mutation. Dysfunction of the leptin axis, as evidenced by the Lep(ob) and the Lepr (db) mutations, markedly reduced gallstone formation in a    genetically susceptible background strain, indicating that in mice with this genetic background, physiologic leptin homeostasis is a requisite for cholesterol cholelithogenesis. In contrast, the Cpe (fat) mutation enhanced the prevalence of    cholelithiasis markedly when compared with the background strain. Since CPE converts many prohormones to hormones, a deficiency of biologically active cholecystokinin is a likely contributor to enhanced susceptibility to cholelithiasis through    compromising gallbladder contractility and small intestinal motility. Because some murine models of obesity increased, whereas others decreased cholesterol gallstone susceptibility, we establish that cholesterol cholelithiasis in mice is not    simply a secondary consequence of obesity per se. Rather, specific genes and distinct pathophysiological pathways are responsible for the shared susceptibility to both of these common diseases.</p>

	]]>
</description>

<author>G Bouchard et al.</author>


</item>


<item>
<title>Insulin-like growth factor I is required for the anabolic actions of parathyroid hormone on mouse bone.</title>
<link>http://mouseion.jax.org/stfb2000_2009/890</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/890</guid>
<pubDate>Tue, 08 May 2012 19:55:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Parathyroid hormone (PTH) is a potent anabolic agent for bone, but the mechanism(s) by which it works remains imperfectly understood. Previous studies have indicated that PTH stimulates insulin-like growth factor (IGF) I production,    but it remains uncertain whether IGF-I mediates some or all of the skeletal actions of PTH. To address this question, we examined the skeletal response to PTH in IGF-I-deficient (knockout [k/o]) mice. These mice and their normal littermates    (NLMs) were given daily injections of PTH (80 microg/kg) or vehicle for 2 weeks after which their tibias were examined for fat-free weight (FFW), bone mineral content, bone structure, and bone formation rate (BFR), and their femurs were assessed    for mRNA levels of osteoblast differentiation markers. In wild-type mice, PTH increased FFW, periosteal BFR, and cortical thickness (C.Th) of the proximal tibia while reducing trabecular bone volume (BV); these responses were not seen in the k/o    mice. The k/o mice had normal mRNA levels of the PTH receptor and increased mRNA levels of the IGF-I receptor but markedly reduced basal mRNA levels of the osteoblast markers. Surprisingly, these mRNAs in the k/o bones increased several-fold more    in response to PTH than the mRNAs in the bones from their wild-type littermates. These results indicate that IGF-I is required for the anabolic actions of PTH on bone formation, but the defect lies distal to the initial response of the osteoblast    to PTH.</p>

	]]>
</description>

<author>D D. Bikle et al.</author>


</item>


<item>
<title>Craniosynostosis in Twist heterozygous mice: a model for Saethre-Chotzen syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/889</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/889</guid>
<pubDate>Tue, 08 May 2012 19:55:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Saethre-Chotzen syndrome is a common autosomal dominant form of craniosynostosis, the premature fusion of the sutures of the calvarial bones of the skull. Most Saethre-Chotzen syndrome cases are caused by haploinsufficiency for the    TWIST gene. Mice heterozygous for a null mutation of the Twist gene replicate certain features of Saethre-Chotzen syndrome, but have not been reported to exhibit craniosynostosis. We demonstrate that Twist heterozygous mice exhibit fusions of the    coronal suture and other cranial suture abnormalities, indicating that Twist heterozygous mice constitute a better animal model for Saethre-Chotzen syndrome than was previously appreciated.</p>

	]]>
</description>

<author>E A. Carver et al.</author>


</item>


<item>
<title>A compendium of mouse knockouts with inner ear defects.</title>
<link>http://mouseion.jax.org/stfb2000_2009/888</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/888</guid>
<pubDate>Tue, 08 May 2012 19:55:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetically engineered strains of mice, modified by gene targeting (knockouts), are increasingly being employed as alternative effective research tools in elucidating the genetic basis of human deafness. An impressive array of    auditory and vestibular mouse knockouts is already available as a valuable resource for studying the ontogenesis, morphogenesis and function of the mammalian inner ear. This article provides a current catalog of mouse knockouts with inner ear    morphogenetic malformations and hearing or balance deficits resulting from ablation of genes that are regionally expressed in the inner ear and/or within surrounding tissues, such as the hindbrain, neural crest and mesenchyme.</p>

	]]>
</description>

<author>A V. Anagnostopoulos</author>


</item>


<item>
<title>The Snell dwarf mutation Pit1(dw) can increase life span in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/887</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/887</guid>
<pubDate>Tue, 08 May 2012 19:54:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Over the past 30 years, the Snell dwarf mutation (Pit1(dw)) has been reported to shorten, to have no effect on, or to increase life span in various colonies; however, few details of these disparate results have been published. We    now report that mean, median, and maximum life spans are increased by 40-50% for Snell dwarf (Pit1(dw)/Pit1(dw)) DW/J females, and 25-50% for dwarf DWC3F1 males and females with the compound heterozygous Pit1(dw)/Pit1(dw-J) genotype. We    previously observed aspects of delayed senescence in Snell dwarf (Pit1(dw)/Pit1(dw)) DW/J males; however, their median life span was shortened by about 25% (Genetic Effects on Aging II, 1990, The Telford Press, Caldwell, NJ, pp. 435-456).  This    short life span was not an intrinsic effect of the mutation, but a consequence of housing male dwarfs with normal-sized male littermates; our present results demonstrate that Snell dwarf males attain very long life spans when housed with    normal-sized females. We conclude that the dwarf mutation interacts with environmental factors to alter life spans and, probably, rates of ageing, over an extremely broad range. We propose that this variation in the effect of the Snell dwarf    mutation results from a tradeoff between physical vigor and life span that is mediated by pituitary hormones, and that growth hormone, thyroid hormone, and possibly prolactin regulate mechanisms that schedule mortality in mammals.</p>

	]]>
</description>

<author>K Flurkey et al.</author>


</item>


<item>
<title>A reduced peripheral blood CD4(+) lymphocyte proportion is a consistent ageing phenotype.</title>
<link>http://mouseion.jax.org/stfb2000_2009/886</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/886</guid>
<pubDate>Tue, 08 May 2012 19:54:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Peripheral blood leukocyte composition was measured in young, middle-aged and old C57BL/6J (B6) and BALB/cByJ (BALB) mice by flow cytometry to test the hypothesis that ageing is associated with declines in the proportions of    peripheral blood T lymphocytes. In both B6 and BALB mice, increasing age is associated with a significant and continuous decline in the proportions of CD4(+) lymphocytes, a moderate decline in the proportion of CD8(+) lymphocytes, a significant    increase in the proportion of Gr1(+) granulocytes and an almost unchanged proportion of B lymphocytes. As expected, the proportion of CD44(low) naive T lymphocytes decreased with age. Expression of Fas (CD95(+)) on CD4(+) and CD8(+) lymphocytes    showed no consistent change with age. We also measured peripheral blood CD4(+) and CD8(+) lymphocyte proportions in young and old A/J, CBA/CaJ, DBA/2J, DW/J and (DWxC3H) F1 mice. The CD4(+) lymphocyte proportion decreased from young to old age in    these strains by 56,65,72,78 and 68%, respectively.  The CD8(+) lymphocyte proportion decreased moderately with age in all the inbred strains tested but not in the (DWxC3H) F1 hybrid. Thus, a reduced proportion of peripheral blood CD4(+)    lymphocytes is a consistent ageing phenotype in a wide range of Mus musculus strains.</p>

	]]>
</description>

<author>J Chen et al.</author>


</item>


<item>
<title>Annotation of human chromosome 21 for relevance to Down syndrome: gene structure and expression analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/885</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/885</guid>
<pubDate>Tue, 08 May 2012 19:54:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Down syndrome is caused by an extra copy of human chromosome 21 and the resultant dosage-related overexpression of genes contained within it. To efficiently direct experiments to determine specific gene-phenotype correlations, it is    necessary to identify all genes within 21q and assess their functional associations and expression patterns. Analysis of the complete finished sequence of 21q resulted in annotated 225 genes and gene models, most of which were incomplete and/or    had little or no experimental verification. Here we correct or complete the genomic structures of 16 genes, 4 of which were not reported in the annotation of the complete sequence. Our data include the identification of six genes encoding short    or ambiguous open reading frames; the identification of three cases in which alternative splicing produces two structurally unrelated protein sequences; and the identification of six genes encoding proteins with functional motifs, two genes with    unusually low similarity to their orthologous mouse proteins, and four genes with significant conservation in Drosophila melanogaster. We further demonstrate that an additional nine gene models represent bona fide transcripts and develop    expression patterns for these genes plus nine additional novel chromosome 21 genes and four paralogous genes mapping elsewhere in the human genome. These data have implications for generating complete transcript maps of chromosome 21 and for the    entire human genome, and for defining expression abnormalities in Down syndrome and mouse models.</p>

	]]>
</description>

<author>K Gardiner et al.</author>


</item>


<item>
<title>The family of toxin-related ecto-ADP-ribosyltransferases in humans and the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/884</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/884</guid>
<pubDate>Tue, 08 May 2012 19:53:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>ADP-ribosyltransferases including toxins secreted by Vibrio cholera, Pseudomonas aerurginosa, and other pathogenic bacteria inactivate the function of human target proteins by attaching ADP-ribose onto a critical amino acid residue.    Cross-species polymerase chain reaction (PCR) and database mining identified the orthologs of these ADP-ribosylating toxins in humans and the mouse. The human genome contains four functional toxin-related ADP-ribosyltransferase genes (ARTs) and    two related intron-containing pseudogenes; the mouse has six functional orthologs. The human and mouse ART genes map to chromosomal regions with conserved linkage synteny. The individual ART genes reveal highly restricted expression patterns,    which are largely conserved in humans and the mouse.  We confirmed the predicted extracellular location of the ART proteins by expressing recombinant ARTs in insect cells. Two human and four mouse ARTs contain the active site motif (R-S-EXE)    typical of arginine-specific ADP-ribosyltransferases and exhibit the predicted enzyme activities. Two other human ARTs and their murine orthologues deviate in the active site motif and lack detectable enzyme activity. Conceivably, these ARTs may    have acquired a new specificity or function. The position-sensitive iterative database search program PSI-BLAST connected the mammalian ARTs with most known bacterial ADP-ribosylating toxins. In contrast, no related open reading frames occur in    the four completed genomes of lower eucaryotes (yeast, worm, fly, and mustard weed). Interestingly, these organisms also lack genes for ADP-ribosylhydrolases, the enzymes that reverse protein ADP-ribosylation. This suggests that the two enzyme    families that catalyze reversible mono-ADP-ribosylation either were lost from the genomes of these nonchordata eucaryotes or were subject to horizontal gene transfer between kingdoms.</p>

	]]>
</description>

<author>G Glowacki et al.</author>


</item>


<item>
<title>Meta-analyses of therapies for postmenopausal osteoporosis. IX: Summary of meta-analyses of therapies for postmenopausal osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/883</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/883</guid>
<pubDate>Tue, 08 May 2012 19:53:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>This section summarizes the results of the seven systematic reviews of osteoporosis therapies published in this series [calcium, vitamin D, hormone replacement therapy (HRT), alendronate, risedronate, raloxifene, and calcitonin] and    systematic reviews of etidronate and fluoride we have published elsewhere. We highlight the methodological strengths and weaknesses of the individual studies, and summarize the effects of treatments on the risk of vertebral and nonvertebral    fractures and on bone density, including effects in different patient subgroups. We provide an estimate of the expected impact of antiosteoporosis interventions in prevention and treatment populations using the number needed to treat (NNT) as a    reference. In addition to the evidence, judgements about the relative weight that one places on weaker and stronger evidence, attitudes toward uncertainty, circumstances of patients' and societal values or preferences will, and should, play an    important role in decision-making regarding anti-osteoporosis therapy.</p>

	]]>
</description>

<author>A Cranney et al.</author>


</item>


<item>
<title>Translational repression by MSY4 inhibits spermatid differentiation in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/882</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/882</guid>
<pubDate>Tue, 08 May 2012 19:53:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>In developing male germ cells, newly synthesized protamine mRNAs are stored for up to 7 days before translational activation. Translational repression of protamine 1 (Prm1) mRNA requires sequences present in its 3' untranslated    region (UTR) and substantial evidence suggests a role for the murine Y-box protein MSY4 in this process. To determine if MSY4 can mediate translational repression in vivo, we generated transgenic mice in which the temporal window of MSY4    expression was extended during spermatogenesis. Expression of MSY4 disrupted the normal completion of spermatogenesis and caused dominant sterility. Immunocytochemical analysis of several markers, including the protamines, indicated that MSY4    prevented normal activation of translation. mRNAs whose translation was inhibited contained at least one MSY4 RNA recognition site, suggesting sequence-dependent translational repression. Altered translational activation resulted in defective    processing of protamine 2 and severe defects in sperm morphogenesis. These results suggest that MSY4 plays an active role in translational repression of several mRNAs in differentiating spermatids.</p>

	]]>
</description>

<author>F Giorgini et al.</author>


</item>


<item>
<title>Modulation of the notch signaling by Mash1 and Dlx1/2 regulates sequential specification and differentiation of progenitor cell types in the subcortical telencephalon.</title>
<link>http://mouseion.jax.org/stfb2000_2009/881</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/881</guid>
<pubDate>Tue, 08 May 2012 19:52:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Notch signaling has a central role in cell fate specification and differentiation. We provide evidence that the Mash1 (bHLH) and Dlx1 and Dlx2 (homeobox) transcription factors have complementary roles in regulating Notch signaling,    which in turn mediates the temporal control of subcortical telencephalic neurogenesis in mice. We defined progressively more mature subcortical progenitors (P1, P2 and P3) through their combinatorial expression of MASH1 and DLX2, as well as the    expression of proliferative and postmitotic cell markers at E10.5-E11.5. In the absence of Mash1, Notch signaling is greatly reduced and 'early' VZ progenitors (P1 and P2) precociously acquire SVZ progenitor (P3) properties. Comparing the    molecular phenotypes of the delta-like 1 and Mash1 mutants, suggests that Mash1 regulates early neurogenesis through Notch-and Delta-dependent and -independent mechanisms. While Mash1 is required for early neurogenesis (E10.5), Dlx1 and Dlx2 are    required to downregulate Notch signaling during specification and differentiation steps of 'late' progenitors (P3). We suggest that alternate cell fate choices in the developing telencephalon are controlled by coordinated functions of bHLH and    homeobox transcription factors through their differential affects on Notch signaling.</p>

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</description>

<author>K Yun et al.</author>


</item>


<item>
<title>The early topography of thalamocortical projections is shifted in Ebf1 and Dlx1/2 mutant mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/880</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/880</guid>
<pubDate>Tue, 08 May 2012 19:52:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The prevailing model to explain the formation of topographic projections in the nervous system stipulates that this process is governed by information located within the projecting and targeted structures. In mammals, different    thalamic nuclei establish highly ordered projections with specific neocortical domains and the mechanisms controlling the initial topography of these projections remain to be characterized. To address this issue, we examined Ebf1(-/-) embryos in    which a subset of thalamic axons does not reach the neocortex. We show that the projections that do form between thalamic nuclei and neocortical domains have a shifted topography, in the absence of regionalization defects in the thalamus or    neocortex. This shift is first detected inside the basal ganglia, a structure on the path of thalamic axons, and which develops abnormally in Ebf1(-/-) embryos. A similar shift in the topography of thalamocortical axons inside the basal ganglia    and neocortex was observed in Dlx1/2(-/-) embryos, which also have an abnormal basal ganglia development. Furthermore, Dlx1 and Dlx2 are not expressed in the dorsal thalamus or in cortical projections neurons. Thus, our study shows that: (1)    different thalamic nuclei do not establish projections independently of each other; (2) a shift in thalamocortical topography can occur in the absence of major regionalization defects in the dorsal thalamus and neocortex; and (3) the basal    ganglia may contain decision points for thalamic axons' pathfinding and topographic organization. These observations suggest that the topography of thalamocortical projections is not strictly determined by cues located within the neocortex and    may be regulated by the relative positioning of thalamic axons inside the basal ganglia.</p>

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</description>

<author>S Garel et al.</author>


</item>


<item>
<title>A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9.</title>
<link>http://mouseion.jax.org/stfb2000_2009/879</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/879</guid>
<pubDate>Tue, 08 May 2012 19:52:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Constitutive activation of tyrosine kinases, such as the BCR/ABL fusion associated with t(9;22)(q34;q22), is a hallmark of chronic myeloid leukemia (CML) syndromes in humans. Expression of BCR/ABL is both necessary and sufficient to    cause a chronic myeloproliferative syndrome in murine bone marrow transplantation models, and absolutely depends on kinase activity. Progression of CML to acute leukemia (blast crisis) in humans has been associated with acquisition of secondary    chromosomal translocations, including the t(7;11)(p15;p15) resulting in the NUP98/HOXA9 fusion protein. We demonstrate that BCR/ABL cooperates with NUP98/HOXA9 to cause blast crisis in a murine model. The phenotype depends both on expression of    BCR/ABL and NUP98/HOXA9, but tumors retain sensitivity to the ABL inhibitor STI571 in vitro and in vivo. This paradigm is applicable to other constitutively activated tyrosine kinases such as TEL/PDGFbetaR. These experiments document cooperative    effects between constitutively activated tyrosine kinases, which confer proliferative and survival properties to hematopoietic cells, with mutations that impair differentiation, such as the NUP98/HOXA9, giving rise to the acute myeloid leukemia    (AML) phenotype. Furthermore, these data indicate that despite acquisition of additional mutations, CML blast crisis cells retain their dependence on BCR/ABL for proliferation and survival.</p>

	]]>
</description>

<author>A B. Dash et al.</author>


</item>


<item>
<title>Critical role for Gab2 in transformation by BCR/ABL.</title>
<link>http://mouseion.jax.org/stfb2000_2009/878</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/878</guid>
<pubDate>Tue, 08 May 2012 19:51:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>The BCR/ABL oncogene causes chronic myelogenous leukemia (CML) in humans and a CML-like disease, as well as lymphoid leukemia, in mice. p210 BCR/ABL is an activated tyrosine kinase that phosphorylates itself and several cellular    signaling proteins. The autophosphorylation site tyrosine 177 binds the adaptor Grb2 and helps determine the lineage and severity of BCR/ABL disease: Tyr177 mutation (BCR/ABL-Y177F) dramatically impairs myeloid leukemogenesis, while diminishing    lymphoid leukemogenesis. The critical signal(s) from Tyr177 has remained unclear. We report that Tyr177 recruits the scaffolding adaptor Gab2 via a Grb2/Gab2 complex. Compared to BCR/ABL-expressing Ba/F3 cells, BCR/ABL-Y177F cells exhibit    markedly reduced Gab2 tyrosine phosphorylation and association of phosphatidylinositol-3 kinase (PI3K) and Shp2 with Gab2 and BCR/ABL, and decreased PI3K/Akt and Ras/Erk activation, cell proliferation, and spontaneous migration. Remarkably, bone    marrow myeloid progenitors from Gab2 (-/-) mice are resistant to transformation by BCR/ABL, whereas lymphoid transformation is diminished as a consequence of markedly increased apoptosis. BCR/ABL-evoked PI3K/Akt and Ras/Erk activation also are    impaired in Gab2 (-/-) primary myeloid and lymphoid cells. Our results identify Gab2 and its associated proteins as key determinants of the lineage and severity of BCR/ABL transformation.</p>

	]]>
</description>

<author>M Sattler et al.</author>


</item>


<item>
<title>Epithelial-mesenchymal transitions and cancer</title>
<link>http://mouseion.jax.org/stfb2000_2009/877</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/877</guid>
<pubDate>Tue, 08 May 2012 19:51:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E A, Gridley Carver</author>


</item>


<item>
<title>Mitotic chromosome preparations from mouse cells for karyotyping.</title>
<link>http://mouseion.jax.org/stfb2000_2009/876</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/876</guid>
<pubDate>Tue, 08 May 2012 19:51:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>This unit contains protocols for the preparation of mitotic chromosomes from mouse peripheral blood, Giemsa banding of those chromosomes, and classification into a karyotype, including recognition of some common pitfalls of    misidentification and information for determining aberrant chromosomes. The methods described can be used to identify visible chromosomal rearrangements and their precise cytological breakpoints in the living mouse. In conjunction with    fluorescent in situ hybridization (FISH), the metaphase spreads can also be used for the linear placement of loci on a chromosome and for determining the insertion site(s) of a foreign transgene.</p>

	]]>
</description>

<author>E C. Akeson et al.</author>


</item>


<item>
<title>The NOD mouse: a model for insulin-dependent diabetes mellitus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/875</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/875</guid>
<pubDate>Tue, 08 May 2012 19:50:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nonobese diabetic (NOD) mice spontaneously develop autoimmune T cell-mediated insulin-dependent diabetes mellitus (IDDM). This unit presents a protocol for maintaining NOD mice under conditions permissive to full expression of their    autoimmune potential. Methods are also described for diagnosing IDDM on the basis of glycosuria and glycosemia as well as for the semiquantitation of insulitis, a valuable subphenotype diagnostic of prediabetes in these mice, including a    procedure for aldehyde fuchsin staining to identify beta granules in beta islet cells for diagnostic purposes. An adoptive-transfer method is also included in which leukocytes, purified T cells, or T cell infiltrates obtained from the insulitic    pancreas tissue of NOD mice are injected into prediabetic NOD or diabetes-resistant F1 mice, which then develop disease in an accelerated fashion.  This protocol also includes alternative steps in which bone-marrow cells from NOD mice are    transferred to syngeneic, irradiated NOD mice, allowing for reconstitution with a diabetogenic immune system. Steps for isolating pancreatic islet cells, which can then be used for a variety of purposes (e.g., as a source of islet antigens to    establish and maintain autoreactive T cell lines) are included. Finally, steps are outlined that can be used to introduce transgenes into NOD mice. This protocol also discusses important considerations for introduction of targeted mutations    produced in embryonic stem cells derived from other inbred strains, or introduction of other genes from non-diabetes-prone strains.</p>

	]]>
</description>

<author>E H. Leiter</author>


</item>


<item>
<title>Transgenic studies of pain and analgesia: mutation or background genotype?</title>
<link>http://mouseion.jax.org/stfb2000_2009/874</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/874</guid>
<pubDate>Tue, 08 May 2012 19:50:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>The application of transgenic (knockout) technology to the study of pain is rapidly expanding. Despite its power, this technique has several shortcomings that complicate the interpretation of the data obtained. Although compensation    by other genes is a well recognized problem, issues related to the background genotype of the mutant mice are less well appreciated. This review describes these confounds as they apply to studies of pain and pain inhibition. We show that the 129    and C57BL/6 mouse strains, which provide the default genetic background on which null mutants are constructed, display significant and sometimes extreme phenotypic differences in many assays of nociception, hypersensitivity, and analgesia.    Although problems related to the differential responsiveness of the two strains are minimized by placing knockouts onto "pure" 129 and/or C57BL/6 backgrounds, we also illustrate that neither of these strains are particularly representative of    inbred mice in general. Procedures to reduce confounds and converging evidence must be used to accurately determine the functions of the targeted genes in pain-related phenomena.</p>

	]]>
</description>

<author>W R. Lariviere et al.</author>


</item>


<item>
<title>In silico mapping of mouse quantitative trait loci.</title>
<link>http://mouseion.jax.org/stfb2000_2009/873</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/873</guid>
<pubDate>Tue, 08 May 2012 19:49:55 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E J. Chesler et al.</author>


</item>


<item>
<title>PDGF autocrine stimulation dedifferentiates cultured astrocytes and induces oligodendrogliomas and oligoastrocytomas from neural progenitors and astrocytes in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/872</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/872</guid>
<pubDate>Tue, 08 May 2012 19:49:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present evidence that some low-grade oligodendrogliomas may be comprised of proliferating glial progenitor cells that are blocked in their ability to differentiate, whereas malignant gliomas have additionally acquired other    mutations such as disruption of cell cycle arrest pathways by loss of Ink4a-Arf.  We have modeled these effects in cell culture and in mice by generating autocrine stimulation of glia through the platelet-derived growth factor receptor (PDGFR).     In cell culture, PDGF signaling induces proliferation of glial precursors and blocks their differentiation into oligodendrocytes and astrocytes. In addition, coexpression of PDGF and PDGF receptors has been demonstrated in human gliomas, implying    that autocrine stimulation may be involved in glioma formation. In this study, using somatic cell type-specific gene transfer we investigated the functions of PDGF autocrine signaling in gliomagenesis by transferring the overexpression of PDGF-B    into either nestin-expressing neural progenitors or glial fibrillary acidic protein (GFAP)-expressing astrocytes both in cell culture and in vivo. In cultured astrocytes, overexpression of PDGF-B caused significant increase in proliferation rate    of both astrocytes and neural progenitors.  Furthermore, PDGF gene transfer converted cultured astrocytes into cells with morphologic and gene expression characteristics of glial precursors. In vivo, gene transfer of PDGF to neural progenitors    induced the formation of oligodendrogliomas in about 60% of mice by 12 wk of age; PDGF transfer to astrocytes induced the formation of either oligodendrogliomas or mixed oligoastrocytomas in about 40% of mice in the same time period. Loss of    Ink4a-Arf, a mutation frequently found in high-grade human gliomas, resulted in shortened latency and enhanced malignancy of gliomas. The highest percentage of PDGF-induced malignant gliomas arose from of Ink4a-Arf null progenitor cells.  These    data suggest that chronic autocrine PDGF signaling can promote a proliferating population of glial precursors and is potentially sufficient to induce gliomagenesis. Loss of Ink4a-Arf is not required for PDGF-induced glioma formation but promotes    tumor progression toward a more malignant phenotype.</p>

	]]>
</description>

<author>C Dai et al.</author>


</item>


<item>
<title>Glioma models.</title>
<link>http://mouseion.jax.org/stfb2000_2009/871</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/871</guid>
<pubDate>Tue, 08 May 2012 19:49:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gliomas are primary central nervous system tumors that arise from astrocytes, oligodendrocytes or their precursors. Gliomas can be classified into several groups according to their histologic characteristics, the most malignant of    the gliomas is glioblastoma multiforme. In contrast to the long-standing and well-defined histopathology, the underlying molecular and genetic bases for gliomas are only just emerging. Many genetic alterations have been identified in human    gliomas, however, establishing unequivocal correlation between these genetic alterations and gliomagenesis requires accurate animal models for this disease. Here we are reviewing the existing animal models for gliomas with different strategies    and our current knowledge on the important issues about this disease, such as activation of signal transduction pathways, disruption of cell cycle arrest pathways, cell-of-origin of gliomas, and therapeutic strategies.</p>

	]]>
</description>

<author>C Dai et al.</author>


</item>


<item>
<title>The NOD mouse: a model for insulin-dependent diabetes mellitus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/870</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/870</guid>
<pubDate>Tue, 08 May 2012 19:48:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nonobese diabetic (NOD) mice spontaneously develop autoimmune T cell-mediated insulin-dependent diabetes mellitus (IDDM). This unit presents a protocol for maintaining NOD mice under conditions permissive to full expression of their    autoimmune potential. Methods are also described for diagnosing IDDM on the basis of glycosuria and glycosemia as well as for the semiquantitation of insulitis, a valuable subphenotype diagnostic of prediabetes in these mice, including a    procedure for aldehyde fuchsin staining to identify beta granules in beta islet cells for diagnostic purposes. An adoptive-transfer method is also included in which leukocytes, purified T cells, or T cell infiltrates obtained from the insulitic    pancreas tissue of NOD mice are injected into prediabetic NOD or diabetes-resistant F1 mice, which then develop disease in an accelerated fashion.  This protocol also includes alternative steps in which bone-marrow cells from NOD mice are    transferred to syngeneic, irradiated NOD mice, allowing for reconstitution with a diabetogenic immune system. Steps for isolating pancreatic islet cells, which can then be used for a variety of purposes (e.g., as a source of islet antigens to    establish and maintain autoreactive T cell lines) are included. Finally, steps are outlined that can be used to introduce transgenes into NOD mice. This protocol also discusses important considerations for introduction of targeted mutations    produced in embryonic stem cells derived from other inbred strains, or introduction of other genes from non-diabetes-prone strains.</p>

	]]>
</description>

<author>E H. Leiter</author>


</item>


<item>
<title>Mediums Change, Fears Stay the Same</title>
<link>http://digitalcommons.colby.edu/honorstheses/627</link>
<guid isPermaLink="true">http://digitalcommons.colby.edu/honorstheses/627</guid>
<pubDate>Tue, 08 May 2012 19:48:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although generally dismissed by scholars as being overly sentimental or superstitious, the gothic genre has survived for over four centuries and maintained significant cultural appeal, outlasting the sentimental novel and the travelogue as popular literature. What, then, makes this genre different? What is so special about the gothic?</p>
<p>In my thesis, I examine the evolving cultural appeal of the gothic genre that keeps it attractive and relevant for readers by tracing the gothic text, <em>The Woman in Black</em> by Susan Hill, through its initial inception and its subsequent adaptations. As a novel, <em>The Woman in Black</em> both repeats and revises the gothic genre, revealing which themes and concerns were still relevant in 1983. The theatrical adaptation of <em>The Woman in Black</em> (1987) by Stephen Mallatratt shows how these motifs and anxieties have evolved from the early 1980s to the late 1980s. Finally, James Watkins’ 2012 film adaptation of <em>The Woman in Black</em> further emphasizes the importance and timelessness of Hill’s original subject, the question of what it means to be a good parent.</p>
<p>The gothic genre continuously evolves to express the tacit fears of each generation, examining the extreme consequences of life’s oppositions, retaining its relevance over the ages.</p>

	]]>
</description>

<author>Lucy Wilhelms</author>


</item>


<item>
<title>A novel model of murine mucopolysaccharidosis type VII due to an intracisternal a particle element transposition into the beta-glucuronidase gene: clinical and pathologic findings.</title>
<link>http://mouseion.jax.org/stfb2000_2009/869</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/869</guid>
<pubDate>Tue, 08 May 2012 19:48:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>We describe the clinical and pathologic findings in a murine model of mucopolysaccharidosis VII (Sly disease) that arose spontaneously in the C3H/HeOuJ mouse strain. Affected gus(mps2J)/gus(mps2J) mice are deficient in    beta-glucuronidase because of insertion of an intracisternal A particle element into intron 8 of the gus structural gene. This is the first model of a human lysosomal storage disease caused by an intracisternal A particle element insertion. Mice    with the gus(mps2J)/gus(mps2J) genotype have < 1% of normal beta-glucuronidase activity and secondary elevations of other lysosomal enzymes. The phenotype includes shortened life-span, dysmorphic features, and skeletal dysplasia. Lysosomal    storage of glycosaminoglycans is widespread and affects the brain, skeleton, eye, ear, heart valves, aorta, and the fixed tissue macrophage system. Thus the phenotypic and pathologic alterations in gus(mps2J)/gus(mps2J) mice are similar to those    in patients with mucopolysaccharidosis VII. The finding of antibodies to beta-glucuronidase in some older gus(mps2J)/gus(mps2J) mice suggests the mice produce sufficient enzyme to elicit an immune response. The gus(mps2J)/gus(mps2J) model    provides another well-defined genetic system for the study of the pathophysiology of mucopolysaccharidosis and for evaluation of experimental therapies for lysosomal storage diseases. The disease in gus(mps2J)/gus(mps2J) mice is less severe than    that seen in the previously characterized B6.C-H2(bm1)/ByBir-gus(mps)/gus(mps) mouse model. Furthermore, unlike gus(mps)/gus(mps) mice, gus(mps2J)/gus(mps2J) mice are fertile and breed to produce litters, all of which are mucopolysaccharidosis    VII pups. This feature makes them extremely useful for testing intrauterine therapies.</p>

	]]>
</description>

<author>C Vogler et al.</author>


</item>


<item>
<title>Treatment of alopecia areata in C3H/HeJ mice with the topical immunosuppressant FK506 (Tacrolimus).</title>
<link>http://mouseion.jax.org/stfb2000_2009/868</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/868</guid>
<pubDate>Tue, 08 May 2012 19:48:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata-like hair loss has been observed in C3H/HeJ mice and can be defined as a tissue-restricted T cell mediated disease of the hair follicle. Because FK506 has been described as suppressing T cell mediated autoimmune    diseases, we addressed the question whether topical treatment of C3H/HeJ mice with FK506 has a beneficial effect on alopecia areata (AA). For this purpose six C3H/HeJ mice with AA were treated topically with 0.1% FK506 ointment, four mice    received the vehicle only. Four of six FK506-treated mice showed complete hair regrowth, whereas 1/4 vehicle-treated mice regrew hair. Mice treated successfully with FK506 had reduced perifollicular infiltrates of CD4+ and CD8+ cells and a    decreased expression of MHC class I and II and ICAM-1 on hair follicle epithelium, compared to control mice. We conclude that topical treatment with FK506 is able to induce hair regrowth in AA of C3H/HeJ mice, most likely by suppressing the T    cell mediated immune response.</p>

	]]>
</description>

<author>Paul P. Freyschmidt et al.</author>


</item>


<item>
<title>Brown adipose tissue-specific insulin receptor knockout shows diabetic phenotype without insulin resistance.</title>
<link>http://mouseion.jax.org/stfb2000_2009/867</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/867</guid>
<pubDate>Tue, 08 May 2012 19:47:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although insulin regulates metabolism in both brown and white adipocytes, the role of these tissues in energy storage and utilization is quite different. Recombination technology using the Cre-loxP approach allows inactivation of    the insulin receptor in a tissue-specific manner. Mice lacking insulin receptors in brown adipocytes show an age-dependent loss of interscapular brown fat but increased expression of uncoupling protein-1 and -2. In parallel, these mice develop an    insulin-secretion defect resulting in a progressive glucose intolerance, without insulin resistance. This model provides direct evidence for not only a role for the insulin receptors in brown fat adipogenesis, the data also suggest a novel role    of brown adipose tissue in the regulation of insulin secretion and glucose homeostasis.</p>

	]]>
</description>

<author>C Guerra et al.</author>


</item>


<item>
<title>Effects of ectopias and their cortical location on several measures of learning in BXSB mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/866</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/866</guid>
<pubDate>Tue, 08 May 2012 19:47:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>About half of BXSB/MpJ-Yaa mice have ectopias, which are misplaced clusters of neurons located in layer I of cortex. This study replicated several previous findings showing that there are learning differences between mice with    ectopias and those without. In addition, we had sufficient numbers of ectopic mice to investigate if ectopics learned differently depending on the cortical location of the ectopia(s). Mice with at least one ectopia located in prefrontal cortex    were initially impaired in learning the Morris maze, as well as relearning the Lashley maze when it was inverted, but learned better in the radial-arm maze when compared to ectopic mice with ectopias located in nonprefrontal regions of cortex.    Mice with at least one ectopia in motor cortex learned the Lashley maze better than mice with ectopias located outside motor cortex. In sum, the cortical location of the ectopia(s) affected learning performance in certain tasks within the ectopic    group, but regardless of the cortical location of the ectopia(s), ectopics still learned differently than nonectopics in several tasks.</p>

	]]>
</description>

<author>L A. Hyde et al.</author>


</item>


<item>
<title>Murine mucopolysaccharidosis VIL: impact of therapies on the phenotype, clinical course, and pathology in a model of a lysosomal storage disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/865</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/865</guid>
<pubDate>Tue, 08 May 2012 19:47:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mucopolysaccharidoses are a group of lysosomal storage diseases caused by deficiency of an enzyme required for the normal degradation of glycosaminoglycans. Patients with mucopolysaccharidosis typically have widespread lysosomal    storage, skeletal and central nervous system disease, and hepatosplenomegaly. Some patients with mucopolysaccharidosis may benefit from enzyme replacement therapy or bone marrow transplantation.  Animal models of mucopolysaccharidosis have proven    valuable for the evaluation of the effectiveness of potential treatments for patients with lysosomal storage disease. A murine model of MPS VII (Sly syndrome) has proven particularly useful because of its well-defined genetics and its    well-characterized clinical, pathologic, and biochemical alterations, which resemble those seen in patients with mucopolysaccharidosis.  Correction of these alterations forms the basis for evaluation of the effectiveness of novel treatments. A    wide range of therapies have been tested using this model, including enzyme replacement therapy, bone marrow, stem cell, and neural progenitor cell transplantation, and a variety of viral-mediated gene therapies. The inferences drawn from these    therapeutic studies using the murine MPS VII model are likely generalizable to other lysosomal storage diseases.</p>

	]]>
</description>

<author>C Vogler et al.</author>


</item>


<item>
<title>Requirement for the murine zinc finger protein ZFR in perigastrulation growth and survival.</title>
<link>http://mouseion.jax.org/stfb2000_2009/864</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/864</guid>
<pubDate>Tue, 08 May 2012 19:46:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The transition from preimplantation to postimplantation development leads to the initiation of complex cellular differentiation and morphogenetic movements, a dramatic decrease in cell cycle length, and a commensurate increase in    the size of the embryo. Accompanying these changes is the need for the transfer of nutrients from the mother to the embryo and the elaboration of sophisticated genetic networks that monitor genomic integrity and the homeostatic control of    cellular growth, differentiation, and programmed cell death. To determine the function of the murine zinc finger protein ZFR in these events, we generated mice carrying a null mutation in the gene encoding it. Homozygous mutant embryos form    normal-appearing blastocysts that implant and initiate the process of gastrulation. Mutant embryos form mesoderm but they are delayed in their development and fail to form normal anterior embryonic structures. Loss of ZFR function leads to both    an increase in programmed cell death and a decrease in mitotic index, especially in the region of the distal tip of the embryonic ectoderm. Mutant embryos also have an apparent reduction in apical vacuoles in the columnar visceral endoderm cells    in the extraembryonic region. Together, these cellular phenotypes lead to a dramatic development delay and embryonic death by 8 to 9 days of gestation, which are independent of p53 function.</p>

	]]>
</description>

<author>M J. Meagher et al.</author>


</item>


<item>
<title>Packaging paternal chromosomes with protamine.</title>
<link>http://mouseion.jax.org/stfb2000_2009/863</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/863</guid>
<pubDate>Tue, 08 May 2012 19:46:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R E. Braun</author>


</item>


<item>
<title>A highly conserved sequence essential for translational repression of the protamine 1 messenger rna in murine spermatids.</title>
<link>http://mouseion.jax.org/stfb2000_2009/862</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/862</guid>
<pubDate>Tue, 08 May 2012 19:46:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Translational regulation of the protamine 1 mRNA is mediated by sequences in its 3' untranslated region. In this study, we demonstrate that a highly conserved sequence, the translational control element, is solely responsible for    protamine 1 translational regulation. Mutation of the conserved sequence causes premature translation of a transgene containing a fusion between the human growth hormone coding sequence and the protamine 1 3' untranslated region. Temporal    expression of the transgene was monitored in prepubertal animals by Northern and Western blotting and in adult animals by immunocytochemistry. Messenger RNAs lacking the translational control element sediment in the messenger ribonucleoprotein    particle and ribosomal fractions of polysome gradients, suggesting that the translational control element is required for translational repression but not for incorporation of mRNAs into ribonucleoprotein particles.</p>

	]]>
</description>

<author>J Zhong et al.</author>


</item>


<item>
<title>MSY2 and MSY4 bind a conserved sequence in the 3&apos; untranslated region of protamine 1 mRNA in vitro and in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/861</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/861</guid>
<pubDate>Tue, 08 May 2012 19:45:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Y-box proteins are major constituents of ribonucleoprotein particles (RNPs) which contain translationally silent mRNAs in gametic cells. We have recently shown that a sequence-specific RNA binding activity present in spermatogenic    cells contains the two Y-box proteins MSY2 and MSY4. We show here that MSY2 and MSY4 bind a sequence, 5'-UCCAUCA-3', present in the 3' untranslated region of the translationally repressed protamine 1 (Prm1) mRNA. Using pre- and post-RNase    T1-digested substrate RNAs, it was determined that MSY2 and MSY4 can bind an RNA of eight nucleotides containing the MSY2 and MSY4 binding site. Single nucleotide mutations in the sequence eliminated the binding of MSY2 and MSY4 in an    electrophoretic mobility shift assay, and the resulting mutants failed to compete for binding in a competition assay. A consensus site of U(AC)C(A)CAU(C)CA(CU) (subscripts indicate nucleotides which do not disrupt YRS binding by MSY2 and MSY4),    denoted the Y-box recognition site (YRS), was defined from this mutational analysis. These mutations in the YRS were further characterized in vivo using a novel application of the yeast three-hybrid system.  Experiments with transgenic mice show    that disruption of the YRS in vivo relieves Prm1-like repression of a reporter gene. The conservation of the RNA binding motifs among Y-box protein family members raises the possibility that other Y-box proteins may have previously unrecognized    sequence-specific RNA binding activities.</p>

	]]>
</description>

<author>F Giorgini et al.</author>


</item>


<item>
<title>Absence of germline infection in male mice following intraventricular injection of adenovirus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/860</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/860</guid>
<pubDate>Tue, 08 May 2012 19:45:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The possibility of inadvertent exposure of gonadal tissue to gene therapy vectors has raised safety concerns about germline infection. We show here that the receptor for coxsackie B viruses and adenoviruses 2 and 5 (CXADR) is    expressed in mouse germ cells, suggesting the possibility that these viruses could infect germ cells. To directly assess the risk of germline infection in vivo, we injected an adenovirus carrying the germ-cell-specific protamine promoter fused to    the bacterial lacZ reporter gene into the left ventricular cavity of mice and then monitored expression of the reporter gene in germ cells. To differentiate between infection of stem cells and differentiating spermatogenic cells, we analyzed    expression of the reporter cassette at different times after viral delivery. Under all conditions tested, mice did not express the Escherichia coli beta-galactosidase protein in developing spermatids or in mature epididymal spermatozoa. Primary    germ cells cultured in vitro were also refractory to adenoviral infection. Our data suggest that the chance of vertical germline transmission and insertional mutagenesis is highly unlikely following intracoronary adenoviral    delivery.</p>

	]]>
</description>

<author>A H. Peters et al.</author>


</item>


<item>
<title>Gsh2 and Pax6 play complementary roles in dorsoventral patterning of the mammalian telencephalon.</title>
<link>http://mouseion.jax.org/stfb2000_2009/859</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/859</guid>
<pubDate>Tue, 08 May 2012 19:44:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>The telencephalon has two major subdivisions, the pallium and subpallium.  The pallium, which primarily consists of glutamatergic cortical structures, expresses dorsal molecular markers, whereas the subpallium, which primarily    consists of the GABAergic basal ganglia, expresses ventral molecular markers. Here, we present evidence that the progenitor and postmitotic cells flanking the pallial/subpallial boundary (PSB) in the embryonic mouse can be subdivided into    multiple regions that express unique combinations of transcription factors. The domains that immediately flank the PSB are the ventral pallium (VP) and the dorsal lateral ganglionic eminence (dLGE). The early expression of the Pax6 and Gsh2    homeobox transcription factors overlaps in the region of the dLGE.  Analyses of mice that lack functional alleles of either Gsh2 or Pax6 demonstrate that these genes have complementary roles in patterning the primordia flanking the PSB. In the    Gsh2 mutants, the dLGE is respecified into a VP-like structure, whereas in the Pax6 mutants the VP is respecified into a dLGE-like structure. The role of Pax6 in dorsalizing the telencephalon is similar to its role in the spinal cord, supporting    the hypothesis that some dorsoventral patterning mechanisms are used at all axial levels of the central nervous system.</p>

	]]>
</description>

<author>K Yun et al.</author>


</item>


<item>
<title>Induction of myeloproliferative disease in mice by tyrosine kinase fusion oncogenes does not require granulocyte-macrophage colony-stimulating factor or interleukin-3.</title>
<link>http://mouseion.jax.org/stfb2000_2009/858</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/858</guid>
<pubDate>Tue, 08 May 2012 19:44:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Tyrosine kinase fusion oncogenes that occur as a result of chromosomal translocations have been shown to activate proliferative and antiapoptotic pathways in leukemic cells, but the importance of autocrine and paracrine expression    of hematopoietic cytokines in leukemia pathogenesis is not understood. Evidence that leukemic transformation may be, at least in part, cytokine dependent includes data from primary human leukemia cells, cell culture experiments, and murine models    of leukemia. This report demonstrates that interleukin (IL)-3 plasma levels are elevated in myeloproliferative disease (MPD) caused by the TEL/tyrosine kinase fusions TEL/platelet-derived growth factor beta receptor (PDGFbetaR), TEL/Janus kinase    2 (JAK2), and TEL/neurotrophin-3 receptor (TRKC). Plasma granulocyte-macrophage colony-stimulating factor (GM-CSF) levels were elevated by TEL/PDGFbetaR and TEL/JAK2. However, all of the fusions tested efficiently induced MPD in mice genetically    deficient for both GM-CSF and IL-3, demonstrating that these cytokines are not necessary for the development of disease in this model system. Furthermore, in experiments using normal marrow transduced with TEL/PDGFbetaR retrovirus mixed with    marrow transduced with an enhanced green fluorescent protein (EGFP) retrovirus, the MPD induced in these mice demonstrated minimal stimulation of normal myelopoiesis by the TEL/PDGFbetaR-expressing cells. In contrast, recipients of mixed    GM-CSF-transduced and EGFP-transduced marrow exhibited significant paracrine expansion of EGFP-expressing cells. Collectively, these data demonstrate that, although cytokine levels are elevated in murine bone marrow transplant models of leukemia    using tyrosine kinase fusion oncogenes, GM-CSF and IL-3 are not required for myeloproliferation by any of the oncogenes tested.</p>

	]]>
</description>

<author>M H. Tomasson et al.</author>


</item>


<item>
<title>Interleukin 3 and granulocyte-macrophage colony-stimulating factor are not required for induction of chronic myeloid leukemia-like myeloproliferative disease in mice by BCR/ABL.</title>
<link>http://mouseion.jax.org/stfb2000_2009/857</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/857</guid>
<pubDate>Tue, 08 May 2012 19:44:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Primitive hematopoietic progenitors from some patients with Philadelphia chromosome (Ph)-positive chronic myeloid leukemia (CML) express aberrant transcripts for interleukin 3 (IL-3) and granulocyte colony-stimulating factor    (G-CSF), and exhibit autonomous proliferation in serum-free cultures that is inhibited by anti-IL-3 and anti-IL-3 receptor antibodies.  Expression of the product of the Ph chromosome, the BCR/ABL oncogene, in mice by retroviral bone marrow    transduction and transplantation induces CML-like leukemia, and some leukemic mice have increased circulating IL-3, and perhaps granulocyte-macrophage colony-stimulating factor (GM-CSF).  These observations raise the possibility of autocrine or    paracrine cytokine production in the pathogenesis of human CML. Mice with homozygous inactivation of the Il-3 gene, the Gm-csf gene, or both, were used to test the requirement for these cytokines for induction of CML-like disease by BCR/ABL.    Neither IL-3 nor GM-CSF was required in donor, recipient, or both for induction of CML-like leukemia by p210 BCR/ABL. Use of novel mice deficient in both IL-3 and GM-CSF demonstrated that the lack of effect on leukemogenesis was not due to    redundancy between these hematopoietic growth factors. Analysis of cytokine levels in leukemic mice where either donor or recipient was Il-3(-/-) indicated that the increased IL-3 originated from the recipient, suggestive of a host reaction to    the disease. These results demonstrate that IL-3 and GM-CSF are not required for BCR/ABL-induced CML-like leukemia in mice and suggest that autocrine production of IL-3 does not play a role in established chronic phase CML in    humans.</p>

	]]>
</description>

<author>S Li et al.</author>


</item>


<item>
<title>Experimental design for gene expression microarrays.</title>
<link>http://mouseion.jax.org/stfb2000_2009/856</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/856</guid>
<pubDate>Tue, 08 May 2012 19:43:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>We examine experimental design issues arising with gene expression microarray technology. Microarray experiments have multiple sources of variation, and experimental plans should ensure that effects of interest are not confounded    with ancillary effects. A commonly used design is shown to violate this principle and to be generally inefficient. We explore the connection between microarray designs and classical block design and use a family of ANOVA models as a guide to    choosing a design. We combine principles of good design and A-optimality to give a general set of recommendations for design with microarrays. These recommendations are illustrated in detail for one kind of experimental objective, where we also    give the results of a computer search for good designs.</p>

	]]>
</description>

<author>M K. Kerr et al.</author>


</item>


<item>
<title>Post-transcriptional control and male infertility.</title>
<link>http://mouseion.jax.org/stfb2000_2009/855</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/855</guid>
<pubDate>Tue, 08 May 2012 19:43:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R E. Braun</author>


</item>


<item>
<title>A sequence-specific RNA binding complex expressed in murine germ cells contains MSY2 and MSY4.</title>
<link>http://mouseion.jax.org/stfb2000_2009/854</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/854</guid>
<pubDate>Tue, 08 May 2012 19:43:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>The protamine mRNAs are stored for up to 8 days as translationally repressed ribonucleoprotein particles during murine spermatogenesis. Translational repression of the protamine 1, Prm1, mRNA is controlled by sequences in its    3'-untranslated region (UTR). In this study we used the yeast three-hybrid system to clone Msy4, which encodes a novel member of the Y box family of nucleic acid binding proteins. MSY4 specifically binds to a site within the 5' most 37    nucleotides in the Prm1 3' UTR. Msy4 is highly expressed in the testis, and the protein is detected in the cytoplasm of germ cells in both the testis and the ovary, where repressed messages are stored. Analysis of a previously described 48/50-kDa    binding activity in testis extracts by electrophoretic mobility shift assays and immunoprecipitation indicates the activity is composed of MSY4 and MSY2, another mouse Y box protein. Polysome analysis demonstrates MSY4 is associated with mRNPs,    consistent with MSY4 having a role in storing repressed messages.</p>

	]]>
</description>

<author>H G. Davies et al.</author>


</item>


<item>
<title>Offspring’s leukocyte telomere length, paternal age, and telomere elongation in sperm</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1035</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1035</guid>
<pubDate>Tue, 08 May 2012 19:42:53 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Masayuki Kimura et al.</author>


</item>


<item>
<title>Sex differences in thermal nociception and morphine antinociception in rodents depend on genotype.</title>
<link>http://mouseion.jax.org/stfb2000_2009/853</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/853</guid>
<pubDate>Tue, 08 May 2012 19:42:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>It has been appreciated for some time that the sexes can differ in their sensitivity to pain and its inhibition. Both the human and rodent literatures remain quite contentious, with many investigators failing to observe sex    differences that others document clearly. Recent data from our laboratory have pointed to an interaction between sex and genotype in rodents, such that sex differences are observed in some strains but not others. However, these studies employed    inbred mouse strains and are thus not directly relevant to existing data. We presently examined whether the observation of statistically significant sex differences in nociception and morphine antinociception might depend on the particular    outbred rodent population chosen for study. Rats of both sexes and three common outbred strains were obtained from three suppliers (Long Evans, Simonsen; Sprague Dawley, Harlan; Wistar Kyoto, Taconic) and tested for nociceptive sensitivity on the    49 degrees C tail-withdrawal assay, and antinociception following morphine (1-10mg/kg, i.p.). In further studies, three outbred populations of mice (CD-1, Harlan; Swiss Webster, Harlan; Swiss Webster, Simonsen) were bred in our vivarium for    several generations and tested for tail-withdrawal sensitivity and morphine antinociception (1-20male, and no significant difference. In a separate study in which the estrous cycle was tracked in female mice, we found evidence for an interaction    between genotype and estrous phase relevant to morphine antinociception. However, estrous cyclicity did not explain the observed sex differences. These data are discussed with respect to the existing sex difference and pain literature, and also    as they pertain to future investigations of these phenomena.</p>

	]]>
</description>

<author>J S. Mogil et al.</author>


</item>


<item>
<title>Combined activation of Ras and Akt in neural progenitors induces glioblastoma formation in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/852</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/852</guid>
<pubDate>Tue, 08 May 2012 19:42:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gliomas are the most common primary malignant brain tumours and are classified into four clinical grades, with the most aggressive tumours being grade 4 astrocytomas (also known as glioblastoma multiforme; GBM). Frequent genetic    alterations in GBMs (refs 2-5) result in stimulation of common signal transduction pathways involving Ras, Akt and other proteins. It is not known which of these pathways, if any, are sufficient to induce GBM formation. Here we transfer, in a    tissue-specific manner, genes encoding activated forms of Ras and Akt to astrocytes and neural progenitors in mice. We found that although neither activated Ras nor Akt alone is sufficient to induce GBM formation, the combination of activated Ras    and Akt induces high-grade gliomas with the histological features of human GBMs. These tumours appear to arise after gene transfer to neural progenitors, but not after transfer to differentiated astrocytes. Increased activity of RAS is found in    many human GBMs (ref. 11), and we show here that Akt activity is increased in most of these tumours, implying that combined activation of these two pathways accurately models the biology of this disease.</p>

	]]>
</description>

<author>E C. Holland et al.</author>


</item>


<item>
<title>Astrocytes give rise to oligodendrogliomas and astrocytomas after gene transfer of polyoma virus middle T antigen in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/851</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/851</guid>
<pubDate>Tue, 08 May 2012 19:42:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>The cells of origin for oligodendrogliomas and astrocytomas are not known but are presumed to be oligodendrocyte and astrocyte precursors, respectively. In this paper we report the generation of mixed gliomas from in vivo    transformation of glial fibrillary acidic protein (GFAP)-positive cells (differentiated astrocytes) with polyoma virus middle T antigen (MTA). MTA is a powerful oncogene that activates a number of signal transduction pathways, including those    proposed to be involved in gliomagenesis, and has been shown to induce tumors in many cell types. We have achieved transfer of MTA expression specifically to GFAP(+) cells in vivo using somatic cell gene transfer, and find resultant formation of    anaplastic gliomas with mixed astrocytoma and oligodendroglioma morphological features. We conclude that GFAP- expressing astrocytes, with appropriate signaling abnormalities, can serve as the cell of origin for oligodendrogliomas, astrocytomas,    or mixed gliomas.</p>

	]]>
</description>

<author>E C. Holland et al.</author>


</item>


<item>
<title>A sequence-specific RNA binding complex expressed in murine germ cells contains MSY2 and MSY4.</title>
<link>http://mouseion.jax.org/stfb2000_2009/850</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/850</guid>
<pubDate>Tue, 08 May 2012 19:41:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>Temporal control of protein synthesis during spermatogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/849</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/849</guid>
<pubDate>Tue, 08 May 2012 19:41:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>During oogenesis and spermatogenesis transcription ceases prior to the differentiation of the mature cells. To complete germ cell differentiation and initiate early embryogenesis, proteins are synthesized from pre-existing mRNAs    that are stored for several days. It is well established that important regulatory elements functioning in spatial localization, temporal translation or messenger RNA stability are located in the 3' untranslated region (3' UTR) of mRNAs. During    mammalian spermatogenesis temporal translational regulation of the protamine 1 (Prm1) mRNA is dependent on a highly conserved sequence located in the distal region of its 3' UTR. The 17-nucleotide translational control element (TCE) mediates    translational repression of the Prm1 mRNA. Mutation of the TCE causes premature synthesis of protamine protein and sterility.  The Prm1 mRNA is stored as a cytoplasmic ribonucleoprotein (mRNP) particle in spermatids. Contained within the particle    are several members of the Y box family of nucleic acid binding proteins. In the yeast three-hybrid system the murine Y box proteins MSY1, MSY2 and MSY4 bind in a sequence-dependent manner to a conserved region in the proximal portion of the Prm1    3' UTR. Sequence-specific binding by MSY4 to the Y box recognition sequence (YRS) is dependent on the highly conserved cold shock domain, possibly through the RNP1 and RNP2 motifs present within it. The Y box proteins may function as    translational repressors in vivo.  Alternatively, their primary function may be to protect mRNAs from degradation during their extended period of storage. Translational activation of stored mRNAs is essential for the completion of gametogenesis.    Proper translational activation of the Prm1 mRNA in elongated spermatids requires the cytoplasmic double-stranded RNA binding protein TARBP2. Tarbp2 is expressed at low levels in many cells but is expressed at robust levels in late stage meiotic    cells and in postmeiotic spermatids. Mice mutant for Tarbp2 are defective in proper translational activation of the Prm1 and Prm2 mRNAs and are sterile. Current studies are designed to determine the mechanism by which proteins bound to the 3' UTR    communicate with the 5' end of the message to control translational silencing and activation.</p>

	]]>
</description>

<author>R E. Braun</author>


</item>


<item>
<title>Fanconi anemia complementation group C is required for proliferation of murine primordial germ cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/848</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/848</guid>
<pubDate>Tue, 08 May 2012 19:41:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fanconi anemia is a polygenic trait hypothesized to be a DNA damage repair disease. We show that all three Fanconi anemia loci that have been cloned are expressed in the embryonic gonad during the period of primordial germ cell    proliferation. Mice mutant for the Fanconi anemia complementation group C locus (Fancc) have reduced germ cell numbers as early as embryonic day E12.5, suggesting the Fancc protein functions prior to meiosis in both sexes. Depletion in the mutant    occurs at a time when all three loci would be expressed in a wild-type gonad, implying a function in the early germline. Determination of the mitotic index of primordial germ cells by BrdU incorporation shows that germ cells in Fancc(-/-) mice    proliferate significantly more slowly than littermate controls. This study demonstrates Fancc is required for mitotic proliferation of primordial germ cells.</p>

	]]>
</description>

<author>J J. Nadler et al.</author>


</item>


<item>
<title>Male contraception: views to the 21st century, Bethesda, MD, USA, 9-10 September 1999.</title>
<link>http://mouseion.jax.org/stfb2000_2009/847</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/847</guid>
<pubDate>Tue, 08 May 2012 19:40:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>For men who still wish to father children, the contraceptive options currently available are withdrawal and the condom. Although significant progress has been made on hormonal and vaccine-related approaches to male contraception, a    marketed product is, at best, several years away.  Therefore, the National Institute of Child Health and Human Development convened a workshop to discuss novel strategies for development of male contraceptives that focused on the testis and    epididymis. Participants recognized that exploration of these new approaches will necessitate considerable investment of funds and research efforts.</p>

	]]>
</description>

<author>L V. DePaolo et al.</author>


</item>


<item>
<title>Repositories of mouse mutations and inbred, congenic, and recombinant inbred strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/846</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/846</guid>
<pubDate>Tue, 08 May 2012 19:40:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M T. Davisson et al.</author>


</item>


<item>
<title>Identification of ZFR, an ancient and highly conserved murine chromosome-associated zinc finger protein.</title>
<link>http://mouseion.jax.org/stfb2000_2009/845</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/845</guid>
<pubDate>Tue, 08 May 2012 19:40:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>In a screen for RNA binding proteins expressed during murine spermatogenesis, we cloned a novel, ancient zinc finger protein possessing a region common to a small class of RNA binding proteins. Zfr (zinc finger RNA binding) encodes    a protein of 1052 amino acids with three widely spaced Cys2His2 zinc fingers. Outside of the zinc fingers, ZFR shares a region that is highly conserved between several RNA binding proteins containing copies of the double-stranded RNA binding    motif. By northern blotting, Zfr is expressed at highest levels within the testis, ovary and brain. Immunohistochemistry and confocal microscopy were used to show that ZFR is highly expressed during meiosis I in males and females and is    chromosome associated. Zfr is also expressed in Sertoli cells in the testis and granulosa cells in the ovary where it is localized to the nucleus. Using fluorescent in situ hybridization we mapped Zfr to chromosome 15 region A. ZFR appears to be    an ancient protein, as apparent homologs exist in invertebrates (D. melanogaster) nematodes (C. elegans) and humans (H. sapiens).</p>

	]]>
</description>

<author>M J. Meagher et al.</author>


</item>


<item>
<title>Cloning and characterization of the mouse interleukin enhancer binding factor 3 (Ilf3) homolog in a screen for RNA binding proteins.</title>
<link>http://mouseion.jax.org/stfb2000_2009/844</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/844</guid>
<pubDate>Tue, 08 May 2012 19:39:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>In a screen for RNA-binding proteins expressed during murine spermatogenesis, we have identified a cDNA that encodes a protein of 911 amino acids that contains two copies of the double-stranded RNA-binding motif and has 80% identity    with human Interleukin Enhancer Binding Factor 3 (ILF3). Linkage and cytogenetic analyses localized the Ilf3 cDNA to a portion of mouse Chr 9, which shows conserved synteny with a region of human Chr 19 where the human ILF3 gene had been    previously localized, supporting that we had cloned the murine homolog of ILF3. Northern analysis indicated the Ilf3 gene is ubiquitously expressed in mouse adult tissues with high levels of expression in the brain, thymus, testis, and ovary.    Polyclonal antibodies detected multiple protein species in a subset of the tissues expressing Ilf3 RNA. Immunoreactive species are present at high levels in the thymus, testis, ovary, and the spleen to a lesser extent. The high degree of sequence    similarity between the mouse ILF3 protein and other dsRNA binding motif-containing proteins suggests a role in RNA metabolism, while the differential expression indicates the mouse ILF3 protein predominantly functions in tissues containing    developing lymphocyte and germ cells.</p>

	]]>
</description>

<author>F W. Buaas et al.</author>


</item>


<item>
<title>A double-stranded RNA binding protein required for activation of repressed messages in mammalian germ cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/843</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/843</guid>
<pubDate>Tue, 08 May 2012 19:39:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chromatin packaging in mammalian spermatozoa requires an ordered replacement of the somatic histones by two classes of spermatid-specific basic proteins, the transition proteins and the protamines. Temporal expression of transition    proteins and protamines during spermatid differentiation is under translational control, and premature translation of protamine 1 leads to precocious nuclear condensation and sterility. We have previously suggested that the double-stranded (ds)    RNA binding protein Prbp (encoded by the gene Tarbp2) functions as a translational regulator during mouse spermatogenesis. Here we show that Prbp is required for proper translational activation of the mRNAs encoding the protamines. We generated    mice that carry a targeted disruption of Tarbp2 and determined that they were sterile and severely oligospermic. Using immunohistological analysis, we determined that the endogenous Prm2 mRNA and a reporter mRNA carrying protamine 1    translational-control elements were translated in a mosaic pattern. We showed that failure to synthesize the protamines resulted in delayed replacement of the transition proteins and subsequent failure of spermiation. The timing of Prbp    expression suggests that it may function as a chaperone in the assembly of specific translationally regulated ribonucleoprotein particles.</p>

	]]>
</description>

<author>J Zhong et al.</author>


</item>


<item>
<title>Differential origins of neocortical projection and local circuit neurons: role of Dlx genes in neocortical interneuronogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/842</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/842</guid>
<pubDate>Tue, 08 May 2012 19:38:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Herein we review the evidence that neocortical projection neurons and interneurons are derived from distinct regions within the telencephalon.  While neocortical projection neurons are derived from the ventricular zone of the    neocortex, neocortical interneurons appear to be derived from the germinal zone of the basal ganglia. These interneurons follow a tangential migratory pathway from the ganglionic eminences to the cortex.  Interneurons of the olfactory bulb follow    a distinct tangential migration from the basal ganglia. The Dlx homeobox genes, which are essential for basal ganglia differentiation, are also required for the development of neocortical and olfactory bulb interneurons. Furthermore, evidence is    presented that retroviral-mediated expression of DLX2 in neocortical cells can induce GABAergic interneuron differentiation.</p>

	]]>
</description>

<author>S Anderson et al.</author>


</item>


<item>
<title>The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/841</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/841</guid>
<pubDate>Tue, 08 May 2012 19:38:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The product of the Philadelphia chromosome (Ph) translocation, the BCR/ABL oncogene, exists in three principal forms (P190, P210, and P230 BCR/ABL) that are found in distinct forms of Ph-positive leukemia, suggesting the three    proteins have different leukemogenic activity. We have directly compared the tyrosine kinase activity, in vitro transformation properties, and in vivo leukemogenic activity of the P190, P210, and P230 forms of BCR/ABL. P230 exhibited lower    intrinsic tyrosine kinase activity than P210 and P190. Although all three oncogenes transformed both myeloid (32D cl3) and lymphoid (Ba/F3) interleukin (IL)-3-dependent cell lines to become independent of IL-3 for survival and growth, their    ability to stimulate proliferation of Ba/F3 lymphoid cells differed and correlated directly with tyrosine kinase activity. In a murine bone marrow transduction/transplantation model, the three forms of BCR/ABL were equally potent in the induction    of a chronic myeloid leukemia (CML)-like myeloproliferative syndrome in recipient mice when 5-fluorouracil (5-FU)-treated donors were used. Analysis of proviral integration showed the CML-like disease to be polyclonal and to involve multiple    myeloid and B lymphoid lineages, implicating a primitive multipotential target cell.  Secondary transplantation revealed that only certain minor clones gave rise to day 12 spleen colonies and induced disease in secondary recipients, suggesting    heterogeneity among the target cell population. In contrast, when marrow from non- 5-FU-treated donors was used, a mixture of CML-like disease, B lymphoid acute leukemia, and macrophage tumors was observed in recipients. P190 BCR/ABL induced    lymphoid leukemia with shorter latency than P210 or P230. The lymphoid leukemias and macrophage tumors had provirus integration patterns that were oligo- or monoclonal and limited to the tumor cells, suggesting a lineage-restricted target cell    with a requirement for additional events in addition to BCR/ABL transduction for full malignant transformation. These results do not support the hypothesis that P230 BCR/ABL induces a distinct and less aggressive form of CML in humans, and    suggest that the rarity of P190 BCR/ABL in human CML may reflect infrequent BCR intron 1 breakpoints during the genesis of the Ph chromosome in stem cells, rather than intrinsic differences in myeloid leukemogenicity between P190 and    P210.</p>

	]]>
</description>

<author>S Li et al.</author>


</item>


<item>
<title>Cell migration and chick limb development: chemotactic action of FGF-4 and the AER.</title>
<link>http://mouseion.jax.org/stfb2000_2009/840</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/840</guid>
<pubDate>Tue, 08 May 2012 19:38:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Experiments have been carried out to investigate the role of the apical ectodermal ridge (AER) and FGF-4 on the control of cell migration during limb bud morphogenesis. By coupling DiI cell labeling with ectopic implantation of    FGF-4 microcarrier beads we have found that FGF-4 acts as a potent and specific chemoattractive agent for mesenchymal cells of the limb bud. The response to FGF-4 is dose dependent in both the number of cells stimulated to migrate and the    distance migrated. The cell migration response to FGF-4 appears to be independent of the known inductive activity of FGF-4 on Shh gene expression. We investigated the role of the AER in controlling cell migration by characterizing the migration    pattern of DiI-labeled subapical cells during normal limb outgrowth and following partial AER removal. Subapical cells within 75 micrometer of the AER migrate to make contact with the AER and are found intermingled with nonlabeled cells. Thus,    the progress zone is dynamic with cells constantly altering their neighbor relationships during limb outgrowth. AER removal studies show that cell migration is AER dependent and that subapical cells redirect their path of migration toward a    functional AER. These studies indicate that the AER has a chemoattractive function and regulates patterns of cell migration during limb outgrowth. Our results suggest that the chemoattractive activity of the AER is mediated in part by the    production of FGF-4.</p>

	]]>
</description>

<author>S Li et al.</author>


</item>


<item>
<title>Post-transcriptional control of gene expression during spermatogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/839</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/839</guid>
<pubDate>Tue, 08 May 2012 19:37:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>The synthesis and storage of mRNAs prior to their translation is a necessity during spermatogenesis as global transcription ceases several days prior to the completion of spermatid differentiation. Post-transcriptional control can    be mediated by sequences in the 5' and 3' untranslated regions of mRNAs, and in some cases separate elements may regulate translational repression and translational activation. Translational repression is essential for spermatid differentiation    as premature translation can lead to an arrest in spermatid differentiation and cause dominant male sterility.</p>

	]]>
</description>

<author>R E. Braun</author>


</item>


<item>
<title>Spermatid perinuclear ribonucleic acid-binding protein binds microtubules in vitro and associates with abnormal manchettes in vivo in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/838</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/838</guid>
<pubDate>Tue, 08 May 2012 19:37:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Spermatid perinuclear RNA-binding protein (SPNR) is a microtubule-associated RNA-binding protein that localizes to the manchette in developing spermatids. The RNA target of SPNR in vivo is unknown, although we have previously    suggested the possibility that SPNR is involved in the translational activation of the protamine 1 mRNA in elongated spermatids. To increase our understanding of SPNR's association with the manchette, we sought to determine SPNR's subcellular    localization in several mouse mutants that show reduced fertility or sterility and that have structurally abnormal manchettes. We show here that despite the highly abnormal manchettes and microtubule aggregates formed in azh, hop-sterile, tw2,    and tw8 mutants, SPNR remains associated with the manchettes. Localization of SPNR to the abnormal manchettes suggests that SPNR is tightly bound to the manchette. SPNR could bind manchette microtubules directly, or it could bind indirectly via    an interaction with a microtubule-associated protein (MAP). We sought to determine whether SPNR binds microtubules in vitro, and if so, whether it requires a MAP. We show by Western analysis that the endogenous SPNR protein can be pelleted with    murine testis microtubules in a taxol-dependent manner in vitro. A recombinant version of SPNR produced in bacteria can also be pelleted with testis microtubules, as well as microtubules polymerized from purified bovine brain tubulin, an    association that is salt-sensitive. These results suggest that SPNR, in addition to its function as an RNA-binding protein, is also a bona fide MAP.</p>

	]]>
</description>

<author>J M. Schumacher et al.</author>


</item>


<item>
<title>The gene encoding PRBP, the mouse homolog of human TRBP, maps to distal chromosome 15.</title>
<link>http://mouseion.jax.org/stfb2000_2009/837</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/837</guid>
<pubDate>Tue, 08 May 2012 19:37:05 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J Zhong et al.</author>


</item>


<item>
<title>Every sperm is sacred--or is it?</title>
<link>http://mouseion.jax.org/stfb2000_2009/836</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/836</guid>
<pubDate>Tue, 08 May 2012 19:36:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R E. Braun</author>


</item>


<item>
<title>Genetics and immunogenetics of NOD mice and related strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/835</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/835</guid>
<pubDate>Tue, 08 May 2012 19:36:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E H. Leiter</author>


</item>


<item>
<title>NOD mice and related strains: origins, husbandry and biology introduction.</title>
<link>http://mouseion.jax.org/stfb2000_2009/834</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/834</guid>
<pubDate>Tue, 08 May 2012 19:36:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E H. Leiter</author>


</item>


<item>
<title>NOD Mice and Related Strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/833</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/833</guid>
<pubDate>Tue, 08 May 2012 19:35:45 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>Separate elements in the 3&apos; untranslated region of the mouse protamine 1 mRNA regulate translational repression and activation during murine spermatogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/832</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/832</guid>
<pubDate>Tue, 08 May 2012 19:35:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse protamine mRNAs, Prm-1 and Prm-2, are translationally repressed for several days during male germ cell differentiation. The translational delay of mouse Prm-1 mRNA has previously been shown to be dependent upon cis-acting    elements that reside in the last 62 nucleotides of the Prm-1 3' untranslated region (3' UTR). We have previously identified a 48/50-kDa protein that binds the 3' UTRs of both Prm-1 and Prm-2 mRNAs in a sequence-specific manner, is present in    cytoplasmic fractions of postmeiotic round spermatids where the protamine mRNAs are translationally silent, and is markedly reduced in elongated spermatids where the protamine mRNAs become activated for translation. Surprisingly, the binding site    for this activity maps to a region of the Prm-1 3' UTR not contained within the functional 62 nucleotides described above. In this report we show that the binding site for the 48/50-kDa protein can also delay translation of a reporter RNA in    vivo, suggesting that the 48/50-kDa protein can repress the translation of Prm-1 mRNA during murine spermatogenesis. This observation proves that two separate regions of the Prm-1 3' UTR are sufficient to repress Prm-1 translation. In addition,    immunocytochemistry and polysome analysis have revealed that this transgenic reporter mRNA fails to undergo proper translational activation. These results suggest that an additional region of the Prm-1 3' UTR is required for proper translational    activation and that Prm-1 translational repression elements can be separated from those involved in translational activation.</p>

	]]>
</description>

<author>M A. Fajardo et al.</author>


</item>


<item>
<title>Impact of Room Ventilation Rates on Mouse Cage Ventilation and Microenvironment.</title>
<link>http://mouseion.jax.org/stfb2000_2009/831</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/831</guid>
<pubDate>Tue, 08 May 2012 19:35:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>To assess the impact of room ventilation on animal cage microenvironment, intracage ventilation rate, temperature, humidity, and concentrations of carbon dioxide and ammonia were monitored in nonpressurized, bonnet-topped mouse    cages.  Cages on the top, middle, and bottom rows of a mouse rack were monitored at room ventilation rates of 0, 5, 10, and 20 air changes/h (ACH). Ventilation inside the animal cage increased somewhat from 12.8 to 18.9 ACH as room ventilation    rate in- creased from 0 to 20 ACH, but the differences were not statistically significant, and most of the increase occurred in cages in the top row nearest to the fresh air supply. Cages containing mice had ventilation rate between 10 and 15 ACH    even when room ventilation was reduced to 0 ACH; this ventilation is a result of the thermal heat load of the mice. After 6 days of soiled bedding, intracage ammonia concentration was c 3 ppm at all room ventilation rates and was not affected by    increasing room ventilation. Temperature inside cages did not change with increasing ventilation. Humidity inside cages significantly decreased with increasing ventilation, from 55% relative humidity at 5 ACH to 36% relative humidity at 20 ACH.    Carbon dioxide concentration decreased from 2,500 ppm to 1,900 ppm when ventilation rate increased from 5 ACH to 10 ACH, but no further significant decrease was observed at 20 ACH. In conclusion, increasing the room ventilation rate higher than 5    ACH did not result in significant improvements in the cage microenvironment.</p>

	]]>
</description>

<author>C K. Reeb et al.</author>


</item>


<item>
<title>A testis cytoplasmic RNA-binding protein that has the properties of a translational repressor.</title>
<link>http://mouseion.jax.org/stfb2000_2009/830</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/830</guid>
<pubDate>Tue, 08 May 2012 19:34:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Translation of the mouse protamine 1 (Prm-1) mRNA is repressed for several days during male germ cell differentiation. With the hope of cloning genes that regulate the translational repression of Prm-1, we screened male germ cell    cDNA expression libraries with the 3' untranslated region of the Prm-1 RNA. From this screen we obtained two independent clones that encode Prbp, a Prm-1 RNA-binding protein. Prbp contains two copies of a double-stranded-RNA-binding domain. In    vitro, the protein binds to a portion of the Prm-1 3' untranslated region previously shown to be sufficient for translational repression in transgenic mice, as well as to poly(I). poly(C). Prbp protein is present in multiple forms in cytoplasmic    extracts prepared from wild-type mouse testes and is absent from testes of germ cell-deficient mouse mutants, suggesting that Prbp is restricted to the germ cells of the testis. Immunocytochemical localization confirmed that Prbp is present in    the cytoplasmic compartment of late-stage meiotic cells and haploid round spermatids. Recombinant Prbp protein inhibits the translation of multiple mRNAs in a wheat germ lysate, suggesting that Prbp acts to repress translation in round    spermatids. While this protein lacks complete specificity for Prm-1-containing RNAs in vitro, the properties of Prbp are consistent with it acting as a general repressor of translation.</p>

	]]>
</description>

<author>K Lee et al.</author>


</item>


<item>
<title>Germ cell defects and hematopoietic hypersensitivity to gamma-interferon in mice with a targeted disruption of the Fanconi anemia C gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/829</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/829</guid>
<pubDate>Tue, 08 May 2012 19:34:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fanconi anemia (FA) is an autosomal recessive chromosome instability syndrome characterized by progressive bone marrow (BM) failure, skeletal defects, and increased susceptibility to malignancy. FA cells are hypersensitive to DNA    cross-linking agents, oxygen and have cell cycle abnormalities. To develop an animal model of the disease we generated mice homozygous for a targeted deletion of exon 9 of the murine FA complementation group C gene (fac). Mutant mice had normal    neonatal viability and gross morphology, but their cells had the expected chromosome breakage and DNA cross-linker sensitivity. Surprisingly, male and female mutant mice had reduced numbers of germ cells and females had markedly impaired    fertility. No anemia was detectable in the peripheral blood during the first year of life, but the colony forming capacity of marrow progenitor cells was abnormal in vitro in mutant mice. Progenitor cells from fac knock-out mice were    hypersensitive to interferon gamma. This previously unrecognized phenotype may form the basis for BM failure in human FA.</p>

	]]>
</description>

<author>M A. Whitney et al.</author>


</item>


<item>
<title>Spnr, a murine RNA-binding protein that is localized to cytoplasmic microtubules.</title>
<link>http://mouseion.jax.org/stfb2000_2009/828</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/828</guid>
<pubDate>Tue, 08 May 2012 19:33:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous studies in transgenic mice have established the importance of the 3' untranslated region (UTR) of the spermatid-specific protamine-1 (Prm-1) mRNA in its translational control during male germ cell development. To clone    genes that mediate the translational repression or activation of the Prm-1 mRNA, we screened cDNA expression libraries made with RNA from pachytene spermatocytes and round spermatids, with an RNA probe corresponding to the 3' UTR of Prm-1. We    obtained six independent clones that encode Spnr, a spermatid perinuclear RNA-binding protein. Spnr is a 71-kD protein that contains two previously described RNA binding domains. The Spnr mRNA is expressed at high levels in the testis, ovary, and    brain, and is present in multiple forms in those tissues. Immunolocalization of the Spnr protein within the testis shows that it is expressed exclusively in postmeiotic germ cells and that it is localized to the manchette, a spermatid-specific    microtubular array. Although the Spnr protein is expressed too late to be directly involved in the translational repression of Prm-1 specifically, we suggest that the Spnr protein may be involved in other aspects of spermatid RNA metabolism, such    as RNA transport or translational activation.</p>

	]]>
</description>

<author>J M. Schumacher et al.</author>


</item>


<item>
<title>Distribution of Tenr, an RNA-binding protein, in a lattice-like network within the spermatid nucleus in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/827</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/827</guid>
<pubDate>Tue, 08 May 2012 19:33:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>In a molecular screen for cDNAs that encode protamine RNA-binding proteins, we obtained seven independent clones that encode Tenr, a testis nuclear RNA-binding protein. Tenr is a 72-kDa protein that has one copy of a previously    described RNA-binding domain. Northwestern blotting experiments showed that a maltose-binding protein-Tenr fusion binds to a variety of RNAs in vitro and that it does not bind to single-stranded or double-stranded DNA. The Tenr gene is    transcribed exclusively in the testis, and its mRNA is restricted to cells from the pachytene spermatocyte stage through the round spermatid stage.  Immunolocalization of the Tenr protein within the testis showed that it is first detected    postmeiotically, demonstrating that the Tenr mRNA is under translational control. The Tenr protein is localized to round and early elongating spermatid cells, and confocal microscopy revealed a lattice-like nuclear distribution suggesting    association with the nuclear scaffold. We suggest that the Tenr protein may be involved in testis-specific nuclear posttranscriptional processes such as heterogeneous nuclear RNA (hnRNA) packaging, alternative splicing, or nuclear/cytoplasmic    transport of mRNAs.</p>

	]]>
</description>

<author>J M. Schumacher et al.</author>


</item>


<item>
<title>Premature translation of protamine 1 mRNA causes precocious nuclear condensation and arrests spermatid differentiation in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/826</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/826</guid>
<pubDate>Tue, 08 May 2012 19:33:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Translational control is a major form of regulating gene expression during gametogenesis and early development in many organisms. We sought to determine whether the translational repression of the protamine 1 (Prm1) mRNA is    necessary for normal spermatid differentiation in mice. To accomplish this we generated transgenic animals that carry a Prm1 transgene lacking its normal 3' untranslated region. Premature translation of Prm1 mRNA caused precocious condensation of    spermatid nuclear DNA, abnormal head morphogenesis, and incomplete processing of Prm2 protein. Premature accumulation of Prm1 within syncytial spermatids in mice hemizygous for the transgene caused dominant male sterility, which in some cases was    accompanied by a complete arrest in spermatid differentiation. These results demonstrate that correct temporal synthesis of Prm1 is necessary for the transition from nucleohistones to nucleoprotamines.</p>

	]]>
</description>

<author>K Lee et al.</author>


</item>


<item>
<title>Molecular genetic analysis of mammalian spermatid differentiation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/825</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/825</guid>
<pubDate>Tue, 08 May 2012 19:32:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R E. Braun et al.</author>


</item>


<item>
<title>Germ cell-specific proteins interact with the 3&apos; untranslated regions of Prm-1 and Prm-2 mRNA.</title>
<link>http://mouseion.jax.org/stfb2000_2009/824</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/824</guid>
<pubDate>Tue, 08 May 2012 19:32:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>The testis-specific mouse protamine genes (Prm-1 and Prm-2) are transcribed in haploid round spermatids, their mRNAs stored as cytoplasmic ribonucleoprotein particles and translated about 1 week later in elongating spermatids. We    have compared the in vitro translational efficiencies of deproteinized Prm-1 mRNA isolated from purified populations of germ cells and found that Prm-1 mRNA from round spermatids translates as efficiently as Prm-1 mRNA from elongating spermatids,    suggesting that translation of Prm-1 mRNA is normally repressed in round spermatids. Previous studies in transgenic mice have shown that the 3' UTR of Prm-1 mRNA is necessary and sufficient for its translational control (Braun et al., 1989). In    this manuscript, we have used an RNA band shift assay to identify an activity, present in cytoplasmic fractions of meiotic spermatocytes and postmeiotic round spermatids, that binds the 3'UTRs of both Prm-1 and Prm-2 mRNA.  We have used 3' UTR    deletion variants to map the binding site to a 22-nt region within the Prm-1 3' UTR and to a 20-nt region within the Prm-2 3' UTR. uv cross-linking of the RNA band shift activities detected with the Prm-1 and Prm-2 3' UTRs generated the same two    RNA/protein complexes of 53 and 55 kDa. The presence of the binding activity in the cell type and subcellular compartment associated with Prm-1 and Prm-2 mRNA storage suggest that the activity may be actively engaged in translational repression    of these mRNAs.</p>

	]]>
</description>

<author>M A. Fajardo et al.</author>


</item>


<item>
<title>Phonological awareness, letter knowledge and literacy development in Indonesian beginner readers and spellers</title>
<link>http://epubs.scu.edu.au/hahs_pubs/1116</link>
<guid isPermaLink="true">http://epubs.scu.edu.au/hahs_pubs/1116</guid>
<pubDate>Tue, 08 May 2012 19:32:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H Winskel et al.</author>


</item>


<item>
<title>Initiator (DnaA) protein concentration as a function of growth rate in Escherichia coli and Salmonella typhimurium.</title>
<link>http://mouseion.jax.org/stfb2000_2009/823</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/823</guid>
<pubDate>Tue, 08 May 2012 19:31:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>The DnaA protein concentration was determined in five different Escherichia coli strains and in Salmonella typhimurium LT2 growing at different growth rates. The DnaA protein concentration was found to be invariant over a wide range    of growth rates in the four E. coli K-12 strains and in S. typhimurium. In E. coli B/r the DnaA protein concentration was generally higher than in the K-12 strains, and it increased with decreasing growth rates. For all the strains, there appears    to be a correlation between the DnaA protein concentration and the initiation mass.  This supports the concept of the concentration of DnaA protein setting the initiation mass and, thus, that the DnaA protein is a key molecule in the regulation    of initiation of chromosome replication in members of the family Enterobacteriaceae.</p>

	]]>
</description>

<author>F G. Hansen et al.</author>


</item>


<item>
<title>Germ-line intrachromosomal recombination restores fertility in transgenic MyK-103 male mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/822</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/822</guid>
<pubDate>Tue, 08 May 2012 19:31:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Males of the MyK-103 line of transgenic mice are fertile and sire litters of normal size, but they never transmit the transgene, whereas females transmit the transgene with normal frequency. The chromosome originally bearing the    transgene can be transmitted through the male germ line, but only after the transgene is deleted or rearranged by intrachromosomal recombination. The transgene encodes a functional herpes simplex virus (HSV) thymidine kinase gene that causes    sperm infertility when expressed in postmeiotic germ cells. Immunocytochemistry revealed clones of germ cells that fail to express HSV thymidine kinase. We postulate that these cells arose by transgene deletion in embryonic germ cells and    postnatal spermatogonial stem cells and that they are responsible for the normal fertility of MyK-103 males. The frequency of recombination events at the integration locus suggests that it contains a hotspot for mitotic    recombination.</p>

	]]>
</description>

<author>T M. Wilkie et al.</author>


</item>


<item>
<title>Infertility in male transgenic mice: disruption of sperm development by HSV-tk expression in postmeiotic germ cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/821</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/821</guid>
<pubDate>Tue, 08 May 2012 19:31:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous experiments revealed that male transgenic mice bearing a cosmid that included the Class II E alpha gene, about 35 kb of 5' flanking DNA, and the cosmid vector sequences were sterile. To ascertain the cause of the sterility,    various subfragments of the cosmid were tested in transgenic mice. Only those pieces of DNA that included some of the E alpha flanking chromosomal DNA and the herpes simplex virus (HSV)-thymidine kinase (tk) gene that was in the vector resulted    in male sterility. Histological analysis revealed abnormalities in nuclear morphology of elongating spermatids and retention of mature spermatids within the seminiferous epithelium. Immunocytochemical studies showed that the HSV-tk gene was    expressed at low levels in postmeiotic round spermatids and at higher levels in more mature elongating spermatids. To determine whether expression of HSV-tk in spermatids might be responsible for the sterility, the protamine gene promoter was    used to direct the expression of HSV-tk to postmeiotic germ cells. Since the mice so treated were also sterile, the data suggest that expression of this enzyme in spermatids is responsible for the sterility phenotype.</p>

	]]>
</description>

<author>R E. Braun et al.</author>


</item>


<item>
<title>Temporal translational regulation of the protamine 1 gene during mouse spermatogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/820</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/820</guid>
<pubDate>Tue, 08 May 2012 19:30:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Temporal translational control is an important mechanism of gene regulation during mouse spermatogenesis. Studies of the protamine 1 gene, one member of a class of translationally regulated genes, have shown that it is first    transcribed post-meiotically in round spermatids, and that the mRNA is stored in an untranslatable form as an inactive ribonucleoprotein particle for up to 1 week before it is translated. The analysis of the expression of fusions between the    protamine gene and reporter genes in transgenic mice has demonstrated that sequences mapping in the 3'-untranslated region of the protamine mRNA are sufficient to confer protamine-like translational regulation on the chimeric mRNAs. It is    proposed that sequence-specific RNA-binding proteins interact with the protamine 3'-untranslated region and mediate the temporal translational control. Future progress at elucidating the mechanism of translational regulation will come from the    identification of translational control factors and their study in vitro and in vivo.</p>

	]]>
</description>

<author>R E. Braun</author>


</item>


<item>
<title>Targeted correction of a major histocompatibility class II E alpha gene by DNA microinjected into mouse eggs.</title>
<link>http://mouseion.jax.org/stfb2000_2009/819</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/819</guid>
<pubDate>Tue, 08 May 2012 19:30:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>DNA molecules containing the 5' end of a functional major histocompatibility class II E alpha gene were injected into mouse eggs bearing E alpha genes with 630-base-pair (bp) deletions encompassing the promoter and first exon. The    deletion was corrected by homologous recombination in 1 of about 500 transgenic mice that incorporated the injected DNA. The corrected E alpha gene was transmitted to progeny, which were bred to homozygosity. Southern blot analysis, polymerase    chain reaction amplification of the DNA spanning the deletion, and sequence analysis revealed that the corrected allele resembles the wild-type E alpha gene. At sites of single-base-pair polymorphisms, there was apparently random conversion to    either the donor or recipient sequence. In addition, many point mutations were introduced. mRNAs were produced from the corrected allele in a tissue-specific manner, but their sizes were different from the wild-type allele, and they did not    produce detectable E alpha protein. This experiment demonstrates the feasibility of targeting foreign DNA to a gene that is completely inactive in fertilized mouse eggs.</p>

	]]>
</description>

<author>R L. Brinster et al.</author>


</item>


<item>
<title>Protamine 3&apos;-untranslated sequences regulate temporal translational control and subcellular localization of growth hormone in spermatids of transgenic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/818</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/818</guid>
<pubDate>Tue, 08 May 2012 19:30:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although the mouse protamine 1 gene (mP1) is first transcribed in round spermatids, its mRNA is not translated until about 1 week later in elongating spermatids. To determine what mP1 sequences are important for its transcriptional    and translational regulation, we have constructed fusions between mP1 and the human growth hormone (hGH) structural gene and analyzed their expression in transgenic mice. We show that mP1 sequences 5' to the start of transcription are sufficient    to confer spermatid-specific expression on the hGH gene. We also show that 156 nucleotides of mP1 3'-untranslated sequence is sufficient to confer mP1-like translational regulation on the hGH mRNA. Interestingly, the subcellular localization of    hGH was dependent on the time during spermiogenesis that it was made. Synthesis of hGH in early round spermatids resulted in localization in the acrosome, whereas synthesis in late elongating spermatids resulted in intracellular, but not    acrosomal, localization.</p>

	]]>
</description>

<author>R E. Braun et al.</author>


</item>


<item>
<title>Genetically haploid spermatids are phenotypically diploid.</title>
<link>http://mouseion.jax.org/stfb2000_2009/817</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/817</guid>
<pubDate>Tue, 08 May 2012 19:29:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Because chromosomal homologues segregate from one another during meiosis, spermatids are genetically different. Post-meiotic gene expression could lead to gametic differences, some of which might lead to preferential transmission of    certain alleles over others. In both insects and mammals, however, all the cells derived from a single spermatogonial cell develop within a common syncytium formed as a result of incomplete cytokinesis at each of the mitotic and meiotic cell    divisions. It has been proposed that the intercellular bridges connecting the cells, which are about 1 micron in diameter, permit the sharing of cytoplasmic constituents, thus ensuring the synchronous development of a clone of cells and gametic    equivalence between haploid spermatids. By analysing the product of a transgene which is expressed exclusively in post-meiotic germ cells in hemizygous transgenic mice, we have shown that genetically distinct spermatids share the product of the    transgene and hence can be phenotypically equivalent.</p>

	]]>
</description>

<author>R E. Braun et al.</author>


</item>


<item>
<title>Cloning and characterization of dnaA(Cs), a mutation which leads to overinitiation of DNA replication in Escherichia coli K-12.</title>
<link>http://mouseion.jax.org/stfb2000_2009/816</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/816</guid>
<pubDate>Tue, 08 May 2012 19:29:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>The product of the dnaA gene is essential for the initiation of chromosomal DNA replication in Escherichia coli K-12. A cold-sensitive mutation, dnaA(Cs), was originally isolated as a putative intragenic suppressor of the    temperature sensitivity of a dnaA46 mutant (G. Kellenberger-Gujer, A. J. Podhajska, and L. Caro, Mol. Gen. Genet. 162:9-16, 1978). The cold sensitivity of the dnaA(Cs) mutant was attributed to a loss of replication control resulting in    overinitiation of DNA replication. We cloned and sequenced the dnaA gene from the dnaA(Cs) mutant and showed that it contains three point mutations in addition to the original dnaA46(Ts) mutation. The dnaA(Cs) mutation was dominant to the    wild-type allele. Overproduction of the DnaA(Cs) protein blocked cell growth. In contrast, overproduction of wild-type DnaA protein reduced the growth rate of cells but did not stop cell growth. Thus, the effect of elevated levels of the DnaA(Cs)    protein was quite different from that of the wild-type protein under the same conditions.</p>

	]]>
</description>

<author>R E. Braun et al.</author>


</item>


<item>
<title>DNA methylation differentially enhances the expression of one of the two E. coli dnaA promoters in vivo and in vitro.</title>
<link>http://mouseion.jax.org/stfb2000_2009/815</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/815</guid>
<pubDate>Tue, 08 May 2012 19:28:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The promoter/regulatory region of the dnaA gene, whose gene product is required for the initiation of DNA replication in Escherichia coli K-12, contains an unusually large number of Dam methylation sites. In this paper we report    that the expression of the dnaA gene is decreased in Dam- strains of E. coli. The decrease in the expression of dnaA was measured in vivo using a dnaA-lacZ gene fusion. In vivo S1 nuclease mapping demonstrated that the decrease was due to a    differential decrease in expression from the more proximal of the two dnaA promoters, dnaA2P.  Comparison of the strengths of the two dnaA promoters in an in vitro transcription system using methylated and unmethylated DNA templates suggests that    the effect of methylation on dnaA2P is probably at the level of RNA polymerase/DNA interaction. We suggest that this effect of methylation may be important in controlling the expression of dnaA during the E. coli cell cycle.</p>

	]]>
</description>

<author>R E. Braun et al.</author>


</item>


<item>
<title>Autoregulation of the DNA replication gene dnaA in E. coli K-12.</title>
<link>http://mouseion.jax.org/stfb2000_2009/814</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/814</guid>
<pubDate>Tue, 08 May 2012 19:28:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>The dnaA gene in E. coli K-12 is required for the initiation of DNA replication.  Although the specific function of the dnaA protein is unknown, it has been suggested that it is a regulator of the frequency of initiation. In this    paper we report that the expression of both a dnaA-lacZ translational fusion and a dnaA-trpA-lacZ transcriptional fusion in vivo are sensitive to changes in the level of functional dnaA protein. Overproduction of the dnaA gene product leads to a    reduction in expression from both fusions while introduction of dnaA- alleles results in an increased expression. Results from a deletion analysis of the dnaA promoter/regulatory region suggest that both dnaA promoters are regulated by the dnaA    gene product and that a site between the two promoters is responsible for the regulation. DNAase protection experiments showed that the dnaA protein binds to DNA in the region of the two dnaA promoters. Our results indicate that the dnaA gene    product regulates its own synthesis by inhibiting transcription from both of its promoters.</p>

	]]>
</description>

<author>R E. Braun et al.</author>


</item>


<item>
<title>The public and smoking: fear or calm deliberation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/813</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/813</guid>
<pubDate>Tue, 08 May 2012 19:27:41 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C C. LITTLE</author>


</item>


<item>
<title>Smoking and lung cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/812</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/812</guid>
<pubDate>Tue, 08 May 2012 19:27:12 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C C. LITTLE</author>


</item>


<item>
<title>Training at Bar Harbor.</title>
<link>http://mouseion.jax.org/stfb2000_2009/811</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/811</guid>
<pubDate>Tue, 08 May 2012 19:26:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C C. Little</author>


</item>


<item>
<title> Age-related increases in calcium-binding protein immunoreactivity in the cochlear nucleus of hearing impaired C57BL/6J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/810</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/810</guid>
<pubDate>Tue, 08 May 2012 19:26:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Aging C57BL/6J (C57) mice (1-30 months old), were used to study calcium-binding protein immunoreactivity (parvalbumin, calbindin and calretinin) in the cochlear nucleus. A quantitative stereological method, the optical fractionator    was used to determine the total number of neurons, and the total number of immunostained neurons in the posteroventral- and dorsal cochlear nuclei (PVCN and DCN). A statistically significant age-related decrease of the total number of neurons was    found in the PVCN and DCN using Nissl staining. In the DCN, an age-related increase in the total number of parvalbumin-positive neurons was found, while no changes in the total number of calbindin or calretinin positive neurons were demonstrated.    In the PVCN, the total number of parvalbumin, calbindin, or calretinin positive neurons remained stable with increasing age. The percentage of parvalbumin, calbindin, and calretinin positive neurons significantly increased in the DCN, and the    percentage of parvalbumin and calbindin-positive neurons increased in the PVCN. These findings imply that there is a relative up-regulation of calcium-binding proteins in neurons that had not previously expressed these proteins. This plastic    response in the profoundly hearing impaired C57 mouse may be a survival strategy for cochlear nucleus neurons.</p>

	]]>
</description>

<author>E Idrizbegovic et al.</author>


</item>


<item>
<title> Genetic and phenotypic analysis of seizure susceptibility in PL/J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/809</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/809</guid>
<pubDate>Tue, 08 May 2012 19:25:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Epilepsy is one of the most common but genetically complex neurological disorders in humans. Identifying animal models that recapitulate human epilepsies is important for pharmacological studies of anticonvulsants, dissection of    molecular and biochemical pathogenesis of epilepsy, and discovery of epilepsy susceptibility genes. We discovered that the PL/J inbred mouse strain is susceptible to handling- and rhythmic tossing-induced seizure. The tonic-clonic and generalized    seizures observed after induction were accompanied by abnormal EEGs, similar to seizures observed in EL and SWXL-4 mice. PL/J mice also had an extremely low threshold to electroconvulsive seizures compared to other strains and showed variable    sensitivity to pentylenetetrazole-induced seizures. Gross neurostructural abnormalities were not found in PL/J mice. Crosses with the seizure-resistant C57BL/6 J strain revealed semidominant inheritance of the rhythmic tossing seizure trait with    low penetrance. F2 progeny indicated that the genetic inheritance of seizure susceptibility in PL/J is non-Mendelian. We crossed DBA/2 J mice, which are resistant to rhythmic tossing seizure but susceptible to audiogenic seizures, to PL/J. We    found that seizure penetrance in (DBA/2 J x PL/J)F1 mice was similar to the penetrance in (C57BL/6 J x PL/J)F1 mice but the severity and frequency of seizure were higher in (DBA/2 J x PL/J)F1 mice. The PL/J strain serves as an interesting new    model for studying the genetics, neurobiology, and pharmacology of epilepsy.</p>

	]]>
</description>

<author>T Kitami et al.</author>


</item>


<item>
<title> Genetically increasing Myoc expression supports a necessary pathologic role of abnormal proteins in glaucoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/808</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/808</guid>
<pubDate>Tue, 08 May 2012 19:25:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite the importance of MYOC for glaucoma, the protein's normal function(s) and the pathogenic mechanism(s) of MYOC mutations are not clear. Elevated intraocular pressure (IOP) and glaucoma are sometimes induced by    corticosteroids, and corticosteroid use can result in substantially increased MYOC expression. It has been suggested, therefore, that steroid-induced MYOC protein levels cause steroid-induced glaucoma and that protein level-increasing mutations    in MYOC contribute to glaucoma not associated with steroid use. A causative role of elevated MYOC levels in steroid-induced glaucoma is controversial, however, and it is not clear if elevated MYOC levels can result in IOP elevation. To directly    test if increased levels of MYOC can cause IOP elevation and glaucoma, we generated bacterial artificial chromosome transgenic mice that overexpress Myoc at a level similar to that induced by corticosteroid use. These mice do not develop elevated    IOP or glaucoma. Our present findings, along with the absence of glaucoma in mice completely lacking MYOC, show that changing the level of MYOC is not pathogenic (from absent to approximately 15 times normal). These findings suggest that    noncoding sequence variants are unlikely to influence glaucoma and that disease pathogenesis in primary open-angle glaucoma patients is dependent upon the expression of abnormal mutant proteins. This work does not support a causative role for    increased MYOC levels or the MYOC gene in steroid-induced glaucoma.</p>

	]]>
</description>

<author>D B. Gould et al.</author>


</item>


<item>
<title> Retrotransposons regulate host genes in mouse oocytes and preimplantation embryos.</title>
<link>http://mouseion.jax.org/stfb2000_2009/807</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/807</guid>
<pubDate>Tue, 08 May 2012 19:24:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>A comprehensive analysis of transposable element (TE) expression in mammalian full-grown oocytes reveals that LTR class III retrotransposons make an unexpectedly high contribution to the maternal mRNA pool, which persists in    cleavage stage embryos. The most abundant transcripts in the mouse oocyte are from the mouse transcript (MT) retrotransposon family, and expression of this and other TE families is developmentally regulated.  Furthermore, TEs act as alternative    promoters and first exons for a subset of host genes, regulating their expression in full-grown oocytes and cleavage stage embryos. To our knowledge, this is the first example of TEs initiating synchronous, developmentally regulated expression of    multiple genes in mammals. We propose that differential TE expression triggers sequential reprogramming of the embryonic genome during the oocyte to embryo transition and in preimplantation embryos.</p>

	]]>
</description>

<author>A E. Peaston et al.</author>


</item>


<item>
<title> Pitfalls of animal model systems in ageing research.</title>
<link>http://mouseion.jax.org/stfb2000_2009/806</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/806</guid>
<pubDate>Tue, 08 May 2012 19:24:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Often, reports of anti-ageing research using animal models are overly optimistic and incomplete. Without having the details of the study (issues inherent with the animal models, the condition of the animal colony, the replicability    of the findings, for example), even the educated public can find it difficult to interpret the reports accurately. This chapter provides background information about ageing research and animal models in general and arms readers with guidelines    they can use to assist them when analyzing reports of ageing research using those models. The article also uses the guidelines to briefly evaluate three anti-ageing treatment candidates: one in the very early stages of testing (resveratrol), one    that has been proven unfounded as an anti-ageing intervention by testing [dehydroepiandrosterone (DHEA)] and one that has undergone testing successfully (l-deprenyl).</p>

	]]>
</description>

<author>K Flurkey et al.</author>


</item>


<item>
<title> Using ANOVA to analyze microarray data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/805</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/805</guid>
<pubDate>Tue, 08 May 2012 19:23:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>ANOVA provides a general approach to the analysis of single and multiple factor experiments on both one- and two-color microarray platforms. Mixed model ANOVA is important because in many microarray experiments there are multiple    sources of variation that must be taken into consideration when constructing tests for differential expression of a gene. The genome is large, and the signals of expression change can be small, so we must rely on rigorous statistical methods to    distinguish signal from noise. We apply statistical tests to ensure that we are not just making up stories based on seeing patterns where there may be none.</p>

	]]>
</description>

<author>G A. Churchill</author>


</item>


<item>
<title> Enhanced pathogenicity of diabetogenic T cells escaping a non-MHC gene-controlled near death experience.</title>
<link>http://mouseion.jax.org/stfb2000_2009/804</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/804</guid>
<pubDate>Tue, 08 May 2012 19:23:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>For unknown reasons, the common MHC class I variants encoded by the H2g7 haplotype (Kd, Db) aberrantly elicit autoreactive CD8 T cell responses essential to type 1 diabetes development when expressed in NOD mice, but not other    strains. In this study, we show that interactive non-MHC genes allow a NOD-derived diabetogenic CD8 T cell clonotype (AI4) to be negatively selected at far greater efficiency in C57BL/6 mice congenically expressing H2g7 (B6.H2g7). However, the    few AI4 T cells escaping negative selection in B6.H2g7 mice are exported from the thymus more efficiently, and are more functionally aggressive than those of NOD origin. This provides mechanistic insight to previous findings that resistant mouse    strains carry some genes conferring greater diabetes susceptibility than the corresponding NOD allele. In the B6.H2g7 stock, non-MHC gene-controlled elevations in TCR expression are associated with both enhanced negative selection of diabetogenic    CD8 T cells and increased aggressiveness of those escaping this process. An implication of this finding is that the same phenotype, in this case relatively high TCR expression levels, could have double-edged sword effects, contributing to type 1    diabetes resistance at one level of T cell development, but at another actually promoting pathogenesis.</p>

	]]>
</description>

<author>Rossi C. Choisy et al.</author>


</item>


<item>
<title> Regulation of skin and islet allograft survival in mice treated with costimulation blockade is mediated by different CD4+ cell subsets and different mechanisms.</title>
<link>http://mouseion.jax.org/stfb2000_2009/803</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/803</guid>
<pubDate>Tue, 08 May 2012 19:23:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Donor-specific transfusion (DST) and a brief course of anti-CD154 monoclonal antibody (mAb) induces permanent islet and prolonged skin allograft survival in mice. Induction of skin allograft survival requires the    presence of CD4 cells and deletion of alloreactive CD8 cells.  The specific roles of CD4 and CD4CD25 cells and the mechanism(s) by which they act are not fully understood. METHODS: We used skin and islet allografts, a CD8 T cell receptor (TCR)    transgenic model system, and in vivo depleting antibodies to analyze the role of CD4 cell subsets in regulating allograft survival in mice treated with DST and anti-CD154 mAb.  RESULTS: Deletion of CD4 or CD25 cells during costimulation blockade    induced rapid rejection of skin but only minimally shortened islet allograft survival. Deletion of CD4 or CD25 cells had no effect upon survival of healed-in islet allografts, and CD25 cell deletion had no effect upon healed-in skin allograft    survival. In the TCR transgenic model, DST plus anti-CD154 mAb treatment deleted alloreactive CD8 T cells, and anti-CD4 mAb treatment prevented that deletion. In contrast, injection of anti-CD25 mAb did not prevent alloreactive CD8 T cell    deletion.  CONCLUSIONS: These data document that (1) both CD4CD25 and CD4CD25 cells are required for induction of skin allograft survival, (2) CD4CD25 T cells are not required for alloreactive CD8 T cell deletion, and (3) CD4CD25 regulatory cells    are not critical for islet allograft tolerance. It appears that skin and islet transplantation tolerance are mediated by different CD4 cell subsets and different mechanisms.</p>

	]]>
</description>

<author>S J. Banuelos et al.</author>


</item>


<item>
<title> Homologous recombinational repair proteins in mouse meiosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/802</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/802</guid>
<pubDate>Tue, 08 May 2012 19:22:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Eukaryotic meiotic recombination requires numerous biochemical processes, including break initiation, end resection, strand invasion and heteroduplex formation, and, finally, crossover resolution. In this review, we discuss    primarily those proteins involved in the initial stages of homologous recombination, including SPO11, MRE11, RAD50, NBS1, DMC1, RAD51, RAD51 paralogs, RAD52, RPA, RAD54, and RAD54B. Focusing on the mouse as a model organism, we discuss what is    known about the conserved roles of these proteins in vertebrate somatic cells and in mammalian meiosis. We consider such information as gene expression in gonadal tissue, protein localization patterns on chromosomal cores in meiocyte nuclei, and    information gleaned from mouse models.</p>

	]]>
</description>

<author>L A. Bannister et al.</author>


</item>


<item>
<title> Quantitative trait loci that determine plasma lipids and obesity in C57BL/6J and 129S1/SvImJ inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/801</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/801</guid>
<pubDate>Tue, 08 May 2012 19:21:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>The plasma lipid concentrations and obesity of C57BL/6J (B6) and 129S1/SvImJ (129) inbred mouse strains fed a high-fat diet containing 15% dairy fat, 1% cholesterol, and 0.5% cholic acid differ markedly. To identify the loci    controlling these traits, we conducted a quantitative trait loci (QTL) analysis of 294 (B6 x 129) F(2) females fed a high-fat diet for 14 weeks. Non-HDL cholesterol concentrations were affected by five significant loci: Nhdlq1 [chromosome 8, peak    centimorgan (cM) 38, logarithm of odds [LOD] 4.4); Nhdlq4 (chromosome 10, cM 70, LOD 4.0); Nhdlq5 (chromosome 6, cM 0) interacting with Nhdlq4; Nhdlq6 (chromosome 7, cM 10) interacting with Nhdlq1; and Nhdlq7 (chromosome 15, cM 0) interacting    with Nhdlq4. Triglyceride (TG) concentrations were affected by three significant loci: Tgq1 (chromosome 18, cM 42, LOD 3.2) and Tgq2 (chromosome 9, cM 66) interacting with Tgq3 (chromosome 4, cM 58). Obesity measured by percentage of body fat    mass and body mass index was affected by two significant loci: Obq16 (chromosome 8, cM 48, LOD 10.0) interacting with Obq18 (chromosome 9, cM 65). Knowing the genes for these QTL will enhance our understanding of obesity and lipid    metabolism.</p>

	]]>
</description>

<author>N Ishimori et al.</author>


</item>


<item>
<title> Requirement for both H-2Db and H-2Kd for the induction of diabetes by the promiscuous CD8+ T cell clonotype AI4.</title>
<link>http://mouseion.jax.org/stfb2000_2009/800</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/800</guid>
<pubDate>Tue, 08 May 2012 19:21:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>The NOD mouse is a model for autoimmune type 1 diabetes in humans. CD8(+) T cells are essential for the destruction of the insulin-producing pancreatic beta cells characterizing this disease. AI4 is a pathogenic CD8(+) T cell    clone, isolated from the islets of a 5-wk-old female NOD mouse, which is capable of mediating overt diabetes in the absence of CD4(+) T cell help. Recent studies using MHC-congenic NOD mice revealed marked promiscuity of the AI4 TCR, as the    selection of this clonotype can be influenced by multiple MHC molecules, including some class II variants.  The present work was designed, in part, to determine whether similar promiscuity also characterizes the effector function of mature AI4    CTL.  Using splenocyte and bone marrow disease transfer models and in vitro islet-killing assays, we report that efficient recognition and destruction of beta cells by AI4 requires the beta cells to simultaneously express both H-2D(b) and H-2K(d)    class I MHC molecules. The ability of the AI4 TCR to interact with both H-2D(b) and H-2K(d) was confirmed using recombinant peptide libraries. This approach also allowed us to define a mimotope peptide recognized by AI4 in an H-2D(b)-restricted    manner. Using ELISPOT and mimotope/H-2D(b) tetramer analyses, we demonstrate for the first time that AI4 represents a readily detectable T cell population in the islet infiltrates of prediabetic NOD mice. Our identification of a ligand for    AI4-like T cells will facilitate further characterization and manipulation of this pathogenic and promiscuous T cell population.</p>

	]]>
</description>

<author>T Takaki et al.</author>


</item>


<item>
<title> Sex- and lineage-specific inheritance of depression-like behavior in the rat.</title>
<link>http://mouseion.jax.org/stfb2000_2009/799</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/799</guid>
<pubDate>Tue, 08 May 2012 19:20:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Wistar-Kyoto (WKY) rat exhibits physiological and behavioral similarities to endophenotypes of human depression. In the forced swim test (FST), a well-characterized antidepressant-reversible test for behavioral despair in    rodents, WKYs express characteristics of behavioral despair; increased immobility, and decreased climbing. To map genetic loci linked to behavior in the FST, we conducted a quantitative trait loci (QTL) analysis of the segregating F2 generation    of a WKY x Fisher 344 (F344) reciprocal intercross. Using linear-model-based genome scans to include covariate (sex or lineage)-by-QTL interaction effects, four significant QTL influencing climbing behavior were identified. In addition, we    identified three, seven, and two suggestive QTL for climbing, immobility, and swimming, respectively. One of these loci was pleiotropic, affecting both immobility and climbing. As found in human linkage studies, several of these QTL showed sex-    and/or lineage-dependent effects. A simultaneous search strategy identified three epistatic locus pairs for climbing. Multiple regression analysis was employed to characterize the joint contributions of these QTL and to clarify the sex- and    lineage-dependent effects. As expected for complex traits, FST behavior is influenced by multiple QTL of small effect, each contributing 5%-10%, accounting for a total 10%-30% of the phenotypic variance. A number of loci mapped in this study    share overlapping candidate regions with previously identified emotionality QTL in mice as well as with susceptibility loci recognized by linkage or genome scan analyses for major depression or bipolar disorder in humans. The presence of these    loci across species suggests that these QTL may represent universal genetic factors contributing to mood disorders.</p>

	]]>
</description>

<author>L C. Solberg et al.</author>


</item>


<item>
<title> Phenotypic and molecular assessment of seven patients with 6p25 deletion syndrome: relevance to ocular dysgenesis and hearing impairment.</title>
<link>http://mouseion.jax.org/stfb2000_2009/798</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/798</guid>
<pubDate>Tue, 08 May 2012 19:20:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Thirty-nine patients have been described with deletions involving chromosome 6p25. However, relatively few of these deletions have had molecular characterization. Common phenotypes of 6p25 deletion syndrome patients    include hydrocephalus, hearing loss, and ocular, craniofacial, skeletal, cardiac, and renal malformations. Molecular characterization of deletions can identify genes that are responsible for these phenotypes. METHODS: We report the clinical    phenotype of seven patients with terminal deletions of chromosome 6p25 and compare them to previously reported patients. Molecular characterization of the deletions was performed using polymorphic marker analysis to determine the extents of the    deletions in these seven 6p25 deletion syndrome patients. RESULTS: Our results, and previous data, show that ocular dysgenesis and hearing impairment are the two most highly penetrant phenotypes of the 6p25 deletion syndrome. While deletion of    the forkhead box C1 gene (FOXC1) probably underlies the ocular dysgenesis, no gene in this region is known to be involved in hearing impairment. CONCLUSIONS: Ocular dysgenesis and hearing impairment are the two most common phenotypes of 6p25    deletion syndrome. We conclude that a locus for dominant hearing loss is present at 6p25 and that this locus is restricted to a region distal to D6S1617.  Molecular characterization of more 6p25 deletion patients will aid in refinement of this    locus and the identification of a gene involved in dominant hearing loss.</p>

	]]>
</description>

<author>D B. Gould et al.</author>


</item>


<item>
<title> Disruption of muscle membrane and phenotype divergence in two novel mouse models of dysferlin deficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/797</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/797</guid>
<pubDate>Tue, 08 May 2012 19:19:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Limb girdle muscular dystrophy type 2B and Miyoshi myopathy are clinically distinct forms of muscular dystrophy that arise from defects in the dysferlin gene. Here, we report two novel lines of dysferlin-deficient mice obtained by    (a) gene targeting and (b) identification of an inbred strain, A/J, bearing a retrotransposon insertion in the dysferlin gene.  The mutations in these mice were located at the 3' and 5' ends of the dysferlin gene. Both lines of mice lacked    dysferlin and developed a progressive muscular dystrophy with histopathological and ultrastructural features that closely resemble the human disease. Vital staining with Evans blue dye revealed loss of sarcolemmal integrity in both lines of mice,    similar to that seen in mdx and caveolin-3 deficient mice. However, in contrast to the latter group of animals, the dysferlin-deficient mice have an intact dystrophin glycoprotein complex and normal levels of caveolin-3. Our findings indicate    that muscle membrane disruption and myofiber degeneration in dysferlinopathy were directly mediated by the loss of dysferlin via a new pathogenic mechanism in muscular dystrophies.  We also show that the mutation in the A/J mice arose between the    late 1970s and the early 1980s, and had become fixed in the production breeding stocks. Therefore, all studies involving the A/J mice or mice derived from A/J, including recombinant inbred, recombinant congenic and chromosome substitution    strains, should take into account the dysferlin defect in these strains. These new dysferlin-deficient mice should be useful for elucidating the pathogenic pathway in dysferlinopathy and for developing therapeutic strategies.</p>

	]]>
</description>

<author>M Ho et al.</author>


</item>


<item>
<title> Transcription profiling of inner ears from Pou4f3(ddl/ddl) identifies Gfi1 as a target of the Pou4f3 deafness gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/796</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/796</guid>
<pubDate>Tue, 08 May 2012 19:19:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pou4f3 (Brn3.1, Brn3c) is a class IV POU domain transcription factor that has a central function in the development of all hair cells in the human and mouse inner ear sensory epithelia. A mutation of POU4F3 underlies human    autosomal dominant non-syndromic progressive hearing loss DFNA15.  Through a comparison of inner ear gene expression profiles of E16.5 wild-type and Pou4f3 mutant deaf mice using a high density oligonucleotide microarray, we identified the gene    encoding growth factor independence 1 (Gfi1) as a likely in vivo target gene regulated by Pou4f3. To validate this result, we performed semi-quantitative RT-PCR and in situ hybridizations for Gfi1 on wild-type and Pou4f3 mutant mice. Our results    demonstrate that a deficiency of Pou4f3 leads to a statistically significant reduction in Gfi1 expression levels and that the dynamics of Gfi1 mRNA abundance closely follow the pattern of expression for Pou4f3.  To examine the role of Gfi1 in the    pathogenesis of Pou4f3-related deafness, we performed comparative analyses of the embryonic inner ears of Pou4f3 and Gfi1 mouse mutants using immunohistochemistry and scanning electron microscopy. The loss of Gfi1 results in outer hair cell    degeneration, which appears comparable to that observed in Pou4f3 mutants.  These results identify Gfi1 as the first downstream target of a hair cell specific transcription factor and suggest that outer hair cell degeneration in Pou4f3 mutants is    largely or entirely a result of the loss of expression of Gfi1.</p>

	]]>
</description>

<author>R Hertzano et al.</author>


</item>


<item>
<title> Rejection of human islets and human HLA-A2.1 transgenic mouse islets by alloreactive human lymphocytes in immunodeficient NOD-scid and NOD-Rag1(null)Prf1(null) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/795</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/795</guid>
<pubDate>Tue, 08 May 2012 19:18:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Immunodeficient NOD mice engrafted with human peripheral blood mononuclear cells (PBMCs) were used in two models of human islet allograft rejection.  Model one: human PBMCs were engrafted into chemically diabetic NOD-scid mice    bearing established subrenal human islet allografts. Inflammation and often complete islet allograft rejection were observed. Model 2 incorporated three key advances. First, we developed a new immunodeficient recipient, NOD-RagI(null)Prf1(null)    mice. Second, graft-lymphocyte interactions were optimized by intrasplenic co-transplantation of islets and human PBMC. Third, NOD-scid islets expressing human HLA-A2.1 were used as allograft targets. Diabetic NOD-RagI(null)Prf1(null) recipients    of HLA-A2.1 transgenic mouse islets, alone or co-engrafted with HLA-A2-positive human PBMC, exhibited durable graft survival and euglycemia. Contrastingly, co-transplantation with HLA-A2-negative human PBMC led to islet graft rejection without    evidence of graft-vs.-host disease (GVHD). We propose that diabetic NOD-RagI(null)Prf1(null) mice co-engrafted with HLA-A2 mouse transgenic islets and allogeneic human PBMC provide an effective in vivo model of human islet allograft    rejection.</p>

	]]>
</description>

<author>S J. Banuelos et al.</author>


</item>


<item>
<title> Maternal beta-catenin and E-cadherin in mouse development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/794</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/794</guid>
<pubDate>Tue, 08 May 2012 19:18:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The oocyte to embryo transition in metazoans depends on maternal proteins and transcripts to ensure the successful initiation of development, and the correct and timely activation of the embryonic genome. We conditionally    eliminated the maternal gene encoding the cell adhesion molecule E-cadherin and partially eliminated the beta-catenin gene from the mouse oocyte. Oocytes lacking E-cadherin, or expressing a truncated allele of beta-catenin without the N-terminal    part of the protein, give rise to embryos whose blastomeres do not adhere. Blastomere adhesion is restored after translation of protein from the wild-type paternal alleles: at the morula stage in embryos lacking maternal E-cadherin, and at the    late four-cell stage in embryos expressing truncated beta-catenin. This suggests that adhesion per se is not essential in the early cleavage stage embryos, that embryos develop normally if compaction does not occur until the morula stage, and    that the zona pellucida suffices to maintain blastomere proximity. Although maternal E-cadherin is not essential for the completion of the oocyte-to-embryo transition, absence of wild-type beta-catenin in oocytes does statistically compromise    developmental success rates. This developmental deficit is alleviated by the simultaneous absence of maternal E-cadherin, suggesting that E-cadherin regulates nuclear beta-catenin availability during embryonic genome activation.</p>

	]]>
</description>

<author>Vries W. De et al.</author>


</item>


<item>
<title> Haplotype analysis in multiple crosses to identify a QTL gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/793</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/793</guid>
<pubDate>Tue, 08 May 2012 19:17:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Identifying quantitative trait locus (QTL) genes is a challenging task.  Herein, we report using a two-step process to identify Apoa2 as the gene underlying Hdlq5, a QTL for plasma high-density lipoprotein cholesterol (HDL) levels    on mouse chromosome 1. First, we performed a sequence analysis of the Apoa2 coding region in 46 genetically diverse mouse strains and found five different APOA2 protein variants, which we named APOA2a to APOA2e. Second, we conducted a haplotype    analysis of the strains in 21 crosses that have so far detected HDL QTLs; we found that Hdlq5 was detected only in the nine crosses where one parent had the APOA2b protein variant characterized by an Ala61-to-Val61 substitution. We then found    that strains with the APOA2b variant had significantly higher (P < or = 0.002) plasma HDL levels than those with either the APOA2a or the APOA2c variant. These findings support Apoa2 as the underlying Hdlq5 gene and suggest the Apoa2    polymorphisms responsible for the Hdlq5 phenotype.  Therefore, haplotype analysis in multiple crosses can be used to support a candidate QTL gene.</p>

	]]>
</description>

<author>X Wang et al.</author>


</item>


<item>
<title> Mouse development and cell proliferation in the absence of D-cyclins.</title>
<link>http://mouseion.jax.org/stfb2000_2009/792</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/792</guid>
<pubDate>Tue, 08 May 2012 19:17:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>D-type cyclins (cyclins D1, D2, and D3) are regarded as essential links between cell environment and the core cell cycle machinery. We tested the requirement for D-cyclins in mouse development and in proliferation by generating    mice lacking all D-cyclins. We found that these cyclin D1(-/-)D2(-/-)D3(-/-) mice develop until mid/late gestation and die due to heart abnormalities combined with a severe anemia. Our analyses revealed that the D-cyclins are critically required    for the expansion of hematopoietic stem cells. In contrast, cyclin D-deficient fibroblasts proliferate nearly normally but show increased requirement for mitogenic stimulation in cell cycle re-entry. We found that the proliferation of cyclin    D1(-/-)D2(-/-)D3(-/-) cells is resistant to the inhibition by p16(INK4a), but it critically depends on CDK2. Lastly, we found that cells lacking D-cyclins display reduced susceptibility to the oncogenic transformation. Our results reveal the    presence of alternative mechanisms that allow cell cycle progression in a cyclin D-independent fashion.</p>

	]]>
</description>

<author>K Kozar et al.</author>


</item>


<item>
<title> In vivo and in vitro evidence that the high osteoblastic activity in C3H/HeJ mice compared to C57BL/6J mice is intrinsic to bone cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/791</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/791</guid>
<pubDate>Tue, 08 May 2012 19:17:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Two inbred mouse strains, C3H/HeJ (C3H) and C57BL/6J (B6), displayed a profound difference in femoral peak bone density. We have previously shown that the difference could be attributed to a greater bone formation rate (BFR) that    was due to a higher osteoblastic activity [measured by a mineral apposition rate (MAR)] in the C3H (high density) than B6 (low density) mice. The present study sought to determine (1) whether the BFR/MAR differences between the two mouse strains    present in weight-loaded endochondral bones are also seen in less weight-loaded membranous bones and (2) whether the difference in osteoblastic activity was seen in vitro in the absence of systemic factors. To address the first objective, we    performed histomorphometric measurements on the weakly loaded membranous bones (i.e., parietal bones of the calvaria) to determine if there were similar differences in MAR and BFR of membranous bones as those of highly loaded, endochondral bones.    The parietal bones of adult C3H mice showed similar increases in MAR and BFR as the endochondral bones, compared to B6 mice of same age, suggesting that the differences in the MAR and BFR in the two mouse strains are probably not related to    differences in mechanical strain. These findings also suggest that the gene(s) responsible for the difference in MAR between strains may not be a mechanical response gene. With respect to the second objective, we isolated osteoblasts from the    parietal bones and determined their differentiation status (i.e., ALP-specific activity) and bone-forming ability (i.e., mineralized nodule formation) in vitro. Consistent with the premise that C3H osteoblasts have an intrinsic, higher    differentiation status and bone-forming ability than B6 osteoblasts, osteoblasts isolated from C3H mice as compared with those from B6 mice had a significantly greater ALP-specific activity and a greater ability to form mineralized nodules in    vitro in the absence of systemic factors. Because differences in ALP activity, bone-forming ability, cortical bone width, and osteoblastic activity were detected at birth, the different MAR/BFR phenotypes develop at very early life and even    perhaps during embryogenesis. In conclusion, we have for the first time provided evidence that the genetic differences responsible for the observed MAR/BFR phenotype in the C3H-B6 strains are intrinsic to osteoblasts and might not depend on    responses to mechanical loading and/or alterations in systemic factors.</p>

	]]>
</description>

<author>M H. Sheng et al.</author>


</item>


<item>
<title> The knockout mouse project.</title>
<link>http://mouseion.jax.org/stfb2000_2009/790</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/790</guid>
<pubDate>Tue, 08 May 2012 19:16:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mouse knockout technology provides a powerful means of elucidating gene function in vivo, and a publicly available genome-wide collection of mouse knockouts would be significantly enabling for biomedical discovery. To date,    published knockouts exist for only about 10% of mouse genes.  Furthermore, many of these are limited in utility because they have not been made or phenotyped in standardized ways, and many are not freely available to researchers. It is time to    harness new technologies and efficiencies of production to mount a high-throughput international effort to produce and phenotype knockouts for all mouse genes, and place these resources into the public domain.</p>

	]]>
</description>

<author>C P. Austin et al.</author>


</item>


<item>
<title> Submission of microarray data to public repositories.</title>
<link>http://mouseion.jax.org/stfb2000_2009/789</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/789</guid>
<pubDate>Tue, 08 May 2012 19:16:13 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C A. Ball et al.</author>


</item>


<item>
<title> Standards for microarray data: an open letter.</title>
<link>http://mouseion.jax.org/stfb2000_2009/788</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/788</guid>
<pubDate>Tue, 08 May 2012 19:15:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C Ball et al.</author>


</item>


<item>
<title> An efficient SNP system for mouse genome scanning and elucidating strain relationships.</title>
<link>http://mouseion.jax.org/stfb2000_2009/787</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/787</guid>
<pubDate>Tue, 08 May 2012 19:15:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>A set of 1638 informative SNP markers easily assayed by the Amplifluor genotyping system were tested in 102 mouse strains, including the majority of the common and wild-derived inbred strains available from The Jackson Laboratory.    Selected from publicly available databases, the markers are on average approximately 1.5 Mb apart and, whenever possible, represent the rare allele in at least two strains. Amplifluor assays were developed for each marker and performed on two    independent DNA samples from each strain.  The mean number of polymorphisms between strains was 608+/-136 SD. Several tests indicate that the markers provide an effective system for performing genome scans and quantitative trait loci analyses in    all but the most closely related strains. Additionally, the markers revealed several subtle differences between closely related mouse strains, including the groups of several 129, BALB, C3H, C57, and DBA strains, and a group of wild-derived    inbred strains representing several Mus musculus subspecies. Applying a neighbor-joining method to the data, we constructed a mouse strain family tree, which in most cases confirmed existing genealogies.</p>

	]]>
</description>

<author>P M. Petkov et al.</author>


</item>


<item>
<title>Culture and everyday explanations of behavior</title>
<link>http://epubs.scu.edu.au/hahs_pubs/1115</link>
<guid isPermaLink="true">http://epubs.scu.edu.au/hahs_pubs/1115</guid>
<pubDate>Tue, 08 May 2012 19:15:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H Winskel</author>


</item>


<item>
<title> Biological nomenclatures: a source of lexical knowledge and ambiguity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/786</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/786</guid>
<pubDate>Tue, 08 May 2012 19:14:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>There has been increased work in developing automated systems that involve natural language processing (NLP) to recognize and extract genomic information from the literature. Recognition and identification of biological entities is    a critical step in this process. NLP systems generally rely on nomenclatures and ontological specifications as resources for determining the names of the entities, assigning semantic categories that are consistent with the corresponding ontology,    and assignment of identifiers that map to well-defined entities within a particular nomenclature. Although nomenclatures and ontologies are valuable for text processing systems, they were developed to aid researchers and are heterogeneous in    structure and semantics. A uniform resource that is automatically generated from diverse resources, and that is designed for NLP purposes would be a useful tool for the field, and would further database interoperability. This paper presents work    towards this goal. We have automatically created lexical resources from four model organism nomenclature systems (mouse, fly, worm, and yeast), and have studied performance of the resources within an existing NLP system, GENIES. Using    nomenclatures is not straightforward because issues concerning ambiguity, synonymy, and name variations are quite challenging.  In this paper we focus mainly on ambiguity. We determined that the number of ambiguous gene names within the    individual nomenclatures, across the four nomenclatures, and with general English ranged from 0%-10.18%, 1.187%-20.30%, and 0%-2.49% respectively. When actually processing text, we found the rate of ambiguous occurrences (not counting ambiguities    stemming from English words) to range from 2.4%-32.9% depending on the organisms considered.</p>

	]]>
</description>

<author>O Tuason et al.</author>


</item>


<item>
<title> Effects of prolonged exposure to an augmented acoustic environment on the auditory system of middle-aged C57BL/6J mice: cochlear and central histology and sex differences.</title>
<link>http://mouseion.jax.org/stfb2000_2009/785</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/785</guid>
<pubDate>Tue, 08 May 2012 19:13:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic progressive sensorineural hearing loss in mice of the C57BL/6J (B6) inbred strain begins at high frequencies during young adulthood and is severe by 12 months (middle age). Nightly treatment with an augmented acoustic    environment (AAE)--12-hour periods of exposure to repetitive noise bursts of moderate intensity, begun at age 25 days--resulted in less severe hearing loss compared with control mice. Cochlear histopathological correlates of AAE treatment,    assessed at 12-14 months of age, included lessened severity of progressive loss of outer hair cells in both sexes as well as small savings of spiral ganglion cells in females and inner hair cells in males. AAE effects on the number of surviving    neurons (age 12-14 months) in the anterior ventral cochlear nucleus (AVCN) depended on sex.  Compared with controls, the loss of AVCN neurons that typically accompanies the initial period of hearing loss (between 2 and 7 months of age) was not    significantly affected by AAE treatment in females. In contrast, males treated with the AAE exhibited more severe loss of neurons in the dorsal and ventral extremes of the AVCN than male controls of the same age. AAE treatment begun at age 3-5    months resulted in significant but less severe loss of AVCN neurons in 1-year-old male mice.</p>

	]]>
</description>

<author>J F. Willott et al.</author>


</item>


<item>
<title> Transgenic Cre expression mice for generation of erythroid-specific gene alterations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/784</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/784</guid>
<pubDate>Tue, 08 May 2012 19:13:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Transgenic mice that express Cre recombinase in erythroid cell lineages were developed so that genes affecting erythropoiesis/hematopoiesis may be altered without necessarily affecting fetus viability. A micro-LCR    cassette-beta-globin promoter-Cre recombinase gene (microLCR-betapr-Cre) construct was synthesized and used to generate transgenic mice.  Concurrently, we produced mice containing a microLCR-loxP-flanked beta sickle gene    (microLCR-loxP-beta(S)-loxP) construct. microLCR-betapr-Cre mice with intact transgenes in variable copy number were identified. Cre expression was assessed by RNAse protection and RT-PCR. Cre function was ascertained by breeding to    microLCR-loxP-beta(S)-loxP mice. We demonstrate that beta(S) expression was not detected in the blood of bigenics, but the gene was present in nonerythroid cells. Thus, excision of the loxP-flanked beta(S) gene was restricted to erythroid cell    lineages.</p>

	]]>
</description>

<author>K R. Peterson et al.</author>


</item>


<item>
<title> Mast cells, Fc epsilon RI, and IL-13 are required for development of airway hyperresponsiveness after aerosolized allergen exposure in the absence of adjuvant.</title>
<link>http://mouseion.jax.org/stfb2000_2009/783</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/783</guid>
<pubDate>Tue, 08 May 2012 19:12:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>In certain models of allergic airway disease, mast cells facilitate the development of inflammation and airway hyper-responsiveness (AHR). To define the role of the high affinity IgE receptor (FcepsilonRI) in the development of    AHR, mice with a disruption of the alpha subunit of the high affinity IgE receptor (FcepsilonRI(-/-)) were exposed on 10 consecutive days to nebulized OVA. Forty-eight hours after the last nebulization, airway responsiveness was monitored by the    contractile response of tracheal smooth muscle to electrical field stimulation (EFS).  After the 10-day OVA challenge protocol, wild-type mice demonstrated increased responsiveness to EFS, whereas similarly challenged FcepsilonRI(-/-) mice showed    a low response to EFS, similar to nonexposed animals. Further, allergen-challenged FcepsilonRI(-/-) mice showed less airway inflammation, goblet cell hyperplasia, and lower levels of IL-13 in lung homogenates compared with the controls.    IL-13-deficient mice failed to develop an increased response to EFS or goblet cell hyperplasia after the 10-day OVA challenge. We transferred bone marrow-derived mast cells from wild-type mice to FcepsilonRI(-/-) mice 1 day before initiating the    challenge protocol. After the 10-day OVA challenge, recipient FcepsilonRI(-/-) mice demonstrated EFS-induced responses similar to those of challenged wild-type mice. Transferred mast cells could be detected in tracheal preparations. These results    show that FcepsilonRI is important for the development of AHR after an aerosolized allergen sensitization protocol and that this effect is mediated through FcepsilonRI on mast cells and production of IL-13 in the lung.</p>

	]]>
</description>

<author>C Taube et al.</author>


</item>


<item>
<title> Adult-onset Alopecia areata is a complex polygenic trait in the C3H/HeJ mouse model.</title>
<link>http://mouseion.jax.org/stfb2000_2009/782</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/782</guid>
<pubDate>Tue, 08 May 2012 19:12:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata (AA) is an autoimmune disease that targets actively growing (anagen) hair follicles in humans and other mammals. C3H/HeJ, but not C57BL/6J, mice spontaneously develop an adult-onset form of AA. A segregating    population of C3HB6F2 female mice (n=1096), generated from crossing these two strains, was used for genome-wide linkage analysis to identify AA genetic susceptibility. Previous analysis identified susceptibility intervals on chromosomes 17    (Alaa1) and 9 (Alaa2). Using additional markers in these intervals and saturation mapping purported intervals on chromosomes 8 and 15, two additional regions were identified (Alaa3 and Alaa4, respectively). Human gene association studies    identified specific human leukocyte antigen intervals comparable with those (major histocompatibility complex) found in Alaa1 in the mouse. Other human studies identified genes not found in this linkage study, but these human transcription    factors are directly regulated by genes within Alaa1. These results indicate the necessity of integrating both gene association and genome-wide linkage studies in both mice and humans to understand the complex nature of these and other polygenic    diseases.</p>

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</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title> The inner nuclear membrane protein lamin B receptor forms distinct microdomains and links epigenetically marked chromatin to the nuclear envelope.</title>
<link>http://mouseion.jax.org/stfb2000_2009/781</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/781</guid>
<pubDate>Tue, 08 May 2012 19:11:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Using heterochromatin-enriched fractions, we have detected specific binding of mononucleosomes to the N-terminal domain of the inner nuclear membrane protein lamin B receptor. Mass spectrometric analysis reveals that LBR-associated    particles contain complex patterns of methylated/acetylated histones and are devoid of "euchromatic" epigenetic marks. LBR binds heterochromatin as a higher oligomer and forms distinct nuclear envelope microdomains in vivo. The organization of    these membrane assemblies is affected significantly in heterozygous ic (ichthyosis) mutants, resulting in a variety of structural abnormalities and nuclear defects.</p>

	]]>
</description>

<author>D Makatsori et al.</author>


</item>


<item>
<title> Altered oxidative stress response of the long-lived Snell dwarf mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/780</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/780</guid>
<pubDate>Tue, 08 May 2012 19:11:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Several single gene mutations in mice that increase the murine life span have been identified, including the Pit-1 mutation which results in the Snell dwarf (Pit1(dw/dw)), however, the biological mechanism of this life-span    extension is still unclear. Based on studies that show oxidative stress plays an important role in the aging process, we hypothesized that the increased longevity seen in Snell dwarf mice may result from a resistance to oxidative stress. We    report that Snell dwarf mice respond to oxidative stress induced by 3-NPA differently than their wild type littermates. This altered response results in diminished activation of the MEK-ERK kinase cascade and virtually no phosphorylation of c-Jun    at Ser63 in dwarf mice after 3-NPA treatment, despite a robust phosphorylation of Ser63 in wild type mice. We propose that this altered management of oxidative stress in dwarf mice is partially responsible for the increased longevity in Snell    dwarf mice.</p>

	]]>
</description>

<author>M A. Madsen et al.</author>


</item>


<item>
<title> Liver-specific expression of the agouti gene in transgenic mice promotes liver carcinogenesis in the absence of obesity and diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/779</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/779</guid>
<pubDate>Tue, 08 May 2012 19:10:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The agouti protein is a paracrine factor that is normally present in the skin of many species of mammals. Agouti regulates the switch between black and yellow hair pigmentation by signalling through the melanocortin 1    receptor (Mc1r) on melanocytes. Lethal yellow (Ay) and viable yellow (Avy) are dominant regulatory mutations in the mouse agouti gene that cause the wild-type protein to be produced at abnormally high levels throughout the body. Mice harboring    these mutations exhibit a pleiotropic syndrome characterized by yellow coat color, obesity, hyperglycemia, hyperinsulinemia, and increased susceptibility to hyperplasia and carcinogenesis in numerous tissues, including the liver.  The goal of    this research was to determine if ectopic expression of the agouti gene in the liver alone is sufficient to recapitulate any aspect of this syndrome. For this purpose, we generated lines of transgenic mice expressing high levels of agouti in the    liver under the regulatory control of the albumin promoter. Expression levels of the agouti transgene in the liver were quantified by Northern blot analysis. Functional agouti protein in the liver of transgenic mice was assayed by its ability to    inhibit binding of the alpha-melanocyte stimulating hormone (alphaMSH) to the Mc1r. Body weight, plasma insulin and blood glucose levels were analyzed in control and transgenic mice. Control and transgenic male mice were given a single    intraperitoneal injection (10 mg/kg) of the hepatocellular carcinogen, diethylnitrosamine (DEN), at 15 days of age. Mice were euthanized at 36 or 40 weeks after DEN injection and the number of tumors per liver and total liver weights were    recorded. RESULTS: The albumin-agouti transgene was expressed at high levels in the livers of mice and produced a functional agouti protein. Albumin-agouti transgenic mice had normal body weights and normal levels of blood glucose and plasma    insulin, but responded to chemical initiation of the liver with an increased number of liver tumors compared to non-transgenic control mice.  CONCLUSIONS: The data demonstrate that liver-specific expression of the agouti gene is not sufficient to    induce obesity or diabetes, but, in the absence of these factors, agouti continues to promote hepatocellular carcinogenesis.</p>

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</description>

<author>A I. Kuklin et al.</author>


</item>


<item>
<title> Lymphotoxin and TNF produced by B cells are dispensable for maintenance of the follicle-associated epithelium but are required for development of lymphoid follicles in the Peyer&apos;s patches.</title>
<link>http://mouseion.jax.org/stfb2000_2009/778</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/778</guid>
<pubDate>Tue, 08 May 2012 19:10:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Organogenesis of Peyer's patches (PP), follicle-associated epithelium, and M cells is impaired in mice lacking B cells. At the same time, lymphotoxin (LT) and TNF are known to be critical for the development of PP. To directly    address the function of LT and TNF expressed by B cells in the maintenance of PP structure, we studied the de novo formation of PP in B cell-deficient mice after the transfer of bone marrow from mice with targeted mutations in LT, TNF, or their    combinations. We found that although the compartmentalization of T and B cell zones and development of follicular dendritic cells were affected by the lack of B cell-derived LT and TNF, the development of follicle-associated epithelium and M    cells in PP was completely independent of LT/TNF production by B cells.</p>

	]]>
</description>

<author>A V. Tumanov et al.</author>


</item>


<item>
<title> ATRX, a member of the SNF2 family of helicase/ATPases, is required for chromosome alignment and meiotic spindle organization in metaphase II stage mouse oocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/777</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/777</guid>
<pubDate>Tue, 08 May 2012 19:09:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>ATRX is a centromeric heterochromatin binding protein belonging to the SNF2 family of helicase/ATPases with chromatin remodeling activity.  Mutations in the human ATRX gene result in X-linked alpha-thalassaemia with mental    retardation (ATRX) syndrome and correlate with changes in methylation of repetitive DNA sequences. We show here that ATRX also functions to regulate key stages of meiosis in mouse oocytes. At the germinal vesicle (GV) stage, ATRX was found    associated with the perinucleolar heterochromatin rim in transcriptionally quiescent oocytes.  Phosphorylation of ATRX during meiotic maturation is dependent upon calcium calmodulin kinase (CamKII) activity. Meiotic resumption also coincides with    deacetylation of histone H4 at lysine 5 (H4K5 Ac) while ATRX and histone H3 methylated on lysine 9 (H3K9) remained bound to the centromeres and interstitial regions of condensing chromosomes, respectively. Inhibition of histone deacetylases    (HDACs) with trichostatin A (TSA) disrupted ATRX binding to the centromeres of hyperacetylated chromosomes resulting in abnormal chromosome alignments at metaphase II (MII). Similarly, while selective ablation of ATRX by antibody microinjection    and RNA interference (RNAi) had no effect on the progression of meiosis, it had severe consequences for the alignment of chromosomes on the metaphase II spindle. These results suggest that genome-wide epigenetic modifications such as global    histone deacetylation are essential for the binding of ATRX to centromeric heterochromatin.  Moreover, centromeric ATRX is required for correct chromosome alignment and organization of a bipolar meiotic metaphase II spindle.</p>

	]]>
</description>

<author>La Fuente De et al.</author>


</item>


<item>
<title> Hair cycle-specific immunolocalization of retinoic acid synthesizing enzymes Aldh1a2 and Aldh1a3 indicate complex regulation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/776</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/776</guid>
<pubDate>Tue, 08 May 2012 19:09:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Retinoic acid has long been known to alter skin and hair growth but an exact mechanism is unclear. This study was performed to examine the sites of endogenous retinoic acid synthesis in the cycling hair follicle to better    understand the role retinoic acid plays in this process. Retinal dehydrogenases (Aldh1a1, 2, and 3, formerly Raldh 1, 2, and 3) are the enzymes responsible for the last step in retinoic acid synthesis.  Immunohistochemistry was performed on adult    C57BL/6J mouse skin sections with antibodies against Aldh1a2 and Aldh1a3. Aldh1a2 expression was seen primarily in the outer root sheath and basal/spinous layer during all stages of the hair cycle, and in the bulge during anagen and early    catagen, whereas Aldh1a3 expression was primarily in the dermal papilla, pre-cortex, and hair shaft during mid-late anagen. The expression patterns of these two similar retinoic acid synthesizing enzymes at specific follicular sites suggest that    they mediate and are regulated by different epithelial proliferation and differentiation signaling pathways.</p>

	]]>
</description>

<author>H B. Everts et al.</author>


</item>


<item>
<title> Hepatic ABCG5 and ABCG8 overexpression increases hepatobiliary sterol transport but does not alter aortic atherosclerosis in transgenic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/775</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/775</guid>
<pubDate>Tue, 08 May 2012 19:08:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The individual roles of hepatic versus intestinal ABCG5 and ABCG8 in sterol transport have not yet been investigated. To determine the specific contribution of liver ABCG5/G8 to sterol transport and atherosclerosis, we generated    transgenic mice that overexpress human ABCG5 and ABCG8 in the liver but not intestine (liver G5/G8-Tg) in three different genetic backgrounds: C57Bl/6, apoE-KO, and low density lipoprotein receptor (LDLr)-KO. Hepatic overexpression of ABCG5/G8    enhanced hepatobiliary secretion of cholesterol and plant sterols by 1.5-2-fold, increased the amount of intestinal cholesterol available for absorption and fecal excretion by up to 27%, and decreased the accumulation of plant sterols in plasma    by approximately 25%. However, it did not alter fractional intestinal cholesterol absorption, fecal neutral sterol excretion, hepatic cholesterol concentrations, or hepatic cholesterol synthesis.  Consequently, overexpression of ABCG5/G8 in only    the liver had no effect on the plasma lipid profile, including cholesterol, HDL-C, and non-HDL-C, or on the development of proximal aortic atherosclerosis in C57Bl/6, apoE-KO, or LDLr-KO mice. Thus, liver ABCG5/G8 facilitate the secretion of    liver sterols into bile and serve as an alternative mechanism, independent of intestinal ABCG5/G8, to protect against the accumulation of dietary plant sterols in plasma. However, in the absence of changes in fractional intestinal cholesterol    absorption, increased secretion of sterols into bile induced by hepatic overexpression of ABCG5/G8 was not sufficient to alter hepatic cholesterol balance, enhance cholesterol removal from the body or to alter atherogenic risk in liver G5/G8-Tg    mice. These findings demonstrate that overexpression of ABCG5/G8 in the liver profoundly alters hepatic but not intestinal sterol transport, identifying distinct roles for liver and intestinal ABCG5/G8 in modulating sterol    metabolism.</p>

	]]>
</description>

<author>J E. Wu et al.</author>


</item>


<item>
<title> Human neonatal Fc receptor mediates transport of IgG into luminal secretions for delivery of antigens to mucosal dendritic cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/774</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/774</guid>
<pubDate>Tue, 08 May 2012 19:08:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mucosal secretions of the human gastrointestinal, respiratory, and genital tracts contain significant quantities of IgG. The mechanism by which IgG reaches luminal secretions and the function of IgG in these locations are unknown.    Here, we find that the human neonatal Fc receptor (FcRn) is the vehicle that transports IgG across the intestinal epithelial barrier into the lumen where the IgG can bind cognate antigen. The FcRn can then recycle the IgG/antigen complex back    across the intestinal barrier into the lamina propria for processing by dendritic cells and presentation to CD4(+) T cells in regional organized lymphoid structures. These results explain how IgG is secreted onto mucosal surfaces and scavenges    luminal antigens for recognition by the immune system.</p>

	]]>
</description>

<author>M Yoshida et al.</author>


</item>


<item>
<title> Characterization of the progressive skin disease and inflammatory cell infiltrate in mice with inhibited NF-kappaB signaling.</title>
<link>http://mouseion.jax.org/stfb2000_2009/773</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/773</guid>
<pubDate>Tue, 08 May 2012 19:07:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>A growth inhibitory role in skin development for the NF-kappaB proteins has been established in recent years. We have previously shown that inhibition of NF-kappaB by overexpression of degradation-resistant IkappaB-alpha in the    skin results in the development of squamous cell carcinomas (SCC). In this paper, we characterize the progressive skin disease leading to cancer development in mice with inhibited NF-kappaB signaling in the skin. Increased proliferation and a    strong inflammatory response were evident in transgenic skin. A mixed inflammatory cell infiltrate dominated by polymorphonuclear leukocytes was observed in concurrence with an upregulation of the proinflammatory cytokine tumor necrosis    factor-alpha. This genetically engineered mouse mutation may be a useful tool to test the efficacy of cytokine therapies for SCC in the future.</p>

	]]>
</description>

<author>H o. van et al.</author>


</item>


<item>
<title> A new murine model of humoral immuno-deficiency specifically affects class switching to T-independent antigens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/772</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/772</guid>
<pubDate>Tue, 08 May 2012 19:07:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Immunoglobulin (Ig) isotype deficiencies are among the most common and least characterized humoral immunodeficiencies. A thorough understanding of their immunological and genetic features has been hampered by their extreme    heterogeneity and the paucity of suitable animal models. Here, we report the initial characterization of a new mouse model with selective Ig deficiency. SENCARA mice display low serum IgG3 levels as well as severely deficient IgG3 responses to T    cell-independent (TI) type 1 and 2 antigens.  However, despite the significant block in class switching, expression of activation-induced deaminase and gamma3 germ-line transcription after TI antigen immunization are normal. IgG3 production in    response to in vitro LPS stimulation was also normal, ruling out a specific defect in the Cgamma3 switch machinery. A decrease in the number of peritoneal B1a cells and enlarged splenic marginal zones were observed. The immunodeficiency is    inherited as an autosomal, semi-dominant, essentially monogenic trait in SENCARA x C57BL/6 crosses. The SENCARA humoral immunodeficiency constitutes a novel immune phenotype, resembling human conditions such as IgG2 deficiency. This new mouse    model will be of interest for the understanding of mechanisms involved in TI immune responses and may provide new insights into the molecular basis of human Ig deficiencies.</p>

	]]>
</description>

<author>I I. Kuzin et al.</author>


</item>


<item>
<title> New mouse genetic models for human contraceptive development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/771</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/771</guid>
<pubDate>Tue, 08 May 2012 19:06:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic strategies for the post-genomic sequence age will be designed to provide information about gene function in a myriad of physiological processes. Here an ENU mutagenesis program (http://reprogenomics.jax.org) is described    that is generating a large resource of mutant mouse models of infertility; male and female mutants with defects in a wide range of reproductive processes are being recovered. Identification of the genes responsible for these defects, and the    pathways in which these genes function, will advance the fields of reproduction research and medicine.  Importantly, this program has potential to reveal novel human contraceptive targets.</p>

	]]>
</description>

<author>C Lessard et al.</author>


</item>


<item>
<title> Systems biology of the 2-cell mouse embryo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/770</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/770</guid>
<pubDate>Tue, 08 May 2012 19:06:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>The transcriptome of the 2-cell mouse embryo was analyzed to provide insight into the molecular networks at play during nuclear reprogramming and embryonic genome activation. Analysis of ESTs from a 2-cell cDNA library identified    nearly 4,000 genes, over half of which have not been previously studied. Transcripts of mobile elements, especially those of LTR retrotransposons, are abundantly represented in 2-cell embryos, suggesting their possible role in introducing genomic    variation, and epigenetic restructuring of the embryonic genome. Analysis of Gene Ontology of the 2-cell-stage expressed genes outlines the major biological processes that guide the oocyte-to-embryo transition. These results provide a foundation    for understanding molecular control at the onset of mammalian development.</p>

	]]>
</description>

<author>A V. Evsikov et al.</author>


</item>


<item>
<title> The MHC class I-like Fc receptor promotes humorally mediated autoimmune disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/769</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/769</guid>
<pubDate>Tue, 08 May 2012 19:05:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>The MHC class I family-like Fc receptor, FcRn, is normally responsible for extending the life span of serum IgG Ab's, but whether this molecule contributes to autoimmune pathogenesis remains speculative. To determine directly    whether this function contributes to humoral autoimmune disease, we examined whether a deficiency in the FcRn heavy chain influences autoimmune arthritis in the K/BxN mouse model. FcRn deficiency conferred either partial or complete protection in    the arthritogenic serum transfer and the more aggressive genetically determined K/BxN autoimmune arthritis models. The protective effects of an FcRn deficiency could be overridden with excessive amounts of pathogenic IgG Ab's. The therapeutic    saturation of FcRn by high-dose intravenous IgG (IVIg) also ameliorated arthritis, directly implicating FcRn blockade as a significant mechanism of IVIg's anti-inflammatory action. The results suggest that FcRn is a potential therapeutic target    that links the initiation and effector phases of humoral autoimmune disease.</p>

	]]>
</description>

<author>S Akilesh et al.</author>


</item>


<item>
<title> Contributions of dysregulated energy metabolism to type 2 diabetes development in NZO/H1Lt mice with polygenic obesity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/768</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/768</guid>
<pubDate>Tue, 08 May 2012 19:05:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>New Zealand Obese (NZO) male mice develop a polygenic juvenile-onset obesity and maturity-onset hyperinsulinemia and hyperglycemia (diabesity).  Here we report on metabolic and molecular changes associated with the antidiabesity    action of CL316,243 (CL), a beta(3)-adrenergic receptor agonist. Dietary CL treatment initiated at weaning reduced the peripubertal rise in body weight and adiposity while promoting growth without suppressing hyperphagia. The changes in    adiposity, in turn, suppressed development of hyperinsulinemia, hyperleptinemia, hyperlipidemia, and hyperglycemia. These CL-induced alterations were reflected by decreased adipose tissue mass, increased expression of transcripts for uncoupling    protein-1 (UCP-1), peroxisome proliferator-activated receptor alpha (PPARalpha), peroxisome proliferater-activated receptor coactivator-1 (PGC-1), and robust development of brown adipocyte function in white fat. Increased drug-mediated energy    dissipation elicited a 1.5 degrees C increase in whole body temperature under conditions of increased food intake but with no change in physical activity. Indirect calorimetry of mice treated with CL showed both increased energy expenditure and a    restoration of a prominent diurnal pattern in the respiratory exchange ratio suggesting improved nutrient sensing. Our data suggest that CL promotes increased energy dissipation in white and brown fat depots by augmenting thermogenesis and by    metabolic re-partitioning of energy in a diabesity-protective fashion. This is the first report demonstrating the effects of dietary beta(3)-agonist in preventing the onset of diabesity in a polygenic rodent model of type 2    diabetes.</p>

	]]>
</description>

<author>R A. Koza et al.</author>


</item>


<item>
<title> Prolonged survival of neonatal porcine islet xenografts in mice treated with a donor-specific transfusion and anti-CD154 antibody.</title>
<link>http://mouseion.jax.org/stfb2000_2009/767</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/767</guid>
<pubDate>Tue, 08 May 2012 19:04:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Combined treatment with a single donor-specific transfusion (DST) and a brief course of anti-mouse CD154 monoclonal antibody (mAb) to induce co-stimulation blockade leads to long-term murine islet allograft survival.    The authors hypothesized that this protocol could also induce long-term survival of neonatal porcine islet cell clusters (NPCC) in chemically diabetic immunocompetent mice and allow their differentiation into functional insulin-producing cells.    METHODS: Pancreata from 1- to 3-day-old pigs were collagenase digested and cultured for 8 days. NPCC were recovered and transplanted into the renal subcapsular space.  Recipients included chemically diabetic nonobese diabetic (NOD)-scid and    C57BL/6 mice that were otherwise untreated, treated with anti-CD154 mAb alone, or treated with DST plus anti-CD154 mAb. Plasma glucose concentration and body weight were measured, and xenografts were examined histologically. RESULTS: NPCC fully    differentiated and restored normoglycemia in four of five diabetic NOD-scid recipients but were uniformly rejected by diabetic C57BL/6 recipients. Anti-CD154 mAb monotherapy restored normoglycemia in 4 of 10 (40%) NPCC-engrafted, chemically    diabetic C57BL/6 mice, but combined treatment with DST and anti-CD154 mAb restored normoglycemia in 12 of 13 (92%) recipients.  Reversal of diabetes required 5 to 12 weeks. Surviving grafts were essentially free of inflammatory infiltrates 15    weeks after transplantation. CONCLUSIONS: Combination therapy with a single DST and a brief course of anti-mouse CD154 mAb without maintenance immunosuppression permits survival and differentiation of NPCC in diabetic C57BL/6 mice.  Successful    grafts were associated with durable restoration of normoglycemia and the absence of graft inflammation.</p>

	]]>
</description>

<author>M C. Appel et al.</author>


</item>


<item>
<title> Three ENU-induced neurological mutations in the pore loop of sodium channel Scn8a (Na(v)1.6) and a genetically linked retinal mutation, rd13.</title>
<link>http://mouseion.jax.org/stfb2000_2009/766</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/766</guid>
<pubDate>Tue, 08 May 2012 19:03:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>The goal of The Jackson Laboratory Neuroscience Mutagenesis Facility is to generate mouse models of human neurological disease. We describe three new models obtained from a three-generation screen for recessive mutations.     Homozygous mutant mice from lines nmf2 and nmf5 exhibit hind limb paralysis and juvenile lethality. Homozygous nmf58 mice exhibit a less severe movement disorder that includes sustained dystonic postures. The mutations were mapped to the distal    region of mouse Chromosome (Chr) 15.  Failure to complement a mutant allele of a positional candidate gene, Scn8a, demonstrated that the mutations are new alleles of Scn8a. Missense mutations of evolutionarily conserved residues of the sodium    channel were identified in the three lines, with the predicted amino acid substitutions N1370T, I1392F, and L1404H. These residues are located within the pore loop of domain 3 of sodium channel Na(v)1.6. The lethal phenotypes suggest that the new    alleles encode proteins with partial or complete loss of function. Several human disorders are caused by mutation in the pore loop of domain 3 of paralogous sodium channel genes. Line nmf5 contains a second, independent mutation in the rd13 locus    that causes a reduction in cell number in the outer nuclear layer of the retina. rd13 was mapped to the distal 4 Mb of Chr 15. No coding or splice site mutations were detected in Pde1b, a candidate gene for rd13. The generation of three    independent Scn8a mutations among 1100 tested G3 families demonstrates that the Scn8a locus is highly susceptible to ENU mutagenesis. The new alleles of Scn8a will be valuable for analysis of sodium channel physiology and disease.</p>

	]]>
</description>

<author>D A. Buchner et al.</author>


</item>


<item>
<title> Bio-ontologies-fast and furious.</title>
<link>http://mouseion.jax.org/stfb2000_2009/765</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/765</guid>
<pubDate>Tue, 08 May 2012 19:03:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J Blake</author>


</item>


<item>
<title> The developmental transcription factor slug is widely expressed in tissues of adult mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/764</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/764</guid>
<pubDate>Tue, 08 May 2012 19:02:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Slug transcription factor plays an important role in epithelial-mesenchymal transformation during embryogenesis and is expressed in adult tissues during carcinogenesis. By detecting expression of a Slug-beta-galactosidase    fusion protein, we have now demonstrated that Slug is also re-expressed in a variety of normal tissues in the adult mouse. Slug is expressed at relatively high levels in patchy stretches of basal cells in stratified and pseudostratified    epithelium, including skin, oral mucosa, esophagus, stomach, rectum, cervix, and trachea. Slug is also found at variable levels in fibroblasts and stromal smooth muscle cells in many tissues. Sites of more intense Slug expression in mesenchymal    tissues include cartilage, kidney glomeruli, lung, ovary, and uterus. Therefore, Slug expression is not restricted to the period of embryonic development or to pathological processes. The pattern of localization to basal cells in various    epithelia suggests that Slug may play a role in the cell migration that occurs during continual renewal of these tissues.</p>

	]]>
</description>

<author>A E. Parent et al.</author>


</item>


<item>
<title> Reductions in linker histone levels are tolerated in developing spermatocytes but cause changes in specific gene expression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/763</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/763</guid>
<pubDate>Tue, 08 May 2012 19:02:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>H1 linker histones are involved in packaging chromatin into 30-nm fibers and higher order structures. Most eukaryotic cells contain nearly one H1 molecule for each nucleosome core particle. Male germ cells in mammals contain large    amounts of a germ cell-specific linker histone, HIST1HT, herein denoted H1t, which is particularly abundant in pachytene spermatocytes. Despite its abundance in male germ cells and significant divergence in primary sequence from other H1    subtypes, inactivation of the H1t gene in mice showed that it is not required for spermatogenesis.  Analysis of germ cell chromatin from H1t null mice showed that other H1 subtypes, especially the testis-enriched HIST1H1A, herein denoted as the    H1a subtype, were able to compensate for the absence of H1t to maintain a normal total H1 to nucleosome core ratio. To disrupt the compensation, we generated H1t and H1a double null mice by two sequential gene-targeting steps in embryonic stem    cells. Elimination of both H1t and H1a led to a 25% decrease in the ratio of H1 to nucleosome cores in double null germ cells. Surprisingly, the reduction in H1 did not perturb spermatogenesis or produce detectable defects in meiotic processes.    Microarray analysis of gene expression showed that the reduced linker histone levels did not affect global gene expression, but it did cause changes in expression of specific genes. Our results indicate that a partial reduction in linker    histone-nucleosome core particle stoichiometry is tolerated in developing male germ cells.</p>

	]]>
</description>

<author>Q Lin et al.</author>


</item>


<item>
<title> Dual effect of p53 on radiation sensitivity in vivo: p53 promotes hematopoietic injury, but protects from gastro-intestinal syndrome in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/762</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/762</guid>
<pubDate>Tue, 08 May 2012 19:01:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ionizing radiation (IR) induces p53-dependent apoptosis in radiosensitive tissues, suggesting that p53 is a determinant of radiation syndromes. In fact, p53-deficient mice survive doses of IR that cause lethal hematopoietic    syndrome in wild-type animals. Surprisingly, p53 deficiency results in sensitization of mice to higher doses of IR, causing lethal gastro-intestinal (GI) syndrome. While cells in the crypts of p53-wild-type epithelium undergo prolonged growth    arrest after irradiation, continuous cell proliferation ongoing in p53-deficient epithelium correlates with accelerated death of damaged cells followed by rapid destruction of villi and accelerated lethality. p21-deficient mice are also    characterized by increased sensitivity to GI syndrome-inducing doses of IR. We conclude that p53/p21-mediated growth arrest plays a protective role in the epithelium of small intestine after severe doses of IR. Pharmacological inhibition of p53    by a small molecule that can rescue from lethal hematopoietic syndrome has no effect on the lethality from gastro-intestinal syndrome, presumably because of a temporary and reversible nature of its action.</p>

	]]>
</description>

<author>E A. Komarova et al.</author>


</item>


<item>
<title> Transgenic rescue of neurogenic atrophy in the nmd mouse reveals a role for Ighmbp2 in dilated cardiomyopathy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/761</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/761</guid>
<pubDate>Tue, 08 May 2012 19:01:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Immunoglobulin mu binding protein 2 (IGHMBP2) is a DNA/RNA helicase with a putative role in transcriptional regulation and splicing. A recessive mutation of the Ighmbp2 gene in neuromuscular degeneration (nmd) mice causes    progressive neurogenic atrophy of limb muscles. Affected mice show significant loss of motor neurons with large caliber axons and a moderate reduction of neurons with small caliber axons in the ventral nerve roots of the spinal cord. To    investigate the role of Ighmbp2 in the pathogenesis of neuromuscular degeneration, we generated two independent lines of transgenic mice expressing the full-length Ighmbp2 cDNA specifically in neurons. Histopathological evaluation of L4 ventral    nerve roots revealed that transgenic expression of the Ighmbp2 cDNA prevented primary motor neuron degeneration, while restoring the normal axonal morphology and density in nmd mice. A similar neuronal improvement is found in mutant mice carrying    the CAST/EiJ-derived modifier of nmd (Mnm(C)). Intriguingly, both the transgenic and modified nmd mice went on to develop a previously unobserved cardiac and skeletal myopathy. Necropsy of nmd mice in end-stage heart failure revealed a primary    dilated cardiomyopathy with secondary respiratory failure that was confirmed by in vivo ECG and echocardiographic measures. Our results suggest that reduced levels of IGHMBP2 in nmd mice compromise the integrity and function not only of motor    neurons but also of skeletal and cardiac myocytes. These findings highlight the important role of IGHMBP2 in the maintenance and survival of these terminally differentiated cell types.</p>

	]]>
</description>

<author>T P. Maddatu et al.</author>


</item>


<item>
<title> The XY body: a specialized meiotic chromatin domain.</title>
<link>http://mouseion.jax.org/stfb2000_2009/760</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/760</guid>
<pubDate>Tue, 08 May 2012 19:00:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The sex chromosomes of mammalian spermatocytes form a specialized nuclear territory known as the XY body, where both transcription and homologous recombination are restricted. The array of proteins assembled into the XY body is    typical of heterochromatin. This special subnuclear domain is in distinct contrast to the autosomal domain of the spermatocyte nucleus, where both homologous recombination and transcription occur. The special features of the XY body might reflect    absence of homology between the sex chromosomes, rather than any form of dosage compensation, and may also serve to mark parental origin of the paternal X chromosome.</p>

	]]>
</description>

<author>M A. Handel</author>


</item>


<item>
<title> Duration of alloantigen presentation and avidity of T cell antigen recognition correlate with immunodominance of CTL response to minor histocompatibility antigens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/759</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/759</guid>
<pubDate>Tue, 08 May 2012 19:00:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>CD8 T lymphocytes (CTL) responsive to immunodominant minor histocompatibility (minor H) Ags are thought to play a disproportionate role in allograft rejection in MHC-identical solid and bone marrow transplant settings. Although    many studies have addressed the mechanisms underlying immunodominance in models of infectious diseases, cancer immunotherapy, and allograft immunity, key issues regarding the molecular basis of immunodominance remain poorly understood. In this    study, we exploit the minor H Ag system to understand the relationship of the various biochemical parameters of Ag presentation and recognition to immunodominance. We show that the duration of individual minor H Ag presentation and the avidity of    T cell Ag recognition influence the magnitude and, hence, the immunodominance of the CTL response to minor H Ags. These properties of CTL Ag presentation and recognition that contribute to immunodominance have implications not only for tissue    transplantation, but also for autoimmunity and tumor vaccine design.</p>

	]]>
</description>

<author>Y Yoshimura et al.</author>


</item>


<item>
<title> Stage-dependent effects of oocytes and growth differentiation factor 9 on mouse granulosa cell development: advance programming and subsequent control of the transition from preantral secondary follicles to early antral tertiary
   follicles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/758</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/758</guid>
<pubDate>Tue, 08 May 2012 18:59:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>The development of an ovarian follicle requires a complex set of reciprocal interactions between the oocyte and granulosa cells in order for both types of cells to develop properly. These interactions are largely orchestrated by    the oocyte via paracrine factors such as growth differentiation factor 9 (GDF9). To examine these interactions further, a study was conducted of the effects of oocytes at different stages of development on proteins synthesized by mouse granulosa    cells during the transition of granulosa cells (GCs) from preantral, secondary (2 degrees ) follicles (2 degrees GCs) to mural granulosa cells (3 degrees GCs) of antral tertiary (3 degrees ) follicles. The ability of recombinant GDF9 to mimic the    effects of oocytes was also determined. Effects were evaluated by high- resolution, two-dimensional protein gel electrophoresis coupled to computer-assisted, quantitative gel image analysis. Coculture of the 2 degrees GCs with growing oocytes    (GOs) from 2 degrees follicles brought about many of the changes in granulosa cell phenotype associated with the 2 degrees to 3 degrees follicle transition. GDF9 likewise brought about many of these changes, but only a subset of GDF9-affected    protein spots were also affected by coculture with GOs. Coculture of 2 degrees GCs with the nearly fully grown oocytes (FGOs) from 3 degrees follicles had a reduced effect on 2 degrees GC phenotype, in comparison with coculture with GOs. For some    proteins, oocyte coculture or GDF9 treatment appeared to have opposite effects on 2 degrees GCs and 3 degrees GCs. Additional effects of GDF9 and oocytes were seen in cultures of 2 degrees GCs for proteins other than those that differed between    untreated control 2 degrees and 3 degrees GCs. These results indicate that GOs and GDF9 can each induce 2 degrees GCs to shift their phenotype toward that of 3 degrees GCs. The ability of the oocyte to produce this effect is diminished with    oocyte development. The transition in the GC phenotype promoted by oocytes appears stable because differences in 2 degrees GCs promoted by oocytes and GDF9 were observed in untreated 3 degrees GCs. We conclude that the influence of the oocyte on    GCs changes with the progression of their development, and so too does the response of the GCs to the oocyte. Moreover, by acting on the 2 degrees GCs, GOs are able to influence stably the phenotype of 3 degrees GCs. Thus, at or near the 2    degrees to 3 degrees follicle transition, signals from the growing  oocyte contribute to the development of the mural GC phenotype.</p>

	]]>
</description>

<author>K E. Latham et al.</author>


</item>


<item>
<title>Breakdown of the Dipole Approximation in Soft-X-Ray Photoemission</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/35</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/35</guid>
<pubDate>Tue, 08 May 2012 18:59:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although breakdowns in the dipole approximation in the soft-X-ray photon-energy range (<em>h</em>ν≤5 keV) were first observed 30 years ago and have been studied theoretically for many years, their significance at low energies has remained generally unappreciated within the broader photoemission community. Advances in gas-phase photoemission experiments using synchrotron radiation have recently highlighted nondipole effects at relatively low energies while probing the limits of the dipole approximation. Breakdowns in this approximation are manifested primarily as deviations from dipolar angular distributions of photoelectrons. Detailed new results demonstrate nondipolar angular-distribution effects are easily observable in atomic gases at energies well below 1 keV, and, in molecules, a previously unexpected phenomenon greatly enhances the breakdown of the dipole approximation just above core-level ionization thresholds. A progress report on this newly burgeoning area from an experimental perspective is presented here, including a brief history, a description of recent advances, graphical representations of nondipolar angular distributions, a re-evaluation of the classic first experiment in the soft-X-ray range and a look to the future.</p>

	]]>
</description>

<author>Dennis W. Lindle et al.</author>


</item>


<item>
<title> Meiosis-activating sterol promotes the metaphase I to metaphase II transition and preimplantation developmental competence of mouse oocytes maturing in vitro.</title>
<link>http://mouseion.jax.org/stfb2000_2009/757</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/757</guid>
<pubDate>Tue, 08 May 2012 18:59:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>The objective of this study was to determine the effects of a sterol found in ovarian follicular fluid, known as meiosis-activating sterol (FF-MAS), on the maturation of mouse oocytes in vitro. Possible effects of FF-MAS in    promoting the metaphase I (MI) to metaphase II (MII) transition (nuclear maturation) and the competence of oocytes to complete preimplantation embryo development to the blastocyst stage (cytoplasmic maturation) were assessed. Cumulus    cell-enclosed oocytes that were compromised in their ability to undergo nuclear maturation and subsequent development because of the age or genotype of the female were isolated at the germinal vesicle stage and matured in vitro using media    supplemented with 0 to 20 microM FF-MAS. Oocytes that progressed to MII were inseminated in vitro, and the percentages developing to the 2-cell and blastocyst stages were determined. The sterol was omitted from the media used for oocyte    insemination or preimplantation development. FF-MAS promoted a significantly higher percentage of oocytes in all groups to progress to MII in vitro. Moreover, FF-MAS treatment of oocytes maturing in vitro dramatically increased the competence of    all but one of the groups of oocytes to complete preimplantation development. Therefore, FF-MAS improved mouse oocyte quality by promoting both nuclear and cytoplasmic maturation in vitro.</p>

	]]>
</description>

<author>Bivens C. Marin et al.</author>


</item>


<item>
<title> Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/756</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/756</guid>
<pubDate>Tue, 08 May 2012 18:58:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Abl kinase inhibitor imatinib mesylate is the preferred treatment for Philadelphia chromosome-positive (Ph(+)) chronic myeloid leukemia (CML) in chronic phase but is much less effective in CML blast crisis or Ph(+) B-cell acute    lymphoblastic leukemia (B-ALL). Here, we show that Bcr-Abl activated the Src kinases Lyn, Hck and Fgr in B-lymphoid cells. BCR-ABL1 retrovirus-transduced marrow from mice lacking all three Src kinases efficiently induced CML but not B-ALL in    recipients. The kinase inhibitor CGP76030 impaired the proliferation of B-lymphoid cells expressing Bcr-Abl in vitro and prolonged survival of mice with B-ALL but not CML. The combination of CGP76030 and imatinib was superior to imatinib alone in    this regard. The biochemical target of CGP76030 in leukemia cells was Src kinases, not Bcr-Abl. These results implicate Src family kinases as therapeutic targets in Ph(+) B-ALL and suggest that simultaneous inhibition of Src and Bcr-Abl kinases    may benefit individuals with Ph(+) acute leukemia.</p>

	]]>
</description>

<author>Y Hu et al.</author>


</item>


<item>
<title> Gravity receptor function in mice with graded otoconial deficiencies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/755</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/755</guid>
<pubDate>Tue, 08 May 2012 18:57:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of the present study was to examine gravity receptor function in mutant mouse strains with variable deficits in otoconia: lethal milk (lm), pallid (pa), tilted (tlt), mocha (mh), and muted (mu). Control animals were    either age-matched heterozygotes or C57BL/6J (abbr. B6) mice.  Gravity receptor function was measured using linear vestibular evoked potentials (VsEPs). Cage and swimming behaviors were also documented.  Temporal bones were cleared to assess the    overall otoconial deficit and to correlate structure and function for lm mice. Results confirmed the absence of VsEPs for mice that lacked otoconia completely. VsEP thresholds and amplitudes varied in mouse strains with variable loss of otoconia.     Some heterozygotes also showed elevated VsEP thresholds in comparison to B6 mice. In lm mice, which have absent otoconia in the utricle and a variable loss of otoconia in the saccule, VsEPs were present and average P1/N1 amplitudes were highly    correlated with the average loss of saccular otoconia (R = 0.77,p < 0.001). Cage and swimming behavior were not adversely affected in those animals with recordable VsEPs. Most, but not all, mice with absent VsEPs were unable to swim. Some animals    were able to swim despite having no measurable gravity receptor response. The latter finding underscores the remarkable adaptive potential exhibited by neurobehavioral systems following profound sensory loss. It also shows that behavior alone may    be an unreliable indicator of the extent of gravity receptor deficits.</p>

	]]>
</description>

<author>S M. Jones et al.</author>


</item>


<item>
<title> A genome end-game: understanding gene function in the nervous system.</title>
<link>http://mouseion.jax.org/stfb2000_2009/754</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/754</guid>
<pubDate>Tue, 08 May 2012 18:57:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C Bult et al.</author>


</item>


<item>
<title> B cell selection defects underlie the development of diabetogenic APCs in nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/753</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/753</guid>
<pubDate>Tue, 08 May 2012 18:56:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>One mechanism whereby B cells contribute to type 1 diabetes in nonobese diabetic (NOD) mice is as a subset of APCs that preferentially presents MHC class II-bound pancreatic beta cell Ags to autoreactive CD4 T cells.  This results    from their ability to use cell surface Ig to specifically capture beta cell Ags. Hence, we postulated a diabetogenic role for defects in the tolerance mechanisms normally blocking the maturation and/or activation of B cells expressing    autoreactive Ig receptors. We compared B cell tolerance mechanisms in NOD mice with nonautoimmune strains by using the IgHEL and Ig3-83 transgenic systems, in which the majority of B cells recognize one defined Ag. NOD- and nonautoimmune-prone    mice did not differ in ability to delete or receptor edit B cells recognizing membrane-bound self Ags. However, in contrast to the nonautoimmune-prone background, B cells recognizing soluble self Ags in NOD mice did not undergo partial deletion    and were also not efficiently anergized. The defective induction of B cell tolerance to soluble autoantigens is most likely responsible for the generation of diabetogenic APC in NOD mice.</p>

	]]>
</description>

<author>P A. Silveira et al.</author>


</item>


<item>
<title> Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/752</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/752</guid>
<pubDate>Tue, 08 May 2012 18:56:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have developed a genotyping system for detecting genetic contamination in the laboratory mouse based on assaying single-nucleotide polymorphism (SNP) markers positioned on all autosomes and the X chromosome. This system provides    a fast, reliable, and cost-effective way for genetic monitoring, while maintaining a very high degree of confidence. We describe the allelic distribution of 235 SNPs in 48 mouse strains, thereby creating a database of polymorphisms useful for    genotyping purposes. The SNP markers used in this study were chosen from publicly available SNP databases. Four genotyping methods were evaluated, and dynamic two-tube allele-specific PCR assays were developed for each marker and tested on a set    of 48 inbred mouse strains. The minimal number of assays sufficient to distinguish groups consisting of different numbers of mouse strains was estimated, and a panel of 28 SNPs sufficient to distinguish virtually all of the inbred strains tested    was selected. Amplifluor SNP detection assays were developed for these markers and tested on an extended list of 96 strains. This panel was used as a genetic quality control approach to monitor the genotypes of nearly 300 inbred, wild-derived,    congenic, consomic, and recombinant inbred strains maintained at The Jackson Laboratory. We have concluded that this marker panel is sufficient for genetic contamination monitoring in colonies containing a large number of genetically diverse    mouse strains and that reduced versions of the panel could be implemented in facilities housing a lower number of strains.</p>

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</description>

<author>P M. Petkov et al.</author>


</item>


<item>
<title> Endogenous oncogenic K-ras(G12D) stimulates proliferation and widespread neoplastic and developmental defects.</title>
<link>http://mouseion.jax.org/stfb2000_2009/751</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/751</guid>
<pubDate>Tue, 08 May 2012 18:55:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Activating mutations in the ras oncogene are not considered sufficient to induce abnormal cellular proliferation in the absence of cooperating oncogenes. We demonstrate that the conditional expression of an endogenous K-ras(G12D)    allele in murine embryonic fibroblasts causes enhanced proliferation and partial transformation in the absence of further genetic abnormalities. Interestingly, K-ras(G12D)-expressing fibroblasts demonstrate attenuation and altered regulation of    canonical Ras effector signaling pathways. Widespread expression of endogenous K-ras(G12D) is not tolerated during embryonic development, and directed expression in the lung and GI tract induces preneoplastic epithelial hyperplasias. Our results    suggest that endogenous oncogenic ras is sufficient to initiate transformation by stimulating proliferation, while further genetic lesions may be necessary for progression to frank malignancy.</p>

	]]>
</description>

<author>D A. Tuveson et al.</author>


</item>


<item>
<title> Genetic contributors to lipoprotein cholesterol levels in an intercross of 129S1/SvImJ and RIIIS/J inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/750</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/750</guid>
<pubDate>Tue, 08 May 2012 18:55:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>To determine the genetic contribution to variation among lipoprotein cholesterol levels, we performed quantitative trait locus (QTL) analyses on an intercross between mouse strains RIIIS/J and 129S1/SvImJ. Male mice of the parental    strains and the reciprocal F1 and F2 populations were fed a high-cholesterol, cholic acid-containing diet for 8-12 wk. At the end of the feeding period, plasma total, high-density lipoprotein (HDL), and non-HDL cholesterol were determined. For    HDL cholesterol, we identified three significant QTLs on chromosomes (Chrs) 1 (D1Mit507, 88 cM, 72-105 cM, 4.8 LOD), 9 (D11Mit149, 14 cM, 10-25 cM, 9.4 LOD), and 12 (D12Mit60, 20 cM, 0-50 cM, 5.0 LOD). These QTLs were considered identical to QTLs    previously named Hdlq5, Hdlq17, and Hdlq18, respectively, in crosses sharing strain 129. For total cholesterol, we identified two significant QTLs on Chrs 1 and 9, which were named Chol10 (D1Mit507, 88 cM, 10-105 cM, 3.9 LOD) and Chol11    (D11Mit149, 14 cM, 0-30 cM, 4.4 LOD), respectively. In addition, for total cholesterol, we identified two suggestive QTLs on Chrs 12 (distal) and 17, which remain unnamed. For non-HDL cholesterol, we identified and named one new QTL on Chr 17,    Nhdlq3 (D17Mit221, 58 cM, 45-60 cM, 3.4 LOD). Nhdlq3 colocalized with orthologous human QTLs for lipoprotein phenotypes, and with Abcg5 and Abcg8. Overall, we detected eight QTLs for lipoprotein cholesterol concentrations on Chrs 1, 9, 12, and 17    (each two per chromosome), including a new QTL for non-HDL cholesterol, Nhdlq3, on Chr 17.</p>

	]]>
</description>

<author>M A. Lyons et al.</author>


</item>


<item>
<title> Influence of sex and diet on quantitative trait loci for HDL cholesterol levels in an SM/J by NZB/BlNJ intercross population.</title>
<link>http://mouseion.jax.org/stfb2000_2009/749</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/749</guid>
<pubDate>Tue, 08 May 2012 18:54:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>To investigate the dependence of HDL quantitative trait loci (QTL) on sex and diet, we generated a large intercross population of mice from parental strains SM/J and NZB/BlNJ. We measured HDL levels in progeny fed a chow diet and    measured them again after 6, 12, and 16 weeks of feeding a high-fat, high-cholesterol diet. QTL analysis was performed on the 260 female and 253 male F(2) progeny. A total of 13 significant QTL were found. Four QTL were specific to female mice:    Hdlq23 (Chr 6, 26 cM), Hdlq26 (Chr 10, 70 cM), Hdlq27 (Chr 15, 48 cM), and Hdlq32 (Chr 19, 40 cM). One significant QTL was specific to male mice: Hdlq29 (Chr 17, 36 cM). In addition, several QTL were found to have effects that were dependent on    diet. Sex- and diet-dependent effects were characterized using a linear model-based genome scan method that avoids the potential pitfalls of subdivided data analysis. The dependence of QTL effects on sex suggests an important role for the sex    hormones in HDL regulation. We recommend that sex should be explicitly accounted for in future studies in the genetics of HDL regulation in both mice and humans.</p>

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</description>

<author>R Korstanje et al.</author>


</item>


<item>
<title> Identification of quantitative trait loci that modify the severity of hereditary spherocytosis in wan, a new mouse model of band-3 deficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/748</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/748</guid>
<pubDate>Tue, 08 May 2012 18:54:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Defects in red blood cell (RBC) membrane skeleton components cause hereditary spherocytosis (HS). Clinically, HS varies significantly even among individuals with identical gene defects, illustrating the profound effects of genetic    background on disease severity. We exploited a new spontaneous mouse model, wan, which arose on the inbred C3H/HeJ strain, to identify quantitative trait loci (QTL) that modify the HS phenotype.  Homozygous wan mice have severe HS due to a    complete deficiency of erythroid band 3. A QTL analysis of RBC count, hemoglobin, hematocrit, mean corpuscular volume (MCV), and mean corpuscular hemoglobin content (MCHC) was performed in wan/wan mice from an F2 intercross between C3H/HeJ(+/wan)    and CAST/Ei(+/+) F1 hybrids. Hematologic and survival data from C3H, CAST/Ei F2 wan homozygotes support the hypothesis that genetic modifiers significantly influence the band-3 null HS phenotype.  Significant QTL were identified for the MCV trait    only, suggesting that RBC membrane characteristics are a target for modifier gene action. The most significant quantitative trait locus, Hsm1 (hereditary spherocytosis modifier 1), localizes to mouse Chromosome 12 and is dominant. The peak LOD    score was obtained with a marker for Spnb1 encoding erythroid beta-spectrin, an obvious candidate gene.</p>

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</description>

<author>L L. Peters et al.</author>


</item>


<item>
<title> Nitric oxide regulates receptor activator of nuclear factor-kappaB ligand and osteoprotegerin expression in bone marrow stromal cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/747</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/747</guid>
<pubDate>Tue, 08 May 2012 18:53:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bone remodeling reflects an equilibrium between bone resorption and formation. The local expression of receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) in bone determines the entry of monoblastic    precursors into the osteoclast lineage and subsequent bone resorption. Nitric oxide (NO) inhibits osteoclastic bone resorption in vitro and regulates bone remodeling in vivo. An interaction of NO with RANKL and OPG has not been studied. Here, we    show that treatment of ST-2 murine stromal cells with the NO donor sodium nitroprusside (100 microm) for 24 h inhibited 1,25 dihydroxyvitamin D(3)-induced RANKL mRNA to less than 33 +/- 7% of control level, whereas OPG mRNA increased to 204 +/-    19% of control. NOR-4 replicated these NO effects. The effects of NO were dose dependent and associated with changes in protein levels: RANKL protein decreased and OPG protein increased after treatment with NO. PTH-induced RANKL expression in    primary stromal cells was inhibited by sodium nitroprusside, indicating that the NO effect did not require vitamin D. NO donor did not change the stability of RANKL or OPG mRNAs, suggesting that NO affected transcription. Finally, cGMP, which can    function as a second messenger for NO, did not reproduce the NO effect, nor did inhibition of endogenous guanylate cyclase prevent the NO effect on these osteoactive genes. The effect of NO to decrease the RANKL/OPG equilibrium should lead to    decreased recruitment of osteoclasts and positive bone formation. Thus, drugs and conditions that cause local increase in NO formation in bone may have positive effects on bone remodeling.</p>

	]]>
</description>

<author>X Fan et al.</author>


</item>


<item>
<title> Cholesterol synthesis inhibition distal to squalene upregulates biliary phospholipid secretion and counteracts cholelithiasis in the genetically prone C57L/J mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/746</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/746</guid>
<pubDate>Tue, 08 May 2012 18:52:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND AND AIMS: Newly synthesised cholesterol contributes poorly to biliary lipid secretion but may assume greater importance when the rate limiting enzyme 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) is upregulated. As    this occurs in the gall stone susceptible C57L/J inbred mouse, we employed two cholesterol biosynthesis inhibitors, Tu 2208 and Ro 48-8071, potent inhibitors of squalene epoxidase and oxidosqualene-lanosterol cyclase, respectively, to assess    their potential in preventing cholesterol cholelithiasis in the C57L/J mouse strain. Mice were fed a lithogenic diet comprising a balanced nutrient intake with 15% dairy fat, 1% cholesterol, and 0.5% cholic acid added. METHODS: We determined gall    stone phenotype, HMGR activity, biliary lipid secretion rates, and counterregulatory events in male C57L/J mice and gall stone resistant AKR treated with Tu 2208 (30-60 mg/kg/day) or Ro 48-8071 (30-100 mg/kg/day), while ingesting chow or the    lithogenic diet. RESULTS: Both agents reduced the gall stone prevalence rate from 73% to 17% in C57L/J mice, inhibited HMGR activity, and decreased hepatic cholesterol concentrations without appreciably influencing biliary cholesterol secretion.    In C57L as well as AKR mice, both agents increased biliary phospholipid (which is mostly phosphatidylcholine) secretion rates and at the highest doses effectively reduced the biliary cholesterol saturation index. CONCLUSIONS: Cholesterol    biosynthesis inhibitors acting distally to squalene do not reduce biliary cholesterol secretion rates despite reductions in cholesterol biosynthesis and hepatocellular levels. However, they effectively prevent gall stone formation through    stimulation of pathways that lead to enhanced biliary phospholipid secretion.</p>

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</description>

<author>G A. Clarke et al.</author>


</item>


<item>
<title> Marking Xs, together and separately.</title>
<link>http://mouseion.jax.org/stfb2000_2009/745</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/745</guid>
<pubDate>Tue, 08 May 2012 18:52:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M A. Handel</author>


</item>


<item>
<title>Electric-octupole and pure-electric-quadrupole effects in soft x-ray photoemission</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/34</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/34</guid>
<pubDate>Tue, 08 May 2012 18:51:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Second-order [ O(k<sup>2</sup>), k = ω/c] nondipole effects in soft-x-ray photoemission are demonstrated via an experimental and a theoretical study of angular distributions of neon valence photoelectrons in the 100–1200 eV photon-energy range. A newly derived theoretical expression for nondipolar angular distributions characterizes the second-order effects using four new parameters with primary contributions from pure-quadrupole and octupole-dipole interference terms. Independent-particle calculations of these parameters account for a significant portion of the existing discrepancy between experiment and theory for Ne 2p first-order nondipole parameters.</p>

	]]>
</description>

<author>Andrei Derevianko et al.</author>


</item>


<item>
<title> Age-related hearing loss and the ahl locus in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/744</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/744</guid>
<pubDate>Tue, 08 May 2012 18:51:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>C57BL/6 (B6) mice experience hearing loss and cochlear degeneration beginning about mid-life, whereas CAST/Ei (CAST) mice retain normal hearing until old age. A locus contributing to the hearing loss of B6 mice, named age-related    hearing loss (ahl), was mapped to Chromosome 10. A homozygous, congenic strain of mice (B6.CAST-+ahl ), generated by crossing B6 (ahl/ahl) and CAST (+ahl/+ahl) mice has the same genomic material as the B6 mice except in the region of the ahl    locus, which is derived from CAST. In this study, we have determined the extent of the CAST-derived region of Chromosome 10 in the congenic strain and have examined mice of all three strains for hearing loss and cochlear morphology between 9 and    25 months of age. Results for B6 mice were similar to those described previously. CAST mice showed no detectable hearing loss even at 24 months of age; however, they had a small amount of ganglion cell degeneration.  B6.CAST-+ahl mice were    protected from early onset hearing loss and basal turn degeneration, but older animals did show some hearing loss and ganglion cell degeneration. We conclude that loci in addition to ahl contribute to the differences in hearing loss between B6    and CAST mice.  These results illustrate the complex inheritance of age-related hearing loss in mice and may have implications for the study of human presbycusis.</p>

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</description>

<author>E M. Keithley et al.</author>


</item>


<item>
<title> Genetic analysis of blood pressure in C3H/HeJ and SWR/J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/743</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/743</guid>
<pubDate>Tue, 08 May 2012 18:50:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hypertension is a complex phenotype induced by multiple environmental and genetic factors. Quantitative trait locus (QTL) analysis is a powerful method for identifying genomic regions underlying complex diseases. We conducted a QTL    analysis of blood pressure in mice using 217 F(2) progeny (males and females) from a cross between the normotensive C3H/HeJ and hypertensive SWR/J inbred strains. Our analysis identified significant QTL controlling blood pressure on chromosome 1    [Chr 1; Bpq8; peak 78 cM; 95% confidence interval 64-106 cM; logarithm of the odds ratio (LOD) 3.5; peak marker D1Mit105] and on Chr 16 (Bpq9; peak 56 cM; 95% confidence interval 46-58 cM; LOD 3.6; peak marker D16Mit158). Bpq8 was previously    identified in a cross between C57BL/6J and A/J mice, and we narrowed this QTL from 42 to 18 cM (95% confidence interval 68-86 cM) by combining the data from these crosses. By examining Bpq8 for regions where ancestral alleles were conserved among    the high allele strains (C57BL/6J, SWR/J) and different from the low allele strains (A/J, C3H/HeJ), we identified a 2.3-cM region where the high allele strains shared a common haplotype. Bpq8 is concordant with known QTL in both rat and human,    suggesting that the causal gene underlying Bpq8 may be conserved as a disease gene in human hypertension.</p>

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</description>

<author>K DiPetrillo et al.</author>


</item>


<item>
<title> Mitogen-activated protein kinase dynamics during the meiotic G2/MI transition of mouse spermatocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/742</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/742</guid>
<pubDate>Tue, 08 May 2012 18:50:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cellular and genetic approaches were used to investigate the requirements for activation during spermatogenesis of the extracellular signal-regulated protein kinases (ERKs), more commonly known as the mitogen-activated protein    kinases (MAPKs). The MAPKS and their activating kinases, the MEKs, are expressed in specific developmental patterns. The MAPKs and MEK2 are expressed in all premeiotic germ cells and spermatocytes, while MEK1 is not expressed abundantly in    pachytene spermatocytes. Phosphorylated (active) variants of these kinases are diminished in pachytene spermatocytes. Treatment of pachytene spermatocytes with okadaic acid (OA), to induce transition from meiotic prophase to metaphase I (G2/MI),    resulted in phosphorylation and enzymatic activation of ERK1/2. However, U0126, an inhibitor of the ERK-activating kinases, MEK1/2, did not inhibit OA-induced MAPK activation or chromosome condensation. Analysis of spermatocytes lacking MOS, a    mitogen-activated protein kinase kinase kinase responsible for MEK and MAPK activation, revealed that MOS is not required for OA-induced activation of the MAPKs.  OA-induced MAPK activation was inhibited by butyrolactone I, an inhibitor of    cyclin-dependent kinases 1 and 2 (CDK1, CDK2); thus, these kinases may regulate MAPK activity. Additionally, spermatocytes lacking CDC25C condensed bivalent chromosomes and activated both MPF and MAPKs in response to OA treatment; therefore,    there is a CDC25C-independent pathway for MPF and MAPK activation. These studies reveal that spermatocytes do not require either MOS or CDC25C for onset of the meiotic division phase or for activation of MPF and the MAPKs, thus implicating a    novel pathway for activation of the ERK1/2 MAPKs in spermatocytes.</p>

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</description>

<author>A Inselman et al.</author>


</item>


<item>
<title> The relative levels of translin-associated factor X (TRAX) and testis brain RNA-binding protein determine their nucleocytoplasmic distribution in male germ cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/741</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/741</guid>
<pubDate>Tue, 08 May 2012 18:49:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Testis brain RNA-binding protein (TB-RBP), the mouse orthologue of human translin, is an RNA and single-stranded DNA-binding protein abundant in testis and brain. Translin-associated factor X (TRAX) was identified as a protein that    interacts with TB-RBP and is dependent upon TB-RBP for stabilization. Using immunohistochemistry to investigate the subcellular locations of TB-RBP and TRAX during spermatogenesis, both proteins localize in nuclei in meiotic pachytene    spermatocytes and in the cytoplasm of subsequent meiotic and post-meiotic cells. An identical subcellular distribution is seen in female germ cells. Western blot analysis of germ cell protein extracts reveals an increased ratio of TRAX to TB-RBP    in meiotic pachytene spermatocytes compared with the post-meiotic round and elongated spermatids. Using COS-1 cells and mouse embryonic fibroblasts derived from TB-RBP null mice as model systems to examine the shuttling of TB-RBP and TRAX, we    demonstrate that TRAX contains a functional nuclear localization signal and TB-RBP contains a functional nuclear export signal. Coexpression of both proteins in COS-1 cells and TB-RBP-deficient mouse embryonic fibroblasts reveals that the ratio    of TRAX to TB-RBP determines their subcellular locations, i.e. increased TRAX to TB-RBP ratios lead to nuclear localizations, whereas TRAX remains in the cytoplasm when TB-RBP levels are elevated. These subcellular distributions require    interaction between TB-RBP and TRAX. We propose that the subcellular locations of TB-RBP and TRAX in male germ cells are modulated by the relative ratios of TRAX and TB-RBP.</p>

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</description>

<author>Y S. Cho et al.</author>


</item>


<item>
<title> Antibodies that label paraffin-embedded mouse tissues: a collaborative endeavor.</title>
<link>http://mouseion.jax.org/stfb2000_2009/740</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/740</guid>
<pubDate>Tue, 08 May 2012 18:49:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Histology and immunohistochemistry are important tools in the study of human diseases and their respective animal models. The study of mouse models has been hampered by the absence of a large set of mouse-specific antibodies    adapted to paraffin-embedded tissues. A total of 196 antibodies were tested on paraffin-embedded mouse tissues preserved in five different fixatives (Fekete's acid-alcohol-formalin, 10% neutral buffered formalin, 4% paraformaldehyde, IHC Zinc    Fixative, and Bouin's fixative). The antibodies were targeted to proteins of the cytoplasm (n = 100), plasma membrane (n = 48), nucleus (n = 36), extracellular compartment (n = 5), cytoplasm/cell membrane (n = 4), and viral proteins (n = 3). A    total of 83 antibodies provided an adequate signal to noise ratio. Of these, adequate labeling required heat-mediated epitope retrieval or enzymatic digestion for 32 and 8 antibodies, respectively. Epitope recognition was best for tissues fixed    with Fekete's acid-alcohol-formalin. However, some proteins could be detected only in IHC Zinc Fixative, confirming that there is no single fixative suitable for the preservation of all epitopes. Four of 13 antibodies that failed to label their    cellular targets on tissue sections successfully labeled whole-mount tissues, indicating that tissue processing plays an important role in epitope degradation. Regularly updated information on immunohistochemistry of normal and neoplastic mouse    tissues is accessible online at (http://tumor.informatics.jax.org); links to antibody suppliers' web sites are provided.</p>

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</description>

<author>I Mikaelian et al.</author>


</item>


<item>
<title> First cleavage plane of the mouse egg is not predetermined but defined by the topology of the two apposing pronuclei.</title>
<link>http://mouseion.jax.org/stfb2000_2009/739</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/739</guid>
<pubDate>Tue, 08 May 2012 18:48:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Studies of experimentally manipulated embryos have led to the long-held conclusion that the polarity of the mouse embryo remains undetermined until the blastocyst stage. However, recent studies reporting that the    embryonic-abembryonic axis of the blastocyst arises perpendicular to the first cleavage plane, and hence to the animal-vegetal axis of the zygote, have led to the claim that the axis of the mouse embryo is already specified in the egg. Here we    show that there is no specification of the axis in the egg. Time-lapse recordings show that the second polar body does not mark a stationary animal pole, but instead, in half of the embryos, moves towards a first cleavage plane. The first    cleavage plane coincides with the plane defined by the two apposing pronuclei once they have moved to the centre of the egg. Pronuclear transfer experiments confirm that the first cleavage plane is not determined in early interphase but rather is    specified by the newly formed topology of the two pronuclei. The microtubule networks that allow mixing of parental chromosomes before dividing into two may be involved in these processes.</p>

	]]>
</description>

<author>T Hiiragi et al.</author>


</item>


<item>
<title> Insulin-like growth factor I and bone mineral density: experience from animal models and human observational studies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/738</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/738</guid>
<pubDate>Tue, 08 May 2012 18:48:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>The insulin-like growth factor (IGF) system has been linked to the process of bone acquisition through epidemiological analyses of large cohorts and in vitro studies of bone cells. However, the precise relationship between the    expression of IGF-I in bone and skeletal homeostasis or pathological conditions such as osteoporosis, remains poorly defined. Recent advances in genomic engineering have resulted in the development of better in vivo models for testing the role of    IGF-I during development and the maintenance of the adult skeleton. Evidence from conditional mutagenesis studies of IGF-I has opened up a new area of in vivo analysis. These studies suggest that serum IGF-I levels may represent more than a    storage depot or permissive factor during skeletal acquisition and that tissue IGF-I is essential for normal bone formation. The implications from these animal models are far-reaching and suggest that newer approaches for manipulating the IGF    regulatory system may one day be useful as therapeutic adjuncts for the treatment of osteoporosis.</p>

	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title> Quantitative gene expression profiling implicates genes for susceptibility and resistance to alveolar bone loss.</title>
<link>http://mouseion.jax.org/stfb2000_2009/737</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/737</guid>
<pubDate>Tue, 08 May 2012 18:47:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Periodontal disease is one of the most prevalent chronic inflammatory diseases. There is a genetic component to susceptibility and resistance to this disease. Using a mouse model, we investigated the progression of alveolar bone    loss by gene expression profiling of susceptible and resistant mouse strains (BALB/cByJ and A/J, respectively). We employed a novel and sensitive quantitative real-time PCR method to compare basal RNA transcription of a 48-gene set in the gingiva    and the spleen and the subsequent changes in gene expression due to Porphyromonas gingivalis oral infection. Basal expression of interleukin-1 beta (Il1b) and tumor necrosis factor alpha (Tnf) mRNA was higher in the gingiva of the susceptible    BALB/cByJ mice than in the gingiva of resistant A/J mice.  Gingival Il1b gene expression increased further and Stat6 gene expression was turned on after P. gingivalis infection in BALB/cByJ mice but not in A/J mice. The basal expression of    interleukin-15 (Il15) in the gingiva and the basal expression of p-selectin (Selp) in the spleen were higher in the resistant A/J mice than in the susceptible BALB/cByJ mice. In the resistant A/J mice the expression of no genes detectably changed    in the gingiva after infection. These results suggest a molecular phenotype in which discrete sets of differentially expressed genes are associated with genetically determined susceptibility (Il1b, Tnf, and Stat6) or resistance (Il15 and Selp) to    alveolar bone loss, providing insight into the genetic etiology of this complex disease.</p>

	]]>
</description>

<author>G T. Hart et al.</author>


</item>


<item>
<title> Islet allograft survival induced by costimulation blockade in NOD mice is controlled by allelic variants of Idd3.</title>
<link>http://mouseion.jax.org/stfb2000_2009/736</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/736</guid>
<pubDate>Tue, 08 May 2012 18:47:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>NOD mice develop type 1 autoimmune diabetes and exhibit genetically dominant resistance to transplantation tolerance induction. These two phenotypes are genetically separable. Costimulation blockade fails to prolong skin allograft    survival in (NOD x C57BL/6)F1 mice and in NOD-related strains made diabetes-resistant by congenic introduction of protective major histocompatibility complex (MHC) or non-MHC Idd region genes. Here, we tested the hypothesis that the genetic basis    for the resistance of NOD mice to skin allograft tolerance also applies to islet allografts. Surprisingly, costimulation blockade induced permanent islet allograft survival in (NOD x C57BL/6)F1 mice but not in NOD mice. After costimulation    blockade, islet allograft survival was prolonged in diabetes-resistant NOD.B6 Idd3 mice and shortened in diabetes-free C57BL/6 mice congenic for the NOD Idd3 variant. Islet allograft tolerance could not be induced in diabetes-resistant NOD.B10    Idd5 and NOD.B10 Idd9 mice.  The data demonstrate that 1) NOD mice resist islet allograft tolerance induction; 2) unlike skin allografts, resistance to islet allograft tolerance is a genetically recessive trait; 3) an Idd3 region gene(s) is an    important determinant of islet allograft tolerance induction; and 4) there may be overlap in the mechanism by which the Idd3 resistance locus improves self-tolerance and the induction of allotolerance.</p>

	]]>
</description>

<author>T Pearson et al.</author>


</item>


<item>
<title> Complement activation is critical to airway hyperresponsiveness after acute ozone exposure.</title>
<link>http://mouseion.jax.org/stfb2000_2009/735</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/735</guid>
<pubDate>Tue, 08 May 2012 18:46:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ozone (O3) can induce airway hyperresponsiveness (AHR) and neutrophilic inflammation. We evaluated the role of complement in development of AHR and inflammation after acute O3 exposure in mice. Mice were exposed to O3 at 2 ppm for    3 hours, and airway responsiveness to methacholine was measured 8 hours after O3 exposure. Complement was depleted or inhibited by intraperitoneal injection of cobra venom factor (CVF) or complement receptor-related gene y (Crry)-Ig, a potent C3    convertase inhibitor; neutrophils were depleted using an antineutrophil monoclonal antibody. CVF attenuated the development of AHR by O3. Administration of Crry-Ig also prevented the development of AHR. Bronchoalveolar lavage (BAL) fluid    neutrophilia after O3 exposure was significantly decreased by administration of either CVF or Crry-Ig. Increased BAL fluid total protein after O3 exposure was lowered by depletion or inhibition of complement. In contrast to the effects of    complement inhibition or depletion, depletion of BAL neutrophil counts by more than 90% with the monoclonal antibody did not affect the development of AHR after O3 exposure. These data indicated that activation of the complement system follows    acute O3 exposure and is important to the development of AHR and airway neutrophilia. However, this neutrophil response does not appear necessary for the development of AHR.</p>

	]]>
</description>

<author>J W. Park et al.</author>


</item>


<item>
<title> The hypolipidemic natural product Commiphora mukul and its component guggulsterone inhibit oxidative modification of LDL.</title>
<link>http://mouseion.jax.org/stfb2000_2009/734</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/734</guid>
<pubDate>Tue, 08 May 2012 18:46:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is accumulating evidence that LDL oxidation is essential for atherogenesis, and that antioxidants that prevent this oxidation may either slow down or prevent atherogenesis. In the present study, we found that Commiphora mukul    and its cholesterol-lowering component, guggulsterone, effectively inhibited LDL oxidation mediated by either catalytic copper ions, free radicals generated with the azo compound 2,2'-azobis-(2-amidinopropane)dihydrochloride (AAPH), soybean    lipoxygenase enzymatically, or mouse peritoneal macrophages. This inhibition was assessed by the decrease in the following parameters describing LDL oxidation: conjugated dienes, relative electrophoretic mobility (REM), thiobarbituric acid    reactive substances, lipid hydroperoxides, oxidation-specific immune epitopes as detected with a monoclonal antibody against oxidized LDL, and the accumulation of LDL derived cholesterol esters in mouse peritoneal macrophages. We concluded that    C. mukul and its lipid-lowering component, guggulsterone, significantly inhibit LDL oxidation. The combination of antioxidant and lipid-lowering properties of C. mukul and guggulsterone makes them especially beneficial against    atherogenesis.</p>

	]]>
</description>

<author>X Wang et al.</author>


</item>


<item>
<title> New intragenic deletions in the Phex gene clarify X-linked hypophosphatemia-related abnormalities in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/733</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/733</guid>
<pubDate>Tue, 08 May 2012 18:45:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>X-linked hypophosphatemic rickets (XLH) in humans is caused by mutation in the PHEX gene. Previously, three mutations in the mouse Phex gene have been reported: Phex(Hyp), Gy, and Phex(Ska1). Here we report analysis of two new    spontaneous mutation in the mouse Phex gene, Phex(Hyp-2J) and Phex(Hyp-Duk). Phex(Hyp-2J) and Phex(Hyp-Duk) involve intragenic deletions of at least 7.3 kb containing exon 15, and 30 kb containing exons 13 and 14, respectively. Both mutations    cause similar phenotypes in males, including shortened hind legs and tail, a shortened square trunk, hypophosphatemia, hypocalcemia, and rachitic bone disease. In addition, mice carrying the Phex(Hyp-Duk) mutation exhibit background-dependent    variable expression of deafness, circling behavior, and cranial dysmorphology, demonstrating the influence of modifying genes on Phex-related phenotypes. Cochlear cross-sections from Phex(Hyp-2J)/Y and Phex(Hyp-Duk)/Y males reveal a thickening of    the temporal bones surrounding the cochlea with the presence of a precipitate in the scala tympani. Evidence of the degeneration of the organ of Corti and spiral ganglion also are present in the hearing-impaired Phex(Hyp-Duk)/Y mice, but not in    the normal-hearing Phex(Hyp-2J)/Y mice. Analysis of the phenotypes noted in Phex(Hyp-Duk)/Y and Phex(Hyp-2J)/Y males, together with those noted in Phex(Ska1)/Y and Phex(Hyp)/Y males, now allow XLH-related phenotypes to be separated from    non-XLH-related phenotypes, such as those noted in Gy/Y males. Also, identification of the genetic modifiers of hearing and craniofacial dysmorphology in Phex(Hyp-Duk)/Y mice could provide insight into the phenotypic variation of XLH in    humans.</p>

	]]>
</description>

<author>Depiereux B. Lorenz et al.</author>


</item>


<item>
<title> ExQuest, a novel method for displaying quantitative gene expression from ESTs.</title>
<link>http://mouseion.jax.org/stfb2000_2009/732</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/732</guid>
<pubDate>Tue, 08 May 2012 18:45:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is a pressing need for interactive bioinformatics tools that empower investigators with the means to extract information and organize it in a simplified but meaningful format. A wealth of mammalian gene expression data is    readily accessible, much of which is based on expressed sequence tags (ESTs). Many mammalian ESTs are derived from tissue-specific cDNA libraries in which the number of ESTs representing a specific gene approximates the transcriptional expression    level in the source tissue.  Our program ExQuest (Expressional Quantification of ESTs) organizes the public EST database (dbEST) into hierarchical tissue classes and reports tissue or developmental gene expression patterns for both mRNA and    genomic sequences. ExQuest also displays tissue expression patterns of genes in the context of assembled chromosomes. These interactive "transcriptome" maps provide a novel tool for investigating the genomic basis of gene expression as well as    prioritizing candidate genes within genetically mapped mutant and quantitative trait loci.</p>

	]]>
</description>

<author>A C. Brown et al.</author>


</item>


<item>
<title> Restoration of hair growth in mice with an alopecia areata-like disease using topical anthralin.</title>
<link>http://mouseion.jax.org/stfb2000_2009/731</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/731</guid>
<pubDate>Tue, 08 May 2012 18:44:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Anthralin is a widely used topical anti-psoriatic drug that may have an immunomodulating effect on alopecia areata (AA) as it does in psoriasis.  The aims of the present study were to investigate the effects of anthralin on hair    growth in balding C3H/HeJ mice affected by an AA-like disease and to study the underlying mechanisms. Affected C3H/HeJ mice were treated daily for 10 weeks on half of the dorsal skin with 0.2% anthralin and the contra-lateral side was treated    with the vehicle ointment. The percentage of surface hair coverage and hair density was graded weekly for both sides and hair growth indices were calculated using these two variables. Hair regrowth was observed in 9/14 mice on the treated sides.    Four mice displayed near complete replacement of normal density and length hairs.  All the vehicle-treated sides showed either no change or continued hair loss. An RNase protection assay (RPA) showed that expression of tumor necrosis factor-alpha    (TNF-alpha) and -beta were inhibited by anthralin upon successful treatment. It appears that anthralin may be an effective therapy for C3H/HeJ mice with AA and certain cytokines may be involved in the therapeutic effects of anthralin on restoring    hair regrowth in AA-affected C3H/HeJ mice.</p>

	]]>
</description>

<author>L Tang et al.</author>


</item>


<item>
<title> Hepatic overexpression of murine Abcb11 increases hepatobiliary lipid secretion and reduces hepatic steatosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/730</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/730</guid>
<pubDate>Tue, 08 May 2012 18:44:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abcb11 encodes for the liver bile salt export pump, which is rate-limiting for hepatobiliary bile salt secretion. We employed transthyretin-Abcb11 and BAC-Abcb11 transgenes to develop mice overexpressing the bile salt export pump    in the liver. The mice manifest increases in bile flow and biliary secretion of bile salts, phosphatidylcholine, and cholesterol.  Hepatic gene expression of cholesterol 7alpha-hydroxylase and ileal expression of the apical sodium bile salt    transporter are markedly reduced, whereas gene expression of targets of the nuclear bile salt receptor FXR (ileal lipid-binding protein, short heterodimer partner (SHP) is increased. Because these changes in gene expression are associated with an    increased overall hydrophobicity of the bile salt pool and a 4-fold increase of the FXR ligand taurodeoxycholate, they reflect bile salt-mediated regulation of FXR and SHP target genes. Despite the increased biliary secretion of bile salts, fecal    bile salt excretion is unchanged, suggestive of an enhanced enterohepatic cycling of bile salts.  Abcb11 transgenic mice fed a lithogenic (high cholesterol/fat/cholic acid) diet display markedly reduced hepatic steatosis compared with wild-type    controls. We conclude that mice overexpressing Abcb11 display an increase in biliary bile salt secretion and taurodeoxycholate content, which is associated with FXR/SHP-mediated changes in hepatic and ileal gene expression. Because these mice are    resistant to hepatic lipid accumulation, regulation of Abcb11 may be important for the pathogenesis and treatment of steatohepatitis.</p>

	]]>
</description>

<author>A Figge et al.</author>


</item>


<item>
<title> Hypertriglyceridaemia in Alstrom&apos;s syndrome: causes and associations in 37 cases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/729</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/729</guid>
<pubDate>Tue, 08 May 2012 18:43:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: To document frequency of severe hypertriglyceridaemia in Alstrom's syndrome (AS) and its relationship to hepatic and renal function, glycaemia and insulin resistance. PATIENTS AND METHODS: Thirty-seven subjects with AS    aged 5-35 years, 51% male, were assessed at multidisciplinary clinics in Canada, UK and Italy. Diagnostic criteria were: severe cone/rod dystrophy leading to severe visual impairment in early childhood, sensorineural deafness, moderate overall    obesity and normal intelligence. Three patients were treated with thyroxine for primary hypothyroidism and one female patient for secondary amenorrhoea with 20 micro g ethinyloestradial combined oral contraceptive. Two male patients were    receiving monthly intramuscular testosterone enanthate for secondary hypogonadism. Fasting bloods were taken for serum insulin, serum glucose, serum triglycerides, hepatic and renal function and glycosylated Hb. Triglyceride levels > 8 mmol/l and    fasting serum insulin levels > 16 microunits/ml were considered to represent severe hypertriglyceridaemia and severe insulin resistance, respectively. All subjects with (23) hypertriglyceridaemia also had high insulin resistance, as measured by    HOMA modelling. However, there was no significant correlation between log tyriglyceride and log serum insulin or HOMA in the whole group (P = 0.2 and 0.14, respectively). There was no clear relationship between serum triglyceride levels and age,    body mass index (BMI), hepatic or renal impairment or glycaemia. CONCLUSION: The first overview of serum triglyceride levels in a significant number of reported cases of Alstrom Syndrome shows an overlap between severe hypertriglyceridaemia and    severe hyperinsulinism, but not a direct correlation between the two nor with insulin resistance measured by HOMA. Triglyceride levels were not related to glycaemia, hepatic or renal dysfunction.</p>

	]]>
</description>

<author>R B. Paisey et al.</author>


</item>


<item>
<title> Differential levels of diabetogenic stress in two new mouse models of obesity and type 2 diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/728</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/728</guid>
<pubDate>Tue, 08 May 2012 18:43:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genetic basis for the more common forms of human obesity predisposing to insulin resistance and development of type 2 diabetes is multigenic rather than monogenic in origin. New mouse "diabesity" models have been created by    combining independent diabetes risk-conferring quantitative trait loci from two unrelated parental strains: New Zealand Obese (NZO/HlLt) and Nonobese Nondiabetic (NON/Lt). F1 hybrid males, heterozygous at all polymorphic autosomal loci    distinguishing the two parental strains, are driven to obesity-induced diabetes (diabesity) at high frequencies. This review focuses on two new recombinant congenic strains (RCSs) developed by introgressing multiple NZO/HlLt chromosomal segments    into the nominally diabesity-resistant NON/Lt strain background.  Both RCSs gain more weight than NON animals. Although exhibiting comparable weight gain and adiposity, only one of the two RCSs develops diabetes. Hence, these two RCSs will be    instructive in elucidating genetic and pathophysiological differences underlying uncomplicated obesity syndromes versus diabetogenic obesity (diabesity) syndromes. Unlike mice with null mutations in a single gene producing morbid obesity, the new    models develop a more moderate obesity produced by the interaction of numerous genes with relatively small effects. These RCSs are differentially sensitive to adverse side effects of thiazolidinediones and thus should be particularly useful for    pharmacogenetic analyses.</p>

	]]>
</description>

<author>E H. Leiter et al.</author>


</item>


<item>
<title> ALS/Lt: a new type 2 diabetes mouse model associated with low free radical scavenging potential.</title>
<link>http://mouseion.jax.org/stfb2000_2009/727</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/727</guid>
<pubDate>Tue, 08 May 2012 18:42:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Outbred CD-1 mice carry a spectrum of genetic susceptibilities for obesity and type 2 diabetes. ALS is an inbred strain with low antioxidant defenses produced by inbreeding CD-1 mice, with selection for susceptibility to alloxan, a    generator of highly reactive oxygen free radicals and a potent beta-cell toxin. The objective of this study was to determine if the low ability to diffuse free radical stress would contribute to spontaneous type 2 diabetes development in    alloxan-untreated males. Indeed, both hyperinsulinemia and impaired glucose tolerance developed spontaneously between 6 and 8 weeks of age in alloxan-untreated males. Further aging was accompanied by increases in body mass, progressively more    severe hyperinsulinemia, and development of overt hyperglycemia. Transition from impaired glucose tolerance to overt hyperglycemia correlated with a decreased ratio of reduced to oxidized glutathione. Evidence that the increased oxidative burden    elicited the type 2 diabetes syndrome was obtained by the systemic elevation of the antioxidative capacity through daily administration of R-lipoic acid. R-lipoic acid (30 mg/kg) prevented hyperglycemia, reduced insulin levels, and increased free    radical scavenging potential. This mouse model with reduced ability to diffuse free radical stress is of obvious interest because free radical-mediated damage is implicated in the pathogenesis and complications of both type 1 and type 2    diabetes.</p>

	]]>
</description>

<author>C E. Mathews et al.</author>


</item>


<item>
<title> BRCA2 deficiency in mice leads to meiotic impairment and infertility.</title>
<link>http://mouseion.jax.org/stfb2000_2009/726</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/726</guid>
<pubDate>Tue, 08 May 2012 18:42:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The role of Brca2 in gametogenesis has been obscure because of embryonic lethality of the knockout mice. We generated Brca2-null mice carrying a human BAC with the BRCA2 gene. This construct rescues embryonic lethality and the mice    develop normally. However, there is poor expression of the transgene in the gonads and the mice are infertile, allowing examination of the function of BRCA2 in gametogenesis. BRCA2-deficient spermatocytes fail to progress beyond the early    prophase I stage of meiosis.  Observations on localization of recombination-related and spermatogenic-related proteins suggest that the spermatocytes undergo early steps of recombination (DNA double strand break formation), but fail to complete    recombination or initiate spermiogenic development. In contrast to the early meiotic prophase arrest of spermatocytes, some mutant oocytes can progress through meiotic prophase I, albeit with a high frequency of nuclear abnormalities, and can be    fertilized and produce embryos. Nonetheless, there is marked depletion of germ cells in adult females. These studies provide evidence for key roles of the BRCA2 protein in mammalian gametogenesis and meiotic success.</p>

	]]>
</description>

<author>S K. Sharan et al.</author>


</item>


<item>
<title> Mouse strains with an active H2-Ea meiotic recombination hot spot exhibit increased levels of H2-Ea-specific DNA breaks in testicular germ cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/725</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/725</guid>
<pubDate>Tue, 08 May 2012 18:41:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>We devised a sensitive method for the site-specific detection of rare meiotic DNA strand breaks in germ cell-enriched testicular cell populations from mice that possess or lack an active recombination hot spot at the H2-Ea gene.    Using germ cells from adult animals, we found an excellent correlation between the frequency of DNA breaks in the 418-bp H2-Ea hot spot and crossover activity. The temporal appearance of DNA breaks was also studied in 7- to 18-day-old mice with    an active hot spot during the first waves of spermatogenesis. The number of DNA breaks detected rose as leptotene and zygotene spermatocytes populate the testis with a peak at day 14 postpartum, when leptotene, zygotene, and early pachytene    spermatocytes are the most common meiotic prophase I cell types.  The number of DNA breaks drops precipitously 1 day later, when middle to late pachytene spermatocytes become the dominant subtype. The recombination-related breaks in the hot spot    likely reflect SPO11-induced double-strand breaks and/or recombination intermediates containing free 3' hydroxyl groups.</p>

	]]>
</description>

<author>J Qin et al.</author>


</item>


<item>
<title> Genetically based influences on the site-specific regulation of trabecular and cortical bone morphology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/724</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/724</guid>
<pubDate>Tue, 08 May 2012 18:41:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>The degree of site-specificity by which genes influence bone quantity and architecture was investigated in the femur of three strains of mice.  Morphological indices were highly dependent on both genetic makeup as well as    anatomical location showing that the assessment of bone structure from a single site cannot be extrapolated to other sites even within a single bone. INTRODUCTION: The identification of genes responsible for establishing peak BMD will yield    critical information on the regulation of bone quantity and quality. Whereas such knowledge may eventually uncover novel molecular drug targets or enable the identification of individuals at risk of osteoporosis, the site-specificity by which    putative genotypes cause low or high bone mass (and effective bone morphology) is essentially unknown. MATERIALS AND METHODS: microCT was used to determine morphological and microarchitectural features of the femora harvested from three    genetically distinct strains of 4-month-old female mice, each with distinct skeletal mass (low: C57BL/6J [B6], medium: BALB/cByJ [BALB], high: C3H/HeJ [C3H]). Two trabecular regions (distal epiphysis and metaphysis) were considered in addition to    four cortical regions within the metaphysis and diaphysis. RESULTS AND CONCLUSIONS: Comparing morphological properties of the different trabecular and cortical femoral regions between the three strains of mice, it was apparent that high or low    values of specific parameters of bone morphology could not be consistently attributed to the same genetic strain. Trabecular metaphyseal bone volume, for instance, was 385% larger in C3H mice than in B6 mice, yet the two strains displayed similar    bone volume fractions in the epiphysis. Similarly, BALB mice had 48% more trabecular bone than C3H mice in the epiphysis, but there were no strain-specific differences in cortical bone area at the diaphysis. These data suggest that the genetic    control of bone mass and morphology, even within a given bone, is highly site-specific and that a comprehensive search for genes that are indicative of bone quantity and quality may also have to occur on a very site-specific basis.</p>

	]]>
</description>

<author>S Judex et al.</author>


</item>


<item>
<title> Genetically linked site-specificity of disuse osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/723</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/723</guid>
<pubDate>Tue, 08 May 2012 18:40:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genetic influence on bone loss in response to mechanical unloading was investigated within diaphyseal and distal femoral regions in three genetically distinct strains of mice. One mouse strain failed to lose bone after removal    of function, whereas osteopenia was evident in multiple regions of the remaining two strains but in different areas of the bone.  INTRODUCTION: It is well recognized that susceptibility to osteoporosis is, in large measure, determined by the    genome, but whether this influence is systemic or site-specific is not yet known. Here, the extent to which genetic variations influence regional bone loss caused by disuse was studied in the femora of adult female mice from three inbred strains.     MATERIALS AND METHODS: Adult C57BL/6J (B6), C3H/HeJ (C3H), and BALB/cByJ (BALB) mice were subjected to 15-21 days of disuse, achieved by hindlimb suspension, and six distinct anatomical regions of the femur were analyzed by high-resolution    microCT. RESULTS AND CONCLUSIONS: In B6 mice, the amount of disuse stimulated bone loss was relatively uniform across all regions, with 20% loss of trabecular bone and 10% loss of cortical bone.  The degree of bone loss in BALB mice varied    greatly, ranging from 59% in the metaphysis to 3% in the proximal diaphysis. In this strain, the nonuniformity of bone loss was directly related to the nonuniform distribution of baseline bone morphology (r2 = 0.94). In direct contrast with BALB    and B6, disuse failed to produce significant losses of bone in any of the analyzed regions of the C3H mice. Instead, these animals displayed a unique compensatory mechanism to disuse, where the large loss of calcified tissue from the endocortical    surface (-24%) was compensated for by an expansion of the periosteal envelope (10%). These data indicate a strong, yet complex, genetic dependence of the site-specific regulation of bone remodeling in response to a powerful catabolic signal.     Consequently, the skeletal region of interest and the genetic make-up of the individual may have to be considered interdependently when considering the pathogenesis of osteoporosis or the efficacy of an intervention to prevent or recover bone    loss.</p>

	]]>
</description>

<author>S Judex et al.</author>


</item>


<item>
<title> A new allele of the mouse hairless gene interferes with Hox/LacZ transgene regulation in hair follicle primordia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/722</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/722</guid>
<pubDate>Tue, 08 May 2012 18:40:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>A new autosomal recessive mouse mutation, causing loss of hair in homozygous mice 2-3 weeks after birth, arose spontaneously in a colony at the National Institute for Medical Research (NIMR), Mill Hill, London in early 1998.    Complementation analysis confirmed that this mutation was an allele of the hairless gene (hr). The gene symbol hr(rhbm) (hairless-rhino-bald Mill Hill) was assigned to reflect the source of the colony. Here we show the molecular defect in these    mutants, which is a substantial deletion at the 3'-end of the hairless gene. Morphological and immunological analysis of the new hairless mutation was performed at early postnatal stages. In an effort to address the molecular and cellular    mechanisms of the hairless phenotype, we analysed developmental stages before the establishment of alopecia. Using a HoxLacZ reporter line of transgenic mice, epidermal placode formation was followed in embryos.  Homozygous mutant embryos    (hr(rhbmh)/hr(rhbmh)), containing the LacZ reporter under the control of a Hoxb4 gene enhancer, display sharp loss of LacZ staining in epidermal cells invaginating to form the embryonic hair follicle placode. In the light of targeted mutagenesis    data involving a Hox gene in the hair development, we discuss the potential implication of the hr(rhbmh) locus in cascades of Hox gene regulation during embryogenesis.</p>

	]]>
</description>

<author>M V. Brancaz et al.</author>


</item>


<item>
<title> Vestibular defects in head-tilt mice result from mutations in Nox3, encoding an NADPH oxidase.</title>
<link>http://mouseion.jax.org/stfb2000_2009/721</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/721</guid>
<pubDate>Tue, 08 May 2012 18:39:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The vestibular system of the inner ear is responsible for the perception of motion and gravity. Key elements of this organ are otoconia, tiny biomineral particles in the utricle and the saccule. In response to gravity or linear    acceleration, otoconia deflect the stereocilia of the hair cells, thus transducing kinetic movements into sensorineural action potentials. Here, we present an allelic series of mutations at the otoconia-deficient head tilt (het) locus, affecting    the gene for NADPH oxidase 3 (Nox3). This series of mutations identifies for the first time a protein with a clear enzymatic function as indispensable for otoconia morphogenesis.</p>

	]]>
</description>

<author>R Paffenholz et al.</author>


</item>


<item>
<title> Prostate pathology of genetically engineered mice: definitions and classification. The consensus report from the Bar Harbor meeting of the Mouse Models of Human Cancer Consortium Prostate Pathology Committee.</title>
<link>http://mouseion.jax.org/stfb2000_2009/720</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/720</guid>
<pubDate>Tue, 08 May 2012 18:39:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Pathological Classification of Prostate Lesions in Genetically Engineered Mice (GEM) is the result of a directive from the National Cancer Institute Mouse Models of Human Cancer Consortium Prostate Steering Committee to provide    a hierarchical taxonomy of disorders of the mouse prostate to facilitate classification of existing and newly created mouse models and the translation to human prostate pathology. The proposed Bar Harbor Classification system is the culmination    of three meetings and workshops attended by various members of the Prostate Pathology Committee of the Mouse Models of Human Cancer Consortium. A 2-day Pathology Workshop was held at The Jackson Laboratory in Bar Harbor, Maine, in October 2001,    in which study sets of 93 slides from 22 GEM models were provided to individual panel members. The comparison of mouse and human prostate anatomy and disease demonstrates significant differences and considerable similarities that bear on the    interpretation of the origin and natural history of their diseases. The recommended classification of mouse prostate pathology is hierarchical, and includes developmental, inflammatory, benign proliferative, and neoplastic disorders. Among the    neoplastic disorders, preinvasive, microinvasive, and poorly differentiated neoplasms received the most attention. Specific criteria were recommended and will be discussed. Transitions between neoplastic states were of particular concern.    Preinvasive neoplasias of the mouse prostate were recognized as focal, atypical, and progressive lesions.  These lesions were designated as mouse prostatic intraepithelial neoplasia (mPIN). Some atypical lesions were identified in mouse models    without evidence of progression to malignancy. The panel recommended that mPIN lesions not be given histological grades, but that mPIN be further classified as to the absence or presence of documented associated progression to invasive carcinoma.    Criteria for recognizing microinvasion, for classification of invasive gland-forming adenocarcinomas, and for characterizing poorly differentiated tumors, including neuroendocrine carcinomas, were developed and are discussed. The uniform    application of defined terminology is essential for correlating results between different laboratories and models. It is recommended that investigators use the Bar Harbor Classification system when characterizing new GEM models or when conducting    experimental interventions that may alter the phenotype or natural history of lesion progression in existing models.</p>

	]]>
</description>

<author>S B. Shappell et al.</author>


</item>


<item>
<title> A new role for the mitotic RAD21/SCC1 cohesin in meiotic chromosome cohesion and segregation in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/719</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/719</guid>
<pubDate>Tue, 08 May 2012 18:38:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>The evolutionarily conserved cohesin complex is required for the establishment and maintenance of sister chromatid cohesion, in turn essential for proper chromosome segregation. RAD21/SCC1 is a regulatory subunit of the mitotic    cohesin complex, as it links together all other subunits of the complex. The destruction of RAD21/SCC1 along chromosomal arms and later at centromeres results in the dissociation of the cohesin complex, facilitating chromosome segregation. Here,    we report for the first time that mammalian RAD21/SCC1 associates with the axial/lateral elements of the synaptonemal complex along chromosome arms and on centromeres of mouse spermatocytes. Importantly, RAD21/SCC1 is lost from chromosome arms in    late prophase I but persists on centromeres. The loss of centromeric RAD21/SCC1 coincides with the separation of sister chromatids at anaphase II. These findings support a role for mammalian RAD21/SCC1 in maintaining sister chromatid cohesion in    meiosis.</p>

	]]>
</description>

<author>H Xu et al.</author>


</item>


<item>
<title> Classification of proliferative pulmonary lesions of the mouse: recommendations of the mouse models of human cancers consortium.</title>
<link>http://mouseion.jax.org/stfb2000_2009/718</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/718</guid>
<pubDate>Tue, 08 May 2012 18:38:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rapid advances in generating new mouse genetic models for lung neoplasia provide a continuous challenge for pathologists and investigators.  Frequently, phenotypes of new models either have no precedents or are arbitrarily    attributed according to incongruent human and mouse classifications. Thus, comparative characterization and validation of novel models can be difficult. To address these issues, a series of discussions was initiated by a panel of human,    veterinary, and experimental pathologists during the Mouse Models of Human Cancers Consortium (NIH/National Cancer Institute) workshop on mouse models of lung cancer held in Boston on June 20-22, 2001. The panel performed a comparative evaluation    of 78 cases of mouse and human lung proliferative lesions, and recommended development of a new practical classification scheme that would (a) allow easier comparison between human and mouse lung neoplasms, (b) accommodate newly emerging mouse    neoplasms, and (c) address the interpretation of benign and preinvasive lesions of the mouse lung.  Subsequent discussions with additional experts in pulmonary pathology resulted in the current proposal of a new classification. It is anticipated    that this classification, as well as the complementary digital atlas of virtual histological slides, will help investigators and pathologists in their characterization of new mouse models, as well as stimulate further research aimed at a better    understanding of proliferative lesions of the lung.</p>

	]]>
</description>

<author>A Y. Nikitin et al.</author>


</item>


<item>
<title>Colby Undergraduate Research Symposium 2011 Program &amp; Abstracts</title>
<link>http://digitalcommons.colby.edu/ugrs/69</link>
<guid isPermaLink="true">http://digitalcommons.colby.edu/ugrs/69</guid>
<pubDate>Tue, 08 May 2012 18:37:50 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title> Mapping quantitative trait loci for vertebral trabecular bone volume fraction and microarchitecture in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/717</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/717</guid>
<pubDate>Tue, 08 May 2012 18:37:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>BMD, which reflects both cortical and cancellous bone, has been shown to be highly heritable; however, little is known about the specific genetic factors regulating trabecular bone. Genome-wide linkage analysis of vertebral    trabecular bone traits in 914 adult female mice from the F2 intercross of C57BL/6J and C3H/HeJ inbred strains revealed a pattern of genetic regulation derived from 13 autosomes, with 5-13 QTLs associated with each of the traits. Ultimately,    identification of genes that regulate trabecular bone traits may yield important information regarding mechanisms that regulate mechanical integrity of the skeleton.  INTRODUCTION: Both cortical and cancellous bone influence the mechanical    integrity of the skeleton, with the relative contribution of each varying with skeletal site. Whereas areal BMD, which reflects both cortical and cancellous bone, has been shown to be highly heritable, little is known about the genetic    determinants of trabecular bone density and architecture. MATERIALS AND METHODS: To identify heritable determinants of vertebral trabecular bone traits, we evaluated the fifth lumbar vertebra from 914 adult female mice from the F2 intercross of    C57BL/6J (B6) and C3H/HeJ (C3H) progenitor strains. High-resolution microCT was used to assess total volume (TV), bone volume (BV), bone volume fraction (BV/TV), trabecular thickness (Tb.Th), separation (Tb.Sp), and number (Tb.N) of the    trabecular bone in the vertebral body in the progenitors (n = 8/strain) and female B6C3H-F2 progeny (n = 914). Genomic DNA from F2 progeny was screened for 118 PCR-based markers discriminating B6 and C3H alleles on all 19 autosomes. RESULTS AND    CONCLUSIONS: Despite having a slightly larger trabecular bone compartment, C3H progenitors had dramatically lower vertebral trabecular BV/TV (-53%) and Tb.N (-40%) and higher Tb.Sp (71%) compared with B6 progenitors (p < 0.001 for all).    Genome-wide quantitative trait analysis revealed a pattern of genetic regulation derived from 13 autosomes, with 5-13 quantitative trait loci (QTLs) associated with each of the vertebral trabecular bone traits, exhibiting adjusted LOD scores    ranging from 3.1 to 14.4. The variance explained in the F2 population by each of the individual QTL after adjusting for contributions from other QTLs ranged from 0.8% to 5.9%. Taken together, the QTLs explained 22-33% of the variance of the    vertebral traits in the F2 population. In conclusion, we observed a complex pattern of genetic regulation for vertebral trabecular bone volume fraction and microarchitecture using the F2 intercross of the C57BL/6J and C3H/HeJ inbred mouse strains    and identified a number of QTLs, some of which are distinct from those that were previously identified for total femoral and vertebral BMD.  Identification of genes that regulate trabecular bone traits may ultimately yield important information    regarding the mechanisms that regulate the acquisition and maintenance of mechanical integrity of the skeleton.</p>

	]]>
</description>

<author>M L. Bouxsein et al.</author>


</item>


<item>
<title> A dynamic switch in Rb+/- mediated neuroendocrine tumorigenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/716</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/716</guid>
<pubDate>Tue, 08 May 2012 18:37:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rb+/- mice develop a complex spectrum of neuroendocrine tumors on a mixed genetic (129Sv x C57BL/6) background. To understand how the 129Sv and C57BL/6 contributions affect Rb+/- tumorigenesis, we serially backcrossed Rb+/- animals    to the 129Sv or C57BL/6 strain, and analysed their pathological profiles. Strikingly, the length of survival and the penetrance, severity and multiplicity of neuroendocrine tumors switch dramatically between Rb+/- animals from the two genetic    backgrounds. In fact, the 129Sv background significantly enhances both the initiation and progression of tumorigenesis in the intermediate lobe of the pituitary (ILP) in Rb+/- animals. This is due to the surprising fact that ILPs from wild-type    129Sv animals are inherently abnormal, and thus greatly predisposed to neoplasia. This is likely to explain the high incidence of ILP tumors, an otherwise rare tumor type in wild-type mice, in numerous knockout studies performed on the 129Sv    strain, and raises the intriguing possibility that the classic Rb+/- neuroendocrine tumors may fade away in another as of yet unidentified inbred strain. Finally, we have increased the utility of the Rb+/- tumor model, since Rb+/- animals on the    C57BL/6 background develop high-penetrance tumors of the anterior lobe of the pituitary, a class of tumors estimated to occur in 20-25% of humans.Oncogene (2004) 23, 3296-3307. doi:10.1038/sj.onc.1207457 Published online 15 March    2004</p>

	]]>
</description>

<author>S W. Leung et al.</author>


</item>


<item>
<title> The effect of dietary glutathione and coenzyme Q10 on the prevention and treatment of inflammatory bowel disease in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/715</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/715</guid>
<pubDate>Tue, 08 May 2012 18:36:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Because reactive oxygen species have been implicated as mediators of inflammatory bowel disease (IBD), we evaluated the potential preventive and therapeutic effects of two dietary antioxidants, glutathione (GSH) and coenzyme Q10    (CoQ10) on dextran sulfate sodium (DSS)-induced colitis in mice. Fifty female 8-wk old Swiss-Webster mice were randomly assigned to 4 groups for a pre-treatment "prevention" study: (1) GSH (1% of diet); (2) CoQ10 (200 mg/kg/d); (3) DSS only (3%    of drinking water); (4) control (no treatment). The mice in groups 1 and 2 were fed with GSH or CoQ10 for 21 wks, and the mice in groups 1, 2 and 3 were provided DSS from wk 7 for 4 cycles (1 cycle = 1 wk DSS followed by 2-wk water). Another 50    mice were randomly assigned to 4 groups for a 21-wk "treatment" study where the mice in groups 1, 2, and 3 were administered DSS for 6 cycles (18 wks) to induce colitis. GSH and CoQ10 were added from wk 7 until the completion of the protocol.    Loose stools and hemocult positivity were modestly but significantly reduced with GSH or CoQ10 at several periods during the intervention in both the prevention and treatment studies. In contrast, histological evaluation revealed increases in    colonic dysplasia and ulceration with GSH or CoQ10. Thus, in this mouse model, GSH and CoQ10 appear to have a beneficial effect on acute signs of IBD, but may have an adverse impact on the chronic pathophysiology of the disease. Further studies    using additional animal models are required to determine whether GSH or CoQ10 provide a favorable or unfavorable benefit:risk ratio in the prevention or treatment of IBD.</p>

	]]>
</description>

<author>C Liu et al.</author>


</item>


<item>
<title> Regulation of postsurgical fibrosis by the programmed death-1 inhibitory pathway.</title>
<link>http://mouseion.jax.org/stfb2000_2009/714</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/714</guid>
<pubDate>Tue, 08 May 2012 18:36:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Surgical adhesions are a common and often severe complication of abdominal or pelvic injury that cause pelvic pain, bowel obstruction, and infertility in women. Current treatments are of limited effectiveness because little is    known about the cellular and subcellular processes underlying adhesiogenesis. Recently, we showed that Th1 alpha beta CD4(+) T cells mediate the pathogenesis of adhesion formation in a rodent model of this disease process. In this study, we    demonstrate that in mice these T cells home directly to the site of surgically induced adhesions and control local chemokine production in a manner dependent on the CD28 T cell costimulatory pathway. Conversely, the inhibitory programmed death-1    pathway plays a central role in limiting adhesiogenesis, as programmed death-1 blockade was associated with increased T cell infiltration, chemokine production, and a concomitant exacerbation of disease. Our results reveal for the first time that    the development of postsurgical fibrosis is under the tight control of positive and negative T cell costimulation, and suggest that targeting these pathways may provide promising therapies for the prevention of adhesion formation.</p>

	]]>
</description>

<author>M A. Holsti et al.</author>


</item>


<item>
<title> Many ribosomal protein genes are cancer genes in zebrafish.</title>
<link>http://mouseion.jax.org/stfb2000_2009/713</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/713</guid>
<pubDate>Tue, 08 May 2012 18:35:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have generated several hundred lines of zebrafish (Danio rerio), each heterozygous for a recessive embryonic lethal mutation. Since many tumor suppressor genes are recessive lethals, we screened our colony for lines that display    early mortality and/or gross evidence of tumors. We identified 12 lines with elevated cancer incidence. Fish from these lines develop malignant peripheral nerve sheath tumors, and in some cases also other tumor types, with moderate to very high    frequencies. Surprisingly, 11 of the 12 lines were each heterozygous for a mutation in a different ribosomal protein (RP) gene, while one line was heterozygous for a mutation in a zebrafish paralog of the human and mouse tumor suppressor gene,    neurofibromatosis type 2. Our findings suggest that many RP genes may act as haploinsufficient tumor suppressors in fish. Many RP genes might also be cancer genes in humans, where their role in tumorigenesis could easily have escaped detection up    to now.</p>

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</description>

<author>A Amsterdam et al.</author>


</item>


<item>
<title>Successful Pioneers: Irish Catholic Settlers in the Township of Hibbert, Ontario, 1845-1887</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6938</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6938</guid>
<pubDate>Tue, 08 May 2012 18:35:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Successful Pioneers: Irish Catholic Settlers in the Township of Hibbert, Ontario, 1845-1887. The study of Irish Catholic immigrants is interesting as a part of the wider issue that has consumed Canada since its inception - immigration and immigrant communities. By testing the assumptions of historical literature, we can see how different stories have been told about the Irish Catholic immigrant experience in Canada and the variety of reasons given for the communities' relative successes or failures. The Township of Hibbert affords an opportunity to study Irish Catholic Immigrants in somewhat uniquely promising socioeconomic, dernographic and geographic circumstances. The settlers developed into a strong and confident rural community. And though many of the articles and monographs published in the past twenty years have discredited the assumptions of the earlier cultural deterministic models of Irish Canadian studies, the literature concerning the nineteenth century rural experience continues to place Irish Catholics on the periphery. This despite the fact that most Irish Catholics in Canada during this era lived in rural communities. The central thesis of this paper is that the Irish Catholic community in the Township of Hibbert were not as downtrodden as the historical literature ,concerning the subject of Irish Catholics usually suggests. The Irish Catholics, of the Township of Hibbert were economically, politically and socially more secure than any other community discussed in the Canadian historical literature. They found it was neither necessary nor desirable to publicly demand recognition, as an ethnic or cultural group, from their local society and therefore expressed moderation concerning the issues of Irish nationalism and religious rights. It is this story that this paper will attempt to discuss.</p>

	]]>
</description>

<author>Derek Tucker</author>


</item>


<item>
<title> Comparative pathology of nerve sheath tumors in mouse models and humans.</title>
<link>http://mouseion.jax.org/stfb2000_2009/712</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/712</guid>
<pubDate>Tue, 08 May 2012 18:35:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite the progress made in our understanding of the biology of neurofibromatosis (NF), the long-term clinical outcome for affected patients has not changed significantly in the past decades, and both NF1 and NF2 are still    associated with a significant morbidity and a decreased life span. A number of NF1 and NF2 murine models have been generated to aid in the study of NF tumor biology and in the development of targeted therapies for NF patients. A single, universal    pathological classification of the lesions generated in these murine models is essential for the validation of the models, for their analysis and comparison with other models, and for their future effective use in preclinical treatment trials.    For the formulation of a pathological classification of these lesions, the WHO classification of human tumors was used as a reference.  However, it was not adopted for the classification of the GEM lesions because of some important differences    between the human and murine lesions. A novel classification scheme for peripheral nerve sheath tumors in murine models was therefore devised.</p>

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</description>

<author>Rachamimov A. Stemmer et al.</author>


</item>


<item>
<title> Lymphomagenesis and female-specific lethality in p53-deficient mice occur independently of E2f1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/711</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/711</guid>
<pubDate>Tue, 08 May 2012 18:34:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E H. Wloga et al.</author>


</item>


<item>
<title> Absence of a reductase, NCB5OR, causes insulin-deficient diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/710</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/710</guid>
<pubDate>Tue, 08 May 2012 18:34:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>NCB5OR is a highly conserved NAD(P)H reductase that contains a cytochrome b5-like domain at the N terminus and a cytochrome b5 reductase-like domain at the C terminus. The enzyme is located in the endoplasmic reticulum (ER) and is    widely expressed in organs and tissues. Targeted inactivation of this gene in mice has no impact on embryonic or fetal viability. At 4 weeks of age, Ncb5or-/- mice have normal blood glucose levels but impaired glucose tolerance. Isolated    Ncb5or-/- islets have markedly impaired glucose- or arginine-stimulated insulin secretion. By 7 weeks of age, these mice develop severe hyperglycemia with markedly decreased serum insulin levels and nearly normal insulin tolerance. As the animals    age, there is a progressive loss of beta cells in pancreatic islets, but there is no loss of alpha, delta, or PP cells. Electron microscopy reveals degranulation of beta cells and hypertrophic and hyperplastic mitochondria, some of which contain    electron dense inclusions.  Four-week-old Ncb5or-/- mice have enhanced sensitivity to the diabetogenic agent streptozotocin. NCB5OR appears to play a critical role in protecting pancreatic beta cells against oxidant stress.</p>

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</description>

<author>J Xie et al.</author>


</item>


<item>
<title> Initial stages of mammary tumor virus infection are superantigen independent.</title>
<link>http://mouseion.jax.org/stfb2000_2009/709</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/709</guid>
<pubDate>Tue, 08 May 2012 18:33:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Exogenous mouse mammary tumor virus (MMTV) is transmitted via the milk from infected mothers to newborn pups. Efficient MMTV transmission is dependent on proliferation of T cells with particular TCR beta-chains, which occurs upon    recognition of virally encoded superantigen (SAg) bound to MHC class II molecules. It is assumed that infection of these dividing cells favors MMTV amplification. SAg is important for MMTV infection, as mice that lack SAg-cognate T cells due to    expression of endogenous Mtv loci or mice that express inappropriate MHC haplotypes unable to present viral SAg efficiently were shown to be resistant to MMTV infection.  However, this resistance was not absolute, as these mice developed late    onset MMTV-induced mammary tumors. In this study, we show that the success of initial MMTV infection in neonates is independent of SAg function but depends on the developmentally regulated proliferation of target cells.  However, SAg was    absolutely required for virus spread following completion of this proliferative stage.</p>

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</description>

<author>Y Pobezinskaya et al.</author>


</item>


<item>
<title> Moving forward with chemical mutagenesis in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/708</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/708</guid>
<pubDate>Tue, 08 May 2012 18:32:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>The study of genetic variation in mice offers a powerful experimental platform for understanding gene function. Complex trait analysis, gene-targeting and gene-trapping technologies, as well as insertional and chemical mutagenesis    approaches are becoming increasingly sophisticated and provide a variety of options for cataloguing gene activities and interactions. In this review we discuss fundamental and practical concepts related to chemical mutagenesis and we highlight    the growing list of strategies for performing mutagenesis screens in mice. Gene-driven and diverse types of phenotype-driven screens provide several options for the recovery of the invaluable variety of alleles generated by chemical mutagenesis.    The unique advantages offered using chemical mutagenesis compare favourably to and complement the spectrum of approaches available for functional annotation of the mammalian genome.</p>

	]]>
</description>

<author>T P. O&apos;Brien et al.</author>


</item>


<item>
<title> The Gene Ontology (GO) database and informatics resource.</title>
<link>http://mouseion.jax.org/stfb2000_2009/707</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/707</guid>
<pubDate>Tue, 08 May 2012 18:32:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Gene Ontology (GO) project (http://www. geneontology.org/) provides structured, controlled vocabularies and classifications that cover several domains of molecular and cellular biology and are freely available for community use    in the annotation of genes, gene products and sequences.  Many model organism databases and genome annotation groups use the GO and contribute their annotation sets to the GO resource. The GO database integrates the vocabularies and contributed    annotations and provides full access to this information in several formats. Members of the GO Consortium continually work collectively, involving outside experts as needed, to expand and update the GO vocabularies. The GO Web resource also    provides access to extensive documentation about the GO project and links to applications that use GO data for functional analyses.</p>

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</description>

<author>M A. Harris et al.</author>


</item>


<item>
<title> The Mouse Genome Database (MGD): integrating biology with the genome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/706</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/706</guid>
<pubDate>Tue, 08 May 2012 18:31:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Database (MGD) is one component of the Mouse Genome Informatics (MGI) system (http://www.informatics.jax.org), a community database resource for the laboratory mouse. MGD strives to provide a comprehensive    knowledgebase about the mouse with experiments and data annotated from both literature and online sources. MGD curates and presents consensus and experimental data representations of genetic, genotype (sequence) and phenotype information    including highly detailed reports about genes and gene products. Primary foci of integration are through representations of relationships between genes, sequences and phenotypes. MGD collaborates with other bioinformatics groups to curate a    definitive set of information about the laboratory mouse and to build and implement the data and semantic standards that are essential for comparative genome analysis. Recent developments in MGD discussed here include an extensive integration of    the mouse sequence data and substantial revisions in the presentation, query and visualization of sequence data.</p>

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</description>

<author>C J. Bult et al.</author>


</item>


<item>
<title> The mouse Gene Expression Database (GXD): updates and enhancements.</title>
<link>http://mouseion.jax.org/stfb2000_2009/705</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/705</guid>
<pubDate>Tue, 08 May 2012 18:31:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Gene Expression Database (GXD) is a community resource for gene expression information in the laboratory mouse. By collecting and integrating different types of expression data, GXD provides information about expression    profiles in different mouse strains and mutants.  Participation in the Gene Ontology (GO) project classifies genes and gene products with regard to molecular functions, biological processes, and cellular components. Integration with other Mouse    Genome Informatics (MGI) databases places the gene expression information in the context of mouse genetic, genomic and phenotypic information. The integration of these types of information enables valuable insights into the molecular biology that    underlies development and disease. The utility of GXD has been improved by the daily addition of new data and through the implementation of new query and display features. These improvements make it easier for users to interrogate and visualize    expression data in the context of their specific needs. GXD is accessible through the MGI website at http://www.informatics.jax.org/ or directly at http://www.  informatics.jax.org/menus/expression_menu.shtml.</p>

	]]>
</description>

<author>D P. Hill et al.</author>


</item>


<item>
<title> RIII/Sa mice with a high incidence of mammary tumors express two exogenous strains and one potential endogenous strain of mouse mammary tumor virus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/704</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/704</guid>
<pubDate>Tue, 08 May 2012 18:31:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The inbred mouse strain RIII has long been known for shedding large amounts of mouse mammary tumor virus (MMTV) particles in milk and for the development of hormone-dependent early mammary tumors at a very high incidence (>90%). We    have established one RIII subline (RIII/Sa) that shows a pattern of virus expression and tumor incidence similar to that in RIII mice. In the present study, we analyzed the milk and mammary tumors of RIII/Sa mice for virus characterization by    reverse transcriptase PCR (RT-PCR) cloning and sequencing of the open reading frame (ORF) of the MMTV long terminal repeats (LTRs). Our results show that these mice express a mixture of at least three different MMTV strains, two of which,    designated here as RIII/Sa MMTV-1 and RIII/Sa MMTV-2, are exogenous. The third virus, RIII/Sa MMTV-3, appears to carry the signature of an endogenous provirus, Mtv-17. Similar studies done with the milk and mammary glands of another subline,    RIIIS/J, revealed that they do not express MMTV in their milk. The RIII/Sa and RIIIS/J mice also exhibited differences in their endogenous proviral contents. Twelve spontaneously developed mammary tumors of RIII/Sa mice were examined for possible    Wnt-1 and/or int-2/Fgf3 mutations that are usually found to occur in most mouse mammary tumors as a consequence of MMTV proviral integration. This work led to the isolation of one MMTV-Wnt-1 junction fragment and one MMTV-int-2/Fgf3 junction    fragment from 2 of the 12 tumors. Further analyses showed that both junction fragments contained the RIII/Sa MMTV-2-specific LTR ORF, indicating that this virus was involved in the development of both tumors. Whether RIII/Sa MMTV-1 and/or RIII/Sa    MMTV-3 plays any role in mammary tumor development in RIII/Sa mice remains to be established. Overall, the present study demonstrates, to our surprise, that (i) RIII/Sa mice express, unlike other native mouse strains, three strains of MMTVs; and    (ii) the virions are completely different from the virus expressed by another subline of RIII mice, the BR6 mice.</p>

	]]>
</description>

<author>N H. Sarkar et al.</author>


</item>


<item>
<title> Quantitative trait locus mapping of genes that regulate phospholipid transfer activity in SM/J and NZB/BlNJ inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/703</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/703</guid>
<pubDate>Tue, 08 May 2012 18:30:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: Phospholipid transfer protein (PLTP), an important protein in the transfer of phospholipids between lipoprotein particles and in the remodeling of HDL, is regulated at both the transcriptional and the protein level. We    performed quantitative trait locus (QTL) analysis to identify genomic loci regulating PLTP activity in mice. METHODS AND RESULTS: Plasma PLTP activity was measured in 217 male F2 progeny from a SM/J x NZB/B1NJ intercross. Two QTL for plasma PLTP    activity in mice fed chow (Pltpq1 and Pltpq2) were found on chromosomes 3 (34 cM, logarithm of odds [LOD] 3.5) and 10 (66 cM, LOD 4.1); two additional QTL in mice fed atherogenic diet (Pltpq3 and Pltpq4) were found on chromosomes 9 (56 cM, LOD    4.5) and 15 (34 cM, LOD 5.0); and one QTL (Pltiq1) for the inducibility of PLTP activity was found on chromosome 4 (70 cM, LOD 3.7).  Several candidate genes for these 5 QTL were tested by sequence comparison and expression studies. CONCLUSIONS:    We identified five significant loci involved in PLTP activity in the mouse and provided supporting evidence for the candidacy of Nr1h4 and Apof as the genes underlying Pltpq2.</p>

	]]>
</description>

<author>R Korstanje et al.</author>


</item>


<item>
<title> Quantitative trait loci analysis for plasma HDL-cholesterol concentrations and atherosclerosis susceptibility between inbred mouse strains C57BL/6J and 129S1/SvImJ.</title>
<link>http://mouseion.jax.org/stfb2000_2009/702</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/702</guid>
<pubDate>Tue, 08 May 2012 18:29:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: The C57BL/6 (B6) and 129 mouse inbred strains differ markedly in plasma HDL-cholesterol concentrations and atherosclerosis susceptibility after a high-fat diet consumption. To identify loci controlling these traits, we    performed quantitative trait loci (QTL) analysis. METHODS AND RESULTS: We fed a high-fat diet to 294 (B6x129S1/SvImJ)F2 females for 14 weeks, measured plasma HDL concentrations and size of aortic fatty-streak lesions, genotyped F2 females, and    performed QTL analysis. HDL concentrations were affected by six loci: Hdlq14 and Hdlq15 on chromosome 1 (peaks cM 80 and cM 104, logarithm of odds [LOD] 5.3 and 9.7, respectively); Hdlq16 on chromosome 8 (cM 44, LOD 2.6); Hdlq17 on chromosome 9    (cM 24, LOD 2.9); Hdlq18 on chromosome 12 (cM 20, LOD 5.9); and Hdlq19 on chromosome 2 (cM 90), which interacted with Hdlq15. Atherosclerosis susceptibility was affected by five loci: Ath17 on chromosome 10 (cM 34, LOD 6.6); Ath18 on chromosome    12 (cM 16, LOD 3.7); Ath19 (chromosome 11, cM 60), which interacted with Ath18; and Ath20 (chromosome 10, cM 10), which interacted with Ath21 (chromosome 12, cM 50). CONCLUSIONS: We identified six loci for HDL and five loci for atherosclerosis    susceptibility in a (B6x129S1/SvImJ)F2 intercross.</p>

	]]>
</description>

<author>N Ishimori et al.</author>


</item>


<item>
<title> Caspase-1 is not required for type 1 diabetes in the NOD mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/701</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/701</guid>
<pubDate>Tue, 08 May 2012 18:29:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Interleukin (IL)-1 beta and IL-18 are two cytokines associated with the immunopathogenesis of diabetes in NOD mice. Both of these cytokines are cleaved by caspase-1 to their biologically active forms. IL-1 is a proinflammatory    cytokine linked to beta-cell damage, and IL-18 stimulates production of interferon (IFN)gamma in synergy with IL-12. To examine the effects produced by caspase-1 deficiency on diabetes development in NOD/Lt mice, a disrupted Casp1 gene was    introduced by a speed congenic technique.  Casp1(-/-) bone marrow-derived macrophages stimulated with lipopolysaccharide produced no detectable IL-18, fourfold lower IL-1 beta, and 20-30% less IL-1 alpha than macrophages from wild-type Casp1(+/+)    or Casp1(+/-) controls. Unexpectedly, despite reduced IL-1 and IL-18, there was no change in the rate of diabetes or in total incidence as compared with that in wild-type NOD mice. IL-1 reportedly makes an important pathological contribution in    the multidose streptozotocin model of diabetes; however, there was no difference in sensitivity to streptozotocin between NOD mice and NOD.Casp1(-/-) mice at 40 mg/kg body wt or at 25 mg/kg body wt dosage levels. These findings show that    caspase-1 processing of IL-1 beta and IL-18 is not absolutely required for mediation of spontaneous or chemically induced diabetes pathogenesis in the NOD mouse.</p>

	]]>
</description>

<author>W H. Schott et al.</author>


</item>


<item>
<title> Quantitative trait loci that determine lipoprotein cholesterol levels in an intercross of 129S1/SvImJ and CAST/Ei inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/700</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/700</guid>
<pubDate>Tue, 08 May 2012 18:28:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>To identify genetic determinants of lipoprotein levels, we are performing quantitative trait locus (QTL) analysis on a series of mouse intercrosses in a "daisy chain" experimental design, to increase the power of detecting QTL and    to identify common variants that should segregate in multiple intercrosses. In this study, we intercrossed strains CAST/Ei and 129S1/SvImJ, determined HDL, total, and non-HDL cholesterol levels, and performed QTL mapping using Pseudomarker    software. For HDL cholesterol, we identified two significant QTL on chromosome (Chr) 1 (Hdlq5, 82 cM, 60-100 cM) and Chr 4 (Hdlq10, 20 cM, 10-30 cM). For total cholesterol, we identified three significant QTL on Chr 1 (Chol7, 74 cM, 65-80 cM),    Chr 4 (Chol8, 12 cM, 0-30 cM), and Chr 17 (Chol9, 54 cM, 20-60 cM). For non-HDL cholesterol, we identified significant QTL on Chr 8 (Nhdlq1, 34 cM, 20-60 cM) and Chr X (Nhdlq2, 6 cM, 0-18 cM). Hdlq10 was the only QTL detected in two intercrosses    involving strain CAST/Ei. Hdlq5, Hdlq10, Nhdlq1, and two suggestive QTL at D7Mit246 and D15Mit115 coincided with orthologous human lipoprotein QTL. Our analysis furthers the knowledge of the genetic control of lipoprotein levels and points to the    importance of Hdlq10, which was detected repeatedly in multiple studies.</p>

	]]>
</description>

<author>M A. Lyons et al.</author>


</item>


<item>
<title> Operant conditioning in the Ts65Dn mouse: learning.</title>
<link>http://mouseion.jax.org/stfb2000_2009/699</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/699</guid>
<pubDate>Tue, 08 May 2012 18:28:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ts65Dn and littermate controls were trained to respond (nose-poke) under operant schedules of reinforcement. A small difference was observed in the initial operant training of the Ts65Dn mouse that disappeared with training under a    fixed-ratio 15 schedule of milk presentation. No difference was observed in a position reversal task in which mice initially trained to respond upon one photocell had to learn to respond on a previously inactive photocell. Under an incremental    repeated acquisition of behavioral chains schedule, no difference was observed when one or two responses were required to complete the sequence. However, when three or four responses were required to complete the sequence, a marked deficit was    observed in the Ts65Dn mice. These results show that both Ts65Dn and littermate controls can be trained to respond under operant schedules of reinforcement, but that Ts65Dn mice have a learning deficit that is correlated with task    difficulty.</p>

	]]>
</description>

<author>G R. Wenger et al.</author>


</item>


<item>
<title> Loss of NFAT5 results in renal atrophy and lack of tonicity-responsive gene expression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/698</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/698</guid>
<pubDate>Tue, 08 May 2012 18:28:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>The transcription factor NFAT5/TonEBP, a member of the NFAT/Rel family of transcription factors, has been implicated in diverse cellular responses, including the response to osmotic stress, integrin-dependent cell migration, T cell    activation, and the Ras pathway in Drosophila. To clarify the in vivo role of NFAT5, we generated NFAT5-null mice.  Homozygous mutants were genetically underrepresented after embryonic day 14.5. Surviving mice manifested a progressive and    profound atrophy of the kidney medulla with impaired activation of several osmoprotective genes, including those encoding aldose reductase, Na+/Cl--coupled betaine/gamma-aminobutyric acid transporter, and the Na+/myo-inositol cotransporter. The    aldose reductase gene is controlled by a tonicity-responsive enhancer, which was refractory to hypertonic stress in fibroblasts lacking NFAT5, establishing this enhancer as a direct transcriptional target of NFAT5. Our findings demonstrate a    central role for NFAT5 as a tonicity-responsive transcription factor required for kidney homeostasis and function.</p>

	]]>
</description>

<author>Rodriguez C. Lopez et al.</author>


</item>


<item>
<title> Pathbase: a database of mutant mouse pathology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/697</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/697</guid>
<pubDate>Tue, 08 May 2012 18:27:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pathbase is a database that stores images of the abnormal histology associated with spontaneous and induced mutations of both embryonic and adult mice including those produced by transgenesis, targeted mutagenesis and chemical    mutagenesis. Images of normal mouse histology and strain-dependent background lesions are also available. The database and the images are publicly accessible (http://www.pathbase.net) and linked by anatomical site, gene and other identifiers to    relevant databases; there are also facilities for public comment and record annotation. The database is structured around a novel ontology of mouse disorders (MPATH) and provides high-resolution downloadable images of normal and diseased tissues    that are searchable through orthogonal ontologies for pathology, developmental stage, anatomy and gene attributes (GO terms), together with controlled vocabularies for type of genetic manipulation or mutation, genotype and free text annotation    for mouse strain and additional attributes. The database is actively curated and data records assessed by pathologists in the Pathbase Consortium before publication. The database interface is designed to have optimal browser and platform    compatibility and to interact directly with other web-based mouse genetic resources.</p>

	]]>
</description>

<author>P N. Schofield et al.</author>


</item>


<item>
<title> MHC class II molecules play a role in the selection of autoreactive class I-restricted CD8 T cells that are essential contributors to type 1 diabetes development in nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/696</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/696</guid>
<pubDate>Tue, 08 May 2012 18:27:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Development of autoreactive CD4 T cells contributing to type 1 diabetes (T1D) in both humans and nonobese diabetic (NOD) mice is either promoted or dominantly inhibited by particular MHC class II variants. In addition, it is now    clear that when co-expressed with other susceptibility genes, some common MHC class I variants aberrantly mediate autoreactive CD8 T cell responses also essential to T1D development. However, it was unknown whether the development of diabetogenic    CD8 T cells could also be dominantly inhibited by particular MHC variants. We addressed this issue by crossing NOD mice transgenically expressing the TCR from the diabetogenic CD8 T cell clone AI4 with NOD stocks congenic for MHC haplotypes that    dominantly inhibit T1D. High numbers of functional AI4 T cells only developed in controls homozygously expressing NOD-derived H2(g7) molecules. In contrast, heterozygous expression of some MHC haplotypes conferring T1D resistance anergized AI4 T    cells through decreased TCR (H2(b)) or CD8 expression (H2(q)). Most interestingly, while AI4 T cells exert a class I-restricted effector function, H2(nb1) MHC class II molecules can contribute to their negative selection. These findings provide    insights to how particular MHC class I and class II variants interactively regulate the development of diabetogenic T cells and the TCR promiscuity of such autoreactive effectors.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title> Functional annotation of mouse mutations in embryonic stem cells by use of expression profiling.</title>
<link>http://mouseion.jax.org/stfb2000_2009/695</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/695</guid>
<pubDate>Tue, 08 May 2012 18:27:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Expression profiling offers a potential high-throughput phenotype screen for mutant mouse embryonic stem (ES) cells. We have assessed the ability of expression arrays to distinguish among heterozygous mutant ES cell lines and to    accurately reflect the normal function of the mutated genes.  Two ES cell lines hemizygous for overlapping regions of mouse Chromosome (Chr) 5 differed substantially from the wildtype parental line and from each other. Expression differences    included frequent downregulation of hemizygous genes and downstream effects on genes mapping to other chromosomes. Some genes were affected similarly in each deletion line, consistent with the overlap of the deletions. To determine whether such    downstream effects reveal pathways impacted by a mutation, we examined ES cell lines heterozygous for mutations in either of two well-characterized genes. A heterozygous mutation in the gene encoding the cell cycle regulator, cyclin D kinase 4 (    Cdk4), affected expression of many genes involved in cell growth and proliferation. A heterozygous mutation in the ATP binding cassette transporter family A, member 1 ( Abca1) gene, altered genes associated with lipid homeostasis, the    cytoskeleton, and vesicle trafficking. Heterozygous Abca1 mutation had similar effects in liver, indicating that ES cell expression profile reflects changes in fundamental processes relevant to mutant gene function in multiple cell    types.</p>

	]]>
</description>

<author>D J. Symula et al.</author>


</item>


<item>
<title> Forward Genetic Screens for Meiotic and Mitotic Recombination-Defective Mutants in Mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/694</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/694</guid>
<pubDate>Tue, 08 May 2012 18:26:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>The goal of understanding the function of all mammalian genes is best accomplished through mutational analyses. Although the sequence of the mouse genome is now available and many genes have been identified, it is not possible to    ascribe functions accurately to these genes in silico.  Gene targeting using embryonic stem cells is ideal for analysis of individual genes selected on the basis of sequence features, but it is impractical for identifying novel genes involved    in particular biological processes. Phenotype-based random mutagenesis of the genome is well suited for this goal. In the mouse, N-ethyl-N-nitrosourea (ENU) induces point mutations at a high frequency in the mouse germline. In this chapter,    we describe methods for detecting and characterizing recombination mutations in mice produced by ENU mutagenesis. Potential meiotic recombination mutants are identified in a hierarchical fashion, by performing a screen for infertility, then gonad    histology to determine whether meiotic arrest occurs, and finally by immunohistochemical analysis of meiotic chromosome with a battery of antibody markers. Screening for mutations potentially required for recombinational repair of DNA damage in    somatic cells is performed using a flow cytometry-based micronucleus assay. Both strategies have proved effective in identifying desired classes of mutations.</p>

	]]>
</description>

<author>L Reinholdt et al.</author>


</item>


<item>
<title> Increased erythrocyte adhesion in mice and humans with hereditary spherocytosis and hereditary elliptocytosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/693</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/693</guid>
<pubDate>Tue, 08 May 2012 18:26:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice with disruptions of the red blood cell (RBC) cytoskeleton provide severe hemolytic anemia models in which to study multiorgan thrombosis and infarction. The incidence of cerebral infarction ranges from 70% to 100% in mice with    alpha-spectrin deficiency. To determine whether mutant RBCs abnormally bind adhesive vascular components, we measured adhesion of mouse and human RBCs to immobilized human thrombospondin (TSP) and laminin (LM) under controlled flow conditions.    Mutant RBCs had at least 10-fold higher adhesion to TSP compared with normal RBCs (P <.006). Mutant relative to unaffected RBC adhesion to LM was significantly (P <.01) increased as well. Treatment of RBCs with the anionic polysaccharide dextran    sulfate inhibited mutant RBC adhesion to TSP (P <.001). Treatment of RBCs with antibodies to CD47 or the CD47-binding TSP peptide 4N1K did not inhibit TSP adhesion of RBCs. Previously, we have shown that infarcts in alpha-spectrin-deficient    sph/sph mice become histologically evident beginning at 6 weeks of age. TSP adhesion of RBCs from 3- to 4- and 6- to 8-week-old sph/sph mice was significantly higher than RBCs from adult mice (> 12 weeks old; P <.005). While the mechanism of    infarction in these mice is unknown, we speculate that changes in RBC adhesive characteristics contribute to this pathology.</p>

	]]>
</description>

<author>N J. Wandersee et al.</author>


</item>


<item>
<title> Electrocardiographic and other cardiac anomalies in beta-glucuronidase-null mice corrected by nonablative neonatal marrow transplantation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/692</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/692</guid>
<pubDate>Tue, 08 May 2012 18:25:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cardiovascular manifestations of lysosomal storage disease (LSD) are a significant health problem for affected patients. Infantile-onset cardiac disease, because of its rapid progression, is usually treated symptomatically. Therapy    in older patients includes valve replacement and bone marrow (BM) transplantation, both of which are life threatening in the already debilitated patients. Enzyme replacement therapy has potential benefit but has not yet been demonstrated to    provide long-term relief for cardiac disease. Here, we demonstrate prevention of severe cardiac manifestations in beta-glucuronidase (GUSB) null mice BM-transplanted i.v.  as neonates without myeloablative pretreatment. The mice, a model of    mucopolysaccharidosis type VII (MPSVII, Sly syndrome), develop progressive LSD unless provided with GUSB early in life. The BM recipients retained GUSB+ donor cells in the peripheral blood and heart until necropsy at > or = 11 months of age. The    enzyme beta-hexosamindase increased in tissues of GUSB null MPSVII mice was reduced significantly (P = 0.001) in treated MPSVII hearts. Electrocardiography demonstrated normalization of heart rate, PR, PQ, and QRS intervals in BM recipients.    Storage was markedly reduced in the stroma of heart valves, adventitial cells of the aortic root, perivascular and interstitial cells of the myocardium, and interstitial cells of the conduction tissue. Heart/body weight ratio normalized. The    aortic root was still grossly distended, and the conductive myocytes retained storage, suggesting neither plays a major role in ECG normalization. We conclude that transplantation of MPSVII neonates without toxic intervention can prevent many of    the cardiovascular manifestations of LSD.</p>

	]]>
</description>

<author>A J. Schuldt et al.</author>


</item>


<item>
<title> Evidence for a conserved function in synapse formation reveals Phr1 as a candidate gene for respiratory failure in newborn mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/691</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/691</guid>
<pubDate>Tue, 08 May 2012 18:25:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic studies using a set of overlapping deletions centered at the piebald locus on distal mouse chromosome 14 have defined a genomic region associated with respiratory distress and lethality at birth. We have isolated and    characterized the candidate gene Phr1 that is located within the respiratory distress critical genomic interval. Phr1 is the ortholog of the human Protein Associated with Myc as well as Drosophila highwire and Caenorhabditis elegans regulator of    presynaptic morphology 1. Phr1 is expressed in the embryonic and postnatal nervous system. In mice lacking Phr1, the phrenic nerve failed to completely innervate the diaphragm. In addition, nerve terminal morphology was severely disrupted,    comparable with the synaptic defects seen in the Drosophila hiw and C. elegans rpm-1 mutants. Although intercostal muscles were completely innervated, they also showed dysmorphic nerve terminals. In addition, sensory neuron terminals in the    diaphragm were abnormal. The neuromuscular junctions showed excessive sprouting of nerve terminals, consistent with inadequate presynaptic stimulation of the muscle. On the basis of the abnormal neuronal morphology seen in mice, Drosophila, and    C. elegans, we propose that Phr1 plays a conserved role in synaptic development and is a candidate gene for respiratory distress and ventilatory disorders that arise from defective neuronal control of breathing.</p>

	]]>
</description>

<author>R W. Burgess et al.</author>


</item>


<item>
<title> Netrin 1-mediated chemoattraction regulates the migratory pathway of LHRH neurons.</title>
<link>http://mouseion.jax.org/stfb2000_2009/690</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/690</guid>
<pubDate>Tue, 08 May 2012 18:24:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Luteinizing hormone-releasing hormone (LHRH) neurons migrate from the vomeronasal organ (VNO) to the forebrain in all mammals studied. In mice, the direction of LHRH neuron migration is dependent upon axons that originate in the    VNO, but bypass the olfactory bulb and project caudally into the basal forebrain. Thus, factors that guide this unique subset of vomeronasal axons that comprise the caudal vomeronasal nerve (cVNN) are candidates for regulating the migration of    LHRH neurons. We previously showed that deleted in colorectal cancer (DCC) is expressed by neurons that migrate out of the VNO during development [Schwarting et al. (2001) J. Neurosci., 21, 911-919]. We examined LHRH neuron migration in Dcc-/-    mice and found that trajectories of the cVNN and positions of LHRH neurons are abnormal. Here we extend these studies to show that cVNN trajectories and LHRH cell migration in netrin 1 (Ntn1) mutant mice are also abnormal.  Substantially reduced    numbers of LHRH neurons are found in the basal forebrain and many LHRH neurons migrate into the cerebral cortex of Ntn1 knockout mice. In contrast, migration of LHRH cells is normal in Unc5h3rcm mutant mice. These results are consistent with the    idea that the chemoattraction of DCC+ vomeronasal axons by a gradient of netrin 1 protein in the ventral forebrain guides the cVNN, which, in turn, determines the direction of LHRH neuron migration in the forebrain. Loss of function through a    genetic deletion in either Dcc or Ntn1 results in the migration of many LHRH neurons to inappropriate destinations.</p>

	]]>
</description>

<author>G A. Schwarting et al.</author>


</item>


<item>
<title> Transplanted ER-MP12(hi)20(-)58(med/hi) myeloid progenitors produce resident macrophages from marrow that are therapeutic for lysosomal storage disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/689</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/689</guid>
<pubDate>Tue, 08 May 2012 18:24:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lysosomal storage diseases (LSD) respond to bone marrow (BM) transplantation when donor-derived cells deliver needed enzyme.  Hypothetically, the ubiquitous resident macrophages (MPhi) are the primary delivery vehicle of    therapeutic protein. In mucopolysaccharidosis type VII (MPS VII) mice with LSD, transplanted mature MPhi reduce undegraded glycosaminoglycans (GAG) in the lysosome but are incapable of self-renewal, leading to return of storage after 1 month. We    show here that a population of early BM-derived myeloid progenitors devoid of long-term hematopoietic stem cells (LT-HSC) engrafted MPS VII BM, released monocytes into peripheral blood (PBL), and engrafted tissues at known sites of resident MPhi.    These primitive Mac-1(-) cells were sorted from normal whole BM and were defined by ER-MP12(hi)20(-)58(med/hi) labeling.  Lysosomal storage was reduced in liver, spleen, thymus, heart, kidney, and bone. Cells persisted for 3 months, suggesting    self-renewal capacity or a long half-life. Cells sorted from BM by ER-MP12(-)20(hi) marker expression (which are maturer myeloid cells that express Mac-1) engrafted tissues instead of BM and quantitatively repopulated less than cells derived from    the ER-MP12(hi)20(-)58(med/hi) population. Also, reduction of lysosomal storage was variable and generally less when compared to that following transplantation of immature ER-MP12(hi)20(-)58(med/hi) cells. We conclude that primitive myeloid    progenitors are more therapeutic for LSD than mature myeloid cells due to their greater longevity and increased capacity to seed tissues. The ability of cells derived from these primitive precursors to seed deep within tissues make them excellent    candidates for both cellular therapy and gene transfer techniques to cure a wide range of metabolic diseases.</p>

	]]>
</description>

<author>B W. Soper et al.</author>


</item>


<item>
<title> Book review: Making Mice: Standardizing Animals for American Biomedical Research, 1900-1955.</title>
<link>http://mouseion.jax.org/stfb2000_2009/688</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/688</guid>
<pubDate>Tue, 08 May 2012 18:23:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K Paigen</author>


</item>


<item>
<title>Lifetime effects on the dissociation of core-excited N2 and CO molecules</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/33</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/33</guid>
<pubDate>Tue, 08 May 2012 18:23:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Vibrational-resolved ion and ion-pair yield spectra of N<sub>2</sub> and CO taken at their 1s⃗π<sup>*</sup> resonance excitations reveal decay-channel-dependent core hole lifetimes. The linewidths of the yield spectra tend to be shortened when the number of electrons ejected in the deexcitation process increases, finally becoming narrower than the total ion yield or absorption natural lifetime width of the core-excited states of N<sub>2</sub> and CO, respectively. In contrast to this, the linewidths of the yield spectra for the singly charged molecular ions, N<sub>2</sub><sup>+</sup> and CO<sup>+</sup>, are shown to be broader than their corresponding natural linewidths. This linewidth shortening and broadening observed in the ion yield spectra are explained by the effect of different internuclear distances on the lifetime of an excited molecular state.</p>

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</description>

<author>N. Saito et al.</author>


</item>


<item>
<title> Approaches to handling, breeding, strain preservation, genotyping, and drug administration for mouse models of cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/687</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/687</guid>
<pubDate>Tue, 08 May 2012 18:23:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D Boggess et al.</author>


</item>


<item>
<title> Presentation of antigen by endothelial cells and chemoattraction are required for homing of insulin-specific CD8+ T cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/686</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/686</guid>
<pubDate>Tue, 08 May 2012 18:23:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Activated insulin-specific CD8(+) T cells (IS-CD8(+) cells) home to the pancreas, destroy beta cells, and cause rapid diabetes upon transfer into diabetes-prone NOD mice. Surprisingly, they also cause diabetes in mouse strains that    are free of preexistent inflammation. Thus, we hypothesized that islet-specific homing may be in part dependent on IS-CD8(+) cells' recognition of the cognate major histocompatibility complex (MHC)/peptide complexes presented by pancreatic    endothelial cells, which acquire the antigen (insulin) from beta cells. In fact, islet-specific homing was abrogated in mice that lack MHC class I expression, or presentation of the specific peptide, or have impaired insulin secretion. Moreover,    we found that IS-CD8(+) cells directly recognized pancreatic endothelial cells in islet organ cultures. Triggering of IS-CD8(+) cells' T cell receptor (TCR) led to activation of integrins expressed by these cells. In addition, chemokines,    particularly SLC (CCL21), were also required for IS-CD8(+) cells' adhesion to endothelial monolayers and for successful homing in vivo. Thus, signaling through TCR and chemokine receptors work in concert to assure firm adhesion of T cells to the    pancreatic endothelium. The antigen cross-presentation ability of endothelia may therefore contribute to the specificity of homing of activated T lymphocytes to the tissues where antigens are generated by other cell types.</p>

	]]>
</description>

<author>A Y. Savinov et al.</author>


</item>


<item>
<title>The categorisation of objects into numeral classifier categories: a discrimination task using Malay</title>
<link>http://epubs.scu.edu.au/hahs_pubs/1114</link>
<guid isPermaLink="true">http://epubs.scu.edu.au/hahs_pubs/1114</guid>
<pubDate>Tue, 08 May 2012 18:22:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K Salehuddin</author>


</item>


<item>
<title> Transformations for cDNA microarray data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/685</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/685</guid>
<pubDate>Tue, 08 May 2012 18:22:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>X Q. Cui et al.</author>


</item>


<item>
<title> Love at first site.</title>
<link>http://mouseion.jax.org/stfb2000_2009/684</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/684</guid>
<pubDate>Tue, 08 May 2012 18:21:57 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>L Bonetta et al.</author>


</item>


<item>
<title> Mouse genetics as a tool for elucidating molecular pathways involved in hearing loss.</title>
<link>http://mouseion.jax.org/stfb2000_2009/683</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/683</guid>
<pubDate>Tue, 08 May 2012 18:21:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>A Ikeda et al.</author>


</item>


<item>
<title> A rare complex DNA rearrangement in the murine Steel gene results in exon duplication and a lethal phenotype.</title>
<link>http://mouseion.jax.org/stfb2000_2009/682</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/682</guid>
<pubDate>Tue, 08 May 2012 18:20:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Kit ligand (Kitl), encoded by the Steel (Sl) locus, plays an essential role in hematopoiesis, gametogenesis, and melanogenesis during both embryonic and adult life. We have characterized a new spontaneous mutant of the Sl locus in    mice designated KitlSl-20J that arose in the breeding colony at Jackson Laboratories. Heterozygous KitlSl-20J mice display a white belly spot and intercrossing results in an embryonic lethal phenotype in the homozygous state. Analysis of    homozygous embryos demonstrated a significant reduction in fetal liver cellularity, colony forming unit-erythroid (CFU-E) progenitors, and a total absence of germ cells. Although expressed in vivo, recombinant mutant protein demonstrated loss of    bioactivity that was correlated with lack of receptor binding.  Analysis of the Sl gene transcripts in heterozygous KitlSl-20J mice revealed an in-frame tandem duplication of exon 3. A long-range polymerase chain reaction (PCR) strategy using    overlapping primers in exon 3 amplified an approximately 7-kilobase (kb) product from DNA isolated from heterozygous KitlSl-20J mice but not from wild-type DNA that contained sequences from both introns 2 and 3 and an inverted intron 2 sequence,    suggesting a complex rearrangement as the mechanism of the mutation.  "Complexity analysis" of the sequence of the amplified product strongly suggests that local DNA motifs may have contributed to the generation of this spontaneous KitlSl-20J    allele, likely mediated by a 2-step process.  The KitlSl-20J mutation is a unique KitlSl allele and represents an unusual mechanism of mutation.</p>

	]]>
</description>

<author>S Chandra et al.</author>


</item>


<item>
<title> Peroxisome proliferator-activated receptor-gamma-deficient heterozygous mice develop an exacerbated neural antigen-induced Th1 response and experimental allergic encephalomyelitis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/681</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/681</guid>
<pubDate>Tue, 08 May 2012 18:20:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear receptor transcription factor that regulates cell growth, differentiation, and homeostasis. PPARgamma agonists are potent therapeutic agents for type 2    diabetes, obesity, and inflammation. Experimental allergic encephalomyelitis (EAE) is a Th1 cell-mediated inflammatory demyelinating autoimmune disease model of multiple sclerosis. We have shown recently that PPARgamma agonists inhibit EAE by    blocking IL-12 production, IL-12 signaling, and neural Ag-induced Th1 differentiation. In this study, we show that the PPARgamma-deficient heterozygous mice develop an exacerbated EAE with prolonged clinical symptoms than the wild-type    littermates, following immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 peptide. The exacerbation of EAE in PPARgamma(+/-) mice associates with an increased expansion of CD4(+) and CD8(+) T cells and expression of CD40 and MHC    class II molecules in response to MOGp35-55 Ag. The PPARgamma(+/-) mice also showed an increase in T cell proliferation and Th1 response to MOGp35-55 Ag than the wild-type littermates. These findings suggest that PPARgamma be a critical    physiological regulator of CNS inflammation and demyelination in EAE and perhaps multiple sclerosis and other Th1 cell-mediated autoimmune diseases.</p>

	]]>
</description>

<author>J J. Bright et al.</author>


</item>


<item>
<title> Adipose-specific peroxisome proliferator-activated receptor gamma knockout causes insulin resistance in fat and liver but not in muscle.</title>
<link>http://mouseion.jax.org/stfb2000_2009/680</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/680</guid>
<pubDate>Tue, 08 May 2012 18:19:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Syndrome X, typified by obesity, insulin resistance (IR), dyslipidemia, and other metabolic abnormalities, is responsive to antidiabetic thiazolidinediones (TZDs). Peroxisome proliferator-activated receptor (PPAR) gamma, a target    of TZDs, is expressed abundantly in adipocytes, suggesting an important role for this tissue in the etiology and treatment of IR. Targeted deletion of PPARgamma in adipose tissue resulted in marked adipocyte hypocellularity and hypertrophy,    elevated levels of plasma free fatty acids and triglyceride, and decreased levels of plasma leptin and ACRP30. In addition, increased hepatic glucogenesis and IR were observed.  Despite these defects, blood glucose, glucose and insulin tolerance,    and insulin-stimulated muscle glucose uptake were all comparable to those of control mice. However, targeted mice were significantly more susceptible to high-fat diet-induced steatosis, hyperinsulinemia, and IR.  Surprisingly, TZD treatment    effectively reversed liver IR, whereas it failed to lower plasma free fatty acids. These results suggest that syndrome X may be comprised of separable PPARgamma-dependent components whose origins and therapeutic sites may reside in distinct    tissues.</p>

	]]>
</description>

<author>W He et al.</author>


</item>


<item>
<title> Severe hypocalcemia after intravenous bisphosphonate therapy in occult vitamin D deficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/679</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/679</guid>
<pubDate>Tue, 08 May 2012 18:19:31 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title> Synopsis: XVIIth Testis Workshop, &quot;Functional Genomics of Male Reproduction&quot;.</title>
<link>http://mouseion.jax.org/stfb2000_2009/678</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/678</guid>
<pubDate>Tue, 08 May 2012 18:19:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M A. Handel et al.</author>


</item>


<item>
<title> Mice and more.</title>
<link>http://mouseion.jax.org/stfb2000_2009/677</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/677</guid>
<pubDate>Tue, 08 May 2012 18:18:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>A report on the Mouse Initiatives V meeting 'Genomics of Complex Systems in Biomedical Research', The Jackson Laboratory, Bar Harbor, USA, 30 July-2 August 2003.</p>

	]]>
</description>

<author>C J. Bult</author>


</item>


<item>
<title> Public stem cell banks: considerations of justice in stem cell research and therapy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/676</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/676</guid>
<pubDate>Tue, 08 May 2012 18:17:53 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R R. Faden et al.</author>


</item>


<item>
<title> Factors related to the use of bone densitometry: survey responses of 494 primary care physicians in New England.</title>
<link>http://mouseion.jax.org/stfb2000_2009/675</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/675</guid>
<pubDate>Tue, 08 May 2012 18:17:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Large population-based surveys have shown that approximately 30% of people over age 65 years have osteoporosis and that 17% of the population over 65 years will sustain a fracture during their lifetime. Many people with    osteoporosis are never being evaluated even though effective treatments are available. We examined why primary care physicians order few bone mineral density scans. We conducted a cross-sectional survey of primary care physicians practicing in    any of the six New England states. Target physician specialties included internal medicine, general practitioners/family physicians, and obstetrician-gynecologists who had a facsimile number listed with the American Medical Association.     Demographics, practice characteristics, use of bone densitometry, and attitudes regarding osteoporosis, bone densitometry and health maintenance were assessed by questionnaire. Twelve percent ( n=494) of the physicians responded to the    questionnaire. Respondents were similar to non-respondents with respect to years of practice, training and geographical state, though they were more likely to be female ( p</p>

	]]>
</description>

<author>D H. Solomon et al.</author>


</item>


<item>
<title> Paracrine overexpression of IGFBP-4 in osteoblasts of transgenic mice decreases bone turnover and causes global growth retardation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/674</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/674</guid>
<pubDate>Tue, 08 May 2012 18:16:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Insulin-like growth factor binding protein 4 (IGFBP-4) is abundantly expressed in bone and is generally believed to function as an inhibitor of IGF action. To investigate the function of locally produced IGFBP-4 in bone in vivo, we    targeted expression of IGFBP-4 to osteoblasts using a human osteocalcin promoter to direct transgene expression. IGFBP-4 protein levels in calvaria of transgenic (OC-BP4) mice as measured by Western ligand blot were increased 25-fold over the    endogenous level.  Interestingly, levels of IGFBP-5 were decreased in the OC-BP4 mice, possibly because of a compensatory alteration in IGF-1 action.  Morphometric measurements showed a decrease in femoral length and total bone volume in    transgenic animals compared with the controls. Quantitative histomorphometry at the distal femur disclosed a striking reduction in bone turnover in the OC-BP4 mice. Osteoblast number/bone length and bone formation rate/bone surface in OC-BP4 mice    were approximately one-half that seen in control mice. At birth, OC-BP4 mice were of normal size and weight but exhibited striking postnatal growth retardation. Organ allometry (mg/g body weight) analysis revealed that, whereas most organs    exhibited a proportional reduction in weight, calvarial and femoral wet weights were disproportionally small (approximately 70% and 80% of control, respectively). In conclusion, paracrine overexpression of IGFBP-4 in the bone microenvironment    markedly reduced cancellous bone formation and turnover and severely impaired overall postnatal skeletal and somatic growth. We attribute these effects to the sequestration of IGF-1 by IGFBP-4 and consequent impairment of IGF-1 action in skeletal    tissue.</p>

	]]>
</description>

<author>M Zhang et al.</author>


</item>


<item>
<title> The cellular and clinical parameters of anabolic therapy for osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/673</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/673</guid>
<pubDate>Tue, 08 May 2012 18:16:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>A new era in the management of osteoporosis began with the recent approval of parathyroid hormone (PTH) for the treatment of postmenopausal osteoporosis. This peptide holds promise as the first in a series of anabolic growth    factors that promote bone formation, enhance mineralization,and stimulate periosteal growth, yet exert relatively limited effects on bone resorption. Daily intermittent PTH treatment for postmenopausal women results in a dramatic increase in bone    mineral density (BMD) (i.e., 10-15% improvement in spine BMD) and a significant decline (i.e., a risk reduction of nearly 2/3) in the occurrence of fragility fractures. The mechanism of PTH's anabolic action on the skeleton is complex and    involves multiple pathways linked to common signaling peptides that affect gene transcription in osteoblasts. One fascinating aspect of PTH, both at the clinical and molecular level, is the relationship between the frequency of PTH treatment and    the bone response. Depending on the type of PTH exposure, there can be an anabolic or catabolic skeletal phenotype that can then be recapitulated by certain in vivo and in vitro model systems. Transcriptional events following ligand binding to    the PTH/PTHrP1 receptor have been studied, with particular interest in target genes such as IGF-I that can regulate both bone formation and resorption. Novel in vivo strategies, including temporal and conditional mutagenesis, will almost    certainly lead to newer therapeutic paradigms for the treatment of postmenopausal osteoporosis.</p>

	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title> Mouse genetic approaches to access pathways important in retinal function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/672</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/672</guid>
<pubDate>Tue, 08 May 2012 18:15:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>The laboratory mouse is a premier research tool for understanding human biology and disease. With the availability of the first complete draft sequences of the mouse genome and ongoing large scale screens for new mouse mutations to    serve as novel models, the usefulness of the mouse will only increase. The vision research field, in particular, which has identified many human diseases for which no models are yet available, will benefit from the newly developed tools in mouse    molecular genetics.</p>

	]]>
</description>

<author>P M. Nishina et al.</author>


</item>


<item>
<title> Towards understanding the function of the tubby gene family in the retina.</title>
<link>http://mouseion.jax.org/stfb2000_2009/671</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/671</guid>
<pubDate>Tue, 08 May 2012 18:15:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>S Ikeda et al.</author>


</item>


<item>
<title> Meiosis in male PL/J mice: a genetic model for gametic aneuploidy.</title>
<link>http://mouseion.jax.org/stfb2000_2009/670</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/670</guid>
<pubDate>Tue, 08 May 2012 18:14:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sperm from mice of the PL/J strain have a high frequency of sperm-head morphology abnormalities. Fluorescence in situ hybridization (FISH) methods revealed that PL/J sperm are also characterized by a high frequency of aneuploidy.    The traits of abnormal sperm head morphology and aneuploidy are associated with numerous meiotic abnormalities.  Spermatocytes of PL/J mice exhibit chromosome asynapsis during meiotic prophase as well as reduced crossing over, revealed by    analysis of both MLH1 foci in pachytene spermatocytes and chiasmata seen at the first meiotic metaphase. During the first meiotic division, roughly one-third of the PL/J spermatocytes exhibit aberrant spindle morphology, with abnormalities    including monopolar spindles, split spindle poles, and incomplete spindle formation and centrosomal abnormalities. F1 progeny of a cross between PL/J and C57BL/6J did not exhibit a high frequency of either sperm aneuploidy or sperm head    morphology aberrations, as would be expected if the PL/J traits were dominant. Among progeny of a backcross of F1 mice to PL/J, none of 16 males assessed exhibited elevated frequencies of sperm head morphology abnormalities. Four of the    individuals exhibited elevated sperm aneuploidy, but not at the levels of the PL/J parents.  Thus, it is likely that the aberrant PL/J traits are due to several genes and/or modifiers affecting the generation of both sperm aneuploidy and abnormal    sperm head morphology.</p>

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</description>

<author>A Pyle et al.</author>


</item>


<item>
<title> Growth hormone rising: did we quit too quickly?</title>
<link>http://mouseion.jax.org/stfb2000_2009/669</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/669</guid>
<pubDate>Tue, 08 May 2012 18:14:06 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title> Integrating computationally assembled mouse transcript sequences with the Mouse Genome Informatics (MGI) database.</title>
<link>http://mouseion.jax.org/stfb2000_2009/668</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/668</guid>
<pubDate>Tue, 08 May 2012 18:13:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Databases of experimentally generated and computationally derived transcript sequences are valuable resources for genome analysis and annotation. The utility of such databases is enhanced when the sequences they contain are    integrated with such biological information as genomic location, gene function, gene expression and phenotypic variation. We present the analysis and results of a semi-automated process of connecting transcript assemblies with highly curated    biological information for mouse genes that is available through the Mouse Genome Informatics (MGI) database.</p>

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</description>

<author>Y Zhu et al.</author>


</item>


<item>
<title> Skeletal unloading induces resistance to insulin-like growth factor I on bone formation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/667</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/667</guid>
<pubDate>Tue, 08 May 2012 18:13:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Skeletal unloading results in an inhibition of bone formation associated with a decrease in osteoblast number, impaired mineralization of bone, and altered proliferation and differentiation of osteoprogenitor cells.  Although such    changes are likely to be mediated by multiple factors, resistance to the growth-promoting action of insulin-like growth factor I (IGF-I) has been hypothesized to play an important role. To determine whether skeletal unloading induces resistance    to IGF-I on bone formation, we examined the response of unloaded (hindlimb elevation) and normally loaded tibia and femur to IGF-I administration. To eliminate the variable of endogenous growth hormone production and secretion during exogenous    IGF-I administration, we used growth hormone-deficient dwarf rats (dw-4).  The rats were given IGF-I (2.5 mg/kg/day) or vehicle during 7 and 14 days of unloading or normal loading. This significantly increased the serum level of IGF-I in both the    normally loaded and unloaded rats. Unloading did not affect the serum level of IGF-I in the vehicle-treated rats. IGF-I markedly increased periosteal bone formation at the tibiofibular junction of normally loaded rats. Unloading decreased bone    formation in the vehicle-treated rats, and blocked the ability of IGF-I to increase bone formation. On the other hand, IGF-I increased periosteal bone formation at the midpoint of the humerus (normally loaded in this model) in both    hindlimb-elevated and normally loaded rats. IGF-I significantly increased osteogenic colony number, total ALP activity, and total mineralization in bone marrow osteoprogenitor (BMOp) cells of normally loaded rats.  Unloading reduced these    parameters in the vehicle-treated rats, and blocked the stimulation by IGF-I. Furthermore, IGF-I administration (10 ng/ml) in vitro significantly increased cell proliferation of the BMOp cells isolated from normally loaded bone, but not that of    cells from unloaded bone. These results indicate that skeletal unloading induces resistance to IGF-I on bone formation.</p>

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</description>

<author>T Sakata et al.</author>


</item>


<item>
<title> Clustering of multiple specific genes and gene-rich R-bands around SC-35 domains: evidence for local euchromatic neighborhoods.</title>
<link>http://mouseion.jax.org/stfb2000_2009/666</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/666</guid>
<pubDate>Tue, 08 May 2012 18:12:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Typically, eukaryotic nuclei contain 10-30 prominent domains (referred to here as SC-35 domains) that are concentrated in mRNA metabolic factors.  Here, we show that multiple specific genes cluster around a common SC-35 domain,    which contains multiple mRNAs. Nonsyntenic genes are capable of associating with a common domain, but domain "choice" appears random, even for two coordinately expressed genes. Active genes widely separated on different chromosome arms associate    with the same domain frequently, assorting randomly into the 3-4 subregions of the chromosome periphery that contact a domain. Most importantly, visualization of six individual chromosome bands showed that large genomic segments ( approximately 5    Mb) have striking differences in organization relative to domains. Certain bands showed extensive contact, often aligning with or encircling an SC-35 domain, whereas others did not. All three gene-rich reverse bands showed this more than the    gene-poor Giemsa dark bands, and morphometric analyses demonstrated statistically significant differences. Similarly, late-replicating DNA generally avoids SC-35 domains. These findings suggest a functional rationale for gene clustering in    chromosomal bands, which relates to nuclear clustering of genes with SC-35 domains. Rather than random reservoirs of splicing factors, or factors accumulated on an individual highly active gene, we propose a model of SC-35 domains as functional    centers for a multitude of clustered genes, forming local euchromatic "neighborhoods."</p>

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</description>

<author>L S. Shopland et al.</author>


</item>


<item>
<title> An investigation of the predictors of bone mineral density and response to therapy with alendronate in osteoporotic men.</title>
<link>http://mouseion.jax.org/stfb2000_2009/665</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/665</guid>
<pubDate>Tue, 08 May 2012 18:12:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Male osteoporosis is an important disease, with 25-30% of all hip fractures occurring in men. In a recent randomized, placebo-controlled study of osteoporotic males, alendronate 10 mg daily for 2 yr led to significant increments in    bone mineral density (BMD), of a similar magnitude to those observed in postmenopausal women. In this study, specimens collected at intervals during the recent trial of alendronate in male osteoporosis, from 197 of the original 241 participants,    were assayed for testosterone, estradiol, IGF-I, IGF binding protein 3 (IGFBP-3), bone-specific alkaline phosphatase [BSAP (serum)], and N-telopeptide of type I collagen corrected for creatinine [NTx (urine)]. Together with fracture and    densitometry data from the original study, relationships were examined between BMD and serum IGF-I, IGFBP-3, testosterone, estradiol, BSAP, and urine NTx, both at baseline and during treatment with alendronate, to gain possible insights into the    pathogenesis of male osteoporosis. Statistically significant (P</p>

	]]>
</description>

<author>W M. Drake et al.</author>


</item>


<item>
<title> Temporal expression of cell cycle-related proteins during spermatogenesis: establishing a timeline for onset of the meiotic divisions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/664</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/664</guid>
<pubDate>Tue, 08 May 2012 18:11:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>During spermatogenesis, the complex events of the first meiotic prophase and division phase bring about dramatic changes in nuclear organization.  One factor frustrating mechanistic dissection of these events is lack of knowledge    about precisely what events occur, in what order they occur, and how they may be interrelated by temporal sequence; in other words, a precise timeline is lacking. This temporal ordering problem can be tackled by following expression and    localization in mouse spermatocytes of proteins critical to events of the meiotic cell division process. These include ones that are primarily chromosomal and related to pairing and recombination, as well as kinases and substrates that mediate    the cell cycle transition. Distinct and protein-specific patterns occur with respect to expression and localization throughout meiotic prophase and division and dramatic relocalization of proteins occurs as spermatocytes enter the meiotic    division phase. This information provides a foundation for a meiotic timeline that can be augmented to provide, eventually, a complete catalog of meiotic events and their temporal sequence. Such a framework can clarify mechanisms of normal    meiosis as well as mutant phenotypes and aberrations of the meiotic process that lead to aneuploidy.</p>

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</description>

<author>A Inselman et al.</author>


</item>


<item>
<title> From mouse to man: redefining the role of insulin-like growth factor-I in the acquisition of bone mass.</title>
<link>http://mouseion.jax.org/stfb2000_2009/663</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/663</guid>
<pubDate>Tue, 08 May 2012 18:11:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>The insulin-like growth factor system (IGF) has been linked to the process of bone acquisition through epidemiologic analyses of large cohorts and in vitro studies of bone cells. But the exact relationship between expression of    IGF-I in bone and skeletal homeostasis or pathologic conditions, such as osteoporosis, remains poorly defined. Recent advances in genomic engineering have resulted in the development of better in vivo models to test the role of IGF-I during    development and maintenance of the adult skeleton. It is now established that skeletal expression of IGF-I is critical for differentiative bone cell function. It may also be essential for the full anabolic effects of parathyroid hormone on    trabecular bone and for some component of biomineralization. Evidence from conditional mutagenesis studies suggests that serum IGF-I may represent more than a storage depot or permissive factor during the final phase of skeletal acquisition. This    work re-examines the original tenets of the "somatomedin hypothesis" in light of these newer mouse models and their remarkable skeletal phenotypes. The implications are far reaching and suggest that newer approaches for manipulating the IGF    regulatory system may one day be useful as therapeutic adjuncts for the treatment of osteoporosis.</p>

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</description>

<author>S Yakar et al.</author>


</item>


<item>
<title> Mapping of rabbit microsatellite markers using chromosome-specific libraries.</title>
<link>http://mouseion.jax.org/stfb2000_2009/662</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/662</guid>
<pubDate>Tue, 08 May 2012 18:10:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recently, rabbit microsatellite markers were developed from a chromosome 1-specific library, and seven new markers were incorporated into the genetic map of the rabbit. We have now developed microsatellite markers from chromosomes    3-, 5-, 6-, 7-, 12-, and 19-specific libraries. Linkage analysis was performed with use of these new markers, five recently physically mapped markers (PMP2, TCRB, ALOX15, MT1, and Sol33), microsatellite markers located in the HBA gene cluster,    the MHC region and FABP6 gene, and seven biochemical markers (Es-1, Es-3, Est-2, Est-4, Est-6, Est-X, and HP). This analysis enabled us to verify the specificity of the libraries and to determine the position and orientation of the linkage groups    on the chromosomes.</p>

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</description>

<author>R Korstanje et al.</author>


</item>


<item>
<title> New leptin receptor mutations in mice: Lepr(db-rtnd), Lepr(db-dmpg) and Lepr(db-rlpy).</title>
<link>http://mouseion.jax.org/stfb2000_2009/661</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/661</guid>
<pubDate>Tue, 08 May 2012 18:10:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Three new spontaneous recessive mouse mutations in the leptin receptor gene (Lepr), Lepr(db-rtnd), Lepr(db-dmpg) and Lepr(db-rlpy), originated in the CBA/J (CBA), B10.D2-H8(b)(57N)/Sn (B10) and NU/J strains, respectively.    Lepr(db-rtnd) and Lepr(db-dmpg) were maintained on C57BL/6J (B6), resulting in congenic lines of B6.CBA-Lepr(db-rtnd) and B6.B10-Lepr(db-dmpg). Lepr(db-rtnd) was also maintained on CBA post F1 generation of a cross between the B6 and the CBA,    generating the congenic line CBA.B6CBA-Lepr(db-rtnd). Lepr(db-rlpy) was maintained as a coisogenic strain. The aims of this study were to determine the molecular bases for these new Lepr mutations and to characterize the new mutant stocks, with    respect to obesity and diabetes. Mutations were analyzed by Southern blot analysis, reverse transcriptase-polymerase chain reaction and sequencing.  Body weights and plasma glucose and insulin levels were measured, and the histology of the    pancreas was carried out. Lepr(db-rtnd) contained one G deletion in exon 4 of Lepr, introducing a frameshift and premature termination. Lepr(db-dmpg) had a deletion in the extracellular domain of LEPR: Lepr(db-rlpy) exhibited a large DNA    deletion, leading to a complete lack of LEPR: All three mutations led to morbid obesity and diabetes. It is noteworthy that Lepr(db-rtnd) caused milder hyperglycemia accompanied by higher plasma and pancreatic insulin contents on B6 compared to    that on CBA backgrounds. In summary, we discovered three new mutations of Lepr, providing new mouse models for obesity and diabetes. Furthermore, our mutant stocks will be useful in elucidating the effects of the genetic background on the Lepr    mutations and in testing the specificity of antibodies to LEPR.</p>

	]]>
</description>

<author>J H. Kim et al.</author>


</item>


<item>
<title> Complete nucleotide sequence of the chloroplast genome from a leptosporangiate fern, Adiantum capillus-veneris L.</title>
<link>http://mouseion.jax.org/stfb2000_2009/660</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/660</guid>
<pubDate>Tue, 08 May 2012 18:09:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>We determined the complete nucleotide sequence of the chloroplast genome of the leptosporangiate fern, Adiantum capillus-veneris L. (Pteridaceae).  The circular genome is 150,568 bp, with a large single-copy region (LSC) of 82,282    bp, a small-single copy region (SSC) of 21,392 bp and inverted repeats (IR) of 23,447 bp each. We compared the sequence to other published chloroplast genomes to infer the location of putative genes.  When the IR is considered only once, we    assigned 118 genes, of which 85 encode proteins, 29 encode tRNAs and 4 encode rRNAs. Four protein-coding genes, all four rRNA genes and six tRNA genes occur in the IR. Most (57) putative protein-coding genes appear to start with an ATG codon, but    we also detected five other possible start codons, some of which suggest tRNA editing. We also found 26 apparent stop codons in 18 putative genes, also suggestive of RNA editing. We found all but one of the tRNA genes necessary to encode the    complete repertoire required for translation. The missing trnK gene appears to have been disrupted by a large inversion, relative to other published chloroplast genomes. We detected several structural rearrangements that may provide useful    information for phylogenetic studies.</p>

	]]>
</description>

<author>P G. Wolf et al.</author>


</item>


<item>
<title> Mouse nomenclature and maintenance of genetically engineered mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/659</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/659</guid>
<pubDate>Tue, 08 May 2012 18:09:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Modern genetic engineering technologies enable us to manipulate the mouse genome in increasingly complex ways to model human biology and disease. As a result, the number of mouse strains carrying transgenes or induced mutations has    increased markedly. Thorough understanding of strain and gene nomenclature is essential to ensure that investigators know what kind of mouse they have, and what to expect in terms of phenotype. Genetically engineered mice alter gene function by    over-expressing, eliminating, or modifying a gene product. The resulting phenotype is often unexpected and not completely understood, necessitating special care and potentially complex breeding and husbandry strategies. Animal care technicians    responsible for routine maintenance of the colony, facility managers, veterinarians, and research personnel working with mice should be well informed about the nature of the mutation, distinguishing characteristics, and necessary precautions in    handling the mice. Personnel working with mice also must be aware of the multitude of factors intrinsic to the mouse and present in the environment that can influence reproductive performance. Finally, diligent adherence to the maintenance of    genetic quality in conjunction with cryopreservation of germplasm is the best insurance against loss of a colony.</p>

	]]>
</description>

<author>C C. Linder</author>


</item>


<item>
<title> CDS annotation in full-length cDNA sequence.</title>
<link>http://mouseion.jax.org/stfb2000_2009/658</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/658</guid>
<pubDate>Tue, 08 May 2012 18:08:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The identification of coding sequences (CDS) is an important step in the functional annotation of genes. CDS prediction for mammalian genes from genomic sequence is complicated by the vast abundance of intergenic sequence in the    genome, and provides little information about how different parts of potential CDS regions are expressed. In contrast, mammalian gene CDS prediction from cDNA sequence offers obvious advantages, yet encounters a different set of complexities when    performed on high-throughput cDNA (HTC) sequences, such as the set of 60,770 cDNAs isolated from full-length enriched libraries of the FANTOM2 project. We developed a CDS annotation strategy that uses a variety of different CDS prediction    programs to annotate the CDS regions of FANTOM2 cDNAs. These include rsCDS, which uses sequence similarity to known proteins; ProCrest; Longest-ORF and Truncated-ORF, which are ab initio based predictors; and finally, DECODER and NCBI CDS    predictor, which use a combination of both principles. Aided by graphical displays of these CDS prediction results in the context of other sequence similarity results for each cDNA, FANTOM2 CDS inspection by curators and follow-up quality control    procedures resulted in high quality CDS predictions for a total of 14,345 FANTOM2 clones.</p>

	]]>
</description>

<author>M Furuno et al.</author>


</item>


<item>
<title>Linguistic relativity: from chasing frogs to eating spaghetti</title>
<link>http://epubs.scu.edu.au/hahs_pubs/1113</link>
<guid isPermaLink="true">http://epubs.scu.edu.au/hahs_pubs/1113</guid>
<pubDate>Tue, 08 May 2012 18:08:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H Winskel</author>


</item>


<item>
<title> Development and evaluation of an automated annotation pipeline and cDNA annotation system.</title>
<link>http://mouseion.jax.org/stfb2000_2009/657</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/657</guid>
<pubDate>Tue, 08 May 2012 18:08:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Manual curation has long been held to be the "gold standard" for functional annotation of DNA sequence. Our experience with the annotation of more than 20,000 full-length cDNA sequences revealed problems with this approach,    including inaccurate and inconsistent assignment of gene names, as well as many good assignments that were difficult to reproduce using only computational methods. For the FANTOM2 annotation of more than 60,000 cDNA clones, we developed a number    of methods and tools to circumvent some of these problems, including an automated annotation pipeline that provides high-quality preliminary annotation for each sequence by introducing an "uninformative filter" that eliminates uninformative    annotations, controlled vocabularies to accurately reflect both the functional assignments and the evidence supporting them, and a highly refined, Web-based manual annotation tool that allows users to view a wide array of sequence analyses and to    assign gene names and putative functions using a consistent nomenclature. The ultimate utility of our approach is reflected in the low rate of reassignment of automated assignments by manual curation. Based on these results, we propose a new    standard for large-scale annotation, in which the initial automated annotations are manually investigated and then computational methods are iteratively modified and improved based on the results of manual curation.</p>

	]]>
</description>

<author>T Kasukawa et al.</author>


</item>


<item>
<title> The aging auditory system: anatomic and physiologic changes and implications for rehabilitation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/656</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/656</guid>
<pubDate>Tue, 08 May 2012 18:07:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Over the last century, research in the area of age-related hearing loss has provided a vast amount of knowledge regarding age-related effects on the anatomy and physiology of the auditory system. As we enter the new millennium,    researchers are beginning to shift their attention towards developing methods of modulating the effects of age-related hearing loss and the development of efficacious intervention strategies to meet all of an individual's hearing-related    rehabilitative needs. The purpose of this review is to provide a framework for considering how the biological aspects of the aging auditory system interact with the most common current therapeutic intervention for age-related hearing loss--the    use of amplification--and also how the biological aspects point to other potential intervention strategies.</p>

	]]>
</description>

<author>T H. Chisolm et al.</author>


</item>


<item>
<title> Rh-RhAG/ankyrin-R, a new interaction site between the membrane bilayer and the red cell skeleton, is impaired by Rh(null)-associated mutation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/655</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/655</guid>
<pubDate>Tue, 08 May 2012 18:07:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Several studies suggest that the Rh complex represents a major interaction site between the membrane lipid bilayer and the red cell skeleton, but little is known about the molecular basis of this interaction. We report here that    ankyrin-R is capable of interacting directly with the C-terminal cytoplasmic domain of Rh and RhAG polypeptides. We first show that the primary defect of ankyrin-R in normoblastosis (nb/nb) spherocytosis mutant mice is associated with a sharp    reduction of RhAG and Rh polypeptides.  Secondly, our flow cytometric analysis of the Triton X-100 extractability of recombinant fusion proteins expressed in erythroleukemic cell lines suggests that the C-terminal cytoplasmic domains of Rh and    RhAG are sufficient to mediate interaction with the erythroid membrane skeleton.  Using the yeast two-hybrid system, we demonstrate a direct interaction between the cytoplasmic tails of Rh and RhAG and the second repeat domain (D2) of ankyrin-R.    This finding is supported by the demonstration that the substitution of Asp-399 in the cytoplasmic tail of RhAG, a mutation associated with the deficiency of the Rh complex in one Rhnull patient, totally impaired interaction with domain D2 of    ankyrin-R. These results identify the Rh/RhAG-ankyrin complex as a new interaction site between the red cell membrane and the spectrin-based skeleton, the disruption of which might result in the stomato-spherocytosis typical of Rhnull red    cells.</p>

	]]>
</description>

<author>V Nicolas et al.</author>


</item>


<item>
<title> The SCAN domain defines a large family of zinc finger transcription factors.</title>
<link>http://mouseion.jax.org/stfb2000_2009/654</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/654</guid>
<pubDate>Tue, 08 May 2012 18:06:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The SCAN domain is a highly conserved dimerization motif that is vertebrate-specific and found near the N-terminus of C(2)H(2) zinc finger proteins (SCAN-ZFP). Although the function of most SCAN-ZFPs is unknown, some have been    implicated in the transcriptional regulation of growth factors, genes involved in lipid metabolism, as well as other genes involved in cell survival and differentiation. Here we utilize a bioinformatics approach to define the structures and gene    locations of the 71 members of the human SCAN domain family, as well as to assess the conserved syntenic segments in the mouse genome and identify potential orthologs. The genes encoding SCAN domains are clustered, often in tandem arrays, in both    the human and mouse genomes and are capable of generating isoforms that may affect the function of family members. Twenty-three members of the mouse SCAN family appear to be orthologous with human family members, and human-specific cluster    expansions were observed.  Remarkably, the SCAN domains in lower vertebrates are not associated with C(2)H(2) zinc finger genes, but are contained in large retrovirus-like polyproteins. Collectively, these studies define a large family of    vertebrate-specific transcriptional regulators that may have rapidly expanded during recent evolution.</p>

	]]>
</description>

<author>T L. Sander et al.</author>


</item>


<item>
<title> G protein-coupled receptor genes in the FANTOM2 database.</title>
<link>http://mouseion.jax.org/stfb2000_2009/653</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/653</guid>
<pubDate>Tue, 08 May 2012 18:06:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>G protein-coupled receptors (GPCRs) comprise the largest family of receptor proteins in mammals and play important roles in many physiological and pathological processes. Gene expression of GPCRs is temporally and spatially    regulated, and many splicing variants are also described. In many instances, different expression profiles of GPCR gene are accountable for the changes of its biological function. Therefore, it is intriguing to assess the complexity of the    transcriptome of GPCRs in various mammalian organs. In this study, we took advantage of the FANTOM2 (Functional Annotation Meeting of Mouse cDNA 2) project, which aimed to collect full-length cDNAs inclusively from mouse tissues, and found 410    candidate GPCR cDNAs. Clustering of these clones into transcriptional units (TUs) reduced this number to 213. Out of these, 165 genes were represented within the known 308 GPCRs in the Mouse Genome Informatics (MGI) resource. The remaining 48    genes were new to mouse, and 14 of them had no clear mammalian ortholog. To dissect the detailed characteristics of each transcript, tissue distribution pattern and alternative splicing were also ascertained. We found many splicing variants of    GPCRs that may have a relevance to disease occurrence. In addition, the difficulty in cloning tissue-specific and infrequently transcribed GPCRs is discussed further.</p>

	]]>
</description>

<author>Y Kawasawa et al.</author>


</item>


<item>
<title> Human disease genes and their cloned mouse orthologs: exploration of the FANTOM2 cDNA sequence data set.</title>
<link>http://mouseion.jax.org/stfb2000_2009/652</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/652</guid>
<pubDate>Tue, 08 May 2012 18:05:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The FANTOM2 cDNA sequence data set is an excellent model to demonstrate the power of large-scale cDNA sequencing, with the goal of providing a full-length transcript sequence for each mouse gene. This data set enhances the use of    the mouse as a model for human disease. Here we identify mouse cDNA sequences in the FANTOM2 data set for a set of 67 human disease genes that as of May 2002 had no corresponding mouse cDNA annotated in the Mouse Genome Informatics (MGI)    database. These 67 human disease genes include genes related to neurological and eye disorders and cancer. We also present a list of the human disease genes and their cloned mouse orthologs found in two public databases, LocusLink and MGI.    Allelic variant and gene functional information available in MGI provides additional information relative to these mouse models, whereas computed sequence-based connections at NCBI support facile navigation through multiple    genomes.</p>

	]]>
</description>

<author>L M. Schriml et al.</author>


</item>


<item>
<title> Customized molecular phenotyping by quantitative gene expression and pattern recognition analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/651</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/651</guid>
<pubDate>Tue, 08 May 2012 18:05:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Description of the molecular phenotypes of pathobiological processes in vivo is a pressing need in genomic biology. We have implemented a high-throughput real-time PCR strategy to establish quantitative expression profiles of a    customized set of target genes. It enables rapid, reproducible data acquisition from limited quantities of RNA, permitting serial sampling of mouse blood during disease progression. We developed an easy to use statistical algorithm--Global    Pattern Recognition--to readily identify genes whose expression has changed significantly from healthy baseline profiles. This approach provides unique molecular signatures for rheumatoid arthritis, systemic lupus erythematosus, and graft versus    host disease, and can also be applied to defining the molecular phenotype of a variety of other normal and pathological processes.</p>

	]]>
</description>

<author>S Akilesh et al.</author>


</item>


<item>
<title> Variations in yeast 3&apos;-processing cis-elements correlate with transcript stability.</title>
<link>http://mouseion.jax.org/stfb2000_2009/650</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/650</guid>
<pubDate>Tue, 08 May 2012 18:04:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>A large set of yeast mRNA 3'-processing regulatory sequences was analyzed statistically, revealing a systematic variation that correlates with measured mRNA stability. Transcripts with relatively short half-lives have a high    frequency of inclusion of 3'-processing elements that include the core sequence of binding sites for the PUF proteins, which enhance mRNA turnover. These results suggest that regulatory sequence variation, typically modeled as random, could arise    instead from the necessity or advantage of specifying multiple functions in a common sequence element.</p>

	]]>
</description>

<author>J H. Graber</author>


</item>


<item>
<title> Sustained hepatic expression of FoxM1B in transgenic mice has minimal effects on hepatocellular carcinoma development but increases cell proliferation rates in preneoplastic and early neoplastic lesions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/649</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/649</guid>
<pubDate>Tue, 08 May 2012 18:04:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Increased hepatic expression of the Forkhead transcription factor FoxM1B in adult mice accelerates hepatocyte proliferation after partial hepatectomy, while in hepatocytes in intact liver the transgenic (Tg) protein is inactive and    has no effect on proliferation. To investigate the influence of FoxM1B on liver tumor formation, we examined the effect of sustained enrichment of FoxM1B in the hepatocytes of mice treated with a diethylnitrosamine (DEN)/phenobarbital tumor    induction protocol. Tg enrichment of FoxM1B in hepatocytes did not increase the proliferation rate in normal liver tissue even when the protein was localized to the nucleus. However, it did cause an increase in the proliferation rate and size of    preneoplastic and early neoplastic lesions, although having no effects on the total numbers of these lesions. As tumors progressed to hepatocellular carcinomas, the additional Tg FoxM1B protein had no effect on cell proliferation, and there was    no increase in tumor burden compared to wild-type animals. This suggests that the artificial enrichment of FoxM1B in the liver, which has been suggested as a gene therapy protocol for liver dysfunction with aging, may not be tumorigenic in that    organ.</p>

	]]>
</description>

<author>O A. Kalinina et al.</author>


</item>


<item>
<title> Cutaneous smooth muscle tumors in the dog and cat.</title>
<link>http://mouseion.jax.org/stfb2000_2009/648</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/648</guid>
<pubDate>Tue, 08 May 2012 18:03:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cutaneous smooth muscle tumors may arise from arrector pili muscles and from smooth muscles of the dermal vasculature. This report describes histologic and immunohistochemical features of eight arrector pili hamartomas in 8 dogs,    15 piloleiomyomas in 10 dogs and 3 cats, 10 piloleiomyosarcomas in 9 dogs and 1 cat, 1 angioleiomyoma in 1 cat, and 9 angioleiomyosarcomas in 6 dogs and 3 cats. Hamartomas and tumors arising from arrector pili muscles preferentially originated    from the dorsal trunk. 5/5 (100%) arrector pili hamartomas, 10/12 (83%) piloleiomyomas, 4/5 (80%) piloleiomyosarcomas, 1/1 (100%) angioleiomyoma, and 6/7 (86%) angioleiomyosarcomas were positive for smooth muscle actin. 5/5 (100%) arrector pili    hamartomas, 10/12 (83%) piloleiomyomas, 4/5 (80%) piloleiomyosarcomas, 1/1 (100%) angioleiomyoma, and 1/7 (14%) angioleiomyosarcomas were positive for desmin. Two incompletely excised canine angioleiomyosarcomas recurred locally. Metastases were    not reported.</p>

	]]>
</description>

<author>S M. Liu et al.</author>


</item>


<item>
<title> Muscle-specific Pparg deletion causes insulin resistance.</title>
<link>http://mouseion.jax.org/stfb2000_2009/647</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/647</guid>
<pubDate>Tue, 08 May 2012 18:03:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Thiazolidinediones (TZDs) are insulin-sensitizing drugs and are potent agonists of the nuclear peroxisome proliferator-activated receptor-gamma (PPAR-gamma). Although muscle is the major organ responsible for insulin-stimulated    glucose disposal, PPAR-gamma is more highly expressed in adipose tissue than in muscle. To address this issue, we used the Cre-loxP system to knock out Pparg, the gene encoding PPAR-gamma, in mouse skeletal muscle. As early as 4 months of age,    mice with targeted disruption of PPAR-gamma in muscle showed glucose intolerance and progressive insulin resistance. Using the hyperinsulinemic-euglycemic clamp technique, the in vivo insulin-stimulated glucose disposal rate (IS-GDR) was reduced    by approximately 80% and was unchanged by 3 weeks of TZD treatment. These effects reveal a crucial role for muscle PPAR-gamma in the maintenance of skeletal muscle insulin action, the etiology of insulin resistance and the action of    TZDs.</p>

	]]>
</description>

<author>A L. Hevener et al.</author>


</item>


<item>
<title> Mouse parvovirus: survival of the fittest.</title>
<link>http://mouseion.jax.org/stfb2000_2009/646</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/646</guid>
<pubDate>Tue, 08 May 2012 18:02:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R O. Jacoby et al.</author>


</item>


<item>
<title> The ichq mutant mouse, a model for the human skin disorder harlequin ichthyosis: mapping, keratinocyte culture, and consideration of candidate genes involved in epidermal growth regulation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/645</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/645</guid>
<pubDate>Tue, 08 May 2012 18:02:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Harlequin ichthyosis (HI) is a rare and usually fatal scaling skin disorder. The HI mutant mouse (ichq/ichq) has many similarities to the human disorder and provides an important model to identify candidate genes. In this study, we    report refined mapping of the mouse ichq locus and consideration of the candidate genes: calpain 1 (Capn1), phospholipase C beta 3 (Plcb3), and Rela and Ikka/Chuk that encode components of the nuclear factor-kappa B (NF-kappaB) pathway. Each are    strong candidates because of epidermal expression and/or changes in expression in human HI.  All candidates are linked to the ichq locus on mouse Chromosome 19, although Ikka is located more distally. Genetic mapping in mouse has narrowed the    ichq critical region to 4 cM. Keratinocytes from skin of +/+, +/ichq and ichq/ichq mice were cultured; all genotypes had similar expression of epidermal differentiation markers. RT-PCR amplification and sequence analysis of each candidate gene    did not reveal any mutations in the ichq mouse. Mutational screening of CAPN1 cDNA from different human HI cases revealed a R433P change, but analysis of 50 normal samples demonstrated that this was an apparent polymorphism. Sequence of RELA in    five unrelated human HI cases was normal. The results provide compelling evidence that none of these genes are the primary defect in the ichq mouse and that CAPN1 and RELA are not mutated in the human disorder.</p>

	]]>
</description>

<author>M Dunnwald et al.</author>


</item>


<item>
<title> Mouse Phenome Project: understanding human biology through mouse genetics and genomics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/644</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/644</guid>
<pubDate>Tue, 08 May 2012 18:02:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M Bogue</author>


</item>


<item>
<title>Interaction between language and cognition</title>
<link>http://epubs.scu.edu.au/hahs_pubs/1112</link>
<guid isPermaLink="true">http://epubs.scu.edu.au/hahs_pubs/1112</guid>
<pubDate>Tue, 08 May 2012 18:02:08 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H Winskel</author>


</item>


<item>
<title> Epigenesis versus preformation during mammalian development. Introduction.</title>
<link>http://mouseion.jax.org/stfb2000_2009/643</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/643</guid>
<pubDate>Tue, 08 May 2012 18:01:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R L. Gardner et al.</author>


</item>


<item>
<title>On the angular distributions of electrons photoejected from fixed-in-space and randomly oriented molecules</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/32</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/32</guid>
<pubDate>Tue, 08 May 2012 18:01:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>New theoretical expressions are devised from a dynamical perspective for molecular photoionization cross sections differential in electron ejection angles which facilitate comparisons between theory and experiment and provide a convenient basis for ab initio calculations. The cross sections obtained for fixed-in-space molecules, including the lowest-order (nondipole) effects of retardation, are given in terms of invariant molecular body-frame transition moments and related normalized angular-distribution amplitudes which can be calculated employing interaction-prepared states without reference to specific scattering boundary conditions. Corresponding expressions for molecular dipole and nondipole anisotropy factors appropriate for randomly oriented molecules are obtained in closed forms involving expectation values of harmonic polynomials over the fixed-in-space body-frame angular-distribution amplitudes. The expressions are seen to be in the spirit of corresponding results for atomic photoionization anisotropy factors, to which they reduce in appropriate limits. Interpretations of recently measured angular distributions of photoelectrons from the K-shell of molecular nitrogen illustrate how the development relates measurements on randomly oriented molecules to those performed on fixed-in-space molecules. The theoretical formalism provides results in excellent accord with measurements of the molecular nitrogen K-shell dipole anisotropy factor, and accounts for the origins of large nondipole effects observed at relatively low photon energies (ℏ<em>ω</em>≤500 eV) in the measured angular distributions.</p>

	]]>
</description>

<author>P. W. Langhoff et al.</author>


</item>


<item>
<title> Comment on &quot; &apos;Stemness&apos;: transcriptional profiling of embryonic and adult stem cells&quot; and &quot;a stem cell molecular signature&quot;.</title>
<link>http://mouseion.jax.org/stfb2000_2009/642</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/642</guid>
<pubDate>Tue, 08 May 2012 18:01:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>A V. Evsikov et al.</author>


</item>


<item>
<title> Osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/641</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/641</guid>
<pubDate>Tue, 08 May 2012 18:01:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Osteoporosis is a disease that may have a tremendous impact on the lives of many postmenopausal women. It is encouraging that effective treatments for this disease abound and the challenge is to ensure that those most in need of    diagnosis or therapy obtain adequate care. Further research is expected to clarify the role of combination therapy or sequential use of different agents for the maximum benefit in fracture protection. There is an array of efficacious options to    consider when diagnosing and treating osteoporosis so that patients and their caregivers can remain optimistic about the management of this chronic disease and prevention of future fractures.</p>

	]]>
</description>

<author>S A. Brown et al.</author>


</item>


<item>
<title> Dietary soy oil content and soy-derived phytoestrogen genistein increase resistance to alopecia areata onset in C3H/HeJ mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/640</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/640</guid>
<pubDate>Tue, 08 May 2012 18:01:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata (AA) is a complex, multi-factorial disease where genes and the environment may affect susceptibility and severity. Diet is an environmental factor with the potential to influence disease susceptibility. We    considered dietary soy (soya) oil content and the soy-derived phytoestrogen genistein as potential modifying agents for C3H/HeJ mouse AA. Normal haired C3H/HeJ mice were grafted with skin from spontaneous AA affected mice, a method previously    shown to induce AA.  Grafted mice were given one of three diets containing 1%, 5% or 20% soy oil and observed for AA development. In a separate study, mice on a 1% soy oil diet were injected with 1 mg of genistein three times per week for 10    weeks or received the vehicle as a control. Of mice on 1%, 5%, and 20% soy oil diets, 43 of 50 mice (86%), 11 of 28 mice (39%), and 2 of 11 mice (18%) developed AA, respectively. Four of 10 mice injected with genistein and 9 of 10 controls    developed AA. Mice with AA had hair follicle inflammation consistent with observations for spontaneous mouse AA, but no significant association was observed between the extent of hair loss and diet or genistein injection. Mice that failed to    develop AA typically experience white hair regrowth from their skin grafts associated with a moderate macrophage and dendritic cell infiltration. Soy oil and derivatives have previously been reported to modify inflammatory conditions.    Hypothetically, soy oil compounds may act on C3H/HeJ mice through modulating estrogen-dependent mechanisms and/or inflammatory activity to modify AA susceptibility.</p>

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</description>

<author>K J. McElwee et al.</author>


</item>


<item>
<title> Follicular stem cell carcinoma: histologic, immunohistochemical, ultrastructural, and clinical characterization in 30 dogs.</title>
<link>http://mouseion.jax.org/stfb2000_2009/639</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/639</guid>
<pubDate>Tue, 08 May 2012 18:00:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Diagnostic records of 30 primary and one metastatic follicular stem cell carcinomas in 30 dogs were reviewed. Neoplastic cells had a clear cytoplasm and formed lobules and nests surrounded by a basement membrane.     Trichoepitheliomatous and apocrine differentiations were noted in 22 of 30 (73%) and 21 of 30 (70%) primary tumors, respectively. Glycogen was present in 20 of 20 (100%) tumors tested, suggesting tricholemmal differentiation. Antibodies against    AE1/AE3 cytokeratin, vimentin, and melanA/MART1 stained 29 of 30 (97%), 29 of 30 (97%), and 12 of 27 (44%) primary tumors, respectively. Small amounts of melanin were identified in 14 primary tumors, either on the hematoxylin and eosin-stained    section (n = 6), or on the Fontana-stained section (n = 8 of 14). Ultrastructural features of neoplastic cells included cell junction complexes, swollen mitochondria, neuroendocrine-like granules, and intracytoplasmic non-membrane-bound    accumulation of proteinaceous material. Features of this neoplasm are consistent with a follicular stem cell origin. Follow-up information was available for eight dogs. Metastases developed in the draining lymph node at the time of excision of    the primary tumor (n = 1) or subsequently (n = 3).</p>

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</description>

<author>I Mikaelian et al.</author>


</item>


<item>
<title> CRB1 is essential for external limiting membrane integrity and photoreceptor morphogenesis in the mammalian retina.</title>
<link>http://mouseion.jax.org/stfb2000_2009/638</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/638</guid>
<pubDate>Tue, 08 May 2012 18:00:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations within the CRB1 gene have been shown to cause human retinal diseases including retinitis pigmentosa and Leber congenital amaurosis. We have recently identified a mouse model, retinal degeneration 8 (rd8) with a single    base deletion in the Crb1 gene. This mutation is predicted to cause a frame shift and premature stop codon which truncates the transmembrane and cytoplasmic domain of CRB1. Like in Drosophila crumbs (crb) mutants, staining for adherens junction    proteins known to localize to the external limiting membrane, the equivalent of the zonula adherens in the mammalian retina, is discontinuous and fragmented. Shortened photoreceptor inner and outer segments are observed as early as 2 weeks after    birth, suggesting a developmental defect in these structures rather than a degenerative process. Photoreceptor degeneration is observed only within regions of retinal spotting, which is seen predominantly in the inferior nasal quadrant of the    eye, and is caused by retinal folds and pseudorosettes. Photoreceptor dysplasia and degeneration in Crb1 mutants strongly vary with genetic background, suggesting that the variability in phenotypes of human patients that carry mutations in CRB1    may be due to interactions with background modifiers in addition to allelic variations.  The Crb1rd8 mouse model will facilitate the analysis of Crb1 function in the neural retina and the identification of interacting factors as candidate retinal    disease genes.</p>

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</description>

<author>A K. Mehalow et al.</author>


</item>


<item>
<title> Insulin-like growth factor I and calcium balance: evolving concepts of an evolutionary process.</title>
<link>http://mouseion.jax.org/stfb2000_2009/637</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/637</guid>
<pubDate>Tue, 08 May 2012 17:59:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title> Adenomatous hyperplasia of the thyroid gland in beluga whales (Delphinapterus leucas) from the St. Lawrence Estuary and Hudson Bay, Quebec, Canada.</title>
<link>http://mouseion.jax.org/stfb2000_2009/636</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/636</guid>
<pubDate>Tue, 08 May 2012 17:59:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>We evaluated thyroid gland lesions in beluga whales (Delphinapterus leucas) from the St. Lawrence Estuary (n = 16) and Hudson Bay (n = 14).  Follicular cysts and nodules of adenomatous hyperplasia of the thyroid gland were found in    eight and nine adults from the St. Lawrence Estuary (n = 10), respectively, and in four and six adults from Hudson Bay (n = 14), respectively. The total volume of the lesions of thyroid adenomatous hyperplasia was positively correlated with age    in both populations.  Comparison between populations could not be performed because of differences in age structures of sample groups. Beluga whales from both populations have unique thyroid lesions among marine mammals.</p>

	]]>
</description>

<author>I Mikaelian et al.</author>


</item>


<item>
<title>Arbitrium Humanum: Liberum vel Liberandum? An Historical-Theological Study of John Calvin&apos;s Doctrine of the Will</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6937</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6937</guid>
<pubDate>Tue, 08 May 2012 17:58:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>John Calvin, the sixteenth-century reformer, taught that the fall into sin left the human will bound in a miserable slavery to depravity, unless it is liberated by Jesus Christ. Recently, Dewey J. Hoitenga Jr. has argued that Calvin retains so little of the will as it was created that he cannot adequately account for humanity's moral responsibility. However, a careful examination of Calvin's writings reveals that this reformer develops an understanding of the human will which is more nuanced than Hoitenga would lead one to believe. Like his mentor, Augustine, Calvin distinguishes between a will that is free from external coercion and a will that is equally free to choose either good or evil. In his debate with the Roman Catholic theologian, Albert Pighius, Calvin upholds the former while rejecting the latter. Furthermore, in this same debate, Geneva's reformer voices his agreement with the libertqs in externis - the liberty of the will in earthly matters - as it is expressed, for instance, in the Augsburg Confession Calvin also ardently avoids the kind of deterministic fatalism which some radical reformers, particularly the Libertines, adopted. At the same time, none of these distinctions and qualifications detract him from his fundamental conviction that the fallen human will, of itself, cannot even begin to take the first steps towards salvation. Redemption is not a co-operative venture between the will of God and the will of human beings. Rather, it includes a sovereign work of God's grace upon the human will. Hoitenga's critique raises important questions; however, it fails to pay sufficient attention to the historical and polemical context in which Calvin develops his doctrine of the will. when that context is investigated, it becomes clear that Calvin teaches the depravity, not the destruction, of the human will. A depraved will cannot save itself, but it remains morally responsible for the actions it initiates.</p>

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</description>

<author>Jason Vliet</author>


</item>


<item>
<title> Regulation of human short-term repopulating cell (STRC) engraftment in NOD/SCID mice by host CD122+ cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/635</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/635</guid>
<pubDate>Tue, 08 May 2012 17:58:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: NOD/SCID and NOD/SCID B2m(null) mice are used for the in vivo study of human hematopoietic stem cells (HSC). A previously unrecognized HSC in cord blood, termed short-term repopulating cell (STRC), has been identified    using NOD/SCID B2m(null) mice. However, only low levels of STRC engraft in NOD/SCID mice, presumably due to their higher levels of NK cell activity. The objective of these studies was to deplete NK cells both by genetic manipulation of the hosts    and by antibody depletion of cell populations that may regulate engraftment with human STRC. METHODS: C57BL/6-SCID mice and immunodeficient NOD mice genetically deleted in NK cell activity were injected intravenously with human cord blood cells    to quantify STRC engraftment. Cohorts of these mice were also treated with anti-NK1.1 or anti-CD122 (IL-2r beta-chain) antibodies. RESULTS: Human STRC fail to engraft in C57BL/6-SCID mice treated with anti-NK1.1 or with anti-CD122 antibody that    targets mouse NK and myeloid cells. NOD/SCID mice, NOD-Rag1(null) mice, and NOD-Rag1(null)Pfp(null) mice that are genetically deleted in NK cell cytotoxic activity support only low levels of STRC engraftment. In contrast, STRC engraft at high    levels in all three strains of immunodeficient NOD mice treated with anti-CD122 antibody.  CONCLUSION: Injection of anti-CD122 antibody leads to high levels of STRC engraftment in immunodeficient NOD mice, but not in C57BL/6-SCID mice.  These    data document that depletion of NK cells is required, and that additional murine host innate immune factors, presumably myeloid cells, are important in regulating human STRC engraftment.</p>

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</description>

<author>L D. Shultz et al.</author>


</item>


<item>
<title> Metaphase FISHing of transgenic mice recommended: FISH and SKY define BAC-mediated balanced translocation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/634</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/634</guid>
<pubDate>Tue, 08 May 2012 17:58:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The evolving trend to use larger transgenes and their associated increased chance of unexpected genetic events mandates more careful characterization of transgenic mice. In characterizing our five new mouse strains transgenic for    the BAC, bEMS4, we have identified the highest copy number reported to date: the stable incorporation of approximately 40 copies of a 194-kb expressed transgene in a single insertion site. We caution, however, that standard molecular techniques    failed to identify a balanced translocation in another strain, and an inappropriate site of insertion in a third. Molecular cytogenetic analysis using metaphase FISH was the minimum level of characterization needed to reveal these unexpected    genetic events. In addition, we combined FISH and SKY to identify the transgene at the breakpoints of the balanced translocation, t(3;9). This is the first description of a BAC-mediated chromosomal rearrangement and the first application of SKY    to identify transgene-induced chromosomal rearrangements.</p>

	]]>
</description>

<author>B S. Abrahams et al.</author>


</item>


<item>
<title> Cutaneous fibropapilloma in a mountain lion (Felis concolor).</title>
<link>http://mouseion.jax.org/stfb2000_2009/633</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/633</guid>
<pubDate>Tue, 08 May 2012 17:57:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>A 12-yr-old mountain lion (Felis concolor) developed a 0.5-cm3 raised nonpigmented and nonulcerated mass between the lip and the nasal planum.  The tumor was surgically removed and diagnosed histologically as a fibropapilloma. The    tumor recurred 1 yr later, at which time it was again excised, and the diagnosis was reconfirmed by biopsy. Frozen tissue from the second excision was submitted for polymerase chain reaction testing for papillomavirus. The 176-base pair    polymerase chain reaction product recovered from the tumor was cloned and sequenced. The papillomavirus had 96% homology with a papillomavirus previously retrieved from a fibropapilloma in a domestic cat and is the next most closely related to    bovine papillomavirus type 1. This is the first report of a virus-associated fibropapilloma in a mountain lion.</p>

	]]>
</description>

<author>F Y. Schulman et al.</author>


</item>


<item>
<title> Mouse model of subretinal neovascularization with choroidal anastomosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/632</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/632</guid>
<pubDate>Tue, 08 May 2012 17:57:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: To characterize the phenotype and report a reliable genetic model of retinal angiogenesis and subretinal neovascularization in the mouse.  METHODS: The mouse phenotype was characterized using ophthalmoscopy, fundus    photography, fluorescein angiography, electroretinography, histology, gene sequencing, and linkage analysis. RESULTS: Scattered pink-gray retinal lesions were found on ophthalmoscopy and were confirmed to be subretinal neovascularization on    fluorescein angiography. On histologic examination, outer plexiform retinal neovascularization with growth into the subretinal space was found as early as postnatal Day 15.  On genetic analysis, homozygosity of the Vldlr mutation always    segregated with the retinal angiogenesis, whereas normal and heterozygous mice had no neovascularization. The histologic studies 15 to 18 days consistently showed new outer plexiform neovascular vessels drawn to the subretinal space by 20 days,    and by 30 to 50 days, subretinal hemorrhages and choroidal anastomoses were common. Mice by 8 months had increased vascularity of the iris and ciliary body. CONCLUSIONS: The Vldlr mutation in the mouse provides a good model for retinal    angiogenesis and subretinal neovascularization. Finding a strong association between retinal angiogenesis and a very low density lipid receptor mutation is new, and study of lipid receptor physiology may broaden the understanding of retinal    angiogenesis.</p>

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</description>

<author>J R. Heckenlively et al.</author>


</item>


<item>
<title> Progress toward understanding the genetic and biochemical mechanisms of inherited photoreceptor degenerations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/631</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/631</guid>
<pubDate>Tue, 08 May 2012 17:56:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>More than 80 genes associated with human photoreceptor degenerations have been identified. Attention must now turn toward defining the mechanisms that lead to photoreceptor death, which occurs years to decades after the birth of    the cells. Consequently, this review focuses on topics that offer insights into such mechanisms, including the one-hit or constant risk model of photoreceptor death; topological patterns of photoreceptor degeneration; mutations in ubiquitously    expressed splicing factor genes associated only with photoreceptor degeneration; disorders of the retinal pigment epithelium; modifier genes; and global gene expression analysis of the retina, which will greatly increase our understanding of the    downstream events that occur in response to a mutation.</p>

	]]>
</description>

<author>L R. Pacione et al.</author>


</item>


<item>
<title> The pathogenesis of alopecia areata in rodent models.</title>
<link>http://mouseion.jax.org/stfb2000_2009/630</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/630</guid>
<pubDate>Tue, 08 May 2012 17:56:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rodent models of human disease provide an important tool in the investigation of genetic and environmental activation factors, disease pathogenesis, and the development of new and improved treatments. Up to 20% of aged C3H/HeJ mice    and 70% of Dundee Experimental Bald Rats (DEBR) develop alopecia areata (AA), a nonscarring, inflammatory hair loss disease with a suspected autoimmune pathogenesis. These rodent models are currently employed in determining the genetic basis of    AA, understanding the mechanisms of disease initiation and progression, and defining potential endogenous and environmental influences. Induction of AA by skin graft transfer between affected and unaffected mice has been employed to examine skin    and immune system changes during AA pathogenesis.  Manipulation of inflammatory cells in vivo indicates AA is primarily a cell mediated disease with auto-antibody production as a secondary event.  Whether the AA activating factors are exogenous    or endogenous antigens, or involve normal or aberrant epitope expression remains to be elucidated.  However, current research suggests a self contained disease cycle involving four key events: (1) Failure of the putative anagen stage hair    follicle immune privilege and exposure of hair follicle located AA inciting epitopes to the immune system; (2) Antigen presentation, costimulation, and activation of responsive lymphocytes by antigen presenting cells; (3) Activated inflammatory    cell migration to, and infiltration of, hair follicles; (4) The subsequent disruptive actions of the inflammatory cell infiltrate on the hair follicles. Each of these events is vulnerable to therapeutic intervention, and rodent models will be    fundamentally involved in developing new treatments for AA.</p>

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</description>

<author>K J. McElwee et al.</author>


</item>


<item>
<title> Animal and in vitro models for the study of hair follicles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/629</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/629</guid>
<pubDate>Tue, 08 May 2012 17:56:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Since the way in which the hair follicle functions is not well understood, many hair disorders are poorly controlled. A range of in vitro and in vivo models have therefore been developed to investigate the cell biological and    biochemical mechanisms involved in the organization of this complex tissue. These range from cultures of a single cell type, such as those of the regulatory, mesenchyme-derived dermal papilla, through organ culture of isolated follicles to    natural or genetically manipulated animal models.  Each system has advantages and disadvantages for studying particular aspects of follicular function and some are potentially useful for the development of novel treatments for hair    disorders.</p>

	]]>
</description>

<author>V A. Randall et al.</author>


</item>


<item>
<title> Fas-deficient C3.MRL-Tnfrsf6(lpr) mice and Fas ligand-deficient C3H/HeJ-Tnfsf6(gld) mice are relatively resistant to the induction of alopecia areata by grafting of alopecia areata-affected skin from C3H/HeJ mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/628</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/628</guid>
<pubDate>Tue, 08 May 2012 17:55:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata is suspected to be a T cell-mediated autoimmune disease of the hair follicle, where Fas is expressed on hair follicles and Fas ligand on perifollicular infiltrates. To elucidate whether the Fas/Fas ligand pathway is    of pathogenetic significance in alopecia areata, we investigated whether alopecia areata can be induced in Fas-deficient and Fas ligand-deficient mice and whether alopecia areata develops in Fas-deficient and Fas ligand-deficient skin. Therefore,    we induced alopecia areata by grafting alopecia areata-affected C3H/HeJ mouse skin on to C3H/HeJ mice (control), on to Fas ligand-deficient C3H/HeJ-Tnfsf6(gld) mice or Fas-deficient C3.MRL-Tnfrsf6(lpr) mice. All control mice developed alopecia    areata, whereas no Fas-deficient mice showed hair loss and two of seven Fas ligand-deficient mice developed only transitory, limited alopecia areata. Moreover, skin from C3H/HeJ mice (control), C3H/HeJ-Tnfsf6(gld) mice, and C3.MRL-Tnfrsf6(lpr)    mice was grafted on to C3H/HeJ mice with extensive alopecia areata. Skin grafts from control mice developed hair loss, whereas Fas-deficient and Fas ligand-deficient skin grafts were spared from alopecia areata. Terminal deoxynucleotidyl    transferase-mediated deoxyuridine triphosphate nick end-labeling and immunofluorescence studies revealed an increased number of apoptotic cells and expression of Fas on hair follicles as well as expression of Fas ligand on cells of the    perifollicular infiltrate in C3H/HeJ mice with alopecia areata, whereas in Fas-deficient and Fas ligand-deficient mice apoptotic cells were virtually absent in hair follicles. The results suggest that the Fas/Fas ligand pathway plays an important    pathogenetic role in alopecia areata.</p>

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</description>

<author>Paul P. Freyschmidt et al.</author>


</item>


<item>
<title> Manipulation of stem cell proliferation and lineage commitment: visualisation of label-retaining cells in wholemounts of mouse epidermis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/627</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/627</guid>
<pubDate>Tue, 08 May 2012 17:55:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mammalian epidermis is maintained by stem cells that have the ability to self-renew and generate daughter cells that differentiate along the lineages of the hair follicles, interfollicular epidermis and sebaceous gland. As stem    cells divide infrequently in adult mouse epidermis, they can be visualised as DNA label-retaining cells (LRC). With whole-mount labelling, we can examine large areas of interfollicular epidermis and many hair follicles simultaneously, enabling us    to evaluate stem cell markers and examine the effects of different stimuli on the LRC population. LRC are not confined to the hair follicle, but also lie in sebaceous glands and interfollicular epidermis. LRC reside throughout the permanent    region of the hair follicle, where they express keratin 15 and lie in a region of high alpha6beta4 integrin expression. LRC are not significantly depleted by successive hair growth cycles. They can, nevertheless, be stimulated to divide by    treatment with phorbol ester, resulting in near complete loss of LRC within 12 days. Activation of Myc stimulates epidermal proliferation without depleting LRC and induces differentiation of sebocytes within the interfollicular epidermis.     Expression of N-terminally truncated Lef1 to block beta-catenin signalling induces transdifferentiation of hair follicles into interfollicular epidermis and sebocytes and causes loss of LRC primarily through proliferation. We conclude that LRC    are more sensitive to some proliferative stimuli than others and that changes in lineage can occur with or without recruitment of LRC into cycle.</p>

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</description>

<author>K M. Braun et al.</author>


</item>


<item>
<title> Genetic separation of the transplantation tolerance and autoimmune phenotypes in NOD mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/626</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/626</guid>
<pubDate>Tue, 08 May 2012 17:54:45 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T Pearson et al.</author>


</item>


<item>
<title> New paths to human ES cells?</title>
<link>http://mouseion.jax.org/stfb2000_2009/625</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/625</guid>
<pubDate>Tue, 08 May 2012 17:54:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D Solter</author>


</item>


<item>
<title> Alloimmune injury and rejection of human skin grafts on human peripheral blood lymphocyte-reconstituted non-obese diabetic severe combined immunodeficient beta2-microglobulin-null mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/624</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/624</guid>
<pubDate>Tue, 08 May 2012 17:53:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Small animal models with the capacity to support engraftment of a functional human immune system are needed to facilitate studies of human alloimmunity. In the present investigation, non-obese diabetic (NOD) severe combined    immunodeficient (scid) beta2-microglobulin-null (B2mnull) mice engrafted with human peripheral blood lymphocytes (hu-PBL-NOD-scid B2mnull mice) were used as in vivo models for studying human skin allograft rejection. Hu-PBL-NOD-scid B2mnull mice    were established by injection of human spleen cells or PBLs and transplanted with full-thickness allogeneic human skin. Human cell engraftment was enhanced by injection of anti-mouse CD122 antibody. The respective contributions of human CD4+ and    CD8+ cells in allograft rejection were determined using depleting antibodies. Human skin grafts on unmanipulated NOD-scid B2mnull mice uniformly survived but on chimeric hu-PBL-NOD-scid B2mnull mice exhibited severe immune-mediated injury that    often progressed to complete rejection. The alloaggressive hu-PBLs did not require prior in vitro sensitization to elicit targeted effector cell activity. Extensive mononuclear cell infiltration directed towards human-origin endothelium was    associated with thrombosis and fibrin necrosis. No evidence of graft-versus-host disease was detected. Either CD4+ or CD8+ T cells may mediate injury and alloimmune rejection of human skin grafts on hu-PBL-NOD-scid B2mnull mice. It is proposed    that Hu-PBL-NOD-scid B2mnull mice engrafted with human skin will provide a useful model for analysis of interventions designed to modulate human allograft rejection.</p>

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</description>

<author>N A. Turgeon et al.</author>


</item>


<item>
<title> NOD/LtSz-Rag1nullPfpnull mice: a new model system with increased levels of human peripheral leukocyte and hematopoietic stem-cell engraftment.</title>
<link>http://mouseion.jax.org/stfb2000_2009/623</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/623</guid>
<pubDate>Tue, 08 May 2012 17:53:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: A critical need exists for effective small-animal models that accept engraftment of human hematopoietic progenitor cells and mature lymphocytes. The purpose of this study was to determine the phenotypic effects of    perforin (Pfp) deficiency on nonobese diabetic (NOD)-Rag1null mice and to evaluate the ability of NOD/LtSz-Rag1nullPfpnull recipients to support engraftment with human hematolymphoid cells. METHODS: A new genetic stock of NOD mice doubly    homozygous for targeted mutations at the recombination activating gene (Rag)-1 and Pfp genes was developed.  NOD/LtSz-Rag1nullPfpnull mice were studied for immunopathologic and hematologic abnormalities. The ability of these mice to support    engraftment with human peripheral blood mononuclear cells (PBMC) and umbilical-cord blood hematopoietic progenitor cells was assessed. RESULTS: NOD/LtSz-Rag1nullPfpnull mice lacked mature B cells, T cells, natural killer (NK) cell cytotoxic    activity and were devoid of serum immunoglobulin (Ig) throughout a 37-week lifespan. These mice supported heightened engraftment with human PBMC as compared with NOD/LtSz-Rag1null controls as evidenced by a 4- to 5-fold increase in percentages of    human lymphocytes and a 7- to 13-fold increase in percentages of CD4+ T cells in the peripheral blood and spleen. Total numbers of human CD4+ T cells were increased approximately 20-fold in the spleens of NOD/LtSz-Rag1nullPfpnull mice. These mice    also showed approximately 12-fold higher levels of engraftment with human umbilical-cord blood cells compared with NOD/LtSz-Rag1null mice. CONCLUSIONS: NOD/LtSz-Rag1nullPfpnull mice are devoid of mature B cell, T cell, and NK cell cytotoxic    activity, engraft at high levels with human PBMC, and hematopoietic progenitor cells and provide a new NK cell-deficient model for human hematolymphoid cell engraftment.</p>

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</description>

<author>L D. Shultz et al.</author>


</item>


<item>
<title> Bombesin/gastrin-releasing peptide receptor: a potential target for antibody-mediated therapy of small cell lung cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/622</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/622</guid>
<pubDate>Tue, 08 May 2012 17:53:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Bombesin/gastrin releasing peptide (BN/GRP) is a growth factor for small cell lung cancer (SCLC). The receptor (R) for BN/GRP is overexpressed on SCLC cells and other solid tumors. BN/GRP and its receptor form an autocrine    loop to promote tumor growth. We developed a novel immunotherapeutic approach targeting cell surface BN/GRP-R on SCLC cells and an immune trigger molecule on host immune effector cells to direct immune effector cells to SCLC cells and mediate    targeted cancer cell destruction. Targeted immunotherapy combined with chemotherapy enhanced cell killing. EXPERIMENTAL DESIGN: We designed a synthetic BN/GRP antagonist (Antag 2) and constructed a bispecific molecule (BsMol), H22xAntag 2    (humanized monoclonal antibody) for FcgammaRI. We tested the binding of the BsMol to several SCLC cell lines, its ability to mediate cytotoxicity of SCLC by IFN-gamma-activated human monocytes with chemotherapy, and BsMol-mediated immunotherapy    in an animal model of SCLC human xenograft. RESULTS: Common chemotherapy (cisplatin, etoposide, and paclitaxel) inhibited thymidine uptake into SCLC cells in a dose-dependent pattern. Antibody-dependent cellular cytotoxicity mediated by the BsMol    inhibited thymidine uptake into SCLC cells and was largely dependent on E:T cell ratio. When SCLC cells were treated with antibody-dependent cellular cytotoxicity followed by exposure to chemotherapy agents an additional 25-40% inhibition of    thymidine uptake into SCLC cells was observed consistently. With BsMol and IFN-gamma-activated human monocytes, tumor burdens were reduced significantly in immunodeficient mice bearing human SCLC xenografts. CONCLUSIONS: Combined chemotherapy and    immunotherapy targeting BN/GRP-R with a BsMol significantly enhances targeted SCLC cell killing.</p>

	]]>
</description>

<author>J Zhou et al.</author>


</item>


<item>
<title> Mouse alopecia areata models: an array of data on mechanisms and genetics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/621</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/621</guid>
<pubDate>Tue, 08 May 2012 17:52:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Laboratory mice have become the premier animal model for most human and domestic animal diseases, and they have long been the model of choice for studying mammalian genetics, especially since the advent of genetic engineering. Many    remarkable discoveries have been made through intense study of these wonderful small mammals, and undoubtably many more will be made. It is no surprise that one mouse model for alopecia areata (AA) has been found possibly many more will be, some    of which exhibit rare phenotypes found in subpopulations of humans with the disease, such as nail deformities, thyroid disease, inflammatory bowel disease, and autoimmune polyendocrine syndrome type 1. Intense investigation by many groups into    the first model, the adult onset form of AA (using the C3H/HeJ inbred strain), found similarities as well as differences with commonly held ideas concerning human AA. Regardless of some of the controversies, much insight has been gained from    studying these and other rodent and domestic animal models which has opened up new ideas and discussions of AA and its treatment.</p>

	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title> Old wine in new bottles: reviving old therapies for alopecia areata using rodent models.</title>
<link>http://mouseion.jax.org/stfb2000_2009/620</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/620</guid>
<pubDate>Tue, 08 May 2012 17:52:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata is regarded as a tissue-restricted autoimmune disease of hair follicles in which follicular activity is arrested because of the continued activity of lymphocytic infiltrates. Actual loss of hair follicles does not    occur, even in hairless lesions. A variety of immunomodulating therapies, including contact sensitizers and immunomodulators, are part of the usual armamentarium for this disorder.  None of these treatments have been consistent in their efficacy,    and many have untoward side effects. Nevertheless, their uses in valid animal models provide a tool to dissect out molecular mechanisms of therapeutic effects. For several decades, both mechlorethamine (for the treatment of cutaneous T cell    lymphoma) and anthralin (for the treatment of psoriasis) have been used successfully. When these therapies were tested in rat and mouse alopecia areata models, we found anthralin and mechlorethamine to be the most effective topical modalities,    respectively. The underlying cellular mechanisms may act through targeting infiltrative lymphocytes, and the molecular mechanisms may involve specific cytokine expression changes. These visible, accessible, and unilaterally treated animal model    systems are ideal for studying novel alopecia areata therapies, particularly in terms of their in vivo molecular mechanisms of action.</p>

	]]>
</description>

<author>L Tang et al.</author>


</item>


<item>
<title> Safety issues in cell-based intervention trials.</title>
<link>http://mouseion.jax.org/stfb2000_2009/619</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/619</guid>
<pubDate>Tue, 08 May 2012 17:52:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>We report on the deliberations of an interdisciplinary group of experts in science, law, and philosophy who convened to discuss novel ethical and policy challenges in stem cell research. In this report we discuss the ethical and    policy implications of safety concerns in the transition from basic laboratory research to clinical applications of cell-based therapies derived from stem cells. Although many features of this transition from lab to clinic are common to other    therapies, three aspects of stem cell biology pose unique challenges. First, tension regarding the use of human embryos may complicate the scientific development of safe and effective cell lines. Second, because human stem cells were not    developed in the laboratory until 1998, few safety questions relating to human applications have been addressed in animal research. Third, preclinical and clinical testing of biologic agents, particularly those as inherently complex as mammalian    cells, present formidable challenges, such as the need to develop suitable standardized assays and the difficulty of selecting appropriate patient populations for early phase trials. We recommend that scientists, policy makers, and the public    discuss these issues responsibly, and further, that a national advisory committee to oversee human trials of cell therapies be established.</p>

	]]>
</description>

<author>L Dawson et al.</author>


</item>


<item>
<title> Cappuccino, a mouse model of Hermansky-Pudlak syndrome, encodes a novel protein that is part of the pallidin-muted complex (BLOC-1).</title>
<link>http://mouseion.jax.org/stfb2000_2009/618</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/618</guid>
<pubDate>Tue, 08 May 2012 17:51:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hermansky-Pudlak syndrome (HPS) is a disorder of organelle biogenesis affecting 3 related organelles-melanosomes, platelet dense bodies, and lysosomes. Four genes causing HPS in humans (HPS1-HPS4) are known, and at least 15    nonallelic mutations cause HPS in the mouse. Where their functions are known, the HPS-associated proteins are involved in some aspect of intracellular vesicular trafficking, that is, protein sorting and vesicle docking and fusion. Biochemical and    genetic evidence indicates that the HPS-associated genes encode components of at least 3 distinct protein complexes: the adaptor complex AP-3; the HPS1/HPS4 complex; and BLOC-1 (biogenesis of lysosome-related organelles complex-1), consisting of    the proteins encoded at 2 mouse HPS loci, pallid (pa) and muted (mu), and at least 3 other unidentified proteins. Here, we report the cloning of the mouse HPS mutation cappuccino (cno). We show that the wild-type cno gene encodes a novel,    ubiquitously expressed cytoplasmic protein that coassembles with pallidin and the muted protein in the BLOC-1 complex.  Further, we identify a frameshift mutation in mutant cno/cno mice. The C-terminal 81 amino acids are replaced with 72    different amino acids in the mutant CNO protein, and its ability to interact in BLOC-1 is abolished. We performed mutation screening of patients with HPS and failed to identify any CNO defects. Notably, although defects in components of the    HPS1/HPS4 and the AP-3 complexes are associated with HPS in humans, no defects in the known components of BLOC-1 have been identified in 142 patients with HPS screened to date, suggesting that BLOC-1 function may be critical in    humans.</p>

	]]>
</description>

<author>S L. Ciciotte et al.</author>


</item>


<item>
<title> Mice with targeted mutation of peroxiredoxin 6 develop normally but are susceptible to oxidative stress.</title>
<link>http://mouseion.jax.org/stfb2000_2009/617</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/617</guid>
<pubDate>Tue, 08 May 2012 17:51:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Reactive oxygen species, especially hydrogen peroxide, are important in cellular signal transduction. However, excessive amounts of these species damage tissues and cells by oxidizing virtually all important biomolecules.    Peroxiredoxin 6 (PRDX6) (also called antioxidant protein 2, or AOP2) is a novel peroxiredoxin family member whose function in vivo is unknown. Through immunohistochemistry, we have determined that the PRDX6 protein was widely expressed in every    tissue examined, most abundantly in epithelial cells. It was found in cytosol, but not in membranes, organelles, and nuclei fractions. Prdx6 mRNA was also expressed in every tissue examined. The widespread expression of Prdx6 suggested that its    functions were quite important. To determine these functions, we generated Prdx6-targeted mutant (Prdx6-/-) mice, confirmed the gene disruption by Southern blots, PCR, RT-PCR, Western blots, and immunohistochemistry, and compared the effects of    paraquat, hydrogen peroxide, and t-butyl hydroperoxide on Prdx6-/- and wild-type (Prdx6+/+) macrophages, and of paraquat on Prdx6-/- and Prdx6+/+ mice. Prdx6-/- macrophages had higher hydrogen peroxide levels, and lower survival rates; Prdx6-/-    mice had significantly lower survival rates, more severe tissue damage, and higher protein oxidation levels. Additionally, there were no differences in the mRNA expression levels of other peroxiredoxins, glutathione peroxidases, catalase,    superoxide dismutases, thioredoxins, and glutaredoxins between normal Prdx6-/- and Prdx6+/+ mice and those injected with paraquat. Our study provides in vivo evidence that PRDX6 is a unique non-redundant antioxidant that functions independently    of other peroxiredoxins and antioxidant proteins.</p>

	]]>
</description>

<author>X Wang et al.</author>


</item>


<item>
<title> Distinct osteoclast precursors in the bone marrow and extramedullary organs characterized by responsiveness to Toll-like receptor ligands and TNF-alpha.</title>
<link>http://mouseion.jax.org/stfb2000_2009/616</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/616</guid>
<pubDate>Tue, 08 May 2012 17:50:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Osteoclasts are derived from hemopoietic stem cells and play critical roles in bone resorption and remodeling. Multinucleated osteoclasts are attached tightly to bone matrix, whereas precursor cells with the potential to    differentiate into osteoclasts in culture are widely distributed. In this study, we assessed the characteristics of osteoclast precursors in bone marrow (BM) and in extramedullary organs as indicated by their responsiveness to ligands for    Toll-like receptors (TLRs) and to TNF-alpha. Development of osteoclasts from precursor cells in the BM was inhibited by CpG oligonucleotides, a ligand for TLR9, but not by LPS, a ligand for TLR4. BM osteoclasts were induced by TNF-alpha as well    as receptor activator of NF-kappaB ligand in the presence of M-CSF. Splenic osteoclast precursors, even in osteoclast-deficient osteopetrotic mice, differentiated into mature osteoclasts following exposure to TNF-alpha or receptor activator of    NF-kappaB ligand. However, splenic osteoclastogenesis was inhibited by both LPS and CpG. Osteoclastogenesis from peritoneal precursors was inhibited by not only these TLR ligands but also TNF-alpha. The effects of peptidoglycan, a ligand for    TLR2, were similar to those of LPS. BM cells precultured with M-CSF were characterized with intermediate characteristics between those of splenic and peritoneal cavity precursors. Taken together, these findings demonstrate that osteoclast    precursors are not identical in the tissues examined. To address the question of why mature osteoclasts occur only in association with bone, we may characterize not only the microenvironment for osteoclastogenesis, but also the osteoclast    precursor itself in intramedullary and extramedullary tissues.</p>

	]]>
</description>

<author>S Hayashi et al.</author>


</item>


<item>
<title> Alopecia areata in C3H/HeJ mice involves leukocyte-mediated root sheath disruption in advance of overt hair loss.</title>
<link>http://mouseion.jax.org/stfb2000_2009/615</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/615</guid>
<pubDate>Tue, 08 May 2012 17:50:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata (AA) can be induced in C3H/HeJ mice by grafting full-thickness AA-affected skin. An 8- to 12-week delay between surgery and overt hair loss onset provides an opportunity to examine disease pathogenesis. Normal    haired C3H/HeJ mice were sham-grafted or grafted with AA-affected skin. Mice were euthanatized 2, 4, 6, 8, 10, and 12 weeks after surgery along with chronic AA-affected mice as a positive control.  Until 6 weeks after grafting, inflammation was    only evident around anagen-stage hair follicles in host skin adjacent to but not distant from the AA-affected graft. From 8 weeks on, AA-grafted but not sham-grafted mice exhibited a diffuse dermal inflammation at distant sites that progressively    focused on anagen-stage hair follicles at 10 and 12 weeks.  Perifollicular inflammation was primarily composed of CD4+ and CD8+ cells associated with follicular epithelium intercellular adhesion molecule -1 expression. Only CD8+ cells penetrated    intrafollicularly by 12 weeks after surgery, although both CD4+ and CD8+ intrafollicular cells were observed in chronic AA-affected mice. Under electron microscopy, intrafollicular lymphocyte and macrophage infiltration associated with hair    follicle dystrophy was prominent 10 weeks after surgery, primarily within the differentiating outer and inner root sheaths. This study shows that focal follicular inflammation develops some time in advance of overt hair loss and focuses on the    differentiating root sheaths in C3H/HeJ mice. The severity of inflammation and the degree of hair follicle dystrophy induced by the infiltrate appear to reach a threshold level before overt hair loss occurs.</p>

	]]>
</description>

<author>K J. McElwee et al.</author>


</item>


<item>
<title> Restoration of hair growth with topical diphencyprone in mouse and rat models of alopecia areata.</title>
<link>http://mouseion.jax.org/stfb2000_2009/614</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/614</guid>
<pubDate>Tue, 08 May 2012 17:50:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The contact sensitizer, diphencyprone (DPCP), is one of the most effective therapies for the more severe forms of alopecia areata (AA). OBJECTIVE: The purpose of this study was to determine the efficacy of topical DPCP    on the 2 available rodent models for AA, and to determine the underlying therapeutic mechanisms. METHODS: AA-affected mice and rats were treated unilaterally with topical DPCP on the ventral and dorsal surface, respectively. The opposite sides    were treated with vehicle alone.  Skin biopsy specimens were collected from both sides for histologic analysis. RESULTS: Hair regrowth was observed on the treated sides in the majority of the animals of both species. Immunohistochemical analyses    revealed reduction of intrafollicular CD8(+) lymphocyte infiltrates after successful treatment in mice. CONCLUSION: The AA-like hair disorder of these 2 rodent models can be used as a tool for furthering our understanding of human AA and the    therapeutic actions of DPCP.</p>

	]]>
</description>

<author>L Tang et al.</author>


</item>


<item>
<title> Effects of pressure overload on extracellular matrix expression in the heart of the atrial natriuretic peptide-null mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/613</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/613</guid>
<pubDate>Tue, 08 May 2012 17:49:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study tested the hypothesis that atrial natriuretic peptide has direct antihypertrophic actions on the heart by modulating expression of genes involved in cardiac hypertrophy and extracellular matrix production.  Hearts of    male, atrial natriuretic peptide-null and control wild-type mice that had been subjected to pressure overload after transverse aortic constriction and control unoperated hearts were weighed and subjected to microarray, Northern blot, and    immunohistochemical analyses. Microarray and Northern blot analyses were used to identify genes that are regulated differentially in response to stress in the presence and absence of atrial natriuretic peptide. Immunohistochemical analysis was    used to identify and localize expression of the protein products of these genes. Atrial natriuretic peptide-null mice demonstrated cardiac hypertrophy at baseline and an exaggerated hypertrophic response to transverse aortic constriction    associated with increased expression of the extracellular matrix molecules periostin, osteopontin, collagen I and III, and thrombospondin, as well as the extracellular matrix regulatory proteins, matrix metalloproteinase-2 and tissue inhibitor of    metalloproteinase-3, and the novel growth factor pleiotrophin compared with wild-type controls. These results support the hypothesis that atrial natriuretic peptide protects against pressure overload-induced cardiac hypertrophy and remodeling by    negative modulation of genes involved in extracellular matrix deposition.</p>

	]]>
</description>

<author>D Wang et al.</author>


</item>


<item>
<title> Mapping cholesterol gallstone susceptibility (Lith) genes in inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/612</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/612</guid>
<pubDate>Tue, 08 May 2012 17:49:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The individual risk for developing cholesterol gallstones in response to specific environmental factors is determined by complex genetics involving multiple genes. In this review, we introduce inbred mice as a model to localise and    identify the murine genes that harbour cholesterol gallstone susceptibility alleles (Lith genes). These genes are associated with increased risk of gallstone formation when mice are fed a lithogenic diet containing cholesterol and cholic acid. We    summarise the steps involved in localising the chromosomal regions that harbour Lith genes, focusing particularly on the initial step known as quantitative trait locus mapping, which employs breeding crosses of gallstone-susceptible and    gallstone-resistant inbred mouse strains. Subsequent steps to narrow the chromosomal regions of the quantitative trait loci and identify the underlying Lith genes are outlined, with particular reference to the examples of Lith1 and Lith2, the    first discovered quantitative trait loci associated with murine cholesterol cholelithiasis. We have now reported five quantitative trait loci for murine cholelithogenesis, which are officially named Lith1 through Lith5. Once the genes underlying    these quantitative trait loci and other chromosomal loci from ongoing mouse crosses are identified and confirmed, the 'road-map' for discovery of orthologous human LITH genes will be available and, thereafter, their putative roles in cholesterol    gallstone formation can be tested in selected human populations.</p>

	]]>
</description>

<author>H Wittenburg et al.</author>


</item>


<item>
<title> Assessing the risk of transmission of three infectious agents among mice housed in a negatively pressurized caging system.</title>
<link>http://mouseion.jax.org/stfb2000_2009/611</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/611</guid>
<pubDate>Tue, 08 May 2012 17:49:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous studies from our institution have shown that ventilated caging run at negative pressure to a mouse room dramatically reduced exposure of personnel to the major mouse allergen, Mus m 1. The current study was designed to    determine whether negative cage ventilation posed an inordinate risk for spread of infectious agents between cages and/or racks. B6;129S-Tnfsf5(tm1Imx)/J (TNF) mice, which were naturally and persistently infected with Pneumocystis carinii,    Helicobacter bilis, and Pasteurella pneumotropica, were used as the source of infections.  Uninfected C3Smn.CB17-Prkdc(scid)/J (SCID) mice with severe combined immunodeficiency were used to detect transmission. The following methods were used to    detect transmission of infections: polymerase chain reaction (PCR) amplification and histological examination of lungs for P. carinii; PCR of fecal specimens or cecal contents for H. bilis; and culture of oropharyngeal, tracheal, or vaginal swabs    for P. pneumotropica. We determined whether transmission of the three agents occurred via direct contact (cohabitation), exposure to soiled bedding, and/or by handling naive SCID mice after handling infected TNF mice. During a 12-week period, all    three infectious agents were readily transmitted to uninfected mice by cohabitation. Transmission was much less efficient and occurred later among mice exposed to contaminated bedding. Transmission did not occur as a result of handling. We then    studied transmission of the three infectious agents among mice housed in individually ventilated cages run at negative pressure in a small, crowded mouse room. Transmission of P. carinii was detected at the end of the 12-month study in the    densely populated room, probably because the exhaust from the changing station passed over soiled cages and caused aerosolization of particulates. Caging systems run at negative pressure effectively reduce personnel exposure to allergens and may    also inhibit the transmission of infectious diseases.</p>

	]]>
</description>

<author>D D. Myers et al.</author>


</item>


<item>
<title> Reducing exposure to laboratory animal allergens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/610</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/610</guid>
<pubDate>Tue, 08 May 2012 17:48:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Laboratory animal allergy is a serious health problem. We examined several possible allergen-reducing strategies that might be effective in the working mouse room. Ambient allergen concentrations were measured when mice were    maintained under several conditions: conventional housing versus ventilated cage racks operated under negative or positive pressure. We found that housing mice in ventilated cages operated under negative pressure and using ventilated changing    tables reduced ambient mouse allergen (Mus m 1) concentrations tenfold, compared with values when mice were housed in conventional caging and using a conventional (non-ventilated) changing table. Housing mice in positively pressurized cages    versus conventional cages did not reduce ambient allergen values.  Cleaning mouse rooms at an accelerated frequency also did not reduce ambient Mus m 1 concentration. We also quantified ambient allergen values in several areas of The Jackson    Laboratory. A facility-wide survey of Mus m 1 concentrations indicated that allergen concentrations were undetectable in control areas, but ranged from a mean (+/- SEM) 0.11 +/- 0.02 ng/m3 to 5.40 +/- 0.30 ng/m3 in mouse rooms with different cage    types. The percentage of animal caretakers reporting allergy symptoms correlated significantly with ambient allergen concentrations: 12.9% reported symptoms in the rooms with the lowest allergen concentration (0.14 +/- 0.02 ng/m3), but 45.9%    reported symptoms in rooms with the highest concentration (2.3 +/- 0.4 ng/m3). These data indicate that existing technology can significantly reduce exposure to laboratory animal allergens and improve the health of animal    caretakers.</p>

	]]>
</description>

<author>I B. Schweitzer et al.</author>


</item>


<item>
<title> Connecting sequence and biology in the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/609</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/609</guid>
<pubDate>Tue, 08 May 2012 17:48:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Sequencing Consortium and the RIKEN Genome Exploration Research grouphave generated large sets of sequence data representing the mouse genome and transcriptome, respectively. These data provide a valuable    foundation for genomic research. The challenges for the informatics community are how to integrate these data with the ever-expanding knowledge about the roles of genes and gene products in biological processes, and how to provide useful views to    the scientific community. Public resources, such as the National Center for Biotechnology Information (NCBI; http://www.ncbi.nih.gov), and model organism databases, such as the Mouse Genome Informatics database (MGI;    http://www.informatics.jax.org), maintain the primary data and provide connections between sequence and biology. In this paper, we describe how the partnership of MGI and NCBI LocusLink contributes to the integration of sequence and biology,    especially in the context of the large-scale genome and transcriptome data now available for the laboratory mouse. In particular, we describe the methods and results of integration of 60,770 FANTOM2 mouse cDNAs with gene records in the databases    of MGI and LocusLink.</p>

	]]>
</description>

<author>R M. Baldarelli et al.</author>


</item>


<item>
<title> Development of an enhanced GFP-based dual-color reporter to facilitate genetic screens for the recovery of mutations in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/608</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/608</guid>
<pubDate>Tue, 08 May 2012 17:48:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutagenesis screens to isolate a variety of alleles leading to null and non-null phenotypes represent an important approach for the characterization of gene function. Genetic schemes that use visible markers permit the efficient    recovery of chemically induced mutations. We have developed a universal reporter system to visibly mark chromosomes for genetic screens in the mouse. The dual-color reporter is based on a single vector that drives the ubiquitous coexpression of    the enhanced GFP (EGFP) spectral variants yellow and cyan. We show that widespread expression of the dual-color reporter is readily detected in embryonic stem cells, mice, and throughout developmental stages. CRE-loxP- and FLPe-FRT-mediated    deletion of each color cassette demonstrates the modular design of the marker system. Random integration followed by plasmid rescue and sequence-based mapping was used to introduce the marker to a defined genomic location. Thus, single-step    placement will simplify the construction of a genomewide bank of marked chromosomes. The dual-color nature of the marker permits complete identification of genetic classes of progeny as embryos or mice in classic regionally directed screens. The    design also allows for more efficient and novel schemes, such as marked suppressor screens, in the mouse. The result is a versatile reporter that can be used independently or in combination with the growing sets of deletion and inversion    resources to enhance the design and application of a wide variety of genetic schemes for the functional dissection of the mammalian genome.</p>

	]]>
</description>

<author>A C. Frank et al.</author>


</item>


<item>
<title> An essential role of Th1 responses and interferon gamma in infection-mediated suppression of neoplastic growth.</title>
<link>http://mouseion.jax.org/stfb2000_2009/607</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/607</guid>
<pubDate>Tue, 08 May 2012 17:47:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>We had previously demonstrated that in mice acute toxoplasmosis leads to systemic inhibition of angiogenesis and, consequently, strong suppression of neoplastic growth. Here we investigated the role of Th1 cytokines, in particular    interferon gamma (IFN-gamma), in this phenomenon. Besides toxoplasma, neoplastic growth was readily blocked during acute infection with other Th1 response-inducing pathogens such as Listeria monocytogenes and lymphocytic choriomeningitis virus    (LCMV). In contrast, chronic infection with LCMV (when Th1 responses were strongly suppressed) and acute infection with Schistosoma mansoni (when Th2 responses predominated) afforded no anti-tumor protection. To corroborate the involvement of Th1    cytokines in infection-mediated suppression of neoplastic growth, we utilized mice deficient in interleukin-10 (IL10), a suppressor of Th1 responses. When challenged with B16 cells concomitantly with toxoplasma infection, both IL10-null and wild    type mice exhibited resistance to neoplastic growth. However, tumors borne by IL10-null animals were even smaller than those borne by their wild type counterparts. This enhanced resistance correlated with dramatically elevated levels of    circulating IFN-gamma, a principal Th1 cytokine. Furthermore, while interleukin-12 and tumor necrosis factor a were dispensable for tumor suppression, in animals deficient in IFN-gamma production or signaling, tumor growth and neovascularization    were markedly enhanced. Interestingly, the enhancement was also apparent in uninfected animals suggesting that IFN-gamma and its anti-angiogenic effects underlie both infection-dependent and -independent tumor surveillance.</p>

	]]>
</description>

<author>E B. Rankin et al.</author>


</item>


<item>
<title> The nature and identification of quantitative trait loci: a community&apos;s view.</title>
<link>http://mouseion.jax.org/stfb2000_2009/606</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/606</guid>
<pubDate>Tue, 08 May 2012 17:47:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>This white paper by eighty members of the Complex Trait Consortium presents a community's view on the approaches and statistical analyses that are needed for the identification of genetic loci that determine quantitative traits.    Quantitative trait loci (QTLs) can be identified in several ways, but is there a definitive test of whether a candidate locus actually corresponds to a specific QTL?</p>

	]]>
</description>

<author>O Abiola et al.</author>


</item>


<item>
<title> Quantitative PCR genotyping assay for the Ts65Dn mouse model of Down syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/605</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/605</guid>
<pubDate>Tue, 08 May 2012 17:47:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Ts65Dn mouse is a segmentally trisomic model for Down syndrome. Until now, Ts65Dn mice have been identified by the laborious methods of either chromosomal analysis of cultured peripheral lymphocytes or fluorescent in situ    hybridization (FISH). We report here a quantitative PCR method for genotyping Ts65Dn mice, as well as a phenotypic description for visually preclassifying mice to be genotyped.</p>

	]]>
</description>

<author>D P. Liu et al.</author>


</item>


<item>
<title> In collaboration: the Jackson Laboratory Craniofacial Resource.</title>
<link>http://mouseion.jax.org/stfb2000_2009/604</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/604</guid>
<pubDate>Tue, 08 May 2012 17:46:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dr. Sandy C. Marks, Jr., has been a longtime collaborator of the Mouse Mutant Resource at The Jackson Laboratory and, most recently, was involved in the development of a Craniofacial Resource at TJL. The goals of this resource are    to discover and supply to the scientific community mouse models of human craniofacial disease. A brief description of this collaboration is presented in Sandy's honor.</p>

	]]>
</description>

<author>J D. Bauschatz et al.</author>


</item>


<item>
<title> X-linked and lineage-dependent inheritance of coping responses to stress.</title>
<link>http://mouseion.jax.org/stfb2000_2009/603</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/603</guid>
<pubDate>Tue, 08 May 2012 17:46:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Coping-or how one routinely deals with stress-is a complex behavioral trait with bearing on chronic disease and susceptibility to psychiatric disorders. This complexity is a result of not only underlying multigenic factors, but    also important non-genetic ones. The defensive burying (DB) test, although originally developed as a test of anxiety, can accurately measure differences in coping strategies by assaying an animal's behavioral response to an immediate threat with    ethological validity.  Using offspring derived from reciprocal crosses of two inbred rat strains differing in DB behaviors, we provide convergent phenotypic and genotypic evidence that coping styles are inherited in an X-linked fashion. We find    that first-generation (F(1)) males, but not females, show maternally derived coping styles, and second-generation (F(2)) females, but not males, show significant differences in coping styles when separated by grandmaternal lineage. By using a    linear modeling approach to account for covariate effects (sex and lineage) in QTL analysis, we map three quantitative trait loci (QTL) on the X Chromosome (Chr) ( Coping-1, Approach-1, and Approach-2) associated with coping behaviors in the DB    paradigm. Distinct loci were associated with different aspects of coping, and their effects were modulated by both the sex and lineage of the animals, demonstrating the power of the general linear modeling approach and the important interplay of    allelic and non-allelic factors in the inheritance of coping behaviors.</p>

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</description>

<author>N Ahmadiyeh et al.</author>


</item>


<item>
<title> Positional cloning and characterization of Mei1, a vertebrate-specific gene required for normal meiotic chromosome synapsis in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/602</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/602</guid>
<pubDate>Tue, 08 May 2012 17:46:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse meiotic mutant Mei1 was isolated in a screen for infertile mice descended from chemically mutagenized embryonic stem cells. Homozygotes of both sexes are sterile due to meiotic arrest caused by defects in chromosome    synapsis. Notably, RAD51 protein does not load onto Mei1 mutant meiotic chromosomes, suggesting that there is a defect in either recombinational repair or the production of double-strand breaks (DSBs) that require such repair. Here, we show that    treatment of mutant males with cisplatin restores RAD51 loading, suggesting that mutant spermatocytes have intact recombinational repair mechanisms. Levels of histone H2AX phosphorylation (gammaH2AX) at leptonema are significantly reduced    compared with wild-type controls but comparable to that seen in animals deficient for SPO11, the molecule required for catalyzing DSB formation during meiosis. These observations provide evidence that genetically programmed DSB induction is    defective in Mei1 leptotene spermatocytes. We also report the positional cloning of Mei1, which encodes a product without significant homology to any known protein.  Expressed almost exclusively in gonads, Mei1 has no apparent homologs in yeast,    worms, or flies. However, Mei1 orthologs are present in the genomes of mammals, chickens, and zebrafish. Thus, Mei1 is required for vertebrate meiosis. To our knowledge, Mei1 is the first meiosis-specific mutation identified by forward genetic    approaches in mammals.</p>

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</description>

<author>B J. Libby et al.</author>


</item>


<item>
<title> Islet cell autoimmunity and transplantation tolerance: two distinct mechanisms?</title>
<link>http://mouseion.jax.org/stfb2000_2009/601</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/601</guid>
<pubDate>Tue, 08 May 2012 17:45:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recent advances in islet transplantation have enabled physicians to cure type 1 autoimmune diabetes, but at the cost of lifelong immunosuppression with its attendant side effects and long-term health risks. To eliminate the need    for immunosuppression, researchers have developed methods for inducing tolerance to transplanted allografts. Tolerance-based transplantation using costimulation blockade has proven remarkably successful in many animal model systems. The most    widely used animal model system for studying islet transplantation in type 1-like autoimmune diabetes is the NOD mouse. Unfortunately, this strain has proven resistant to costimulation blockade-based transplantation tolerance protocols that are    successful in chemically diabetic mice given islet grafts. It has been assumed that resistance to transplantation tolerance in the NOD mouse is (1) related to autoimmunity directed against its pancreatic beta cells, (2) a consequence of that    autoimmunity, and (3) under the control of the same genes that control autoimmunity. In this review, we provide arguments to challenge these assumptions. We describe a new animal model and a new conceptual framework based on data indicating that    the mechanisms responsible for resistance to transplantation tolerance and beta cell autoimmunity are not identical. We believe that the recent discoveries we describe will have important implications for the development of tolerance-based    transplantation therapies and their translation from the laboratory to the clinic.</p>

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</description>

<author>T Pearson et al.</author>


</item>


<item>
<title> Overlapping deletions spanning the proximal two-thirds of the mouse t complex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/600</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/600</guid>
<pubDate>Tue, 08 May 2012 17:45:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chromosome deletion complexes in model organisms serve as valuable genetic tools for the functional and physical annotation of complex genomes. Among their many roles, deletions can serve as mapping tools for simple or quantitative    trait loci (QTLs), genetic reagents for regional mutagenesis experiments, and, in the case of mice, models of human contiguous gene deletion syndromes. Deletions also are uniquely suited for identifying regions of the genome containing    haploinsufficient or imprinted loci. Here we describe the creation of new deletions at the proximal end of mouse Chromosome (Chr) 17 by using the technique of ES cell irradiation and the extensive molecular characterization of these and    previously isolated deletions that, in total, cover much of the mouse t complex. The deletions are arranged in five overlapping complexes that collectively span about 25 Mbp. Furthermore, we have integrated each of the deletion complexes with    physical data from public and private mouse genome sequences, and our own genetic data, to resolve some discrepancies. These deletions will be useful for characterizing several phenomena related to the t complex and t haplotypes, including    transmission ratio distortion, male infertility, and the collection of t haplotype embryonic lethal mutations. The deletions will also be useful for mapping other loci of interest on proximal Chr 17, including T-associated sex reversal ( Tas) and    head-tilt ( het). The new deletions have thus far been used to localize the recently identified t haplolethal ( Thl1) locus to an approximately 1.3-Mbp interval.</p>

	]]>
</description>

<author>D E. Bergstrom et al.</author>


</item>


<item>
<title> Appearance of human plasma cells following differentiation of human B cells in NOD/SCID mouse spleen.</title>
<link>http://mouseion.jax.org/stfb2000_2009/599</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/599</guid>
<pubDate>Tue, 08 May 2012 17:44:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Relatively little is known for the differentiation and maturation process of human B cells to plasma cells. This is particularly important in reconstitution work involving transfer of autoantibodies. To address this issue, we    transplanted human peripheral blood mononuclear cells (PBMC) directly into the spleen of irradiated NOD/SCID mice depleted of natural killer cell activity. Within 6 weeks, naive B cells differentiated into memory B cells and, importantly, the    numbers of human CD138+ plasma cells in spleen increased by 100 fold after transplantation. Plasma cell numbers correlated with the detection of human IgM and IgG in serum, indicating that human B cells had differentiated into mature plasma cells    in the murine spleen. In addition to CD19+ plasma cells, a distinct CD19- plasma cell population was detected, suggesting that downregulation of CD19 associated with maturation of plasma cells occurred. When purified human B cells were    transplanted, those findings were not observed. Our results indicate that differentiation and maturation of human B cells and plasma cells can be investigated by transplantation of human PBMC into the spleen of NOD/SCID mice. The model will be    useful for studying the differentiation of human B cells and generation of plasma cells.</p>

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</description>

<author>K Kikuchi et al.</author>


</item>


<item>
<title> Fluorescence imaging of multiple myeloma cells in a clinically relevant SCID/NOD in vivo model: biologic and clinical implications.</title>
<link>http://mouseion.jax.org/stfb2000_2009/598</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/598</guid>
<pubDate>Tue, 08 May 2012 17:44:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The in vivo preclinical testing of investigational therapies for multiple myeloma (MM) is hampered by the fact that models generated to recapitulate the development of diffuse skeletal lesions after i.v. injections of tumor cells    do not allow for ready detection of the exact site(s) of lesions or for comprehensive monitoring of their progression. We therefore developed an in vivo MM model in severe combined immunodeficient/nonobese diabetic mice in which diffuse MM    lesions developed after tail vein i.v. injection of human RPMI-8226/S MM cells stably transfected with a construct for green fluorescent protein (GFP). Using whole-body real-time fluorescence imaging to detect autofluorescent GFP(+) MM cells (and    confirming the sensitivity and specificity of these findings both histologically and by flow cytometric detection of GFP(+) cells), we serially monitored, in a cohort of 75 mice, the development and progression of MM tumors. Their anatomical    distribution and pathophysiological manifestations were consistent with the clinical course of MM in human patients, i.e., hallmarked by major involvement of the axial skeleton (e.g., spine, skull, and pelvis) and frequent development of    paralysis secondary to spinal lesions without significant tumor spread to lungs, liver, spleen, or kidney. This model both recapitulates the diffuse bone disease of human MM and allows for serial whole-body visualization of its spatiotemporal    progression. It therefore provides a valuable in vivo system to elucidate the molecular mechanisms underlying the marked osteotropism of MM, particularly for the axial skeleton, and for assessment of in vivo activity of novel anti-MM    therapeutics.</p>

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</description>

<author>C S. Mitsiades et al.</author>


</item>


<item>
<title> Genetic effects for femoral biomechanics, structure, and density in C57BL/6J and C3H/HeJ inbred mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/597</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/597</guid>
<pubDate>Tue, 08 May 2012 17:44:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genome-wide QTL analysis for bone density, structure, and biomechanical phenotypes was performed in 999 (B6xC3H)F2 mice. Multivariate phenotypes were also derived to test for pleiotropic QTL effects. Highly significant QTLs were    detected with pleiotropic effects on many of these phenotypes, and QTLs with unique effects on specific phenotypes were found as well.  INTRODUCTION: The inbred C57BL/6J (B6) and C3H/HeJ (C3H) mouse strains were previously shown to segregate    quantitative trait loci (QTLs) for femoral bone density. MATERIALS AND METHODS: The 999 s filial (F2) mouse progeny were further phenotyped for measures of femoral biomechanics (load to failure, Fu; work to failure, U; stiffness, S), structure    (polar moment of inertia, Ip; moment of inertia ratio, Ir), and more specific femoral midshaft bone density measures (cortical and total vBMD). Two novel multivariate phenotypes were computed using principal component analysis, thus aiding in the    exploration of pleiotropic effects of the QTLs detected. RESULTS AND CONCLUSIONS: Results of a genome-wide analysis provided strong evidence of pleiotropic QTL effects on chromosome 4, with six of the seven primary phenotypic measures,    representing femoral biomechanics, density, and structure, producing LOD scores greater than 8.  Chromosomes 1, 8, 13, and 14 were also identified as harboring QTLs that affect phenotypes in two of the three aspects of bone properties. QTLs    uniquely contributing to variability in biomechanical measures were identified on chromosomes 10 and 12, whereas a QTL solely affecting structure was found on chromosome 17. Analysis of the evidence for pleiotropic effects using principal    component analysis revealed pleiotropic QTLs on chromosomes 4 and 14, influencing nearly all the bone phenotypes measured and revealed QTLs on chromosomes 1, 8, 13, and 17 with pleiotropic effects restricted to either density or the structure and    stiffness phenotypes. The use of multivariate phenotypes has allowed us to identify pleiotropic effects of several QTLs previously linked in studies of other mouse strains and in human studies of bone mineral density and femoral structure, which    will provide important insight regarding the importance of allelic variation on the entire skeleton.</p>

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</description>

<author>D L. Koller et al.</author>


</item>


<item>
<title> Perturbations in bone formation and resorption in insulin-like growth factor binding protein-3 transgenic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/596</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/596</guid>
<pubDate>Tue, 08 May 2012 17:43:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>IGF-I and their binding proteins are important in bone health. Examination of BMD, osteoblast proliferation, and markers of bone resorption in transgenic mice that constitutively overexpress IGFBP-3 indicates that overexpression of    IGFBP-3 increases osteoclast number and bone resorption, impairs osteoblast proliferation, and has a significant negative effect on bone formation. INTRODUCTION: Low serum insulin-like growth factor I (IGF-I) levels correlate with an increased    risk of osteoporotic fractures.  Serum IGF-I is largely bound to IGF-binding protein-3 (IGFBP-3), which can inhibit IGF-I action and enhance delivery of IGF-I to tissues. Its role in bone biology is unclear. METHODS: Bone mineral density (BMD),    osteoblast proliferation, and markers of bone resorption were examined in transgenic (Tg) mice that constitutively overexpressed human IGFBP-3 cDNA driven by either the cytomegalovirus (CMV) or phosphoglycerate kinase (PGK) promoter. RESULTS:    Cultured calvarial osteoblasts from Tg mice expressed the transgene and grew more slowly than cells from wild-type (Wt) mice, and the mitogenic response to IGF-I was attenuated in osteoblasts from Tg mice. Total volumetric BMD and cortical BMD,    measured in the femur using peripheral quantitative computed tomography (pQCT) were significantly reduced in both Tg mouse strains compared with Wt mice. PGKBP-3 Tg mice showed the most marked reduction in bone density. Osteocalcin levels were    similar in Wt and CMVBP-3 Tg mice but were significantly reduced in PGKBP-3 Tg mice. Urinary deoxypyridinoline and osteoclast perimeter, markers of bone resorption, were significantly increased in both Tg mouse strains compared with Wt mice.    Using double labeling with tetracycline, we demonstrated that pericortical and endocortical mineral apposition rate was significantly reduced in PGKBP-3 Tg mice compared with Wt mice.  CONCLUSIONS: These data show that overexpression of IGFBP-3    increases osteoclast number and bone resorption, impairs osteoblast proliferation, and has a significant negative effect on bone formation.</p>

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</description>

<author>J V. Silha et al.</author>


</item>


<item>
<title> Congenic mice reveal sex-specific genetic regulation of femoral structure and strength.</title>
<link>http://mouseion.jax.org/stfb2000_2009/595</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/595</guid>
<pubDate>Tue, 08 May 2012 17:43:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic linkage studies in C3H/HeJ (C3H) and C57BL/6J (B6) mice identified several chromosomal locations or quantitative trait loci (QTL) linked to femoral volumetric bone mineral density (vBMD). From QTL identified on chromosomes    (chr) 1, 4, 6, 13, and 18, five congenic mouse strains were developed. In each of these mice, genomic DNA from the QTL region of the donor C3H strain was transferred into the recipient B6 strain. Here we report the effects of donated C3H QTL on    femoral structure, cortical vBMD and bending strength. Femoral structure was quantified by the polar moment of inertia (Ip) at the mid-diaphysis, which reflects the bending or torsional rigidity of the femur. Although the C3H progenitor mice have    a smaller Ip than B6 progenitor mice, the congenic mice carrying the C3H segment at Chr 4 had significantly increased Ip in both males and females, giving these mice stronger femora. In female mice from the congenic Chr 1 strain, Ip was increased    whereas male mice from the Chr 1 strain had smaller femoral cross-sections and significantly reduced Ip. This sex-specific effect on femoral structure was seen to a lesser extent in Chr 18 congenic mice. In addition, cortical vBMD was measured    using peripheral quantitative computed tomography. Cortical vBMD was similar among most congenic strains except in Chr 6 congenic mice, where cortical vBMD was significantly less in females, but not in males. We conclude that (1) chromosomal QTL    from C3H mice, which are genetically linked to total femoral vBMD, also regulate femoral structure; (2) the QTL on Chr 4 improves femoral structure and strength; (3) QTL on Chr 1 and 18 impart sex-specific effects on femoral structure; and (4)    the QTL on Chr 6 imparts a sex-specific effect on cortical vBMD and femoral strength.</p>

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</description>

<author>C H. Turner et al.</author>


</item>


<item>
<title> Normoblastosis, a murine model for ankyrin-deficient hemolytic anemia, is caused by a hypomorphic mutation in the erythroid ankyrin gene Ank1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/594</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/594</guid>
<pubDate>Tue, 08 May 2012 17:43:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ankyrin deficiency is one of the most common causes of hereditary spherocytosis in humans. A spontaneous mutation, normoblastosis (Ank1nb), discovered in 1969 in a mouse stock maintained at the Jackson Laboratory, provides an    important animal model for these human ankyrin-deficient anemias. Study of this model has led to the finding of multiple isoforms of Ank1 as well as Ank1nb-related pathology in nonerythroid tissues. To enhance the usefulness of this model, we    have identified the Ank1nb mutation as the deletion of a guanosine residue in exon 36 of the erythroid ankyrin gene (Ank1). This results in a frame shift that introduces a stop 13 codons downstream and predicts a 157 kDa nb-ankyrin lacking the    regulatory domain but including intact membrane- and spectrin-binding domains. By epitope scanning on immunoblots, we show that a previously reported protein (p150) found in nb reticulocytes is the predicted nb-ankyrin. Existing evidence    indicates that this protein is functional, making the normoblastosis mutation a hypomorph rather than a null as originally thought. The nb-ankyrin provides an explanation for the milder phenotype displayed by nb/nb animals relative to the murine    spectrin-deficient anemias, spherocytosis (Spna1(sph), Spna1(sph-1J), Spna1(sph-2BC), Spna1(sph-DEM)) and jaundiced (Spnb1(ja)), and suggests that truncated ankyrins could be useful in gene replacement therapy.</p>

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</description>

<author>C S. Birkenmeier et al.</author>


</item>


<item>
<title> High-resolution genetic map of X-linked juvenile-type granulosa cell tumor susceptibility genes in mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/593</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/593</guid>
<pubDate>Tue, 08 May 2012 17:42:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>SWR/Bm (SWR) female mice spontaneously develop early-onset ovarian granulosa cell (GC) tumors that can progress to metastatic carcinoma and thus provide a model system for human, juvenile-type GC tumors. In SWR mice, GC tumor    susceptibility is an inherited, polygenic trait that appears at a low frequency. A dramatic increase in tumor frequency occurs when the autosomal SWR genetic complement is combined with the X-linked Gct4 allele of the mouse strain SJL/Bm (SJL).    The modifier effect of the SJL Gct4 allele (Gct4(J)) also shows a strong parent-of-origin effect, occurring only when the Gct4(J) allele is paternally inherited. To genetically localize Gct4, we generated seven congenic mouse strains (SWR.SJL-X1    through -X7) that contained a defined segment of the SJL X chromosome (Chr) on the SWR autosomal strain background and mapped Gct4 to a 3 cM region. To better define the location of Gct4, we created an additional congenic strain (SWR.CAST-X) that    contains most of the genetically polymorphic Chr X from the strain CAST/Ei. From crosses of the SWR.CAST-X and SWR.SJL-X congenic strains, we derived males carrying unique combinations of SJL-X and CAST-X segments. Progeny testing subsequently    revealed a second SJL-derived, GC tumor frequency modifier gene, Gct6, located 6.5 cM distal to Gct4 on Chr X. In summary, we have mapped two modifier genes on the mouse Chr X that cause high-frequency, juvenile-type GC tumor development in    female mice. The identity of these genes will provide a solid foundation for determination of tumor susceptibility genes in human cases of juvenile-type GC tumors.</p>

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</description>

<author>A M. Dorward et al.</author>


</item>


<item>
<title> A single nucleotide polymorphism in the Emp3 gene defines the H4 minor histocompatibility antigen.</title>
<link>http://mouseion.jax.org/stfb2000_2009/592</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/592</guid>
<pubDate>Tue, 08 May 2012 17:42:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Minor histocompatibility antigens (minor H antigen) elicit strong T-cell-mediated responses during both graft rejection and graft versus leukemia (GvL) among MHC-matched individuals (where MHC is major histocompatibility complex).    Employing expression-cloning methodology, we have identified a cDNA clone, MI-35, encoding the immunodominant H4b minor H antigen within the classical mouse H4 complex. The minimal antigenic epitope derived from H4b presented on Kb class I MHC is    SGIVYIHL (SYL8) and the polymorphism is due to C-->T nucleotide modification in p3 resulting in the change of threonine (ACT) to isoleucine (ATT). The results presented here demonstrate that amino acid variation in the allelic epitopes results in    the low abundance of H4a peptide. The differential peptide copy number resulted in an immunodominant cytotoxic T cells (CTL) response directed against H4b while the anti-B6 response directed against H4a was easily dominated. These results provide    a molecular mechanism for the H4 minor H antigen and suggest a novel mechanism by which alloantigenic disparity caused by conservative amino acid changes can be augmented by posttranslational antigen processing events.</p>

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</description>

<author>B Luedtke et al.</author>


</item>


<item>
<title> PERK eIF2alpha kinase regulates neonatal growth by controlling the expression of circulating insulin-like growth factor-I derived from the liver.</title>
<link>http://mouseion.jax.org/stfb2000_2009/591</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/591</guid>
<pubDate>Tue, 08 May 2012 17:42:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Humans afflicted with the Wolcott-Rallison syndrome and mice deficient for PERK (pancreatic endoplasmic reticulum eIF2alpha kinase) show severe postnatal growth retardation. In mice, growth retardation in Perk-/- mutants is    manifested within the first few days of neonatal development.  Growth parameters of Perk-/- mice, including comparison of body weight to length and organ weights, are consistent with proportional dwarfism. Tibia growth plates exhibited a    reduction in proliferative and hypertrophic chondrocytes underlying the longitudinal growth retardation. Neonatal Perk-/- deficient mice show a 75% reduction in liver IGF-I mRNA and serum IGF-I within the first week, whereas the expression of    IGF-I mRNA in most other tissues is normal. Injections of IGF-I partially reversed the growth retardation of the Perk-/- mice, whereas GH had no effect. Transgenic rescue of PERK activity in the insulin- secreting beta-cells of the Perk-/- mice    reversed the juvenile but not the neonatal growth retardation. We provide evidence that circulating IGF-I is derived from neonatal liver but is independent of GH at this stage. We propose that PERK is required to regulate the expression of IGF-I    in the liver during the neonatal period, when IGF-I expression is GH-independent, and that the lack of this regulation results in severe neonatal growth retardation.</p>

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</description>

<author>Y Li et al.</author>


</item>


<item>
<title> The effects of parathyroid hormone and alendronate alone or in combination in postmenopausal osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/590</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/590</guid>
<pubDate>Tue, 08 May 2012 17:41:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Parathyroid hormone increases bone strength primarily by stimulating bone formation, whereas antiresorptive drugs reduce bone resorption. We conducted a randomized, double-blind clinical study of parathyroid hormone and    alendronate to test the hypothesis that the concurrent administration of the two agents would increase bone density more than the use of either one alone. METHODS: A total of 238 postmenopausal women (who were not using bisphosphonates) with low    bone mineral density at the hip or spine (a T score of less than -2.5, or a T score of less than -2.0 with an additional risk factor for osteoporosis) were randomly assigned to daily treatment with parathyroid hormone (1-84) (100 microg; 119    women), alendronate (10 mg; 60 women), or both (59 women) and were followed for 12 months. Bone mineral density at the spine and hip was assessed by dual-energy x-ray absorptiometry and quantitative computed tomography. Markers of bone turnover    were measured in fasting blood samples. RESULTS: The bone mineral density at the spine increased in all the treatment groups, and there was no significant difference in the increase between the parathyroid hormone group and the    combination-therapy group. The volumetric density of the trabecular bone at the spine increased substantially in all groups, but the increase in the parathyroid hormone group was about twice that found in either of the other groups.  Bone    formation increased markedly in the parathyroid hormone group but not in the combination-therapy group. Bone resorption decreased in the combination-therapy group and the alendronate group. CONCLUSIONS: There was no evidence of synergy between    parathyroid hormone and alendronate.  Changes in the volumetric density of trabecular bone, the cortical volume at the hip, and levels of markers of bone turnover suggest that the concurrent use of alendronate may reduce the anabolic effects of    parathyroid hormone. Longer-term studies of fractures are needed to determine whether and how antiresorptive drugs can be optimally used in conjunction with parathyroid hormone therapy.</p>

	]]>
</description>

<author>D M. Black et al.</author>


</item>


<item>
<title> Another view of T cell antigen recognition: cooperative engagement of glycolipid antigens by Va14Ja18 natural TCR.</title>
<link>http://mouseion.jax.org/stfb2000_2009/589</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/589</guid>
<pubDate>Tue, 08 May 2012 17:41:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Va14Ja18 natural T (iNKT) cells rapidly elicit a robust effector response to different glycolipid Ags, with distinct functional outcomes.  Biochemical parameters controlling iNKT cell function are partly defined.  However, the    impact of iNKT cell receptor beta-chain repertoire and how alpha-galactosylceramide (alpha-GalCer) analogues induce distinct functional responses have remained elusive. Using altered glycolipid ligands, we discovered that the Vb repertoire of    iNKT cells impacts recognition and Ag avidity, and that stimulation with suboptimal avidity Ag results in preferential expansion of high-affinity iNKT cells. iNKT cell proliferation and cytokine secretion, which correlate with iNKT cell receptor    down-regulation, are induced within narrow biochemical thresholds. Multimers of CD1d1-alphaGalCer- and alphaGalCer analogue-loaded complexes demonstrate cooperative engagement of the Va14Ja18 iNKT cell receptor whose structure and/or organization    appear distinct from conventional alphabeta TCR. Our findings demonstrate that iNKT cell functions are controlled by affinity thresholds for glycolipid Ags and reveal a novel property of their Ag receptor apparatus that may have an important role    in iNKT cell activation.</p>

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</description>

<author>A K. Stanic et al.</author>


</item>


<item>
<title> Hepatic lipase expression in macrophages contributes to atherosclerosis in apoE-deficient and LCAT-transgenic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/588</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/588</guid>
<pubDate>Tue, 08 May 2012 17:41:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hepatic lipase (HL) has a well-established role in lipoprotein metabolism.  However, its role in atherosclerosis is poorly understood. Here we demonstrate that HL deficiency raises the proatherogenic apoB-containing lipoprotein    levels in plasma but reduces atherosclerosis in lecithin cholesterol acyltransferase (LCAT) transgenic (Tg) mice, similar to results previously observed with HL-deficient apoE-KO mice. These findings suggest that HL has functions that modify    atherogenic risk that are separate from its role in lipoprotein metabolism. We used bone marrow transplantation (BMT) to generate apoE-KO and apoE-KO x HL-KO mice, as well as LCAT-Tg and LCAT-Tg x HL-KO mice, chimeric for macrophage HL gene    expression. Using in situ RNA hybridization, we demonstrated localized production of HL by donor macrophages in the artery wall. We found that expression of HL by macrophages enhances early aortic lesion formation in both apoE-KO and LCAT-Tg    mice, without changing the plasma lipid profile, lipoprotein lipid composition, or HL and lipoprotein lipase activities. HL does, however, enhance oxidized LDL uptake by peritoneal macrophages.  These combined data demonstrate that    macrophage-derived HL significantly contributes to early aortic lesion formation in two independent mouse models and identify a novel mechanism, separable from the role of HL in plasma lipoprotein metabolism, by which HL modulates atherogenic    risk in vivo.</p>

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</description>

<author>Z Nong et al.</author>


</item>


<item>
<title> Adoptive transfer of islet antigen-autoreactive T cell clones to transgenic NOD.Ea(d)mice induces diabetes indicating a lack of I-E mediated protection against activated effector T cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/587</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/587</guid>
<pubDate>Tue, 08 May 2012 17:40:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Transgenic insertion of the MHC class II Ea(d)gene in NOD mice restores I-E expression and prevents T-cell-mediated autoimmune diabetes (IDDM).  The specific molecular and cellular mechanisms responsible for the diabetes resistance    of transgenic NOD.Ea(d)mice remain unclear. We adoptively transferred islet antigen-specific T cell clones into NOD and transgenic NOD.Ea(d)mice to evaluate the level of protection provided by I-E expression against activated effector T cells. We    have found that neither neonatal or 3-5-week-old I-E-expressing NOD.Ea(d)mice can completely inhibit the diabetogenic activities of activated islet antigen-specific T cell clones. These data indicate that Ealpha protein expression in NOD antigen    presenting cells (APC) does not reduce islet autoantigen presentation in the context of I-A(g7)below the threshold required for stimulation of effector/memory diabetogenic T cells. Our results suggest that the mechanism of Ealpha protein-mediated    diabetes resistance in NOD mice may be "antigen ignorance," in which the quantity of islet autoantigens presented in the context of I-A(g7)by APC is reduced below the threshold required to activate nai;ve islet antigen-specific T    cells.</p>

	]]>
</description>

<author>S A. Roberts et al.</author>


</item>


<item>
<title> Tracking autoimmune T cells in diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/586</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/586</guid>
<pubDate>Tue, 08 May 2012 17:40:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Insulin-dependent diabetes mellitus is usually caused by the autoimmune destruction of pancreatic beta cells by T cells. Methodologies to track the development, migration, and functional activation of one class of such T cells (CD4    T cells) have been limited. However, it now appears that this limitation has been overcome.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title> Overexpression of Prdx6 reduces H2O2 but does not prevent diet-induced atherosclerosis in the aortic root.</title>
<link>http://mouseion.jax.org/stfb2000_2009/585</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/585</guid>
<pubDate>Tue, 08 May 2012 17:40:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mammalian 1-Cys peroxiredoxin (Prdx6) is a unique member of the peroxiredoxin family of proteins capable of protecting cells from metal-catalyzed oxidative damage. We recently identified Prdx6 as a candidate for the    quantitative trait locus Ath1, a gene responsible for a difference in diet-induced atherosclerosis susceptibility in mice. To investigate the role of Prdx6 in atherosclerosis, we generated transgenic mice that overexpress the Prdx6 allele from    the Ath1-resistant 129/SvJ strain on an Ath1-susceptible C57BL/6J background. These mice expressed significantly elevated levels of Prdx6 mRNA and protein in multiple tissues including liver, aorta, and peritoneal macrophages, which accumulated    significantly lower levels of hydrogen peroxide, revealing an enhanced antioxidant activity in these mice. However, overexpression of Prdx6 had no protective effect on LDL oxidation in vitro, and transgenic mice fed an atherogenic diet for 10    weeks did not possess an increased resistance to atherosclerosis nor did they maintain the high prediet plasma HDL levels consistent with the Ath1-resistant phenotype. In addition, the Prdx6 allele from the susceptible strain was shown to have a    higher antioxidant activity than that of the resistant strains. These data suggest that the increased peroxidase activity attributable to Prdx6 overexpression in transgenic mice is not sufficient to protect mice from atherosclerosis, and that    Prdx6 is not likely to be the gene underlying Ath1.</p>

	]]>
</description>

<author>S A. Phelan et al.</author>


</item>


<item>
<title> Expansion of hematopoietic stem cell phenotype and activity in Trp53-null mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/584</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/584</guid>
<pubDate>Tue, 08 May 2012 17:40:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVES: To study the effects of transformation-related protein 53 (Trp53) and other genes on hematopoiesis and hematopoietic stem cells (HSCs). METHODS: Frequencies of murine bone marrow cells (BMCs) with the    Lin(-)Sca-1(+)c-kit(+)CD34- phenotype were analyzed by flow cytometry, and were increased in mice with germ-line deletion of the Trp53 (Trp53(-/-)) gene but not in 25 other deletions of genes involved in cell cycling, development, cancer, or    hematopoiesis. Therefore, Trp53(-/-) and wild-type Trp53(+/+) mice were compared using the following assays: complete blood counts, day-9 colony-forming unit spleen (CFU-S), and competitive repopulation. In the latter assay, donor repopulating    ability was analyzed at one, three, and five months, while recipient survival and recipient blood and bone marrow cell composition were analyzed at five months, after transplantation. RESULTS: In comparison to wild-type controls, Trp53(-/-) mice    had normal blood and bone marrow cell counts, increased CD11b(+), and decreased CD45R(+) cell proportions in blood and bone marrow, twice as many Lin(-)Sca-1(+)c-kit(+)CD34(-) BMCs, and 37% more day-9 CFU-S. In the competitive repopulation assay,    Trp53(-/-) BMCs engrafted lethally irradiated recipients two to four times better than Trp53(+/+) BMCs. The Trp53(-/-) engraftment advantage increased with time in the recipients.  Recipients of Trp53(-/-) donors had two to three times more    Lin(-)Sca-1(+)c-kit(+)CD34(-) BMCs than recipients of Trp53(+/+) donors at five months after transplantation. However, only 44% of recipients of Trp53(-/-) donors survived five months after trans-plantation, compared with 92% of recipients of    Trp53(+/+) donors. CONCLUSION: The Trp53-null allele expands bone marrow Lin(-)Sca-1(+)c-kit(+)CD34(-) cells and the overall activity of HSCs; however, it increases recipient mortality.</p>

	]]>
</description>

<author>M TeKippe et al.</author>


</item>


<item>
<title> Association of cadherin 23 with polygenic inheritance and genetic modification of sensorineural hearing loss.</title>
<link>http://mouseion.jax.org/stfb2000_2009/583</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/583</guid>
<pubDate>Tue, 08 May 2012 17:39:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Age-related hearing loss (AHL) in common inbred mouse strains is a genetically complex quantitative trait. We found a synonymous single-nucleotide polymorphism in exon 7 of Cdh23 that shows significant association with AHL and the    deafness modifier mdfw (modifer of deafwaddler). The hypomorphic Cdh23(753A) allele causes in-frame skipping of exon 7. Altered adhesion or reduced stability of CDH23 may confer susceptibility to AHL. Homozygosity at Cdh23(753A) or in combination    with heterogeneous secondary factors is a primary determinant of AHL in mice.</p>

	]]>
</description>

<author>Trauth K. Noben et al.</author>


</item>


<item>
<title> Acoustic startle and prepulse inhibition in 40 inbred strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/582</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/582</guid>
<pubDate>Tue, 08 May 2012 17:39:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>A high-throughput phenotype screening protocol was used to measure the acoustic startle response (ASR) and prepulse inhibition (PPI) in mice.  ASRs were evoked by noise bursts; prepulses for PPI were 70 dB sound pressure level    tones of 4, 12, and 20 kHz. Forty inbred strains of mice were tested (in most cases using 10 males and 10 females of each strain).  The data on both the ASR and PPI had high internal and test-retest reliability and showed large differences among    inbred strains, indicative of strong genetic influences. Previously obtained measures of hearing sensitivity in the same inbred strains were not significantly correlated with ASR or PPI measures.</p>

	]]>
</description>

<author>J F. Willott et al.</author>


</item>


<item>
<title> Molecular control of the oocyte to embryo transition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/581</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/581</guid>
<pubDate>Tue, 08 May 2012 17:39:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>The elucidation of the molecular control of the initiation of mammalian embryogenesis is possible now that the transcriptomes of the full-grown oocyte and two-cell stage embryo have been prepared and analysed.  Functional    annotation of the transcriptomes using gene ontology vocabularies, allows comparison of the oocyte and two-cell stage embryo between themselves, and with all known mouse genes in the Mouse Genome Database. Using this methodology one can outline    the general distinguishing features of the oocyte and the two-cell stage embryo. This, when combined with oocyte-specific targeted deletion of genes, allows us to dissect the molecular networks at play as the differentiated oocyte and sperm    transit into blastomeres with unlimited developmental potential.</p>

	]]>
</description>

<author>B B. Knowles et al.</author>


</item>


<item>
<title> Characterization of protein kinase C-delta in mouse oocytes throughout meiotic maturation and following egg activation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/580</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/580</guid>
<pubDate>Tue, 08 May 2012 17:38:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Changes in protein kinase C (PKC) activity influence the progression of meiosis; however, the specific function of the various PKC isoforms in female gametes is not known. In the current study, the protein expression and    subcellular distribution profile of PKC-delta (PKC-delta), a novel isoform of the PKC family, was determined in mouse oocytes undergoing meiotic maturation and following egg activation. The full-length protein was observed as a doublet (76 and 78    kDa) on Western blot analysis. A smaller (47 kDa) carboxyl-terminal fragment, presumably the truncated catalytic domain of PKC-delta, was also strongly expressed. Both the full-length protein and the catalytic fragment became phosphorylated    coincident with the resumption of meiosis and remained phosphorylated throughout metaphase II (MII) arrest. Immunofluorescence staining showed PKC-delta distributed diffusely throughout the cytoplasm of oocytes during maturation and associated    with the spindle apparatus during the first meiotic division. Discrete foci of the protein also localized with the chromosomes in some mature eggs. Following the completion of meiosis, PKC-delta became dephosphorylated within 2 h of in vitro    fertilization or parthenogenetic activation. The protein also accumulated in the nuclei of early embryos and was phosphorylated during M-phase of the initial mitotic cleavage division. By the two-cell stage, expression of the truncated catalytic    fragment was minimal. These data demonstrate that the subcellular distribution and posttranslational modification of PKC-delta is cell cycle dependent, suggesting that its activity and/or function likely vary with the progression of meiosis and    egg activation.</p>

	]]>
</description>

<author>M M. Viveiros et al.</author>


</item>


<item>
<title> Toward the genetics of mammalian reproduction: induction and mapping of gametogenesis mutants in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/579</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/579</guid>
<pubDate>Tue, 08 May 2012 17:38:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genetic control of mammalian gametogenesis is inadequately characterized because of a lack of mutations causing infertility. To further the discovery of genes required for mammalian gametogenesis, phenotype-driven screens were    performed in mice using random chemical mutagenesis of whole animals and embryonic stem cells. Eleven initial mutations are reported here that affect proliferation of germ cells, meiosis, spermiogenesis, and spermiation. Nine of the mutations    have been mapped genetically. These preliminary studies provide baselines for estimating the number of genes required for gametogenesis and offer guidance in conducting new genetic screens that will accelerate and optimize mutant discovery. This    report demonstrates the efficacy and expediency of mutagenesis to identify new genes required for mammalian gamete development.</p>

	]]>
</description>

<author>J O. Ward et al.</author>


</item>


<item>
<title> Mouse models of USH1C and DFNB18: phenotypic and molecular analyses of two new spontaneous mutations of the Ush1c gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/578</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/578</guid>
<pubDate>Tue, 08 May 2012 17:38:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>We mapped two new recessive mutations causing circling behavior and deafness to the same region on chromosome 7 and showed they are allelic by complementation analysis. One was named 'deaf circler' (allele symbol dfcr) and the    other 'deaf circler 2 Jackson' (allele symbol dfcr-2J). Both were shown to be mutations of the Ush1c gene, the mouse ortholog of the gene responsible for human Usher syndrome type IC and for the non-syndromic deafness disorder DFNB18. The Ush1c    gene contains 28 exons, 20 that are constitutive and eight that are alternatively spliced. The dfcr mutation is a 12.8 kb intragenic deletion that eliminates three constitutive and five alternatively spliced exons. The dfcr-2J mutation is a 1 bp    deletion in an alternatively spliced exon that creates a transcriptional frame shift, changing 38 amino acid codons before introducing a premature stop codon. Both mutations cause congenital deafness and severe balance deficits due to inner ear    dysfunction. The stereocilia of cochlear hair cells are disorganized and splayed in mutant mice, with subsequent degeneration of the hair cells and spiral ganglion cells. Harmonin, the protein encoded by Ush1c, has been shown to bind, by means of    its PDZ-domains, with the products of other Usher syndrome genes, including Myo7a, Cdh23 and Sans. The complexes formed by these protein interactions are thought to be essential for maintaining the integrity of hair cell stereocilia. The Ush1c    mutant mice described here provide a means to directly investigate these interactions in vivo and to evaluate gene structure-function relationships that affect inner ear and eye phenotypes.</p>

	]]>
</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title> Hematopoietic senescence is postponed and hematopoietic stem cell function is enhanced by dietary restriction.</title>
<link>http://mouseion.jax.org/stfb2000_2009/577</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/577</guid>
<pubDate>Tue, 08 May 2012 17:37:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: The aim of this study was to test dietary restriction (DR) as an intervention to alleviate senescence-associated functional defects in hematopoietic stem cells (HSCs). MATERIALS AND METHODS: BALB/cByJ (BALB) mice were    fed ad libitum (AL) or were diet restricted (DR) to 75% of the AL food intake after 1 month of age. Peripheral blood and bone marrow cell compositions were compared in 3- and 25-month-old AL (AL-3, AL-25) mice and in 25-month-old DR (DR-25) mice    using fluorescence-activated cell staining. Relative HSC functions in vivo were compared using competitive repopulation, and were also tested in 6-month-old BALB mice to measure the effects of short-term DR. RESULTS: Compared to AL-3, AL-25 blood    had significantly lower levels of red blood cells and hemoglobin. AL-25 marrow contained less than half the concentration of Lin(-)CD34(-)Sca1(+)CD117(+) HSCs and showed only half the in vivo functional ability of AL-3 marrow.  In vivo, AL-25    HSCs failed to produce the strong correlations over time that demonstrate clonal stability during competitive repopulation. These correlations were shown in AL-3 HSCs. DR for 24 months alleviated hematopoietic deficiencies in the blood, increased    concentrations of bone marrow Lin(-)CD34(-)Sca1(+)CD117(+) HSCs and improved HSC functional abilities in DR-25 mice to values far greater than those in normally aged mice. Surprisingly, HSC function in 25-month-old DR mice was better than that in    young adults. Degrees of recipient repopulation by HSCs from DR-25 mice also correlated well over time, demonstrating clonal stability.  Short-term DR for 5 months also improved HSC function, but to a much smaller degree. CONCLUSIONS: Aged BALB    mice show hematopoietic and HSC senescence and clonal succession. Lifelong DR slows hematopoietic senescence and prevents HSC aging.</p>

	]]>
</description>

<author>J Chen et al.</author>


</item>


<item>
<title> TCF and Groucho-related genes influence pituitary growth and development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/576</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/576</guid>
<pubDate>Tue, 08 May 2012 17:37:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the prophet of PIT1 gene (PROP1) are the most common cause of multiple pituitary hormone deficiency in humans; however, the mechanism of PROP1 action is not well understood. We report that Prop1 is essential for    dorsally restricted expression of a Groucho-related gene, transducin-like enhancer of split 3 (Tle3), which encodes a transcriptional corepressor.  Deficiency of a related gene, amino terminal enhancer of split (Aes), causes pituitary anomalies    and growth insufficiency. TLE3 and AES have been shown to interact with TCF/LEF (transcripiton factors of the T cell-specific and lymphoid enhancer specific group) family members in cell culture systems. In the absence of TCF4 (Tcf7L2), Prop1    levels are elevated, pituitary hyperplasia ensues and palate closure is abnormal.  Thus, we demonstrate that Tcf4 and Aes influence pituitary growth and development, and place Tcf4 and Tle3 in the genetic hierarchy with Prop1.</p>

	]]>
</description>

<author>M L. Brinkmeier et al.</author>


</item>


<item>
<title> Phenotypic heterogeneity in the stargazin allelic series.</title>
<link>http://mouseion.jax.org/stfb2000_2009/575</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/575</guid>
<pubDate>Tue, 08 May 2012 17:37:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>The stargazer mutant mouse is characterized by its ataxic gait, head tossing, and absence seizures. The mutation was identified in the gamma 2 subunit gene of the high voltage-dependent calcium channel, Cacng2.  Subsequently, two    allelic variants of stargazer have arisen, waggler and stargazer 3J. In this study, we have compared these new alleles to the original stargazer allele. All three mutations affect the Cacng2 mRNA levels as they all arise from disruptions within    the introns of this gene.  Our results show that the mutations cause reduced Cacng2 mRNA and protein levels. Stargazer and waggler mice have the least amount of mRNA and undetectable protein, whereas stargazer 3J appears to be the mildest allele,    both in terms of the phenotype and protein expression.  Electroencephalographic (EEG) analysis confirmed that stargazer has frequent spike-wave discharges (SWDs); the average duration of each discharge burst is 5 seconds and recurs every minute.    The waggler allele causes a greater variation in SWD activity depending on the individual mouse, and the stargazer 3J mouse has no SWDs. The preliminary characterization of this heterogeneous allelic series provides a basis to explore more    biochemical and physiological parameters relating to the role of the Cacng2 product in calcium channel activity, AMPA receptor localization, and cerebellar disturbances.</p>

	]]>
</description>

<author>V A. Letts et al.</author>


</item>


<item>
<title> Oocyte-dependent activation of mitogen-activated protein kinase (ERK1/2) in cumulus cells is required for the maturation of the mouse oocyte-cumulus cell complex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/574</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/574</guid>
<pubDate>Tue, 08 May 2012 17:36:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Luteinizing hormone (LH) induces maturational processes in oocyte-cumulus cell complexes (OCC) of preovulatory follicles that include both resumption of meiosis in the oocyte and expansion (mucification) of the cumulus oophorus.    Both processes require activation of mitogen-activated protein kinase (MAPK) in granulosa cells. Here, it is reported that inhibition of MAPK activation prevented gonadotropin-stimulated resumption of meiosis as well as the rise in expression of    two genes whose products are necessary for normal cumulus expansion, Has2 and Ptgs2. However, inhibition of MAPK did not block gonadotropin-induced elevation of granulosa cell cAMP, indicating that the activation of MAPK required for inducing GVB    and cumulus expansion is downstream of cAMP. Moreover, activation of MAPK in cumulus cells requires one or more paracrine factors from the oocyte to induce GVB and cumulus expansion; MAPK activation alone is not sufficient to initiate these    maturational processes. This study demonstrates a remarkable interaction between the oocyte and cumulus cells that is essential for gonadotropin-induced maturational processes in OCC.  By enabling gonadotropin-dependent MAPK activation in    granulosa cells, oocytes promote the generation of a return signal from these cells that induces the resumption of meiosis. It also appears that an oocyte-dependent pathway downstream from oocyte-enabled activation of MAPK, and distinct from that    promoting the resumption of meiosis, governs cumulus expansion.</p>

	]]>
</description>

<author>Y Q. Su et al.</author>


</item>


<item>
<title> Characterization of Notch3-deficient mice: Normal embryonic development and absence of genetic interactions with a Notch1 mutation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/573</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/573</guid>
<pubDate>Tue, 08 May 2012 17:36:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Notch signaling pathway is an evolutionarily conserved signaling mechanism and mutations in its components disrupt cell fate specification and embryonic development in many organisms. To analyze the in vivo role of the Notch3    gene in mice, we created a deletion allele by gene targeting. Embryos homozygous for this mutation developed normally and homozygous mutant adults were viable and fertile. We also examined whether we could detect genetic interactions during early    embryogenesis between the Notch3 mutation and a targeted mutation of the Notch1 gene. Double homozygous mutant embryos exhibited defects normally observed in Notch1-deficient embryos, but we detected no obvious synergistic effects in the double    mutants. These data demonstrate that the Notch3 gene is not essential for embryonic development or fertility in mice, and does not have a redundant function with the Notch1 gene during early embryogenesis.  genesis 37:139-143,    2003.</p>

	]]>
</description>

<author>L T. Krebs et al.</author>


</item>


<item>
<title> Lith6: a new QTL for cholesterol gallstones from an intercross of CAST/Ei and DBA/2J inbred mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/572</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/572</guid>
<pubDate>Tue, 08 May 2012 17:36:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>A complex genetic basis determines the individual predisposition to develop cholesterol gallstones in response to environmental factors. We employed quantitative trait locus/loci (QTL) analyses of an intercross between inbred    strains CAST/Ei (susceptible) and DBA/2J (resistant) to determine the subset of gallstone susceptibility (Lith) genes these strains possess. Parental and first filial generation mice of both genders and male intercross offspring were evaluated    for gallstone formation after feeding a lithogenic diet. Linkage analysis was performed using a form of multiple interval mapping. One significant QTL colocalized with Lith1 [chromosome (chr) 2, 50 cM], a locus identified previously.    Significantly, new QTL were detected and named Lith10 (chr 6, 4 cM), Lith6 (chr 6, 54 cM), and Lith11 (chr 8, 58 cM). Statistical and genetic analyses suggest that Lith6 comprises two QTL in close proximity. Our molecular and genetic data support    the candidacy of peroxisome proliferator-activated receptor gamma (Pparg) and Slc21a1, encoding Pparg, and the basolateral bile acid transporter SLC21A1 (Slc21a1/Oatp1), respectively, as genes underlying Lith6.</p>

	]]>
</description>

<author>M A. Lyons et al.</author>


</item>


<item>
<title> New quantitative trait loci that contribute to cholesterol gallstone formation detected in an intercross of CAST/Ei and 129S1/SvImJ inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/571</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/571</guid>
<pubDate>Tue, 08 May 2012 17:35:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cholesterol gallstone formation is a response to interactions between multiple genes and environmental stimuli. To determine the subset of cholesterol gallstone susceptibility (Lith) genes possessed by strains CAST/Ei (susceptible)    and 129S1/SvImJ (resistant), we conducted quantitative trait locus (QTL) analyses of an intercross between these strains. Parental strains and F(1) mice of both genders were evaluated for gallstone formation after consumption of a lithogenic diet    for 8 wk.  Gallstone susceptibility of strain CAST was predominantly due to cholesterol hypersecretion. Male intercross offspring were genotyped and phenotyped for cholesterol gallstone formation after consumption of the lithogenic diet for 10    wk. Linkage analysis was performed using PSEUDOMARKER software. One significant, new QTL was detected and named Lith13 [chromosome (Chr) 5, 30 cM]. Statistical analyses and QTL fine mapping suggest this QTL may comprise two closely linked loci.    We confirmed the presence of Lith6 (Chr 6). Suggestive QTL were detected on Chrs 1, 2, 5, 14, and 16. The QTL on Chrs 2 and 16 confirmed previously identified, suggestive QTL. Therefore, they were named Lith12 (101 cM) and Lith14 (42 cM),    respectively. We identified candidate genes based on known function and location and performed mRNA expression analyses using both parental strains and intercross progeny for preliminary evaluation of their contributions to gallstone formation.    Cebpb (Lith12), Pparg (Lith6), and Slc21a1 (Lith6) displayed expression differences. Our work continues to demonstrate the genetic complexity and to elucidate the pathophysiology of cholesterol gallstone formation. It should facilitate the    development of new approaches for treating this common human disorder.</p>

	]]>
</description>

<author>M A. Lyons et al.</author>


</item>


<item>
<title> A goodbye to Charlie Janeway: Charles A. Janeway Jr (1943-2003).</title>
<link>http://mouseion.jax.org/stfb2000_2009/570</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/570</guid>
<pubDate>Tue, 08 May 2012 17:35:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>A S. Rudensky et al.</author>


</item>


<item>
<title>Interchannel coupling in the photoionization of the M-shell of Kr well above threshold: Experiment and Theory</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/31</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/31</guid>
<pubDate>Tue, 08 May 2012 17:35:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Photoionization cross sections and asymmetry (β) parameters for Kr 3s, 3p, and 3d subshells have been measured and calculated in the 300–1300-eV photon energy range. Good agreement between experiment and theory is found for both cross-section branching ratios and β parameters. Interchannel coupling among the channels arising from 3s, 3p, and 3d subshells is found to be necessary for quantitative accuracy of the theory. This shows that the interchannel coupling phenomenology far above threshold, found previously for outer shells of Ne and Ar, is also operative for inner atomic shells.</p>

	]]>
</description>

<author>H. S. Chakraborty et al.</author>


</item>


<item>
<title> FXR and ABCG5/ABCG8 as determinants of cholesterol gallstone formation from quantitative trait locus mapping in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/569</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/569</guid>
<pubDate>Tue, 08 May 2012 17:35:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND & AIMS: Cholesterol gallstone formation is a complex genetic trait. To identify additional cholesterol gallstone susceptibility loci, we performed a quantitative trait locus analysis using an intercross of PERA/Ei and    I/LnJ inbred strains of mice. METHODS: Mice of both sexes were examined for gallstone weight and evaluated according to a scoring system for the physical chemistry of cholelithiasis during feeding of a lithogenic diet. Intercross offspring were    genotyped, and linkage analysis was performed by interval mapping. Differences in messenger RNA expression of positional candidate genes were determined using reverse-transcription and real-time polymerase chain reaction. RESULTS: We identified    significant loci associated with gallstone weight on chromosomes 10 and 4, named Lith7 and Lith8, respectively (both susceptibility alleles conferred by strain I/LnJ). Positional candidate genes with higher expression in I/LnJ mice are Fxr    (official symbol, Nr1h4), encoding the nuclear bile salt receptor, on chromosome 10 and Shp1 (official symbol, Nr0b2), encoding the small heterodimer partner 1, on chromosome 4. A significant locus associated with gallstone score on chromosome    17, named Lith9 (susceptibility allele conferred by strain PERA/Ei), colocalizes with the genes Abcg5 and Abcg8 that encode the canalicular cholesterol transporter.  Higher hepatic messenger RNA expression of Abcg5 and Abcg8 in strain PERA/Ei    correlates positively with higher biliary cholesterol levels.  CONCLUSIONS: Our findings suggest a primary role of the nuclear bile salt receptor FXR and the canalicular cholesterol transporter ABCG5/ABCG8 in the genetic susceptibility and    pathogenesis of cholesterol cholelithiasis in these strains of inbred mice.</p>

	]]>
</description>

<author>H Wittenburg et al.</author>


</item>


<item>
<title> Pleiotropy, homeostasis, and functional networks based on assays of cardiovascular traits in genetically randomized populations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/568</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/568</guid>
<pubDate>Tue, 08 May 2012 17:35:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>A major problem in studying biological traits is understanding how genes work together to provide organismal structures and functions. Conventional reductionist paradigms attribute functions to particular proteins, motifs, and    amino acids. An equally important but harder problem involves the synthesis of data at fundamental levels of biological systems to understand functionality at higher levels. We used subtle, naturally occurring, multigenic variation of    cardiovascular (CV) properties in a panel of genetically randomized strains that are derived from the A/J and C57BL/6J strains of mice to perturb CV functions in nonpathologic ways. In this proof-of-concept study, computational analysis correctly    identified the known relations among CV properties and revealed functionality at higher levels of the CV system. The network was then used to account for pleiotropies and homeostatic responses in single gene mutant mice and in mice treated with a    pharmacologic agent (anesthesia). The CV network accounted for functional dependencies in complementary ways to the insights obtained from genetic networks and biochemical pathways. These networks are therefore an important approach for defining    and characterizing functional relations in complex biological systems in health and disease.</p>

	]]>
</description>

<author>J H. Nadeau et al.</author>


</item>


<item>
<title> Using advanced intercross lines for high-resolution mapping of HDL cholesterol quantitative trait loci.</title>
<link>http://mouseion.jax.org/stfb2000_2009/567</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/567</guid>
<pubDate>Tue, 08 May 2012 17:34:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mapping quantitative trait loci (QTLs) with high resolution facilitates identification and positional cloning of the underlying genes. The novel approach of advanced intercross lines (AILs) generates many more recombination events    and thus can potentially narrow QTLs significantly more than do conventional backcrosses and F2 intercrosses. In this study, we carried out QTL analyses in (C57BL/6J x NZB/BlNJ) x C57BL/6J backcross progeny fed either chow or an atherogenic diet    to detect QTLs that regulate high-density lipoprotein cholesterol (HDL)concentrations, and in (C57BL/6J x NZB/BlNJ) F11 AIL progeny to confirm and narrow those QTLs.  QTLs for HDL concentrations were found on chromosomes 1, 5, and 16. AIL not    only narrowed the QTLs significantly more than did a conventional backcross but also resolved a chromosome 5 QTL identified in the backcross into two QTLs, the peaks of both being outside the backcross QTL region.  We tested 27 candidate genes    and found significant mRNA expression differences for 12 (Nr1i3, Apoa2, Sap, Tgfb2, Fgfbp1, Prom, Ppargc1, Tcf1, Ncor2, Srb1, App, and Ifnar). Some of these underlay the same QTL, indicating that expression differences are common and not    sufficient to identify QTL genes. All the major HDL QTLs in our study had homologous counterparts in humans, implying that their underlying genes regulate HDL in humans.</p>

	]]>
</description>

<author>X Wang et al.</author>


</item>


<item>
<title> Donor cell expansion is delayed following nonablative in utero transplantation to treat murine mucopolysaccharidosis type VII.</title>
<link>http://mouseion.jax.org/stfb2000_2009/566</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/566</guid>
<pubDate>Tue, 08 May 2012 17:34:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>To block development of progressive childhood diseases, in utero transplantation (IUTx) requires immediate and significant donor peripheral blood (PB) cell amplification. To date, negligible and nontherapeutic donor PB cell levels    have been observed postnatally, except in patients with immunodeficiency diseases. Donor cell fate in utero still is not clear. Ease of identifying and quantifying beta-glucuronidase (GUSB)-expressing donor cells in GUSB-null    mucopolysaccharidosis type VII (MPSVII) mouse recipients allowed us to evaluate temporal donor cell engraftment and amplification post-IUTx. Like humans, MPSVII mice are unable to catabolize lysosomal glycosaminoglycans and progressively develop    severe storage disease unless they are treated early in life.IUTx recipients were nonablated MPSVII fetuses and genetically stem cell-deficient, and hence myeloablated, W(41)/W(41) MPSVII fetuses. Donor GUSB+ cells were identified and counted in    histochemical tissue sections.  Quantitative results were confirmed by flow cytometry, enzyme analysis, and histopathology.Whereas GUSB+ cells engraft in most tissues in utero, significant amplification does not occur until the first postnatal    week in the nonablated MPSVII hosts. In contrast, genetically myeloablated MPSVII recipients display widely distributed donor cell replacement accompanied by extensive amplification in utero. In both models, storage is alleviated in adult tissues    with significant donor cell repopulation.To become therapeutic, IUTx must overcome the limitations of donor cell expansion in the highly competitive fetal environment. Fortunately, nonablative mechanisms to amplify cells in utero are coming on    line.</p>

	]]>
</description>

<author>J E. Barker et al.</author>


</item>


<item>
<title> Mouse models of Down syndrome: how useful can they be? Comparison of the gene content of human chromosome 21 with orthologous mouse genomic regions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/565</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/565</guid>
<pubDate>Tue, 08 May 2012 17:34:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>With an incidence of approximately 1 in 700 live births, Down syndrome (DS) remains the most common genetic cause of mental retardation. The phenotype is assumed to be due to overexpression of some number of the >300 genes encoded    by human chromosome 21. Mouse models, in particular the chromosome 16 segmental trisomies, Ts65Dn and Ts1Cje, are indispensable for DS-related studies of gene-phenotype correlations. Here we compare the updated gene content of the finished    sequence of human chromosome 21 (364 genes and putative genes) with the gene content of the homologous mouse genomic regions (291 genes and putative genes) obtained from annotation of the public sector C57Bl/6 draft sequence. Annotated genes fall    into one of three classes. First, there are 170 highly conserved, human/mouse orthologues. Second, there are 83 minimally conserved, possible orthologues. Included among the conserved and minimally conserved genes are 31 antisense transcripts.    Third, there are species-specific genes: 111 spliced human transcripts show no orthologues in the syntenic mouse regions although 13 have homologous sequences elsewhere in the mouse genomic sequence, and 38 spliced mouse transcripts show no    identifiable human orthologues. While these species-specific genes are largely based solely on spliced EST data, a majority can be verified in RNA expression experiments. In addition, preliminary data suggest that many human-specific transcripts    may represent a novel class of primate-specific genes. Lastly, updated functional annotation of orthologous genes indicates genes encoding components of several cellular pathways are dispersed throughout the orthologous mouse chromosomal regions    and are not completely represented in the Down syndrome segmental mouse models.  Together, these data point out the potential for existing mouse models to produce extraneous phenotypes and to fail to produce DS-relevant phenotypes.</p>

	]]>
</description>

<author>K Gardiner et al.</author>


</item>


<item>
<title> A missense mutation in the mouse Col2a1 gene causes spondyloepiphyseal dysplasia congenita, hearing loss, and retinoschisis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/564</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/564</guid>
<pubDate>Tue, 08 May 2012 17:33:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>A missense mutation in the mouse Col2a1 gene has been discovered, resulting in a mouse phenotype with similarities to human spondyloepiphyseal dysplasia (SED) congenita. In addition, SED patients have been identified with a similar    molecular mutation in human COL2A1.  This mouse model offers a useful tool for molecular and biological studies of bone development and pathology. INTRODUCTION: A new mouse autosomal recessive mutation has been discovered and named    spondyloepiphyseal dysplasia congenita (gene symbol sedc). MATERIALS AND METHODS: Homozygous sedc mice can be identified at birth by their small size and shortened trunk. Adults have shortened noses, dysplastic vertebrae, femora, and tibias, plus    retinoschisis and hearing loss. The mutation was mapped to Chr15, and Col2a1 was identified as a candidate gene. RESULTS: Sequence analyses revealed that the affected gene is Col2a1, which has a missense mutation at exon 48 causing an amino acid    change of arginine to cysteine at position 1417. Two human patients with spondyloepiphyseal dysplasia (SED) congenita have been reported with the same amino acid substitution at position 789 in the human COL2A1 gene. CONCLUSIONS: Thus, sedc/sedc    mice provide a valuable model of human SED congenita with molecular and phenotypic homology. Further biochemical analyses, molecular modeling, and cell culture studies using sedc/sedc mice could provide insight into mechanisms of skeletal    development dependent on Col2a1 and its role in fibril formation and cartilage template organization.</p>

	]]>
</description>

<author>L R. Donahue et al.</author>


</item>


<item>
<title> Successful allogeneic neonatal bone marrow transplantation devoid of myeloablation requires costimulatory blockade.</title>
<link>http://mouseion.jax.org/stfb2000_2009/563</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/563</guid>
<pubDate>Tue, 08 May 2012 17:33:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>A significant number of nonmalignant, progressive childhood disorders respond to bone marrow transplantation (BMT). Toxic myeloablative pretreatment regimens, graft failure, and graft-vs-host disease complicate the utility of BMT    for neonatal treatment. We recently demonstrated high-dose BMT in neonatal animals enables chimeric engraftment without toxic myeloablation. Reagents that block T cell costimulation (anti-CD40L mAb and/or CTLA-4Ig) establish tolerant allogeneic    engraftment in adult recipients. Donor lymphocyte infusion (DLI) re-establishes failing grafts and treats malignant relapse via a graft-vs-leukemia response. In this study, we tested the hypothesis that combining these approaches would allow    tolerant allogeneic engraftment devoid of myeloablation in neonatal normal and mutant mice with lysosomal storage disease. Tolerant chimeric allogeneic engraftment was achieved before DLI only in the presence of both anti-CD40L mAb and CTLA-4Ig.    DLI amplified allografts to full donor engraftment long-term. DLI-treated mice either maintained long-term tolerance or developed late-onset chronic graft-vs-host disease. This combinatorial approach provides a nontoxic method to establish    tolerant allogeneic engraftment for treatment of progressive childhood diseases.</p>

	]]>
</description>

<author>B W. Soper et al.</author>


</item>


<item>
<title> E2F3 loss has opposing effects on different pRB-deficient tumors, resulting in suppression of pituitary tumors but metastasis of medullary thyroid carcinomas.</title>
<link>http://mouseion.jax.org/stfb2000_2009/562</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/562</guid>
<pubDate>Tue, 08 May 2012 17:33:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>The E2F transcription factors are key downstream targets of the retinoblastoma protein (pRB) tumor suppressor. We have previously shown that E2F3 plays a critical role in mediating the mitogen-induced activation of E2F-responsive    genes and contributes to both the inappropriate proliferation and the p53-dependent apoptosis that arise in pRB-deficient embryos. Here we show that E2F3 also has a significant effect on the phenotype of tumor-prone Rb(+/-) mice. The absence of    E2F3 results in a significant expansion in the life spans of these animals that correlates with a dramatic alteration in the tumor spectrum. E2F3 loss suppresses the development of the pituitary tumors that normally account for the death of    Rb(+/-) mice. However, it also promotes the development of medullary thyroid carcinomas yielding metastases at a high frequency.  This increased aggressiveness does not seem to result from any change in p53 levels or activity in these tumors. We    show that, instead, E2F3 loss leads to an increase in the rate of tumor initiation. Finally, analysis of Rb(+/-); E2f3(+/-) mice shows that this tumor-suppressive function of E2F3 is dose dependent.</p>

	]]>
</description>

<author>U Ziebold et al.</author>


</item>


<item>
<title>A new statistic to evaluate imputation reliability</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1034</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1034</guid>
<pubDate>Tue, 08 May 2012 17:32:53 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Peng Lin et al.</author>


</item>


<item>
<title> Cyclin E ablation in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/561</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/561</guid>
<pubDate>Tue, 08 May 2012 17:32:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>E type cyclins (E1 and E2) are believed to drive cell entry into the S phase. It is widely assumed that the two E type cyclins are critically required for proliferation of all cell types. Here, we demonstrate that E type cyclins    are largely dispensable for mouse development. However, endoreplication of trophoblast giant cells and megakaryocytes is severely impaired in the absence of cyclin E. Cyclin E-deficient cells proliferate actively under conditions of continuous    cell cycling but are unable to reenter the cell cycle from the quiescent G(0) state. Molecular analyses revealed that cells lacking cyclin E fail to normally incorporate MCM proteins into DNA replication origins during G(0)-->S progression. We    also found that cyclin E-deficient cells are relatively resistant to oncogenic transformation. These findings define a molecular function for E type cyclins in cell cycle reentry and reveal a differential requirement for cyclin E in normal versus    oncogenic proliferation.</p>

	]]>
</description>

<author>Y Geng et al.</author>


</item>


<item>
<title> Autoimmunity as the consequence of a spontaneous mutation in Rasgrp1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/560</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/560</guid>
<pubDate>Tue, 08 May 2012 17:32:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>A mouse strain was identified with a recessive genetic lesion, which spontaneously developed a lymphoproliferative autoimmune syndrome exhibiting features of systemic lupus erythematosus. Positional mapping of the    disease-associated locus revealed a lesion in Rasgrp1 that prevented the translation of the RasGRP1 protein. T cells from these mice failed to activate Ras or proliferate vigorously following antigen encounter and showed defects in positive    selection. Peripheral RasGRP1lag T cells spontaneously adopted a memory phenotype and were able to transfer disease to lymphopenic recipient mice. CD4+ T cells accumulated in the lymphoid tissues of older RasGRP1lag mice and were resistant to    activation-induced cell death. RasGRP1lag B cells were functionally normal, but activated B cells were detected in older mice, as were autoantibodies directed against self-antigens. Our findings indicate that Ras signaling pathways are required    to maintain T cell tolerance and to prevent autoimmune disease.</p>

	]]>
</description>

<author>K Layer et al.</author>


</item>


<item>
<title> Retroposon compensatory mechanism hypothesis not supported: Zfa knockout mice are fertile.</title>
<link>http://mouseion.jax.org/stfb2000_2009/559</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/559</guid>
<pubDate>Tue, 08 May 2012 17:31:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>It is hypothesized that autosomal retroposons compensate for the loss of their inactivated essential X-chromosome progenitors during spermatogenesis. Here we test this Retroposon Compensatory Mechanism (RCM) hypothesis using the    Zfy gene family. The mouse autosomal retroposon Zfa is expressed in testes at the same developmental time points at which Zfx levels decline, which correspond to the time of male sex chromosome inactivation, suggesting that Zfa may compensate for    the loss of Zfx during spermatogenesis. We examined the effect of Zfa-targeted mutagenesis on spermatogenesis in three genetically distinct mouse strains.  Surprisingly, Zfa knockout mice showed no detectable fertility, sperm count, or testes    morphology defects. We therefore conclude that Zfa is not an essential gene for spermatogenesis and fertility. This surprising finding now challenges the RCM hypothesis at least for the Zfy gene family. It also forces us to reevaluate the    original data underpinning the RCM hypothesis for this family and to propose alternative hypotheses.</p>

	]]>
</description>

<author>K G. Banks et al.</author>


</item>


<item>
<title> Essential role for the peroxiredoxin Prdx1 in erythrocyte antioxidant defence and tumour suppression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/558</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/558</guid>
<pubDate>Tue, 08 May 2012 17:31:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Reactive oxygen species are involved in many cellular metabolic and signalling processes and are thought to have a role in disease, particularly in carcinogenesis and ageing. We have generated mice with targeted inactivation of    Prdx1, a member of the peroxiredoxin family of antioxidant enzymes. Here we show that mice lacking Prdx1 are viable and fertile but have a shortened lifespan owing to the development beginning at about 9 months of severe haemolytic anaemia and    several malignant cancers, both of which are also observed at increased frequency in heterozygotes. The haemolytic anaemia is characterized by an increase in erythrocyte reactive oxygen species, leading to protein oxidation, haemoglobin    instability, Heinz body formation and decreased erythrocyte lifespan. The malignancies include lymphomas, sarcomas and carcinomas, and are frequently associated with loss of Prdx1 expression in heterozygotes, which suggests that this protein    functions as a tumour suppressor.  Prdx1-deficient fibroblasts show decreased proliferation and increased sensitivity to oxidative DNA damage, whereas Prdx1-null mice have abnormalities in numbers, phenotype and function of natural killer cells.     Our results implicate Prdx1 as an important defence against oxidants in ageing mice.</p>

	]]>
</description>

<author>C A. Neumann et al.</author>


</item>


<item>
<title> Rb and N-ras function together to control differentiation in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/557</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/557</guid>
<pubDate>Tue, 08 May 2012 17:31:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>The product of the retinoblastoma tumor suppressor gene (Rb) can control cell proliferation and promote differentiation. Murine embryos nullizygous for Rb die midgestation with defects in cell cycle regulation, control of    apoptosis, and terminal differentiation of several tissues, including skeletal muscle, nervous system, and lens. Previous cell culture-based experiments have suggested that the retinoblastoma protein (pRb) and Ras operate in a common pathway to    control cellular differentiation. Here we have tested the hypothesis that the proto-oncogene N-ras participates in Rb-dependent regulation of differentiation by generating and characterizing murine embryos deficient in both N-ras and Rb. We show    that deletion of N-ras rescues a unique subset of the developmental defects associated with nullizygosity of Rb, resulting in a significant extension of life span. Rb(-/-); N-ras(-/-) skeletal muscle has normal fiber density, myotube length and    thickness, in contrast to Rb-deficient embryos. Additionally, Rb(-/-); N-ras(-/-) muscle shows a restoration in the expression of the late muscle-specific gene MCK, and this correlates with a significant potentiation of MyoD transcriptional    activity in Rb(-/-); N-ras(-/-), compared to Rb(-/-) myoblasts in culture. The improved differentiation of skeletal muscle in Rb(-/-); N-ras(-/-) embryos occurs despite evidence of deregulated proliferation and apoptosis, as seen in Rb-deficient    animals. Our findings suggest that the control of differentiation and proliferation by Rb are genetically separable.</p>

	]]>
</description>

<author>C Takahashi et al.</author>


</item>


<item>
<title> Donor cell replacement in mice transplanted in utero is limited by immune-independent mechanisms.</title>
<link>http://mouseion.jax.org/stfb2000_2009/556</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/556</guid>
<pubDate>Tue, 08 May 2012 17:30:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>In utero transplantation (IUTx) therapy with allogeneic cells results in negligible peripheral blood (PBL) chimerism in nonablated humans with progressive diseases. IUTx has been successful only in immunocompromised fetuses.    Because early treatment has great potential for halting disease progression, mechanisms preventing cell expansion must be identified and corrected. The hypothesis that factors in addition to allogenicity are responsible for low-level expansion is    tested here by transplanting congenic cells into nonablated normal and mucopolycaccharidosis type VII (MPSVII) murine fetuses. MPSVII mice lack the enzyme beta-glucuronidase (GUSB-), accumulate glycosaminoglycans, and progressively develop severe    storage disease. Low levels of enzyme can reverse storage. Evidence presented elsewhere showed that allogeneic donor cells overexpressing GUSB are negligible and their corrective effects are lost post-IUTx in MPSVII mice. We find that (1)    congenic donor PBL cells, like allogeneic cells, are negligible in PBL of normal GUSB+ and MPSVII GUSB- hosts post-IUTx; (2) congenic, unlike allogeneic cells, are retained long term in both GUSB+ and GUSB- recipients; and (3) sufficient GUSB is    produced to alleviate storage for up to 11.5 months in multiple tissues of GUSB- hosts. GUSB+ and GUSB- animals repopulate to a similar extent, indicating that donor GUSB enzyme does not initiate an immune response in the MPSVII null recipients.    We conclude that the initial expansion of congenic and allogeneic cells is limited post-IUTx by non-immune-related mechanisms and the level of PBL cells is not necessarily indicative of graft failure following congenic IUTx. The mechanism    limiting initial expansion may differ from that supporting long-term cell retention.</p>

	]]>
</description>

<author>J E. Barker et al.</author>


</item>


<item>
<title> Genome function and nuclear architecture: from gene expression to nanoscience.</title>
<link>http://mouseion.jax.org/stfb2000_2009/555</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/555</guid>
<pubDate>Tue, 08 May 2012 17:30:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Biophysical, chemical, and nanoscience approaches to the study of nuclear structure and activity have been developing recently and hold considerable promise. A selection of fundamental problems in genome organization and function    are reviewed and discussed in the context of these new perspectives and approaches. Advancing these concepts will require coordinated networks of physicists, chemists, and materials scientists collaborating with cell, developmental, and genome    biologists.</p>

	]]>
</description>

<author>T P. O&apos;Brien et al.</author>


</item>


<item>
<title> Identification of the beta cell antigen targeted by a prevalent population of pathogenic CD8+ T cells in autoimmune diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/554</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/554</guid>
<pubDate>Tue, 08 May 2012 17:29:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Type 1 diabetes is an autoimmune disease in which autoreactive T cells attack and destroy the insulin-producing pancreatic beta cells. CD8+ T cells are essential for this beta cell destruction, yet their specific antigenic targets    are largely unknown. Here, we reveal that the autoantigen targeted by a prevalent population of pathogenic CD8+ T cells in nonobese diabetic mice is islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP). Through tetramer    technology, IGRP-reactive T cells are readily detected in islets and peripheral blood directly ex vivo. The human IGRP gene maps to a diabetes susceptibility locus, suggesting that IGRP also may be an antigen for pathogenic T cells in human type    1 diabetes and, thus, a new, potential target for diagnostic and therapeutic approaches.</p>

	]]>
</description>

<author>S M. Lieberman et al.</author>


</item>


<item>
<title> Genetic disassociation of autoimmunity and resistance to costimulation blockade-induced transplantation tolerance in nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/553</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/553</guid>
<pubDate>Tue, 08 May 2012 17:29:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Curing type 1 diabetes by islet transplantation requires overcoming both allorejection and recurrent autoimmunity. This has been achieved with systemic immunosuppression, but tolerance induction would be preferable.  Most islet    allotransplant tolerance induction protocols have been tested in nonobese diabetic (NOD) mice, and most have failed. Failure has been attributed to the underlying autoimmunity, assuming that autoimmunity and resistance to transplantation    tolerance have a common basis. Out of concern that NOD biology could be misleading in this regard, we tested the hypothesis that autoimmunity and resistance to transplantation tolerance in NOD mice are distinct phenotypes. Unexpectedly, we    observed that (NOD x C57BL/6)F(1) mice, which have no diabetes, nonetheless resist prolongation of skin allografts by costimulation blockade. Further analyses revealed that the F(1) mice shared the dendritic cell maturation defects and abnormal    CD4(+) T cell responses of the NOD but had lost its defects in macrophage maturation and NK cell activity. We conclude that resistance to allograft tolerance induction in the NOD mouse is not a direct consequence of overt autoimmunity and that    autoimmunity and resistance to costimulation blockade-induced transplantation tolerance phenotypes in NOD mice can be dissociated genetically. The outcomes of tolerance induction protocols tested in NOD mice may not accurately predict outcomes in    human subjects.</p>

	]]>
</description>

<author>T Pearson et al.</author>


</item>


<item>
<title> Genetic evidence that relative synaptic efficacy biases the outcome of synaptic competition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/552</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/552</guid>
<pubDate>Tue, 08 May 2012 17:28:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Synaptic activity drives synaptic rearrangement in the vertebrate nervous system; indeed, this appears to be a main way in which experience shapes neural connectivity. One rearrangement that occurs in many parts of the nervous    system during early postnatal life is a competitive process called 'synapse elimination'. At the neuromuscular junction, where synapse elimination has been analysed in detail, muscle fibres are initially innervated by multiple axons, then all but    one are withdrawn and the 'winner' enlarges. In support of the idea that synapse elimination is activity dependent, it is slowed or speeded when total neuromuscular activity is decreased or increased, respectively. However, most hypotheses about    synaptic rearrangement postulate that change depends less on total activity than on the relative activity of the competitors. Intuitively, it seems that the input best able to excite its postsynaptic target would be most likely to win the    competition, but some theories and results make other predictions. Here we use a genetic method to selectively inhibit neurotransmission from one of two inputs to a single target cell. We show that more powerful inputs are strongly favoured    competitors during synapse elimination.</p>

	]]>
</description>

<author>M Buffelli et al.</author>


</item>


<item>
<title> PPARdelta is a very low-density lipoprotein sensor in macrophages.</title>
<link>http://mouseion.jax.org/stfb2000_2009/551</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/551</guid>
<pubDate>Tue, 08 May 2012 17:28:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although triglyceride-rich particles, such as very low-density lipoprotein (VLDL), contribute significantly to human atherogenesis, the molecular basis for lipoprotein-driven pathogenicity is poorly understood. We demonstrate that    in macrophages, VLDL functions as a transcriptional regulator via the activation of the nuclear receptor peroxisome proliferator-activated receptor delta. The signaling components of native VLDL are its triglycerides, whose activity is enhanced    by lipoprotein" lipase. Generation of peroxisome proliferator-activated receptor delta null macrophages verifies the absolute requirement of this transcription factor in mediating the VLDL response. Thus, our data reveal a pathway through which    dietary triglycerides and VLDL can directly regulate gene expression in atherosclerotic lesions.</p>

	]]>
</description>

<author>A Chawla et al.</author>


</item>


<item>
<title> Effect of heterozygous PPARgamma deficiency and TZD treatment on insulin resistance associated with age and high-fat feeding.</title>
<link>http://mouseion.jax.org/stfb2000_2009/550</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/550</guid>
<pubDate>Tue, 08 May 2012 17:27:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Peroxisome proliferator-activated receptor-gamma (PPARgamma) is the target receptor for thiazolidinedione (TZD) compounds, which are a class of insulin-sensitizing drugs used in the treatment of type 2 diabetes.  Paradoxically,    however, mice deficient in PPARgamma (PPARgamma(+/-)) are more insulin sensitive than their wild-type (WT) littermates, not less, as would be predicted. To determine whether PPARgamma deficiency could prevent the development of the insulin    resistance associated with increasing age or high-fat (HF) feeding, insulin sensitivity was assessed in PPARgamma(+/-) and WT mice at 2, 4, and 8 mo of age and in animals fed an HF diet. Because TZDs elicit their effect through PPARgamma    receptor, we also examined the effect of troglitazone (a TZD) in these mice. Glucose metabolism was assessed by hyperinsulinemic euglycemic clamp and oral glucose tolerance test. Insulin sensitivity declined with age for both groups. However, the    decline in the PPARgamma(+/-) animals was substantially less than that of the WT animals, such that, by 8 mo of age, the PPARgamma(+/-) mice were markedly more insulin sensitive than the WT mice. This greater sensitivity in PPARgamma(+/-) mice    was lost with TZD treatment. HF feeding led to marked adipocyte hypertrophy and peripheral tissue and hepatic insulin resistance in WT mice but also in PPARgamma(+/-) mice. Treatment of these mice with troglitazone completely prevented the    adipocyte hypertrophy and normalized insulin action. In conclusion, PPARgamma deficiency partially protects against age-related insulin resistance but does not protect against HF diet-induced insulin resistance.</p>

	]]>
</description>

<author>P D. Miles et al.</author>


</item>


<item>
<title> Subversion of the innate immune system by a retrovirus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/549</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/549</guid>
<pubDate>Tue, 08 May 2012 17:27:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Retroviruses evolve rapidly to avoid the immune response of the infected host. We show here that the wild-type mouse mammary tumor virus MMTV(C3H) persisted indefinitely in C3H/HeN mice. However, it was rapidly lost in" mice of the    closely related C3H/HeJ strain and was replaced by a virus recombinant with an endogenous Mtv provirus. Maintenance of the wild-type virus was dependent on Toll-like receptor-4 (TLR4) signaling, which" triggered production of the    immunosuppressive cytokine interleukin-10. In the presence of mutant TLR4 in C3H/HeJ mice, wild-type virus was" eliminated by the cytotoxic immune response, promoting selection of the" immune escape recombinant MMTV variants. Thus, subversion of    the innate" immune system is yet another survival strategy used by retroviruses.</p>

	]]>
</description>

<author>B A. Jude et al.</author>


</item>


<item>
<title> The role of B lymphocytes as key antigen-presenting cells in the development of T cell-mediated autoimmune type 1 diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/548</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/548</guid>
<pubDate>Tue, 08 May 2012 17:27:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title> A band 3-based macrocomplex of integral and peripheral proteins in the RBC membrane.</title>
<link>http://mouseion.jax.org/stfb2000_2009/547</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/547</guid>
<pubDate>Tue, 08 May 2012 17:26:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have studied the membrane proteins of band 3 anion exchanger (AE1)-deficient mouse and human red blood cells. It has been shown previously that proteins of the band 3 complex are reduced or absent in these cells. In this study    we show that proteins of the Rh complex are also greatly reduced (Rh-associated glycoprotein, Rh polypeptides, CD47, glycophorin B) or absent (LW). These observations suggest that the Rh complex is associated with the band 3 complex in healthy    RBCs. Mouse band 3(-/-) RBCs differed from the human band 3-deficient RBCs in that they retained CD47. Aquaporin 1 was reduced, and its glycosylation was altered in mouse and human band 3-deficient RBCs. Proteins of the glycophorin C complex, and    other proteins with independent cytoskeletal interactions, were present in normal or increased amounts. To obtain direct evidence for the association of the band 3 and the Rh protein complexes in the RBC, we examined whether Rh complex proteins    were coimmunoprecipitated with band 3 from membranes. RhAG and Rh were found to be efficiently coimmunoprecipitated with band 3 from deoxycholate-solubilized membranes.  Results suggest that band 3 forms the core of a macrocomplex of integral and    peripheral RBC membrane proteins. The presence of these proteins in a single structural macrocomplex makes it likely that they have linked functional or regulatory roles. We speculate that this macrocomplex may function as an integrated    CO(2)/O(2) gas exchange unit (metabolon) in the erythrocyte.</p>

	]]>
</description>

<author>L J. Bruce et al.</author>


</item>


<item>
<title>May 2012 World Transit Research Newsletter</title>
<link>http://www.worldtransitresearch.info/newsletter/12</link>
<guid isPermaLink="true">http://www.worldtransitresearch.info/newsletter/12</guid>
<pubDate>Tue, 08 May 2012 17:26:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Institute of Transport Studies (Monash University)</author>


</item>


<item>
<title> Loss of the Tg737 protein results in skeletal patterning defects.</title>
<link>http://mouseion.jax.org/stfb2000_2009/546</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/546</guid>
<pubDate>Tue, 08 May 2012 17:26:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Tg737 mutant mice exhibit pathologic conditions in numerous tissues along with skeletal patterning defects. Herein, we characterize the skeletal pathologic conditions and confirm a role for Tg737 in skeletal patterning through    transgenic rescue. Analyses were conducted in both the hypomorphic Tg737(orpk) allele that results in duplication of digit one and in the null Tg737(Delta2-3betaGal) allele that is an embryonic lethal mutation exhibiting eight digits per limb. In    early limb buds, Tg737 expression is detected throughout the mesenchyme becoming concentrated in precartilage condensations at later stages. In situ analyses indicate that the Tg737(orpk) mutant limb defects are not associated with changes in    expression of Shh, Ihh, HoxD11-13, Patched, BMPs, or Glis. Likewise, in Tg737(Delta2-3betaGal) mutant embryos, there was no change in Shh expression. However, in both alleles, Fgf4 was ectopically expressed on the anterior apical ectodermal    ridge. Collectively, the data argue for a dosage effect of Tg737 on the limb phenotypes and that the polydactyly is independent of Shh misexpression. Developmental Dynamics 227:78-90, 2003.</p>

	]]>
</description>

<author>Q Zhang et al.</author>


</item>


<item>
<title> Statistical tests for differential expression in cDNA microarray experiments.</title>
<link>http://mouseion.jax.org/stfb2000_2009/545</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/545</guid>
<pubDate>Tue, 08 May 2012 17:26:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Extracting biological information from microarray data requires appropriate statistical methods. The simplest statistical method for detecting differential expression is the t test, which can be used to compare two conditions when    there is replication of samples. With more than two conditions, analysis of variance (ANOVA) can be used, and the mixed ANOVA model is a general and powerful approach for microarray experiments with multiple factors and/or several sources of    variation.</p>

	]]>
</description>

<author>X Cui et al.</author>


</item>


<item>
<title> Effect of age on susceptibility to azoxymethane-induced colonic aberrant crypt foci formation in C57BL/6JNIA mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/544</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/544</guid>
<pubDate>Tue, 08 May 2012 17:25:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>To determine the effect of age on susceptibility to azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) formation and its underlying mechanism, young and old mice were injected with AOM weekly for 4 or 5 weeks and    euthanized 5 or 6 weeks later. Given the same (12 or 15) mg/kg body weight dose of AOM, old mice had significantly more ACF than young mice. However, given the same total dose of AOM (to avoid confounding effect of higher dose to heavier old    mice), at a low total dose (1.5 mg) there was no age difference, but at higher total doses (1.8 and 2.2 mg) young mice had significantly more ACF than old mice. These results indicate that the age-related susceptibility to AOM differs depending    on whether administration of the carcinogen is based on weight or total dose. These age differences are not due to variations in cyclooxygenase-2 expression, cell proliferation, or AOM hydroxylase activity.</p>

	]]>
</description>

<author>H Chung et al.</author>


</item>


<item>
<title> T cells are required for host protection against Brugia malayi but need not produce or respond to interleukin-4.</title>
<link>http://mouseion.jax.org/stfb2000_2009/543</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/543</guid>
<pubDate>Tue, 08 May 2012 17:25:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>T cells are known to be required for host protection in mouse models of Brugia malayi infection. Several independent studies in murine models have also highlighted the rapid induction of Th2-like responses after infection with B.    malayi or B. pahangi. Previous data from our laboratory have described a significant increase in permissiveness in the absence of interleukin-4 (IL-4), the "prototypical" Th2 cytokine, involved in both the induction and maintenance of Th2    responses. These observations led to our hypothesis that T cells involved in murine host protection would respond to IL-4 signaling and differentiate into cells of the "type 2" phenotype. As such, these cells would presumably also act as major    sources of IL-4. To investigate these hypotheses, we performed several adoptive transfers in which we controlled the cell population(s) able to produce or respond to IL-4. We show here that, in contrast to our original hypotheses, IL-4 production    and IL-4 receptor expression by T cells are both dispensable for T-cell-mediated host protection. Instead, our data imply that T cells may be required for eosinophil accumulation at the site of infection.</p>

	]]>
</description>

<author>L Spencer et al.</author>


</item>


<item>
<title> The human DDX and DHX gene families of putative RNA helicases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/542</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/542</guid>
<pubDate>Tue, 08 May 2012 17:25:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nucleic acid helicases are characterized by the presence of the helicase domain containing eight motifs. The sequence of the helicase domain is used to classify helicases into families. To identify members of the DEAD and DEAH    families of human RNA helicases, we used the helicase domain sequences to search the nonredundant peptide sequence database. We report the identification of 36 and 14 members of the DEAD and DEAH families of putative RNA helicases, including    several novel genes. The gene symbol DDX had been used previously for both DEAD- and DEAH-box families. We have now adopted DDX and DHX symbols to denote DEAD- and DEAH-box families, respectively. Members of human DDX and DHX families of putative    RNA helicases play roles in differentiation and carcinogenesis.</p>

	]]>
</description>

<author>M Abdelhaleem et al.</author>


</item>


<item>
<title> Sry Expression Level and Protein Isoform Differences Play a Role in Abnormal Testis Development in C57BL/6J Mice Carrying Certain Sry Alleles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/541</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/541</guid>
<pubDate>Tue, 08 May 2012 17:24:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Transfer of certain Mus domesticus-derived Y chromosomes (Sry(DOM) alleles, e.g., Sry(POS) and Sry(AKR)) onto the C57BL/6J (B6) mouse strain causes abnormal gonad development due to an aberrant interaction between the Sry(DOM)    allele and the B6-derived autosomal (tda) genes. For example, B6 XY(POS) fetuses develop ovaries and ovotestes and B6 XY(AKR) fetuses have delayed testis cord development. To test whether abnormal testis development is caused by insufficient    Sry(DOM) expression, two approaches were used. First, gonad development and relative Sry expression levels were examined in fetal gonads from two strains of B6 mice that contained a single M. domesticus-derived and a single M. musculus-derived    Sry allele (B6-Y(POS,RIII) and B6-Y(AKR,RIII)). In both cases, presence of the M. musculus Sry(RIII) allele corrected abnormal testis development. On the B6 background, Sry(POS) was expressed at about half the level of Sry(RIII) whereas Sry(AKR)    and Sry(RIII) were equally expressed. On an F(1) hybrid background, both Sry(POS) and Sry(RIII) expression increased, but Sry(POS) expression increased to a greater extent. Second, sexual development and Sry expression levels were determined in    XX mice carrying a transgene expressing Sry(POS) controlled by POS-derived or MUS-derived regulatory regions. In both cases one B6 transgenic line was recovered in which XX transgenic mice developed only testicular tissue but cord development was    delayed despite normal Sry transcriptional initiation and overexpression.  For three transgenes where B6 XX transgenic mice developed as females, hermaphrodites, or males, the percentage of XX transgenic males increased on an F(1) background. For    the one transgene examined, Sry expression increased on an F(1) background. These results support a model in which delayed testis development is caused by the presence of particular DOM SRY protein isoforms and this, combined with insufficient    Sry expression, causes sex reversal. These results also indicate that at least one tda gene regulates Sry expression, possibly by directly binding to Sry regulatory regions.</p>

	]]>
</description>

<author>K H. Albrecht et al.</author>


</item>


<item>
<title> On the normalization of RNA equilibrium free energy to the length of the sequence.</title>
<link>http://mouseion.jax.org/stfb2000_2009/540</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/540</guid>
<pubDate>Tue, 08 May 2012 17:24:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is no universal definition of stability for RNA secondary structures. Here we present an approach that is based on normalization of the equilibrium free energy to the length of the sequence: a segment of RNA is said to be    stable if the ratio of the equilibrium free energy to the length of the segment is greater than a certain threshold value.  Discarding the segments whose normalized equilibrium free energies are smaller than the threshold allows us to view the    secondary structure at different levels of stability. Confined to only highly stable structures, the algorithm for secondary structure prediction admits a number of simplifications that make it computationally tractable for large sequences and    advantageous over most other methods on a genome-wide scale. This method was applied to the Caenorhabditis elegans genome to localize the regions that encode stable secondary structures. In particular, 36 of 56 previously reported micro-RNAs were    localized to 4% of the genome. A fraction of long (>or=400 nt) stable inverted repeats in the genomic sequence of C.elegans was found. Their distribution is very uneven, and skewed towards the ends of chromosomes. This method can be used for    genome-wide detection of transcription termination signals, putative micro-RNAs, and other regulatory elements that involve stable RNA secondary structures.</p>

	]]>
</description>

<author>D D. Pervouchine et al.</author>


</item>


<item>
<title> Graft-versus-host disease can be separated from graft-versus-lymphoma effects by control of lymphocyte trafficking with FTY720.</title>
<link>http://mouseion.jax.org/stfb2000_2009/539</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/539</guid>
<pubDate>Tue, 08 May 2012 17:24:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Graft-versus-host disease (GvHD) mediated by donor T cells recognizing host alloantigens is associated with beneficial graft-versus-tumor effects in recipients of allogeneic hematopoietic cell transplants. Since leukemias and    lymphomas reside largely within the lymphohematopoietic system, we have proposed that the desired graft-versus-leukemia or graft-versus-lymphoma effect can be separated from the complication of GvHD by confinement of the graft-versus-host    alloresponse to the lymphohematopoietic tissues. Since the new sphingosine-1-phosphate receptor agonist immunosuppressive drug FTY720 leads to trapping of T cells in secondary lymphoid tissues, we evaluated the possibility that this drug could    diminish GvHD, a disease involving epithelial target tissues, while permitting a beneficial alloresponse to take place within the lymphohematopoietic system, leading to graft-versus-lymphoma effects.  We demonstrate here that FTY720 markedly    reduces GvHD in a clinically relevant, haploidentical strain combination, while permitting antitumor effects against a T cell lymphoma of unshared host MHC haplotype to proceed unhindered. These results establish a potential new immunotherapeutic    approach to separating graft-versus-leukemia effects from GvHD.</p>

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</description>

<author>Y M. Kim et al.</author>


</item>


<item>
<title> Cell-specific mitotic defect and dyserythropoiesis associated with erythroid band 3 deficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/538</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/538</guid>
<pubDate>Tue, 08 May 2012 17:23:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Most eukaryotic cell types use a common program to regulate the process of cell division. During mitosis, successful partitioning of the genetic material depends on spatially coordinated chromosome movement and cell cleavage. Here    we characterize a zebrafish mutant, retsina (ret), that exhibits an erythroid-specific defect in cell division with marked dyserythropoiesis similar to human congenital dyserythropoietic anemia.  Erythroblasts from ret fish show binuclearity and    undergo apoptosis due to a failure in the completion of chromosome segregation and cytokinesis.  Through positional cloning, we show that the ret mutation is in a gene (slc4a1) encoding the anion exchanger 1 (also called band 3 and AE1), an    erythroid-specific cytoskeletal protein. We further show an association between deficiency in Slc4a1 and mitotic defects in the mouse. Rescue experiments in ret zebrafish embryos expressing transgenic slc4a1 with a variety of mutations show that    the requirement for band 3 in normal erythroid mitosis is mediated through its protein 4.1R-binding domains.  Our report establishes an evolutionarily conserved role for band 3 in erythroid-specific cell division and illustrates the concept of    cell-specific adaptation for mitosis.</p>

	]]>
</description>

<author>B H. Paw et al.</author>


</item>


<item>
<title> Glycerol regulates stratum corneum hydration in sebaceous gland deficient (asebia) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/537</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/537</guid>
<pubDate>Tue, 08 May 2012 17:23:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The only known function of human sebaceous glands is the provocation of acne. We assessed here whether sebum influences stratum corneum hydration or permeability barrier function in asebia J1 and 2 J mice, with profound sebaceous    gland hypoplasia. Asebia J1 mice showed normal permeability barrier homeostasis and extracellular lamellar membrane structures, but they displayed epidermal hyperplasia, inflammation, and decreased (>50%) stratum corneum hydration, associated    with a reduction in sebaceous gland lipids (wax diesters/monoesters, sterol esters). The triglyceride content of both asebia and control stratum corneum was low, consistent with high rates of triglyceride hydrolysis within the normal    pilosebaceous apparatus, despite high rates of triglyceride synthesis. Although a mixture of synthetic, sebum-like lipids (sterol/wax esters, triglycerides) did not restore normal stratum corneum hydration to asebia skin, topical glycerol, the    putative product of triglyceride hydrolysis in sebaceous glands, normalized stratum corneum hydration, and the glycerol content of asebia stratum corneum was 85% lower than in normal stratum corneum. In contrast, another potent endogenous    humectant (urea) did not correct the abnormality. The importance of glycerol generation from triglyceride in sebaceous glands for stratum corneum hydration was demonstrated further by (i) the absence of sebaceous-gland-associated lipase activity    in asebia mice, whereas abundant enzyme activity was present in the glands of control mice; and (ii) the inability of high concentrations of topical triglyceride to correct the hydration abnormality, despite the presence of abundant lipase    activity in asebia stratum corneum. These results show that sebaceous-gland-derived glycerol is a major contributor to stratum corneum hydration.</p>

	]]>
</description>

<author>J W. Fluhr et al.</author>


</item>


<item>
<title> Major Locus on Mouse Chromosome 17 and Minor Locus on Chromosome 9 are Linked with Alopecia Areata in C3H/HeJ Mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/536</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/536</guid>
<pubDate>Tue, 08 May 2012 17:23:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata is an autoimmune disease that targets actively growing (anagen) hair follicles in humans, mice, rats, dogs, horses, and cattle.  C3H/HeJ mice spontaneously develop alopecia areata from 5 mo of age and older in    females and later in males. Frequency of disease approached 20% in a colony by 18 mo of age. C57BL/6J mice do not develop alopecia areata.  A segregating F2 population of female mice (n=1096) was generated from crossing these two strains.    Alopecia areata (n=138) and clinically normal (n=214) mice were genotyped at 12 mo of age using 211 microsatellite probes. The peak logarithm of odds ratio score on mouse chromosome 17 (10.9) was around marker D17Mit134 at 16.9 cM from the    centromere. The mouse histocompatibility locus, H2, the mouse equivalent of human leukocyte antigen in humans, was a likely candidate. Twelve-month-old C3H.SW-H2b/SnJ mice (C3H/HeJ congenic mice in which the H2k purported susceptibility locus was    replaced with the H2b purported resistance locus) did not develop alopecia areata, supporting this locus as being important in alopecia areata. A suggestive linkage was also found on mouse Chromosome 9 (logarithm of odds ratio score 2.0) around    D9Mit206, 20 cM from the centromere. The interval on mouse Chromosome 17 contains several orthologous genes potentially associated with human alopecia areata.</p>

	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title> Notch signaling regulates left-right asymmetry determination by inducing Nodal expression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/535</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/535</guid>
<pubDate>Tue, 08 May 2012 17:22:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Generation of left-right asymmetry is an integral part of the establishment of the vertebrate body plan. Here we show that the Notch signaling pathway plays a primary role in the establishment of left-right asymmetry in mice by    directly regulating expression of the Nodal gene.  Embryos mutant for the Notch ligand Dll1 or doubly mutant for the Notch1 and Notch2 receptors exhibit multiple defects in left-right asymmetry.  Analysis of the enhancer regulating node-specific    Nodal expression revealed the presence of binding sites for the RBP-J protein, the primary transcriptional mediator of Notch signaling. Mutation of these sites destroyed the ability of this enhancer to direct node-specific gene expression in    transgenic mice. Our results demonstrate that Dll1-mediated Notch signaling is essential for generation of left-right asymmetry, and that the Notch pathway acts upstream of Nodal expression during left-right asymmetry determination in    mice.</p>

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</description>

<author>L T. Krebs et al.</author>


</item>


<item>
<title> By Altering Ocular Immune Privilege, Bone Marrow-derived Cells Pathogenically Contribute to DBA/2J Pigmentary Glaucoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/534</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/534</guid>
<pubDate>Tue, 08 May 2012 17:22:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pigment dispersion syndrome causes iris pigment release and often progresses to elevated intraocular pressure and pigmentary glaucoma (PG).  Because melanin pigment can have adjuvant like properties and because the Gpnmb gene,    which contributes to pigment dispersion in DBA/2J (D2) mice, is expressed in dendritic cells, we tested the hypothesis that ocular immune abnormalities participate in PG phenotypes. Strikingly, we show that D2 eyes exhibit defects of the normally    immunosuppressive ocular microenvironment including inability of aqueous humor to inhibit T cell activation, failure to support anterior chamber (AC)-associated immune deviation, and loss of ocular immune privilege. Histologic analysis    demonstrates infiltration of inflammatory leukocytes into the AC and their accumulation within the iris, whereas clinical indications of inflammation are typically very mild to undetectable. Importantly, some of these abnormalities precede    clinical indications of pigment dispersal, suggesting an early role in disease etiology. Using bone marrow chimeras, we show that lymphohematopoietic cell lineages largely dictate the progression of pigment dispersion, the ability of the eye to    support induction of AC-associated immune deviation, and the integrity of the blood/ocular barrier. These results suggest previously unsuspected roles for bone marrow-derived cells and ocular immune privilege in the pathogenesis of    PG.</p>

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</description>

<author>J S. Mo et al.</author>


</item>


<item>
<title> Novel anterior segment phenotypes resulting from forkhead gene alterations: evidence for cross-species conservation of function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/533</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/533</guid>
<pubDate>Tue, 08 May 2012 17:22:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Mutations in murine and human versions of an ancestrally related gene usually result in similar phenotypes. However, interspecies differences exist, and in the case of two forkhead transcription factor genes (FOXC1 and    FOXC2), these differences include corneal or anterior segment phenotypes, respectively. This study was undertaken to determine whether such discrepancies provide an opportunity for identifying novel human-murine ocular phenotypes. METHODS: Four    pedigrees with early-onset glaucoma phenotypes secondary to segmental chromosomal duplications or deletions encompassing FOXC1 and 18 individuals from 9 FOXC2 mutation pedigrees underwent detailed ocular phenotyping. Subsequently, mice with    mutations in Foxc1 or a related forkhead gene, Foxe3, were assessed for features of the human phenotypes. RESULTS: A significant increase in central corneal thickness was present in affected individuals from the segmental duplication pedigrees    compared with their unaffected relatives (mean increase 13%, maximum 35%, P < 0.05). Alterations in corneal thickness were present in mice heterozygous and homozygous for Foxe3 mutations but neither in Foxc1 heterozygotes nor the small human    segmental deletion pedigree. Mutations in FOXC2 resulted in ocular anterior segment anomalies. These were more severe and prevalent with mutations involving the forkhead domain. CONCLUSIONS: Normal corneal development is dependent on the precise    dose and levels of activity of certain forkhead transcription factors. The altered corneal thickness attributable to increased forkhead gene dosage is particularly important, because it may affect the clinical management of certain glaucoma    subtypes and lead to excessive treatment. The FOXC1 and Foxe3 data, taken together with the novel ocular phenotypes of FOXC2 mutations, highlight the remarkable cross-species conservation of function among forkhead genes.</p>

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</description>

<author>O J. Lehmann et al.</author>


</item>


<item>
<title> Intrinsic requirement for zinc finger transcription factor Gfi-1 in neutrophil differentiation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/532</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/532</guid>
<pubDate>Tue, 08 May 2012 17:21:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>We report essential roles of zinc finger transcription factor Gfi-1 in myeloid development. Gene-targeted Gfi-1(-/-) mice lack normal neutrophils and are highly susceptible to abscess formation by gram-positive bacteria.  Arrested,    morphologically atypical, Gr1(+)Mac1(+) myeloid cells expand with age in the bone marrow. RNAs encoding primary but not secondary or tertiary neutrophil (granulocyte) granule proteins are expressed. The atypical Gr1(+)Mac1(+) cell population    shares characteristics of both the neutrophil and macrophage lineages and exhibits phagocytosis and respiratory burst activity. Reexpression of Gfi-1 in sorted Gfi-1(-/-) progenitors ex vivo rescues neutrophil differentiation in response to    G-CSF. Thus, Gfi-1 not only promotes differentiation of neutrophils but also antagonizes traits of the alternate monocyte/macrophage program.</p>

	]]>
</description>

<author>H Hock et al.</author>


</item>


<item>
<title> Insulin-like growth factor regulates peak bone mineral density in mice by both growth hormone-dependent and -independent mechanisms.</title>
<link>http://mouseion.jax.org/stfb2000_2009/531</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/531</guid>
<pubDate>Tue, 08 May 2012 17:21:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>To evaluate the relative contribution of the GH/IGF axis to the development of peak bone mineral density (BMD), we measured skeletal changes in IGF-I knockout (KO), IGF-II KO, and GH-deficient lit/lit mice and their corresponding    control mice at d 23 (prepubertal), 31 (pubertal), and 56 (postpubertal) in the entire femur by dual energy x-ray absorptiometry and in the mid-diaphysis by peripheral quantitative computed tomography. Lack of growth factors resulted in different    degrees of failure of skeletal growth depending on the growth period and the growth factor involved. At d 23, femoral length, size, and BMD were reduced by 25-40%, 15-17%, and 8-10%, respectively, in mice deficient in IGF-I, IGF-II, and GH    compared with the control mice. During puberty, BMD increased by 40% in control mice and by 15% in IGF-II KO and GH-deficient mice, whereas it did not increase in the IGF-I KO mice. Disruption of IGF-I, but not IGF-II, completely prevented the    periosteal expansion that occurs during puberty, whereas it was reduced by 50% in GH-deficient mice.  At d 56, femoral length, size, and BMD were reduced by 40-55%, 11-18%, and 25-32%, respectively, in mice deficient in IGF-I, IGF-II, and GH    compared with the control mice. Our data demonstrate that: 1) mice deficient in IGF-I exhibit a greater impairment in bone accretion than mice deficient in IGF-II or GH; 2) GH/IGF-I, but not IGF-II, is critical for puberty-induced bone growth;    and 3) IGF-I effects on bone accretion during prepuberty are mediated predominantly via mechanisms independent of GH, whereas during puberty they are mediated via both GH-dependent and GH-independent mechanisms.</p>

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</description>

<author>S Mohan et al.</author>


</item>


<item>
<title> Quantitative trait loci that determine lipoprotein cholesterol levels in DBA/2J and CAST/Ei inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/530</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/530</guid>
<pubDate>Tue, 08 May 2012 17:20:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>To investigate genetic contributions to individual variations of lipoprotein cholesterol concentrations, we performed quantitative trait locus/loci (QTL) analyses of an intercross of CAST/Ei and DBA/2J inbred mouse strains after    feeding a high-cholesterol cholic acid diet for 10 weeks. In total, we identified four QTL for HDL cholesterol. Three of these were novel and were named Hdlq10 [20 centimorgans (cM), chromosome 4], Hdlq11 (48 cM, chromosome 6), and Hdlq12 (68 cM,    chromosome 6). The fourth QTL, Hdl1 (48 cM, chromosome 2), confirmed a locus discovered previously using a breeding cross that employed different inbred mouse strains. In addition, we identified one novel QTL for total and non-HDL cholesterol (8    cM, chromosome 9) that we named Chol6. Hdlq10, colocalized with a mutagenesis-induced point mutation (Lch), also affecting HDL. We provide molecular evidence for Abca1 as the gene underlying Hdlq10 and Ldlr as the gene underlying Chol6 that,    coupled with evidence generated by other researchers using knockout and transgenic models, causes us to postulate that polymorphisms of these genes, different from the mutations leading to Tangier's disease and familial hypercholesterolemia,    respectively, are likely primary genetic determinants of quantitative variation of lipoprotein levels in mice and, by orthology, in the human population.</p>

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</description>

<author>M A. Lyons et al.</author>


</item>


<item>
<title> Delayed occurrence of fatal neoplastic diseases in ames dwarf mice: correlation to extended longevity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/529</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/529</guid>
<pubDate>Tue, 08 May 2012 17:20:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ames dwarf mice have drawn much attention in aging research because of their marked life extension. Studies demonstrate that some of the physiological characteristics of Ames dwarf mice are similar to those of dietary restricted    mice. Because dietary restriction has been shown to suppress and/or delay the occurrence of various age-related diseases, we investigated age-related pathological changes in Ames dwarf mice. We observed Ames dwarf mice to have a delayed    occurrence of presumably fatal neoplastic disease compared with their normal siblings. In addition to the delayed occurrence, we found that the incidence of presumably fatal adenocarcinoma in lung was significantly lower in Ames dwarf mice than    for their normal siblings. The delayed occurrence of total neoplastic lesions and reduced incidence of adenocarcinoma in lung possibly could be attributed to the retardation of tumor development by changes in the levels of growth hormone and    insulin-like growth factor-1, and thereby be a major contributing factor to the extended life span observed in these mice.</p>

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</description>

<author>Y Ikeno et al.</author>


</item>


<item>
<title> Desmoglein 4 in hair follicle differentiation and epidermal adhesion.  Evidence from inherited hypotrichosis and acquired pemphigus vulgaris.</title>
<link>http://mouseion.jax.org/stfb2000_2009/528</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/528</guid>
<pubDate>Tue, 08 May 2012 17:20:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cell adhesion and communication are interdependent aspects of cell behavior that are critical for morphogenesis and tissue architecture. In the skin, epidermal adhesion is mediated in part by specialized cell-cell junctions known    as desmosomes, which are characterized by the presence of desmosomal cadherins, known as desmogleins and desmocollins. We identified a cadherin family member, desmoglein 4, which is expressed in the suprabasal epidermis and hair follicle. The    essential role of desmoglein 4 in skin was established by identifying mutations in families with inherited hypotrichosis, as well as in the lanceolate hair mouse. We also show that DSG4 is an autoantigen in pemphigus vulgaris. Characterization of    the phenotype of naturally occurring mutant mice revealed disruption of desmosomal adhesion and perturbations in keratinocyte behavior. We provide evidence that desmoglein 4 is a key mediator of keratinocyte cell adhesion in the hair follicle,    where it coordinates the transition from proliferation to differentiation.</p>

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</description>

<author>A Kljuic et al.</author>


</item>


<item>
<title> An immunodominant minor histocompatibility alloantigen that initiates corneal allograft rejection.</title>
<link>http://mouseion.jax.org/stfb2000_2009/527</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/527</guid>
<pubDate>Tue, 08 May 2012 17:19:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Murine orthotopic corneal allografts experience immune privilege and have good survival as compared with skin allografts.  However, privilege is not complete, and some grafts are still rejected.  Unexpectedly, corneas    expressing minor histocompatibility (H) alloantigens are rejected at a higher rate than major histocompatibility complex (MHC) disparate grafts. We hypothesize that certain immunodominant minor H alloantigens are extremely immunogenic when    expressed in corneal tissue, terminate ocular immune privilege, and initiate corneal allograft rejection. METHODS AND RESULTS: Corneal allograft survival and the role of CD4+ T cells and CD8+ T cells were examined in corneal transplants that    expressed genetically defined minor H3 alloantigens. The H3 locus contains at least two minor H genes. H3a is presented by MHC class I and recognized exclusively by CD8+ T cells. H3b is presented by class II and recognized exclusively by CD4+ T    cells. Congenic strains that differ from C57BL/10 at (1) H3a, (2) H3b, or (3) H3a+H3b were used for orthotopic corneal and skin transplants. Donor corneas expressing either H3a or H3a+H3b experienced immune privilege and survived longer than skin    allografts. By contrast, donor corneas expressing H3b (recognized by CD4+ T cells) experienced vigorous rejection and were eliminated faster than skin allografts.  CONCLUSION: There are minor H alloantigens that terminate ocular immune privilege    and initiate corneal allograft rejection. These minor H alloantigens are more immunogenic when expressed in corneal tissue than when they are expressed in skin allografts.</p>

	]]>
</description>

<author>Z Haskova et al.</author>


</item>


<item>
<title>Multiple loci within the major histocompatibility complex confer risk of psoriasis</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1033</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1033</guid>
<pubDate>Tue, 08 May 2012 17:19:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bing-Jian Feng et al.</author>


</item>


<item>
<title> R/qtl: QTL mapping in experimental crosses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/526</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/526</guid>
<pubDate>Tue, 08 May 2012 17:19:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Summary: R/qtl is an extensible, interactive environment for mapping quantitative trait loci (QTLs) in experimental populations derived from inbred lines. It is implemented as an add-on package for the freely-available statistical    software, R, and includes functions for estimating genetic maps, identifying genotyping errors, and performing single-QTL and two-dimensional, two-QTL genome scans by multiple methods, with the possible inclusion of covariates. Availability: The    package is freely available at http://www.biostat.jhsph.edu/~kbroman/qtl. Contact: kbroman@jhsph.edu</p>

	]]>
</description>

<author>K W. Broman et al.</author>


</item>


<item>
<title> The H4(b) Minor Histocompatibility Antigen Is Caused by a Combination of Genetically Determined and Posttranslational Modifications.</title>
<link>http://mouseion.jax.org/stfb2000_2009/525</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/525</guid>
<pubDate>Tue, 08 May 2012 17:19:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Minor histocompatibility (H) Ag disparities result in graft-vs-host disease and chronic solid allograft rejection in MHC-identical donor-recipient combinations. Minor H Ags are self protein-derived peptides presented by MHC class I    molecules. Most arise as a consequence of allelic variation in the bound peptide (p) that results in TCR recognizing the p/MHC as foreign. We used a combinational peptide screening approach to identify the immune dominant H2K(b)-restricted    epitope defining the mouse H4(b) minor H Ag. H4(b) is a consequence of a P3 threonine to isoleucine change in the MHC-bound peptide derived from epithelial membrane protein-3. This allelic variation also leads to phosphorylation of the H4(b) but    not the H4(a) epitope. Further, ex vivo CD8(+) T lymphocytes bind phosphorylated Ag tetramers with high efficiency. Although we document the above process in the minor H Ag system, posttranslational modifications made possible by subtle amino    acid changes could also contribute to immunogenicity and immune dominance in tumor immunotherapeutic settings.</p>

	]]>
</description>

<author>R Yadav et al.</author>


</item>


<item>
<title> Proapoptotic BID is required for myeloid homeostasis and tumor suppression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/524</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/524</guid>
<pubDate>Tue, 08 May 2012 17:18:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>The proper expansion and contraction of hematopoietic cells requires tight regulation of cell death. BID, a "BH3-only" molecule, amplifies death receptor signals connecting the extrinsic to intrinsic pathways by triggering the    mitochondrial pathway of apoptosis. Bid-deficient mice, as they age, spontaneously develop a myeloproliferative disorder, which progresses from myeloid hyperplasia to a fatal, clonal malignancy closely resembling chronic myelomonocytic leukemia    (CMML). Thus, an apoptotic defect can result in myeloid leukemogenesis. Premalignant Bid-/- myeloid precursor cells are resistant to death receptor-induced apoptosis.  Furthermore, a competitive reconstitution assay demonstrates that    Bid-deficient long-term repopulating cells give rise to expanded myelomonocytic cells in vivo. Surprisingly, a single BH3-only molecule operating in the extrinsic death receptor pathway proved essential in vivo for physiologic cell death required    to maintain myeloid homeostasis.  Moreover, progression to CMML indicates that an upstream BH3-only molecule, BID, is required to suppress tumorigenesis.</p>

	]]>
</description>

<author>S S. Zinkel et al.</author>


</item>


<item>
<title> Zygote arrest 1 (Zar1) is a novel maternal-effect gene critical for the oocyte-to-embryo transition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/523</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/523</guid>
<pubDate>Tue, 08 May 2012 17:18:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The female gamete (the oocyte) serves the distinct purpose of transmitting the maternal genome and other maternal factors that are critical for post-ovulation events. Through the identification and characterization of    oocyte-specific factors, we are beginning to appreciate the diverse functions of oocytes in ovarian folliculogenesis, fertilization and embryogenesis. To understand these processes further, we identified genes called zygote arrest 1 (Zar1 and    ZAR1 in mouse and human, respectively) as novel oocyte-specific genes. These encode proteins of 361 amino acids and 424 amino acids, respectively, which share 59% amino-acid identity and an atypical plant homeo-domain (PHD) motif. Although    Zar1-null (Zar1(-/-)) mice are viable and grossly normal, Zar1(-/-) females are infertile.  Ovarian development and oogenesis through the early stages of fertilization are evidently unimpaired, but most embryos from Zar1(-/-) females arrest at    the one-cell stage. Distinct pronuclei form and DNA replication initiates, but the maternal and paternal genomes remain separate in arrested zygotes. Fewer than 20% of the embryos derived from Zar1(-/-) females progress to the two-cell stage and    show marked reduction in the synthesis of the transcription-requiring complex, and no embryos develop to the four-cell stage. Thus, Zar1 is the first identified oocyte-specific maternal-effect gene that functions at the oocyte-to-embryo    transition and, as such, offers new insights into the initiation of embryonic development and fertility control in mammals.</p>

	]]>
</description>

<author>X Wu et al.</author>


</item>


<item>
<title> Ru2 and Ru encode mouse orthologs of the genes mutated in human Hermansky-Pudlak syndrome types 5 and 6.</title>
<link>http://mouseion.jax.org/stfb2000_2009/522</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/522</guid>
<pubDate>Tue, 08 May 2012 17:18:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hermansky-Pudlak syndrome (HPS) is a genetically heterogeneous disease involving abnormalities of melanosomes, platelet dense granules and lysosomes. Here we have used positional candidate and transgenic rescue approaches to    identify the genes mutated in ruby-eye 2 and ruby-eye mice (ru2 and ru, respectively), two 'mimic' mouse models of HPS. We also show that these genes are orthologs of the genes mutated in individuals with HPS types 5 and 6, respectively, and that    their protein products directly interact. Both genes are previously unknown and are found only in higher eukaryotes, and together represent a new class of genes that have evolved in higher organisms to govern the synthesis of highly specialized    lysosome-related organelles.</p>

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</description>

<author>Q Zhang et al.</author>


</item>


<item>
<title> Necropsy procedures with histopathologic evaluation of tissues are fundamentally the same regardless of species.</title>
<link>http://mouseion.jax.org/stfb2000_2009/521</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/521</guid>
<pubDate>Tue, 08 May 2012 17:18:05 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J P. Sundberg</author>


</item>


<item>
<title> Evidence for a skeletal mechanosensitivity gene on mouse chromosome 4.</title>
<link>http://mouseion.jax.org/stfb2000_2009/520</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/520</guid>
<pubDate>Tue, 08 May 2012 17:17:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Differences in skeletal mechanical adaptation between C3H/HeJ (C3H) and C57BL/6J (B6) mouse strains suggest that these mice can be used to elucidate the genes involved in mechanosensitivity regulation. The C3H and B6 skeletons also    differ in bone size, and several quantitative trait loci (QTL) have been mapped for bone size. We hypothesized that genes controlling bone size (external diameter) might exert their effect by influencing mechanosensitivity. The hypothesis was    tested by applying mechanical loads to the ulnae of the B6.C3H-4T (4T) congenic mouse strain, which is genetically 98.4% B6 and carries the C3H chromosome 4 (Chr. 4) QTL genomic DNA. Mechanical strain was measured at the midshaft ulna in separate    calibration animals. 4T mice were significantly more responsive to mechanical stimulation than B6 control mice, as assessed by changes in bone geometry and fluorochrome-derived bone formation rates. Bone formation rates were also greater in the    ulnae and femora of 6-wk-old 4T mice engaged in normal cage activity compared with age-matched B6 mice.  Collectively, the results might explain why 4T mice have wider femora and ulnae than do B6 control mice and suggest that mouse Chr. 4    contains a genetic locus that modulates the mechanosensitivity of bone tissue.</p>

	]]>
</description>

<author>A G. Robling et al.</author>


</item>


<item>
<title> Contribution of Fas to diabetes development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/519</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/519</guid>
<pubDate>Tue, 08 May 2012 17:17:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fas (Tnfrsf6, Apo-1, CD95) is a death receptor involved in apoptosis induced in many cell types. Fas have been shown to be expressed by insulin-producing beta cells in mice and humans. However, the importance of Fas in the    development of autoimmune diabetes remains controversial. To further evaluate the importance of Fas in pathogenesis of diabetes, we generated NOD mice (nonobese diabetic mice developing spontaneous autoimmune diabetes) with beta cell-specific    expression of a dominant-negative point mutation in a death domain of Fas, known as lpr(cg) or Fas(cg). Spontaneous diabetes was significantly delayed in NOD mice expressing Fas(cg), and the effect depended on the expression level of the    transgene. However, Fas(cg)-bearing mice were still sensitive to diabetes transferred by splenocytes from overtly diabetic NOD mice. At the same time, Fas(cg) expression did neutralize the accelerating effect of transgenic Fas-ligand expressed by    the same beta cells. Thus, both Fas-dependent and -independent mechanisms are involved in beta cell destruction, but interference with the Fas pathway early in disease development may retard or prevent diabetes progression.</p>

	]]>
</description>

<author>A Y. Savinov et al.</author>


</item>


<item>
<title> Unique resistance of I/LnJ mice to a retrovirus is due to sustained interferon gamma-dependent production of virus-neutralizing antibodies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/518</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/518</guid>
<pubDate>Tue, 08 May 2012 17:17:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Selection of immune escape variants impairs the ability of the immune system to sustain an efficient antiviral response and to control retroviral infections. Like other retroviruses, mouse mammary tumor virus (MMTV) is not    efficiently eliminated by the immune system of susceptible mice. In contrast, MMTV-infected I/LnJ mice are capable of producing IgG2a virus-neutralizing antibodies, sustain this response throughout their life, and secrete antibody-coated virions    into the milk, thereby preventing infection of their progeny. Antibodies were produced in response to several MMTV variants and were cross-reactive to them.  Resistance to MMTV infection was recessive and was dependent on interferon (IFN)-gamma    production, because I/LnJ mice with targeted deletion of the INF-gamma gene failed to produce any virus-neutralizing antibodies. These findings reveal a novel mechanism of resistance to retroviral infection that is based on a robust and sustained    IFN-gamma-dependent humoral immune response.</p>

	]]>
</description>

<author>A Purdy et al.</author>


</item>


<item>
<title> Paralytic Autoimmune Myositis Develops in Nonobese Diabetic Mice Made Th1 Cytokine-Deficient by Expression of an IFN-gamma Receptor beta-Chain Transgene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/517</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/517</guid>
<pubDate>Tue, 08 May 2012 17:16:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nonobese diabetic (NOD) mice and some human type 1 diabetes (T1D) patients manifest low to high levels of other autoimmune pathologies. Skewing their cytokine production from a Th1 (primarily IFN-gamma) to a Th2 (primarily IL-4 and    IL-10) pattern is a widely proposed approach to dampen the pathogenicity of autoreactive diabetogenic T cells. However, it is important that altered cytokine balances not enhance any other autoimmune proclivities to dangerous levels. Murine CD4 T    cells are characterized by a reciprocal relationship between the production of IFN-gamma and expression of the beta-chain component of its receptor (IFN-gammaRB).  Thus, NOD mice constitutively expressing a CD2 promoter-driven IFN-gammaRB    transgene in all T cells are Th1-deficient. Unexpectedly, NOD.IFN-gammaRB Tg mice were found to develop a lethal early paralytic syndrome induced by a CD8 T cell-dependent autoimmune-mediated myositis. Furthermore, pancreatic insulitis levels    were not diminished in 9-wk-old NOD.IFN-gammaRB Tg females, and overt T1D developed in the few that survived to an older age. Autoimmune-mediated myositis is only occasionally detected in standard NOD mice. Hence, some manipulations diminishing    Th1 responses can bring to the forefront what are normally secondary autoimmune pathologies in NOD mice, while also failing to dependably abrogate pancreatic beta cell destruction. This should raise a cautionary note when considering the use of    protocols that induce alterations in cytokine balances as a means of blocking progression to overt T1D in at-risk humans.</p>

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</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title> The MHC Class I-Like IgG Receptor Controls Perinatal IgG Transport, IgG Homeostasis, and Fate of IgG-Fc-Coupled Drugs.</title>
<link>http://mouseion.jax.org/stfb2000_2009/516</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/516</guid>
<pubDate>Tue, 08 May 2012 17:16:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abs of the IgG isotype are efficiently transported from mother to neonate and have an extended serum t(1/2) compared with Abs of other isotypes.  Circumstantial evidence suggests that the MHC class I-related protein, the neonatal    FcR (FcRn), is the FcR responsible for both in vivo functions. To understand the phenotypes imposed by FcRn, we produced and analyzed mice with a defective FcRn gene. The results provide direct evidence that perinatal IgG transport and protection    of IgG from catabolism are mediated by FcRn, and that the latter function is key to IgG homeostasis, essential for generating a potent IgG response to foreign Ags, and the basis of enhanced efficacy of Fc-IgG-based therapeutics. FcRn is therefore    a promising therapeutic target for enhancing protective humoral immunity, treating autoimmune disease, and improving drug efficacy.</p>

	]]>
</description>

<author>D C. Roopenian et al.</author>


</item>


<item>
<title> Phenotype-based identification of mouse chromosome instability mutants.</title>
<link>http://mouseion.jax.org/stfb2000_2009/515</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/515</guid>
<pubDate>Tue, 08 May 2012 17:16:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is increasing evidence that defects in DNA double-strand-break (DSB) repair can cause chromosome instability, which may result in cancer. To identify novel DSB repair genes in mice, we performed a phenotype-driven mutagenesis    screen for chromosome instability mutants using a flow cytometric peripheral blood micronucleus assay. Micronucleus levels were used as a quantitative indicator of chromosome damage in vivo. Among offspring derived from males mutagenized with the    germline mutagen N-ethyl-N-nitrosourea (ENU), we identified a recessive mutation conferring elevated levels of spontaneous and radiation- or mitomycin C-induced micronuclei. This mutation, named chaos1 (chromosome aberration occurring    spontaneously 1), was genetically mapped to a 1.3-Mb interval on chromosome 16 containing Polq, encoding DNA polymerase theta. We identified a nonconservative mutation in the ENU-derived allele, making it a strong candidate for chaos1. POLQ is    homologous to Drosophila MUS308, which is essential for normal DNA interstrand crosslink repair and is unique in that it contains both a helicase and a DNA polymerase domain.  While cancer susceptibility of chaos1 mutant mice is still under    investigation, these data provide a practical paradigm for using a forward genetic approach to discover new potential cancer susceptibility genes using the surrogate biomarker of chromosome instability as a screen.</p>

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</description>

<author>N Shima et al.</author>


</item>


<item>
<title> Genetic models in applied physiology: selected contribution: effects of spaceflight on immunity in the C57BL/6 mouse. I. Immune population distributions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/514</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/514</guid>
<pubDate>Tue, 08 May 2012 17:15:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>There are several aspects of the spaceflight environment that may lead to changes in immunity: mission-related psychological stress, radiation, and changes in gravity. On December 5, 2001, the space shuttle Endeavor launched for a    12-day mission to examine these effects on C57BL/6 mice for the first time. On their return, assays were performed on the spleen, blood, and bone marrow. In response to flight, there were no significant differences in the general circulating    leukocyte proportions. In contrast, there was an increase in splenic lymphocyte percentages, with a corresponding decrease in granulocytes. There was an overall shift in splenic lymphocytes away from T cells toward B cells, and a decrease in the    CD4-to-CD8 ratios due to a decrease in T helpers. In contrast, there were proportional increases in bone marrow T cells, with decreases in B cells. Although the blast percentage and count were decreased in flight mice, the CD34(+) population was    increased. The data were more consistent with a shift in bone marrow populations rather than a response to changes in the periphery. Many of the results are similar to those using other models. Clearly, spaceflight can influence immune parameters    ranging from hematopoiesis to mature leukocyte mechanisms.</p>

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</description>

<author>M J. Pecaut et al.</author>


</item>


<item>
<title> NOD congenic mice genetically protected from autoimmune diabetes remain resistant to transplantation tolerance induction.</title>
<link>http://mouseion.jax.org/stfb2000_2009/513</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/513</guid>
<pubDate>Tue, 08 May 2012 17:15:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The loss of self-tolerance leading to autoimmune type 1 diabetes in the NOD mouse model involves at least 19 genetic loci. In addition to their genetic defects in self-tolerance, NOD mice resist peripheral transplantation tolerance    induced by costimulation blockade using donor-specific transfusion and anti-CD154 antibody. Hypothesizing that these two abnormalities might be related, we investigated whether they could be uncoupled through a genetic approach.    Diabetes-resistant NOD and C57BL/6 stocks congenic for various reciprocally introduced Idd loci were assessed for their ability to be tolerized. Surprisingly, in NOD congenic mice that are almost completely protected from diabetes, costimulation    blockade failed to prolong skin allograft survival. In reciprocal C57BL/6 congenic mice with NOD-derived Idd loci, skin allograft survival was readily prolonged by costimulation blockade. These data indicate that single or multiple combinations    of evaluated Idd loci that dramatically reduce diabetes frequency do not correct resistance to peripheral transplantation tolerance induced by costimulation blockade. We suggest that mechanisms controlling autoimmunity and transplantation    tolerance in NOD mice are not completely overlapping and are potentially distinct, or that the genetic threshold for normalizing the transplantation tolerance defect is higher than that for preventing autoimmune diabetes.</p>

	]]>
</description>

<author>T Pearson et al.</author>


</item>


<item>
<title> Slug expression during organogenesis in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/512</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/512</guid>
<pubDate>Tue, 08 May 2012 17:15:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The vertebrate Slug gene encodes a zinc finger-containing transcriptional repressor. Here we report expression of the mouse Slug gene during organogenesis and late fetal development using histochemical detection of    beta-galactosidase expressed from a targeted Slug(lacZ) knock-in allele.  The Slug gene is highly expressed in the mesenchymal or stromal component of numerous organs. It is also highly expressed in craniofacial mesenchyme, in bone of both    mesodermal and neural crest origin, and in the outflow tract and the endocardial cushions of the heart. Anat Rec Part A 271A:189-191, 2003.</p>

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</description>

<author>K F. Oram et al.</author>


</item>


<item>
<title> One Hundred Years of Mouse Genetics. An intellectual history. i. the classical period (1902-1980).</title>
<link>http://mouseion.jax.org/stfb2000_2009/511</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/511</guid>
<pubDate>Tue, 08 May 2012 17:14:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K Paigen</author>


</item>


<item>
<title> Genetic models in applied physiology: selected contribution: effects of spaceflight on immunity in the C57BL/6 mouse. II. Activation, cytokines, erythrocytes, and platelets.</title>
<link>http://mouseion.jax.org/stfb2000_2009/510</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/510</guid>
<pubDate>Tue, 08 May 2012 17:14:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>This portion of the study quantified the effects of a 12-day space shuttle mission (Space Transport System-108/UF-1) on body and lymphoid organ masses, activation marker expression, cytokine secretion, and erythrocyte and    thrombocyte characteristics in C57BL/6 mice. Animals in flight (Flt group) had 10-12% lower body mass compared with ground controls housed either in animal enclosure modules or under standard vivarium conditions (P < 0.001) and the smallest    thymus and spleen masses. Percentages of CD25(+) lymphocytes, CD3(+)/CD25(+) T cells, and NK1.1(+)/CD25(+) natural killer cells from Flt mice were higher compared with both controls (P < 0.05). In contrast, CD71 expression was depressed in the    Flt and animal enclosure module control mice compared with vivarium control animals (P < 0.001). Secretion of interferon-gamma, IL-2, and IL-4, but not tumor necrosis factor-alpha and IL-5, by splenocytes from Flt mice was decreased relative to    either one or both ground controls (P < 0.05). Flt mice also had high red blood cell and thrombocyte counts compared with both sets of controls; low red blood cell volume and distribution width, percentage of reticulocytes, and platelet volume    were also noted (P < 0.05) and were consistent with dehydration. These data indicate that relatively short exposure to the spaceflight environment can induce profound changes that may become significant during long-term space    missions.</p>

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</description>

<author>D S. Gridley et al.</author>


</item>


<item>
<title> Overlapping deletions define novel embryonic lethal loci in the mouse t complex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/509</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/509</guid>
<pubDate>Tue, 08 May 2012 17:14:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Summary: The t complex region of mouse chromosome 17 contains genetic information critical for embryonic development. To identify and map loci required for normal embryogenesis, a set of overlapping deletions (D17Aus9(df10J),    D17Aus9(df12J), and D17Aus9(df13J)) surrounding the D17Aus9 locus and one encompassing the T locus, Del(17)T(7J), were bred in various combinations and the consequences of nullizygosity in overlapping regions were examined. The results indicated    that there are at least two functional units within 1 cM of D17Aus9. l17J1 is a peri-implantation lethal mutation within the region deleted in D17Aus9(df13J), whereas l17J2 is a later-acting lethal defined by the region of overlap between    Del(17)T(7J) and D17Aus9(df12J). Del(17)T(7J)/D17Aus9(df12J) embryos die around 10.5 dpc. The development of the mutant embryos is characterized by lack of axial rotation, an abnormal notochord structure, and a ballooning pericardium. These    studies demonstrate the value of overlapping deletion complexes, as opposed to individual deletion complexes, for the identification, mapping, and analysis of genes required for embryonic development. genesis 35:133-142, 2003.</p>

	]]>
</description>

<author>H H. Chao et al.</author>


</item>


<item>
<title> Continuous infusion of endostatin inhibits differentiation, mobilization, and clonogenic potential of endothelial cell progenitors.</title>
<link>http://mouseion.jax.org/stfb2000_2009/508</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/508</guid>
<pubDate>Tue, 08 May 2012 17:14:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: We investigated the effect of endostatin on differentiation, mobilization, and clonogenic potential of circulating endothelial cell (EC) progenitors, and whether the effect of endostatin was improved by continuous infusion    (CI) versus bolus administration. EXPERIMENTAL DESIGN: Four-color flow cytometry and clonogenic EC cultures were used to study EC progenitors in tumor-free mice, tumor-bearing immunodeficient mice, and immunodeficient mice xenotransplanted with    human bone marrow (BM) cells.  RESULTS: Endostatin significantly reduced the number of circulating EC progenitors in tumor-free BALB/c mice. The effect of endostatin on EC progenitors was enhanced significantly in mice treated with CI drug    treatment. When immunodeficient mice xenotransplanted with human BM cells were treated with CI of endostatin we observed a significant decrease in the engraftment and differentiation of human BM-derived EC progenitors.  Numbers of circulating EC    progenitors increased 7-fold in immunodeficient mice bearing human lymphoma. In this preclinical model, treatment with CI of endostatin inhibited host murine EC progenitor mobilization and human tumor growth. Furthermore, the clonogenic potential    of EC progenitors was impaired severely. CONCLUSIONS: Endostatin is a potent inhibitor of the mobilization and clonogenic potential of human and murine EC progenitors, and its preclinical activity is increased significantly in CI compared with    bolus administration. These observations might be useful in the design of future clinical trials.</p>

	]]>
</description>

<author>M Capillo et al.</author>


</item>


<item>
<title> Curly bare (cub), a new mouse mutation on chromosome 11 causing skin and hair abnormalities, and a modifier gene (mcub) on chromosome 5.</title>
<link>http://mouseion.jax.org/stfb2000_2009/507</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/507</guid>
<pubDate>Tue, 08 May 2012 17:13:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the outcrossing of a new recessive mouse mutation causing hair loss, a new wavy-coated phenotype appeared. The two distinct phenotypes were shown to be alternative manifestations of the same gene mutation and attributable to a    single modifier locus. The new mutation, curly bare (cub), was mapped to distal Chr 11 and the modifier (mcub) was mapped to Chr 5. When homozygous for the recessive mcub allele, cub/cub mice appear hairless. A single copy of the dominant Mcub    allele confers a full, curly coat in cub/cub mice. Reciprocal transfer of full-thickness skin grafts between mutant and control animals showed that the skin phenotype was tissue autonomous. The hairless cub/cub mcub/mcub mice show normal contact    sensitivity responses to oxazolone. The similarity of the wavy coat phenotype to those of Tgfa and Egfr mutations and the map positions of cub and mcub suggest candidate genes that interact in the EGF receptor signal transduction    pathway.</p>

	]]>
</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title> Dp1 is required for extra-embryonic development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/506</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/506</guid>
<pubDate>Tue, 08 May 2012 17:13:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Release of E2F1/DP1 heterodimers from repression mediated by the retinoblastoma tumor suppressor (pRB) triggers cell cycle entry into S phase, suggesting that E2F1 and DP1 proteins must act in unison, either to facilitate or to    suppress cell-cycle progression. In stark contrast to the milder phenotypes that result from inactivation of E2Fs, we report that loss of Dp1 leads to death in utero because of the failure of extra-embryonic development. Loss of Dp1 compromises    the trophectoderm-derived tissues - specifically, the expansion of the ectoplacental cone and chorion, and endoreduplication in trophoblast giant cells. Inactivation of p53 is unable to rescue the Dp1-deficient embryonic lethality. Thus, DP1 is    absolutely required for extra-embryonic development and consequently embryonic survival, consistent with E2F/DP1 normally acting to promote growth in vivo.</p>

	]]>
</description>

<author>M J. Kohn et al.</author>


</item>


<item>
<title> A revised protocol for in vitro development of mouse oocytes from primordial follicles dramatically improves their developmental competence.</title>
<link>http://mouseion.jax.org/stfb2000_2009/505</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/505</guid>
<pubDate>Tue, 08 May 2012 17:13:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The objective of this study was to improve the conditions for oocyte development in vitro beginning with the primordial follicles of newborn mice. Previous studies showed that oocytes competent of meiotic maturation, fertilization,    and preimplantation could develop in vitro from primordial follicles. However, the success rates were low and only one live offspring was produced (0.5% of embryos transferred). A revised protocol was compared with the original protocol using    oocyte maturation and preimplantation development as end points. The percentage of oocytes maturing to metaphase II and developing to the blastocyst stage was significantly improved using the revised protocol. In addition, we compared the    production of offspring from two-cell stage embryos derived from in vitro-grown and in vivo-grown oocytes. Of 1160 transferred two-cell stage embryos derived from in vitro-grown oocytes, 66 (5.7%) developed to term and 7 pups (10.6%) died at    birth. The remaining 59 pups (27 females, 32 males) survived to adulthood. By comparison, of 437 transferred two-cell stage embryos derived from in vivo-grown oocytes, 76 (17.4%) developed to term and 4 (5.3%) died at birth. The remaining 72 pups    (35 females, 37 males) survived to adulthood. These studies provide proof of the principle that fully competent mammalian oocytes can develop in vitro from primordial follicles and present a significant advance in oocyte culture    technology.</p>

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</description>

<author>M J. O&apos;Brien et al.</author>


</item>


<item>
<title> Notch signaling and inherited disease syndromes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/504</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/504</guid>
<pubDate>Tue, 08 May 2012 17:12:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Notch signaling pathway is an evolutionarily conserved, intercellular signaling mechanism essential for proper embryonic development in organisms as diverse as insects, nematodes, echinoderms and mammals.  Disruptions in    conserved developmental pathways frequently result in inherited congenital anomalies in humans. Mutations in genes encoding Notch pathway components underlie three inherited human diseases: Alagille syndrome, spondylocostal dysostosis, and    cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. Mouse models for these three diseases have been developed, and are leading to novel insights into the pathology of these diseases in    humans.</p>

	]]>
</description>

<author>T Gridley</author>


</item>


<item>
<title> Spontaneous deletion of epilepsy gene orthologs in a mutant mouse with a low electroconvulsive threshold.</title>
<link>http://mouseion.jax.org/stfb2000_2009/503</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/503</guid>
<pubDate>Tue, 08 May 2012 17:12:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The electroconvulsive threshold (ECT) test has been used extensively to determine the protection conferred by antiepileptic drug candidates against induced seizures in rodents. Despite its clinical relevance, the potential of ECT    to identify mouse epilepsy models in genetic studies has not been thoroughly assessed. We adopted the ECT test to screen the progeny of ethylnitrosourea treated male C57BL/6J mice. In a small-scale screen, several mutant lines conferring a low    threshold to ECT minimal clonic seizures were mapped to the telomeric region of mouse chromosome 2 in independent founder families. This high incidence was suggestive of a single spontaneous event that pre-existed in the founders of mutagenized    stock. Genetic and physical mapping led to the discovery that several lines shared a single mutation, Szt1 (seizure threshold-1), consisting of a 300 kb deletion of genomic DNA involving three known genes. Two of these genes, Kcnq2 and Chrna4,    are known to be mutated in human epilepsy families. Szt1 homozygotes and heterozygotes display similar phenotypes to those found in the respective Kcnq2 knockout mutant mice, suggesting that Kcnq2 haploinsufficiency is at the root of the Szt1    seizure sensitivity.  Our results provide a novel genetic model for epilepsy research and demonstrate that the approach of using ECT to study seizures in mice has the potential to lead to the identification of human epilepsy susceptibility    genes.</p>

	]]>
</description>

<author>Y Yang et al.</author>


</item>


<item>
<title> Aberrant actin cytoskeleton leads to accelerated proliferation of corneal epithelial cells in mice deficient for destrin (actin depolymerizing factor).</title>
<link>http://mouseion.jax.org/stfb2000_2009/502</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/502</guid>
<pubDate>Tue, 08 May 2012 17:12:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Corneal disease is the most common cause of bilateral blindness in the world. Visual loss in this condition is often due to changes in morphology and function of the corneal epithelial surface. Corneal disease-1 (corn1) and    corn1(2J) are spontaneous mouse mutants that develop irregular thickening of the corneal epithelium, similar to that observed in human corneal surface disease. These autosomal-recessive mutations cause an increase in the rate of proliferation of    the corneal epithelial cells.  Here, we report that the phenotypes in both mutants are caused by mutations within the destrin gene (also known as actin-depolymerizing factor). By positional cloning, we identified a deletion encompassing the    entire coding sequence of the destrin gene in corn1 mice, and a point mutation (Pro106Ser) in the coding sequence of destrin in corn1(2J) mice.  In situ analysis showed that destrin is highly expressed in the corneal epithelium. Consistent with    the cellular roles for destrin, an essential regulator of actin filament turnover that acts by severing and enhancing depolymerization of actin filament, we observed that the corn1 mutations increased the content of filamentous actin in corneal    epithelial cells.  Our results suggest an in vivo connection between remodeling of the actin cytoskeleton and the control of cell proliferation, and a new pathway through which an aberrant actin cytoskeleton can cause epithelial    hyperproliferation.</p>

	]]>
</description>

<author>S Ikeda et al.</author>


</item>


<item>
<title> One Hundred Years of Mouse Genetics. An intellectual history. ii. the molecular revolution (1981-2002).</title>
<link>http://mouseion.jax.org/stfb2000_2009/501</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/501</guid>
<pubDate>Tue, 08 May 2012 17:12:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K Paigen</author>


</item>


<item>
<title> Roles of NPM2 in chromatin and nucleolar organization in oocytes and embryos.</title>
<link>http://mouseion.jax.org/stfb2000_2009/500</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/500</guid>
<pubDate>Tue, 08 May 2012 17:11:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Upon fertilization, remodeling of condensed maternal and paternal gamete DNA occurs to form the diploid genome. In Xenopus laevis, nucleoplasmin 2 (NPM2) decondenses sperm DNA in vitro. To study chromatin remodeling in vivo, we    isolated mammalian NPM2 orthologs. Mouse NPM2 accumulates in oocyte nuclei and persists in preimplantation embryos. Npm2 knockout females have fertility defects owing to failed preimplantation embryo development. Although sperm DNA decondensation    proceeds without NPM2, abnormalities are evident in oocyte and early embryonic nuclei. These defects include an absence of coalesced nucleolar structures and loss of heterochromatin and deacetylated histone H3 that normally circumscribe nucleoli    in oocytes and early embryos, respectively. Thus, Npm2 is a maternal effect gene critical for nuclear and nucleolar organization and embryonic development.</p>

	]]>
</description>

<author>K H. Burns et al.</author>


</item>


<item>
<title> Adenovirus Early Region 3 Antiapoptotic 10.4K, 14.5K, and 14.7K Genes Decrease the Incidence of Autoimmune Diabetes in NOD Mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/499</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/499</guid>
<pubDate>Tue, 08 May 2012 17:11:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genes in the early region 3 (E3) of the adenovirus genome allow the virus to evade host immune responses by interfering with major histocompatibility (MHC) class I-mediated antigen presentation and tumor necrosis factor-alpha    (TNF-alpha)- or Fas-induced apoptosis of infected cells. Autoimmune type 1 diabetes (T1D) is inhibited in NOD mice transgenically expressing all E3 genes under control of a rat insulin promoter (RIPE3/NOD). For dissecting the protective    mechanisms afforded by various E3 genes, they were subdivided into RIP-driven transgene constructs. Strong T1D protection mediated at the beta-cell level characterized DL704/NOD mice lacking the E3 gp19K gene suppressing MHC class I expression    but retaining the 10.4K, 14.5K, and 14.7K genes inhibiting Fas- or TNF-alpha-induced apoptosis and TNF-alpha-induced NF-kB activation. Much weaker protection characterized DL309/NOD mice expressing the gp19K but not the 10.4K, 14.5K, and 14.7K    genes. While RIPE3/NOD splenocytes had an unexpected decrease in ability to adoptively transfer T1D, splenocytes from both the DL704 and DL309 stocks efficiently did so.  These findings indicate that all E3 genes must be expressed to inhibit the    diabetogenic potential of NOD immune cells. They also demonstrate that the antiapoptotic E3 genes most effectively protect pancreatic beta-cells from diabetogenic immune responses.</p>

	]]>
</description>

<author>M A. Pierce et al.</author>


</item>


<item>
<title> Topical mechlorethamine restores autoimmune-arrested follicular activity in mice with an alopecia areata-like disease by targeting infiltrated lymphocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/498</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/498</guid>
<pubDate>Tue, 08 May 2012 17:11:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata is an autoimmune disease targeted at hair follicles with infiltrated T lymphocytes probably playing an important role in the pathogenesis. It was reported in 1985 that mechlorethamine was effective on alopecia    areata patients. This has never been confirmed since. The aims of the study were to investigate the effects of mechlorethamine on balding C3H/HeJ mice affected with an alopecia-areata-like disease and to study the underlying mechanisms. Mice were    treated on half of the dorsal skin with mechlorethamine and the contralateral side was treated with the vehicle ointment. After 10 wk of mechlorethamine therapy, a full pelage of hair covered the treated side in all the mice and was maintained    during the study, whereas the vehicle-treated sides showed either no change or continued hair loss. Immunohistochemistry revealed that infiltrated CD4+ and CD8+ lymphocytes were eliminated from the treated side. In vitro cell viability assay    showed that lymphocytes were much more sensitive to the cytotoxic effects of mechlorethamine than skin and hair follicular cells.  RNase protection assay and real-time reverse transcription polymerase chain reaction showed that tumor necrosis    factor alpha/beta, interleukin-12, and interferon-gamma were inhibited by mechlorethamine upon successful treatment. Our findings support that mechlorethamine restores follicular activity by selectively targeting infiltrated lymphocytes in vivo    in alopecia-areata-affected mice.</p>

	]]>
</description>

<author>L Tang et al.</author>


</item>


<item>
<title> Restoring aging bones.</title>
<link>http://mouseion.jax.org/stfb2000_2009/497</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/497</guid>
<pubDate>Tue, 08 May 2012 17:11:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title> The Development of a Highly Informative Mouse Simple Sequence Length Polymorphism (SSLP) Marker Set and Construction of a Mouse Family Tree Using Parsimony Analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/496</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/496</guid>
<pubDate>Tue, 08 May 2012 17:10:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>To identify highly informative markers for a large number of commonly employed murine crosses, we selected a subset of the extant mouse simple sequence length polymorphism (SSLP) marker set for further development.  Primer pairs    for 314 SSLP markers were designed and typed against 54 inbred mouse strains. We designed new PCR primer sequences for the markers selected for multiplexing using the fluorescent dyes FAM, VIC, NED, and ROX. The number of informative markers for    C57BL/6J x DBA/2J is 217, with an average spacing of 6.8 centiMorgans (cM). For all other pairs of strains, the mean number of informative markers per cross is 197.0 (SD 37.8) with a mean distance between markers of 6.8 cM (SD 1.1). To confirm    map positions of the 224 markers in our set that are polymorphic between Mus musculus and Mus spretus, we used The Jackson Laboratory (TJL) interspecific backcross mapping panel (TJL BSS); 168 (75%) of these markers had not been previously mapped    in this cross by other investigators, adding new information to this community map resource. With this large data set, we sought to reconstruct a phylogenetic history of the laboratory mouse using Wagner parsimony analysis. Our results are    largely congruent with the known history of inbred mouse strains. [The following individuals kindly provided reagents, samples, or unpublished information as indicated in the paper: E. Eicher, T. Golovkina, J. Cheverud, S. Cropp, P. Denny, and A.    Southwell.]</p>

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</description>

<author>P D. Witmer et al.</author>


</item>


<item>
<title> Presentation of Antigen by Endothelial Cells and Chemoattraction Are Required for Homing of Insulin-specific CD8(+) T Cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/495</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/495</guid>
<pubDate>Tue, 08 May 2012 17:10:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Activated insulin-specific CD8(+) T cells (IS-CD8(+) cells) home to the pancreas, destroy beta cells, and cause rapid diabetes upon transfer into diabetes-prone NOD mice. Surprisingly, they also cause diabetes in mouse strains that    are free of preexistent inflammation. Thus, we hypothesized that islet-specific homing may be in part dependent on IS-CD8(+) cells' recognition of the cognate major histocompatibility complex (MHC)/peptide complexes presented by pancreatic    endothelial cells, which acquire the antigen (insulin) from beta cells. In fact, islet-specific homing was abrogated in mice that lack MHC class I expression, or presentation of the specific peptide, or have impaired insulin secretion. Moreover,    we found that IS-CD8(+) cells directly recognized pancreatic endothelial cells in islet organ cultures. Triggering of IS-CD8(+) cells' T cell receptor (TCR) led to activation of integrins expressed by these cells. In addition, chemokines,    particularly SLC (CCL21), were also required for IS-CD8(+) cells' adhesion to endothelial monolayers and for successful homing in vivo. Thus, signaling through TCR and chemokine receptors work in concert to assure firm adhesion of T cells to the    pancreatic endothelium. The antigen cross-presentation ability of endothelia may therefore contribute to the specificity of homing of activated T lymphocytes to the tissues where antigens are generated by other cell types.</p>

	]]>
</description>

<author>A Y. Savinov et al.</author>


</item>


<item>
<title> Flow cytometric and immunoblot assays for cell surface ADP-ribosylation using a monoclonal antibody specific for ethenoadenosine.</title>
<link>http://mouseion.jax.org/stfb2000_2009/494</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/494</guid>
<pubDate>Tue, 08 May 2012 17:10:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>NAD-dependent ADP-ribosylation is one of the posttranslational protein modifications. On mammalian cells, glycosylphosphatidylinositol-anchored cell surface ADP-ribosyltransferases (ARTs) ADP-ribosylate other cell surface proteins    and thereby affect important cellular functions. Here we describe convenient flow-cytometric and immunoblot assays for monitoring ADP-ribosylation of cell surface proteins on living cells by exploiting the capacity of ARTs to utilize etheno-NAD    as substrate.  Etheno-ADP-ribosylation of cell surface proteins can be detected by flow cytometry with 1G4, a monoclonal antibody specific for ethenoadenosine.  Labeling of cells with 1G4 is dependent on the expression of cell surface ARTs and    occurs only after incubation of ART-expressing cells with etheno-NAD and not with etheno-ADP-ribose. Dose-response analyses show efficient 1G4 staining of ART-expressing cells at micromolar etheno-NAD concentrations. Half-maximal staining is    obtained with 1-2&mgr;M etheno-NAD, saturation is reached at 5-20&mgr;M etheno-NAD. Immunoblot analyses confirm that ART-expressing cells incorporate ethenoadenosine covalently (i.e., SDS resistant) into several cell surface proteins. The    flow-cytometric 1G4 staining assay can be used to identify subpopulations of cells expressing cell surface ART activity and to select ART(hi) cell variants. The immunoblot 1G4 staining assay can also be used to identify etheno-ADP-ribosylated    target proteins. These new assays hold promise for many interesting applications in biochemistry and cell biology.</p>

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</description>

<author>C Krebs et al.</author>


</item>


<item>
<title> Oxidative stress, cell cycle, and neurodegeneration.</title>
<link>http://mouseion.jax.org/stfb2000_2009/493</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/493</guid>
<pubDate>Tue, 08 May 2012 17:10:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J A. Klein et al.</author>


</item>


<item>
<title> Mechanisms of anemia in SHP-1 protein tyrosine phosphatase-deficient &quot;viable motheaten&quot; mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/492</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/492</guid>
<pubDate>Tue, 08 May 2012 17:09:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Viable motheaten mice (abbreviated gene symbol me(v)) are deficient in SHP-1, a critical negative regulator of signal transduction in hematopoietic cells. These mice exhibit severe immune dysfunction accompanied by    hyperproliferation of myeloid cells, widespread inflammatory lesions, and regenerative anemia. The aim of this study was to investigate the mechanisms underlying anemia in me(v)/me(v) mice.Multiple hematologic parameters, osmotic fragility, and    erythropoietin levels were measured to characterize the anemia in me(v)/me(v) mice. B-cell-deficient me(v)/me(v) Igh-6(null) mice were generated to assess the role of anti-erythrocyte antibodies. Coombs assays and flow cytometry were carried out    for detection of anti-erythrocyte antibodies. Oxidant production by macrophages, glutathione levels, and lipid peroxidation products in erythrocytes were measured, as was the impact of oxidant on the ultrastructure of me(v)/me(v) erythrocytes.     Erythroid maturation and erythrocyte plasma membrane integrity were assessed with flow cytometry by evaluating CD71 expression and annexin V labeling.The regenerative anemia of me(v)/me(v) mice was associated with erythrocyte changes that were    independent of the presence of anti-erythrocyte antibodies. Erythrocytes from me(v)/me(v) mice had increased fragility and heightened susceptibility to oxidant damage.  Macrophages from me(v)/me(v) mice demonstrated a higher basal level of    oxidant production and enhanced production after stimulation. Oxidant damage in me(v)/me(v) erythrocytes was evidenced by a significant elevation of lipid peroxidation and diminished levels of glutathione.Our results support the hypothesis that    as a consequence of severe inflammatory disease, me(v)/me(v) erythrocytes are subject to exceptionally high oxidative stress resulting in oxidation of phospholipids in the erythrocyte membrane with subsequent hemolysis.</p>

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</description>

<author>B L. Lyons et al.</author>


</item>


<item>
<title> Novel secreted isoform of adhesion molecule ICAM-4: potential regulator of membrane-associated ICAM-4 interactions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/491</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/491</guid>
<pubDate>Tue, 08 May 2012 17:09:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Intercellular adhesion molecule-4 (ICAM-4), a newly characterized adhesion molecule, is expressed early in human erythropoiesis and functions as a ligand for binding alpha4beta1 and alphaV integrin-expressing cells.  Within the    bone marrow, erythroblasts surround central macrophages forming erythroblastic islands. Evidence suggests that these islands are highly specialized subcompartments where cell adhesion events, in concert with cytokines, play critical roles in    regulating erythropoiesis and apoptosis.  Since erythroblasts express alpha4beta1 and ICAM-4 and macrophages exhibit alphaV, ICAM-4 is an attractive candidate for mediating cellular interactions within erythroblastic islands. To determine whether    ICAM-4 binding properties are conserved across species, we first cloned and sequenced the murine homologue. The translated amino acid sequence showed 68% overall identity with human ICAM-4. Using recombinant murine ICAM-4 extracellular domains,    we discovered that hematopoietic alpha4beta1- expressing HEL cells and nonhematopoietic alphaV-expressing FLY cells adhered to mouse ICAM-4. Cell adhesion studies showed that FLY and HEL cells bound to mouse and human proteins with similar    avidity. These data strongly suggest conservation of integrin-binding properties across species. Importantly, we characterized a novel second splice cDNA that would be predicted to encode an ICAM-4 isoform, lacking the membrane-spanning domain.    Erythroblasts express both isoforms of ICAM-4.  COS-7 cells transfected with green flourescent protein constructs of prototypic or novel ICAM-4 cDNA showed different cellular localization patterns. Moreover, analysis of tissue culture medium    revealed that the novel ICAM-4 cDNA encodes a secreted protein. We postulate that secretion of this newly described isoform, ICAM-4S, may modulate binding of membrane-associated ICAM-4 and could thus play a critical regulatory role in    erythroblast molecular attachments.</p>

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</description>

<author>G Lee et al.</author>


</item>


<item>
<title> Conditional mutation of Rb causes cell cycle defects without apoptosis in the central nervous system.</title>
<link>http://mouseion.jax.org/stfb2000_2009/490</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/490</guid>
<pubDate>Tue, 08 May 2012 17:09:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Targeted disruption of the retinoblastoma gene in mice leads to embryonic lethality in midgestation accompanied by defective erythropoiesis. Rb(-/-) embryos also exhibit inappropriate cell cycle activity and apoptosis in the    central nervous system (CNS), peripheral nervous system (PNS), and ocular lens. Loss of p53 can prevent the apoptosis in the CNS and lens; however, the specific signals leading to p53 activation have not been determined. Here we test the    hypothesis that hypoxia caused by defective erythropoiesis in Rb-null embryos contributes to p53-dependent apoptosis.  We show evidence of hypoxia in CNS tissue from Rb(-/-) embryos. The Cre-loxP system was then used to generate embryos in which    Rb was deleted in the CNS, PNS and lens, in the presence of normal erythropoiesis. In contrast to the massive CNS apoptosis in Rb-null embryos at embryonic day 13.5 (E13.5), conditional mutants did not have elevated apoptosis in this tissue.    There was still significant apoptosis in the PNS and lens, however. Rb(-/-) cells in the CNS, PNS, and lens underwent inappropriate S-phase entry in the conditional mutants at E13.5. By E18.5, conditional mutants had increased brain size and    weight as well as defects in skeletal muscle development. These data support a model in which hypoxia is a necessary cofactor in the death of CNS neurons in the developing Rb mutant embryo.</p>

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</description>

<author>D MacPherson et al.</author>


</item>


<item>
<title> Loss of myosin VI reduces secretion and the size of the Golgi in fibroblasts from Snell&apos;s waltzer mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/489</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/489</guid>
<pubDate>Tue, 08 May 2012 17:09:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Golgi morphology and function are dependent on an intact microtubule and actin cytoskeleton. Myosin VI, an unusual actin-based motor protein moving towards the minus ends of actin filaments, has been localized to the Golgi complex    at the light and electron microscopic level. Myosin VI is present in purified Golgi membranes as a peripheral membrane protein, targeted by its globular tail domain. To investigate the function of myosin VI at the Golgi complex, immortal    fibroblastic cell lines of Snell's waltzer mice lacking myosin VI were established. In these cell lines, where myosin VI is absent, the Golgi complex is reduced in size by approximately 40% compared with wild-type cells. Furthermore, protein    secretion of a reporter protein from Snell's waltzer cells is also reduced by 40% compared with wild-type cells. Rescue experiments showed that fully functional myosin VI was able to restore Golgi complex morphology and protein secretion in    Snell's waltzer cells to the same level as that observed in wild-type cells.</p>

	]]>
</description>

<author>C L. Warner et al.</author>


</item>


<item>
<title> The major histocompatibility complex-related Fc receptor for IgG (FcRn) binds albumin and prolongs its lifespan.</title>
<link>http://mouseion.jax.org/stfb2000_2009/488</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/488</guid>
<pubDate>Tue, 08 May 2012 17:08:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The inverse relationship between serum albumin concentration and its half-life suggested to early workers that albumin would be protected from a catabolic fate by a receptor-mediated mechanism much like that proposed for IgG. We    show here that albumin binds FcRn in a pH dependent fashion, that the lifespan of albumin is shortened in FcRn-deficient mice, and that the plasma albumin concentration of FcRn-deficient mice is less than half that of wild-type mice. These    results affirm the hypothesis that the major histocompatibility complex-related Fc receptor protects albumin from degradation just as it does IgG, prolonging the half-lives of both.</p>

	]]>
</description>

<author>C Chaudhury et al.</author>


</item>


<item>
<title>Courtyard</title>
<link>http://elibrary.law.psu.edu/home_gallery/6</link>
<guid isPermaLink="true">http://elibrary.law.psu.edu/home_gallery/6</guid>
<pubDate>Tue, 08 May 2012 17:08:40 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>Katz Hall Courtroom</title>
<link>http://elibrary.law.psu.edu/home_gallery/5</link>
<guid isPermaLink="true">http://elibrary.law.psu.edu/home_gallery/5</guid>
<pubDate>Tue, 08 May 2012 17:08:40 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>Lewis Katz Building</title>
<link>http://elibrary.law.psu.edu/home_gallery/4</link>
<guid isPermaLink="true">http://elibrary.law.psu.edu/home_gallery/4</guid>
<pubDate>Tue, 08 May 2012 17:08:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>Lewis Katz Building at Night</title>
<link>http://elibrary.law.psu.edu/home_gallery/3</link>
<guid isPermaLink="true">http://elibrary.law.psu.edu/home_gallery/3</guid>
<pubDate>Tue, 08 May 2012 17:08:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>Study Area</title>
<link>http://elibrary.law.psu.edu/home_gallery/2</link>
<guid isPermaLink="true">http://elibrary.law.psu.edu/home_gallery/2</guid>
<pubDate>Tue, 08 May 2012 17:08:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>UP Library</title>
<link>http://elibrary.law.psu.edu/home_gallery/1</link>
<guid isPermaLink="true">http://elibrary.law.psu.edu/home_gallery/1</guid>
<pubDate>Tue, 08 May 2012 17:08:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title> Congenic strains of mice for verification and genetic decomposition of quantitative trait loci for femoral bone mineral density.</title>
<link>http://mouseion.jax.org/stfb2000_2009/487</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/487</guid>
<pubDate>Tue, 08 May 2012 17:08:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Peak femoral volumetric bone mineral density (femoral bone mineral density) in C57BL/6J (B6) 4-month-old female mice is 50% lower than in C3H/HeJ (C3H) and 34% lower than in CAST/EiJ (CAST) females. Genome-wide analyses of (B6 x    C3H)F2 and (B6 x CAST)F2 4-month-old female progeny demonstrated that peak femoral bone mineral density is a complex quantitative trait associated with genetic loci (QTL) on numerous chromosomes (Chrs) and with trait heritabilities of 83% (C3H)    and 57% (CAST). To test the effect of each QTL on femoral bone mineral density, two sets of loci (six each from C3H and CAST) were selected to make congenic strains by repeated backcrossing of donor mice carrying a given QTL-containing    chromosomal region to recipient mice of the B6 progenitor strain. At the N6F1 generation, each B6.C3H and B6.CAST congenic strain (statistically 98% B6-like in genomic composition) was intercrossed to obtain N6F2 progeny for testing the effect of    each QTL on femoral bone mineral density. In addition, the femoral bone mineral density QTL region on Chr 1 of C3H was selected for congenic subline development to facilitate fine mapping of this strong femoral bone mineral density locus.  In 11    of 12 congenic strains, 6 B6.C3H and 5 B6.CAST, femoral bone mineral density in mice carrying c3h or cast alleles in the QTL regions was significantly different from that of littermates carrying b6 alleles.  Differences also were observed in body    weight, femoral length, and mid-diaphyseal periosteal circumference among these 11 congenic strains when compared with control littermates; however, these latter three phenotypes were not consistently correlated with femoral bone mineral density.    Analyses of eight sublines derived from the B6.C3H-1T congenic region revealed two QTLs: one located between 36.9 and 49.7 centiMorgans (cM) and the other located between 73.2 and 100.0 cM distal to the centromere. In conclusion, these congenic    strains provide proof of principle that many QTLs identified in the F2 analyses for femoral bone mineral density exert independent effects when transferred and expressed in a common genetic background. Furthermore, significant differences in    femoral bone mineral density among the congenic strains were not consistently accompanied by changes in body weight, femur length, or periosteal circumference. Finally, decomposition of QTL regions by congenic sublines can reveal additional loci    for phenotypes assigned to a QTL region and can markedly refine genomic locations of quantitative trait loci, providing the opportunity for candidate gene testing.</p>

	]]>
</description>

<author>K L. Shultz et al.</author>


</item>


<item>
<title> Primed Peritoneal B Lymphocytes Are Sufficient To Transfer Protection against Brugia pahangi Infection in Mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/486</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/486</guid>
<pubDate>Tue, 08 May 2012 17:08:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lymphatic filariasis is a tropical disease caused by the nematode parasites Wuchereria bancrofti and Brugia malayi. Whereas the protective potential of T lymphocytes in filarial infection is well documented, investigation of the    role of B lymphocytes in antifilarial immunity has been neglected. In this communication, we examine the role of B lymphocytes in antifilarial immunity, using Brugia pahangi infections in the murine peritoneal cavity as a model. We find that B    lymphocytes are required for clearance of primary and challenge infections with B. pahangi third-stage larvae (L3). We assessed the protective potential of peritoneal B lymphocytes by adoptive transfer experiments. Primed but not naive peritoneal    B cells from wild-type mice that had been immunized with B. pahangi L3 protected athymic recipients from challenge infection. We evaluated possible mechanisms by which B cells mediate protection.  Comparisons of cytokine mRNA expression between    B-lymphocyte-deficient and immunocompetent mice following B. pahangi infection suggest that B cells are required for the early production of Th2-type cytokines by peritoneal cells. In addition, B-cell-deficient mice demonstrate a defect in    inflammatory cell recruitment to the peritoneal cavity following B. pahangi infection. The data demonstrate a critical role of B lymphocytes in antifilarial immunity in naive mice and in the memory response in primed mice.</p>

	]]>
</description>

<author>N Paciorkowski et al.</author>


</item>


<item>
<title> Antioxidant protein 2 prevents methemoglobin formation in erythrocyte hemolysates.</title>
<link>http://mouseion.jax.org/stfb2000_2009/485</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/485</guid>
<pubDate>Tue, 08 May 2012 17:08:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Antioxidant protein 2 (AOP2) is a member of a family of thiol-specific antioxidants, recently renamed peroxiredoxins, that evolved as part of an elaborate system to counteract and control detrimental effects of oxygen radicals.    AOP2 is found in endothelial cells, erythrocytes, monocytes, T and B cells, but not in granulocytes. AOP2 was found solely in the cytoplasm and was not associated with the nuclear or membrane fractions; neither was it detectable in plasma.    Further experiments focused on the function of AOP2 in erythrocytes where it is closely associated with the hemoglobin complex, particularly with the heme. An investigation of the mechanism of this interaction demonstrated that the conserved    cysteine-47 in AOP2 seems to play a role in AOP2-heme interactions. Recombinant AOP2 prevented induced as well as noninduced methemoglobin formation in erythrocyte hemolysates, indicating its antioxidant properties. We conclude that AOP2 is part    of a sophisticated system developed to protect and support erythrocytes in their many physiological functions.</p>

	]]>
</description>

<author>K M. Stuhlmeier et al.</author>


</item>


<item>
<title> Modification of ocular defects in mouse developmental glaucoma models by tyrosinase.</title>
<link>http://mouseion.jax.org/stfb2000_2009/484</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/484</guid>
<pubDate>Tue, 08 May 2012 17:07:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the cytochrome P450 family 1, subfamily B, polypeptide 1 (CYP1B1) gene are a common cause of human primary congenital glaucoma (PCG). Here we show that Cyp1b1-/- mice have ocular drainage structure abnormalities    resembling those reported in human PCG patients. Using Cyp1b1-/- mice, we identified the tyrosinase gene (Tyr) as a modifier of the drainage structure phenotype, with Tyr deficiency increasing the magnitude of dysgenesis. The severe dysgenesis in    eyes lacking both CYP1B1 and TYR was alleviated by administration of the tyrosinase product dihydroxyphenylalanine (l-dopa). Tyr also modified the drainage structure dysgenesis in mice with a mutant Foxc1 gene, which is also involved in PCG.    These experiments raise the possibility that a tyrosinase/l-dopa pathway modifies human PCG, which could open new therapeutic avenues.</p>

	]]>
</description>

<author>R T. Libby et al.</author>


</item>


<item>
<title> Genetic Models in Applied Physiology: Invited Review: Identifying new mouse models of cardiovascular disease: a review of high-throughput screens of mutagenized and inbred strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/483</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/483</guid>
<pubDate>Tue, 08 May 2012 17:07:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse is a proven model for studying human disease. Many strains exist that exhibit either natural or engineered genetic variation and thereby enable the elucidation of pathways involved in the development of cardiovascular    disease. Although those mouse models have been fundamental to advancing our knowledge base, we are still at an early stage in understanding how genes contribute to complex disorders. There remains a need for new animal models that closely    represent human disease. To expedite their development, we have established the Center for New Mouse Models of Heart, Lung, Blood, and Sleep Disorders at The Jackson Laboratory. We are using a phenotype-driven approach to identify mutations    leading to atherosclerosis, hypertension, obesity, blood disorders, lung dysfunction, thrombosis, and disordered sleep. Our high-throughput, comprehensive phenotyping draws from two sources for new models: 1) the natural variation among over 40    inbred mouse strains and 2) chemically induced, whole-genome mutagenized mice. Here, we review our cardiovascular screens and present some hypertensive, obese, and cardiovascular models identified with this approach.</p>

	]]>
</description>

<author>K L. Svenson et al.</author>


</item>


<item>
<title> Evidence that the red cell skeleton protein 4.2 interacts with the Rh membrane complex member CD47.</title>
<link>http://mouseion.jax.org/stfb2000_2009/482</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/482</guid>
<pubDate>Tue, 08 May 2012 17:07:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rh(null) red cells are characteristically stomato-spherocytic. This and other evidence suggest that the Rh complex represents a major attachment site between the membrane lipid bilayer and the erythroid skeleton. As an attempt to    identify the linking protein(s) between the red cell skeleton and the Rh complex, we analyzed the expression of Rh, RhAG, CD47, LW, and glycophorin B proteins in red cells from patients with hereditary spherocytosis associated with complete    protein 4.2 deficiency but normal band 3 (4.2(-)HS). Flow cytometric and immunoblotting analysis revealed a severe reduction of CD47 (up to 80%) and a slower mobility of RhAG on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, possibly    reflecting an overglycosylation state. Unexpectedly, 4.2(-/-) mice, which are anemic, displayed a normal red cell expression of CD47 and RhAG. These results suggest that human protein 4.2, through interaction with CD47, is involved in the    skeleton linkage and/or membrane translocation of the Rh complex. However, these potential role(s) of protein 4.2 might be not conserved across species. Finally, the absence or low expression of red cell CD47 in CD47(-/-) mice and in some humans    carrying RHCE gene variants (D--, D., and R(N)), respectively, had no detectable effect on protein 4.2 and RhAG expression. Since these cells are morphologically normal with no sign of hemolysis, it is assumed that CD47 deficiency per se is not    responsible for the cell shape abnormalities and for the compensated hemolytic anemia typical of 4.2(-) and Rh(null) red cells.</p>

	]]>
</description>

<author>Chanteloup I. Mouro et al.</author>


</item>


<item>
<title> Mutations in the murine erythroid alpha -spectrin gene alter spectrin mRNA and protein levels and spectrin incorporation into the red blood cell membrane skeleton.</title>
<link>http://mouseion.jax.org/stfb2000_2009/481</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/481</guid>
<pubDate>Tue, 08 May 2012 17:07:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Tetramers of alpha- and beta-spectrin heterodimers, linked by intermediary proteins to transmembrane proteins, stabilize the red blood cell cytoskeleton. Deficiencies of either alpha- or beta-spectrin can result in severe    hereditary spherocytosis (HS) or hereditary elliptocytosis (HE) in mice and humans. Four mouse mutations, sph, sph(Dem), sph(2BC), and sph(J), affect the erythroid alpha-spectrin gene, Spna1, on chromosome 1 and cause severe HS and HE. Here we    describe the molecular alterations in alpha-spectrin and their consequences in sph(2BC)/sph(2BC) and sph(J)/sph(J) erythrocytes. A splicing mutation, sph(2BC) initiates the skipping of exon 41 and premature protein termination before the site    required for dimerization of alpha-spectrin with beta-spectrin. A nonsense mutation in exon 52, sph(J) eliminates the COOH-terminal 13 amino acids.  Both defects result in instability of the red cell membrane and loss of membrane surface area. In    sph(2BC)/sph(2BC), barely perceptible levels of messenger RNA and consequent decreased synthesis of alpha-spectrin protein are primarily responsible for the resultant hemolysis. By contrast, sph(J)/sph(J) mice synthesize the truncated    alpha-spectrin in which the 13-terminal amino acids are deleted at higher levels than normal, but they cannot retain this mutant protein in the cytoskeleton. The sph(J) deletion is near the 4.1/actin-binding region at the junctional complex    providing new evidence that this 13-amino acid segment at the COOH-terminus of alpha-spectrin is crucial to the stability of the junctional complex.</p>

	]]>
</description>

<author>N J. Wandersee et al.</author>


</item>


<item>
<title> Ribosomal protein S19 expression during erythroid differentiation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/480</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/480</guid>
<pubDate>Tue, 08 May 2012 17:06:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The gene encoding ribosomal protein S19 (RPS19) has been shown to be mutated in 25% of the patients affected by Diamond-Blackfan anemia (DBA), a congenital erythroblastopenia. As the role of RPS19 in erythropoiesis is still to be    defined, we performed studies on RPS19 expression during terminal erythroid differentiation. Comparative analysis of the genomic sequences of human and mouse RPS19 genes enabled the identification of 4 conserved sequence elements in the 5'    region. Characterization of transcriptional elements allowed the identification of the promoter in the human RPS19 gene and the localization of a strong regulatory element in the third conserved sequence element. By Northern blot and Western blot    analyses of murine splenic erythroblasts infected with the anemia-inducing strain Friend virus (FAV cells), RPS19 mRNA and protein expression were shown to decrease during terminal erythroid differentiation. We anticipate that these findings will    contribute to further development of our understanding of the contribution of RPS19 to erythropoiesis.</p>

	]]>
</description>

<author>Costa L. Da et al.</author>


</item>


<item>
<title> The comprehensive mouse radiation hybrid map densely cross-referenced to the recombination map: a tool to support the sequence assemblies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/479</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/479</guid>
<pubDate>Tue, 08 May 2012 17:06:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have developed a unique comprehensive mouse radiation hybrid (RH) map of nearly 23,000 markers integrating data from three international genome centers and over 400 independent laboratories. We have cross-referenced this map to    the 0.5-cM resolution recombination-based Jackson Laboratory (TJL) backcross panel map, building a complete set of RH framework chromosome maps based on a high density of known-ordered anchor markers.  We have systematically typed markers to    improve coverage and resolve discrepancies, and have reanalyzed data sets as needed. The cross-linking of the RH and recombination maps has resulted in a highly accurate genome-wide map with consistent marker order. We have compared these linked    framework maps to the Ensembl mouse genome sequence assembly, and show that they are a useful medium resolution tool for both validating sequence assembly and elucidating chromosome biology. [Supplemental material is available online at    www.genome.org.]</p>

	]]>
</description>

<author>L B. Rowe et al.</author>


</item>


<item>
<title> Our small relative.</title>
<link>http://mouseion.jax.org/stfb2000_2009/478</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/478</guid>
<pubDate>Tue, 08 May 2012 17:06:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T O&apos;Brien et al.</author>


</item>


<item>
<title> Mutations at the mouse ichthyosis locus are within the lamin B receptor gene: a single gene model for human Pelger-Huet anomaly.</title>
<link>http://mouseion.jax.org/stfb2000_2009/477</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/477</guid>
<pubDate>Tue, 08 May 2012 17:06:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>The nature of the wild-type gene product at the mouse ichthyosis (ic) locus has been of great interest because mutations at this locus cause marked abnormalities in nuclear heterochromatin, similar to those observed in Pelger-Huet    anomaly (PHA). We recently found that human PHA is caused by mutations in the gene (LBR) encoding lamin B receptor, an evolutionarily conserved inner nuclear membrane protein involved in nuclear assembly and chromatin binding. Mice homozygous for    deleterious alleles at the ichthyosis (ic) locus present with a blood phenotype similar to PHA, and develop other phenotypic abnormalities, including alopecia, variable expression of syndactyly and hydrocephalus. The ic locus on mouse chromosome    1 shares conserved synteny with the chromosomal location of the human LBR locus on human chromosome 1. In this study, we identified one nonsense (815ins) and two frameshift mutations (1088insCC and 1884insGGAA) within the Lbr gene of mice    homozygous for either of three independent mutations (ic, ic(J) and ic(4J), respectively) at the ichthyosis locus. These allelic mutations are predicted to result in truncated or severely impaired LBR protein. Our studies of mice homozygous for    the ic(J) mutation revealed a complete loss of LBR protein as shown by immunofluorescence microscopy and immunoblotting. The findings provide the molecular basis for the heterochromatin clumping and other distinct phenotypes caused by ic    mutations. These spontaneous Lbr mutations confirm the molecular basis of human PHA and provide a small animal model for determination of the precise function of LBR in normal and pathological states.</p>

	]]>
</description>

<author>L D. Shultz et al.</author>


</item>


<item>
<title> Genetic modulation of tau phosphorylation in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/476</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/476</guid>
<pubDate>Tue, 08 May 2012 17:05:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The axonal microtubule stabilizing protein tau is hyperphosphorylated in several neurodegenerative conditions, including Alzheimer's disease, yet the genes that regulate tau phosphorylation are largely unknown.  Disabled-1 (Dab1)    is a cytoplasmic adapter protein that interacts with apolipoprotein E (ApoE) receptors and controls neuronal positioning during embryonic brain development. We have investigated the role of Dab1 in tau phosphorylation. We found that wild-type    Dab1, but not a mutant lacking tyrosine phosphorylation sites, protects mice from the hyperphosphorylation of tau. However, the absence of Dab1 is not sufficient to cause tau hyperphosphorylation, because hyperphosphorylation is manifested only    when Dab1 is mutated in specific mouse strain backgrounds. Tau hyperphosphorylation correlates with early death in susceptible mouse strains, and it occurs in the neurons of the hippocampus and dentate gyrus. By quantitative trait locus (QTL)    analysis of Dab1-deficient mice on a hybrid strain background, we uncovered one significant and three suggestive chromosomal loci that modulate tau phosphorylation. Two of these QTL regions contain genes that are defective in early onset    Alzheimer's disease. Our findings suggest that Dab1 gene disruption sensitizes mice to tau hyperphosphorylation contingent on specific haplotypes that are linked to Alzheimer's disease loci. Dab1 mutant mice provide an animal model for studying    the relationships between ApoE receptors, tau hyperphosphorylation, and Alzheimer's disease.</p>

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</description>

<author>J Brich et al.</author>


</item>


<item>
<title> MGD: the Mouse Genome Database.</title>
<link>http://mouseion.jax.org/stfb2000_2009/475</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/475</guid>
<pubDate>Tue, 08 May 2012 17:05:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Database (MGD) (http://www.informatics.jax.org) one component of a community database resource for the laboratory mouse, a key model organism for interpreting the human genome and for understanding human biology.    MGD strives to provide an extensively integrated information resource with experimental details annotated from both literature and on-line genomic data sources. MGD curates and presents the consensus representation of genotype (sequence) to    phenotype information including highly detailed information about genes and gene products.  Primary foci of integration are through representations of relationships between genes, sequences and phenotypes. MGD collaborates with other    bioinformatics groups to curate a definitive set of information about the laboratory mouse. Recent developments include a general implementation of database structures for controlled vocabularies and the integration of a phenotype classification    system.</p>

	]]>
</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title> &apos;Cyclic alopecia&apos; in Msx2 mutants: defects in hair cycling and hair shaft differentiation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/474</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/474</guid>
<pubDate>Tue, 08 May 2012 17:05:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Msx2-deficient mice exhibit progressive hair loss, starting at P14 and followed by successive cycles of wavelike regrowth and loss. During the hair cycle, Msx2 deficiency shortens anagen phase, but prolongs catagen and telogen.    Msx2-deficient hair shafts are structurally abnormal.  Molecular analyses suggest a Bmp4/Bmp2/Msx2/Foxn1 acidic hair keratin pathway is involved. These structurally abnormal hairs are easily dislodged in catagen implying a precocious exogen.    Deficiency in Msx2 helps to reveal the distinctive skin domains on the same mouse. Each domain cycles asynchronously - although hairs within each skin domain cycle in synchronized waves. Thus, the combinatorial defects in hair cycling and    differentiation, together with concealed skin domains, account for the cyclic alopecia phenotype.</p>

	]]>
</description>

<author>L Ma et al.</author>


</item>


<item>
<title> MAANOVA: A software package for the analysis of spotted cDNA microarray experiments.</title>
<link>http://mouseion.jax.org/stfb2000_2009/473</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/473</guid>
<pubDate>Tue, 08 May 2012 17:05:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H Wu et al.</author>


</item>


<item>
<title> Hidden projection properties of some nonregular fractional factorial designs and their applications.</title>
<link>http://mouseion.jax.org/stfb2000_2009/472</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/472</guid>
<pubDate>Tue, 08 May 2012 17:05:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D A. Bulutoglu et al.</author>


</item>


<item>
<title> Mouse and rat genome informatics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/471</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/471</guid>
<pubDate>Tue, 08 May 2012 17:04:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title> T cell knockout mice have diminished alveolar bone loss after oral infection with Porphyromonas gingivalis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/470</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/470</guid>
<pubDate>Tue, 08 May 2012 17:04:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Periodontal diseases are chronic inflammatory diseases that can result in resorption of the alveolar bone of the jaw. We have developed a murine model in which alveolar bone loss is induced by oral infection with Porphyromonas    gingivalis, an oral anaerobic bacterium associated with periodontal disease in humans. Here we compared a strain of immunocompetent mice (C57BL/6J) to the same strain of mice made T cell deficient by genetic deletion of the alpha chain of their T    cell receptors (C57BL/6J-Tcra). T cell deficiency did not affect the ability of P. gingivalis to implant in the oral cavity. The two strains of mice had equal percentages of P. gingivalis among their cultivable anaerobes 7 weeks after infection.    The same bacterial load led to much less bone resorption in the T cell deficient mice than in the immune normal mice, measured as either the number of sites with significant loss, or as the total amount of bone resorbed. T cell deficient mice    lost bone at only three out of 14 measurement sites, compared with eight out of 14 sites in the wild-type mice. The total amount of bone lost was 70% less in the T cell deficient mice. T cell deficient mice had lower titers of P.    gingivalis-specific IgG than the wild-type mice after oral infection did, but the same titers of specific IgA. Lower titers did not correlate with greater bone loss. Antigen-activated T lymphocytes are known to induce osteoclastogenesis; here we    demonstrate that T cell deletion decreases the amount of alveolar bone loss induced by infection of the murine oral cavity.</p>

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</description>

<author>P J. Baker et al.</author>


</item>


<item>
<title> Genetic susceptibility to chronic periodontal disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/469</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/469</guid>
<pubDate>Tue, 08 May 2012 17:04:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Evidence suggests that there is a significant genetic component to susceptibility and resistance to chronic periodontal disease. Data from both clinical studies and studies using animal models are reviewed here.  Also outlined are    the genomic methods that are now available for identifying susceptibility and resistance loci.</p>

	]]>
</description>

<author>P J. Baker et al.</author>


</item>


<item>
<title> Standards for microarray data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/468</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/468</guid>
<pubDate>Tue, 08 May 2012 17:04:06 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C A. Ball et al.</author>


</item>


<item>
<title> The underlying principles of scientific publication.</title>
<link>http://mouseion.jax.org/stfb2000_2009/467</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/467</guid>
<pubDate>Tue, 08 May 2012 17:03:55 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C A. Ball et al.</author>


</item>


<item>
<title> Members of the synaptobrevin/vesicle-associated membrane protein (VAMP) family in Drosophila are functionally interchangeable in vivo for neurotransmitter release and cell viability.</title>
<link>http://mouseion.jax.org/stfb2000_2009/466</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/466</guid>
<pubDate>Tue, 08 May 2012 17:03:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Synaptobrevins or VAMPs are vesicle-associated membrane proteins, often called v-SNARES, that are important for vesicle transport and fusion at the plasma membrane. Drosophila has two characterized members of this gene family:    synaptobrevin (syb) and neuronal synaptobrevin (n-syb). Mutant phenotypes and gene-expression patterns indicate that n-Syb is exclusively neuronal and required only for synaptic vesicle secretion, whereas Syb is ubiquitous and, as shown here,    essential for cell viability. When the eye precursor cells were made homozygous for syb(-), the eye failed to develop. In contrast, n-syb(-) eye clones developed appropriately but failed to activate downstream neurons. To determine whether the    two proteins are structurally specialized to accomplish these distinct in vivo functions, we have driven the expression of each gene in the absence of the other to look for phenotypic rescue. We find that expression of n-syb during eye    development can rescue the cell lethality of the syb mutations, as can rat VAMP2 and cellubrevin. Expression of syb can restore synaptic transmission to n-syb mutants as assayed both by electroretinogram and recordings of excitatory junctional    currents at the neuromuscular junction. Therefore, we find that Syb, which usually is not involved in synaptic function, can mediate Ca(2+)-triggered synaptic activity and that no particular specialization of the v-SNARE is required to    differentiate synaptic exocytosis from other forms.</p>

	]]>
</description>

<author>S Bhattacharya et al.</author>


</item>


<item>
<title> Mapping sites responsible for interactions of agrin with neurons.</title>
<link>http://mouseion.jax.org/stfb2000_2009/465</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/465</guid>
<pubDate>Tue, 08 May 2012 17:03:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The multidomain proteoglycan agrin is a critical organizer of postsynaptic differentiation at the skeletal neuromuscular junction. Agrin is also abundant in the brain, but its roles there are unknown. As a step toward understanding    these roles, we mapped sites responsible for interactions of neurons with agrin. First, we used a series of recombinant agrin fragments to show that at least four sites on agrin interact with chick ciliary neurons. Use of blocking antibodies and    peptides indicated that neurons adhere to a site in the second of three G domains by means of alphaVbeta1 integrin, and to a site in the last of four epidermal growth factor (EGF) repeats via a distinct beta1 integrin. A third,    integrin-independent adhesion site is near to but distinct from the site that induces postsynaptic differentiation in muscles. These domains are insufficient, however, to account for neurite outgrowth-inhibiting properties of full-length agrin,    which are mediated by the N-terminal half of the molecule. We then used a second set of agrin mutants to demonstrate and map a transmembrane domain in the amino-terminus of the SN-isoform of agrin. The extracellular matrix-bound form of agrin,    called LN, bears an amino-terminus required for secretion and binding to laminin. The SN form, which is selectively expressed by neurons, bears a variant amino terminus that converts agrin from a secreted, matrix-associated protein to a type-II    transmembrane protein, providing a mechanism for presenting agrin in central, as opposed to neuromuscular, synaptic clefts. The SN-amino terminus can mediate externalization and membrane anchoring of heterologous proteins, but is insufficient to    target them to the synapse.  Together, these studies define sites that contribute to the subcellular localization of and signaling by neuronal agrin.</p>

	]]>
</description>

<author>R W. Burgess et al.</author>


</item>


<item>
<title> What is the &apos;true&apos; function of skin?</title>
<link>http://mouseion.jax.org/stfb2000_2009/464</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/464</guid>
<pubDate>Tue, 08 May 2012 17:03:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Conventional textbook wisdom portrays the skin as an organ that literally enwraps whatever each of us stands for as a more or less functional, individual member of the mammalian species, and has it that the skin primarily    establishes, controls and transmits contacts with the external world. In addition, the skin has long been recognized to protect the organism from deleterious environmental impacts (physical, chemical,microbiological), and is well-known as crucial    for the maintenance of temperature, electrolyte and fluid balance. Now, ever more studies are being published that show the skin to also operate as a huge and highly active biofactory for the synthesis,processing and/or metabolism of an    astounding range of e.g. structural proteins, glycans, lipids and signaling molecules. Increasingly, it becomes appreciated that the skin, furthermore, is an integral component of the immune, nervous and endocrine systems, with numerous lines of    cross-talk between these systems established intracutaneously (e.g. Ann NY Acad Sci Vol 885, 1999; Endocrine Rev 21:457-487, 2000; Physiol Rev 80:980-1020, 2001; Exp Dermatol 10: 349-367, 2001). All these emerging cutaneous functions beyond the    classical image of the skin as a barrier and sensory organ are immediately relevant for many of the quandaries that clinical dermatology, dermatopathology, and dermatopharmacology are still struggling with to-date, and offer the practising    dermatologist attractive new targets for therapeutic intervention. Yet, many of these skin functions are not even mentioned in dermatology textbooks and await systematic therapeutic targeting. Following a suggestion by Enno Christophers, the    current 'Controversies' feature brings together an unusually diverse council of biologists and clinicians, who share their thought-provoking views with the readers and allow us to peek into the future of research in cutaneous biology, not the    least by reminding us of the -- often ignored -- evolutionary and embryonal origins of our favorite organ. Hopefully, this unique discussion feature will foster an understanding of the 'true' skin functions that is both more comprehensive and    more profound than conventional teaching on this topic, and will stimulate more than 'skin-deep' reflections on the full range of skin functions.</p>

	]]>
</description>

<author>C M. Chuong et al.</author>


</item>


<item>
<title> Mutations in the gene encoding the lamin B receptor produce an altered nuclear morphology in granulocytes (Pelger-Huet anomaly).</title>
<link>http://mouseion.jax.org/stfb2000_2009/463</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/463</guid>
<pubDate>Tue, 08 May 2012 17:03:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pelger-Huet anomaly (PHA; OMIM *169400) is an autosomal dominant disorder characterized by abnormal nuclear shape and chromatin organization in blood granulocytes. Affected individuals show hypolobulated neutrophil nuclei with    coarse chromatin. Presumed homozygous individuals have ovoid neutrophil nuclei, as well as varying degrees of developmental delay, epilepsy and skeletal abnormalities. Homozygous offspring in an extinct rabbit lineage showed severe    chondrodystrophy, developmental anomalies and increased pre- and postnatal mortality. Here we show, by carrying out a genome-wide linkage scan, that PHA is linked to chromosome 1q41-43. We identified four splice-site, two frameshift and two    nonsense mutations in LBR, encoding the lamin B receptor. The lamin B receptor (LBR), a member of the sterol reductase family, is evolutionarily conserved and integral to the inner nuclear membrane; it targets heterochromatin and lamins to the    nuclear membrane. Lymphoblastoid cells from heterozygous individuals affected with PHA show reduced expression of the lamin B receptor, and cells homozygous with respect to PHA contain only trace amounts of it. We found that expression of the    lamin B receptor affects neutrophil nuclear shape and chromatin distribution in a dose-dependent manner. Our findings have implications for understanding nuclear envelope-heterochromatin interactions, the pathogenesis of Pelger-like conditions in    leukemia, infection and toxic drug reactions, and the evolution of neutrophil nuclear shape.</p>

	]]>
</description>

<author>K Hoffmann et al.</author>


</item>


<item>
<title> Brugian infections in the peritoneal cavities of laboratory mice: kinetics of infection and cellular responses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/462</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/462</guid>
<pubDate>Tue, 08 May 2012 17:03:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Standard, immunocompetent, inbred strains of mice are non-permissive for infection with the human filarial nematode, Brugia malayi or the closely related Brugia pahangi. This non-permissiveness allows one to address the    mechanism(s) that might be used by mammalian hosts to eliminate large, multicellular, metazoan, extracellular invertebrate pathogens. We describe here the time course of intraperitoneal Brugian infections in naive and primed +/+ mice from two    commonly used, inbred laboratory strains (C57BL/6J and BALB/cByJ). We believe that this documentation of the course of infection in normal mice will serve as a reference for future studies using mice with gene-targeted immunological deficits or    which have been pharmacologically or immunologically manipulated to manifest such deficits. Our data show that even though both strains of mice eliminate the parasite before the onset of patency, there are significant differences in the time    course of infection and in the fractions of input larvae that can be recovered at any time after infection. In a secondary infection, the time course of elimination is accelerated. We examined the cells in the peritoneal cavity, the site of    infection, by flow microfluorimetry using forward and side scatter properties and cell surface antigen expression using fluorescent antibodies. These studies reveal a complex cellular pattern, predominated by B lymphocytes, macrophages, and    eosinophils. The most notable gross morphological findings at necropsy during the phase of elimination of the parasite are nodules of tissue containing larvae, which appear viable in some cases and undergoing various stages of disintegration in    others. These nodules, which are histologically granulomas, are primarily composed of macrophages and eosinophils, with few if any lymphocytes. Transmission electron micrographs reveal that eosinophils can penetrate under the cuticles of the    larvae and be seen in close approximation with internal structures.  These granulomas may represent an important mechanism by which worms are eliminated.</p>

	]]>
</description>

<author>T V. Rajan et al.</author>


</item>


<item>
<title> In vitro and in vivo hematopoietic potential of human stem cells residing in muscle tissue.</title>
<link>http://mouseion.jax.org/stfb2000_2009/461</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/461</guid>
<pubDate>Tue, 08 May 2012 17:02:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: We studied the in vitro and in vivo hematopoietic potential of human stem cells residing in muscle tissue collected from adults with head and neck cancer. MATERIALS AND METHODS: Adherent muscle cells were cultured in F12    medium with 10% fetal bovine serum and transplanted into immunodeficient mice. RESULTS: On day 12 we obtained a median of 500,000 adherent cells per gram muscle sample. Thy-1, endoglin, HER2/neu, and P1H12 were expressed in the majority of cells.    CD34, VEGFR2, c-kit, VCAM-1, and CXCR4 were expressed in 0.5-1.5%, 1-5%, 1-15%, 9-15%, and 30% of cells, respectively. Immunodeficient mice transplanted with fresh muscle cells or less than 500,000 cultured cells showed little or no human    engraftment. In mice transplanted with more than 500,000 cultured cells, up to 14% human CD45(+) hematopoietic cells (including myeloid and lymphoid subsets) were detected by flow cytometry. Engraftment was confirmed by polymerase chain reaction,    Southern blotting, and DNA sequencing. Liver, muscle, and spleen evaluated for human DNA were positive in the majority of mice showing hematopoietic engraftment in the bone marrow. In vivo hematopoietic engraftment potential was maintained in    cultured CD45(-) muscle cells transduced with the green fluorescence protein gene. CONCLUSIONS: Human stem cells residing in muscle tissue can generate multilineage hematopoiesis in immunodeficient mice. Surprisingly, this hematopoietic potential    increased in cultured versus fresh cells from muscle tissue.</p>

	]]>
</description>

<author>C Dell&apos;Agnola et al.</author>


</item>


<item>
<title> Gene array profiling and immunomodulation studies define a cell-mediated immune response underlying the pathogenesis of alopecia areata in a mouse model and humans.</title>
<link>http://mouseion.jax.org/stfb2000_2009/460</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/460</guid>
<pubDate>Tue, 08 May 2012 17:02:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alopecia areata is a suspected autoimmune hair loss disease. In a rodent model, alopecia areata can be induced in normal haired C3H/HeJ mice by transfer of skin grafts from mice with spontaneous alopecia areata. At weeks 2, 4, 6,    and 10 after surgery, grafted mice were euthanized, skin collected and processed for histology, and RNA extracted. Age-matched sham-grafted mice, and mice with and without spontaneous alopecia areata, were similarly processed. For comparison,    skin biopsies from alopecia areata and androgenetic alopecia affected humans were also collected. Skin mRNA processed to cDNA was analyzed using Affymetrix mouse 11K and human 6800 gene chip(R) array technology. Microarray results indicated 42    known genes upregulated or downregulated during onset of mouse alopecia areata consistent with an inflammatory cell-mediated disease pathogenesis involving antigen presentation, costimulation, and a T helper 1 lymphocyte response. In contrast,    114 genes, many regulating immunoglobulin response, were altered late in disease development. In alopecia areata affected humans, 95 genes were significantly modulated. As confirmation of microarray analysis results, lymph node and spleen cells    from alopecia areata affected mice injected into normal haired littermates transferred the alopecia areata phenotype. Alopecia areata onset could be inhibited in skin-grafted mice by modulation with B7.1- and B7.2-specific monoclonal antibodies.    In addition, depletion of CD4+ CD8+ expressing cells in chronic alopecia areata affected mice using monoclonal antibodies permitted hair regrowth. The results consistently demonstrated the importance of an immune cell-mediated disease mechanism    in alopecia areata pathogenesis and suggested targeting antigen-presenting cells and reactive lymphocytes may be effective in alopecia areata treatment.</p>

	]]>
</description>

<author>J M. Carroll et al.</author>


</item>


<item>
<title> Establishment and characterization of a new osteogenic cell line (MOS-J) from a spontaneous C57BL/6J mouse osteosarcoma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/459</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/459</guid>
<pubDate>Tue, 08 May 2012 17:02:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this paper we describe the establishment and characterization of a transplantable cell line derived from a spontaneously occurring chondroblastic osteosarcoma in a C57BL/6J mouse. The tumor line, MOS-J, forms solid tumors when    injected intramuscularly into immunocompetent syngeneic hosts, mimicking endochondral bone development. These transplantable tumors have the capacity to destroy and invade existing bone and invade vessels in close proximity to the tumor. In    culture, MOS-J cells form layers of pleomorphic cells with high mitotic activity. These cells have marked alkaline phosphatase activity and form calcified foci in vitro that stain with alizarin red. MOS-J cells also promote osteoclast development    in vitro from normal bone marrow cells. These characteristics indicate the potential utility of the MOS-J osteosarcoma cell line as a model for studies of human osteosarcoma and bone biology.</p>

	]]>
</description>

<author>M J. Joliat et al.</author>


</item>


<item>
<title> Increased frequency of pre-pro B cells in the bone marrow of New Zealand Black (NZB) mice: implications for a developmental block in B cell differentiation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/458</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/458</guid>
<pubDate>Tue, 08 May 2012 17:02:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Reductions in populations of both Pre-B cell (Hardy fractions D) and Pro-B cells (Hardy fractions B-C) have been described in association with murine lupus. Recent studies of B cell populations, based on evaluation of B cell    differentiation markers, now allow the enumeration and enrichment of other stage specific precursor cells. In this study we report detailed analysis of the ontogeny of B cell lineage subsets in New Zealand black (NZB) and control strains of mice.    Our data suggest that B cell development in NZB mice is partially arrested at the fraction A Pre-Pro B cell stage. This arrest at the Pre-Pro B cell stage is secondary to prolonged lifespan and greater resistance to spontaneous apoptosis. In    addition, expression of the gene encoding the critical B cell development transcription factor BSAP is reduced in the Pre-Pro B cell stage in NZB mice. This impairment may influence subsequent B cell development to later stages, and thereby    accounts for the down-regulation of the B cell receptor component Ig alpha (mb-1). Furthermore, levels of expression of the Rug2, lambda5 and Ig beta (B29) genes are also reduced in Pre-Pro B cells of NZB mice. The decreased frequency of    precursor B cells in the Pre-Pro B cell population occurs at the most primitive stage of B cell differentiation.</p>

	]]>
</description>

<author>Z X. Lian et al.</author>


</item>


<item>
<title> Functional evidence for the mediation of diabetogenic T cell responses by HLA-A2.1 MHC class I molecules through transgenic expression in NOD mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/457</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/457</guid>
<pubDate>Tue, 08 May 2012 17:01:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Particular major histocompatibility complex (MHC) class II alleles clearly contribute to T cell-mediated autoimmune type 1 diabetes (T1D) in both humans and nonobese diabetic (NOD) mice. However, studies in NOD mice indicate MHC    class I-restricted T cell responses are also essential to T1D development. In humans, epidemiological studies have suggested that some common class I alleles, including HLA-A2.1 (A*02011), may confer increased susceptibility to T1D when expressed    in conjunction with certain class II alleles. We show here that when HLA-A2.1 molecules are transgenically expressed in NOD mice, A2-restricted T cell responses arise against pancreatic beta cells, leading to an earlier onset of T1D. The    accelerated onset of T1D in the NOD.HLA-A2.1 transgenic mice is not due to nonspecific effects of expressing a third class I molecule, because a stock of NOD mice transgenically expressing HLA-B27 class I molecules showed no such acceleration of    T1D, but rather were significantly protected from disease.  These findings provide the first functional evidence that certain human MHC class I molecules can contribute to the development of T1D.</p>

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</description>

<author>M P. Marron et al.</author>


</item>


<item>
<title> Probabilistic prediction of Saccharomyces cerevisiae mRNA 3&apos;-processing sites.</title>
<link>http://mouseion.jax.org/stfb2000_2009/456</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/456</guid>
<pubDate>Tue, 08 May 2012 17:01:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present a tool for the prediction of mRNA 3'-processing (cleavage and polyadenylation) sites in the yeast Saccharomyces cerevisiae, based on a discrete state-space model or hidden Markov model. Comparison of predicted sites with    experimentally verified 3'-processing sites indicates good agreement. All predicted or known yeast genes were analyzed to find probable 3'-processing sites. Known alternative 3'-processing sites, both within the 3'-untranslated region and within    the protein coding sequence were successfully identified, leading to the possibility of prediction of previously unknown alternative sites. The lack of an apparent 3'-processing site calls into question the validity of some predicted genes. This    is specifically investigated for predicted genes with overlapping coding sequences.</p>

	]]>
</description>

<author>J H. Graber et al.</author>


</item>


<item>
<title> A ubiquitous and conserved signal for RNA localization in chordates.</title>
<link>http://mouseion.jax.org/stfb2000_2009/455</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/455</guid>
<pubDate>Tue, 08 May 2012 17:01:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>During oogenesis in Xenopus laevis, several RNAs that localize to the vegetal cortex via one of three temporally defined pathways have been identified. Although individual mRNAs utilize only one pathway, there is functional overlap    and apparent continuity between them, suggesting that common cis-acting sequences may exist. Because previous work with the Vg1 mRNA revealed that short nontandem repeats are important for localization, we developed a new computer program, called    REPFIND, to expedite the identification of repeated motifs in other localized RNAs. Here we show that clusters of short CAC-containing motifs characterize the localization elements (LEs) of virtually all mRNAs localized to the vegetal cortex of    Xenopus oocytes. A search for this signal in GenBank [9] resulted in the identification of new localized mRNAs, demonstrating the applicability of REPFIND to predict localized RNAs. CAC-rich LEs are also found in ascidians and other vertebrates,    indicating that these cis regulatory elements are conserved in chordates. Interestingly, biochemical evidence shows that distinct CAC-containing motifs have different functions in the localization process. Thus, clusters of CAC-containing motifs    are a ubiquitous signal for RNA localization and can signal localization in a variety of pathways through slight variations in sequence composition.</p>

	]]>
</description>

<author>J N. Betley et al.</author>


</item>


<item>
<title> Mouse genetic model for bone strength and size phenotypes: NZB/B1NJ and RF/J inbred strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/454</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/454</guid>
<pubDate>Tue, 08 May 2012 17:01:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The relationships of bone size, bone strength, and bone formation were investigated in two strains of mice, NZB/B1NJ and RF/J. Measurement of the femur midshaft size by peripheral quantitative computed tomography (pQCT) showed that    the RF/J mice had a 32% greater cross-sectional area than NZB/B1NJ mice at 10 weeks of age, and a 38% greater cross-sectional area at 22 weeks of age. Body weight in the RF/J mice was 10% higher at 10 weeks but 9% lower at 22 weeks. Bone strength    was determined by a three-point bending method. In agreement with the difference in bone cross-sectional area, the femurs of the RF/J mice were stronger (80% greater) and stiffer (80% greater) than the bones of the NZB/B1NJ mice. To determine    whether periosteal bone formation played a role in the greater size of the RF/J mice, the mice were injected with tetracycline to label areas of new bone formation. Histomorphometrical analysis of the femur diaphysis demonstrated higher rates of    periosteal bone formation (131% greater) and of periosteal forming surface (81% greater) in RF/J than in NZB/B1NJ mice. We conclude that a high rate of periosteal bone formation increases bone size and strength in RF/J mice when compared with    NZB/B1NJ mice. The NZB/B1NJ and RF/J mice should be an excellent model to investigate the genes that regulate femur size and strength.</p>

	]]>
</description>

<author>J E. Wergedal et al.</author>


</item>


<item>
<title> Roles of neurotransmitter in synapse formation: development of neuromuscular junctions lacking choline acetyltransferase.</title>
<link>http://mouseion.jax.org/stfb2000_2009/453</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/453</guid>
<pubDate>Tue, 08 May 2012 17:00:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Activity-dependent and -independent signals collaborate to regulate synaptogenesis, but their relative contributions are unclear. Here, we describe the formation of neuromuscular synapses at which neurotransmission is completely    and specifically blocked by mutation of the neurotransmitter-synthesizing enzyme choline acetyltransferase. Nerve terminals differentiate extensively in the absence of neurotransmitter, but neurotransmission plays multiple roles in synaptic    differentiation.  These include influences on the numbers of pre- and postsynaptic partners, the distribution of synapses in the target field, the number of synaptic sites per target cell, and the number of axons per synaptic site.     Neurotransmission also regulates the formation or stability of transient acetylcholine receptor-rich processes (myopodia) that may initiate nerve-muscle contact. At subsequent stages, neurotransmission delays some steps in synaptic maturation but    accelerates others. Thus, neurotransmission affects synaptogenesis from early stages and coordinates rather than drives synaptic maturation.</p>

	]]>
</description>

<author>T Misgeld et al.</author>


</item>


<item>
<title>Index</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/16</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/16</guid>
<pubDate>Tue, 08 May 2012 17:00:32 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<source></source>

</item>


<item>
<title>The Influence of Groundwater Sample Flow Rate on Suspended Solids, Geochemical and Contaminant Concentrations and its Effect on Trend Analysis</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/15</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/15</guid>
<pubDate>Tue, 08 May 2012 17:00:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adherence to a standard groundwater sampling method is a fundamental requirement for the accurate assessment of contaminated sites. Confidence in expensive analytical results relied upon to evaluate contaminant fate, transport and risk potential is lost when possible sampling error is suspected. A correlation between suspended solids content and elevated fuel oil hydrocarbon concentrations was observed at sites where aggressive groundwater sampling methods were employed. This relationship was not observed when suspended solids were removed via filtration or at gasoline release sites, independent of filtration. The higher octanol-water coefficient of middle distillate petroleum compounds was attributed to the additive effect imparted by suspended solid-bound contaminants on dissolved phase concentrations. To further explore potential groundwater sampling induced error associated with aggressive purge and sample collection flow rates independent of turbidity, a controlled experiment was conducted over a range of groundwater flow rates at a gasoline impacted site. Volatile petroleum hydrocarbon (VPH) and geochemical parameter levels varied substantially between sampling treatments that ranged from 50 to 1,000 ml/min (including hand bailing) despite achieving stabilization of the geochemical parameters during each treatment. Sample precision was greatest for the 100 ml/min purge and sample flow rate. Possible sources of VPH concentration variability among the various treatments are discussed along with the importance of developing and adhering to site-specific sampling protocols, and the challenge of not doing so to trend analysis.</p>

	]]>
</description>

<author>Tease, Bruce et al.</author>

<source></source>

</item>


<item>
<title>New Continuous Monitoring Technologies for Vapor Intrusion,</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/14</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/14</guid>
<pubDate>Tue, 08 May 2012 17:00:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Typically, site investigation is carried out by using handheld or transportable field instruments coupled with offsite lab analyses. When using field instruments, the data generated represents a snapshot in time and space. Often, as with a PID or FID, data is presented as a total of contaminates present at that time and place. More sophisticated field equipment such as GC/MS can provide speciation, but still suffer from poor spatial and temporal resolution.</p>
<p>As an alternative, investigators can choose methods such as Summa canisters that sample for a fixed period, say 24 hours, followed by lab analysis. The data generated provides speciation but the concentrations represent an average for the sampling period.</p>
<p>Investigators are aware that environmental conditions such as pressure, temperature, water level and air movement substantially affect concentrations on a range of timescales, therefore uncertainty will always exist when using methods that lack temporal resolution.</p>
<p>The presentation describes instrumentation that provides real time continuous data both down hole and ambient for multiple parameters such as VOCs, methane, oxygen, carbon dioxide, hydrogen sulfide and carbon monoxide together with atmospheric and borehole pressure. Data is presented from field work carried out by, among other, the Maine DEP, for applications such as vapor intrusion, recovery well monitoring and landfill gas migration.</p>
<p>A comparison between spot sampling and continuous monitoring raises questions about the value of limited spot sampling.</p>

	]]>
</description>

<author>Smith, Thomas H. et al.</author>

<source></source>

</item>


<item>
<title>PCDDs/PCDFs in Soils at a Former Tannery Site-- Profiles as Evidence of PCP Contamination</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/13</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/13</guid>
<pubDate>Tue, 08 May 2012 17:00:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>PCDDs/PCDFs contamination in soils at a former tannery site in Eastern Massachusetts was found to be widespread.  PCDDs/PCDFs concentrations (the sum as (Cl<sub>4</sub> – Cl<sub>8</sub>); tetra-octachloro totals) in the majority of the soil samples (17/32) far exceeded concentrations (10-1000 times) typically found in soils in industrial/urban settings worldwide (1-10 ppb). The distribution pattern of PCDDs/PCDFs in site soils in combination with highly elevated concentrations did not indicate significant influences from off-site sources (e.g. aerial distribution pattern).  Widespread chromium contamination in soils often collocated with elevated concentrations of OCDD suggested that both contaminants could be attributed to a common industrial source:  the former tannery operations. (total chromium concentrations in the soil samples ranged from 22.2 – 3,457 mg/kg).</p>
<p>Elevated PCDDs/PCDFs concentrations predominated by OCDD were most likely attributable to the historical use of pentachlorophenol (PCP) and/or products containing PCP.  PCP was likely used as a fungicide/biocide in tannery processes that took place at the site. PCP origins were established through comparison of PCDDs/PCDFs profiles found in soils to those characteristic of PCP products as reported in the open literature (PCDDs/PCDFs profiles found in PCP products are predominated by hexa, hepta and octa congeners). Elevated OCDD concentrations present in site soils may not be solely attributable to historical use of PCP.  OCDD, which is the most common PCDDs/PCDFs congener present as a contaminant (artifact of PCP production chemistry) in PCP may also be formed photochemically.  The latter reaction takes place over time in surface soils with PCP serving as the precursor compound.  The extent to which this reaction has contributed to OCDD levels found in soils has been estimated by comparison of profiles found in site soils to those characteristic of commercial PCP products.</p>

	]]>
</description>

<author>Hunt, Gary T. et al.</author>

<source></source>

</item>


<item>
<title>Southern Caspian Sea Coasts, Morphology, Sediment Characteristics, and Sea Level Change</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/12</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/12</guid>
<pubDate>Tue, 08 May 2012 17:00:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>As the world's largest closed body of water, considerable changes in the Caspian Sea water level make it an unique laboratory to study all aspects of coastal zones. This research was aimed at evaluating the linkage between sea level changes and sediment characteristics of the south Caspian Sea coast. Initially, three field surveys were made along 700 km of the southern Caspian Sea coast. In addition to nearshore sampling, land forms were mapped. On the basis of the field reconnaissance, eight principal sampling stations were chosen. Sediments were sampled by divers along profiles at right angles to the coast at 5 depths (2, 4, 6, 8,10 meters). Hydrographic profiles also were surveyed. Laboratory tests on the sediment samples were made, and the sediment characteristics and morphological features were divided into distinct zones based on their response to sea level changes.</p>
<p><br><strong></strong></p>

	]]>
</description>

<author>Firoozfar, Alireza et al.</author>

<source></source>

</item>


<item>
<title>Risk Considerations Related To Environmental Arsenic Exposure:  Drinking Water Ingestion Versus Dietary Intake Or Soil Exposure</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/11</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/11</guid>
<pubDate>Tue, 08 May 2012 17:00:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The February 2010 release of the Draft Toxicological Review of Inorganic Arsenic by the U.S. Environmental Protection Agency provoked discussion of a potential significant downward revision of the arsenic cancer slope factor (CSF), which would be applicable to many oral exposure evaluations.  Given the extreme variability in soil cleanup guidelines that are in use throughout the United States and internationally for arsenic, it may be appropriate to more seriously consider bifurcating the manner in which arsenic is evaluated in environmental media.  In much the same fashion by which manganese and cadmium presently are evaluated from a risk perspective, arsenic may lend itself to similar evaluation from a drinking water exposure standpoint separately from a dietary or an environmental soil route of exposure.  This paper examines the basis for the current oral toxicological guidance with respect to specific exposure route and environmental medium of exposure, and addresses possible means for alternative toxicity guidance related to arsenic, based on differences in exposure through soil or the diet.</p>

	]]>
</description>

<author>Teaf, Christopher M. et al.</author>

<source></source>

</item>


<item>
<title>Sampling Strategy and Risk Evaluation of PAHs in Soil Near a Former Pipeline in Maine</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/10</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/10</guid>
<pubDate>Tue, 08 May 2012 17:00:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>In 1952 a 7.25-mile long jet propulsion fuel (JP-5) supply pipeline was built within a 30-foot wide easement from the fuel farm at Defense Fuel Support Point, Casco Bay to Naval Air Station Brunswick, Maine. This subterranean pipeline, which spanned 115 private properties in Harpswell, Maine, was in operation until 1991 when it was decommissioned and abandoned in place. During construction, the pipeline was wrapped with an asbestos covering and, to eliminate any potential threat to humans from exposure to this covering, a decision was made to remove the pipeline. The pipeline remained in place until the Maine Congressional delegation acquired funding in 2007 for the removal. Pipeline removal began on February 8, 2010 and was completed by May 18, 2010.</p>
<p>Polycyclic aromatic hydrocarbons (PAHs) were detected in soil during routine monitoring associated with pipeline removal. Whereas the source of PAHs was originally thought to have been JP-5 fuel oil releases, the project team determined that this was not the case and searched for another source of PAHs. This paper describes the planning and conduct of an environmental investigation that was necessary to evaluate the nature and extent of pipeline-related PAH contamination and potential human health risks from exposure to PAHs in easement soil. Collaboration between Maine Department of Environmental Protection (MEDEP) and the Navy was a key component in minimizing investigative costs while ensuring that the health of local residents was protected. A statistically based sampling design and statistical data analyses supported the project.</p>

	]]>
</description>

<author>Race, Charles D. et al.</author>

<source></source>

</item>


<item>
<title>Remediation of a Former MGP Site in Norwich New York: a Case Study</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/9</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/9</guid>
<pubDate>Tue, 08 May 2012 17:00:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Former Manufactured Gas Plant (MGP) production from circa 1860s through the 1950s at a site in Norwich, New York, resulted in impacts to both on-site and off-site soils and groundwater.  Site remediation includes four phases of treatment: in situ solidification (ISS) of on-site source materials; recovery of NAPL from off-site; in-situ chemical oxidation (ISCO) of off-site areas; and enhanced bioremediation of off-site groundwater.</p>
<p>Approximately 52,103 cubic yards (39,835 cubic meters) of impacted sand and gravel were solidified in-situ using auger mixing technology, and over 54,000 gallons (210,000 liters) of NAPL have been recovered to date.  An ISCO bench-scale study revealed that four applications of hydrogen peroxide will reduce BTEX and naphthalene by 99% and TPH by 50%.  Full-scale ISCO application will occur upon completion of NAPL recovery, followed by enhanced bioremediation of dissolved phase contamination (benzene and naphthalene).</p>

	]]>
</description>

<author>Underhill, Scott A. et al.</author>

<source></source>

</item>


<item>
<title> The Alstrom syndrome: is it a rare or unknown disease?</title>
<link>http://mouseion.jax.org/stfb2000_2009/452</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/452</guid>
<pubDate>Tue, 08 May 2012 17:00:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Alstrom syndrome is a rare, autosomal recessive disorder characterized by retinal degeneration, obesity, progressive hearing impairment, non-insulin-dependent diabetes mellitus and kidney and heart failure.  Mental retardation    is absent and the extremities are normal. The Alstrom syndrome gene located on chromosome 2, has been recently identified. The Alstrom syndrome involves multiple organ systems with a complex interaction between pathways. Phenotypic expression    varies considerably, even within sibships. Manifestations observed in some, but not all, Alstrom syndrome patients include acanthosis nigricans, alopecia, short stature, scoliosis, kyphosis, hyperostosis frontalis interna, muscle dystonia,    advanced bone age and subcapsular cataract. Other metabolic and endocrinological abnormalities have been described: hypothyroidism, hypogonadism, diabetes insipidus, growth hormone deficiency, hyperuricemia and hyperlipidemia. In the final stages    of the disease, affected individuals exhibit progressive chronic nephropathy with eventual kidney failure. The most frequent causes of death include hepatic dysfunction and congestive heart failure secondary to dilated cardiomyopathy. We have    summarized our personal clinical data and the information from the scientific literature on the topic in order to provide an up-to-date review on the Alstrom syndrome.</p>

	]]>
</description>

<author>P Maffei et al.</author>


</item>


<item>
<title>Dechlorination of Pentachlorophenol by Zero Valent Iron and Bimetals: Effect of Surface Characteristics and Bimetal Preparation Procedure</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/8</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/8</guid>
<pubDate>Tue, 08 May 2012 17:00:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Treatment of Pentachlorophenol (PCP) is challenging due to its hydrophobic nature and the stability of the carbon-chlorine bond, particularly in aromatic molecules. Zero Valent Iron (ZVI) has been used as an effective in situ passive treatment process for PCP contaminated groundwater. However, ZVI applications can experience a decrease in degradation rates over time due to: ZVI surface passivation, the formation of non-conducting iron oxides on the ZVI surface, and the accumulation of less chlorinated intermediates. In this study, ZVI modification by acid washing and formation of bimetallic systems by the incorporation of Nickel (Ni) was explored to overcome these limitations.</p>
<p>PCP degradation was investigated in batch tests using ZVI as received (unwashed or UW) and acid washed (AW) ZVI. Two forms of bimetals were tested - one in which the Ni powder and ZVI (UW or AW) were physically mixed (Ni<sub>S</sub>/Fe) and the other in which the Ni was coated onto acid washed ZVI (Ni<sub>C</sub>/Fe) by reacting ZVI with NiSO<sub>4</sub> solutions. PCP dechlorination was confirmed by gas chromatography quantifying PCP and all intermediates formed. Raman spectroscopy was used to characterise the ZVI surfaces.</p>

	]]>
</description>

<author>Gunawardana, Buddhika et al.</author>

<source></source>

</item>


<item>
<title>Interpretation of Biological Data on Indoor Air Quality:  Presence Doesn&apos;t Equate to Significance</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/7</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/7</guid>
<pubDate>Tue, 08 May 2012 17:00:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Based on results of residential air tests, homeowners may be advised that a significant mold problem exists in their home, and that extensive cleanup or remediation is required.  Those living in such homes may attribute perceived or actual health conditions to reported levels of, or exposure to, molds.  Consensus numerical guidelines or agency standards for evaluation of mold exposure do not exist.  Toxicological evidence does not support a contention that healthy individuals are at significant health risk from common mold levels. Putative sensitive populations are not well-documented, and the literature is controversial or inconsistent.  Factors influencing likelihood that indoor mold exposure contributes to adverse health effects include indoor vs. outdoor mold levels, concentration/types of mold species indoors vs. outdoors, number of samples collected indoors vs. outdoors, and number of sample events.  For situations in which prevalence and speciation of indoor mold is indistinguishable from or less than outdoors, adverse health effects cannot be solely or predominantly a result of indoor exposures.  Mold concentration data are reviewed from several residences where mold test results were presented as indicating a "mold problem".  We conclude, despite the fact that extensive and expensive remediation efforts and protracted litigation occurred, these data do not support allegations of adverse health effects from potential exposure to indoor mold in the observed homes.</p>

	]]>
</description>

<author>Teaf, Christopher M. et al.</author>

<source></source>

</item>


<item>
<title>How Overly Cautious Risk Assessment Methods Overstate Risk from PCBs in Indoor Air</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/6</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/6</guid>
<pubDate>Tue, 08 May 2012 17:00:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The past use of building materials that contained polychlorinated biphenyls (PCBs) is prompting public concern and expensive PCB removal projects.  Building materials that may contain PCBs include paint, caulk, floor finishes and many other interior and exterior construction components manufactured before 1972. While initial concern about PCBs in buildings has focused on schools, it is likely that PCB-containing materials will also be found in many residential, commercial, and industrial structures.</p>
<p>In buildings, the primary route of human exposure is the inhalation of PCBs that volatilize out of building materials. The USEPA has indicated that inhalation of airborne PCBs may pose a significant human exposure pathway in schools. EPA’s approach to PCBs in schools is evolving quickly.  Initial estimates of health risk from indoor PCBs were calculated using risk assessment methods and EPA published toxicity factors. Recently, EPA established guidance titled “Public Health Levels for PCBs in Indoor School Air” to assist school systems in remediation efforts.  These criteria are intended to be “prudent public health levels that maintain PCB exposures below the 'reference dose' – the amount of PCB exposure that EPA does not believe will cause harm."</p>
<p>This article considers two factors central to the accurate assessment of PCB indoor air risk: 1) the difference in the chemical make up of PCBs in air compared to the chemical make up of the PCBs in the building materials they originated from; and 2) how the variability in certain commercial lots of PCBs (Aroclors) can result in different degrees of toxicity.  Each of these factors may act to significantly modify the level of risk associated with the inhalation of PCBs in buildings.  At the present time, EPA has not incorporated these factors into its calculation of its Public Health Levels.</p>

	]]>
</description>

<author>Okun, James D. et al.</author>

<source></source>

</item>


<item>
<title>Mercury Exposure Considerations: Evaluating the Chemical Form and Activities of the Individual</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/5</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/5</guid>
<pubDate>Tue, 08 May 2012 17:00:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Evaluation of exposure to mercury in an environmental or an occupational context is more complex than that for many other substances, insofar as it requires consideration of a combination of factors including the form of mercury present and the associated toxicology (e.g., elemental vs. organic vs. inorganic), as well as characteristics of the individual/exposure being evaluated (e.g., route, frequency, duration, and magnitude of exposure). Given the major differences in absorption of mercury forms by route, it is not sufficient to discuss simply “mercury exposure”, as often occurs in media reports. Methods for addressing each of these characteristics are discussed, and specific case studies are presented to illustrate the practical significance of differences in contact with several common mercury forms that may be encountered under variable exposure circumstances. In addition, a discussion is presented of the variability of responses between adults and children to selected mercury forms, with attention to similarities or differences in observed effects. Finally, common sources of mercury exposure to the general population are discussed, for purposes of comparison with potential exposures in the workplace.</p>

	]]>
</description>

<author>Teaf, Christopher M. et al.</author>

<source></source>

</item>


<item>
<title>Monitoring Sources of Mercury in the Atmosphere</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/4</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/4</guid>
<pubDate>Tue, 08 May 2012 17:00:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>In Virginia and most other states, rain and snow collection stations have been used to determine the concentration of mercury in precipitation. These mercury measurements are distributed by the National Atmospheric Deposition Program through the Illinois State Water Survey (http://nadp.sws.uiuc.edu). Mercury deposition data has been gathered for over a decade and may be compared to the on-line data currently reported from collection sites. Coal-burning power plants are thought to contribute most of the atmospheric mercury, and it was thought that the precipitation collections would prove this hypothesis. In Virginia, this hypothesis is supported. It has been found that the atmospheric content of mercury increases during prolonged intervals without precipitation. In this study, it was found that the atmospheric content of mercury was exceptionally low following an unusually prolonged precipitation event.</p>

	]]>
</description>

<author>Metcalf, James et al.</author>

<source></source>

</item>


<item>
<title>Assessing the Bioavailability of Arsenic in Sediments for Use in Human Health Risk Assessment</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/3</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/3</guid>
<pubDate>Tue, 08 May 2012 17:00:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Arsenic concentrations in sediments in a wetlands located downgradient from a landfill in northeastern Massachusetts were found to be over 1,000 mg/kg in several locations with a maximum detected concentration of 4,500 mg/kg. The elevated arsenic in sediment is likely the result of the dissolution of iron and arsenic in the underlying rock under reducing conditions mobilized with the groundwater and co-precipitating out into the sediments when groundwater reaches the oxidizing surface water, producing an iron and arsenic bearing floc. Approximately 15 acres of wetlands appear to be impacted from elevated arsenic concentrations. To assess the potential impacts to human health and to determine the extent of acreage requiring remedial action, a site-specific bioavailability factor was developed using an <em>in vitro</em> laboratory assessment.  While <em>in vivo</em> (live animal) studies are considered to be the most accurate measures of bioavailability for assessing absorption of contaminants by humans, the <em>in vivo</em> studies are expensive and lengthy. The <em>in vitro</em> approach undertaken for this assessment simulates digestive activity in the stomach, including residence time, pH, temperature, agitation, and solid to liquid ratio.  This <em>in vitro</em> laboratory approach coupled with an adjustment based on <em>in vivo</em> data, along with a mineralogical characterization of the impacted sediments, served to develop a site-specific bioavailability factor that resulted in more accurate human health risk characterization results.</p>

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</description>

<author>Lamie, Pamela O.</author>

<source></source>

</item>


<item>
<title>Characteristics of Soils and Heavy Metal Content of Vegetation in Oil Spill Impacted Land in Nigeria</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/2</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/2</guid>
<pubDate>Tue, 08 May 2012 17:00:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study examined the impact of an oil spill on soil characteristics and heavy metal content of vegetation. Soil and vegetation were sampled using a 1 metre square quadrant at distances of 1 m, 10 m, 20 m and 30 m from the oil spill. After vegetation identification, they were separated into leaves, stems and roots. Analysis of soil characteristics and heavy metals (Pb, Cd and Zn) content of the vegetation was carried out. The data were analyzed using descriptive statistics and ANOVA. <em>Calopogonium mucunoides, Axonopus compressus and Sida acuta </em>were identified. Leaves had higher heavy metals content followed by stems and roots. Concentrations of heavy metals in the soils with respect to distances were in the order of 1 m > 10 m > 20 m > 30 m. Soil organic carbon content ranged from 18.75 – 27. 30 g/kg. The soils heavy metal concentrations ranged from 0.10 – 0.18 mgCd/kg, 0.34 – 0.46 mgZn/kg and 0.28 – 0.44 mgPb/kg.</p>

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</description>

<author>Bada, Babatunde Saheed et al.</author>

<source></source>

</item>


<item>
<title>Front Matter</title>
<link>http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/1</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/soilsproceedings/vol17/iss1/1</guid>
<pubDate>Tue, 08 May 2012 17:00:16 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<source></source>

</item>


<item>
<title> Elizabeth S. Russell, May 1, 1913 - May 28, 2001.</title>
<link>http://mouseion.jax.org/stfb2000_2009/451</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/451</guid>
<pubDate>Tue, 08 May 2012 17:00:01 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J E. Barker et al.</author>


</item>


<item>
<title> During the early prediabetic period in NOD mice, the pathogenic CD8(+) T-cell population comprises multiple antigenic specificities.</title>
<link>http://mouseion.jax.org/stfb2000_2009/450</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/450</guid>
<pubDate>Tue, 08 May 2012 16:59:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the NOD mouse model of type 1 diabetes, major histocompatibilitycomplex (MHC) class I-restricted CD8(+) T cells are essential for disease development. However, the extent of diversity of their antigenic specificities during    early pathogenesis remains unclear. An insulin-derived peptide was recently identified as the epitope for the NOD-derived diabetogenic T-cell clone G9C8. To explore the possibility that the early pathogenic CD8(+) T-cell population comprises    additional antigenic specificities, we employed the T-cell clones AI4 and NY8.3, both of which are pathogenic and represent specificities present in early insulitic lesions. The clones responded to distinct fractions of chromatographically    separated class I MHC-bound peptides purified from NOD-derived NIT-1 beta cells, and neither clone recognized the insulin-derived peptide. NIT-1 cells represent an unlimited peptide source that will allow for the future isolation and sequencing    of the novel multiple epitopes targeted early in the autoimmune response by pathogenic CD8(+) T cells.</p>

	]]>
</description>

<author>T P. DiLorenzo et al.</author>


</item>


<item>
<title> Development of mice expressing a single D-type cyclin.</title>
<link>http://mouseion.jax.org/stfb2000_2009/449</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/449</guid>
<pubDate>Tue, 08 May 2012 16:59:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>D-cyclins (cyclins D1, D2, and D3) are components of the core cell cycle machinery. To directly test the ability of each D-cyclin to drive development of various lineages, we generated mice expressing only cyclin D1, or only cyclin    D2, or only cyclin D3. We found that these "single-cyclin" embryos develop normally until late gestation. Our analyses revealed that in single-cyclin embryos, the tissue-specific expression pattern of D-cyclins was lost. Instead, mutant embryos    ubiquitously expressed the remaining D-cyclin. These findings suggest that the functions of the three D-cyclins are largely exchangeable at this stage. Later in life, single-cyclin mice displayed focused abnormalities, resulting in premature    mortality. "Cyclin D1-only" mice developed severe megaloblastic anemia, "cyclin D2-only" mice presented neurological abnormalities, and "cyclin D3-only" mice lacked normal cerebella. Analyses of the affected tissues revealed that these    compartments failed to sufficiently up-regulate the remaining, intact D-cyclin. In particular, we found that in cerebellar granule neuron precursors, the N-myc transcription factor communicates with the cell cycle machinery via cyclins D1 and D2,    but not D3, explaining the inability of D3-only mice to up-regulate cyclin D3 in this compartment. Hence, the requirement for a particular cyclin in a given tissue is likely caused by specific transcription factors, rather than by unique    properties of cyclins.</p>

	]]>
</description>

<author>M A. Ciemerych et al.</author>


</item>


<item>
<title> Vitamin D(3) receptor ablation sensitizes skin to chemically induced tumorigenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/448</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/448</guid>
<pubDate>Tue, 08 May 2012 16:59:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>1,25-Dihydroxyvitamin D(3) (1,25D(3)) is the biologically active form of vitamin D(3) that interacts with the nuclear vitamin D(3) receptor (VDR) to modulate gene expression in a tissue-specific fashion. 1,25D(3) is a potent    regulator of cell proliferation, differentiation and apoptosis in a variety of cell types, including keratinocytes. In these studies, we assessed the sensitivity of mice homozygous for a null allele of the VDR (VDR(-/-) mice) and their wild-type    counterparts (VDR(+/+) mice) to oral administration of the carcinogen 7,12-dimethylbenzanthracene (DMBA).  Although the protocol was optimized for the induction of mammary tumors, 85% of VDR(-/-) mice developed persistent skin tumors within 60    days of carcinogen exposure. In VDR(-/-) mice exposed to DMBA, papillomas arose on all areas of the body, with an average tumor burden of 5.3 papillomas/mouse. No papillomas or any other skin lesions were observed in age- and sex-matched VDR(+/+)    mice dosed with DMBA and followed for 6 months. The majority (80%) of skin tumors that developed in VDR(-/-) mice were classified histologically as sebaceous, squamous or follicular papillomas. Other types of lesions, including basal cell    carcinoma, hemangioma and melanotic foci, were occasionally observed in VDR(-/-) mice (but not in VDR(+/+) mice) exposed to DMBA. Quantification of epidermal thickness and BrdU incorporation indicated that skin from VDR(-/-) mice exhibited    hyperproliferation beginning at 7 weeks of age, which was exacerbated by DMBA treatment. Untreated aging VDR(-/-) mice did not exhibit tumor formation, but did develop a progressive skin phenotype characterized by thickened wrinkled skin, dermoid    cysts and long curly nails. Together with previous reports that 1,25D(3) inhibits papilloma formation induced by topical DMBA-TPA regimens, our observation of enhanced sensitivity of VDR(-/-) mice to chemically induced skin carcinogenesis offers    compelling evidence that disruption of VDR signaling predisposes to neoplasia.</p>

	]]>
</description>

<author>G M. Zinser et al.</author>


</item>


<item>
<title> The preferential ability of B lymphocytes to act as diabetogenic APC in NOD mice depends on expression of self-antigen-specific immunoglobulin receptors.</title>
<link>http://mouseion.jax.org/stfb2000_2009/447</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/447</guid>
<pubDate>Tue, 08 May 2012 16:58:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>B lymphocytes partially contribute to autoimmune type 1 diabetes (T1D) as a subset of APC with a preferential ability to trigger pathogenic CD4 T cells. We hypothesized that this resulted from the unique ability of B lymphocytes to    take up pancreatic beta cell proteins through Ig mediated capture. T1D was significantly delayed, but not prevented, in a NOD stock in which the B lymphocyte Ig repertoire was strongly restricted because of the allelic exclusion induced by    transgenic Ig molecules specific for the disease irrelevant hen egg lysozyme (HEL) protein (NOD.IgHEL mice).  However, introducing the Ig(mu)null mutation to eliminate the small residual numbers of non-transgenic B lymphocytes in the NOD.IgHEL    stock strongly suppressed T1D to the same low levels that characterize B lymphocyte deficient NOD.Ig(mu)null mice. In contrast to standard NOD mice, both the NOD.IgHEL.Ig(mu)null and NOD.Ig(mu)null stocks were unable to generate T cell responses    against the candidate diabetes autoantigen, glutamic acid decarboxylase. These results indicate that Ig-mediated capture of beta cell autoantigens accounts for why B lymphocytes have a greater capacity than other APC subtypes to trigger    diabetogenic T cells.  Hence, defects in B lymphocyte, as well as T lymphocyte, tolerance induction mechanisms may contribute to T1D in NOD mice.</p>

	]]>
</description>

<author>P A. Silveira et al.</author>


</item>


<item>
<title> Age-related alterations in the lymphohematopoietic and B-lineage precursor populations in NZB mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/446</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/446</guid>
<pubDate>Tue, 08 May 2012 16:58:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Significant disturbances in B lineage populations of New Zealand Black (NZB) mice have been reported, both with respect to their phenotypes as well as to their function. Notably, there is a profound age-dependent decrease in B-cell    precursors in this strain of lupus prone mice. In efforts to characterize the impact of this disturbance in disease, we performed an intensive phenotypic and B-cell population analysis in young and old NZB mice. Our results revealed that there    was a significant age-dependent decrease in B cell precursors at all levels of the B-cell-lineage developmental pathway. Analysis of the proliferative capacity of these cell populations showed a comparative decrease in cycling activity in the    B-cell-lineage populations of old NZB mice.  Furthermore, these cell subsets were much more susceptible to spontaneous apoptosis when compared with similar populations from age-matched BALB/c or young NZB mice. Since the frequency of cells that    express the interleukin-7 receptor (IL-7R) declines as NZB mice age, we hypothesize that impairment of IL-7R signal transduction pathways could contribute to severe perturbations of B-cell function in aged NZB mice.</p>

	]]>
</description>

<author>Z X. Lian et al.</author>


</item>


<item>
<title> QTL analysis of self-selected macronutrient diet intake: fat, carbohydrate, and total kilocalories.</title>
<link>http://mouseion.jax.org/stfb2000_2009/445</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/445</guid>
<pubDate>Tue, 08 May 2012 16:58:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The present study investigated the inheritance of dietary fat, carbohydrate, and kilocalorie intake traits in an F(2) population derived from an intercross between C57BL/6J (fat-preferring) and CAST/EiJ (carbohydrate-preferring)    mice. Mice were phenotyped for self-selected food intake in a paradigm which provided for 10 days a choice between two macronutrient diets containing 78/22% of energy as a composite of either fat/protein or carbohydrate/protein. Quantitative    trait locus (QTL) analysis identified six significant loci for macronutrient intake: three for fat intake on chromosomes (Chrs) 8 (Mnif1), 18 (Mnif2), and X (Mnif3), and three for carbohydrate intake on Chrs 17 (Mnic1), 6 (Mnic2), and X (Mnic3).    An absence of interactions among these QTL suggests the existence of separate mechanisms controlling the intake of fat and carbohydrate. Two significant QTL for cumulative kilocalorie intake, adjusted for baseline body weight, were found on Chrs    17 (Kcal1) and 18 (Kcal2). Without body weight adjustment, another significant kcal locus appeared on distal Chr 2 (Kcal3). These macronutrient and kilocalorie QTL, with the exception of loci on Chrs 8 and X, encompassed chromosomal regions    influencing body weight gain and adiposity in this F2 population. These results provide new insight into the genetic basis of naturally occurring variation in nutrient intake phenotypes.</p>

	]]>
</description>

<author>Richards B. Smith et al.</author>


</item>


<item>
<title> Large-scale, high-throughput screening for coagulation and hematologic phenotypes in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/444</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/444</guid>
<pubDate>Tue, 08 May 2012 16:58:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Phenome Project is an international effort to systematically gather phenotypic data for a defined set of inbred mouse strains. For such large-scale projects the development of high-throughput screening protocols that    allow multiple tests to be performed on a single mouse is essential. Here we report hematologic and coagulation data for more than 30 inbred strains. Complete blood counts were performed using an Advia 120 analyzer. For coagulation testing, we    successfully adapted the Dade Behring BCS automated coagulation analyzer for use in mice by lowering sample and reagent volume requirements. Seven automated assay procedures were developed. Small sample volume requirements make it possible to    perform multiple tests on a single animal without euthanasia, while reductions in reagent volume requirements reduce costs. The data show that considerable variation in many basic hematological and coagulation parameters exists among the inbred    strains. These data, freely available on the World Wide Web, allow investigators to knowledgeably select the most appropriate strain(s) to meet their individual study designs and goals.</p>

	]]>
</description>

<author>L L. Peters et al.</author>


</item>


<item>
<title> Loss of cell adhesion in Dsg3bal-Pas mice with homozygous deletion mutation (2079del14) in the desmoglein 3 gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/443</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/443</guid>
<pubDate>Tue, 08 May 2012 16:57:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pemphigus encompasses a group of autoimmune blistering diseases with circulating pathogenic autoantibodies recognizing several proteins, including the desmosomal cadherin, desmoglein 3. Targeted disruption of the Dsg3 gene by    homologous recombination (Dsg3tm1stan) in mouse results in fragility of the skin and oral mucous membranes, analogous to the human disease. In addition, the Dsg3tm1stan mice develop phenotypic runting and hair loss, identical to that of the mouse    mutant, Dsg3bal-2J. The Dsg3bal-2J mice are homozygous for a 1 bp insertion (2275insT) in the Dsg3 gene resulting in a nonfunctional Dsg3 mRNA. In this study, we characterized an allelic mutation, Dsg3bal-Pas, with clinical features similar to    those in Dsg3bal-2J. We have identified a 14 bp deletion in exon 13 of the Dsg3 gene resulting in a frameshift and premature termination codon 7 bp downstream from the site of the deletion and causing a truncation of the desmoglein 3 polypeptide    by 199 amino acids, eliminating virtually all of the intracellular domain. We demonstrate that, although a Dsg3 mRNA transcript was detectable in Dsg3bal-Pas skin, the corresponding protein for desmoglein 3 was completely absent in the oral    mucosal epithelium of homozygous Dsg3bal-Pas compared with that of +/Dsg3bal-Pas mice. No significant changes in the expression of desmogleins 1 and 2 were detected. To elucidate a potential mechanism causing loss of cell adhesion in the    Dsg3bal-Pas mice, we generated a myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein and expressed it in keratinocytes. The myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein was found predominantly in the cytoplasm possibly due to increased    proteolytic degradation. Cell surface staining was also detected but was jagged, not linear along the cell-cell border like that observed for the full-length desmoglein 3. The expression of the myc-tagged truncated Dsg3bal-Pas desmoglein 3    protein resulted in a reduction in staining of other desmosomal proteins, including desmoglein 1 and 2, plakophilin 2, and plakoglobin. In addition, the cells expressing myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein underwent dramatic    changes in cell morphology and exhibited striking extensive filopodia. Collectively, these data showed that the perturbation of desmoglein 3 found in the Dsg3bal-Pas mice resulted in disadhesion of keratinocytes manifested with blistering    phenotype.</p>

	]]>
</description>

<author>L Pulkkinen et al.</author>


</item>


<item>
<title> Resistance to alopecia areata in C3H/HeJ mice is associated with increased expression of regulatory cytokines and a failure to recruit CD4+ and CD8+ cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/442</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/442</guid>
<pubDate>Tue, 08 May 2012 16:57:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Grafting alopecia areata affected C3H/HeJ mouse skin to littermates induces alopecia areata, but high dietary soy oil reduces alopecia areata susceptibility. Alopecia areata affected and resistant mice were characterized to    evaluate possible mechanisms involved in alopecia areata resistance. Of 44 mice that received alopecia areata affected skin grafts but failed to develop alopecia areata, only two of 22 receiving further alopecia areata affected skin grafts    developed alopecia areata, whereas 39 of 44 controls developed alopecia areata. Alopecia areata affected skin contained increased numbers of CD4+ and CD8+ cells, increases in pro inflammatory T helper 1 and T helper 2 type cytokines, and    upregulation of CD28, CD40L, and their ligands. In draining lymph nodes, a relatively high number of antigen-presenting cells was recovered, whereas several CD44v variants were downregulated. In contrast, alopecia areata resistant mouse skin did    not display increased numbers of CD4+ and CD8+ cells, whereas counter-regulatory cytokines interleukins 4 and 10 were upregulated. High expression of CD28, CD80, CD86, CD40, CTLA4, CD44v variants, and FasL occurred in alopecia areata resistant    mouse spleens. In vitro, lymph node cells of susceptible and resistant mice responded equally to a mitogenic stimulus, but only lymph node cells from alopecia areata affected mice displayed an increased response with T cell receptor stimulation    via anti-CD3 cross-linking. These results suggest alopecia areata is a cell-mediated autoimmune disease, but alopecia areata affected skin graft hosts may resist alopecia areata onset through active counter-regulatory mechanisms. Because alopecia    areata resistant mice showed unimpaired responsiveness and a transient inflammatory response towards the graft, it is suggested that alopecia areata develops as a consequence of an inappropriate immune response regulation.</p>

	]]>
</description>

<author>K J. McElwee et al.</author>


</item>


<item>
<title> Initial sequencing and comparative analysis of the mouse genome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/441</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/441</guid>
<pubDate>Tue, 08 May 2012 16:57:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The sequence of the mouse genome is a key informational tool for understanding the contents of the human genome and a key experimental tool for biomedical research. Here, we report the results of an international collaboration to    produce a high-quality draft sequence of the mouse genome. We also present an initial comparative analysis of the mouse and human genomes, describing some of the insights that can be gleaned from the two sequences. We discuss topics including the    analysis of the evolutionary forces shaping the size, structure and sequence of the genomes; the conservation of large-scale synteny across most of the genomes; the much lower extent of sequence orthology covering less than half of the genomes;    the proportions of the genomes under selection; the number of protein-coding genes; the expansion of gene families related to reproduction and immunity; the evolution of proteins; and the identification of intraspecies    polymorphism.</p>

	]]>
</description>

<author>R H. Waterston et al.</author>


</item>


<item>
<title> Analysis of the mouse transcriptome based on functional annotation of 60,770 full-length cDNAs.</title>
<link>http://mouseion.jax.org/stfb2000_2009/440</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/440</guid>
<pubDate>Tue, 08 May 2012 16:57:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Only a small proportion of the mouse genome is transcribed into mature messenger RNA transcripts. There is an international collaborative effort to identify all full-length mRNA transcripts from the mouse, and to ensure that each    is represented in a physical collection of clones. Here we report the manual annotation of 60,770 full-length mouse complementary DNA sequences. These are clustered into 33,409 'transcriptional units', contributing 90.1% of a newly established    mouse transcriptome database. Of these transcriptional units, 4,258 are new protein-coding and 11,665 are new non-coding messages, indicating that non-coding RNA is a major component of the transcriptome. 41% of all transcriptional units showed    evidence of alternative splicing. In protein-coding transcripts, 79% of splice variations altered the protein product. Whole-transcriptome analyses resulted in the identification of 2,431 sense-antisense pairs.  The present work, completely    supported by physical clones, provides the most comprehensive survey of a mammalian transcriptome so far, and is a valuable resource for functional genomics.</p>

	]]>
</description>

<author>Y Okazaki et al.</author>


</item>


<item>
<title> Cloning and genomic characterization of Felis domesticus papillomavirus type 1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/439</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/439</guid>
<pubDate>Tue, 08 May 2012 16:56:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>A novel papillomavirus was cloned from hyperkeratotic cutaneous lesions of a Persian domestic cat. The Felis domesticus papillomavirus (FdPV-1) genome counts 8300 bp and has a typical genome structure with an early region (E1, E2,    E4, E6, E7), a late region (L1, L2), and a noncoding upstream regulatory region (URR or NCR1) between the end of L1 and the beginning of E6. The FdPV-1 also shows an unusual second noncoding region (NCR2) of 1.3 kb, situated between the end of E2    and the beginning of L2.  This NCR2 is uniquely related to a similar region in the canine oral papillomavirus (COPV). Phylogenetic analysis places FdPV-1 together with COPV, the cottontail rabbit papillomavirus, human papillomavirus type 1    (HPV-1), and HPV-63 in the group of the benign cutaneous papillomaviruses.  The position of FdPV-1 in the phylogenetic tree allows us to hypothesize that already in an early phase of the papillomavirus molecular evolution, a split occurred into    viruses with a dual tropism primarily for cutaneous epithelia but also secondarily for mucosal surfaces, and viruses with a specific monotropism for mucosal surfaces. The close relationship between FdPV-1 and COPV, and between their Canidae and    Felidae hosts, supports the hypothesis that papillomaviruses have speciated and coevolved together with their hosts throughout vertebrate evolution. A papillomavirus mutation rate of 0.73 to 0.96 x 10(-8) nucleotide substitutions per base per    year was calculated.</p>

	]]>
</description>

<author>R Tachezy et al.</author>


</item>


<item>
<title> Real-time T-cell profiling identifies H60 as a major minor histocompatibility antigen in murine graft-versus-host disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/438</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/438</guid>
<pubDate>Tue, 08 May 2012 16:56:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although CD8 T cells are thought to be a principal effector population of graft-versus-host disease (GVHD), their dynamics and specificity remain a mystery. Using a mouse model in which donor and recipient were incompatible at many    minor histocompatibility antigens (minor H Ags), the CD8 T-cell response was tracked temporally and spatially through the course of GVHD. Donor CD8 T cells in the circulation, spleen, lung, and liver demonstrated virtually identical kinetics:    rapid expansion and then decline prior to morbidity. Remarkably, up to one fourth of the CD8 T cells were directed against a single minor antigen, H60. Extreme H60 immunodominance occurred regardless of sampling time, site, and genetic    background. This study is the first to analyze the T cells participating in GVHD in "real-time," demonstrates the exceptional degree to which immunodominance of H60 can occur, and suggests that such superdominant minor H Ags could be risk factors    for GVHD.</p>

	]]>
</description>

<author>E Y. Choi et al.</author>


</item>


<item>
<title> Interleukin-10-deficient mice are less susceptible to the induction of alopecia areata.</title>
<link>http://mouseion.jax.org/stfb2000_2009/437</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/437</guid>
<pubDate>Tue, 08 May 2012 16:56:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Paul P. Freyschmidt et al.</author>


</item>


<item>
<title> Effects of oral dehydroepiandrosterone on bone density in young women with anorexia nervosa: a randomized trial.</title>
<link>http://mouseion.jax.org/stfb2000_2009/436</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/436</guid>
<pubDate>Tue, 08 May 2012 16:55:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Young women with anorexia nervosa (AN) have subnormal levels of dehydroepiandrosterone (DHEA) and estrogen that may be mechanistically linked to the bone loss seen in this disease. The purpose of this study was to compare the    effects of a 1-yr course of oral DHEA treatment vs.  conventional hormonal replacement therapy (HRT) in young women with AN.  Sixty-one young women were randomly assigned to receive oral DHEA (50 mg/d) or HRT (20 micro g ethinyl estradiol/0.1 mg    levonorgestrel).  Anthropometric, nutrition, and exercise data were acquired every 3 months, and bone mineral density (BMD) and body composition were measured by dual energy x-ray absorptiometry (DXA) every 6 months over 1 yr. Serum samples were    obtained for measurements of hormones, proresorptive cytokines, and bone formation markers, and urine was collected for determinations of bone resorption markers at each visit. In initial analyses, total hip BMD increased significantly and    similarly (+1.7%) in both groups. Hip BMD increases were positively correlated with increases in IGF-I (r = 0.44; P = 0.030) and the bone formation marker, bone-specific alkaline phosphatase increased significantly only in the DHEA treatment    group (P = 0.003).  However, both groups gained significant amounts of weight over the year of therapy, and after controlling for weight gain, no treatment effect was detectable. There was no significant change in lumbar BMD in either group.     Both bone formation markers, bone-specific alkaline phosphatase and osteocalcin, increased transiently at 6-9 months in those subjects receiving DHEA compared with the estrogen-treated group (P < 0.05). Both DHEA and HRT significantly reduced    levels of the bone resorption markers, urinary N-telopeptides (P < 0.05). There was a positive correlation between changes in IGF-I and changes in weight, body fat determined by DXA, and estradiol for both groups. In addition, patients receiving    DHEA exhibited improvement on three validated psychological instruments (Eating Attitudes Test, Anorexia Nervosa Subtest, and Spielberger Anxiety Inventory). Both DHEA and HRT had similar effects on hip and spinal BMD.  Over the year of    treatment, maintenance of both hip and spinal BMD was seen, but there was no significant increase after accounting for weight gain. Compared with HRT, DHEA appeared to have anabolic effects, evidenced by the positive correlation between increases    in hip DXA measurements and IGF-I and significant increases in bone formation markers. Both therapies significantly decreased bone resorption. Replicating results from studies of the elderly, DHEA resulted in improvements in specific    psychological parameters in these young women.</p>

	]]>
</description>

<author>C M. Gordon et al.</author>


</item>


<item>
<title> Confirmation and high resolution mapping of an atherosclerosis susceptibility gene in mice on Chromosome 1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/435</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/435</guid>
<pubDate>Tue, 08 May 2012 16:55:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previously, we demonstrated that Ath1 is a quantitative trait locus for aortic fatty streak formation, located on Chromosome (chr) 1, with susceptibility in C57BL/6J mice and resistance in C3H/HeJ and BALB/cJ mice fed an    atherogenic diet. In this study, we find an atherosclerosis susceptibility locus in the same region of Chr 1 by constructing two congenic strains with the resistance phenotype transferred from different resistant strains, PERA/EiJ or SPRETUS/EiJ.    By backcrossing one congenic strain to C57BL/6J and testing recombinant animals, we reduced the distance of the atherosclerosis susceptibility region to 2.3 cM between D1Mit14 and D1Mit10. Further testing of nine recombinant animals showed that    eight of the nine were consistent with a further narrowing between D1Mit159 and D1Mit398 a distance of 0.66 cM. This region encompasses a number of potential candidate genes including the thiol-specific antioxidant gene Aop2, also known as    peroxiredoxin 5 (Prdx5). AOP2 is capable of reducing hydroperoxides and lipid peroxides in the cell. To investigate Aop2 as a potential candidate, we mapped Aop2 in our backcross and localized it to the atherosclerosis susceptibility interval. We    determined that Aop2 is highly expressed in atherosclerosis-related tissues including liver and heart. We also found an inverse correlation between Aop2 mRNA in liver and atherosclerosis phenotype for strains C57BL/6 and the resistant congenic    derived from SPRETUS/EiJ. Since LDL oxidation has been implicated in the pathogenesis of this disease, and AOP2 possesses antioxidant activity, we suggest the role of Aop2 in atherosclerosis susceptibility needs to be further    explored.</p>

	]]>
</description>

<author>S A. Phelan et al.</author>


</item>


<item>
<title> Immunodominance of H60 is caused by an abnormally high precursor T cell pool directed against its unique minor histocompatibility antigen peptide.</title>
<link>http://mouseion.jax.org/stfb2000_2009/434</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/434</guid>
<pubDate>Tue, 08 May 2012 16:55:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The H60 minor histocompatibility (H) antigen peptide is derived from a glycoprotein that serves as a ligand for the stimulatory NKG2D receptor.  We show that this peptide is remarkably immunodominant in that it competes effectively    with MHC alloantigens, is efficiently crosspresented by host antigen-presenting cells (APCs), and readily elicits naive CD8 T cell responses in vitro. H60 immunodominance is neither a consequence of NKG2D engagement nor competition among minor H    antigens on APCs. Instead, H60 immunodominance is a consequence of an abnormally high naive precursor frequency of H60 peptide reactive CD8 T cells. Understanding why the H60 peptide is so immunogenic has important implications in tissue    transplantation and vaccine design.</p>

	]]>
</description>

<author>E Y. Choi et al.</author>


</item>


<item>
<title> Melanosome morphologies in murine models of hermansky-pudlak syndrome reflect blocks in organelle development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/433</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/433</guid>
<pubDate>Tue, 08 May 2012 16:54:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hermansky-Pudlak syndrome is an autosomal recessive disease characterized by pigment dilution and prolonged bleeding time. At least 15 mutant mouse strains have been classified as models of Hermansky-Pudlak syndrome. Some of the    genes are implicated in intracellular vesicle trafficking: budding, targeting, and secretion. Many of the Hermansky-Pudlak syndrome genes remain uncharacterized and their functions are unknown. Clues to the functions of these genes can be found    by analyzing the physiologic and cellular phenotypes. Here we have examined the morphology of the melanosomes in the skin of 10 of the mutant mouse Hermansky-Pudlak syndrome strains by transmission electron microscopy. We demonstrate that the    morphologies reflect inhibition of organelle maturation or transfer.  The Hermansky-Pudlak syndrome strains are classified into morphologic groups characterized by the step at which melanosome biogenesis or transfer to keratinocytes is inhibited,    with the cappuccino strain observed to be blocked at the earliest step and gunmetal blocked at the latest step. We show that all Hermansky-Pudlak syndrome mutant strains except gunmetal have an increase in unpigmented or hypopigmented immature    melanosomal forms, leading to the hypopigmented coat colors seen in these strains. In contrast, the hypopigmentation seen in the gunmetal strain is due to the retention of melanosomes in melanocytes, and inefficient transfer into    keratinocytes.</p>

	]]>
</description>

<author>T Nguyen et al.</author>


</item>


<item>
<title> Extension and integration of the gene ontology (GO): combining GO vocabularies with external vocabularies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/432</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/432</guid>
<pubDate>Tue, 08 May 2012 16:54:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Structured vocabulary development enhances the management of information in biological databases. As information grows, handling the complexity of vocabularies becomes difficult. Defined methods are needed to manipulate, expand and    integrate complex vocabularies. The Gene Ontology (GO) project provides the scientific community with a set of structured vocabularies to describe domains of molecular biology. The vocabularies are used for annotation of gene products and for    computational annotation of sequence data sets. The vocabularies focus on three concepts universal to living systems, biological process, molecular function and cellular component. As the vocabularies expand to incorporate terms needed by diverse    annotation communities, species-specific terms become problematic. In particular, the use of species-specific anatomical concepts remains unresolved. We present a method for expansion of GO into areas outside of the three original universal    concept domains. We combine concepts from two orthogonal vocabularies to generate a larger, more specific vocabulary. The example of mammalian heart development is presented because it addresses two issues that challenge GO; inclusion of    organism-specific anatomical terms, and proliferation of terms and relationships. The combination of concepts from orthogonal vocabularies provides a robust representation of relevant terms and an opportunity for evaluation of hypothetical    concepts.</p>

	]]>
</description>

<author>D P. Hill et al.</author>


</item>


<item>
<title> Generation of a new congenic mouse strain to test the relationships among serum insulin-like growth factor I, bone mineral density, and skeletal morphology in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/431</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/431</guid>
<pubDate>Tue, 08 May 2012 16:54:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Insulin-like growth factor (IGF) I is a critical peptide for skeletal growth and consolidation. However, its regulation is complex and, in part, heritable. We previously indicated that changes in both serum and skeletal IGF-I were    related to strain-specific differences in total femoral bone mineral density (BMD) in mice. In addition, we defined four quantitative trait loci (QTLs) that contribute to the heritable determinants of the serum IGF-I phenotype in F2 mice derived    from progenitor crosses between C3H/HeJ (C3H; high total femoral BMD and high IGF-I) and C57BL/6J (B6; low total femoral BMD and low IGF-I) strains. The strongest QTL, IGF-I serum level 1 (Igflsl-1; log10 of the odds ratio [LOD] score,    approximately 9.0), is located on the middle portion of chromosome (Chr) 6. For this locus, C3H alleles are associated with a significant reduction in serum IGF-I. To test the effect of this QTL in vivo, we generated a new congenic strain    (B6.C3H-6T [6T]) by placing the Chr 6 QTL region (D6Mit93 to D6Mit150) from C3H onto the B6 background. We then compared serum and skeletal IGF-I levels, body weight, and several skeletal phenotypes from the N9 generation of 6T congenic mice    against B6 control mice. Female 6T congenic mice had 11-21% lower serum IGF-I levels at 6, 8, and 16 weeks of age compared with B6 (p < 0.05 for all). In males, serum IGF-I levels were similar in 6T congenics and B6 controls at 6 weeks and 8    weeks but were lower in 6T congenic mice at 16 weeks (p < 0.02). In vitro, there was a 40% reduction in secreted IGF-I in the conditioned media (CMs) from 6T calvaria osteoblasts compared with B6 cells (p < 0.01). Total femoral BMD as measured by    peripheral quantitative computed tomography (pQCT) was lower in both 6T male (-4.8%, p < 0.01) and 6T female (-2.3%, p = 0.06) congenic mice. Geometric features of middiaphyseal cortical bone were reduced in 6T congenic mice compared with control    mice. Femoral cancellous bone volume (BV) density and trabecular number (Tb.N) were 50% lower, whereas trabecular separation (Tb.Sp) was 90% higher in 8-week-old female 6T congenic mice compared with B6 control  mice (p < 0.01 for all).     Similarly, vertebral cancellous BV density and Tb.N were lower (-29% and -19%, respectively), whereas Tb.Sp was higher (+29%) in 16-week-old female 6T congenic mice compared with B6 control mice (p < 0.001 for all).  Histomorphometric evaluation    of the proximal tibia indicated that 6T congenics had reduced BV fraction, labeled surface, and bone formation rates compared with B6 congenic mice. In summary, we have developed a new congenic mouse strain that confirms the Chr 6 QTL as a major    genetic regulatory determinant for serum IGF-I. This locus also influences bone density and morphology, with more dramatic effects in cancellous bone than in cortical bone.</p>

	]]>
</description>

<author>M L. Bouxsein et al.</author>


</item>


<item>
<title> QTL associated with blood pressure, heart rate, and heart weight in CBA/CaJ and BALB/cJ mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/430</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/430</guid>
<pubDate>Tue, 08 May 2012 16:53:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>To better understand the genetic basis of essential hypertension, we conducted a quantitative trait locus (QTL) analysis of a population of 207 (BALB/cJ x CBA/CaJ) F(2) male mice to identify genomic regions that regulate blood    pressure, heart rate, and heart weight. We identified two loci, Bpq6 (blood pressure quantitative locus 6) on chromosome 15 (Chr 15; peak, 16 cM; 95% confidence interval, 0-25 cM) and Bpq7 on Chr 7 (peak, 42 cM; 95% confidence interval, 35-50 cM)    that were significantly associated with blood pressure. We also identified two loci, Hrq1 (heart rate quantitative locus 1) and Hrq2, on D2Mit304 (peak, 72 cM; 95% confidence interval 60-80 cM) and D15Mit184 (peak, 25 cM; 95% confidence interval    20-35 cM), respectively, that were significantly associated with heart rate. A significant gene-gene interaction for heart rate was found between Hrq1 and D1Mit10 (peak, 57 cM; 95% confidence interval, 45-75 cM); the latter QTL was named Hrq3. We    identified a significant locus for heart weight, Hwq1 (heart weight quantitative locus 1), at D14Mit67 (peak, 38 cM; 95% confidence interval, 20-43 cM). Identification of the genes for these QTL should lead to a better understanding of the causes    of essential hypertension.</p>

	]]>
</description>

<author>F Sugiyama et al.</author>


</item>


<item>
<title> Genetic predisposition to low bone mass is paralleled by an enhanced sensitivity to signals anabolic to the skeleton.</title>
<link>http://mouseion.jax.org/stfb2000_2009/429</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/429</guid>
<pubDate>Tue, 08 May 2012 16:53:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The structure of the adult skeleton is determined, in large part, by its genome. Whether genetic variations may influence the effectiveness of interventions to combat skeletal diseases remains unknown. The differential response of    trabecular bone to an anabolic (low-level mechanical vibration) and a catabolic (disuse) mechanical stimulus were evaluated in three strains of adult mice. In low bone-mineral-density C57BL/6J mice, the low-level mechanical signal caused    significantly larger bone formation rates (BFR) in the proximal tibia, but the removal of functional weight bearing did not significantly alter BFR. In mid-density BALB/cByJ mice, mechanical stimulation also increased BFR, whereas disuse    significantly decreased BFR. In contrast, neither anabolic nor catabolic mechanical signals influenced any index of bone formation in high-density C3H/HeJ mice. Together, data from this study indicate that the sensitivity of trabecular tissue to    both anabolic and catabolic stimuli is influenced by the genome. Extrapolated to humans, these results may explain in part why prophylaxes for low bone mass are not universally effective, yet also indicate that there may be a genotypic indication    of people who are at reduced risk of suffering from bone loss.</p>

	]]>
</description>

<author>S Judex et al.</author>


</item>


<item>
<title> Differential effects of environmental enrichment on behavior and learning of male and female Ts65Dn mice, a model for Down syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/428</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/428</guid>
<pubDate>Tue, 08 May 2012 16:53:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have assessed the effects of enriched environment (EE) upon behavioral and cognitive performances of partially trisomic Ts65Dn (TS) mice and their control (CO) littermates. Enriched environment was applied to pups for 7 weeks    after weaning. Circadian spontaneous activity (actimetry), exploratory behavior (hole board), activity in the open field and spatial memory (Morris Water Maze, repeated acquisition and cued paradigms) were analyzed in 86 female and 75 male mice,    starting 15 days after completing enrichment. For each gender, mice were distributed in non-enriched and enriched control and trisomic groups. Enriched environment reduced in trisomic females and enhanced in trisomic males' circadian activity.     Exploratory behavior was increased by enrichment in all groups, regardless of gender or presence of trisomy. In the Morris Water Maze, a significant improvement of the spatial memory was observed in enriched-control females, but not in    enriched-control male mice, as assessed by distances traveled. Performances in the four groups of control animals were also consistently and significantly better than those of matching trisomic mice. In the acquisition trials, enrichment improved    performance in trisomic female animals, but deteriorated in trisomic male mice. In all groups, changes in escape latencies and distances induced by enrichment were accounted for by changes in the total time spent in the periphery of the pool,    indicating changes in learning strategy. Working memory was the function more affected by enrichment. It is concluded that enriched environment induces behavioral and learning changes in trisomic mice, although gender plays a significant    modulatory role.</p>

	]]>
</description>

<author>Cue C. Martinez et al.</author>


</item>


<item>
<title> Genetics of colitis susceptibility in IL-10-deficient mice: backcross versus F2 results contrasted by principal component analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/427</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/427</guid>
<pubDate>Tue, 08 May 2012 16:53:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Interleukin-10-deficient (Il10(-/-)) mice on a C3H/HeJBir genetic background develop more severe colitis than those on a C57BL/6J background. We performed genome screens for quantitative trait loci (QTLs) regulating colitis    susceptibility in this model system using two first backcross populations derived from these two strains. To reduce the complexity of this analysis, the information from numerous histologic phenotypes was summarized by principal component    analysis. A similar approach was applied to previously published data from an F2 intercross (involving the same progenitor strains), which allowed us to ascertain all six previously reported cytokine-deficiency-induced colitis susceptibility loci    (Cdcs1-6) with main and/or interacting effects on chromosomes 3, 1, 2, 8, 17, and 18. The colitogenic effect of Cdcs1 was confirmed in the backcross to C3H/HeJBir-Il10(-/-). Its effect was epistatically modified by another locus on chromosome 12.    In addition, three main effect QTLs on chromosomes 4, 5, and 12 were identified in the backcross to C57BL/6J-Il10(-/-). Analyses of the modes of inheritance in these crosses revealed colitogenic contributions by both parental genomes. These    findings show the complexity of inheritance underlying susceptibility to colitis and illustrate why detection of human inflammatory bowel disease loci has proven to be so difficult.</p>

	]]>
</description>

<author>M Mahler et al.</author>


</item>


<item>
<title> Variation in gene expression within and among natural populations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/426</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/426</guid>
<pubDate>Tue, 08 May 2012 16:52:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Evolution may depend more strongly on variation in gene expression than on differences between variant forms of proteins. Regions of DNA that affect gene expression are highly variable, containing 0.6% polymorphic sites.  These    naturally occurring polymorphic nucleotides can alter in vivo transcription rates. Thus, one might expect substantial variation in gene expression between individuals. But the natural variation in mRNA expression for a large number of genes has    not been measured. Here we report microarray studies addressing the variation in gene expression within and between natural populations of teleost fish of the genus Fundulus. We observed statistically significant differences in expression between    individuals within the same population for approximately 18% of 907 genes. Expression typically differed by a factor of 1.5, and often more than 2.0. Differences between populations increased the variation.  Much of the variation between    populations was a positive function of the variation within populations and thus is most parsimoniously described as random. Some genes showed unexpected patterns of expression--changes unrelated to evolutionary distance. These data suggest that    substantial natural variation exists in gene expression and that this quantitative variation is important in evolution.</p>

	]]>
</description>

<author>M F. Oleksiak et al.</author>


</item>


<item>
<title> Distinct role of surface lymphotoxin expressed by B cells in the organization of secondary lymphoid tissues.</title>
<link>http://mouseion.jax.org/stfb2000_2009/425</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/425</guid>
<pubDate>Tue, 08 May 2012 16:52:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>In order to definitively ascertain the functional contribution of lymphotoxin (LT) expressed by B cells, we produced mice with the LTbeta gene deleted from B cells (B-LTbeta KO mice). In contrast to systemic LTbeta deletion, in    B-LTbeta KO mice only splenic microarchitecture was affected, while lymph nodes and Peyer's patches (PP) were normal, except for PP's reduced size. Even though B-LTbeta KO spleens retained a small number of follicular dendritic cells (FDC) which    appeared to be dependent on LTbeta produced by T cells, IgG responses to sheep red blood cells were markedly reduced. Thus, the organogenic function of B-LTbeta is almost entirely restricted to spleen, where it supports the correct lymphoid    architecture that is critical for an effective humoral immune response.</p>

	]]>
</description>

<author>A Tumanov et al.</author>


</item>


<item>
<title> Characterization of a novel murine retrovirus mixture that facilitates hematopoiesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/424</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/424</guid>
<pubDate>Tue, 08 May 2012 16:52:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>A new virus previously arose in BALB/c females mated repeatedly to C57BL/6 (B6) males and then injected with fixed, activated B6 male spleen cells (V. S. Ter-Grigorov, O. Krifuks, E. Liubashevsky, A. Nyska, Z. Trainin, and V.    Toder, Nat. Med. 3:37-41, 1997). In the present study, BALB/cJ mice inoculated with virus-containing plasma from affected mice developed splenomegaly, which was caused by increased numbers of Sca-1(+) Lin(-) hematopoietic stem cells (HSC) and    their differentiated progeny.  Biological and molecular analyses of a new virus revealed a mixture of murine leukemia viruses (MuLVs). These MuLVs comprised ecotropic and mink lung cell focus-forming (MCF) virus classes and are termed    Rauscher-like MuLVs because they bear numerous similarities to the ecotropic and MCF viruses of the Rauscher MuLV complex but do not include a spleen focus-forming virus. The ecotropic virus component alone transferred some disease    characteristics, while MCF virus alone did not. Thus, we have described a novel virus mixture, termed Rauscher-like MuLV, that causes an increase in hematopoiesis due to activation of pluripotent HSC.  Experiments using mice and a protocol that    replicated the pregnancy and immunization strategy of the original experiment demonstrated that endogenous BALB/c mouse ecotropic and xenotropic MuLVs are activated by these treatments. Emv1 was expressed in the spleens of multiparous mice but    not in those of virgin mice, and Bxv1Emv1-pseudotyped MuLVs were recovered following injection of fixed, activated B6 cells. Thus, multiple pregnancies and allostimuli appear to have provided the signals required for activation of and    recombination among endogenous viruses and could have resulted in generation of the Rauscher-like MuLV mixture.</p>

	]]>
</description>

<author>L M. Hook et al.</author>


</item>


<item>
<title> The effects of piracetam on cognitive performance in a mouse model of Down&apos;s syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/423</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/423</guid>
<pubDate>Tue, 08 May 2012 16:51:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Piracetam is a nootropic agent that has been shown to improve cognitive performance in a number of animal model systems. Piracetam is reported to be used widely as a means of improving cognitive function in children with Down's    syndrome (DS). In order to provide a preclinical assessment of the potential efficacy of piracetam, we examined the effects of a dose range of piracetam in the Ts65Dn mouse model of DS. Ts65Dn mice are trisomic for a region of mouse chromosome 16    with homology to human chromosome 21.  Daily piracetam treatment at doses of 0, 75, 150, and 300 mg/kg ip was initiated in 6-week-old male Ts65Dn and euploid control mice. Following 4 weeks of treatment, mice were tested in the visible and    hidden-platform components of the Morris water maze and were placed overnight in computerized activity chambers to assess effects on overall activity.  Piracetam treatment was continued through the 4 weeks of testing. In control mice, 75 and 150    mg/kg/day piracetam improved performance in both the visible- and hidden-platform tasks. Although low doses of piracetam reduced search time in the visible-platform component in Ts65Dn mice, all piracetam doses prevented trial-related    improvements in performance in Ts65Dn mice. The 300-mg/kg/day-piracetam dose was associated with a reversal of the nocturnal spontaneous hyperactivity in Ts65Dn. These data do not provide support for piracetam treatment for individuals with    DS.</p>

	]]>
</description>

<author>T H. Moran et al.</author>


</item>


<item>
<title> Fundamentals of experimental design for cDNA microarrays.</title>
<link>http://mouseion.jax.org/stfb2000_2009/422</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/422</guid>
<pubDate>Tue, 08 May 2012 16:51:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Microarray technology is now widely available and is being applied to address increasingly complex scientific questions. Consequently, there is a greater demand for statistical assessment of the conclusions drawn from microarray    experiments. This review discusses fundamental issues of how to design an experiment to ensure that the resulting data are amenable to statistical analysis. The discussion focuses on two-color spotted cDNA microarrays, but many of the same issues    apply to single-color gene-expression assays as well.</p>

	]]>
</description>

<author>G A. Churchill</author>


</item>


<item>
<title> Regulation of bone volume is different in the metaphyses of the femur and vertebra of C3H/HeJ and C57BL/6J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/421</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/421</guid>
<pubDate>Tue, 08 May 2012 16:51:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The C3H/HeJ (C3H) mice exhibited a greater bone formation rate (BFR) and a greater mineral apposition rate (MAR) in the cortical bone of the midshafts of the femur and tibia than did C57BL/6J (B6) mice. This study sought to    determine if these strain-related differences would also be observed in cancellous bone. Metaphyses of the femur and lumbar vertebra (L5-6) from C3H and B6 mice, 6 and 12 weeks of age, were analyzed by histomorphometry. Similar to cortical bone,    the bone volume in the femoral metaphysis of C3H mice was greater (by 54% and 65%, respectively) than that of B6 mice at both 6 and 12 weeks of age. Higher BFR and mineral apposition rate (MAR) contributed to the higher bone volume in the C3H    mice compared with the B6 mice. In contrast, bone volume (by 59% and 13%, respectively, p < 0.001) and trabecular number (by 55% and 35%, respectively, p < 0.001) in the vertebrae were lower in the C3H mice than in B6 mice at 6 and 12 weeks of    age. At 6 weeks of age, MAR was higher (by 43%, p = 0.004) in C3H mice, but because of a low trabecular number, the BFR (by 37%, p = 0.026) and tetracycline-labeled bone surface (by 52%, p < 0.001) per tissue were lower in the vertebrae of C3H    mice than B6 mice.  The low bone volume in vertebrae of C3H mice was probably not due to a higher bone resorption, because the osteoclast number (by 55%, p < 0.001) and eroded surface (by 61%, p <0.001) per tissue area in the C3H mice were also    lower in B6 mice. At 12 weeks, the trabecular thickness had increased (by 36%, p < 0.001) in the C3H mice and the difference in bone volume between strains was less than that at 6 weeks. These contrasting and apparently opposing strain-related    differences in trabecular bone parameters between femur and vertebra in these two mouse strains suggest that the genetic regulation of bone volume in the metaphyses of different skeletal sites is different between C3H and B6 mice.</p>

	]]>
</description>

<author>M H. Sheng et al.</author>


</item>


<item>
<title> Gene expression between a congenic strain that contains a quantitative trait locus of high bone density from CAST/EiJ and its wild-type strain C57BL/6J.</title>
<link>http://mouseion.jax.org/stfb2000_2009/420</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/420</guid>
<pubDate>Tue, 08 May 2012 16:51:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Peak bone density is an important determining factor of future osteoporosis risk. We previously identified a quantitative trait locus (QTL) that contributes significantly to high bone density on mouse chromosome 1 from a cross    between C57BL/6J (B6) and CAST/EiJ (CAST) mouse strains. We then generated a congenic strain, B6.CAST-1T, in which the chromosomal fragment containing this QTL had been transferred from CAST to the B6 background. The congenic mice have a    significantly higher bone density than the B6 mice. In this study we performed cDNA microarray analysis to evaluate the gene expression profile that might yield insights into the mechanisms controlling the high bone density by this QTL. This    study led to several interesting observations. First, approximately 60% of 8,734 gene accessions on GEM I chips were expressed in the femur of B6 mice. The expression and function of two-thirds of these expressed genes and ESTs have not been    documented previously. Second, expression levels of genes related to bone formation were lower in congenic than in B6 mice.  These data are consistent with a low bone formation in the congenic mice, a possibility that is confirmed by reduced    skeletal alkaline phosphatase activity in serum compared with B6 mice. Third, expression levels of genes that might have negative regulatory action on bone resorption were higher in congenic than in B6 mice. Together these findings suggest that    the congenic mice might have a lower bone turnover rate than B6 mice and raise the possibility that the high bone density in the congenic mice could be due to reduced bone resorption rather than increased bone formation.</p>

	]]>
</description>

<author>W Gu et al.</author>


</item>


<item>
<title> Construction of a BAC contig for a 3 cM biologically significant region of mouse chromosome 1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/419</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/419</guid>
<pubDate>Tue, 08 May 2012 16:51:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>One QTL and genes and phenotypes have been localized in the region between 92 cM and 95cM of mouse chromosome 1. The QTL locus contributes to approximately 40% of the variation of the peak bone density between C57BL/6J (B6) and    CAST/EiJ (CAST) strains. Other loci located in this chromosomal region include a neural tube defect mutant loop-tail (Lp), a lymphocyte-stimulating determinant (Lsd), and the Transgelin 2 (Tagln 2).  The human chromosome region homologous to this    region is 1q21-23, which also contains a QTL locus for high bone mineral density (BMD).  Furthermore, it has been reported that this region may have duplicated several times in the mouse genome. Therefore, genomic sequencing of this region will    provide important information for mouse genome structure, for positional cloning of mouse genes, and for the study of human homologous genes. In order to provide a suitable template for genomic sequencing by the NIH-sponsored genomic centers, we    have constructed a BAC contig of this region using the RPCI-23 library. We have also identified the currently available mouse genomic sequences localized in our BAC contig.  Further analysis of these sequences and BAC clones indicated a high    frequency of repetitive sequences within this chromosomal area. This region also contains L1 retrotransposon sequences, providing a potential mechanism for the repetitive sequences described in the literature.</p>

	]]>
</description>

<author>W K. Gu et al.</author>


</item>


<item>
<title> Neuronal loss and brain atrophy in mice lacking cathepsins B and L.</title>
<link>http://mouseion.jax.org/stfb2000_2009/418</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/418</guid>
<pubDate>Tue, 08 May 2012 16:50:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cathepsins B and L are widely expressed cysteine proteases implicated in both intracellular proteolysis and extracellular matrix remodeling.  However, specific roles remain to be validated in vivo. Here we show that combined    deficiency of cathepsins B and L in mice is lethal during the second to fourth week of life. Cathepsin B(-/-)/L(-/-) mice reveal a degree of brain atrophy not previously seen in mice. This is because of massive apoptosis of select neurons in the    cerebral cortex and the cerebellar Purkinje and granule cell layers. Neurodegeneration is accompanied by pronounced reactive astrocytosis and is preceded by an accumulation of ultrastructurally and biochemically unique lysosomal bodies in large    cortical neurons and by axonal enlargements. Our data demonstrate a pivotal role for cathepsins B and L in maintenance of the central nervous system.</p>

	]]>
</description>

<author>U Felbor et al.</author>


</item>


<item>
<title> Deletion in Catna2, encoding alpha N-catenin, causes cerebellar and hippocampal lamination defects and impaired startle modulation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/417</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/417</guid>
<pubDate>Tue, 08 May 2012 16:50:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice homozygous for the cerebellar deficient folia (cdf) mutation are ataxic and have cerebellar hypoplasia and abnormal lobulation of the cerebellum. In the cerebella of cdf/cdf homozygous mice, approximately 40% of Purkinje cells    are located ectopically in the white matter and inner granule-cell layer. Many hippocampal pyramidal cells are scattered in the plexiform layers, and those that are correctly positioned are less densely packed than are cells in wild-type mice. We    show that fear conditioning and prepulse inhibition of the startle response are also disrupted in cdf/cdf mice. We identify a deletion on chromosome 6 that removes approximately 150 kb in the cdf critical region. The deletion includes part of    Catna2, encoding alpha N-catenin, a protein that links the classical cadherins to the neuronal cytoskeleton. Expression of a Catna2 transgene in cdf/cdf mice restored normal cerebellar and hippocampal morphology, prepulse inhibition and fear    conditioning. The findings suggest that catenin cadherin cell-adhesion complexes are important in cerebellar and hippocampal lamination and in the control of startle modulation.</p>

	]]>
</description>

<author>C Park et al.</author>


</item>


<item>
<title> Delayed administration of carrier marrow can decrease competition on donor stem cells during engraftment and maintain radioprotection of the host.</title>
<link>http://mouseion.jax.org/stfb2000_2009/416</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/416</guid>
<pubDate>Tue, 08 May 2012 16:50:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: The goal of this study was to determine if competitive pressure was placed on hematopoietic stem cells (HSC) by a coinjected "carrier" population that maintains short-term survival of the host. Our hypothesis was that    delayed introduction of "carrier" cells would increase engraftment of donor HSC. MATERIALS AND METHODS: Competitive repopulation assays were performed using genetically distinguishable whole bone marrow (BM) populations. Donor BM was competed    against carrier BM that was coinjected or injected 3 or 4 days later. Radioprotection with delayed carrier injection also was examined by performing the initial HSC transplantation with Hoechst(lo) side population (SP) cells. SP HSC incubated    with cytokines and BM stroma to stimulate cell cycling before transplantation also were tested using coinjection or delayed carrier administration. RESULTS: Delayed introduction of carrier whole BM increased peripheral expansion of donor whole    BM, freshly isolated HSC, or cytokine-stimulated HSC compared to coinjection with carrier cells. A 3-day delay in carrier administration maintained radioprotection in 100% of lethally irradiated recipients of highly enriched HSC, whereas a 4-day    delay did not rescue these recipients from death. When recipients are rescued, recovering host marrow can compete against donor HSC unless sufficient donor cells are injected. CONCLUSIONS: Delayed introduction of carrier BM significantly    increases donor HSC engraftment and peripheral expansion by reducing competition in the host. Competition by a coinjected carrier cell population or recovery of host marrow significantly reduces the therapeutic efficacy of normal or in vitro    manipulated donor HSC.</p>

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</description>

<author>B W. Soper et al.</author>


</item>


<item>
<title> IGF-I regulates osteoprotegerin (OPG) and receptor activator of nuclear factor-kappaB ligand in vitro and OPG in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/415</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/415</guid>
<pubDate>Tue, 08 May 2012 16:49:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>IGF-I, a ubiquitous polypeptide, plays a key role in longitudinal bone growth and acquisition. The most predominant effect of skeletal IGF-I is acceleration of the differentiation program for osteoblasts. However, in vivo studies    using recombinant human (rh) IGF-I and/or rhGH have demonstrated stimulation of both bone formation and resorption, thereby potentially limiting the usefulness of these peptides in the treatment of osteoporosis. In this study, we hypothesized    that IGF-I modulates bone resorption by regulating expression of osteoprotegerin (OPG) and receptor activator of nuclear factor-kappaB (RANK) ligand (RANKL) in bone cells.  Using Northern analysis in ST2 cells, we found that human IGF-I    suppressed OPG mRNA in a time- and dose-dependent manner: 100 micro g/LIGF-I (13 nM) decreased OPG expression by 37.0 +/- 1.8% (P < 0.002). The half maximal inhibitory dose of IGF-I was reached at 50 micro g/liter ( approximately 6.5 nM) with no    effect of IGF-I on OPG message stability. Conditioned media from ST2 cells confirmed that IGF-I decreased secreted OPG, reducing levels by 42%, from 12.1-7 ng/ml at 48 h (P < 0.05). Similarly, IGF-I at 100 micro g/liter (13 nM) increased RANKL    mRNA expression to 353 +/- 74% above untreated cells as assessed by real-time PCR. In vivo, low doses of rhGH when administered to elderly postmenopausal women only modestly raised serum IGF-I (to concentrations of 18-26 nM) and did not affect    circulating OPG concentrations; however, administration of rhIGF-I (30 micro g/kg.d) for 1 yr to older women resulted in a significant increase in serum IGF-I (to concentrations of 39-45 nM) and a 20% reduction in serum OPG (P < 0.05). In    summary, we conclude that IGF-I in a dose- and time-dependent manner regulates OPG and RANKL in vitro and in vivo. These data suggest IGF-I may act as a coupling factor in bone remodeling by activating both bone formation and bone resorption; the    latter effect appears to be mediated through the OPG/RANKL system in bone.</p>

	]]>
</description>

<author>J Rubin et al.</author>


</item>


<item>
<title> Circulating levels of IGF-1 directly regulate bone growth and density.</title>
<link>http://mouseion.jax.org/stfb2000_2009/414</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/414</guid>
<pubDate>Tue, 08 May 2012 16:49:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>IGF-1 is a growth-promoting polypeptide that is essential for normal growth and development. In serum, the majority of the IGFs exist in a 150-kDa complex including the IGF molecule, IGF binding protein 3 (IGFBP-3), and the acid    labile subunit (ALS). This complex prolongs the half-life of serum IGFs and facilitates their endocrine actions. Liver IGF-1-deficient (LID) mice and ALS knockout (ALSKO) mice exhibited relatively normal growth and development, despite having 75%    and 65% reductions in serum IGF-1 levels, respectively. Double gene disrupted mice were generated by crossing LID+ALSKO mice. These mice exhibited further reductions in serum IGF-1 levels and a significant reduction in linear growth. The proximal    growth plates of the tibiae of LID+ALSKO mice were smaller in total height as well as in the height of the proliferative and hypertrophic zones of chondrocytes. There was also a 10% decrease in bone mineral density and a greater than 35% decrease    in periosteal circumference and cortical thickness in these mice. IGF-1 treatment for 4 weeks restored the total height of the proximal growth plate of the tibia.  Thus, the double gene disruption LID+ALSKO mouse model demonstrates that a    threshold concentration of circulating IGF-1 is necessary for normal bone growth and suggests that IGF-1, IGFBP-3, and ALS play a prominent role in the pathophysiology of osteoporosis.</p>

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</description>

<author>S Yakar et al.</author>


</item>


<item>
<title> The harlequin mouse mutation downregulates apoptosis-inducing factor.</title>
<link>http://mouseion.jax.org/stfb2000_2009/413</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/413</guid>
<pubDate>Tue, 08 May 2012 16:49:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Harlequin (Hq) mutant mice have progressive degeneration of terminally differentiated cerebellar and retinal neurons. We have identified the Hq mutation as a proviral insertion in the apoptosis-inducing factor (Aif) gene, causing    about an 80% reduction in AIF expression. Mutant cerebellar granule cells are susceptible to exogenous and endogenous peroxide-mediated apoptosis, but can be rescued by AIF expression.  Overexpression of AIF in wild-type granule cells further    decreases peroxide-mediated cell death, suggesting that AIF serves as a free radical scavenger. In agreement, dying neurons in aged Hq mutant mice show oxidative stress. In addition, neurons damaged by oxidative stress in both the cerebellum and    retina of Hq mutant mice re-enter the cell cycle before undergoing apoptosis. Our results provide a genetic model of oxidative stress-mediated neurodegeneration and demonstrate a direct connection between cell cycle re-entry and oxidative stress    in the ageing central nervous system.</p>

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</description>

<author>J A. Klein et al.</author>


</item>


<item>
<title> APC-dependent suppression of colon carcinogenesis by PPARgamma.</title>
<link>http://mouseion.jax.org/stfb2000_2009/412</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/412</guid>
<pubDate>Tue, 08 May 2012 16:49:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Activation of PPARgamma by synthetic ligands, such as thiazolidinediones, stimulates adipogenesis and improves insulin sensitivity. Although thiazolidinediones represent a major therapy for type 2 diabetes, conflicting studies    showing that these agents can increase or decrease colonic tumors in mice have raised concerns about the role of PPARgamma in colon cancer. To analyze critically the role of this receptor, we have used mice heterozygous for Ppargamma with both    chemical and genetic models of this malignancy. Heterozygous loss of PPARgamma causes an increase in beta-catenin levels and a greater incidence of colon cancer when animals are treated with azoxymethane. However, mice with preexisting damage to    Apc, a regulator of beta-catenin, develop tumors in a manner insensitive to the status of PPARgamma. These data show that PPARgamma can suppress beta-catenin levels and colon carcinogenesis but only before damage to the APC/beta-catenin pathway.    This finding suggests a potentially important use for PPARgamma ligands as chemopreventative agents in colon cancer.</p>

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</description>

<author>G D. Girnun et al.</author>


</item>


<item>
<title> Cln3(Deltaex7/8) knock-in mice with the common JNCL mutation exhibit progressive neurologic disease that begins before birth.</title>
<link>http://mouseion.jax.org/stfb2000_2009/411</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/411</guid>
<pubDate>Tue, 08 May 2012 16:48:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Juvenile-onset neuronal ceroid lipofuscinosis (JNCL; Batten disease) features hallmark membrane deposits and loss of central nervous system (CNS) neurons. Most cases of the disease are due to recessive inheritance of an    approximately 1 kb deletion in the CLN3 gene, encoding battenin. To investigate the common JNCL mutation, we have introduced an identical genomic DNA deletion into the murine CLN3 homologue (Cln3) to create Cln3( Deltaex7/8) knock-in mice. The    Cln3( Deltaex7/8) allele produced alternatively spliced mRNAs, including a variant predicting non-truncated protein, as well as mutant battenin that was detected in the cytoplasm of cells in the periphery and CNS. Moreover, Cln3( Deltaex7/8)    homozygotes exhibited accrual of JNCL-like membrane deposits from before birth, in proportion to battenin levels, which were high in liver and select neuronal populations. However, liver enzymes and CNS development were normal. Instead, Cln3(    Deltaex7/8) mice displayed recessively inherited degenerative changes in retina, cerebral cortex and cerebellum, as well as neurological deficits and premature death. Thus, the harmful impact of the common JNCL mutation on the CNS was not well    correlated with membrane deposition per se, suggesting instead a specific battenin activity that is essential for the survival of CNS neurons.</p>

	]]>
</description>

<author>S L. Cotman et al.</author>


</item>


<item>
<title> Distinct roles for CREB-binding protein and p300 in hematopoietic stem cell self-renewal.</title>
<link>http://mouseion.jax.org/stfb2000_2009/410</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/410</guid>
<pubDate>Tue, 08 May 2012 16:48:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hematopoietic stem cells (HSC) are tightly regulated through, as yet, undefined mechanisms that balance self-renewal and differentiation. We have identified a role for the transcriptional coactivators CREB-binding protein (CBP) and    p300 in such HSC fate decisions. A full dose of CBP, but not p300, is crucial for HSC self-renewal. Conversely, p300, but not CBP, is essential for proper hematopoietic differentiation. Furthermore, in chimeric mice, hematologic malignancies    emerged from both CBP(-/-) and p300(-/-) cell populations. Thus, CBP and p300 play essential but distinct roles in maintaining normal hematopoiesis, and, in mice, both are required for preventing hematologic tumorigenesis.</p>

	]]>
</description>

<author>V I. Rebel et al.</author>


</item>


<item>
<title> Slug, a highly conserved zinc finger transcriptional repressor, protects hematopoietic progenitor cells from radiation-induced apoptosis in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/409</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/409</guid>
<pubDate>Tue, 08 May 2012 16:48:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>We show here that a zinc finger transcriptional repressor, Slug, which is aberrantly upregulated by the E2A-HLF oncoprotein in pro-B cell acute leukemia, functions as an antiapoptotic factor in normal hematopoietic progenitor    cells. Slug(-/-) mice were much more radiosensitive than wild-type mice, dying earlier and showing accentuated decreases in peripheral blood cell counts, as well as abundant microhemorrhages and widely disseminated bacterial microabscesses    throughout the body. Slug expression was detected in diverse subsets of hematopoietic progenitors, but not in more differentiated B and T lymphoid cells, and there was a significant increase in apoptotic (TUNEL-positive) bone marrow progenitor    cells in irradiated Slug(-/-) mice compared to wild-type controls. These results implicate Slug in a novel survival pathway that protects hematopoietic progenitors from apoptosis after DNA damage.</p>

	]]>
</description>

<author>A Inoue et al.</author>


</item>


<item>
<title> Deletion of the GATA domain of TRPS1 causes an absence of facial hair and provides new insights into the bone disorder in inherited tricho-rhino-phalangeal syndromes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/408</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/408</guid>
<pubDate>Tue, 08 May 2012 16:48:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>GATA transcription factors mediate cell differentiation in diverse tissues, and their dysfunction is associated with certain congenital human disorders. The six classical vertebrate GATA proteins, GATA-1 to GATA-6, are highly    homologous, bear two tandem zinc fingers of the C(4) (GATA) type, and activate transcription. TRPS1, the only other vertebrate protein with the GATA motif, is a large, multitype zinc finger protein that harbors a single DNA-binding GATA domain    and represses transcription.  Monoallelic TRPS1 mutations cause two dominantly inherited human developmental disorders of the hair, face, and digits, tricho-rhino-phalangeal syndrome (TRPS) types I (MIM 190350) and III (MIM 190351); missense GATA    domain mutations account for the more severe type III form. Here we report that heterozygous mice with deletions of the TRPS1 GATA domain (TRPS1(+/Deltagt)) display facial anomalies that overlap with findings for TRPS, whereas    TRPS1(Deltagt/Deltagt) mice additionally reveal a complete absence of vibrissae. Unexpectedly, TRPS1(Deltagt/Deltagt) mice die of neonatal respiratory failure resulting from abnormalities of the thoracic spine and ribs. Heterozygotes also develop    thoracic kyphoscoliosis with age and reveal structural deficits in cortical and trabecular bones. These findings directly implicate the GATA type zinc finger of TRPS1 in regulation of bone and hair development and suggest that skeletal    abnormalities emphasized in descriptions of TRPS are only the extreme manifestations of a generalized bone dysplasia.</p>

	]]>
</description>

<author>T H. Malik et al.</author>


</item>


<item>
<title> The netrin 1 receptors Unc5h3 and Dcc are necessary at multiple choice points for the guidance of corticospinal tract axons.</title>
<link>http://mouseion.jax.org/stfb2000_2009/407</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/407</guid>
<pubDate>Tue, 08 May 2012 16:47:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Migrating axons require the correct presentation of guidance molecules, often at multiple choice points, to find their target. Netrin 1, a bifunctional cue involved in both attracting and repelling axons, is involved in many cell    migration and axon pathfinding processes in the CNS.  The netrin 1 receptor DCC and its Caenorhabditis elegans homolog UNC-40 have been implicated in directing the guidance of axons toward netrin sources, whereas the C. elegans UNC-6 receptor,    UNC-5 is necessary for migrations away from UNC-6. However, a role of vertebrate UNC-5 homologs in axonal migration has not been demonstrated. We demonstrate that the Unc5h3 gene product, shown previously to regulate cerebellar granule cell    migrations, also controls the guidance of the corticospinal tract, the major tract responsible for coordination of limb movements. Furthermore, we show that corticospinal tract fibers respond differently to loss of UNC5H3. In addition, we observe    corticospinal tract defects in mice homozygous for a spontaneous mutation that truncates the Dcc transcript.  Postnatal day 0 netrin 1 mutant mice also demonstrate corticospinal tract abnormalities. Last, interactions between the Dcc and Unc5h3    mutations were observed in gene dosage experiments. This is the first evidence of an involvement in axon guidance for any member of the vertebrate unc-5 family and confirms that both the cellular and axonal guidance functions of C. elegans unc-5    have been conserved in vertebrates.</p>

	]]>
</description>

<author>J H. Finger et al.</author>


</item>


<item>
<title> A model scientist.</title>
<link>http://mouseion.jax.org/stfb2000_2009/406</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/406</guid>
<pubDate>Tue, 08 May 2012 16:47:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>A A. Kandutsch</author>


</item>


<item>
<title> New mouse model to study islet transplantation in insulin-dependent diabetes mellitus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/405</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/405</guid>
<pubDate>Tue, 08 May 2012 16:47:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Islet transplantation studies with diabetic rodents frequently use treatment with diabetogens such as alloxan or streptozotocin to render hosts hyperglycemic. These chemicals produce unwanted toxic side effects, which    complicate interpretations of damage produced by hyperglycemia versus direct toxin-induced damage. A mouse that spontaneously developed insulin-sensitive diabetes without beta-cell autoimmunity would provide an excellent vehicle for testing    beta-cell replacement protocols. The Ins2Akita mutation disrupts normal insulin processing and causes a failure in secretion of mature insulins, which results in the early development of hyperglycemia. This report examines the insulin sensitivity    of mice that carry Ins2Akita and their responsiveness to engraftment with syngeneic pancreatic islets. METHODS: Ten-week-old C57BL/6J-Ins2Akita/+ males were given 1 unit of insulin to determine insulin sensitivity. Also, 10-week-old,    hyperglycemic B6-Ins2Akita/+ received either 400 islets isolated from syngeneic C57BL/6J males (n=7) or from allogeneic BALB/cJ males (n=5) under the renal capsule. These mice were followed for 8 weeks after engraftment or until remission of    euglycemia. Nephrectomy of the graft-containing kidney was performed on mice that remained euglycemic.  These mice were then followed for 2 weeks for return of hyperglycemia.  RESULTS: B6-Ins2Akita/+ mice are insulin responsive. Insulin treatment    of hyperglycemic B6-Ins2Akita/+ males significantly lowered blood glucose values within 1 hr. In addition, B6-Ins2Akita/+ recipients of syngeneic islet grafts reversed their diabetic state in less than 72 hr. These islet-engrafted mice remained    normoglycemic until removal of the graft-containing kidney. Removal of the graft resulted in a return to hyperglycemia. Mice that received allogeneic grafts efficiently rejected the graft. CONCLUSIONS: Our data support the hypothesis that    B6-Ins2Akita/+ mice are insulin sensitive and provide an excellent model for islet transplantation studies. In addition, the reduced beta-cell mass and the absence of beta-cell autoimmunity, coupled to the fact that these mice also reject    allografts, suggest that these mice may be useful for a variety of other applications, including testing functionality of human islets prepared for transplantation and perhaps also for exploring beta-cell restorative therapy using pancreatic    islet stem cells.</p>

	]]>
</description>

<author>C E. Mathews et al.</author>


</item>


<item>
<title> The SJL/J mouse is not a model for PBC.</title>
<link>http://mouseion.jax.org/stfb2000_2009/404</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/404</guid>
<pubDate>Tue, 08 May 2012 16:47:13 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M Sasaki et al.</author>


</item>


<item>
<title> Growth defect in Grg5 null mice is associated with reduced Ihh signaling in growth plates.</title>
<link>http://mouseion.jax.org/stfb2000_2009/403</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/403</guid>
<pubDate>Tue, 08 May 2012 16:46:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gene-targeted disruption of Grg5, a mouse homologue of Drosophila groucho (gro), results in postnatal growth retardation in mice. The growth defect, most striking in approximately half of the Grg5 null mice, occurs during the first    4-5 weeks of age, but most mice recover retarded growth later.  We used the nonlinear mixed-effects model to fit the growth data of wild-type, heterozygous, and Grg5 null mice. On the basis of preliminary evidence suggesting an interaction    between Grg5 and the transcription factor Cbfa1/Runx2, critical for skeletal development, we further investigated the skeleton in the mice. A long bone growth plate defect was identified, which included shorter zones of proliferative and    hypertrophic chondrocytes and decreased trabecular bone formation. This decreased trabecular bone formation is likely caused by a reduced recruitment of osteoblasts into the growth plate region of Grg5 null mice. Like the growth defect, the    growth plate and trabecular bone abnormality improved as the mice grew older. The growth plate defect was associated with reduced Indian hedgehog expression and signaling. We suggest that Grg5, a transcriptional coregulator, modulates the    activities of transcription factors, such as Cbfa1/Runx2 in vivo to affect Ihh expression and the function of long bone growth plates.</p>

	]]>
</description>

<author>W F. Wang et al.</author>


</item>


<item>
<title> Fierce: a new mouse deletion of Nr2e1; violent behaviour and ocular abnormalities are background-dependent.</title>
<link>http://mouseion.jax.org/stfb2000_2009/402</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/402</guid>
<pubDate>Tue, 08 May 2012 16:46:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>A new spontaneous mouse mutation named fierce (frc) is deleted for the nuclear receptor Nr2e1 gene (also known as Tlx, mouse homolog of Drosophila tailless). The fierce mutation is genetically and phenotypically similar to Nr2e1    targeted mutations previously studied on segregating genetic backgrounds. However, we have characterized the fierce brain, eye, and behavioural phenotypes on three defined genetic backgrounds (C57BL/6J, 129P3/JEms, and B6129F1). The data revealed    many novel and background-dependent phenotypic characteristics. Whereas abnormalities in brain development, hypoplasia of cerebrum and olfactory lobes, were consistent on all three backgrounds, our novel finding of enlarged ventricles in 100% and    overt hydrocephalus in up to 30% of fierce mice were unique to the C57BL/6J background. Developmental eye abnormalities were also background-dependent with B6129F1-frc mice having less severe thinning of optic layers and less affected    electroretinogram responses. Impaired regression of hyaloid vessels was observed in all backgrounds. Furthermore, retinal vessels were deficient in size and number in 129P3/JEms-frc and B6129F1-frc mice but almost entirely absent in C57BL/6J-frc    mice. We present the first standardized behavioural tests conducted on Nr2e1 mutant mice and show that C57BL/6J-frc and B6129F1-frc mice have deficits in sensorimotor assays and are hyperaggressive in both sexes and backgrounds. However,    C57BL/6J-frc mice were significantly more aggressive than B6129F1-frc mice. Overall, this extensive characterization of the fierce mutation is essential to its application for the study of behavioural, and brain and eye developmental disorders.    In addition, the background-dependent differences revealed will enable the identification of important genetic modifiers.</p>

	]]>
</description>

<author>K A. Young et al.</author>


</item>


<item>
<title> Quantitative trait locus mapping of genes that regulate HDL cholesterol in SM/J and NZB/B1NJ inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/401</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/401</guid>
<pubDate>Tue, 08 May 2012 16:46:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>To investigate the quantitative trait loci (QTL) regulating plasma cholesterol, the female progeny of an (SMxNZB/ B1NJ)xNZB/B1NJ backcross were fed an atherogenic diet. After 18 wk, plasma total cholesterol and high-density    lipoprotein cholesterol (HDL-C) was measured. HDL-C concentrations were greater in NZB than in SM mice. For standard chow-fed mice, QTL were found near D5Mit370 and D18Mit34. For mice fed an atherogenic diet, a QTL was found near D5Mit239. The    QTL for chow-fed and atherogenic-fed mice on chromosome 5 seem to be two different loci. We used a multitrait analysis to rule out pleiotropy in favor of a two-QTL hypothesis. Furthermore, the HDL-C in these strains was induced by the high-fat    diet. For inducible HDL-C, one significant locus was found near D15Mit39. The gene for an HDL receptor, Srb1, maps close to the HDL-C QTL at D5Mit370, but the concentrations of Srb1 mRNA and SR-B1 protein and the gene sequence of NZB/B1NJ and    SM/J did not support Srb1 as a candidate gene. With these QTL, we have identified chromosomal regions that affect lipoprotein profiles in these strains.</p>

	]]>
</description>

<author>W A. Pitman et al.</author>


</item>


<item>
<title> Anterior segment dysgenesis and the developmental glaucomas are complex traits.</title>
<link>http://mouseion.jax.org/stfb2000_2009/400</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/400</guid>
<pubDate>Tue, 08 May 2012 16:46:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Glaucoma refers to a heterogeneous group of disorders that involve retinal ganglion cell death, optic nerve damage, and loss of visual field.  Glaucoma is a leading cause of vision loss worldwide, affecting an estimated 67 million    people. Elevated intraocular pressure is a major risk factor for glaucoma. Individuals with malformations of structures of the anterior segment of the eye frequently develop elevated intraocular pressure and glaucoma. In this review, we focus on    the developmental glaucomas, the subset of glaucomas associated with anterior segment dysgenesis. To minimize overlap with other reviews in this issue and elsewhere, we highlight the complex, multifactorial nature of these diseases and recent    advances using mice.</p>

	]]>
</description>

<author>D B. Gould et al.</author>


</item>


<item>
<title> Genetic modifiers of vision and hearing.</title>
<link>http://mouseion.jax.org/stfb2000_2009/399</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/399</guid>
<pubDate>Tue, 08 May 2012 16:46:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The identification of 'disease genes' and the mutations within them has greatly enhanced our understanding of normal function in the eye and ear.  At the same time, it has become clear that these single-gene mutations must reside    in a permissive genetic background for a disease phenotype to manifest. Segregating background genes can also modify the age of onset, rate of progression or severity of these diseases. These background genes that interact with the disease    mutation and that are responsible for the specific phenotypes observed are commonly called genetic modifiers.  Identification of these modifier genes may define the biological pathways that lead from the primary genetic defect to the aberrant    phenotype. Once the identities of modifier genes that suppress vision or hearing loss become known, the door opens to new potential therapeutic targets, since these modifier genes may be more amenable to treatment than the primary mutant    gene.</p>

	]]>
</description>

<author>N B. Haider et al.</author>


</item>


<item>
<title> Mapping of the mouse hyh gene to a YAC/BAC contig on proximal Chromosome 7.</title>
<link>http://mouseion.jax.org/stfb2000_2009/398</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/398</guid>
<pubDate>Tue, 08 May 2012 16:45:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice that are homozygous for the autosomal recessive hydrocephaly with hop gait (hyh) mutation on Chromosome (Chr) 7 have congenital hydrocephalus characterized by an interhemispheric cyst arising from the third ventricle and    agenesis of the corpus callosum. Analysis of more than 500 backcross and intercross progeny maps the hyh locus to proximal Chr 7, approximately 13 cM centromeric to its originally reported map position. Analysis of recombinants at several MIT    microsatellite markers localized the hyh locus between D7Mit75 and D7Mit56. Development of several new SSLP markers allowed us to refine the hyh candidate interval to a region defined by the cone-rod homeobox ( Crx) gene proximally and D7Mit56    distally. A contig of yeast artificial chromosome (YAC) clones and bacterial artificial chromosome (BAC) clones spanning this entire region has been developed, and a number of potential candidate genes for hyh within this interval have been    identified. Gene content is conserved between this region of mouse Chr 7 and human Chr 19q13.3. Physical mapping of the regions around D7Mit75 and D7Mit56 has also determined the order of a number of MIT markers that remain unresolved on the    Mouse Genome Database (MGD) map. Our physical map and transcript map may be useful for positional cloning of genes in this unusually gene-rich region of the genome.</p>

	]]>
</description>

<author>T H. Chae et al.</author>


</item>


<item>
<title> Understanding the human condition: experimental strategies in Mammalian genetics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/397</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/397</guid>
<pubDate>Tue, 08 May 2012 16:45:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice have become the mammalian model of choice for the application of genetics in biomedical research due to the evolutionary conservation of physiological systems and their attendant pathologies among all mammals as well as the    exceptional power of genetic research technologies in the species. Beginning from aberrant phenotypes, a large number of mouse mutants and natural polymorphisms have been cloned, providing much information about the molecular basis of    physiological processes.  Additionally, the variable expression of these mutations in different inbred strain backgrounds has demonstrated the importance of modifier genes, which are also susceptible to cloning. Research efforts are keeping pace    with these developments. In the area of gene discovery, large, government-funded mutagenesis programs now exist, and as a matter of great practical importance, recent evidence suggests that the same genes may be involved in the natural    polymorphisms affecting disease in mice and humans. In parallel, dramatic advances are also being made in our ability to measure physiological processes in mice, and the advent of expression profiling promises revolutionary advances in    understanding phenotype at the molecular level. Gene-driven approaches have relied on engineering the mouse genome, including adding, subtracting, and replacing genes and, most recently, the ability to control gene activity reversibly. Together,    these multiple advances in our technical abilities have created extraordinary opportunities for future discovery.</p>

	]]>
</description>

<author>K Paigen</author>


</item>


<item>
<title> Novel Sxr(a) ES cell line offers hope for Y chromosome gene-targeted mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/396</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/396</guid>
<pubDate>Tue, 08 May 2012 16:45:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>A mouse targeted for a Y Chromosome gene has not been reported. Because the Y Chromosome is present in only one copy, and most of its genes are critical for germ cell development, such a mouse would likely be infertile. Thus, we    describe a new reproductive strategy to enable transmission of targeted Y Chromosome genes to subsequent generations. The strategy uses two segregating copies of Y Chromosome genes to mimic the autosomal condition. To achieve this, we developed a    new embryonic stem cell line from the XYSxr(a) mouse, which carries a duplication of the gene-rich Y Chromosome short arm. Importantly, we demonstrate germ line transmission of the YSxr(a) chromosome and describe this significant new tool as a    practical solution to enable reproduction in mice targeted for Y Chromosome genes.</p>

	]]>
</description>

<author>E M. Simpson et al.</author>


</item>


<item>
<title> Molecular and phenotypic analysis of 25 recessive, homozygous-viable alleles at the mouse agouti locus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/395</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/395</guid>
<pubDate>Tue, 08 May 2012 16:45:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Agouti is a paracrine-acting, transient antagonist of melanocortin 1 receptors that specifies the subapical band of yellow on otherwise black hairs of the wild-type coat. To better understand both agouti structure/function and the    germline damage caused by chemicals and radiation, an allelic series of 25 recessive, homozygous-viable agouti mutations generated in specific-locus tests were characterized. Visual inspection of fur, augmented by quantifiable chemical analysis    of hair melanins, suggested four phenotypic categories (mild, moderate, umbrous-like, severe) for the 18 hypomorphs and a single category for the 7 amorphs (null). Molecular analysis indicated protein-coding alterations in 8 hypomorphs and 6    amorphs, with mild-moderate phenotypes correlating with signal peptide or basic domain mutations, and more devastating phenotypes resulting from C-terminal lesions. Ten hypomorphs and one null demonstrated wild-type coding potential, suggesting    that they contain mutations elsewhere in the > or = 125-kb agouti locus that either reduce the level or alter the temporal/spatial distribution of agouti transcripts. Beyond the notable contributions to the field of mouse germ cell mutagenesis,    analysis of this allelic series illustrates that complete abrogation of agouti function in vivo occurs most often through protein-coding lesions, whereas partial loss of function occurs slightly more frequently at the level of gene expression    control.</p>

	]]>
</description>

<author>R J. Miltenberger et al.</author>


</item>


<item>
<title> Tumor suppression by a severely truncated species of retinoblastoma protein.</title>
<link>http://mouseion.jax.org/stfb2000_2009/394</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/394</guid>
<pubDate>Tue, 08 May 2012 16:44:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rb(+/+):Rb(-/-) chimeric mice are healthy until early in adulthood when they develop lethal pituitary tumors composed solely of Rb(-/-) cells. In an effort to delineate the minimal structures of the retinoblastoma protein necessary    for RB tumor suppression function, chimeric animals derived from stably transfected RB(-/-) embryonic stem (ES) cells were generated. One such ES cell transfectant expressed a human RB allele encoding a stable, truncated nuclear derivative    lacking residues 1 to 378 (Delta 1-378). Others encoded either wild-type human RB or an internally deleted derivative of the Delta 1-378 mutant. All gave rise to viable chimeric animals with comparable degrees of chimerism. However, unlike    control mice derived, in part, from naive Rb(-/-) ES cells or from ES cells transformed by the double RB mutant, Delta 1-378/Delta exon22, animals derived from either wild-type RB- or Delta 1-378 RB-producing ES cells failed to develop pituitary    tumors. Thus, in this setting, a substantial fraction of the RB sequence is unnecessary for RB-mediated tumor suppression.</p>

	]]>
</description>

<author>H Yang et al.</author>


</item>


<item>
<title>The Influences of Chernyshevsky, Tkachev, and Nechaev on the political thought of V.I. Lenin.</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6936</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6936</guid>
<pubDate>Tue, 08 May 2012 16:44:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>The collapse of the Soviet Union has challenged Marxist political theory. Many people saw the collapse of the Soviet Union as a defeat of Marxism. Most scholars of Political Theory realize that Lenin did not follow Marxist writings. However, most still consider Lenin as predominately a Marxist. This thesis will examine the source of Lenin's ideas on Class, the Party, and the Revolution, and will trace these differences with Marx to chernyshevsky, Tkachev, and Nechaev. It will irrustrate the extent of the influence of Lenin's Russian, non-Marxist, predecessors. Lenin did indeed study and adopt aspects of Marxism, but he differed with him in some important areas, particularly Class, the Party, and the Revolution. Marx, writing in western Europe, sought human emancipation, while Lenin, in backward, autocratic Russia, sought political emancipation from the Tsarist autocracy. This resulted in differences between the thought and writings of Lenin and Marx.</p>

	]]>
</description>

<author>Ian Wallace</author>


</item>


<item>
<title> Reaching for excellence at adolescence: journal of clinical densitometry at year 5.</title>
<link>http://mouseion.jax.org/stfb2000_2009/393</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/393</guid>
<pubDate>Tue, 08 May 2012 16:44:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title> North American male reference population for speed of sound in bone at multiple skeletal sites.</title>
<link>http://mouseion.jax.org/stfb2000_2009/392</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/392</guid>
<pubDate>Tue, 08 May 2012 16:44:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alternatives to dual-energy X-ray absorptiometry (DXA) have been sought to increase access to low-cost osteoporosis risk assessment. Early quantitative ultrasound (QUS) systems measured speed of sound (SOS) and broadband ultrasound    attenuation (BUA) at the calcaneus, and these were demonstrated to be good predictors of hip fracture risk. Recent studies have demonstrated the usefulness of other peripheral sites to assess bone status. The Sunlight Omnisense (Sunlight Medical,    Rehovot, Israel) is a portable, inexpensive QUS device capable of multiple-site SOS measurement.  To provide a robust male reference database, 588 healthy Caucasian males aged 20-90 yr were recruited from 6 centers across North America. SOS    measurements were taken at the distal 1/3 radius, proximal third phalanx, midshaft tibia, and fifth metatarsal. A female reference database has previously been collected at North American sites. The results indicate that SOS in males exhibits an    age-related decline beginning in the fifth decade at the radius, phalanx, and metatarsal, whereas the tibial SOS remains nearly constant until the ninth decade. Although females reach a higher-peak SOS than males at most sites, SOS is higher in    males at all sites after the sixth decade, as a result of a more gradual decline in SOS. Longitudinal monitoring of healthy men should be performed to confirm these cross-sectional results.</p>

	]]>
</description>

<author>S R. Hayman et al.</author>


</item>


<item>
<title> Implications for the insulin signaling pathway in Snell dwarf mouse longevity: a similarity with the C. elegans longevity paradigm.</title>
<link>http://mouseion.jax.org/stfb2000_2009/391</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/391</guid>
<pubDate>Tue, 08 May 2012 16:44:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutation analyses in the nematode, Caenorhabditis elegans, and mice have identified genes that increase their life-span via hormonal signal transduction, i.e. the insulin/insulin-like growth factor-1 (IGF-1) pathway in nematodes,    and the growth hormone (GH)-thyriod stimulating hormone (TSH)-prolactin system in Snell dwarf mouse mutants. We have shown that the GH deficiency due to Pit1 mutation in the long-lived Snell dwarf mice may decrease circulating insulin levels,    thereby resulting in a decreased activity of the insulin/IGF-1 signaling pathway. The data presented are consistent with our hypothesis that the decreased circulating insulin levels resulting from the Pit1 mutation mimics a physiological state    similar to that proposed to occur in the long-lived C. elegans, daf-2 mutant. Our studies demonstrate a series of changes in components of the insulin/IGF-1-signaling pathway that suggest a reduction-of-function of this pathway in the aged dwarf.    These include a decreased IRS-2 pool level, a decrease in PI3K activity and its association with IRS-2 and decreased docking of p85alpha to IRS-2. Our data also suggest a preferential docking of IRS-2-p85alpha-p110alpha in the aged dwarf liver    and IRS-2-p85alpha-p110beta in the aged control. We speculate that the preference for the p110alpha-containing complex may be a specific characteristic of a downstream segment of the longevity-signaling cascade. We conclude that the Pit1 mutation    may result in physiological homeostasis that favors longevity, and that the Snell dwarf mutant conforms to the nematode longevity paradigm.</p>

	]]>
</description>

<author>C C. Hsieh et al.</author>


</item>


<item>
<title> Effects of the Pit1 mutation on the insulin signaling pathway: implications on the longevity of the long-lived Snell dwarf mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/390</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/390</guid>
<pubDate>Tue, 08 May 2012 16:44:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in Caenorhabditis elegans and mice have identified candidate genes that increase their lifespan via hormonal signal transduction, i.e.  the insulin/IGF-1-like pathway. In this study we propose that longevity of the Snell    dwarf (Pit1(dw)/Pit1(dw)) mouse is associated with a decrease of the insulin/IGF-1 signaling pathway caused by the Pit1 mutation. We recently demonstrated that the growth hormone deficiency of the dwarf mouse alters circulating insulin levels,    thereby resulting in a decreased activity of the insulin/IGF-1 signaling pathway, which is a determining factor in the increased nematode lifespan. The decreased activity of the insulin/IGF-1 signaling pathway is indicated by decrease of (a)    IRS-two pool levels; (b) docking of p85alpha to IRS-2; (c) docking of p85alpha to p110alpha or p110beta, and (d) IRS-2-associated PI3K activity. In this study we present data suggesting that the InRbeta-IRS-1-PI3K pathway is attenuated in the    Snell dwarf mouse liver. Our data show that the PI3K activity associated with IRS-1, the docking of IRS-1 to InRbeta and the docking of p85alpha to IRS-1 are attenuated in the aged Snell dwarf. Our studies suggest that the Pit1 mutation results    in a decreased activity of the insulin/IGF-1 pathway; that this plays a key role in the longevity of the Snell dwarf mouse and conforms to the nematode longevity paradigm.</p>

	]]>
</description>

<author>C C. Hsieh et al.</author>


</item>


<item>
<title> International Workshop on Lessons from Animal Models for Human Type 1 Diabetes: analyzing target autoantigens of humoral immunity in nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/389</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/389</guid>
<pubDate>Tue, 08 May 2012 16:43:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The aim of this workshop was to identify autoantibody assays that could provide useful markers of autoimmunity in the NOD mouse model for type 1 diabetes. It was demonstrated that insulin autoantibodies measured by sensitive    radiobinding assay are a marker of autoimmunity in NOD mice and draw into question the true nature of GADA and IA-2A in this animal model.</p>

	]]>
</description>

<author>E Bonifacio et al.</author>


</item>


<item>
<title> Cloning v. clowning.</title>
<link>http://mouseion.jax.org/stfb2000_2009/388</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/388</guid>
<pubDate>Tue, 08 May 2012 16:43:42 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D Solter</author>


</item>


<item>
<title> Molecular phenotyping for analyzing subtle genetic effects in mice: application to an angiotensinogen gene titration.</title>
<link>http://mouseion.jax.org/stfb2000_2009/387</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/387</guid>
<pubDate>Tue, 08 May 2012 16:43:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The angiotensinogen M235T polymorphism in humans is linked to differential expression of the human angiotensinogen gene (AGT) gene and hypertension, but the homeostatic responses resulting from this polymorphism are not known. We    therefore investigated how mice respond to five genetically determined levels of mouse angiotensinogen gene (Agt) expression covering the range associated with the M235T variants. By using high-throughput molecular phenotyping, tissue RNAs were    assayed for expression of 10 genes important in hypertension. Significant positive and negative responses occurred in both sexes as Agt expression increased twofold, including a three-fold increase in aldosterone synthase expression in adrenal    gland, and a two-fold decrease in renin expression in kidney. In males, cardiac expression of the precursor of atrial natriuretic peptide B and of adrenomedullin also increased approximately twofold. The relative expression of all genes studied    except Agt differed significantly in the two sexes, and several unexpected relationships were encountered. A highly significant correlation between renal expression of the angiotensin type 1a receptor and kallikrein, independent of Agt genotype,    is present in females (P < 0.0001) but not males (P = 0.4). The correlation between blood pressure (BP) and liver Agt expression within the five Agt genotypes is significant in females (P = 0.0005) but not in males (P = 0.2), whereas correlation    of BP with differences between the genotypes is less in females (P = 0.06) than in males (P = 0.001). The marked gender differences in gene expression in wild-type mice and the changes induced by moderate alterations in Agt expression and BP    emphasize the need to look for similar differences in humans.</p>

	]]>
</description>

<author>H S. Kim et al.</author>


</item>


<item>
<title> Musculoskeletal effects of the recombinant human IGF-I/IGF binding protein-3 complex in osteoporotic patients with proximal femoral fracture: a double-blind, placebo-controlled pilot study.</title>
<link>http://mouseion.jax.org/stfb2000_2009/386</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/386</guid>
<pubDate>Tue, 08 May 2012 16:43:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>The administration of recombinant human IGF-I complexed with its predominant binding protein IGF binding protein-3 (rhIGF-I/IGFBP-3) may allow the safe administration of higher doses of IGF-I than can be accomplished with rhIGF-I    alone. The aim of this randomized, double-blind, placebo- controlled pilot study was to evaluate the short-term safety and musculoskeletal effects of rhIGF-I/IGFBP-3 in older women (aged 65-90 yr) with recent hip fracture. Within 72 h after the    event, 30 patients received continuous administration of either placebo (n = 10), 0.5 mg/kg.d rhIGF-I/IGFBP-3 (n = 9), or 1 mg/kg.d rhIGF-I/IGFBP-3 (n = 11). Treatment was administered by sc infusion through a portable mini-pump for a total of 8    wk after hip fracture surgery, with patient follow-up to 6 months after surgery. Efficacy evaluations included a contralateral hip bone density determination, markers of bone turnover (including serum osteocalcin and urinary excretion of    N-telopeptide), grip strength, and tests of functional ability. During the administration of rhIGF-I/IGFBP-3, mean serum levels of IGF-I significantly (P < 0.001) increased from 83 ng/ml to 289 ng/ml (0.5 mg/kg.d) and 393 ng/ml (1 mg/kg.d),    respectively.  Both doses were well tolerated, and no hypoglycemia or other therapy-induced side effects were observed. After an initial loss of hip bone density after hip fracture surgery, patients treated with 1 mg/kg.d rhIGF-I/IGFBP-3 regained    a substantial portion of their femoral bone mass.  At 6 months postfracture (4 months after the 2-month infusion), they showed a statistically not significant decrease from baseline in hip bone density (-2.6%, P = 0.53). Placebo-treated patients,    on the other hand, failed to regain lost bone: at 6 months postfracture, bone density in the placebo group had declined by 6.1% (P = 0.04). Additionally, in patients treated with 1.0 mg/kg.d rhIGF-I/IGFBP-3, grip strength had increased from    baseline by 11.4% by the end of the study (P = 0.04) whereas patients on placebo lost 11.6% from baseline (P = 0.16). This increase in muscle strength in the high-dose group was associated with a positive effect on functional recovery. We    conclude that a 2-month infusion of rhIGF-I/IGFBP-3 in patients with recent hip fracture is feasible, safe, and well tolerated. Analyzing the effects on bone mass, muscle strength, and functional ability, we observed beneficial trends. In the    context of a small exploratory study, these findings should be interpreted with caution, but they support the need for future trials to further assess the therapeutic potential of rhIGF-I/IGFBP-3 in elderly subjects with    osteoporosis.</p>

	]]>
</description>

<author>S Boonen et al.</author>


</item>


<item>
<title> Mutations in ALMS1 cause obesity, type 2 diabetes and neurosensory degeneration in Alstrom syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/385</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/385</guid>
<pubDate>Tue, 08 May 2012 16:43:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alstrom syndrome is a homogeneous autosomal recessive disorder that is characterized by childhood obesity associated with hyperinsulinemia, chronic hyperglycemia and neurosensory deficits. The gene involved in Alstrom syndrome    probably interacts with genetic modifiers, as subsets of affected individuals present with additional features such as dilated cardiomyopathy, hepatic dysfunction, hypothyroidism, male hypogonadism, short stature and mild to moderate    developmental delay, and with secondary complications normally associated with type 2 diabetes, such as hyperlipidemia and atherosclerosis. Our detection of an uncharacterized transcript, KIAA0328, led us to identify the gene ALMS1, which    contains sequence variations, including four frameshift mutations and two nonsense mutations, that segregate with Alstrom syndrome in six unrelated families.  ALMS1 is ubiquitously expressed at low levels and does not share significant sequence    homology with other genes reported so far. The identification of ALMS1 provides an entry point into a new pathway leading toward the understanding of both Alstrom syndrome and the common diseases that characterize it.</p>

	]]>
</description>

<author>G B. Collin et al.</author>


</item>


<item>
<title> Mutant mouse models reveal the relative roles of E2F1 and E2F3 in vivo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/384</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/384</guid>
<pubDate>Tue, 08 May 2012 16:42:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The E2F1, -2, and -3 transcription factors are key downstream targets of the retinoblastoma protein (pRB) tumor suppressor that drive expression of proliferation-associated genes. Here we use mutant mouse strains to investigate    E2F3's role in vivo. We show that E2F3 is essential for embryonic viability in the pure 129/Sv background but the presence of C57BL/6 alleles yields some adult survivors. Although growth retarded, surviving E2f3(-/-) animals are initially    healthy. However, they die prematurely, exhibiting no obvious tumor phenotype but with the typical signs of congestive heart failure. The defects are completely distinct from those arising in E2f1 mutant mice (S. J. Field et al., Cell 85:549-561;    1996; L. Yamasaki et al., Cell 85:537-548, 1996), supporting the prevailing view that these E2Fs must have some unique biological functions in vivo. To test this model, we examined the phenotypes of E2f1 E2f3 compound mutant mice. Almost all of    the developmental and age-related defects arising in the individual E2f1 or E2f3 mice were exacerbated by the mutation of the other E2f. Thus, E2F1 and E2F3 appear to play critical, overlapping roles in the development and maintenance of a    variety of tissues. Importantly, this study did identify one major difference in the properties of E2F1 and E2F3: either alone or in combination with E2F1 loss, E2f3 mutation did not increase the incidence of tumor formation. These data strongly    suggest that tumor suppression is a specific property of E2F1 and not E2F3.</p>

	]]>
</description>

<author>J E. Cloud et al.</author>


</item>


<item>
<title> Mutant laboratory mice with abnormalities in pigmentation: annotated tables.</title>
<link>http://mouseion.jax.org/stfb2000_2009/383</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/383</guid>
<pubDate>Tue, 08 May 2012 16:42:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mammalian pigment cell research has recently entered a phase of significantly increased activity due largely to the exploitation of the many mutant mouse stocks that are coming on stream. Numerous transgenic, targeted mutagenesis    (so-called 'knockouts'), conditional (so-called 'gene switch') and spontaneous mutant mice develop abnormal coat color phenotypes. The number of mice that exhibit such abnormalities is increasing exponentially as genetic engineering methods    become routine.  Since defined abnormalities in such mutant mice provide important clues to the as yet often poorly understood functional roles of many gene products, this overview includes a corresponding, annotated table of mutant mice with    pigmentation alterations. These range from early developmental defects via a large array of coat color abnormalities to a melanoma metastasis model. This overview should provide helpful pointers to investigators who are looking for mouse models    to explore or to compare functional activities of genes of interest and for comparing coat color phenotypes of spontaneous or genetically engineered mouse mutants with novel ones. Secondly, this review includes a table of mouse models of specific    human diseases with genetically defined pigmentation abnormalities. In summary, this annotated table should serve as a useful reference for anyone interested in the molecular controls of pigmentation.</p>

	]]>
</description>

<author>M Nakamura et al.</author>


</item>


<item>
<title> Rules and guidelines for mouse gene, allele, and mutation nomenclature: a condensed version.</title>
<link>http://mouseion.jax.org/stfb2000_2009/382</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/382</guid>
<pubDate>Tue, 08 May 2012 16:42:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>L J. Maltais et al.</author>


</item>


<item>
<title> Absence of the CD44 Gene Prevents Sarcoma Metastasis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/381</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/381</guid>
<pubDate>Tue, 08 May 2012 16:42:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>To test the role of the CD44 gene in tumorigenesis, mice with the min mutationof the APC gene or with the tm1 mutation of the p53 gene were crossedwith CD44 knockout mice. The absence of CD44 gene products did not affect tumor    incidence or survival; however, mice with disruption of the CD44 gene showed virtually aborted metastasis formation of osteosarcomas.  This is in agreement with the role attributed to CD44 variants in the spread of cancer. Therefore, CD44 gene    products are not essential for tumor incidence and growth but are important in regulating metastasis formation.</p>

	]]>
</description>

<author>G F. Weber et al.</author>


</item>


<item>
<title> Segmentation defects of Notch pathway mutants and absence of a synergistic phenotype in lunatic fringe/radical fringe double mutant mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/380</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/380</guid>
<pubDate>Tue, 08 May 2012 16:42:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Summary: The Notch signaling pathway is important in regulating formation and anterior-posterior patterning of somites in vertebrate embryos. Here we show that distinct segmentation defects are displayed in embryos mutant for the    Notch pathway genes Notch1, Lunatic fringe (Lfng), Delta-like 1 (Dll1), and Delta-like 3 (Dll3). Lfng-deficient mice and Dll3-deficient mice exhibit very similar defects, and marker analysis suggests that progression of the segmentation clock is    disrupted in Dll3 mutants. We also show that Radical fringe (Rfng)-deficient mice exhibit no obvious phenotypic defects. To assess whether the absence of a phenotype in Rfng-deficient mice was the result of functional redundancy with the Lfng    gene, we generated Lfng/Rfng double homozygous mutant mice. These mice exhibit the skeletal defects normally observed in Lfng-deficient mice, but we detected no obvious synergistic or additive effects in the double mutant animals. genesis    33:21-28, 2002. Copyright 2002 Wiley-Liss, Inc.</p>

	]]>
</description>

<author>N Zhang et al.</author>


</item>


<item>
<title> Loss of Pin1 function in the mouse causes phenotypes resembling cyclin D1-null phenotypes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/379</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/379</guid>
<pubDate>Tue, 08 May 2012 16:41:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Phosphorylation of proteins on serine/threonine residues preceding proline is a key signaling mechanism. The conformation and function of a subset of these phosphorylated proteins is regulated by the prolyl isomerase Pin1 through    isomerization of phosphorylated Ser/Thr-Pro bonds. Although young Pin1(-/-) mice have been previously shown to develop normally, we show here that they displayed a range of cell-proliferative abnormalities, including decreased body weight and    testicular and retinal atrophies.  Furthermore, in Pin1(-/-) adult females, the breast epithelial compartment failed to undergo the massive proliferative changes associated with pregnancy. Interestingly, many of these Pin1-deficient phenotypes    such as retinal hypoplasia and mammary gland impairment are also the characteristic of cyclin D1-deficient mice. Cyclin D1 levels were significantly reduced in many tissues in Pin1-deficient mice, including retina and breast epithelial cells from    pregnant mice. Moreover, Pin1 directly bound to cyclin D1 phosphorylated on Thr-286-Pro increased cyclin D1 in the nucleus and stabilized cyclin D1. These results indicate that Pin1 positively regulates cyclin D1 function at the transcriptional    level, as demonstrated previously, and also through posttranslational stabilization, which together explain why Pin1 loss-of-function phenotypes in the mouse resemble cyclin D1-null phenotypes. Our results provide genetic evidence for an    essential role of Pin1 in maintaining cell proliferation and regulating cyclin D1 function.</p>

	]]>
</description>

<author>Y C. Liou et al.</author>


</item>


<item>
<title> Crossover interference in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/378</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/378</guid>
<pubDate>Tue, 08 May 2012 16:41:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present an analysis of crossover interference in the mouse genome, on the basis of high-density genotype data from two reciprocal interspecific backcrosses, comprising 188 meioses. Overwhelming evidence was found for strong    positive crossover interference with average strength greater than that implied by the Carter-Falconer map function. There was some evidence for interchromosomal variation in the level of interference, with smaller chromosomes exhibiting stronger    interference. We further compared the observed numbers of crossovers to previous cytological observations on the numbers of chiasmata and evaluated evidence for the obligate chiasma hypothesis.</p>

	]]>
</description>

<author>K W. Broman et al.</author>


</item>


<item>
<title> Cutting edge: the minor histocompatibility antigen H60 peptide interacts with both H-2Kb and NKG2D.</title>
<link>http://mouseion.jax.org/stfb2000_2009/377</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/377</guid>
<pubDate>Tue, 08 May 2012 16:41:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Minor histocompatibility Ags elicit cell-mediated immune responses and graft rejection in individuals receiving MHC-matched tissues. H60 represents a dominant Ag that elicits a strong CTL response in C57BL/6 mice immunized against    BALB.B. An 8-aa peptide in the H60 protein is presented by H-2K(b) and this is recognized by the TCR as an alloantigen.  The intact H60 glycoprotein is a ligand for the costimulatory NKG2D receptor that is expressed by activated CD8(+) T cells.    Thus, H60 may provide both an allogeneic peptide and its own costimulation. We show that mutation of an H-2K(b)-binding anchor residue in the H60 peptide completely abrogates binding of H60 glycoprotein to NKG2D and a synthetic H60 peptide    partially blocks the binding of NKG2D to its ligand. Ligands of the human NKG2D receptor are remarkably polymorphic, suggesting that these may also serve as minor histocompatibility Ags.</p>

	]]>
</description>

<author>A Cerwenka et al.</author>


</item>


<item>
<title> Absence of CD5 Dramatically Reduces Progression of Pulmonary Inflammatory Lesions in SHP-1 Protein-Tyrosine Phosphatase-Deficient &apos;Viable Motheaten&apos; Mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/376</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/376</guid>
<pubDate>Tue, 08 May 2012 16:41:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice homozygous for the viable motheaten (Hcph(me-v)) mutation are deficient in SHP-1 protein-tyrosine phosphatase, resulting in severe systemic autoimmunity and immune dysfunction. A high percentage of B-cells in viable motheaten    mice express the cell surface glycoprotein CD5, in contrast to wild type mice that express CD5 on only a small percentage of B-cells. CD5(+) B-cells have been associated with autoantibody production.  To determine the role of CD5 in the    development of the inflammatory disease in me(v)/ me(v) mice, we created a stock of CD5(null)me(v)/ me(v) mice. The longevity of CD5(null)me(v)/ me(v) mice was increased 69% in comparison to me(v)/ me(v) mice on a similar (B6;129) background. The    increased lifespan was associated with a marked reduction in pulmonary inflammation. Flow cytometry analysis of spleen cells from CD5(null)me(v)/ me(v) mice at 9-12 weeks of age revealed significant decreases in percentages of IgM/B220 double    positive B-cells, Mac-1/Gr-1 double positive cells and CD4(+) T-cells compared with me(v)/ me(v) mice.  CD5(null)me(v)/ me(v) mice also had significantly lower serum IgM levels in comparison to me(v)/ me(v) mice. Study of CD5(null)me(v)/ me(v)    mice may provide further insight into the role of CD5 in cell signaling and may help explain the observed association of CD5(+) B-cells with autoimmune disease. Copyright 2002 Elsevier Science Ltd.</p>

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</description>

<author>M J. Joliat et al.</author>


</item>


<item>
<title> T Cell Developmental Defects in &apos;Viable Motheaten&apos; Mice Deficient in SHP-1 Protein-Tyrosine Phosphatase. Developmental Defects are Corrected in vitro in the Presence of Normal Hematopoietic-Origin Stromal Cells and in vivo by
   Exogenous IL-7.</title>
<link>http://mouseion.jax.org/stfb2000_2009/375</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/375</guid>
<pubDate>Tue, 08 May 2012 16:40:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Defects in the gene that encodes SHP-1 protein tyrosine phosphatase result in multiple hematopoietic abnormalities and generalized autoimmunity in viable motheaten (me(v)) mice. These mice also exhibit early thymic involution and    abnormalities in T cell development. Here, we describe the use of fetal thymic organ culture (FTOC) and bone marrow adoptive transfer to study the effects of SHP-1 deficiency on thymocyte development.  Chimeric FTOC established with normal bone    marrow placed onto deoxyguanosine-treated fetal thymic lobes or onto scid fetal thymic lobes generated T cells. Bone marrow from SHP-1-deficient me(v)/ me(v) mice generated decreased numbers of T cells in chimeric FTOC established using    deoxyguanosine-treated thymi but generated normal numbers in chimeric FTOC established using scid thymi. However, scid fetal thymi seeded with me(v)/ me(v) bone marrow also exhibited morphological abnormalities and contained elevated numbers of    macrophages. Addition of IL-7 to me(v)/ me(v) bone marrow-seeded scid FTOC led to increased cell numbers, particularly of macrophages. Intrathymic injection of IL-7 partially restored the ability of progenitor cells in me(v)/ me(v) bone marrow to    populate the thymus of adoptive recipients. We conclude that abnormal T cell development in me(v)/ me(v) mice may in part be due to defects in the ability of bone marrow-derived accessory cells to provide bioavailable IL-7 to developing    thymocytes. Copyright 2002 Elsevier Science Ltd.</p>

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</description>

<author>S W. Christianson et al.</author>


</item>


<item>
<title> Mice with targeted gene disruptions or gene insertions for diabetes research: problems, pitfalls, and potential solutions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/374</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/374</guid>
<pubDate>Tue, 08 May 2012 16:40:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse has been a favoured organism for molecular manipulation in studies seeking to establish the genetic bases and pathophysiologic mechanisms underlying both Type I (insulin-dependent) and Type II (non-insulin-dependent)    diabetes mellitus. Gene targeting and transgenesis are the two powerful molecular technologies used in these endeavours.  Interpretation of results generated from such studies, either entailing an altered phenotype or the absence of a phenotypic    change, is not always simple. This review focuses on certain complications inherent in the methodologies, and outlines steps that can be taken to distinguish effects of the genetic manipulation from unexpected contributions from the genetic    background. [Diabetologia (2002) 45: 296-308]</p>

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</description>

<author>E H. Leiter</author>


</item>


<item>
<title> Microtubule-associated protein 1A is a modifier of tubby hearing (moth1).</title>
<link>http://mouseion.jax.org/stfb2000_2009/373</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/373</guid>
<pubDate>Tue, 08 May 2012 16:40:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Once a mutation in the gene tub was identified as the cause of obesity, retinal degeneration and hearing loss in tubby mice, it became increasingly evident that the members of the tub gene family (tulps) influence maintenance and    function of the neuronal cell lineage. Suggested molecular functions of tubby-like proteins include roles in vesicular trafficking, mediation of insulin signaling and gene transcription. The mechanisms through which tub functions in neurons,    however, have yet to be elucidated. Here we report the positional cloning of an auditory quantitative trait locus (QTL), the modifier of tubby hearing 1 gene (moth1), whose wildtype alleles from strains AKR/J, CAST/Ei and 129P2/OlaHsd protect    tubby mice from hearing loss. Through a transgenic rescue experiment, we verified that sequence polymorphisms in the neuron-specific microtubule-associated protein 1a gene (Mtap1a) observed in the susceptible strain C57BL/6J (B6) are crucial for    the hearing-loss phenotype. We also show that these polymorphisms change the binding efficiency of MTAP1A to postsynaptic density molecule 95 (PSD95), a core component in the cytoarchitecture of synapses. This indicates that at least some of the    observed polymorphisms are functionally important and that the hearing loss in C57BL/6J-tub/tub (B6-tub/tub) mice may be caused by impaired protein interactions involving MTAP1A. We therefore propose that tub may be associated with synaptic    function in neuronal cells.</p>

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</description>

<author>A Ikeda et al.</author>


</item>


<item>
<title> Sex does not seem to influence the formation of aortic lesions in the P-407-induced mouse model of hyperlipidemia and atherosclerosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/372</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/372</guid>
<pubDate>Tue, 08 May 2012 16:39:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Coronary heart disease secondary to atherosclerosis is the leading cause of death for men in the United States. Using a new, nontransgenic, non-fat-fed mouse model of hyperlipidemia and atherosclerosis developed in our laboratory,    we investigated the effect of sex on lipid profiles and subsequent aortic atherosclerotic lesion formation. Female and male C57BL/6 mice, which consumed a low-fat diet, were treated with either normal saline or poloxamer 407 (P-407), a triblock    copolymer comprised of poly(oxyethylene) and poly(oxypropylene) units, for 4 months. Blood samples were obtained at 0, 1, 2, 3, and 4 months, whereas hearts and livers were harvested only at 4 months, because this model requires approximately 4    months for significant atheroma formation. P-407-treated mice of either sex demonstrated a profound increase in plasma cholesterol and triglyceride; at 3 and 4 months the plasma lipids were significantly (p < 0.05) higher for male mice compared    with female mice. Aortas retrieved from P-407-treated mice of either sex after 4 months demonstrated a significant (p < 0.001) increase in the mean atherosclerotic lesion size compared with their respective saline-treated controls, but there was    no significant (p > 0.05) difference between lesion sizes for P-407-treated male mice (1.02 +/- 0.074 x 10(5) microm(2)) compared with P-407-treated female mice (1.14 +/- 0.28 x 10(5) microm(2)). Livers harvested at 4 months from either sex of    P-407-treated mice displayed no damage to hepatocytes but increased proliferation of macrophages (Kupffer cells), which contained sequestered lipids. Thus, male C57BL/6 mice form atherosclerotic lesions as extensive as female mice in the P-407    mouse model of atherosclerosis.</p>

	]]>
</description>

<author>T P. Johnston et al.</author>


</item>


<item>
<title> The mammalian oocyte orchestrates the rate of ovarian follicular development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/371</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/371</guid>
<pubDate>Tue, 08 May 2012 16:39:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>The development of both the mammalian oocyte and the somatic cell compartments of the ovarian follicle is highly coordinated; this coordination ensures that the ovulated oocyte is ready to undergo fertilization and subsequent    embryogenesis. Disruption of this synchrony results in oocyte developmental failure. Communication between the oocyte and companion somatic cells is essential for successful development of both follicular compartments. However, it was not    previously known whether one cell type, either the somatic or the germ cell compartment, determines the overall rate of follicular development. To test the hypothesis that the oocyte orchestrates the rate of follicle development, mid-sized    oocytes isolated from secondary follicles were transferred back to primordial follicles, the earliest stage of follicular development. This transfer doubled the rate of follicular development and the differentiation of follicular somatic cells.    Oocyte development in these accelerated follicles appeared normal; recovered oocytes were competent to undergo fertilization and embryonic development. These results demonstrate that oocytes orchestrate and coordinate the development of mammalian    ovarian follicles and that the rate of follicular development is based on a developmental program intrinsic to the oocyte.</p>

	]]>
</description>

<author>J J. Eppig et al.</author>


</item>


<item>
<title> Purkinje cell degeneration (pcd) phenotypes caused by mutations in the axotomy-induced gene, Nna1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/370</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/370</guid>
<pubDate>Tue, 08 May 2012 16:39:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>The classical recessive mouse mutant, Purkinje cell degeneration (pcd), exhibits adult-onset degeneration of cerebellar Purkinje neurons, retinal photoreceptors, olfactory bulb mitral neurons, and selected thalamic neurons, and has    defective spermatogenesis. Here we identify Nna1 as the gene mutated in the original pcd and two additional pcd alleles (pcd2J and pcd3J). Nna1 encodes a putative nuclear protein containing a zinc carboxypeptidase domain initially identified by    its induction in spinal motor neurons during axonal regeneration. The present study suggests an unexpected molecular link between neuronal degeneration and regeneration, and its results have potential implications for neurodegenerative diseases    and male infertility.</p>

	]]>
</description>

<author>Gonzalez A. Fernandez et al.</author>


</item>


<item>
<title> The Mouse Tumor Biology Database: a public resource for cancer genetics and pathology of the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/369</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/369</guid>
<pubDate>Tue, 08 May 2012 16:39:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Developing genetic mouse models for cancer research has been recognized as an "exceptional opportunity" by the National Cancer Institute. The establishment of bioinformatics resources to facilitate access to published and    unpublished data on the genetics and pathology of cancer in different strains of the laboratory mouse is critical to developing and using mouse models of human disease. In this article, we review the Mouse Tumor Biology Database (MTB), a public    resource for information on cancer genetics, epidemiology, and pathology in genetically defined mice. We outline current content, data acquisition strategies, and query mechanisms for MTB. MTB is accessible on-line at    http://tumor.informatics.jax.org.</p>

	]]>
</description>

<author>D Naf et al.</author>


</item>


<item>
<title> Targeted disruption of NBS1 reveals its roles in mouse development and DNA repair.</title>
<link>http://mouseion.jax.org/stfb2000_2009/368</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/368</guid>
<pubDate>Tue, 08 May 2012 16:39:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nijmegen breakage syndrome (NBS) is an autosomal recessive hereditary disease that shares some common defects with ataxia-telangiectasia. The gene product mutated in NBS, named NBS1, is a component of the Mre11 complex that is    involved in DNA strand-break repair. To elucidate the physiological roles of NBS1, we disrupted the N-terminal exons of the NBS1 gene in mice. NBS1(m/m) mice are viable, growth retarded and hypersensitive to ionizing radiation (IR). NBS1(m/m)    mice exhibit multiple lymphoid developmental defects, and rapidly develop thymic lymphoma. In addition, female NBS1(m/m) mice are sterile due to oogenesis failure.  NBS1(m/m) cells are impaired in cellular responses to IR and defective in    cellular proliferation. Most systematic and cellular defects identified in NBS1(m/m) mice recapitulate those in NBS patients, and are essentially identical to those observed in Atm(-/-) mice. In contrast to Atm(-/-) mice, spermatogenesis is    normal in NBS1(m/m) mice, indicating that distinct roles of ATM have differential requirement for NBS1 activity.  Thus, NBS1 and ATM have overlapping and distinct functions in animal development and DNA repair.</p>

	]]>
</description>

<author>J Kang et al.</author>


</item>


<item>
<title> Evidence that multifunctional calcium/calmodulin-dependent protein kinase II (CaM KII) participates in the meiotic maturation of mouse oocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/367</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/367</guid>
<pubDate>Tue, 08 May 2012 16:38:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Calcium-dependent signaling pathways are thought to be involved in the regulation of mammalian oocyte meiotic maturation. However, the molecular linkages between the calcium signal and the processes driving meiotic maturation are    not clearly defined. The present study was conducted to test the hypothesis that the multi-functional calcium/calmodulin-dependent protein kinase II (CaM KII) functions as one of these key linkers. Mouse oocytes were treated with a    pharmacological CaM KII inhibitor, KN-93, or a peptide CaM KII inhibitor, myristoylated AIP, and assessed for the progression of meiosis. Two systems for in vitro oocyte maturation were used: (1) spontaneous gonadotropin-independent maturation    and (2) follicle-stimulating hormone (FSH)-induced reversal of hypoxanthine-mediated meiotic arrest. FSH-induced, but not spontaneous germinal vesicle breakdown (GVB) was dose-dependently inhibited by both myristoylated AIP and KN-93, but not its    inactive analog, KN-92. However, emission of the first polar body (PB1) was inhibited by myristoylated AIP and KN-93 in both oocyte maturation systems. Oocytes that failed to produce PB1 exhibited normal-appearing metaphase I chromosome    congression and spindles indicating that CaM KII inhibitors blocked the metaphase I to anaphase I transition. Similar results were obtained when the oocytes were treated with a calmodulin antagonist, W-7, and matured spontaneously.  These results    suggest that CaM KII, and hence the calcium signaling pathway, is potentially involved in regulating the meiotic maturation of mouse oocytes. This kinase both participates in gonadotropin-induced resumption of meiosis, as well as promoting the    metaphase I to anaphase I transition. Further evidence is therefore, provided of the critical role of calcium-dependent pathways in mammalian oocyte maturation. Copyright 2002 Wiley-Liss, Inc.</p>

	]]>
</description>

<author>Y Q. Su et al.</author>


</item>


<item>
<title> Allogenic fetal liver cells have a distinct competitive engraftment advantage over adult bone marrow cells when infused into fetal as compared with adult severe combined immunodeficient recipients.</title>
<link>http://mouseion.jax.org/stfb2000_2009/366</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/366</guid>
<pubDate>Tue, 08 May 2012 16:38:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>In utero transplantation (IUT) is becoming a viable option for the treatment of various immune and metabolic disorders diagnosed early in gestation. In this study, donor fetal liver cells had a 10-fold competitive engraftment    advantage relative to adult bone marrow in allogeneic fetal severe combined immunodeficient (SCID) recipients compared with adult recipients. In contrast, adult bone marrow cells engrafted slightly better than fetal liver cells in allogeneic    adult SCID transplant recipients. By using different ratios of fetal and adult cell mixtures, fetal liver cells repopulated 8.2 times better than adult bone marrow cells in fetal recipients, but only 0.8 times as well in adult recipients. Fetal    SCID recipients were more permissive to an allogeneic donor graft than adult recipients. These data indicate that the recipient microenvironment may regulate the engraftment efficiency of a given stem cell source and suggest that the use of cord    blood should be tested in clinical IUT.</p>

	]]>
</description>

<author>P A. Taylor et al.</author>


</item>


<item>
<title> A haplolethal locus uncovered by deletions in the mouse T complex.</title>
<link>http://mouseion.jax.org/stfb2000_2009/365</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/365</guid>
<pubDate>Tue, 08 May 2012 16:38:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Proper levels of gene expression are important for normal mammalian development. Typically, altered gene dosage caused by karyotypic abnormalities results in embryonic lethality or birth defects. Segmental aneuploidy can be    compatible with life but often results in contiguous gene syndromes. The ability to manipulate the mouse genome allows the systematic exploration of regions that are affected by alterations in gene dosage. To explore the effects of segmental    haploidy in the mouse t complex on chromosome 17, radiation-induced deletion complexes centered at the Sod2 and D17Leh94 loci were generated in embryonic stem (ES) cells. A small interval was identified that, when hemizygous, caused specific    embryonic lethal phenotypes (exencephaly and edema) in most fetuses. The penetrance of these phenotypes was background dependent. Additionally, evidence for parent-of-origin effects was observed. This genetic approach should be useful for    identifying genes that are imprinted or whose dosage is critical for normal embryonic development.</p>

	]]>
</description>

<author>V L. Browning et al.</author>


</item>


<item>
<title> Deconstructing and reconstructing obesity-induced diabetes (diabesity) in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/364</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/364</guid>
<pubDate>Tue, 08 May 2012 16:38:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Obesity-driven type 2 diabetes (diabesity) involves complex genetic and environmental interactions to trigger disease. Here, we combine variable numbers of known quantitative trait loci (QTL) for obesity and diabetes contributed by    New Zealand Obese (NZO/HlLt) and Nonobese Nondiabetic (NON/Lt) strains in the form of 10 interval-directed recombinant congenic strains (RCS), with NON/Lt as the background strain, to dissect the genetic interactions involved. All 10 RCS gain    significantly more weight than the NON parental strain, but none are as obese as the parental, diabetes-prone NZO. Diabetes development in these RCS at F12 ranges between 0 and 100%, depending on genetic constitution. RCS-2, -1, and -10 represent    a step-wise increase in numbers of specific diabetogenic QTL, resulting in a step-wise increase in diabetes incidence. RCS-10 recreates the 100% incidence seen in (NZOxNON)F1 males, but with less weight gain.  Similarly, RCS-6, -7, -8, and -9    represent diabetes-prone strains with different combinations of diabetogenic QTL. RCS-3, -4, and -5 represent obese strains that do not transit to diabetes. Because these obesity and diabetes syndromes reflect different collections of QTL, rather    than null mutations in the leptin or leptin receptor genes, they are extremely relevant as models for the polygenic obesity/diabesity syndromes in humans.</p>

	]]>
</description>

<author>P C. Reifsnyder et al.</author>


</item>


<item>
<title> A Gja8 (Cx50) point mutation causes an alteration of alpha3 connexin (Cx46) in semi-dominant cataracts of Lop10 mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/363</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/363</guid>
<pubDate>Tue, 08 May 2012 16:37:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations of connexin alpha8 (GJA8 or Cx50) and connexin alpha3 (GJA3 or Cx46) in humans have been reported to cause cataracts with semi-dominant inheritance patterns. Targeted null mutations in Gja8 and Gja3 in mice cause    cataracts with recessive inheritance. The molecular bases for these differences in inheritance patterns and the mechanism for cataractogenesis in these mutants are poorly understood. We recently mapped an autosomal semi-dominant cataract [lens    opacity 10 (Lop10)] mutation to mouse chromosome 3 and identified a missense mutation (Gright arrowC) in the Gja8 gene, which causes glycine at codon 22 to be replaced with arginine (G22R). Moreover, we demonstrated that the alpha8 G22R isoform    is a loss-of-function mutant for alpha8, as well as a dominant mutation for reducing the phosphorylated forms of alpha3 connexin in vivo. To test the hypothesis that the alteration of endogenous alpha3 connexin in Lop10 mice led to a unique lens    phenotype, we generated double mutant offspring between Lop10 and the Gja3(tm1) (alpha3(--/--)) mice. The double homozygous mutant mice (Lop10/Lop10 alpha3(--/--)) showed relatively normal lens cortical fibers compared to the Lop10 mice. A    functional impairment of endogenous alpha3 connexin is therefore partly responsible for cellular phenotypes in the Lop10 mice. This study has provided some novel molecular insights into mouse and human cataractogenesis caused by alpha8 and alpha3    mutations. These mouse models will be useful for investigating the mechanistic relationship between gap junction impairment and cataract formation.</p>

	]]>
</description>

<author>B Chang et al.</author>


</item>


<item>
<title> A goniolens for clinical monitoring of the mouse iridocorneal angle and optic nerve.</title>
<link>http://mouseion.jax.org/stfb2000_2009/362</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/362</guid>
<pubDate>Tue, 08 May 2012 16:37:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Due to the increasing importance of mouse models and mouse genetics in ophthalmic research, we have developed a goniolens for mice.  METHODS: The size and basic design parameters of a human goniolens were adapted to the    mouse eye. RESULTS: The goniolens is straightforward to use and allows non-invasive visualization of the structures of the anterior chamber angle, including Schlemm's canal, trabecular meshwork, iris and anterior surface of the peripheral ciliary    body. Goniophotography using the mouse lens allows documentation of anterior chamber angle abnormalities, and facilitates comparisons of changes to these structures in the same eye over time. In addition, high quality magnified views of the optic    nerve, retinal vessels and posterior retina are easily obtained.  CONCLUSIONS: This goniolens is an important new tool for studying the genetic and clinical etiology of anterior segment dysgenesis and glaucoma in mice.</p>

	]]>
</description>

<author>R S. Smith et al.</author>


</item>


<item>
<title> Intraocular teratoma in a mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/361</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/361</guid>
<pubDate>Tue, 08 May 2012 16:37:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>A 4.5-month-old male B6.129S2-Trp53tm1Tyj mouse developed an enlarged left eye. After euthanasia, the eye was removed and found to contain a teratoma composed of smooth muscle, white fat, neural tissue, and villous intestinal    epithelium with appearance similar to that of the small intestine. Many normal intraocular structures were absent. To our knowledge, this represents the first reported intraocular teratoma in a mouse.</p>

	]]>
</description>

<author>R S. Smith et al.</author>


</item>


<item>
<title> The mouse meiotic mutation mei1 disrupts chromosome synapsis with sexually dimorphic consequences for meiotic progression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/360</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/360</guid>
<pubDate>Tue, 08 May 2012 16:37:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>mei1 (meiosis defective 1) is the first meiotic mutation in mice derived by phenotype-driven mutagenesis. It was isolated by using a novel technology in which embryonic stem (ES) cells were chemically mutagenized and used to    generate families of mice that were screened for infertility.  We report here that mei1/mei1 spermatocytes arrest at the zygotene stage of meiosis I, exhibiting failure of homologous chromosomes to properly synapse. Notably, RAD51 failed to    associate with meiotic chromosomes in mutant spermatocytes, despite evidence for the presence of chromosomal breaks. Transcription of genes that are markers for the leptotene and zygotene stages, but not genes that are markers for the pachytene    stage, was observed. mei1/mei1 females are sterile, and their oocytes also show severe synapsis defects. Nevertheless, unlike arrested spermatocytes, a small number of mutant oocytes proved capable of progressing to metaphase I and attempting the    first meiotic division. However, their chromosomes were unpaired and were not organized properly at the metaphase plate or along the spindle fibers during segregation. mei1 was genetically mapped to chromosome (Chr) 15 in an interval that is    syntenic to human Chr 22q13.  This region, which has been completely sequenced, contains no known homologs of genes specifically required for meiosis in model organisms.  Thus, mei1 may be a novel meiotic gene.</p>

	]]>
</description>

<author>B J. Libby et al.</author>


</item>


<item>
<title> Interacting QTLs for cholesterol gallstones and gallbladder mucin in AKR and SWR strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/359</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/359</guid>
<pubDate>Tue, 08 May 2012 16:36:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>We employed quantitative trait locus (QTL) mapping in a backcross between gallstone-susceptible SWR/J and gallstone-resistant AKR/J inbred mice to identify additional susceptibility loci for cholesterol gallstone formation. After    12 wk of feeding the mice a lithogenic diet, we phenotyped 330 backcross progeny for gallstones, gallbladder mucin accumulation, liver weight, and body weight. Marker-based regression analysis revealed significant single QTLs associated with    gallstone formation on chromosome 9 and the liver weight/body weight ratio on chromosomes 5 and X. A search for gene pairs detected significant gene-gene interactions for mucin accumulation between loci on chromosomes 5 and 11 and suggestive    gene-gene interactions linked to gallstone formation between the QTL on chromosome 9 and loci on chromosomes 6 and 15. These findings uncover new QTLs for cholesterol gallstones, reveal independent loci for mucin accumulation, and demonstrate the    importance of considering gene-gene interactions in cholesterol cholelithiasis.  According to standard nomenclature, the gallstone QTL on chromosome 9 is named Lith5.</p>

	]]>
</description>

<author>H Wittenburg et al.</author>


</item>


<item>
<title> Retinal degeneration mutants in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/358</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/358</guid>
<pubDate>Tue, 08 May 2012 16:36:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Jackson Laboratory, having the world's largest collection of mouse mutant stocks and genetically diverse inbred strains, is an ideal place to look for genetically determined eye variations and disorders. Through ophthalmoscopy,    electroretinography and histology, we have discovered disorders affecting all aspects of the eye including the lid, cornea, iris, lens and retina, resulting in corneal disorders, cataracts, glaucoma and retinal degenerations. Mouse models of    retinal degeneration have been investigated for many years in the hope of understanding the causes of photoreceptor cell death. Sixteen naturally occurring mouse mutants that manifest degeneration of photoreceptors in the retina with preservation    of all other retinal cell types have been found: retinal degeneration (formerly rd, identical with rodless retina, r, now Pde6b(rd1)); Purkinje cell degeneration (pcd); nervous (nr); retinal degeneration slow (rds, now Prph(Rd2)); retinal    degeneration 3 (rd3); motor neuron degeneration (mnd); retinal degeneration 4 (Rd4); retinal degeneration 5 (rd5, now tub); vitiligo (vit, now Mitf(mi-vit)); retinal degeneration 6 (rd6); retinal degeneration 7 (rd7, now Nr2e3(rd7)); neuronal    ceroid lipofuscinosis (nclf); retinal degeneration 8 (rd8); retinal degeneration 9 (Rd9); retinal degeneration 10 (rd10, now Pde6b(rd10)); and cone photoreceptor function loss (cpfl1). In this report, we first review the genotypes and phenotypes    of these mutants and second, list the mouse strains that carry each mutation. We will also provide detailed information about the cpfl1 mutation. The phenotypic characteristics of cpfl1 mice are similar to those observed in patients with complete    achromatopsia (ACHM2, OMIM 216900) and the cpfl1 mutation is the first naturally-arising mutation in mice to cause cone-specific photoreceptor function loss. cpfl1 mice may provide a model for congenital achromatopsia in humans.</p>

	]]>
</description>

<author>B Chang et al.</author>


</item>


<item>
<title> Corralling conditional mutations: A unified resource for mouse phenotypes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/357</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/357</guid>
<pubDate>Tue, 08 May 2012 16:36:13 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J T. Eppig et al.</author>


</item>


<item>
<title> A mouse model of Alagille syndrome: Notch2 as a genetic modifier of Jag1 haploinsufficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/356</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/356</guid>
<pubDate>Tue, 08 May 2012 16:35:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alagille syndrome is a human autosomal dominant developmental disorder characterized by liver, heart, eye, skeletal, craniofacial and kidney abnormalities. Alagille syndrome is caused by mutations in the Jagged 1 (JAG1) gene, which    encodes a ligand for Notch family receptors. The majority of JAG1 mutations seen in Alagille syndrome patients are null alleles, suggesting JAG1 haploinsufficiency as a primary cause of this disorder. Mice homozygous for a Jag1 null mutation die    during embryogenesis and Jag1/+ heterozygous mice exhibit eye defects but do not exhibit other phenotypes characteristic of Alagille syndrome patients ( Xue, Y., Gao, X., Lindsell, C. E., Norton, C. R., Chang, B., Hicks, C., Gendron-Maguire, M.,    Rand, E. B., Weinmaster, G. and Gridley, T. (1999) HUM: Mol. Genet. 8, 723-730). Here we report that mice doubly heterozygous for the Jag1 null allele and a Notch2 hypomorphic allele exhibit developmental abnormalities characteristic of Alagille    syndrome. Double heterozygous mice exhibit jaundice, growth retardation, impaired differentiation of intrahepatic bile ducts and defects in heart, eye and kidney development. The defects in bile duct epithelial cell differentiation and    morphogenesis in the double heterozygous mice are similar to defects in epithelial morphogenesis of Notch pathway mutants in Drosophila, suggesting that a role for the Notch signaling pathway in regulating epithelial morphogenesis has been    conserved between insects and mammals. This work also demonstrates that the Notch2 and Jag1 mutations interact to create a more representative mouse model of Alagille syndrome and provides a possible explanation of the variable phenotypic    expression observed in Alagille syndrome patients.</p>

	]]>
</description>

<author>B McCright et al.</author>


</item>


<item>
<title> The tubby-like proteins, a family with roles in neuronal development and function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/355</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/355</guid>
<pubDate>Tue, 08 May 2012 16:35:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The identification of a mutation at the tubby (Tub) locus, which causes obesity and neurosensory degeneration, led to the discovery of the tubby-like proteins (TULPs). Tub and the genes that encode three tubby-like proteins (TULP1-    TULP3) form a novel, small gene family that plays an important role in maintenance and function of neuronal cells during development and post-differentiation. Although exploration of the molecular function of these genes is still in its infancy,    recent biochemical studies have provided 'entry points' into pathways whose elucidation will further our understanding of TULP action. In addition, mRNA expression and translocation of the TUB protein have been shown to be regulated by thyroid    hormone and by G-protein-coupled receptor signaling, respectively. These latter findings may help to link the cellular function of TUB to known mechanisms for energy homeostasis.</p>

	]]>
</description>

<author>A Ikeda et al.</author>


</item>


<item>
<title> Efficient generation and mapping of recessive developmental mutations using ENU mutagenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/354</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/354</guid>
<pubDate>Tue, 08 May 2012 16:35:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Treatment with N-ethyl-N-nitrosourea (ENU) efficiently generates single-nucleotide mutations in mice. Along with the renewed interest in this approach, much attention has been given recently to large screens with broad aims;    however, more finely focused studies have proven very productive as well. Here we show how mutagenesis together with genetic mapping can facilitate the rapid characterization of recessive loci required for normal embryonic development. We    screened third-generation progeny of mutagenized mice at embryonic day (E) 18.5 for abnormalities of organogenesis. We ascertained 15 monogenic mutations in the 54 families that were comprehensively analyzed. We carried out the experiment as an    outcross, which facilitated the genetic mapping of the mutations by haplotype analysis. We mapped seven of the mutations and identified the affected locus in two lines. Using a hierarchical approach, it is possible to maximize the efficiency of    this analysis so that it can be carried out easily with modest infrastructure and resources.</p>

	]]>
</description>

<author>B J. Herron et al.</author>


</item>


<item>
<title> The Muscular Dystrophy with Myositis (mdm) Mouse Mutation Disrupts a Skeletal Muscle-Specific Domain of Titin.</title>
<link>http://mouseion.jax.org/stfb2000_2009/353</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/353</guid>
<pubDate>Tue, 08 May 2012 16:34:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Muscular dystrophy with myositis (mdm) is a recessive mouse mutation that causes severe and progressive muscular degeneration. Here we report the identification of the mdm mutation as a complex rearrangement that includes a    deletion and a LINE insertion in the titin (Ttn) gene. Mutant allele-specific splicing results in the deletion of 83 amino acids from the N2A region of TTN, a domain thought to bind calpain-3 (CAPN3) the product of the human limb-girdle muscular    dystrophy type 2A (LGMD2A) gene.  The Ttn(mdm) mutant mouse may serve as a model for human tibial muscular dystrophy, which maps to the TTN locus at 2q31 and shows a secondary reduction of CAPN3 similar to that observed in mdm skeletal muscle.    This is the first demonstration that a mutation in Ttn is associated with muscular dystrophy and provides a novel animal model to test for functional interactions between TTN and CAPN3.</p>

	]]>
</description>

<author>S M. Garvey et al.</author>


</item>


<item>
<title> Atrichia with papular lesions resulting from mutations in the rhesus macaque (Macaca mulatta) hairless gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/352</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/352</guid>
<pubDate>Tue, 08 May 2012 16:34:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Atrichia with papular lesions (APL) is a rare form of hair loss with an autosomal recessive mode of inheritance that is characterized by the absence of normal hair follicles, and formation of intradermal cystic structures.    Mutations in the hairless (hr) gene in mice and humans have been implicated in the development of this phenotype. Hairless is a putative transcription factor containing a single zinc-finger DNA binding domain, with restricted expression in brain    and skin. Here, we describe the complete hr cDNA sequence from the rhesus macaque (Macaca mulatta) and report the identification of a compound heterozygous mutation in a hairless rhesus macaque born from unrelated parents. Cutaneous biopsy    samples from the affected macaque revealed abnormalities, including the replacement of normal hair follicles with dermal cysts and comedones, reminiscent of the skin phenotype observed in hairless mice and humans with APL.</p>

	]]>
</description>

<author>W Ahmad et al.</author>


</item>


<item>
<title> The cerebellar deficient folia (cdf) gene acts intrinsically in Purkinje cell migrations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/351</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/351</guid>
<pubDate>Tue, 08 May 2012 16:34:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cerebellar deficient folia (cdf) is a recently identified mouse mutation causing ataxia and cerebellar abnormalities including lobulation defects and abnormal placement of a specific subset of Purkinje cells. To understand the    etiology of the cerebellar defects in cdf mutant mice, we examined postnatal development of the cdf/cdf cerebellum. Our results demonstrate that Purkinje cell ectopia and foliation defects are apparent at birth, suggesting the cdf mutation    disrupts the positioning of many, but not all, Purkinje cells during development. In addition to cerebellar abnormalities, we observed lamination defects in the hippocampus of cdf mutant mice, although neocortical defects were not seen.    Furthermore, ectopic Purkinje cells in cdf/cdf mice express an increased level of Dab1 protein, as previously observed in mice with mutations in genes in the reelin signaling pathway. Lastly, analysis of cdf <-->ROSA26 chimeric mice demonstrated    that the cdf mutation is intrinsic to Purkinje cells. We suggest that the cdf gene product is required in a subset of Purkinje cells, possibly to respond to Reelin signals.</p>

	]]>
</description>

<author>C Park et al.</author>


</item>


<item>
<title> It&apos;s a knockout! Male infertility and neuropathology.</title>
<link>http://mouseion.jax.org/stfb2000_2009/350</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/350</guid>
<pubDate>Tue, 08 May 2012 16:33:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>An increasing number of genetically engineered animals are produced worldwide for use in both basic and applied research. Here, I provide an update of some of the latest mouse knockouts in The Jackson Laboratory Transgenic/Targeted    Mutation Database (TBASE), concentrating on those associated with male infertility and neuropathology.</p>

	]]>
</description>

<author>A V. Anagnostopoulos</author>


</item>


<item>
<title> Quantitative trait loci regulating relative lymphocyte proportions in mouse peripheral blood.</title>
<link>http://mouseion.jax.org/stfb2000_2009/349</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/349</guid>
<pubDate>Tue, 08 May 2012 16:33:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Relative proportions of peripheral blood (PB) B lymphocytes (B220%) as well as CD4 (CD4%) and CD8 (CD8%) T lymphocytes differ significantly among inbred mouse strains: B220% is high in C57BL/6J (B6) and C57BR/cdJ, intermediate in    BALB/cByJ (BALB) and DBA/2J (D2), and low in NOD/LtJ (NOD) and SJL/J (SJL) mice, whereas CD4% and CD8% are high in NOD and SJL mice and low in the other 4 strains. By following segregating genetic markers linked to these traits in (B6 x D2)    recombinant inbred (BXD RI) mice, the study defined 2 quantitative trait loci (QTLs) for the B220% phenotype: Pbbcp1 (peripheral blood B cell percentage 1, logarithm of odds [LOD] 4.1, P <.000 01) and Pbbcp2 (LOD 3.7, P <.000 04) on chromosome 1    (Chr 1) at about 63 cM and 48 cM; one suggestive locus for the CD4% phenotype (LOD 2.6, P <.000 57) on Chr 8 at about 73 cM; and one QTL for the CD8% phenotype: Pbctlp1 (peripheral blood cytotoxic T lymphocyte percentage 1, LOD 3.8, P <.000 02)    on Chr 19 at about 12 cM. The study further segregated PB lymphocyte proportions in B6SJLF2 mice by using DNA markers adjacent to these mapped QTLs and found that the Pbbcp1 locus (LOD 5.6, P <.000 01) was also important in this mouse population.    In both BXD RI and B6SJLF2 mice, QTLs regulating B-cell proportions showed no significant effect on T-cell proportions and vice versa. Thus, PB B- and T-lymphocyte proportions are regulated separately by different genetic elements.</p>

	]]>
</description>

<author>J Chen et al.</author>


</item>


<item>
<title> Mutations in a novel CLN6-encoded transmembrane protein cause variant neuronal ceroid lipofuscinosis in man and mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/348</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/348</guid>
<pubDate>Tue, 08 May 2012 16:33:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>The CLN6 gene that causes variant late-infantile neuronal ceroid lipofuscinosis (vLINCL), a recessively inherited neurodegenerative disease that features blindness, seizures, and cognitive decline, maps to 15q21-23. We have used    multiallele markers spanning this approximately 4-Mb candidate interval to reveal a core haplotype, shared in Costa Rican families with vLINCL but not in a Venezuelan kindred, that highlighted a region likely to contain the CLN6 defect.    Systematic comparison of genes from the minimal region uncovered a novel candidate, FLJ20561, that exhibited DNA sequence changes specific to the different disease chromosomes: a G-->T transversion in exon 3, introducing a stop codon on the Costa    Rican haplotype, and a codon deletion in exon 5, eliminating a conserved tyrosine residue on the Venezuelan chromosome. Furthermore, sequencing of the murine homologue in the nclf mouse, which manifests recessive NCL-like disease, disclosed a    third lesion-an extra base pair in exon 4, producing a frameshift truncation on the nclf chromosome. Thus, the novel approximately 36-kD CLN6-gene product augments an intriguing set of unrelated membrane-spanning proteins, whose deficiency causes    NCL in mouse and man.</p>

	]]>
</description>

<author>H Gao et al.</author>


</item>


<item>
<title> Vaginal transmission of cell-associated HIV-1 in the mouse is blocked by a topical, membrane-modifying agent.</title>
<link>http://mouseion.jax.org/stfb2000_2009/347</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/347</guid>
<pubDate>Tue, 08 May 2012 16:32:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Because both HIV-1 virions and HIV-infected cells are present in the semen and cervical mucus of infected individuals, HIV-1 prevention strategies must consider both cell-free and cell-associated virus. Antibodies that target HIV-1    virions have been shown to prevent vaginal transmission of cell-free virus in macaques, but since cell-associated transmission has not been reliably demonstrated in this model system, no strategies to prevent such transmission have been tested.    We have employed a mouse model in which SCID mice carry human peripheral blood leukocytes (HuPBLs). In these mice, vaginal transmission of cell-associated, but not cell-free, HIV-1 transmission occurs, mediated by transepithelial migration of    HIV-infected cells. Topical application of beta-cyclodextrin (beta-CD), a cholesterol-sequestering agent that interferes with cell migration and budding of virus from lipid rafts, blocks transmission of cell-associated HIV-1. The HuPBL-SCID model    of vaginal HIV-1 transmission should prove useful for investigating cell-associated HIV-1 transmucosal HIV-1 transmission, as well as for screening reagents for their potential efficacy in preventing sexual HIV-1 transmission.</p>

	]]>
</description>

<author>K V. Khanna et al.</author>


</item>


<item>
<title> The Mouse Genome Database (MGD): the model organism database for the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/346</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/346</guid>
<pubDate>Tue, 08 May 2012 16:32:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Database (MGD) is the community database resource for the laboratory mouse, a key model organism for interpreting the human genome and for understanding human biology and disease (http://www.informatics.jax.org).    MGD strives to provide a highly curated, highly integrated information resource that not only includes the consensus view of current knowledge about the mouse, but also provides comparative genomic information particularly for human and rat    genomes.  MGD includes extensive information about mouse genes, supporting all gene attribute assertions with experimental data, statements of evidence and citation. Detailed information about alleles and mouse mutants includes genotype,    molecular variant and phenotype descriptions. Extensive collaboration with other data providers such as NCBI, RIKEN and SWISS-PROT provides standardization of gene:sequence associations and robust interconnections between large information    systems based on shared sequence curation. Recent integration of large datasets of mouse full-length cDNAs and radiation-hybrid mapped ESTs, the continued development and use of extensive structured vocabularies and the expansion of the    representation of phenotypes highlight this year's developments.</p>

	]]>
</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title> Rat Genome Database (RGD): mapping disease onto the genome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/345</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/345</guid>
<pubDate>Tue, 08 May 2012 16:32:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Rat Genome Database (RGD, http://rgd.mcw.edu) is an NIH-funded project whose stated mission is 'to collect, consolidate and integrate data generated from ongoing rat genetic and genomic research efforts and make these data    widely available to the scientific community'. In a collaboration between the Bioinformatics Research Center at the Medical College of Wisconsin, the Jackson Laboratory and the National Center for Biotechnology Information, RGD has been created    to meet these stated aims.  The rat is uniquely suited to its role as a model of human disease and the primary focus of RGD is to aid researchers in their study of the rat and in applying their results to studies in a wider context. In support of    this we have integrated a large amount of rat genetic and genomic resources in RGD and these are constantly being expanded through ongoing literature and bulk dataset curation. RGD version 2.0, released in June 2001, includes curated data on rat    genes, quantitative trait loci (QTL), microsatellite markers and rat strains used in genetic and genomic research. VCMap, a dynamic sequence-based homology tool was introduced, and allows researchers of rat, mouse and human to view mapped genes    and sequences and their locations in the other two organisms, an essential tool for comparative genomics. In addition, RGD provides tools for gene prediction, radiation hybrid mapping, polymorphic marker selection and more. Future developments    will include the introduction of disease-based curation expanding the curated information to cover popular disease systems studied in the rat. This will be integrated with the emerging rat genomic sequence and annotation pipelines to provide a    high-quality disease-centric resource, applicable to human and mouse via comparative tools such as VCMap. RGD has a defined community outreach focus with a Visiting Scientist program and the Rat Community Forum, a web-based forum for rat    researchers and others interested in using the rat as an experimental model. Thus, RGD is not only a valuable resource for those working with the rat but also for researchers in other model organisms wishing to harness the existing genetic and    physiological data available in the rat to complement their own work.</p>

	]]>
</description>

<author>S Twigger et al.</author>


</item>


<item>
<title> The ATP binding cassette transporter A1 (ABCA1) modulates the development of aortic atherosclerosis in C57BL/6 and apoE-knockout mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/344</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/344</guid>
<pubDate>Tue, 08 May 2012 16:31:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Identification of mutations in the ABCA1 transporter (ABCA1) as the genetic defect in Tangier disease has generated interest in modulating atherogenic risk by enhancing ABCA1 gene expression. To investigate the role of ABCA1 in    atherogenesis, we analyzed diet-induced atherosclerosis in transgenic mice overexpressing human ABCA1 (hABCA1-Tg) and spontaneous lesion formation in hABCA1-Tg x apoE-knockout (KO) mice. Overexpression of hABCA1 in C57BL/6 mice resulted in a    unique anti-atherogenic profile characterized by decreased plasma cholesterol (63%), cholesteryl ester (63%), free cholesterol (67%), non-high density lipoprotein (HDL)-cholesterol (53%), and apolipoprotein (apo) B (64%) but markedly increased    HDL-cholesterol (2.8-fold), apoA-I (2.2-fold), and apoE (2.8-fold) levels. These beneficial changes in the lipid profile led to significantly lower (65%) aortic atherosclerosis in hABCA1-Tg mice. In marked contrast, ABCA1 overexpression had a    minimal effect on the plasma lipid profile of apoE-KO mice and resulted in a 2- to 2.6-fold increase in aortic lesion area. These combined results indicate that overexpression of ABCA1 in C57BL/6 mice on a high cholesterol diet results in an    atheroprotective lipoprotein profile and decreased atherosclerosis, and thus provide previously undocumented in vivo evidence of an anti-atherogenic role for the ABCA1 transporter. In contrast, overexpression of ABCA1 in an apoE-KO background led    to increased atherosclerosis, further substantiating the important role of apoE in macrophage cholesterol metabolism and atherogenesis. In summary, these results establish that, in the presence of apoE, overexpression of ABCA1 modulates HDL as    well as apoB-containing lipoprotein metabolism and reduces atherosclerosis in vivo, and indicate that pharmacological agents that will increase ABCA1 expression may reduce atherogenic risk in humans.</p>

	]]>
</description>

<author>C W. Joyce et al.</author>


</item>


<item>
<title> Effects of peroxisome proliferator-activated receptor delta on placentation, adiposity, and colorectal cancer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/343</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/343</guid>
<pubDate>Tue, 08 May 2012 16:31:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Targeting of the nuclear prostaglandin receptor peroxisome proliferator-activated receptor delta (PPARdelta) by homologous recombination results in placental defects and frequent (>90%) midgestation lethality. Surviving    PPARdelta(-/-) mice exhibit a striking reduction in adiposity relative to wild-type levels. This effect is not reproduced in mice harboring an adipose tissue-specific deletion of PPARdelta, and thus likely reflects peripheral PPARdelta functions    in systemic lipid metabolism. Finally, we observe that PPARdelta is dispensable for polyp formation in the intestine and colon of APC(min) mice, inconsistent with its recently proposed role in the establishment of colorectal tumors. Together,    these observations reveal specific roles for PPARdelta in embryo development and adipocyte physiology, but not cancer.</p>

	]]>
</description>

<author>Y Barak et al.</author>


</item>


<item>
<title> Activation of beta -catenin signaling in differentiated mammary secretory cells induces transdifferentiation into epidermis and squamous metaplasias.</title>
<link>http://mouseion.jax.org/stfb2000_2009/342</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/342</guid>
<pubDate>Tue, 08 May 2012 16:31:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mammary anlagen are formed in the embryo as a derivative of the epidermis, a process that is controlled by Lef-1 and therefore possibly by beta-catenin. To investigate the role of beta-catenin signaling in mammary alveolar    epithelium, we have stabilized endogenous beta-catenin in differentiating alveolar epithelium through the deletion of exon 3 (amino acids 5-80) of the beta-catenin gene. This task was accomplished in mice carrying a floxed beta-catenin gene and a    Cre transgene under control of the mammary-specific whey acidic protein (WAP) gene promoter or the mouse mammary tumor virus-long terminal repeat (MMTV-LTR). Stabilized beta-catenin was obtained during the first pregnancy, and its presence    resulted in the dedifferentiation of alveolar epithelium followed by a transdifferentiation into epidermal and pilar structures. Extensive squamous metaplasia, but no adenocarcinomas, developed upon beta-catenin activation during pregnancy and    persisted throughout involution. These data demonstrate that the activation of beta-catenin signaling induces a program that results in loss of mammary epithelial cell differentiation and induction of epidermal structures.</p>

	]]>
</description>

<author>K Miyoshi et al.</author>


</item>


<item>
<title> Mutations in genes encoding melanosomal proteins cause pigmentary glaucoma in DBA/2J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/341</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/341</guid>
<pubDate>Tue, 08 May 2012 16:30:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pigmentary glaucoma is a significant cause of human blindness. Abnormally liberated iris pigment and cell debris enter the ocular drainage structures, leading to increased intraocular pressure (IOP) and glaucoma.  DBA/2J (D2) mice    develop a form of pigmentary glaucoma involving iris pigment dispersion (IPD) and iris stromal atrophy (ISA). Using high-resolution mapping techniques, sequencing and functional genetic tests, we show that IPD and ISA result from mutations in    related genes encoding melanosomal proteins. IPD is caused by a premature stop codon mutation in the Gpnmb (GpnmbR150X) gene, as proved by the occurrence of IPD only in D2 mice that are homozygous with respect to GpnmbR150X; otherwise, similar D2    mice that are not homozygous for GpnmbR150X do not develop IPD. ISA is caused by the recessive Tyrp1b mutant allele and rescued by the transgenic introduction of wildtype Tyrp1. We hypothesize that IPD and ISA alter melanosomes, allowing toxic    intermediates of pigment production to leak from melanosomes, causing iris disease and subsequent pigmentary glaucoma. This is supported by the rescue of IPD and ISA in D2 eyes with substantially decreased pigment production. These data indicate    that pigment production and mutant melanosomal protein genes may contribute to human pigmentary glaucoma. The fact that hypopigmentation profoundly alleviates the D2 disease indicates that therapeutic strategies designed to decrease pigment    production may be beneficial in human pigmentary glaucoma.</p>

	]]>
</description>

<author>M G. Anderson et al.</author>


</item>


<item>
<title> How H13 histocompatibility peptides differing by a single methyl groug and lacking conventional MHC binding anchor motifs determine self-nonself discrimination.</title>
<link>http://mouseion.jax.org/stfb2000_2009/340</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/340</guid>
<pubDate>Tue, 08 May 2012 16:30:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse H13 minor histocompatibility (H) Ag, originally detected as a barrier to allograft transplants, is remarkable in that rejection is a consequence of an extremely subtle interchange, P4(Val/Ile), in a nonamer H2-D(b)-bound    peptide. Moreover, H13 peptides lack the canonical P5(Asn) central anchor residue normally considered important for forming a peptide/MHC complex. To understand how these noncanonical peptide pMHC complexes form physiologically active TCR    ligands, crystal structures of allelic H13 pD(b) complexes and a P5(Asn) anchored pD(b) analog were solved to high resolution. The structures show that the basis of TCRs to distinguish self from nonself H13 peptides is their ability to    distinguish a single solvent-exposed methyl group. In addition, the structures demonstrate that there is no need for H13 peptides to derive any stabilization from interactions within the central C pocket to generate fully functional pMHC    complexes. These results provide a structural explanation for a classical non-MHC-encoded H Ag, and they call into question the requirement for contact between anchor residues and the major MHC binding pockets in vaccine design.</p>

	]]>
</description>

<author>D A. Ostrov et al.</author>


</item>


<item>
<title>The Future of the Oocyte</title>
<link>http://mouseion.jax.org/stfb2000_2009/339</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/339</guid>
<pubDate>Tue, 08 May 2012 16:30:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title> Genetics and bone using the mouse understand man.</title>
<link>http://mouseion.jax.org/stfb2000_2009/338</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/338</guid>
<pubDate>Tue, 08 May 2012 16:29:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W G. Beamer et al.</author>


</item>


<item>
<title> Motoneuron survival is enhanced in the absence of neuromuscular junction formation in embryos.</title>
<link>http://mouseion.jax.org/stfb2000_2009/337</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/337</guid>
<pubDate>Tue, 08 May 2012 16:29:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Approximately half of the motoneurons produced during development die before birth or shortly after birth. Although it is believed that survival depends on a restricted supply of a trophic sustenance produced by the synaptic target    tissue (i.e., muscle), it is unclear whether synapse formation per se is involved in motoneuron survival. To address this issue, we counted cranial motoneurons in a set of mutant mice in which formation of neuromuscular junctions is dramatically    impaired (i.e., null mutants for agrin, nerve-derived agrin, rapsyn, and MuSK). We demonstrate that in the absence of synaptogenesis, there is an 18-34% increase in motoneuron survival in the facial, trochlear, trigeminal motor, and hypoglossal    nuclei; the highest survival occurred in the MuSK-deficient animals in which synapse formation is most severely compromised. There was no change in the size of the mutant motoneurons as compared with control animals, and the morphology of the    mutant motoneurons appeared normal. We postulate that the increased axonal branching observed in these mutants leads to a facilitated "access" of the motoneurons to muscle-derived trophic factors at sites other than synapses or that inactivity    increases the production of such factors. Finally, we examined motoneurons in double mutants of CNTFRalpha(-/-) (in which there is a partial loss of motoneurons) and MuSK(-/-) (in which there is an increased survival of motoneurons). The    motoneuron numbers in the double mutants parallel those of the single MuSK-deficient mice, indicating that synapse disruption can even overcome the deleterious effect of CNTFRalpha ablation.</p>

	]]>
</description>

<author>J Terrado et al.</author>


</item>


<item>
<title> Distinct roles of nerve and muscle in postsynaptic differentiation of the neuromuscular synapse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/336</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/336</guid>
<pubDate>Tue, 08 May 2012 16:29:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>The development of chemical synapses is regulated by interactions between pre- and postsynaptic cells. At the vertebrate skeletal neuromuscular junction, the organization of an acetylcholine receptor (AChR)-rich postsynaptic    apparatus has been well studied. Much evidence suggests that the nerve-derived protein agrin activates muscle-specific kinase (MuSK) to cluster AChRs through the synapse-specific cytoplasmic protein rapsyn. But how postsynaptic differentiation is    initiated, or why most synapses are restricted to an 'end-plate band' in the middle of the muscle remains unknown. Here we have used genetic methods to address these issues. We report that the initial steps in postsynaptic differentiation and    formation of an end-plate band require MuSK and rapsyn, but are not dependent on agrin or the presence of motor axons. In contrast, the subsequent stages of synaptic growth and maintenance require nerve-derived agrin, and a second nerve-derived    signal that disperses ectopic postsynaptic apparatus.</p>

	]]>
</description>

<author>W Lin et al.</author>


</item>


<item>
<title> The mouse Ames waltzer hearing-loss mutant is caused by mutation of Pcdh15, a novel protocadherin gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/335</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/335</guid>
<pubDate>Tue, 08 May 2012 16:29:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The neuroepithelia of the inner ear contain hair cells that function as mechanoreceptors to transduce sound and motion signals. Mutations affecting these neuroepithelia cause deafness and vestibular dysfuction in humans. Ames    waltzer (av) is a recessive mutation found in mice that causes deafness and a balance disorder associated with the degeneration of inner ear neuroepithelia. Here we report that the gene that harbours the av mutation encodes a novel protocadherin.    Cochlear hair cells in the av mutants show abnormal stereocilia by 10 days after birth (P10). This is the first evidence for the requirement of a protocadherin for normal function of the mammalian inner ear.</p>

	]]>
</description>

<author>K N. Alagramam et al.</author>


</item>


<item>
<title> Expression of Pcdh15 in the inner ear, nervous system and various epithelia of the developing embryo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/334</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/334</guid>
<pubDate>Tue, 08 May 2012 16:28:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>We previously determined that Protocadherin 15 (Pcdh15) is associated with the Ames waltzer mutation in the mouse. Here we describe where the Pcdh15 gene is expressed at specific times during mouse development using RNA in situ    hybridization. The expression of Pcdh15 is found in the sensory epithelium in the developing inner ear, in Rathke's pouch, and broadly throughout the brain with the highest level of expression being detected at embryonic day 16 (E16). Pcdh15    transcripts are also found in the developing eye, dorsal root ganglion, and the dorsal aspect of the neural tube, floor plate and ependymal cells adjacent to the neural canal.  Additionally, expression is also detected in the developing glomeruli    of the kidney, surface of the tongue, vibrissae, bronchi of the lung, and in the epithelium of the olfactory apparatus, gut and lung.</p>

	]]>
</description>

<author>C L. Murcia et al.</author>


</item>


<item>
<title> Mutations in the novel protocadherin PCDH15 cause Usher syndrome type 1F.</title>
<link>http://mouseion.jax.org/stfb2000_2009/333</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/333</guid>
<pubDate>Tue, 08 May 2012 16:28:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have determined the molecular basis for Usher syndrome type 1F (USH1F) in two families segregating for this type of syndromic deafness. By fluorescence in situ hybridization, we placed the human homolog of the mouse    protocadherin Pcdh15 in the linkage interval defined by the USH1F locus. We determined the genomic structure of this novel protocadherin, and found a single-base deletion in exon 10 in one USH1F family and a nonsense mutation in exon 2 in the    second. Consistent with the phenotypes observed in these families, we demonstrated expression of PCDH15 in the retina and cochlea by RT-PCR and immunohistochemistry. This report shows that protocadherins are essential for maintenance of normal    retinal and cochlear function.</p>

	]]>
</description>

<author>K N. Alagramam et al.</author>


</item>


<item>
<title> Phenotypic variations of orpk mutation and chromosomal localization of modifiers influencing kidney phenotype.</title>
<link>http://mouseion.jax.org/stfb2000_2009/332</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/332</guid>
<pubDate>Tue, 08 May 2012 16:28:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Oak Ridge polycystic kidney (orpk) mutant mouse model resulted from a transgene insertion into the Tg737 gene and exhibits a pleiotropic syndrome with lesions in the kidney, liver, and pancreas. We found marked differences in    the phenotypic expression of the orpk mutation when bred on different genetic backgrounds. In the FVB/N background, the phenotype is very severe for kidney, pancreas, and liver lesions. To evaluate better how genetic background might influence    the expressivity of the orpk phenotype, we bred the transgene into the C3HeB/FeJLe (C3H) genetic background. We performed a genome-wide scan using backcross and intercross populations with more than 150 markers to map the chromosomal location of    the modifier genes that differ in the FVB/N and C3H genetic backgrounds that affect the severity of kidney disease in the orpk mouse.  Low-resolution interval mapping was performed using the Map Manager QTb program, with the interval explaining a    significant portion of the variance being the distal end of chromosome 4.</p>

	]]>
</description>

<author>C Sommardahl et al.</author>


</item>


<item>
<title> Genes and cellular requirements for autoimmune diabetes susceptibility in nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/331</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/331</guid>
<pubDate>Tue, 08 May 2012 16:27:56 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title> Evidence that Sry is expressed in pre-Sertoli cells and Sertoli and granulosa cells have a common precursor.</title>
<link>http://mouseion.jax.org/stfb2000_2009/330</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/330</guid>
<pubDate>Tue, 08 May 2012 16:27:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The expression of Sry in the undifferentiated, bipotential genital ridges of mammalian XY fetuses initiates testis development and is hypothesized to do so by directing supporting cell precursors to develop as Sertoli cells and not    as granulosa cells. To directly test this hypothesis, transgenic mice expressing EGFP under the control of the Sry promoter were produced. After establishing that the transgene was expressed in fetal gonads similarly to endogenous Sry, the    spatial and temporal expression of the Sry-EGFP transgene was investigated in developing gonads by using confocal microscopy and immunofluorescent histochemistry. This analysis indicated: (1) Sry is first expressed in cells located centrally in    the genital ridge and then later in cells located at the cranial and caudal poles, (2) Sry is expressed exclusively in pre-Sertoli cells in the urogenital ridge, and (3) Sertoli and granulosa cells develop from a common precursor. These results    support the hypothesis that Sry initiates testis differentiation by directing the development of supporting cell precursors as Sertoli rather than granulosa cells. Furthermore, the Sry expression pattern explains the nonrandom distribution of    testicular and ovarian tissue in mammalian ovotestes.</p>

	]]>
</description>

<author>K H. Albrecht et al.</author>


</item>


<item>
<title> The nude mouse skin phenotype: the role of Foxn1 in hair follicle development and cycling.</title>
<link>http://mouseion.jax.org/stfb2000_2009/329</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/329</guid>
<pubDate>Tue, 08 May 2012 16:27:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>The original nude mouse mutation has proven to be an incredibly valuable biomedical tool since its discovery in 1966. Initially its value was as a tool to study the immune system. The immunodeficiency in this mutant mouse made nude    mice valuable as hosts for xenografts, primarily for cancer research. More recently, the most obvious clinical feature of this mutant mouse, lack of hair, has been capitalized on to define the role of Foxn1 in normal and pathological skin and    hair follicle physiology.</p>

	]]>
</description>

<author>L Mecklenburg et al.</author>


</item>


<item>
<title> Phenotypic characterization of Lith genes that determine susceptibility to cholesterol cholelithiasis in inbred mice: soluble pronucleating proteins in gallbladder and hepatic biles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/328</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/328</guid>
<pubDate>Tue, 08 May 2012 16:26:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND/AIMS: Gallstone susceptibility is high in C57L inbred mice (males > females) and low in AKR mice, related to variant lithogenic (Lith) genes. We examined the relationship between biliary crystallization-promoting    proteins and gallstone susceptibility. METHODS: Biliary protein and lipid concentrations were determined at 0, 7,14, 21, 28 and 56 days on a lithogenic diet. RESULTS: Protein and soluble mucin concentrations in gallbladder biles increased    markedly in males, but remained low in females of both strains and correlated with the cholesterol saturation index (CSI). In all groups, IgA and IgM concentrations decreased initially, but increased at later stages. There were no consistent    changes in IgG concentrations, but aminopeptidase-N levels were higher in AKR than in C57L. During the lithogenic diet period, the CSI was > or = 2 in C57L males, approximately 1.5 in AKR males, and 1 in females of both strains. Taurodeoxycholate    and taurochenodeoxycholate rose sharply in C57L, but remained low in AKR. CONCLUSIONS: Hydrophobic bile salts, cholesterol supersaturation, and possibly, high mucin concentrations are associated with gallstone formation. In vitro    crystallization-promoting immunoglobulins and aminopeptidase-N do not appear to be major factors in murine gallstone pathogenesis, in line with the observation that genes encoding these proteins do not co-localize with any known Lith    locus.</p>

	]]>
</description>

<author>Erpecum K. van et al.</author>


</item>


<item>
<title>Anionic Photofragmentation of CO: A Selective Probe of Core-Level Resonances</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/30</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/30</guid>
<pubDate>Tue, 08 May 2012 16:26:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Anion-yield spectroscopy using x rays is shown to be a selective probe of molecular core-level processes, providing unique experimental verification of shape resonances. For CO, partial anion and cation yields are presented for photon energies near the C K edge. The O<sup>-</sup> yield exhibits features above threshold related only to doubly excited states, in contrast to cation yields which also exhibit pronounced structure due to the well-known σ<sup>*</sup> shape resonance. Because the shape resonance is completely suppressed for O<sup>-</sup>, anion spectroscopy thus constitutes a highly selective probe, yielding information unobtainable with absorption or electron spectroscopy.</p>

	]]>
</description>

<author>Wayne C. Stolte et al.</author>


</item>


<item>
<title> Mapping of rabbit chromosome 1 markers generated from a microsatellite-enriched chromosome-specific library.</title>
<link>http://mouseion.jax.org/stfb2000_2009/327</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/327</guid>
<pubDate>Tue, 08 May 2012 16:26:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>A genomic DNA library was produced from flow-sorted rabbit chromosome 1 and enriched for fragments containing CA-repeats. Clones containing CA-repeats were identified and primers for amplification of the microsatellite were    developed after sequencing the clone. The degree of polymorphism was tested in rabbits from different breeds. This approach identified 12 microsatellite markers which could be used for studying linkage relationships in the progeny of an    F(2)-intercross: (AX/JUxIIIVO/JU) F(2), and two backcrosses: (OS/JxX/J)X/J and (WH/JxX/J)X/J. Seven of these markers were mapped on chromosome 1.</p>

	]]>
</description>

<author>R Korstanje et al.</author>


</item>


<item>
<title> Tyrosine phosphorylation of Grb2 by Bcr/Abl and epidermal growth factor receptor: a novel regulatory mechanism for tyrosine kinase signaling.</title>
<link>http://mouseion.jax.org/stfb2000_2009/326</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/326</guid>
<pubDate>Tue, 08 May 2012 16:26:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Growth factor receptor-binding protein-2 (Grb2) plays a key role in signal transduction initiated by Bcr/Abl oncoproteins and growth factors, functioning as an adaptor protein through its Src homology 2 and 3 (SH2 and SH3) domains.    We found that Grb2 was tyrosine-phosphorylated in cells expressing BCR/ABL and in A431 cells stimulated with epidermal growth factor (EGF). Phosphorylation of Grb2 by Bcr/Abl or EGF receptor reduced its SH3-dependent binding to Sos in vivo, but    not its SH2-dependent binding to Bcr/Abl. Tyr209 within the C-terminal SH3 domain of Grb2 was identified as one of the tyrosine phosphorylation sites, and phosphorylation of Tyr209 abolished the binding of the SH3 domain to a proline-rich Sos    peptide in vitro. In vivo expression of a Grb2 mutant where Tyr209 was changed to phenylalanine enhanced BCR/ABL-induced ERK activation and fibroblast transformation, and potentiated and prolonged Grb2-mediated activation of Ras,    mitogen-activated protein kinase and c-Jun N-terminal kinase in response to EGF stimulation. These results suggest that tyrosine phosphorylation of Grb2 is a novel mechanism of down-regulation of tyrosine kinase signaling.</p>

	]]>
</description>

<author>S Li et al.</author>


</item>


<item>
<title> Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras.</title>
<link>http://mouseion.jax.org/stfb2000_2009/325</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/325</guid>
<pubDate>Tue, 08 May 2012 16:26:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adenocarcinoma of the lung is the most common form of lung cancer, but the cell of origin and the stages of progression of this tumor type are not well understood. We have developed a new model of lung adenocarcinoma in mice    harboring a conditionally activatable allele of oncogenic K-ras. Here we show that the use of a recombinant adenovirus expressing Cre recombinase (AdenoCre) to induce K-ras G12D expression in the lungs of mice allows control of the timing and    multiplicity of tumor initiation.  Through the ability to synchronize tumor initiation in these mice, we have been able to characterize the stages of tumor progression. Of particular significance, this system has led to the identification of a    new cell type contributing to the development of pulmonary adenocarcinoma.</p>

	]]>
</description>

<author>E L. Jackson et al.</author>


</item>


<item>
<title> Interleukin-4 receptor-Stat6 signaling in murine infections with a tissue-dwelling nematode parasite.</title>
<link>http://mouseion.jax.org/stfb2000_2009/324</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/324</guid>
<pubDate>Tue, 08 May 2012 16:25:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Interleukin-4 (IL-4) has been shown to be crucial in parasite expulsion in several gastrointestinal nematode infection models. Data from both epidemiological studies with humans and experimental infections in animals imply a    critical role for the type II helper response, dominated by IL-4, in host protection. Here we utilized inbred mice on two distinct backgrounds to document the involvement of IL-4 in the clearance of a primary infection of Brugia from the murine    host. Our data from infections of IL-4 receptor(-/-) and Stat6(-/-) mice further indicate that IL-4 exerts its effects by activating the Stat6 molecule in host target cells, a finding which links clearance requirements of a gastrointestinal    tract-dwelling nematode with those of a tissue-dwelling nematode.  Additionally, we show that the requirements for IL-4 receptor binding and Stat6 activation extend to accelerated clearance of a secondary infection as well. The data shown here,    including analysis of cell populations at the site of infection and infection of immunoglobulin E (IgE)(-/-) mice, lead us to suggest that deficiencies in eosinophil recruitment and isotype switching to IgE production may be at least partially    responsible for slower parasite clearance in the absence of IL-4.</p>

	]]>
</description>

<author>L Spencer et al.</author>


</item>


<item>
<title> Defining the genetics of osteoporosis: using the mouse to understand man.</title>
<link>http://mouseion.jax.org/stfb2000_2009/323</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/323</guid>
<pubDate>Tue, 08 May 2012 16:25:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Very low bone mineral density (BMD) is now considered as diagnostic of osteoporosis. Moreover, many women who are osteopenic eventually develop osteoporotic fractures. Hence, bone density testing has occupied center stage in the    diagnosis and treatment of this disorder. In addition, over the last several years, BMD has been utilized as the phenotype of choice for defining heritable markers for osteoporotic fractures. However, genetic studies in humans have been limited    to some degree by the tremendous heterogeneity among populations, as well as multiple genetic, heritable and environmental determinants of the BMD phenotype. Recent advances in technology have afforded investigators the opportunity to study    acquisition and maintenance of BMD in small animals. Along with newer knockout and transgenic strategies, quantification of mouse bone mass has advanced our understanding of both the biologic and genetic determinants of bone density. In this    review, we will examine the use of the mouse to map the heritable factors that regulate bone acquisition. We will also examine the role of newer technology to decompose the bone density phenotype into components that are amenable to genetic    studies.  This review will focus on three models: (1) healthy inbred (2) recombinant inbred, and (3) congenic strains of mice. Progress in this area with these strains has been rapid, and a summary of several quantitative trait loci (QTLs) is    provided. The future of the mouse as a tool to map the genes that define the osteoporosis syndrome is extremely promising.</p>

	]]>
</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title> Oocyte control of ovarian follicular development and function in mammals.</title>
<link>http://mouseion.jax.org/stfb2000_2009/322</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/322</guid>
<pubDate>Tue, 08 May 2012 16:25:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>A new perspective on ovarian follicular development has emerged over the last decade. Whereas the oocyte was previously considered only a passive recipient of developmental signals from oocyte-associated granulosa cells, it is now    clear that communication between oocytes and granulosa cells is bidirectional. A complex interplay of regulatory factors governs the development of both types of cell. This interplay is essential not only for oocyte development but also for    follicular development, beginning with the initial assembly of the primordial follicle and continuing throughout ovulation. The existence of an oocyte-granulosa cell regulatory loop, essential for normal follicular differentiation as well as for    the production of an oocyte competent to undergo fertilization and embryogenesis, is proposed. Although gonadotrophins are essential for driving the differentiation of granulosa cell phenotypes, within its sphere of influence, the oocyte is    probably the dominant factor determining the direction of differentiation and the function of the granulosa cells associated with it.</p>

	]]>
</description>

<author>J J. Eppig</author>


</item>


<item>
<title> The skeletal structure of insulin-like growth factor I-deficient mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/321</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/321</guid>
<pubDate>Tue, 08 May 2012 16:25:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The importance of insulin-like growth factor I (IGF-I) for growth is well established. However, the lack of IGF-I on the skeleton has not been examined thoroughly. Therefore, we analyzed the structural properties of bone from mice    rendered IGF-I deficient by homologous recombination (knockout [k/o]) using histomorphometry, peripheral quantitative computerized tomography (pQCT), and microcomputerized tomography (muCT).  The k/o mice were 24% the size of their wild-type    littermates at the time of study (4 months). The k/o tibias were 28% and L1 vertebrae were 26% the size of wild-type bones. Bone formation rates (BFR) of k/o tibias were 27% that of the wild-type littermates. The k/o bones responded normally to    growth hormone (GH; 1.7-fold increase) and supranormally to IGF-I (5.2-fold increase) with respect to BFR. Cortical thickness of the proximal tibia was reduced 17% in the k/o mouse. However, trabecular bone volume (bone volume/total volume    [BV/TV]) was increased 23% (male mice) and 88% (female mice) in the k/o mice compared with wild-type controls as a result of increased connectivity, increased number, and decreased spacing of the trabeculae. These changes were either less or not    found in L1. Thus, lack of IGF-I leads to the development of a bone structure, which, although smaller, appears more compact.</p>

	]]>
</description>

<author>D Bikle et al.</author>


</item>


<item>
<title> T-cell contributions to alveolar bone loss in response to oral infection with Porphyromonas gingivalis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/320</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/320</guid>
<pubDate>Tue, 08 May 2012 16:25:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have previously shown that mice lacking CD4+, but not CD8+, T cells lose less alveolar bone loss in response to oral infection with Porphyromonas gingivalis than do immunocompetent mice of the same genetic background, indicating    that CD4+ T cells contribute to bone resorption.  The CD4+ and CD8+ T-cell knockouts were produced by targeted deletions of, respectively, major histocompatibility complex II (MHCII) or beta2-microglobulin (producing non-expression of MHCI).    Because MHC deletions can have other effects in addition to those on T-cell selection, we wanted to confirm that the lessened bone loss was truly an effect of the lack of T cells. Consequently, we repeated our experiments with C57B1 /6J-Tcra mice    that have a targeted deletion of the alpha chain of the T-cell receptor (Tcra). Six weeks after oral infection with P. gingivalis ATCC 53977 the total bone loss at buccal maxillary sites was 0.28 mm in infected immunocompetent mice (P=0.002    compared with sham-infected mice), whereas in Tcra knockouts the bone loss was only 0.08 mm (P=0.04 compared with shams). The T-cell-deficient mice thus lost 70% less bone after infection than did genetically matched immunocompetent mice (P    =0.003).  These experiments confirm that T cells, and their responses to oral infection with P. gingivalis, help to push bone remodeling in the direction of net loss of bone.</p>

	]]>
</description>

<author>P J. Baker et al.</author>


</item>


<item>
<title> Targeted Disruption of the Myocilin Gene (Myoc) Suggests that Human Glaucoma-Causing Mutations Are Gain of Function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/319</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/319</guid>
<pubDate>Tue, 08 May 2012 16:25:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Glaucoma is a heterogeneous eye disease and a major cause of blindness worldwide. Recently, primary open angle glaucoma (POAG)-associated mutations have been found in the trabecular meshwork inducible glucocorticoid response gene    (TIGR), also known as the myocilin gene (MYOC), at the GLC1A locus on chromosome 1q21-q31. These mutations occurred in a subset of patients with juvenile- and adult-onset POAG and exhibited autosomal dominant inheritance. Ocular expression and    its involvement in POAG suggest that TIGR/MYOC may have a role(s) in regulating intraocular pressure (IOP). Here, we report the generation and analysis of mice heterozygous and homozygous for a targeted null mutation in Myoc. Our study shows that    Myoc mutant mice are both viable and fertile. Our in vivo findings further demonstrate that Myoc is not required for normal IOP or normal ocular morphology. The lack of a discernable phenotype in both Myoc-heterozygous and Myoc-null mice suggests    that haploinsufficiency is not a critical mechanism for POAG in individuals with mutations in MYOC. Instead, disease-causing mutations in humans likely act by gain of function.</p>

	]]>
</description>

<author>B S. Kim et al.</author>


</item>


<item>
<title> The mouse snail gene encodes a key regulator of the epithelial-mesenchymal transition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/318</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/318</guid>
<pubDate>Tue, 08 May 2012 16:24:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Snail family genes encode DNA binding zinc finger proteins that act as transcriptional repressors. Mouse embryos deficient for the Snail (Sna) gene exhibit defects in the formation of the mesoderm germ layer. In Sna(-/-) mutant    embryos, a mesoderm layer forms and mesodermal marker genes are induced but the mutant mesoderm is morphologically abnormal.  Lacunae form within the mesoderm layer of the mutant embryos, and cells lining these lacunae retain epithelial    characteristics. These cells resemble a columnar epithelium and have apical-basal polarity, with microvilli along the apical surface and intercellular electron-dense adhesive junctions that resemble adherens junctions. E-cadherin expression is    retained in the mesoderm of the Sna(-/-) embryos. These defects are strikingly similar to the gastrulation defects observed in snail-deficient Drosophila embryos, suggesting that the mechanism of repression of E-cadherin transcription by Snail    family proteins may have been present in the metazoan ancestor of the arthropod and mammalian lineages.</p>

	]]>
</description>

<author>E A. Carver et al.</author>


</item>


<item>
<title> A major quantitative trait locus on chromosome 3 controls colitis severity in IL-10-deficient mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/317</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/317</guid>
<pubDate>Tue, 08 May 2012 16:24:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Colitic lesions are much more severe in C3H/HeJBir (C3H) than C57BL/6J (B6) mice after 10 backcrosses of a disrupted interleukin-10 (Il10) gene.  This study identified cytokine deficiency-induced colitis susceptibility (Cdcs)    modifiers by using quantitative trait locus (QTL) analysis. A segregating F(2) population (n = 408) of IL-10-deficient mice was genotyped and necropsied at 6 weeks of age. A major C3H-derived colitogenic QTL (Cdcs1) on chromosome (Chr.)  3    contributed to lesions in both cecum [logarithm of odds ratio (LOD) = 14.6)] and colon (LOD = 26.5) as well as colitis-related phenotypes such as spleen/body weight ratio, mesenteric lymph node/body weight ratio, and secretory IgA levels.     Evidence for other C3H QTL on Chr. 1 (Cdcs2) and Chr. 2 (Cdcs3) was obtained. Cdcs1 interacted epistatically or contributed additively with loci on other chromosomes. The resistant B6 background also contributed colitogenic QTL: Cdcs4 (Chr. 8),    Cdcs5 (Chr. 17, MHC), and Cdcs6 (Chr.  18). Epistatic interactions between B6 QTL on Chr. 8 and 18 contributing to cecum hyperplasia were particularly striking. In conclusion, a colitogenic susceptibility QTL on Chr. 3 has been shown to    exacerbate colitis in combination with modifiers contributed from both parental genomes. The complex nature of interactions among loci in this mouse model system, coupled with separate deleterious contributions from both parental strains,    illustrates why detection of human inflammatory bowel disease linkages has proven to be so difficult. A human ortholog of the Chr. 3 QTL, if one exists, would map to Chr. 4q or 1p.</p>

	]]>
</description>

<author>M A. Farmer et al.</author>


</item>


<item>
<title> Establishing an ENU mutagenesis screen for the piebald region of mouse Chromosome 14.</title>
<link>http://mouseion.jax.org/stfb2000_2009/316</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/316</guid>
<pubDate>Tue, 08 May 2012 16:24:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Greenberg A. Hagge et al.</author>


</item>


<item>
<title> A genomic-systems biology map for cardiovascular function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/315</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/315</guid>
<pubDate>Tue, 08 May 2012 16:24:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>With the draft sequence of the human genome available, there is a need to better define gene function in the context of systems biology. We studied 239 cardiovascular and renal phenotypes in 113 male rats derived from an F2    intercross and mapped 81 of these traits onto the genome. Aggregates of traits were identified on chromosomes 1, 2, 7, and 18. Systems biology was assessed by examining patterns of correlations ("physiological profiles") that can be used for gene    hunting, mechanism-based physiological studies, and, with comparative genomics, translating these data to the human genome.</p>

	]]>
</description>

<author>M Stoll et al.</author>


</item>


<item>
<title> Haploinsufficient Bmp4 ocular phenotypes include anterior segment dysgenesis with elevated intraocular pressure.</title>
<link>http://mouseion.jax.org/stfb2000_2009/314</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/314</guid>
<pubDate>Tue, 08 May 2012 16:24:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Glaucoma is a blinding disease usually associated with high intraocular pressure (IOP). In some families, abnormal anterior segment development contributes to glaucoma. The genes causing anterior segment dysgenesis and    glaucoma in most of these families are not identified and the affected developmental processes are poorly understood. Bone morphogenetic proteins (BMPs) participate in various developmental processes. We tested the importance of Bmp4 gene dosage    for ocular development and developmental glaucoma. RESULTS: Bmp4+/- mice have anterior segment abnormalities including malformed, absent or blocked trabecular meshwork and Schlemm's canal drainage structures. Mice with severe drainage structure    abnormalities, over 80% or more of their angle's extent, have elevated IOP. The penetrance and severity of abnormalities is strongly influenced by genetic background, being most severe on the C57BL/6J background and absent on some other    backgrounds. On the C57BL/6J background there is also persistence of the hyaloid vasculature, diminished numbers of inner retinal cells, and absence of the optic nerve.  CONCLUSIONS: We demonstrate that heterozygous deficiency of BMP4 results in    anterior segment dysgenesis and elevated IOP. The abnormalities are similar to those in human patients with developmental glaucoma. Thus, BMP4 is a strong candidate to contribute to Axenfeld-Rieger anomaly and other developmental conditions    associated with human glaucoma. BMP4 also participates in posterior segment development and wild-type levels are usually critical for optic nerve development on the C57BL/6J background.  Bmp4+/- mice are useful for studying various components of    ocular development, and may allow identification of strain specific modifiers affecting a variety of ocular phenotypes.</p>

	]]>
</description>

<author>B Chang et al.</author>


</item>


<item>
<title> Sex, flies and microarrays.</title>
<link>http://mouseion.jax.org/stfb2000_2009/313</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/313</guid>
<pubDate>Tue, 08 May 2012 16:23:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>In a typical microarray study, experimental RNA samples are compared to a reference sample and expression ratios are clustered. A new study of the effects of sex, aging and genotype on gene expression in Drosophila melanogaster    departs from this paradigm. Highly replicated comparisons generate measures of expression that are analyzed using classical analysis of variance (ANOVA) techniques, revealing substantial differences in gene expression between the two sexes as    well as smaller effects of age and strain. Moreover, this study demonstrates that replication and experimental design are essential to detecting small but biologically important differences in expression patterns.</p>

	]]>
</description>

<author>G A. Churchill et al.</author>


</item>


<item>
<title> Observed incidence of tumorigenesis in long-term rodent studies of rAAV vectors.</title>
<link>http://mouseion.jax.org/stfb2000_2009/312</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/312</guid>
<pubDate>Tue, 08 May 2012 16:23:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gene therapy using recombinant adeno-associated virus vectors (rAAV) is generally considered safe. During the course of a study designed to determine the long-term efficacy of rAAV-mediated gene therapy initiated in newborn mice    with the lysosomal storage disease, mucopolysaccharidosis type VII (MPSVII), a significant incidence of hepatocellular carcinomas and angiosarcomas was discovered. A hepatocellular carcinoma was first detected in a 35-week-old mouse and by 72    weeks of age, three out of five rAAV-treated MPSVII mice had similar lesions. These types of tumors had not been seen previously in long-term studies of MPSVII mice using recombinant enzyme or bone marrow transplantation. In an attempt to    ascertain whether mouse strain or GUSB expression confers susceptibility to tumor formation, we histopathologically examined untreated normal mice of the same strain, untreated MPSVII mice, and normal mice overexpressing human GUSB for the    presence of tumors and increased hepatocyte replication. The results of these studies do not indicate that MPSVII mice or mice overexpressing human GUSB are susceptible to tumor formation; however, the number of animals examined is too small to    draw definitive conclusions. Results from quantitative PCR performed on the tumor samples suggest that the tumors are probably not caused by an insertional mutagenesis event followed by the clonal expansion of a transformed cell.  In a separate    study, a relatively large group of mice injected with varying doses and types of rAAV vectors had no evidence of hepatic or vascular tumors. Although the mechanism of tumor formation is currently unknown, the tumorigenic potential of rAAV vectors    must be rigorously determined in long-term in vivo studies.</p>

	]]>
</description>

<author>A Donsante et al.</author>


</item>


<item>
<title> N-WASP deficiency reveals distinct pathways for cell surface projections and microbial actin-based motility.</title>
<link>http://mouseion.jax.org/stfb2000_2009/311</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/311</guid>
<pubDate>Tue, 08 May 2012 16:23:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Wiskott-Aldrich syndrome protein (WASP) family of molecules integrates upstream signalling events with changes in the actin cytoskeleton. N-WASP has been implicated both in the formation of cell-surface projections (filopodia)    required for cell movement and in the actin-based motility of intracellular pathogens. To examine N-WASP function we have used homologous recombination to inactivate the gene encoding murine N-WASP.  Whereas N-WASP-deficient embryos survive    beyond gastrulation and initiate organogenesis, they have marked developmental delay and die before embryonic day 12. N-WASP is not required for the actin-based movement of the intracellular pathogen Listeria but is absolutely required for the    motility of Shigella and vaccinia virus. Despite these distinct defects in bacterial and viral motility, N-WASP-deficient fibroblasts spread by using lamellipodia and can protrude filopodia. These results imply a crucial and non-redundant role    for N-WASP in murine embryogenesis and in the actin-based motility of certain pathogens but not in the general formation of actin-containing structures.</p>

	]]>
</description>

<author>S B. Snapper et al.</author>


</item>


<item>
<title> Oxidative stress in aging in the C57B16/J mouse cochlea.</title>
<link>http://mouseion.jax.org/stfb2000_2009/310</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/310</guid>
<pubDate>Tue, 08 May 2012 16:23:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Presbycusis is a complex of high frequency hearing loss and disproportionate loss of speech discrimination that is seen concomitantly with physical signs of aging. Among the most extensively characterized strains of mice that show    an early hearing loss is the C57B16/J strain, a strain that shows early onset of high frequency hearing loss at age 6 months and complete hearing loss by 1 year of age. The histopathology of this strain consists of loss of hair cells and spiral    ganglion neurons in the basal turn, with a progression of loss of hair cells and ganglion neurons towards the apical portion of the cochlea as the animal ages. The process of aging has been extensively studied and although details differ in    various organisms the consensus today is that oxidative stress, i.e.  free radical-mediated tissue damage, is one of the core mechanisms of aging. Aerobic metabolism results in the creation of hydrogen peroxide and reactive oxygen species. These    are normally detoxified by a variety of enzymes and free radical scavengers, including superoxide dismutase (SOD), catalase and glutathione. To determine whether oxidative stress plays a role in the pathophysiology of hearing loss in this mouse    model of presbycusis we determined the relative change in mRNA production for selected free radical detoxifying enzymes in the C57B16/J mouse cochlea.  Using semi-quantitative RT-PCR with tubulin mRNA as a control, relative levels of antioxidant    enzyme mRNAs were determined. There was an overall increase in SOD1 mRNA levels when comparing 1 and 9 month time points, and a transient increase in the expression level of catalase mRNA. B6.CAST+ Ahl mice, which carry the C57B16/J genome but    receive their Ahl gene from CAST mice, do not show these alteractions in antioxidant enzyme production. Our results suggest that at an age of 9 months, at which point significant hearing loss has developed, the C57B16/J mouse cochlea is exposed    to increased levels of free radicals and that the Ahl gene of the C57B16/J mouse mediates this decrease in protective enzymes and therefore increase in levels of oxidative stress.</p>

	]]>
</description>

<author>H Staecker et al.</author>


</item>


<item>
<title> Monoallelic gene expression in mice: who? When? How? Why?</title>
<link>http://mouseion.jax.org/stfb2000_2009/309</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/309</guid>
<pubDate>Tue, 08 May 2012 16:22:57 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J Schimenti</author>


</item>


<item>
<title> Evolutionary breakpoints on human chromosome 21.</title>
<link>http://mouseion.jax.org/stfb2000_2009/308</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/308</guid>
<pubDate>Tue, 08 May 2012 16:22:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Segments of the long arm of human chromosome 21 are conserved, centromere to telomere, in mouse chromosomes 16, 17, and 10. There have been 28 genes identified in human chromosome 21 between TMPRSS2, whose orthologue is the most    distal gene mapped to mouse chromosome 16, and PDXK, whose orthologue is the most proximal gene mapped to mouse chromosome 10. Only 6 of these 28 genes have been mapped in mouse, and all are located on chromosome 17.  To better define the    chromosome 17 segment and the 16 to 17 transition, we used a combination of mouse radiation hybrid panel mapping and physical mapping by mouse: human genomic sequence comparison. We have determined the mouse chromosomal location of an additional    12 genes, predicted the location of 7 more,and defined the endpoints of the mouse chromosome 17 region. The mouse chromosome 16/chromosome 17 evolutionary breakpoint is between human genes ZNF295 and UMODL1, showing there are seven genes in the    chromosome 16 segment distal to Tmprss2. The chromosome 17/chromosome 10 breakpoint seems to have involved a duplication of the gene PDXK, which on chromosome 21 lies immediately distal to the KIAA0179 gene. These data suggest that there may be    as few as 21 functional genes in the mouse chromosome 17 segment. This information is important for defining existing and constructing more complete mouse models of Down syndrome.</p>

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</description>

<author>M T. Davisson et al.</author>


</item>


<item>
<title> Use of coisogenic host blastocysts for efficient establishment of germline chimeras with C57BL/6J ES cell lines.</title>
<link>http://mouseion.jax.org/stfb2000_2009/307</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/307</guid>
<pubDate>Tue, 08 May 2012 16:22:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gene targeting in embryonic stem (ES) cells allows the production of mice with specified genetic mutations. Currently, germline-competent ES cell lines are available from only a limited number of mouse strains, and inappropriate ES    cell/host blastocyst combinations often restrict the efficient production of gene-targeted mice. Here, we describe the derivation of C57BL/6J (B6) ES lines and compare the effectiveness of two host blastocyst donors, FVB/NJ (FVB) and the    coisogenic strain C57BL/6-Tyr(c)-2J (c2J), for the production of germline chimeras. We found that when B6 ES cells were injected into c2J host blastocysts, a high rate of coat-color chimerism was detected, and germline transmission could be    obtained with few blastocyst injections. In all but one case, highly chimeric mice transmitted to 100% of their offspring. The injection of B6 ES cells into FVB blastocysts produced some chimeric mice. However; the proportion of coat-color    chimerism was low, with many more blastocyst injections required to generate chimeras capable of germline transmission.  Our data support the use of the coisogenic albino host strain, c2J, for the generation of germline-competent chimeric mice    when using B6 ES cells.</p>

	]]>
</description>

<author>Gossler K. Schuster et al.</author>


</item>


<item>
<title> The mouse Hoxd13(spdh) mutation, a polyalanine expansion similar to human type II synpolydactyly (SPD), disrupts the function but not the expression of other Hoxd genes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/306</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/306</guid>
<pubDate>Tue, 08 May 2012 16:22:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Polyalanine expansion in the human HOXD13 gene induces synpolydactyly (SPD), an inherited congenital limb malformation. A mouse model was isolated, which showed a spontaneous alanine expansion due to a 21-bp duplication at the    corresponding place in the mouse gene. This mutation (synpolydactyly homolog, spdh), when homozygous, causes malformations in mice similar to those seen in affected human patients. We have studied the genetics of this condition, by using several    engineered Hoxd alleles, as well as by looking at the expression of Hox and other marker genes. We show that the mutated SPDH protein induces a gain-of-function phenotype, likely by behaving as a dominant negative over other Hox genes. The    mutation, however, seems to act independently from Hoxa13 and doesn't appear to affect Hox gene expression, except for a slight reduction of the HOXD13 protein itself. Developmental studies indicate that the morphological effect is mostly due to    a severe retardation in the growth and ossification of the bony elements, in agreement with a general impairment in the function of posterior Hoxd genes.</p>

	]]>
</description>

<author>S Bruneau et al.</author>


</item>


<item>
<title> Fas deficiency delays the resolution of airway hyperresponsiveness after allergen sensitization and challenge.</title>
<link>http://mouseion.jax.org/stfb2000_2009/305</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/305</guid>
<pubDate>Tue, 08 May 2012 16:22:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: In asthma, persistent inflammation might be the result of (1) an impaired ability to clear inflammatory cells from the airways and/or (2) impaired apoptotic responses. OBJECTIVE: In a mouse model, we investigated the    regulatory role of Fas (CD95)-induced apoptosis in the development and resolution of airway inflammation and airway hyperresponsiveness (AHR). METHODS: Mice that were either Fas-sufficient (wild-type; WT) or Fas-deficient (lpr ) were sensitized    by intraperitoneal injections of ovalbumin (OVA) and challenged once intranasally with OVA (IP-IN mice). Control (IN) mice were challenged only. RESULTS: IP-IN WT mice developed AHR at 48 hours; changes in airway resistance resolved by 96 hours.    Airway responsiveness at 48 hours in IP-IN lpr mice was similar to that in IP-IN WT mice. However, in contrast to WT mice, IP-IN lpr mice sustained significant AHR at 96 hours in comparison with IN lpr mice; the AHR resolved by 6 days.    Bronchoalveolar lavage fluid cell composition was similar in all of the different groups at 48 hours and 96 hours. Both IP-IN WT mice and lpr mice exhibited similar tissue eosinophilia, whereas IP-IN lpr mice had significantly lower numbers of    TdT-mediated dUTP nick end labeling (TUNEL)-positive cells in comparison with IP-IN WT mice at 48 hours. Anti-IL-5 antibody given to IP-IN lpr mice 48 hours and 72 hours after the challenge significantly decreased AHR and eosinophilic    inflammation and increased TUNEL-positive cell numbers at 96 hours.  CONCLUSION: These results suggest that Fas expression can regulate the onset and resolution of AHR through an increase in eosinophil apoptosis.</p>

	]]>
</description>

<author>C Duez et al.</author>


</item>


<item>
<title> Of mice and genome sequence.</title>
<link>http://mouseion.jax.org/stfb2000_2009/304</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/304</guid>
<pubDate>Tue, 08 May 2012 16:21:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Availability of the mouse genome sequence will have a major impact on the study of vertebrate evolution, mammalian biology, and animal models of human disease. Resources to explore genome biology in mice will maximize the effect of    this watershed event.</p>

	]]>
</description>

<author>B A. Hamilton et al.</author>


</item>


<item>
<title> Reciprocal mouse and human limb phenotypes caused by gain- and loss-of-function mutations affecting lmbr1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/303</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/303</guid>
<pubDate>Tue, 08 May 2012 16:21:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>The major locus for dominant preaxial polydactyly in humans has been mapped to 7q36. In mice the dominant Hemimelic extra toes (Hx) and Hammertoe (Hm) mutations map to a homologous chromosomal region and cause similar limb defects.    The Lmbr1 gene is entirely within the small critical intervals recently defined for both the mouse and human mutations and is misexpressed at the exact time that the mouse Hx phenotype becomes apparent during limb development. This result    suggests that Lmbr1 may underlie preaxial polydactyly in both mice and humans. We have used deletion chromosomes to demonstrate that the dominant mouse and human limb defects arise from gain-of-function mutations and not from haploinsufficiency.    Furthermore, we created a loss-of-function mutation in the mouse Lmbr1 gene that causes digit number reduction (oligodactyly) on its own and in trans to a deletion chromosome. The loss of digits that we observed in mice with reduced Lmbr1    activity is in contrast to the gain of digits observed in Hx mice and human polydactyly patients. Our results suggest that the Lmbr1 gene is required for limb formation and that reciprocal changes in levels of Lmbr1 activity can lead to either    increases or decreases in the number of digits in the vertebrate limb.</p>

	]]>
</description>

<author>R M. Clark et al.</author>


</item>


<item>
<title>Caring for Place: Negotiating World Heritage on Lord Howe Island</title>
<link>http://ro.uow.edu.au/thsci/23</link>
<guid isPermaLink="true">http://ro.uow.edu.au/thsci/23</guid>
<pubDate>Tue, 08 May 2012 16:21:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lord Howe Island, located 700 kilometres north east of Sydney, New South Wales, is part of the World Heritage listed Lord Howe Island Group. In 1982 the Lord Howe Island Group was listed under the World Heritage Convention for its outstanding ‘natural’ heritage values. Since the listing, the World Heritage Convention has revisited the concept of ‘nature’ as the sole criterion for the designation of World Heritage, by embracing the concept of ‘cultural landscape’. However, this has no retrospective effect and therefore has not affected the listing of the Lord Howe Island Group. Consequently, despite a cultural heritage of over 180 years of European settlement, Lord Howe Island’s ‘cultural landscape’ and ‘intangible heritage’ are not valued in the process of managing it as a World Heritage Site.</p>
<p>This thesis explores the consequences of environmental management processes arising from World Heritage listing which presently operate to marginalise, if not silence, Islander knowledge and how Islanders and other residents care for the Island. To do so, the project invited all Island residents, including those employed in ‘environmental management’ positions, to talk about <em>what </em>and <em>how </em>they care for the Island. The project required the development of a methodology that employed mixed-methods, and, crucially, was mindful of the concept of <em>islandness</em>, that is the cultural protocols of island places. Applying a form of narrative analysis, the results explore the differences and similarities between how ‘Islanders’ and other residents, on the one hand, and ‘environmental managers’ on the other, talk about nature, the Island, boundaries, plants, animals and World Heritage. Case studies illustrate how ‘environmental managers’ and other Island residents, particularly ‘Islanders’, draw on different knowledge-making practices to care for the Island and how this often results in disagreement over what should be protected, and what belongs and does not belong on the Island. This thesis suggests contemporary concepts of World Heritage, including ‘cultural landscape’ and ‘intangible heritage’, offer a mechanism whereby the process of environmental management of Lord Howe Island can engage with different knowledges of caring for the Island.</p>

	]]>
</description>

<author>Lucy Farrier</author>


</item>


<item>
<title> Efficient chromosomal mapping of a methylcholanthrene- induced tumor antigen by ctl immunoselection.</title>
<link>http://mouseion.jax.org/stfb2000_2009/302</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/302</guid>
<pubDate>Tue, 08 May 2012 16:21:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>It has been difficult to genetically map the genes encoding tumor Ags because they arise as a consequence of somatic mutational events.  CTL-mediated immunoselection can impose potent immunoselective pressure against tumor cells,    resulting in the survival of rare tumor Ag-loss variants. We subjected a heterozygous 3-methylcholanthrene-induced murine sarcoma cell line to CTL immunoselection, selecting for the loss of a tumor-specific Ag, recognized antigen from MCA-induced    tumor 1 (Ram1).  Several variants eluded CTL recognition by genetic loss of the hemizygously expressed tumor-specific Ag epitope. A frequently observed genetic escape mechanism was spontaneous mitotic recombination resulting in loss of    heterozygosity on chromosome 4. Higher density genetic analyses along with functional confirmation with an independently produced chromosome 4 loss of heterozygosity variant positioned the Ram1 locus to a distal 7.1 cM interval on chromosome 4.    This region of the mouse genome is rich in tumor-modifier genes and this positioning of Ram1 may thus provide insight into the genetic basis of 3-methycholanthrene-induced tumor Ags.</p>

	]]>
</description>

<author>S Akilesh et al.</author>


</item>


<item>
<title> Pemphigus: an unfolding story.</title>
<link>http://mouseion.jax.org/stfb2000_2009/301</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/301</guid>
<pubDate>Tue, 08 May 2012 16:20:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>S A. Grando et al.</author>


</item>


<item>
<title> International Workshop on Lessons From Animal Models for Human Type 1 Diabetes: identification of insulin but not glutamic acid decarboxylase or IA-2 as specific autoantigens of humoral autoimmunity in nonobese diabetic
   mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/300</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/300</guid>
<pubDate>Tue, 08 May 2012 16:20:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Several self-antigens have been reported as targets of the autoimmune response in nonobese diabetic (NOD) mice. The aim of this workshop was to identify autoantibody assays that could provide useful markers of autoimmunity in this    animal model for type 1 diabetes. More than 400 serum samples from NOD (4, 8, and 12 weeks of age and at diabetes onset), BALB/c, and B6 mice were collected from six separate animal facilities, coded, and distributed to five laboratories for    autoantibody measurement.  Insulin autoantibodies (IAA) were measured by radiobinding assay (RBA) by four laboratories and by enzyme-linked immunosorbent assay (ELISA) in one laboratory. Using the 99th percentile of BALB/c and B6 control mice as    the threshold definition of positivity, IAA by RBA were detected in NOD mice at frequencies ranging from 10 to 30% at age 4 weeks, from 26 to 56% at 8 weeks, from 42 to 56% at 12 weeks, and from 15 to 75% at diabetes onset.  With ELISA, IAA    signals differed significantly between control mouse strains and increased with age in both control and NOD mice, with frequencies in NOD animals being 0% at 4 weeks, 14% at 8 weeks, 19% at 12 weeks, and 42% at diabetes onset. For IAA, the ELISA    results were relatively discordant with those of RBA. GAD autoantibody (GADA) and IA-2 autoantibody (IA-2A) signals obtained by RBA were low (maximum 2.5% of total) but were increased in NOD mice compared with control mice at diabetes onset (GADA    29-50%; IA-2A 36-47%). ELISA also detected GADA (42%) and IA-2A (50%) at diabetes onset, with results concordant with those of RBA. Remarkably, GADA and IA-2A frequencies varied significantly with respect to the source colony of NOD mice.    Furthermore, whereas neither GADA nor IA-2A correlated with IAA, there was strong concordance between GADA and IA-2A in individual mice. Sera with increased binding to GAD and IA-2 also had increased binding to the unrelated antigen myelin    oligodendrocyte glycoprotein, and binding to GAD could not be inhibited with excess unlabeled antigen, suggesting nonspecific interactions. In sum, this workshop demonstrated that IAA measured by sensitive RBA are a marker of autoimmunity in NOD    mice and draw into question the true nature of GADA and IA-2A in this animal model.</p>

	]]>
</description>

<author>E Bonifacio et al.</author>


</item>


<item>
<title> Availability and characterization of transgenic and knockout mice with behavioral manifestations: where to look and what to search for.</title>
<link>http://mouseion.jax.org/stfb2000_2009/299</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/299</guid>
<pubDate>Tue, 08 May 2012 16:20:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice altered by transgenesis or gene targeting ('knockouts') have increasingly been employed as alternative effective tools in elucidating the genetic basis of neurophysiology and behavior. Standardization of specific behavioral    paradigms and phenotyping strategies will ensure that these behavioral mouse mutants offer robust models for evaluating the efficacy of novel therapeutics in the treatment of hereditary neurological disorders. The Induced Mutant Resource (IMR) at    The Jackson Laboratory (Bar Harbor, Maine, USA) imports, cryopreserves, develops, maintains, and distributes to the research community biomedically valuable stocks of transgenic and targeted mutant mice. Information on behavioral and neurological    strains-including a phenotypic synopsis, husbandry requirements, strain availability, and genetic typing protocols-is available through the IMR database (http://www.jax.org/resources/documents/imr/). A current catalog of available strains is    readily accessible via the JAX(R)Mice Web site at http://jaxmice.jax.org/index.shtml. In addition, The Jackson Laboratory is now home to TBASE (http://tbase.jax.org/), a comprehensive, community database whose primary focus is on mouse knockouts.    TBASE accommodates an exhaustive bibliographical resource for transgenic and knockout mice and provides a detailed phenotypic characterization of numerous behavioral knockouts that is primarily extracted from the literature. Concerted efforts to    merge the two resources into a new, schematically reformed database are underway.</p>

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</description>

<author>A V. Anagnostopoulos et al.</author>


</item>


<item>
<title> The molecular bases of spontaneous immunological mutations in the mouse and their homologous human diseases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/298</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/298</guid>
<pubDate>Tue, 08 May 2012 16:20:08 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M J. Joliat et al.</author>


</item>


<item>
<title> A null mutation in inositol polyphosphate 4-phosphatase type I causes selective neuronal loss in weeble mutant mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/297</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/297</guid>
<pubDate>Tue, 08 May 2012 16:19:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Weeble mutant mice have severe locomotor instability and significant neuronal loss in the cerebellum and in the hippocampal CA1 field. Genetic mapping was used to localize the mutation to the gene encoding inositol polyphosphate    4-phosphatase type I (Inpp4a), where a single nucleotide deletion results in a likely null allele. The substrates of INPP4A are intermediates in a pathway affecting intracellular Ca(2+) release but are also involved in cell cycle regulation    through binding the Akt protooncogene; dysfunction in either may account for the neuronal loss of weeble mice. Although other mutations in phosphoinositide enzymes are associated with synaptic defects without neuronal loss, weeble shows that    Inpp4a is critical for the survival of a subset of neurons during postnatal development in mice.</p>

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</description>

<author>A Nystuen et al.</author>


</item>


<item>
<title> Desmutagenic and bio-antimutagenic activity of docosahexaenoic acid and eicosapentaenoic acid in cultured Chinese hamster V79 cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/296</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/296</guid>
<pubDate>Tue, 08 May 2012 16:19:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The antimutagenic activities of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were examined by studying their effects on induction of 6-thioguanine (6TG)-resistant mutations by ethyl methanesulfonate (EMS) in cultured    Chinese hamster V79 cells. DRA had a remarkable inhibitory effect against the cytotoxicity of EMS, when cells were simultaneously-treated with EMS, showing a blocking or scavenging activity of DHA in reduction of surviving fraction of cells. DHA    had not so significant effect, when cells were treated before and after treatment with EMS. On the other hand, EPA had marked inhibiting effects against cytotoxicity of EMS, when cells were treated with EPA, before, simultaneous and after    treatment with EMS. Against the induction of mutations by EMS, an antimutagenic activity of DHA was found when cells were pre-treated, simultaneously-treated or post-treated with DHA. EPA was also effective in reducing EMS-induced 6TG-resistant    mutations when the cells were treated using the three different treatment procedures described above. The results suggest that in cultured Chinese hamster V79 cells, DHA and EPA may have both desmutagenic activity, which inactivates EMS    chemically and/or enzymatically and bio-antimutagenic activity which suppresses mutation fixation after DNA is damaged by EMS.</p>

	]]>
</description>

<author>Y Kuroda et al.</author>


</item>


<item>
<title> A statistical framework for quantitative trait mapping.</title>
<link>http://mouseion.jax.org/stfb2000_2009/295</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/295</guid>
<pubDate>Tue, 08 May 2012 16:19:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>We describe a general statistical framework for the genetic analysis of quantitative trait data in inbred line crosses. Our main result is based on the observation that, by conditioning on the unobserved QTL genotypes, the problem    can be split into two statistically independent and manageable parts. The first part involves only the relationship between the QTL and the phenotype. The second part involves only the location of the QTL in the genome. We developed a simple    Monte Carlo algorithm to implement Bayesian QTL analysis. This algorithm simulates multiple versions of complete genotype information on a genomewide grid of locations using information in the marker genotype data. Weights are assigned to the    simulated genotypes to capture information in the phenotype data. The weighted complete genotypes are used to approximate quantities needed for statistical inference of QTL locations and effect sizes. One advantage of this approach is that only    the weights are recomputed as the analyst considers different candidate models. This device allows the analyst to focus on modeling and model comparisons. The proposed framework can accommodate multiple interacting QTL, nonnormal and multivariate    phenotypes, covariates, missing genotype data, and genotyping errors in any type of inbred line cross. A software tool implementing this procedure is available. We demonstrate our approach to QTL analysis using data from a mouse backcross    population that is segregating multiple interacting QTL associated with salt-induced hypertension.</p>

	]]>
</description>

<author>S Sen et al.</author>


</item>


<item>
<title> Maximum life spans in mice are extended by wild strain alleles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/294</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/294</guid>
<pubDate>Tue, 08 May 2012 16:19:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genes that control basic aging mechanisms in mammals are unknown. By using two four-way crosses, each including a strain derived from wild, undomesticated stocks, we identified two quantitative trait loci that extend murine    life spans by approximately 10%. In one cross, the longest-lived 18% of carriers of the D8Mit171 marker allele from the MOLD/Rk strain, Mus m. molossinus, outlived the longest lived 18% of noncarriers by 129 days (P = 5.4 x 10(-5)); in a second    cross, carriers of the D10Mit267 allele from the CAST/Ei strain, Mus m. castaneus, outlived noncarriers by 125 days ( P = 1.6 x 10(-6)). In both crosses, P < 1.0 x 10(-4 )is considered significant. Because these life span increases required that    all essential biological systems function longer than normal, these alleles most likely retarded basic aging mechanisms in multiple biological systems simultaneously.</p>

	]]>
</description>

<author>S Klebanov et al.</author>


</item>


<item>
<title> Transgenic rescue implicates beta 2-microglobulin as a diabetes susceptibility gene in nonobese diabetic (NOD) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/293</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/293</guid>
<pubDate>Tue, 08 May 2012 16:18:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Type 1 diabetes in both humans and nonobese diabetic (NOD) mice results from T-cell-mediated autoimmune destruction of insulin-producing pancreatic beta cells. Linkage studies have shown that type 1 diabetes in NOD mice is a    polygenic disease involving more than 15 chromosomal susceptibility regions. Despite extensive investigation, the identification of individual susceptibility genes either within or outside the major histocompatibility complex region has proven    problematic because of the limitations of linkage analysis. In this paper, we provide evidence implicating a single diabetes susceptibility gene, which lies outside the major histocompatibility complex region. Using allelic reconstitution by    transgenic rescue, we show that NOD mice expressing the beta(2) microglobulin (beta(2)M)(a) allele develop diabetes, whereas NOD mice expressing a murine beta(2)M(b) or human allele are protected. The murine beta(2)M(a) allele differs from the    beta(2)M(b) allele only at a single amino acid. Mechanistic studies indicate that the absence of the NOD beta(2)M(a) isoform on nonhematopoietic cells inhibits the development or activation of diabetogenic T cells.</p>

	]]>
</description>

<author>Williams E. Hamilton et al.</author>


</item>


<item>
<title> Mutations in the Human Orthologue of the Mouse underwhite Gene (uw) Underlie a New Form of Oculocutaneous Albinism, OCA4.</title>
<link>http://mouseion.jax.org/stfb2000_2009/292</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/292</guid>
<pubDate>Tue, 08 May 2012 16:18:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Oculocutaneous albinism (OCA) affects approximately 1/20,000 people worldwide. All forms of OCA exhibit generalized hypopigmentation. Reduced pigmentation during eye development results in misrouting of the optic nerves, nystagmus,    alternating strabismus, and reduced visual acuity. Loss of pigmentation in the skin leads to an increased risk for skin cancer.  Two common forms and one infrequent form of OCA have been described. OCA1 (MIM 203100) is associated with mutations    of the TYR gene encoding tyrosinase (the rate-limiting enzyme in the production of melanin pigment) and accounts for approximately 40% of OCA worldwide. OCA2 (MIM 203200), the most common form of OCA, is associated with mutations of the P gene    and accounts for approximately 50% of OCA worldwide. OCA3 (MIM 203290), a rare form of OCA and also known as "rufous/red albinism," is associated with mutations in TYRP1 (encoding tyrosinase-related protein 1). Analysis of the TYR and P genes in    patients with OCA suggests that other genes may be associated with OCA. We have identified the mouse underwhite gene (uw) and its human orthologue, which underlies a new form of human OCA, termed "OCA4." The encoded protein, MATP (for    "membrane-associated transporter protein") is predicted to span the membrane 12 times and likely functions as a transporter.</p>

	]]>
</description>

<author>J M. Newton et al.</author>


</item>


<item>
<title> Structure, chromosomal localization, and expression of the gene for mouse ecto-mono(ADP-ribosyl)transferase ART5.</title>
<link>http://mouseion.jax.org/stfb2000_2009/291</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/291</guid>
<pubDate>Tue, 08 May 2012 16:18:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mono(ADP-ribosyl)transferases regulate the function of target proteins by attaching ADP-ribose to specific amino acid residues in their target proteins. The purpose of this study was to determine the structure, chromosomal    localization, and expression profile of the gene for mouse ecto-ADP-ribosyltransferase ART5. Southern blot analyses indicate that Art5 is a single copy gene which maps to mouse chromosome 7 at offset 49.6 cM in close proximity to the Art1, Art2a    and Art2b genes. Northern blot and RT-PCR analyses demonstrate prominent expression of Art5 in testis, and lower levels in cardiac and skeletal muscle. Sequence analyses reveal that the Art5 gene encompasses six exons spanning 8 kb of genomic    DNA. The 5' end of the Art5 gene overlaps with that of the Art1 gene. A single long exon encodes the predicted ART5 catalytic domain. Separate exons encode the N-terminal leader peptide and a hydrophilic C-terminal extension.  Sequencing of    RT-PCR products and ESTs identified six splice variants. The deduced amino acid sequence of ART5 shows 87% sequence identity to its orthologue from the human, and 37 and 32% identity to its murine paralogues ART1 and ART2. Unlike ART1 and ART2,    ART5 lacks a glycosylphosphatidylinositol-anchor signal sequence and is predicted to be a secretory enzyme. This prediction was confirmed by transfecting an Art5 cDNA expression construct into Sf9 insect cells. The secreted epitope-tagged ART5    protein resembled rat ART2 in exhibiting potent NAD-glycohydrolase activity. This study provides important experimental tools to further elucidate the function of ART5.</p>

	]]>
</description>

<author>G Glowacki et al.</author>


</item>


<item>
<title> Insulin-like growth factor binding proteins in femoral and vertebral bone marrow stromal cells: expression and regulation by thyroid hormone and dexamethasone.</title>
<link>http://mouseion.jax.org/stfb2000_2009/290</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/290</guid>
<pubDate>Tue, 08 May 2012 16:17:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Insulin-like growth factor (IGF)-I is an important regulator of bone metabolism. Clinical observations suggest that different anatomic sites within the adult skeleton respond differently to hormonal and therapeutic treatment, and    recent studies on bone marrow stromal cells in culture show that there are skeletal site-dependent differences in the gene expression of IGF-I. The actions of IGF-I and -II on bone cells are known to be modulated by the IGF binding proteins    (IGFBP)-1 through -6 and the Type I and Type II IGF receptors. Therefore, we compared the expression of IGFBP-1 through -6 in adult female rat bone marrow stromal cell cultures derived from two separate skeletal sites: vertebrae and femurs. The    cultures were maintained simultaneously under conditions that support osteoblast differentiation from osteoprogenitors present in the femoral and vertebral marrow cell populations. We also addressed whether IGFBP messenger RNA levels are    regulated by thyroid hormone (T(3)) and dexamethasone (dex) treatment in femoral vs. vertebral marrow stromal cells in vitro, since steroid hormones play an important role in skeletal function. Northern blot analyses revealed that there are    distinct skeletal site differences in the gene expression of IGFBPs. The vertebral marrow cultures express IGFBP-2 through -6 mRNAs, with IGFBP-2, IGFBP-4, and IGFBP-6 mRNAs predominating. The femoral marrow stromal cell cultures express only    IGFBP-4 and IGFBP-6. Importantly, vertebral marrow cultures have much higher IGFBP mRNA steady-state levels than femoral cultures for all the detected IGFBP transcripts. IGFBP-1 is not detected in either femoral or vertebral cultures. In addition    to a skeletal site difference, we show that T(3) and dex regulate the expression of specific IGFBP mRNAs.  T(3) treatment also upregulates IGF-I protein secretion by vertebral marrow stromal cell cultures. Interestingly, the type I receptor for    IGF-I was expressed equivalently in cultures from the two skeletal sites. These findings have important implications for the anatomical site specificities of hormonal responses that are noted in the skeleton. Copyright 2001 Wiley-Liss,    Inc.</p>

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</description>

<author>M Milne et al.</author>


</item>


<item>
<title> Ts65Dn -- localization of the translocation breakpoint and trisomic gene content in a mouse model for Down syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/289</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/289</guid>
<pubDate>Tue, 08 May 2012 16:17:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fluorescent in situ hybridization (FISH) -- using mouse chromosome paints, probes for the mouse major centromeric satellite DNA, and probes for genes on chromosomes (Chr) 16 and 17 -- was employed to locate the breakpoint in a    translocation used to produce a mouse model for Down syndrome. The Ts65Dn trisomy is derived from the reciprocal translocation T(16;17)65Dn.  The Ts65Dn mouse carries a marker chromosome containing the distal segment of Chr 16, a region that    shows linkage conservation with human Chr 21, and the proximal end of Chr 17. This chromosome confers trisomy for most of the genes in the Chr 16 segment and Ts65Dn mice show many of the phenotypic features characteristic of Down syndrome. We    used FISH on metaphase chromosomes from translocation T65Dn/+ heterozygotes and Ts65Dn mice to show that the Chr 17 breakpoint is distal to the heterochromatin of Chr 17, that the Ts65Dn marker chromosome contains a small portion of Chr 17    euchromatin, that the Chr 16 breakpoint lies between the Ncam2 and Gabpa/App genes, and that the Ts65Dn chromosome contains >80% of the human Chr 21 homologs. The significance of this finding is discussed in terms of the utility of this mouse    model.</p>

	]]>
</description>

<author>E C. Akeson et al.</author>


</item>


<item>
<title> Intraocular pressure in genetically distinct mice: an update and strain survey.</title>
<link>http://mouseion.jax.org/stfb2000_2009/288</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/288</guid>
<pubDate>Tue, 08 May 2012 16:17:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Little is known about genetic factors affecting intraocular pressure (IOP) in mice and other mammals. The purpose of this study was to determine the IOPs of genetically distinct mouse strains, assess the effects of    factors such as age, sex and time of day on IOP in specific strain backgrounds, and to assess the effects of specific candidate gene mutations on IOP. RESULTS: Based on over 30 studied mouse strains, average IOP ranges from approximately 10 to 20    mmHg. Gender does not typically affect IOP and aging results in an IOP decrease in some strains. Most tested strains exhibit a diurnal rhythm with IOP being the highest during the dark period of the day. Homozygosity for a null allele of the    carbonic anhydrase II gene (Car2n) does not alter IOP while homozygosity for a mutation in the leptin receptor gene (Leprdb) that causes obesity and diabetes results in increased IOP. Albino C57BL/6J mice homozygous for a tyrosinase mutation    (Tyrc-2J) have higher IOPs than their pigmented counterparts. CONCLUSIONS: Genetically distinct mouse strains housed in the same environment have a broad range of IOPs. These IOP differences are likely due to interstrain genetic differences that    create a powerful resource for studying the regulation of IOP. Age, time of day, obesity and diabetes have effects on mouse IOP similar to those in humans and other species. Mutations in two of the assessed candidate genes (Lepr and Tyr) result    in increased IOP. These studies demonstrate that mice are a practical and powerful experimental system to study the genetics of IOP regulation and disease processes that raise IOP to harmful levels.</p>

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</description>

<author>O V. Savinova et al.</author>


</item>


<item>
<title> The mouse Hoxd13(spdh) mutation, a polyalanine expansion similar to human type II synpolydactyly (SPD), disrupts the function but not the expression of other Hoxd genes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/287</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/287</guid>
<pubDate>Tue, 08 May 2012 16:17:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Polyalanine expansion in the human HOXD13 gene induces synpolydactyly (SPD), an inherited congenital limb malformation. A mouse model was isolated, which showed a spontaneous alanine expansion due to a 21-bp duplication at the    corresponding place in the mouse gene. This mutation (synpolydactyly homolog, spdh), when homozygous, causes malformations in mice similar to those seen in affected human patients. We have studied the genetics of this condition, by using several    engineered Hoxd alleles, as well as by looking at the expression of Hox and other marker genes. We show that the mutated SPDH protein induces a gain-of-function phenotype, likely by behaving as a dominant negative over other Hox genes. The    mutation, however, seems to act independently from Hoxa13 and doesn't appear to affect Hox gene expression, except for a slight reduction of the HOXD13 protein itself. Developmental studies indicate that the morphological effect is mostly due to    a severe retardation in the growth and ossification of the bony elements, in agreement with a general impairment in the function of posterior Hoxd genes.</p>

	]]>
</description>

<author>S Bruneau et al.</author>


</item>


<item>
<title> Relatively normal human lymphopoiesis but rapid turnover of newly formed B cells in transplanted nonobese diabetic/SCID mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/286</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/286</guid>
<pubDate>Tue, 08 May 2012 16:16:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human B lineage lymphocyte precursors in chimeric nonobese diabetic/SCID mice transplanted with umbilical cord blood cells were directly compared with those present in normal bone marrow. All precursor subsets were represented and    in nearly normal proportions. Cell cycle activity and population dynamics were investigated by staining for the Ki-67 nuclear Ag as well as by incorporation experiments using 5-bromo-2'-deoxyuridine.  Again, this revealed that human B    lymphopoiesis in chimeras parallels that in normal marrow with respect to replication and progression through the lineage. Moreover, sequencing of Ig gene rearrangement products showed that a diverse repertoire of V(H) genes was utilized by the    newly formed lymphocytes but there was no evidence for somatic hypermutation. The newly formed B cells frequently acquired the CD5 Ag and had a short life span in the periphery. Thus, all molecular requirements for normal B lymphocyte formation    are present in nonobese diabetic/SCID mice, but additional factors are needed for recruitment of B cells into a fully mature, long-lived pool. The model can now be exploited to learn about species restricted and conserved environmental cues for    human B lymphocyte production.</p>

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</description>

<author>M I. Rossi et al.</author>


</item>


<item>
<title> Does one gene determine whether a C57BL/6J-Y(POS) mouse will develop as a female or as an hermaphrodite?</title>
<link>http://mouseion.jax.org/stfb2000_2009/285</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/285</guid>
<pubDate>Tue, 08 May 2012 16:16:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Two studies were conducted to further our understanding of the inherited condition in mice known as C57BL/6J-Y(POS) (B6-Y(POS)) sex reversal. One study determined what proportion of B6 XY(POS) mice develop as females or    hermaphrodites. We found that 75% develop as females and the remainder develop as hermaphrodites regardless of whether the analysis is conducted at 14.5-16 days of embryonic development (based on gonad phenotype) or at weaning (based on the    appearance of external genitalia and presence of mammary-associated yellow pigmented hair). We also found that 75 % of the gonads in B6 XY(POS) mice develop as ovaries and the remainder develop as ovotestes; none develop as a testis. We conclude    that if any testicular tissue develops, sufficient testosterone is produced to cause at least some masculinization of the external genitalia. The second study tested the hypothesis that development of testicular tissue in B6 XY(POS) mice is due    to the presence of a POS-derived gene, whereas B6 homozygosity of this gene guarantees ovarian development. The results did not support the POS gene theory. Therefore, we conclude it is a matter of chance that 75 % of B6 XY(POS) mice develop as    females and 25 % develop as hermaphrodites.</p>

	]]>
</description>

<author>E M. Eicher et al.</author>


</item>


<item>
<title> Creating the gene ontology resource: design and implementation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/284</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/284</guid>
<pubDate>Tue, 08 May 2012 16:16:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The exponential growth in the volume of accessible biological information has generated a confusion of voices surrounding the annotation of molecular information about genes and their products. The Gene Ontology (GO) project seeks    to provide a set of structured vocabularies for specific biological domains that can be used to describe gene products in any organism. This work includes building three extensive ontologies to describe molecular function, biological process, and    cellular component, and providing a community database resource that supports the use of these ontologies. The GO Consortium was initiated by scientists associated with three model organism databases: SGD, the Saccharomyces Genome database;    FlyBase, the Drosophila genome database; and MGD/GXD, the Mouse Genome Informatics databases. Additional model organism database groups are joining the project. Each of these model organism information systems is annotating genes and gene    products using GO vocabulary terms and incorporating these annotations into their respective model organism databases. Each database contributes its annotation files to a shared GO data resource accessible to the public at    http://www.geneontology.org/.  The GO site can be used by the community both to recover the GO vocabularies and to access the annotated gene product data sets from the model organism databases. The GO Consortium supports the development of the GO    database resource and provides tools enabling curators and researchers to query and manipulate the vocabularies. We believe that the shared development of this molecular annotation resource will contribute to the unification of biological    information.</p>

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</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title> Tumor formation and inactivation of RIZ1, an Rb-binding member of a nuclear protein-methyltransferase superfamily.</title>
<link>http://mouseion.jax.org/stfb2000_2009/283</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/283</guid>
<pubDate>Tue, 08 May 2012 16:16:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>The retinoblastoma protein-interacting zinc finger gene RIZ (PRDM2) is a member, by sequence homology, of a nuclear protein-methyltransferase (MTase) superfamily involved in chromatin-mediated gene expression. The gene produces two    protein products, RIZ1 that contains a conserved MTase domain and RIZ2 that lacks the domain. RIZ1 gene expression is frequently silenced in human cancers, and the gene is also a common target of frameshift mutation in microsatellite-unstable    cancers. We now report studies of mice with a targeted mutation in the RIZ1 locus. The mutation inactivates RIZ1 but not RIZ2. These RIZ1 mutant mice were viable and fertile but showed a high incidence of diffuse large B-cell lymphomas (DLBL) and    a broad spectrum of unusual tumors. RIZ1 deficiency also accelerated tumorigenesis in p53 heterozygous mutant mice. Finally, several missense mutations of RIZ1 were found in human tumor tissues and cell lines; one of these was particularly common    in human DLBL tumors.  These missense mutations, as well as the previously described frameshift mutation, all mapped to the MTase functional domains. All abolished the capacity of RIZ1 to enhance estrogen receptor activation of transcription.     These data suggest a direct link between tumor formation and the MTase domain of RIZ1 and describe for the first time a tumor susceptibility gene among methyltransferases.</p>

	]]>
</description>

<author>Perkins G. Steele et al.</author>


</item>


<item>
<title> Transgenic and knockout databases. Behavioral profiles of mouse mutants.</title>
<link>http://mouseion.jax.org/stfb2000_2009/282</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/282</guid>
<pubDate>Tue, 08 May 2012 16:15:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetically engineered strains of mice, modified by transgenesis or gene targeting ("knockouts") are being generated at an impressive rate and used, among other areas, as premiere research tools in deciphering the genetic basis of    behavior. As behavioral phenotyping strategies continue to evolve, characterization of these "designer" mice will provide models to evaluate the efficacy of new pharmacological and gene therapy treatments in human hereditary diseases. Reported    behavioral profiles include aberrant social, reproductive, and parental behaviors, learning and memory deficits, feeding disorders, aggression, anxiety-related behaviors, pain/analgesia, and altered responses to antidepressants, antipsychotics,    ethanol, and psychostimulant drugs of abuse. The Induced Mutant Resource (IMR) at The Jackson Laboratory (TJL, Bar Harbor, ME, USA) imports, cryopreserves, develops, maintains, and distributes biomedically important stocks of transgenic and    targeted mutant mice to the research community. Information on neurological/behavioral strains - including behavioral performance, husbandry requirements, strain availability, and genetic typing protocols - is provided through the IMR database    (http://www.jax.org/resources/documents/imr/). A catalog of available strains is readily accessible via the JAX(R) Mice website at http://jaxmice.jax.org/index.shtml. In addition, TJL is now host to TBASE (http://tbase.jax.org/), a comprehensive,    public-domain database with primary emphasis on mouse knockouts. TBASE contains an exhaustive list of knockout-related citations and provides an extensive phenotypic characterization of numerous behavioral mutants that is extracted directly from    the literature. Present efforts to merge the two resources into a novel, schematically enhanced database, provisionally named Transgenic and Targeted Mutation Database (TTMD), will be briefly discussed.</p>

	]]>
</description>

<author>A V. Anagnostopoulos et al.</author>


</item>


<item>
<title> Elizabeth S. Russell 1913-2001.</title>
<link>http://mouseion.jax.org/stfb2000_2009/281</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/281</guid>
<pubDate>Tue, 08 May 2012 16:15:31 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J E. Barker</author>


</item>


<item>
<title> PPAR-gamma dependent and independent effects on macrophage-gene expression in lipid metabolism and inflammation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/280</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/280</guid>
<pubDate>Tue, 08 May 2012 16:15:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is highly expressed in lipid-accumulating macrophages of the coronary artery. In light of this, the wide-spread clinical use of thiazolidinediones (TZDs) in the    treatment of type II diabetes raises concerns about the role of PPAR-gamma in macrophage function and disease progression. To define the role of PPAR-gamma in macrophage biology, we used homologous recombination to create embryonic stem cells    that were homozygous for a null mutation in the PPAR-gamma gene. We demonstrate here that PPAR-gamma is neither essential for nor substantially affects the development of the macrophage lineage both in vitro and in vivo. In contrast, we show it    is an important regulator of the scavenger receptor CD36, which has been genetically linked to lipid accumulation in macrophages. Both 15-deoxy-Delta12,14prostaglandin J2 and thiazolidinediones have anti-inflammatory effects that are independent    of PPAR-gamma. We show that PPAR-gamma is required for positive effects of its ligands in modulating macrophage lipid metabolism, but that inhibitory effects on cytokine production and inflammation may be receptor independent.</p>

	]]>
</description>

<author>A Chawla et al.</author>


</item>


<item>
<title> A PPAR gamma-LXR-ABCA1 pathway in macrophages is involved in cholesterol efflux and atherogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/279</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/279</guid>
<pubDate>Tue, 08 May 2012 16:14:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous work has implicated PPAR gamma in the regulation of CD36 expression and macrophage uptake of oxidized LDL (oxLDL). We provide evidence here that in addition to lipid uptake, PPAR gamma regulates a pathway of cholesterol    efflux. PPAR gamma induces ABCA1 expression and cholesterol removal from macrophages through a transcriptional cascade mediated by the nuclear receptor LXR alpha. Ligand activation of PPAR gamma leads to primary induction of LXR alpha and to    coupled induction of ABCA1. Transplantation of PPAR gamma null bone marrow into LDLR -/- mice results in a significant increase in atherosclerosis, consistent with the hypothesis that regulation of LXR alpha and ABCA1 expression is protective in    vivo. Thus, we propose that PPAR gamma coordinates a complex physiologic response to oxLDL that involves particle uptake, processing, and cholesterol removal through ABCA1.</p>

	]]>
</description>

<author>A Chawla et al.</author>


</item>


<item>
<title> Bootstrapping cluster analysis: assessing the reliability of conclusions from microarray experiments.</title>
<link>http://mouseion.jax.org/stfb2000_2009/278</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/278</guid>
<pubDate>Tue, 08 May 2012 16:14:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>We introduce a general technique for making statistical inference from clustering tools applied to gene expression microarray data. The approach utilizes an analysis of variance model to achieve normalization and estimate    differential expression of genes across multiple conditions.  Statistical inference is based on the application of a randomization technique, bootstrapping. Bootstrapping has previously been used to obtain confidence intervals for estimates of    differential expression for individual genes. Here we apply bootstrapping to assess the stability of results from a cluster analysis. We illustrate the technique with a publicly available data set and draw conclusions about the reliability of    clustering results in light of variation in the data. The bootstrapping procedure relies on experimental replication. We discuss the implications of replication and good design in microarray experiments.</p>

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</description>

<author>M K. Kerr et al.</author>


</item>


<item>
<title> Experimental and computational approaches yield a high-resolution, 1-Mb physical map of the region harboring the mouse t haplotype sterility factor, tcs1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/277</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/277</guid>
<pubDate>Tue, 08 May 2012 16:14:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>A Planchart et al.</author>


</item>


<item>
<title> Variables to predict engraftment of umbilical cord blood into immunodeficient mice: usefulness of the non-obese diabetic--severe combined immunodeficient assay.</title>
<link>http://mouseion.jax.org/stfb2000_2009/276</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/276</guid>
<pubDate>Tue, 08 May 2012 16:13:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Umbilical cord blood is an alternative stem cell source for patients without matched family donors. In this study, we examined several parameters that have not been studied in detail -- radiation dose, cell dose, age of mice, and    maternal and neonatal characteristics of the cord blood donor -- that affect engraftment of cord blood in non-obese diabetic-severe combined immunodeficient (NOD--scid) mice. Engraftment, measured using flow cytometry analyses of human CD45(+)    cells, was highest in 400 cGy-treated mice. Successful engraftment was demonstrated up to 6 months, with a mean engraftment of 31% (range 0--67%) of human cells in recipient bone marrow. Engraftment was skewed to B lymphocytes. The radiation dose    of 350 cGy resulted in superior survival of the murine recipients compared with 400 cGy (P = 0.03). The sex of the NOD--scid recipients had a significant effect on survival (female superior to male, P = 0.01), but not on engraftment. There were    high levels of variability among different cord units and among animals injected with the same cord unit. This variability may limit the clinical usefulness of the NOD--scid mice as hosts for the quantification of human stem cells.</p>

	]]>
</description>

<author>K K. Ballen et al.</author>


</item>


<item>
<title> DelBank: a mouse ES-cell resource for generating deletions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/275</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/275</guid>
<pubDate>Tue, 08 May 2012 16:13:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>N C. Goodwin et al.</author>


</item>


<item>
<title> Ducky mouse phenotype of epilepsy and ataxia is associated with mutations in the Cacna2d2 gene and decreased calcium channel current in cerebellar Purkinje cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/274</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/274</guid>
<pubDate>Tue, 08 May 2012 16:13:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse mutant ducky, a model for absence epilepsy, is characterized by spike-wave seizures and ataxia. The ducky gene was mapped previously to distal mouse chromosome 9. High-resolution genetic and physical mapping has resulted    in the identification of the Cacna2d2 gene encoding the alpha2delta2 voltage-dependent calcium channel subunit. Mutations in Cacna2d2 were found to underlie the ducky phenotype in the original ducky (du) strain and in a newly identified strain    (du(2J)). Both mutations are predicted to result in loss of the full-length alpha2delta2 protein.  Functional analysis shows that the alpha2delta2 subunit increases the maximum conductance of the alpha1A/beta4 channel combination when coexpressed    in vitro in Xenopus oocytes. The Ca(2+) channel current in acutely dissociated du/du cerebellar Purkinje cells was reduced, with no change in single-channel conductance. In contrast, no effect on Ca(2+) channel current was seen in cerebellar    granule cells, results consistent with the high level of expression of the Cacna2d2 gene in Purkinje, but not granule, neurons. Our observations document the first mammalian alpha2delta mutation and complete the association of each of the major    classes of voltage-dependent Ca(2+) channel subunits with a phenotype of ataxia and epilepsy in the mouse.</p>

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</description>

<author>J Barclay et al.</author>


</item>


<item>
<title> Cardiac conduction abnormalities in a mouse model of Lyme borreliosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/273</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/273</guid>
<pubDate>Tue, 08 May 2012 16:12:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Borrelia Burgdorferi (BB) induces cardiac conduction abnormalities in infected humans. Mice models of Lyme disease have been developed, however their electrophysiologic (EP) properties of conduction are unknown.    METHODS: Seventy-six C3H/J mice (BB infected and age- and gender-matched controls) underwent blinded in vivo EP studies. In a first phase of the study, 40 male C3H/J mice were divided into 2 groups: Group (A) mice were infected at age 3 (weeks)    and studied at 5, and Group (B) mice were infected at 9 and studied at 11. In a second phase, 36 female mice were divided into 2 groups: Group (C) mice were infected at 3 weeks and studied at 5, and Group (D) mice were infected at 3 and studied    at 11.  RESULTS: Infected mice of group (A) and (C) had wider QRS complexes (21.0+/-1.6 versus 17.3+/-1.3ms, p< or =0.0001 and 20.3+/-2.1 versus 18.5+/-1.7, p = 0.05, respectively) compared to the healthy controls (HC).  Infected mice of group    (B) and group (D) were similar to the HC. In all groups, the presence of conduction abnormalities correlated very closely with the amount of inflammation on pathology. CONCLUSION: This study describes the first EP mouse model of Lyme carditis.    C3H/J mice exhibit conduction abnormalities that are reversible 8 weeks after inoculation, closely paralleling the resolution of inflammation on pathology. This model can be a valuable tool in the developing and testing of new modalities for the    prevention and treatment of Lyme carditis.</p>

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</description>

<author>S Saba et al.</author>


</item>


<item>
<title> Mouse paracentric inversion In(3)55Rk mutates the urate oxidase gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/272</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/272</guid>
<pubDate>Tue, 08 May 2012 16:12:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>The paracentric inversion In(3)55Rk on mouse Chromosome 3 (Chr 3) was induced by cesium irradiation. Genetic crosses indicate the proximal breakpoint cosegregates with D3Mit324 and D3Mit92; the distal breakpoint cosegregates with    D3Mit127, D3Mit160, and D3Mit200. Giemsa-banded chromosomes show the inversion spans approximately 80% of Chr 3. The proximal breakpoint occurs within band 3A2, not 3B as reported previously; the distal breakpoint occurs within band 3H3. Mice    homozygous for the inversion exhibit nephropathy indicative of uricase deficiency. Southern blot analyses of urate oxidase, Uox, show two RFLPs of genomic mutant DNA: an EcoRI site between exons 4-8 and a BamHI site 3' to exon 6. Mutant cDNA    fails to amplify downstream of base 844 at the 3' end of exon 7. FISH analysis of chromosomes from inversion heterozygotes, using a cosmid clone containing genomic wild-type DNA for Uox exons 2-4, shows that a 5' segment of the mutated Uox allele    on the inverted chromosome has been transposed from the distal breakpoint region to the proximal breakpoint region. Clinical, histopathological, and Northern analyses indicate that our radiation-induced mutation, uox(In), is a putative null.    Copyright 2001 S. Karger AG, Basel</p>

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</description>

<author>S A. Cook et al.</author>


</item>


<item>
<title> Excess cone cell proliferation due to lack of a functional NR2E3 causes retinal dysplasia and degeneration in rd7/rd7 mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/271</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/271</guid>
<pubDate>Tue, 08 May 2012 16:11:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>The rd7 mouse is a model for hereditary retinal degeneration characterized clinically by retinal spotting throughout the fundus and late onset retinal degeneration, and histologically by retinal dysplasia manifesting as folds and    whorls in the photoreceptor layer. This study demonstrates that the rd7 phenotype results from a splicing error created by a genomic deletion of an intron and part of an exon. Hematoxylin/eosin staining of rd7 tissue shows that the whorls in the    outer nuclear layer of the retina do not appear during embryonic development but manifest by postnatal day 12.5 (P12.5). Furthermore, in situ hybridization data indicates that the Nr2e3 message is first present at barely discernable levels at    embryonic day 18.5, becomes abundant by P2.5, and reaches maximal adult levels by P10.5. Results from these experiments indicate that Nr2e3 message is expressed prior to the development of S-cones. This data coincides with studies in humans    showing that mutations in Nr2e3 result in a unique type of retinal degeneration known as enhanced S-cone syndrome, where patients have a 30-fold increase in S-cone sensitivity compared to normal.  Immunohistochemical staining of cone cells    demonstrates that rd7 retinas have an increased number of cone cells compared to wild-type retinas.  Thus, Nr2e3 may function by regulating genes involved in cone cell proliferation, and mutations in this gene lead to retinal dysplasia and    degeneration by disrupting normal photoreceptor cell topography as well as cell-cell interactions.</p>

	]]>
</description>

<author>N B. Haider et al.</author>


</item>


<item>
<title>Book Reviews.</title>
<link>http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/8</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/8</guid>
<pubDate>Tue, 08 May 2012 16:11:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>The Battle Amulet of the North American Indians.</title>
<link>http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/7</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/7</guid>
<pubDate>Tue, 08 May 2012 16:11:23 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>William Thornton Parker</author>


</item>


<item>
<title> Inhibition of autoimmune diabetes in nonobese diabetic mice by transgenic restoration of h2-e mhc class ii expression: additive, but unequal, involvement of multiple apc subtypes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/270</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/270</guid>
<pubDate>Tue, 08 May 2012 16:11:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Transgenic restoration of normally absent H2-E MHC class II molecules on APC dominantly inhibits T cell-mediated autoimmune diabetes (IDDM) in nonobese diabetic (NOD) mice. We analyzed the minimal requirements for transgenic H2-E    expression on APC subtypes (B lymphocytes vs macrophages/dendritic cells (DC)) to inhibit IDDM. This issue was addressed through the use of NOD stocks transgenically expressing high levels of H2-E and/or made genetically deficient in B    lymphocytes in a series of genetic intercross and bone marrow/lymphocyte chimera experiments. Standard (H2-E(null)) NOD B lymphocytes exert a pathogenic function(s) necessary for IDDM. However, IDDM was inhibited in mixed chimeras where H2-E was    solely expressed on all B lymphocytes.  Interestingly, this resistance was abrogated when even a minority of standard NOD H2-E(null) B lymphocytes were also present. In contrast, in NOD chimeras where H2-E expression was solely limited to    approximately half the macrophages/DC, an active immunoregulatory process was induced that inhibited IDDM. Introduction of a disrupted IL-4 gene into the NOD-H2-E transgenic stock demonstrated that induction of this Th2 cytokine does not    represent the IDDM protective immunoregulatory process mediated by H2-E expression. In conclusion, high numbers of multiple subtypes of APC must express H2-E MHC class II molecules to additively inhibit IDDM in NOD mice. This raises a high    threshold for success in future intervention protocols designed to inhibit IDDM by introduction of putatively protective MHC molecules into hemopoietic precursors of APC.</p>

	]]>
</description>

<author>E A. Johnson et al.</author>


</item>


<item>
<title>War Charms and Kindred Amulets.</title>
<link>http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/6</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/6</guid>
<pubDate>Tue, 08 May 2012 16:11:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. Ahrens</author>


</item>


<item>
<title>An Autonomous Ukraine.</title>
<link>http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/5</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/5</guid>
<pubDate>Tue, 08 May 2012 16:11:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>Relativistic effects on interchannel coupling in atomic photoionization: the photoelectron angular distribution of Xe</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/29</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/29</guid>
<pubDate>Tue, 08 May 2012 16:11:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Measurements of the photoelectron angular-distribution asymmetry parameter β for Xe 5s photoionization have been performed in the 80–200 eV photon-energy region. The results show a substantial deviation from the nonrelativistic value of β=2 and provide a clear signature of significant relativistic effects in interchannel coupling.</p>

	]]>
</description>

<author>Oliver Hemmers et al.</author>


</item>


<item>
<title>The Constitution on the Defensive.</title>
<link>http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/4</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/4</guid>
<pubDate>Tue, 08 May 2012 16:11:16 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Homer Hoyt</author>


</item>


<item>
<title>Fads in Philosophy.</title>
<link>http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/3</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/3</guid>
<pubDate>Tue, 08 May 2012 16:11:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Paul Carus</author>


</item>


<item>
<title>Hebrew Education in the Family After the Exile.</title>
<link>http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/2</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/2</guid>
<pubDate>Tue, 08 May 2012 16:11:12 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Fletcher H. Swift</author>


</item>


<item>
<title>Henri Dunant, Founder of the Red Cross.</title>
<link>http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/1</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/ocj/vol1918/iss1/1</guid>
<pubDate>Tue, 08 May 2012 16:11:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Paul Grunberg</author>


</item>


<item>
<title> CD40-mediated activation of T cells accelerates, but is not required for, encephalitogenic potential of myelin basic protein-recognizing T cells in a model of progressive experimental autoimmune encephalomyelitis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/269</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/269</guid>
<pubDate>Tue, 08 May 2012 16:11:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>CD40 ligand-CD40 interactions are important in the development of experimental autoimmune encephalomyelitis (EAE), but it is unclear whether this interaction is critical for de novo recruitment of T cells, entry of T cells into the    central nervous system (CNS), or effector function of T cells in vivo. In this report we define the role of CD40 in a model of progressive EAE that does not depend on epitope spread or recruitment of new myelin-specific T cells into the CNS.    Results show that CD40 is not required for trans-migration of activated T cells through the endothelial blood-brain barrier, and in its absence T cells will both enter the CNS and induce disease. However, interaction with CD40 is critical for    optimal activation and encephalitogenicity of cloned Th1 cells. In its presence, Th1 cells enter the CNS earlier and induce more severe disease. Inclusion of IL-12 during activation of Th1 cells in the absence of CD40 can override the otherwise    suboptimal level of encephalitogenicity observed.  The implication of these findings for therapeutic use of agents designed to block this pathway is discussed.</p>

	]]>
</description>

<author>Leeman S. Abromson et al.</author>


</item>


<item>
<title> Emerging anabolic treatments for osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/268</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/268</guid>
<pubDate>Tue, 08 May 2012 16:10:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Therapy for osteoporosis is principally centered on the use of agents that block bone resorption and supplementation with vitamin D and calcium.  Although these drugs are effective in reducing the risk of subsequent fractures, and    modestly increasing bone density, most patients being treated for osteoporosis still have low bone mass and a greater risk of fracture. Anabolic agents stimulate bone formation, strength, and mass. In addition, there is emerging evidence that    anabolic agents can reduce subsequent fracture risk. The two most promising agents, parathyroid hormone (PTH) and GH/IGF-I, act to increase osteoblast mediated bone formation. A review of the potential usefulness of PTH and GH/IGF-I is    presented.</p>

	]]>
</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title> Apoptosis in ultrasound-produced threshold lesions in the rabbit brain.</title>
<link>http://mouseion.jax.org/stfb2000_2009/267</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/267</guid>
<pubDate>Tue, 08 May 2012 16:10:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Focused ultrasound (US) surgery has been used to induce high temperature elevations in tissue to coagulate the proteins and kill the tissue. The introduction of noninvasive online temperature monitoring has made it possible to    induce well-controlled thermal exposures. In this study, we used magnetic resonance imaging (MRI) thermometry to monitor thermal exposures near the threshold of tissue damage, and then investigated if apoptosis was induced. Rabbit brains were    sonicated with an eight-sector phased array to create a large region of uniform temperature elevation at the end of a 30-s sonication. Histological examination demonstrated that apoptosis was induced in some cells. At 4 h after the sonications,    the apoptotic cells constituted 9 +/- 7% of identifiable cells. By 48 h after the sonications, the number of apoptotic cells had increased up to 17 +/- 9%. The impact of this finding for therapy needs to be explored further.</p>

	]]>
</description>

<author>N Vykhodtseva et al.</author>


</item>


<item>
<title> Primary hyperparathyroidism caused by parathyroid-targeted overexpression of cyclin D1 in transgenic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/266</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/266</guid>
<pubDate>Tue, 08 May 2012 16:09:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The relationship between abnormal cell proliferation and aberrant control of hormonal secretion is a fundamental and poorly understood issue in endocrine cell neoplasia. Transgenic mice with parathyroid-targeted overexpression of    the cyclin D1 oncogene, modeling a gene rearrangement found in human tumors, were created to determine whether a primary defect in this cell-cycle regulator can cause an abnormal relationship between serum calcium and parathyroid hormone    response, as is typical of human primary hyperparathyroidism. We also sought to develop an animal model of hyperparathyroidism and to examine directly cyclin D1's role in parathyroid tumorigenesis. Parathyroid hormone gene regulatory    region--cyclin D1 (PTH--cyclin D1) mice not only developed abnormal parathyroid cell proliferation, but also developed chronic biochemical hyperparathyroidism with characteristic abnormalities in bone and, notably, a shift in the relationship    between serum calcium and PTH. Thus, this animal model of human primary hyperparathyroidism provides direct experimental evidence that overexpression of the cyclin D1 oncogene can drive excessive parathyroid cell proliferation and that this    proliferative defect need not occur solely as a downstream consequence of a defect in parathyroid hormone secretory control by serum calcium, as had been hypothesized. Instead, primary deregulation of cell-growth pathways can cause both the    hypercellularity and abnormal control of hormonal secretion that are almost inevitably linked together in this common disorder.</p>

	]]>
</description>

<author>Y Imanishi et al.</author>


</item>


<item>
<title> Reduced incidence of thrombosis in mice with hereditary spherocytosis following neonatal treatment with normal hematopoietic cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/265</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/265</guid>
<pubDate>Tue, 08 May 2012 16:09:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Thrombosis is a life-threatening complication of hemolytic anemia in humans. Cardiac thrombi are present in all adult alpha-spectrin-deficient (sph/sph) mice with severe hereditary spherocytosis, providing a model for events    preceding thrombosis. The current study evaluated (1) the timing of thrombosis initiation and (2) the effect of postnatal transplantation of normal cells on life span and thrombotic incidence in adult mice. Thrombi are detected histologically    following necropsy in untreated sph/sph mice of various ages and are not observed until 6 weeks of age. Thrombotic incidence increases from 50% at 6 to 7 weeks of age to 100% at 9 weeks of age. As a potential therapy, nonablated sph/sph neonates    were transfused with either genetically marked normal peripheral blood (PB), bone marrow (BM), or both and assessed for donor cells and thrombosis. A single transfusion of PB, with or without BM, significantly increases the percentage of sph/sph    mice that survive to weaning (4 weeks of age).  Replacement in all sph/sph recipients is limited to red blood cells (RBCs). RBCs derived from donor PB are lost within 5 weeks. PB plus BM prolongs high-level donor PB cell production better than BM    alone.  Thrombotic incidence is significantly reduced in all sph/sph mice treated with PB, BM, or both. Hence, the presence of normal blood cells in the peripheral circulation of neonatal and adult sph/sph mice rescues the former and abrogates    the development of thrombosis in the latter. (Blood.  2001;97:3972-3975)</p>

	]]>
</description>

<author>N J. Wandersee et al.</author>


</item>


<item>
<title> Neural tube defects and neuroepithelial cell death in Tulp3 knockout mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/264</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/264</guid>
<pubDate>Tue, 08 May 2012 16:08:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The tubby-like protein 3 (Tulp3) gene has been identified as a member of a small novel gene family which is primarily neuronally expressed. Mutations in two of the family members, tub and tulp1, have been shown to cause    neurosensory disorders. To determine the in vivo function of Tulp3, we have generated a germline mutation in the mouse Tulp3 gene by homologous recombination. Embryos homozygous for the Tulp3 mutant allele exhibit failure of neural tube closure,    and die by embryonic day 14.5. Failure of cranial neural tube closure coincided with increased neuroepithelial apoptosis specifically in the hindbrain and the caudal neural tube. In addition, the number of betaIII-tubulin positive cells is    significantly decreased in the hindbrain of Tulp3(-/-) embryos. These results suggest that disruption of the Tulp3 gene affects the development of a neuronal cell population. Interestingly, some Tulp3 heterozygotes also manifest embryonic    lethality with neuroepithelial cell death. Our results demonstrate that the Tulp3 gene is essential for embryonic development in mice.</p>

	]]>
</description>

<author>A Ikeda et al.</author>


</item>


<item>
<title> Animal models for male pattern (androgenetic) alopecia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/263</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/263</guid>
<pubDate>Tue, 08 May 2012 16:08:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>The stump-tailed macaque (Macaca arctoides) appears to be a suitable biological model for human androgenetic alopecia. The expense, danger, and low availability compromise its value but macaques currently remain the model of    choice. Rodent models, both testosterone induced alopecia and various xenograft approaches, show promise for elucidating fundamental information on normal and abnormal hair growth as well as serving as models to develop new therapies to treat    hair loss.</p>

	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title> Morphology of hair in normal and mutant laboratory mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/262</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/262</guid>
<pubDate>Tue, 08 May 2012 16:07:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inbred laboratory mice are mammals and therefore are haired. Mice develop many of the same diseases as humans and have become the premier in vivo model for studying biology, pathology, genetics, and molecular mechanisms.  Mice are    useful tools to study hair biology. Examples of characterized mutant mice with abnormal pilosebaceous unit phenotypes are presented to illustrate the value of these animals as models to help understand human diseases of the skin and    hair.</p>

	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title> Regulation of prostaglandin-endoperoxide synthase 2 messenger ribonucleic acid expression in mouse granulosa cells during ovulation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/261</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/261</guid>
<pubDate>Tue, 08 May 2012 16:07:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Normal ovulation in mice requires PG-endoperoxide synthase 2 (cyclooxygenase-2; COX-2) expression. This study examined the role of the oocyte and other factors in regulating steady state levels of COX-2 messenger RNA (mRNA) in    granulosa cells. Multiphasic changes in the expression pattern of COX-2 mRNA were found, with peaks of expression 4 and 12 h after hCG treatment. Changes in relative expression levels in cumulus cells and mural granulosa cells occurred over time,    with similar mRNA levels at 4 h, but higher levels in cumulus cells compared with mural granulosa cells at 8 and 12 h post-hCG. In cultured mural granulosa cells, LH, FSH, and oocytes promoted COX-2 mRNA expression concurrent with the first    expression peak in vivo. At the same time, FSH, but not LH, treatment of cultured cumulus-oocyte complexes (COC) promoted COX-2 mRNA expression in cumulus cells. This response of cumulus cells to FSH treatment was largely dependent on the    presence of either fully grown germinal vesicle stage or maturing oocytes, but not growing oocytes. At 8 h, COX-2 mRNA expression in FSH-stimulated COC was lower than at 4 h; however, oocyte coculture promoted COX-2 mRNA expression in cumulus    cells.  No second peak in expression occurred in cultured COC. However, coculture of COC with follicle walls promoted COX-2 mRNA expression in Cumulus cells 12 h post-hCG; an effect augmented by oocytes. Therefore, the oocyte resident within    ovulatory follicles produces a factor(s) that promotes expression of COX-2 mRNA by cumulus cells and possibly by mural granulosa cells. Thus, the oocyte probably plays an important role in promoting ovulation. However, the multiphasic changes in    the pattern of COX-2 expression appear orchestrated by non-oocyte-derived factors.</p>

	]]>
</description>

<author>I M. Joyce et al.</author>


</item>


<item>
<title> Evidence that protein kinase C (PKC) participates in the meiosis I to meiosis II transition in mouse oocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/260</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/260</guid>
<pubDate>Tue, 08 May 2012 16:07:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Oocytes from LTXBO mice exhibit a delayed entry into anaphase I and frequently enter interphase after the first meiotic division. This unique oocyte model was used to test the hypothesis that protein kinase C (PKC) may regulate the    meiosis I-to-meiosis II transition. PKC activity was detected in LTXBO oocytes at prophase I and increased with meiotic maturation, with the highest (P < 0.05) activity observed at late metaphase I (MI). Treatment of late MI-stage oocytes with    the PKC inhibitor, bisindolylmaleimide I (BIM), transiently reduced (P < 0.05) M-phase-promoting factor (MPF) activity and promoted (P X 0.05) progression to metaphase II (MII), while mitogen-activated protein kinase (MAPK) activity remained    elevated during the MI-to-MII transition.  Confocal microscopy analysis of LTXBO oocytes during this transition showed PKC-delta associated with the meiotic spindle and then with the chromosomes at MII. Inhibition of PKC activity also prevented    untimely entry into interphase, but only when PKC activity was reduced in oocytes before the progression to MII and thus indicates that the transition into interphase is directly associated with the delayed triggering of anaphase I. Moreover, the    defect(s) that initiate activation occur upstream of MAPK, as suppression of PKC activity failed to prevent activation by Mos(tm1Ev)/ Mos(tm1Ev) LTXBO oocytes expressing no detectable MAPK activity. In summary, PKC participates in the regulatory    mechanisms that delay entry into anaphase I in LTXBO oocytes, and the disruption promotes untimely entry into interphase. Thus, loss of regulatory control over PKC activity during oocyte maturation disrupts the critical MI-to-MII transition,    leading to a precocious exit from meiosis. Copyright 2001 Academic Press.</p>

	]]>
</description>

<author>M M. Viveiros et al.</author>


</item>


<item>
<title> B Cells are Selectively Associated with Thymic Cortical but not Medullary Pathology in NZB Mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/259</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/259</guid>
<pubDate>Tue, 08 May 2012 16:07:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abnormal expansion of autoantibody-synthesizing B cells and self-reactive T cells, which most likely escape negative selection within the thymus, have both been characterized and reasoned to play a role in the pathogenesis of    autoimmunity in NZB mice. Support for this thesis has been our observation that NZB mice have severe cortical and medullary thymic microarchitectural defects. As a means to dissect the roles of T and B cells in the induction of such    abnormalities, B cell-deficient NZB mice were bred by backcrossing the Igh6(null)allele on to the NZB background (NZB-&mgr;MT mice). Such mice showed undetectable levels of autoantibodies. NZB-&mgr;MT mice, as compared to wild-type NZB mice, had    lower absolute numbers of CD4(+)T cells. Furthermore, thymic abnormalities in NZB-&mgr;MT mice were restricted to the medulla. These data suggest that, while B cells may play a role in thymic cortical abnormalities, the medullary abnormalities    are induced by other mechanisms. Copyright 2001 Academic Press.</p>

	]]>
</description>

<author>N Taguchi et al.</author>


</item>


<item>
<title> Increased Expression of mXBP-1 (TREB-5) in Thymic B Cells in New Zealand Mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/258</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/258</guid>
<pubDate>Tue, 08 May 2012 16:06:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>New Zealand Black mice as well as several other murine models of murine lupus are well known for premature degeneration of thymus and development of autoimmunity. To focus on molecular events unique to murine lupus, we performed    differential display using arbitrary primer pairs to distinguish NZB versus BALB/c thymus at 5 weeks of age. Following an extensive analysis of DNA bands that were either consistently up or downregulated and from studies of expression pattern of    thymic genes by in situ nucleic acid hybridization, we focused on one clone that was consistently differentially expressed between NZB and BALB/c thymus. This clone was isolated, sequenced, and identified as the murine homologue of the human X    box binding protein (hXBP-1), also known as TREB 5. mXBP-1 was found to be consistently upregulated in B cells in the thymic cortex of NZB and (NZBxNZW)F1, but not BALB/c, C3H/HeJ or C57BL/6 mice. In addition, it was dramatically elevated in MRL/    lpr but not MRL/++ mice; similarly, it was increased in BXSB/ Yaa male but not BXSB female thymic cortex. Of particular interest was an absence of mXBP-1 expression in the thymus of NZB/ Bln- Igh6(null)homozygotes. mXBP-1 has several putative    functions, including the regulation of MHC class II expression and by virtue of its ability to recognize CRE-like elements shown to be involved in HTLV-1 transcription. Copyright 2001 Academic Press.</p>

	]]>
</description>

<author>N Taguchi et al.</author>


</item>


<item>
<title> Quantitative trait loci for femoral and lumbar vertebral bone mineral density in C57BL/6J and C3H/HeJ inbred strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/257</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/257</guid>
<pubDate>Tue, 08 May 2012 16:06:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Significant differences in vertebral (9%) and femoral (50%) adult bone mineral density (BMD) between the C57BL/6J (B6) and C3H/HeJ (C3H) inbred strains of mice have been subjected to genetic analyses for quantitative trait loci    (QTL). Nine hundred eighty-six B6C3F2 females were analyzed to gain insight into the number of genes that regulate peak BMD and their locations. Femurs and lumbar vertebrae were isolated from 4-month-old B6C3F2 females at skeletal maturity and    then BMD was determined by peripheral quantitative computed tomography (pQCT). Estimates of BMD heritability were 83% for femurs and 72% for vertebrae. Genomic DNA from F2 progeny was screened for 107 polymerase chain reaction (PCR)-based markers    discriminating B6 and C3H alleles on all 19 autosomes. The regression analyses of markers on BMD revealed ten chromosomes (1, 2, 4, 6, 11, 12, 13, 14, 16, and 18) carrying QTLs for femurs and seven chromosomes (1, 4, 7, 9, 11, 14, and 18)    carrying QTLs for vertebrae, each with log10 of the odds ratio (LOD) scores of 2.8 or better. The QTLs on chromosomes (Chrs) 2, 6, 12, 13, and 16 were unique to femurs, whereas the QTLs on Chrs 7 and 9 were unique to vertebrae. When the two bone    sites had a QTL on the same chromosome, the same marker had the highest, although different, LOD score. A pairwise comparison by analysis of variance (ANOVA) did not reveal significant gene x gene interactions between QTLs for either bone site.    BMD variance accounted for by individual QTLs ranged from 1% to 10%. Collectively, the BMD QTLs for femurs accounted for 35.1% and for vertebrae accounted for 23.7 % of the F2 population variances in these bones. When mice were homozygous c3/c3    in the QTL region, 8 of the 10 QTLs increased, while the remaining two QTLs on Chrs 6 and 12 decreased, femoral BMD. Similarly, when mice were homozygous c3/c3 in the QTL region for the vertebrae, five of the seven QTLs increased, while two QTLs    on Chrs 7 and 9 decreased, BMD. These findings show the genetic complexity of BMD with multiple genes participating in its regulation.  Although 5 of the 12 QTLs are considered to be skeleton-wide loci and commonly affect both femurs and    vertebrae, each of the bone sites also exhibited unique QTLs. Thus, the BMD phenotype can be Partitioned into its genetic components and the effects of these loci on normal bone biology can be determined. Importantly, the BMD QTLs that we have    identified are in regions of the mouse genome that have known human homology, and the QTLs will become useful experimental tools for mechanistic and therapeutic analyses of bone regulatory genes.</p>

	]]>
</description>

<author>W G. Beamer et al.</author>


</item>


<item>
<title> Changing patterns of cell surface mono (ADP-ribosyl) transferase antigen ART2.2 on resting versus cytopathically-activated T cells in NOD/Lt mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/256</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/256</guid>
<pubDate>Tue, 08 May 2012 16:06:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>AIMS/HYPOTHESIS: ART2.2 is a mouse T-cell surface ectoenzyme [mono (ADP-ribosyl) transferase] shed upon strong activation. We analysed temporal changes in ART2.2 expression in unmanipulated and cyclophosphamide-treated NOD/Lt mice    compared with diabetes-resistant control strains. We used NAD, the ART2.2 substrate, to test whether ART-mediated ADP-ribosylation could retard diabetogenic activation of islet-reactive T cells in vitro. METHODS: ART2.2 and CD38, another    NAD-utilizing enzyme, were measured by flow cytometry. ADP-ribosylation from ethano-NAD was followed by flow cytometry using a reagent specific for etheno-ADP ribose. RESULTS: Although mature NOD CD4 + and C D8 + T cells expressed ART2.2, this    expression was delayed in young NOD mice when compared with control strains. This ontological delay at 3 weeks of age correlated with an early burst of CD25 expression unique to NOD splenic T cells. This pattern was reproduced in    cyclophosphamide-accelerated diabetes in young NOD/Lt males, wherein a retarded repopulation of ART2.2 T cells in spleen and islets correlated with development of heavy insulitis and diabetes. NAD inhibited anti-CD3 induced activation of splenic    T cells in vitro and also retarded killing of beta-cell targets by NOD islet-reactive CD8 effectors in vitro at concentrations equal to or greater than 1 micromol/l. Evidence suggested that CD38 on B lymphocytes competes with ART2.2 for substrate    needed by B lymphocytes for ADP ribosylation. CONCLUSIONS: ART2.2 on T cells may not simply mark the resting state, but could also contribute to it via ADP-ribosylation.</p>

	]]>
</description>

<author>V Ablamunits et al.</author>


</item>


<item>
<title> Analysis of glomerulosclerosis and atherosclerosis in lecithin cholesterol acyltransferase-deficient mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/255</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/255</guid>
<pubDate>Tue, 08 May 2012 16:05:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>To evaluate the biochemical and molecular mechanisms leading to glomerulosclerosis and the variable development of atherosclerosis in patients with familial lecithin cholesterol acyl transferase (LCAT) deficiency, we generated LCAT    knockout (KO) mice and cross-bred them with apolipoprotein (apo) E KO, low density lipoprotein receptor (LDLr) KO, and cholesteryl ester transfer protein transgenic mice. LCAT-KO mice had normochromic normocytic anemia with increased reticulocyte    and target cell counts as well as decreased red blood cell osmotic fragility. A subset of LCAT-KO mice accumulated lipoprotein X and developed proteinuria and glomerulosclerosis characterized by mesangial cell proliferation, sclerosis, lipid    accumulation, and deposition of electron dense material throughout the glomeruli. LCAT deficiency reduced the plasma high density lipoprotein (HDL) cholesterol (-70 to -94%) and non-HDL cholesterol (-48 to -85%) levels in control, apoE-KO,    LDLr-KO, and cholesteryl ester transfer protein-Tg mice. Transcriptome and Western blot analysis demonstrated up-regulation of hepatic LDLr and apoE expression in LCAT-KO mice. Despite decreased HDL, aortic atherosclerosis was significantly    reduced (-35% to -99%) in all mouse models with LCAT deficiency. Our studies indicate (i) that the plasma levels of apoB containing lipoproteins rather than HDL may determine the atherogenic risk of patients with hypoalphalipoproteinemia due to    LCAT deficiency and (ii) a potential etiological role for lipoproteins X in the development of glomerulosclerosis in LCAT deficiency. The availability of LCAT-KO mice characterized by lipid, hematologic, and renal abnormalities similar to    familial LCAT deficiency patients will permit future evaluation of LCAT gene transfer as a possible treatment for glomerulosclerosis in LCAT-deficient states.</p>

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</description>

<author>G Lambert et al.</author>


</item>


<item>
<title> A new spectrin, beta IV, has a major truncated isoform that associates with promyelocytic leukemia protein nuclear bodies and the nuclear matrix.</title>
<link>http://mouseion.jax.org/stfb2000_2009/254</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/254</guid>
<pubDate>Tue, 08 May 2012 16:05:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>We isolated cDNAs that encode a 77-kDa peptide similar to repeats 10-16 of beta-spectrins. Its gene localizes to human chromosome 19q13.13-q13.2 and mouse chromosome 7, at 7.5 centimorgans. A 289-kDa isoform, similar to full-length    beta-spectrins, was partially assembled from sequences in the human genomic DNA data base and completely cloned and sequenced. RNA transcripts are seen predominantly in the brain, and Western analysis shows a major peptide that migrates as a    72-kDa band. This new gene, spectrin betaIV, thus encodes a full-length minor isoform (SpbetaIVSigma1) and a truncated major isoform (SpbetaIVSigma5). Immunostaining of cells shows a micropunctate pattern in the cytoplasm and nucleus. In    mesenchymal stem cells, the staining concentrates at nuclear dots that stain positively for the promyelocytic leukemia protein (PML). Expression of SpbetaIVSigma5 fused to green fluorescence protein in cells produces nuclear dots that include all    PML bodies, which double in number in transfected cells. Deletion analysis shows that partial repeats 10 and 16 of SpbetaIVSigma5 are necessary for nuclear dot formation. Immunostaining of whole-mount nuclear matrices reveals diffuse positivity    with accentuation at PML bodies. Spectrin betaIV is the first beta-spectrin associated with a subnuclear structure and may be part of a nuclear scaffold to which gene regulatory machinery binds.</p>

	]]>
</description>

<author>W T. Tse et al.</author>


</item>


<item>
<title> Cytomegalovirus infection increases development of atherosclerosis in Apolipoprotein-E knockout mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/253</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/253</guid>
<pubDate>Tue, 08 May 2012 16:05:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cytomegalovirus (CMV) infection has been associated with coronary artery disease, but it is unknown whether the virus can causally contribute to atherogenesis. To determine whether the virus has this capacity, we infected an    atherosclerotic-prone mouse strain (C57BL/6J apoE-/-) with murine CMV. At 14 days of age, 30 mice received CMV (30000 pfu) ip and 30 received virus free media. At 13 and 16 weeks atherosclerotic lesion size was measured from aortic sinus    cross-sections. Infection did not alter plasma levels of cholesterol, triglycerides, and high density lipoprotein (HDL); however, 4 weeks after infection IFNgamma levels were elevated (infection vs control: 156+/-49 vs 50+/-22 pg/ml, P=0.04). No    differences in lesion size were present at 13 weeks post infection. However, by 16 weeks mean aortic sinus lesion area (mm(2)x10(3)+/-SEM; N=75) in the CMV-infected mice was significantly greater than in uninfected mice (74+/-6 vs 57+/-6;    P=0.04). CMV caused the greatest increase (34%) in lesion size in females (103+/-9 vs 77+/-10; P=0.05; N=35). These results provide additional evidence implicating CMV as a causal agent of atherosclerosis, at least in an animal    model.</p>

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</description>

<author>E Hsich et al.</author>


</item>


<item>
<title> Mapping of microsatellite loci and association of aorta atherosclerosis with LG VI markers in the rabbit.</title>
<link>http://mouseion.jax.org/stfb2000_2009/252</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/252</guid>
<pubDate>Tue, 08 May 2012 16:05:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Twenty-three rabbit microsatellites were extracted from the EMBL nucleotide database. Nine of these markers, together with nine earlier published microsatellite markers, were found to be polymorphic between the AX/JU and IIIVO/JU    inbred strains. By using an F(2) intercross we could integrate five markers into the rabbit linkage map. One anonymous microsatellite marker could be assigned to chromosome 1, and one microsatellite marker, located within the metallothionein-1    gene, could be added to linkage group VI (LG VI). Three microsatellite markers (one anonymous, one located within the PMP2 gene, and one located within the FABP6 gene) constitute a new linkage group (LG XI). We also measured the degree of dietary    cholesterol-induced aorta atherosclerosis in the F(2) animals. A significant cosegregation was found between the degree of aorta atherosclerosis and the allelic variation of the biochemical marker Est-2 on LG VI in male rabbits. This association    was not found in female rabbits.</p>

	]]>
</description>

<author>R Korstanje et al.</author>


</item>


<item>
<title> Abnormal dispersion of a purkinje cell subset in the mouse mutant cerebellar deficient folia (cdf).</title>
<link>http://mouseion.jax.org/stfb2000_2009/251</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/251</guid>
<pubDate>Tue, 08 May 2012 16:05:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Purkinje cells of different molecular phenotypes subdivide the cortex of the cerebellum both rostrocaudally into parasagittal bands and mediolaterally into transverse zones. Superimposed on the Purkinje cell compartmentation, the    cerebellar cortex is pleated into a reproducible array of lobes and lobules. During cerebellar development, Purkinje cell bands are formed through the rostrocaudal dispersal of embryonic clusters, triggered primarily by a Reelin-dependent    signaling pathway. In the naturally occurring mouse mutant cerebellar deficient folia (cdf), there is a failure of Purkinje cell dispersion that results in widespread Purkinje cell ectopia in the adult. The ectopia is restricted primarily to that    subset of Purkinje cells that does not express zebrin II/aldolase C and that forms ectopic clusters in among the cerebellar nuclei. Most Purkinje cells that express zebrin II are located normally in a monolayer.  Thus, the cerebellum of cdf    mutants has a failure of Purkinje cell dispersion that is confined primarily to a zebrin II-negative (zebrin II(-)) subpopulation. Despite the Purkinje cell ectopia, the parasagittal band organization of the cerebellum is still clear. The    shortening of the cortex is distributed evenly over all lobules, with the result that transverse expression boundaries are relocated with respect to the lobules and fissures. The number of Purkinje cells in the cdf/cdf cerebellum is similar to    the number in littermate controls. Therefore, it appears that the lesion in cdf results in the failure of a zebrin II(-) Purkinje cell subset to disperse either due to a cell intrinsic defect or due to an abnormal interaction between the Purkinje    cells and either granule cells or afferent inputs.</p>

	]]>
</description>

<author>E Beierbach et al.</author>


</item>


<item>
<title> Genetic analysis of a new mouse model for non-insulin-dependent diabetes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/250</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/250</guid>
<pubDate>Tue, 08 May 2012 16:04:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The TallyHo (TH) mouse strain is a newly established model for non-insulin-dependent diabetes mellitus (NIDDM). TH mice show obesity, hyperinsulinemia, hyperlipidemia, and male-limited hyperglycemia. A genetic dissection of the    diabetes syndrome has been carried out using male backcross 1 progeny obtained from crosses between (C57BL/6J x TH)F1 and TH mice or (CAST/Ei x TH)F1 and TH mice. A genome-wide scan reveals three quantitative trait loci (QTLs), Tanidd1-3    (TH-associated NIDDM) linked to hyperglycemia. The major QTL (common in both crosses), Tanidd1, maps to chromosome (Chr) 19. Additionally, gene-gene interactions contributing to hyperglycemia have been observed between Tanidd1 and a locus on Chr    18 as well as between Tanidd2 and a locus on Chr 16. The overt hyperglycemia in TH mice is, therefore, likely due to a mutation in a major diabetes susceptibility locus on Chr 19, which interacts with additional genes to lead to an observable    phenotype. Copyright 2001 Academic Press.</p>

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</description>

<author>J H. Kim et al.</author>


</item>


<item>
<title> Electroconvulsive thresholds of inbred mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/249</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/249</guid>
<pubDate>Tue, 08 May 2012 16:04:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>The electroconvulsive threshold (ECT) test is used commonly in the screening of anti-epileptic drugs in rodent models, but little is known about its genetic or mechanistic basis. Thresholds for minimal clonic, maximal tonic, or    psychomotor (partial) seizures were determined in 16 different inbred mouse strains in two different laboratories. A wide range of thresholds was observed, suggesting that a variety of neuroexcitability alleles exist in inbred strains. Although    there was generally good cross-strain correlation between the three seizure types, several outlier strains were detected, showing that genetically encoded differences can affect the ability of a particular seizure type to spread through the    brain. Furthermore, the relative seizure susceptibility of a strain was comparable between the two laboratories, suggesting that despite different test sites, instrumentation, and personnel, the ECT assay is portable and that common inbred    strains can often be relied upon as calibration standards. Last, the ECT paradigm was also sensitive enough to detect single locus differences, laying the groundwork for mutation screens for new neuroexcitability models. Copyright 2001 Academic    Press.</p>

	]]>
</description>

<author>W N. Frankel et al.</author>


</item>


<item>
<title> Fine mapping of Ath6, a quantitative trait locus for atherosclerosis in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/248</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/248</guid>
<pubDate>Tue, 08 May 2012 16:03:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ath6 is a novel quantitative trait locus associated with differences in susceptibility to atherosclerosis between C57BL/6J (B6) and C57BLKS/J (BKS) inbred mouse strains. Combining data from an intercross and a backcross (1593    meioses) between mice from B6 and BKS strains and from The Jackson Laboratory interspecific backcross panels, (C57BL/6J x Mus spretus) F1 x C57BL/6J and (C57BL/6J x SPRET/Ei) F1 x SPRET/Ei, we constructed a consensus genetic map and narrowed Ath6    to a 1.07 +/- 0.26 cM interval between the anonymous DNA marker D12Pgn4 and the gene Nmyc1.  This region is near the proximal end of murine Chromosome (Chr) 12, which is homologous to the human chromosomal region 2p24-p25. Marker order in the    Ath6 region was concordant among the two crosses and The Jackson Laboratory interspecific backcross panels. This high resolution map rules out candidate genes encoding apolipoprotein B, syndecan 1, and Adam17. The two Ath6 crosses have a combined    potential resolution of 0.06 cM.</p>

	]]>
</description>

<author>M K. Purcell et al.</author>


</item>


<item>
<title> Naturally variant autosomal and sex-linked loci determine the severity of iron overload in beta 2-microglobulin-deficient mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/247</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/247</guid>
<pubDate>Tue, 08 May 2012 16:03:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hereditary hemochromatosis (HH) is a common chronic human genetic disorder whose hallmark is systemic iron overload. Homozygosity for a mutation in the MHC class I heavy chain paralogue gene HFE has been found to be a primary cause    of HH. However, many individuals homozygous for the defective allele of HFE do not develop iron overload, raising the possibility that genetic variation in modifier loci contributes to the HH phenotype. Mice deficient in the product of the    beta(2)-microglobulin (beta(2)M) class I light chain fail to express HFE and other MHC class I family proteins, and they have been found to manifest many characteristics of the HH phenotype. To determine whether natural genetic variation plays a    role in controlling iron overload, we performed classical genetic analysis of the iron-loading phenotype in beta(2)M-deficient mice in the context of different genetic backgrounds. Strain background was found to be a major determinant in iron    loading. Sex played a role that was less than that of strain background but still significant. Resistance and susceptibility to iron overload segregated as complex genetic traits in F(1) and back-cross progeny. These results suggest the existence    of naturally variant autosomal and Y chromosome-linked modifier loci that, in the context of mice genetically predisposed by virtue of a beta(2)M deficiency, can profoundly influence the severity of iron loading. These results thus provide a    genetic explanation for some of the variability of the HH phenotype.</p>

	]]>
</description>

<author>T J. Sproule et al.</author>


</item>


<item>
<title> Comparison of permeating and nonpermeating cryoprotectants for mouse sperm cryopreservation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/246</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/246</guid>
<pubDate>Tue, 08 May 2012 16:03:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mouse sperm has proven to be more difficult to cryopreserve than sperm of other mammalian species. Published reports show that only three cryoprotectant agents (CPAs), alone or combined, have been studied: glycerol and dimethyl    sulfoxide (DMSO), as permeating agents, and raffinose, as a nonpermeating agent. To date, the most consistent results for mouse sperm cryopreservation have been achieved by use of raffinose/skim milk as cryoprotectant with rapid cooling at 20    degrees C per minute. In this study, we compared the cryoprotection provided by permeating (glycerol, formamide, propanediol, DMSO, adonitol) or nonpermeating (lactose, raffinose, sucrose, trehalose, d-mannitol) compounds for freezing mouse    sperm. Different solutions were made using 3% skim milk solution as the buffer or extender in which all different cryoprotectant agents were dissolved at a concentration of 0.3 M, with a final osmolality of approx. 400 mOsm. Sperm samples from    CB6F1 (hybrid) and C57BL/6J (inbred) mice collected directly into each CPA were frozen/thawed under identical conditions. After thawing and CPA elimination (centrifugation) raffinose (59%), trehalose (61%), and sucrose (61%) sustained the best    motility (P = < 0.1) of the nonpermeating agents, whereas the best of the permeating agents was DMSO (42%). Membrane integrity was analyzed and showed that the simple exposure (prefreeze) to sugars was less harmful than the exposure to glycols.    Coincidentally, sperm frozen in trehalose (41%), raffinose (40.5%), and sucrose (37.5%) were the samples less injured among all different postthawed CPA tested.  The in vitro fertilization results demonstrated that hybrid mouse spermatozoa frozen    with sugars (lactose 80%, raffinose 80%, trehalose 79% of two-cell embryos production) were more fertile than those frozen with glycols (glycerol 11%). Copyright 2001 Academic Press.</p>

	]]>
</description>

<author>J M. Sztein et al.</author>


</item>


<item>
<title> Intercellular communication via connexin43 gap junctions is required for ovarian folliculogenesis in the mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/245</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/245</guid>
<pubDate>Tue, 08 May 2012 16:02:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ovarian follicle in mammals is a functional syncytium, with the oocyte being coupled with the surrounding cumulus granulosa cells, and the cumulus cells being coupled with each other and with the mural granulosa cells, via gap    junctions. The gap junctions coupling granulosa cells in mature follicles contain several different connexins (gap junction channel proteins), including connexins 32, 43, and 45. Connexin43 immunoreactivity can be detected from the onset of    folliculogenesis just after birth and persists through ovulation. In order to assess the importance of connexin43 gap junctions for postnatal folliculogenesis, we grafted ovaries from late gestation mouse fetuses or newborn pups lacking    connexin43 (Gja1(-)/Gja1(-)) into the kidney capsules of adult females and allowed them to develop for up to 3 weeks (this was necessitated by the neonatal lethality caused by the mutation). By the end of the graft period, tertiary (antral)    follicles had developed in grafted normal (wild-type or heterozygote) ovaries. Most follicles in Gja1(-)/Gja1(-) ovaries, however, failed to become multilaminar, with the severity of the effect depending on strain background. Dye transfer    experiments indicated that intercellular coupling between granulosa cells is reduced, but not abolished, in the absence of connexin43, consistent with the presence of additional connexins. These results suggest that coupling between granulosa    cells mediated specifically by connexin43 channels is required for continued follicular growth. Measurements of oocyte diameters revealed that oocyte growth in mutant follicles is retarded, but not arrested, despite the arrest of    folliculogenesis. The mutant follicles are morphologically abnormal: the zona pellucida is poorly developed, the cytoplasm of both granulosa cells and oocytes is vacuolated, and cortical granules are absent from the oocytes. Correspondingly, the    mutant oocytes obtained from 3-week grafts failed to undergo meiotic maturation and could not be fertilized, although half of the wild-type oocytes from 3-week grafted ovaries could be fertilized. We conclude that connexin43-containing gap    junction channels are required for expansion of the granulosa cell population during the early stages of follicular development and that failure of the granulosa cell layers to develop properly has severe consequences for the oocyte. Copyright    2001 Academic Press.</p>

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</description>

<author>C L. Ackert et al.</author>


</item>


<item>
<title> Cutting edge: systemic inhibition of angiogenesis underlies resistance to tumors during acute toxoplasmosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/244</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/244</guid>
<pubDate>Tue, 08 May 2012 16:02:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ability of various infections to suppress neoplastic growth has been well documented. This phenomenon has been traditionally attributed to infection-induced concomitant, cell-mediated antitumor immunity. We found that infection    with Toxoplasma gondii effectively blocked neoplastic growth of a nonimmunogenic B16.F10 melanoma. Moreover, this effect was independent of cytotoxic T or NK cells, production of NO by macrophages, or the function of the cytokines IL-12 and    TNF-alpha. These findings suggested that antitumor cytotoxicity was not the primary mechanism of resistance. However, infection was accompanied by strong, systemic suppression of angiogenesis, both in a model system and inside the nascent tumor.    This suppression resulted in severe hypoxia and avascular necrosis that are incompatible with progressive neoplastic growth. Our results identify the suppression of tumor neovascularization as a novel mechanism critical for infection-induced    resistance to tumors.</p>

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</description>

<author>C A. Hunter et al.</author>


</item>


<item>
<title> Notch signaling during vascular development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/243</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/243</guid>
<pubDate>Tue, 08 May 2012 16:02:01 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T Gridley</author>


</item>


<item>
<title> Mutations of the mouse Twist and sy (fibrillin 2) genes induced by chemical mutagenesis of ES cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/242</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/242</guid>
<pubDate>Tue, 08 May 2012 16:01:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>A prior phenotype-based screen of mice derived from ethylmethanesulfonate-mutagenized embryonic stem cells yielded two mouse limb defect mutants. Animals heterozygous for the polydactyly ems (Pde) mutation display preaxial    polydactyly of the hindlimbs, and homozygous syndactyly ems (sne) animals are characterized by a fusion of the middle digits of their hindlimbs and sometimes forelimbs. We now report that Pde is a new allele of the basic helix-loop-helix protein    gene Twist.  Sequencing the full-length cDNA and several hundred basepairs of genomic DNA upstream of the coding region failed to reveal a mutation, suggesting that the lesion may be in a regulatory element of the gene. sne is a new fused    phalanges (fp) allele of the shaker-with-syndactylism deletion complex (sy), and we show that the genomic lesion is a small deletion removing an entire exon, coincident with the insertion of the 3' end of a LINE element belonging to the TF    subfamily. Copyright 2001</p>

	]]>
</description>

<author>V L. Browning et al.</author>


</item>


<item>
<title> High-resolution genetic and physical mapping of modifier-of-deafwaddler (mdfw) and Waltzer (Cdh23v).</title>
<link>http://mouseion.jax.org/stfb2000_2009/241</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/241</guid>
<pubDate>Tue, 08 May 2012 16:01:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Modifier-of-deafwaddler (mdfw) and waltzer (Cdh23v) are loci on mouse chromosome 10 encoding factors that are essential for the function of auditory hair cells. The BALB/cByJ-specific mdfw allele encodes a necessary and sufficient    modifier that induces progressive early onset hearing loss in CBy-dfw2J heterozygotes. Recessive mutations in the waltzer locus result in circling behavior and congenital deafness. In this report we present a high-resolution integrated genetic    and physical map of mdfw and Cdh23(v). Our genetic analyses localize mdfw between markers D10Mit60 and 148M13T7 within a 1.01-cM region. The Cdh23v critical interval is fully contained within the mdfw region and localizes between markers 146O23T7    and 148M13T7 within a 0.35-cM interval that is represented in an approximately 500-kb BAC contig. Our data suggest that mdfw and Cdh23v are allelic. Copyright 2001 Academic Press.</p>

	]]>
</description>

<author>E C. Bryda et al.</author>


</item>


<item>
<title> Expression of genes involved in mammalian meiosis during the transition from egg to embryo.</title>
<link>http://mouseion.jax.org/stfb2000_2009/240</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/240</guid>
<pubDate>Tue, 08 May 2012 16:00:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ooplasm of higher eukaryotes provides substances necessary for completing the last stages of meiosis and initiating the first mitotic division. These processes are firmly attuned to other events in the egg and newly formed    embryo, such as switching from the use of maternal transcripts to the onset of zygotic transcription. In mammals little is known about the molecular mechanisms guiding this transition, largely due to the lack of information about genes expressed    in the egg and early embryos. Studies of yeast mitosis have contributed much of what is known about the vertebrate cell cycle, and recent reports indicate that homologs of yeast DNA repair genes also function during mammalian gametogenesis. To    examine whether this conservation can be expanded to include genes operative in oocyte meiosis, we performed a computer-based search for homologs of yeast genes that are induced during sporulation in C. elegans, Drosophila, and mammals. Results    from this study suggest that yeast and higher eukaryotes share genes that coordinate the overall process of meiosis. However intriguing differences exist, reflecting the distinctive mechanisms governing the progression of meiosis in each    organism. ESTs representing more than half of the mammalian homologs are present in mouse cDNA libraries that contains genes controlling the meiosis/mitosis transition. About 50% of these genes contain potential cis-elements for cytoplasmic    polyadenylation in their 3'-UTR, suggesting the importance of controlled translation in the egg and zygote. Mol. Reprod. Dev.  59:144-158, 2001. Copyright 2001 Wiley-Liss, Inc.</p>

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</description>

<author>S Y. Hwang et al.</author>


</item>


<item>
<title> Unusual resistance of ALR/Lt mouse beta cells to autoimmune destruction: role for beta cell-expressed resistance determinants.</title>
<link>http://mouseion.jax.org/stfb2000_2009/239</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/239</guid>
<pubDate>Tue, 08 May 2012 16:00:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic analysis of autoimmune insulin-dependent diabetes mellitus (IDDM) has focused on genes controlling immune functions, with little investigation of innate susceptibility determinants expressed at the level of target beta    cells. The Alloxan (AL) Resistant (R) Leiter (Lt) mouse strain, closely related to the IDDM-prone nonobese diabetic (NOD)/Lt strain, demonstrates the importance of such determinants. ALR mice are unusual in their high constitutive expression of    molecules associated with dissipation of free-radical stress systemically and at the beta-cell level. ALR islets were found to be remarkably resistant to two different combinations of beta-cytotoxic cytokines (IL-1beta, tumor necrosis factor    alpha, and IFN-gamma) that destroyed islets from the related NOD and alloxan-susceptible strains. The close MHC relatedness between the NOD and ALR strains (H2-Kd and H2-Ag7 identical) allowed us to examine whether ALR islet cells could survive    autoimmune destruction by NOD-derived Kd-restricted diabetogenic cytotoxic T lymphocyte clones (AI4 and the insulin-reactive G9C8 clones). Both clones killed islet cells from all Kd-expressing strains except ALR. ALR resistance to diabetogenic    immune systems was determined in vivo by means of adoptive transfer of the G9C8 clone or by chimerizing lethally irradiated ALR or reciprocal (ALR x NOD)F1 recipients with NOD bone marrow. In all in vivo systems, ALR and F1 female recipients of    NOD marrow remained IDDM free; in contrast, all of the NOD recipients became diabetic. In conclusion, the ALR mouse presents a unique opportunity to identify dominant IDDM resistance determinants expressed at the beta cell level.</p>

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</description>

<author>C E. Mathews et al.</author>


</item>


<item>
<title> Distinguishing self from nonself: immunogenicity of the murine H47 locus is determined by a single amino acid substitution in an unusual peptide.</title>
<link>http://mouseion.jax.org/stfb2000_2009/238</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/238</guid>
<pubDate>Tue, 08 May 2012 15:59:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Histocompatibility (H) Ags are responsible for chronic graft rejection and graft vs host disease in solid tissue and bone marrow transplantation among MHC-matched individuals. Here we defined the molecular basis of self-nonself    discrimination for the murine chromosome 7 encoded H47 histocompatibility locus, known by its trait of graft-rejection for over 40 years. H47 encodes a novel, highly conserved cell surface protein containing the SCILLYIVI (SII9) nonapeptide in    its transmembrane region.  The p7 isoleucine-to-phenylalanine substitution in SII9 defined the antigenic polymorphism and T cell specificity. Despite absence of the canonical consensus motif and weak binding to D(b) MHC I, both H47 peptides were    presented to CTLs. However, unlike all the other known H loci, the relative immunogenicity of both H47 alleles varied dramatically and was profoundly influenced by neighboring H loci. The results provide insights into the peptide universe that    defines nonself and the basis of histoincompatibility.</p>

	]]>
</description>

<author>L M. Mendoza et al.</author>


</item>


<item>
<title>Time-of-Flight Photoelectron Spectroscopy of Atoms and Molecules</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/28</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/28</guid>
<pubDate>Tue, 08 May 2012 15:59:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Following the advent of third-generation synchrotron-radiation sources with ultra-high brightness and X-ray pulse widths of a few picoseconds, the technique of time-of-flight (TOF) electron spectroscopy has experienced a dramatic enhancement in energy resolution. Using soft-X-ray beams focused to 100 μm or less, a new gas-phase TOF-photoelectron apparatus in operation at the Advanced Light Source (ALS) has demonstrated electron energy resolution as high as 8000 (<em>E</em>/Δ<em>E</em>), comparable to some of the best electrostatic analyzers, while maintaining the traditional efficiency of the TOF technique. This apparatus is being used to probe limitations of basic approximations in X-ray photoemission: (1) the independent-particle approximation, and (2) the dipole approximation. In both cases, new limits of these approximations have been discovered in unexpected photon-energy regimes. This paper includes an overview of the TOF technique as well as a summary of results from the ALS on limits of these basic approximations.</p>

	]]>
</description>

<author>Dennis W. Lindle et al.</author>


</item>


<item>
<title> Maximum life spans in mice are extended by wild strain alleles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/237</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/237</guid>
<pubDate>Tue, 08 May 2012 15:59:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genes that control basic aging mechanisms in mammals are unknown. By using two four-way crosses, each including a strain derived from wild, undomesticated stocks, we identified two quantitative trait loci that extend murine    life spans by approximately 10%. In one cross, the longest-lived 18% of carriers of the D8Mit171 marker allele from the MOLD/Rk strain, Mus m. molossinus, outlived the longest lived 18% of noncarriers by 129 days (P = 5.4 x 10(-5)); in a second    cross, carriers of the D10Mit267 allele from the CAST/Ei strain, Mus m. castaneus, outlived noncarriers by 125 days ( P = 1.6 x 10(-6)). In both crosses, P < 1.0 x 10(-4 )is considered significant. Because these life span increases required that    all essential biological systems function longer than normal, these alleles most likely retarded basic aging mechanisms in multiple biological systems simultaneously.</p>

	]]>
</description>

<author>S Klebanov et al.</author>


</item>


<item>
<title> Autoreactive diabetogenic T-cells in NOD mice can efficiently expand from a greatly reduced precursor pool.</title>
<link>http://mouseion.jax.org/stfb2000_2009/236</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/236</guid>
<pubDate>Tue, 08 May 2012 15:59:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>A broad repertoire of pancreatic beta-cell autoreactive T-cells normally contributes to the development of type 1 diabetes in NOD mice. However, it has been unknown if a large reduction in the precursor pool from which autoreactive    T-cells are drawn would inhibit the development of type 1 diabetes. To address this issue, we reduced the precursor frequency of autoreactive T-cells in NOD mice through allelic exclusion induced by transgenic expression of an H2-Db class    I-restricted T-cell receptor (TCR) specific for a pathologically irrelevant lymphocytic choriomeningitis virus (LCMV) peptide. TCR allelic exclusion greatly reduced the pool of T-cells from which diabetogenic effectors could be derived in these    NODxLCMV TCR Tg mice. Surprisingly, this did not impair their type 1 diabetes susceptibility. Furthermore, a diabetogenic CD8 T-cell population that is prevalent in standard NOD mice was present at essentially equivalent levels in pancreatic    islets of NODxLCMV TCR Tg mice. Other data indicated that the antigenic specificity of these CD8 T-cells is primarily the function of a shared TCR-alpha chain. Although the percentage of TCR transgenic T-cells decreased in NOD versus B6,D2    control mice, much higher total numbers of both the TCR transgenic and the nontransgenic T-cells accumulated in the NOD strain. This transgenic T-cell accumulation in the absence of the cognate peptide indicated that the NOD genetic background    preferentially promotes a highly efficient antigen-independent T-cell expansion. This might allow diabetogenic T-cells in NOD mice to undergo an efficient expansion before encountering antigen, which would represent an important and previously    unconsidered aspect of pathogenesis.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title> Combined histologic and molecular features reveal previously unappreciated subsets of lymphoma in AKXD recombinant inbred mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/235</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/235</guid>
<pubDate>Tue, 08 May 2012 15:58:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hematopoietic neoplasms developing in AKXD recombinant inbred, NFS.V(+) and ICSBP knockout mice were assessed using morphologic, cytologic and molecular criteria that relate these disorders to human lymphoma and leukemia. Lymphoma    types included precursor T-cell and B-cell lymphoblastic, small lymphocytic, splenic marginal zone, follicular, and diffuse large cell (DLCL). In addition to previously defined subtypes of DLCL composed of centroblasts or immunoblasts, two    additional subtypes are defined here: lymphoblastic lymphoma like (LL) and lymphoma characterized by a histiocytic reaction (HS). DLCL(HS) were distinguished from true histiocytic lymphomas by the presence of clonal Ig gene    rearrangements.</p>

	]]>
</description>

<author>H C. Morse et al.</author>


</item>


<item>
<title> Biochemical and biophysical evidence for gamma 2 subunit association with neuronal voltage-activated Ca2+ channels.</title>
<link>http://mouseion.jax.org/stfb2000_2009/234</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/234</guid>
<pubDate>Tue, 08 May 2012 15:58:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>A novel gene (Cacng2; gamma(2)) encoding a protein similar to the voltage-activated Ca(2+) channel gamma(1) subunit was identified as the defective gene in the epileptic and ataxic mouse, stargazer. In this study, we analyzed the    association of this novel neuronal gamma(2) subunit with Ca(2+) channels of rabbit brain, and the function of the gamma(2) subunit in recombinant neuronal Ca(2+) channels expressed in Xenopus oocytes. Our results showed that the gamma(2) subunit    and a closely related protein (called gamma(3)) co-sedimented and co-immunoprecipitated with neuronal Ca(2+) channel subunits in vivo. Electrophysiological analyses showed that gamma(2) co-expression caused a significant decrease in the current    amplitude of both alpha(1B)(alpha(1)2.2)-class (36.8%) and alpha(1A)(alpha(1)2.1)-class (39.7%) Ca(2+) channels (alpha(1)beta(3)alpha(2)delta). Interestingly, the inhibitory effects of the gamma(2) subunit on current amplitude were dependent on    the co-expression of the alpha(2)delta subunit. In addition, co-expression of gamma(2) or gamma(1) also significantly decelerates the activation kinetics of alpha(1B)-class Ca(2+) channels. Taken together, these results suggest that the gamma(2)    subunit is an important constituent of the neuronal Ca(2+) channel complex and that it down-regulates neuronal Ca(2+) channel activity. Furthermore, the gamma(2) subunit likely contributes to the fine-tuning of neuronal Ca(2+) channels by    counterbalancing the effects of the alpha(2)delta subunit.</p>

	]]>
</description>

<author>M G. Kang et al.</author>


</item>


<item>
<title> Role of protein synthesis in the development of a transcriptionally permissive state in one-cell stage mouse embryos.</title>
<link>http://mouseion.jax.org/stfb2000_2009/233</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/233</guid>
<pubDate>Tue, 08 May 2012 15:57:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The time of onset of gene transcription in the mouse embryo is temporally regulated. A prominent feature of this regulation is a change during the one-cell stage from a transcriptionally nonpermissive state to a transcriptionally    permissive state. During the early one-cell stage, the cytoplasm is either inadequate or suppressive for nuclear gene transcription, but by the late one-cell stage, the cytoplasm acquires the ability to support gene transcription either in    endogenous nuclei or exogenous nuclei introduced microsurgically. We have investigated the role of protein synthesis in this cytoplasmic transition. Nuclei from two-cell stage embryos treated with alpha-amanitin were used to evaluate the    transcriptional permissiveness of late one-cell stage cytoplasm, as indicated by the production of transcripts from four genes that are specifically transcribed at elevated rates during the two-cell stage. Two of these genes were transcribed    following nuclear transfer to late one-cell stage cytoplasm, and two were not transcribed. Treatment of the recipient cytoplasm with cycloheximide to inhibit protein synthesis from the early to the late one-cell stage inhibited the transcription    of the two genes that were transcribed in the untreated, late one-cell stage recipients. These results indicate that acquisition of the transcriptionally permissive state during the one-cell stage is facilitated by protein synthesis, and that the    transcriptional permissiveness in the late one-cell stage cytoplasm is limited to certain genes.</p>

	]]>
</description>

<author>Q Wang et al.</author>


</item>


<item>
<title> C57BL/6J-T-Associated Sex Reversal in Mice Is Caused by Reduced Expression of a Mus domesticus Sry Allele.</title>
<link>http://mouseion.jax.org/stfb2000_2009/232</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/232</guid>
<pubDate>Tue, 08 May 2012 15:57:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>C57BL/6J-T-associated sex reversal (B6-TAS) in XY mice results in ovarian development and involves (1) hemizygosity for Tas, a gene located in the region of Chromosome 17 deleted in T(hp) and T(Orl), (2) homozygosity for one or    more B6-derived autosomal genes, and (3) the presence of the AKR Y chromosome. Here we report results from experiments designed to investigate the Y chromosome component of this sex reversal. Testis development was restored in B6 T(Orl)/+ XY(AKR)    mice carrying a Mus musculus Sry transgene. In addition, two functionally different classes of M. domesticus Sry alleles were identified among eight standard and two wild-derived inbred strains. One class, which includes AKR, did not initiate    normal testis development in B6 T(Orl)/+ XY mice, whereas the other did. DNA sequence analysis of the Sry ORF and a 5' 800-bp segment divided these inbred strains into the same groups. Finally, we found that Sry is transcribed in B6 T(Orl)/+    XY(AKR) fetal gonads but at a reduced level. These results pinpoint Sry as the Y-linked component of B6-TAS. We hypothesize that the inability of specific M. domesticus Sry alleles to initiate normal testis development in B6 T(Orl)/+ XY(AKR) mice    results from a biologically insufficient level of Sry expression, allowing the ovarian development pathway to proceed.</p>

	]]>
</description>

<author>L L. Washburn et al.</author>


</item>


<item>
<title> p35 and p39 are essential for cyclin-dependent kinase 5 function during neurodevelopment.</title>
<link>http://mouseion.jax.org/stfb2000_2009/231</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/231</guid>
<pubDate>Tue, 08 May 2012 15:56:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cyclin-dependent kinase 5 (Cdk5) plays a pivotal role in brain development and neuronal migration. Cdk5 is abundant in postmitotic, terminally differentiated neurons. The ability of Cdk5 to phosphorylate substrates is dependent on    activation by its neuronal-specific activators p35 and p39.  There exist striking differences in the phenotypic severity of Cdk5-deficient mice and p35-deficient mice. Cdk5-null mutants show a more severe disruption of lamination in the cerebral    cortex, hippocampus, and cerebellum. In addition, Cdk5-null mice display perinatal lethality, whereas p35-null mice are viable. These discrepancies have been attributed to the function of other Cdk5 activators, such as p39. To understand the    roles of p39 and p35, we created p39-null mice and p35/p39 compound-mutant mice. Interestingly, p39-null mice show no obvious detectable abnormalities, whereas p35(-/-)p39(-/-) double-null mutants are perinatal lethal. We show here that the    p35(-/-)p39(-/-) mutants exhibit phenotypes identical to those of the Cdk5-null mutant mice. Other compound-mutant mice with intermediate phenotypes allow us to determine the distinct and redundant functions between p35 and p39. Our data strongly    suggest that p35 and p39 are essential for Cdk5 activity during the development of the nervous system. Thus, p35 and p39 are likely to be the principal, if not the only, activators of Cdk5.</p>

	]]>
</description>

<author>J Ko et al.</author>


</item>


<item>
<title> A Y-encoded subunit of the translation initiation factor Eif2 is essential for mouse spermatogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/230</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/230</guid>
<pubDate>Tue, 08 May 2012 15:56:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>In mouse and man, deletions of specific regions of the Y chromosome have been linked to early failure of spermatogenesis and consequent sterility; the Y chromosomal gene(s) with this essential early role in spermatogenesis have not    been identified. The partial deletion of the mouse Y short arm (the Sxrb deletion) that occurred when Tp(Y)1CtSxr-b (hereafter Sxrb) arose from Tp(Y)1CTSxr-b (hereafter Sxra) defines Spy, a Y chromosomal factor essential for normal spermatogonial    proliferation.  Molecular analysis has identified six genes that lie within the deletion: Ube1y1 (refs. 4,5), Smcy, Uty, Usp9y (also known as Dffry), Eif2s3y (also known as Eif-2gammay) and Dby10; all have closely similar X-encoded homologs. Of    the Y-encoded genes, Ube1y1 and Dby have been considered strong candidates for mouse Spy function, whereas Smcy has been effectively ruled out as a candidate. There is no Ube1y1 homolog in man, and DBY, either alone or in conjunction with USP9Y,    is the favored candidate for an early spermatogenic role. Here we show that introduction of Ube1y1 and Dby as transgenes into Sxrb-deletion mice fails to overcome the spermatogenic block. However, the introduction of Eif2s3y restores normal    spermatogonial proliferation and progression through meiotic prophase. Therefore, Eif2s3y, which encodes a subunit of the eukaryotic translation initiation factor Eif2, is Spy.</p>

	]]>
</description>

<author>S Mazeyrat et al.</author>


</item>


<item>
<title> Somatic activation of the K-ras oncogene causes early onset lung cancer in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/229</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/229</guid>
<pubDate>Tue, 08 May 2012 15:55:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>About 30% of human tumours carry ras gene mutations. Of the three genes in this family (composed of K-ras, N-ras and H-ras), K-ras is the most frequently mutated member in human tumours, including adenocarcinomas of the pancreas (    approximately 70-90% incidence), colon (approximately 50%) and lung ( approximately 25-50%). To construct mouse tumour models involving K-ras, we used a new gene targeting procedure to create mouse strains carrying oncogenic alleles of K-ras that    can be activated only on a spontaneous recombination event in the whole animal. Here we show that mice carrying these mutations were highly predisposed to a range of tumour types, predominantly early onset lung cancer. This model was further    characterized by examining the effects of germline mutations in the tumour suppressor gene p53, which is known to be mutated along with K-ras in human tumours. This approach has several advantages over traditional transgenic strategies, including    that it more closely recapitulates spontaneous oncogene activation as seen in human cancers.</p>

	]]>
</description>

<author>L Johnson et al.</author>


</item>


<item>
<title> Statistical design and the analysis of gene expression microarray data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/228</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/228</guid>
<pubDate>Tue, 08 May 2012 15:55:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gene expression microarrays are an innovative technology with enormous promise to help geneticists explore and understand the genome. Although the potential of this technology has been clearly demonstrated, many important and    interesting statistical questions persist. We relate certain features of microarrays to other kinds of experimental data and argue that classical statistical techniques are appropriate and useful. We advocate greater attention to experimental    design issues and a more prominent role for the ideas of statistical inference in microarray studies.</p>

	]]>
</description>

<author>M K. Kerr et al.</author>


</item>


<item>
<title> A glutamic acid decarboxylase 65-specific Th2 cell clone immunoregulates autoimmune diabetes in nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/227</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/227</guid>
<pubDate>Tue, 08 May 2012 15:55:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Several studies have provided indirect evidence in support of a role for beta cell-specific Th2 cells in regulating insulin-dependent diabetes (IDDM). Whether a homogeneous population of Th2 cells having a defined beta cell Ag    specificity can prevent or suppress autoimmune diabetes is still unclear. In fact, recent studies have demonstrated that beta cell-specific Th2 cell clones can induce IDDM. In this study we have established Th cell clones specific for glutamic    acid decarboxylase 65 (GAD65), a known beta cell autoantigen, from young unimmunized nonobese diabetic (NOD) mice. Adoptive transfer of a GAD65-specific Th2 cell clone (characterized by the secretion of IL-4, IL-5, and IL-10, but not IFN-gamma or    TGF-beta) into 2- or 12-wk-old NOD female recipients prevented the progression of insulitis and subsequent development of overt IDDM. This prevention was marked by the establishment of a Th2-like cytokine profile in response to a panel of beta    cell autoantigens in cultures established from the spleen and pancreatic lymph nodes of recipient mice. The immunoregulatory function of a given Th cell clone was dependent on the relative levels of IFN-gamma vs IL-4 and IL-10 secreted.  These    results provide direct evidence that beta cell-specific Th2 cells can indeed prevent and suppress autoimmune diabetes in NOD mice.</p>

	]]>
</description>

<author>R Tisch et al.</author>


</item>


<item>
<title> Lifespan extension and delayed immune and collagen aging in mutant mice with defects in growth hormone production.</title>
<link>http://mouseion.jax.org/stfb2000_2009/226</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/226</guid>
<pubDate>Tue, 08 May 2012 15:54:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Single-gene mutations that extend lifespan provide valuable tools for the exploration of the molecular basis for age-related changes in cell and tissue function and for the pathophysiology of age-dependent diseases. We show here    that mice homozygous for loss-of-function mutations at the Pit1 (Snell dwarf) locus show a >40% increase in mean and maximal longevity on the relatively long-lived (C3H/HeJ x DW/J)F(1) background. Mutant dw(J)/dw animals show delays in    age-dependent collagen cross-linking and in six age-sensitive indices of immune system status. These findings thus demonstrate that a single gene can control maximum lifespan and the timing of both cellular and extracellular senescence in a    mammal. Pituitary transplantation into dwarf mice does not reverse the lifespan effect, suggesting that the effect is not due to lowered prolactin levels. In contrast, homozygosity for the Ghrhr(lit) mutation, which like the Pit1(dw) mutation    lowers plasma growth hormone levels, does lead to a significant increase in longevity. Male Snell dwarf mice, unlike calorically restricted mice, become obese and exhibit proportionately high leptin levels in old age, showing that their    exceptional longevity is not simply due to alterations in adiposity per se. Further studies of the Pit1(dw) mutant, and the closely related, long-lived Prop-1(df) (Ames dwarf) mutant, should provide new insights into the hormonal regulation of    senescence, longevity, and late life disease.</p>

	]]>
</description>

<author>K Flurkey et al.</author>


</item>


<item>
<title> Program description: Strategies for biological annotation of mammalian systems: implementing gene ontologies in mouse genome informatics.</title>
<link>http://mouseion.jax.org/stfb2000_2009/225</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/225</guid>
<pubDate>Tue, 08 May 2012 15:54:14 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D P. Hill et al.</author>


</item>


<item>
<title> Genome-wide epistatic interaction analysis reveals complex genetic determinants of circadian behavior in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/224</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/224</guid>
<pubDate>Tue, 08 May 2012 15:53:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic heterogeneity underlies many phenotypic variations observed in circadian rhythmicity. Continuous distributions in measures of circadian behavior observed among multiple inbred strains of mice suggest that the inherent    contributions to variability are polygenic in nature. To identify genetic loci that underlie this complex behavior, we have carried out a genome-wide complex trait analysis in 196 (C57BL/6J X BALB/cJ)F(2) hybrid mice. We have characterized    variation in this panel of F(2) mice among five circadian phenotypes: free-running circadian period, phase angle of entrainment, amplitude of the circadian rhythm, circadian activity level, and dissociation of rhythmicity. Our genetic analyses of    these phenotypes have led to the identification of 14 loci having significant effects on this behavior, including significant main effect loci that contribute to three of these phenotypic measures: period, phase, and amplitude. We describe an    additional locus detection method, genome-wide genetic interaction analysis, developed to identify locus pairs that may interact epistatically to significantly affect phenotype. Using this analysis, we identified two additional pairs of loci that    have significant effects on dissociation and activity level; we also detected interaction effects in loci contributing to differences of period, phase, and amplitude. Although single gene mutations can affect circadian rhythms, the analysis of    interstrain variants demonstrates that significant genetic complexity underlies this behavior. Importantly, most of the loci that we have detected by these methods map to locations that differ from the nine known clock genes, indicating the    presence of additional clock-relevant genes in the mammalian circadian system. These data demonstrate the analytical value of both genome-wide complex trait and epistatic interaction analyses in further understanding complex phenotypes, and point    to promising approaches for genetic analysis of such phenotypes in other mammals, including humans.</p>

	]]>
</description>

<author>K Shimomura et al.</author>


</item>


<item>
<title> Characterization of the murine lbx2 promoter, identification of the human homologue, and evaluation as a candidate for alstrom syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/223</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/223</guid>
<pubDate>Tue, 08 May 2012 15:53:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>The murine Lbx2 gene is a member of the ladybird family of homeobox genes, which is expressed in the developing urogenital system, eye, and brain.  Using transgenic mice, we demonstrate that 9 kb of the 5' flanking region of mouse    Lbx2 is able to direct expression of a reporter gene in a tissue-specific manner recapitulating the endogenous expression pattern.  This regulatory region provides a novel reagent allowing for transgenic expression in the developing urogenital    ridge. In addition, we describe the identification of the human homologue, LBX2. Comparison of the human LBX2 and mouse Lbx2 sequences upstream of the coding regions reveals sequence conservation suggesting conserved regulatory regions. Both the    human LBX2 and the mouse Lbx2 genes have similar genomic structures and are composed of two exons separated by an intron. We mapped the mouse Lbx2 gene to 35 cM on chromosome 6 and the human LBX2 gene to a homologous region of chromosome 2p13.    This is a candidate region for several inherited disorders, including Alstrom syndrome, a disorder that includes ocular, urogenital, and renal abnormalities. Given the expression pattern of Lbx2, the chromosomal location in humans, and the    potential function of mammalian ladybird genes, we have begun to analyze patients with ocular disorders and those with Alstrom syndrome for mutations in LBX2. Although polymorphisms were identified, our results indicate that mutations in the    coding region of LBX2 do not account for Alstrom syndrome in the six kindreds analyzed. Copyright 2001 Academic Press.</p>

	]]>
</description>

<author>F Chen et al.</author>


</item>


<item>
<title> Molecular and functional mapping of the piebald deletion complex on mouse chromosome 14.</title>
<link>http://mouseion.jax.org/stfb2000_2009/222</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/222</guid>
<pubDate>Tue, 08 May 2012 15:52:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>The piebald deletion complex is a set of overlapping chromosomal deficiencies surrounding the endothelin receptor B locus collected during the Oak Ridge specific-locus-test mutagenesis screen. These chromosomal deletions represent    an important resource for genetic studies to dissect the functional content of a genomic region, and several developmental defects have been associated with mice homozygous for distinct piebald deletion alleles. We have used molecular markers to    order the breakpoints for 20 deletion alleles that span a 15.7-18-cM region of distal mouse chromosome 14. Large deletions covering as much as 11 cM have been identified that will be useful for regionally directed mutagenesis screens to reveal    recessive mutations that disrupt development. Deletions identified as having breakpoints positioned within previously described critical regions have been used in complementation studies to further define the functional intervals associated with    the developmental defects.  This has focused our efforts to isolate genes required for newborn respiration and survival, skeletal patterning and morphogenesis, and central nervous system development.</p>

	]]>
</description>

<author>J J. Roix et al.</author>


</item>


<item>
<title> Diverse repertoire of the MHC class II-peptide complexes is required for presentation of viral superantigens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/221</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/221</guid>
<pubDate>Tue, 08 May 2012 15:52:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Among other features, peptides affect MHC class II molecules, causing changes in the binding of bacterial superantigens (b-Sag). Whether peptides can alter binding of viral superantigens (v-Sag) to MHC class II was not known. Here    we addressed the question of whether mutations limiting the diversity of peptides bound by the MHC class II molecules influenced the presentation of v-Sag and, subsequently, the life cycle of the mouse mammary tumor virus (MMTV). T cells reactive    to v-Sag were found in mice lacking DM molecules as well as in A(b)Ep-transgenic mice in which MHC class II binding grooves were predominantly occupied by an invariant chain fragment or Ealpha(52-68) peptide, respectively. APCs from the mutant    mice failed to present v-Sag, as determined by the lack of Sag-specific T cell activation, Sag-induced T cell deletion, and by the aborted MMTV infection. In contrast, mice that express I-A(b) with a variety of bound peptides presented v-Sag and    were susceptible to MMTV infection. Comparison of v-Sag and b-Sag presentation by the same mutant cells suggested that presentation of v-Sag had requirements similar to that for presentation of toxic shock syndrome toxin-1. Thus, MHC class II    peptide repertoire is critical for recognition of v-Sag by the T cells and affects the outcome of infection with a retrovirus.</p>

	]]>
</description>

<author>T Golovkina et al.</author>


</item>


<item>
<title> Scd3--a novel gene of the stearoyl-CoA desaturase family with restricted expression in skin.</title>
<link>http://mouseion.jax.org/stfb2000_2009/220</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/220</guid>
<pubDate>Tue, 08 May 2012 15:52:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Stearoyl-coenzyme A (CoA) desaturase (SCD) is a key enzyme involved in the conversion of saturated fatty acids into monounsaturated fatty acids.  Previously, two members of this gene family, namely, Scd1 and Scd2, have been    reported. Here we report the identification and characterization of a skin, specifically to the sebaceous gland. The Scd3 gene codes for a transcript of approximately 4.9 kb with an open reading frame that results in a 359-amino-acid protein.    Scd3 shares 91 and 88% identity in the protein-coding region with Scd1 and Scd2, respectively, and maps to mouse chromosome 19 in very close proximity to Scd1 and Scd2. Unlike Scd1, Scd3 expression is higher in male mouse skin than in female    mouse skin. The promoter sequence of Scd3 reveals similarity with Scd1 in the proximal region but also possesses several distinctive features including the polyunsaturated fatty acid-response element. Scd3 is expressed in the skin of young asebia    mutant mice (Scd1(ab2J)/Scd1(ab2J)) in the absence of Scd1. Scd3 expression changes during the mouse hair cycle but not as dramatically as Scd1. The tissue-specific and sex-dependent expression of Scd3 suggests the presence of gene- and    hormonal-specific control mechanisms. Copyright 2001 Academic Press.</p>

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</description>

<author>Y Zheng et al.</author>


</item>


<item>
<title> The impact of reduced frequency of cage changes on the health of mice housed in ventilated cages.</title>
<link>http://mouseion.jax.org/stfb2000_2009/219</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/219</guid>
<pubDate>Tue, 08 May 2012 15:51:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Our purpose in this investigation was to determine if we could reduce cage changing frequency without adversely affecting the health of mice. We housed mice at three different cage changing frequencies: 7, 14, and 21 days, each at    three different cage ventilation rates: 30, 60 and 100 air changes per hour (ACH), for a total of nine experimental conditions. For each condition, we evaluated the health of 12 breeding pairs and 12 breeding trios of C57BL/6J mice for 7 months.    Health was assessed by breeding performance, weanling weight and growth, plasma corticosterone levels, immune function, and histological examination of selected organs.  Over a period of 4 months, we monitored the cage microenvironment for    ammonia and carbon dioxide concentrations, relative humidity, and temperature one day prior to changing the cage. The relative humidity, carbon dioxide concentrations, and temperature of the cages at all conditions were within acceptable levels.    Ammonia concentrations remained below 25 ppm (parts per million) in most cages, but, even at higher concentrations, did not adversely affect the health of mice. Frequency of cage changing had only one significant effect; pup mortality with pair    matings was greater at the cage changing frequency of 7 days compared with 14 or 21 days. In addition, pup mortality with pair matings was higher at 30 ACH compared with other ventilation rates. In conclusion, under the conditions of this study,    cage changes once every 14 days and ventilation rates of 60 ACH provide optimum conditions for animal health and practical husbandry.</p>

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</description>

<author>Whitaker C. Reeb et al.</author>


</item>


<item>
<title> Transgenic mice for the preparation of puromycin-resistant primary embryonic fibroblast feeder layers for embryonic stem cell selection.</title>
<link>http://mouseion.jax.org/stfb2000_2009/218</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/218</guid>
<pubDate>Tue, 08 May 2012 15:51:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E R. Linnell et al.</author>


</item>


<item>
<title> Rat xenograft survival in mice treated with donor-specific transfusion and anti-CD154 antibody is enhanced by elimination of host CD4+ cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/217</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/217</guid>
<pubDate>Tue, 08 May 2012 15:50:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Treatment with a donor-specific transfusion (DST) and a brief course of anti-mouse CD154 (anti-CD40-ligand) monoclonal antibody (mAb) prolongs the survival of both allografts and rat xenografts in mice. The mechanism by    which allograft survival is prolonged is incompletely understood, but depends in part on the presence of CD4+ cells and the deletion of alloreactive CD8+ T cells. Less is known about the mechanism by which this protocol prolongs xenograft    survival. METHODS: We measured rat islet and skin xenograft survival in euthymic and thymectomized mice treated with combinations of DST, anti-CD154 mAb, anti-CD4 mAb, and anti-CD8 mAb. Recipients included C57BL/6, C57BL/6-scid, C57BL/6-CD4null,    and C57BL/6-CD8null mice. RESULTS: Pretreatment with a depleting anti-CD4 mAb markedly prolonged the survival of both skin and islet xenografts in mice given DST plus anti-CD154 mAb. Comparable prolongation of xenograft survival was obtained in    C57BL/6-CD4null recipients treated with DST and anti-CD154 mAb. In contrast, anti-CD8 mAb did not prolong the survival of either islet or skin xenografts in mice treated with DST and anti-CD154 mAb. Thymectomy did not influence xenograft survival    in any treatment group. Adoptive transfer of splenocytes from C57BL/6-CD4null recipients treated with DST and anti-CD154 mAb and bearing long-term skin xenografts revealed the presence of residual xenoreactive cells. CONCLUSIONS: These data    suggest that treatment with DST and anti-CD154 mAb induces a state of "functional" transplantation tolerance. They also support the hypothesis that both the induction and maintenance of graft survival based on this protocol depend on different    cellular mechanisms in allogeneic and xenogeneic model systems.</p>

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</description>

<author>E J. Gordon et al.</author>


</item>


<item>
<title> Sequence interpretation.  Functional annotation of mouse genome sequences.</title>
<link>http://mouseion.jax.org/stfb2000_2009/216</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/216</guid>
<pubDate>Tue, 08 May 2012 15:50:31 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J H. Nadeau et al.</author>


</item>


<item>
<title> Classification, clinical manifestations, and immunopathological mechanisms of the epithelial variant of paraneoplastic autoimmune multiorgan syndrome: a reappraisal of paraneoplastic pemphigus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/215</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/215</guid>
<pubDate>Tue, 08 May 2012 15:50:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Recent studies suggest that paraneoplastic pemphigus (PNP) is a heterogeneous autoimmune syndrome involving several internal organs and that the pathophysiological mechanisms mediating cutaneous, mucosal, and internal    lesions are not limited to autoantibodies targeting adhesion molecules. OBJECTIVE: To classify the diverse mucocutaneous and respiratory presentations of PNP and characterize the effectors of humoral and cellular autoimmunity mediating epithelial    tissue damage. METHODS: We examined 3 patients manifesting the lichen planus pemphigoideslike subtype of PNP. A combination of standard immunohistochemical techniques, enzyme-linked immunosorbent assay with desmoglein (DSG) baculoproteins, and an    immunoprecipitation assay were used to characterize effectors of humoral and cellular autoimmunity in patients with PNP and in neonatal wild-type and DSG3-knockout mice with PNP phenotype induced by passive transfer of patients' IgGs. RESULTS: In    addition to the known "PNP antigenic complex," epithelial targets recognized by PNP antibodies included 240-, 150-, 130-, 95-, 80-, 70-, 66-, and 40/42-kd proteins but excluded DSG1 and DSG3. In addition to skin and the epithelium lining upper    digestive and respiratory tract mucosa, deposits of autoantibodies were found in kidney, urinary bladder, and smooth as well as striated muscle. Autoreactive cellular cytotoxicity was mediated by CD8(+) cytotoxic T lymphocytes, CD56(+) natural    killer cells, and CD68(+) monocytes/macrophages. Inducible nitric oxide synthase was visualized both in activated effectors of cellular cytotoxicity and their targets. Keratin 14-positive basal epithelial cells sloughed from the large airways and    obstructed small airways. CONCLUSIONS: The paraneoplastic disease of epithelial adhesion known as PNP in fact represents only 1 manifestation of a heterogeneous autoimmune syndrome in which patients, in addition to small airway occlusion and    deposition of autoantibodies in different organs, may display a spectrum of at least 5 different clinical and immunopathological mucocutaneous variants (ie, pemphiguslike, pemphigoidlike, erythema multiforme-like, graft-vs-host disease-like, and    lichen planus-like). We suggest that the more encompassing term "paraneoplastic autoimmune multiorgan syndrome," or PAMS, be applied. The pathophysiological mechanisms of PAMS involve both humoral and cellular autoimmunity responses. Epithelial    cell membrane antigens other than DSG1 or DSG3 are targeted by effectors of PAMS autoimmunity. Apoptosis of damaged basal cells mediates epithelial clefting, and respiratory failure results possibly from obstruction of small airways with sloughed    epithelial cells.</p>

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</description>

<author>V T. Nguyen et al.</author>


</item>


<item>
<title> Clinical review 123: Anabolic therapy for osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/214</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/214</guid>
<pubDate>Tue, 08 May 2012 15:49:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>All currently available, approved therapies for osteoporosis inhibit bone resorption. By acting at this site in the bone remodeling cycle, estrogens, selective estrogen receptor modulators, calcitonin, and the bisphosphonates all    have the capacity to increase bone mineral density and to reduce the risk of new fractures. There can be no doubt that these agents have had an enormous impact on our diagnostic and therapeutic approach to osteoporosis. Despite their great value,    the antiresorptives are generally not associated with dramatic increases in bone mass, and their action to reduce fracture risk, although highly significant, is rarely more than 50% of the baseline risk. Another approach is anabolic therapy, in    which bone formation is directly stimulated. In this review we will summarize the anabolic agents that have been studied and present a current view of their current standing. Fluoride, GH, insulin-like growth factor I, the statins, and PTH will    be reviewed. Although still in development, approaches to combination therapy with antiresorptives and anabolic agents are also promising.</p>

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</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title> Cytotoxicity of anti-cd64-ricin a chain immunotoxin against human acute myeloid leukemia cells in vitro and in scid mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/213</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/213</guid>
<pubDate>Tue, 08 May 2012 15:49:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Blast cells from patients with acute myeloid leukemia (AML) commonly express CD64, the high-affinity receptor for immunoglobulin G (FcgammaRI).  An immunotoxin (MDX-44) was constructed by coupling humanized anti-CD64 monoclonal    antibody (mAb) H22 via a bivalent linker to deglycosylated ricin A-chain (RA). Human leukemia cell lines were incubated with MDX-44 or H22/free RA. The effect of MDX-44 on the proliferation of leukemia cells was assessed by [(3)H]thymidine    incorporation. In the presence of interferon-gamma (IFN-gamma), MDX-44 significantly inhibited the proliferation of CD64(+) HL-60, NB4, and U937 cells in 72-h cultures in a dose-dependent manner. The mechanism of action appeared to be the    induction of apoptosis, as measured by propidium iodide staining and flow cytometry analysis. However, CD64(-) KG-1a and Daudi cells were not affected by MDX-44/IFN-gamma. Incubating HL-60 cells with MDX-44/IFN-gamma resulted in a 99% decrease in    colony-forming units, whereas colony-forming cells in normal bone marrow were not significantly suppressed by such treatment. Cells from 60% of AML patients (6/10) were inhibited by MDX-44/IFN-gamma, and the inhibition was correlated with CD64    expression on these cells (r = 0.65). In a human AML model in NOD/SCID mice, MDX-44/IFN-gamma inhibited 95-98% of peritoneal exudate AML cell proliferation and 85-90% of solid leukemia masses. The effect of MDX-44 on AML cells was dependent on    activation of cells by IFN-gamma.  MDX-44/IFN-gamma may have value in the therapy of AML cells expressing cell-surface CD64.</p>

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</description>

<author>R K. Zhong et al.</author>


</item>


<item>
<title> Transcriptional repression and developmental functions of the atypical vertebrate GATA protein TRPS1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/212</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/212</guid>
<pubDate>Tue, 08 May 2012 15:48:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Known vertebrate GATA proteins contain two zinc fingers and are required in development, whereas invertebrates express a class of essential proteins containing one GATA-type zinc finger. We isolated the gene encoding TRPS1, a    vertebrate protein with a single GATA-type zinc finger.  TRPS1 is highly conserved between XENOPUS: and mammals, and the human gene is implicated in dominantly inherited tricho-rhino-phalangeal (TRP) syndromes. TRPS1 is a nuclear protein that    binds GATA sequences but fails to transactivate a GATA-dependent reporter. Instead, TRPS1 potently and specifically represses transcriptional activation mediated by other GATA factors. Repression does not occur from competition for DNA binding    and depends on a C-terminal region related to repressive domains found in Ikaros proteins. During mouse development, TRPS1 expression is prominent in sites showing pathology in TRP syndromes, which are thought to result from TRPS1    haploinsufficiency. We show instead that truncating mutations identified in patients encode dominant inhibitors of wild-type TRPS1 function, suggesting an alternative mechanism for the disease. TRPS1 is the first example of a GATA protein with    intrinsic transcriptional repression activity and possibly a negative regulator of GATA-dependent processes in vertebrate development.</p>

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</description>

<author>T H. Malik et al.</author>


</item>


<item>
<title> Positional cloning of a novel gene on chromosome 16q causing Bardet-Biedl syndrome (BBS2).</title>
<link>http://mouseion.jax.org/stfb2000_2009/211</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/211</guid>
<pubDate>Tue, 08 May 2012 15:48:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bardet-Biedl syndrome (BBS) is a genetically heterogeneous autosomal recessive disorder with the primary clinical features of obesity, pigmented retinopathy, polydactyly, hypogenitalism, mental retardation and renal anomalies.    Associated features of the disorder include diabetes mellitus, hypertension and congenital heart disease. There are six known BBS loci, mapping to chromosomes 2, 3, 11, 15, 16 and 20. The BBS2 locus was initially mapped to an 18 cM interval on    chromosome 16q21 with a large inbred Bedouin kindred. Further analysis of the Bedouin population allowed fider or the fine mapping of this locus to a 2 cM region distal to marker D16S408. Physical mapping and sequence analysis of this region    resulted in the identification of a number of known genes and expressed sequence tag clusters. Mutation screening of a novel gene (BBS2) with a wide pattern of tissue expression revealed homozygous mutations in two inbred pedigrees, including the    large Bedouin kindred used to initially identify the BBS2 locus. In addition, mutations were found in three of 18 unrelated BBS probands from small nuclear families.</p>

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</description>

<author>D Y. Nishimura et al.</author>


</item>


<item>
<title> Development and function of diabetogenic T-cells in B-cell-deficient nonobese diabetic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/210</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/210</guid>
<pubDate>Tue, 08 May 2012 15:48:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Insulin-dependent diabetes (type 1 diabetes) in the NOD mouse is a T-cell-mediated autoimmune disease. However, B-cells may also play a critical role in disease pathogenesis, as genetically B-cell-deficient NOD mice (NOD.microMT)    have been shown to be protected from type 1 diabetes and to display reduced responses to certain islet autoantigens. To examine the requirements for B-cells in the development of type 1 diabetes, we generated a B-cell-naive T-cell repertoire by    transplantation of NOD fetal thymuses (FTs) into NOD.scid recipients. Surprisingly, these FT-derived NOD T-cells were diabetogenic in 36% of NOD.scid recipients, despite the absence of B-cells. In addition, T-cells isolated from NOD.microMT mice    were diabetogenic in 22% of NOD.scid recipients. Together, these results indicate that B-cells are not an absolute requirement for the generation or effector function of an islet-reactive T-cell repertoire in NOD mice.  We suggest that conditions    favoring rapid lymphocyte expansion can reveal autoreactive T-cell activity and precipitate disease in genetically susceptible individuals.</p>

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</description>

<author>P P. Chiu et al.</author>


</item>


<item>
<title> Effects of dietary restriction on appendicular bone in the SENCAR mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/209</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/209</guid>
<pubDate>Tue, 08 May 2012 15:47:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Peptide hormones, cytokines, and growth factors regulate cellular metabolism by stimulating second messenger signal transduction cascades in target tissues. A mutation in the regulatory domain of protein kinase C (PKC) in SENCAR    (sensitive to carcinogenesis) mice renders them extremely sensitive to diacylglycerol and phorbol esters, resulting in rapid growth, high free radical generation, carcinogenesis, and metabolic bone disease.  Dietary restriction (DR) normalizes    PKC and ameliorates adverse downstream effects, including carcinogenesis, in SENCAR mice. We hypothesized that DR sufficient to ameliorate carcinogenesis would prevent or delay the early onset of metabolic bone disease in SENCAR mice. Male mice    were assigned to 1 of 4 feeding groups from 10 to 16 weeks of age (the critical period when metabolic bone disease develops): ad libitum (AL)-fed; AL antioxidant (0.07% thioproline)-fed; 40% DR; or 40% DR antioxidant-fed. Femoral bone mass was    determined gravimetrically. Tibial total, cortical, and trabecular bone mineral density (BMD) were determined by quantitative computed tomography. Body weight, femoral bone mass, and tibial cortical BMD were lower in DR than in AL mice. However,    tibial total and trabecular BMD were higher in DR than in AL mice. Serum calcitonin, the hormone that inhibits the osteoclastic bone resorption that is most notable in trabecular bone, was 2-fold higher in DR than in AL-fed mice. Dietary    thioproline had no major effects. Thus, DR sufficient to ameliorate carcinogenesis in SENCAR mice did not prevent early-onset metabolic bone disease, but it had a beneficial effect on tibial trabecular BMD that occurred at the apparent expense of    cortical BMD. DR in SENCAR mice was also associated with elevated serum calcitonin, which may inhibit osteoclastic resorption and account for trabecular bone conservation in this model. In conclusion, PKC or the downstream metabolic processes    regulated by it appear to play previously unrecognized roles in the regulation of tibial trabecular BMD and serum calcitonin in SENCAR mice.  Copyright 2001 by W.B. Saunders Company</p>

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</description>

<author>Murray E. Brochmann et al.</author>


</item>


<item>
<title> Unique design for fixed ventilated changing station.</title>
<link>http://mouseion.jax.org/stfb2000_2009/208</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/208</guid>
<pubDate>Tue, 08 May 2012 15:47:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Jackson Laboratory animal colonies present a unique challenge for the design and operation of an animal changing station that maximizes protection of animal health and welfare while also protecting the health and safety of the    animal caretaker. The authors describe the modification of a fixed ventilated changing station for improved animal health, reduced ergonomic strain, and decreased allergen exposure.</p>

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</description>

<author>T Peterson et al.</author>


</item>


<item>
<title> Mice deficient in methylenetetrahydrofolate reductase exhibit hyperhomocysteinemia and decreased methylation capacity, with neuropathology and aortic lipid deposition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/207</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/207</guid>
<pubDate>Tue, 08 May 2012 15:47:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hyperhomocysteinemia, a risk factor for cardiovascular disease, is caused by nutritional and/or genetic disruptions in homocysteine metabolism. The most common genetic cause of hyperhomocysteinemia is the 677C-->T mutation in the    methylenetetrahydrofolate reductase (MTHFR) gene. This variant, with mild enzymatic deficiency, is associated with an increased risk for neural tube defects and pregnancy complications and with a decreased risk for colon cancer and leukemia.    Although many studies have reported that this variant is also a risk factor for vascular disease, this area of investigation is still controversial. Severe MTHFR deficiency results in homocystinuria, an inborn error of metabolism with    neurological and vascular complications. To investigate the in vivo pathogenetic mechanisms of MTHFR deficiency, we generated mice with a knockout of MTHFR: Plasma total homocysteine levels in heterozygous and homozygous knockout mice are 1.6-    and 10-fold higher than those in wild-type littermates, respectively.  Both heterozygous and homozygous knockouts have either significantly decreased S-adenosylmethionine levels or significantly increased S-adenosylhomocysteine levels, or both,    with global DNA hypomethylation.  The heterozygous knockout mice appear normal, whereas the homozygotes are smaller and show developmental retardation with cerebellar pathology.  Abnormal lipid deposition in the proximal portion of the aorta was    observed in older heterozygotes and homozygotes, alluding to an atherogenic effect of hyperhomocysteinemia in these mice.</p>

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</description>

<author>Z Chen et al.</author>


</item>


<item>
<title> Nonablative neonatal marrow transplantation attenuates functional and physical defects of beta-glucuronidase deficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/206</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/206</guid>
<pubDate>Tue, 08 May 2012 15:46:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>The toxicity of preparative regimens render neonatal bone marrow transplantation (BMT) for progressive childhood diseases a controversial treatment. Ablative BMT in neonatal mice with or without the lysosomal storage disease    mucopolysaccharidosis type VII (MPS VII) show high morbidity and developmental disruption of both brain and bone structure.  In this investigation, BMT was performed with a high dose of congenic, normal bone marrow into nonablated newborn mice.    Recipients had lifelong, multilineage, peripheral blood chimerism with the donor beta-glucuronidase-positive (GUS(+)) cells that was both well tolerated and therapeutic. Three daily injections of normal adult marrow increased the average life    span by at least 6 months and corrected the functional breeding deficits typical of the MPS VII mice. Twelve months after injection, several structural features of femurs were more like that of normal mice than of untreated MPS VII mice.    Periosteal circumference and bone cortical thickness were significantly improved in males and cortical density did not differ significantly from values in normal females.  Significant reduction of lysosomal glycosaminoglycan storage corresponded    directly with GUS enzyme activity and percentage of histochemically GUS(+) cells in visceral organs and hematopoietic tissues such as thymus, spleen, peripheral blood, and bone marrow. By all criteria tested, BMT into neonatal MPS VII mice in the    absence of any preparative regimen is a successful therapy.</p>

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</description>

<author>B W. Soper et al.</author>


</item>


<item>
<title> Mouse strain differences determine severity of iron accumulation in Hfe knockout model of hereditary hemochromatosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/205</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/205</guid>
<pubDate>Tue, 08 May 2012 15:46:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hereditary hemochromatosis (HH) is a common disorder of iron metabolism caused by mutation in HFE, a gene encoding an MHC class I-like protein.  Clinical studies demonstrate that the severity of iron loading is highly variable    among individuals with identical HFE genotypes. To determine whether genetic factors other than Hfe genotype influence the severity of iron loading in the murine model of HH, we bred the disrupted murine Hfe allele onto three different    genetically defined mouse strains (AKR, C57BL/6, and C3H), which differ in basal iron status and sensitivity to dietary iron loading. Serum transferrin saturations (percent saturation of serum transferrin with iron), hepatic and splenic iron    concentrations, and hepatocellular iron distribution patterns were compared for wild-type (Hfe +/+), heterozygote (Hfe +/-), and knockout (Hfe -/-) mice from each strain. Although the Hfe -/- mice from all three strains demonstrated increased    transferrin saturations and liver iron concentrations compared with Hfe +/+ mice, strain differences in severity of iron accumulation were striking. Targeted disruption of the Hfe gene led to hepatic iron levels in Hfe -/- AKR mice that were 2.5    or 3.6 times higher than those of Hfe -/- C3H or Hfe -/- C57BL/6 mice, respectively. The Hfe -/- mice also demonstrated strain-dependent differences in transferrin saturation, with the highest values in AKR mice and the lowest values in C3H mice.    These observations demonstrate that heritable factors markedly influence iron homeostasis in response to Hfe disruption. Analysis of mice from crosses between C57BL/6 and AKR mice should allow the mapping and subsequent identification of genes    modifying the severity of iron loading in this murine model of HH.</p>

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</description>

<author>R E. Fleming et al.</author>


</item>


<item>
<title> The mouse anterior chamber angle and trabecular meshwork develop without cell death.</title>
<link>http://mouseion.jax.org/stfb2000_2009/204</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/204</guid>
<pubDate>Tue, 08 May 2012 15:46:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The iridocorneal angle forms in the mammalian eye from undifferentiated mesenchyme between the root of the iris and cornea. A major component is the trabecular meshwork, consisting of extracellular matrix organized into    a network of beams, covered in trabecular endothelial cells. Between the beams, channels lead to Schlemm's canal for the drainage of aqueous humor from the eye into the blood stream. Abnormal development of the iridocorneal angle that interferes    with ocular fluid drainage can lead to glaucoma in humans. Little is known about the precise mechanisms underlying angle development. There are two main hypotheses.  The first proposes that morphogenesis involves mainly cell differentiation,    matrix deposition and assembly of the originally continuous mesenchymal mass into beams, channels and Schlemm's canal. The second, based primarily on rat studies, proposes that cell death and macrophages play an important role in forming channels    and beams. Mice provide a potentially useful model to understand the origin and development of angle structures and how defective development leads to glaucoma. Few studies have assessed the normal structure and development of the mouse angle. We    used light and electron microscopy and a cell death assay to define the sequence of events underlying formation of the angle structures in mice. RESULTS: The mouse angle structures and developmental sequence are similar to those in humans. Cell    death was not detectable during the period of trabecular channel and beam formation. CONCLUSIONS: These results support morphogenic mechanisms involving organization of cellular and extracellular matrix components without cell death or    atrophy.</p>

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</description>

<author>R S. Smith et al.</author>


</item>


<item>
<title> How to study pathologic phenotypes of knockout mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/203</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/203</guid>
<pubDate>Tue, 08 May 2012 15:45:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R T. Bronson</author>


</item>


<item>
<title> Genetically engineered mice. Husbandry and resources.</title>
<link>http://mouseion.jax.org/stfb2000_2009/202</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/202</guid>
<pubDate>Tue, 08 May 2012 15:45:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J J. Sharp et al.</author>


</item>


<item>
<title> Deletion of the p27Kip1 gene restores normal development in cyclin D1-deficient mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/201</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/201</guid>
<pubDate>Tue, 08 May 2012 15:45:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>D-type cyclins (cyclins D1, D2, and D3) are key components of cell cycle machinery in mammalian cells. These proteins are believed to drive cell cycle progression by associating with their kinase partners, cyclin-dependent kinases,    and by directing phosphorylation of critical cellular substrates. In addition, D-cyclins play a kinase-independent role by sequestering cell cycle inhibitors p27(Kip1) and p21(Cip1). In the past, we and others generated cyclin D1-deficient mice    and have shown that these mice display developmental abnormalities, hypoplastic retinas, and pregnancy-insensitive mammary glands. To test the significance of cyclin D1-p27(Kip1) interaction within a living mouse, we crossed cyclin D1-deficient    mice with mice lacking p27(Kip1), and we generated double-mutant cyclin D1(-/-)p27(-/-) animals. Here we report that ablation of p27(Kip1) restores essentially normal development in cyclin D1-deficient mice. Our results provide genetic evidence    that p27(Kip1) functions downstream of cyclin D1.</p>

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</description>

<author>Y Geng et al.</author>


</item>


<item>
<title> Previously undetected human hematopoietic cell populations with short-term repopulating activity selectively engraft NOD/SCID-beta2 microglobulin-null mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/200</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/200</guid>
<pubDate>Tue, 08 May 2012 15:44:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Increasing use of purified or cultured human hematopoietic cells as transplants has revealed an urgent need for better methods to predict the speed and durability of their engraftment potential. We now show that NOD/SCID-beta2    microglobulin-null (NOD/SCID-beta2m-/-) mice are sequentially engrafted by two distinct and previously unrecognized populations of transplantable human short-term repopulating hematopoietic cells (STRCs), neither of which efficiently engraft    NOD/SCID mice. One is predominantly CD34+CD38+ and is myeloid-restricted; the other is predominantly CD34+CD38- and has broader lymphomyeloid differentiation potential. In contrast, the long-term repopulating human cells that generate lymphoid    and myeloid progeny in NOD/SCID mice engraft and self-renew in NOD/SCID-beta2m-/- mice equally efficiently. In short-term expansion cultures of adult bone marrow cells, myeloid-restricted STRCs were preferentially amplified (greater than tenfold)    and, interestingly, both types of STRC were found to be selectively elevated in mobilized peripheral blood harvests. These results suggest an enhanced sensitivity of STRCs to natural killer cell-mediated rejection. They also provide new in vivo    assays for different types of human STRC that may help to predict the engraftment potential of clinical transplants and facilitate future investigation of early stages of human hematopoietic stem cell differentiation.</p>

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</description>

<author>H Glimm et al.</author>


</item>


<item>
<title> Antigen-specific mediated suppression of beta cell autoimmunity by plasmid DNA vaccination.</title>
<link>http://mouseion.jax.org/stfb2000_2009/199</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/199</guid>
<pubDate>Tue, 08 May 2012 15:44:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this study, we have investigated the use of plasmid DNA (pDNA) vaccination to elicit Th2 effector cell function in an Ag-specific manner and in turn prevent insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD)    mice. pDNA recombinants were engineered encoding a secreted fusion protein consisting of a fragment of glutamic acid decarboxylase 65 (GAD65) linked to IgGFc, and IL-4. Intramuscular injection of pDNA encoding GAD65-IgGFc and IL-4 effectively    prevented diabetes in NOD mice treated at early or late preclinical stages of IDDM. This protection was GAD65-specific since NOD mice immunized with pDNA encoding hen egg lysozyme-IgGFc and IL-4 continued to develop diabetes. Furthermore, disease    prevention correlated with suppression of insulitis and induction of GAD65-specific regulatory Th2 cells. Importantly, GAD65-specific immune deviation was dependent on pDNA-encoded IL-4. In fact, GAD65-specific Th1 cell reactivity was    significantly enhanced in animals immunized with pDNA encoding only GAD65-IgGFc. Finally, NOD.IL4(null) mice treated with pDNA encoding GAD65-IgGFc and IL-4 continued to develop diabetes, indicating that endogenous IL-4 was also required for    disease prevention. These results demonstrate that pDNA vaccination is an effective strategy to elicit beta cell-specific Th2 regulatory cell function for the purpose of preventing IDDM even at a late stage of disease development.</p>

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</description>

<author>R Tisch et al.</author>


</item>


<item>
<title> A nuclear-mitochondrial DNA interaction affecting hearing impairment in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/198</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/198</guid>
<pubDate>Tue, 08 May 2012 15:44:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The pathophysiologic pathways and clinical expression of mitochondrial DNA (mtDNA) mutations are not well understood. This is mainly the result of the heteroplasmic nature of most pathogenic mtDNA mutations and of the absence of    clinically relevant animal models with mtDNA mutations. mtDNA mutations predisposing to hearing impairment in humans are generally homoplasmic, yet some individuals with these mutations have severe hearing loss, whereas their maternal relatives    with the identical mtDNA mutation have normal hearing. Epidemiologic, biochemical and genetic data indicate that nuclear genes are often the main determinants of these differences in phenotype. To identify a mouse model for maternally inherited    hearing loss, we screened reciprocal backcrosses of three inbred mouse strains, A/J, NOD/LtJ and SKH2/J, with age-related hearing loss (AHL). In the (A/J x CAST/Ei) x A/J backcross, mtDNA derived from the A/J strain exerted a significant    detrimental effect on hearing when compared with mtDNA from the CAST/Ei strain. This effect was not seen in the (NOD/LtJ x CAST/Ei) x NOD/LtJ and (SKH2/J x CAST/Ei) x SKH2/J backcrosses. Genotyping revealed that this effect was seen only in mice    homozygous for the A/J allele at the Ahl locus on mouse chromosome 10. Sequencing of the mitochondrial genome in the three inbred strains revealed a single nucleotide insertion in the tRNA-Arg gene (mt-Tr) as the probable mediator of the    mitochondrial effect. This is the first mouse model with a naturally occurring mtDNA mutation affecting a clinical phenotype, and it provides an experimental model to dissect the pathophysiologic processes connecting mtDNA mutations to hearing    loss.</p>

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</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title> Characterization of Corn1 mice: Alteration of epithelial and stromal cell gene expression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/197</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/197</guid>
<pubDate>Tue, 08 May 2012 15:44:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Corn1 is an autosomal recessive mutation characterized by corneal epithelial hyperplasia and stromal neovascularization. The aim of the present study is to examine the expression patterns of specific epithelial and stromal    proteins in corn/corn1 mutant mice. METHODS: Immunohistochemistry with antibodies directed against keratins 1, 4, 5, 12, and 14 as well as loricrin, filaggrin, and involucrin were performed in corn1/corn1 and wild type, A.By/SnJ strain, mice at 4    weeks of age.  Western blot hybridization was performed to confirm the presence of involucrin in corneas. In situ and northern blot hybridization were used to evaluate the expression of keratin 12, lumican, and keratocan in these mice. RESULTS:    In corn1/corn1 mice, focal areas of corneal epithelial hyperplasia alternate with epithelium with normal appearance. Both regions of normal and hyperplastic corneal epithelium were labeled by anti-keratin 12 antibodies through all corneal    epithelial layers. The anti-keratin 14 antibody only labeled the basal cell layer in normal epithelial areas, whereas it labeled both basal and suprabasal cell layers in hyperplastic areas. In wild type mice, anti-keratin 12 antibodies labeled    all corneal epithelial layers, whereas anti-keratin 14 labeled the basal corneal epithelial cells only. Positive staining by anti-involucrin antibody was demonstrated in the basal corneal epithelial layer of wild type mice and normal areas of    corn1/corn1 mice. Similarly, as observed with anti-keratin 14 antibody, the anti-involucrin antibody labeled both basal and suprabasal cell layers of hyperplastic corneal epithelium of corn1/corn1 mice. Antibodies against keratin 1, keratin 4,    loricrin, and fillagrin did not label the corneas of wild type mice or corn1/corn1 mice. Northern hybridization indicated that the expressions of keratocan and lumican mRNA levels were up regulated in corn1/corn1 mice, but keratin 12 mRNA    remained similar to that of the wild type mice. In situ hybridization revealed that the lumican mRNA was detected in epithelial and stromal cells of corn1/corn1 mice, whereas keratocan mRNA was only detected in stromal cells. CONCLUSIONS:    Hyperproliferative epithelial cells of corn1/corn1 mice have increased levels of expression of keratin 14 and involucrin, but do not exhibit the phenotypical characteristics of cornification. These observations indicate that factors associated    with the phenotypes of corn1/corn1 mice do not alter the cornea-type epithelial differentiation of keratin 12 expression, but cause aberrant expression of lumican by corneal epithelial cells.</p>

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</description>

<author>I Wang et al.</author>


</item>


<item>
<title> Chromosomal organization of candidate genes involved in cholesterol gallstone formation: a murine gallstone map.</title>
<link>http://mouseion.jax.org/stfb2000_2009/196</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/196</guid>
<pubDate>Tue, 08 May 2012 15:43:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Epidemiologic and family studies indicate that cholesterol gallstone formation is in part genetically determined. The major contribution to our current understanding of gallstone genes derives from animal studies, particularly    cross-breeding experiments in inbred mouse strains that differ in genetic susceptibility to cholesterol gallstone formation (quantitative trait loci mapping). In this review we summarize how the combined use of genomic strategies and phenotypic    studies in inbred mice has proven to be a powerful means of dissecting the complex pathophysiology of this common disease. We present a "gallstone map" for the mouse, consisting of all genetic loci that have been identified to confer gallstone    susceptibility as well as putative candidate genes.  Translation of the genetic loci and genes between mouse and human predicts chromosomal regions in the human genome that are likely to harbor gallstone genes. Both the number and the precise    understanding of gallstone genes are expected to further increase with rapid progress of the genome projects, and multiple new targets for early diagnosis and prevention of gallstone disease should become possible.</p>

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</description>

<author>F Lammert et al.</author>


</item>


<item>
<title> Functional annotation of a full-length mouse cDNA collection.</title>
<link>http://mouseion.jax.org/stfb2000_2009/195</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/195</guid>
<pubDate>Tue, 08 May 2012 15:43:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The RIKEN Mouse Gene Encyclopaedia Project, a systematic approach to determining the full coding potential of the mouse genome, involves collection and sequencing of full-length complementary DNAs and physical mapping of the    corresponding genes to the mouse genome. We organized an international functional annotation meeting (FANTOM) to annotate the first 21,076 cDNAs to be analysed in this project. Here we describe the first RIKEN clone collection, which is one of    the largest described for any organism. Analysis of these cDNAs extends known gene families and identifies new ones.</p>

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</description>

<author>M Ashburner et al.</author>


</item>


<item>
<title>The Origin of the Settlement of Niagara-on-the-Lake</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6935</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6935</guid>
<pubDate>Tue, 08 May 2012 15:43:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis describes the major policies that contributed to the creation of the settlement at Niagara on-the-Lake, Ontario. These policies, that involved the blending of political, historical and geographical ingredients, were in general executed during the administration of Sir Frederick Haldimand within the framework of British colonial policy. The settlement that resulted was a unique expression of the response of an eighteenth century policy-maker to two major factors: the American War of Independence and the continuance of a British fur trade monopoly in North America- Research aimed at isolating the principal locational policies that led to the development of the settlement; firstly as a means of understanding the choice of locational site, and secondly, as an example of the degree of influence that one administrator can have on past and present Iocational patterns. The thesis has focused on the significant contribution made by Frederick Haldimand to the political and historical geography of Canada; a contribution that has been largely overlooked in historical and geographical literature. It has also shown that the historical, political and geographical administrative framework can contribute to an understanding of present day patterns of settlement, and in fact has had far more influence on such patterns than previously indicated by the literature.</p>

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</description>

<author>Faye Whitfield</author>


</item>


<item>
<title> Controlling exposure to laboratory animal allergens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/194</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/194</guid>
<pubDate>Tue, 08 May 2012 15:43:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Laboratory animal allergy (LAA) is a significant occupational disease that may affect up to one third of personnel exposed to laboratory animals.  Research has characterized the relative risks of exposure, in terms of intensity,    frequency, and duration, associated with given tasks and work areas in the animal facility. Studies have shown that reduced exposure to animal allergens can reduce the incidence of LAA and relieve symptoms among affected workers. A combination of    measures to eliminate or control allergen exposure, including engineering and administrative controls and personal protective equipment, have been integral components of effective LAA management programs. The author provides a comprehensive    review of exposure control options, considerations, and " best practices" relative to laboratory animal allergen in the context of traditional industrial hygiene methods.</p>

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</description>

<author>D J. Harrison</author>


</item>


<item>
<title> Mouse models for the Wolf-Hirschhorn deletion syndrome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/193</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/193</guid>
<pubDate>Tue, 08 May 2012 15:42:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Wolf-Hirschhorn syndrome (WHS) is a deletion syndrome caused by segmental haploidy of chromosome 4p16.3. Its hallmark features include a 'Greek warrior helmet' facial appearance, mental retardation, various midline defects and    seizures. The WHS critical region (WHSCR) lies between the Huntington's disease gene, HD, and FGFR3. In mice, the homologs of these genes map to chromosome 5 in a region of conserved synteny with human 4p16.3. To derive mouse models of WHS and    map genes responsible for subphenotypes of the syndrome, five mouse lines bearing radiation-induced deletions spanning the WHSCR syntenic region were generated and characterized. Similar to WHS patients, these animals were growth-retarded, were    susceptible to seizures and showed midline (palate closure, tail kinks), craniofacial and ocular anomalies (colobomas, corneal opacities). Other phenotypes included cerebellar hypoplasia and a shortened cerebral cortex. Expression of WHS-like    traits was variable and influenced by strain background and deletion size. These mice represent the first animal models for WHS. This collection of nested chromosomal deletions will be useful for mapping and identifying loci responsible for the    various subphenotypes of WHS, and provides a paradigm for the dissection of other deletion syndromes using the mouse.</p>

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</description>

<author>D Naf et al.</author>


</item>


<item>
<title> Concordance of murine quantitative trait loci for salt-induced hypertension with rat and human loci.</title>
<link>http://mouseion.jax.org/stfb2000_2009/192</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/192</guid>
<pubDate>Tue, 08 May 2012 15:42:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>To investigate the genetic control of salt-induced hypertension, we performed a quantitative trait locus analysis on male mice from a reciprocal backcross between the salt-sensitive C57BL/6J and the normotensive A/J inbred mouse    strains after they were provided with water containing 1% salt for 2 weeks. Genome-wide scans performed on these mice and analyzed with a combination of conventional marker-based regressions and a novel simultaneous search for pairs revealed six    significant quantitative trait loci associated with salt-induced blood pressure, two of which were interacting loci. These six loci, named Bpq1-6 for blood pressure quantitative trait loci, mapped to D1Mit334, D1Mit14, D4Mit164, D5Mit31, D6Mit15,    and D15Mit13. Furthermore, five of these six loci were concordant with hypertension loci in rats, and four were concordant with hypertension loci in humans, suggesting that quantitative trait loci mapping in model organisms can be used to guide    the search for human blood pressure genes. Copyright 2001 Academic Press.</p>

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</description>

<author>F Sugiyama et al.</author>


</item>


<item>
<title> Mouse models of blood pressure regulation and hypertension.</title>
<link>http://mouseion.jax.org/stfb2000_2009/191</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/191</guid>
<pubDate>Tue, 08 May 2012 15:42:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human essential hypertension is recognized as a multifactorial disease involving many genes, but the causative genes have not yet been identified. For many years hypertension was studied primarily in the rat, but more recently    several candidate genes for hypertension have been used to produce transgenic mice for gain of function and gene-targeted mice for loss of function studies. These genetically engineered mouse strains with hypertension or hypotension are providing    insights into the mechanisms of blood pressure regulation. However, genetically engineered mice are used to study one gene at a time, and another complementary approach is needed for polygenic inheritance and gene interaction. The    phenotype-driven approach to hypertension studies uses the natural variation among inbred strains and crosses to find quantitative trait loci. The four mouse crosses carried out so far have found several quantitative trait loci that are    concordant with hypertension loci found in rats and humans.</p>

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</description>

<author>F Sugiyama et al.</author>


</item>


<item>
<title> Atherosclerosis in apoE knockout mice infected with multiple pathogens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/190</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/190</guid>
<pubDate>Tue, 08 May 2012 15:41:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cytomegalovirus (CMV) and Chlamydia pneumoniae (CP) possibly contribute to atherosclerosis. Murine CMV (MCMV) and CP increase lesion size in apoE knockout mice. In this study, apoE knockout mice were infected with MCMV and CP to    determine whether infection with multiple pathogens increases lesion size to a greater extent than either pathogen alone and whether infection with MCMV changes serum cytokine levels in a manner that could increase lesion development. One group    of mice received MCMV at 2 weeks of age, followed by 2 doses of CP at 6 and 8 weeks of age. Additional groups received only MCMV or CP. Animals were killed at 16 weeks of age to determine lesion area. Infection with MCMV alone, CP alone, and both    MCMV and CP increased lesion size 84% (P<.001), 70% (P<.0001), and 45% (P<.01), respectively. The MCMV-induced increase in circulating levels of interferon-gamma may have contributed to this increase.</p>

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</description>

<author>M S. Burnett et al.</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/233</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/233</guid>
<pubDate>Tue, 08 May 2012 15:41:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/232</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/232</guid>
<pubDate>Tue, 08 May 2012 15:41:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/231</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/231</guid>
<pubDate>Tue, 08 May 2012 15:41:23 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title> Transcriptional activity of the mouse oocyte genome: companion granulosa cells modulate transcription and chromatin remodeling.</title>
<link>http://mouseion.jax.org/stfb2000_2009/189</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/189</guid>
<pubDate>Tue, 08 May 2012 15:41:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chromatin configuration in the germinal vesicle (GV) undergoes dynamic changes during oocyte growth, yet little is known about the mechanisms regulating chromatin remodeling in mouse oocytes. The hypothesis that companion granulosa    cells play a role in modulating chromatin configuration and subsequent transcriptional activity in the oocyte genome was tested. Analysis of transcriptional activity, as determined by Br-UTP incorporation, revealed a similar percentage of    transcriptionally active and inactive oocytes present in the large antral follicles of mature females. However, gonadotropin stimulation of follicular development induced an increase in the proportion of transcriptionally inactive oocytes.    Interestingly, a similar proportion of stage-matched, oocyte-granulosa cell complexes grown in vitro without gonadotropin stimulation displayed chromatin redistribution around the nucleolus and no transcriptional activity. In contrast, when    cultured in the absence of companion granulosa cells, transcriptional activity remained unabated in the majority of denuded GV stage oocytes. Extended prophase arrest in fully grown transcriptionally inactive oocyte-granulosa cell complexes had    no effect on the progression of meiosis after in vitro maturation.  However, it reduced the competence to complete preimplantation embryo development. These results indicate that chromatin redistribution around the nucleolus is associated with    transcriptional repression in the GV of both fully grown in vivo-derived oocytes and cultured oocyte-granulosa cell complexes. Moreover, the results presented here suggest that some aspects of intraovarian control mechanisms were abrogated during    culture of oocyte-granulosa cell complexes, resulting in a higher proportion of oocytes with "mature" chromatin. Most importantly, companion granulosa cells played an active role in modulating the transcriptional activity of the oocyte    genome.</p>

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</description>

<author>La Fuente De et al.</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/230</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/230</guid>
<pubDate>Tue, 08 May 2012 15:41:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/229</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/229</guid>
<pubDate>Tue, 08 May 2012 15:41:16 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Impact Fees</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/224</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/224</guid>
<pubDate>Tue, 08 May 2012 15:40:59 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title> Lutheran blood group glycoprotein and its newly characterized mouse homologue specifically bind alpha5 chain-containing human laminin with high affinity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/188</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/188</guid>
<pubDate>Tue, 08 May 2012 15:40:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lutheran blood group glycoproteins (Lu gps) are receptors for the extracellular matrix protein, laminin. Studies suggest that Lu gps may contribute to vaso-occlusion in sickle cell disease and it has recently been shown that sickle    cells adhere to laminin isoforms containing the alpha5 chain (laminin 10/11). Laminin alpha5 is present in the subendothelium and is also a constituent of bone marrow sinusoids, suggesting a role for the Lu/laminin interaction in erythropoiesis.    The objectives of the current study were to define more precisely the molecular interactions of the extracellular and intracellular regions of human Lu and to clone and characterize a mouse homologue. To this end, complementary DNA and genomic    clones for the mouse homologue were sequenced and the mouse Lu gene mapped to a region on chromosome 7 with conserved synteny with human 19q13.2. Mouse and human Lu gps are highly conserved (72% identity) at the amino acid sequence level and both    mouse and human Lu gps specifically bind laminin 10/11 with high affinity.  Furthermore, the first 3, N-terminal, immunoglobulin superfamily domains of human Lu are critical for this interaction. The results indicated that the cytoplasmic domain    of BRIC 221-labeled human Lu gp is linked with the spectrin-based skeleton, affording the speculation that this interaction may be critical for signal transduction. These results further support a role for Lu gps in sickle cell disease and    indicate the utility of mouse models to explore the function of Lu gp-laminin 10/11 interaction in normal erythropoiesis and in sickle cell disease.</p>

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</description>

<author>S F. Parsons et al.</author>


</item>


<item>
<title>Land Use Regulation of Religious Institutions:  Balancing Planning Concerns with Constitutional and Statutory Safeguards for Religious Freedom</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/223</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/223</guid>
<pubDate>Tue, 08 May 2012 15:40:55 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Adult Entertainment Zoning Issues</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/222</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/222</guid>
<pubDate>Tue, 08 May 2012 15:40:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Religious Land Use and RLUIPA Update</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/221</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/221</guid>
<pubDate>Tue, 08 May 2012 15:40:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Legal Issues in the Regulation of On-Premise Signs</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/220</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/220</guid>
<pubDate>Tue, 08 May 2012 15:40:44 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein et al.</author>


</item>


<item>
<title>First Amendment Zoning Issues:  Regulation of Signs, Adult Entertainment &amp; Religious Uses</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/219</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/219</guid>
<pubDate>Tue, 08 May 2012 15:40:41 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title> Mutation of the hematopoietic cell phosphatase (Hcph) gene is associated with resistance to gamma-irradiation-induced apoptosis in Src homology protein tyrosine phosphatase (SHP)-1-deficient &quot;motheaten&quot; mutant mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/187</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/187</guid>
<pubDate>Tue, 08 May 2012 15:40:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>To determine the role of Src homology protein tyrosine phosphatase (SHP-1) in the ionizing radiation-induced stress response, we analyzed the apoptotic response and cell cycle function in irradiated spleen cells of motheaten    (me/me) mice. The defect in me/me mice has been attributed to mutations of the HCPH: gene, which encodes SHP-1. Homozygotes develop severe systemic autoimmune and inflammatory disease, whereas heterozygotes live longer and develop hematopoietic    and lymphoid malignance. Spleen cells from C57BL/6 (B6)-me/me and B6-+/+ controls were analyzed after gamma-irradiation from a (137)Cs source. B6-me/me cells were significantly more resistant than B6-+/+ cells to gamma-irradiation-induced    apoptosis exhibiting a higher LD(50). The defective apoptosis response of the B6-me/me cells was exhibited by T and B cells and macrophages. Of the Bcl-2 family members analyzed, a significant difference was observed in the transcription of Bax    mRNA, which was up-regulated early after irradiation in B6-+/+ cells, but not B6-me/me cells. Analysis of 3,3'-dihexyloxacarbocyanine iodide revealed resistance to the gamma-irradiation-induced mitochondrial transmembrane permeability transition    in the B6-me/me cells. The blocking of the cell cycle in the G(0)/G(1) phase characteristic of the irradiated B6-+/+ cells was not observed in the B6-me/me cells. There was decreased phosphorylation of p38 mitogen-activated protein kinase and    increased phosphorylation of p53 from spleen cell lysates of irradiated B6-me/me mice compared with wild-type mice. These data suggest that SHP-1 plays an important role in regulation of apoptosis and cell cycle arrest after a    gamma-irradiation-induced stress response.</p>

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</description>

<author>H C. Hsu et al.</author>


</item>


<item>
<title>Due Process and Equal Protection,</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/216</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/216</guid>
<pubDate>Tue, 08 May 2012 15:40:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein et al.</author>


</item>


<item>
<title>Anti-Defamation League of B&apos;Nai B&apos;rith</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/215</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/215</guid>
<pubDate>Tue, 08 May 2012 15:40:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Zoning Laws and Freedom of Speech</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/214</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/214</guid>
<pubDate>Tue, 08 May 2012 15:40:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>O&apos;Brien Content-Neutral Free Speech</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/212</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/212</guid>
<pubDate>Tue, 08 May 2012 15:40:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Low-Value Speech</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/211</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/211</guid>
<pubDate>Tue, 08 May 2012 15:40:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title> Th1 to Th2 cytokine shifts in nonobese diabetic mice: sometimes an outcome, rather than the cause, of diabetes resistance elicited by immunostimulation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/186</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/186</guid>
<pubDate>Tue, 08 May 2012 15:40:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Numerous immunostimulatory protocols inhibit the development of T cell-mediated autoimmune insulin-dependent diabetes mellitus (IDDM) in the nonobese diabetic (NOD) mouse model. Many of these protocols, including treatment with the    nonspecific immunostimulatory agents CFA or bacillus Calmette-Guerin (BCG) vaccine, have been reported to mediate protection by skewing the pattern of cytokines produced by pancreatic beta-cell autoreactive T cells from a Th1 (IFN-gamma) to a Th2    (IL-4 and IL-10) profile. However, most of these studies have documented associations between such cytokine shifts and disease protection rather than a cause/effect relationship. To partially address this issue we produced NOD mice genetically    deficient in IFN-gamma, IL-4, or IL-10. Elimination of any of these cytokines did not significantly alter the rate of spontaneous IDDM development. Additional experiments using these mice confirmed that CFA- or BCG-elicited diabetes protection is    associated with a decreased IFN-gamma to IL-4 mRNA ratio within T cell-infiltrated pancreatic islets, but this is a secondary consequence rather than the cause of disease resistance. Unexpectedly, we also found that the ability of BCG and, to a    lesser extent, CFA to inhibit IDDM development in standard NOD mice is actually dependent upon the presence of the Th1 cytokine, IFN-gamma.  Collectively, our studies demonstrate that while Th1 and Th2 cytokine shifts may occur among beta-cell    autoreactive T cells of NOD mice protected from overt IDDM by various immunomodulatory therapies, it cannot automatically be assumed that this is the cause of their disease resistance.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title>Eminent Domain, Takings and Exactions</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/209</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/209</guid>
<pubDate>Tue, 08 May 2012 15:40:01 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein et al.</author>


</item>


<item>
<title>Rescuing Space Tourists:  A Humanitarian Duty and Business Need</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/208</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/208</guid>
<pubDate>Tue, 08 May 2012 15:39:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper explores the controversial topic of the duty to rescue under existing space law treaties and makes the case for an expansive interpretation of the treaties that would require states to rescue space tourists. This being said, space companies are advised not to rely on state action to rescue tourists in distress, but are instead urged to make their own arrangements to help ensure the safety of their customers and, in turn, limit their exposure to liability. To assist companies in this task, this paper sets forth the essential components of a rescue policy that should be adopted by every space tourism company.</p>

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</description>

<author>Mark J. Sundahl</author>


</item>


<item>
<title>State Courts and Supplemental Jurisdiction Under the Civil Rights Act of 1991</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/203</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/203</guid>
<pubDate>Tue, 08 May 2012 15:39:40 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title> Defective spectrin integrity and neonatal thrombosis in the first mouse model for severe hereditary elliptocytosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/185</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/185</guid>
<pubDate>Tue, 08 May 2012 15:39:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations affecting the conversion of spectrin dimers to tetramers result in hereditary elliptocytosis (HE), whereas a deficiency of human erythroid alpha- or beta-spectrin results in hereditary spherocytosis (HS). All spontaneous    mutant mice with cytoskeletal deficiencies of spectrin reported to date have HS. Here, the first spontaneous mouse mutant, sph(Dem)/ sph(Dem), with severe HE is described. The sph(Dem) mutation is the insertion of an intracisternal A particle    element in intron 10 of the erythroid alpha-spectrin gene. This causes exon skipping, the in-frame deletion of 46 amino acids from repeat 5 of alpha-spectrin and alters spectrin dimer/tetramer stability and osmotic fragility. The disease is more    severe in sph(Dem)/sph(Dem) neonates than in alpha-spectrin-deficient mice with HS. Thrombosis and infarction are not, as in the HS mice, limited to adults but occur soon after birth. Genetic background differences that exist between HE and HS    mice are suspect, along with red blood cell morphology differences, as modifiers of thrombosis timing.  sph(Dem)/sph(Dem) mice provide a unique model for analyzing spectrin dimer- to-tetramer conversion and identifying factors that influence    thrombosis.</p>

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</description>

<author>N J. Wandersee et al.</author>


</item>


<item>
<title>Litigating Section  1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/202</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/202</guid>
<pubDate>Tue, 08 May 2012 15:39:37 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>The Impact of Heck v. Humphrey on Section 1983 Litigation</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/201</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/201</guid>
<pubDate>Tue, 08 May 2012 15:39:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>An Introduction to State Court § 1983 Litigation</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/199</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/199</guid>
<pubDate>Tue, 08 May 2012 15:39:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Litigating Section  1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/198</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/198</guid>
<pubDate>Tue, 08 May 2012 15:39:23 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/197</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/197</guid>
<pubDate>Tue, 08 May 2012 15:39:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Section 1983 Wrongful Death Remedies</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/196</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/196</guid>
<pubDate>Tue, 08 May 2012 15:39:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title> Genetic analysis of case/control data using estimated haplotype frequencies: application to APOE locus variation and Alzheimer&apos;s disease.</title>
<link>http://mouseion.jax.org/stfb2000_2009/184</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/184</guid>
<pubDate>Tue, 08 May 2012 15:39:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is growing debate over the utility of multiple locus association analyses in the identification of genomic regions harboring sequence variants that influence common complex traits such as hypertension and diabetes. Much of    this debate concerns the manner in which one can use the genotypic information from individuals gathered in simple sampling frameworks, such as the case/control designs, to actually assess the association between alleles in a particular genomic    region and a trait. In this paper we describe methods for testing associations between estimated haplotype frequencies derived from multilocus genotype data and disease endpoints assuming a simple case/control sampling design. These proposed    methods overcome the lack of phase information usually associated with samples of unrelated individuals and provide a comprehensive way of assessing the relationship between sequence or multiple-site variation and traits and diseases within    populations. We applied the proposed methods in a study of the relationship between polymorphisms within the APOE gene region and Alzheimer's disease. Cases and controls for this study were collected from the United States and France. Our results    confirm the known association between the APOE locus and Alzheimer's disease, even when the epsilon 4 polymorphism is not contained in the tested haplotypes. This suggests that, in certain situations, haplotype information and linkage    disequilibrium-induced associations between polymorphic loci that neighbor loci harboring functional sequence variants can be exploited to identify disease-predisposing alleles in large, freely mixing populations via estimated haplotype frequency    methods.</p>

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</description>

<author>D Fallin et al.</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/194</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/194</guid>
<pubDate>Tue, 08 May 2012 15:39:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>An Introduction to State Court Section 1983 Litigation</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/193</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/193</guid>
<pubDate>Tue, 08 May 2012 15:39:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Credit Rating Organizations, Their Role in the Current Calamity, and Future Prospects for Reform</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/192</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/192</guid>
<pubDate>Tue, 08 May 2012 15:39:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Christopher Sagers et al.</author>


</item>


<item>
<title>Environmental Justice:  The Social and Demographic Impact of Environmental Choices</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/190</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/190</guid>
<pubDate>Tue, 08 May 2012 15:38:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Heidi Gorovitz Robertson</author>


</item>


<item>
<title>Controlling Existing Facilities</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/189</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/189</guid>
<pubDate>Tue, 08 May 2012 15:38:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>This chapter first will address the environmental grandfather clauses that allow older, existing facilities to pollute more heavily than newer facilities of the same type. It will discuss allegations of unequal government enforcement as a driver of environmental inequity. It will then address the statutory, administrative, and common law methods citizens might use to control existing facilities that degrade the environment in low-income and minority communities. Finally, it will briefly address methods for controlling existing facilities that are available only to government entities.</p>

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</description>

<author>Heidi Gorovitz Robertson</author>


</item>


<item>
<title> Defects in development of the kidney, heart and eye vasculature in mice homozygous for a hypomorphic Notch2 mutation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/183</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/183</guid>
<pubDate>Tue, 08 May 2012 15:38:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Notch gene family encodes large transmembrane receptors that are components of an evolutionarily conserved intercellular signaling mechanism. To assess the in vivo role of the Notch2 gene, we constructed a targeted mutation,    Notch2(del1). Unexpectedly, we found that alternative splicing of the Notch2(del1) mutant allele leads to the production of two different in-frame transcripts that delete either one or two EGF repeats of the Notch2 protein, suggesting that this    allele is a hypomorphic Notch2 mutation. Mice homozygous for the Notch2(del1) mutation died perinatally from defects in glomerular development in the kidney.  Notch2(del1)/Notch2(del1 )mutant kidneys were hypoplastic and mutant glomeruli lacked a    normal capillary tuft. The Notch ligand encoded by the Jag1 gene was expressed in developing glomeruli in cells adjacent to Notch2-expressing cells. We show that mice heterozygous for both the Notch2(del1) and Jag1(dDSL) mutations exhibit a    glomerular defect similar to, but less severe than, that of Notch2(del1)/Notch2(del1 )homozygotes.  The co-localization and genetic interaction of Jag1 and Notch2 imply that this ligand and receptor physically interact, forming part of the signal    transduction pathway required for glomerular differentiation and patterning. Notch2(del1)/Notch2(del1 )homozygotes also display myocardial hypoplasia, edema and hyperplasia of cells associated with the hyaloid vasculature of the eye. These data    identify novel developmental roles for Notch2 in kidney, heart and eye development.</p>

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</description>

<author>B McCright et al.</author>


</item>


<item>
<title>Cleveland</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/187</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/187</guid>
<pubDate>Tue, 08 May 2012 15:38:48 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Heidi Gorovitz Robertson</author>


</item>


<item>
<title>The First and Fourth Amendment Rights of Students</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/185</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/185</guid>
<pubDate>Tue, 08 May 2012 15:38:42 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>The First and Fourth Amendment Rights of Students</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/184</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/184</guid>
<pubDate>Tue, 08 May 2012 15:38:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>The First and Fourth Amendment Rights of Students</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/183</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/183</guid>
<pubDate>Tue, 08 May 2012 15:38:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title> Genetic modification of glaucoma associated phenotypes between AKXD-28/Ty and DBA/2J mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/182</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/182</guid>
<pubDate>Tue, 08 May 2012 15:38:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Glaucoma is a common disease but its molecular etiology is poorly understood. It involves retinal ganglion cell death and optic nerve damage that is often associated with elevated intraocular pressure.  Identifying    genes that modify glaucoma associated phenotypes is likely to provide insights to mechanisms of glaucoma. We previously reported glaucoma in DBA/2J mice caused by recessive alleles at two loci, isa and ipd, that cause iris stromal atrophy and    iris pigment dispersion, respectively. A approach for identifying modifier genes is to study the effects of specific mutations in different mouse strains. When the phenotypic effect of a mutation is modified upon its introduction into a new    strain, crosses between the parental strains can be used to identify modifier genes. The purpose of this study was to determine if the effects of the DBA/2J derived isa and ipd loci are modified in strain AKXD-28/Ty.  RESULTS: AKXD-28/Ty mice    develop glaucoma characterized by intraocular pressure elevation, retinal ganglion loss, and optic nerve excavation. In AKXD-28/Ty, isa causes an iris stromal atrophy phenotype as in DBA/2J.  However, the iris pigment dispersion phenotype    associated with ipd in DBA/2J does not occur in AKXD-28/Ty. Additionally, a greater severity and speed of retinal and optic nerve damage following intraocular pressure elevation in AKXD-28/Ty compared to DBA/2J mice suggests that AKXD-28/Ty is    more susceptible to pressure-induced cell death. CONCLUSIONS: The consequences of the ipd and isa mutations are modified in the AKXD-28/Ty background. These strains provide a resource for the identification of modifier genes that modulate pigment    dispersion and susceptibility to pressure-induced cell death.</p>

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</description>

<author>M G. Anderson et al.</author>


</item>


<item>
<title>The First and Fourth Amendment Rights of Students</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/182</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/182</guid>
<pubDate>Tue, 08 May 2012 15:38:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>The First and Fourth Amendment Rights of Students</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/181</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/181</guid>
<pubDate>Tue, 08 May 2012 15:38:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>The Regulation of Public Protest:  Picketing, Parades, and Demonstrations</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/180</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/180</guid>
<pubDate>Tue, 08 May 2012 15:38:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>The First and Fourth Amendment Rights of Students</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/178</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/178</guid>
<pubDate>Tue, 08 May 2012 15:38:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>Time, Place, and Manner Restrictions</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/177</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/177</guid>
<pubDate>Tue, 08 May 2012 15:38:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>Viewpoint Discrimination</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/176</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/176</guid>
<pubDate>Tue, 08 May 2012 15:38:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>True Threats</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/175</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/175</guid>
<pubDate>Tue, 08 May 2012 15:38:13 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title> The Mouse Genome Database (MGD): integration nexus for the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/181</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/181</guid>
<pubDate>Tue, 08 May 2012 15:38:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Database (MGD) is the community database resource for the laboratory mouse, a key model organism for interpreting the human genome and for understanding human biology and disease (http://www.informatics.jax.org).    MGD provides standard nomenclature and consensus map positions for mouse genes and genetic markers; it provides a curated set of mammalian homology records, user-defined chromosomal maps, experimental data sets and the definitive mouse 'gene to    sequence' reference set for the research community. The integration and standardization of these data sets facilitates the transition between mouse DNA sequence, gene and phenotype annotations. A recent focus on allele and phenotype    representations enhances the ability of MGD to organize and present data for exploring the relationship between genotype and phenotype. This link between the genome and the biology of the mouse is especially important as phenotype information    grows from large mutagenesis projects and genotype information grows from large-scale sequencing projects.</p>

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</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title>Mobile/Manufactured Home Laws</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/170</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/170</guid>
<pubDate>Tue, 08 May 2012 15:37:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kenneth J. Kowalski</author>


</item>


<item>
<title>Disparate Treatment</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/169</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/169</guid>
<pubDate>Tue, 08 May 2012 15:37:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kenneth J. Kowalski</author>


</item>


<item>
<title> Web-based access to mouse models of human cancers: the Mouse Tumor Biology (MTB) Database.</title>
<link>http://mouseion.jax.org/stfb2000_2009/180</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/180</guid>
<pubDate>Tue, 08 May 2012 15:37:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Tumor Biology (MTB) Database serves as a curated, integrated resource for information about tumor genetics and pathology in genetically defined strains of mice (i.e., inbred, transgenic and targeted mutation strains).    Sources of information for the database include the published scientific literature and direct data submissions by the scientific community. Researchers access MTB using Web-based query forms and can use the database to answer such questions as    'What tumors have been reported in transgenic mice created on a C57BL/6J background?', 'What tumors in mice are associated with mutations in the Trp53 gene?' and 'What pathology images are available for tumors of the mammary gland regardless of    genetic background?'. MTB has been available on the Web since 1998 from the Mouse Genome Informatics web site (http://www.informatics.jax.org). We have recently implemented a number of enhancements to MTB including new query options, redesigned    query forms and results pages for pathology and genetic data, and the addition of an electronic data submission and annotation tool for pathology data.</p>

	]]>
</description>

<author>C J. Bult et al.</author>


</item>


<item>
<title>Contributing Editor</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/168</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/168</guid>
<pubDate>Tue, 08 May 2012 15:37:50 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sandra J. Kerber</author>


</item>


<item>
<title>Responding to the Impact of Downtown Development:  Linkage Programs and Comprehensive Planning</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/167</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/167</guid>
<pubDate>Tue, 08 May 2012 15:37:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. Dennis Keating</author>


</item>


<item>
<title>Rent Control in the United States</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/166</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/166</guid>
<pubDate>Tue, 08 May 2012 15:37:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. Dennis Keating et al.</author>


</item>


<item>
<title>Cleveland: Post-Populist Public-Private Partnerships</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/165</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/165</guid>
<pubDate>Tue, 08 May 2012 15:37:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. Dennis Keating et al.</author>


</item>


<item>
<title>Rent Control:  Fair Return, Landlord Hardship, and Regulatory Takings</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/163</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/163</guid>
<pubDate>Tue, 08 May 2012 15:37:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. Dennis Keating</author>


</item>


<item>
<title> The Mouse Gene Expression Database (GXD).</title>
<link>http://mouseion.jax.org/stfb2000_2009/179</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/179</guid>
<pubDate>Tue, 08 May 2012 15:37:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Gene Expression Database (GXD) is a community resource of gene expression information for the laboratory mouse. By combining the different types of expression data, GXD aims to provide increasingly complete information about    the expression profiles of genes in different mouse strains and mutants, thus enabling valuable insights into the molecular networks that underlie normal development and disease. GXD is integrated with the Mouse Genome Database (MGD). Extensive    interconnections with sequence databases and with databases from other species, and the development and use of shared controlled vocabularies extend GXD's utility for the analysis of gene expression information. GXD is accessible through the    Mouse Genome Informatics web site at http://www.informatics.jax.org/ or directly at http://www.informatics.jax.org/menus/expression_menu. shtml.</p>

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</description>

<author>M Ringwald et al.</author>


</item>


<item>
<title>Community Development Corporations in the United States:  Their Role in Housing and Urban Redevelopment</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/161</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/161</guid>
<pubDate>Tue, 08 May 2012 15:37:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. Dennis Keating et al.</author>


</item>


<item>
<title>Post-Populist Public-Private Partnerships</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/159</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/159</guid>
<pubDate>Tue, 08 May 2012 15:37:13 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. Dennis Keating et al.</author>


</item>


<item>
<title>Open Housing in Metropolitan Cleveland</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/158</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/158</guid>
<pubDate>Tue, 08 May 2012 15:37:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W. Dennis Keating</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/157</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/157</guid>
<pubDate>Tue, 08 May 2012 15:37:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/156</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/156</guid>
<pubDate>Tue, 08 May 2012 15:37:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/155</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/155</guid>
<pubDate>Tue, 08 May 2012 15:36:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title> The future of genetic case-control studies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/178</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/178</guid>
<pubDate>Tue, 08 May 2012 15:36:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The case-control study design has been a veritable workhorse in epidemiological research since its inception and acceptance as a valid and valued field of inquiry. The reasons for this owe to the simplicity of the required sampling    and the (potential) ease of analysis and interpretation of results. Unfortunately, there are a number of problems that plague the use of the case-control design in assessing relationships between genetic variation and disease susceptibility in    the population at large. Many of these problems are entirely analogous to problems that inhere in applications of the case-control design in nongenetic settings. These problems include stratification, the assessment of statistical significance,    heterogeneity, and the interpretation of multiple outcomes or phenotypic information. In this chapter we describe 10 problems thought to plague genetic case-control studies and offer potential solutions to each. Many of our proposed solutions    require the use of multiple DNA markers to accommodate the genetic background of the individuals sampled as cases and controls. It is hoped that our discussions and proposals will spark further debate about the analysis and ultimate utility of    the case-control study in genetic epidemiology research.</p>

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</description>

<author>N J. Schork et al.</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/154</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/154</guid>
<pubDate>Tue, 08 May 2012 15:36:53 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/153</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/153</guid>
<pubDate>Tue, 08 May 2012 15:36:49 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Biomedical Matching Gui Development</title>
<link>http://scholarworks.boisestate.edu/electrical_gradproj/1</link>
<guid isPermaLink="true">http://scholarworks.boisestate.edu/electrical_gradproj/1</guid>
<pubDate>Tue, 08 May 2012 15:36:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Biomedical researchers constantly search for new methods to diagnose the extent of joint injuries in live human subjects. In order to achieve this, the researchers need to know the accurate three dimensional kinematic data of bones and joints and to accurately quantify how bones in a joint move relative to one another during dynamic activities. Algorithms have been developed previously to estimate the exact spatial position and movement of the bones. These methods involved generation of digitally reconstructed radiographs (DRR) from a three dimensional CT scan image of human joint with known position and orientation and comparing it with the original two dimensional video fluoroscopy (video X-ray) image. This way, a DRR image could be found which looks similar to the fluoroscopy frame of the knee joint and thus the position and orientation of the bone could be discovered.</p>
<p>Previous research has been done for finding the dimensions and the orientation of the bone by making use of a sequential Monte Carlo method [1] and Swarm Intelligence techniques in a parallel computing environment [2]. These methods are a little hard to understand by a person not involved in image processing. This project is about developing a user friendly GUI to help people understand the scope of the problem on which researchers are working. The GUI displays the bones in both three dimensional and two dimensional space, allowing the human user to do the search which was previously done automatically by the computer using image feature information. The user of the GUI will estimate the position of a given bone, given images of a bone in 3D and 2D space viewed at perspectives chosen by the user.</p>

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</description>

<author>Nazia Sarang</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/152</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/152</guid>
<pubDate>Tue, 08 May 2012 15:36:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Section 1983 Wrongful Death Remedies</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/151</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/151</guid>
<pubDate>Tue, 08 May 2012 15:36:42 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Tax Increment Financing</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/150</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/150</guid>
<pubDate>Tue, 08 May 2012 15:36:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Powers of Planning Commissions and Planning Boards</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/149</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/149</guid>
<pubDate>Tue, 08 May 2012 15:36:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title> Genome partitioning and whole-genome analysis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/177</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/177</guid>
<pubDate>Tue, 08 May 2012 15:36:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Standard DNA marker-based approaches to mapping genes that influence complex traits typically consider a limited number of hypotheses. Most of these hypotheses concentrate on the effect of a single individual locus (or relatively    few loci) on the trait of interest. Although of tremendous importance scientifically, such hypotheses do not accommodate the full range of genetic phenomena that may contribute to phenotypic expression.  We present novel approaches to complex    trait analysis that make as complete use of marker information as is possible. The proposed methodologies can be used to entertain a wide variety of hypotheses, including those that engage, for example, the contribution of a particular    chromosome, genome-wide heterozygosity, and multiple genomic regions, to phenotypic expression. We consider a number of possible extensions of the proposed methods as well as their limitations. Although we discuss many methodological details in    the context of quantitative trait locus mapping involving sampling units such as human pedigrees and hybrids resulting from crosses between inbred strains of model organisms, our procedures can be easily adapted to standard sibpair and other    sampling unit-based designs. Ultimately, the proposed approaches not only have the potential to increase power to identify individual loci that harbor trait-influencing genes, but also present a framework for testing a number of hypotheses about    the nature of the genetic determinants of phenotypes in general.</p>

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</description>

<author>N J. Schork</author>


</item>


<item>
<title>Land Use Regulation of Religious Institutions:  Balancing Planning Concerns with Constitutional and Statutory Safeguards for Religious Freedom</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/147</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/147</guid>
<pubDate>Tue, 08 May 2012 15:36:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Religious Land Use and RLUIPA Update</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/145</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/145</guid>
<pubDate>Tue, 08 May 2012 15:36:18 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Legal Issues in the Regulation of On-Premise Signs</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/144</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/144</guid>
<pubDate>Tue, 08 May 2012 15:36:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein et al.</author>


</item>


<item>
<title>Recent Developments Concerning RLUIPA</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/142</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/142</guid>
<pubDate>Tue, 08 May 2012 15:36:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>First Amendment Zoning Issues:  Regulation of Signs, Adult Entertainment &amp; Religious Uses</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/141</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/141</guid>
<pubDate>Tue, 08 May 2012 15:36:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title> Comparative mapping: tracking gene homologues among mammals.</title>
<link>http://mouseion.jax.org/stfb2000_2009/176</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/176</guid>
<pubDate>Tue, 08 May 2012 15:35:58 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J T. Eppig</author>


</item>


<item>
<title>Anti-Defamation League of B&apos;Nai B&apos;rith</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/139</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/139</guid>
<pubDate>Tue, 08 May 2012 15:35:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Property Rights, Police Power, Nuisance and Vested Rights</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/137</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/137</guid>
<pubDate>Tue, 08 May 2012 15:35:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein et al.</author>


</item>


<item>
<title>O&apos;Brien Content-Neutral Free Speech</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/136</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/136</guid>
<pubDate>Tue, 08 May 2012 15:35:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Low-Value Speech</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/135</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/135</guid>
<pubDate>Tue, 08 May 2012 15:35:40 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein</author>


</item>


<item>
<title>Freedom of Religion and Expression</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/134</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/134</guid>
<pubDate>Tue, 08 May 2012 15:35:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein et al.</author>


</item>


<item>
<title>Eminent Domain, Takings and Exactions</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/133</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/133</guid>
<pubDate>Tue, 08 May 2012 15:35:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan C. Weinstein et al.</author>


</item>


<item>
<title> Defective mesonephric cell migration is associated with abnormal testis cord development in C57BL/6J XY(Mus domesticus) mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/175</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/175</guid>
<pubDate>Tue, 08 May 2012 15:35:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>During the critical period of mouse sex determination, mesenchymal cells migrate from the mesonephros into the adjacent developing testis. This process is thought to initiate cord development and is dependent on Sry.  The presence    of Sry, however, does not always guarantee normal testis development. For example, transfer of certain Mus domesticus-derived Y chromosomes, i.e., M. domesticus Sry alleles, onto the C57BL/6J (B6) inbred mouse strain results in abnormal testis    development. We tested the hypothesis that mesonephric cell migration was impaired in three cases representing a range of aberrant testis development: B6 XY(AKR), B6 XY(POS), and (BXD-21 x B6-Y(POS))F1 XY(POS). In each case, mesonephric cell    migration was abnormal. Furthermore, the timing, extent, and position of migrating cells in vitro and cord development in vivo were coincident, supporting the hypothesis that mesonephric cells are critical for cord development. Additional    experiments indicated that aberrant testis development results from the inability of Sry(M. domesticus) to initiate normal cell migration, but that downstream signal transduction mechanisms are intact. These experiments provide new insight into    the mechanism of C57BL/6J-Y(M. domesticus) sex reversal. We present a model incorporating these findings as they relate to mammalian sex determination.</p>

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</description>

<author>K H. Albrecht et al.</author>


</item>


<item>
<title>The Cape Town Convention: Unleashing Capital for the Space Industry</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/131</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/131</guid>
<pubDate>Tue, 08 May 2012 15:35:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mark J. Sundahl</author>


</item>


<item>
<title>Litigating Section  1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/130</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/130</guid>
<pubDate>Tue, 08 May 2012 15:35:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Litigating Section  1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/129</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/129</guid>
<pubDate>Tue, 08 May 2012 15:35:18 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>The Civil Rights Act of 1991 and the Judicial Improvements Act of 1990: Their Impact on State Court Practice and on the Supplemental Jurisdiction of the Federal Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/128</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/128</guid>
<pubDate>Tue, 08 May 2012 15:35:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>State Courts and Supplemental Jurisdiction Under the Civil Rights Act of 1991</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/127</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/127</guid>
<pubDate>Tue, 08 May 2012 15:35:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title> Insulin-like growth factor I and bone: from mouse to man.</title>
<link>http://mouseion.jax.org/stfb2000_2009/174</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/174</guid>
<pubDate>Tue, 08 May 2012 15:35:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Serum insulin-like growth factor I (IGF-I) is regulated by numerous variables, including growth hormone (GH), nutritional status, gonadal steroids and other hormones. However, the circulating IGF-I phenotype is also under heritable    regulation, and several genetic determinants may be important in defining tissue-specific expression of the gene encoding this peptide. A very strong correlation has been found between serum IGF-I concentration and bone acquisition in both mice    and humans. Based on previous studies as well as ongoing work with mice, it has been hypothesized that regulation of the serum IGF-I phenotype includes non-GH-dependent factors and, furthermore, that these determinants are also involved in the    acquisition of bone mass. This paper reports that, by performing intercrosses between two inbred strains of mice of similar age, size and length, but with different serum levels of IGF-I, we have identified regulatory loci for serum IGF-I and    established their relationship to putative quantitative trait loci for bone mineral density.  Mapping these quantitative trait loci will help refine our understanding of disorders related to IGF-I.</p>

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</description>

<author>W G. Beamer et al.</author>


</item>


<item>
<title>Litigating Section  1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/124</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/124</guid>
<pubDate>Tue, 08 May 2012 15:35:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>An Introduction to State Court § 1983 Litigation</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/123</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/123</guid>
<pubDate>Tue, 08 May 2012 15:34:59 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title>Litigating Section 1983 Actions in State Courts</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/119</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/119</guid>
<pubDate>Tue, 08 May 2012 15:34:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Steven H. Steinglass</author>


</item>


<item>
<title> Spontaneous fracture (sfx): a mouse genetic model of defective peripubertal bone formation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/173</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/173</guid>
<pubDate>Tue, 08 May 2012 15:34:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>A new mouse model of stage-specific bone growth failure and fracture has been recovered as an autosomal recessive mutation, designated spontaneous fracture (sfx). The sfx/sfx mice are phenotypically normal until shortly after    weaning, when reduced mobility and impaired somatic growth are first noted. By 6 weeks of age, body, spleen, and thymus weights, as well as hematocrits and serum calcium, inorganic phosphate, total alkaline phosphatase, insulin-like growth    factor-I, and osteocalcin levels are decreased. The sfx/sfx mice also show reduced femoral cortical density and diaphyseal circumference, as well as a paucity of mature osteoblasts on bone surfaces. Histological analyses of the femur and tibia in    the mutants show subtle reduction of chondrocyte numbers in epiphyseal-plate columns, reduction of matrix, and near absence of osteoid below the differentiated chondrocytes. Trabeculae in proximal tibiae, iliacs, and vertebral bodies are sparse    and thin. Cortical bone thickness of mutants is markedly thinned in all sites examined. By 7-8 weeks, radiographic films routinely show spontaneous impact fractures of the distal femur accompanied by callus formation, whereas complete fractures    are less commonly observed.  Volumetric bone mineral density (BMD) of mutant femurs is similar to +/?  littermates in the center of the femoral diaphysis, but BMD declines as either end of the femoral diaphysis is approached. We have mapped the    gene responsible for this phenotype to central Chromosome 14. Reduced bone mass, impaired bone formation, abnormalities of bone architecture, and a disposition to spontaneous fracture identify sfx/sfx mice as a useful model for understanding the    mechanisms responsible for peripubertal bone formation.</p>

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</description>

<author>W G. Beamer et al.</author>


</item>


<item>
<title>What&apos;s New About &quot;Past Practices?</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/115</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/115</guid>
<pubDate>Tue, 08 May 2012 15:34:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan Miles Ruben</author>


</item>


<item>
<title>Environmental Justice:  The Social and Demographic Impact of Environmental Choices</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/114</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/114</guid>
<pubDate>Tue, 08 May 2012 15:34:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Heidi Gorovitz Robertson</author>


</item>


<item>
<title>William Ruckelshaus</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/112</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/112</guid>
<pubDate>Tue, 08 May 2012 15:34:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Heidi Gorovitz Robertson</author>


</item>


<item>
<title> Heterogeneity of Porphyromonas gingivalis strains in the induction of alveolar bone loss in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/172</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/172</guid>
<pubDate>Tue, 08 May 2012 15:34:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>These experiments examine alveolar bone loss in a model in which specific pathogen-free mice are exposed orally with Porphyromonas gingivalis.  Alveolar bone loss was induced as a result of a specific infection with P. gingivalis,    rather than other environmental antigens. Infection with live P. gingivalis was required, as significant bone loss did not follow gavage with formalin-killed P. gingivalis. The virulence of different strains of P. gingivalis was compared. Two    laboratory strains of the bacteria (ATCC 53977 and W50) and a mutant strain lacking the 43-kDa fimbrillin (strain DPG3) induced bone loss. P. gingivalis 381, however, did not induce bone loss. There was a strong immunoglobulin G (IgG) antibody    response to infection with each strain but a significant serum IgA response only to strain 381. These studies show that in mice with a background oral microflora bone loss is induced by a specific infection with P. gingivalis and that bacterial    strain variation is important in determining whether alveolar bone loss will ensue.</p>

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</description>

<author>P J. Baker et al.</author>


</item>


<item>
<title>Controlling Existing Facilities</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/110</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/110</guid>
<pubDate>Tue, 08 May 2012 15:34:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>This chapter first will address the environmental grandfather clauses that allow older, existing facilities to pollute more heavily than newer facilities of the same type. It will discuss allegations of unequal government enforcement as a driver of environmental inequity. It will then address the statutory, administrative, and common law methods citizens mights use to control existing facilities that degrade the environment in low-income and minority communities. Finally, it will briefly address methods for controlling existing facilities that are available only to government entities.</p>

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</description>

<author>Heidi Gorovitz Robertson</author>


</item>


<item>
<title>The First and Fourth Amendment Rights of Students</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/108</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/108</guid>
<pubDate>Tue, 08 May 2012 15:34:12 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>The First and Fourth Amendment Rights of Students</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/106</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/106</guid>
<pubDate>Tue, 08 May 2012 15:34:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>The First and Fourth Amendment Rights of Students</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/105</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/105</guid>
<pubDate>Tue, 08 May 2012 15:34:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title> How to study pathologic phenotypes of knockout mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/171</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/171</guid>
<pubDate>Tue, 08 May 2012 15:34:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>R T. Bronson</author>


</item>


<item>
<title>The Regulation of Public Protest:  Picketing, Parades, and Demonstrations</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/104</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/104</guid>
<pubDate>Tue, 08 May 2012 15:33:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>A First Amendment Compass:  Navigating the Speech Clause with a Five-Step Analytical Framework</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/103</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/103</guid>
<pubDate>Tue, 08 May 2012 15:33:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title>Prisons</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/98</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/98</guid>
<pubDate>Tue, 08 May 2012 15:33:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kevin F. O&apos;Neill</author>


</item>


<item>
<title> Agrin isoforms with distinct amino termini: differential expression, localization, and function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/170</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/170</guid>
<pubDate>Tue, 08 May 2012 15:33:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The proteoglycan agrin is required for postsynaptic differentiation at the skeletal neuromuscular junction, but is also associated with basal laminae in numerous other tissues, and with the surfaces of some neurons. Little is known    about its roles at sites other than the neuromuscular junction, or about how its expression and subcellular localization are regulated in any tissue. Here we demonstrate that the murine agrin gene generates two proteins with different NH(2)    termini, and present evidence that these isoforms differ in subcellular localization, tissue distribution, and function. The two isoforms share approximately 1,900 amino acids (aa) of common sequence following unique NH(2) termini of 49 or 150    aa; we therefore call them short NH(2)-terminal (SN) and long NH(2)-terminal (LN) isoforms. In the mouse genome, LN-specific exons are upstream of an SN-specific exon, which is in turn upstream of common exons. LN-agrin is expressed in both    neural and nonneural tissues. In spinal cord it is expressed in discrete subsets of cells, including motoneurons. In contrast, SN-agrin is selectively expressed in the nervous system but is widely distributed in many neuronal cell types. Both    isoforms are externalized from cells but LN-agrin assembles into basal laminae whereas SN-agrin remains cell associated. Differential expression of the two isoforms appears to be transcriptionally regulated, whereas the unique SN and LN sequences    direct their distinct subcellular localizations.  Insertion of a "gene trap" construct into the mouse genome between the LN and SN exons abolished expression of LN-agrin with no detectable effect on expression levels of SN-agrin or on SN-agrin    bioactivity in vitro. Agrin protein was absent from all basal laminae in mice lacking LN-agrin transcripts. The formation of the neuromuscular junctions was as drastically impaired in these mutants as in mice lacking all forms of agrin. Thus,    basal lamina-associated LN-agrin is required for neuromuscular synaptogenesis, whereas cell-associated SN-agrin may play distinct roles in the central nervous system.</p>

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</description>

<author>R W. Burgess et al.</author>


</item>


<item>
<title>Case Law Supplement</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/97</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/97</guid>
<pubDate>Tue, 08 May 2012 15:33:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>divorce, pensions</p>

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</description>

<author>Karin Mika</author>


</item>


<item>
<title>Cybermedicine, Telemedicine, and Data Protection in the United States</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/96</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/96</guid>
<pubDate>Tue, 08 May 2012 15:33:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>This chapter provides an overview of law relating to online and Internet medical practice, data protection, and consumer information privacy. It provides a comprehensive overview of federal (HIPAA) and state privacy laws, concluding that both those legal resources leave gaps in consumer protection and provide no real penalties for violating the laws. The authors educate the readers to the legal and data protection problems consumers will encounter in purchasing medical and health services on the Internet. Furthermore, the authors recount some actual case studies and follow those with expert advice for those Internet consumers who wish to be not merely informed, but also safe. The authors not only educate the readers to the lack of protection afforded to them but also advocate throughout the chapter that the United States must enact more federal protection for the consumer in order to deter privacy violations and punish criminal, negligent, and wilful violations of personal consumer privacy.</p>

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</description>

<author>Karin Mika et al.</author>


</item>


<item>
<title>Teaching Persuasion and Critical Thinking Using the State of the Union Address</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/95</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/95</guid>
<pubDate>Tue, 08 May 2012 15:33:27 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Claire May</author>


</item>


<item>
<title>Disparate Treatment</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/93</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/93</guid>
<pubDate>Tue, 08 May 2012 15:33:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kenneth J. Kowalski</author>


</item>


<item>
<title> Analysis of variance for gene expression microarray data.</title>
<link>http://mouseion.jax.org/stfb2000_2009/169</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/169</guid>
<pubDate>Tue, 08 May 2012 15:33:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Spotted cDNA microarrays are emerging as a powerful and cost-effective tool for large-scale analysis of gene expression. Microarrays can be used to measure the relative quantities of specific mRNAs in two or more tissue samples for    thousands of genes simultaneously. While the power of this technology has been recognized, many open questions remain about appropriate analysis of microarray data. One question is how to make valid estimates of the relative expression for genes    that are not biased by ancillary sources of variation. Recognizing that there is inherent "noise" in microarray data, how does one estimate the error variation associated with an estimated change in expression, i.e., how does one construct the    error bars? We demonstrate that ANOVA methods can be used to normalize microarray data and provide estimates of changes in gene expression that are corrected for potential confounding effects. This approach establishes a framework for the general    analysis and interpretation of microarray data.</p>

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</description>

<author>M K. Kerr et al.</author>


</item>


<item>
<title>Dispersion and Adaptation:  The California Experience</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/87</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/87</guid>
<pubDate>Tue, 08 May 2012 15:33:02 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. Dennis Keating</author>


</item>


<item>
<title>Downtown Linkage Policies: A Case Study of Developers&apos; Opinions on San Francisco&apos;s Program</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/86</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/86</guid>
<pubDate>Tue, 08 May 2012 15:32:58 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. Dennis Keating</author>


</item>


<item>
<title> Genotype-based screen for ENU-induced mutations in mouse embryonic stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/168</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/168</guid>
<pubDate>Tue, 08 May 2012 15:32:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ability to generate mutations is a prerequisite to functional genetic analysis. Despite a long history of using mice as a model system for genetic analysis, the scientific community has not generated a comprehensive collection    of multiple alleles for most mouse genes. The chemical mutagen of choice for mouse has been N-ethyl-N-nitrosourea (ENU), an alkylating agent that mainly causes base substitutions in DNA, and therefore allows for recovery of complete and partial    loss-, as well as gain-, of-function alleles . Specific locus tests designed to detect recessive mutations showed that ENU is the most efficient mutagen in mouse with an approximate mutation rate of 1 in 1,000 gametes. In fact, several    genome-wide and region-specific screens based on phenotypes have been carried out. The anticipation of the completion of the human and mouse genome projects, however, now emphasizes genotype-driven genetics--from sequence to mutants. To take    advantage of the mutagenicity of ENU and its ability to create allelic series of mutations, we have developed a complementary approach to generating mutations using mouse embryonic stem (ES) cells. We show that a high mutation frequency can be    achieved and that modulating DNA-repair activities can enhance this frequency. The treated cells retain germline competency, thereby rendering this approach applicable for efficient generation of an allelic series of mutations pivotal to a    fine-tuned dissection of biological pathways.</p>

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</description>

<author>Y Chen et al.</author>


</item>


<item>
<title>Cleveland: Post-Populist Public-Private Partnerships</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/83</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/83</guid>
<pubDate>Tue, 08 May 2012 15:32:49 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. Dennis Keating et al.</author>


</item>


<item>
<title>Linkage:  Tying Downtown Development to Community Housing Needs</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/82</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/82</guid>
<pubDate>Tue, 08 May 2012 15:32:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. Dennis Keating</author>


</item>


<item>
<title>The Impact of Regulatory Takings Law on Municipal Exactions Policy: The Cases of Boston and Los Angeles </title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/80</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/80</guid>
<pubDate>Tue, 08 May 2012 15:32:40 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. Dennis Keating</author>


</item>


<item>
<title>Management of Neighborhood Development: Community Development Corporations</title>
<link>http://engagedscholarship.csuohio.edu/fac_book_contributions/78</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/fac_book_contributions/78</guid>
<pubDate>Tue, 08 May 2012 15:32:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. Dennis Keating et al.</author>


</item>


<item>
<title> The Oak Ridge Polycystic Kidney (orpk) disease gene is required for left-right axis determination.</title>
<link>http://mouseion.jax.org/stfb2000_2009/167</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/167</guid>
<pubDate>Tue, 08 May 2012 15:32:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Analysis of several mutations in the mouse is providing useful insights into the nature of the genes required for the establishment of the left-right axis during early development. Here we describe a new targeted allele of the    mouse Tg737 gene, Tg737(Delta)2-3(beta)Gal), which causes defects in left-right asymmetry and other abnormalities during embryogenesis. The Tg737 gene was originally identified based on its association with the mouse Oak Ridge Polycystic Kidney    (orpk) insertional mutation, which causes polycystic kidney disease and other defects.  Complementation tests between the original orpk mutation and the new targeted knock-out mutation demonstrate that Tg737(Delta)2-3(beta)Gal) behaves as an    allele of Tg737. The differences in the phenotype between the two mutations suggest that the orpk mutation is a hypomorphic allele of the Tg737 gene. Unlike the orpk allele, where all homozygotes survive to birth, embryos homozygous for the    Tg737(Delta)2-3(beta)Gal) mutation arrest in development at mid-gestation and exhibit neural tube defects, enlargement of the pericardial sac and, most notably, left-right asymmetry defects. At mid-gestation the direction of heart looping is    randomized, and at earlier stages in development lefty-2 and nodal, which are normally expressed asymmetrically, exhibit symmetrical expression in the mutant embryos. Additionally, we determined that the ventral node cells in mutant embryos fail    to express the central cilium, which is a characteristic and potentially functional feature of these cells. The expression of both Shh and Hnf3(beta) is downregulated in the midline at E8.0, indicating that there are significant alterations in    midline development in the Tg737(Delta)2-3(beta)Gal) homozygous embryos. We propose that the failure of ventral node cells to fully mature alters their ability to undergo differentiation as they migrate out of the node to contribute to the    developing midline structures. Analysis of this new knockout allele allows us to define a critical role for the Tg737 gene during early embryogenesis. We have named the product of the Tg737 gene Polaris, which is based on the various polarity    related defects associated with the different alleles of the Tg737 gene.</p>

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</description>

<author>N S. Murcia et al.</author>


</item>


<item>
<title> Neuroepithelial defects of the inner ear in a new allele of the mouse mutation Ames waltzer.</title>
<link>http://mouseion.jax.org/stfb2000_2009/166</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/166</guid>
<pubDate>Tue, 08 May 2012 15:32:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>This report presents new findings regarding a recessive insertional mutation in the transgenic line TgN2742Rpw that causes deafness and circling behavior in mice homozygous for the mutation. The mutant locus was mapped to a region    on mouse chromosome 10 close to three spontaneous recessive mutations causing deafness: Ames waltzer (av), Waltzer (v), and Jackson circler (jc). Complementation testing revealed that the TgN2742Rpw mutation is allelic with av. Histological and    auditory brainstem response (ABR) evaluation of animals that have the new allele balanced with the av(J) allele (called compound heterozygotes, TgN2742Rpw/av(J)) supports our genetic analysis. ABR evaluation shows complete absence of auditory    response throughout the life span of TgN2742Rpw/av(J) compound heterozygotes. Scanning electron microscopy revealed abnormalities of inner and outer hair cell stereocilia in the cochleae of TgN2742Rpw mutants at 10 days after birth (DAB). The    organ of Corti subsequently undergoes degeneration, leading to nearly complete loss of the cochlear neuroepithelium in older mutants by about 50 DAB. The vestibular neuroepithelia remain morphologically normal until at least 30 DAB.  However, by    50 days, degenerative changes are evident in the saccular macula, which progresses to total loss of the saccular neuroepithelium in older animals. The new allele of av reported here will be designated av(TgN2742Rpw).</p>

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</description>

<author>K N. Alagramam et al.</author>


</item>


<item>
<title> Persistent hyperplastic tunica vasculosa lentis and persistent hyperplastic primary vitreous in transgenic line TgN3261Rpw.</title>
<link>http://mouseion.jax.org/stfb2000_2009/165</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/165</guid>
<pubDate>Tue, 08 May 2012 15:31:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Persistent hyperplastic tunica vasculosa lentis and persistent hyperplastic primary vitreous are congenital ocular anomalies that can lead to cataract formation. A line of insertional mutant mice, TgN3261Rpw, generated at the Oak    Ridge National Laboratory in a large-scale insertional mutagenesis program was found to have a low incidence (8/243; 3.29%) of multiple developmental ocular abnormalities. The ocular abnormalities include persistent hyperplastic primary vitreous,    persistent hyperplastic tunica vasculosa lentis, failure of cleavage of the anterior segment, retrolental fibrovascular membrane, posterior polar cataract, and detached retina. This transgenic mouse line provides an ontogenetic model because of    the high degree of similarity of this entity in humans, dogs, and mice.</p>

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</description>

<author>C M. Colitz et al.</author>


</item>


<item>
<title> Mouse chromosome 15.</title>
<link>http://mouseion.jax.org/stfb2000_2009/164</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/164</guid>
<pubDate>Tue, 08 May 2012 15:31:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>K Huppi et al.</author>


</item>


<item>
<title> Heritability of life span in mice and its implication for direct and indirect selection for longevity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/163</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/163</guid>
<pubDate>Tue, 08 May 2012 15:30:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>We found high narrow-sense heritability of life span based on the regression of offspring on average parental (midparent) life spans. In two mouse populations prepared using the 4-way-cross design, mean +/- SE heritabilities were    62 +/- 11% (P < 0.001) and 44 +/- 15% (P < 0.01). To reflect inherited rates of aging, rather than resistance to early disease, data from the first 25% to die were deleted, so that only about 40% of families were used for offspring-midparent    regressions. Heritabilities still remained high, 38% and 55%, for the same two populations, respectively. Populations studied in two other experiments did not show nearly as high heritabilities; in one case probably due to environmental stress,    and in the other probably because the strains used did not have sufficient additive variance in genes regulating longevity. Significant heritabilities occurred only when a wild derived inbred strain was included in the 4-way cross. The age when a    female ceased to reproduce appeared to be related to the life spans of her offspring, but only weakly, not approaching significance for any individual experiment. The age when a female became infertile was related to her life span, but the    relationship disappeared when short-lived mice were excluded from the analysis. Our findings indicate that, in sufficiently diverse mouse populations, selection for increased longevity should be possible and that the direct selection for parental    life span will be a more efficient strategy than selection for female reproductive life span.</p>

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</description>

<author>S Klebanov et al.</author>


</item>


<item>
<title> Improved insulin-sensitivity in mice heterozygous for PPAR-gamma deficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/162</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/162</guid>
<pubDate>Tue, 08 May 2012 15:30:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The thiazolidinedione class of insulin-sensitizing, antidiabetic drugs interacts with peroxisome proliferator-activated receptor gamma (PPAR-gamma). To gain insight into the role of this nuclear receptor in insulin resistance and    diabetes, we conducted metabolic studies in the PPAR-gamma gene knockout mouse model. Because homozygous PPAR-gamma-null mice die in development, we studied glucose metabolism in mice heterozygous for the mutation (PPAR-gamma(+/-) mice). We    identified no statistically significant differences in body weight, basal glucose, insulin, or FFA levels between the wild-type (WT) and PPAR-gamma(+/-) groups. Nor was there a difference in glucose excursion between the groups of mice during    oral glucose tolerance test, but insulin concentrations of the WT group were greater than those of the PPAR-gamma(+/-) group, and insulin-induced increase in glucose disposal rate was significantly increased in PPAR-gamma(+/-) mice. Likewise, the    insulin-induced suppression of hepatic glucose production was significantly greater in the PPAR-gamma(+/-) mice than in the WT mice. Taken together, these results indicate that - counterintuitively - although pharmacological activation of    PPAR-gamma improves insulin sensitivity, a similar effect is obtained by genetically reducing the expression levels of the receptor.</p>

	]]>
</description>

<author>P D. Miles et al.</author>


</item>


<item>
<title> Cryopreservation of murine spermatozoa.</title>
<link>http://mouseion.jax.org/stfb2000_2009/161</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/161</guid>
<pubDate>Tue, 08 May 2012 15:30:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cryopreservation of mouse sperm provides an economic option for preserving the large number of mouse strains now being generated by transgenic and targeted mutation methodologies. The ability of a spermatozoan cell to survive    cryobiological preservation depends on general biophysical constraints that apply to all cells, such as the avoidance or minimization of the formation of intracellular ice during cooling. This action is typically achieved by use of cryoprotectant    substances and by controlled, slow rates of cooling. Superimposed on those general constraints may be special characteristics of mouse spermatozoa, such as more narrow, osmotically driven volume tolerance limits and the fact that relatively    successful freezing can be obtained without the use of a permeating cryoprotective agent. The lack of important information regarding sperm cells fundamental cryobiological properties, including their osmotic and membrane permeability    characteristics, has hindered progress in developing anything but empirically derived methods. Genetic differences between inbred mouse strains are reflected in motility and fertility characteristics of mouse sperm and contribute to the    difficulty of developing successful cryopreservation methods. Recovery of live young from frozen sperm has been much more successful with sperm from hybrid mice than from most inbred strains. There have been no published reports of successful    cryopreservation of rat sperm. Nevertheless, in mice, success in deriving live young from intracytoplasmic sperm injection using sperm frozen under suboptimal conditions raises the possibility of using this technique for the ultimate rescue of    sperm regardless of the success of cryopreservation. This technique, however, requires additional development and verification of its efficacy before it will be suitable for general laboratory use. Although cryopreservation of mouse sperm is not    yet universally successful, it can be used reliably to supplement cryopreservation of embryos and other germline cells or tissues for preserving biomedically important strains of mice for research.</p>

	]]>
</description>

<author>J K. Critser et al.</author>


</item>


<item>
<title> Effects of physiological versus pharmacological beta-carotene supplementation on cell proliferation and histopathological changes in the lungs of cigarette smoke-exposed ferrets.</title>
<link>http://mouseion.jax.org/stfb2000_2009/160</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/160</guid>
<pubDate>Tue, 08 May 2012 15:29:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>There remains a remarkable discordance between the results of observational epidemiological studies and intervention trials using beta-carotene as a potential chemopreventive agent. One question that needs to be examined is whether    the adverse outcomes of human beta-carotene trials are related to the large doses of beta-carotene that were administered. In the present study, ferrets were given a physiological (low) dose or a pharmacological (high) dose of beta-carotene    supplementation (0.43 mg versus 2.4 mg/kg body wt/day, which is equivalent to 6 mg versus 30 mg/day in humans) and exposed to cigarette smoke for 6 months. We investigated the effects of these doses of beta-carotene on retinoid concentrations,    expression of retinoic acid receptors (RARs), activator protein 1 (AP-1; c-Jun and c-Fos), cyclin D1, proliferating cellular nuclear antigen (PCNA), and histopathological changes in the lungs of both normal and cigarette smoke-exposed ferrets.    Thirty-six male ferrets were treated in six groups-control, smoke-exposed (SM), low-dose beta-carotene (LBC), high-dose beta-carotene (HBC), low-dose beta-carotene plus smoke exposure (LBC+SM) or high-dose beta-carotene plus smoke exposure    (HBC+SM)-for 6 months. Retinoic acid concentration and RAR beta gene expression, but not expression of RAR alpha and RAR gamma, was reduced in the lung tissue of HBC+SM, HBC, SM and LBC+SM ferrets, but not in that of LBC ferrets, as compared with    the control group. Expression of AP-1 and PCNA was greater in HBC+SM, HBC, SM and LBC+SM ferrets, but not in the LBC ferrets, as compared with the control group. Increased amounts of cyclin D1 and keratinized squamous metaplasia were observed in    the lung tissue of HBC+SM, HBC and SM groups but not in that of the LBC+SM, LBC or control groups. These data suggest that, in contrast with a pharmacological dose of beta-carotene, a physiological dose of beta-carotene in smoke-exposed ferrets    has no potentially detrimental effects and may afford weak protection against lung damage induced by cigarette smoke.</p>

	]]>
</description>

<author>C Liu et al.</author>


</item>


<item>
<title> Heritable susceptibility for colitis in mice induced by IL-10 deficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/159</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/159</guid>
<pubDate>Tue, 08 May 2012 15:29:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Severity of inflammatory bowel disease in IL-10 gene-targeted mice is in part determined by genetic background. In the current study, a targeted IL-10 gene was transferred into the C3H/HeJBir substrain, known to exhibit high T-cell    and B-cell responses to enteric flora, and to be highly sensitive to colitigenic stress. IL-10-deficient C3H/HeJBir mice developed early onset colitis in contrast to IL-10-deficient C57BL/6J congenic mice Histopathologic analysis of disease in    C3H/HeJBir.Il10-/- and C57BL/6J.Il10-/- mice showed significant differences at all ages studied.  Hybrids of these congenic strains (F1.Il10-/-) were produced to study the mode of inheritance as well as subphenotypes that correlated with    histopathology. Lesions in F1 mice were intermediate between parental strains. C3H-contributed subphenotypes that correlated best with histopathology were peripheral blood granulocyte percentage, serum amyloid A concentration, spleen weight/body    weight ratio, and mesenteric lymph node weight/ body weight ratio. Neither enhanced humoral immunity (secretory IgA, anti-Escherichia coli cellular membrane Ig) characteristic of C3H/HeJBir, nor T-cell percentages in peripheral blood correlated    as well. This study represents a necessary step in elucidating murine genetic modifiers controlling colitis sensitivity.</p>

	]]>
</description>

<author>I J. Bristol et al.</author>


</item>


<item>
<title> Linkage mapping in populations with karyotypic rearrangements.</title>
<link>http://mouseion.jax.org/stfb2000_2009/158</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/158</guid>
<pubDate>Tue, 08 May 2012 15:28:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>A simulation study was used to examine the consequences of karyotypic rearrangements on molecular genetic map construction. Two groups of 50 datasets were created for F2 populations segregating for a reciprocal translocation of    chromosomal segments or a reciprocal translocation and inversion. Multiple attempts were made to construct maps for each dataset using MapMaker/EXP. As expected, the markers from segments involved in the translocation formed one linkage group.    Maps that corresponded to the known marker order within a segment could be constructed by the following method. The separation of markers distal to the translocation breakpoints into their respective segments could be made by constructing    multiple maps, using distinct orders of marker entry, and observing the variances in intermarker distances: variances between pairs of markers from the same segment were an order of magnitude less compared to pairs where markers were from    different segments. The order of markers within a segment could be determined from combining the pairwise linkage results from multiple maps, or from maps including all markers from a segment. No bias in map distances was observed. These results    indicate that, under conditions similar to those tested, genetic maps corresponding to the segments conserved in translocations can be constructed.</p>

	]]>
</description>

<author>K D. Livingstone et al.</author>


</item>


<item>
<title> Loss of normal profilaggrin and filaggrin in flaky tail (ft/ft) mice: an animal model for the filaggrin-deficient skin disease ichthyosis vulgaris.</title>
<link>http://mouseion.jax.org/stfb2000_2009/157</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/157</guid>
<pubDate>Tue, 08 May 2012 15:28:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Flaky tail (gene symbol ft) is an autosomal recessive mutation in mice that results in a dry, flaky skin, and annular tail and paw constrictions in the neonatal period. Previous studies demonstrated that the ft mutation maps to the    central region of mouse chromosome 3, in the vicinity of the epidermal differentiation complex, a gene locus that includes many nonkeratin genes expressed in epidermis. In this study we report a detailed characterization of the flaky tail mouse.    Affected homozygous ft/ft mice exhibit large, disorganized scales on tail and paw skin, marked attenuation of the epidermal granular layer, mild acanthosis, and orthokeratotic hyperkeratosis. Biochemical analysis demonstrated that ft/ft mice    lacked normal high molecular profilaggrin (approximately 500 kDa), and instead expressed a lower molecular weight form of profilaggrin (220 kDa) that is not proteolytically processed to profilaggrin intermediates or filaggrin. Mutant mice lacked    the large, irregular F-type keratohyalin granules that contain profilaggrin, and filaggrin was absent from the cornified layers of ft/ft epidermis. The expression of epidermal keratins was unchanged, whereas the cornified envelope proteins    involucrin and loricrin were increased in ft/ft epidermis. Cultured ft/ft keratinocytes also synthesized reduced amounts of profilaggrin mRNA and protein, demonstrating that the defect in profilaggrin expression is intrinsic to epidermal cells.    These findings demonstrate that flaky tail mice express an abnormal profilaggrin polypeptide that does not form normal keratohyalin F-granules and is not proteolytically processed to filaggrin. We propose that the absence of filaggrin, and in    particular the hygroscopic, filaggrin-derived amino acids that are thought to function in epidermal hydration, underlies the dry, scaly skin characteristic of ft/ft mice. This animal model provides a tool for understanding the role of filaggrin    in normal epidermal function and may provide insight into the molecular basis of the filaggrin-deficient human skin disorder ichthyosis vulgaris.</p>

	]]>
</description>

<author>R B. Presland et al.</author>


</item>


<item>
<title> Characterization of a hematopoietic stem cell with engraftment advantage</title>
<link>http://mouseion.jax.org/stfb2000_2009/156</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/156</guid>
<pubDate>Tue, 08 May 2012 15:28:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>In studying hematopoietic stem cell (HSC) function in vivo, we discovered that HSCs from CXB-12/HiaJ (CXB-12) mice have 14 times the total long term repopulating ability found in the best of 11 other CXB recombinant inbred (RI)    lines. This was determined using the competitive repopulation assay where bone marrow cells (BMCs) from each RI line donor were mixed with gentically marked competitor BMCs from the (BALBx B6) F1 (F1) hybrid, the mice used to produce the RI    lines, and the mixtures repopulated lethally irradiated F1 recipients. After six months, percentages of donor type erythrocytes and lymphoytes gave a measure of the long term repopulating abilities of the donor RI lines relative to the F1    competitor. When high doses of BMCs were used, CXB-12 cells repopulated 6-12 times better than the F1 competitor cells, while when a low dose of BMCs were used in competitive dilution, CXB-12 donors had 2.4 times the number of HSCs as the F1    competitor, and each CXB-12 HSC repopulated 1.4 times as well. The CXB-12 HSC engraftment advantage is associated with a 50% increase in cobblestone area forming cell frequency and an one fold increase in the number of side population cells    revealed by Hoechst 33342 vital dye staining. There was no effect on day 12 spleen colony forming units. The CXB-12 HSC engraftment advantage appears to result from increased HSC proliferation and differentiation abilities which are caused either    by a unique recombination of parental genes or by specific mutations in the CXB-12 genome.</p>

	]]>
</description>

<author>J Chen et al.</author>


</item>


<item>
<title> Mouse mutagenesis is &apos;in&apos;. Sharing experience and resources in large-scale functional genomics: mutagenesis of the mouse genome, Georgia Genetics Symposium II, Athens, Georgia, 6-9 September 2000.</title>
<link>http://mouseion.jax.org/stfb2000_2009/155</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/155</guid>
<pubDate>Tue, 08 May 2012 15:27:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W N. Frankel</author>


</item>


<item>
<title> Calorie restriction increases light-dependent photoreceptor cell loss in the neural retina of fischer 344 rats.</title>
<link>http://mouseion.jax.org/stfb2000_2009/154</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/154</guid>
<pubDate>Tue, 08 May 2012 15:27:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>We investigated the effect of > or = 8 months of 40% caloric restriction (CR) on photoreceptor cell loss in 12, 18, and 24 month-old Fischer 344 rats (N = 154). Rats were reared at the NIA Biomarkers Program, National Center for    Toxicological Research. Photoreceptor cell density, assessed histologically, declined with age in both the CR-fed and ad lib (AL)-fed cohorts (P < 0.000), but declines were more pronounced in the CR cohort (P < 0.0005). The deleterious effect of    CR was most pronounced in the central as opposed to the peripheral retina (P = 0.008), suggesting a light-dependent mechanism. Photoreceptor cell density was inversely associated with rearing under bright light (300-750 lux) as compared with    rearing under lower illuminance (< or = 200 lux) (P < 0.0005). However, the deleterious effect of bright light on photoreceptor cell density was more pronounced in the CR cohort (P = 0.04). Effects of CR on circadian activity are likely to    increase the actual light exposure of the CR cohort and may explain the apparent inability of CR to delay retinal aging in albino rats.</p>

	]]>
</description>

<author>M Obin et al.</author>


</item>


<item>
<title> Related function of mouse SOX3, SOX9, and SRY HMG domains assayed by male sex determination.</title>
<link>http://mouseion.jax.org/stfb2000_2009/153</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/153</guid>
<pubDate>Tue, 08 May 2012 15:26:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sox genes encode proteins related to each other, and to the sex determining gene Sry, by the presence of a DNA binding motif known as the HMG domain. Although HMG domains can bind to related DNA sequences, Sox gene products may    achieve target gene specificity by binding to preferred target sequences or by interacting with specific partner proteins. To assess their functional similarities, we replaced the HMG box of Sry with the HMG box of Sox3 or Sox9 and tested whether    these constructs caused sex reversal in XX mice. Our results indicate that such chimeric transgenes can functionally replace Sry and elicit development of testis cords, male patterns of gene expression, and elaboration of male secondary sexual    characteristics. This implies that chimeric SRY proteins with SOX HMG domains can bind to and regulate SRY target genes and that potential SRY partner factor interactions are not disrupted by HMG domain substitutions.</p>

	]]>
</description>

<author>D E. Bergstrom et al.</author>


</item>


<item>
<title> Primitive hematopoietic stem cell function in vivo is uniquely high in the CXB-12 mouse strain.</title>
<link>http://mouseion.jax.org/stfb2000_2009/152</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/152</guid>
<pubDate>Tue, 08 May 2012 15:26:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bone marrow cells (BMCs) from CXB-12/HiaJ (CXB-12) mice had 14 times the total long-term repopulating ability found in the best of 11 other CXB recombinant inbred (RI) lines. BMCs from each RI line donor were mixed with genetically    marked standard competitor BMCs from the BALB/cByxC57BL/6 F1 (CByB6F1) hybrid, the mice used to produce the RI lines, and the mixtures repopulated lethally irradiated CByB6F1 recipients. Percentages of donor-type erythrocytes and lymphocytes    measured the actual long-term repopulating functions of the donor RI lines relative to the standard competitor. CXB-12 BMCs repopulated better after 3 or 6 months than after 1 month, suggesting that the most primitive precursors were involved.     Compared to CByB6F1 standard competitor cells, CXB-12 cells repopulated 3 to 12 times as well, with their advantage increasing when higher doses of cells were transplanted, probably because of hybrid resistance of the recipient against low doses.    This was far better than expected, because F1 cells normally function 2 to 3 times as well as cells from an inbred strain. In competitive dilution, the advantage resulted from 2 factors: more precursor cells and more function per precursor. In    the model that best fit the data, CXB-12 donors had 2.4 times the concentration of hematopoietic stem cells (HSCs) as the CByB6F1 standard, and each HSC repopulated 1.4 times as well. CXB-12 mice did not have elevated erythrocyte and lymphocyte    numbers in blood and marrow and did not have unusually elevated concentrations of colony-forming unit spleen, cobblestone colonies, and long-term colony-initiating cells in marrow.</p>

	]]>
</description>

<author>J Chen et al.</author>


</item>


<item>
<title> Defects in the cappuccino (cno) gene on mouse chromosome 5 and human 4p cause Hermansky-Pudlak syndrome by an AP-3-independent mechanism.</title>
<link>http://mouseion.jax.org/stfb2000_2009/151</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/151</guid>
<pubDate>Tue, 08 May 2012 15:26:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Defects in a triad of organelles (melanosomes, platelet granules, and lysosomes) result in albinism, prolonged bleeding, and lysosome abnormalities in Hermansky-Pudlak syndrome (HPS). Defects in HPS1, a protein of unknown function,    and in components of the AP-3 complex cause some, but not all, cases of HPS in humans. There have been 15 inherited models of HPS described in the mouse, underscoring its marked genetic heterogeneity. Here we characterize a new spontaneous    mutation in the mouse, cappuccino (cno), that maps to mouse chromosome 5 in a region conserved with human 4p15-p16. Melanosomes of cno/cno mice are immature and dramatically decreased in number in the eye and skin, resulting in severe    oculocutaneous albinism. Platelet dense body contents (adenosine triphosphate, serotonin) are markedly deficient, leading to defective aggregation and prolonged bleeding. Lysosomal enzyme concentrations are significantly elevated in the kidney    and liver. Genetic, immunofluorescence microscopy, and lysosomal protein trafficking studies indicate that the AP-3 complex is intact in cno/cno mice. It was concluded that the cappuccino gene encodes a product involved in an AP-3-independent    mechanism critical to the biogenesis of lysosome-related organelles.  (Blood. 2000;96:4227-4235)</p>

	]]>
</description>

<author>B Gwynn et al.</author>


</item>


<item>
<title> Mammalian cloning: advances and limitations.</title>
<link>http://mouseion.jax.org/stfb2000_2009/150</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/150</guid>
<pubDate>Tue, 08 May 2012 15:25:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>For many years, researchers cloning mammals experienced little success, but recent advances have led to the successful cloning of several mammalian species. However, cloning by the transfer of nuclei from adult cells is still a    hit-and-miss procedure, and it is not clear what technical and biological factors underlie this. Our understanding of the molecular basis of reprogramming remains extremely limited and affects experimental approaches towards increasing the    success rate of cloning.  Given the future practical benefits that cloning can offer, the time has come to address what should be done to resolve this problem.</p>

	]]>
</description>

<author>D Solter</author>


</item>


<item>
<title> Linkage disequilibrium analysis of biallelic DNA markers, human quantitative trait loci, and threshold-defined case and control subjects.</title>
<link>http://mouseion.jax.org/stfb2000_2009/149</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/149</guid>
<pubDate>Tue, 08 May 2012 15:25:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Linkage disequilibrium (LD) mapping has been applied to many simple, monogenic, overtly Mendelian human traits, with great success. However, extensions and applications of LD mapping approaches to more complex human quantitative    traits have not been straightforward. In this article, we consider the analysis of biallelic DNA marker loci and human quantitative trait loci in settings that involve sampling individuals from opposite ends of the trait distribution. The purpose    of this sampling strategy is to enrich samples for individuals likely to possess (and not possess) trait-influencing alleles. Simple statistical models for detecting LD between a trait-influencing allele and neighboring marker alleles are derived    that make use of this sampling scheme. The power of the proposed method is investigated analytically for some hypothetical gene-effect scenarios. Our studies indicate that LD mapping of loci influencing human quantitative trait variation should    be possible in certain settings.  Finally, we consider possible extensions of the proposed methods, as well as areas for further consideration and improvement.</p>

	]]>
</description>

<author>N J. Schork et al.</author>


</item>


<item>
<title> The mouse brain transcriptome by SAGE: differences in gene expression between P30 brains of the partial trisomy 16 mouse model of Down syndrome (Ts65Dn) and normals.</title>
<link>http://mouseion.jax.org/stfb2000_2009/148</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/148</guid>
<pubDate>Tue, 08 May 2012 15:25:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Trisomy 21, or Down syndrome (DS), is the most common genetic cause of mental retardation. Changes in the neuropathology, neurochemistry, neurophysiology, and neuropharmacology of DS patients' brains indicate that there is probably    abnormal development and maintenance of central nervous system structure and function. The segmental trisomy mouse (Ts65Dn) is a model of DS that shows analogous neurobehavioral defects. We have studied the global gene expression profiles of    normal and Ts65Dn male and normal female mice brains (P30) using the serial analysis of gene expression (SAGE) technique. From the combined sample we collected a total of 152,791 RNA tags and observed 45,856 unique tags in the mouse brain    transcriptome. There are 14 ribosomal protein genes (nine under expressed) among the 330 statistically significant differences between normal male and Ts65Dn male brains, which possibly implies abnormal ribosomal biogenesis in the development and    maintenance of DS phenotypes. This study contributes to the establishment of a mouse brain transcriptome and provides the first overall analysis of the differences in gene expression in aneuploid versus normal mammalian brain    cells.</p>

	]]>
</description>

<author>R Chrast et al.</author>


</item>


<item>
<title> Antibodies against keratinocyte antigens other than desmogleins 1 and 3 can induce pemphigus vulgaris-like lesions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/147</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/147</guid>
<pubDate>Tue, 08 May 2012 15:24:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pemphigus is an autoimmune disease of skin adhesion associated with autoantibodies against a number of keratinocyte antigens, such as the adhesion molecules desmoglein (Dsg) 1 and 3 and acetylcholine receptors.  The notion that    anti-Dsg antibodies alone are responsible for blisters in patients with pemphigus vulgaris (PV) stems from the ability of rDsg1 and rDsg3 to absorb antibodies that cause PV-like skin blisters in neonatal mice. Here, we demonstrate that PV IgGs    eluted from rDsg1-Ig-His and rDsg3-Ig-His show similar antigenic profiles, including the 38-, 43-, 115-, and 190-kDa keratinocyte proteins and a non-Dsg 3 130-kDa polypeptide present in keratinocytes from Dsg 3 knockout mouse. We injected into    Dsg 3-lacking mice the PV IgGs that did not cross-react with the 160-kDa Dsg 1 or its 45-kDa immunoreactive fragment and that showed no reactivity with recombinant Dsg 1. We used both the Dsg3(null) mice with a targeted mutation of the Dsg3 gene    and the "balding" Dsg3(bal)/Dsg3(bal) mice that carry a spontaneous null mutation in Dsg3. These PV IgGs caused gross skin blisters with PV-like suprabasal acantholysis and stained perilesional epidermis in a fishnet-like pattern, indicating that    the PV phenotype can be induced without anti-Dsg 3 antibody. The anti-Dsg 1 antibody also was not required, as its presence in PV IgG does not alter the PV-like phenotype in skin organ cultures and because pemphigus foliaceus IgGs produce a    distinct phenotype in Dsg3(null) mice. Therefore, mucocutaneous lesions in PV patients could be caused by non-Dsg antibodies.</p>

	]]>
</description>

<author>V T. Nguyen et al.</author>


</item>


<item>
<title> TNF-alpha induces osteoclastogenesis by direct stimulation of macrophages exposed to permissive levels of RANK ligand.</title>
<link>http://mouseion.jax.org/stfb2000_2009/146</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/146</guid>
<pubDate>Tue, 08 May 2012 15:24:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>While TNF-alpha is pivotal to the pathogenesis of inflammatory osteolysis, the means by which it recruits osteoclasts and promotes bone destruction are unknown. We find that a pure population of murine osteoclast precursors fails    to undergo osteoclastogenesis when treated with TNF-alpha alone. In contrast, the cytokine dramatically stimulates differentiation in macrophages primed by less than one percent of the amount of RANKL (ligand for the receptor activator of    NF-kappaB) required to induce osteoclast formation. Mirroring their synergistic effects on osteoclast differentiation, TNF-alpha and RANKL markedly potentiate NF-kappaB and stress-activated protein kinase/c-Jun NH(2)-terminal kinase activity, two    signaling pathways essential for osteoclastogenesis. In vivo administration of TNF-alpha prompts robust osteoclast formation in chimeric animals in which ss-galactosidase positive, TNF-responsive macrophages develop within a TNF-nonresponsive    stromal environment. Thus, while TNF-alpha alone does not induce osteoclastogenesis, it does so both in vitro and in vivo by directly targeting macrophages within a stromal environment that expresses permissive levels of RANKL. Given the    minuscule amount of RANKL sufficient to synergize with TNF-alpha to promote osteoclastogenesis, TNF-alpha appears to be a more convenient target in arresting inflammatory osteolysis.</p>

	]]>
</description>

<author>J Lam et al.</author>


</item>


<item>
<title> Skeletal muscle deformity and neuronal disorder in Trio exchange factor-deficient mouse embryos.</title>
<link>http://mouseion.jax.org/stfb2000_2009/145</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/145</guid>
<pubDate>Tue, 08 May 2012 15:23:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dbl-homology guanine nucleotide exchange factors (DH-GEFs) regulate actin cytoskeletal reorganization, cell adhesion, and gene transcription via activation of Rho GTPases. However, little is known about the physiological role of    mammalian DH-GEFs during development. The DH-GEF family member Trio is of particular interest because it is a multifunctional protein possessing two GEF domains, as well as a protein serine/threonine kinase domain, and trio-like genes in    Caenorhabditis elegans and Drosophila were shown to function in neural migration and axon guidance. To determine the role of Trio during mammalian development, we generated a mouse trio loss-of-function mutation (trio(-/-)). Trio function is    essential during late embryonic development as genotype analysis indicated that trio(-/-) embryos died between embryonic day (E)-15.5 and birth, or shortly thereafter. In the trio(-/-) embryos, primary skeletal myofibers were relatively normal at    E14.5, but by E18.5 highly unusual spherical myofibers accumulated. Trio deficiency may cause a defect in secondary myogenesis, as the appearance of the abnormal trio(-/-) skeletal myofibers temporally coincided with the onset of secondary    myogenesis, and smaller secondary myofibers located adjacent to the primary myofibers were absent. The proliferation of trio(-/-) secondary myoblasts appeared normal, suggesting that Trio may regulate secondary myoblast alignment or fusion.    trio(-/-) embryos also displayed aberrant organization in several regions within the brain, including the hippocampal formation and olfactory bulb. We thus conclude that Trio is essential for late embryonic development, and that Trio functions in    fetal skeletal muscle formation and in the organization of neural tissues.</p>

	]]>
</description>

<author>S P. O&apos;Brien et al.</author>


</item>


<item>
<title> The information content of a character under a Markov model of evolution.</title>
<link>http://mouseion.jax.org/stfb2000_2009/144</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/144</guid>
<pubDate>Tue, 08 May 2012 15:23:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>The rate of evolutionary change associated with a character determines its utility for the reconstruction of phylogenetic history. For a given age of lineage splits, we examine the information content of a character to assess the    magnitude and range of an optimal rate of substitution. On the one hand an optimal transition rate must provide sufficiently many character changes to distinguish subclades, whereas on the other hand changes must be sufficiently rare that    reversals on a single branch (and hence homoplasy) are uncommon. In this study, we evolve binary characters over three tree topologies with fixed branch lengths, while varying transition rate as a parameter. We use the character state    distribution obtained to measure the "information content" of a character given a transition rate. This is done with respect to several criteria-the probability of obtaining the correct tree using parsimony, the probability of infering the    correct ancestral state, and Shannon-Weaver and Fisher information measures on the configuration of probability distributions.  All of the information measures suggest the intuitive result of the existence of optimal rates for phylogeny    reconstruction. This nonzero optimum is less pronounced if one conditions on there having been a change, in which case the parsimony-based results of minimum change being the most informative tends to hold.</p>

	]]>
</description>

<author>M Shpak et al.</author>


</item>


<item>
<title> The insulin gene VNTR is associated with fasting insulin levels and development of juvenile obesity.</title>
<link>http://mouseion.jax.org/stfb2000_2009/143</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/143</guid>
<pubDate>Tue, 08 May 2012 15:23:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>In millions of people, obesity leads to type 2 diabetes (T2D; also known as non-insulin-dependent diabetes mellitus). During the early stages of juvenile obesity, the increase of insulin secretion in proportion to accumulated fat    balances insulin resistance and protects patients from hyperglycaemia. After several decades, however,beta-cell function deteriorates and T2D develops in approximately 20% of obese patients. In modern societies, obesity has thus become the    leading risk factor for T2D (ref. 5). The factors that predispose obese patients to alteration of insulin secretion upon gaining weight remain unknown. To determine which genetic factors predispose obese patients to beta-cell dysfunction, and    possibly T2D, we studied single-nucleotide polymorphisms (SNPs) in the region of the insulin gene (INS) among 615 obese children. We found that, in the early phase of obesity, alleles of the INS variable number of tandem repeat (VNTR) locus are    associated with different effects of body fatness on insulin secretion. Young obese patients homozygous for class I VNTR alleles secrete more insulin than those with other genotypes.</p>

	]]>
</description>

<author>Stunff C. Le et al.</author>


</item>


<item>
<title> A major gene affecting age-related hearing loss is common to at least ten inbred strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/142</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/142</guid>
<pubDate>Tue, 08 May 2012 15:22:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inbred strains of mice offer promising models for understanding the genetic basis of human presbycusis or age-related hearing loss (AHL). We previously mapped a major gene affecting AHL in C57BL/6J mice. Here, we show that the same    Chromosome 10 gene (Ahl) is a major contributor to AHL in nine other inbred mouse strains-129P1/ReJ, A/J, BALB/cByJ, BUB/BnJ, C57BR/cdJ, DBA/2J, NOD/LtJ, SKH2/J, and STOCK760. F1 hybrids between each of these inbred strains and the normal-hearing    inbred strain CAST/Ei retain good hearing, indicating that inheritance of AHL is recessive. To follow segregation of hearing loss, F1 hybrids were backcrossed to the parental strains with AHL. Auditory-evoked brain-stem response thresholds were    used to assess hearing in more than 1500 N2 mice and analyzed as quantitative traits for linkage associations with Chromosome 10 markers.  Highly significant linkage was found in all nine strain backcrosses, with the highest probability (LOD >    70) near the marker D10Mit112. This map position for Ahl is near the waltzer mutation (v) and the modifier of deaf waddler locus (mdfw), suggesting the possibility of allelism. Results from an intercross of C57BL/6J and NOD/LtJ mice indicate that    the 6- to 10-month difference in AHL onset between these two strains is not due to allelic heterogeneity of the Ahl gene.</p>

	]]>
</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title> Interferon-gamma receptor signaling is dispensable in the development of autoimmune type 1 diabetes in NOD mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/141</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/141</guid>
<pubDate>Tue, 08 May 2012 15:22:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>There have been two previous conflicting reports that the development of T-cell-mediated autoimmune diabetes (type 1 diabetes) was respectively unaffected or inhibited in NOD mice genetically deficient in the T-helper (Th) 1    cytokine interferon (IFN)-gamma or the alpha-chain subunit of its receptor. Our goal was to resolve this conundrum by congenically transferring, from a 129 donor strain to the NOD background, a functionally inactivated gene for the beta-chain    signaling (located on chromosome 16) rather than the alpha-chain ligand binding domain (located on chromosome 10) of the IFN-gamma receptor. These NOD.IFNgammaRBnull mice were characterized by normal patterns of leukocyte development and T-cells    that produced greatly enhanced levels of the putatively type 1 diabetes-protective Th2 cytokine interleukin (IL)-4. However, despite being unable to respond to the primary Thl cytokine IFN-gamma and having T-cells that produce greatly enhanced    levels of IL-4, NOD.IFNgammaRBnull mice remained highly susceptible to type 1 diabetes. This result indicated that the previously reported inhibition of type 1 diabetes in NOD mice carrying a functionally inactivated IFN-gamma receptor    alpha-chain gene may have been due to a closely linked and previously unidentified diabetes resistance allele. Furthermore, our results indicate that the pathogenicity of diabetogenic T-cells in NOD mice is not dampened by an inability to respond    to IFN-gamma and a concurrent shift to greatly enhanced Th2 cytokine production. This finding calls into question whether clinical protocols designed to shift beta-cell autoreactive T-cells from a Thl to Th2 cytokine production profile will truly    be safe and efficacious in blocking the development of type 1 diabetes in humans.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title> A common promoter variant of the leptin gene is associated with changes in the relationship between serum leptin and fat mass in obese girls.</title>
<link>http://mouseion.jax.org/stfb2000_2009/140</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/140</guid>
<pubDate>Tue, 08 May 2012 15:21:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the leptin gene lead to rare obese syndromes of Mendelian inheritance in humans and rodents. However, no relevant mutations are found in the coding region of leptin gene DNA in patients with common multifactorial    obesity. These obese patients tend to have an elevation of serum leptin proportional to their adiposity but with a rather wide dispersion of leptin levels for a given body fat content, which in part is attributable to sexual dimorphism. The    current study, performed in two independent Caucasian cohorts of obese girls, shows that a frequent promoter variant of the leptin gene is associated with changes in the relationship between serum leptin and body fatness. Girls of comparable    adiposity have different circulating leptin levels, depending on their genotype at this locus. Girls with the -/- Lep -2,549 genotype have 25% lower mean leptin levels than the girls with other genotypes, as reflected by differences in the    regression slopes of leptin-to-fat mass. Therefore, genetic factors related to the leptin gene may be important in defining the set point of obese individuals (i.e., the circulating leptin level for a given degree of body fatness). This    definition may be of both physiological and therapeutic relevance, although a phenotypic association with an individual single-nucleotide polymorphism is not sufficient to assign function to this particular nucleotide site.</p>

	]]>
</description>

<author>Stunff C. Le et al.</author>


</item>


<item>
<title> Grey intense: a new mouse mutation affecting pigmentation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/139</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/139</guid>
<pubDate>Tue, 08 May 2012 15:21:16 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M T. Davisson et al.</author>


</item>


<item>
<title> Comparison of bone formation responses to parathyroid hormone(1-34), (1-31), and (2-34) in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/138</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/138</guid>
<pubDate>Tue, 08 May 2012 15:20:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this study we used a mouse model system to compare the in vivo effects of parathyroid hormone(1-34) [PTH(1-34)] with that of PTH(1-31) or PTH(2-34) analogs. Daily subcutaneous administration of PTH(1-34) for 15 days caused a    dose-dependent increase in the serum osteocalcin level and bone extract alkaline phosphatase activity, markers of bone formation.  PTH(2-34) was much less potent, whereas PTH(1-31) was equipotent in stimulating bone formation parameters in mice.    PTH(1-34) caused significant increases in serum calcium (after 4 h) and tartrate-resistant acid phosphatase activity in bone extract (after 4 h), whereas PTH(2-34) and PTH(1-31) were less potent. Because PTH(1-31) caused a smaller increase in    bone resorption parameters compared to PTH(1-34), despite similar effects on bone formation parameters, we evaluated the long-term anabolic effects of PTH(1-31) and PTH(1-34) in mice. Weekly evaluations of serum osteocalcin levels demonstrated    that daily injections of PTH(1-34) and PTH(1-31) at 80 &mgr;g/kg body weight increased serum osteocalcin levels within 1 week of the start of treatment, which were maintained during the entire 22 week treatment. Assessment of bone density at the    end of the treatment period with peripheral quantitated computed tomography (pQCT) revealed that PTH(1-34) caused a significantly greater increase in femoral bone density compared to PTH(1-31) at the middiaphysis (18% vs. 9% over vehicle control;    p < 0.001). Both PTH(1-34) and PTH(1-31) increased periosteal circumference compared to vehicle (p < 0.01) without a significant difference between the two treatments. In contrast, PTH(1-34) caused a significantly greater reduction in endosteal    circumference than PTH(1-31) (p < 0.001). Both analogs significantly increased maximum load and area of moment of inertia over the vehicle group. In conclusion, our findings suggest that PTH(1-34) and PTH(1-31) may exhibit different anabolic    effects at the periosteum vs. endosteum in the long bones of mice.</p>

	]]>
</description>

<author>S Mohan et al.</author>


</item>


<item>
<title> Mapping quantitative trait loci for serum insulin-like growth factor-1 levels in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/137</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/137</guid>
<pubDate>Tue, 08 May 2012 15:20:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Serum insulin-like growth factor-1 (IGF-1) and femoral bone mineral density (BMD) differ between two inbred strains of mice, C3H/HeJ (C3H) and C57BL/6J (B6), by approximately 30% and 50%, respectively. Similarly, skeletal IGF-1    content, bone formation, mineral apposition, and marrow stromal cell numbers are higher in C3H than in B6 mice. Because IGF-1 and several bone parameters cosegregate, we hypothesize that the serum IGF-1 phenotype has a strong heritable component    and that genetic determinants for serum IGF-1 are involved in the regulation of bone mass. We intercrossed (B6 x C3H)F1 hybrids and analyzed 682 F2 female offspring at 4 months of age for serum IGF-1 by radioimmunoassay and femoral BMD by    peripheral quantitative computerized tomography (pQCT). Genomic DNA was assayed by polymerase chain reaction (PCR) to determine alleles for 114 Mit markers inherited in F2 mice at average distances of 14 centimorgans (cM) along each chromosome    (Chr). Serum IGF-1 levels in the F2 progeny were relatively normal in distribution, but showed a greater range than either progenitor, indicating that serum IGF-1 level is a polygenic trait with an estimated heritability of 52%. Serum IGF-1    correlated with femoral length (r = 0.266, p < 0.0001) and femoral BMD (r = 0.267, p < 0.0001).  Whole genome scans for main effects associated with serum IGF-1 levels revealed three significant QTLs (in order of significance) on mouse Chrs 6,    15, and 10. The QTL on Chr 6 showed a significant reduction in IGF-1 associated with increasing C3H allele number, whereas the Chr 15 and Chr 10 loci showed additive effects with increasing C3H allele number. A genome-wide search for interacting    marker pairs identified a significant interaction between the Chr 6 QTL and a locus on Chr 11. This interactive effect suggested that when the Chr 11 locus was homozygous for C3H, there was no effect of the Chr 6 locus on serum IGF-1; however,    the combination of C3H alleles on Chr 6 with B6 alleles on Chr 11 was associated with reduced serum IGF-1 concentrations. To test this in vivo, we tested congenic mice carrying the Chr 6 QTL region from C3H on a B6 background (B6.C3H-6). Both    serum IGF-1 and femoral BMD were significantly lower in female congenic than progenitor B6 mice. In summary, we identified three major QTLs on mouse Chrs 6, 10, and 15, and noted a major locus-locus interaction between Chrs 6 and 11. We named    these QTLs IGF-1 serum levels (Igf1sl1 to Igf1sl4). Functional isolation of the Igf1sl1 QTL on Chr 6 for IGF-1 in B6.C3H-6 congenic mice demonstrated effects on both the IGF-1 and BMD phenotypes. The genetic determinants of these Igf1sl QTLs will    provide much insight into the regulation of IGF-1 and the subsequent acquisition of peak bone mass.</p>

	]]>
</description>

<author>C J. Rosen et al.</author>


</item>


<item>
<title> The adhesion signaling molecule p190 RhoGAP is required for morphogenetic processes in neural development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/136</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/136</guid>
<pubDate>Tue, 08 May 2012 15:19:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rho GTPases direct actin rearrangements in response to a variety of extracellular signals. P190 RhoGAP (GTPase activating protein) is a potent Rho regulator that mediates integrin-dependent adhesion signaling in cultured cells. We    have determined that p190 RhoGAP is specifically expressed at high levels throughout the developing nervous system. Mice lacking functional p190 RhoGAP exhibit several defects in neural development that are reminiscent of those described in mice    lacking certain mediators of neural cell adhesion. The defects reflect aberrant tissue morphogenesis and include abnormalities in forebrain hemisphere fusion, ventricle shape, optic cup formation, neural tube closure, and layering of the cerebral    cortex. In cells of the neural tube floor plate of p190 RhoGAP mutant mice, polymerized actin accumulates excessively, suggesting a role for p190 RhoGAP in the regulation of +Rho-mediated actin assembly within the neuroepithelium. Significantly,    several of the observed tissue fusion defects seen in the mutant mice are also found in mice lacking MARCKS, the major substrate of protein kinase C (PKC), and we have found that p190 RhoGAP is also a PKC substrate in vivo. Upon either direct    activation of PKC or in response to integrin engagement, p190 RhoGAP is rapidly translocated to regions of membrane ruffling, where it colocalizes with polymerized actin. Together, these results suggest that upon activation of neural adhesion    molecules, the action of PKC and p190 RhoGAP leads to a modulation of Rho GTPase activity to direct several actin-dependent morphogenetic processes required for normal neural development.</p>

	]]>
</description>

<author>M R. Brouns et al.</author>


</item>


<item>
<title> Hypoglycaemia, liver necrosis and perinatal death in mice lacking all isoforms of phosphoinositide 3-kinase p85 alpha.</title>
<link>http://mouseion.jax.org/stfb2000_2009/135</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/135</guid>
<pubDate>Tue, 08 May 2012 15:19:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Phosphoinositide 3-kinases produce 3'-phosphorylated phosphoinositides that act as second messengers to recruit other signalling proteins to the membrane. Pi3ks are activated by many extracellular stimuli and have been implicated    in a variety of cellular responses. The Pi3k gene family is complex and the physiological roles of different classes and isoforms are not clear. The gene Pik3r1 encodes three proteins (p85 alpha, p55 alpha and p50 alpha) that serve as regulatory    subunits of class IA Pi3ks (ref.  2). Mice lacking only the p85 alpha isoform are viable but display hypoglycaemia and increased insulin sensitivity correlating with upregulation of the p55 alpha and p50 alpha variants. Here we report that loss    of all protein products of Pik3r1 results in perinatal lethality. We observed, among other abnormalities, extensive hepatocyte necrosis and chylous ascites. We also noted enlarged skeletal muscle fibres, brown fat necrosis and calcification of    cardiac tissue. In liver and muscle, loss of the major regulatory isoform caused a great decrease in expression and activity of class IA Pi3k catalytic subunits; nevertheless, homozygous mice still displayed hypoglycaemia, lower insulin levels    and increased glucose tolerance. Our findings reveal that p55 alpha and/or p50 alpha are required for survival, but not for development of hypoglycaemia, in mice lacking p85 alpha.</p>

	]]>
</description>

<author>D A. Fruman et al.</author>


</item>


<item>
<title> Multiple seizure susceptibility genes on chromosome 7 in SWXL-4 congenic mouse strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/134</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/134</guid>
<pubDate>Tue, 08 May 2012 15:18:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The SWXL-4 recombinant inbred mouse strain is unusually sensitive to recurrent tonic-clonic seizures upon routine handling and to seizures induced by chemoconvulsants. In a conventional intercross with the ABP/Le strain, we    previously mapped a SWXL-4-derived quantitative trait locus called Szf1 (seizure frequency 1) to Chromosome 7. In the present study, we confirm the existence of Szf1 in both an independent cross and a congenic strain. However, derivative congenic    recombinant strains show that an interaction between at least two genes on Chromosome 7-each of which has a very small effect on its own-account for Szf1.</p>

	]]>
</description>

<author>M E. Legare et al.</author>


</item>


<item>
<title> Comparison of recombinant growth differentiation factor-9 and oocyte regulation of KIT ligand messenger ribonucleic acid expression in mouse ovarian follicles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/133</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/133</guid>
<pubDate>Tue, 08 May 2012 15:18:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Oocytes secrete factors that regulate the development of the surrounding granulosa cells in ovarian follicles. KIT ligand (KL) mRNA expression in granulosa cells is thought to be regulated by oocytes; however, the factor(s) that    mediate this effect are not known. One candidate is the oocyte-specific gene product growth differentiation factor-9 (GDF-9). This study examined the effect of recombinant GDF-9 (rGDF-9) on steady-state KL mRNA expression levels in preantral and    mural granulosa cells in vitro.  Furthermore, the study compared the effect of rGDF-9 with that of coculture with oocytes at different developmental stages. As determined by RNase protection assay, both KL-1 and KL-2 mRNA levels in preantral and    mural granulosa cells were suppressed by 25-250 ng/ml rGDF-9. Fully grown oocytes also suppressed both KL-1 and KL-2 mRNA expression levels. Partly grown oocytes isolated from 7-, 10-, or 12-day-old mice either had no effect on KL mRNA levels or    promoted KL-1 mRNA steady-state expression. It is concluded that GDF-9 is likely to mediate the action of fully grown, but not partly grown, oocytes on granulosa cell KL mRNA expression.</p>

	]]>
</description>

<author>I M. Joyce et al.</author>


</item>


<item>
<title> In vitro fertilization with cryopreserved inbred mouse sperm.</title>
<link>http://mouseion.jax.org/stfb2000_2009/132</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/132</guid>
<pubDate>Tue, 08 May 2012 15:17:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sperm from C57BL/6J, DBA/2J, BALB/cJ, 129S3/SvImJ, and FVB/NJ inbred mice were cryopreserved in 3% skim milk/18% raffinose cryoprotectant solution.  The post-thaw sperm from all strains were evaluated for their viability and    fertility by comparing them against B6D2F1 sperm used as a control.  The protocol used for freezing mouse sperm was effective in different strains, because the motility was decreased by 50% after cryopreservation similar to other mammalian sperm.    However, the progressive motility and the fertility of each inbred strain were affected differently. The C57BL/6J, BALB/cJ, and 129S3/SvImJ strains were the most affected; their fertility (two-cell cleavage) decreased from 70%, 34%, and 84% when    using freshly collected sperm to 6%, 12%, and 6% when using frozen/thawed sperm, respectively. Live newborns derived from frozen/thawed sperm were obtained from all strains in the study. These results corroborate the genetic variation among    strains with regard to fertility and susceptibility to cryopreservation.</p>

	]]>
</description>

<author>J M. Sztein et al.</author>


</item>


<item>
<title> Murine hematopoietic stem cell characterization and its regulation in BM transplantation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/131</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/131</guid>
<pubDate>Tue, 08 May 2012 15:17:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Using 5-color fluorescence-activated cell sorting, we isolated a subset of murine pluripotent hematopoietic stem cells (PHSC) with the phenotype Lin(-) Sca(+) kit(+) CD38(+) CD34(-) that appears to fulfill the criteria for most    primitive PHSC. In the presence of whole bone marrow (BM) competitor cells, these cells produced reconstitution in lethally irradiated primary, secondary, and tertiary murine transplant recipients over the long term. However, these cells alone    could not produce reconstitution in lethally irradiated recipients. Rapid proliferation of these cells after BM transplantation required the assistance of another BM cell subset, which has the phenotype Lin(-) Sca(+) kit(+) CD38(-)    CD34(+).</p>

	]]>
</description>

<author>Y Zhao et al.</author>


</item>


<item>
<title> Hereditary spherocytosis in zebrafish riesling illustrates evolution of erythroid beta-spectrin structure, and function in red cell morphogenesis and membrane stability.</title>
<link>http://mouseion.jax.org/stfb2000_2009/130</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/130</guid>
<pubDate>Tue, 08 May 2012 15:16:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Spectrins are key cytoskeleton proteins with roles in membrane integrity, cell morphology, organelle transport and cell polarity of varied cell types during development. Defects in erythroid spectrins in humans result in congenital    hemolytic anemias with altered red cell morphology. Although well characterized in mammals and invertebrates, analysis of the structure and function of non-mammalian vertebrate spectrins has been lacking. The zebrafish riesling (ris) suffers from    profound anemia, where the developing red cells fail to assume terminally differentiated erythroid morphology. Using comparative genomics, erythroid beta-spectrin (sptb) was identified as the gene mutated in ris. Zebrafish Sptb shares 62.3%    overall identity with the human ortholog and phylogenetic comparisons suggest intragenic duplication and divergence during evolution. Unlike the human and murine orthologs, the pleckstrin homology domain of zebrafish Sptb is not removed in red    cells by alternative splicing. In addition, apoptosis and abnormal microtubule marginal band aggregation contribute to hemolysis of mutant erythrocytes, which are features not present in mammalian red cells with sptb defects. This study presents    the first genetic characterization of a non-mammalian vertebrate sptb and demonstrates novel features of red cell hemolysis in non-mammalian red cells. Further, we propose that the distinct mammalian erythroid morphology may have evolved from    specific modifications of Sptb structure and function.</p>

	]]>
</description>

<author>E C. Liao et al.</author>


</item>


<item>
<title> In vivo kinetics of murine hemopoietic stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/129</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/129</guid>
<pubDate>Tue, 08 May 2012 15:16:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>We used stochastic modeling and computer simulation to study the replication, apoptosis, and differentiation of murine hemopoietic stem cells (HSCs) in vivo. This approach allows description of the behavior of an unobserved    population (ie, HSCs) on the basis of the behavior of observed progeny cells (ie, granulocytes and lymphocytes). The results of previous limiting-dilution, competitive-repopulation studies in 44 mice were compared with the results of simulated    transplantation studies to identify parameters that led to comparable outcomes. Using this approach, we estimated that murine HSCs replicate (on average) once every 2.5 weeks and that the frequency of murine HSCs is 8 per 10(5) nucleated marrow    cells. If it is assumed that short-term repopulating cells are distinct from HSCs, that they contribute to hemopoiesis early after transplantation, and that they are independently regulated, a frequency of 4 HSCs per 10(5) nucleated marrow cells    also allows simulations that best approximate the observed data. When stochastic modeling and computer simulation were applied to limiting-dilution, autologous-transplantation studies in cats heterozygous for glucose-6-phosphate-dehydrogenase,    different estimates of HSC replication rate (1 per 8.3-10 weeks) and frequency (6 per 10(7) cells) were derived. Therefore, it appears that these parameters vary inversely with increased longevity, size, or both.  An implication of these data is    that human HSCs may be less frequent and replicate more slowly. These findings on cell kinetics have several implications.</p>

	]]>
</description>

<author>J L. Abkowitz et al.</author>


</item>


<item>
<title> Quantitative trait loci mapping for cholesterol gallstones in AKR/J and C57L/J strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/128</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/128</guid>
<pubDate>Tue, 08 May 2012 15:15:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Quantitative trait locus (QTL) mapping was used to locate genes that determine the difference in cholesterol gallstone disease between the gallstone-susceptible strain C57L/J and the gallstone-resistant strain AKR/J. Gallstone    weight was determined in 231 male (AKR x C57L) F(1) x AKR backcross mice fed a lithogenic diet containing 1% cholesterol, 0.5% cholic acid, and 15% butterfat for 8 wk. Mice having no stones and mice having the largest stones were genotyped at    approximately 20-cM intervals to find the loci determining cholesterol gallstone formation. The major locus, Lith1, mapped near D2Mit56 and was confirmed by constructing a congenic strain, AK. L-Lith1(s). Another locus, Lith2, mapped near    D19Mit58 and was also confirmed by constructing a congenic strain AK.L-Lith2(s). Other suggestive, but not statistically significant, loci mapped to chromosomes 6, 7, 8, 10, and X. The identification of these Lith genes will elucidate the    pathophysiology of cholesterol gallstone formation.</p>

	]]>
</description>

<author>B Paigen et al.</author>


</item>


<item>
<title> Disruption of Eph/ephrin signaling affects migration and proliferation in the adult subventricular zone</title>
<link>http://mouseion.jax.org/stfb2000_2009/127</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/127</guid>
<pubDate>Tue, 08 May 2012 15:14:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The subventricular zone (SVZ) of the lateral ventricles, the largest remaining germinal zone of the adult mammalian brain, contains an extensive network of neuroblasts migrating rostrally to the olfactory bulb. Little is known    about the endogenous proliferation signals for SVZ neural stem cells or guidance cues along the migration pathway. Here we show that the receptor tyrosine kinases EphB1-3 and EphA4 and their transmembrane ligands, ephrins-B2/3, are expressed by    cells of the SVZ.  Electron microscopy revealed ephrin-B ligands associated with SVZ astrocytes, which function as stem cells in this germinal zone. A three-day infusion of the ectodomain of either EphB2 or ephrin-B2 into the lateral ventricle    disrupted migration of neuroblasts and increased cell proliferation. These results suggest that Eph/ephrin signaling is involved in the migration of neuroblasts in the adult SVZ and in either direct or indirect regulation of cell    proliferation.</p>

	]]>
</description>

<author>J C. Conover et al.</author>


</item>


<item>
<title> Single nucleotide polymorphisms and the future of genetic epidemiology</title>
<link>http://mouseion.jax.org/stfb2000_2009/126</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/126</guid>
<pubDate>Tue, 08 May 2012 15:14:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this review, we consider the motivation behind contemporary single nucleotide polymorphism (SNP) initiatives. Many of these initiatives are projected to involve large, population-based surveys. We therefore emphasize the utility    of SNPs for genetic epidemiology studies. We start by offering an overview of genetic polymorphism and discuss the historical use of polymorphism in the identification of disease-predisposing genes via meiotic mapping. We next consider some of    the unique aspects of SNPs, and their relative advantages and disadvantages in human population-based analyses. In this context, we describe and critique the following six different areas of application for SNP technologies: Gene discovery and    mapping. Association-based candidate polymorphism testing. Diagnostics and risk profiling. Prediction of response to environmental stimuli, xenobiotics and diet. Homogeneity testing and epidemiological study design. Physiologic genomics. We focus    on key issues within each of these areas in an effort to point out potential problems that might plague the use of SNPs (or other forms of polymorphism) within them. However, we make no claim that our list of considerations are exhaustive.    Rather, we believe that they may provide a starting point for further dialog about the ultimate utility of SNP technologies. In addition, although our emphasis is placed on applications of SNPs to the understanding of human phenotypes, we    acknowledge that SNP maps and technologies applied to other species (e.g. the mouse genome, pathogen genomes, plant genomes, etc.)  are also of tremendous interest.</p>

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</description>

<author>N J. Schork et al.</author>


</item>


<item>
<title> Metalloprotease-mediated shedding of enzymatically active mouse ecto-ADP-ribosyltransferase ART2.2 upon T cell activation [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/125</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/125</guid>
<pubDate>Tue, 08 May 2012 15:13:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>T cells proteolytically shed the ectodomains of several cell surface proteins and, thereby, can alter their responsiveness and can release soluble intercellular regulators. ART2.2 is a GPI-anchored ecto-ADP-ribosyltransferase (ART)    related to ADP-ribosylating bacterial toxins. ART2.2 is expressed exclusively by mature T cells. Here we show that ART2.2 is shed from the cell surface in enzymatically active form upon activation of T cells. Shedding of ART2.2 resembles that of    L-selectin (CD62L) in dose response, kinetics of release, and sensitivity to the metalloprotease inhibitor Immunex Compound 3, suggesting that ART2.2, like CD62L, is cleaved by TNF-alpha-converting enzyme or by another metalloprotease. ART2.2    shed from activated T cells migrates slightly faster in SDS-PAGE analyses than does ART2.2 released upon cleavage of the GPI anchor. This indicates that shedding of ART2.2 is mediated by proteolytic cleavage close to its membrane anchor. Shed    ART2.2 is enzymatically active and ADP-ribosylates several substrates in vitro.  Thus, shedding of ART2.2 releases a potential intercellular regulator.  Finally, using a new FACS assay for monitoring ADP-ribosylation of cell surface proteins, we    demonstrate that shedding of ART2.2 correlates with a reduced sensitivity of T cell surface proteins to ADP-ribosylation. Our findings suggest that by shedding ART2.2 the activated T cell not only releases a potential intercellular regulator but    also may alter its responsiveness to immune regulation by ART2.2-mediated ADP-ribosylation of cell surface proteins.</p>

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</description>

<author>S Kahl et al.</author>


</item>


<item>
<title>Wavelet-Based Segmentation of Fluorescence Microscopy Images in Two and Three Dimensions</title>
<link>http://digitalcommons.library.umaine.edu/etd/1022</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1022</guid>
<pubDate>Tue, 08 May 2012 15:13:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Interphase chromosomes are organized into discrete chromosome territories (CTs) that may occupy preferred sub-nuclear positions. While chromosome size and gene density appear to influence positioning, the biophysical mechanisms behind CT localization, especially the relationship between morphology and positioning, remain obscure. One reason for this has been the difficulty in imaging, segmenting, and analyzing structures with variable or imprecise boundaries. This prompted us to develop a novel approach, based on the two-dimensional (2D) wavelet-transform modulus maxima (WTMM) method, adapted to perform objective and rigorous CT segmentation from nuclear background. The wavelet-transform acts as a mathematical microscope to characterize spatial image information over a continuous range of size scales. This space-scale nature, combined with full objectivity of the formalism, makes it more accurate than intensity-based segmentation algorithms and more appropriate than manual intervention. Using the WTMM method in two dimensions, we show that CTs have a highly nonspherical 3D morphology, that CT positioning is nonrandom, and favors heterologous CT groupings. Once we have fully developed and tested the method in two dimensions, we modify it to perform three-dimensional segmentation and reconstruction of c. <em>elegans</em> embryonic nuclei. The c. <em>elegans</em> nematode provides an opportunity to study cellular development at the molecular level in a rather narrow temporal frame. Interest in automated cell lineage tracing in c. <em>elegans</em> has led to the development of systems to perform this function using intensity thresholding image analysis techniques on time-lapse 3D images of histone-GFP labeled cells/nuclei. We attempt to improve this process by using the 2D WTMM method developed to segment mouse CTs. We modify the method to find and segment any number of objects within a particular size range (on the order of cell nuclei) in an image. We perform this segmentation on every image in a 3D image stack of GFP-fluoresced widefield images and then automatically sort these segmented objects into individual nuclei folders with the goal of recreating the 3D nuclei spheres.</p>

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</description>

<author>Jeremy Grant</author>


</item>


<item>
<title>Roller-Coaster Failure Rates and Mean Residual Life Functions</title>
<link>http://digitalcommons.library.umaine.edu/etd/1021</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1021</guid>
<pubDate>Tue, 08 May 2012 15:13:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The investigation in this paper was motivated by an extended generalized inverse Gaussian (EGIG) distribution which has more than one turning point of the failure rate for certain values of the parameters. We present some general results for studying the reationship between the change points of Glaser's eta function, the failure rate and the MRLF. Also, we establish an ordering between the number of change points of Glaser's eta function, the hazard rate and the MRLF. These results are used to investigate, in detail, the monotonicity of the three functions in the case of the EGIG. The EGIG model has one additional parameter, S, than the generalized inverse Gaussian (GIG) model's three parameters; see (Jorgensen, 1982). For the EGIG model, the maximum likelihood estimation of the four parameters is discussed and a score test is developed for testing the importance of the additional parameter, S. An example is provided to illustrate that the EGIG model fits the data better than the GIG of (Jorgensen, 1982).</p>

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</description>

<author>Weston D. Viles</author>


</item>


<item>
<title> Development of spontaneous arthritis in beta2-microglobulin-deficient mice without expression of HLA-B27: association with deficiency of endogenous major histocompatibility complex class I expression [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/124</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/124</guid>
<pubDate>Tue, 08 May 2012 15:13:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: Mice deficient in beta2-microglobulin (beta2m), but expressing the human major histocompatibility complex (MHC) class I molecule HLA-B27, have been reported to develop spontaneous inflammatory arthritis (SA). We sought    to determine whether, under certain conditions, beta2m deficiency alone was sufficient to cause SA, and if this might be a result of class I deficiency. METHODS: The following types of mice were produced: mice of the MHC b haplotype genetically    deficient in beta2m (beta2m(0)) on several genetic backgrounds (C57BL/6J [B6], BALB/cJ, SJL/J, MRL/MpJ, and B6,129), mice deficient in the transporter associated with antigen processing (TAP1(0)) on a B6,129 background, and HLA-B27-transgenic    beta2m(0) mice on a B6 background. Cohorts were transferred from specific pathogen-free (SPF) to conventional (non-SPF) animal rooms, and evaluated clinically and histologically for the development of SA. RESULTS: SA occurred in TAP1(0) and    beta2m(0)/class I-deficient mice with a mixed B6,129 genome at a developed this arthropathy. MRL/ MpJ beta2m(0) mice were unaffected.  Expression of B27 did not increase the frequency of SA in B27-transgenic B2m(0) B6 mice compared with that in    beta2m(0) B6 controls. CONCLUSION: Class I deficiency is sufficient to cause SA in mice. The frequency of disease, as well as B27-specific SA, is markedly dependent on a non-MHC genetic background. These results suggest that class I deficiency in    a genetically susceptible mouse can mimic B27-associated arthropathy.</p>

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</description>

<author>D J. Kingsbury et al.</author>


</item>


<item>
<title>The Profile Likelihood Method in Finding Confidence Intervals and its Comparison with the Bootstrap Percentile Method</title>
<link>http://digitalcommons.library.umaine.edu/etd/1020</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1020</guid>
<pubDate>Tue, 08 May 2012 15:12:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>In many ecological research studies, abundance data, which usually contain a large number of zeros, are skewed. Therefore, it has been recently advocated that profile likelihood confidence intervals, which are generally not symmetric, be used in studies of such kind of data. Fletcher et al. (2007) shows how to numerically calculate the profile likelihood confidence intervals, using the Lagrange multiplier method. Following the authors' footprint, I not only succeed in understanding the deep wisdom by filling in the theoretical proofs, but am able to extend this method to a more complicated data set as well. On the other hand, there is actually an alternative approach to get asymmetric confidence intervals. This approach is called the bootstrap method, which is a recently developed computer-based method for assigning measures of accuracy to statistical estimates. The whole bootstrap methodology provides more than ten slightly different ways to get confidence intervals. Among all of them, I choose the bootstrap percentile method, based on which I make a direct comparison to the profile likelihood method.</p>

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</description>

<author>Chenglu Dai</author>


</item>


<item>
<title>Estimation of Extra Risk and Benchmark Dose in Dose Response Models</title>
<link>http://digitalcommons.library.umaine.edu/etd/1019</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1019</guid>
<pubDate>Tue, 08 May 2012 15:12:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>An important goal in quantitative risk/safety analysis of chemical toxins or pharmaceutical agents is determination of toxic risk posed by exposure to the agent. For purpose of assessing exposure risks, the extra risk function is defined as the risk above the background level corrected for non-response in the unexposed population. Our interest, in this thesis, is in statistical methods for obtaining upper confidence limits on the extra risk and lower confidence limits on the dose level at which a certain benchmark risk is achieved. Existing method on the above problem is examined and several examples from literature are provided. In addition, a new method of obtaining the desired confidence intervals is investigated and the results are compared with those obtained by the existing method.</p>

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</description>

<author>Na Wang</author>


</item>


<item>
<title> Maternal environment and genotype interact to establish diabesity in mice [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/123</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/123</guid>
<pubDate>Tue, 08 May 2012 15:12:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Obesity, a major risk factor for type II diabetes, is becoming more prevalent in Western populations consuming high calorie diets while expending less energy both at the workplace and at home. Most human obesity, and probably most    type II diabetes as well, reflects polygenic rather than monogenic inheritance. We have genetically dissected a polygenic mouse model of obesity-driven type II diabetes by outcrossing the obese, diabetes-prone, NZO (New Zealand Obese)/HlLt strain    to the relatively lean NON (Nonobese Nondiabetic)/Lt strain, and then reciprocally backcrossing obese F1 mice to the lean NON/Lt parental strain. A continuous distribution of body weights was observed in a population of 203 first backcross males.    The 22% of first backcross males developing overt diabetes showed highest peripubertal weight gains and earliest development of hyperinsulinemia. We report a complex diabetes-predisposing ("diabesity") QTL (Quantitative Trait Loci) on chromosome    1 contributing significant main effects to increases in body weight, plasma insulin, and plasma glucose. NZO contributed QTL with significant main effects on adiposity parameters on chromosomes 12 and 5.  A NON QTL on chromosome 14 interacted    epistatically with the NZO obesity QTL on chromosome 12 to increase adiposity. Although the main effect of the diabetogenic QTL on chromosome 1 was on rapid growth rather than adiposity, it interacted epistatically with the obesity QTL on    chromosome 12 to increase plasma glucose levels. Additional complex epistatic interactions eliciting significant increases in body weight and/or plasma glucose were found between the NZO-contributed QTL on chromosome 1 and other NZO-contributed    QTL on chromosomes 15 and 17, as well as with an NON-contributed QTL on chromosome 2. We further show that certain of these intergenic interactions are predicated on, or enhanced by, the maternal postparturitional environment. We show by    cross-fostering experiments that the maternal environmental influence in part is because of the presence of early obesity-inducing factors in the milk of obese F1 dams. We also discuss a strategy for using recombinant congenic strains to separate    and reassemble interacting QTL for future study.</p>

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</description>

<author>P C. Reifsnyder et al.</author>


</item>


<item>
<title> The roads from phenotypic variation to gene discovery: mutagenesis versus QTLs.</title>
<link>http://mouseion.jax.org/stfb2000_2009/122</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/122</guid>
<pubDate>Tue, 08 May 2012 15:11:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>In model organisms, chemical mutagenesis provides a powerful alternative to natural, polygenic variation (for example, quantitative trait loci (QTLs)) for identifying functional pathways and complex disease genes.  Despite recent    progress in QTLs, we expect that mutagenesis is will ultimately prove more effective because the prospects of gene identification are high and every gene affecting a trait is potentially a target.</p>

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</description>

<author>J H. Nadeau et al.</author>


</item>


<item>
<title> Timely translation during the mouse oocyte-to-embryo transition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/121</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/121</guid>
<pubDate>Tue, 08 May 2012 15:11:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the mouse, completion of oocyte maturation and the initiation of preimplantation development occur during transcriptional silence and depend on the presence and translation of stored mRNAs transcribed in the growing oocyte. The    Spin gene has three transcripts, each with an identical open reading frame and a different 3' untranslated region (UTR) (Beta)-galactosidase-tagged reporter transcripts containing each of the different Spin 3'UTRs were injected into oocytes and    zygotes and (beta)-galactosidase activity was monitored. Results from these experiments suggest that differential polyadenylation and translation occurs at two critical points in the oocyte-to-embryo transition - upon oocyte maturation and    fertilization - and is dependent on sequences in the 3'UTR. The stability and mobility shifts of ten other maternal transcripts were monitored by reprobing a northern blot of oocytes and embryos collected at 12 hour intervals after fertilization.    Some are more stable than others and the upward mobility shift associated with polyadenylation correlates with the presence of cytoplasmic polyadenylation elements (CPEs) within about 120 nucleotides of the nuclear polyadenylation signal.  A    survey of the 3' UTRs of expressed sequence tag clusters from a mouse 2-cell stage cDNA library indicates that about one third contain CPEs. We suggest that differential transcript stability and a translational control program can supply the    diversity of protein products necessary for oocyte maturation and the initiation of development.</p>

	]]>
</description>

<author>B Oh et al.</author>


</item>


<item>
<title> Expression and immune recognition of SV40 Tag in transgenic mice that develop metastatic osteosarcomas [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/120</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/120</guid>
<pubDate>Tue, 08 May 2012 15:10:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mature adult mice of the C57BL/6-TgN(Amy1TAg)501Knw transgenic mouse lineage, 501, containing a liver alpha-amylase promoted-SV40 Tag hybrid gene, routinely develop SV40 Tag-induced metastatic osteosarcomas. This form of    alpha-amylase was known to be expressed in the liver, salivary glands, pancreas, and fat. Cells in the normal rib adjacent to the periosteum also express alpha-amylase suggesting that transgene expression is correctly targeted to generate    osteosarcomas. 501 mice express SV40 Tag in the salivary glands but do not develop abnormalities in these organs by the time of their death from SV40-induced osteosarcomas. Mice of the C57BL/6 strain make a strong and effective anti-tumor immune    response to SV40 Tag immunization. However, immunization of 501 mice with SV40 Tag early in life does not alter or prevent SV40 Tag-induced osteosarcomagenesis. 501 mice mount a significantly less effective cytotoxic T-lymphocyte response    following SV40 Tag immunization while 501 osteosarcoma-derived cells are fully susceptible to SV40 Tag-specific T-cell lysis. This suggests that partial tolerance, not loss of antigen presentation by tumor cells, characterizes this mouse model of    endogenous bone tumor development. To determine whether the immune recognition of endogenous SV40 Tag could influence tumorigenesis, the metastatic potential and time of death from tumor was investigated in CD4-null mutant 501 mice and beta-2    microglobulin-null mutant 501 mice. The size and number of metastases in these strains and longevity of these strains varied. We suggest that components of both the innate and adaptive immune response control tumor appearance and    progression.</p>

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</description>

<author>I Marton et al.</author>


</item>


<item>
<title> E2F4 is essential for normal erythrocyte maturation and neonatal viability.</title>
<link>http://mouseion.jax.org/stfb2000_2009/119</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/119</guid>
<pubDate>Tue, 08 May 2012 15:09:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>The retinoblastoma protein (pRB) plays a key role in the control of normal development and proliferation through the regulation of the E2F transcription factors. We generated a mutant mouse model to assess the in vivo role of the    predominant E2F family member, E2F4. Remarkably, loss of E2F4 had no detectable effect on either cell cycle arrest or proliferation. However, E2F4 was essential for normal development. E2f4-/- mice died of an increased susceptibility to    opportunistic infections that appeared to result from craniofacial defects. They also displayed a variety of erythroid abnormalities that arose from a cell autonomous defect in late stage maturation. This suggests that E2F4 makes a major    contribution to the control of erythrocyte development by the pRB tumor suppressor.</p>

	]]>
</description>

<author>P O. Humbert et al.</author>


</item>


<item>
<title>Hurricane Wilma: A Love Story</title>
<link>http://digitalcommons.fiu.edu/etd/607</link>
<guid isPermaLink="true">http://digitalcommons.fiu.edu/etd/607</guid>
<pubDate>Tue, 08 May 2012 15:09:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hurricane Wilma: A Love Story is a coming-of-age memoir about the two years the narrator spent rebuilding his hurricane-damaged condo in Miami Beach in order to provide a home for the woman he would eventually marry. The torturous rebuilding process forced the narrator to confront his deepest insecurities, to overcome a lifelong mother dependency and to assume adult responsibility. He learns to accept and even love the imperfections and particularities of his apartment, just as he does those of his girlfriend. The writing style aspires to the elegance of Tobias Wolff’s <em>This Boy’s Life</em>, the integrity of William Finnegan’s <em>Crossing the Line</em>, the irreverence of Carl Hiaasen’s <em>Basket Case </em>and the insight of Calvin Trillin’s <em>Remembering Denny</em>. The memoir is a tale of growing up despite oneself, of a young journalist who comes to learn, through a series of missteps and misadventures, the true meaning of home.</p>

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</description>

<author>Dan A. Grech</author>


</item>


<item>
<title>Modeling of Crosstalk in High Speed Planar Structure Parallel Data Buses and Suppression by Uniformly Spaced Short Circuits</title>
<link>http://digitalcommons.fiu.edu/etd/606</link>
<guid isPermaLink="true">http://digitalcommons.fiu.edu/etd/606</guid>
<pubDate>Tue, 08 May 2012 15:09:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>The aim of this thesis is to identify coupling mechanisms for three line microstrip, stripline and microstrip with dielectric overlay structures as either inductive or capacitive, quantify through simulation and measurement the amount of crosstalk to be expected in terms of scattering parameters. A new method of crosstalk suppression is implemented into each three line structure by placing uniformly spaced short circuits down the length of the center transmission line.</p>
<p>All structures were simulated over various physical and electrical parameters. Select microstrip structures, shielded and unshielded, were fabricated and measured to validate the effectiveness of the shielding technique. Shielding effectiveness was calculated from the measurements, and their results showed that the isolation between lines was increased by up to 20dB.</p>

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</description>

<author>Gabriel A. Solana</author>


</item>


<item>
<title>Vitamin D levels, vitamin D receptor polymorphisms and HOMA2 model in Cuban Americans, Haitian Americans, and African Americans with and without type 2 Diabetes</title>
<link>http://digitalcommons.fiu.edu/etd/605</link>
<guid isPermaLink="true">http://digitalcommons.fiu.edu/etd/605</guid>
<pubDate>Tue, 08 May 2012 15:09:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>This cross sectional study investigated the association between 25-hydroxyvitamin D (25(OH)D) levels, vitamin D receptor (VDR) polymorphisms, HOMA2 and diabetes status in Cuban Americans, Haitian Americans, and African Americans. The sample for the study included a total of 885 participants (Cuban American = 370; Haitian American = 259; African American = 256). Serum 25(OH)D levels were determined using a commercial ELISA kit from Immunodiagnostic Systems Limited. Polymerase chain reaction-restriction fragment length polymorphism (PCR- RFLP) was used for genotyping<em> BsmI </em>and<em> TaqI,</em> Real-time- Polymerase chain reaction (RT-PCR) was used for <em>ApaI</em>. HOMA2 model calculations were used as a surrogate marker for insulin resistance, insulin sensitivity and β-cell function. All statistical analyses were performed using SPSS (Version 18.0, Chicago, IL, U.S.). Student’s <em>t</em>-test and analysis of variance (ANOVA), c<sup>2</sup> test and logistic regression analysis were used.</p>
<p>We found that Cuban Americans without T2D had significantly lower odds of having insufficient 25(OH)D compared to all other groups. Participants with darker skin (Haitian Americans and African Americans) and those with T2D had the greatest risk of having insufficient levels of 25(OH)D. Cuban Americans with T2D had a protective factor for vitamin D insufficiency if they carried the <em>TaqI </em>genotype (tt) (<em>p </em>< 0.02) and Cuban Americans without T2D had the highest β-cell function levels (<em>p </em>< 0.05).</p>
<p>Further investigation is needed to have a better understanding of the role vitamin D, VDR polymorphisms and the role HOMA2 model plays in the three ethnicities. Awareness of the high prevalence of vitamin D insufficiency among Haitian Americans and African Americans and also in those with T2D may sensitize physicians and dietitians to increase efforts to prevent vitamin D insufficiency. Further research to investigate the role and mechanism of action of vitamin D and diabetes is warranted.</p>

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</description>

<author>Lamya Shaban</author>


</item>


<item>
<title> Genetic control of susceptibility to porphyromonas gingivalis-induced alveolar bone loss in mice [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/118</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/118</guid>
<pubDate>Tue, 08 May 2012 15:08:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Periodontal disease affects a large percentage of the human population.  Resorption of the alveolar bone of the jaw is a pivotal sequela of periodontal disease, because this bone is the attachment site for the periodontal ligaments    that anchor the teeth. Using a murine model in which alveolar bone loss is induced by oral infection with Porphyromonas gingivalis, a gram-negative bacterium associated with human adult periodontal disease, we provide evidence suggesting that    susceptibility to such bone loss is a genetically determined trait. AKR/J, DBA/2J, and BALB/cByJ or BALB/cJ mice were highly susceptible, while A/J, A/HeJ, 129/J, SJL/J, and C57BL/6J mice were much more resistant. When susceptible BALB/cJ and    BALB/cByJ mice were crossed to resistant strains, two patterns were observed. (BALBc/ByJ x C57BL/6J)F(1) offspring were susceptible, suggesting C57BL/6J has recessive resistance alleles, while (BALB/cJ x A/J)F(1) mice were all resistant,    suggesting that A/J mice have dominant resistance alleles. These results suggest a tractable genetic basis for P. gingivalis-induced alveolar bone loss and open the possibility of exploiting the mouse model to identify loci important for host    susceptibility and resistance to periodontal disease.</p>

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</description>

<author>P J. Baker et al.</author>


</item>


<item>
<title>The longitudinal influence of physical activity on adolescent alcohol use</title>
<link>http://digitalcommons.fiu.edu/etd/604</link>
<guid isPermaLink="true">http://digitalcommons.fiu.edu/etd/604</guid>
<pubDate>Tue, 08 May 2012 15:08:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this research was to explore the influence of physical activity on depressive symptomatology and adolescent alcohol use during an underexplored transition from middle school to high school. The study initiative is supported by the fact that research has shown a unique and simultaneous decrease in physical activity (CDC, 2010), increase in depressive symptomatology (SAMHSA, 2010) and increase in alcohol use (USDHHS, 2011) during middle adolescence. A risk and resilience framework was used in efforts to conceptualize how these variables may be inter-related.</p>
<p>Data from waves I and II of the National Longitudinal Study of Adolescent Health (Add Health, Bearman et al., 1997; Udry, 1997) was used (N = 2,054; aged 13-15 years). The sample was ethnically and racially diverse (58.2% White, 24% African American, 11.7% Hispanic, and 6.1% other). Structural equation models were developed to test the potential influence physical activity has on adolescent alcohol use (e.g., frequency of alcohol use and binge alcohol use) and whether any of the relationship was mediated by depressive symptomatology or varied as a function of gender.</p>
<p>Results demonstrated that there was a significant influence of structured physical activity (e.g., sports) on adolescent alcohol use. However, contrary to the proposed hypothesis, engaging in structured physical activity appeared to contribute to greater binge drinking among adolescents. Instead of demonstrating a protective feature, the findings suggest that engaging in structured physical activity places adolescents at risk for binge drinking. Furthermore, no significant relationships, positive or negative, were found for the influence of physical activity (structured and unstructured) on frequency of alcohol use. The findings regarding mediation revealed binge drinking as a mediator between physical activity (structured) and depressive symptomatology. These findings provide support for research, practice, and policy initiatives focused on developing a more comprehensive understanding of alcohol use drinking behaviors, physical activity involvement, and depressive symptomatology among adolescents, which this study demonstrates are all associated with one another. Results represent an initial step toward evaluating these relationships at a much younger age.</p>

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</description>

<author>Beverly A. Ruffin</author>


</item>


<item>
<title> Neuromuscular ataxia: a new spontaneous mutation in the mouse [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/117</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/117</guid>
<pubDate>Tue, 08 May 2012 15:08:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Neuromuscular ataxia, nma, is a new autosomal recessive mutation that arose spontaneously in CBA/J inbred mice at The Jackson Laboratory. The mutation, now maintained on the B6C3FeF(1) hybrid background, when homozygous, causes    small size, uncoordinated gait, dysmetria, dystonia, general weakness, and death shortly after weaning. No biochemical or morphological abnormalities have been detected. We used an intercross between the B6C3FeF(1) mutant and CAST/Ei to map the    nma mutation to the proximal end of Chr 12. The most likely gene order places the mutation between D12Mit270 and D12Mit54, non-recombinant with D12Mit2 in 96 tested meioses.</p>

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</description>

<author>Bailey P. Ward et al.</author>


</item>


<item>
<title> A new spontaneous mouse mutation in the kcne1 gene [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/116</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/116</guid>
<pubDate>Tue, 08 May 2012 15:07:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>A new mouse mutant, punk rocker (allele symbol Kcne1(pkr)), arose spontaneously on a C57BL/10J inbred strain background and is characterized by a distinctive head-tossing, circling, and ataxic phenotype. It is also profoundly and    bilaterally deaf. The mutation resides in the Kcne1 gene on Chromosome (Chr) 16 and has been identified as a single base change within the coding region of the third exon. The C to T nucleotide substitution causes an arginine to be altered to a    termination codon at amino acid position 67, and predictably this will result in a significantly truncated protein product. The Kcne1(pkr) mutant represents the first spontaneous mouse model for the human disorder, Jervell and Lange-Nielsen    syndrome, associated with mutations in the homologous KCNE1 gene on human Chr 21.</p>

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</description>

<author>V A. Letts et al.</author>


</item>


<item>
<title> Cross-referencing radiation hybrid data to the recombination map: lessons from mouse chromosome 18 [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/115</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/115</guid>
<pubDate>Tue, 08 May 2012 15:06:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>We are building a framework map of known-order anchor markers between the mouse T31 radiation hybrid (RH) panel and the recombination map based on The Jackson Laboratory (TJL) interspecific backcross panels using the established    genetic order to evaluate and strengthen the RH results. In making this map comparison, we have elucidated several problems inherent in RH mapping and minimized these by careful attention to data gathering and interpretation methods. We describe    lessons and pitfalls of developing radiation hybrid maps, using the example of mouse Chromosome 18, for which we have built a framework map of microsatellite anchor loci spanning the entire chromosome at significant LOD with no gaps. Sixty-five    D18Mit- simple sequence length polymorphism (SSLP) markers form a continuous linkage along the T31 RH Chromosome 18 (RH map length 1598 cR, genetic length 41 cM) with all LODs greater than 6. These markers are also placed on TJL interspecific    backcrosses, and the order of the markers in the two systems is in complete agreement. We are continuing to cross-reference the RH data to TJL backcross data for the other mouse chromosomes to improve further the power of RH mapping and to    integrate more precisely the extensive existing recombination mapping data for the mouse with the incoming radiation hybrid map data. Copyright 2000 Academic Press.</p>

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</description>

<author>L B. Rowe et al.</author>


</item>


<item>
<title> Genetic and physical mapping of the cerebellar deficient folia (cdf) locus on mouse chromosome 6 [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/114</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/114</guid>
<pubDate>Tue, 08 May 2012 15:06:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cerebellar deficient folia (cdf) is a recessive mouse mutation causing ataxia and cerebellar cytoarchitectural abnormalities, including hypoplasia, foliation defects, and Purkinje cell ectopia. To identify the cdf gene, we have    generated a high-resolution genetic map of a 3.24 +/- 0.55 cM (95% CI) region encompassing the cdf gene using 1997 F2 mice generated from a (C3H/HeSnJ-cdf/cdf x CAST/Ei)F1 intercross. Linkage analysis showed that the cdf gene cosegregates with    D6Mit208, D6Mit359, and D6Mit225. A contig of five YACs, nine BACs, and three P1s was constructed across the cdf nonrecombinant region. Based on genetic and physical maps, the cdf gene was localized to the 0.28 +/- 0.23 cM (95% CI) interval    between D6Mit209 and D6Ack1. These results will greatly facilitate the map-based cloning of the cdf gene, which in turn should further knowledge of the molecular mechanisms of neuronal positioning and foliation during cerebellar development.    Copyright 2000 Academic Press.</p>

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</description>

<author>C Park et al.</author>


</item>


<item>
<title> The mouse fidgetin gene defines a new role for AAA family proteins in mammalian development [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/113</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/113</guid>
<pubDate>Tue, 08 May 2012 15:05:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse mutation fidget arose spontaneously in a heterogeneous albino stock. This mutant mouse is characterized by a side-to-side head-shaking and circling behaviour, due to reduced or absent semicircular canals.  Fidget mice    also have small eyes, associated with cell-cycle delay and insufficient growth of the retinal neural epithelium, and lower penetrance skeletal abnormalities, including pelvic girdle dysgenesis, skull bone fusions and polydactyly. By positional    cloning, we found the gene mutated in fidget mice, fidgetin (Fign), which encodes a new member of the 'meiotic' or subfamily-7 (SF7; ref. 7) group of ATPases associated with diverse cellular activities (AAA proteins). We also discovered two    closely related mammalian genes. AAA proteins are molecular chaperones that facilitate a variety of functions, including membrane fusion, proteolysis, peroxisome biogenesis, endosome sorting and meiotic spindle formation, but functions for the    SF7 AAA proteins are largely unknown. Fidgetin is the first mutant AAA protein found in a mammalian developmental mutant, thus defining a new role for these proteins in embryonic development.</p>

	]]>
</description>

<author>G A. Cox et al.</author>


</item>


<item>
<title> Differences that matter: major cytotoxic T cell-stimulating minor histocompatibility antigens.</title>
<link>http://mouseion.jax.org/stfb2000_2009/112</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/112</guid>
<pubDate>Tue, 08 May 2012 15:04:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite thousands of genetic polymorphisms among MHC matched mouse strains, a few unknown histocompatibility antigens are targeted by the cytotoxic T cells specific for tissue grafts. We isolated the cDNA of a novel BALB.B antigen    gene that defines the polymorphic H28 locus on chromosome 3 and yields the naturally processed ILENFPRL (IFL8) peptide for presentation by Kb MHC to C57BI/6 CTL. The CTL specific for the IFL8/Kb and our previously identified H60/Kb complexes    represent a major fraction of the B6 anti-BALB.B immune response. The immunodominance of these antigens can be explained by their differential transcription in the donor versus the host strains and their expression in professional donor    antigen-presenting cells.</p>

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</description>

<author>S Malarkannan et al.</author>


</item>


<item>
<title> Accuracy of haplotype frequency estimation for biallelic loci, via the expectation-maximization algorithm for unphased diploid genotype data [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/111</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/111</guid>
<pubDate>Tue, 08 May 2012 15:03:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Haplotype analyses have become increasingly common in genetic studies of human disease because of their ability to identify unique chromosomal segments likely to harbor disease-predisposing genes. The study of haplotypes is also    used to investigate many population processes, such as migration and immigration rates, linkage-disequilibrium strength, and the relatedness of populations. Unfortunately, many haplotype-analysis methods require phase information that can be    difficult to obtain from samples of nonhaploid species. There are, however, strategies for estimating haplotype frequencies from unphased diploid genotype data collected on a sample of individuals that make use of the expectation-maximization    (EM) algorithm to overcome the missing phase information. The accuracy of such strategies, compared with other phase-determination methods, must be assessed before their use can be advocated. In this study, we consider and explore sources of    error between EM-derived haplotype frequency estimates and their population parameters, noting that much of this error is due to sampling error, which is inherent in all studies, even when phase can be determined. In light of this, we focus on    the additional error between haplotype frequencies within a sample data set and EM-derived haplotype frequency estimates incurred by the estimation procedure. We assess the accuracy of haplotype frequency estimation as a function of a number of    factors, including sample size, number of loci studied, allele frequencies, and locus-specific allelic departures from Hardy-Weinberg and linkage equilibrium.  We point out the relative impacts of sampling error and estimation error, calling    attention to the pronounced accuracy of EM estimates once sampling error has been accounted for. We also suggest that many factors that may influence accuracy can be assessed empirically within a data set-a fact that can be used to create    "diagnostics" that a user can turn to for assessing potential inaccuracies in estimation.</p>

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</description>

<author>D Fallin et al.</author>


</item>


<item>
<title> Genetics of mouse mammary tumor virus-induced mammary tumors: linkage of tumor induction to the gag gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/110</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/110</guid>
<pubDate>Tue, 08 May 2012 15:03:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Retroviruses are believed to induce tumors by acting as insertional mutagens that activate expression of cellular protooncogenes. Indeed, almost 90% of mouse mammary tumor virus (MMTV)-induced mammary tumors in C3H/He mice show    upregulation of Int protooncogenes. We have analyzed three different MMTV variants [MMTV(C3H), MMTV(HeJ), and a genetically engineered MMTV hybrid provirus (HP)] for tumorigenicity in mice from two distinct genetic backgrounds. All three viruses    were tumor causing in BALB/cJ mice. However, only MMTV(C3H), but not MMTV(HeJ) or HP, induced mammary tumors in C3H/He mice. All of the viruses were infectious on either background and up-regulated expression of Int genes in tumors they induced.    Like HP, MMTV(HeJ) was found to be a genetic recombinant between endogenous Mtv1 provirus and exogenous MMTV(C3H). Sequence comparison of MMTV variants linked the tumorigenicity of MMTV(C3H) to the gag region of the retrovirus.</p>

	]]>
</description>

<author>L M. Hook et al.</author>


</item>


<item>
<title> Amelioration of severe hereditary spherocytosis in nonablated adult mice by marrow transplantation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/109</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/109</guid>
<pubDate>Tue, 08 May 2012 15:02:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human severe hereditary spherocytosis (sHS) is life threatening and transfusion dependent. sHS is lethal within 6 days of birth for 99% of jaundiced (ja/ja) mice, making these mice excellent models for early therapeutic    interventions. Nonablated ja/ja neonates simultaneously transfused and given intravenous injections of normal marrow become chimeric for donor cells. Significant improvement of red blood cell parameters occurs but is temporary because the donor    marrow-derived cells gradually disappear from the circulation. The average lifespan, however, is increased to 8.7 months. We postulate that donor cells are diluted by rapidly proliferating host cells during postnatal growth. Here, we test this    hypothesis by determining whether treatment of adults improves long-term therapy. Nonablated ja/ja adults rescued by a single neonatal transfusion were injected intravenously with 1 x 10(10) normal, genetically marked donor marrow cells/kg body    weight. Donor cell implantation and blood parameters were monitored periodically and tissue histopathology was determined at necropsy.sHS recipients with 100% donor erythroid cells have significantly improved red blood cell counts throughout life    when compared with ja/ja controls transfused once at birth. Total serum iron and bilirubin levels are corrected in ja/ja marrow recipients. Donor-implanted HS mice necropsied at 16 to 21 months of age have normal mean cell hemoglobin    concentration and dramatically decreased tissue iron deposits. Reticulocyte counts but not red cell counts normalize, suggesting the HS mice reset their response to hypoxia.Nonablative transplantation performed after cessation of host postnatal    red blood cell amplification can be therapeutic long term for transfusion-dependent hemolytic anemias.</p>

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</description>

<author>J E. Barker et al.</author>


</item>


<item>
<title> Mice mutant for ppap2c, a homolog of the germ cell migration regulator wunen, are viable and fertile [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/108</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/108</guid>
<pubDate>Tue, 08 May 2012 15:01:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Summary: Phosphatidic acid phosphatases (PAPs) catalyze the conversion of phosphatidic acid to diacylglycerol and inorganic phosphate and have been postulated to function both in lipid biosynthesis and in cellular signal    transduction. In Drosophila melanogaster, the Type 2 phosphatidic acid phosphatase protein encoded by the wunen gene, negatively regulates primordial germ cell migration. We recently described the cloning and characterization of the mouse Ppap2c    gene, which encodes the Type 2 phosphatidic acid phosphatase Pap2c (Zhang et al., Genomics 63:142-144).  To analyze the in vivo role of the Ppap2c gene we constructed a null mutation by gene targeting. Ppap2c(-/-) homozygous mutant mice were    viable, fertile, and exhibited no obvious phenotypic defects. These data demonstrate that the Ppap2c gene is not essential for embryonic development or fertility in mice. genesis 27:137-140, 2000.</p>

	]]>
</description>

<author>N Zhang et al.</author>


</item>


<item>
<title> Development of mouse and rat oocytes in chimeric reaggregated ovaries after interspecific exchange of somatic and germ cell components [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/107</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/107</guid>
<pubDate>Tue, 08 May 2012 15:00:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>The germ cell and somatic cell compartments of newborn rat and mouse ovaries, which contain only primordial stage follicles, were completely exchanged and reaggregated to produce xenogeneic chimeric ovaries. The reaggregated    ovaries were grafted beneath the renal capsules of ovariectomized SCID mice to develop for periods up to 21 days. Xenogeneic follicles developed with essentially normal morphological characteristics Both rat and mouse oocytes with    species-specific characteristics grew within follicles that were composed of somatic cells exclusively of the alternative species. Rat oocytes grown in mouse follicles became competent to resume meiosis, and progressed to metaphase II when they    were removed from follicles and cultured. In addition, mouse oocytes grown in rat follicles underwent fertilization and preimplantation development in vitro, and developed to term after embryos were transferred to pseudopregnant mouse foster    mothers. Therefore, despite an estimated 11 million years of divergent evolution, oocytes and somatic cells of rat and mouse ovaries can be exchanged and can produce functional oocytes. It is concluded that factors involved in oocyte-somatic cell    interactions necessary to support oocyte development and appropriate differentiation of the oocyte-associated granulosa cells are conserved between rats and mice.  Moreover, although granulosa cells play important roles in oocyte development, the    development of species-specific characteristics of oocytes occurs without apparent modification by a xenogeneic follicular environment.</p>

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</description>

<author>J J. Eppig et al.</author>


</item>


<item>
<title> Treatment with an anti-CD44v10-specific antibody inhibits the onset of alopecia areata in C3H/HeJ mice [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/106</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/106</guid>
<pubDate>Tue, 08 May 2012 14:59:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>A murine CD44v10-neutralizing antibody has been reported to impair delayed-type hypersensitivity reactions. Because alopecia areata is characterized by a delayed-type hypersensitivity-like T cell mediated immune response, we    addressed the question whether an anti-CD44v10-antibody influences the onset of alopecia areata. Therefore, we used the C3H/HeJ mouse model with the induction of alopecia areata in unaffected mice by the grafting of lesional alopecia areata mouse    skin.  Six grafted mice were injected (intraperitoneally) with anti-CD44v10, six grafted mice with anti-CD44standard, and six with phosphate-buffered saline only. After 11 wk phosphate-buffered saline injected animals on average had developed    alopecia areata on 36.8% of their body. The onset of hair loss was slightly delayed and its extent reduced to 17.2% of their body in anti-CD44standard-treated mice. By contrast, five of six anti-CD44v10-treated mice did not show any hair loss and    one mouse developed alopecia areata on only 1% of the body. Immunohistochemical examination revealed a marked reduction of perifollicular CD8+ lymphocytes and, to a lesser degree, CD4+ cells as well as a decreased expression of major    histocompatibility complex class I on hair follicle epithelium in anti-CD44v10-treated mice as compared with phosphate-buffered saline or anti-CD44 standard-treated mice. Our data show that anti-CD44v10 is able to inhibit the onset of alopecia    areata in C3H/HeJ mice. This might be accomplished by an anti-CD44v10-triggered impairment of immune cell homing (e.g., CD8+ T cells), resulting in a decrease of their number in target tissues.</p>

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</description>

<author>Paul P. Freyschmidt et al.</author>


</item>


<item>
<title> GFP-tagged expression and immunohistochemical studies to determine the subcellular localization of the tubby gene family members [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/105</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/105</guid>
<pubDate>Tue, 08 May 2012 14:59:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The tubby gene family consists of four members, TUB, TULP1, TULP2 and TULP3, with unknown function. However, a splice junction mutation within the mouse tub gene leads to retinal and cochlear degeneration, as well as maturity onset    obesity and insulin resistance. Mutations within human TULP1 have also been shown to co-segregate in several cases of autosomal recessive retinitis pigmentosa (RP) and TULP1 deficiency in mice leads to retinal degeneration. The primary amino acid    sequences of the tubby family members do not predict a likely biochemical function. As a first step in defining their function, we present a detailed characterization of the cellular and subcellular localization of the human (TUB) and mouse (tub)    homologous gene products. We report the isolation of TUB splice variants which have different subcellular localizations (nuclear versus cytoplasmic) and which define a nuclear localization signal. In addition, using green fluorescent protein    (GFP) tags, we observe a nuclear localization for TULP1, similar to TUB splicing forms TUB 561 and TUB 506.  Finally, we report tubby expression in mouse brain by in situ hybridization and by immunohistochemistry with polyclonal antibodies.     Protein was found in both the hypothalamic satiety centers and in a variety of other CNS structures including the cortex, cerebellum, olfactory bulb and hippocampus. Both nuclear and cytoplasmic signals were detected with a series of    independently generated polyclonal antibodies, consistent with the presence of multiple alternatively spliced isoforms within the CNS.</p>

	]]>
</description>

<author>W He et al.</author>


</item>


<item>
<title> Quantitative trait locus mapping of genes regulating pulmonary PKC activity and PKC-alpha content.</title>
<link>http://mouseion.jax.org/stfb2000_2009/104</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/104</guid>
<pubDate>Tue, 08 May 2012 14:58:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Strain A/J mice, which are predisposed to experimentally induced asthma and adenocarcinoma, have the lowest pulmonary protein kinase (PK) C activity and content among 22 inbred mouse strains. PKC in neonatal A/J mice is similar to    that in other strains, so this difference reflects strain-dependent postnatal regulation. PKC activity is 60% higher in C57BL/6J (B6) than in A/J lungs, and the protein and mRNA concentrations of PKC-alpha, the major pulmonary PKC isozyme, are    two- to threefold higher in B6 mice. These differences result from more than a single gene as assessed in F(1), F(2), and backcross progeny of B6 and A/J parents.  Quantitative trait locus (QTL) analysis of 23 AxB and BxA recombinant inbred    strains derived from B6 and A/J progenitors indicates a major locus regulating lung PKC-alpha content that maps near the Pkcalpha structural gene on chromosome 11 (D11MIT333; likelihood ratio statistic = 12.5) and a major locus controlling PKC    activity that maps on chromosome 3 (D3MIT19; likelihood ratio statistic = 15.4). The chromosome 11 QTL responsible for low PKC-alpha content falls within QTLs for susceptibilities to lung tumorigenesis and ozone-induced toxicity.</p>

	]]>
</description>

<author>Nield L. Dwyer et al.</author>


</item>


<item>
<title> Timely translation during the mouse oocyte-to-embryo transition.</title>
<link>http://mouseion.jax.org/stfb2000_2009/103</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/103</guid>
<pubDate>Tue, 08 May 2012 14:57:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the mouse, completion of oocyte maturation and the initiation of preimplantation development occur during transcriptional silence and depend on the presence and translation of stored mRNAs transcribed in the growing oocyte. The    Spin gene has three transcripts, each with an identical open reading frame and a different 3' untranslated region (UTR) (Beta)-galactosidase-tagged reporter transcripts containing each of the different Spin 3'UTRs were injected into oocytes and    zygotes and (beta)-galactosidase activity was monitored. Results from these experiments suggest that differential polyadenylation and translation occurs at two critical points in the oocyte-to-embryo transition - upon oocyte maturation and    fertilization - and is dependent on sequences in the 3'UTR. The stability and mobility shifts of ten other maternal transcripts were monitored by reprobing a northern blot of oocytes and embryos collected at 12 hour intervals after fertilization.    Some are more stable than others and the upward mobility shift associated with polyadenylation correlates with the presence of cytoplasmic polyadenylation elements (CPEs) within about 120 nucleotides of the nuclear polyadenylation signal.  A    survey of the 3' UTRs of expressed sequence tag clusters from a mouse 2-cell stage cDNA library indicates that about one third contain CPEs. We suggest that differential transcript stability and a translational control program can supply the    diversity of protein products necessary for oocyte maturation and the initiation of development.</p>

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</description>

<author>B Oh et al.</author>


</item>


<item>
<title> Effects of macrophage-colony-stimulating factor deficiency on the maturation of microglia and brain macrophages and on their expression of scavenger receptor.</title>
<link>http://mouseion.jax.org/stfb2000_2009/102</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/102</guid>
<pubDate>Tue, 08 May 2012 14:57:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Macrophage-colony-stimulating factor (M-CSF) regulates the survival, proliferation and differentiation of the mononuclear phagocyte lineage.  Osteopetrotic (op/op) mice defective in producing functional M-CSF were used in order to    investigate the role of M-CSF on the development of microglia and brain macrophages and the expression of scavenger receptor (SR). Adult op/op and littermate mice at 10-47 weeks of age were investigated by immunohistochemistry with a panel of    monoclonal antibodies (F4/80, Mac-1, anti-major histocompatibility complex (MHC) class II and anti-SR), electron microscopy and reverse transcriptase-polymerase chain reaction (RT-PCR). Microglia were weakly immunolabeled with F4/80 and Mac-1 in    op/op and littermate mice, but the number of microglia in op/op mice was reduced in the cerebrum, cerebellum and brainstem compared with that of normal littermates. The numbers of Mac-1-positive microglia in op/op mice was 39% (pons) and 30%    (cerebellar cortex) lower than that in normal littermates (P<0.05). In addition, the microglia cell processes in op/op mice were often shorter than those in control mice. In op/op and littermate mice, both MHC class II and SR were present in    perivascular cells and macrophages of the leptomeninx and choroid plexus.  Ultrastructurally, perivascular cells appeared to be immature, since their cytoplasm was narrow and contained few inclusion bodies compared with those of control mice.    Reverse transcriptase-polymerase chain reaction showed a weak expression for SR mRNA in the brains of op/op mice as well as littermate mice. These results indicate that microglia are partly dependent on M-CSF for their proliferation and    differentiation and that M-CSF has no significant effect on the expression of SR in the physiological brain. The study also suggests that M-CSF affects the maturation of perivascular cells at the ultrastructural level.</p>

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</description>

<author>A Sasaki et al.</author>


</item>


<item>
<title> Nf1;Trp53 mutant mice develop glioblastoma with evidence of strain-specific effects [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/101</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/101</guid>
<pubDate>Tue, 08 May 2012 14:56:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K M. Reilly et al.</author>


</item>


<item>
<title> Targeted overexpression of insulin-like growth factor I to osteoblasts of transgenic mice: increased trabecular bone volume without increased osteoblast proliferation.</title>
<link>http://mouseion.jax.org/stfb2000_2009/100</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/100</guid>
<pubDate>Tue, 08 May 2012 14:55:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Insulin-like growth factor I (IGF-I) is an important growth factor for bone, yet the mechanisms that mediate its anabolic activity in the skeleton are poorly understood. To examine the effects of locally produced IGF-I in bone in    vivo, we targeted expression IGF-I to osteoblasts of transgenic mice using a human osteocalcin promoter. The IGF-I transgene was expressed in bone osteoblasts in OC-IGF-I transgenic mice at high levels in the absence of any change in serum IGF-I    levels, or of total body growth. Bone formation rate at the distal femur in 3-week-old OC-IGF-I transgenic mice was approximately twice that of controls. By 6 weeks, bone mineral density as measured by dual energy x-ray, and quantitative computed    tomography was significantly greater in OC-IGF-I transgenic mice compared with controls. Histomorphometric measurements revealed a marked (30%) increase femoral cancellous bone volume in the OC-IGF-I transgenic mice, but no change in the total    number of osteoblasts or osteoclasts. Transgenic mice also demonstrated an increase in the osteocyte lacunea occupancy, suggesting that IGF-I may extend the osteocyte life span. We conclude that IGF-I produced locally in bone osteoblasts exerts    its anabolic effect primarily by increasing the activity of resident osteoblasts.</p>

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</description>

<author>G Zhao et al.</author>


</item>


<item>
<title> Branchial cysts in laboratory mice [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/99</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/99</guid>
<pubDate>Tue, 08 May 2012 14:55:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Large solitary cysts in the superficial tissues of the ventral neck are described in five laboratory mice of two inbred strains and one outbred line. The cysts were lined by cuboidal to columnar epithelium similar to that in    branchial cysts reported in other animal species but distinct from the stratified squamous epithelium with prominent lymphoid tissue typical of branchial cysts in man. These findings suggest that the lesion referred to as a branchial cyst in    animals differs slightly from the lesion of the same name in man. Copyright 2000 Harcourt Publishers Ltd.</p>

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</description>

<author>M P. France et al.</author>


</item>


<item>
<title>An Extension of the Rishon Model</title>
<link>http://digitalcommons.unl.edu/physicsfinkler/1</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsfinkler/1</guid>
<pubDate>Tue, 08 May 2012 14:54:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present an extension of the Rishon Model of Harari, et. al. [1] [2] [3] In that model, the first generation leptons and quarks are each made from three rishons of two varieties, T and V as follows: <em>v</em><sub>e</sub> = V V V , e<sup>+</sup> = T T T , <em>d</em> = T V V , and <em>u</em> = T T V . In addition to the original rishons and their anti-rishons T and V , we introduce the dark rishon X and its anti-rishon X; all have spin 1/2.</p>
<p>An exciting possibility that emerges from this idea is the possiblity of ‘beams’ of dark matter coming from the decays of higher generation fermions – much in the same way as ‘beams’ of neutrinos are made. The result of such collisions could produce known particles via color/hypercolor interactions or another - as yet unknown - interaction of dark rishons.</p>

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</description>

<author>Paul Finkler</author>


</item>


<item>
<title> Distinct regulatory elements direct delta1 expression in the nervous system and paraxial mesoderm of transgenic mice [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/98</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/98</guid>
<pubDate>Tue, 08 May 2012 14:54:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Delta1 gene encodes one of the Notch ligands in mice. Delta1 is expressed during early embryogenesis in a complex and dynamic pattern in the paraxial mesoderm and neuroectoderm, and is essential for normal somitogenesis and    neuronal differentiation. Molecular components thought to act in response to ligand binding and Notch activation have been identified in different species. In contrast, little is known about the transcriptional regulation of Notch receptors and    their ligands. As a first step to identify upstream factors regulating Delta1 expression in different tissues, we searched for cis-regulatory regions in the Delta1 promoter able to direct heterologous gene expression in a tissue specific manner    in transgenic mice. Our results show that a 4.3 kb genomic DNA fragment of the Delta1 gene is sufficient in a lacZ reporter transgene to reproduce most aspects of Delta1 expression from the primitive streak stage to early organogenesis. Using a    minimal Delta1 promoter we also show that this upstream region contains distinct regulatory modules that individually direct tissue-specific transgene expression in subdomains of the endogenous expression pattern. It appears that expression in    the paraxial mesoderm depends on the interaction of multiple positive and negative regulatory elements. We also find that at least some regulatory sequences required for transgene expression in subdomains of the neural tube have been maintained    during the evolution of mammals and teleost fish, suggesting that part of the regulatory network that controls expression of Delta genes may be conserved.</p>

	]]>
</description>

<author>J Beckers et al.</author>


</item>


<item>
<title> The mouse rib-vertebrae mutation disrupts anterior-posterior somite patterning and genetically interacts with a delta1 null allele [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/97</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/97</guid>
<pubDate>Tue, 08 May 2012 14:53:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rib-vertebrae (rv) is an autosomal recessive mutation in mouse that affects the morphogenesis of the vertebral column. Axial skeleton defects vary along the anterior-posterior body axis, and include split vertebrae and neural    arches, and fusions of adjacent segments. Here, we show that defective somite patterning underlies the vertebral malformations and altered Notch signaling may contribute to the phenotype. Somites in affected regions are irregular in size and    shape, epithelial morphology is disrupted, and anterior-posterior somite patterning is abnormal, reminiscent of somite defects obtained in loss-of-function alleles of Notch signaling pathway components. Expression of Dll1, Dll3, Lfng and Notch1    is altered in rv mutant embryos, and rv and Dll1(lacZ), a null allele of the Notch ligand Delta1, genetically interact. Mice double heterozygous for rv and Dll1(lacZ), show vertebral defects, and one copy of Dll1(lacZ) on the homozygous rv    background enhances the mutant phenotype and is lethal in the majority of cases. However, fine genetic mapping places rv into an interval on chromosome seven that does not contain a gene encoding a known component of the Notch signaling    pathway.</p>

	]]>
</description>

<author>J Beckers et al.</author>


</item>


<item>
<title> Positioning of five genes (CASK, ARX, SAT, IMAGE cDNAs 248928 and 253949) from the human X chromosome short arm with respect to evolutionary breakpoints on the mouse X chromosome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/96</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/96</guid>
<pubDate>Tue, 08 May 2012 14:53:01 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H J. Blair et al.</author>


</item>


<item>
<title> Feline papillomas and papillomaviruses.</title>
<link>http://mouseion.jax.org/stfb2000_2009/95</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/95</guid>
<pubDate>Tue, 08 May 2012 14:52:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Papillomaviruses (PVs) are highly species- and site-specific pathogens of stratified squamous epithelium. Although PV infections in the various Felidae are rarely reported, we identified productive infections in six cat species.    PV-induced proliferative skin or mucous membrane lesions were confirmed by immunohistochemical screening for papillomavirus-specific capsid antigens. Seven monoclonal antibodies, each of which reacts with an immunodominant antigenic determinant    of the bovine papillomavirus L1 gene product, revealed that feline PV capsid epitopes were conserved to various degrees. This battery of monoclonal antibodies established differential expression patterns among cutaneous and oral PVs of snow    leopards and domestic cats, suggesting that they represent distinct viruses.  Clinically, the lesions in all species and anatomic sites were locally extensive and frequently multiple. Histologically, the areas of epidermal hyperplasia were flat    with a similarity to benign tumors induced by cutaneotropic, carcinogenic PVs in immunosuppressed human patients.  Limited restriction endonuclease analyses of viral genomic DNA confirmed the variability among three viral genomes recovered from    available frozen tissue. Because most previous PV isolates have been species specific, these studies suggest that at least eight different cat papillomaviruses infect the oral cavity (tentative designations: Asian lion, Panthera leo, P1PV; snow    leopard, Panthera uncia, PuPV-1; bobcat, Felis rufus, FrPV; Florida panther, Felis concolor, FcPV; clouded leopard, Neofelis nebulosa NnPV; and domestic cat, Felis domesticus, FdPV-2) or skin (domestic cat, F. domesticus, FdPV-1; and snow    leopard, P. uncia, PuPV-2).</p>

	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title> The C3H/HeJBir mouse model: a high susceptibility phenotype for colitis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/94</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/94</guid>
<pubDate>Tue, 08 May 2012 14:51:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>C3H/HeJBir is a substrain of C3H/HeJ mice that was generated by selective breeding for the phenotype of spontaneous colitis. These mice show increased B cell and T cell reactivity to antigens of the enteric bacterial flora. CD4+ T    cells from this strain cause colitis, when activated by enteric bacterial antigens and transferred to histocompatible severe combined immunodeficient recipients. The expression of the disease phenotype of spontaneous colitis is greatly influenced    by housing conditions and probably requires an immunostimulatory enteric flora. This strain seems to carry multiple susceptibility genes for colitis as does the parental C3H/HeJ strain; the genes involved are being mapped. This strain represents    a high susceptibility phenotype for colitis that is providing insight into the interactions among immune, environmental and genetic factors that can result in IBD.</p>

	]]>
</description>

<author>C O. Elson et al.</author>


</item>


<item>
<title> Intercellular adhesion molecule-1 and hair follicle regression.</title>
<link>http://mouseion.jax.org/stfb2000_2009/93</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/93</guid>
<pubDate>Tue, 08 May 2012 14:51:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although the intercellular adhesion molecule-1 (ICAM-1) is recognized for its pivotal role in inflammation and immune responses, its role in developmental systems, such as the cyclic growth (anagen) and regression (catagen) of the    hair follicle, remains to be explored. Here we demonstrate that ICAM-1 expression in murine skin is even more widespread and more developmentally regulated than was previously believed. In addition to endothelial cells, selected epidermal and    follicular keratinocyte subpopulations, as well as interfollicular fibroblasts, express ICAM-1. Murine hair follicles express ICAM-1 only late during morphogenesis. Thereafter, morphologically identical follicles markedly differ in their ICAM-1    expression patterns, which become strikingly hair cycle-dependent in both intra- and extrafollicular skin compartments.  Minimal ICAM-1 and leukocyte function-associated (LFA-1) protein and mRNA expression is observed during early anagen and    maximal expression during late anagen and catagen. Keratinocytes of the distal outer root sheath, fibroblasts of the perifollicular connective tissue sheath, and perifollicular blood vessels exhibit maximal ICAM-1 immunoreactivity during catagen,    which corresponds to changes of LFA-1 expression on perifollicular macrophages. Finally, ICAM-1-deficient mice display significant catagen acceleration compared to wild-type controls.  Therefore, ICAM-1 upregulation is not limited to pathological    situations but is also important for skin and hair follicle remodeling. Collectively this suggests a new and apparently nonimmunological function for ICAM-1-related signaling in cutaneous biology.</p>

	]]>
</description>

<author>Rover S. Muller et al.</author>


</item>


<item>
<title> Ornithine decarboxylase transgenic mice as a model for human atrichia with papular lesions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/92</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/92</guid>
<pubDate>Tue, 08 May 2012 14:50:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>The hair follicle is characterized by cyclic transformations from active growth and hair fiber production through regression into a resting phase.  The growth phase, known as anagen, is associated with rapid rates of cell turnover,    and variations in the rate of DNA synthesis in mouse skin throughout the hair cycle are accompanied by changes in the activity of ornithine decarboxylase (ODC), a key enzyme in the synthesis of polyamines, which are actively involved in    regulation of normal cell division, differentiation, and growth. Previously, a transgenic mouse was created that overexpressed ODC in the skin using a K6 promoter. The first hair cycle in neonatal transgenic mice appeared to be normal, but by the    third week of postnatal life transgenic pups begin to progressively lose hair. The lower portion of the hair follicle was progressively replaced with enlarging cystic structures located in the deep dermis, and the transgenic mice exhibited    excessive growth of skin mass resulting in pronounced wrinkling and folding. Interestingly, these findings bore striking resemblance to the rhino mouse phenotype and to human patients with papular atrichia, a rare congenital ectodermal disorder    characterized by progressive and irreversible hair loss in early childhood. The similarities in phenotype between transgenic mice and human atrichia with papular lesions suggest that ODC transgenics may represent a useful model for studying this    disorder. It appears that ODC plays a functionally important, yet still obscure role in a complex metabolic pathway that is critical in hair follicle function not only in mice, but in humans as well.</p>

	]]>
</description>

<author>A A. Panteleyev et al.</author>


</item>


<item>
<title> Calorie restriction modulates age-dependent changes in the retinas of brown norway rats [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/91</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/91</guid>
<pubDate>Tue, 08 May 2012 14:49:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>The present study examined the effect of a 40% reduction in caloric intake (CR) versus ad libitum (AL) feeding on retinal aging. CR- and AL-fed Brown Norway (BN) rats were obtained at 12, 24 and 30 months of age from the National    Center for Toxicological Research (NCTR). Age-dependent declines in outer nuclear layer (ONL=photoreceptor) cell densities, ONL height, inner nuclear layer (INL) cell densities, and thicknesses of the inner retina and whole retina were quantified    in thick sections at six loci across the circumference of the sensory retina (four peripheral, two central). Data were analyzed by repeated measures, general linear models.  Aging in both diet groups was associated with declines in ONL cell    density, ONL height, peripheral INL cell density and total retinal thickness (P</p>

	]]>
</description>

<author>M Obin et al.</author>


</item>


<item>
<title>Search for first generation leptoquark pair production in the electron + missing
energy + jets final state</title>
<link>http://digitalcommons.unl.edu/physicsbloom/319</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsbloom/319</guid>
<pubDate>Tue, 08 May 2012 14:49:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present a search for the pair production of first generation scalar leptoquarks (<em>LQ</em>) in data corresponding to an integrated luminosity of 5.4 fb<sup>-1</sup> collected with the D0 detector at the Fermilab Tevatron Collider in <em>pp</em> collisions at √<em>s</em>= 1.96 TeV. In the channel <em>LQLQ</em> → eqv<sub>e</sub>q<sup>1</sup>, where q, q<sup>1</sup> are u or d quarks, no significant excess of data over background is observed, and we set a 95% C.L. lower limit of 326 GeV on the <em>LQ</em> mass, assuming equal probabilities of <em>LQ</em> decays to eq and v<sub>e</sub>q<sup>1</sup>.</p>

	]]>
</description>

<author>V. M. Abazov et al.</author>


</item>


<item>
<title> Bisphosphonates: safety and efficacy in the treatment and prevention of osteoporosis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/90</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/90</guid>
<pubDate>Tue, 08 May 2012 14:49:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Osteoporosis affects more than 28 million Americans. With the advent of accessible and affordable diagnostic studies, awareness and recognition of this disease by patients and clinicians are growing. Osteoporotic fractures of the    spine and hip are costly and associated with significant morbidity and mortality. Over the past decade, a surge of new antiosteoporotic drugs have been labeled or are awaiting labeling by the U.S. Food and Drug Administration. One class of agents    used to treat osteoporosis is the bisphosphonates, which inhibit bone resorption, cause an increase in bone mineral density and reduce the risk of future fractures caused by aging, estrogen deficiency and corticosteroid use.  Overall,    bisphosphonates have been shown to have a strong safety and tolerability profile.</p>

	]]>
</description>

<author>S L. Greenspan et al.</author>


</item>


<item>
<title> Mice, mutations and mammary glands.</title>
<link>http://mouseion.jax.org/stfb2000_2009/89</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/89</guid>
<pubDate>Tue, 08 May 2012 14:48:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>B J. Tennent et al.</author>


</item>


<item>
<title> Peaks and troughs in linkage mapping for the rheumatic diseases [editorial]</title>
<link>http://mouseion.jax.org/stfb2000_2009/88</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/88</guid>
<pubDate>Tue, 08 May 2012 14:47:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J S. Lanchbury et al.</author>


</item>


<item>
<title> Localization of tubby-like protein 1 in developing and adult human retinas.</title>
<link>http://mouseion.jax.org/stfb2000_2009/87</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/87</guid>
<pubDate>Tue, 08 May 2012 14:47:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: To localize tubby-like protein 1 (TULP1) in developing and adult human retinas. METHODS: TULP1 was localized by immunofluorescence microscopy in human retinas, aged 8.4 fetal weeks to adult. TULP1-positive cells were    identified by double labeling with antibodies specific for cones, rods, and astrocytes. RESULTS: In adult retinas, anti-TULP1 labels cone and rod inner segments, somata, and synapses; outer segments are TULP1-negative. A few inner nuclear and    ganglion cells are weakly TULP1-positive. In fetal retinas, cells at the outer retinal border are TULP1-positive at 8.4 weeks. At 11 weeks, the differentiating central cones are strongly TULP1-reactive and some are positive for blue cone opsin.    At 15.4 weeks, all central cones are strongly positive for TULP1 and many are reactive for red/green cone opsin. At 17.4 weeks, central rods are weakly TULP-reactive. In peripheral retina at 15.4 weeks to 1 month after birth, displaced cones in    the nerve fiber layer are positive for TULP1, recoverin, and blue cone opsin. Some ganglion cells are weakly reactive for TULP1 at 11 weeks and later, but astrocytes and the optic nerve are TULP1-negative at all ages examined. CONCLUSIONS: The    finding of TULP1 labeling of cones before they are reactive for blue or red/green cone opsin suggests an important role for TULP1 in development. TULP1 expression in both developing and mature cones and rods is consistent with a primary    photoreceptor defect in retinitis pigmentosa (RP) caused by TULP1 mutations. Weak TULP1-immunolabeling of some inner retinal neurons in developing and adult retinas suggests that optic disc changes in patients with RP who have TULP1 mutations may    be primary as well as secondary to photoreceptor degeneration.</p>

	]]>
</description>

<author>A H. Milam et al.</author>


</item>


<item>
<title> Metaphase I arrest and spontaneous parthenogenetic activation of strain LTXBO oocytes: chimeric reaggregated ovaries establish primary lesion in oocytes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/86</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/86</guid>
<pubDate>Tue, 08 May 2012 14:46:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Oocytes of strain LT mice, and related strains such as LTXBO, exhibit a high incidence of arrest in the progression of meiosis at metaphase I (MI) and in spontaneous parthenogenetic activation. Activation of these oocytes within    the ovary leads to the formation of ovarian teratomas. In this study, the role of the oocyte's companion granulosa cells, the cumulus cells, was investigated using fully grown oocytes matured in vitro after isolation from LTXBO mice. Results    showed that the role of cumulus cells in MI arrest is dichotomous. Cumulus cells temporarily helped to sustain MI arrest, but they also promoted a delayed progression to metaphase II.  Cumulus cells also promoted parthenogenetic activation that    occurred in association with the delayed progression to metaphase II. Next, the question of whether the lesion(s) promoting MI arrest and spontaneous activation is due to defects in the somatic cells or is intrinsic to the oocyte was addressed    using chimeric reaggregated ovaries. An improved method for completely exchanging the germ cell and the somatic cell compartments of ovaries from newborn mice is described. These chimeric reaggregated ovaries, grafted beneath the renal capsule of    SCID mice, allowed the complete development of LTXBO oocytes to occur in association with somatic cells from control (B6SJLF(1)) ovaries and development of control oocytes in association with LTXBO somatic cells. Oocyte growth and follicular    development appeared generally normal in reaggregated ovaries.  High incidences of MI arrest and spontaneous activation of LTXBO oocytes occurred regardless of the genotype of the somatic cells. Moreover, there was a low incidence of MI arrest    and spontaneous activation of control oocytes, even though they underwent complete development and maturation associated with LTXBO somatic cells. It is concluded that the phenotypes of MI arrest and parthenogenetic activation in LTXBO oocytes    are defects caused by lesions intrinsic to the oocyte. Nevertheless, the oocyte's companion somatic cells play crucial roles in the expression of these lesions. Copyright 2000 Academic Press.</p>

	]]>
</description>

<author>J J. Eppig et al.</author>


</item>


<item>
<title> Interdigitated deletion complexes on mouse chromosome 5 induced by irradiation of embryonic stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/85</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/85</guid>
<pubDate>Tue, 08 May 2012 14:46:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chromosome deletions have several applications in the genetic analysis of complex organisms. They can be used as reagents in region-directed mutagenesis, for mapping of simple or complex traits, or to identify biological    consequences of segmental haploidy, the latter being relevant to human contiguous gene syndromes and imprinting. We have generated three deletion complexes in ES (Embryonic Stem) cells that collectively span approximately 40 cM of proximal mouse    chromosome 5. The deletion complexes were produced by irradiation of F(1) hybrid ES cells containing herpes simplex virus thymidine kinase genes (tk) integrated at the Dpp6, Hdh (Huntington disease locus), or Gabrb1 loci, followed by selection    for tk-deficient clones. Deletions centered at the adjacent Hdh and Dpp6 loci ranged up to approximately 20 cM or more in length and overlapped in an interdigitated fashion. However, the interval between Hdh and Gabrb1 appeared to contain a locus    haploinsufficient for ES cell viability, thereby preventing deletions of either complex from overlapping. In some cases, the deletions resolved the order of markers that were previously genetically inseparable. A subset of the ES cell-bearing    deletions was injected into blastocysts to generate germline chimeras and establish lines of mice segregating the deletion chromosomes. At least 11 of the 26 lines injected were capable of producing germline chimeras. In general, those that    failed to undergo germline transmission bore deletions larger than the germline-competent clones, suggesting that certain regions of chromosome 5 contain haploinsufficient developmental genes, and/or that overall embryonic viability is    cumulatively decreased as more genes are rendered hemizygous. Mice bearing deletions presumably spanning the semidominant hammertoe locus (Hm) had no phenotype, suggesting that the classic allele is a dominant, gain-of-function mutation.    Overlapping deletion complexes generated in the fashion described in this report will be useful as multipurpose genetic tools and in systematic functional mapping of the mouse genome.</p>

	]]>
</description>

<author>J C. Schimenti et al.</author>


</item>


<item>
<title> Algorithms for mutant sorting: the need for phenotype vocabularies.</title>
<link>http://mouseion.jax.org/stfb2000_2009/84</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/84</guid>
<pubDate>Tue, 08 May 2012 14:45:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>For effectively annotated phenotypes for mouse, a number of detailed phenotypic classification systems are needed. The rapidly increasing number of phenotypically described characteristics of both normal and mutant mice are    providing a rich data set for comparison and analysis.  However, we cannot rely on text descriptions that are subject to the word-usage style of the writer if we are to do large-scale comparative analysis of traits and diseases. The rationale for    developing vocabularies and examples of several vocabularies being developed are described.  Finally, the critical nature of community participation in both building and applying phenotype vocabularies is discussed.</p>

	]]>
</description>

<author>J T. Eppig</author>


</item>


<item>
<title> Toward the yeastification of mouse genetics: chemical mutagenesis of embryonic stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/83</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/83</guid>
<pubDate>Tue, 08 May 2012 14:45:06 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Y Chen et al.</author>


</item>


<item>
<title> Gene transfer to ankyrin-deficient bone marrow corrects spherocytosis in vitro.</title>
<link>http://mouseion.jax.org/stfb2000_2009/82</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/82</guid>
<pubDate>Tue, 08 May 2012 14:44:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: The goal of this study was to transfer by retroviral vector the cDNA for ankyrin to progenitors from normal bone marrow and from the nb/nb spherocytosis mutant deficient in expression of full-length ankyrin to achieve    erythroid expression of functional ankyrin protein. MATERIALS AND METHODS: A minigene composed of the human ankyrin promoter, murine ankyrin cDNA, and the 3' human domain corresponding to the ankyrin 2.2 isoform was assembled in the retroviral    vector, pG1. Murine erythroleukemia (MEL) cells, normal murine bone marrow cells, 3T3 fibroblasts, and nb/nb mutant bone marrow and spleen cells were transduced with the retroviral supernatant. Transduced mutant cells were induced to    differentiate in liquid culture. Gene transfer was assessed by colony polymerase chain reaction (PCR) and reverse transcriptase (RT)-PCR, immunofluorescence, and Southern, Northern, and Western blot analysis. RESULTS: MEL cells, normal bone    marrow progenitors, and nb/nb cells were all successfully transduced and expressed ankyrin by RT-PCR and Western blot. Transduced murine 3T3 fibroblasts and MEL cells exhibited cell membrane staining by immunofluorescence. Colony RT-PCR    demonstrated dependence of expression on erythropoietin. In vitro, the transduced nb/nb cells matured to polychromatophils, whereas nontransduced nb/nb cells matured to microspherocytes. CONCLUSION: Retroviral transfer of ankyrin corrected the    defect leading to formation of microspherocytes in erythroid differentiation cultures from the nb/nb mutant. The human ankyrin promoter conferred erythropoietin-dependent expression in normal and mutant erythroid progenitors, which could have    implications for the gene therapy of human hemolytic anemias.</p>

	]]>
</description>

<author>G J. Dooner et al.</author>


</item>


<item>
<title> Acceleration of type 1 diabetes by a coxsackievirus infection requires a preexisting critical mass of autoreactive T-cells in pancreatic islets [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/81</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/81</guid>
<pubDate>Tue, 08 May 2012 14:43:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Coxsackievirus infections have been proposed as an environmental trigger for the development of T-cell-mediated autoimmune (type 1) diabetes by either providing a molecular mimic of the candidate pancreatic beta-cell autoantigen    GAD or inducing bystander inflammation in the pancreas. In this study in the NOD mouse model, we found that infection with a pancreatrophic coxsackievirus isolate can accelerate type 1 diabetes development through the induction of a bystander    activation effect, but only after a critical threshold level of insulitic beta-cell-autoreactive T-cells has accumulated. Thus, coxsackievirus infections do not appear to initiate beta-cell autoreactive immunity but can accelerate the process    once it is underway. These findings indicate that the timing of a coxsackievirus infection, rather than its simple presence or absence, may have important etiological implications for the development of T-cell-mediated autoimmune type 1 diabetes    in humans.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title> Erythroid phosphatidyl serine exposure is not predictive of thrombotic risk in mice with hemolytic anemia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/80</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/80</guid>
<pubDate>Tue, 08 May 2012 14:43:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Thrombosis is a major complication of human hemolytic anemias such as sickle cell disease, thalassemia, and severe hereditary spherocytosis (HS). Mice with severe HS and severe hereditary elliptocytosis (HE) also suffer from    thrombosis, with incidences ranging from 15 and 22% in beta-spectrin- and ankyrin-deficient mice, respectively, to 85 to 100% in alpha-spectrin-deficient and band 3 knockout mice. A contributing factor to thrombosis could be loss of phospholipid    asymmetry of the mutant red blood cells (RBCs), with concomitant exposure of the aminophospholipid phosphatidylserine (PS). Increased PS exposure occurs in RBCs from sickle cell and thalassemia patients and in RBCs from band 3-deficient mice. To    determine if increased PS exposure correlates with thrombotic risk in HS and HE mice with ankyrin, beta-spectrin, and alpha-spectrin deficiencies, measurements of FITC-labeled annexin V binding to externalized PS on RBCs were performed. PS    exposure is elevated in all mice with HS and HE, but the percentage of RBCs with exposed PS does not correlate with thrombotic risk in these mice. Copyright 2000 Academic Press.</p>

	]]>
</description>

<author>N J. Wandersee et al.</author>


</item>


<item>
<title> Th1 and Th2 mediate acute graft-versus-host disease, each with distinct end-organ targets.</title>
<link>http://mouseion.jax.org/stfb2000_2009/79</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/79</guid>
<pubDate>Tue, 08 May 2012 14:42:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>STAT4 and STAT6 are transcription factors that play crucial roles in responding to IL-12 and IL-4, respectively. STAT4 gene knockout (STAT4(-/-)) mice have markedly reduced Th1 responses and enhanced Th2 responses. STAT6(-/-) mice    show the inverse phenotype. We compared the ability of bone marrow transplantation (BMT) with the inclusion of spleen cells from STAT6(-/-), STAT4(-/-), and wild-type (WT) mice to produce graft-versus-host disease (GVHD) in lethally irradiated    MHC-mismatched recipients. Acute GVHD mortality was more rapid when induced by cells from STAT6(-/-) mice than when induced by STAT4(-/-) cells. However, cells from STAT4(-/-) and STAT6(-/-) donors both induced delayed GVHD mortality compared    with WT controls, or compared with combined STAT4(-/-) and STAT6(-/-) cells, indicating a contribution of both Th1 cells and Th2 cells to acute GVHD. Recipients of STAT6(-/-) BMT showed evidence of acute GVHD with severe diarrhea and marked    weight loss. Recipients of STAT4(-/-) BMT showed signs of GVHD with only initial transient weight loss and later development of severe skin GVHD. Histopathology showed that Th2 responses were required for the induction of both hepatic and severe    skin GVHD. In contrast, both Th1 cells and Th2 cells were capable of causing intestinal pathology of GVHD. Our studies demonstrate an additive role for Th1 and Th2 cells in producing acute GVHD, and suggest a cytokine-directed approach to    treating end-organ manifestations of GVHD.</p>

	]]>
</description>

<author>B Nikolic et al.</author>


</item>


<item>
<title> Segregation distortion of mouse t haplotypes the molecular basis emerges [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/78</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/78</guid>
<pubDate>Tue, 08 May 2012 14:42:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>The t haplotype is an ancestral version of proximal mouse chromosome 17 that has evolved mechanisms to persist as an intact genomic variant in mouse populations. t haplotypes contain mutations that affect embryonic development,    male fertility and male transmission ratio distortion (TRD).  Collectively, these mutations drive the evolutionary success of t haplotypes, a phenomenon that remains one of the longstanding mysteries of mouse genetics. Molecular genetic analysis    of TRD has been confounded by inversions that arose to lock together the various elements of this complex trait. Our first molecular glimpse of the TRD mechanism has finally been revealed with the cloning of the t complex responder (Tcr) locus, a    chimeric kinase with a genetically cis active effect. Whereas + sperm in a +/t male have impaired flagellar function caused by the deleterious action of trans-active, t-haplotype-encoded 'distorters,' the mutant activity of Tcr counterbalances    the distorter effects, maintaining the motility and fertilizing ability of t sperm.</p>

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</description>

<author>J Schimenti</author>


</item>


<item>
<title>Measurement of the B0s Production Cross Section with B0s
→ J/ Decays in pp Collisions at √s = 7 TeV</title>
<link>http://digitalcommons.unl.edu/physicsbloom/318</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsbloom/318</guid>
<pubDate>Tue, 08 May 2012 14:42:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The B<sup>0</sup><sub>s</sub> differential production cross section is measured as functions of the transverse momentum and rapidity in pp collisions at √s= 7 TeV, using the B<sup>0</sup><sub>s</sub> → J/UO decay, and compared with predictions based on perturbative QCD calculations at next-to-leading order. The data sample, collected by the CMS experiment at the LHC, corresponds to an integrated luminosity of 40 pb-1. The B<sup>0</sup><sub>s</sub> is reconstructed from the decays J/U → µ<sup>+</sup>µ<sup>-</sup> and O→ K<sup>+</sup>K<sup>-</sup> The integrated B0s cross section times B0s→ J/UO branching fraction in the range 8B</sup><sub>T</sub>< 50 GeV/c and │y<sup>B</sup> < 2.4 is measured to be 6.9 ± 0.6 ± 0.6 nb, where the first uncertainty is statistical and the second is systematic.</p>

	]]>
</description>

<author>S. Chatrchyan et al.</author>


</item>


<item>
<title> Intramedullary and extramedullary B lymphopoiesis in osteopetrotic mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/77</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/77</guid>
<pubDate>Tue, 08 May 2012 14:41:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adult bone marrow is a major site for hematopoiesis, and reduction of the bone marrow cavity induces hematopoiesis in extramarrow tissues. To investigate the rudimentary intramarrow and the compensatory extramarrow hematopoiesis,    particularly B lymphopoiesis, we used 3 osteopetrotic mouse strains [op/op, mi/mi, and Fos (-/-)], which are severely deficient in functional osteoclasts and therefore form inadequate bone marrow cavities.  We found that bone marrow in these    osteopetrotic mice supports myelopoiesis but not B lymphopoiesis, although cells that have the potential to differentiate into B lineage cells are present in the bone marrow. Although B lymphopoiesis normally occurs both in the spleen and liver    of newborn mice, compensatory B lymphopoiesis in adult op/op and mi/mi mice is observed only in the liver, while myelopoiesis is enhanced in both organs. Interestingly, mice lacking the Fos proto-oncogene exhibit B lymphopoiesis in the spleen as    well as liver. The amounts of expression of steel factor, Flt3/Flk-2 ligand, and interleukin-7 in the bone marrow, spleen, or liver were not significantly affected in these osteopetrotic mutants. These findings suggest that the volume of the bone    marrow cavity regulates B lymphopoiesis without affecting the production of certain hematopoietic growth factors. The splenic microenvironments that support both myelopoiesis and B lymphopoiesis in the neonatal stage are lost in adults and are    not reactivated even in the osteopetrotic adults unless the Fos gene is disrupted.</p>

	]]>
</description>

<author>H Tagaya et al.</author>


</item>


<item>
<title> Narrowing the critical regions for mouse t complex transmission ratio distortion factors by use of deletions [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/76</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/76</guid>
<pubDate>Tue, 08 May 2012 14:41:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previously a deletion in mouse chromosome 17, T(22H), was shown to behave like a t allele of the t complex distorter gene Tcd1, and this was attributed to deletion of this locus. Seven further deletions are studied here, with the    aim of narrowing the critical region in which Tcd1 must lie. One deletion, T(30H), together with three others, T(31H), T(33H), and T(36H), which extended more proximally, caused male sterility when heterozygous with a complete t haplotype and    also enhanced transmission ratio of the partial t haplotype t(6), and this was attributed to deletion of the Tcd1 locus. The deletions T(29H), T(32H), and T(34H) that extended less proximally than T(30H) permitted male fertility when opposite a    complete t haplotype. These results enabled narrowing of the critical interval for Tcd1 to between the markers D17Mit164 and D17Leh48. In addition, T(29H) and T(32H) enhanced the transmission ratio of t(6), but significantly less so than T(30H).    T(34H) had no effect on transmission ratio. These results could be explained by a new distorter located between the breakpoints of T(29H) and T(34H) (between T and D17Leh66E). It is suggested that the original distorter Tcd1 in fact consists of    two loci: Tcd1a, lying between D17Mit164 and D17Leh48, and Tcd1b, lying between T and D17Leh66E.</p>

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</description>

<author>M F. Lyon et al.</author>


</item>


<item>
<title>Interest Based Mutual Gains Bargaining</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/22</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/22</guid>
<pubDate>Tue, 08 May 2012 14:40:50 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Debra Osofsky</author>


</item>


<item>
<title>Annual Legal Update</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/21</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/21</guid>
<pubDate>Tue, 08 May 2012 14:40:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Nicholas DiGiovanni Esq.</author>


</item>


<item>
<title>Advances in Collective Bargaining in AFT Part-Time Locals</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/20</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/20</guid>
<pubDate>Tue, 08 May 2012 14:40:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>AFT represents approximately 55,000 adjuncts. These adjuncts are in a variety of units. There are 99,000 members in 72 full-time/part-time locals; approximately 35,00 of these are part-time adjuncts. There are 10,300 adjuncts in 21 part-time locals that are affiliated with full-time locals. At 20 institutions, AFT represents over 9,800 part-time adjunct faculty in stand-alone units. All of these adjunct locals have contributed much to the union movement, and at the same time, they have put pressure on the union movement for change. It is not surprising, therefore, to see that adjuncts have made gains in their march toward equity with full-time college instructors. These gains have been produced through pressure put on college administrations by the adjuncts themselves and by the full-time faculty who walk hand in hand with them. There have been significant gains made by part-time contingent faculty, but not all of these gains are the result of collective bargaining. Looking at some of the AFT contracts, the state of contingent faculty does indeed appear to be rosy—at least on the surface.</p>

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</description>

<author>Elaine Bobrove</author>


</item>


<item>
<title>Views from Campus: Negotiators</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/19</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/19</guid>
<pubDate>Tue, 08 May 2012 14:40:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Thomas Maraffa</author>


</item>


<item>
<title>Workshop: Collective Bargaining Basics</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/18</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/18</guid>
<pubDate>Tue, 08 May 2012 14:40:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Terrence T. Creamer et al.</author>


</item>


<item>
<title>Negotiations Behind Negotiations: Reaching Out to Constituents</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/17</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/17</guid>
<pubDate>Tue, 08 May 2012 14:40:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Campus administrators and union leaders are well aware of the numerous problems created by multiple years of funding shortfalls. But the general membership of a campus union, going about its business of teaching, researching, serving the community and happily collecting a paycheck every two weeks, may not be aware of the great effort needed to help the campus thrive and to negotiate agreements beneficial to them and to the campus. Overcoming its members’ ignorance of higher education economics and bargaining is only part of the problem for the union. The other part is to convince a diverse membership, each with its own opinions, that the negotiated agreements are the best that can be written at the time.</p>
<p>Getting union members to ratify an agreement that does not contain everything they think they deserve requires: 1) preparation, including a candid analysis of current campus conditions; 2) the exercise of group leadership practices to involve members in the negotiations process; and 3) the adoption of open democratic processes leading to consensus.</p>

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</description>

<author>Nicholas DiObilda</author>


</item>


<item>
<title>Negotiations Behind Negotiations: A System Model</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/16</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/16</guid>
<pubDate>Tue, 08 May 2012 14:40:40 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>William S. Chabala</author>


</item>


<item>
<title>Negotiations Behind Negotiations: Reaching Out to Constituents</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/15</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/15</guid>
<pubDate>Tue, 08 May 2012 14:40:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Reaching consensus within one’s own constituency group, whether from the union or management perspective, is often an overlooked and underappreciated part of the bargaining process. Emphasis is typically on negotiating and getting to “yes” with the other side. While that is the culmination of the process, often the consensus-building that occurs within one’s own membership determines success or failure at the main table. That can be a tall task, given the diverse and at times opposing views and philosophies at play.</p>

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</description>

<author>Robert Zazzali</author>


</item>


<item>
<title>Contingent Faculty Bargaining: Separate but Equal?</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/14</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/14</guid>
<pubDate>Tue, 08 May 2012 14:40:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the 34 years since the PSC formed part-timers have gone from footnote to frontispiece, and our journey has been internal as well as external. What are our services worth? Why are they devalued? What does it mean when we are so fragmented? Why do people in our own departments, whom we have passed in hallways for years, not treat us as colleagues? What does it mean about the profession we’re part of that we're not part of its governance? What does it mean that our passion for our subjects has landed us in a situation where we hardly have time for being creative in them? There is no one to support scholarship, no time to nurture professional development.</p>

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</description>

<author>Marcia Newfield</author>


</item>


<item>
<title>“The One Best Bargaining Unit?”</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/13</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/13</guid>
<pubDate>Tue, 08 May 2012 14:40:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the Chicago area, and Illinois generally, there is not a single bargaining unit that includes both full-time tenure- track (FTTT) and all other contingent faculty of any institution. There are two units that include the FTTT and a large portion, varying by workload, of the contingents. All of the rest of the bargaining units in Illinois are either contingent-only units or FTTT-only, with a few of the contingent units also including academic professionals. Even recent efforts by some local existing FTTT unions to organize the contingents on their campuses have proposed separate units, with only some offering common membership in the same local union. Many of the new bargaining units among contingents in the public sector are of a different union altogether, often NEA contingents and AFT full-time faculty in the community colleges.</p>

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</description>

<author>Joe Berry</author>


</item>


<item>
<title> Physical mapping of male fertility and meiotic drive quantitative trait loci in the mouse t complex using chromosome deficiencies [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/75</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/75</guid>
<pubDate>Tue, 08 May 2012 14:40:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>The t complex spans 20 cM of the proximal region of mouse chromosome 17. A variant form, the t haplotype (t), exists at significant frequencies in wild mouse populations and is characterized by the presence of inversions that    suppress recombination with wild-type (+) chromosomes. Transmission ratio distortion and sterility are associated with t and affect males only. It is hypothesized that these phenomena are caused by trans-acting distorter/sterility factors that    interact with a responder locus (Tcr(t)) and that the distorter and sterility factors are the same because homozygosity of the distorters causes male sterility. One factor, Tcd1, was previously shown to be amorphic using a chromosome deletion. To    overcome limitations imposed by recombination suppression, we used a series of deletions within the t complex in trans to t chromosomes to characterize the Tcd1 region. We find that the distorter activity of Tcd1 is distinct from a linked    sterility factor, originally called tcs1. YACs mapped with respect to deletion breakpoints localize tcs1 to a 1.1-Mb interval flanked by D17Aus9 and Tctex1. We present evidence for the existence of multiple proximal t complex regions that exhibit    distorter activity. These studies demonstrate the utility of chromosome deletions for complex trait analysis.</p>

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</description>

<author>A Planchart et al.</author>


</item>


<item>
<title>It’s All About the Work All the Time: Commonality of Interests in a Common Bargaining Unit</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/12</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/12</guid>
<pubDate>Tue, 08 May 2012 14:40:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lecturers, who are more than half of the 23,000 faculty in the CSU, are committed to their work but are not deluded as to their actual status in the system. Despite some success in encouraging the use of the professional term “Lecturer,” there are plenty of labels—the temps, the adjuncts, the part-time people—to remind contingent faculty of their lack of status. Perhaps the saddest but most accurate label for contingent faculty comes from the term used by academic union leaders in Mexico. Joe Berry used this term—in English, the “precarious” faculty—in a speech he made last January to a large group of contingent faculty in Los Angeles. This term instantly resonated with the audience, who knew all too well how precarious their employment status is, but also saw, with the clear eye of the outsider, the precariousness of the situation of all faculty and indeed of higher education.</p>

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</description>

<author>Elizabeth Hoffman</author>


</item>


<item>
<title>Faculty Specialists/Contingent Faculty at Western Michigan University: A Personal Retrospective</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/11</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/11</guid>
<pubDate>Tue, 08 May 2012 14:40:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the Spring semester, 2005 I took a sabbatical for the second time in my twenty-nine years as a professor at Western Michigan University (WMU). The dictionary defines a sabbatical as “release from normal teaching duties granted to a professor, as for study or travel.” When faculty, friends and relatives ask me what I did on my sabbatical, I first tell them that I spent the month of January in Aruba; basking in the sun, snorkeling, and playing poker. Everyone seems to like and understand that answer. Then I say that I am writing a brief history of the Faculty Specialist employee category, and I get blank stares in return. Two questions are most often asked: “What is a faculty specialist?” and “Why are you doing that?”</p>

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</description>

<author>Gary Mathews</author>


</item>


<item>
<title>Gen X Meets Theory X: What New Scholars Want</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/10</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/10</guid>
<pubDate>Tue, 08 May 2012 14:40:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>“If they can’t understand that I want a kick-ass career and a kick-ass life, then I don’t want to work here,” sums up how many Generation X’ers (born between 1965 and 1980) view their workplace, according to Lancaster and Stillman (2002, p. 107). Further, “Why does it matter when I come and go, as long as I get the work done?” (p. 114). As a group, Gen X’ers are willing to work hard but want to decide when, where, and how. As this generation enters the professoriate in large numbers, some academic institutions may be wondering what hit them. Gen X has met Theory X (a metaphor for a 1960’s workplace) and it is not a pretty sight.</p>

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</description>

<author>Cathy Trower</author>


</item>


<item>
<title>Raising A University Through Collective Bargaining</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/9</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/9</guid>
<pubDate>Tue, 08 May 2012 14:40:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Collective bargaining at its idealist core promises to “love, honor and respect till death do us part.” Historically that has been about as successful as the institution demanding the promise as a condition precedent to the marital union formed. Nevertheless, the progeny of that union, no matter how difficult and imperfect, is the responsibility of that union. Even where there is no duality, there remains a responsibility that is both transparent and undeniable to mold, grow, influence and set an example of excellence for the higher education entity to grow into. This responsibility is then borne of the greatest, purest and most honorable opportunity. It is from this perspective that collective bargaining yields the best results for the entity. It is from this perspective that I approach collective bargaining, however confounding, irritating and obnoxiously particular it seems, as spirit, intent and letter of the rules for the organization to grow by are fashioned.</p>

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</description>

<author>Robert Avery</author>


</item>


<item>
<title>A Disconnect with Fiduciary Responsibility</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/8</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/8</guid>
<pubDate>Tue, 08 May 2012 14:40:28 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mitchell Vogel</author>


</item>


<item>
<title>“And They Call Pennsylvania a Blue State?”</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/7</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/7</guid>
<pubDate>Tue, 08 May 2012 14:40:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>By now, most academicians are aware of the assaults on academic freedom as contained in the Academic Bill of Rights (ABOR) legislation introduced, in some form, in some 24 states. Part of a national movement to muzzle professors deemed too liberal for our colleges and universities, this witch hunt, instigated by former liberal radical David Horowitz, has had a chilling effect on campuses. Some faculty organizations are fighting back; APSCUF (Association of Pennsylvania State College and University Faculties), a union representing some 5,500 faculty and coaches in the Pennsylvania State System of Higher Education (PASSHE), is one of them. This paper outlines what has occurred in Pennsylvania and the measures APSCUF has taken to defuse and debunk Horowitz’s assaults on academic freedom.</p>

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</description>

<author>Pat Heilman</author>


</item>


<item>
<title>Hiring Practices for Faculty</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/6</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/6</guid>
<pubDate>Tue, 08 May 2012 14:40:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Toni Munos et al.</author>


</item>


<item>
<title>Best Practices Language - History of Hiring Practices: 1985-1987 MCCFA Contract</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/5</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/5</guid>
<pubDate>Tue, 08 May 2012 14:40:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bill Newton</author>


</item>


<item>
<title>The Impact of College and University Faculty Collective Bargaining on State Appropriations to Public Higher Education</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/4</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/4</guid>
<pubDate>Tue, 08 May 2012 14:40:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many public college and university faculties have unionized since public employees gained the right to bargain collectively in several states. Most studies of the effects of faculty unionization have been at the institutional level and have included faculty compensation, workload, and other conditions of employment. Although results of these studies are mixed, unionized faculties at four-year institutions experience greater compensation increases in their early years of collective bargaining, but this early advantage subsequently tails off until there is no difference from nonunion counterparts.</p>

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</description>

<author>Jeffrey Franklin Cross</author>


</item>


<item>
<title>The Fiscal Crisis of the Campus: The View from California</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/3</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/3</guid>
<pubDate>Tue, 08 May 2012 14:40:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>The significance of the disinvestment in American baccalaureate, Ph.D. and community college institutions in recent years can hardly be exaggerated. The quandary posed by the attendant reduced funding goes beyond issues of crowded classrooms and dilapidated facilities; ultimately it questions whether our higher education will continue to be a gateway to equality and guarantor of opportunity, a path to broader horizons for citizens—or if it will be transformed into a bulwark of social inequality and vehicle for narrow vocational instruction.</p>
<p>Determining how to successfully grapple with this decline in funding is hindered, however, by the ways in which policy-makers and pundits pose the problem. They reify the forces involved, obscuring the fact that the fiscal problem of the American university is at root a political problem whose resolution requires a political response.</p>

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</description>

<author>R. Jeffrey Lustig</author>


</item>


<item>
<title>Financing Higher Education: Privatization, Resistance and Renewal</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/2</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/2</guid>
<pubDate>Tue, 08 May 2012 14:40:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>The fiscal crisis of higher education currently is being resolved largely through a financing policy of privatization, a pattern that increasingly shifts responsibility to individual students and their families. The politics of privatization makes it ever more difficult for lower-income students to attend college and has become a major financial burden for middle-income people. Beyond the direct financial consequences, privatization has increasingly subordinated the research and educational missions of higher education to the countervailing imperatives of economic growth and competitiveness. Privatization has enhanced the entrepreneurial and corporate features of universities and colleges, increasingly shifting the values of higher education away from notions of common property and the common good to individual self-interest and careerism. The autonomy of higher education institutions has been weakened, both the economic status and professional independence of the faculty have been undermined, and students are increasingly defined as consumers.</p>

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</description>

<author>Gerald Turkel</author>


</item>


<item>
<title>Conference Program</title>
<link>http://thekeep.eiu.edu/jcba/vol0/iss1/1</link>
<guid isPermaLink="true">http://thekeep.eiu.edu/jcba/vol0/iss1/1</guid>
<pubDate>Tue, 08 May 2012 14:40:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>This document is the program of the 33rd annual conference of the National Center for the Study of Collective Bargaining in Higher Education and the Professions.</p>

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</description>


</item>


<item>
<title> Notch signaling is essential for vascular morphogenesis in mice [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/74</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/74</guid>
<pubDate>Tue, 08 May 2012 14:40:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Notch gene family encodes large transmembrane receptors that are components of an evolutionarily conserved intercellular signaling mechanism. To assess the role of the Notch4 gene, we generated Notch4-deficient mice by gene    targeting. Embryos homozygous for this mutation developed normally, and homozygous mutant adults were viable and fertile. However, the Notch4 mutation displayed genetic interactions with a targeted mutation of the related Notch1 gene. Embryos    homozygous for mutations of both the Notch4 and Notch1 genes often displayed a more severe phenotype than Notch1 homozygous mutant embryos. Both Notch1 mutant and Notch1/Notch4 double mutant embryos displayed severe defects in angiogenic vascular    remodeling. Analysis of the expression patterns of genes encoding ligands for Notch family receptors indicated that only the Dll4 gene is expressed in a pattern consistent with that expected for a gene encoding a ligand for the Notch1 and Notch4    receptors in the early embryonic vasculature. These results reveal an essential role for the Notch signaling pathway in regulating embryonic vascular morphogenesis and remodeling, and indicate that whereas the Notch4 gene is not essential during    embryonic development, the Notch4 and Notch1 genes have partially overlapping roles during embryogenesis in mice.</p>

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</description>

<author>L T. Krebs et al.</author>


</item>


<item>
<title> Lanceolate hair-J (lahJ): a mouse model for human hair disorders [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/73</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/73</guid>
<pubDate>Tue, 08 May 2012 14:39:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lanceolate hair-J (lahJ) arose spontaneously in 1994 on the DBA/1LacJ inbred background at The Jackson Laboratory. Mutant mice were runted, alopecic, and lacked vibrissae. As they aged, their skin wrinkled.  Affected mice developed    a noninflammatory, proliferative skin disease with follicular dystrophy. Hair fibers developed a number of abnormalities including periodic nodules along the shaft (trichorrhexis nodosa), compaction resembling trichorrhexis invaginata, spiral    fractures, broken tips, and lance-shaped tips. This mutation exhibits some characteristics that resemble an autosomal recessive ichthyosiform disease that occurs in humans characterized in part by peculiar, invaginating, multinodal, hair shaft    abnormalities known as Netherton's syndrome. Periodic nodules also resemble the human genetic based disease monilethrix. This autosomal recessive mouse mutation, allelic with lanceolate hair (lah), based on breeding studies, is located on mouse    Chromosome 18, within a cluster of genes coding for adhesion molecules. Homozygotes for either of these allelic mouse mutations have elevated serum IgE levels, a feature also common with human Netherton's syndrome.</p>

	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title> N-myc can functionally replace c-myc in murine development, cellular growth, and differentiation [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/72</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/72</guid>
<pubDate>Tue, 08 May 2012 14:39:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Members of the myc family of cellular oncogenes have been implicated as transcriptional regulators in pathways that govern cellular proliferation and death. In addition, N-myc and c-myc are essential for completion of murine    embryonic development. However, the basis for the evolutionary conservation of myc gene family has remained unclear. To elucidate this issue, we have generated mice in which the endogenous c-myc coding sequences have been replaced with N-myc    coding sequences. Strikingly, mice homozygous for this replacement mutation can survive into adulthood and reproduce. Moreover, when expressed from the c-myc locus, N-myc is similarly regulated and functionally complementary to c-myc in the    context of various cellular growth and differentiation processes. Therefore, the myc gene family must have evolved, to a large extent, to facilitate differential patterns of expression.</p>

	]]>
</description>

<author>B A. Malynn et al.</author>


</item>


<item>
<title> A mutation in the lunatic fringe gene suppresses the effects of a jagged2 mutation on inner hair cell development in the cochlea [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/71</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/71</guid>
<pubDate>Tue, 08 May 2012 14:38:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recent studies have demonstrated that the Notch signaling pathway regulates the differentiation of sensory hair cells in the vertebrate inner ear [1] [2] [3] [4] [5] [6] [7] [8] [9]. We have shown previously that in mice homozygous    for a targeted null mutation of the Jagged2 (Jag2) gene, which encodes a Notch ligand, supernumerary hair cells differentiate in the cochlea of the inner ear [7]. Other components of the Notch pathway, including the Lunatic fringe (Lfng) gene,    are also expressed during differentiation of the inner ear in mice [6] [7] [8] [9] [10]. In contrast to the Jag2 gene, which is expressed in hair cells, the Lfng gene is expressed in non-sensory supporting cells in the mouse cochlea [10].  Here    we demonstrate that a mutation in the Lfng gene partially suppresses the effects of the Jag2 mutation on hair cell development. In mice homozygous for targeted mutations of both Jag2 and Lfng, the generation of supernumerary hair cells in the    inner hair cell row is suppressed, while supernumerary hair cells in the outer hair cell rows are unaffected. We also demonstrate that supernumerary hair cells are generated in mice heterozygous for a Notch1 mutation. We suggest a model for the    action of the Notch signaling pathway in regulating hair cell differentiation in the cochlear sensory epithelium.</p>

	]]>
</description>

<author>N Zhang et al.</author>


</item>


<item>
<title> Sequential loss of cytotoxic T lymphocyte responses to simian virus 40 large T antigen epitopes in T antigen transgenic mice developing osteosarcomas.</title>
<link>http://mouseion.jax.org/stfb2000_2009/70</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/70</guid>
<pubDate>Tue, 08 May 2012 14:37:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The role of CTL tolerance in tumor immunity to SV40 large T antigen (T ag)-induced tumors was studied using T ag transgenic mice of the line 501 (H2b). 501 mice express SV40 T ag under the influence of the alpha-amylase promoter,    which leads to the development of osteogenic osteosarcomas late in life and eventual death between 12 and 17 months of age. We determined the ability of 501 mice to respond to the four H2b-restricted T ag CTL epitopes, which include epitope I (T    ag 206-215), epitope II/III (T ag 223-231), the immunorecessive epitope V (T ag 489-497), restricted by H2-Db, and epitope IV (T ag 404-411), restricted by H2-Kb. We demonstrate that 501 mice are partially tolerant to the H2b-restricted T ag    epitopes.  Immunization of 4-month-old 501 mice with T ag-transformed syngeneic cell lines or a recombinant vaccinia virus expressing full-length T ag elicited CTL responses against the H2-Kb-restricted T ag epitope IV only. In contrast,    immunization of 4-month-old 501 mice with recombinant vaccinia viruses expressing individual T ag epitopes as minigenes elicited CTLs against epitopes I, IV, and V, but not against epitope II/III. Complete tolerance to epitopes I, IV, and V    developed in 501 mice, but the age when tolerance was detected varied for each epitope. Tolerance to epitope I occurred by 6 months of age and was accelerated in the absence of CD4+ T cells. Tolerance to the immunorecessive epitope V was observed    in 12-month-old 501 mice but was independent of the presence of osteosarcomas. In contrast, CTLs specific for epitope IV were detected in mice from 3 to 14 months of age but not in mice that had developed osteosarcomas. Analysis of epitope    IV-specific CD8+ cells derived from 3-month-old 501 mice with H2-Kb/epitope IV tetramers revealed decreased numbers of epitope IV-specific CD8+ cells in 501 mice relative to C57BL/6 mice, with a further decrease in older 501 mice. Tumor    progression resulted in loss of H2-Kb/epitope IV tetramer staining CD8+ cells. Thus, progression to tolerance to individual T ag CTL epitopes in 501 mice is epitope dependent.</p>

	]]>
</description>

<author>T D. Schell et al.</author>


</item>


<item>
<title>THE DESIGN AND FABRICATION OF A MICROFLUIDIC REACTOR FOR SYNTHESIS OF CADMIUM SELENIDE QUANTUM DOTS USING SILICON AND GLASS SUBSTRATES</title>
<link>http://digitalcommons.calpoly.edu/theses/720</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/theses/720</guid>
<pubDate>Tue, 08 May 2012 14:37:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>A microfluidic reactor for synthesizing cadmium selenide (CdSe) quantum dots (QDs) was synthesized out of a silicon wafer and Pyrex glass. Microfabrication techniques were used to etch channels into the silicon wafer. Holes were wet-drilled into the Pyrex glass using a diamond-tip drill bit. The Pyrex wafer was anodically bonded to the etched silicon wafer to enclose the microfluidic reactor. Conditions for anodic bonding were created by exposing the stacked substrates to 300V at ~350oC under 5.46N of force. A syringe containing a room temperature CdSe solution was interfaced to the microfluidic reactor by using Poly (dimethylsiloxane) (PDMS) as an interface. The reactor was placed on a hot plate at 225oC, creating thermodynamic conditions for the QD chemical reaction to occur within the etched channels. Tygon® tubing transported solutions in and out of the microfluidic reactor. The CdSe solution was injected into the reactor by a syringe pump at an injection rate of 5 mL/hr, with a channel length of 2.5 cm. While in the microfluidic channels, QD residence time of approximately 30 seconds was sufficient enough for nucleation and growth of QDs to occur. The QD size was characterized by fluorescence full-width-half-maximum (FWHM), which is directly proportional to size distribution. The FWHM of the QDs synthesized was 38 nm, with a peak wavelength of 492 nm. By controlling combinations of pump rate and channel length, a range of QD sizes was able to be consistently synthesized through the microfluidic reactor with significant repeatability and reproducibility.</p>

	]]>
</description>

<author>Peter Robert Gonsalves</author>


</item>


<item>
<title> Asebia-2J (Scd1(ab2J)): a new allele and a model for scarring alopecia.</title>
<link>http://mouseion.jax.org/stfb2000_2009/69</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/69</guid>
<pubDate>Tue, 08 May 2012 14:37:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>A spontaneous, autosomal, recessive mouse mutation exhibiting mild scaly skin, progressive scarring alopecia, slightly runted growth, and photophobia arose at The Jackson Laboratory in 1993 in the inbred mouse strain DBA/1LacJ.    Because this mutant mouse showed genetic, anatomical, and laboratory similarities to the asebia mutation, crosses were done between the new mutant and mice carrying the asebia-J allele. Because the F1 offspring were affected, indicating the two    mutants were allelic, the new mutation was named asebia-2J. Careful histological analysis of skin development of mice homozygous and heterozygous for either asebia-J or asebia-2J revealed that both types of mutant mice are very similar regardless    of their background. Notable histopathological features of mice homozygous for either allele included extreme sebaceous gland hypoplasia, abnormally long anagen follicles, retained inner root sheath, hair fiber perforation of the anagen follicle    base, and progressive follicular replacement by scarring. In this article we present a new pathogenetic hypothesis based on the importance of the sebaceous gland in hair fiber sheath dissociation: in the absence of a functional sebaceous gland    the hair follicle is destroyed. The cutaneous pathology of this mutant mouse underscores the importance of the sebaceous gland to follicular biology and presents an animal model for studying the human scarring alopecias, which characteristically    begin with sebaceous gland ablation.</p>

	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title> Regulation of human cell engraftment and development of EBV-related lymphoproliferative disorders in Hu-PBL-scid mice [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/68</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/68</guid>
<pubDate>Tue, 08 May 2012 14:36:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human PBMC engraft in mice homozygous for the severe combined immunodeficiency (Prkdcscid) mutation (Hu-PBL-scid mice). Hu-PBL-NOD-scid mice generate 5- to 10-fold higher levels of human cells than do Hu-PBL-C.B-17-scid mice, and    Hu-PBL-NOD-scid beta2-microglobulin-null (NOD-scid-B2mnull) mice support even higher levels of engraftment, particularly CD4+ T cells. The basis for increased engraftment of human PBMC and the functional capabilities of these cells in NOD-scid    and NOD-scid-B2mnull mice are unknown. We now report that human cell proliferation in NOD-scid mice increased after in vivo depletion of NK cells. Human cell engraftment depended on CD4+ cells and required CD40-CD154 interaction, but engrafted    CD4+ cells rapidly became nonresponsive to anti-CD3 Ab stimulation. Depletion of human CD8+ cells led to increased human CD4+ and CD20+ cell engraftment and increased levels of human Ig. We further document that Hu-PBL-NOD-scid mice are resistant    to development of human EBV-related lymphoproliferative disorders. These disorders, however, develop rapidly following depletion of human CD8+ cells and are prevented by re-engraftment of CD8+ T cells.  These data demonstrate that 1) murine NK    cells regulate human cell engraftment in scid recipients; 2) human CD4+ cells are required for human CD8+ cell engraftment; and 3) once engrafted, human CD8+ cells regulate human CD4+ and CD20+ cell expansion, Ig levels, and outgrowth of    EBV-related lymphoproliferative disorders. We propose that the Hu-PBL-NOD-scid model is suitable for the in vivo analysis of immunoregulatory interactions between human CD4+ and CD8+ cells.</p>

	]]>
</description>

<author>E J. Wagar et al.</author>


</item>


<item>
<title> Quantitative trait loci modulate renal cystic disease severity in the mouse bpk model [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/67</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/67</guid>
<pubDate>Tue, 08 May 2012 14:36:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Numerous mouse models of polycystic kidney disease (PKD) have been described in which the mutant phenotypes closely resemble human PKD with regard to morphology, cyst localization, and disease progression. As in human PKD, genetic    background affects the disease phenotype in mouse PKD models. Using experimental crosses, these modifying effects can be dissected into discrete genetic factors referred to as quantitative trait loci. The locus for the mouse bpk model was    recently mapped to chromosome (Chr) 10. In the course of these studies, marked variability was observed in the renal cystic disease expressed in F2 bpk/bpk homozygotes of a (BALB/c-+/bpk x CAST/Ei)F1 intercross. The current study was undertaken    to further characterize the renal cystic disease as quantitative trait in this F2 cohort and to map the genetic modifiers that modulate this phenotype. Whole-genome scans revealed a CAST-derived locus on distal Chr 6, near D6Mit14, that affects    renal cystic disease severity. Additional analyses identified loci on Chr 1, Chr 2, and Chr 4, as well as a possible interaction between the Chr 6 locus and a locus on distal Chr 1, near D1Mit17. Interestingly, the gene encoding RGS7, a regulator    of G protein signaling that binds to polycystin-1, was mapped to the same Chr 1 interval. It is concluded that the severity of the bpk renal cystic disease phenotype is modulated by multiple loci and possibly by epistatic interaction among them.    It is hypothesized that the gene encoding the polycystin-binding partner RGS7 is a candidate for the Chr 1 genetic modifier.</p>

	]]>
</description>

<author>Woodford L. Guay et al.</author>


</item>


<item>
<title> Haploinsufficiency of the transcription factors FOXC1 and FOXC2 results in aberrant ocular development.</title>
<link>http://mouseion.jax.org/stfb2000_2009/66</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/66</guid>
<pubDate>Tue, 08 May 2012 14:35:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Anterior segment developmental disorders, including Axenfeld-Rieger anomaly (ARA), variably associate with harmfully elevated intraocular pressure (IOP), which causes glaucoma. Clinically observed dysgenesis does not correlate with    IOP, however, and the etiology of glaucoma development is not understood. The forkhead transcription factor genes Foxc1 (formerly Mf1 ) and Foxc2 (formerly Mfh1 ) are expressed in the mesenchyme from which the ocular drainage structures derive.    Mutations in the human homolog of Foxc1, FKHL7, cause dominant anterior segment defects and glaucoma in various families. We show that Foxc1 (+/-)mice have anterior segment abnormalities similar to those reported in human patients. These    abnormalities include small or absent Schlemm's canal, aberrantly developed trabecular meshwork, iris hypoplasia, severely eccentric pupils and displaced Schwalbe's line. The penetrance of clinically obvious abnormalities varies with genetic    background. In some affected eyes, collagen bundles were half normal diameter, or collagen and elastic tissue were very sparse. Thus, abnormalities in extracellular matrix synthesis or organization may contribute to development of the ocular    phenotypes.  Despite the abnormalities in ocular drainage structures in Foxc1 (+/-)mice, IOP was normal in almost all mice analyzed, on all genetic backgrounds and at all ages. Similar abnormalities were found in Foxc2 (+/-)mice, but no    disease-associated mutations were identified in the human homolog FKHL14 in 32 ARA patients. Foxc1 (+/-)and Foxc2 (+/-)mice are useful models for studying anterior segment development and its anomalies, and may allow identification of genes that    interact with Foxc1 and Foxc2 (or FKHL7 and FKHL14 ) to produce a phenotype with elevated IOP and glaucoma.</p>

	]]>
</description>

<author>R S. Smith et al.</author>


</item>


<item>
<title>The Origin of the Settlement of Niagara-on-the-Lake</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6934</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6934</guid>
<pubDate>Tue, 08 May 2012 14:35:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis describes the major policies that contributed to the creation of the settlement at Niagara on-the-Lake, Ontario. These policies, that involved the blending of political, historical and geographical ingredients, were in general executed during the administration of Sir Frederick Haldimand within the framework of British colonial policy. The settlement that resulted was a unique expression of the response of an eighteenth century policy-maker to two major factors: the American War of Independence and the continuance of a British fur trade monopoly in North America.</p>
<p>Research aimed at isolating the principal locational policies that led to the development of the settlement; firstly as a means of understanding the choice of locational site, and secondly, as an example of the degree of influence that one administrator can have on past and present locational patterns.</p>
<p>The thesis has focused on the significant contribution made by Frederick Haldimand to the political and historical geography of Canada; a contribution that has been largely overlooked in historical and geographical literature. It has also shown that the historical, political and geographical administrative framework can contribute to an understanding of present day patterns of settlement, and in fact has had far more influence on such patterns than previously indicated by the literature.</p>

	]]>
</description>

<author>Faye Vernette Whitfield</author>


</item>


<item>
<title> p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours.</title>
<link>http://mouseion.jax.org/stfb2000_2009/65</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/65</guid>
<pubDate>Tue, 08 May 2012 14:35:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>p73 (ref. 1) has high homology with the tumour suppressor p53 (refs 2-4), as well as with p63, a gene implicated in the maintenance of epithelial stem cells. Despite the localization of the p73 gene to chromosome 1p36.3 a region of    frequent aberration in a wide range of human cancers, and the ability of p73 to transactivate p53 target genes, it is unclear whether p73 functions as a tumour suppressor. Here we show that mice functionally deficient for all p73 isoforms exhibit    profound defects, including hippocampal dysgenesis, hydrocephalus, chronic infections and inflammation, as well as abnormalities in pheromone sensory pathways. In contrast to p53-deficient mice, however, those lacking p73 show no increased    susceptibility to spontaneous tumorigenesis. We report the mechanistic basis of the hippocampal dysgenesis and the loss of pheromone responses, and show that new, potentially dominant-negative, p73 variants are the predominant expression products    of this gene in developing and adult tissues. Our data suggest that there is a marked divergence in the physiological functions of the p53 family members, and reveal unique roles for p73 in neurogenesis, sensory pathways and homeostatic    control.</p>

	]]>
</description>

<author>A Yang et al.</author>


</item>


<item>
<title> Vascular effects following homozygous disruption of p47(phox) : An essential component of NADPH oxidase.</title>
<link>http://mouseion.jax.org/stfb2000_2009/64</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/64</guid>
<pubDate>Tue, 08 May 2012 14:34:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Evidence suggests that the vessel wall contains an oxidase similar, if not identical, to phagocytic NADPH oxidase. We tested the contribution of this specific oxidase to the progression of atherosclerosis and the    regulation of blood pressure. METHODS ABD RESULTS: An examination of aortic rings from wild-type mice and mice with homozygous targeted disruptions in p47(phox) revealed that p47(phox) knockout mice had a reduction in vascular superoxide    production. However, analyses of apoE -/- p47(phox)+/+ and apoE -/- p47(phox) -/- strains of mice demonstrated no significant differences in atherosclerotic lesion sizes. Similarly, analyses of wild-type and p47(phox) knockout mice revealed no    differences in either basal blood pressure or the rise in blood pressure seen after the pharmacological inhibition of nitric oxide synthase. CONCLUSIONS: NADPH oxidase contributes to basal vascular superoxide production. However, the absence of a    functional oxidase does not significantly affect the progression of atherosclerosis in the standard mouse apoE -/- model, nor does it significantly influence basal blood pressure.</p>

	]]>
</description>

<author>E Hsich et al.</author>


</item>


<item>
<title> Mutations in the WRN gene in mice accelerate mortality in a p53-null background.</title>
<link>http://mouseion.jax.org/stfb2000_2009/63</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/63</guid>
<pubDate>Tue, 08 May 2012 14:34:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Werner's syndrome (WS) is a human disease with manifestations resembling premature aging. The gene defective in WS, WRN, encodes a DNA helicase.  Here, we describe the generation of mice bearing a mutation that eliminates    expression of the C terminus of the helicase domain of the WRN protein. Mutant mice are born at the expected Mendelian frequency and do not show any overt histological signs of accelerated senescence. These mice are capable of living beyond 2    years of age. Cells from these animals do not show elevated susceptibility to the genotoxins camptothecin or 4-NQO. However, mutant fibroblasts senesce approximately one passage earlier than controls. Importantly, WRN(-/-);p53(-/-) mice show an    increased mortality rate relative to WRN(+/-);p53(-/-) animals. We consider possible models for the synergy between p53 and WRN mutations for the determination of life span.</p>

	]]>
</description>

<author>D B. Lombard et al.</author>


</item>


<item>
<title> Effect of ex vivo cytokine treatment on human cord blood engraftment in NOD-scid mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/62</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/62</guid>
<pubDate>Tue, 08 May 2012 14:33:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Umbilical cord blood transplantation is considered an alternative to traditional bone marrow transplantation for patients who do not have matched sibling donors. In this study, we examined the effects of ex vivo treatment of human    cord blood cells with cytokine mixtures and assessed the ability of treated cells to engraft in NOD-scid mice. We incubated the cord blood with a four-factor cytokine mixture of interleukin (IL)-3, IL-6, IL-11 and stem cell factor, or with a    two-factor cytokine mixture of thrombopoietin and flt-3. Incubation of cord blood for 48 h with either cytokine mixture did not affect progenitor cell number or proliferative potential as measured by the high proliferative potential (HPP) assay.     Cytokine-treated cord blood injected into irradiated NOD-scid mice resulted in multilineage human engraftment. Overall, incubation with cytokines resulted in variable levels of engraftment with different cord blood samples. Incubation of cord    blood with the four-factor cytokine mixture resulted in increased survival of irradiated NOD-scid recipients.  These results demonstrate that short-term ex vivo treatment of human progenitor cells gives variable results on in vivo multipotential    capabilities.</p>

	]]>
</description>

<author>K Ballen et al.</author>


</item>


<item>
<title> Role of gamma interferon and interleukin-4 in host defense against the human filarial parasite Brugia malayi.</title>
<link>http://mouseion.jax.org/stfb2000_2009/61</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/61</guid>
<pubDate>Tue, 08 May 2012 14:33:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have investigated the roles of gamma interferon (IFN-gamma) and interleukin-4 (IL-4) in host defense against Brugia malayi. Our data suggest that the lack of either IFN-gamma or IL-4 prolongs the time required to achieve sterile    immunity, suggesting that both canonical type 1 and type 2 responses are involved in the clearance of infection.</p>

	]]>
</description>

<author>S Babu et al.</author>


</item>


<item>
<title> Adhesion molecule deficiencies increase Porphyromonas gingivalis-induced alveolar bone loss in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/60</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/60</guid>
<pubDate>Tue, 08 May 2012 14:32:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alveolar bone resorption can be induced in specific-pathogen-free mice by oral infection with Porphyromonas gingivalis (P. J. Baker, R. T. Evans, and D. C. Roopenian, Arch. Oral Biol. 39:1035-1040, 1994). Here we used a mouse    strain, C57BL/6J, which is relatively resistant to P. gingivalis-induced bone loss to examine whether partial or complete deletion of various adhesion molecules would increase susceptibility.  Complete deletion of P-selectin or nearly complete    lack of expression of intercellular adhesion molecule 1 (ICAM-1) led to increased susceptibility to bone resorption after oral infection, while a hypomorphic defect in beta(2)-integrins did not. Both the total amount of bone lost and the number    of sites at which there was significant loss were increased in mice deficient in either ICAM-1 or P-selectin. Each of the three adhesion molecule deficiencies was sufficient to decrease P. gingivalis-specific serum immunoglobulin G responses, but    lower antibody titers did not lead to increased bone loss in partially beta(2)-integrin-deficient mice. In conclusion, P-selectin and ICAM-1 deficiencies increase susceptibility to and severity of alveolar bone loss after P. gingivalis infection.    This finding underscores the importance of innate immunity in protection against P. gingivalis-induced alveolar bone resorption.</p>

	]]>
</description>

<author>P J. Baker et al.</author>


</item>


<item>
<title> Effects of the non-pseudoautosomal region of the Y-chromosome on behavior in female offspring of two congenic strains of mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/59</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/59</guid>
<pubDate>Tue, 08 May 2012 14:32:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>The learning behavior of female offspring of two strains of mice congenic for the Y-chromosome, BXSX/MpJ-Yaa and BXSB/MpJ-Yaa+, was examined.  Significant differences were found in the Morris water maze and the Lashley III maze,    demonstrating that the fathers' Y-chromosome can indirectly affect their daughters' behavior. Approximately half the mice had neocortical ectopias, and females from the two paternal groups reacted differently to the presence or absence of    ectopias. Since females do not have a Y-chromosome, these effects must be through non-genetic mechanisms.  Prenatal factors that could have played a role include possible differences in gonadal growth and the presence of different H-Y antigens.     Postnatally, the sires and male siblings of the two strains may not have behaved the same toward the female offspring and/or the dams, creating differences in behavior.In summary, the behavior of female offspring of two groups of males,    genetically the same except for their Y-chromosomes, was examined. Since females do not receive a Y-chromosome from their fathers, in theory their behavior should not differ. Significant differences were found, indicating that the Y-chromosome,    through some indirect mechanism, can affect females of the next generation.</p>

	]]>
</description>

<author>B J. Hoplight et al.</author>


</item>


<item>
<title> Interaction of Ap1, Ap2, and Sp1 with the regulatory regions of the human pro-alpha1(I) collagen gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/58</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/58</guid>
<pubDate>Tue, 08 May 2012 14:31:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the pro-alpha1(I) collagen gene a number of cis-regulatory elements, which interact with a variety of trans-acting factors, are present in the promoter and first intron. We have undertaken a comprehensive study of Sp1, Ap1, and    Ap2 binding in the region spanning -442 to +1697 nt. DNase I footprinting analysis revealed these factors bind with varying affinities to some of the potential sites: Sp1 binds to 16 of 34 potential sites, Ap2 binds to 22 of 40 potential binding    sites, and Ap1 binds to its only potential site. The Sp1 sites were mostly clustered in the intron region, while the Ap2 sites were clustered in the promoter region. Transmission electron microscopic analysis of DNA-protein complexes not only    confirmed these results, but also clearly showed that heterologous and/or homologous protein-protein interactions between Sp1 and/or Ap2 bring the promoter and intron in contact with each other, with the resulting looping out of the intervening    DNA. This strongly suggests that the DNA-looping model is an explanation for the orientation preference of the enhancing element in the first intron as these interactions possibly create an optimum environment for the binding of the rest of the    transcriptional machinery. Copyright 2000 Academic Press.</p>

	]]>
</description>

<author>W P. Vergeer et al.</author>


</item>


<item>
<title> Genomic, transcriptional and mutational analysis of the mouse microphthalmia locus [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/57</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/57</guid>
<pubDate>Tue, 08 May 2012 14:30:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mouse microphthalmia transcription factor (Mitf) mutations affect the development of four cell types: melanocytes, mast cells, osteoclasts, and pigmented epithelial cells of the eye. The mutations are phenotypically diverse and can    be arranged in an allelic series. In humans, MITF mutations cause Waardenburg syndrome type 2A (WS2A) and Tietz syndrome, autosomal dominant disorders resulting in deafness and hypopigmentation.  Mitf mice thus represent an important model system    for the study of human disease. Here we report the complete exon/intron structure of the mouse Mitf gene and show it to be similar to the human gene. We also found that the mouse gene is transcriptionally complex and is capable of generating at    least 13 different Mitf isoforms. Some of these isoforms are missing important functional domains of the protein, suggesting that they might play an inhibitory role in Mitf function and signal transduction. In addition, we determined the    molecular basis for six microphthalmia mutations. Two of the mutations are reported for the first time here (Mitf(mi-enu198) and Mitf(mi-x39)), while the others (Mitf(mi-ws), Mitf(mi-bws), Mitf(mi-ew), and Mitf(mi-di)) have been described but the    molecular basis for the mutation not determined. When analyzed in terms of the genomic and transcriptional data presented here, it is apparent that these mutations result from RNA processing or transcriptional defects.  Interestingly, three of    the mutations (Mitf(mi-x39), Mitf(mi-bws), and Mitf(mi-ws)) produce proteins that are missing important functional domains of the protein identified in in vitro studies, further confirming a biological role for these domains in the whole    animal.</p>

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</description>

<author>J H. Hallsson et al.</author>


</item>


<item>
<title> Localization of Psoriasis-Susceptibility Locus PSORS1 to a 60-kb Interval Telomeric to HLA-C. [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/56</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/56</guid>
<pubDate>Tue, 08 May 2012 14:30:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recent genome scans have established the presence of a major psoriasis-susceptibility locus in the human leukocyte antigen (HLA) complex on chromosome 6p21.3. To narrow the interval for candidate gene testing, we performed a    linkage-disequilibrium analysis of 339 families, with the use of 62 physically mapped microsatellite markers spanning the major histocompatibility complex (MHC). As detected by use of the transmission/disequilibrium test (TDT), individual markers    yielded significant linkage disequilibrium across most of the MHC. However, the strongest evidence for marker-trait disequilibrium was found in an approximately 300-kb region extending from the MICA gene to the corneodesmosin gene.    Maximum-likelihood haplotypes were constructed across the entire MHC in the original sample and across a 1.2-Mb region of the central MHC in an expanded sample containing 139 additional families.  Short (two- to five-marker) haplotypes were    subjected to the TDT using a "moving-window" strategy that reduced the variability of TDT P values relative to the single-locus results. Furthermore, the expanded sample yielded a sharp peak of evidence for linkage disequilibrium that spanned    approximately 170 kb and that was centered 100 kb telomeric to HLA-C. The 1.2-Mb interval was further dissected by means of recombinant ancestral haplotype analysis. This analysis identified risk haplotype 1 (RH1), which is a 60-kb fragment of    ancestral haplotype 57.1, on all identifiable HLA risk haplotypes. One of these haplotypes exhibits significant linkage disequilibrium with psoriasis but does not carry Cw6, which is the HLA allele most strongly associated with the disease. These    results demonstrate that RH1 is highly likely to carry the disease allele at PSORS1, and they exclude HLA-C and corneodesmosin with a high degree of confidence.</p>

	]]>
</description>

<author>R P. Nair et al.</author>


</item>


<item>
<title> A deletion in a photoreceptor-specific nuclear receptor mRNA causes retinal degeneration in the rd7 mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/55</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/55</guid>
<pubDate>Tue, 08 May 2012 14:29:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The rd7 mouse, an animal model for hereditary retinal degeneration, has some characteristics similar to human flecked retinal disorders. Here we report the identification of a deletion in a photoreceptor-specific nuclear receptor    (mPNR) mRNA that is responsible for hereditary retinal dysplasia and degeneration in the rd7 mouse. mPNR was isolated from a pool of photoreceptor-specific cDNAs originally created by subtractive hybridization of mRNAs from normal and    photoreceptorless rd mouse retinas Localization of the gene corresponding to mPNR to mouse Chr 9 near the rd7 locus made it a candidate for the site of the rd7 mutation. Northern analysis of total RNA isolated from rd7 mouse retinas revealed no    detectable signal after hybridization with the mPNR cDNA probe. However, with reverse transcription-PCR, we were able to amplify different fragments of mPNR from rd7 retinal RNA and to sequence them directly. We found a 380-nt deletion in the    coding region of the rd7 mPNR message that creates a frame shift and produces a premature stop codon. This deletion accounts for more than 32% of the normal protein and eliminates a portion of the DNA-binding domain. In addition, it may result in    the rapid degradation of the rd7 mPNR message by the nonsense-mediated decay pathway, preventing the synthesis of the corresponding protein. Our findings demonstrate that mPNR expression is critical for the normal development and function of the    photoreceptor cells.</p>

	]]>
</description>

<author>N B. Akhmedov et al.</author>


</item>


<item>
<title> beta2 microglobulin-deficient (B2m(null)) NOD/SCID mice are excellent recipients for studying human stem cell function.</title>
<link>http://mouseion.jax.org/stfb2000_2009/54</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/54</guid>
<pubDate>Tue, 08 May 2012 14:28:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human SCID repopulating cells (SRC) are defined based on their functional ability to repopulate the bone marrow of NOD/SCID mice with both myeloid and lymphoid cell populations. The frequency of SRC in umbilical cord blood cells is    1 in 9.3 x 10(5) mononuclear cells. We report that as few as 8 x 10(4) human cord blood mononuclear cells transplanted into NOD/SCID/B2m(null )mice resulted in multilineage differentiation in the murine bone marrow, revealing a more than 11-fold    higher SRC frequency than in NOD/SCID mice. Moreover, as few as 2 to 5 x 10(3) CD34(+) cells recovered from the bone marrow of primary transplanted NOD/SCID mice were sufficient for engrafting secondary NOD/SCID/B2m(null )mice with SRC,    suggesting SRC self-renewal. Thus, by using NOD/SCID/B2m(null )mice as recipients, we established a functional assay for human stem cells capable of engrafting the bone marrow of primary and secondary transplanted immune-deficient mice with SRC,    providing a model that better resembles autologous stem cell transplantation.</p>

	]]>
</description>

<author>O Kollet et al.</author>


</item>


<item>
<title> Granule cells and cerebellar boundaries: analysis of Unc5h3 mutant chimeras.</title>
<link>http://mouseion.jax.org/stfb2000_2009/53</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/53</guid>
<pubDate>Tue, 08 May 2012 14:28:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the Unc5h3 gene, a receptor for the netrin 1 ligand, result in abnormal migrations of both Purkinje and granule cells to regions outside the cerebellum and of granule cells to regions within the cerebellum. Because    both Purkinje and granule cells express this molecule we sought to determine whether one or both of these cell types are the primary target of the mutation. Chimeric mice were made between wild-type ROSA26 transgenic mouse embryos (whose cells    express beta-galactosidase) and Unc5h3 mutant embryos. The resulting chimeric brains exhibited a range of phenotypes. Chimeras that had a limited expression of the extracerebellar phenotype (movement of cerebellar cells into the colliculus and    midbrain tegmentum) and the intracerebellar phenotype (migration of granule cells into white matter) had a normal-appearing cerebellum, whereas chimeras that had more ectopic cells had attenuated anterior cerebellar lobules. Furthermore, the    colonization of colliculus and midbrain tegmentum by cerebellar cells was not equivalent in all chimeras, suggesting different origins for extracerebellar ectopias in these regions. The granule cells of the extracerebellar ectopias were almost    entirely derived from Unc5h3/Unc5h3 mutant embryos, whereas the ectopic Purkinje cells were a mixture of both mutant and wild-type cells.  Intracerebellar ectopias in the chimera were composed exclusively of mutant granule cells. These findings    demonstrate that both inside and outside the cerebellum, the granule cell is the key cell type to demarcate the boundaries of the cerebellum.</p>

	]]>
</description>

<author>D Goldowitz et al.</author>


</item>


<item>
<title> Genetic regulation of primitive hematopoietic stem cell senescence.</title>
<link>http://mouseion.jax.org/stfb2000_2009/52</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/52</guid>
<pubDate>Tue, 08 May 2012 14:27:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: To define effects of strain on PHSC (primitive hematopoietic stem cells) senescence (decline in function with age) in vivo, and to map a locus that regulates PHSC senescence. MATERIALS AND METHODS: Long-term function and    self-renewal were compared in bone marrow cells (BMC) from old and young mice of three strains: BALB/cBy (BALB), DBA/2 (D2) and C57BL/6 (B6), using competitive repopulation and serial transplantation in vivo. BMC from each old or young donor were    mixed with standard doses of congenic, genetically marked BMC and transplanted into lethally recipients. Percentages of donor-type erythrocytes and lymphocytes in the recipients determined the functional ability of donor PHSC relative to the    standard, where one repopulating unit (RU) of donor BMC equals the repopulating ability of 100,000 standard competitor BMC. Using similar techniques, repopulating abilities of old and young recombinant inbred (RI) donors of 12 strains derived    from BALB and B6 were compared in NK-depleted BALBxB6 Fl recipients to map a locus that appears to have a major role in PHSC senescence. RESULTS: PHSC function declined about 2 fold with age in BALB and D2 BMC, and increased more than 2-fold with    age in B6 BMC, with all old/young strain differences significant, p<.01. Ten months after serial transplantation, young B6, BALB, and D2 PHSC had self-renewed 1.6-, 4.2-, and 3.2-fold better than old, with BALB and D2 old/young differences p<.01.    Young B6 PHSC self-renewed 1.9- and 2.9-fold better than young BALB and D2 PHSC. The PHSC senescence phenotypes (old/young RU ratios) for 12 CXB RI strains suggested a genetic linkage to D12Nyul7 on Chromosome 12. CONCLUSION: PHSC senescence is    genetically regulated, and is much delayed in the B6 strain compared to the BALB and D2 strains. A locus on Chromosome 12 may regulate PHSC senescence.</p>

	]]>
</description>

<author>J Chen et al.</author>


</item>


<item>
<title> Th1 and Th2 mediate acute graft-versus-host disease, each with distinct end-organ targets.</title>
<link>http://mouseion.jax.org/stfb2000_2009/51</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/51</guid>
<pubDate>Tue, 08 May 2012 14:27:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>STAT4 and STAT6 are transcription factors that play crucial roles in responding to IL-12 and IL-4, respectively. STAT4 gene knockout (STAT4(-/-)) mice have markedly reduced Th1 responses and enhanced Th2 responses. STAT6(-/-) mice    show the inverse phenotype. We compared the ability of bone marrow transplantation (BMT) with the inclusion of spleen cells from STAT6(-/-), STAT4(-/-), and wild-type (WT) mice to produce graft-versus-host disease (GVHD) in lethally irradiated    MHC-mismatched recipients. Acute GVHD mortality was more rapid when induced by cells from STAT6(-/-) mice than when induced by STAT4(-/-) cells. However, cells from STAT4(-/-) and STAT6(-/-) donors both induced delayed GVHD mortality compared    with WT controls, or compared with combined STAT4(-/-) and STAT6(-/-) cells, indicating a contribution of both Th1 cells and Th2 cells to acute GVHD. Recipients of STAT6(-/-) BMT showed evidence of acute GVHD with severe diarrhea and marked    weight loss. Recipients of STAT4(-/-) BMT showed signs of GVHD with only initial transient weight loss and later development of severe skin GVHD. Histopathology showed that Th2 responses were required for the induction of both hepatic and severe    skin GVHD. In contrast, both Th1 cells and Th2 cells were capable of causing intestinal pathology of GVHD. Our studies demonstrate an additive role for Th1 and Th2 cells in producing acute GVHD, and suggest a cytokine-directed approach to    treating end-organ manifestations of GVHD.</p>

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</description>

<author>B Nikolic et al.</author>


</item>


<item>
<title>Kris Saknussemm</title>
<link>http://digitalcommons.library.unlv.edu/blackmountain_lectures_events/125</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/blackmountain_lectures_events/125</guid>
<pubDate>Tue, 08 May 2012 14:26:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Kris Saknussemm is an Australian-American novelist and media artist. His first novel, <em>Zanesville</em>, became a modern science fiction cult classic. His work has appeared in such publications as <em>The Boston Review, The Hudson Review, The Antioch Review, New Letters</em>, and<em>Prairie Schooner</em>. Kris will be joined by tenor saxophonist, Eric Wyatt, among others, for an original mixed-media performance from Saknussemm's latest novel, <em>Reverend America</em>.</p>

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</description>

<author>Kris Saknussemm</author>


</item>


<item>
<title> Gene ontology: tool for the unification of biology. The Gene Ontology Consortium.</title>
<link>http://mouseion.jax.org/stfb2000_2009/50</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/50</guid>
<pubDate>Tue, 08 May 2012 14:26:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M Ashburner et al.</author>


</item>


<item>
<title> Notch signalling is required for cyclic expression of the hairy-like gene HES1 in the presomitic mesoderm.</title>
<link>http://mouseion.jax.org/stfb2000_2009/49</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/49</guid>
<pubDate>Tue, 08 May 2012 14:25:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Somitic segmentation provides the framework on which the segmental pattern of the vertebrae, some muscles and the peripheral nervous system is established. Recent evidence indicates that a molecular oscillator, the 'segmentation    clock', operates in the presomitic mesoderm (PSM) to direct periodic expression of c-hairy1 and lunatic fringe (l-fng). Here, we report the identification and characterisation of a second avian hairy-related gene, c-hairy2, which also cycles in    the PSM and whose sequence is closely related to the mammalian HES1 gene, a downstream target of Notch signalling in vertebrates. We show that HES1 mRNA is also expressed in a cyclic fashion in the mouse PSM, similar to that observed for c-hairy1    and c-hairy2 in the chick. In HES1 mutant mouse embryos, the periodic expression of l-fng is maintained, suggesting that HES1 is not a critical component of the oscillator mechanism. In contrast, dynamic HES1 expression is lost in mice mutant for    Delta1, which are defective for Notch signalling. These results suggest that Notch signalling is required for hairy-like genes cyclic expression in the PSM.</p>

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</description>

<author>C Jouve et al.</author>


</item>


<item>
<title> Midgestation lethality in mice deficient for the RecA-related gene, Rad51d/Rad51l3.</title>
<link>http://mouseion.jax.org/stfb2000_2009/48</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/48</guid>
<pubDate>Tue, 08 May 2012 14:25:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Homologous recombination (HR) occurs in all organisms, and is important for repair of DNA damage, chromosome segregation during meiosis, and genetic diversification. Genes critical for recombinational DNA repair and meiotic    recombination include members of the RecA/RAD51 family, of which seven have been identified in mammals. Here, we describe the disruption of Rad51d (recently designated Rad51l3) in mice and its phenotypic consequences. Rad51d-deficient mice die    between 8.5 and 11.5 dpc. The affected embryos are smaller than littermates, posteriorly truncated, and developmentally delayed. Embryonic fibroblasts from mutant embryos could not be propagated more than one generation in culture.    Rad51d-deficient blastocysts were not sensitive to gamma radiation or methylmethanesulfonate (MMS) in blastocyst outgrowth experiments. The variable and generalized developmental progression defects in Rad51d-deficient embryos suggests that    mutant cells may undergo delayed or suboptimal repair of DNA damage, resulting in accumulated degrees of mutation and/or cell cycle perturbation that are incompatible with normal embryonic development. genesis 26:167-173, 2000. Copyright 2000    Wiley-Liss, Inc.</p>

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</description>

<author>D L. Pittman et al.</author>


</item>


<item>
<title> Large-scale cDNA analysis reveals phased gene expression patterns during preimplantation mouse development [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/47</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/47</guid>
<pubDate>Tue, 08 May 2012 14:24:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Little is known about gene action in the preimplantation events that initiate mammalian development. Based on cDNA collections made from each stage from egg to blastocyst, 25438 3'-ESTs were derived, and represent 9718 genes, half    of them novel. Thus, a considerable fraction of mammalian genes is dedicated to embryonic expression. This study reveals profound changes in gene expression that include the transient induction of transcripts at each stage. These results raise    the possibility that development is driven by the action of a series of stage-specific expressed genes. The new genes, 798 of them placed on the mouse genetic map, provide entry points for analyses of human and mouse developmental    disorders.</p>

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</description>

<author>M S. Ko et al.</author>


</item>


<item>
<title> GXD: integrated access to gene expression data for the laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2000_2009/46</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/46</guid>
<pubDate>Tue, 08 May 2012 14:24:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M Ringwald et al.</author>


</item>


<item>
<title> Electronic tools for accessing the mouse genome.</title>
<link>http://mouseion.jax.org/stfb2000_2009/45</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/45</guid>
<pubDate>Tue, 08 May 2012 14:23:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J T. Eppig</author>


</item>


<item>
<title>Conscience of a Black Conservative: The 1964 Election and the Rise of the National Negro Republican Assembly</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/90</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/90</guid>
<pubDate>Tue, 08 May 2012 14:23:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>This article explores the activities of black Republicans during and after the 1964 Republican National Convention.  The social turmoil of the 1960s, along with the passage of the 1964 Civil Rights Act and Barry Goldwater’s selection as the GOP’s presidential nominee resulted in an unprecedented massive rejection of the Republican Party by 94 percent of the black electorate. This “6 Percent” moment forced black Republicans to rethink their relationship to the GOP. In turn, this redefinition served as a catalyst for the galvanization of liberal and moderate black party members, who then worked to promote a civil rights agenda within a fundamentally conservative framework.</p>

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</description>

<author>Leah M. Wright</author>


</item>


<item>
<title>December 31, 2007: Death and the End of an Era?</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/89</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/89</guid>
<pubDate>Tue, 08 May 2012 14:23:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Charles C. Lemert</author>


</item>


<item>
<title>“The Spirits in My Mother’s Head”</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/88</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/88</guid>
<pubDate>Tue, 08 May 2012 14:23:32 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Gina Athena Ulysse</author>


<category>Articles</category>

</item>


<item>
<title>“Papa, Patriarchy and Power: Snapshots of a Good Haitian Girl, Feminism and</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/87</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/87</guid>
<pubDate>Tue, 08 May 2012 14:23:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Gina Athena Ulysse</author>


<category>Articles</category>

</item>


<item>
<title>“Conquering Duppies in Kingston: Miss Tiny and Me, Fieldwork Conflicts and</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/86</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/86</guid>
<pubDate>Tue, 08 May 2012 14:23:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Gina Athena Ulysse</author>


<category>Articles</category>

</item>


<item>
<title>Sinners on Trial: Jews and Sacrilege after the Reformation</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/85</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/85</guid>
<pubDate>Tue, 08 May 2012 14:23:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>My book, Sinners on Trial: Jews and Sacrilege after the Reformation tells a story of the process of affirmation of Catholic dogmas after the Reformation, not necessarily though religious education and propaganda but through the application of criminal law, and the courts' treatment of "the sacred" and, thus, also of the "sacrilege."</p>
<p>"Sinners on Trial" combines political, legal, and cultural historical approaches. In Poland, the contest over the sacredness of the Eucharist, a major Catholic dogma challenged by the Reformation, became manifest in lay courts' adjudication of crimes against property and religious symbols, especially those linked to the Eucharistic rituals. The mishandling of sacred symbols and objects transformed sins into crimes and led to harsh sentences, including burning at the stake.</p>
<p>Far more than the Church's efforts to educate the laity, the lay courts' classification of Catholic spaces as the only "sacred spaces" and their adjudication of crimes of "sacrilege," were crucial for the (re)Catholicisation of Poland, and the shaping of the country's religious identity.</p>
<p>"Sinners on Trial" crucially casts a new light on the most infamous case of sacrilege, the accusations against Jews for stealing and desecrating the host, situating it within a broader context of the politics of crime -- most specifically that of sacrilege, illuminating its post-Reformation character.</p>

	]]>
</description>

<author>Magda Teter</author>


<category>Catholic Church and the Jews</category>

<category>Early Modern Jewish History</category>

<category>Early Modern Religious History</category>

<category>Jews and the Reformation</category>

</item>


<item>
<title>Measurement of the anomalous like-sign dimuon charge asymmetry with 9 fb-1 of pp collisions</title>
<link>http://digitalcommons.unl.edu/physicsbloom/317</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsbloom/317</guid>
<pubDate>Tue, 08 May 2012 14:23:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present an updated measurement of the anomalous like-sign dimuon charge asymmetry A<sup>b</sup><sub>Sl</sub> for semileptonic b-hadron decays in 9.0 fb-1 of <em>pp</em> collisions recorded with the D0 detector at a center-of-mass energy of √s= 1.96 TeV at the Fermilab Tevatron collider. We obtain A<sup>b</sup><sub>sl</sub> = (-0.787 ± 0.172 (stat) ± 0.093 (syst)) %. This result differs by 3.9 standard deviations from the prediction of the standard model and provides evidence for anomalously large <em>CP</em> violation in semileptonic neutral <em>B</em> decay. The dependence of the asymmetry on the muon impact parameter is consistent with the hypothesis that it originates from semileptonic <em>b</em>-hadron decays.</p>

	]]>
</description>

<author>V. M. Abazov et al.</author>


</item>


<item>
<title>Sacrilegi e spazi sacri e profane: Ebrei e cristiani in Polonia d’età moderna</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/84</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/84</guid>
<pubDate>Tue, 08 May 2012 14:23:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>As late as the 1926, and perhaps even up to the eve of World War II, on Fridays, in a small church on the Jewish street, a few meters off the main market square in the city of Poznań, the traditional song Kyrie Eleison, God Have Mercy, Christ Have Mercy, was replaced by a song on Jewish desecration of the host in Poznań in 1399. It was a legend, for there is no record of the case; no court room drama, for the trial never took place.  The drama was elsewhere: the set was the city, its geography, and its religious composition.  The protagonists were Carmelite friars who were trying to build in their church of Corpus Christi, and then revive, a eucharistic cult around a legend of host desecration by the Jews. Poznań’s host desecration legend did not just propagate a local eucharistic cult in the post-Reformation era, it also promoted contested tenets of the Catholicism and served as polemics against the Protestants.  More practically, the legend also provided the Carmelites of Poznań whose church of Corpus Christi was located in a remote swampy area outside the city walls with the opportunity to obtain a property they desired within the city—the very site that by the eighteenth century would become the church of the Most Holy Blood of Christ.  All this took place in a very specific time and place, as dogmas were contested, jurisdiction challenged, and competition between Jews and Christians increased.  And the legend that the miraculous hosts had been desecrated by Jews served to affirm the sacredness not only of the Eucharist but also of the Catholic space.</p>

	]]>
</description>

<author>Magda Teter</author>


<category>Catholic Church and the Jews</category>

<category>Early Modern Jewish History</category>

<category>Early Modern Religious History</category>

<category>Jews and the Reformation</category>

<category>Host desecration</category>

</item>


<item>
<title>&quot;I&apos;ll Go The Limit And Then Some:&quot;  Gun Molls, Desire And Danger In The 1930s</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/83</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/83</guid>
<pubDate>Tue, 08 May 2012 14:23:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Claire B. Potter</author>


</item>


<item>
<title> Analysing mouse chromosomal rearrangements with G-banded chromosomes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/44</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/44</guid>
<pubDate>Tue, 08 May 2012 14:23:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E C. Akeson et al.</author>


</item>


<item>
<title>Voyage autour d&apos;une bouteille de sorcier</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/82</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/82</guid>
<pubDate>Tue, 08 May 2012 14:23:13 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Elizabeth McAlister</author>


<category>Articles in French</category>

</item>


<item>
<title>The Jew in the Haitian Imagination: A Popular History of Anti-Judaism and Proto-Racism</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/81</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/81</guid>
<pubDate>Tue, 08 May 2012 14:23:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Elizabeth McAlister</author>


<category>Chapters in Edited Volumes</category>

</item>


<item>
<title>Rara as Popular Army: Hierarchy, Militarism, and Warfare</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/80</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/80</guid>
<pubDate>Tue, 08 May 2012 14:23:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Elizabeth McAlister</author>


<category>Chapters in Edited Volumes</category>

</item>


<item>
<title>Catholic, Vodou, and Protestant: Being Haitian, Becoming American</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/79</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/79</guid>
<pubDate>Tue, 08 May 2012 14:23:04 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Elizabeth McAlister et al.</author>


<category>Chapters in Edited Volumes</category>

</item>


<item>
<title>The Race of Time: DuBois and Reconstruction</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/78</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/78</guid>
<pubDate>Tue, 08 May 2012 14:23:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Charles C. Lemert</author>


</item>


<item>
<title>Understanding Mutual Benefit Societies at the Turn of the Twentieth Century</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/77</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/77</guid>
<pubDate>Tue, 08 May 2012 14:22:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Brian J. Glenn</author>


</item>


<item>
<title>The Two Schools of American Political Development</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/76</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/76</guid>
<pubDate>Tue, 08 May 2012 14:22:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Brian J. Glenn</author>


</item>


<item>
<title>The Shifting Rhetoric of Insurance Denial</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/75</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/75</guid>
<pubDate>Tue, 08 May 2012 14:22:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Brian J. Glenn</author>


</item>


<item>
<title>The Rhetoric of Fraternalism: Its Influence on the Development of the Welfare State,  1900-1935</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/74</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/74</guid>
<pubDate>Tue, 08 May 2012 14:22:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Brian J. Glenn</author>


</item>


<item>
<title>Review of Peter Bernstein. Against the Gods: The Remarkable Story of Risk. (John Wiley &amp; Sons, 1996)</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/73</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/73</guid>
<pubDate>Tue, 08 May 2012 14:22:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Brian J. Glenn</author>


</item>


<item>
<title>Privatization as a Strategy in the United Kingdom, United States, and Beyond,”</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/72</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/72</guid>
<pubDate>Tue, 08 May 2012 14:22:42 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Brian J. Glenn</author>


</item>


<item>
<title>Kansas Politics in the Bigger Picture: A  Review Essay of What’s the Matter with  Kansas?</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/71</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/71</guid>
<pubDate>Tue, 08 May 2012 14:22:39 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Brian J. Glenn</author>


<category>Religion and Social Policy</category>

</item>


<item>
<title> Mapping phenotypic trait loci.</title>
<link>http://mouseion.jax.org/stfb2000_2009/43</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/43</guid>
<pubDate>Tue, 08 May 2012 14:22:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>B A. Taylor</author>


</item>


<item>
<title>The Rise of the Classical Gold Standard: The Role of Focal Points and Synergistic Effects in Spontaneous Order</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/70</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/70</guid>
<pubDate>Tue, 08 May 2012 14:22:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper presents a theory of the invisible hand in homogeneous spontaneous orders.  It does so by answering three fundamental questions: How do spontaneous orders arise? How are they consolidated? Why do they last?  Spontaneous order is conceptualized as a solution to problems of cooperation (i.e., state-of-nature and coordination problems) within variable-sum games in decentralized environments. The processes which solve such cooperation problems must be effective in overcoming various obstacles deriving from limited information, uncertainty, and transaction costs. In the emergence or origin of spontaneous order, certain rules will be selected over others because of social-psychological dispositions (i.e., focal points) among small groups that make those rules desirable as solutions to problems of strategic interdependence. When focal points exist,  problems of information, transaction costs and uncertainty are mitigated as individuals can be secure that the behavioral choices they make are also shared by others in the group, thus reducing their vulnerability from exploitation or poor coordination. Focal points fundamentally condition the formation of preferences in choosing rules which facilitate cooperation. Once certain rules are chosen and perform well in facilitating cooperation within some smaller group (the first--or selection-stage), those rules will become more compelling to the greater or larger social system (the second--or consolidation--stage). The mechanism of consolidation, synergistic effects, gives the rules  a self-propagating quality: i.e., the incentives encouraging individuals to adopt the rules grow in proportion to the number of people that already follow the rules.  Propagation to the larger group will be influenced by the strength of the focal points, with the strongest focal points rendering the most robust propagation process. Once consolidated,  a spontaneous order’s stability will be influenced both by internal as well as external factors.  Internally, perceptions of the desirability of specific rules will be driven by the strength of the focal points which underlie those rules. The stronger the focal points, the greater the stability of the spontaneous order which is founded on those rules. Externally,  conditions in the greater social environment play an important role in determining whether the rules remain viable solutions to the strategic problems facing the group at large.  If these conditions remain fairly static and focal points remain strong, a spontaneous order can be highly stable. Conversely, dynamic conditions and weakening focal points lead to instability.   	The classical gold standard (1880-1914) represents a spontaneous international monetary order whose origin, consolidation, and stability very much reflect the workings of the theory developed herein. The ideology of gold created focal points which made gold attractive as a monetary standard in the latter-19th century. Consolidation of the gold bloc occurred swiftly as supply and demand conditions for precious metals imparted  a robust self-propagating  quality onto gold.  The international monetary order founded on gold remained stable up until World War I as the ideology of gold remained strong and conditions in the greater political economy remained favorable.  	In providing a theory of the process by which spontaneous orders form and exploring the process in the context of an international monetary regime, this paper seeks to fill some important gaps in the study of spontaneous order. First, it offers a theory of the invisible hand in homogeneous spontaneous systems. Second, in doing so, it contributes to a theory of preference formation in social systems. Finally, in presenting a case study in spontaneous (monetary) order, it contributes a much needed historical analysis to a literature dominated by theoretical treatments.</p>

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</description>

<author>Giulio M. Gallarotti</author>


<category>Gold Standard and International Relations</category>

</item>


<item>
<title>The Advent of the Prosperous Society: The Rise of the Guardian State and Structural Change in the World Economy</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/69</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/69</guid>
<pubDate>Tue, 08 May 2012 14:22:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Over the last century there has been a fundamental change in the economic orientation of  industrially advanced democracies, and this has had a pervasive impact on both their macroeconomies and their international economic relations.  Put more starkly, changing expectations about prosperity and the role of government as an economic guardian have fundamentally reshaped the economic geography of the world economy. In humorous tone, it might even be called a cowardly new world, one in which societies refuse to brave the vagaries of unrestrained markets.  This argument presents an alternative to traditional explanations of economics processes and relations in which scholars have studied changes very narrowly and have conceived of them as independent from one another. This article looks at these processes and relations as comprising “economic plates”: i.e., phenomena that are fundamentally linked so that they can be influenced in toto. Macroeconomic processes and international economic relations do occupy the same fundamental plate, and the plate has made significant shifts over the past century as a result of strong underlying forces in the form of changing orientations regarding peoples’ economic fates and governments’ relation to the market.</p>

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</description>

<author>Giulio M. Gallarotti</author>


<category>Politics of Macroeconomics</category>

</item>


<item>
<title>More Revisions in Realism: Hobbesian Anarchy, the Tale of the Fool, and International Relations Theory</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/68</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/68</guid>
<pubDate>Tue, 08 May 2012 14:22:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Thomas Hobbes has been hailed as a major intellectual precursor of realist theory among international relations scholars. Such veneration has brought about ample reactions from various scholars who aver that the use of Hobbes and his vision of anarchy as analogies for building greater theories of international relations is problematic at best. Yet while such critiques of the realist analogy have been abundant, they have devoted scant attention to important passages in the Leviathan (i.e., the tale of the fool in Chapter 15) that would produce greater clarity about Hobbes’ logic regarding the state of nature. Indeed, a careful textual analysis of the tale of the fool demonstrates that Hobbes’ vision of anarchy is even more problematic, then previous critiques suggest, as an analogy for a state of war (i.e., as an environment void of cooperation). Indeed, the tale strongly reinforces critical scholarship that embraces ample opportunities for cooperation (covenants) in a Hobbesian state of nature (i.e., without a Leviathan to impose order). The precise Hobbesian logic evident in this tale, in fact, reflects both strong neoliberal and constructivist elements in what many would consider a least-likely place: in Hobbes’ vision of anarchy. So while Hobbes has been hailed as the first early modern realist, he could also be cited as the first early modern neoliberal and constructivist. In this respect, Hobbes’ own synthesis of elements of realism, constructivism and neoliberalism holds much promise for inspiring a new and more sophisticated vision of international relations: Cosmopolitik.</p>

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</description>

<author>Giulio M. Gallarotti</author>


<category>Power and International Relations</category>

<category>Political Theory and International Relations</category>

</item>


<item>
<title>Monetary Darwinism: The Political Economy of Monetary Relations</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/67</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/67</guid>
<pubDate>Tue, 08 May 2012 14:22:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Giulio M. Gallarotti</author>


<category>Gold Standard and International Relations</category>

</item>


<item>
<title>Hegemons of a Lesser God: The Bank of France and Monetary Leadership Under the Classical Gold Standard</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/66</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/66</guid>
<pubDate>Tue, 08 May 2012 14:22:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Conventional theories of international hegemony all agree on the fact that the stabilizing functions of hegemons (i.e., nations which use their power to maintain orderly relations in a given issue-area) are positively correlated with their power.  The public goods logic upon which this vision is founded posits that as any potential leader becomes more powerful in a given issue area, it will increasingly see its own welfare as synonymous with order in the entire constellation of relations within the issue area itself, and consequently have an incentive to provide the necessary public goods (i.e., the components of stability) to bring such order about. Monetary relations under the classical gold standard (1880-1914), however, demonstrated an entirely different set of circumstances. The principal financial actor of the period (the Bank of England) showed little interest in stabilizing monetary relations during that period. It was in fact the Bank of France, a secondary monetary power, which acted much more robustly as monetary leader under the gold standard in protecting convertibility in gold-club nations. But rather than emanating from a perception of strength, such leadership functions in fact emanated from a sense of financial vulnerability. Hence, monetary leadership under the gold standard significantly tilts conventional hegemonic stability theory in that it reveals relative weakness as a catalyst for stabilizing behavior. Moreover, the stabilization functions of the Bank of France were marshaled for the purpose of keeping France in a secondary financial position to Britain, as a front line status would have placed France in the forefront as an international financial shock absorber, which the Bank sought to avoid for the sake of stability in French finance. In revealing a tendency to relent from enhancing a relative position in financial status, this case also cuts against common tenets of hegemonic stability theory. This article suggests that secondary powers can effectively serve the leadership functions traditionally ascribed to hegemons. Such functions can be carried out both directly (as stabilizers) and indirectly (as facilitators of cooperation).</p>

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</description>

<author>Giulio M. Gallarotti</author>


<category>Gold Standard and International Relations</category>

</item>


<item>
<title>Government Economists as ‘Global Economists’”</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/65</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/65</guid>
<pubDate>Tue, 08 May 2012 14:22:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>With the advent of globalization, economists that serve the U.S. government have had to become more sensitized to the greater internationalization of the challenges facing America's leaders. As this globalized world has turned domestic issues into international issues, the analysis of U.S. government economists has had to concomitantly become more internationalized. Only through such a broad analytical perspective can government economists best understand issues and solve problems in a globalized world.</p>

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</description>

<author>Giulio M. Gallarotti</author>


<category>Economists in Government Service</category>

</item>


<item>
<title>Toward Universal Human Rights and the Rule of Law: The Permanent International Criminal Court</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/64</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/64</guid>
<pubDate>Tue, 08 May 2012 14:22:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>A permanent international criminal court (ICC) was created by an international treaty signed on July 17, 1998 in Rome. This article is an analysis of the newly created ICC.  In it we explore both the institutional weaknesses and strengths of the Court, as well as the sea of political realities within which the Court must navigate, and which ultimately will determine its effectiveness. Finally, we analyze the impact (i.e., advantages and disadvantages) of the Court on the U.S. national interest. As a nation  which has the capacity to play a preponderant role in  making the ICC either effective or ineffective, the U.S., through its support (or lack of), will be in a crucial position of influencing the fate of the Court. Through this analysis we hope to shed light on the potential impact which the ICC will have on the enforcement of international criminal law.</p>

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</description>

<author>Giulio M. Gallarotti et al.</author>


<category>International Criminal Court</category>

</item>


<item>
<title>Politics, International Justice, and the United States: Toward a Permanent International Criminal Court</title>
<link>http://wesscholar.wesleyan.edu/div2facpubs/63</link>
<guid isPermaLink="true">http://wesscholar.wesleyan.edu/div2facpubs/63</guid>
<pubDate>Tue, 08 May 2012 14:22:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>At an address at Carleton University in 1995 Secretary General of the United Nations Boutros Boutros-Ghali declared the need for a “renaissance of international law” as nations face the new challenges of the post-Cold War world. According to Ghali, it is only through international law that the world can “secure a basis for cooperation” and “a lasting foundation for peace.”1 Aspirations for the realization of this lofty rhetoric have centered on the creation of a permanent international criminal court (PICC). The sentiment for a PICC emanates from dissatisfaction with the prevailing practice of international criminal law. Supporters of the court argue that individuals are not being held sufficiently accountable for the most serious crimes against the international community (genocide, war crimes, and crimes against humanity). The use of international tribunals in the 20th century has been ad hoc and temporary, while the present practice of extradite-or-prosecute does not function effectively when nations experience bottlenecks in the prosecution of suspected criminals (i.e., because the suspect is a former head of state, because of civil war, because nations refuse to extradite suspects, or because the requisite judicial institutions are missing). Under such conditions, there is lacking an effective deterrent against criminal acts in the global community because individuals are not being held systematically accountable for their transgressions. A PICC, according to supporters, would provide an ongoing deterrent and thus consolidate a global order based on the respect of international law. To the extent that a PICC became the central player in the prosecution and adjudication of international crime, there would indeed be a major qualitative change in the practice of international criminal law, which has heretofore been principally enforced through sovereign nations.  A permanent court has been proposed by the U.N. International Law Commission in a 1994 draft statute. The statute continues to be negotiated until a June 1998 target date during which it is expected that a majority of nations (led by the U.S.) will sign a formal treaty creating a PICC.  This article is an analysis of the proposed PICC. In it we explore both the institutional weaknesses and strengths of the proposed Court, as well as the sea of political realities within which the Court must navigate, and which ultimately will determine its effectiveness. Finally, we analyze the impact (i.e., advantages and disadvantages) of the Court on the U.S. national interest. As an agent which has the capacity to play a preponderant role in making the PICC either effective or ineffective, U.S. support (or the lack of) will be crucial in determining the influence of the Court. Through this analysis we hope to shed light on the potential impact which the PICC will have on the enforcement of international criminal law.</p>

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</description>

<author>Giulio M. Gallarotti et al.</author>


<category>International Criminal Court</category>

</item>


<item>
<title> The neuronal Golgi apparatus is fragmented in transgenic mice expressing a mutant human SOD1, but not in mice expressing the human NF-H gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/42</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/42</guid>
<pubDate>Tue, 08 May 2012 14:21:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fragmentation of the Golgi apparatus (GA) of motor neurons was first described in sporadic amyotrophic lateral sclerosis (ALS) and later confirmed in transgenic mice expressing the G93A mutation of the gene encoding the enzyme    Cu,Zn superoxide dismutase (SOD1(G93A)) found in some cases of familial ALS. In these transgenic mice, however, the fragmentation of the neuronal GA was associated with cytoplasmic and mitochondrial vacuoles not seen in ALS. The present new    series of transgenic mice expressing 14-17 trans gene copies of SOD1(G93A), compared to 25 copies in the mice we studied previously, showed consistent fragmentation of the GA of spinal cord motor neurons, axonal swellings, Lewy-like body    inclusions in neurons and glia, but none of the cytoplasmic or mitochondrial vacuoles originally reported. Thus, this animal model recapitulates the clinical and most neuropathological findings of sporadic ALS. Neurofilaments (NF) accumulate in    axons and, less often, in neuronal perikarya in most cases of sporadic ALS and they have been implicated in its pathogenesis. In order to investigate whether fragmentation of the neuronal GA also occurs in association with accumulation of    perikaryal NFs, we studied the organelle in transgenic mice expressing the heavy subunit of human neurofilaments (NF-H) which developed a motor neuronopathy resembling ALS. The neuronal GA of mice expressing NF-H, however, was intact despite    massive accumulation of NFs in both perikarya and axons of motor neurons. In contrast, in transgenic mice expressing SOD1(G93A), the GA was fragmented despite the absence of accumulation of perikaryal NFs. These findings suggest that, in    transgenic mice with neuronopathies caused by the expression of mutant SOD1(G93A) or the human NF-H, the GA and the perikaryal NFs are independently involved in the pathogenesis. The evidence suggests that the GA plays a central role in the    pathogenesis of the vast majority of sporadic ALS and in FALS with SOD1 mutations.</p>

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</description>

<author>A Stieber et al.</author>


</item>


<item>
<title> Lop12, a mutation in mouse crygd causing lens opacity similar to human coppock cataract [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/41</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/41</guid>
<pubDate>Tue, 08 May 2012 14:21:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>A new cataract mutation was discovered in an ongoing program to identify new mouse models of hereditary eye disease. Lens opacity 12 (Lop12) is a semidominant mutation that results in an irregular nuclear lens opacity similar to    the human Coppock cataract. Lop12 is associated with a small nonrecombining segment that maps to mouse Chromosome 1 close to the eye lens obsolescence mutation (Cryge(Cat2-Elo)), a member of the gamma-crystallin gene cluster (Cryg). Using a    systemic candidate gene approach to analyze the entire Cryg cluster, a G to A transition was found in exon 3 of Crygd associated with the Lop12 mutation and has been designated Crygd(Lop12). The mutation Crygd(Lop12) leads to the formation of an    in-frame stop codon that produces a truncated protein of 156 amino acids. It is predicted that the defective gene product alters protein folding of the gamma-crystallin(s) and results in lens opacity. Copyright 2000 Academic Press.</p>

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</description>

<author>R S. Smith et al.</author>


</item>


<item>
<title> Identification of a CD8 T cell that can independently mediate autoimmune diabetes development in the complete absence of CD4 T cell helper functions.</title>
<link>http://mouseion.jax.org/stfb2000_2009/40</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/40</guid>
<pubDate>Tue, 08 May 2012 14:20:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous work has indicated that an important component for the initiation of autoimmune insulin-dependent diabetes mellitus (IDDM) in the NOD mouse model entails MHC class I-restricted CD8 T cell responses against pancreatic beta    cell Ags. However, unless previously activated in vitro, such CD8 T cells have previously been thought to require helper functions provided by MHC class II-restricted CD4 T cells to exert their full diabetogenic effects. In this study, we show    that IDDM development is greatly accelerated in a stock of NOD mice expressing TCR transgenes derived from a MHC class I-restricted CD8 T cell clone (designated AI4) previously found to contribute to the earliest preclinical stages of pancreatic    beta cell destruction. Importantly, these TCR transgenic NOD mice (designated NOD.AI4alphabeta Tg) continued to develop IDDM at a greatly accelerated rate when residual CD4 helper T cells were eliminated by introduction of the scid mutation or a    functionally inactivated CD4 allele. In a previously described stock of NOD mice expressing TCR transgenes derived from another MHC class I-restricted beta cell autoreactive T cell clone, IDDM development was retarded by elimination of residual    CD4 T cells. Hence, there is variability in the helper dependence of CD8 T cells contributing to the development of autoimmune IDDM. The A14 clonotype represents the first CD8 T cell with a demonstrated ability to progress from a naive to    functionally activated state and rapidly mediate autoimmune IDDM development in the complete absence of CD4 T cell helper functions.</p>

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</description>

<author>R T. Graser et al.</author>


</item>


<item>
<title> A novel mechanism of resistance to mouse mammary tumor virus infection.</title>
<link>http://mouseion.jax.org/stfb2000_2009/39</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/39</guid>
<pubDate>Tue, 08 May 2012 14:20:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Exogenous mouse mammary tumor virus (MMTV) is carried from the gut of suckling pups to the mammary glands by lymphocytes and induces mammary gland tumors. MMTV-induced tumor incidence in inbred mice of different strains ranges from    0 to as high as 100%. For example, mice of the C3H/HeN strain are highly susceptible, whereas mice of the I/LnJ strain are highly resistant. Of the different factors that together determine the susceptibility of mice to development of    MMTV-induced mammary tumors, genetic elements play a major role, although very few genes that determine a susceptibility-resistance phenotype have been identified so far. Our data indicate that MMTV fails to infect mammary glands in I/LnJ mice    foster nursed on viremic C3H/HeN females, even though the I/LnJ mammary tissue is not refractory to MMTV infection. Lymphocytes from fostered I/LnJ mice contained integrated MMTV proviruses and shed virus but failed to establish infection in the    mammary glands of susceptible syngeneic (I x C3H.JK)F(1) females. Based on the susceptible-resistant phenotype distribution in N(2) females, both MMTV mammary gland infection and mammary gland tumor development in I/LnJ mice are controlled by a    single locus.</p>

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</description>

<author>T V. Golovkina</author>


</item>


<item>
<title> Fluoride and fractures: an ecological fallacy [comment]</title>
<link>http://mouseion.jax.org/stfb2000_2009/38</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/38</guid>
<pubDate>Tue, 08 May 2012 14:19:37 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C J. Rosen</author>


</item>


<item>
<title> B1 B lymphocytes play a critical role in host protection against lymphatic filarial parasites.</title>
<link>http://mouseion.jax.org/stfb2000_2009/37</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/37</guid>
<pubDate>Tue, 08 May 2012 14:18:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Host defense against multicellular, extracellular pathogens such as nematode parasites is believed to be mediated largely, if not exclusively, by T lymphocytes. During our investigations into the course of Brugia malayi and Brugia    pahangi infections in immunodeficient mouse models, we found that mice lacking B lymphocytes were permissive for Brugian infections, whereas immunocompetent mice were uniformly resistant. Mice bearing the Btk(xid) mutation were as permissive as    those lacking all B cells, suggesting that the B1 subset may be responsible for host protection. Reconstitution of immunodeficient recombination activating gene (Rag)-1(-/)- mice with B1 B cells conferred resistance, even in the absence of    conventional B2 lymphocytes and most T cells. These results suggest that B1 B cells are necessary to mediate host resistance to Brugian infection. Our data are consistent with a model wherein early resistance to B. malayi is mediated by humoral    immune response, with a significant attrition of the incoming infectious larval load. Sterile clearance of the remaining parasite burden appears to require cell-mediated immunity. These data raise the possibility that the identification of    molecule(s) recognized by humoral immune mechanisms might help generate prophylactic vaccines.</p>

	]]>
</description>

<author>N Paciorkowski et al.</author>


</item>


<item>
<title> Mice mutant for Egfr and Shp2 have defective cardiac semilunar valvulogenesis.</title>
<link>http://mouseion.jax.org/stfb2000_2009/36</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/36</guid>
<pubDate>Tue, 08 May 2012 14:18:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Atrioventricular and semilunar valve abnormalities are common birth defects, but how cardiac valvulogenesis is directed remains largely unknown. During studies of genetic interaction between Egfr, encoding the epidermal growth    factor receptor, and Ptpn11, encoding the protein-tyrosine-phosphatase Shp2, we discovered that Egfr is required for semilunar, but not atrioventricular, valve development. Although unnoticed in earlier studies, mice homozygous for the    hypomorphic Egfr allele waved-2 (Egfrwa2/wa2) exhibit semilunar valve enlargement resulting from over-abundant mesenchymal cells. Egfr-/- mice (CD1 background) have similar defects. The penetrance and severity of the defects in Egfrwa2/wa2 mice    are enhanced by heterozygosity for a targeted mutation of exon 2 of Ptpn11 (ref. 3). Compound (Egfrwa2/wa2:Ptpn11+/-) mutant mice also show premature lethality. Electrocardiography, echocardiography and haemodynamic analyses showed that affected    mice develop aortic stenosis and regurgitation. Our results identify the Egfr and Shp2 as components of a growth-factor signalling pathway required specifically for semilunar valvulogenesis, support the hypothesis that Shp2 is required for Egfr    signalling in vivo, and provide an animal model for aortic valve disease.</p>

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</description>

<author>B Chen et al.</author>


</item>


<item>
<title> Mouse mutants from chemically mutagenized embryonic stem cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/35</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/35</guid>
<pubDate>Tue, 08 May 2012 14:17:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>The drive to characterize functions of human genes on a global scale has stimulated interest in large-scale generation of mouse mutants.  Conventional germ-cell mutagenesis with N-ethyl-N-nitrosourea (ENU) is compromised by an    inability to monitor mutation efficiency, strain and interlocus variation in mutation induction, and extensive husbandry requirements. To overcome these obstacles and develop new methods for generating mouse mutants, we devised protocols to    generate germline chimaeric mice from embryonic stem (ES) cells heavily mutagenized with ethylmethanesulphonate (EMS). Germline chimaeras were derived from cultures that underwent a mutation rate of up to 1 in 1,200 at the Hprt locus (encoding    hypoxanthine guanine phosphoribosyl transferase). The spectrum of mutations induced by EMS and the frameshift mutagen ICR191 was consistent with that observed in other mammalian cells. Chimaeras derived from ES cells treated with EMS transmitted    mutations affecting several processes, including limb development, hair growth, hearing and gametogenesis. This technology affords several advantages over traditional mutagenesis, including the ability to conduct shortened breeding schemes and to    screen for mutant phenotypes directly in ES cells or their differentiated derivatives.</p>

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</description>

<author>R J. Munroe et al.</author>


</item>


<item>
<title> Cloning, expression, and chromosomal localization of a mouse gene homologous to the germ cell migration regulator wunen and to type 2 phosphatidic acid phosphatases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/34</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/34</guid>
<pubDate>Tue, 08 May 2012 14:17:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>The wunen gene of Drosophila melanogaster encodes a multipass membrane-spanning protein that negatively regulates primordial germ cell migration. Here we describe the cloning of a mouse gene that encodes a protein homologous to    wunen and to the Type 2 phosphatidic acid phosphatases. This gene encodes a 251-amino-acid protein that most closely resembles the human Type 2 phosphatidic acid phosphatase PAP-2c. Northern blot analysis revealed the presence of a single 1.9-kb    Ppap2c transcript.  The Ppap2c gene was localized to the central portion of mouse Chromosome 10 by interspecific backcross analysis. Copyright 2000 Academic Press.</p>

	]]>
</description>

<author>N Zhang et al.</author>


</item>


<item>
<title>Fluoride-promoted ligand exchange in diaryliodonium salts</title>
<link>http://digitalcommons.unl.edu/chemistrydimagno/3</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/chemistrydimagno/3</guid>
<pubDate>Tue, 08 May 2012 14:16:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Diaryliodonium salts are shown to undergo rapid, fluoride-promoted aryl exchange reactions at room temperature in acetonitrile. Aryl exchange is shown to be exquisitely sensitive to the concentration of fluoride ion in solution; fast exchange is observed as the fluoride concentration approaches a stoichiometric amount at 50 mM substrate concentration. The reaction is slowed, but not halted if benzene is the solvent, indicating that free fluoride ion or a four-coordinate anionic I(III) species may be responsible for the exchange. The fluoride-promoted aryl exchange reaction is general and allows direct measurement of the relative stabilities of diaryliodonium salts featuring different aryl substituents. The aryl exchange reaction may be of practical use for the preparation of hitherto inaccessible diaryliodonium salts, thus it also has implications for labeling radiotracers for molecular imaging with <sup>18</sup>F-fluoride (t<sub>1/2</sub> = 109.7 min).</p>

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</description>

<author>Bijia Wang et al.</author>


</item>


<item>
<title>Optimizing the Pedagogical Efficacy of Moodle</title>
<link>http://digitalcommons.csbsju.edu/forum_2012spring/12</link>
<guid isPermaLink="true">http://digitalcommons.csbsju.edu/forum_2012spring/12</guid>
<pubDate>Tue, 08 May 2012 14:16:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Course Management Systems (CMS) such as Moodle, D2L, and Blackboard are often used as auxiliary resources for both traditional and online courses. As CSB/SJU faculty, many of us are developing and using creative CMS resources with the goal of positive pedagogical impact. How is the effectiveness of these resources assessed? Which resources are found most useful by students? How can faculty maximize the pedagogical value of CMS? This Thursday Forum presentation shows participants the results of a study directed toward answering these questions. During three introductory financial accounting courses conducted in 2009, 2010, and 2011, Camtasia videos, assignment solutions, notes, slides, WebEx recordings, homework discussion forums, and other Moodle resources were available to students. Analyses were performed to determine whether student Moodle use correlated with student performance. A pre- and post-course exam was administered to assess student learning as related to Moodle use. In addition, a student survey was conducted to gather evidence about which resources were deemed most useful by students and to compare student perceptions of usefulness with actual use. The forum presentation also shows how to track student use of Moodle resources via the direct and indirect assessment methods used in the study. Examples of student preferred resources are also shown.</p>

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</description>

<author>Michelle Li-Kuehne et al.</author>


</item>


<item>
<title> The bst locus on mouse chromosome 16 is associated with age-related subretinal neovascularization.</title>
<link>http://mouseion.jax.org/stfb2000_2009/33</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/33</guid>
<pubDate>Tue, 08 May 2012 14:16:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ocular neovascularization is the leading cause of blindness in developed countries and often causes rapid loss of vision in age-related macular degeneration. Acute visual loss is most often due to hemorrhage from new vessels that    have extended from the choroid into the subretinal space.  Growth of abnormal vessels beneath the retina in this condition is known as subretinal neovascularization (SRN). Age-related animal models of macular degeneration and SRN have not been    described. Current animal models of SRN depend on chemical or physical stimuli to initiate growth of subretinal vessels. The genes responsible for age-related human macular degeneration with SRN have not been firmly identified. We report an    angiogenic phenotype in Bst/+ mice that is age-related, clinically evident, and resembles human SRN. This represents a spontaneous, genetically determined model of SRN. Bst/+ mice offer the possibility of exploring the molecular mechanisms of SRN    without the need for exogenous agents.</p>

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</description>

<author>R S. Smith et al.</author>


</item>


<item>
<title> Rescue of oocytes from antral follicles of cryopreserved mouse ovaries: competence to undergo maturation, embryogenesis, and development to term.</title>
<link>http://mouseion.jax.org/stfb2000_2009/32</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/32</guid>
<pubDate>Tue, 08 May 2012 14:15:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Only primordial and primary follicles of frozen-thawed mouse ovaries survive after grafting to the ovarian bursa; large secondary follicles and antral follicles together with the oocytes contained in them degenerate.  This study    was undertaken to determine whether fully grown oocytes isolated from the antral follicles of frozen-thawed mouse ovaries are viable and can be rescued to undergo maturation, fertilization, and embryo development in vitro. Ovaries were    cryopreserved after removal from 22-day-old (C57BL/6J x SJL/J)F(1) mice, with or without prior priming with equine chorionic gonadotrophin, and fresh non-frozen ovaries were used as controls. Only cumulus cell-denuded oocytes were recovered from    frozen unprimed ovaries while both cumulus cell-enclosed and denuded oocytes were retrieved from frozen primed ovaries. Oocytes from both groups of frozen-thawed ovaries were able to undergo maturation, fertilization, and development to the    blastocyst stage in vitro, though at lower percentages than oocytes from control unfrozen ovaries. Moreover, 19% of 2-cell stage embryos derived from frozen-thawed primed ovaries, compared with 42% of embryos derived from control primed ovaries,    developed to term after transfer to pseudopregnant foster mothers (not significantly different).  Therefore, fully grown oocytes in antral follicles survive the cryopreservation protocol, as demonstrated by maturation, fertilization and embryo    development in vitro, and development to term after embryo transfer.</p>

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</description>

<author>J M. Sztein et al.</author>


</item>


<item>
<title> Twins. Novel uses to study complex traits and genetic diseases.</title>
<link>http://mouseion.jax.org/stfb2000_2009/31</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/31</guid>
<pubDate>Tue, 08 May 2012 14:14:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>The challenge faced by research into the genetic basis of complex disease is to identify genes of small relative effect against a background of substantial genetic and environmental variation. This has focused interest on a    classical epidemiological design: the study of twins. Through their precise matching for age, the common family environment and background environmental variation, studying diseases in non-identical twin provides a means to enhance the power of    conventional strategies to detect genetic influence through linkage and association. The unique matching of identical twins provides researchers with ways to isolate the function of individual genes involved in disease together with approaches to    understanding how genes and the environment interact.</p>

	]]>
</description>

<author>A J. MacGregor et al.</author>


</item>


<item>
<title>Direct measurement of the mass difference between top and antitop quarks</title>
<link>http://digitalcommons.unl.edu/physicsbloom/316</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsbloom/316</guid>
<pubDate>Tue, 08 May 2012 14:14:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present a direct measurement of the mass difference between top and antitop quarks (∆m) in lepton + jets tt final states using the ‘‘matrix element’’ method. The purity of the lepton + jets sample is enhanced for tt events by identifying at least one of the jets as originating from a b quark. The analyzed data correspond to 3.6 fb-1 of pp collisions at √s = 1.96 TeV acquired by D0 in Run II of the Fermilab Tevatron Collider. The combination of the e + jets and µ + jets channels yields ∆m =0.8 ± 1,8 stat ± 0.5(syst) GeV, which is in agreement with the standard model expectation of no mass difference.</p>

	]]>
</description>

<author>V. M. Abazov et al.</author>


</item>


<item>
<title>Off-label Prescribing: Pediatrician Beliefs and Experience</title>
<link>http://scholarship.shu.edu/dissertations/1800</link>
<guid isPermaLink="true">http://scholarship.shu.edu/dissertations/1800</guid>
<pubDate>Tue, 08 May 2012 14:14:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Elizabeth G. Evola</author>


</item>


<item>
<title> Expression of Cre recombinase in mouse oocytes: a means to study maternal effect genes.</title>
<link>http://mouseion.jax.org/stfb2000_2009/30</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/30</guid>
<pubDate>Tue, 08 May 2012 14:14:23 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Vries W. de et al.</author>


</item>


<item>
<title> Mouse FcgammaRI: identification and functional characterization of five new alleles.</title>
<link>http://mouseion.jax.org/stfb2000_2009/29</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/29</guid>
<pubDate>Tue, 08 May 2012 14:13:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse Fcgr1 gene encoding the high-affinity IgG receptor (FcgammaRI) exists as two known alleles, FcgammaRI-BALB and FcgammaRI-NOD, and these alleles exhibit functional differences. To determine whether other alleles exist in    mouse strains, Fcgr1 coding regions from 35 strains of mice were sequenced and a further five alleles were identified. The FcgammaRI-BALB and NOD alleles are now designated the "a" and "d" alleles, respectively.  Analysis of the five new alleles    revealed that although no polymorphisms were observed in the two leader exons, nucleotide and subsequent amino acid changes were observed in the exons encoding the extracellular domains, and transmembrane and cytoplasmic tail. The cDNA of the    seven alleles (a-g) were isolated and transiently transfected into COS cells, and IgG-binding studies were performed. Receptors encoded by four of the five new alleles (b, c, f, g) bound IgG2a with high affinity, displaying IgG binding    characteristics similar to the a allele (previously FcgammaRI-BALB). The d allele (previously FcgammaRI-NOD) and the e allele [derived from Mus spretus (SPRET/Ei)] encoded receptors which showed broader specificity by binding monomeric IgG2a,    IgG2b, and IgG3.</p>

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</description>

<author>A L. Gavin et al.</author>


</item>


<item>
<title> Identifying T cell-defined histocompatibility antigens by expression cloning.</title>
<link>http://mouseion.jax.org/stfb2000_2009/28</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/28</guid>
<pubDate>Tue, 08 May 2012 14:13:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>L M. Mendoza et al.</author>


</item>


<item>
<title> Sizing up the set of H genes in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/27</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/27</guid>
<pubDate>Tue, 08 May 2012 14:12:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D W. Bailey</author>


</item>


<item>
<title> Lessons from H3, a model autosomal mouse minor histocompatibility locus.</title>
<link>http://mouseion.jax.org/stfb2000_2009/26</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/26</guid>
<pubDate>Tue, 08 May 2012 14:12:03 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D Roopenian</author>


</item>


<item>
<title> Gene dose-dependent control of hematopoiesis and hematologic tumor suppression by CBP.</title>
<link>http://mouseion.jax.org/stfb2000_2009/25</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/25</guid>
<pubDate>Tue, 08 May 2012 14:11:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mice with monoallelic inactivation of the CBP gene develop highly penetrant, multilineage defects in hematopoietic differentiation and, with advancing age, an increased incidence of hematologic malignancies. The latter are    characterized, at least in some cases, by loss of heterozygosity (LOH) at the CBP locus. No such pathology was observed in wild-type or p300 heterozygous null mice of the same age and genetic background. Thus, a full complement of CBP, but not    p300, is required for normal hematopoietic differentiation. These results also provide the first experimental evidence for the hypothesis that CBP has tumor-suppressing activity.</p>

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</description>

<author>A L. Kung et al.</author>


</item>


<item>
<title> NOD/LtSz-Rag1null mice: an immunodeficient and radioresistant model for engraftment of human hematolymphoid cells, HIV infection, and adoptive transfer of NOD mouse diabetogenic T cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/24</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/24</guid>
<pubDate>Tue, 08 May 2012 14:10:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Development of a small animal model for the in vivo study of human immunity and infectious disease remains an important goal, particularly for investigations of HIV vaccine development. NOD/Lt mice homozygous for the severe    combined immunodeficiency (Prkdcscid) mutation readily support engraftment with high levels of human hematolymphoid cells. However, NOD/LtSz-scid mice are highly radiosensitive, have short life spans, and a small number develop functional    lymphocytes with age. To overcome these limitations, we have backcrossed the null allele of the recombination-activating gene (Rag1) for 10 generations onto the NOD/LtSz strain background. Mice deficient in RAG1 activity are unable to initiate    V(D)J recombination in Ig and TCR genes and lack functional T and B lymphocytes. NOD/LtSz-Rag1null mice have an increased mean life span compared with NOD/LtSz-scid mice due to a later onset of lymphoma development, are radioresistant, and lack    serum Ig throughout life.  NOD/LtSz-Rag1null mice were devoid of mature T or B cells. Cytotoxic assays demonstrated low NK cell activity. NOD/LtSz-Rag1null mice supported high levels of engraftment with human lymphoid cells and human hemopoietic    stem cells. The engrafted human T cells were readily infected with HIV.  Finally, NOD/LtSz-Rag1null recipients of adoptively transferred spleen cells from diabetic NOD/Lt+/+ mice rapidly developed diabetes. These data demonstrate the advantages    of NOD/LtSz-Rag1null mice as a radiation and lymphoma-resistant model for long-term analyses of engrafted human hematolymphoid cells or diabetogenic NOD lymphoid cells.</p>

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</description>

<author>L D. Shultz et al.</author>


</item>


<item>
<title> Ermap, a gene coding for a novel erythroid specific adhesion/receptor membrane protein.</title>
<link>http://mouseion.jax.org/stfb2000_2009/23</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/23</guid>
<pubDate>Tue, 08 May 2012 14:10:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ermap (erythroid membrane-associated protein), a gene coding for a novel transmembrane protein produced exclusively in erythroid cells, is described. It is mapped to murine Chromosome 4, 57 cM distal to the centromere. The initial    cDNA clone was isolated from a day 9 murine embryonic erythroid cell cDNA library. The predicted peptide sequence suggests that ERMAP is a transmembrane protein with two extracellular immunoglobulin folds, as well as a highly conserved B30.2    domain and several phosphorylation consensus sequences in the cytoplasmic region.  ERMAP shares a high homology throughout the entire peptide with butyrophilin, a glycoprotein essential for milk lipid droplet formation and release. A GFP-ERMAP    fusion protein was localized to the plasma membrane and cytoplasmic vesicles in transiently transfected 293T cells.  Northern blot analysis and in-situ hybridization demonstrated that Ermap expression was restricted to fetal and adult erythroid    tissues. ERMAP is likely a novel adhesion/receptor molecule specific for erythroid cells.</p>

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</description>

<author>T Z. Ye et al.</author>


</item>


<item>
<title> Modulation of transforming growth factor beta1 gene expression in the mammary gland by insulin-like growth factor I and octreotide.</title>
<link>http://mouseion.jax.org/stfb2000_2009/22</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/22</guid>
<pubDate>Tue, 08 May 2012 14:09:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Transforming growth factor beta1 (TGF-beta1) has been shown to exhibit anti-proliferative activity for mammary gland epithelial cells and for human breast cancer cells. Insulin-like growth factor I (IGF-I), in contrast, is a    well-characterized mitogenic and anti-apoptotic factor involved in mammary gland physiology. In order to examine the hypothesis that IGF-I suppresses TGF-beta1 expression in the mammary gland, we studied the effect of various manipulations of the    growth hormone - IGF-I axis on TGF-beta1 mRNA abundance. Administration of IGF-I to intact animal suppressed TGF-beta1 mRNA levels in a dose-dependent manner to approximately 20% of control levels. Administration of the somatostatin analogue    octreotide in a manner previously shown to acutely suppress the growth hormone - IGF-I axis increased mammary gland TGF-beta1 expression approximately 3-fold. Transgenic mice overexpressing growth hormone expressed TGF-beta1 in the mammary gland    at only approximately 12% of the level of control animals, while mice IGF-I deficient due to the mutation expressed TGF-beta1 at slightly higher levels than control animals. The large differences in TGF-beta1 expression between control and    GH-transgenic animals were correlated with major differences in architecture of the mammary gland, while the appearance of mammary glands of normal and animals was similar. These data document a previously unrecognized relationship between    TGF-beta1 and IGF-I physiology in the mammary gland, and suggest a novel mechanism by which somatostatin analogues influence the proliferative behaviour of breast epithelial cells.</p>

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</description>

<author>H Huynh et al.</author>


</item>


<item>
<title> A new method for characterizing replacement rate variation in molecular sequences. Application of the Fourier and wavelet models to Drosophila and mammalian proteins.</title>
<link>http://mouseion.jax.org/stfb2000_2009/21</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/21</guid>
<pubDate>Tue, 08 May 2012 14:08:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>We propose models for describing replacement rate variation in genes and proteins, in which the profile of relative replacement rates along the length of a given sequence is defined as a function of the site number. We consider    here two types of functions, one derived from the cosine Fourier series, and the other from discrete wavelet transforms. The number of parameters used for characterizing the substitution rates along the sequences can be flexibly changed and in    their most parameter-rich versions, both Fourier and wavelet models become equivalent to the unrestricted-rates model, in which each site of a sequence alignment evolves at a unique rate. When applied to a few real data sets, the new models    appeared to fit data better than the discrete gamma model when compared with the Akaike information criterion and the likelihood-ratio test, although the parametric bootstrap version of the Cox test performed for one of the data sets indicated    that the difference in likelihoods between the two models is not significant. The new models are applicable to testing biological hypotheses such as the statistical identity of rate variation profiles among homologous protein families. These    models are also useful for determining regions in genes and proteins that evolve significantly faster or slower than the sequence average. We illustrate the application of the new method by analyzing human immunoglobulin and Drosophilid alcohol    dehydrogenase sequences.</p>

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</description>

<author>P Morozov et al.</author>


</item>


<item>
<title> NZB mice exhibit a primary T cell defect in fetal thymic organ culture.</title>
<link>http://mouseion.jax.org/stfb2000_2009/20</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/20</guid>
<pubDate>Tue, 08 May 2012 14:08:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Defects in T cell development have been suggested to be a factor in the development of systemic autoimmunity in NZB mice. However, the suggestion of a primary T cell defect has often been by extrapolation, and few direct    observations of T cell precursors in NZB mice have been performed.  Moreover, the capacity of NZB bone marrow T cell precursors to colonize the thymus and the ability of the NZB thymic microenvironment to support T lymphopoiesis have not been    analyzed. To address this important issue, we employed the fetal thymic organ culture system to examine NZB T cell development. Our data demonstrated that NZB bone marrow cells were less efficient at colonizing fetal thymic lobes than those of    control BALB/c or C57BL/6 mice. In addition, NZB bone marrow cells did not differentiate into mature T cells as efficiently as bone marrow cells from BALB/c or C57BL/6 mice. Further analysis revealed that this defect resulted from an intrinsic    deficiency in the NZB Lin-Sca-1+c-kit+ bone marrow stem cell pool to differentiate into T cells in fetal thymic organ culture. Taken together, the data document heretofore unappreciated deficiencies in T cell development that may contribute to    the development of the autoimmune phenotype in NZB mice.</p>

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</description>

<author>Y Hashimoto et al.</author>


</item>


<item>
<title> A major effect QTL determined by multiple genes in epileptic EL mice [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/19</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/19</guid>
<pubDate>Tue, 08 May 2012 14:07:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The EL mouse strain provides a polygenic model for epilepsy. Previous mapping experiments between EL and nonepileptic ABP mice identified, and a congenic strain confirmed, a quantitative trait locus (QTL), El2, which lowered the    threshold to seizures induced by gentle rhythmic tossing. To narrow the map interval further we used a nested strategy to analyze a series of recombinants derived from the congenic strain. The recombinant strains revealed a complex pattern of    inheritance, with at least two independent regions of Chromosome 2 necessary for rhythmic tossing seizures and additional regions associated with unusual gender effects.  Similar results obtained using a completely independent paradigm,    pentylenetetrazole-induced tonic-clonic seizures, exclude the possibility that the genetic complexity was a unique property of the testing assay.  Thus, although conventional QTL mapping efforts detected and appeared to confirm a trait locus with    effects large enough for fine-structure mapping, subsequent dissection revealed multiple loci. Although at least one of these loci was mapped to a 1-cM interval, its individual effect is small, perhaps approaching the practical limits for further    study. Our results in the EL mouse may be prophetic for similar assaults on other polygenic, composite neurological behaviors which vary among inbred strains, begging the consideration of alternative strategies toward gene identification in these    models.</p>

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</description>

<author>M E. Legare et al.</author>


</item>


<item>
<title> Neurotrophin expression by spinal motoneurons in adult and developing rats.</title>
<link>http://mouseion.jax.org/stfb2000_2009/18</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/18</guid>
<pubDate>Tue, 08 May 2012 14:07:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Expression of the neurotrophins NT-4, brain-derived neurotrophic factor (BDNF), and NT-3 in adult rat lumbosacral spinal cord motoneurons is reported. A sensitive in situ hybridization procedure demonstrates localization of the    mRNA for each of these neurotrophins within spinal motoneurons of the adult and in early postnatal development. A majority of adult rat spinal cord lumbar motoneurons (approximately 63%) express NT-4 mRNA as assessed by counting motoneurons in    the L4 and L5 segments of two adult rat spinal cords on adjacent cresyl violet-stained and in situ hybridization sections. Similarly, a majority of lumbar motoneurons (approximately 73%) express BDNF mRNA. Further analyses of adjacent lumbar    spinal cord sections revealed that many, although not all motoneurons coexpress both NT-4 and BDNF mRNAs. At birth, the mRNA encoding NT-3 is expressed in motoneurons, but BDNF mRNA is not apparent until postnatal day 5 (P5) and NT-4 mRNA first    appears at P9. The potential biological significance of neurotrophin mRNA expression in spinal motoneurons is supported by immunohistochemical localization of each neurotrophin protein in adult motoneurons. We discuss the potential role of spinal    cord neurotrophins as autocrine or paracrine factors involved in modulating motoneuron synaptic function. Copyright 2000 Wiley-Liss, Inc.</p>

	]]>
</description>

<author>C R. Buck et al.</author>


</item>


<item>
<title> The mouse adducin gene family: alternative splicing and chromosomal localization.</title>
<link>http://mouseion.jax.org/stfb2000_2009/17</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/17</guid>
<pubDate>Tue, 08 May 2012 14:06:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mouse cDNA sequences encoding alpha, beta, and gamma adducins were cloned from a mouse reticulocyte cDNA library. The purified clones contain alternatively spliced exons from all three adducin genes. In the case of alpha and beta,    the inclusion of the alternatively spliced exons results in truncated polypeptide isoforms (called alpha-2 and beta-2). The mouse predicted amino acid sequences are compared with published rat and human sequences. For completion of this    comparison, cDNA encoding the rat beta-1 carboxy terminus was cloned by PCR. The carboxy terminal region containing MARCKS homology, calmodulin-binding region-2, and spectrin-actin-binding site, is conserved among alpha-1, beta-1, and gamma-1    isoforms in mouse, rat, and humans. We also report here the localization of the gene encoding gamma adducin (Add3) to murine Chr 19, in a region that shows conserved synteny with human Chr 10.</p>

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</description>

<author>S P. Suriyapperuma et al.</author>


</item>


<item>
<title> Retinal degeneration but not obesity is observed in null mutants of the tubby-like protein 1 gene.</title>
<link>http://mouseion.jax.org/stfb2000_2009/16</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/16</guid>
<pubDate>Tue, 08 May 2012 14:05:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>The tub gene is a member of a small, well conserved neuronal gene family of unknown function. Mutations within this gene lead to early-onset blindness and deafness, as well as late-onset obesity and insulin resistance. To test the    hypothesis that mutations within other members of this gene family would lead to similar phenotypes as observed in tubby mice, and hence have similar functional properties, we have generated null mutants of the tubby-like protein ( Tulp ) 1 gene    by homologous recombination. Similarly to tubby mice, Tulp1 (-/-)mice exhibit an early-onset retinal degeneration with a progressive, rapid loss of photoreceptors, further supporting the notion that previously identified mutations within the    human TULP1 gene are indeed causative of retinitis pigmentosa. However, in contrast to tubby mice, Tulp1 (-/-)mice exhibited normal hearing ability and, surprisingly, normal body weight despite the fact that both TUB and TULP1 are expressed in    the same neurons within the hypothalamus in areas known to be involved in feeding behavior and energy homeo stasis. However, TUB and TULP1 show a distinctly different staining pattern in the nucleus of these neurons, perhaps explaining the    difference in body weight between the Tulp1 (-/-)and tubby mutant mice.</p>

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</description>

<author>S Ikeda et al.</author>


</item>


<item>
<title> Gastric hyperplasia in mice lacking the putative Cdc42 effector IQGAP1.</title>
<link>http://mouseion.jax.org/stfb2000_2009/15</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/15</guid>
<pubDate>Tue, 08 May 2012 14:05:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human IQGAP1 is a widely expressed 190-kDa Cdc42-, Rac1-, and calmodulin-binding protein that interacts with F-actin in vivo and that can cross-link F-actin microfilaments in vitro. Recent results have implicated IQGAP1 as a    component of pathways via which Cdc42 or Rac1 modulates cadherin-based cell adhesion (S. Kuroda et al., Science 281:832-835, 1998), whereas yeast IQGAP-related proteins have been found to play essential roles during cytokinesis. To identify    critical in vivo functions of IQGAP1, we generated deficient mice by gene targeting. We demonstrate that IQGAP1 null mutants arise at normal frequency and show no obvious defects during development or for most of their adult life. Loss of IQGAP1    also does not affect tumor development or tumor progression, but mutant mice exhibit a significant (P < 0.0001) increase in late-onset gastric hyperplasia relative to wild-type animals of the same genetic background. While we cannot exclude that    functional redundancy with IQGAP2 contributes to the lack of developmental phenotypes, the restricted expression pattern of IQGAP2 is not obviously altered in adult IQGAP1 mutant mice. Thus, IQGAP1 does not serve any essential nonredundant    functions during murine development but may serve to maintain the integrity of the gastric mucosa in older animals.</p>

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</description>

<author>S Li et al.</author>


</item>


<item>
<title> Urocortin expression in the Edinger-Westphal nucleus is up-regulated by stress and corticotropin-releasing hormone deficiency.</title>
<link>http://mouseion.jax.org/stfb2000_2009/14</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/14</guid>
<pubDate>Tue, 08 May 2012 14:04:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Urocortin is a 40-amino acid mammalian peptide related to CRH and urotensin. The physiological role of urocortin is unknown, but it has been postulated to serve some of the functions previously attributed to CRH. We had earlier    found that urocortin messenger RNA (mRNA) expression within the mouse brain is confined to the region of the Edinger-Westphal (EW) nucleus of the midbrain. To further characterize the regulation of the urocortin gene, we first cloned and    sequenced the mouse gene, confirming the presence of a single gene in the murine genome. A general survey of mouse tissues using Northern blot analysis revealed the presence of urocortin mRNA only within the midbrain. By in situ hybridization    analysis, we found that urocortin mRNA expression in the EW nucleus is responsive to stress, as mRNA levels increased approximately 3-fold after 3 h of restraint. Chronic glucocorticoid treatment, although not affecting basal levels, blocked the    stress-induced rise in urocortin mRNA. Using CRH-deficient [knockout (KO)] mice, we examined the effect of combined CRH and glucocorticoid deficiency upon urocortin mRNA expression. As in wild-type (WT) mice, we had previously found that    urocortin expression in CRHKO mouse brain was not detected outside of the EW nucleus. However, we found that urocortin expression within the EW of CRHKO mice is up-regulated 2- to 3-fold compared with that in WT mice. This up-regulation is not    due to a lack of inhibition by glucocorticoids, as urocortin mRNA levels in the EW nucleus of CRHKO mice did not change after glucocorticoid supplementation. As the EW does not project to any brain regions known to be involved in the behavioral    responses to stress, urocortin expressed in this site is unlikely to mediate stress-induced behaviors. On the other hand, as the EW nucleus may play a role in the regulation of the autonomic nervous system and projects to various brain stem    nuclei that express the CRH receptor, urocortin originating in the EW may play a role in the regulation of the autonomic nervous system during stress.</p>

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</description>

<author>S C. Weninger et al.</author>


</item>


<item>
<title> Mutations in a NIMA-related kinase gene, Nek1, cause pleiotropic effects including a progressive polycystic kidney disease in mice.</title>
<link>http://mouseion.jax.org/stfb2000_2009/13</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/13</guid>
<pubDate>Tue, 08 May 2012 14:04:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>We previously have described a mouse model for polycystic kidney disease (PKD) caused by either of two mutations, kat or kat(2J), that map to the same locus on chromosome 8. The homozygous mutant animals have a latent onset, slowly    progressing form of PKD with renal pathology similar to the human autosomal-dominant PKD. In addition, the mutant animals show pleiotropic effects that include facial dysmorphism, dwarfing, male sterility, anemia, and cystic choroid plexus. We    previously fine-mapped the kat(2J) mutation to a genetic distance of 0.28 +/- 0.12 centimorgan between D8Mit128 and D8Mit129. To identify the underlying molecular defect in this locus, we constructed an integrated genetic and physical map of the    critical region surrounding the kat(2J) mutation. Cloning and expression analysis of the transcribed sequences from this region identified Nek1, a NIMA (never in mitosis A)-related kinase as a candidate gene. Further analysis of the Nek1 gene    from both kat/kat and kat(2J)/kat(2J) mutant animals identified a partial internal deletion and a single-base insertion as the molecular basis for these mutations. The complex pleiotropic phenotypes seen in the homozygous mutant animals suggest    that the NEK1 protein participates in different signaling pathways to regulate diverse cellular processes. Our findings identify a previously unsuspected role for Nek1 in the kidney and open a new avenue for studying cystogenesis and identifying    possible modes of therapy.</p>

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</description>

<author>P Upadhya et al.</author>


</item>


<item>
<title>Is Moderation Possible in American Politics?</title>
<link>http://digitalcommons.library.unlv.edu/blackmountain_lectures_events/124</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/blackmountain_lectures_events/124</guid>
<pubDate>Tue, 08 May 2012 14:03:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Juan Williams, journalist and political analyst, earned a BA degree in Philosophy at Haverford College and has subsequently received an honorary doctorate from Harvard College and State University of New York. He spent twenty-three years with the Washington Post as editorial writer, op-ed columnist, White House and National Correspondent; additionally, he has covered major political campaigns from 1980-2000. Juan has also written for The New York Times and The Wall Street Journal. He has published in The Atlantic Monthly and Time magazine as well as authoring Eyes on the Prize: America's Civil Rights Years, 1954-1965, Thurgood Marshall: American Revolution, and Enough. Juan has earned an Emmy Award for his television documentary work as well as a Political Commentator Award from the American Association of University Women. His television documentaries such as Politics: The New Black Power, A. Philip Randolph: For Jobs and Freedom, Civil Rights and the Press, Riot and Discovery, and Dying for Healthcare have received critical praise. Additionally, Juan has also served many years as NPR's afternoon talk-show host of Talk of the Nation before he expanded his role to become a political analyst for Fox News, appearing as a guest-host for "The O'Reilly Factor," and regular panelist for "Fox News Sunday" and "Special Report with Bret Baier."</p>
<p>Norman J. Ornstein, political scientist and research scholar at the American Enterprise Institute (AEI), earned his Ph.D. from the University of Michigan and has been a regular contributor to the Washington Post as well as writing a weekly column for Roll Call. He has published The Permanent Campaign and Its Future as well as co-authored The Broken Branch: How Congress is Failing America and How to Get it Back on Track and Vital Statistics on Congress 2008. He is also an election analyst for CBS News and sits on many advisory boards including the Institute for Law and Politics at the University of Minnesota Law School and Future of American Democracy Foundation. He is the Founder and Director of the Campaign Finance Work Group, which helped shape the "McCain-Feingold" campaign-financing reform law. He co-directs the Election Reform Party as well as co-directs (with Thomas Mann) the AEI-Brookings Election Reform Packet. He has testified on filibusters to the U.S. Senate Committee on Rules and Administration and on Lobbying Reform to the U.S. House Committee on Rules.</p>
<p>Kathleen Parker won the prestigious H. L. Mencken Writing Award in 1993 and was named one of the nation's Top Five Columnists in both 2004 and 2005 by The Week magazine. In 2010, Kathleen was awarded with the Pulitzer Prize for Commentary for her political opinion columns. Kathleen's work has appeared in the Washington Post, The Weekly Standard, Time, Town & Country, Cosmopolitan, and Fortune Small Business among others. She has been a guest on both The O'Reilly Factor and Chris Matthews Show and sits on the Board of Contributors of USA Today's Forum Page. Kathleen has also been a contributor to The Daily Beast. She earned both a BA and MA degree from Florida State University in Spanish Literature and also studied in Valencia, Spain during part of her undergraduate degree. She was recently the co-host with Elliot Spitzer for <em>ParkerSpitzer</em> show before deciding to devote all of her time and energy to her syndicated column, which is published in over 400 newspapers.</p>
<p>The "Queen of Talk," Patricia Cunningham is the host of the popular radio show, the Patricia Cunningham Show, discussing news and community issues in Las Vegas. A graduate of Ohio State University and an advocate for social justice, she has served or is currently serving as a member of several community groups such as the UNLV President's Task Force on Equity and Diversity, the Nevada State College Diversity Council and the Clark County School District Superintendent's Committee. She is the recipient of the Black Pioneer of Nevada award, a Community Impact Award and the Rose Award by the Professional Black Woman's Alliance, among other numerous accolades. In interviews and other capacities, she has lent her expertise, her voice talents, and her distinct perspective to documentaries such as PBS's Las Vegas: An Unconventional History and other projects ranging in topics from Kwanzaa to AIDS Prevention. Patricia can be heard every Saturday morning at 11:00 on Power 88 (KCEP 88.1).</p>

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</description>

<author>Juan Williams et al.</author>


</item>


<item>
<title> Genealogies of mouse inbred strains.</title>
<link>http://mouseion.jax.org/stfb2000_2009/12</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/12</guid>
<pubDate>Tue, 08 May 2012 14:03:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mouse is a prime organism of choice for modelling human disease. Over 450 inbred strains of mice have been described, providing a wealth of different genotypes and phenotypes for genetic and other studies. As new strains are    generated and others become extinct, it is useful to review periodically what strains are available and how they are related to each other, particularly in the light of available DNA polymorphism data from microsatellite and other markers. We    describe the origins and relationships of inbred mouse strains, 90 years after the generation of the first inbred strain. Given the large collection of inbred strains available, and that published information on these strains is incomplete, we    propose that all genealogical and genetic data on inbred strains be submitted to a common electronic database to ensure this valuable information resource is preserved and used efficiently.</p>

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</description>

<author>J A. Beck et al.</author>


</item>


<item>
<title> Reevaluation of the major histocompatibility complex genes of the NOD-progenitor CTS/Shi strain.</title>
<link>http://mouseion.jax.org/stfb2000_2009/11</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/11</guid>
<pubDate>Tue, 08 May 2012 14:03:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>The common Kd and/or Db alleles of NOD mice contribute to the development of autoimmune diabetes, but their respective contributions are unresolved.  The major histocompatibility complex (MHC) of the CTS/Shi mouse, originally    designated as H2ct, shares MHC class II region identity with the H2g7 haplotype of NOD mice. However, CTS mice were reported to express distinct but undefined MHC class I gene products. Because diabetes frequency was reduced 56% in females of a    NOD stock congenic for H2ct, this partial resistance may have derived from the MHC class I allelic differences. In the present report, we use a combination of serologic analysis and sequencing of MHC class I cDNAs to establish that NOD/Lt and    CTS/Shi share a common H2-Kd allele but differ at the H2-D end of the MHC complex. The H2-D allele of CTS/Shi was identified as the rare H2-Ddx recently described in ALR/Lt, another NOD-related strain. These results in mouse model systems show    that multiple MHC genes confer diabetes resistance and suggest that at least one of the protective MHC or MHC-linked genes in CTS mice may be at the H2-D end of the complex.</p>

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</description>

<author>C E. Mathews et al.</author>


</item>


<item>
<title> The Mouse Genome Database (MGD): expanding genetic and genomic resources for the laboratory mouse. The Mouse Genome Database Group.</title>
<link>http://mouseion.jax.org/stfb2000_2009/10</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/10</guid>
<pubDate>Tue, 08 May 2012 14:02:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Database (MGD) is a comprehensive public database of mouse genomic, genetic and phenotypic information (http://www.  informatics.jax.org). This community database provides information about genes, serves as a    mapping resource of the mouse genome, details mammalian orthologs, integrates experimental data, represents standardized mouse nomenclature for genes and alleles, incorporates links to other genomic resources such as sequence data, and includes a    variety of additional information about the laboratory mouse. MGD scientists and annotators work cooperatively with the research community to provide an integrated, consensus view of the mouse genome while also providing experimental data    including data conflicting with the consensus representation. Recent improvements focus on the representation of phenotypic information and the enhancement of gene and allele descriptions.</p>

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</description>

<author>J A. Blake et al.</author>


</item>


<item>
<title> Mouse tumor biology database (MTB): enhancements and current status.</title>
<link>http://mouseion.jax.org/stfb2000_2009/9</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/9</guid>
<pubDate>Tue, 08 May 2012 14:02:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Tumor Biology Database (MTB) is a Web-based resource that provides access to information on tumor frequency and latency, genetics and pathology in genetically defined mice (transgenics, targeted mutations and inbred    strains). MTB is designed to serve as an information resource for cancer genetics researchers who use the laboratory mouse as a model system for understanding human disease processes. Data in MTB are obtained from the primary scientific    literature and direct submissions by the research community. MTB is accessible from the Mouse Genome Informatics Web site (http://www. informatics.jax.org). User support is available for MTB via Email at    mgi-help@informatics.jax.org</p>

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</description>

<author>C J. Bult et al.</author>


</item>


<item>
<title> GXD: a Gene Expression Database for the laboratory mouse: current status and recent enhancements. The Gene Expresison Database group.</title>
<link>http://mouseion.jax.org/stfb2000_2009/8</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/8</guid>
<pubDate>Tue, 08 May 2012 14:01:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Gene Expression Database (GXD) is a community resource of gene expression information for the laboratory mouse. The database is designed as an open-ended system that can integrate different types of expression data. New    expression data are made available on a daily basis. Thus, GXD provides increasingly complete information about what transcripts and proteins are produced by what genes; where, when and in what amounts these gene products are expressed; and how    their expression varies in different mouse strains and mutants. GXD is integrated with the Mouse Genome Database (MGD). Continuously refined interconnections with sequence databases and with databases from other species place the gene expression    information in the larger biological and analytical context. GXD is accessible through the Mouse Genome Informatics Web site at http://www.informatics.jax.org/ or directly at http://www.informatics.jax.org/menus/expression_menu.shtm    l</p>

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</description>

<author>M Ringwald et al.</author>


</item>


<item>
<title> Sry induces cell proliferation in the mouse gonad [In Process Citation]</title>
<link>http://mouseion.jax.org/stfb2000_2009/7</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/7</guid>
<pubDate>Tue, 08 May 2012 14:01:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sry is the only gene on the Y chromosome that is required for testis formation in mammals. One of the earliest morphological changes that occurs as a result of Sry expression is a size increase of the rudimentary XY gonad relative    to the XX gonad. Using 5'-bromo-2'-deoxyuridine (BrdU) incorporation to label dividing cells, we found that the size increase corresponds with a dramatic increase in somatic cell proliferation in XY gonads, which is not detected in XX gonads.    This male-specific proliferation was observed initially in the cells of the coelomic epithelium and occurred in two distinct stages. During the first stage, proliferation in the XY gonad was observed largely in SF1-positive cells and contributed    to the Sertoli cell population. During the second stage, proliferation was observed in SF1-negative cells at and below the coelomic epithelium and did not give rise to Sertoli cells. Both stages of proliferation were dependent on Sry and    independent of any other genetic differences between male and female gonads, such as X chromosome dosage or other genes on the Y chromosome. The increase in cell proliferation began less than 24 hours after the onset of Sry expression, before the    establishment of male-specific gene expression patterns, and before the appearance of any other known male-specific morphological changes in the XY gonad. Therefore, an increase in cell proliferation in the male coelomic epithelium is the    earliest identified effect of Sry expression.</p>

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</description>

<author>J Schmahl et al.</author>


</item>


<item>
<title> Pathogenesis of cholesterol gallstone disease: role of the liver.</title>
<link>http://mouseion.jax.org/stfb2000_2009/6</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/6</guid>
<pubDate>Tue, 08 May 2012 14:00:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M C. Carey et al.</author>


</item>


<item>
<title> Gene trap strategies in ES cells.</title>
<link>http://mouseion.jax.org/stfb2000_2009/5</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/5</guid>
<pubDate>Tue, 08 May 2012 14:00:05 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W Wurst et al.</author>


</item>


<item>
<title> It&apos;s a knockout!</title>
<link>http://mouseion.jax.org/stfb2000_2009/4</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/4</guid>
<pubDate>Tue, 08 May 2012 13:59:36 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>A V. Anagnostopoulos</author>


</item>


<item>
<title> The mouse genome database: a resource for today and tomorrow.</title>
<link>http://mouseion.jax.org/stfb2000_2009/3</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/3</guid>
<pubDate>Tue, 08 May 2012 13:59:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J T. Eppig et al.</author>


</item>


<item>
<title> Genetically defined risk of salt sensitivity in an intercross of Brown Norway and Dahl S rats.</title>
<link>http://mouseion.jax.org/stfb2000_2009/2</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/2</guid>
<pubDate>Tue, 08 May 2012 13:58:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>A W. Cowley et al.</author>


</item>


<item>
<title>Minor Histocompatibility Antigens: From the Laboratory to the Clinic.</title>
<link>http://mouseion.jax.org/stfb2000_2009/1</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2000_2009/1</guid>
<pubDate>Tue, 08 May 2012 13:57:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>


</item>


<item>
<title>ckn520311d1p2</title>
<link>http://place.asburyseminary.edu/ecommonsfacultylectures/11</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsfacultylectures/11</guid>
<pubDate>Tue, 08 May 2012 13:57:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>ATS</author>


</item>


<item>
<title>Library Focus (Fall 2011)</title>
<link>http://aquila.usm.edu/libraryfocus/2</link>
<guid isPermaLink="true">http://aquila.usm.edu/libraryfocus/2</guid>
<pubDate>Tue, 08 May 2012 13:50:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Ezra Jack Keats Book Awards Move to de Grummond<br>From the Dean</p>

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</description>

<author>University Libraries et al.</author>


</item>


<item>
<title>Index</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/27</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/27</guid>
<pubDate>Tue, 08 May 2012 13:46:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Index</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/27</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/27</guid>
<pubDate>Tue, 08 May 2012 13:46:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Tables</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/26</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/26</guid>
<pubDate>Tue, 08 May 2012 13:46:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Tables</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/26</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/26</guid>
<pubDate>Tue, 08 May 2012 13:46:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Chapter 22: Administration of Justice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/25</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/25</guid>
<pubDate>Tue, 08 May 2012 13:46:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan J. Dimond</author>


</item>


<item>
<title>Chapter 21: Administration of Justice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/25</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/25</guid>
<pubDate>Tue, 08 May 2012 13:46:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan J. Dimond</author>


</item>


<item>
<title>Chapter 21: Evidence</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/24</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/24</guid>
<pubDate>Tue, 08 May 2012 13:46:31 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frederick A. McDermott</author>


</item>


<item>
<title>Chapter 20: Evidence</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/24</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/24</guid>
<pubDate>Tue, 08 May 2012 13:46:31 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frederick A. McDermott</author>


</item>


<item>
<title>Chapter 20: Civil Procedure and Practice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/23</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/23</guid>
<pubDate>Tue, 08 May 2012 13:46:29 PDT</pubDate>
<description>
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</description>

<author>Wendell F. Grimes</author>


</item>


<item>
<title>Chapter 19: Civil Procedure and Practice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/23</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/23</guid>
<pubDate>Tue, 08 May 2012 13:46:29 PDT</pubDate>
<description>
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</description>

<author>Wendell F. Grimes</author>


</item>


<item>
<title>Chapter 19: Workmen&apos;s Compensation</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/22</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/22</guid>
<pubDate>Tue, 08 May 2012 13:46:28 PDT</pubDate>
<description>
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</description>

<author>Maurice F. Shaughnessy</author>


</item>


<item>
<title>Chapter 18: Workmen&apos;s Compensation</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/22</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/22</guid>
<pubDate>Tue, 08 May 2012 13:46:28 PDT</pubDate>
<description>
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</description>

<author>Larry Alan Bear</author>


</item>


<item>
<title>Chapter 18: State and Municipal Government</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/21</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/21</guid>
<pubDate>Tue, 08 May 2012 13:46:26 PDT</pubDate>
<description>
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</description>

<author>Joseph C. Duggan</author>


</item>


<item>
<title>Chapter 17: State and Municipal Government</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/21</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/21</guid>
<pubDate>Tue, 08 May 2012 13:46:26 PDT</pubDate>
<description>
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</description>

<author>Joseph C. Duggan</author>


</item>


<item>
<title>Chapter 17: State Taxation</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/20</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/20</guid>
<pubDate>Tue, 08 May 2012 13:46:25 PDT</pubDate>
<description>
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</description>

<author>David Flower Jr.</author>


</item>


<item>
<title>Chapter 16: Insurance</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/20</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/20</guid>
<pubDate>Tue, 08 May 2012 13:46:25 PDT</pubDate>
<description>
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</description>

<author>J. Albert Burgoyne</author>


</item>


<item>
<title>Chapter 15: State Taxation</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/19</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/19</guid>
<pubDate>Tue, 08 May 2012 13:46:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>David Flower Jr.</author>


</item>


<item>
<title>Chapter 16: Insurance</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/19</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/19</guid>
<pubDate>Tue, 08 May 2012 13:46:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J. Albert Burgoyne et al.</author>


</item>


<item>
<title>Chapter 15: Public Utilities</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/18</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/18</guid>
<pubDate>Tue, 08 May 2012 13:46:22 PDT</pubDate>
<description>
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</description>

<author>Herbert Baer</author>


</item>


<item>
<title>Chapter 14: Public Utilities</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/18</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/18</guid>
<pubDate>Tue, 08 May 2012 13:46:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Herbert Baer</author>


</item>


<item>
<title>Chapter 13: Labor Relations</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/17</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/17</guid>
<pubDate>Tue, 08 May 2012 13:46:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Robert M. Segal</author>


</item>


<item>
<title>Chapter 14: Labor Relations</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/17</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/17</guid>
<pubDate>Tue, 08 May 2012 13:46:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Lawrence M. Kearns</author>


</item>


<item>
<title>Chapter 13: Zoning and Land Use</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/16</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/16</guid>
<pubDate>Tue, 08 May 2012 13:46:19 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Richard G. Huber</author>


</item>


<item>
<title>Chapter 12: Zoning and Land Use</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/16</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/16</guid>
<pubDate>Tue, 08 May 2012 13:46:19 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Richard G. Huber</author>


</item>


<item>
<title>Chapter 12: Administrative Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/15</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/15</guid>
<pubDate>Tue, 08 May 2012 13:46:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John P. Clair</author>


</item>


<item>
<title>Chapter 11: Administrative Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/15</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/15</guid>
<pubDate>Tue, 08 May 2012 13:46:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>George N. Welch</author>


</item>


<item>
<title>Chapter 11: Criminal Law, Procedure and Administration</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/14</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/14</guid>
<pubDate>Tue, 08 May 2012 13:46:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sanford J. Fox</author>


</item>


<item>
<title>Chapter 10: Criminal Law, Procedure and Administration</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/14</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/14</guid>
<pubDate>Tue, 08 May 2012 13:46:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sanford J. Fox</author>


</item>


<item>
<title>Chapter 10: Constitutional Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/13</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/13</guid>
<pubDate>Tue, 08 May 2012 13:46:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John D. O&apos;Reilly</author>


</item>


<item>
<title>Chapter 9: Constitutional Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/13</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/13</guid>
<pubDate>Tue, 08 May 2012 13:46:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John D. O&apos;Reilly Jr.</author>


</item>


<item>
<title>Chapter 9: Security and Mortgages</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/12</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/12</guid>
<pubDate>Tue, 08 May 2012 13:46:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Richard G. Huber</author>


</item>


<item>
<title>Chapter 8: Security and Mortgages</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/12</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/12</guid>
<pubDate>Tue, 08 May 2012 13:46:12 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Austin T. Stickells</author>


</item>


<item>
<title>Chapter 8: Conflict of Laws</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/11</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/11</guid>
<pubDate>Tue, 08 May 2012 13:46:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jean E. De Valpine</author>


</item>


<item>
<title>Chapter 7: Domestic Relations and Persons</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/11</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/11</guid>
<pubDate>Tue, 08 May 2012 13:46:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William J. Greenler Jr.</author>


</item>


<item>
<title>Chapter 7: Domestic Relations and Persons</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/10</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/10</guid>
<pubDate>Tue, 08 May 2012 13:46:10 PDT</pubDate>
<description>
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</description>

<author>Monroe Inker</author>


</item>


<item>
<title>Chapter 6: Commercial Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/10</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/10</guid>
<pubDate>Tue, 08 May 2012 13:46:10 PDT</pubDate>
<description>
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</description>

<author>Alfred I. Maleson</author>


</item>


<item>
<title>Chapter 6: Commercial Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/9</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/9</guid>
<pubDate>Tue, 08 May 2012 13:46:08 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alfred I. Maleson</author>


</item>


<item>
<title>Chapter 5: Corporations</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/9</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/9</guid>
<pubDate>Tue, 08 May 2012 13:46:08 PDT</pubDate>
<description>
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</description>

<author>Bertram H. Loewenberg</author>


</item>


<item>
<title>Chapter 5: Corporations and Partnerships</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/8</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/8</guid>
<pubDate>Tue, 08 May 2012 13:46:07 PDT</pubDate>
<description>
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</description>

<author>Cornelius J. Moynihan</author>


</item>


<item>
<title>Chapter 4: Contracts</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/8</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/8</guid>
<pubDate>Tue, 08 May 2012 13:46:07 PDT</pubDate>
<description>
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</description>

<author>J. Edward Collins</author>


</item>


<item>
<title>Chapter 4: Contracts</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/7</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/7</guid>
<pubDate>Tue, 08 May 2012 13:46:05 PDT</pubDate>
<description>
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</description>

<author>J. Edward Collins</author>


</item>


<item>
<title>Chapter 3: Torts</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/7</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/7</guid>
<pubDate>Tue, 08 May 2012 13:46:05 PDT</pubDate>
<description>
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</description>

<author>James W. Smith</author>


</item>


<item>
<title>Chapter 3: Torts</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/6</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/6</guid>
<pubDate>Tue, 08 May 2012 13:46:03 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James W. Smith</author>


</item>


<item>
<title>Chapter 2: Trusts and Estates</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/6</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/6</guid>
<pubDate>Tue, 08 May 2012 13:46:03 PDT</pubDate>
<description>
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</description>

<author>Emil Slizewski</author>


</item>


<item>
<title>Chapter 2: Trusts and Estates</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/5</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/5</guid>
<pubDate>Tue, 08 May 2012 13:46:02 PDT</pubDate>
<description>
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</description>

<author>Emil Slizewski</author>


</item>


<item>
<title>Chapter 1: Property and Conveyancing</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/5</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/5</guid>
<pubDate>Tue, 08 May 2012 13:46:02 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Cornelius J. Moynihan et al.</author>


</item>


<item>
<title>Chapter 1: Property and Conveyancing </title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/4</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/4</guid>
<pubDate>Tue, 08 May 2012 13:46:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William Schwartz</author>


</item>


<item>
<title>Table of Contents</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/4</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/4</guid>
<pubDate>Tue, 08 May 2012 13:46:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Table of Contents</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/3</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/3</guid>
<pubDate>Tue, 08 May 2012 13:45:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Summary of Contents</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/3</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/3</guid>
<pubDate>Tue, 08 May 2012 13:45:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Summary of Contents</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/2</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/2</guid>
<pubDate>Tue, 08 May 2012 13:45:57 PDT</pubDate>
<description>
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Foreword</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/2</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/2</guid>
<pubDate>Tue, 08 May 2012 13:45:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bailey Aldrich</author>


</item>


<item>
<title>Masthead</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/1</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1960/iss1/1</guid>
<pubDate>Tue, 08 May 2012 13:45:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Masthead</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/1</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1959/iss1/1</guid>
<pubDate>Tue, 08 May 2012 13:45:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>State Versus Federal Government in the Regulation of Immigration: Examining the Constitutionality of Arizona and Alabama’s Immigration Laws</title>
<link>http://scholarworks.sjsu.edu/etd_projects/220</link>
<guid isPermaLink="true">http://scholarworks.sjsu.edu/etd_projects/220</guid>
<pubDate>Tue, 08 May 2012 13:32:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sadaf Siddiq</author>


</item>


<item>
<title>IMPROVING YOUR PUBLICATION STRATEGY: A Two Part Series (Session 1)</title>
<link>http://aisel.aisnet.org/success_strategies/7</link>
<guid isPermaLink="true">http://aisel.aisnet.org/success_strategies/7</guid>
<pubDate>Tue, 08 May 2012 13:27:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kalle Lyytinen et al.</author>


</item>


<item>
<title>IMPROVING YOUR PUBLICATION STRATEGY - Session 2</title>
<link>http://aisel.aisnet.org/success_strategies/6</link>
<guid isPermaLink="true">http://aisel.aisnet.org/success_strategies/6</guid>
<pubDate>Tue, 08 May 2012 13:27:58 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kalle Lyytinen et al.</author>


</item>


<item>
<title>Transepithelial D-glucose and D-fructose Transport Across Lobster Intestine</title>
<link>http://digitalcommons.unf.edu/etd/199</link>
<guid isPermaLink="true">http://digitalcommons.unf.edu/etd/199</guid>
<pubDate>Tue, 08 May 2012 13:26:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>The mechanisms of transepithelial absorption of dietary D-glucose and D-fructose in the American lobster, <em>Homarus americanus</em>, were investigated in this study in order to determine whether sugar transport proteins have been conserved throughout evolution. Whole lobster intestine was isolated and mounted in a perfusion chamber to determine transepithelial mucosal to serosal (MS) and serosal to mucosal (SM) mechanisms of <sup>3</sup>H-D-glucose and <sup>3</sup>H-D-fructose transport across the intestine. Unidirectional MS and SM fluxes were measured by adding variable concentrations of <sup>3</sup>H-D-glucose and <sup>3</sup>H-D-fructose (2.5 to 50uM) to either the perfusate or the bath respectively and sampling the amount of radioactivity that exited the opposite side of the intestine. Both the transepithelial MS and SM transports of <sup>3</sup>H-D-glucose and <sup>3</sup>H-D-fructose were hyperbolic functions of sugar concentration. The net flux of both sugars indicated a net absorption of D-glucose and D-fructose into the serosal compartment. Inhibitory analysis showed that while phloridzin decreased MS <sup>3</sup>H-D-glucose transport via a sodium glucose transport (SGLT 1-like) protein located on the mucosal membrane, <sup>3</sup>H-D-fructose transport was not affected by the drug. Mucosal phloretin decreased MS D-fructose transport but not MS D-glucose transport. Immunohistochemistry analysis revealed the presence of a mucosal GLUT 5 transport protein on the mucosal membrane. Increasing serosal concentrations of phloretin decreased both SM D-glucose and D-fructose transport suggesting the presence of a serosal GLUT 2 used by both sugars. The results of this study support the concept of conserved mechanisms of sugar transport in multicellular animals.</p>

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</description>

<author>Ijeoma Ebelechukwu Obi</author>


</item>


<item>
<title>Misplaced Fidelity</title>
<link>http://scholarship.law.georgetown.edu/facpub/938</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/938</guid>
<pubDate>Tue, 08 May 2012 13:25:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper is a review essay of W. Bradley Wendel's <em>Lawyers and Fidelity to Law</em>, part of a symposium on Wendel's book. Parts I and II aim to situate Wendel's book within the literature on philosophical or theoretical legal ethics. I focus on two points: Wendel's argument that legal ethics should be examined through the lens of political theory rather than moral philosophy, and his emphasis on the role law plays in setting terms of social coexistence in the midst of moral pluralism. Both of these themes lead him to reject viewing legal ethics as an instance of "the problem of role morality." In part III I note the similarity between Wendel's view and that of legal process theorists, and I argue that the view involves too much complacency about the American legal system. Part IV examines the central metaphor of Wendel's book, fidelity to law. I distinguish between two forms of fidelity, personal and interpretive. The former is a relation between persons, while the latter means mimetic accuracy in interpretation, translation, performance of music, portraiture, or other forms of representation. I agree with Wendel's views on the requirement that lawyers exhibit interpretive fidelity toward law, but not personal fidelity. I argue that law is not the kind of thing toward which one can have personal fidelity; rather, the fidelity must be toward other members of the community rather than toward norms as such; and in cases where the law systematically discriminates, or is otherwise systematically unjust, the bonds of reciprocity grounding such a relation are absent, and the kind of unconditional obedience to law that Wendel supports is unjustified. Part V asks where, on Wendel’s view, the morality went. I argue that Wendel's view, which derives from but modifies Joseph Raz's analysis of legal authority as exclusionary reasons, does not succeed—either it begs the question of whether law actually provides exclusionary reasons or, if (as Wendel suggests) the reasons are not wholly exclusionary, Raz’s two levels of reasoning collapse into one, and acting on moral grounds is not in fact excluded by legal authority. I then turn to Wendel's ideas about "moral remainders"—the moral costs that acting on his view of legal ethics may inflict on others. Wendel suggests that some form of atonement can cancel the moral remainder, but I am skeptical that his proposal—atoning through law reform activities—can do the job.</p>

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</description>

<author>David Luban</author>


</item>


<item>
<title>Paradoxical Communication in Office Space</title>
<link>http://digitalcommons.library.umaine.edu/etd/1035</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1035</guid>
<pubDate>Tue, 08 May 2012 13:21:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study explores the phenomenon of paradoxical communication in Office Space. Office Space is a humorous film about several employees who work at a software company called Initech. The film offers many examples of how paradoxical communication functions in an organizational setting and is easily understood by various audiences, specifically those who work in an office setting. The examples in Office Space fall into two categories of paradoxical communication, including the managementemployee paradox and paradoxes of race. This study uses semiotics to analyze the examples in the film. Ultimately, this study attempts to answer the following questions: why is a communication perspective of paradox important and what does this perspective have to offer to the meaning or understanding of paradox? How does paradox function in an organizational setting and how does paradox affect the relationships of those involved in organizational paradox? The study is broken down into four separate chapters. The first chapter introduces the film and follows with a literature review that addresses the foundations of paradox, the importance of context in paradox, and an explanation of paradox in organizations. The second chapter explores semiotics as a method to analyze paradox specifically focusing on signs, codes, signification systems, and ways to identify paradox in the film. Chapter three uses semiotics to analyze the management-employee and racial paradoxes in the film. Finally, chapter four offers conclusions about the communication perspective of paradox, functions of paradox as a communication phenomenon, and insight into further study of paradox.</p>

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</description>

<author>Nikole R. Bonenberger</author>


</item>


<item>
<title>Why Minorities Will Decide the 2012 U.S. Election</title>
<link>http://digitalcommons.library.unlv.edu/brookings_pubs/20</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/brookings_pubs/20</guid>
<pubDate>Tue, 08 May 2012 13:19:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>With Republican Mitt Romney now his party’s presumptive presidential nominee, both his campaign and President Obama’s re-election effort are barnstorming the nation for votes.</p>

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</description>

<author>William H. Frey</author>


</item>


<item>
<title>Mapping U.S. Civic Engagement Discourse: A Geo-Critical Rhetorical Wandering</title>
<link>http://digitalcommons.library.umaine.edu/etd/1034</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1034</guid>
<pubDate>Tue, 08 May 2012 13:16:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>This is a geo-critical wandering into U.S. civic engagement discourse. It is an exploration that uses a hybrid critical and geographical methodology by which to approach U.S. civic engagement discourse. The geo-critical approach is an idiosyncratic combination of historical and spatial orientations that is suited to excavate the historical strata and depth of discourse, as well as the fluctuating, "ahistorical," and "superficial" surface of discourse. From this geo-critical approach this thesis seeks to identify, explore and disturb the ideological structures and potential discursive arrangements that guide and warrant our contemporary understanding and practice of U.S. civic engagement. This thesis attempts to interrogate these structures and arrangements through a combination of ideographic analysis (McGee, 1980) and memetic analysis (Dawkins, 1988; Johnson, 2007). Consisting of an ideographic analysis of three historical and conceptual structures that contain contemporary U.S. civic identity and action, and a supplementary ideographic and memetic analysis of Rock the Vote, a replicating structure on the surface of U.S. civic engagement discourse, this experimentation of methods is productive and indicates that ideographic and memetic analysis are supplementary and complementary. A geo-critical perspective and unique combination of critical and geographical methods, such as the ideograph and meme, is better suited to provide an agile approach, tools, and concepts to interrogate fluid and fragmented contemporary U.S. civic engagement discourse and thus expands "the capacity to represent a wider segment of society and their values" (Deetz, 596).</p>

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</description>

<author>Scott Tulloch</author>


</item>


<item>
<title>DigitalCommons Update for UNL Libraries All-Staff Meeting, May 8, 2012</title>
<link>http://digitalcommons.unl.edu/library_talks/80</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/library_talks/80</guid>
<pubDate>Tue, 08 May 2012 13:15:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Republic of Nauru</p>
<p>More Faraway Places</p>
<p>Most Frequent Visitors</p>
<p>January–April 2012 Totals</p>
<p>What do they want ?</p>
<p>We’re (still) #2 !</p>
<p>We’re now doing Books !</p>

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</description>

<author>Paul Royster</author>


</item>


<item>
<title>A Growing Obsession: An Idealogical Critique of the War on Obesity &amp; Big Medicine</title>
<link>http://digitalcommons.library.umaine.edu/etd/1033</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1033</guid>
<pubDate>Tue, 08 May 2012 13:12:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this project I undertake a rhetorical and ideological criticism of The Learning Channel's (TLC) popular new program, Big Medicine (2007). Approaching this analysis from a critical/cultural studies perspective grounded in feminist theory I explore the gendered and racialized hierarchies established by the program through its representations of gastric bypass surgery candidates and their ability/inability to cope with radically changing their bodies and lives. I argue that Big Medicine (2007) relies on the rhetoric of America's "obesity epidemic" in order to justify the treatment of its "unfit" patients and works to position its successful patients as good cultural citizens. In order to do make this argument I examine the social context in which Big Medicine was created through a historical consideration of diet and weight loss policies created in the U.S. in the 20th and 21st centuries. Following this I enact a discursive ideological critique to further interrogate the social ramifications of Big Medicine and focus on the show's potential "social and political goals" (Hart & Daughton, 2005, p.309). Finally, I conduct a thorough close-textual analysis of the program with focus on the mise-en-scene, cinematography, and narrative of the selected episodes. Through this close textual analysis I explore the implications of representing fatness and weight loss on mainstream U.S. television through the lens of this specific program. Through this analysis I conclude that Big Medicine, as an interpellative force, works to (re)establish hierarchies of power regarding race, gender, and socio-economic status by enforcing (literally and figuratively) the "rules" imposed by U.S. hegemony. In order to do so, the show praises patients who "play by the rules" (i.e. middle-upper class whites) and reassures viewers these patients will inevitably see full recovery. Meanwhile, those who do not capitulate to the bulimic nature of U.S. society (i.e. lowerclass, non-whites) are left to suffer and, in some cases, die from the "disease." In illustrating recovery opportunities in this way the show provokes, as LeBesco (2004) explains, the "racist anxieties" that are associated with "big, profusely round bodies" (p.56) and further stigmatizes obese/overweight individuals.</p>

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</description>

<author>Imke Schessler-Jandreau</author>


</item>


<item>
<title>Following the Evangeline Trail: Acadian Identity Performance Across Borders</title>
<link>http://digitalcommons.library.umaine.edu/etd/1032</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1032</guid>
<pubDate>Tue, 08 May 2012 13:08:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>The poem Evangeline: A Tale of Acadie by Henry Wadsworth Longfellow published in 1847, has had an impact on people for generations. The success of the poem was felt not only by its readership but also by the Acadian culture that the poem, and its heroine, came to represent. Evangeline, as character and poem, has evolved in meaning and popularity over the centuries and still plays a role in the cultural performance of contemporary Acadians. This study of Acadian cultural identity utilizes a performance approach that looks at cultural identity as a performative accomplishment in daily life. The analysis first enacts a performance historiography of the Acadian Deportation in 1755, Longfellow's poetic representation of this historical event, and the contemporary context of performing Evangeline in the Acadian diaspora. Next it examines the storytelling performances of narrative interviews with five Acadians. Three of these Acadians still live in the land of Evangeline, in Grand-Pre, Nova Scotia, and the other two live in Maine. Retellings of the story of Evangeline and reflections on the poem and character by each of the participants were analyzed for meanings which form and inform contemporary performances of Acadian cultural identity. The performance methodology allows for meanings to emerge from the embodied Acadian storytelling and to contextualize them in cultural and political spheres. The analysis reflects both differences as well as commonalities in Acadian identity performance, situated in the contexts the participants inhabit on either side of the international border. The story of Evangeline provides a common vocabulary with which participants on both sides of the border were able to address Acadian identity and the significance of the story in their lives. Differences between Canadian Acadian and Acadian-American retellings suggest how specific history and context shape contemporary performances of cultural identity. Similarities in the storytelling of all the participants indicate that despite identity being multiple and fluid over borders, that there is citationality in the narrative performances which allows for the persistence and stability of Acadian cultural identity. Acadian cultural identity is negotiated under specific and changing contexts and situations. What it means to be Acadian changes with audiences as well as with histories. This performative challenge and achievement makes it possible both to be Acadian and, at the same time, to be different from other Acadians in other locations. This study contributes to the study of how these diasporic people hold on to similar values from the past while simultaneously negotiating future performances of cultural identity as the contexts in which they live change.</p>

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</description>

<author>Adrienne Marie Pidacks</author>


</item>


<item>
<title>Beasts of Burgeon: Animality in the Holocaust Menagerie</title>
<link>http://opus.ipfw.edu/comm_facpres/65</link>
<guid isPermaLink="true">http://opus.ipfw.edu/comm_facpres/65</guid>
<pubDate>Tue, 08 May 2012 13:06:40 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Steven A. Carr PhD</author>


</item>


<item>
<title>Military Lawyers and the Two Cultures Problem</title>
<link>http://scholarship.law.georgetown.edu/facpub/937</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/facpub/937</guid>
<pubDate>Tue, 08 May 2012 13:06:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Military and humanitarian lawyers approach the laws of war—labeled “law of armed conflict” by the former and “international humanitarian law” by the latter—in very different ways. For military lawyers, the starting point is military necessity, and the reigning assumption is that legal regulation of war must accommodate military necessity. For humanitarian lawyers, the starting point is human dignity and human rights. This article argues that from these radically different axioms legal consequences systematically follow regarding treaty interpretation, the sources and reach of customary international law, the nature of international law, deference and discretion to military commanders, and the connection between humanitarian law and human rights law. The result is two interpretive communities that systematically disagree not only over the meaning of particular law-of-war norms, but also over the sources and methods of law that could be used to resolve the disagreements. In recent years the differences between these interpretive communities have grown to outright antagonism—the “two cultures problem” in my title. That raises the question of whether military lawyers’ advice should acknowledge any validity to the contrary views of the “humanitarian” community. (The parallel question arises for humanitarian lawyers, but this article focuses on the military side.) The article argues that the decisive accomplishment of the humanitarian approach is the “civilianization” of the laws of war—the recognition that civilian interests matter just as much as military interests. The article then offers a systematic analysis of the concept of military necessity showing that civilian interests must figure in assessing military necessity itself. Even on its own terms, the military version of the law of war should seek to accommodate the civilian perspectives featured in the humanitarian version. The conclusion explores the possibilities of convergence between the military and humanitarian viewpoints.</p>

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</description>

<author>David Luban</author>


</item>


<item>
<title>Yours are the Hands of God</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/387</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/387</guid>
<pubDate>Tue, 08 May 2012 13:04:29 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Melisa Miller</author>


</item>


<item>
<title>Discourse on Race and Racism: A Phenomenological Analysis of Responses to &lt;em&gt;Black.White.&lt;/em&gt;</title>
<link>http://digitalcommons.library.umaine.edu/etd/1031</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1031</guid>
<pubDate>Tue, 08 May 2012 12:53:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>In 2006. a reality television show aired on FX called <em>Black.White.</em>. In the show. the white Wurgel family and the black Sparks family agreed to share a home for six weeks, frequently swapping racial appearance by changing the color of their skin with the help of advanced make-up artists. The Sparks agreed to live a portion of their lives as white people and the Wurgels agreed to live a portion as black people. The two families struggle with the concept of race throughout the series, declaring at times that race is a big deal, while at other times deciding that they are all just people and should be able to make a connection with others despite the color of their skin. This study looks at how the show stimulates discourse about race and racism, by exploring how audiences talk about it. It answers the question: How do people talk about race and racism? The study consists of six separate chapters. The first chapter takes a look at relevant literature surrounding discourse on race and racism. In this chapter I set up four existing tensions commonly found in discourse on race and racism: Tension 1: Natural vs. Social\Historical\Cultural, Tension 2: Individual Attribute vs. Social Structure, Tension 3: Interpretive Approaches vs. Critical Approaches, Tension 4: Text/Representation vs. Embodiment/Performance. The second chapter explains phenomenology as a methodology and explains the focus group processes used in the study. For the study, four focus groups of mixed ethnicities groups watched the first episode of the show, and they were asked a series of open-ended questions to stimulate discussion about the show. Phenomenology was used as a methodology, as participants' lived experiences were observed and recorded while watching the show and throughout the discussions groups. The third, fourth, and fifth chapters contain a description and reduction of my findings. Chapter three is the first grouping of themes where the participants' comments are specifically about the show. Chapter four is the second grouping of themes where participants' articulate lay theories about race and racism. Chapter five is the last description and reduction chapter, and it is the grouping of themes where the participants share their own personal experiences with race and racism. The sixth chapter is the interpretation of my findings, in this chapter 1 touch on the limitations and contributions of my study. I revisit the research in chapter one and introduce some new tensions that I found structuring our discourse on race and racism.</p>

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</description>

<author>Kristen M. Riley</author>


</item>


<item>
<title>The Satanic Phenomenon: Medieval Representations of Satan</title>
<link>http://scholarship.rollins.edu/mls/28</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/28</guid>
<pubDate>Tue, 08 May 2012 12:50:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>This project deals with the one and only character of Satan, revealing him through the eyes of the medieval world. The ever-evolving, interconnectedness of culture, religion, and superstition make for a truly unique theatrical experience in the middle ages. With limited understanding and access to scripture, medieval Christians generated a blended belief system, in order to make sense of the metaphysical world, which manifests itself in medieval drama‟s representations of Satan. While the medieval character of Satan upholds many of the Church‟s teachings about his nature and purpose, he takes on a new persona when left to the dramatic interpretation of the laity, as opposed to the interpretation of the monastic writer, scholar, or prophetic poet. The literary work of Dante and Milton deliver valuable satanic representations, arguably trumping all others, but something essential is lacking there, when compared to the Satan found on the medieval stage, who now resides not in hell, but in the shadow of Dante and Milton‟s Satan.</p>

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</description>

<author>Morgan A. Matos</author>


</item>


<item>
<title>ckn520311p1</title>
<link>http://place.asburyseminary.edu/ecommonsfacultylectures/10</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsfacultylectures/10</guid>
<pubDate>Tue, 08 May 2012 12:48:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>ATS</author>


</item>


<item>
<title>1,3-Bi-9-anthrylpropane</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/15</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/15</guid>
<pubDate>Tue, 08 May 2012 12:47:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The title compound, C<sub>31</sub>H<sub>24</sub>, with three molecules  in the asymmetric unit. The crystal packing is mainly stabilized by weak  C—H⋯π inter­actions in addition to van der Waals forces.</p>

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</description>

<author>Mustafa Arslan et al.</author>


</item>


<item>
<title>The Communication Experience of Relationship Dissolution: A Grounded Theory Approach</title>
<link>http://digitalcommons.library.umaine.edu/etd/1030</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1030</guid>
<pubDate>Tue, 08 May 2012 12:46:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Leslie Baxter (1982) stated it well when she said: "the breaking up of a relationship is a phenomenon known to most and dreaded by all" (p. 223). One can look at the divorce rate in the United States to see that breaking up and disengaging from close relationships is becoming more of the norm than the exception to life in American society. This research examines the multiple roles and aspects of communication through the process of relationship dissolution and is informed by four theoretical approaches: social exhange, attributional, stage model, and relational dialectics. These four theoretical approaches suggest some specific aspects of the communication roles in the process of relationship dissolution. These specific research questions are kept in mind in the approach to and interpretation of interview data; but, a grounded theory approach is taken in this analysis to examine the communication experience of individuals who have engaged in a relational breakup in the past year. The grounded theory approach is used to build a larger, more complex, inter-connected interpretation of the data based on their perceptions of the communication in these relationships. This analysis is designed to provide a more comprehensive and in-depth analysis of the communication than any of these previously developed approaches. The present model of relationship dissolution examines the beginning, middle, and end phases of a relationship. The beginning phase describes the participants' perceptions prior to the point that they become aware of existing problems in their relationship. Communication is focused on defining "us," the future, and the relationship. The three themes that emerge include expectations, honeymoon, and denial. The middle phase describes the participants' perceptions at the point that their frustrations are becoming increasingly problematic and one or both partners express their concerns to the other. Communication is focused on relationship issues, perceptions, concerns, and communication. The four themes that emerge include frustrations and boiling points, questioning the future, relational problems, communication quality. The end phase describes the participants' perceptions starting at the point that at least one of the partners decides to end the relationship and communicates that to the partner. Communication is focused on re-defining identities, expectations, responsibility, and closure. The four themes that emerge include deciding it's over, communicating the breakup, making sense of the breakup, and closure in re-defining the relationship. The present study supports the findings inherent in the theoretical approaches of social exchange, attribution, stage models, and dialectics concerning relationship dissolution. This study further demonstrates how these approaches can be used together to inform and develop the communication aspects that are inherent in the dissolution process.</p>

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</description>

<author>Sandra M. Fetterman</author>


</item>


<item>
<title>title The Impact of Women Managers on Firm Performance: Evidence from Large U.S. Firms</title>
<link>http://digitalcommons.brockport.edu/bus_facpub/11</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/bus_facpub/11</guid>
<pubDate>Tue, 08 May 2012 12:44:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Drawing on arguments from the management and human resource economics literatures, we hypothesise that the percentage of women managers employed in firms will be positively related to the performance of firms. A correlational research design is employed, and 1992 employment and performance data for 183 U.S. firms is utilised in data analysis. The hypothesis is strongly supported.</p>

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</description>

<author>James J. Cordeiro et al.</author>


</item>


<item>
<title>A predictive model for detection of Agrilus planipennis (Col.,
Buprestidae) larvae in girdled ash (Fraxinus spp.)</title>
<link>http://digitalcommons.unl.edu/usdafsfacpub/153</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/usdafsfacpub/153</guid>
<pubDate>Tue, 08 May 2012 12:42:14 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Agrilus planipennis </em>(emerald ash borer, Coleoptera: Buprestidae) is a pest of ash (<em>Fraxinus</em> spp.) in North America and has caused mortality of ash throughout its introduced range. One technique used for detection of <em>A. planipennis </em>is the establishment and peeling of girdled trap trees. In an effort to reduce the search effort and target detection survey efforts within ash trap trees, a predictive model was created using data from 2007 and validated using data from 2008. In 2007 and 2008, ash trap trees were established, harvested, peeled and inspected for <em>A. planipennis </em>larvae. Gaussian curves were fit to describe the relationship between stem diameter and relative proportion and frequency of larvae. The observed and predicted 2008 relative proportion and frequency of larvae did not differ in paired t-tests. Within the relative proportion and frequency Gaussian models, the curves peaked at approximately 10 cm iameter signifying the greatest proportion and frequency of <em>A.</em> <em>planipennis </em>larvae occurred at 10 cm stem diameter. This peak was then bracketed by 2 cm on each side creating a target stem section with a top diameter of 8 cm and a bottom diameter of 12 cm. A simple linear regression was fit to describe the relationship between the larvae count within the targeted 8–12 cm section of tree and the larvae per cm<sup>3 </sup>of phloem per tree for 2007. The observed and predicted 2008 larvae per cm<sup>3 </sup>did not differ in a paired t-test. Targeting the 8–12 cm diameter section of the trap tree stem will reduce the amount of the tree peeled to less than 45% with more than 50% of <em>A. planipennis </em>larvae within the tree encountered in this targeted section. This reduction in the amount of tree peeled will greatly increase the number of trees and area surveyed for <em>A. planipennis </em>detection and population delimiting surveys.</p>

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</description>

<author>J. M. Marshall et al.</author>


</item>


<item>
<title>Orders That Hold</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/386</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/386</guid>
<pubDate>Tue, 08 May 2012 12:40:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bob Stamps</author>


</item>


<item>
<title>Detecting Inconsistencies in Private Data with Secure Function Evaluation</title>
<link>http://docs.lib.purdue.edu/cstech/1758</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1758</guid>
<pubDate>Tue, 08 May 2012 12:36:30 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Nilothpal Talukder et al.</author>


</item>


<item>
<title>vSlicer: Latency-Aware Virtual Machine Scheduling via Differentiated-Frequency CPU Slicing</title>
<link>http://docs.lib.purdue.edu/cstech/1757</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1757</guid>
<pubDate>Tue, 08 May 2012 12:36:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Cong Xu et al.</author>


</item>


<item>
<title>White Box Sampling in Uncertain Data Processing Enabled by Program Analysis</title>
<link>http://docs.lib.purdue.edu/cstech/1756</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1756</guid>
<pubDate>Tue, 08 May 2012 12:36:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Tao Bao et al.</author>


</item>


<item>
<title>CobWeb: A System for Automated In-Network Cobbling of Web Service Traffic</title>
<link>http://docs.lib.purdue.edu/cstech/1755</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1755</guid>
<pubDate>Tue, 08 May 2012 12:35:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Hitesh Khandelwal et al.</author>


</item>


<item>
<title>An ensemble model for collective classification that reduces learning and inference variance</title>
<link>http://docs.lib.purdue.edu/cstech/1754</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1754</guid>
<pubDate>Tue, 08 May 2012 12:35:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Hoda Eldardiry et al.</author>


</item>


<item>
<title>Who&apos;s Afraid of Virginia Woolf</title>
<link>http://opus.ipfw.edu/theatre_facperform/109</link>
<guid isPermaLink="true">http://opus.ipfw.edu/theatre_facperform/109</guid>
<pubDate>Tue, 08 May 2012 12:34:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Production of Edward Albee's play "Who's Afraid of Virginia Woolf".</p>

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</description>

<author>John O&apos;Connell</author>


</item>


<item>
<title>All My Sons</title>
<link>http://opus.ipfw.edu/theatre_facperform/108</link>
<guid isPermaLink="true">http://opus.ipfw.edu/theatre_facperform/108</guid>
<pubDate>Tue, 08 May 2012 12:34:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>A performance of Arthur Miller's classic play, All My Sons</p>

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</description>

<author>John O&apos;Connell</author>


</item>


<item>
<title>The Good Person of Szechuan</title>
<link>http://opus.ipfw.edu/theatre_facperform/107</link>
<guid isPermaLink="true">http://opus.ipfw.edu/theatre_facperform/107</guid>
<pubDate>Tue, 08 May 2012 12:34:04 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Craig A. Humphrey</author>


</item>


<item>
<title>The Pot Boiler/The Real Inspector Hound</title>
<link>http://opus.ipfw.edu/theatre_facperform/106</link>
<guid isPermaLink="true">http://opus.ipfw.edu/theatre_facperform/106</guid>
<pubDate>Tue, 08 May 2012 12:34:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Craig A. Humphrey</author>


</item>


<item>
<title>Purely Dance 2011</title>
<link>http://opus.ipfw.edu/theatre_facperform/105</link>
<guid isPermaLink="true">http://opus.ipfw.edu/theatre_facperform/105</guid>
<pubDate>Tue, 08 May 2012 12:33:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Craig A. Humphrey</author>


</item>


<item>
<title>All My Sons</title>
<link>http://opus.ipfw.edu/theatre_facperform/104</link>
<guid isPermaLink="true">http://opus.ipfw.edu/theatre_facperform/104</guid>
<pubDate>Tue, 08 May 2012 12:33:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Craig A. Humphrey</author>


</item>


<item>
<title>Network Similarity Decomposition (NSD): A Fast and Scalable Approach to Network Alignment</title>
<link>http://docs.lib.purdue.edu/cstech/1753</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1753</guid>
<pubDate>Tue, 08 May 2012 12:25:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Giorgos Kollias et al.</author>


</item>


<item>
<title>Structured Comparative Analysis of Systems Logs to Diagnose Performance Problems</title>
<link>http://docs.lib.purdue.edu/cstech/1752</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1752</guid>
<pubDate>Tue, 08 May 2012 12:25:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Karthik Nagaraj et al.</author>


</item>


<item>
<title>Accentuating the Positive: Atomicity Inference and Enforcement Using Correct Executions</title>
<link>http://docs.lib.purdue.edu/cstech/1751</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1751</guid>
<pubDate>Tue, 08 May 2012 12:25:30 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Dasarath Weeratunge et al.</author>


</item>


<item>
<title>The TCP Outcast Problem: Exposing Unfairness in Data Center Networks</title>
<link>http://docs.lib.purdue.edu/cstech/1750</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1750</guid>
<pubDate>Tue, 08 May 2012 12:25:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Pawan Prakash et al.</author>


</item>


<item>
<title>1,4-Di-9-anthrylbutane</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/14</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/14</guid>
<pubDate>Tue, 08 May 2012 12:25:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the title compound, C<sub>32</sub>H<sub>26</sub>, the molecule has an  inversion centre at the mid-point of the central C—C bond. Weak  intermolecular C—H...π interactions help to stabilize the crystal  structure.</p>

	]]>
</description>

<author>Mustafa Arslan et al.</author>


</item>


<item>
<title>Consumer-directed health care</title>
<link>http://iris.lib.neu.edu/slaw_fac_pubs/93</link>
<guid isPermaLink="true">http://iris.lib.neu.edu/slaw_fac_pubs/93</guid>
<pubDate>Tue, 08 May 2012 12:25:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>You won’t hear many health experts claim that the American <br>healthcare system is functioning perfectly in terms of core considerations <br>such as cost, access, and quality. The question that arises with <br>the advent of any new policy approach seeking to improve the system <br>is obvious: Does the change represent a step forward or backward? <br>Professors Kristin Madison and Peter Jacobson take up this question in <br>regard to the latest innovation in health care policy—consumer-directed <br>healthcare (CDHC). <br><br>Professor Madison argues that while CDHC is not a panacea, <br>“[e]ven if its shortcomings prevent its full diffusion through the <br>American health care system, CDHC will still . . . help[] to establish a <br>foundation for future reforms in health care finance and delivery, <br>[and] has the potential to improve the health care system in the long <br>run.” Professor Jacobson’s response? “CDHC is a direct attack on the <br>idea that health care differs from other market commodities because <br>of its moral aspirations . . . . For those who believe that equity should <br>be a fundamental attribute of health care delivery, CDHC represents a <br>huge step backwards.” Nonetheless, Professor Madison is convinced <br>that CDHC will be a lightning rod that stirs the American health care <br>system out of its complacency and “forces us to confront the tradeoffs <br>inherent in any health care system in a resource-constrained world.” <br>Professor Jacobson is not content to wait and see how the American <br>public reacts to CDHC: “If the policy focus is on CDHC, equity will be <br>subordinated. If universal coverage dominates, CDHC proponents <br>are probably right that cost and quality issues will be subordinate. For <br>me, it’s an easy choice—helping those without insurance to have a <br>minimal acceptable level of care.”</p>

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</description>

<author>Kristin M. Madison et al.</author>


</item>


<item>
<title>Featherweight Threads for Communication</title>
<link>http://docs.lib.purdue.edu/cstech/1749</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1749</guid>
<pubDate>Tue, 08 May 2012 12:25:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>KC Sivaramakrishnan et al.</author>


</item>


<item>
<title>Privacy Preserving Regression Residual Analysis</title>
<link>http://docs.lib.purdue.edu/cstech/1748</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1748</guid>
<pubDate>Tue, 08 May 2012 12:25:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Ross Wallrabenstein et al.</author>


</item>


<item>
<title>Network Sampling via Edge-based Node Selection with Graph Induction</title>
<link>http://docs.lib.purdue.edu/cstech/1747</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1747</guid>
<pubDate>Tue, 08 May 2012 12:24:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Nesreen Ahmed et al.</author>


</item>


<item>
<title>Geometric Interoperability for Resilient Manufacturing</title>
<link>http://docs.lib.purdue.edu/cstech/1746</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1746</guid>
<pubDate>Tue, 08 May 2012 12:24:50 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Christoph M. Hoffmann et al.</author>


</item>


<item>
<title>Opportunistic Flooding to Improve TCP Transmit Performance in Virtualized Clouds</title>
<link>http://docs.lib.purdue.edu/cstech/1745</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1745</guid>
<pubDate>Tue, 08 May 2012 12:24:42 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sahan Gamage et al.</author>


</item>


<item>
<title>Leave Them Microseconds Alone: Scalable Architecture for Maintaining Packet Latency Measurements</title>
<link>http://docs.lib.purdue.edu/cstech/1744</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1744</guid>
<pubDate>Tue, 08 May 2012 12:24:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Myungjin Lee et al.</author>


</item>


<item>
<title>Using Past Queries for Resource Selection in Distributed Information Retrieval</title>
<link>http://docs.lib.purdue.edu/cstech/1743</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1743</guid>
<pubDate>Tue, 08 May 2012 12:24:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sulleyman Cetintas et al.</author>


</item>


<item>
<title>On the Efficacy of Fine-Grained Traffic Splitting Protocols in Data Center Networks</title>
<link>http://docs.lib.purdue.edu/cstech/1742</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1742</guid>
<pubDate>Tue, 08 May 2012 12:24:18 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Advait Dixit et al.</author>


</item>


<item>
<title>Methods to Determine Node Centrality and Clustering in Graphs with Uncertain Structure</title>
<link>http://docs.lib.purdue.edu/cstech/1741</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1741</guid>
<pubDate>Tue, 08 May 2012 12:24:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph J. Pfeiffer III et al.</author>


</item>


<item>
<title>Query Processing in Private Data Outsourcing Using Anonymization</title>
<link>http://docs.lib.purdue.edu/cstech/1740</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1740</guid>
<pubDate>Tue, 08 May 2012 12:24:02 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ahmet Erhan Nergiz et al.</author>


</item>


<item>
<title>c-Lock: Dynamic Lock-coalescing for Latency-sensitive Distributed Locking</title>
<link>http://docs.lib.purdue.edu/cstech/1739</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1739</guid>
<pubDate>Tue, 08 May 2012 12:23:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Adnan Hassan et al.</author>


</item>


<item>
<title>Sparse Matrix-variate t Process Blockmodels</title>
<link>http://docs.lib.purdue.edu/cstech/1738</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1738</guid>
<pubDate>Tue, 08 May 2012 12:23:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Zenglin Xu et al.</author>


</item>


<item>
<title>Player Piano Piano Player Piano Player Player Piano</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/254</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/254</guid>
<pubDate>Tue, 08 May 2012 12:21:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>A mid-century player piano retrofitted into a switchboard.  11,000 feet of wire, linking 88 devices around a six thousand square foot barn, back to the 88 keys of the piano.  Fans, lights, drills, and saws connected, each with its own note.  And lastly a piano player to bring it to life.  As each note rings out it lights a bulb or drives a motor.  Not a new instrument, but a new experience of the piano, a visual translation of musical interaction.</p>
<p>In this way I hope that I might present to the viewer an entry into some of the experience that I have with playing pianos in general.  I am not a pianist by any means, but I do love to play the piano.  Letting my fingers move across the keyboard, finding notes and embellishing chords, is a great mode of meditation for me, for which I have taken advantage of the Chapel and Bard Hall for the last four years.  It was my aim that each light bulb, drill, and fan would serve as a visual marker of the exploration I embark on at any piano.  As notes unfold from this piano, they are accompanied and bolstered by each electronic device.  Not only is each note aurally unique, as they have always been, but now each note comes with its own function, furthering the potential scope and impact of any given key.<br>        Lastly, through watching the piano player play the piano, or by playing it oneself, I hope that the distance and difference between the piano and the player becomes more thoroughly illuminated.  There are a great many things that the piano, the machine itself, is capable of doing, ways in which it enables it's user to create, and this is brought into relief by the person playing, as they themselves are capable certain things, excelling at some and distorting others. Each individual brings their own style and personality to the act of playing, which results in an entirely different event, even if the notes were entirely the same.  This installation is an attempt to provide an environment for the extension and inspection of this dichotomy.  As I hope my title illuminates, I hope to bring into question which party is controlling which.  Is it the pianist playing the piano, a passive entity, or can it also be the piano allowing or forcing the player to act or perform in its own right.</p>

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</description>

<author>Aaron L. Rogachevsky</author>


</item>


<item>
<title>Signals From Babel: The Influence of Jorge Luis Borges on Metafiction of the Late Twentieth Century</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/253</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/253</guid>
<pubDate>Tue, 08 May 2012 12:21:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>This project examines of the influence of Jorge Luis Borges's approach to the philosophy of George Berkeley on metafictional works by Italo Calvino, Vladimir Nabokov, and Kathy Acker.</p>

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</description>

<author>Emma Stamm</author>


</item>


<item>
<title>Seneca to Shakespeare: Tracking the Influence of Tragedy</title>
<link>http://digitalcommons.bard.edu/senproj_s2011/252</link>
<guid isPermaLink="true">http://digitalcommons.bard.edu/senproj_s2011/252</guid>
<pubDate>Tue, 08 May 2012 12:21:10 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Seneca to Shakespeare</em> examines the English playwright's earliest influence in his tragic compositions. Seneca's effects on Shakespeare can be seen in his themes, psychology of characters, and even in his rich rhetoric. Seneca's early Roman plays launch the art of tragedy in the Elizabethan era.</p>

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</description>

<author>David Wiley</author>


</item>


<item>
<title>Bis(9-ethyl­carbazol-3-yl)methane</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/13</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/13</guid>
<pubDate>Tue, 08 May 2012 12:18:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the title compound, C<sub>29</sub>H<sub>26</sub>N<sub>2</sub>, the  carbazole ring systems are essentially planar. There is no indication of  π–π interactions in the crystal structure, adjacent carbazole groups  being non-parallel.</p>

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</description>

<author>Erol Asker et al.</author>


</item>


<item>
<title>Living the Future 2012: Educational Role of Libraries</title>
<link>http://digitalcommons.library.unlv.edu/libfacpresentation/83</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/libfacpresentation/83</guid>
<pubDate>Tue, 08 May 2012 12:17:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jennifer L. Fabbi et al.</author>


</item>


<item>
<title>9,9′-Diethyl-3,3′-di-9H-carbazol­yl</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/12</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/12</guid>
<pubDate>Tue, 08 May 2012 12:12:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the title compound, C<sub>28</sub>H<sub>24</sub>N<sub>2</sub>, the  carbazole ring systems are essentially planar to within 0.076 (3) Å. The  dihedral angle between the planes of the ring systems is 40.38 (4)°.  The contribution of inter­molecular π–π inter­actions to the mol­ecular  stacking is observed.</p>

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</description>

<author>Erol Asker et al.</author>


</item>


<item>
<title>Switzerland&apos;s nation branding initiative to foster science and technology, higher education and innovation: A case study</title>
<link>http://scholarship.rollins.edu/as_facpub/42</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/as_facpub/42</guid>
<pubDate>Tue, 08 May 2012 12:12:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>This article presents a case study about Switzerland's initiative to promote its science and technology, higher education and innovation environment. This is accomplished through a worldwide network of science and technology outposts run by the Swiss State Secretariat for Education and Research in cooperation with the Federal Department of Foreign Affairs. In this article, we specifically discuss the outpost located in Boston. <em>swissnex</em> Boston acts as a physical and virtual environment to foster closer ties between Switzerland and the Boston region in various fields of interest to academia, industry, business and society. We present the history and mission of <em>swissnex</em> Boston, its role and organizational structure, and a benchmarking analysis of other nations’ initiatives. We further discuss the required leadership and performance measurement of <em>swissnex</em> Boston and the main challenges it has surmounted in its 10 years of operation.</p>

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</description>

<author>Marc Fetscherin et al.</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 34</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/75</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/75</guid>
<pubDate>Tue, 08 May 2012 12:09:37 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 33</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/74</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/74</guid>
<pubDate>Tue, 08 May 2012 12:09:33 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 32</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/73</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/73</guid>
<pubDate>Tue, 08 May 2012 12:09:28 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

	]]>
</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 31</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/72</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/72</guid>
<pubDate>Tue, 08 May 2012 12:09:25 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p>This image captures the sculpture as it begins to topple over.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 30</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/71</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/71</guid>
<pubDate>Tue, 08 May 2012 12:09:22 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><strong><em>Photographer's Notes</em></strong></p>
<p>Onlookers bask in the heat and glow from the burning sculpture.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>On Filling Jars with Water</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/385</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/385</guid>
<pubDate>Tue, 08 May 2012 12:08:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joe Dongell</author>


</item>


<item>
<title>Bis(9-ethyl­carbazol-3-yl)ethane</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/11</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/11</guid>
<pubDate>Tue, 08 May 2012 12:07:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the title compound, C<sub>30</sub>H<sub>28</sub>N<sub>2</sub>, each  carbazole skeleton is essentially planar. The planes of the two  carbazole ring systems are nearly parallel, with a dihedral angle of  2.33 (19)°. The crystal packing is stabilized only by van der Waals  forces and weak C—H⋯π inter­actions.</p>

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</description>

<author>Erol Asker et al.</author>


</item>


<item>
<title>Three-dimensional structure and function of the
&lt;i&gt;Paramecium bursaria&lt;/i&gt; chlorella virus capsid</title>
<link>http://digitalcommons.unl.edu/virologypub/223</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/virologypub/223</guid>
<pubDate>Tue, 08 May 2012 12:03:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>A cryoelectron microscopy 8.5 Å resolution map of the 1,900 Å diameter, icosahedral, internally enveloped <em>Paramecium bursaria</em> chlorella virus was used to interpret structures of the virus at initial stages of cell infection. A fivefold averaged map demonstrated that two minor capsid proteins involved in stabilizing the capsid are missing in the vicinity of the unique vertex. Reconstruction of the virus in the presence of host chlorella cell walls established that the spike at the unique vertex initiates binding to the cell wall, which results in the enveloped nucleocapsid moving closer to the cell. This process is concurrent with the release of the internal viral membrane that was linked to the capsid by many copies of a viral membrane protein in the mature infectous virus. Simultaneously, part of the trisymmetrons around the unique vertex disassemble, probably in part because two minor capsid proteins are absent, causing Paramecium bursaria chlorella virus and the cellular contents to merge, possibly as a result of enzyme(s) within the spike assembly. This may be one of only a few recordings of successive stages of a virus while infecting a eukaryotic host in pseudoatomic detail in three dimensions.</p>
<p>Includes supporting information.</p>

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</description>

<author>Xinzheng Zhang et al.</author>


</item>


<item>
<title>Performative Writing in Performance Studies: Filling in Missing Spaces</title>
<link>http://digitalcommons.library.umaine.edu/etd/1029</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1029</guid>
<pubDate>Tue, 08 May 2012 11:59:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis explores the alternative writing practice known as performative writing as it is enacted within the domain of performance studies. Using Robert Scholes's explication of textual power, I read, interpret, and criticize selected texts of performative writing. I argue that the textual power of performative writing creates spaces of dialogue and resistance through, in part, the indeterminacy and evocativeness of its content. I further explore performative writing by engaging in its practice. Throughout the thesis I create alternative and parallel texts that intersect, overlap, and resist the more traditionally academic portions of the work. These sections are written as letters and side conversations that seek to create self-reflexivity and a reflective relationship of performance and performativity to writing.</p>

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</description>

<author>Margaret A. Haberman</author>


</item>


<item>
<title>9-Ethyl-3-(9H-9-ethyl­carbazol-3-yl)-4-nitro­-9H-carbazole</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/10</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/10</guid>
<pubDate>Tue, 08 May 2012 11:59:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the mol­ecule of the title compound, C<sub>28</sub>H<sub>23</sub>N<sub>3</sub>O<sub>2</sub>,  the nitro group is almost perpendicular to the carbazole ring to which  it is attached. The crystal packing is determined by C—H⋯O and π–π  inter­actions, where the nitrated carbazole ring of one mol­ecule  associates in a shifted parallel planar orientation with the  centrosymmetrically related non-nitrated carbazole ring of a  neighbouring mol­ecule.</p>

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</description>

<author>Erol Asker et al.</author>


</item>


<item>
<title>Sudden Death in Sport at the Secondary School Level:  A Perspective of the Head Football Coach</title>
<link>http://digitalcommons.uconn.edu/gs_theses/245</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/245</guid>
<pubDate>Tue, 08 May 2012 11:59:01 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Context:</strong> Prior research has examined the first aid knowledge and decision making among high school coaches, but little is known about their knowledge of sudden death in sport or their relationship with an athletic trainer. <strong>Objective: </strong>Evaluate the knowledge of the secondary school football coach regarding sudden death in sport and their relationship with their athletic trainer.<strong> Results:</strong> There were four themes from the data: <em>level of preparedness</em>, <em>misconceptions about sudden death in sport, activity modification strategies</em>, and <em>positive coach/athletic trainer relationships</em>. <strong>Conclusion:</strong> The secondary coach is unaware of the potential causes of sudden death in sport and symptoms associated with conditions of sudden death. Athletic trainers working with the secondary coach can have a positive influence on their implementation of strategies to prevent sudden death</p>

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</description>

<author>Benjamin McGrath</author>


</item>


<item>
<title>Hip Abductor Strength and Hip External Rotator Strength Effects on Medial Knee Displacement in Post Pubescent Females</title>
<link>http://digitalcommons.uconn.edu/gs_theses/244</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/244</guid>
<pubDate>Tue, 08 May 2012 11:58:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>ABSTRACT</p>
<p>Hip Abductor Strength and Hip External Rotator Strength Effects on Medial Knee Displacement in Post-Pubescent Females</p>
<p>Megan A. Barry, University of Connecticut</p>
<p><strong>Purpose</strong>: The purpose of the study was to investigate the relationship between hip abductor (ABD) and hip external rotator (ER) strength with medial knee displacement (MKD) when in post-pubescent high school female athletes.</p>
<p><strong>Methods</strong>: Twenty-five post-pubescent high school female athletes (age= 16 ±1, mass= 58.6 kg ± 7.4 kg, height= 166 cm ± 8 cm) volunteered to participate in this study. Maximal isometric hip ABD and ER strength were measured using hand-held dynamometry, and MKD was assessed during a standardized jump-landing task using three-dimensional motion analysis. Participants were instructed to jump off a box, land, and immediately jump upwards for maximal height. Separate correlations were conducted to evaluate the relationship between hip ABD strength and hip ER strength with MKD. Linear regression with forced entry was performed to evaluate if hip ABD and/or hip ER strength significantly predicted MKD.</p>
<p><strong>Results</strong>: Neither hip ABD (r=-0.24, p=0.26) nor hip ER (r=-0.007, p=0.97) strength were significantly correlated with MKD or significantly predicted MKD (R<sup>2</sup>=0.11, p=0.28) in post-pubescent females.</p>
<p><strong>Conclusions</strong>: We found that hip ABD strength and hip ER strength are not significant predictors of MKD. We conclude that increasing hip strength alone is insufficient to prevent ACL and other lower extremity injuries. Strength training of the hip musculature may still need to be addressed in prevention and rehabilitation programs, but should also be combined with teaching proper neuromuscular control through balance, plyometrics, and sport-specific exercises.</p>

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</description>

<author>Megan A. Barry</author>


</item>


<item>
<title>Examining Which Factors Influence the Drinking Culture on College Campuses</title>
<link>http://digitalrepository.trincoll.edu/theses/232</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/232</guid>
<pubDate>Tue, 08 May 2012 11:56:31 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Aaron Westbrooks</author>


</item>


<item>
<title>Differences in Black and White Satisfaction at a Predominantly White Institution</title>
<link>http://digitalrepository.trincoll.edu/theses/231</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/231</guid>
<pubDate>Tue, 08 May 2012 11:56:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Carla Thompkins</author>


</item>


<item>
<title>Who Mentors? Student Involvement and Perceptions of Hartford</title>
<link>http://digitalrepository.trincoll.edu/theses/230</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/230</guid>
<pubDate>Tue, 08 May 2012 11:56:19 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Rachel McHugh</author>


</item>


<item>
<title>Teachers’ Expectations of Middle School Students</title>
<link>http://digitalrepository.trincoll.edu/theses/229</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/229</guid>
<pubDate>Tue, 08 May 2012 11:56:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Melissa Harris</author>


</item>


<item>
<title>Single Sex versus Coeducational Colleges: Who wins the self-esteem battle?</title>
<link>http://digitalrepository.trincoll.edu/theses/228</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/228</guid>
<pubDate>Tue, 08 May 2012 11:56:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Maria Dixon</author>


</item>


<item>
<title>10,10′-Dinitro-10,10′-(propane-1,3-di­yl)di-10H-anthracen-9-one</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/9</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/9</guid>
<pubDate>Tue, 08 May 2012 11:54:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>The title compound, C<sub>31</sub>H<sub>22</sub>N<sub>2</sub>O<sub>6</sub>, was obtained as the decomposition product of (<em>E</em>,<em>E</em>)-1,3-bis­[9,10-dihydro-9-nitro-10-(trinitro­meth­yl)-9-anthr­yl]propane, which was synthesized <em>via</em> a photochemical reaction of 1,3-di-9-anthrylpropane with  tetra­nitro­methane. Inter­molecular C—H⋯O inter­actions are the most  prominent features of the crystal packing; no indications of any  inter­molecular π–π stacking were found.</p>

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</description>

<author>Mustafa Arslan et al.</author>


</item>


<item>
<title>Community: To What End?</title>
<link>http://epublications.marquette.edu/theo_fac/126</link>
<guid isPermaLink="true">http://epublications.marquette.edu/theo_fac/126</guid>
<pubDate>Tue, 08 May 2012 11:53:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Stephen D. Long</author>


</item>


<item>
<title>Environmental Values and Conflict: The Decision-Making Process and Environmental Communication for a Town-Owned Ski Area in the Northeast</title>
<link>http://digitalcommons.library.umaine.edu/etd/1028</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1028</guid>
<pubDate>Tue, 08 May 2012 11:53:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper is a case study analyzing the decision-making process for a small, town-owned ski area in Maine to determine the place of environmental sustainability within it. Key decision-making players are identified and interviewed to determine the environmental knowledge they hold and the ways this knowledge figures into town decisions. Decision-makers are also asked about their views on public participation, a critical element for decisions directly affecting communities. Information gathered through these key interviews is then compared to an analysis of public documents, revealing gaps between decision-maker intentions and sound policy. The community in which the object of analysis resides has unique qualities not only because it owns and operates a ski area but also because it has a strong positive orientation towards the environment. This study discovers that despite community dedication to the environment, environmental awareness is only minimally driven from within the system and is instead steered by external interest groups that apply the pressure needed to create environmental change. Economic issues are consistent decision criterion and environmental issues are only occasional criterion due to a lack of formal policy for the inclusion of environmental topics in town decision-making, In addition to the need to consistently address environmental issues within the town decision-making structure, citizen participation remains critical to maintaining a sound decision-making process. This study analyzes recent "community feedback forums" developed by the ski area in efforts to engage the public and receive input on specific redevelopment needs. A common public participation barrier that was observed is decision-maker satisfaction with the quantity of participation opportunities over the quality of participation. The current participation system appears to serve the decisionmaker need to legitimize decisions responsible to the town instead of building a long-term, trust relationship. This study concludes that the ski area, and the town that owns and operates it, have a strong need for formal environmental policy procedures and the need for public participation review procedures. Differences of opinion among decision-makers and inconsistent levels of environmental attention from interest groups make sustainability efforts inconsistent. Formal policy would lessen the burden on these groups to initiate change and would make environmental and economic conflicts more addressable. Decision-maker preference for voting and other quantity-based forms of public participation hinders organizational trust between the community and the ski area and town. Organizational trust can be achieved should the town adopt a mode of evaluating both the quantity and quality of public participation and use feedback to improve the participation format. The author commends the ski area and town for their strong commitment to environmental sustainability and preservation of natural resources. The suggestions to improve the decision-making system and public participation process will serve to ensure environmental consciousness in town decision-making over time as issues, key leaders, and groups grow and change. The author suggests the town consult outside assistance in order to make more environmentally minded decisions. The expertise of consulting professionals will lessen the burden on the town of making critical environmental decisions on their own.</p>

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</description>

<author>Peter Ingraham Johnson</author>


</item>


<item>
<title>Grain Quality of Brazilian Maize Genotypes as Influenced by Nitrogen Level</title>
<link>http://digitalcommons.unl.edu/foodsciefacpub/114</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/foodsciefacpub/114</guid>
<pubDate>Tue, 08 May 2012 11:50:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Maize (<em>Zea mays </em>L.) is an important crop in Brazil, and concerns  about grain quality are increasingly important with increasing exports  and use of grain for specific end-uses. A wide range of genotypes are  grown and N application is required to produce high yields. The  objectives of these studies were to: (i) determine N application effects  on the kernel hardness and breakage susceptibility of a wide range  of Brazilian genotypes ranging from dent to flint kernel types and  (ii) determine relationships among kernel hardness and breakage  susceptibility tests, yield and N and oil concentration. Three studies were conducted with a broad range of maize genotypes and N application rates of 0, 60, 120, and 180 kg ha<sup>–1</sup>. Grain was harvested and  yields corrected for water content, and grain was evaluated through  a series of chemical and physical quality tests. Application of 180 kg  ha<sup>–1</sup> N application increased grain yield by 747 to 1466 kg ha<sup>–1</sup>,  increased grain N concentration by 0.9 to 2.4 g kg<sup>–1</sup>, and increased  hardness to a lesser extent, while reducing breakage susceptibility by  1.9 to 6.9%. Genotype had a much larger influence on grain quality  parameters than did N rate. The limited correlation between grain  yield, grain N concentration, and grain oil concentration to kernel hardness suggests that development of further improved genotypes  with high maize yields and excellent drymilling grain quality is feasible  in Brazil. The large variation in grain yield and dry milling grain  quality in intermediate kernel-type (semident, semiflint) genotypes  used in Brazil presents short-term potential to select hybrids that  produce both high yield and good dry milling grain quality.</p>

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</description>

<author>Aildson P. Duarte et al.</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 29</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/70</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/70</guid>
<pubDate>Tue, 08 May 2012 11:50:44 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Political Institutions and Economic Policy: Rural Renter Legislation in Argentina, 1912–1942</title>
<link>http://digitalcommons.unf.edu/beco_facpub/1</link>
<guid isPermaLink="true">http://digitalcommons.unf.edu/beco_facpub/1</guid>
<pubDate>Tue, 08 May 2012 11:50:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The importance of political institutions in the economic performance of developing countries is generally overlooked. Argentine economic development in the 19th and early 20th centuries relied on the production of rural exports. The production structure in agriculture was supported by the widespread use of tenancy contracts. This paper uses spatial analysis and logistic regression to study the role of Congress in shaping tenancy legislation for the period 1912 to 1943. The finding is that legislative reform was a product of how political institutions worked in Congress providing veto power to Conservatives over the proposals of Radicals. Electoral fraud in the 1930s stopped tenancy legislation and gave rise to revolutionary changes in the 1940s.</p>

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</description>

<author>Andrés Alberto Gallo</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 28</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/69</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/69</guid>
<pubDate>Tue, 08 May 2012 11:50:41 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p><em><strong></strong></em>A close-up image of the flames reveals detailed carving work.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 27</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/68</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/68</guid>
<pubDate>Tue, 08 May 2012 11:50:38 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><strong><em>Photographer's Notes</em></strong></p>
<p><em></em>A close-up image of the flames reveals detailed carving work.<strong><br></strong></p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 26</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/67</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/67</guid>
<pubDate>Tue, 08 May 2012 11:50:34 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 25</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/66</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/66</guid>
<pubDate>Tue, 08 May 2012 11:50:30 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p>The central pyre visible in <a href="http://digitalcommons.linfield.edu/avcstud_collab/48/" target="_blank" title="Temple of Inner Fire Collaborative Burn Sculpture 07" >Temple of Inner Fire Collaborative Burn Sculpture 07</a> can be seen directing the path of the flames in this image.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 24</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/65</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/65</guid>
<pubDate>Tue, 08 May 2012 11:50:27 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 23</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/64</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/64</guid>
<pubDate>Tue, 08 May 2012 11:50:22 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 22</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/63</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/63</guid>
<pubDate>Tue, 08 May 2012 11:50:18 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 21</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/62</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/62</guid>
<pubDate>Tue, 08 May 2012 11:50:13 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 20</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/61</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/61</guid>
<pubDate>Tue, 08 May 2012 11:50:09 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012, it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p>Taiko drummers accompany the 2012 collaborative burn ceremony.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Audible Identities: Passing and Sound Technologies</title>
<link>http://ecommons.luc.edu/english_facpubs/5</link>
<guid isPermaLink="true">http://ecommons.luc.edu/english_facpubs/5</guid>
<pubDate>Tue, 08 May 2012 11:48:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>At the March 2008 conference of the Association for Recorded Sound Collections held at Stanford University, audio historians played what they claim is the first recording of the human voice. It is a presumably female voice singing <em>Au clair de la lune</em>, though the distorted quality of the 10-second recording renders the words no more decipherable than the singer’s gender to an untutored ear. The recording was made in Paris in April 1860 on a ‘phonautograph’ invented by Édouard-Léon Scott de Martinville (aka Leon Scott), nearly 20 years before Thomas Edison patented the phonograph in 1877. Sound waves captured by a horn attached to a diaphragm vibrated a stiff brush that inscribed the pattern of waves on blackened paper. Scott wanted to produce a <em>visual</em> inscription of human speech but had not yet conceptualised sound as something that could be <em>audibly</em> reproduced; that would be Edison’s contribution when he replaced Scott’s paper with a more pliable and durable substance: tin foil and later wax cylinders. The recent recovery of Scott’s early inscription foregrounds the historicity of listening itself. As many scholars have pointed out, audition is organised differently by sound technology so that how we hear, not just what we hear, changes. Hearing becomes historical not just physiological; listening becomes technique. A new form of listening entails a new concept of sound itself. ‘Phonautograph’ means, literally, sound writing <em>itself</em> (which is the subtitle of Scott’s 1878 book); thus the term ignores the very machine that is reproducing the voice. ‘Phonautograph’ suggests that the sound is literally <em>there</em>, textually inscribed on the blackened paper, and thus, technically, is not a <em>re</em>-production.</p>
<p>Embedded in Scott’s nomenclature is the germ of the debates that sound technology has aroused in the modernist era over the relative value of—and indeed, the very distinction between—original and copy, live and recorded, authentic and mechanically produced, sincerity and fakery, reproduction and representation. The confusion of those borderlines is graphically presented in the image of the dog with his ear to the horn of the gramophone listening to ‘his master’s voice’ (a trademark first acquired by the London Gramophone Company in 1898 and used by Emile Berliner from 1900), as well as in anecdotes, cartoons, photographs and advertisements from the time in which people mistake the talking machine for a person talking, the mimetic representation for the ‘real thing’. That slippage between the live and the recorded, the original and the copy, is precisely the achievement of sound technology; it is not a mistake but what makes it work. In that slippage lies the key to a new, modernist understanding not just of art in the age of mechanical reproduction, but of subjectivity itself. That kind of slippage is one that I have explored elsewhere in terms of ‘passing’.</p>

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</description>

<author>Pamela L. Caughie</author>


</item>


<item>
<title>10,10′-Dinitro-10,10′-(butane-1,4-di­yl)dianthracen-9(10H)-one</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/8</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/8</guid>
<pubDate>Tue, 08 May 2012 11:47:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The title compound, C<sub>32</sub>H<sub>24</sub>N<sub>2</sub>O<sub>6</sub>, was obtained as the decomposition product of (<em>E</em>,<em>E</em>)-1,4-bis­[9,10-dihydro-9-nitro-10-(trinitro­meth­yl)-9-anthr­yl]butane, which was synthesized <em>via</em> a photochemical reaction of 1,4-bis­(9-anthr­yl)butane with  tetra­nitro­methane. The asymmetric unit contains one half-mol­ecule;  the complete mol­ecule is generated by a center of inversion. The  crystal packing is determined mainly by inter­molecular C—H⋯O  inter­actions.</p>

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</description>

<author>Mustafa Arslan et al.</author>


</item>


<item>
<title>Culinary Tourism with Anthony Bourdain: Cultural Colonialism, Masculinity and the Exotic &quot;Other&quot;</title>
<link>http://digitalcommons.library.umaine.edu/etd/1027</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1027</guid>
<pubDate>Tue, 08 May 2012 11:45:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the following thesis, I examine how chef Anthony Bourdain's popular television program, A Cook's Tour (2001), constructs a mediated touristic gazing experience that encourages a hegemonic and privileged Western worldview. I draw upon Bourdain's 2001 written text of the same name to provide secondary evidence when appropriate. Through an ideological criticism of the television program, I demonstrate the ways in which A Cook's Tour presents and normalizes a neo-colonialist discourse between the Western tourist and the Other, and the subsequent positioning of the Other as an appetizing spectacle. As Lindenfeld (2007) states, these representations of food and eating offer a vicarious experience of food culture and thus comprise part of the rhetorical landscape of US tourism. Viewers have the illusion of experiencing ethnicity without ever coming into contact with actual, potentially fear-invoking racialized bodies. This is an interpretive study of the hegemonic discourses of identity and Otherness as constituted through Bourdain's "Western gaze." The interpretation is grounded in the context of a neo-colonialist history. Popular texts dramatize and legitimate the colonialist power dynamics of the West and the Rest. Douglas Keller (2003) explains that media stories [like A Cook's Tour] "provide the symbols, myths and resources through which we constitute a common culture and through the appropriation of which we insert ourselves into this culture. Media spectacles demonstrate who has the power and who is powerless, who is allowed to exercise force and violence and who is not" (p. 9). Developing a critical understanding of how texts position readers/viewers must always extend to helping students understand the social and cultural contexts of viewers and texts: that is, how others might react to, construct and/or resist textual meanings. Media studies are about language and literacy as much as it is about social and cultural studies (Buckingham, 1993).</p>

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</description>

<author>Amy L. Fagan-Cannon</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 19, no. 1</title>
<link>http://collected.jcu.edu/carrollquarterly/57</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/57</guid>
<pubDate>Tue, 08 May 2012 11:45:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 19, no. 2</title>
<link>http://collected.jcu.edu/carrollquarterly/56</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/56</guid>
<pubDate>Tue, 08 May 2012 11:45:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 19, no. 3 and no. 4</title>
<link>http://collected.jcu.edu/carrollquarterly/55</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/55</guid>
<pubDate>Tue, 08 May 2012 11:45:19 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>Mitofusin2 mutations disrupt axonal mitochondrial positioning and promote axon degeneration</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1032</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1032</guid>
<pubDate>Tue, 08 May 2012 11:43:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Albert L. Misko et al.</author>


</item>


<item>
<title>Thalamocortical dysfunction and thalamic injury after asphyxial cardiac arrest in developing rats</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1031</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1031</guid>
<pubDate>Tue, 08 May 2012 11:43:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Michael Shoykhet et al.</author>


</item>


<item>
<title>Spontaneous activity promotes synapse formation in a cell-type-dependent manner in the developing retina</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1030</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1030</guid>
<pubDate>Tue, 08 May 2012 11:43:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Florentina Soto et al.</author>


</item>


<item>
<title>The sodium channel accessory subunit Navβ1 regulates neuronal excitability through modulation of repolarizing voltage-gated K+ channels</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1029</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1029</guid>
<pubDate>Tue, 08 May 2012 11:43:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Céline Marionneau et al.</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 19</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/60</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/60</guid>
<pubDate>Tue, 08 May 2012 11:43:15 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p>Totem Shriver, adjunct professor of 3D design at Linfield College, prepares to launch a flaming arrow to ignite the 2012 collaborative burn sculpture.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Crop Rotation and Soil Amendment Alters
Sorghum Grain Quality</title>
<link>http://digitalcommons.unl.edu/foodsciefacpub/113</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/foodsciefacpub/113</guid>
<pubDate>Tue, 08 May 2012 11:42:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Soybean [<em>Glycine max </em>(L.) Merr.] rotation enhances grain sorghum [<em>Sorghum bicolor </em>(L.) Moench] yield, but infl uence on grain quality has not been measured. The objective was to determine the effect of cropping sequence (CS) and soil amendment (SA) on grain yield and quality. Sorghum grain yield and quality, soil NO<sub>3</sub>–N and water were measured in a rotation study in 2003 and 2004 on a Sharpsburg silty clay loam (fine, smectitic, mesic Typic Argiudoll). Cropping sequences were continuous sorghum, and sorghum rotated with non-nodulating and nodulating soybean. Soil amendments consisted of no amendment, manure (17–26 Mg dry matter ha<sup>−1</sup> yr<sup>−1</sup>), and N (84 kg ha<sup>−1</sup> yr<sup>−1</sup>). CS × SA interaction effects were found for most parameters. Rotation with non-nodulating soybean without SA increased yield by 2.6 to 2.8 Mg ha<sup>−1 </sup>over continuous sorghum without SA. Rotation without SA with nodulating soybean further increased yield by 1.7 to 1.8 Mg ha<sup>−1</sup> over rotation with non-nodulating soybean. Grain N increased by 0.5 to 1.0, 2.5 to 5.0, and 3.3 to 4.9 g kg<sup>−1</sup> for N application to continuous sorghum and sorghum rotated with non-nodulating and nodulating soybean, respectively. Tangential abrasive dehulling device (TADD) removal indicated that continuous sorghum without SA produced the softest grain with 43 to 44% TADD removal, and sorghum rotated with nodulating soybean with manure produced the hardest grain with 22 to 27% TADD removal. As food end-use opportunities for sorghum grain evolve, use of crop rotation and SA application will be important to produce grain with desirable quality attributes.</p>
<p>Includes corrected Table 4.</p>

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</description>

<author>Nanga Mady Kaye et al.</author>


</item>


<item>
<title>An Investigotion of the Prevalence of Rickets among Subadults from the Romon Necropolis of lsola Sacra (1st to 3rd centuries AD), Italy</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6933</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6933</guid>
<pubDate>Tue, 08 May 2012 11:42:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The earliest written reference to rickets comes from Soranus of Ephesus, a Roman medical writer of the early second century AD who describes a high number of children in Rome suffering from rochitic deformities. The current study utilizes two independent forms of evidence, skeletal and historic, to study the prevalence of rickets among the human subadult skeletons of the 1st to 3rd century imperial Roman necropolis of lsola Sacra. The necropolis of lsola Sacra represents the remains of individuals who inhabited imperial Rome's key maritime part', Portus Romae on the Mediterranean coast 23 kilometers west of Rome. One hundred and eighty-two subadult skeletons were examined morphologically and radiographically to search for diagnostic indicators of rickets.</p>
<p>Fifteen percent (27/182) of lsola Sacra subadults, birth to 15 years, show rachitic traits with a wide range of morphological presentation. Most individuals suffered from hyperplastic rickets, less likely due to malnutrition. All age categories and burial types show rachitic traits. No association was found between age and the appearance of rickets. No association was found between burial type and the appearance of rickets.</p>
<p>Roman cultural practices, social values and socioeconomic status of the populace using the necropolis may have predisposed the subadult population of lsola Sacra to rickets. Low maternal vitamin D is likely a strong contributing factor to rickets prevalence in the lsola Sacra sample and wos the result of sociocultural factors influencing maternal vitamin D intake.</p>

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</description>

<author>Carolann C. E. Wood</author>


</item>


<item>
<title>New World Rivals: The Role of the Narragansetts in the Breakdown of Anglo-Native Relations During King Philip’s War</title>
<link>http://digitalcommons.providence.edu/history_students/5</link>
<guid isPermaLink="true">http://digitalcommons.providence.edu/history_students/5</guid>
<pubDate>Tue, 08 May 2012 11:42:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>On June 28, 1675, King Philip’s War officially broke out between the Native Americans and English colonists of southern New England.  The English immediately sought an alliance with the Narragansett tribe of Rhode Island due to their vast power in the area.  However, English actions during this quest for alliance would ultimately turn the Narragansetts into enemies.  The diplomatic and military encounters between the Narragansetts and English serve as a lens to understand dispossession, intercultural conflict, and colonialism during this period.</p>

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</description>

<author>Lauren Sagar</author>


<category>History</category>

</item>


<item>
<title>(E,E)-1,3-Bis[9,10-dihydro-9-nitro-10-(trinitro­meth­yl)-9-anthr­yl]propane</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/7</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/7</guid>
<pubDate>Tue, 08 May 2012 11:40:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The title compound, C<sub>33</sub>H<sub>24</sub>N<sub>8</sub>O<sub>16</sub>,  was obtained as a product of the photoreaction between  1,3-di-9-anthrylpropane and tetra­nitro­methane. The mol­ecule occupies a  special position on a twofold axis. The trinitro­methyl and nitro  substituents on the 9,10-dihydro­acridine system are <em>E</em> oriented.</p>

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</description>

<author>Mustafa Arslan et al.</author>


</item>


<item>
<title>The Virtual World of Social Support: Communicating in Second Life</title>
<link>http://digitalcommons.library.umaine.edu/etd/1026</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1026</guid>
<pubDate>Tue, 08 May 2012 11:39:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The present study extends previous online social support literature by examining the supportive messages found within the Alcoholics Anonymous, Cancer Caregiver and Transgender Identity social support groups within the virtual world of Second Life. Ten Alcoholics Anonymous meetings, 9 Cancer Caregiver meetings and 10 Transgender Identity meetings were recorded and analyzed. Group meetings were coded by utterance based on the social support construct created by Cutrona & Suhr (1992) which codes for tangible, informational, emotional, network and esteem messages. Messages that did not fit into any of the categories were coded as non supportive messages. Statistical analysis revealed significant effects for support between all three groups. The optimal match theory was supported for the majority of the groups by support types. Notable differences involved informational support in the Alcoholics Anonymous group, tangible and esteem support in the Cancer Caregiver group and tangible, emotional and esteem support in the Transgender Identity group. These differences are attributed to use of the Second Life medium as well as the coding of the event that the social support group is based on as either controllable or uncontrollable. Ultimately this study adds to current literature by suggesting that participants in the Alcoholics Anonymous, Cancer Caregiver and Transgender Identity social support groups in Second Life are not seeking the same type of social support as individuals participating in online bulletin boards. Participants in the Second Life support groups are seeking greater amounts of network and esteem social support than their counterparts using other computer-mediated environments. This extends the optimal match theory by showing different groups seek social support within the virtual world of Second Life for different types of support than bulletin boards. Additionally, this study challenges the operationalization of controllability within the optimal match theory by looking at it at both the group and individual levels. Finally, the present study looks at three diverse groups over the same period of time using the same methodology. Other studies have focused on either similar groups or have looked at a variety of groups as reported by other studies using a variety of methodologies.</p>

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</description>

<author>Sara Green-Hamann</author>


</item>


<item>
<title>The Child with a Mental Health Condition</title>
<link>http://opus.ipfw.edu/nursing_facpubs/51</link>
<guid isPermaLink="true">http://opus.ipfw.edu/nursing_facpubs/51</guid>
<pubDate>Tue, 08 May 2012 11:39:41 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Linda M. Finke</author>


</item>


<item>
<title>The Child with a Developmental Disability</title>
<link>http://opus.ipfw.edu/nursing_facpubs/50</link>
<guid isPermaLink="true">http://opus.ipfw.edu/nursing_facpubs/50</guid>
<pubDate>Tue, 08 May 2012 11:39:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Linda M. Finke et al.</author>


</item>


<item>
<title>Curriculum Designs/ Models</title>
<link>http://opus.ipfw.edu/nursing_facpubs/49</link>
<guid isPermaLink="true">http://opus.ipfw.edu/nursing_facpubs/49</guid>
<pubDate>Tue, 08 May 2012 11:39:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Linda M. Finke et al.</author>


</item>


<item>
<title>Architects &amp; Antiquities</title>
<link>http://scholarcommons.sc.edu/rbsc_pubs/27</link>
<guid isPermaLink="true">http://scholarcommons.sc.edu/rbsc_pubs/27</guid>
<pubDate>Tue, 08 May 2012 11:39:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>This catalog accompanied the exhibit of illustrated architectural books from the collections of the Department of Rare Books and Special Collections. The exhibit focused on the career of South Carolina architect Robert Mills (1781-1855), now best-known as architect of the Washington Monument. Several of the titles were among those that Mills himself listed as influencing his development as an architect, while other represented the major schools of architectural influence from which he drew his work.</p>

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</description>

<author>University Libraries--University of South Carolina</author>


</item>


<item>
<title>The effects of the country of brand and the country of manufacturing of automobiles: An experimental study of consumers&apos; brand personality perceptions</title>
<link>http://scholarship.rollins.edu/as_facpub/41</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/as_facpub/41</guid>
<pubDate>Tue, 08 May 2012 11:38:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Purpose: This paper offers a new perspective of country of origin effects on consumers’ brand personality perceptions of domestic and imported automobiles. It assesses the perceived similarities and differences between automobiles from two countries with respect to the country of origin of the brand (COB) and the country of manufacturing (COM) of that same brand.</p>
<p>Design/methodology/approach: An experimental design was used to investigate developed country consumers’ brand personality perceptions of three cars; a domestic car, a car manufactured in a developing country by a developing country manufacturer, and a car from developing country manufacturer that is manufactured in the developed country. Data was collected in the United States and therefore a U.S. car was used as the developed country car. China was selected as the developing country of origin. A structured questionnaire was used to collect primary data.</p>
<p>Findings: Multivariate analysis of variance (MANOVA) indicates that consumers’ brand personality perceptions varied according to the country of origin (COB) of the brand and the country of manufacture (COM) of the brand. We show that the COM of a car influenced the perceived brand personality of the car more than the COB. In some respects the Chinese car made in the U.S. was perceived to have a stronger brand personality than the U.S. car made in China. This suggests that for cars the COM exerts a greater influence on the perceived personality of a brand than the COB.</p>
<p>Research limitations/implications: While this paper offers an exploratory glimpse of potential challenges and opportunities facing domestic and developing country automotive manufacturers, future research should take a larger respondent pool, respondents from other countries, other automotive manufacturers as well as assess the impact of COM and COB on purchase intention and behavior.</p>
<p>Practical implications: Manufacturers of cars must understand the effect of country of origin and country of manufacturing of a brand on consumers’ brand perceptions in order to build, position and protect their brands in various international markets.</p>
<p>Originality/value: This paper provides an important contribution to the existing literature and business practice by providing a new perspective on country of origin research by using the multi-dimensional construct of brand personality and analyzing the relationship between country of origin of a brand and country of manufacturing of that same brand. Moreover, it addressed a timely issue by investigating the challenges and opportunities Chinese and American car manufacturers are facing.</p>

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</description>

<author>Marc Fetscherin et al.</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 18</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/59</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/59</guid>
<pubDate>Tue, 08 May 2012 11:36:49 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p><em><strong></strong></em>Totem Shriver, adjunct professor of 3D design at Linfield College, prepares to take aim at the collaborative burn sculpture.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 17</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/58</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/58</guid>
<pubDate>Tue, 08 May 2012 11:36:46 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p>Totem Shriver, adjunct professor of 3D design at Linfield College, acknowledges the students who built the 2012 collaborative burn sculpture.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 16</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/57</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/57</guid>
<pubDate>Tue, 08 May 2012 11:36:42 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 15</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/56</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/56</guid>
<pubDate>Tue, 08 May 2012 11:36:39 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Hans Christian Andersen (1805-2005): A Bicentennial Selection</title>
<link>http://scholarcommons.sc.edu/rbsc_pubs/26</link>
<guid isPermaLink="true">http://scholarcommons.sc.edu/rbsc_pubs/26</guid>
<pubDate>Tue, 08 May 2012 11:35:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>This catalog accompanied the exhibit of a sample of the author’s works held by the Department of Rare Books and Special Collections. The representative selection of materials contained books from the library’s Historical Children’s Literature Collection and the Augusta Baker Collection of African-American Children’s Literature and Folklore. It included examples of some of the first English translations of Andersen’s writings, as well as several of his classic fairy tales and materials exhibiting the ways in which nineteenth- and twentieth-century children’s book illustrators reacted to and interpreted the text.</p>

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</description>

<author>University Libraries--University of South Carolina</author>


</item>


<item>
<title>Faculy Role in Teaching, Curriculum Development and Evaluation</title>
<link>http://opus.ipfw.edu/nursing_facpubs/48</link>
<guid isPermaLink="true">http://opus.ipfw.edu/nursing_facpubs/48</guid>
<pubDate>Tue, 08 May 2012 11:34:37 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Linda M. Finke</author>


</item>


<item>
<title>Senator Ted Kennedy: A Champion for Mental Health Care and a Friend to Child Psychiatric Nursing</title>
<link>http://opus.ipfw.edu/nursing_facpubs/47</link>
<guid isPermaLink="true">http://opus.ipfw.edu/nursing_facpubs/47</guid>
<pubDate>Tue, 08 May 2012 11:34:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Linda M. Finke</author>


</item>


<item>
<title>A Call for Continued Advocacy to Stop Deep Cuts in Funding for Mental Health Services</title>
<link>http://opus.ipfw.edu/nursing_facpubs/46</link>
<guid isPermaLink="true">http://opus.ipfw.edu/nursing_facpubs/46</guid>
<pubDate>Tue, 08 May 2012 11:34:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Linda M. Finke</author>


</item>


<item>
<title>Interactive Learning Environment: Engaging Students Using Clickers</title>
<link>http://opus.ipfw.edu/nursing_facpubs/45</link>
<guid isPermaLink="true">http://opus.ipfw.edu/nursing_facpubs/45</guid>
<pubDate>Tue, 08 May 2012 11:34:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Educators continue to search for effective methods that will engage students in their learning.  This article presents the integration of clickers using the constructivist approach to foster critical thinking while engaging learners in a large classroom setting.  A 22-item survey was used to measure the perceived value by students to the use of clickers in engaging then in the learning process and fostering critical thinking.  Clickers, also known as personal response systems, created an interactive environment, moving students beyond simple recall to application, analysis, and construction of knowledge.</p>

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</description>

<author>Carol S. Sternberger</author>


</item>


<item>
<title>Toward a Life of Thanksgiving</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/384</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/384</guid>
<pubDate>Tue, 08 May 2012 11:32:55 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bob Stamps</author>


</item>


<item>
<title>A 2:1 complex of 1,3-bis­(9H-carbazol-9-yl)propane and tetra­chloro-p-benzoquinone (p-chloranil)</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/6</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/6</guid>
<pubDate>Tue, 08 May 2012 11:32:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the title electron donor–acceptor complex, C<sub>27</sub>H<sub>22</sub>N<sub>2</sub>·0.5C<sub>6</sub>Cl<sub>4</sub>O<sub>2</sub>, the <em>p</em>-chloranil  mol­ecule lies on a crystallographic inversion center, which is located  at the center of the benzene ring. In the crystal structure, one <em>p</em>-chloranil mol­ecule lies above and below the central rings of each donor group of two neighboring 1,3-bis­(9<em>H</em>-carbazol-9-yl)propane  mol­ecules, with a ring-centroid separation of 3.444 (1) Å. The angle  between the planes of the stacking rings of the carbazole and <em>p</em>-chloranil mol­ecules is 3.4 (2)°.</p>

	]]>
</description>

<author>Mustafa Arslan et al.</author>


</item>


<item>
<title>At Ames Library: A Ghazal</title>
<link>http://digitalcommons.iwu.edu/ames_10anniversary/14</link>
<guid isPermaLink="true">http://digitalcommons.iwu.edu/ames_10anniversary/14</guid>
<pubDate>Tue, 08 May 2012 11:31:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>To commemorate the 10<sup>th</sup> Anniversary of The Ames Library, the library held a poetry contest in which students were asked to submit poems that focused on the library, in an original and creative way. The winning poem, by Madeline Tyner, was read by the author at the 10<sup>th</sup> Anniversary Reception held on April 18, 2012 in the Bates-Merwin Reading Room, Ames Library.</p>

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</description>

<author>Madeline Tyner</author>


</item>


<item>
<title>Minor Myers, Jr. Honors Collection</title>
<link>http://digitalcommons.iwu.edu/ames_10anniversary/13</link>
<guid isPermaLink="true">http://digitalcommons.iwu.edu/ames_10anniversary/13</guid>
<pubDate>Tue, 08 May 2012 11:31:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Created for the Ames Library 10<sup>th</sup> Anniversary Reception on April 18<sup>th</sup>, 2012, this presentation contains a history and description of the collection of books housed in the Bates-Merwin Reading Room. The first of several events celebrating the 10<sup>th</sup> anniversary of the Ames Library, the reception was held in the Bates-Merwin Reading Room, named for longtime trustees and benefactors Davis U. Merwin and Rex James Bates.</p>

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</description>

<author>Sue Stroyan</author>


</item>


<item>
<title>The Ames Library 10th Anniversary Poster</title>
<link>http://digitalcommons.iwu.edu/ames_10anniversary/12</link>
<guid isPermaLink="true">http://digitalcommons.iwu.edu/ames_10anniversary/12</guid>
<pubDate>Tue, 08 May 2012 11:31:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>The poster was created for the Ames Library 10<sup>th</sup> Anniversary Reception, held in the Bates-Merwin Reading Room, on April 18, 2012. The reception was one of several events celebrating the 10<sup>th</sup> anniversary of the library.</p>

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</description>

<author>Stephanie Davis Kahl et al.</author>


</item>


<item>
<title>The Ames Library 10th Anniversary Reception Invitation</title>
<link>http://digitalcommons.iwu.edu/ames_10anniversary/11</link>
<guid isPermaLink="true">http://digitalcommons.iwu.edu/ames_10anniversary/11</guid>
<pubDate>Tue, 08 May 2012 11:31:45 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Karen Schmidt</author>


</item>


<item>
<title>Chaucer and &lt;em&gt;The Canterbury Tales&lt;/em&gt;</title>
<link>http://scholarcommons.sc.edu/rbsc_pubs/25</link>
<guid isPermaLink="true">http://scholarcommons.sc.edu/rbsc_pubs/25</guid>
<pubDate>Tue, 08 May 2012 11:31:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>This catalog accompanied the exhibit of materials from the University of South Carolina’s Department of Rare Books and Special Collections, which featured original material alongside modern high-quality reproductions of the most important of the Chaucer manuscripts and of the early printed editions of his work.</p>

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</description>

<author>University Libraries--University of South Carolina</author>


</item>


<item>
<title>Managing a Successful Academic Career</title>
<link>http://aisel.aisnet.org/success_strategies/5</link>
<guid isPermaLink="true">http://aisel.aisnet.org/success_strategies/5</guid>
<pubDate>Tue, 08 May 2012 11:29:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Viswanath Venkatesh et al.</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 14</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/55</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/55</guid>
<pubDate>Tue, 08 May 2012 11:29:22 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p>Totem Shriver, adjunct professor of 3D design at Linfield, addresses the crowd prior to the burn.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 13</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/54</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/54</guid>
<pubDate>Tue, 08 May 2012 11:29:19 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p><em><strong></strong></em>The 2012 celebration marked the first year that taiko drums were a part of the burn ceremony.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 12</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/53</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/53</guid>
<pubDate>Tue, 08 May 2012 11:29:16 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

	]]>
</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>A Year in the Life: Business Librarians Report on 2008–09</title>
<link>http://repository.cmu.edu/lib_science/87</link>
<guid isPermaLink="true">http://repository.cmu.edu/lib_science/87</guid>
<pubDate>Tue, 08 May 2012 11:28:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>This article summarizes trends and initiatives in the world of academic business librarianship, as reported by the members of the Academic Business Library Directors (ABLD) organization, for the year 2008-9.</p>

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</description>

<author>Roye Werner</author>


</item>


<item>
<title>Eighteenth &amp; Nineteenth Century Books About China</title>
<link>http://scholarcommons.sc.edu/rbsc_pubs/24</link>
<guid isPermaLink="true">http://scholarcommons.sc.edu/rbsc_pubs/24</guid>
<pubDate>Tue, 08 May 2012 11:27:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>This brochure accompanied an exhibit mounted to mark the donation to the University of South Carolina by the People’s Republic of China of an extensive collection of Chinese-language books and reference works, totaling more than 200 volumes. Most of the books displayed were drawn from the library of the original South Carolina College, chartered in 1801. Also displayed were books about China from the personal library of Charles Pinckney (1757-1827), governor of South Carolina, and author of the “Pinckney draft” of the U.S. federal constitution.</p>

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</description>

<author>University Libraries--University of South Carolina</author>


</item>


<item>
<title>Respect Yourself, Protect Yourself</title>
<link>http://opus.ipfw.edu/nursing_facpubs/44</link>
<guid isPermaLink="true">http://opus.ipfw.edu/nursing_facpubs/44</guid>
<pubDate>Tue, 08 May 2012 11:26:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Women of the poor community of Cien Fuegos, Dominican Republic often use folklore or self-treatment for symptoms of vaginitis.  Based on assessment of women in Cien Fuegos, an education program was developed called Respect Yourself, Protect Yourself.  The need to increase empowerment and self respect was clearly evident for the women of this community.  The program focuses on issues of vaginal hygiene, vaginitis, sexually transmitted infections and women's rights and self-protection.  To provide sustainable education, the module will be sent to Cien Fuegos and implemented by local health providers.</p>

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</description>

<author>Mary Gura et al.</author>


</item>


<item>
<title>Hartford’s Southeast Asian Refugee Population: Servicing the Needs of a Growing Community</title>
<link>http://digitalrepository.trincoll.edu/theses/227</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/227</guid>
<pubDate>Tue, 08 May 2012 11:26:57 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Mari Zigas</author>


</item>


<item>
<title>Helpful or Harmful? Teach For America in a Hartford Elementary School</title>
<link>http://digitalrepository.trincoll.edu/theses/226</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/226</guid>
<pubDate>Tue, 08 May 2012 11:26:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Cintli Sanchez</author>


</item>


<item>
<title>Trinity’s Second-Language Requirement: Focusing on students’ perspectives</title>
<link>http://digitalrepository.trincoll.edu/theses/225</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/225</guid>
<pubDate>Tue, 08 May 2012 11:26:45 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Sunny Park</author>


</item>


<item>
<title>Increasing the Arts in Public Schools: The Arkansas Success Story</title>
<link>http://digitalrepository.trincoll.edu/theses/224</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/224</guid>
<pubDate>Tue, 08 May 2012 11:26:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Samantha Moorin</author>


</item>


<item>
<title>Identity Formation of Young Adults: An Oral History Exploration</title>
<link>http://digitalrepository.trincoll.edu/theses/223</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/223</guid>
<pubDate>Tue, 08 May 2012 11:26:33 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Franci Davila</author>


</item>


<item>
<title>Why the School for Young Children? An inside look into the institutional and parental motivations and expectations</title>
<link>http://digitalrepository.trincoll.edu/theses/222</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/222</guid>
<pubDate>Tue, 08 May 2012 11:26:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Kathy Chang</author>


</item>


<item>
<title>Health Care On a Budget: The Rise of Economic Dominance in Health Care Reform</title>
<link>http://digitalrepository.trincoll.edu/theses/221</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/221</guid>
<pubDate>Tue, 08 May 2012 11:26:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Lauren Rice</author>


</item>


<item>
<title>The PKP Caustic at the Trinity College Seismograph Station (TCCT) from the Sumbawa-Indonesia Earthquake on November 8th, 2009</title>
<link>http://digitalrepository.trincoll.edu/theses/220</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/220</guid>
<pubDate>Tue, 08 May 2012 11:26:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>On November 8<sup>th</sup>, 2009 the Trinity College Seismograph Station (TCCT) recorded an earthquake of magnitude Mw = 6.7 with body wave amplitudes that were larger than expected. This earthquake, located in Sumbawa-Indonesia, generated similar body wave amplitudes as earthquakes of the same magnitude (Mw = 6.7) and comparable depth (shallow focus: 0th, 2010 and the Alaska earthquake on July 18<sup>th</sup>, 2010. The large body wave amplitudes were caused by a set of consecutive PKP waves that constructively interfered. The distance from the Sumbawa-Indonesia earthquake to TCCT of 144.96° falls between the lower and higher estimates for the PKP caustic point. The observations at TCCT helped establish a theoretical region, in which future seismic events could create a caustic at or in the proximity of TCCT. It is suggested to use the IRIS network to better estimate the distance to the caustic point for future events occurring in the theoretical region.</p>

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</description>

<author>Daniel Echavarria</author>


</item>


<item>
<title>Impressions Left on Pillows</title>
<link>http://digitalrepository.trincoll.edu/theses/219</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/219</guid>
<pubDate>Tue, 08 May 2012 11:26:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Leslie P. Ahlstrand</author>


</item>


<item>
<title>An Examination of Bacterial Communities in the Upper Respiratory Tracts of Asthmatics and Non-Asthmatics</title>
<link>http://digitalrepository.trincoll.edu/theses/218</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/218</guid>
<pubDate>Tue, 08 May 2012 11:26:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The human body is colonized with commensal microbes that attach to the skin and mucosal membranes and function to protect the host as part of the innate immune response. These indigenous microbiota are able to prevent infections by blocking attachment sites and outcompeting invading pathogens for necessary nutrients. Disturbance of the host-microbe symbiotic balance may increase a host’s susceptibility to disease. In addition, proper colonization of the normal flora has been implicated in playing a vital role in shaping the immune response. It has been hypothesized that reduced exposure to infectious microorganisms early in life can disrupt the development of normal immune regulation. This “hygiene hypothesis” states that the increased prevalence of allergic diseases in developed countries can be attributed to a more hygienic, westernized lifestyle that is characterized by a decrease in microbial challenges. Therefore, the allergic disease asthma, which is characterized by a heightened inflammatory response, could be the result of disturbed microbial colonization, hindrance of immune maturation, and subsequent disregulation of the allergic response. It would be expected that asthmatic individuals would exhibit a less diverse and less abundant population of normal flora as compared to non-asthmatic individuals. This preliminary study investigated the bacterial communities found in the upper respiratory tracts of asthmatic and non-asthmatic subjects. Terminal restriction fragment length polymorphism (tRFLP) was used to examine the composition of bacteria in oropharyngeal samples collected from student volunteers at Trinity College. The tRFLP profiles of asthmatic and non-asthmatic subjects produced conflicting results, and it cannot be concluded if there is a difference in the diversity or abundance of bacterial communities in the upper respiratory tracts of both populations.</p>

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</description>

<author>Kelly O&apos;Brien</author>


</item>


<item>
<title>Trinity Chapel’s Response to Social Issues: Dare to Be True</title>
<link>http://digitalrepository.trincoll.edu/theses/217</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/217</guid>
<pubDate>Tue, 08 May 2012 11:25:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Through examining Trinity’s religious life on campus, this paper will help to explain the Chapel’s response to social issues from 1923 to the present. Over this time period, involvement and advocacy has ebbed and flowed. The responses of the Chapel community have relied heavily on the leadership of the current chaplain and the campus climate of the college. The Chapel’s historical value is embedded in the college’s history and identity. However, the significance the Chapel holds to the college more broadly is changing from a largely Episcopal background to both a social and moral haven for growth. <strong></strong></p>

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</description>

<author>Kathryn T. Van Sickle</author>


</item>


<item>
<title>The direction of hospital case management-searching for a standard definition</title>
<link>http://opus.ipfw.edu/nursing_facpres/52</link>
<guid isPermaLink="true">http://opus.ipfw.edu/nursing_facpres/52</guid>
<pubDate>Tue, 08 May 2012 11:24:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Deborah Poling</author>


</item>


<item>
<title>Defining Advocacy in Nursing</title>
<link>http://opus.ipfw.edu/nursing_facpres/51</link>
<guid isPermaLink="true">http://opus.ipfw.edu/nursing_facpres/51</guid>
<pubDate>Tue, 08 May 2012 11:24:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Deborah Poling</author>


</item>


<item>
<title>Hand Health</title>
<link>http://opus.ipfw.edu/dental_facpubs/64</link>
<guid isPermaLink="true">http://opus.ipfw.edu/dental_facpubs/64</guid>
<pubDate>Tue, 08 May 2012 11:24:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Mary D. Cooper et al.</author>


</item>


<item>
<title>The History of Dental Hygiene in South Korea</title>
<link>http://opus.ipfw.edu/dental_facpubs/63</link>
<guid isPermaLink="true">http://opus.ipfw.edu/dental_facpubs/63</guid>
<pubDate>Tue, 08 May 2012 11:24:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>This historical narrative highlights the origin and development of the dental hygiene profession in South Korea. The legacy of early American missionaries to Korea includes profound and long-lasting contributions in medicine, education and theology. Many of Korea’s top universities today have their roots in the missionary schools of the late nineteenth century, including Yonsei University, home of the first dental hygiene program in Korea. From Yonsei in Seoul, the dental hygiene profession spread throughout the country, including the American missionary-based program in Kwangju in 1977. Contributions included clinical and didactic education, as well as professional leadership and development. American dental missionaries developed the profession of dental hygiene in Korea, and provided guidance to Korean dentists and hygienists for its growth and expansion.</p>

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</description>

<author>Nancy K. Mann</author>


</item>


<item>
<title>Hand Health. How to prevent and manage soft tissue disorders of the   	hands.</title>
<link>http://opus.ipfw.edu/dental_facpubs/62</link>
<guid isPermaLink="true">http://opus.ipfw.edu/dental_facpubs/62</guid>
<pubDate>Tue, 08 May 2012 11:24:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Nancy K. Mann et al.</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 11</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/52</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/52</guid>
<pubDate>Tue, 08 May 2012 11:23:32 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p><em><strong></strong></em>Attendees are encouraged to write messages directly on the sculpture or on slips of paper that are then tucked into the sculpture. Through the ritual act of burning, these sentiments are offered up and released into the universe.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Sex ratios of leatherback turtles: hatchery translocation decreases metabolic heating and female bias</title>
<link>http://opus.ipfw.edu/biology_facpubs/197</link>
<guid isPermaLink="true">http://opus.ipfw.edu/biology_facpubs/197</guid>
<pubDate>Tue, 08 May 2012 11:23:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>ABSTRACT: Many sea turtle nesting colonies are in decline worldwide, and a common conservation practice maximizes hatchling production by translocating eggs from threatened nests to protective beach hatcheries. Typically, translocated eggs are ‘doomed’, or at risk of death due to tidal inundation, predation, or poaching. Sea turtles exhibit temperature-dependent sex determination. We determined how primary sex ratios, estimated from incubation temperatures, were affected by egg clutch translocation to a beach hatchery. We monitored incubation temperatures of eastern Pacific leatherback turtles <em><em><em>Dermochelys coriacea </em></em></em>in hatchery and <em><em><em>in situ </em></em></em>clutches at Playa Grande, Costa Rica, throughout each nesting season from 1998 to 2007. <em><em><em>In situ </em></em></em>clutches were estimated to be 90% female, whereas hatchery clutches (9% of clutches) were estimated to be 64% female. Taking into account differences in hatching success of i<em><em><em>n situ </em></em></em>and hatchery nests, the overall sex ratio was 83% female. The Playa Grande hatchery abiotic environment (sand temperatures, water inputs) was similar to that <em><em><em>in situ </em></em></em>. However, metabolic heating was significantly reduced in hatchery clutches. The most likely explanation is that temperatures in hatchery clutches were cooler (less female-biased) due to decreases in the number of metabolizing embryos since hatchling success was lower in hatchery clutches than <em><em><em>in situ </em></em></em>clutches. Alteration of both primary sex ratios and hatching success is the tradeoff for reducing the risk of death to egg clutches by translocation to a hatchery. This tradeoff is not unique to Playa Grande leatherback turtles, and it is a strong indication that hatchery translocation should be used cautiously.</p>

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</description>

<author>Frank V. Paladino</author>


</item>


<item>
<title>Reproductive output &amp; ultrasonography of endangered population of East Pacific Green Turtles</title>
<link>http://opus.ipfw.edu/biology_facpubs/196</link>
<guid isPermaLink="true">http://opus.ipfw.edu/biology_facpubs/196</guid>
<pubDate>Tue, 08 May 2012 11:23:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Reproductive output is one of the most relevant aspects of life history. We analyzed the reproductive output of the endangered East Pacific green turtle (Chelonia mydas) nesting in Nombre de Jesu´s, Costa Rica. We supplemented beach patrols with ultrasonography to estimate clutch frequency. With ultrasound scans, we classified the stage of turtle ovaries as: early stage (2 or more clutches), late stage (1 clutch), and depleted ovaries (no clutches). We calculated mean (SD) estimated clutch frequency (ECF) to be 3.7 1.8 (n ¼ 24) and an adjusted frequency onsidering individual stage (ECFU; ECF þ number of clutches remaining as observed in the last ultrasound) as 5.1 1.3. This is greater than previously described for East Pacific green turtles. Greater individual output could be representative of a healthier population; but could also indicate a decrease in the estimate population numbers previously reported.<br> 2011 The Wildlife Society.</p>

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</description>

<author>Frank V. Paladino</author>


</item>


<item>
<title>Effects of dietary supplementation of the acidifier Vitoxal-Mionix on growth, survival, immune response and gut microbiota of the Pacific White Shrimp,  Litopenaeus vannamei</title>
<link>http://opus.ipfw.edu/biology_facpubs/195</link>
<guid isPermaLink="true">http://opus.ipfw.edu/biology_facpubs/195</guid>
<pubDate>Tue, 08 May 2012 11:22:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ahmed Mustafa Dr. et al.</author>


</item>


<item>
<title>30 Years of foreign direct investment to China: An interdisciplinary literature review</title>
<link>http://scholarship.rollins.edu/as_facpub/40</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/as_facpub/40</guid>
<pubDate>Tue, 08 May 2012 11:21:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this paper is to examine how scholarly research on Foreign Direct Investment (FDI) to the People’s Republic of China has evolved and been shaped using bibliometrics analysis of 422 journal articles published in 151 journals between 1979 and 2008 on that topic. The literature is dominated by the fields of Economics, followed by Business and Management, Planning and Development and International Relations, which together account for 95% of all publications. Ten percent of the most productive journals are responsible for 40% of all publications and 63% of all citations received. By means of citation mapping, four main research streams have been identified: (1) the motives and determinants of FDI to China; (2) ‘inside’ the multinational enterprise (MNE); (3) the impact of MNE activities; and (4) policy implications for the host country. Emerging research streams have been identified as the effects of inward FDI on (i) corporate social responsibility attitudes of domestic and foreign firms, (ii) environmental and climate issues, (iii) the institutional and societal transformation of China, and (iv) the emergence of Chinese MNEs and its impact on the operations of foreign MNEs in China.</p>

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</description>

<author>Marc Fetscherin et al.</author>


</item>


<item>
<title>Cultural Competence Through Gaming and Literature: Strategies prior to service engagement</title>
<link>http://opus.ipfw.edu/dental_facpres/46</link>
<guid isPermaLink="true">http://opus.ipfw.edu/dental_facpres/46</guid>
<pubDate>Tue, 08 May 2012 11:20:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>To prepare students to be effective practitioners in an increasingly diverse United States, dental hygiene educators must design cross-cultural curricula. One goal of such education is cultural competence, defined as a set of skills that allow individuals to increase their understanding of cultural differences and similarities within, among, and between groups. Cultural competence is a necessity in today’s diverse society and an essential component of clinical practice especially prior to community based learning. Furthermore, the American Dental Association Council on Dental Accreditation standards requires incorporating content related to cultural competence in the dental hygiene curriculum.</p>

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</description>

<author>Nancy K. Mann</author>


</item>


<item>
<title>Clinical Dental Hygiene</title>
<link>http://opus.ipfw.edu/dental_facpres/45</link>
<guid isPermaLink="true">http://opus.ipfw.edu/dental_facpres/45</guid>
<pubDate>Tue, 08 May 2012 11:20:52 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mary D. Cooper</author>


</item>


<item>
<title>Nutrition in Dentistry</title>
<link>http://opus.ipfw.edu/dental_facpres/44</link>
<guid isPermaLink="true">http://opus.ipfw.edu/dental_facpres/44</guid>
<pubDate>Tue, 08 May 2012 11:20:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mary D. Cooper</author>


</item>


<item>
<title>Aging of Polyurethane Foams: IR</title>
<link>http://digitalcommons.library.unlv.edu/chem_fac_articles/84</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/chem_fac_articles/84</guid>
<pubDate>Tue, 08 May 2012 11:19:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>This Compendium contains abstracts written by Advanced Light Source users summarizing research completed or in progress during 2000. Two tables of contents organize the abstracts by beamline and by subject, and a list of funding institutions is also provided. Technical details for each beamline, including whom to contact for additional information, can be found in the beamline information section. The Compendium is intended to complement the Advanced Light Source Activity Report, which presents an overview of the scientific program, ongoing research and development efforts, and operations.</p>

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</description>

<author>A. L. Johnson et al.</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 10</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/51</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/51</guid>
<pubDate>Tue, 08 May 2012 11:17:51 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><strong><em>Photographer's Notes</em></strong></p>
<p>Many attendees, like this drummer, come to the burn in costume.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 09</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/50</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/50</guid>
<pubDate>Tue, 08 May 2012 11:17:48 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p>A member of a student drumming circle provides music prior to the burn.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 08</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/49</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/49</guid>
<pubDate>Tue, 08 May 2012 11:17:45 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012, it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Note</strong></em></p>
<p>Celebration participants stand near their homemade speaker system before the burn begins.</p>

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</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Vision Changes after Space Flight Are Related to Alterations in Folate- and Vitamin B12-Dependent One-Carbon Metabolism</title>
<link>http://opus.ipfw.edu/chemistry_facpubs/52</link>
<guid isPermaLink="true">http://opus.ipfw.edu/chemistry_facpubs/52</guid>
<pubDate>Tue, 08 May 2012 11:17:44 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sara R. Zwart et al.</author>


</item>


<item>
<title>Lessons Learned From an Interdisciplinary Course in Undergraduate Science</title>
<link>http://opus.ipfw.edu/chemistry_facpubs/51</link>
<guid isPermaLink="true">http://opus.ipfw.edu/chemistry_facpubs/51</guid>
<pubDate>Tue, 08 May 2012 11:17:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>This chapter discusses the team teaching of an interdisciplinary science course intended for non-science majors at IPFW.  The course was taught by an interdisciplinary team of scientists and mathematicians (biology, chemistry, geosciences, mathematics, and physics) at IPFW in the early 1990s.</p>

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</description>

<author>Ronald J. Duchovic</author>


</item>


<item>
<title>Type 1 Diabetes impairs Vitamin B6 metabolism at an early stage of women&apos;s adulthood</title>
<link>http://opus.ipfw.edu/chemistry_facpubs/50</link>
<guid isPermaLink="true">http://opus.ipfw.edu/chemistry_facpubs/50</guid>
<pubDate>Tue, 08 May 2012 11:17:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Priscilla G. Masse et al.</author>


</item>


<item>
<title>Pet-Friendly Hotel Add-On Fees As Elements Of Revenue Management</title>
<link>http://opus.ipfw.edu/consumer_facpres/3</link>
<guid isPermaLink="true">http://opus.ipfw.edu/consumer_facpres/3</guid>
<pubDate>Tue, 08 May 2012 11:15:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study is for the purose of measuring the impact of add-on fees for pet-friendly accommodations in the revenue management context.  This data will be developed using STR Trend report of coded pet-friendly and non-pet-friendl properties and analyzed as a function of occupancy, revenue per available room, and average daily revenue data.  It is anticipated that a signficant positve correlation between these variables will indicate the use of add-on fees to be detrimental to pricing as an element within the revenue management context.  Seven markets were used yielding resutlts contrary to the expected findings.</p>

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</description>

<author>Sylvere Hilaire Coussement et al.</author>


</item>


<item>
<title>Internet Marketing Integration For Small Inns:  How Is It Measured?</title>
<link>http://opus.ipfw.edu/consumer_facpres/2</link>
<guid isPermaLink="true">http://opus.ipfw.edu/consumer_facpres/2</guid>
<pubDate>Tue, 08 May 2012 11:15:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>The optimal use of internet resources and revenue management sytems requires financial capabilities generally not affordable by small lodging operations such as bed and breakfast (B&B) inns.  This study addresses the issue of the marketing mix for small hotels.  A survey instrument was used to collect data from this unique niche of inns.  The analysis expected to reveal that a majority of B&B's are successful using only traditional print media, properietary website portals specific to this industry niche, and regional tourism/CVB portals.  However, the use of third party distribution channels i snot expected to be significant.  The examination expects to find that the majority of B&B's make good use of their home website, on-line directories, print materials, and statewide organizations, but cannot afford third party distribution channels.  This information will be useful for business planning purposes and strategic manaement of family run B&B's.</p>

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</description>

<author>Martha Coussement et al.</author>


</item>


<item>
<title>Leveraging Relationships With Industry</title>
<link>http://aisel.aisnet.org/success_strategies/4</link>
<guid isPermaLink="true">http://aisel.aisnet.org/success_strategies/4</guid>
<pubDate>Tue, 08 May 2012 11:14:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Hugh Watson et al.</author>


</item>


<item>
<title>Aging of Polyurethane Foams: XPS and NEXAFS</title>
<link>http://digitalcommons.library.unlv.edu/chem_fac_articles/83</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/chem_fac_articles/83</guid>
<pubDate>Tue, 08 May 2012 11:14:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>This Compendium contains abstracts written by Advanced Light Source users summarizing research completed or in progress during 2000. Two tables of contents organize the abstracts by beamline and by subject, and a list of funding institutions is also provided. Technical details for each beamline, including whom to contact for additional information, can be found in the beamline information section. The Compendium is intended to complement the Advanced Light Source Activity Report, which presents an overview of the scientific program, ongoing research and development efforts, and operations.</p>

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</description>

<author>A. L. Johnson et al.</author>


</item>


<item>
<title>Educators Selection of Pedagogical Strategies to Prepare the Entry Level Athletic Trainer on Techniques Related to Sudden Death in Sport</title>
<link>http://digitalcommons.uconn.edu/gs_theses/243</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/243</guid>
<pubDate>Tue, 08 May 2012 11:10:37 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Educators Selection of Pedagogical Strategies to Prepare the Entry Level Athletic Trainer on Techniques Related to Sudden Death in Sport</strong></p>
<p>Salvatore AS, Mazerolle SM, Yabor TM, Pagnotta KD, Casa DJ: University of Connecticut, Storrs; CT</p>
<p>. <strong></strong></p>
<p><strong>Context:</strong> Educational training is an important factor for the athletic trainer to gain appropriate knowledge and clinical competence. Unfortunately, not all athletic trainers receive proper training and feedback regarding topics related to sudden death in sport, particularly EHS. <strong>Objective:</strong> To gain a more in-depth understanding of the educational training provided to the athletic training student regarding sudden death in sport, beyond EHS. <strong>Design:</strong> An inductive qualitative study utilizing phone interviewing. <strong>Setting:</strong> Athletic Training Education Programs. <strong>Patients or Other Participants:</strong> 12 faculty members (8 males; 4 females) in athletic training programs accredited by Commission on Accreditation of Athletic Training Education (CAATE). Years of Board Certification was 15 ± 9 years, while the average years as a faculty member was 13 ± 8 years, and the average years worked clinically was 11 ± 10. <strong>Data Collection and Analysis:</strong> One-on-one phone interviews following a semi-structured format were conducted with all participants. Interviews were transcribed verbatim and shared with participants prior to analysis. Interviews were analyzed inductively borrowing from the principles of a grounded theory approach and open coding. Multiple analyst triangulation and peer review were included as steps to establish data credibility. <strong>Results:</strong> Two dominant themes emerged from the data: <em>current trends</em> and <em>instructional methods</em>. <em>Current trends</em> were classified as those topics related to sudden death that were considered to be “hot topics” within the media. Although information presented was driven by the NATA Position Statements, considerable attention was spent on cardiac, cervical spine, and head injuries, while limited time was focused on heat illnesses, asthma, or anaphylaxis. The theme was also reflective of regional bias as well as individual professional experiences of the instructors teaching the material. Together these factors influenced how much time was dedicated to and how in-depth each of the conditions of sudden death were covered. <em>Instructional methods</em> reflects the faculty members attempt to provide “real life” learning experiences through simulations and case studies, which ultimately yielded little clinical skill integration and relied more on discourse. Also, educators relied on time spent in clinical education as means to hopefully provide real-time exposure in emergency situations. <strong>Conclusions:</strong> Management of sudden death in sport requires the athletic trainer to be prepared to act quickly, efficiently, while following the recommended practices. Athletic training educators must be prepared, regardless of their previous experiences or personal biases, to provide educational training regarding most causes of sudden death in sport. Furthermore, to facilitate clinical integration and competency, the student must be challenged to implement their knowledge and skill in order to feel prepared to appropriately respond to an emergency situation. Exposure to every medical emergency is implausible, yet opportunities must be afforded to the student to implement their critical decision making abilities. <strong>Word Count</strong>: 449</p>

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</description>

<author>Anthony Salvatore</author>


</item>


<item>
<title>Hypophosphatasia:  Skeletal Presentation In Utero of Non-Lethal Disease</title>
<link>http://opus.ipfw.edu/chemistry_facpubs/49</link>
<guid isPermaLink="true">http://opus.ipfw.edu/chemistry_facpubs/49</guid>
<pubDate>Tue, 08 May 2012 11:09:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hypophosphatasia (HPP), from deactivating mutation(s) within the “tissue nonspecific” alkaline phosphatase (TNSALP) gene, features rickets/osteomalacia and dental disease ranging from <em>in utero</em> absent skeletal mineralization to loss of adult dentition.  Several reports characterize a “benign prenatal” phenotype (BP-HPP).</p>
<p>Seventeen of our 178 pediatric HPP patients have unreported BP-HPP. Here, we describe their prenatal and postnatal findings comparing them to affected siblings, carrier parents, and others with identical <em>TNSALP</em> mutations. New information concerning seven previously published BP-HPP pts is also included with an extensive literature review.</p>
<p>Among our 17 pts, eight autosomal dominant (AD) and nine autosomal recessive (AR) BP-HPP, prenatal ultrasounds had shown normal chest or abdominal circumferences, poor skeletal mineralization, fetal<em> </em>packing, and third trimester improvement.  Postnatally, extremity bowing further improved (13 pts).  BP-HPP severity spanned “infantile” to “odonto” HPP phenotypes, resembling our pts with identical <em>TNSALP</em> mutation(s).  Fourteen of the 15 mothers were HPP carriers or affected. Of 41 cumulative BP-HPP pts (24 literature cases since 1996 meriting a BP-HPP diagnosis, plus our 17), most (26) had AR BP-HPP.  Maternally transmitted HPP affected eleven of the 13 AD BP-HPP probands (p=0.01), including seven of our eight (p=0.035), supporting a maternal <em>in utero</em> effect.</p>
<p>Fetal packing, heterozygosity, and normal fetal mineralization and chest size seem to identify BP-HPP.  However, bowed fetal long bones with AR HPP, specific <em>TNSALP</em> mutations, or poor skeletal mineralization before the third trimester (including in an abortus) do not reliable diagnose HPP lethality.</p>

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</description>

<author>D Wenkert et al.</author>


</item>


<item>
<title>Atypical Femoral Fractures During Bisphosphonate Exposure In Adult Hypophosphatasia</title>
<link>http://opus.ipfw.edu/chemistry_facpubs/48</link>
<guid isPermaLink="true">http://opus.ipfw.edu/chemistry_facpubs/48</guid>
<pubDate>Tue, 08 May 2012 11:09:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>We report a 55-year-old woman who suffered atypical subtrochanteric femoral fractures (ASFFs) after 4 years of exposure to alendronate and then zolendronate given for "osteoporosis." Before alendronate treatment, she had low bone mineral density. After several months of therapy, metatarsal stress fractures began. Bisphosphonate (BP) administration was stopped following the ASFFs, and the adult form of hypophosphatasia (HPP) was diagnosed from low serum alkaline phosphatase (ALP) activity, high endogenous levels of two natural substrates for the "tissue-nonspecific" isoenzyme of ALP (TNSALP), and a heterozygous mutation within the gene that encodes this enzyme. Experience with other HPP families showed that her mutation (Arg71His) with a second defective TNSALP allele can cause severe HPP in infancy, and when heterozygous can cause mild HPP featuring premature loss of deciduous teeth in children. Because the skeletal disease of HPP results from extracellular accumulation of the TNSALP substrate inorganic pyrophosphate (PPi) and its inhibitory effect on mineralization, perhaps HPP patients or carriers will have adverse effects from BPs. BPs are analogues of PPi and can suppress bone turnover but also deactivate TNSALP. Our report is the first of BP exposure preceding ASFFs in adult HPP. To explore a potential role for TNSALP deactivation in ASFFs, mutation analysis of TNSALP should be studied in a cohort of these patients. Meanwhile, clinicians must suspect HPP when clinical or laboratory clues include premature loss of primary dentition, pseudofractures or recurrent poorly healing metatarsal stress fractures, a family history suggestive of HPP, or low serum ALP activity. If HPP is documented, BP treatment might be avoided. To establish the diagnosis of HPP, assays for two natural substrates for TNSALP and TNSALP mutation analysis are available in commercial laboratories. With positive findings, radiological or bone biopsy evidence of acquired osteomalacia would indicate the adult form of this inborn-error-of-metabolism. (c) 2012 American Society for Bone and Mineral Research</p>

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</description>

<author>Roger A.L. Sutton et al.</author>


</item>


<item>
<title>Environment and Hybrid Influences on Rapid-Visco-Analysis Flour Properties of Food-Grade Grain Sorghum</title>
<link>http://digitalcommons.unl.edu/foodsciefacpub/112</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/foodsciefacpub/112</guid>
<pubDate>Tue, 08 May 2012 11:08:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Grain processors would benefi t from information about the production environment and the infl uences of the sorghum [Sorghum bicolor (L.) Moench] hybrid on food-grade fl our properties. The objective of this study was to determine the effects of environment and hybrid on rapid-visco-analysis (RVA) fl our properties of commercially available food-grade sorghum. A randomized complete block experiment was planted in 12 environments, which included the 2004 and 2005 growing seasons and irrigated and dryland water regimes in eastern, central, and west central Nebraska, and a dryland, low-N environment in eastern Nebraska. The environment accounted for 71–85% of the total variation in RVA parameters, while the hybrid accounted for 11–23% and the environmentby- hybrid interaction, 1–3%. Unfortunately, the results of this experiment suggest that it is diffi cult to predict the effect that environment will have on resulting sorghum-fl our parameters. Although of secondary importance in terms of total variation in sorghum-fl our RVA properties, the choice of hybrid predictably and signifi - cantly contributes to sorghum-starch viscosity properties. Food-grade hybrids were grouped based on viscosity properties into those best suited for dry-mill and alkaline-cooked products (Asgrow Orbit; Sorghum Partners NK1486) and those best suited for porridge, consumable alcohol, and ethanol production (Kelly Green Seeds KG6902; NC+ Hybrids 7W92; Asgrow Eclipse; and Fontanelle W-1000). These results were consistent with those previously reported for grain density.</p>

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</description>

<author>Joni K. Griess et al.</author>


</item>


<item>
<title>Environment and Hybrid Influences on Food-Grade Sorghum Grain Yield and Hardness</title>
<link>http://digitalcommons.unl.edu/foodsciefacpub/111</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/foodsciefacpub/111</guid>
<pubDate>Tue, 08 May 2012 11:08:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Few studies have examined grain quality of food-grade sorghum hybrids. The objective of this study was to determine the effects of environment and hybrid on grain quality of commercially available food-grade sorghums. A randomized complete block experiment with three replications was planted in 12 environments, which included the 2004 and 2005 growing seasons and irrigated and dryland water regimes in eastern, central, and west central Nebraska and a dryland low-N environment in eastern Nebraska. Environment accounted for 5 to 140 times greater variation in measured parameters than hybrid, and the hybrid × environment interaction accounted for less than 2% of the total variation. Grain yield and kernel mass varied, with low yields of 1.4 Mg ha<sup>−1</sup> and kernels weighing 9.5 g 1000 kernels<sup>−1</sup> in the low-N 2004 environment, high grain yields of 10.5 Mg ha<sup>−1</sup> under irrigated conditions in central Nebraska in 2005, and kernels weighing 27.8 g 1000 kernels<sup>−1</sup> in the eastern Nebraska dryland 2005 environment. Harder grain was produced in 2005 than in 2004, with the west central and central 2005 environments having the lowest tangential abrasive dehulling device (TADD) removals of 14%. Non-food-grade hybrids produced higher grain yields and kernel mass than food-grade hybrids. Grain hardness was greater for nonfood- grade and medium maturity hybrids when environmental means were lower (i.e., softer) but showed little or no difference in hardness when environmental means were high. Nebraska production environments have the capability to produce high quality food-grade sorghums for specific food uses to benefit both the producer and the food processor.</p>

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</description>

<author>Joni K. Griess et al.</author>


</item>


<item>
<title>Reduced Bone Density Concomitant with Metabolic Abnormalities in Type 1 Diabetic (T1D) Patients</title>
<link>http://opus.ipfw.edu/chemistry_facpres/28</link>
<guid isPermaLink="true">http://opus.ipfw.edu/chemistry_facpres/28</guid>
<pubDate>Tue, 08 May 2012 11:05:30 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>P G. Masse et al.</author>


</item>


<item>
<title>Yearning for Restoration</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/383</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/383</guid>
<pubDate>Tue, 08 May 2012 11:03:49 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Stacy Minger</author>


</item>


<item>
<title>Highly sensitive and reversible silicon nanowire biosensor to study nuclear hormone receptor protein and response element DNA interactions.</title>
<link>http://mouseion.jax.org/stfb2010/171</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/171</guid>
<pubDate>Tue, 08 May 2012 11:02:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>To thoroughly understand the role that estrogen receptors partake in regulation of gene expression, characterization of estrogen receptors (ERs) and estrogen-response elements (EREs) interactions is essential. In the work, we    present a highly sensitive and reusable silicon nanowire (SiNW) biosensor to study the interactions between human ER proteins (ER, alpha and beta subtypes) and EREs (dsDNA). The proteins were covalently immobilized on the SiNW surface.  Various    EREs including wild-type, mutant and scrambled DNA sequences were then applied to the protein-functionalized SiNW surface. Due to negatively charged dsDNA, binding of the EREs to the ERs on the n-type SiNW biosensor leads to the accumulation of    negative charges on the surface, thereby inducing increase in resistance. The results show that the specificity of the ERE-ERalpha binding is higher than that of the ERE-ERbeta binding, what is more, the mutant ERE reduces the binding affinity    for both ERalpha and ERbeta. By applying various concentrations of wild-type ERE to the bound ERalpha, a very low concentration of 10 fM wild-type ERE was found to be able to bind to the ERalpha. The reversible association and dissociation    between ERalpha and wt-ERE was achieved, pointing to a reusable biosensor for protein-DNA binding. Through the study, we have established the SiNW biosensor as a promising method in providing comprehensive study for hormone receptor-response    element interactions.</p>

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</description>

<author>G J. Zhang et al.</author>


</item>


<item>
<title>Multi-variant pathway association analysis reveals the importance of genetic determinants of estrogen metabolism in breast and endometrial cancer susceptibility.</title>
<link>http://mouseion.jax.org/stfb2010/170</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/170</guid>
<pubDate>Tue, 08 May 2012 11:02:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite the central role of estrogen exposure in breast and endometrial cancer development and numerous studies of genes in the estrogen metabolic pathway, polymorphisms within the pathway have not been consistently associated with    these cancers. We posit that this is due to the complexity of multiple weak genetic effects within the metabolic pathway that can only be effectively detected through multi-variant analysis. We conducted a comprehensive association analysis of    the estrogen metabolic pathway by interrogating 239 tagSNPs within 35 genes of the pathway in three tumor samples. The discovery sample consisted of 1,596 breast cancer cases, 719 endometrial cancer cases, and 1,730 controls from Sweden; and the    validation sample included 2,245 breast cancer cases and 1,287 controls from Finland. We performed admixture maximum likelihood (AML)-based global tests to evaluate the cumulative effect from multiple SNPs within the whole metabolic pathway and    three sub-pathways for androgen synthesis, androgen-to-estrogen conversion, and estrogen removal. In the discovery sample, although no single polymorphism was significant after correction for multiple testing, the pathway-based AML global test    suggested association with both breast (p(global) = 0.034) and endometrial (p(global) = 0.052) cancers. Further testing revealed the association to be focused on polymorphisms within the androgen-to-estrogen conversion sub-pathway, for both    breast (p(global) = 0.008) and endometrial cancer (p(global) = 0.014). The sub-pathway association was validated in the Finnish sample of breast cancer (p(global) = 0.015). Further tumor subtype analysis demonstrated that the association of the    androgen-to-estrogen conversion sub-pathway was confined to postmenopausal women with sporadic estrogen receptor positive tumors (p(global) = 0.0003). Gene-based AML analysis suggested CYP19A1 and UGT2B4 to be the major players within the    sub-pathway. Our study indicates that the composite genetic determinants related to the androgen-estrogen conversion are important for the induction of two hormone-associated cancers, particularly for the hormone-driven breast tumour    subtypes.</p>

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</description>

<author>Y L. Low et al.</author>


</item>


<item>
<title>Q&amp;A: ChIP-seq technologies and the study of gene regulation.</title>
<link>http://mouseion.jax.org/stfb2010/169</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/169</guid>
<pubDate>Tue, 08 May 2012 11:02:06 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E T. Liu et al.</author>


</item>


<item>
<title>Cancer genomes.</title>
<link>http://mouseion.jax.org/stfb2010/168</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/168</guid>
<pubDate>Tue, 08 May 2012 11:02:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E P. Diamandis et al.</author>


</item>


<item>
<title>Pyrosequencing enhancement for better detection limit and sequencing homopolymers.</title>
<link>http://mouseion.jax.org/stfb2010/167</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/167</guid>
<pubDate>Tue, 08 May 2012 11:01:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pyrosequencing is a DNA sequencing technique based on sequencing-by-synthesis enabling rapid and real-time sequence determination. Although ample genomic research has been undertaken using pyrosequencing, the requirement of    relatively high amount of DNA template and the difficulty in sequencing the homopolymeric regions limit its key advantages in the applications directing towards clinical research. In this study, we demonstrate that pyrosequencing on homopolymeric    regions with 10 identical nucleotides can be successfully performed with optimal amount of DNA (0.3125-5 pmol) immobilized on conventional non-porous Sepharose beads. We also validate that by using porous silica beads, the sequencing signal    increased 3.5-folds as compared to that produced from same amount of DNA immobilized on solid Sepharose beads. Our results strongly indicate that with optimized quantity of DNA and suitable solid support, the performance of pyrosequencing on    homopolymeric regions and its detection limit has been significantly improved.</p>

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</description>

<author>M Gong et al.</author>


</item>


<item>
<title>The Archon Genomics X PRIZE for whole human genome sequencing.</title>
<link>http://mouseion.jax.org/stfb2010/166</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/166</guid>
<pubDate>Tue, 08 May 2012 11:01:47 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>L Kedes et al.</author>


</item>


<item>
<title>Mutation of Eif4g3, encoding a eukaryotic translation initiation factor, causes male infertility and meiotic arrest of mouse spermatocytes.</title>
<link>http://mouseion.jax.org/stfb2010/165</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/165</guid>
<pubDate>Tue, 08 May 2012 11:01:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ENU-induced repro8 mutation was identified in a screen to uncover genes that control mouse gametogenesis. repro8 causes male-limited infertility, with failure of spermatocytes to exit meiotic prophase via the G2/MI transition.    The repro8 mutation is in the Eif4g3 gene, encoding eukaryotic translation initiation factor 4, gamma 3. Mutant germ cells appear to execute events of meiotic prophase normally, and many proteins characteristic of the prophase-to-metaphase    transition are not obviously depleted. However, activity of CDC2A (CDK1) kinase is dramatically reduced in mutant spermatocytes. Strikingly, HSPA2, a chaperone protein for CDC2A kinase, is absent in mutant spermatocytes in spite of the presence    of Hspa2 transcript, consistent with the observation that the repro8 phenotype is markedly similar to the phenotype of the Hspa2 knockout. Thus, EIF4G3 is required for HSPA2 translation in spermatocytes, a finding that provides the first genetic    evidence for selective translational control of meiotic exit in mammalian spermatocytes.</p>

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</description>

<author>F Sun et al.</author>


</item>


<item>
<title>Expression of the transcription factor, TFII-I, during post-implantation mouse embryonic development.</title>
<link>http://mouseion.jax.org/stfb2010/164</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/164</guid>
<pubDate>Tue, 08 May 2012 11:01:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>ABSTRACT: BACKGROUND: General transcription factor (TFII-I) is a multi-functional transcription factor encoded by the Gtf2i gene, that has been demonstrated to regulate transcription of genes critical for development. Because of the    broad range of genes regulated by TFII-I as well as its potential role in a significant neuro-developmental disorder, developing a comprehensive expression profile is critical to the study of this transcription factor. We sought to define the    timing and pattern of expression of TFII-I in post-implantation embryos at a time during which many putative TFII-I target genes are expressed. FINDINGS: Antibodies to the N-terminus of TFII-I were used to probe embryonic mouse sections. TFII-I    protein is widely expressed in the developing embryo. TFII-I is expressed throughout the period from E8-E16. However, within this period there are striking shifts in localization from cytoplasmic predominant to nuclear.  TFII-I expression varies    in both a spatial and temporal fashion. There is extensive expression in neural precursors at E8. This expression persists at later stages. TFII-I is expressed in developing lung, heart and gut structures.  There is no evidence of isoform    specific expression. Available data regarding expression patterns at both an RNA and protein level throughout development are also comprehensively reviewed. CONCLUSIONS: Our immunohistochemical studies of the temporal and spatial expression    patterns of TFII-I in mouse embryonic sections are consistent with the hypothesis that hemizygous deletion of GTF2I in individuals with Williams-Beuren Syndrome contributes to the distinct cognitive and physiological symptoms associated with the    disorder.</p>

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</description>

<author>I Fijalkowska et al.</author>


</item>


<item>
<title>Principal Component Analysis in the Eigenface Technique for Facial Recognition</title>
<link>http://digitalrepository.trincoll.edu/theses/216</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/216</guid>
<pubDate>Tue, 08 May 2012 11:01:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Several facial recognition algorithms have been explored in the past few decades. Progress has been made towards recognition under varying lighting conditions, poses and facial expressions. In a general context, a facial recognition algorithm and its implementation can be considered as a system. The input to the facial recognition system is a two dimensional image, while the system distinguishes the input image as a user’s face from a pre-determined library of faces. Finally, the output is the discerned face image. In this project, we will examine one particular system: the Eigenface technique.</p>

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</description>

<author>Kevin Huang</author>


</item>


<item>
<title>Pathbase and the MPATH ontology. Community resources for mouse histopathology.</title>
<link>http://mouseion.jax.org/stfb2010/163</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/163</guid>
<pubDate>Tue, 08 May 2012 11:01:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pathbase, the database of mouse histopathology images, was developed as a resource to provide free access to representative images of lesions in background and mutant strains of laboratory mice. When utilized with diagnostic workups    or phenotyping of mutant mice, it can provide a "virtual second opinion" for those working without access to groups of experienced pathologists. This is a community resource, and it facilitates the sharing of expertise and data among members of    the pathology community worldwide. MPATH-the mouse pathology ontology-was developed alongside Pathbase for the annotation of images and now represents an important resource for the coding of diagnoses, permitting sophisticated data retrieval and    computational analysis of mouse phenotypes. In this article, the structure and use of MPATH is discussed, along with current and future challenges for the coding of mutant mouse phenotypes.</p>

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</description>

<author>P N. Schofield et al.</author>


</item>


<item>
<title>La línea divisoria que une: Una exploración de la cultura híbrida en la región fronteriza entre México y los Estados Unidos</title>
<link>http://digitalrepository.trincoll.edu/theses/215</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/215</guid>
<pubDate>Tue, 08 May 2012 11:01:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>With the creation of our “modern world” came the ideology and system of nation-states. Land in its most natural and undivided condition was marked, fenced, walled, and mapped in order to give direct power of territory to a nation-state. The borderline between the United States and Mexico was established not so long ago, in 1857 after the US-Mexico War. The United States seized the opportunity to expand its “borders of freedom,” and waged war in order to conquer land that was part of Mexico. Once half of Mexico’s territory was taken, the borderline was established. However, from these historical roots, a complex and hybrid culture exists in this border region, along with a strong borderlander,<em> fronterizo </em>identity. This region has sparked the interest of many in the past, and has given rise to an extensive body of studies and theories.</p>
<p>For my thesis, I wanted to explore this region’s culture and identity from a unique and interesting angle. My first chapter is a consensus of a variety of studies on the US-Mexico borderland and also an explanation of Even-Zohar’s theory of the laws of cultural interference. In my second chapter I explore the complicated topic of identity in the borderland, which is varied due to southern Mexican and Central American immigration, but a cogent reality for those inhabitants who identify strongly as “borderlanders.” For my final chapter, I applied and evaluated the laws of Even-Zohar’s theory to a set of photographs of the borderland from Alex Webb’s <em>Crossings. </em>In evaluating his theory, I found that although there is a prominence and influence of American culture in the Mexican borderland, there is a balance between Mexican culture and American culture. A hybrid culture truly exists and forms a unique border culture. From this conclusion, I propose that the unity found between the borderlanders and their culture is an example and call for the governments of the United States and Mexico to do the same in order to solve the various drug trafficking and immigration conflicts in this region. More divisions should not be put up; instead, more cooperation is necessary. A borderline wall has not and will not solve anything, and certainly does not stop the flow of cultures. The borderland challenges the power of nation-states and borders, demonstrating the strength and significance culture has.</p>

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</description>

<author>Molly J. Foye</author>


</item>


<item>
<title>A missense mutation in a highly conserved alternate exon of dynamin-1 causes epilepsy in fitful mice.</title>
<link>http://mouseion.jax.org/stfb2010/162</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/162</guid>
<pubDate>Tue, 08 May 2012 11:01:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dynamin-1 (Dnm1) encodes a large multimeric GTPase necessary for activity-dependent membrane recycling in neurons, including synaptic vesicle endocytosis. Mice heterozygous for a novel spontaneous Dnm1 mutation--fitful--experience    recurrent seizures, and homozygotes have more debilitating, often lethal seizures in addition to severe ataxia and neurosensory deficits. Fitful is a missense mutation in an exon that defines the DNM1a isoform, leaving intact the alternatively    spliced exon that encodes DNM1b. The expression of the corresponding alternate transcripts is developmentally regulated, with DNM1b expression highest during early neuronal development and DNM1a expression increasing postnatally with synaptic    maturation. Mutant DNM1a does not efficiently self-assemble into higher order complexes known to be necessary for proper dynamin function, and it also interferes with endocytic recycling in cell culture. In mice, the mutation results in defective    synaptic transmission characterized by a slower recovery from depression after trains of stimulation. The DNM1a and DNM1b isoform pair is highly conserved in vertebrate evolution, whereas invertebrates have only one isoform. We speculate that the    emergence of more specialized forms of DNM1 may be important in organisms with complex neuronal function.</p>

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</description>

<author>R M. Boumil et al.</author>


</item>


<item>
<title>Analysis of Reaction Forces  In a Beam Leaning Against a Wall</title>
<link>http://digitalrepository.trincoll.edu/theses/214</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/214</guid>
<pubDate>Tue, 08 May 2012 11:01:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite the ubiquity of the situation of a ladder standing against a wall, there does not yet exist a universally accepted, valid solution for the mechanical problem. In addition to being a socially relevant problem, it requires the use of interesting analytical techniques in statics and the mechanics of solids to fully address. Here, we present a model of the physics of a ladder and determine the reaction forces on the ladder.</p>

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</description>

<author>Lorenzo Sewanan</author>


</item>


<item>
<title>Clinical ramifications of the MHC family Fc receptor FcRn.</title>
<link>http://mouseion.jax.org/stfb2010/161</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/161</guid>
<pubDate>Tue, 08 May 2012 11:01:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>INTRODUCTION: Knowledge that antibodies of the IgG isotype have remarkably extended persistence in circulation and are able to pass through cell barriers has substantial implications. While it is well established that so-called    neonatal Fc receptor, FcRn, acts throughout life to confer these unusual properties, its ramifications on clinical medicine and therapeutic uses are not broadly appreciated. SCOPE: Here we discuss basic principles and gaps in understanding of    FcRn, including its management of IgG antibodies and along with albumin, its impact on use and design of antibody-based therapeutics, and its genetics.</p>

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</description>

<author>D C. Roopenian et al.</author>


</item>


<item>
<title>Epistasis contributes to the genetic buffering of plasma HDL cholesterol in mice.</title>
<link>http://mouseion.jax.org/stfb2010/160</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/160</guid>
<pubDate>Tue, 08 May 2012 11:01:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Stressful environmental factors, such as a high-fat diet, can induce responses in the expression of genes that act to maintain physiological homeostasis. We observed variation in plasma concentrations of high-density lipoprotein    (HDL) cholesterol across inbred mouse strains in response to high dietary fat intake.  Several strains, including C57BL/6J, have stable levels of plasma HDL independent of diet, whereas other strains, including DBA2/J, show marked changes in    plasma HDL. To explore this phenomenon further, we used publicly available data from a C57BL/6J x DBA/2J intercross to identify genetic factors that associate with HDL under high-fat diet conditions. Our analysis identified an epistatic    interaction that plays a role in the buffering of HDL levels in C57BL/6J mice, and we have identified Arl4d as a candidate gene that mediates this effect. Structural modeling further elucidates the interaction of genetic factors that contribute    to the robustness of HDL in response to high-fat diet in the C57BL/6J strain.</p>

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</description>

<author>R H. Li et al.</author>


</item>


<item>
<title>Effects of Land Use in the Ohio River Basin on the Distribution of Coliform and Antibiotic Resistant Bacteria in the Ohio River</title>
<link>http://mds.marshall.edu/etd/218</link>
<guid isPermaLink="true">http://mds.marshall.edu/etd/218</guid>
<pubDate>Tue, 08 May 2012 11:01:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recent studies indicate that antibiotic resistant bacteria can be useful as indicators of water quality (1, 2, 5, 7, 8, 9, 10). Studies in our laboratory have shown that fecal pollution did not fully explain the distribution or the frequency of antibiotic resistant bacteria in the Ohio River (27, 28). Therefore, it is important to understand the factors that affect the distribution of antibiotic resistant bacteria in aquatic habitat. The purpose of this study was to examine the correlations between land use, water quality, and concentration of antibiotic resistant bacteria in the Ohio River. Mid-channel water samples were collected at five mile intervals in the Ohio River and all major tributaries. Total cultivable bacteria and selected antibiotic resistant bacteria were cultivated on R2A agar. Antibiotic resistant total coliforms and Escherichia coli were enumerated using ColilertÔ reagent (IDEXX Laboratories, Inc., Westbrook, ME) and Quanti-Tray/2000Ô. Land use features were obtained from the national land cover data (NLCD) gathered from the USGS website. The data were then put into ArcGIS® (ESRI, Redlands, CA) and were used with microbiological data to analyze the association between land use and microbial communities. CANOCO 4.5 was used to determine the spatial differences between each site. Linear regression models were used to determine trends between land use and individual microbial communities. The data suggested residential, commercial and, in some cases, wetland land use types have a significant and proportional relationship and that farming and forested areas have a significant but inverse relationship between land use and bacterial abundance.</p>

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</description>

<author>Gene Chou</author>


<category>&lt;p&gt;Bacteria - Ohio River.&lt;/p&gt;
&lt;p&gt;Water quality - Ohio River.&lt;/p&gt;</category>

</item>


<item>
<title>Functional genomics complements quantitative genetics in identifying disease-gene associations.</title>
<link>http://mouseion.jax.org/stfb2010/159</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/159</guid>
<pubDate>Tue, 08 May 2012 11:01:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>An ultimate goal of genetic research is to understand the connection between genotype and phenotype in order to improve the diagnosis and treatment of diseases. The quantitative genetics field has developed a suite of statistical    methods to associate genetic loci with diseases and phenotypes, including quantitative trait loci (QTL) linkage mapping and genome-wide association studies (GWAS). However, each of these approaches have technical and biological shortcomings. For    example, the amount of heritable variation explained by GWAS is often surprisingly small and the resolution of many QTL linkage mapping studies is poor. The predictive power and interpretation of QTL and GWAS results are consequently limited. In    this study, we propose a complementary approach to quantitative genetics by interrogating the vast amount of high-throughput genomic data in model organisms to functionally associate genes with phenotypes and diseases. Our algorithm combines the    genome-wide functional relationship network for the laboratory mouse and a state-of-the-art machine learning method. We demonstrate the superior accuracy of this algorithm through predicting genes associated with each of 1157 diverse phenotype    ontology terms. Comparison between our prediction results and a meta-analysis of quantitative genetic studies reveals both overlapping candidates and distinct, accurate predictions uniquely identified by our approach. Focusing on bone mineral    density (BMD), a phenotype related to osteoporotic fracture, we experimentally validated two of our novel predictions (not observed in any previous GWAS/QTL studies) and found significant bone density defects for both Timp2 and Abcg8 deficient    mice. Our results suggest that the integration of functional genomics data into networks, which itself is informative of protein function and interactions, can successfully be utilized as a complementary approach to quantitative genetics to    predict disease risks. All supplementary material is available at http://cbfg.jax.org/phenotype.</p>

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</description>

<author>Y Guan et al.</author>


</item>


<item>
<title>Disheveled hair and ear (Dhe), a spontaneous mouse Lmna mutation modeling human laminopathies.</title>
<link>http://mouseion.jax.org/stfb2010/158</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/158</guid>
<pubDate>Tue, 08 May 2012 11:01:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Investigations of naturally-occurring mutations in animal models provide important insights and valuable disease models. Lamins A and C, along with lamin B, are type V intermediate filament proteins which constitute the    proteinaceous boundary of the nucleus. LMNA mutations in humans cause a wide range of phenotypes, collectively termed laminopathies. To identify the mutation and investigate the phenotype of a spontaneous, semi-dominant mutation that we have    named Disheveled hair and ear (Dhe), which causes a sparse coat and small external ears in heterozygotes and lethality in homozygotes by postnatal day 10.  FINDINGS: Genetic mapping identified a point mutation in the Lmna gene, causing a single    amino acid change, L52R, in the coiled coil rod domain of lamin A and C proteins. Cranial sutures in Dhe/+ mice failed to close. Gene expression for collagen types I and III in sutures was deficient. Skulls were small and disproportionate.    Skeletons of Dhe/+ mice were hypomineralized and total body fat was deficient in males. In homozygotes, skin and oral mucosae were dysplastic and ulcerated. Nuclear morphometry of cultured cells revealed gene dose-dependent blebbing and    wrinkling. CONCLUSION: Dhe mice should provide a useful new model for investigations of the pathogenesis of laminopathies.</p>

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</description>

<author>P R. Odgren et al.</author>


</item>


<item>
<title>Coordinated expression domains in mammalian genomes.</title>
<link>http://mouseion.jax.org/stfb2010/157</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/157</guid>
<pubDate>Tue, 08 May 2012 11:01:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Gene order in eukaryotic genomes is not random. Genes showing similar expression (coexpression) patterns are often clustered along the genome. The goal of this study is to characterize coexpression clustering in    mammalian genomes and to investigate the underlying mechanisms. METHODOLOGY/PRINCIPAL FINDINGS: We detect clustering of coexpressed genes across multiple scales, from neighboring genes to chromosomal domains that span tens of megabases and, in    some cases, entire chromosomes. Coexpression domains may be positively or negatively correlated with other domains, within and between chromosomes. We find that long-range expression domains are associated with gene density, which in turn is    related to physical organization of the chromosomes within the nucleus. We show that gene expression changes between healthy and diseased tissue samples occur in a gene density-dependent manner. CONCLUSIONS/SIGNIFICANCE: We demonstrate that    coexpression domains exist across multiple scales. We identify potential mechanisms for short-range as well as long-range coexpression domains. We provide evidence that the three-dimensional architecture of the chromosomes may underlie long-range    coexpression domains. Chromosome territory reorganization may play a role in common human diseases such as Alzheimer's disease and psoriasis.</p>

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</description>

<author>Y H. Woo et al.</author>


</item>


<item>
<title>Mouse gestation length is genetically determined.</title>
<link>http://mouseion.jax.org/stfb2010/156</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/156</guid>
<pubDate>Tue, 08 May 2012 11:00:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Preterm birth is an enormous public health problem, affecting over 12% of live births and costing over $26 billion in the United States alone. The causes are complex, but twin studies support the role of genetics in    determining gestation length. Despite widespread use of the mouse in studies of the genetics of preterm birth, there have been few studies that actually address the precise natural gestation length of the mouse, and to what degree the timing of    labor and birth is genetically determined. METHODOLOGY/PRINCIPAL FINDINGS: To further develop the mouse as a genetic model of preterm birth, we developed a high-throughput monitoring system and measured the gestation length in 15 inbred strains.    Our results show an unexpectedly wide variation in overall gestation length between strains that approaches two full days, while intra-strain variation is quite low. Although litter size shows a strong inverse correlation with gestation length,    genetic difference alone accounts for a significant portion of the variation. In addition, ovarian transplant experiments support a primary role of maternal genetics in the determination of gestation length.  Preliminary analysis of gestation    length in the C57BL/6J-Chr#(A/J)/NaJ chromosome substitution strain (B.A CSS) panel suggests complex genetic control of gestation length. CONCLUSIONS/SIGNIFICANCE: Together, these data support the role of genetics in regulating gestation length    and present the mouse as an important tool for the discovery of genes governing preterm birth.</p>

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</description>

<author>S A. Murray et al.</author>


</item>


<item>
<title>Patterns of recombination activity on mouse chromosome 11 revealed by high resolution mapping.</title>
<link>http://mouseion.jax.org/stfb2010/155</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/155</guid>
<pubDate>Tue, 08 May 2012 11:00:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>The success of high resolution genetic mapping of disease predisposition and quantitative trait loci in humans and experimental animals depends on the positions of key crossover events around the gene of interest. In mammals, the    majority of recombination occurs at highly delimited 1-2 kb long sites known as recombination hotspots, whose locations and activities are distributed unevenly along the chromosomes and are tightly regulated in a sex specific manner. The factors    determining the location of hotspots started to emerge with the finding of PRDM9 as a major hotspot regulator in mammals, however, additional factors modulating hotspot activity and sex specificity are yet to be defined. To address this    limitation, we have collected and mapped the locations of 4829 crossover events occurring on mouse chromosome 11 in 5858 meioses of male and female reciprocal F1 hybrids of C57BL/6J and CAST/EiJ mice. This chromosome was chosen for its medium    size and high gene density and provided a comparison with our previous analysis of recombination on the longest mouse chromosome 1. Crossovers were mapped to an average resolution of 127 kb, and thirteen hotspots were mapped to <8 kb. Most crossovers occurred in a small number of the most active hotspots. Females had higher recombination rate than males as a consequence of differences in crossover interference and regional variation of sex specific rates along the chromosome. Comparison with chromosome 1 showed that recombination events tend to be positioned in similar fashion along the centromere-telomere axis but independently of the local gene density. It appears that mammalian recombination is regulated on at least three>levels, chromosome-wide, regional, and at individual hotspots, and these regulation levels are influenced by sex and genetic background but not by gene content.</p>

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</description>

<author>T Billings et al.</author>


</item>


<item>
<title>A mouse model of heritable cerebrovascular disease.</title>
<link>http://mouseion.jax.org/stfb2010/154</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/154</guid>
<pubDate>Tue, 08 May 2012 11:00:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>The study of animal models of heritable cerebrovascular diseases can improve our understanding of disease mechanisms, identify candidate genes for related human disorders, and provide experimental models for preclinical trials. Here    we describe a spontaneous mouse mutation that results in reproducible, adult-onset, progressive, focal ischemia in the brain. The pathology is not the result of hemorrhage, embolism, or an anatomical abnormality in the cerebral vasculature.  The    mutation maps as a single site recessive locus to mouse Chromosome 9 at 105 Mb, a region of shared synteny with human chromosome 3q22. The genetic interval, defined by recombination mapping, contains seven protein-coding genes and one processed    transcript, none of which are changed in their expression level, splicing, or sequence in affected mice. Targeted resequencing of the entire interval did not reveal any provocative changes; thus, the causative molecular lesion has not been    identified.</p>

	]]>
</description>

<author>T J. Sproule et al.</author>


</item>


<item>
<title>Nerve terminal degeneration is independent of muscle fiber genotype in SOD1 mice.</title>
<link>http://mouseion.jax.org/stfb2010/153</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/153</guid>
<pubDate>Tue, 08 May 2012 11:00:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Motor neuron degeneration in SOD1(G93A) transgenic mice begins at the nerve terminal. Here we examine whether this degeneration depends on expression of mutant SOD1 in muscle fibers. METHODOLOGY/PRINCIPAL FINDINGS:    Hindlimb muscles were transplanted between wild-type and SOD1(G93A) transgenic mice and the innervation status of neuromuscular junctions (NMJs) was examined after 2 months.  The results showed that muscles from SOD1(G93A) mice did not induce    motor terminal degeneration in wildtype mice and that muscles from wildtype mice did not prevent degeneration in SOD1(G93A) transgenic mice. Control studies demonstrated that muscles transplanted from SOD1(G93A) mice continued to express mutant    SOD1 protein. Experiments on wildtype mice established that the host supplied terminal Schwann cells (TSCs) at the NMJs of transplanted muscles.  CONCLUSIONS/SIGNIFICANCE: These results indicate that expression of the mutant protein in muscle is    not needed to cause motor terminal degeneration in SOD1(G93A) transgenic mice and that a combination of motor terminals, motor axons and Schwann cells, all of which express mutant protein may be sufficient.</p>

	]]>
</description>

<author>D I. Carrasco et al.</author>


</item>


<item>
<title>CGDSNPdb: a database resource for error-checked and imputed mouse SNPs.</title>
<link>http://mouseion.jax.org/stfb2010/152</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/152</guid>
<pubDate>Tue, 08 May 2012 11:00:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Center for Genome Dynamics Single Nucleotide Polymorphism Database (CGDSNPdb) is an open-source value-added database with more than nine million mouse single nucleotide polymorphisms (SNPs), drawn from multiple sources, with    genotypes assigned to multiple inbred strains of laboratory mice. All SNPs are checked for accuracy and annotated for properties specific to the SNP as well as those implied by changes to overlapping protein-coding genes. CGDSNPdb serves as the    primary interface to two unique data sets, the 'imputed genotype resource' in which a Hidden Markov Model was used to assess local haplotypes and the most probable base assignment at several million genomic loci in tens of strains of mice, and    the Affymetrix Mouse Diversity Genotyping Array, a high density microarray with over 600,000 SNPs and over 900,000 invariant genomic probes.  CGDSNPdb is accessible online through either a web-based query tool or a MySQL public login. Database    URL: http://cgd.jax.org/cgdsnpdb/</p>

	]]>
</description>

<author>L N. Hutchins et al.</author>


</item>


<item>
<title>Finding and sharing: new approaches to registries of databases and services for the biomedical sciences.</title>
<link>http://mouseion.jax.org/stfb2010/151</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/151</guid>
<pubDate>Tue, 08 May 2012 11:00:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>The recent explosion of biological data and the concomitant proliferation of distributed databases make it challenging for biologists and bioinformaticians to discover the best data resources for their needs, and the most efficient    way to access and use them. Despite a rapid acceleration in uptake of syntactic and semantic standards for interoperability, it is still difficult for users to find which databases support the standards and interfaces that they need. To solve    these problems, several groups are developing registries of databases that capture key metadata describing the biological scope, utility, accessibility, ease-of-use and existence of web services allowing interoperability between resources. Here,    we describe some of these initiatives including a novel formalism, the Database Description Framework, for describing database operations and functionality and encouraging good database practise. We expect such approaches will result in improved    discovery, uptake and utilization of data resources. Database URL: http://www.casimir.org.uk/casimir_ddf.</p>

	]]>
</description>

<author>D Smedley et al.</author>


</item>


<item>
<title>Sequence variation at multiple loci influences red cell hemoglobin concentration.</title>
<link>http://mouseion.jax.org/stfb2010/150</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/150</guid>
<pubDate>Tue, 08 May 2012 11:00:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>A substantial genetic contribution underlies variation in baseline peripheral blood counts. We performed quantitative trait locus/loci analyses to identify chromosome regions harboring genes influencing red cell hemoglobin    concentration using the cell hemoglobin concentration mean (CHCM), a directly measured parameter analogous to the mean cell hemoglobin concentration. Fourteen significant loci (gene symbols Chcmq1-Chcmq14) were detected. Seven of these influenced    CHCM in a sex-specific fashion, and 2 showed significant interactive effects (epistasis). For quantitative trait locus/loci detected in multiple crosses, confidence intervals were narrowed using statistical and bioinformatic approaches. Two    strong candidate genes emerged and were further analyzed: adult beta-globin (Hbb) for Chcmq3 on Chr 7, and transferrin (Trf) for Chcmq2 on Chr 9.  High and low allele parental strains in crosses detecting Chcmq3 segregate 100% with the known    ancestral haplotype blocks, hemoglobin (Hb) diffuse (Hbb(d)) and Hb single (Hbb(s)), respectively. Hbb(d) consists of nonidentical major and minor polypeptides and exhibits an increased positive charge relative to Hbb(s) due to the net loss of 2    negative residues in the Hbb(dminor) polypeptide, resulting in a pI of 7.85 versus 7.13. Thus, as shown in human erythrocytes, positively charged Hbs are associated with cell dehydration and increased CHCM in mouse erythrocytes.</p>

	]]>
</description>

<author>L L. Peters et al.</author>


</item>


<item>
<title>A systems-biology approach to modular genetic complexity.</title>
<link>http://mouseion.jax.org/stfb2010/149</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/149</guid>
<pubDate>Tue, 08 May 2012 11:00:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Multiple high-throughput genetic interaction studies have provided substantial evidence of modularity in genetic interaction networks. However, the correspondence between these network modules and specific pathways of information    flow is often ambiguous. Genetic interaction and molecular interaction analyses have not generated large-scale maps comprising multiple clearly delineated linear pathways. We seek to clarify the situation by discerning the difference between    genetic modules and classical pathways. We review a method to optimize the discovery of biologically meaningful genetic modules based on a previously described context-dependent information measure to obtain maximally informative networks. We    compare the results of this method with the established measures of network clustering and find that it balances global and local clustering information in networks. We further discuss the consequences for genetic interaction networks and propose    a framework for the analysis of genetic modularity.</p>

	]]>
</description>

<author>G W. Carter et al.</author>


</item>


<item>
<title>Severe anemia in the Nan mutant mouse caused by sequence-selective disruption of erythroid Kruppel-like factor.</title>
<link>http://mouseion.jax.org/stfb2010/148</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/148</guid>
<pubDate>Tue, 08 May 2012 11:00:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Studies of mouse models of anemia have long provided fundamental insights into red blood cell formation and function. Here we show that the semidominant mouse mutation Nan ("neonatal anemia") carries a single amino acid change    (E339D) within the second zinc finger of the erythroid Kruppel-like factor (EKLF), a critical erythroid regulatory transcription factor. The mutation alters the DNA-binding specificity of EKLF so that it no longer binds promoters of a subset of    its DNA targets. Remarkably, even when mutant Nan and wild-type EKLF alleles are expressed at equivalent levels, the mutant form selectively interferes with expression of EKLF target genes whose promoter elements it no longer binds. This    interference yields a distorted genetic output and selective protein deficiencies that differ from those seen in EKLF-heterozygous and EKLF-null red blood cells and presents a unique and unexpected mechanism of inherited disease.</p>

	]]>
</description>

<author>M Siatecka et al.</author>


</item>


<item>
<title>Humanized nonobese diabetic-scid IL2rgammanull mice are susceptible to lethal Salmonella Typhi infection.</title>
<link>http://mouseion.jax.org/stfb2010/147</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/147</guid>
<pubDate>Tue, 08 May 2012 11:00:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Salmonella enterica serovar Typhi, the cause of typhoid fever, is host-adapted to humans and unable to cause disease in mice. Here, we show that S. Typhi can replicate in vivo in nonobese diabetic (NOD)-scid IL2rgamma(null) mice    engrafted with human hematopoietic stem cells (hu-SRC-SCID mice) to cause a lethal infection with pathological and inflammatory cytokine responses resembling human typhoid. In contrast, S. Typhi does not exhibit net replication or cause illness    in nonengrafted or immunocompetent control animals. Screening of transposon pools in hu-SRC-SCID mice revealed both known and previously unknown Salmonella virulence determinants, including Salmonella Pathogenicity Islands 1, 2, 3, 4, and 6. Our    observations indicate that the presence of human immune cells allows the in vivo replication of S. Typhi in mice. The hu-SRC-SCID mouse provides an unprecedented opportunity to gain insights into S. Typhi pathogenesis and devise strategies for    the prevention of typhoid fever.</p>

	]]>
</description>

<author>S J. Libby et al.</author>


</item>


<item>
<title>Loss of lysophosphatidylcholine acyltransferase 1 leads to photoreceptor degeneration in rd11 mice.</title>
<link>http://mouseion.jax.org/stfb2010/146</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/146</guid>
<pubDate>Tue, 08 May 2012 11:00:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Retinal degenerative diseases, such as retinitis pigmentosa and Leber congenital amaurosis, are a leading cause of untreatable blindness with substantive impact on the quality of life of affected individuals and their families.    Mouse mutants with retinal dystrophies have provided a valuable resource to discover human disease genes and helped uncover pathways critical for photoreceptor function.  Here we show that the rd11 mouse mutant and its allelic strain, B6-JR2845,    exhibit rapid photoreceptor dysfunction, followed by degeneration of both rods and cones. Using linkage analysis, we mapped the rd11 locus to mouse chromosome 13. We then identified a one-nucleotide insertion (c.420-421insG) in exon 3 of the    Lpcat1 gene. Subsequent screening of this gene in the B6-JR2845 strain revealed a seven-nucleotide deletion (c.14-20delGCCGCGG) in exon 1. Both sequence changes are predicted to result in a frame-shift, leading to premature truncation of the    lysophosphatidylcholine acyltransferase-1 (LPCAT1) protein. LPCAT1 (also called AYTL2) is a phospholipid biosynthesis/remodeling enzyme that facilitates the conversion of palmitoyl-lysophosphatidylcholine to dipalmitoylphosphatidylcholine (DPPC).    The analysis of retinal lipids from rd11 and B6-JR2845 mice showed substantially reduced DPPC levels compared with C57BL/6J control mice, suggesting a causal link to photoreceptor dysfunction. A follow-up screening of LPCAT1 in retinitis    pigmentosa and Leber congenital amaurosis patients did not reveal any obvious disease-causing mutations.  Previously, LPCAT1 has been suggested to be critical for the production of lung surfactant phospholipids and biosynthesis of    platelet-activating factor in noninflammatory remodeling pathway. Our studies add another dimension to an essential role for LPCAT1 in retinal photoreceptor homeostasis.</p>

	]]>
</description>

<author>J S. Friedman et al.</author>


</item>


<item>
<title>GRIP1 and 2 regulate activity-dependent AMPA receptor recycling via exocyst complex interactions.</title>
<link>http://mouseion.jax.org/stfb2010/145</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/145</guid>
<pubDate>Tue, 08 May 2012 10:59:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>PSD-95/SAP90/DLG/ZO-1 (PDZ) domain-mediated protein-protein interactions play important roles in regulating AMPA receptor trafficking and neuronal plasticity.  GRIP1 and GRIP2 are homologous multi-PDZ domain-containing proteins that    bind to the C-termini of AMPA-R GluA2 and GluA3 subunits. Previous attempts to determine the cellular roles of GRIP1 and GRIP2 in neurons have been complicated by nonspecific reagents, and by the embryonic lethality of conventional GRIP1 KO mice.    To circumvent these issues we developed a conditional targeted deletion strategy to knock out GRIP1 in postnatal neurons derived from GRIP2 KO mice. Loss of GRIP1 and 2 did not affect normal AMPA-R steady-state trafficking and endocytosis, but    strikingly impaired activity-dependent AMPA-R recycling. This previously uncharacterized role for GRIP1 appears to be mediated by novel interactions with the cellular trafficking machinery via the exocyst protein complex. Indeed, disruption of    GRIP1-exocyst binding caused a strikingly similar deficit in AMPA-R recycling. Together these findings reveal a previously unidentified role for AMPA-R-GRIP1-exocyst protein complexes in activity-dependent AMPA-R trafficking.</p>

	]]>
</description>

<author>L Mao et al.</author>


</item>


<item>
<title>Mutations of the opsin gene (Y102H and I307N) lead to light-induced degeneration of photoreceptors and constitutive activation of phototransduction in mice.</title>
<link>http://mouseion.jax.org/stfb2010/144</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/144</guid>
<pubDate>Tue, 08 May 2012 10:59:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mutations in the Rhodopsin (Rho) gene can lead to autosomal dominant retinitis pigmentosa (RP) in humans. Transgenic mouse models with mutations in Rho have been developed to study the disease. However, it is difficult to know the    source of the photoreceptor (PR) degeneration in these transgenic models because overexpression of wild type (WT) Rho alone can lead to PR degeneration. Here, we report two chemically mutagenized mouse models carrying point mutations in Rho    (Tvrm1 with an Y102H mutation and Tvrm4 with an I307N mutation). Both mutants express normal levels of rhodopsin that localize to the PR outer segments and do not exhibit PR degeneration when raised in ambient mouse room lighting; however, severe    PR degeneration is observed after short exposures to bright light. Both mutations also cause a delay in recovery following bleaching. This defect might be due to a slower rate of chromophore binding by the mutant opsins compared with the WT form,    and an increased rate of transducin activation by the unbound mutant opsins, which leads to a constitutive activation of the phototransduction cascade as revealed by in vitro biochemical assays. The mutant-free opsins produced by the respective    mutant Rho genes appear to be more toxic to PRs, as Tvrm1 and Tvrm4 mutants lacking the 11-cis chromophore degenerate faster than mice expressing WT opsin that also lack the chromophore. Because of their phenotypic similarity to humans with B1    Rho mutations, these mutants will be important tools in examining mechanisms underlying Rho-induced RP and for testing therapeutic strategies.</p>

	]]>
</description>

<author>E Budzynski et al.</author>


</item>


<item>
<title>Oncogenic activation of the Notch1 gene by deletion of its promoter in Ikaros-deficient T-ALL.</title>
<link>http://mouseion.jax.org/stfb2010/143</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/143</guid>
<pubDate>Tue, 08 May 2012 10:59:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Notch pathway is frequently activated in T-cell acute lymphoblastic leukemias (T-ALLs). Of the Notch receptors, Notch1 is a recurrent target of gain-of-function mutations and Notch3 is expressed in all T-ALLs, but it is    currently unclear how these receptors contribute to T-cell transformation in vivo. We investigated the role of Notch1 and Notch3 in T-ALL progression by a genetic approach, in mice bearing a knockdown mutation in the Ikaros gene that    spontaneously develop Notch-dependent T-ALL. While deletion of Notch3 has little effect, T cell-specific deletion of floxed Notch1 promoter/exon 1 sequences significantly accelerates leukemogenesis. Notch1-deleted tumors lack surface Notch1 but    express gamma-secretase-cleaved intracellular Notch1 proteins. In addition, these tumors accumulate high levels of truncated Notch1 transcripts that are caused by aberrant transcription from cryptic initiation sites in the 3' part of the gene.    Deletion of the floxed sequences directly reprograms the Notch1 locus to begin transcription from these 3' promoters and is accompanied by an epigenetic reorganization of the Notch1 locus that is consistent with transcriptional activation.    Further, spontaneous deletion of 5' Notch1 sequences occurs in approximately 75% of Ikaros-deficient T-ALLs. These results reveal a novel mechanism for the oncogenic activation of the Notch1 gene after deletion of its main    promoter.</p>

	]]>
</description>

<author>R Jeannet et al.</author>


</item>


<item>
<title>Zoledronic acid potentiates mTOR inhibition and abolishes the resistance of osteosarcoma cells to RAD001 (Everolimus): pivotal role of the prenylation process.</title>
<link>http://mouseion.jax.org/stfb2010/142</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/142</guid>
<pubDate>Tue, 08 May 2012 10:59:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite recent improvements in therapeutic management of osteosarcoma, ongoing challenges in improving the response to chemotherapy warrants new strategies still needed to improve overall patient survival. In this study, we    investigated in vivo the effects of RAD001 (Everolimus), a new orally available mTOR inhibitor, on the growth of human and mouse osteosarcoma cells either alone or in combination with zoledronate (ZOL), an anti-osteoporotic drug used to treat    bone metastases. RAD001 inhibited osteosarcoma cell proliferation in a dose- and time-dependent manner with no modification of cell-cycle distribution.  Combination with ZOL augmented this inhibition of cell proliferation, decreasing PI3K/mTOR    signaling compared with single treatments. Notably, in contrast to RAD001, ZOL downregulated isoprenylated membrane-bound Ras concomitantly with an increase of nonisoprenylated cytosolic Ras in sensitive and resistant osteosarcoma cell lines to    both drugs. Moreover, ZOL and RAD001 synergized to decrease Ras isoprenylation and GTP-bound Ras levels. Further, the drug combination reduced tumor development in two murine models of osteoblastic or osteolytic osteosarcoma. We found that ZOL    could reverse RAD001 resistance in osteosarcoma, limiting osteosarcoma cell growth in combination with RAD001. Our findings rationalize further study of the applications of mTOR and mevalonate pathway inhibitors that can limit protein prenylation    pathways.</p>

	]]>
</description>

<author>G Moriceau et al.</author>


</item>


<item>
<title>Patent ductus arteriosus in mice with smooth muscle-specific Jag1 deletion.</title>
<link>http://mouseion.jax.org/stfb2010/141</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/141</guid>
<pubDate>Tue, 08 May 2012 10:59:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ductus arteriosus is an arterial vessel that shunts blood flow away from the lungs during fetal life, but normally occludes after birth to establish the adult circulation pattern. Failure of the ductus arteriosus to close after    birth is termed patent ductus arteriosus and is one of the most common congenital heart defects. Mice with smooth muscle cell-specific deletion of Jag1, which encodes a Notch ligand, die postnatally from patent ductus arteriosus. These mice    exhibit defects in contractile smooth muscle cell differentiation in the vascular wall of the ductus arteriosus and adjacent descending aorta. These defects arise through an inability to propagate the JAG1-Notch signal via lateral induction    throughout the width of the vascular wall. Both heterotypic endothelial smooth muscle cell interactions and homotypic vascular smooth muscle cell interactions are required for normal patterning and differentiation of the ductus arteriosus and    adjacent descending aorta. This new model for a common congenital heart defect provides novel insights into the genetic programs that underlie ductus arteriosus development and closure.</p>

	]]>
</description>

<author>X Feng et al.</author>


</item>


<item>
<title>Sub-cubic millimeter intraocular pressure monitoring implant to enable genetic studies on pressure-induced neurodegeneration.</title>
<link>http://mouseion.jax.org/stfb2010/140</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/140</guid>
<pubDate>Tue, 08 May 2012 10:59:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>There is often a strong correlation between elevated levels of intraocular pressure (IOP) and glaucoma; however, the underlying mechanisms that lead to blindness are not well understood. The key may lie in the study of genetic    factors which determine IOP and lead to glaucoma-related blindness. Mice are typically used for genetic research due to their short generation time and accelerated lifespan, manageability, the availability of established and pure lines, and the    ability to manipulate the genome. Post genetic manipulation, IOP monitoring at regular intervals is needed and for large scale testing, on the order of thousands of mice, it is crucial to have at least a partially automated data collection    scheme. This work presents a fully wireless system on a chip that measures 300 microm in its widest dimension, has a wireless microwave-based data and power link, and is capable of relaying digitized pressure recordings to a nearby    base-station.</p>

	]]>
</description>

<author>E Y. Chow et al.</author>


</item>


<item>
<title>Connective tissue growth factor is required for skeletal development and postnatal skeletal homeostasis in male mice.</title>
<link>http://mouseion.jax.org/stfb2010/139</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/139</guid>
<pubDate>Tue, 08 May 2012 10:59:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Connective tissue growth factor (CTGF), a member of the cysteine-rich 61 (Cyr 61), CTGF, nephroblastoma overexpressed (NOV) (CCN) family of proteins, is synthesized by osteoblasts, and its overexpression inhibits osteoblastogenesis    and causes osteopenia. The global inactivation of Ctgf leads to defective endochondral bone formation and perinatal lethality; therefore, the consequences of Ctgf inactivation on the postnatal skeleton are not known. To study the function of    CTGF, we generated Ctgf(+/LacZ) heterozygous null mice and tissue-specific null Ctgf mice by mating Ctgf conditional mice, where Ctgf is flanked by lox sequences with mice expressing the Cre recombinase under the control of the paired-related    homeobox gene 1 (Prx1) enhancer (Prx1-Cre) or the osteocalcin promoter (Oc-Cre). Ctgf(+/LacZ) heterozygous mice exhibited transient osteopenia at 1 month of age secondary to decreased trabecular number. A similar osteopenic phenotype was observed    in 1-month-old Ctgf conditional null male mice generated with Prx1-Cre, suggesting that the decreased trabecular number was secondary to impaired endochondral bone formation. In contrast, when the conditional deletion of Ctgf was achieved by    Oc-Cre, an osteopenic phenotype was observed only in 6-month-old male mice. Osteoblast and osteoclast number, bone formation, and eroded surface were not affected in Ctgf heterozygous or conditional null mice. In conclusion, CTGF is necessary for    normal skeletal development but to a lesser extent for postnatal skeletal homeostasis.</p>

	]]>
</description>

<author>E Canalis et al.</author>


</item>


<item>
<title>Untangling HDL quantitative trait loci on mouse chromosome 5 and identifying Scarb1 and Acads as the underlying genes.</title>
<link>http://mouseion.jax.org/stfb2010/138</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/138</guid>
<pubDate>Tue, 08 May 2012 10:59:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Two high-density lipoprotein cholesterol quantitative trait loci (QTL), Hdlq1 at 125 Mb and Hdlq8 at 113 Mb, were previously identified on mouse distal chromosome 5. Our objective was to identify the underlying genes. We first used    bioinformatics to narrow the Hdlq1 locus to 56 genes. The most likely candidate, Scarb1 (scavenger receptor B1), was supported by gene expression data consistent with knockout and transgenic mouse models. Then we confirmed Hdlq8 as an independent    QTL by detecting it in an intercross between NZB and NZW (LOD = 12.7), two mouse strains that have identical genotypes for Scarb1. Haplotyping narrowed this QTL to 9 genes; the most likely candidate was Acads (acyl-coenzymeA dehydrogenase, short    chain). Sequencing showed that Acads had an amino acid polymorphism, Gly94Asp, in a conserved region; Western blotting showed that protein levels were significantly different between parental strains. A previously known spontaneous deletion    causes loss of ACADS activity in BALB/cBy mice. We showed that HDL levels were significantly elevated in BALB/cBy compared with BALB/c mice and that this HDL difference cosegregated with the Acads mutation. We confirmed that Hdlq1 and Hdlq8 are    independent QTL on mouse chromosome 5 and demonstrated that Scarb1 and Acads are the underlying genes.</p>

	]]>
</description>

<author>Z Su et al.</author>


</item>


<item>
<title>Mutations in sterol O-acyltransferase 1 (Soat1) result in hair interior defects in AKR/J mice.</title>
<link>http://mouseion.jax.org/stfb2010/137</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/137</guid>
<pubDate>Tue, 08 May 2012 10:59:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>B Wu et al.</author>


</item>


<item>
<title>Tropomodulin 1-null mice have a mild spherocytic elliptocytosis with appearance of tropomodulin 3 in red blood cells and disruption of the membrane skeleton.</title>
<link>http://mouseion.jax.org/stfb2010/136</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/136</guid>
<pubDate>Tue, 08 May 2012 10:59:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The short actin filaments in the red blood cell (RBC) membrane skeleton are capped at their pointed ends by tropomodulin 1 (Tmod1) and coated with tropomyosin (TM) along their length. Tmod1-TM control of actin filament length is    hypothesized to regulate spectrin-actin lattice organization and membrane stability. We used a Tmod1 knockout mouse to investigate the in vivo role of Tmod1 in the RBC membrane skeleton. Western blots of Tmod1-null RBCs confirm the absence of    Tmod1 and show the presence of Tmod3, which is normally not present in RBCs. Tmod3 is present at only one-fifth levels of Tmod1 present on wild-type membranes, but levels of actin, TMs, adducins, and other membrane skeleton proteins remain    unchanged. Electron microscopy shows that actin filament lengths are more variable with spectrin-actin lattices displaying abnormally large and more variable pore sizes. Tmod1-null mice display a mild anemia with features resembling hereditary    spherocytic elliptocytosis, including decreased RBC mean corpuscular volume, cellular dehydration, increased osmotic fragility, reduced deformability, and heterogeneity in osmotic ektacytometry. Insufficient capping of actin filaments by Tmod3    may allow greater actin dynamics at pointed ends, resulting in filament length redistribution, leading to irregular and attenuated spectrin-actin lattice connectivity, and concomitant RBC membrane instability.</p>

	]]>
</description>

<author>J D. Moyer et al.</author>


</item>


<item>
<title>An international bioinformatics infrastructure to underpin the Arabidopsis community.</title>
<link>http://mouseion.jax.org/stfb2010/135</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/135</guid>
<pubDate>Tue, 08 May 2012 10:59:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>The future bioinformatics needs of the Arabidopsis community as well as those of other scientific communities that depend on Arabidopsis resources were discussed at a pair of recent meetings held by the Multinational Arabidopsis    Steering Committee and the North American Arabidopsis Steering Committee. There are extensive tools and resources for information storage, curation, and retrieval of Arabidopsis data that have been developed over recent years primarily through    the activities of The Arabidopsis Information Resource, the Nottingham Arabidopsis Stock Centre, and the Arabidopsis Biological Resource Center, among others.  However, the rapid expansion in many data types, the international basis of the    Arabidopsis community, and changing priorities of the funding agencies all suggest the need for changes in the way informatics infrastructure is developed and maintained. We propose that there is a need for a single core resource that is    integrated into a larger international consortium of investigators. We envision this to consist of a distributed system of data, tools, and resources, accessed via a single information portal and funded by a variety of sources, under shared    international management of an International Arabidopsis Informatics Consortium (IAIC). This article outlines the proposal for the development, management, operations, and continued funding for the IAIC.</p>

	]]>
</description>

<author>International Arabidopis Informatics Consortium</author>


</item>


<item>
<title>4Pi microscopy reveals an impaired three-dimensional mitochondrial network of pancreatic islet beta-cells, an experimental model of type-2 diabetes.</title>
<link>http://mouseion.jax.org/stfb2010/134</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/134</guid>
<pubDate>Tue, 08 May 2012 10:59:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Insulin production in pancreatic beta-cells is critically linked to mitochondrial oxidative phosphorylation. Increased ATP production triggered by blood glucose represents the beta-cells' glucose sensor. Type-2 diabetes mellitus    results from insulin resistance in peripheral tissues and impaired insulin secretion.  Pathology of diabetic beta-cells might be reflected by the altered morphology of mitochondrial network. Its characterization is however hampered by the    complexity and density of the three-dimensional (3D) mitochondrial tubular networks in these cell types. Conventional confocal microscopy does not provide sufficient axial resolution to reveal the required details; electron tomography    reconstruction of these dense networks is still difficult and time consuming. However, mitochondrial network morphology in fixed cells can also be studied by 4Pi microscopy, a laser scanning microscopy technique which provides an approximately    7-fold improved axial resolution (approximately 100 nm) over conventional confocal microscopy. Here we present a quantitative study of these networks in insulinoma INS-1E cells and primary beta-cells in Langerhans islets. The former were a    stably-transfected cell line while the latter were transfected with lentivirus, both expressing mitochondrial matrix targeted redox-sensitive GFP.  The mitochondrial networks and their partial disintegration and fragmentation are revealed by    carefully created iso-surface plots and their quantitative analysis.  We demonstrate that beta-cells within the Langerhans islets from diabetic Goto Kakizaki rats exhibited a more disintegrated mitochondrial network compared to those from control    Wistar rats and model insulinoma INS-1E cells. Standardization of these patterns may lead to development of morphological diagnostics for Langerhans islets, for the assessment of beta-cell condition, before their transplantations.</p>

	]]>
</description>

<author>A Dlaskova et al.</author>


</item>


<item>
<title>Sin3a is required by sertoli cells to establish a niche for undifferentiated spermatogonia, germ cell tumors, and spermatid elongation.</title>
<link>http://mouseion.jax.org/stfb2010/133</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/133</guid>
<pubDate>Tue, 08 May 2012 10:58:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Microenvironments support the maintenance of stem cells and the growth of tumors through largely unknown mechanisms. While cell-autonomous chromatin modifications have emerged as important determinants for self-renewal and    differentiation of stem cells, a role for non-cell autonomous epigenetic contributions is not well established. Here, we genetically ablated the chromatin modifier Swi-independent 3a (Sin3a) in fetal Sertoli cells, which partly comprise the niche    for male germline stem cells, and investigated its impact on spermatogenic cell fate and teratoma formation in vivo. Sertoli cell-specific Sin3a deletion resulted in the formation of few undifferentiated spermatogonia after birth while initially    maintaining spermatogenic differentiation. Stem cell-associated markers Plzf, Gfra1, and Oct4 were downregulated in the mutant fetal gonad, while Sertoli cell markers Steel and Gdnf, which support germ cells, were not diminished. Following birth,    markers of differentiating spermatogonia, Kit and Sohlh2, exhibited normal levels, but chemokine-signaling molecules chemokine (C-X-C motif) ligand 12 (CXCL12)/stromal cell-derived factor 1 (SDF1) and chemokine (C-X-C motif) receptor 4 (CXCR4),    expressed in Sertoli cells and germ cells, respectively, were not detected. In the juvenile, mutant testes exhibited a progressive loss of differentiating spermatogonia and a block in spermatid elongation, followed by extensive germ cell    degeneration. Sertoli cell-specific Sin3a deletion also suppressed teratoma formation by fetal germ cells in an in vivo transplantation assay. We conclude that the epigenome of Sertoli cells influences the establishment of a niche for germline    stem cells as well as for tumor initiating cells.</p>

	]]>
</description>

<author>C J. Payne et al.</author>


</item>


<item>
<title>High frequencies of leukemia stem cells in poor-outcome childhood precursor-B acute lymphoblastic leukemias.</title>
<link>http://mouseion.jax.org/stfb2010/132</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/132</guid>
<pubDate>Tue, 08 May 2012 10:58:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>In order to develop a xenograft model to determine the efficacy of new therapies against primary human precursor-B acute lymphoblastic leukemia (ALL) stem cells (LSCs), we used the highly immunodeficient non-obese diabetic    (NOD).Cg-Prkdc(scid)IL2rg(tmlWjl)/SzJ (NOD-severe combined immune deficient (scid) IL2rg(-/-)) mouse strain. Intravenous transplantation of 2 of 2 ALL cell lines and 9 of 14 primary ALL cases generated leukemia-like proliferations in recipient    mice by 1-7 months after transplant. Leukemias were retransplantable, and the immunophenotypes, gene rearrangements and expression profiles were identical or similar to those of the original primary samples. NOD-scid mice transplanted with the    same primary samples developed similar leukemias with only a slightly longer latency than did NOD-scid-IL2Rg(-/-) mice. In this highly sensitive NOD-scid-IL2Rg(-/-)-based assay, 1-100 unsorted primary human ALL cells from five of five tested    patients, four of whom eventually experienced leukemia relapse, generated leukemias in recipient mice. This very high frequency of LSCs suggests that a hierarchical LSC model is not valuable for poor-outcome ALL.</p>

	]]>
</description>

<author>S Morisot et al.</author>


</item>


<item>
<title>Life extension by diet restriction and N-acetyl-L-cysteine in genetically heterogeneous mice.</title>
<link>http://mouseion.jax.org/stfb2010/131</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/131</guid>
<pubDate>Tue, 08 May 2012 10:58:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>We used a heterogeneous stock of mice-UM-HET3, the first generation offspring of CByB6F1/J and C3D2F1/J parents-to test effects of six antiaging treatments on life span. In the first report of diet restriction in a structured,    segregating heterogeneous population, we observed essentially the same increases in mean and maximum life span as found in CByB6F1/J hybrid positive controls. We also report results of treatment with N-acetyl-L-cysteine started at 7 months, and    aspirin, nitroflurbiprofen, 4-hydroxy phenyl N-tert-butyl nitrone, and nordihydroguaiaretic acid, all started at 16-18 months. Only male UM-HET3 mice receiving N-acetyl-L-cysteine had significantly increased life span, and this may have been due    to treatment-related inadvertent diet restriction. The other agents had no significant effects on life span. The use of UM-HET3 mice helps assure that these results are not the result of unresponsiveness of a single genotype but that they more    broadly represent laboratory mice.</p>

	]]>
</description>

<author>K Flurkey et al.</author>


</item>


<item>
<title>A historical perspective on leptin.</title>
<link>http://mouseion.jax.org/stfb2010/130</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/130</guid>
<pubDate>Tue, 08 May 2012 10:58:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>D L. Coleman</author>


</item>


<item>
<title>Achromatopsia as a potential candidate for gene therapy.</title>
<link>http://mouseion.jax.org/stfb2010/129</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/129</guid>
<pubDate>Tue, 08 May 2012 10:58:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Achromatopsia is an autosomal recessive retinal disease involving loss of cone function that afflicts approximately 1 in 30,000 individuals. Patients with achromatopsia usually have visual acuities lower than 20/200 because of the    central vision loss, photophobia, complete color blindness and reduced cone-mediated electroretinographic (ERG) amplitudes. Mutations in three genes have been found to be the primary causes of achromatopsia, including CNGB3 (beta subunit of the    cone cyclic nucleotide-gated cation channel), CNGA3 (alpha subunit of the cone cyclic nucleotide-gated cation channel), and GNAT2 (cone specific alpha subunit of transducin). Naturally occurring mouse models with mutations in Cnga3 (cpfl5 mice)    and Gnat2 (cpfl3 mice) were discovered at The Jackson Laboratory. A natural occurring canine model with CNGB3 mutations has also been found. These animal models have many of the central phenotypic features of the corresponding human diseases.    Using adeno-associated virus (AAV)-mediated gene therapy, we and others show that cone function can be restored in all three models. These data suggest that human achromatopsia may be a good candidate for corrective gene therapy.</p>

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</description>

<author>J J. Pang et al.</author>


</item>


<item>
<title>A novel null allele of mouse DSCAM survives to adulthood on an inbred C3H background with reduced phenotypic variability.</title>
<link>http://mouseion.jax.org/stfb2010/128</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/128</guid>
<pubDate>Tue, 08 May 2012 10:58:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>DSCAMs are cell adhesion molecules that play several important roles in neurodevelopment. Mouse alleles of Dscam identified to date do not survive on an inbred C57BL/6 background, complicating analysis of DSCAM-dependent    developmental processes because of phenotypic variability related to the segregating backgrounds needed for postnatal survival. A novel spontaneous allele of Dscam, hereafter referred to as Dscam(2)(J), has been identified. This allele contains a    four base pair duplication in exon 19, leading to a frameshift and truncation of the open reading frame. Mice homozygous for the Dscam(2)(J) mutant allele survive into adulthood on the C3H/HeJ background on which the mutation was identified.     Using the Dscam(2)(J) allele, retinal phenotypes that have variable severity on a segregating background were examined. A neurite lamination defect similar to that described in chick was discovered in mice. These results indicate that, in the    retina, additional DSCAM-dependent processes can be found by analysis of mutations on different genetic backgrounds.</p>

	]]>
</description>

<author>P G. Fuerst et al.</author>


</item>


<item>
<title>Identification of genetic determinants of IGF-1 levels and longevity among mouse inbred strains.</title>
<link>http://mouseion.jax.org/stfb2010/127</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/127</guid>
<pubDate>Tue, 08 May 2012 10:58:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The IGF-1 signaling pathway plays an important role in regulating longevity. To identify the genetic loci and genes that regulate plasma IGF-1 levels, we intercrossed MRL/MpJ and SM/J, inbred mouse strains that differ in IGF-1    levels.  Quantitative trait loci (QTL) analysis of IGF-1 levels of these F2 mice detected four QTL on chromosomes (Chrs) 9 (48 Mb), 10 (86 Mb), 15 (18 Mb), and 17 (85 Mb).  Haplotype association mapping of IGF-1 levels in 28 domesticated inbred    strains identified three suggestive loci in females on Chrs 2 (13 Mb), 10 (88 Mb), and 17 (28 Mb) and in four males on Chrs 1 (159 Mb), 3 (52 and 58 Mb), and 16 (74 Mb).  Except for the QTL on Chr 9 and 16, all loci co-localized with IGF-1 QTL    previously identified in other mouse crosses. The most significant locus was the QTL on Chr 10, which contains the Igf1 gene and which had a LOD score of 31.8.  Haplotype analysis among 28 domesticated inbred strains revealed a major QTL on Chr    10 overlapping with the QTL identified in the F2 mice. This locus showed three major haplotypes; strains with haplotype 1 had significantly lower plasma IGF-1 and extended longevity (P < 0.05) than strains with haplotype 2 or 3.  Bioinformatic    analysis, combined with sequencing and expression studies, showed that Igf1 is the most likely QTL gene, but that other genes may also play a role in this strong QTL.</p>

	]]>
</description>

<author>M S. Leduc et al.</author>


</item>


<item>
<title>Occupational mouse allergen exposure among non-mouse handlers.</title>
<link>http://mouseion.jax.org/stfb2010/126</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/126</guid>
<pubDate>Tue, 08 May 2012 10:58:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study assessed mouse allergen exposure across a range of jobs, including non-mouse handling jobs, at a mouse facility. Baseline data from 220 new employees enrolled in the Jackson Laboratory (JAXCohort) were analyzed. The    baseline assessment included a questionnaire, allergy skin testing, and spirometry. Exposure assessments consisted of collection of two full-shift breathing zone air samples during a 1-week period. Air samples were analyzed for mouse allergen    content, and the mean concentration of the two shifts represented mouse allergen exposure for that employee. The mean age of the 220 participants was 33 years. Ten percent reported current asthma and 56% were atopic.  Thirty-eight percent were    animal caretakers, 20% scientists, 20% administrative/support personnel, 10% materials/supplies handlers, and 9% laboratory technicians. Sixty percent of the population handled mice. Eighty-two percent of study participants had detectable    breathing zone mouse allergen, and breathing zone mouse allergen concentrations were 1.02 ng/m(3) (0.13-6.91) (median [interquartile range (IQR)]. Although mouse handlers had significantly higher concentrations of breathing zone mouse allergen    than non-handlers (median [IQR]: 4.13 ng/m(3) [0.69-12.12] and 0.21 ng/m(3) [below detection (BD)-0.63], respectively; p < 0.001), 66% of non-handlers had detectable breathing zone mouse allergen. Mouse allergen concentrations among    administrative/support personnel and materials/supplies handlers, jobs that generally do not entail handling mice, were median [IQR]: 0.23 ng/m(3) [BD-0.59] and 0.63 ng/m(3) [BD-18.91], respectively. Seventy-one percent of administrative/support    personnel, and 68% of materials/supplies handlers had detectable breathing zone mouse allergen. As many as half of non-mouse handlers may have levels of exposure that are similar to levels observed among mouse handlers.</p>

	]]>
</description>

<author>Brosnan J. Curtin et al.</author>


</item>


<item>
<title>Quantitative analysis of fitness and genetic interactions in yeast on a genome scale.</title>
<link>http://mouseion.jax.org/stfb2010/125</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/125</guid>
<pubDate>Tue, 08 May 2012 10:58:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Global quantitative analysis of genetic interactions is a powerful approach for deciphering the roles of genes and mapping functional relationships among pathways. Using colony size as a proxy for fitness, we developed a method for    measuring fitness-based genetic interactions from high-density arrays of yeast double mutants generated by synthetic genetic array (SGA) analysis. We identified several experimental sources of systematic variation and developed normalization    strategies to obtain accurate single- and double-mutant fitness measurements, which rival the accuracy of other high-resolution studies. We applied the SGA score to examine the relationship between physical and genetic interaction networks, and    we found that positive genetic interactions connect across functionally distinct protein complexes revealing a network of genetic suppression among loss-of-function alleles.</p>

	]]>
</description>

<author>A Baryshnikova et al.</author>


</item>


<item>
<title>Introduction to laboratory animal genetics.</title>
<link>http://mouseion.jax.org/stfb2010/124</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/124</guid>
<pubDate>Tue, 08 May 2012 10:58:14 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M F. Festing</author>


</item>


<item>
<title>Sex-specific gene expression in the BXD mouse liver.</title>
<link>http://mouseion.jax.org/stfb2010/123</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/123</guid>
<pubDate>Tue, 08 May 2012 10:58:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Differences in clinical phenotypes between the sexes are well documented and have their roots in differential gene expression. While sex has a major effect on gene expression, transcription is also influenced by complex interactions    between individual genetic variation and environmental stimuli. In this study, we sought to understand how genetic variation affects sex-related differences in liver gene expression by performing genetic mapping of genomewide liver mRNA    expression data in a genetically defined population of naive male and female mice from C57BL/6J, DBA/2J, B6D2F1, and 37 C57BL/6J x DBA/2J (BXD) recombinant inbred strains. As expected, we found that many genes important to xenobiotic metabolism    and other important pathways exhibit sexually dimorphic expression. We also performed gene expression quantitative trait locus mapping in this panel and report that the most significant loci that appear to regulate a larger number of genes than    expected by chance are largely sex independent. Importantly, we found that the degree of correlation within gene expression networks differs substantially between the sexes. Finally, we compare our results to a recently released human liver gene    expression data set and report on important similarities in sexually dimorphic liver gene expression between mouse and human. This study enhances our understanding of sex differences at the genome level and between species, as well as increasing    our knowledge of the molecular underpinnings of sex differences in responses to xenobiotics.</p>

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</description>

<author>D M. Gatti et al.</author>


</item>


<item>
<title>Combining QTL data for HDL cholesterol levels from two different species leads to smaller confidence intervals.</title>
<link>http://mouseion.jax.org/stfb2010/122</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/122</guid>
<pubDate>Tue, 08 May 2012 10:58:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Quantitative trait locus (QTL) analysis detects regions of a genome that are linked to a complex trait. Once a QTL is detected, the region is narrowed by positional cloning in the hope of determining the underlying candidate    gene-methods used include creating congenic strains, comparative genomics and gene expression analysis. Combined cross analysis may also be used for species such as the mouse, if the QTL is detected in multiple crosses. This process involves the    recoding of QTL data on a per-chromosome basis, with the genotype recoded on the basis of high- and low-allele status. The data are then combined and analyzed; a successful analysis results in a narrowed and more significant QTL. Using parallel    methods, we show that it is possible to narrow a QTL by combining data from two different species, the rat and the mouse. We combined standardized high-density lipoprotein phenotype values and genotype data for the rat and mouse using information    from one rat cross and two mouse crosses. We successfully combined data within homologous regions from rat Chr 6 onto mouse Chr 12, and from rat Chr 10 onto mouse Chr 11. The combinations and analyses resulted in QTL with smaller confidence    intervals and increased logarithm of the odds ratio scores. The numbers of candidate genes encompassed by the QTL on mouse Chr 11 and 12 were reduced from 1343 to 761 genes and from 613 to 304 genes, respectively. This is the first time that QTL    data from different species were successfully combined; this method promises to be a useful tool for narrowing QTL intervals.</p>

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</description>

<author>A Cox et al.</author>


</item>


<item>
<title>Generation of a conditional null allele of NADPH oxidase activator 1 (NOXA1).</title>
<link>http://mouseion.jax.org/stfb2010/121</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/121</guid>
<pubDate>Tue, 08 May 2012 10:57:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>NADPH oxidase complexes are multiprotein assemblies that generate reactive oxygen species in a variety of mammalian tissues. The canonical phagocytic oxidase consists of a heterodimeric, enzymatic core comprised of the transmembrane    proteins, CYBB andCYBA and is regulated, in part, by an "organizing" function of NCF1 and an "activating" activity of NCF2. In contexts outside of the phagocyte, these regulatory functions may be encoded not only by NCF1 and NCF2, but also    alternatively by their respective paralogues, NOXO1 and NOXA1. To allow tissue-specific dissection of Noxa1 function in mouse, we have generated an allele of Noxa1 suitable for conditional inactivation. Moreover, by crossing Noxa1 conditional    allele carriers to B6.129S4-Meox2(tm1(Cre)Sor)/J mice, we have generated first, Noxa1-null heterozygotes, and ultimately, Noxa1-null homozygotes. Through the thoughtful use of tissue-specific, Cre-expressing mouse strains, the Noxa1 conditional    allele will offer insight into the roles of NOXA1 in the variety of tissues in which it is expressed.</p>

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</description>

<author>J P. Flaherty et al.</author>


</item>


<item>
<title>Critical reasoning on causal inference in genome-wide linkage and association studies.</title>
<link>http://mouseion.jax.org/stfb2010/120</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/120</guid>
<pubDate>Tue, 08 May 2012 10:57:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genome-wide linkage and association studies of tens of thousands of clinical and molecular traits are currently underway, offering rich data for inferring causality between traits and genetic variation. However, the inference    process is based on discovering subtle patterns in the correlation between traits and is therefore challenging and could create a flood of untrustworthy causal inferences. Here we introduce the concerns and show that they are already valid in    simple scenarios of two traits linked to or associated with the same genomic region. We argue that more comprehensive analysis and Bayesian reasoning are needed and that these can overcome some of the pitfalls, although not in every conceivable    case. We conclude that causal inference methods can still be of use in the iterative process of mathematical modeling and biological validation.</p>

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</description>

<author>Y Li et al.</author>


</item>


<item>
<title>Reproductive ageing: Of worms and women.</title>
<link>http://mouseion.jax.org/stfb2010/119</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/119</guid>
<pubDate>Tue, 08 May 2012 10:57:48 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>K Flurkey et al.</author>


</item>


<item>
<title>Mammalian recombination hot spots: properties, control and evolution.</title>
<link>http://mouseion.jax.org/stfb2010/118</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/118</guid>
<pubDate>Tue, 08 May 2012 10:57:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recombination, together with mutation, generates the raw material of evolution, is essential for reproduction and lies at the heart of all genetic analysis.  Recent advances in our ability to construct genome-scale, high-resolution    recombination maps and new molecular techniques for analysing recombination products have substantially furthered our understanding of this important biological phenomenon in humans and mice: from describing the properties of recombination hot    spots in male and female meiosis to the recombination landscape along chromosomes. This progress has been accompanied by the identification of trans-acting systems that regulate the location and relative activity of individual hot    spots.</p>

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</description>

<author>K Paigen et al.</author>


</item>


<item>
<title>Notch signaling in the vasculature.</title>
<link>http://mouseion.jax.org/stfb2010/117</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/117</guid>
<pubDate>Tue, 08 May 2012 10:57:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Notch signaling is an evolutionarily conserved, intercellular signaling mechanism that plays myriad roles during vascular development and physiology in vertebrates. These roles include the regulation of arteriovenous specification    and differentiation in both endothelial cells and vascular smooth muscle cells, regulation of blood vessel sprouting and branching during normal and pathological angiogenesis, and the physiological responses of vascular smooth muscle cells.     Defects in Notch signaling also cause inherited vascular diseases, such as the degenerative vascular disorder cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. This review summarizes recent studies that    highlight the multiple roles the Notch signaling pathway plays during vascular development and physiology.</p>

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</description>

<author>T Gridley</author>


</item>


<item>
<title>Validation of multiplex microbead immunoassay for simultaneous serodetection of multiple infectious agents in laboratory mouse.</title>
<link>http://mouseion.jax.org/stfb2010/116</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/116</guid>
<pubDate>Tue, 08 May 2012 10:57:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Multiplex methodologies enable simultaneous detection of antibodies against several infectious agents allowing sample conservation, cost effectiveness, and amenability to high-throughput/automation. We have previously described a    multiplex microbead immunoassay for serodetection of ten, high-priority mouse infectious pathogens. Here, we present a validation of this multiplex diagnostic system using approximately four hundred serum samples from different groups of mice.    Computer assisted multivariate analysis of the resulting high volume data (8000 data points) was performed. This computational approach enabled presentation of data in a variety of easily interpretable formats (e.g., correlation tables and heat    maps). Importantly, this computer aided approach was instrumental for the evaluation of assay accuracy, sensitivity, specificity, and robustness during the study. Crucial pieces of information were obtained to make timely adjustments for assay    refinement. This progressive approach to developing an implementation-ready clinical assay, facilitated by computational analysis, produced a highly efficient, accurate and dependable serodiagnostics system. This system has effectively replaced    the current state-of-the-art methodology (ELISA) used in mouse colony health management at the University of California and the Jackson Laboratory. A pathway to develop multiplex serology tests for infectious disease diagnosis described here    serves as a model for multiplex immunoassay design, clinical validation, refinement and implementation.</p>

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</description>

<author>R Ravindran et al.</author>


</item>


<item>
<title>High-resolution spectral domain optical coherence tomography images of alstrom syndrome.</title>
<link>http://mouseion.jax.org/stfb2010/115</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/115</guid>
<pubDate>Tue, 08 May 2012 10:57:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alstrom syndrome is a multisystemic disorder characterized by cone-rod dystrophy, hearing loss, obesity, insulin resistance and hyperinsulinemia, type 2 diabetes mellitus, dilated cardiomyopathy, and progressive hepatic and renal    dysfunction.  The cone-rod retinal dystrophy usually develops within a few weeks after birth.  The authors examined a young boy with Alstrom syndrome by means of microperimetry and spectral domain optical coherence tomography (OCT). Instead of    the typical alterations observed in cone-rod dystrophies, the characteristics of the central foveal tissue suggest signs of retinal immaturity, with only a single layer of short, thick cones and rods and immature short outer segments. High-speed    and high-resolution spectral domain OCT allowed a detailed analysis of retinal layers in a young patient with Alstrom syndrome for the first time.</p>

	]]>
</description>

<author>E M. Vingolo et al.</author>


</item>


<item>
<title>New and emerging therapeutic agents for the treatment of fibromyalgia: an update.</title>
<link>http://mouseion.jax.org/stfb2010/114</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/114</guid>
<pubDate>Tue, 08 May 2012 10:57:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fibromyalgia (FM) is a chronic widespread pain condition that is estimated to affect 5 million US adults. Several molecular pathophysiologies are thought to contribute to the symptoms of FM, complicating the development of effective    clinical management techniques. It is now known that abnormalities in both nociceptive and central pain processing systems are necessary (but perhaps not sufficient) to condition the onset and maintenance of FM, producing associated    neuropsychologic symptoms such as pronounced fatigue, sleep abnormalities, cognitive difficulties, stress sensitivity, anxiety, and depression. Current treatment strategies are focused primarily on correcting the pathophysiologic mechanisms    underlying these nervous system abnormalities. Clinical studies demonstrate the safety and efficacy of three drugs recently approved for the treatment of FM: pregabalin (an alpha-2-delta ligand), and duloxetine and milnacipran    (serotonin/norepinephrine reuptake inhibitors). This review describes these pharmaceuticals in detail and discusses their current roles in FM management.</p>

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</description>

<author>J M. Recla</author>


</item>


<item>
<title>Mouse BMD quantitative trait loci show improved concordance with human genome-wide association loci when recalculated on a new, common mouse genetic map.</title>
<link>http://mouseion.jax.org/stfb2010/113</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/113</guid>
<pubDate>Tue, 08 May 2012 10:57:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bone mineral density (BMD) is a heritable trait, and in mice, over 100 quantitative trait loci (QTLs) have been reported, but candidate genes have been identified for only a small percentage. Persistent errors in the mouse genetic    map have negatively affected QTL localization, spurring the development of a new, corrected map. In this study, QTLs for BMD were remapped in 11 archival mouse data sets using this new genetic map. Since these QTLs all were mapped in a comparable    way, direct comparisons of QTLs for concordance would be valid. We then compared human genome-wide association study (GWAS) BMD loci with the mouse QTLs. We found that 26 of the 28 human GWAS loci examined were located within the confidence    interval of a mouse QTL. Furthermore, 14 of the GWAS loci mapped to within 3 cM of a mouse QTL peak. Lastly, we demonstrated that these newly remapped mouse QTLs can substantiate a candidate gene for a human GWAS locus, for which the peak    single-nucleotide polymorphism (SNP) fell in an intergenic region.  Specifically, we suggest that MEF2C (human chromosome 5, mouse chromosome 13) should be considered a candidate gene for the genetic regulation of BMD. In conclusion, use of the    new mouse genetic map has improved the localization of mouse BMD QTLs, and these remapped QTLs show high concordance with human GWAS loci. We believe that this is an opportune time for a renewed effort by the genetics community to identify the    causal variants regulating BMD using a synergistic mouse-human approach.</p>

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</description>

<author>Bicknell C. Ackert et al.</author>


</item>


<item>
<title>Anti-CD4-targeted gold nanoparticles induce specific contrast enhancement of peripheral lymph nodes in X-ray computed tomography of live mice.</title>
<link>http://mouseion.jax.org/stfb2010/112</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/112</guid>
<pubDate>Tue, 08 May 2012 10:57:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Antibody-conjugated gold nanoparticles have been applied as a biologically targeted contrast agent in live mice for one of the most widely used medical imaging methods, X-ray computed tomography. Such nanoprobes directed toward the    CD4 receptor lead to distinctly enhanced X-ray contrast of peripheral lymph nodes. This study demonstrates the general feasibility of biologically specific X-ray imaging in living animals and discusses basic requirements for the use of    nanoparticles as a targeted X-ray contrast agent.</p>

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</description>

<author>W Eck et al.</author>


</item>


<item>
<title>Gene-specific RNA polymerase II phosphorylation and the CTD code.</title>
<link>http://mouseion.jax.org/stfb2010/111</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/111</guid>
<pubDate>Tue, 08 May 2012 10:57:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Phosphorylation of the RNA polymerase (Pol) II C-terminal domain (CTD) repeats (1-YSPTSPS-7) is coupled to transcription and may act as a 'code' that controls mRNA synthesis and processing. To examine the code in budding yeast, we    mapped genome-wide CTD Ser2, Ser5 and Ser7 phosphorylations and the CTD-associated termination factors Nrd1 and Pcf11. Phospho-CTD dynamics are not scaled to gene length and are gene-specific, with highest Ser5 and Ser7 phosphorylation at the 5'    ends of well-expressed genes with nucleosome-occupied promoters. The CTD kinases Kin28 and Ctk1 markedly affect Pol II distribution in a gene-specific way. The code is therefore written differently on different genes, probably under the control    of promoters. Ser7 phosphorylation is enriched on introns and at sites of Nrd1 accumulation, suggesting links to splicing and Nrd1 recruitment.  Nrd1 and Pcf11 frequently colocalize, suggesting functional overlap.  Unexpectedly, Pcf11 is enriched    at centromeres and Pol III-transcribed genes.</p>

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</description>

<author>H Kim et al.</author>


</item>


<item>
<title>miR-22 functions as a micro-oncogene in transformed human bronchial epithelial cells induced by anti-benzo[a]pyrene-7,8-diol-9,10-epoxide.</title>
<link>http://mouseion.jax.org/stfb2010/110</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/110</guid>
<pubDate>Tue, 08 May 2012 10:57:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>MicroRNAs (miRNAs) are small non-coding RNA molecules that negatively control the expression of target genes post-transcriptionally. In this study, transformed human bronchial epithelial cells induced by    anti-benzo[a]pyrene-7,8-diol-9,10-epoxide were characterized for miRNA involved in carcinogenesis. We found miR-22, which was highly expressed in transformed cells, concomitant with downregulation of the tumour suppressor gene PTEN protein. Using    computer-generated and experimental analysis, PTEN was identified as one of the targets of miR-22. Over-expression and inhibition studies of miRNA showed decreased and increased PTEN protein, respectively, with no alteration of PTEN mRNA levels.    These findings suggest that miR-22 regulates PTEN expression through translational repression. A dual-reporter assay confirmed these findings and provided evidence to suggest that miR-22 regulates PTEN expression by binding with a target site in    the PTEN 3'-untranslated region. A mutated seed sequence in the PTEN binding site can abrogate the regulatory role of miR-22 on PTEN.  Moreover, we found that anti-miR-22 promoted cell apoptosis, decreased colony formation and reduced the    motility of malignant cells. Together, the results indicate that miR-22 functions as a micro-oncogene that can invert the functionality of PTEN. Furthermore, the binding site for miR-22 might provide insight into a potential target for gene    therapy.</p>

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</description>

<author>L Liu et al.</author>


</item>


<item>
<title>Beta-endorphin mediates behavioral despair and the effect of ethanol on the tail suspension test in mice.</title>
<link>http://mouseion.jax.org/stfb2010/109</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/109</guid>
<pubDate>Tue, 08 May 2012 10:56:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The opioid peptide beta-endorphin (beta-E) is synthesized and released in response to stressful stimuli as well as acute alcohol administration. The release of beta-E following exposure to an inescapable aversive    situation may mediate behaviors that contribute to allostasis of the stress response. The present study examines the effects of beta-E on immobility in assays involving inescapable stress, both under basal conditions and after acute    administration of EtOH. METHODS: Female and male transgenic mice with varying capacities to translate beta-E were subjected to either the forced swim (FST, Experiment 1) or the tail suspension test (TST, Experiment 2). In Experiment 3, mice were    divided into three groups based on hormonal status (male, female-estrous, and female-nonestrous) and injected with either 1 g/kg EtOH or equivolume saline 14 minutes prior to behavioral assessment on the TST. RESULTS: Experiments 1 and 2    demonstrated a direct relationship between beta-E levels and immobility. There were also sex differences in behavior in these tests, with males displaying more immobility than females. A main effect of genotype in Experiment 3 replicated findings    in Experiments 1 and 2. There was also an effect of EtOH (increasing immobility) and a significant interaction reflecting a particularly robust effect of the drug in mice with low beta-E. In addition, there were interactions between beta-E, EtOH    effects, and hormonal status.  CONCLUSIONS: These findings support the contention that beta-E moderates behavioral responses to stressful stimuli and suggest a role for this peptide in coping behavior. Furthermore, the effects of EtOH on the    response to stress may be mediated by beta-E. Sex differences in this influence may contribute to sex differences in disease susceptibility and expression.</p>

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</description>

<author>E T. Barfield et al.</author>


</item>


<item>
<title>Separate and combined effects of Sod1 and Cdh23 mutations on age-related hearing loss and cochlear pathology in C57BL/6J mice.</title>
<link>http://mouseion.jax.org/stfb2010/108</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/108</guid>
<pubDate>Tue, 08 May 2012 10:56:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Both the ahl allele of Cdh23 and the null mutation of Sod1 have been shown to contribute to age-related hearing loss (AHL) in mice, but mixed strain backgrounds have confounded analyses of their individual and combined effects. To    test for the effects of Sod1 deficiency independently from those of Cdh23(ahl), we produced mice with four digenic genotypes: Sod1(+/+)Cdh23(ahl)(/ahl), Sod1(+/+)Cdh23(+/+), Sod1(-/-)Cdh23(ahl)(/ahl), and Sod1(-/-)Cdh23(+/+), all on a uniform    C57BL(/)6J strain background. We assessed hearing loss by ABR threshold measurements and evaluated cochlear pathologies in age-matched mice of each digenic combination. ABR analysis showed that Sod1(+/+)Cdh23(+/+) mice retain normal hearing up to    15 months of age and that hearing loss of Sod1(+/+)Cdh23(ahl)(/ahl) mice is more age and frequency dependent than that of Sod1(-/-)Cdh23(+/+) mice. ABR results also showed that mice with both gene mutations (Sod1(-/-)Cdh23(ahl)(/ahl)) exhibit the    earliest onset and most severe hearing loss, greater than predicted for strictly additive effects. Histological analysis of cochleas showed that hair cell lesions are most severe in Sod1(-)(/-)Cdh23(ahl)(/ahl) mice followed closely by    Sod1(+)(/+)Cdh23(ahl)(/ahl) mice and much smaller in Sod1(-)(/-)Cdh23(+)(/+) and Sod1(+)(/+)Cdh23(+)(/+) mice. Despite extensive damage to cochlear hair cells, vestibular hair cells appeared remarkably normal in all strains. Although both    Sod1(-/-) and Cdh23(ahl)(/ahl) genotypes had strong effects on hearing loss, the Cdh23(ahl/ahl) genotype was primarily responsible for the increase in hair cell loss, suggesting that the two mutations have different underlying mechanisms of    pathology.</p>

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</description>

<author>K R. Johnson et al.</author>


</item>


<item>
<title>The de-ubiquitinase UCH-L1 is an oncogene that drives the development of lymphoma in vivo by deregulating PHLPP1 and Akt signaling.</title>
<link>http://mouseion.jax.org/stfb2010/107</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/107</guid>
<pubDate>Tue, 08 May 2012 10:56:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>De-ubiquitinating enzymes (DUBs) can reverse the modifications catalyzed by ubiquitin ligases and as such are believed to be important regulators of a variety of cellular processes. Several members of this protein family have been    associated with human cancers; however, there is little evidence for a direct link between deregulated de-ubiquitination and neoplastic transformation.  Ubiquitin C-terminal hydrolase (UCH)-L1 is a DUB of unknown function that is overexpressed in    several human cancers, but whether it has oncogenic properties has not been established. To address this issue, we generated mice that overexpress UCH-L1 under the control of a ubiquitous promoter. Here, we show that UCH-L1 transgenic mice are    prone to malignancy, primarily lymphomas and lung tumors. Furthermore, UCH-L1 overexpression strongly accelerated lymphomagenesis in Emu-myc transgenic mice. Aberrantly expressed UCH-L1 boosts signaling through the Akt pathway by downregulating    the antagonistic phosphatase PHLPP1, an event that requires its de-ubiquitinase activity. These data provide the first in vivo evidence for DUB-driven oncogenesis and suggest that UCH-L1 hyperactivity deregulates normal Akt    signaling.</p>

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</description>

<author>S Hussain et al.</author>


</item>


<item>
<title>Interrogating the transcriptome of oocytes and preimplantation embryos.</title>
<link>http://mouseion.jax.org/stfb2010/106</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/106</guid>
<pubDate>Tue, 08 May 2012 10:56:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>During its growth phase, a mouse oocyte accumulates RNA that is the sole template for new protein synthesis in the transcriptionally silent interval between growth completion and transcriptional activation of the embryonic genome.    Over this transcriptionally silent interval, almost half the quantity of RNA accumulated in the full-grown oocyte is degraded, while stable messages undergo major transcript-specific polyadenylation fluctuations associated with timely translation    of new proteins. These processes, in the background of substantial RNA degradation, create unique pitfalls for transcriptome analysis. Three particular challenges are discussed herein. (1) Systematic errors of relative quantification occur if    standard approaches are used, wherein samples are normalized to a constant quantity of RNA, or when computational analyses are normalized to an apparent "constant" endogenous to the sample. We show that use of a fixed quantity of exogenous RNA    per oocyte or embryo alleviates this problem. (2) Comparison of large-scale expression analyses from widely disparate platforms highlights how the differing protocols produce correspondingly different lists of genes with significant changes in    transcript abundance. Only with careful attention to the differences among experiments can such discrepancies be understood. (3) The complete assessment of changes in expression requires correspondingly comprehensive assessment of the role of    isoform-specific changes.</p>

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</description>

<author>A E. Peaston et al.</author>


</item>


<item>
<title>Response to Drs Foltz and DeLong&apos;s letter to the editor.</title>
<link>http://mouseion.jax.org/stfb2010/105</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/105</guid>
<pubDate>Tue, 08 May 2012 10:56:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>A, Malcolm R. Nicholson</author>


</item>


<item>
<title>Self-complementary AAV-mediated gene therapy restores cone function and prevents cone degeneration in two models of Rpe65 deficiency.</title>
<link>http://mouseion.jax.org/stfb2010/104</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/104</guid>
<pubDate>Tue, 08 May 2012 10:56:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>To test whether fast-acting, self-complimentary (sc), adeno-associated virus-mediated RPE65 expression prevents cone degeneration and/or restores cone function, we studied two mouse lines: the Rpe65-deficient rd12 mouse and the    Rpe65-deficient, rhodopsin null ('that is, cone function-only') Rpe65(-/-)::Rho(-/-) mouse. scAAV5 expressing RPE65 was injected subretinally into one eye of rd12 and Rpe65(-/-)::Rho(-/-) mice at postnatal day 14 (P14).  Contralateral rd12 eyes    were injected later, at P35. Rd12 behavioral testing revealed that rod vision loss was prevented with either P14 or P35 treatment, whereas cone vision was only detected after P14 treatment. Consistent with this observation, P35 treatment only    restored rod electroretinogram (ERG) signals, a result likely due to reduced cone densities at this time point. For Rpe65(-/-)::Rho(-/-) mice in which there is no confounding rod contribution to the ERG signal, cone cells and cone-mediated ERGs    were also maintained with treatment at P14. This work establishes that a self-complimentary AAV5 vector can restore substantial visual function in two genetically distinct models of Rpe65 deficiency within 4 days of treatment. In addition, this    therapy prevents cone degeneration but only if administered before extensive cone degeneration, thus supporting continuation of current Leber's congenital amaurosis-2 clinical trials with an added emphasis on cone subtype analysis and early    intervention.</p>

	]]>
</description>

<author>J Pang et al.</author>


</item>


<item>
<title>Fine mapping in 94 inbred mouse strains using a high-density haplotype resource.</title>
<link>http://mouseion.jax.org/stfb2010/103</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/103</guid>
<pubDate>Tue, 08 May 2012 10:56:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genetics of phenotypic variation in inbred mice has for nearly a century provided a primary weapon in the medical research arsenal. A catalog of the genetic variation among inbred mouse strains, however, is required to enable    powerful positional cloning and association techniques. A recent whole-genome resequencing study of 15 inbred mouse strains captured a significant fraction of the genetic variation among a limited number of strains, yet the common use of hundreds    of inbred strains in medical research motivates the need for a high-density variation map of a larger set of strains. Here we report a dense set of genotypes from 94 inbred mouse strains containing 10.77 million genotypes over 121,433 single    nucleotide polymorphisms (SNPs), dispersed at 20-kb intervals on average across the genome, with an average concordance of 99.94% with previous SNP sets. Through pairwise comparisons of the strains, we identified an average of 4.70 distinct    segments over 73 classical inbred strains in each region of the genome, suggesting limited genetic diversity between the strains. Combining these data with genotypes of 7570 gap-filling SNPs, we further imputed the untyped or missing genotypes of    94 strains over 8.27 million Perlegen SNPs. The imputation accuracy among classical inbred strains is estimated at 99.7% for the genotypes imputed with high confidence. We demonstrated the utility of these data in high-resolution linkage mapping    through power simulations and statistical power analysis and provide guidelines for developing such studies. We also provide a resource of in silico association mapping between the complex traits deposited in the Mouse Phenome Database with our    genotypes. We expect that these resources will facilitate effective designs of both human and mouse studies for dissecting the genetic basis of complex traits.</p>

	]]>
</description>

<author>A Kirby et al.</author>


</item>


<item>
<title>Nrk2b-mediated NAD+ production regulates cell adhesion and is required for muscle morphogenesis in vivo: Nrk2b and NAD+ in muscle morphogenesis.</title>
<link>http://mouseion.jax.org/stfb2010/102</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/102</guid>
<pubDate>Tue, 08 May 2012 10:56:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cell-matrix adhesion complexes (CMACs) play fundamental roles during morphogenesis. Given the ubiquitous nature of CMACs and their roles in many cellular processes, one question is how specificity of CMAC function is modulated. The    clearly defined cell behaviors that generate segmentally reiterated axial skeletal muscle during zebrafish development comprise an ideal system with which to investigate CMAC function during morphogenesis. We found that Nicotinamide riboside    kinase 2b (Nrk2b) cell autonomously modulates the molecular composition of CMACs in vivo. Nrk2b is required for normal Laminin polymerization at the myotendinous junction (MTJ). In Nrk2b-deficient embryos, at MTJ loci where Laminin is not    properly polymerized, muscle fibers elongate into adjacent myotomes and are abnormally long. In yeast and human cells, Nrk2 phosphorylates Nicotinamide Riboside and generates NAD+ through an alternative salvage pathway. Exogenous NAD+ treatment    rescues MTJ development in Nrk2b-deficient embryos, but not in laminin mutant embryos. Both Nrk2b and Laminin are required for localization of Paxillin, but not beta-Dystroglycan, to CMACs at the MTJ. Overexpression of Paxillin in Nrk2b-deficient    embryos is sufficient to rescue MTJ integrity. Taken together, these data show that Nrk2b plays a specific role in modulating subcellular localization of discrete CMAC components that in turn plays roles in musculoskeletal development.    Furthermore, these data suggest that Nrk2b-mediated synthesis of NAD+ is functionally upstream of Laminin adhesion and Paxillin subcellular localization during MTJ development.  These results indicate a previously unrecognized complexity to CMAC    assembly in vivo and also elucidate a novel role for NAD+ during morphogenesis.</p>

	]]>
</description>

<author>M F. Goody et al.</author>


</item>


<item>
<title>Widespread genomic breaks generated by activation-induced cytidine deaminase are prevented by homologous recombination.</title>
<link>http://mouseion.jax.org/stfb2010/101</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/101</guid>
<pubDate>Tue, 08 May 2012 10:56:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Activation-induced cytidine deaminase (AID) is required for somatic hypermutation and immunoglobulin class switching in activated B cells. Because AID has no known target-site specificity, there have been efforts to identify    non-immunoglobulin AID targets. We show here that AID acts promiscuously, generating widespread DNA double-strand breaks (DSBs), genomic instability and cytotoxicity in B cells with less homologous recombination ability. We demonstrate that the    homologous-recombination factor XRCC2 suppressed AID-induced off-target DSBs, promoting B cell survival. Finally, we suggest that aberrations that affect human chromosome 7q36, including XRCC2, correlate with genomic instability in B cell    cancers. Our findings demonstrate that AID has promiscuous genomic DSB-inducing activity, identify homologous recombination as a safeguard against off-target AID action, and have implications for genomic instability in B cell    cancers.</p>

	]]>
</description>

<author>M G. Hasham et al.</author>


</item>


<item>
<title>Research funding. Sustaining the data and bioresource commons.</title>
<link>http://mouseion.jax.org/stfb2010/100</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/100</guid>
<pubDate>Tue, 08 May 2012 10:56:13 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>P N. Schofield et al.</author>


</item>


<item>
<title>The waved with open eyelids (woe) locus is a hypomorphic mouse mutation in Adam17.</title>
<link>http://mouseion.jax.org/stfb2010/99</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/99</guid>
<pubDate>Tue, 08 May 2012 10:56:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>The waved with open eyes (woe) locus is a spontaneous recessive mouse mutation that exhibits wavy fur, eyelids open at birth, and enlarged heart and esophagus.  In this study, we confirmed the previously identified woe phenotypes    and additionally identified anterior eye segment defects, absence of the meibomian glands, and defects in the semilunar cardiac valves. Positional cloning identified a C794T substitution in the Adam17 gene that ablates a putative exonic splicing    enhancer (ESE) sequence in exon 7 resulting in aberrant Adam17 splicing.  The predominant woe transcript, Adam17(Delta)(exon7), lacks exon 7 resulting in an in-frame deletion of 90 bp and a putative Adam17(Delta252-281) protein lacking residues    252-281 from the metalloprotease domain. Western blot analysis in woe identified only the precursor form of Adam17(Delta252-281) protein. Absence of cleavage of the prodomain renders Adam17(Delta252-281) functionally inactive; however,    constitutive and stimulated shedding of Adam17 substrates was detected in woe at significantly reduced levels. This residual Adam17 shedding activity in woe most likely originates from full-length Adam17(T265M) encoded by the Adam17(C794T)    transcript identified expressed at severely reduced levels. These results show that even small amounts of functional Adam17 allow woe mice to survive into adulthood. In contrast to Adam17(-/-) mice that die at birth, the viability of woe mice    provides an excellent opportunity for studying the role of Adam17 throughout postnatal development and homeostasis.</p>

	]]>
</description>

<author>E L. Hassemer et al.</author>


</item>


<item>
<title>Quantitative trait loci for tibial bone strength in C57BL/6J and C3H/HeJ inbred strains of mice.</title>
<link>http://mouseion.jax.org/stfb2010/98</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/98</guid>
<pubDate>Tue, 08 May 2012 10:56:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Three-point bending technology has been widely used in the measurement of bone strength. Quantitative trait loci (QTLs) for bone strength have been identified using mouse femurs. In this study, we investigate the use of mouse tibiae    in identification of QTLs that regulate bone strength. Mouse tibiae were from a F(2) population derived from C57BL/6J (B6) and C3H/HeJ (C3H). Three-point bending was measured using ISO 4049, with the support width adjustable to accommodate    specimen sizes outside the scope of ISO 4049. The strain rate is selectable from 0.05 to 500 mm per min. All stress strain diagrams are recorded and retrieved in digital electronic form. Genome scan was performed in The Jackson Laboratory (TJL).    QTL mapping was conducted using Map Manager QTX software. Data show that (i) both elastic modulus (stiffness) and maximum loading (strength) value appear as normal distributions, suggesting that multiple genetic factors control the bone strength;    (ii) 11 QTLs, accounting for 90% of variation for strength, have been detected. More than half QTLs of three-point bending are located on the same locations of bone density earlier identified from mouse femurs; (iii) a major QTL of femoral and    vertebral bone mineral density (BMD) was not detected for bone strength of tibiae; (iv) the QTL on chromosome 4 has extremely high LOD score of 31.8 and represents 60% of the variation of bone strength; and (v) four QTLs of stiffness (chromosomes    2, 11, 15 and 19) have been identified.</p>

	]]>
</description>

<author>F Jiao et al.</author>


</item>


<item>
<title>Generation of mice with a conditional null allele of the Jagged2 gene.</title>
<link>http://mouseion.jax.org/stfb2010/97</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/97</guid>
<pubDate>Tue, 08 May 2012 10:55:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Notch signaling pathway is an evolutionarily-conserved intercellular signaling mechanism, and mutations in its components disrupt embryonic development in many organisms and cause inherited diseases in humans. The Jagged2 (Jag2)    gene, which encodes a ligand for Notch pathway receptors, is required for craniofacial, limb, and T cell development. Mice homozygous for a Jag2 null allele die at birth from cleft palate, precluding study of Jag2 function in postnatal and adult    mice. We have generated a Jag2 conditional null allele by flanking the first two exons of the Jag2 gene with loxP sites. Cre-mediated deletion of the Jag2(flox) allele generates the Jag2(del2) allele, which behaves genetically as a Jag2 null    allele. This Jag2 conditional null allele will enable investigation of Jag2 function in a variety of tissue-specific contexts.</p>

	]]>
</description>

<author>J Xu et al.</author>


</item>


<item>
<title>myc maintains embryonic stem cell pluripotency and self-renewal.</title>
<link>http://mouseion.jax.org/stfb2010/96</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/96</guid>
<pubDate>Tue, 08 May 2012 10:55:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>While endogenous Myc (c-myc) and Mycn (N-myc) have been reported to be separately dispensable for murine embryonic stem cell (mESC) function, myc greatly enhances induced pluripotent stem (iPS) cell formation and overexpressed c-myc    confers LIF-independence upon mESC. To address the role of myc genes in ESC and in pluripotency generally, we conditionally knocked out both c- and N-myc using myc doubly homozygously floxed mESC lines (cDKO). Both lines of myc cDKO mESC    exhibited severely disrupted self-renewal, pluripotency, and survival along with enhanced differentiation. Chimeric embryos injected with DKO mESC most often completely failed to develop or in rare cases survived but with severe defects.  The    essential nature of myc for self-renewal and pluripotency is at least in part mediated through orchestrating pluripotency-related cell cycle and metabolic programs. This study demonstrates that endogenous myc genes are essential for mESC    pluripotency and self-renewal as well as providing the first evidence that myc genes are required for early embryogenesis, suggesting potential mechanisms of myc contribution to iPS cell formation.</p>

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</description>

<author>N V. Varlakhanova et al.</author>


</item>


<item>
<title>Granulosa cell ligand NPPC and its receptor NPR2 maintain meiotic arrest in mouse oocytes.</title>
<link>http://mouseion.jax.org/stfb2010/95</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/95</guid>
<pubDate>Tue, 08 May 2012 10:55:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Granulosa cells of mammalian Graafian follicles maintain oocytes in meiotic arrest, which prevents their precocious maturation. We show that mouse mural granulosa cells, which line the follicle wall, express natriuretic peptide    precursor type C (Nppc) messenger RNA (mRNA), whereas cumulus cells surrounding oocytes express mRNA of the NPPC receptor NPR2, a guanylyl cyclase. NPPC increased cGMP levels in cumulus cells and oocytes and inhibited meiotic resumption in vitro.    Meiotic arrest was not sustained in most Graafian follicles of Nppc or Npr2 mutant mice, and meiosis resumed precociously. Oocyte-derived paracrine factors promoted cumulus cell expression of Npr2 mRNA. Therefore, the granulosa cell ligand NPPC    and its receptor NPR2 in cumulus cells prevent precocious meiotic maturation, which is critical for maturation and ovulation synchrony and for normal female fertility.</p>

	]]>
</description>

<author>M Zhang et al.</author>


</item>


<item>
<title>Anisotropic regulation of Ankrd2 gene expression in skeletal muscle by mechanical stretch.</title>
<link>http://mouseion.jax.org/stfb2010/94</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/94</guid>
<pubDate>Tue, 08 May 2012 10:55:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>The diaphragm muscles in vivo are subjected to mechanical forces both in the direction of the muscle fibers and in the direction transverse to the fibers.  However, the effect of directional mechanical forces in skeletal muscle gene    regulation is completely unknown. Here, we identified that stretch in the longitudinal and transverse directions to the diaphragm muscle fibers up-regulated Ankrd2 gene expression by two distinct signaling pathways in wild-type (WT) and mdm, a    mouse model of muscular dystrophy with early-onset of progressive muscle-wasting. Stretch in the longitudinal direction activated both NF-kappaB and AP-1 transcription factors, whereas stretch in the transverse direction activated only AP-1    transcription factor. Interestingly, longitudinal stretch activated Ankrd2 promoter only by NF-kappaB, whereas transverse stretch activated Ankrd2 promoter by AP-1. Moreover, we found that longitudinal stretch activated Akt, which up-regulated    Ankrd2 expression through NF-kappaB. However, transverse stretch activated Ras-GTP, Raf-1, and Erk1/2 proteins, which up-regulated Ankrd2 expression through AP-1. Surprisingly, the stretch-activated NF-kappaB and AP-1 signaling pathways was not    involved in Ankrd2 regulation at the basal level, which was high in the mdm mouse diaphragm. Taken together, our data show the anisotropic regulation of Ankrd2 gene expression in the diaphragm muscles of WT and mdm mice via two distinct    mechanosensitive signaling pathways.</p>

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</description>

<author>J S. Mohamed et al.</author>


</item>


<item>
<title>A circadian-regulated gene, Nocturnin, promotes adipogenesis by stimulating PPAR-gamma nuclear translocation.</title>
<link>http://mouseion.jax.org/stfb2010/93</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/93</guid>
<pubDate>Tue, 08 May 2012 10:55:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nocturnin (NOC) is a circadian-regulated protein related to the yeast family of transcription factors involved in the cellular response to nutrient status. In mammals, NOC functions as a deadenylase but lacks a transcriptional    activation domain. It is highly expressed in bone-marrow stromal cells (BMSCs), hepatocytes, and adipocytes. In BMSCs exposed to the PPAR-gamma (peroxisome proliferator-activated receptor-gamma) agonist rosiglitazone, Noc expression was enhanced    30-fold. Previously, we reported that Noc(-/-) mice had low body temperature, were protected from diet-induced obesity, and most importantly exhibited absence of Pparg circadian rhythmicity on a high-fat diet. Consistent with its role in    influencing BMSCs allocation, Noc(-/-) mice have reduced bone marrow adiposity and high bone mass. In that same vein, NOC overexpression enhances adipogenesis in 3T3-L1 cells but negatively regulates osteogenesis in MC3T3-E1 cells. NOC and a    mutated form, which lacks deadenylase activity, bind to PPAR-gamma and markedly enhance PPAR-gamma transcriptional activity. Both WT and mutant NOC facilitate nuclear translocation of PPAR-gamma. Importantly, NOC-mediated nuclear translocation of    PPAR-gamma is blocked by a short peptide fragment of NOC that inhibits its physical interaction with PPAR-gamma. The inhibitory effect of this NOC-peptide was partially reversed by rosiglitazone, suggesting that effect of NOC on PPAR-gamma    nuclear translocation may be independent of ligand-mediated PPAR-gamma activation. In sum, Noc plays a unique role in the regulation of mesenchymal stem-cell lineage allocation by modulating PPAR-gamma activity through nuclear translocation.    These data illustrate a unique mechanism whereby a nutrient-responsive gene influences BMSCs differentiation, adipogenesis, and ultimately body composition.</p>

	]]>
</description>

<author>M Kawai et al.</author>


</item>


<item>
<title>Connective tissue growth factor is required for skeletal development and postnatal skeletal homeostasis in male mice.</title>
<link>http://mouseion.jax.org/stfb2010/92</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/92</guid>
<pubDate>Tue, 08 May 2012 10:55:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Connective tissue growth factor (CTGF), a member of the cysteine-rich 61 (Cyr 61), CTGF, nephroblastoma overexpressed (NOV) (CCN) family of proteins, is synthesized by osteoblasts, and its overexpression inhibits osteoblastogenesis    and causes osteopenia. The global inactivation of Ctgf leads to defective endochondral bone formation and perinatal lethality; therefore, the consequences of Ctgf inactivation on the postnatal skeleton are not known. To study the function of    CTGF, we generated Ctgf(+/LacZ) heterozygous null mice and tissue-specific null Ctgf mice by mating Ctgf conditional mice, where Ctgf is flanked by lox sequences with mice expressing the Cre recombinase under the control of the paired-related    homeobox gene 1 (Prx1) enhancer (Prx1-Cre) or the osteocalcin promoter (Oc-Cre). Ctgf(+/LacZ) heterozygous mice exhibited transient osteopenia at 1 month of age secondary to decreased trabecular number. A similar osteopenic phenotype was observed    in 1-month-old Ctgf conditional null male mice generated with Prx1-Cre, suggesting that the decreased trabecular number was secondary to impaired endochondral bone formation. In contrast, when the conditional deletion of Ctgf was achieved by    Oc-Cre, an osteopenic phenotype was observed only in 6-month-old male mice. Osteoblast and osteoclast number, bone formation, and eroded surface were not affected in Ctgf heterozygous or conditional null mice. In conclusion, CTGF is necessary for    normal skeletal development but to a lesser extent for postnatal skeletal homeostasis.</p>

	]]>
</description>

<author>E Canalis et al.</author>


</item>


<item>
<title>Generation of functional human T-cell subsets with HLA-restricted immune responses in HLA class I expressing NOD/SCID/IL2r gamma(null) humanized mice.</title>
<link>http://mouseion.jax.org/stfb2010/91</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/91</guid>
<pubDate>Tue, 08 May 2012 10:55:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Whereas humanized mouse models have contributed significantly to human immunology research, human T cells developing in mouse thymic environment fail to demonstrate HLA-restricted function. To achieve HLA-restricted human immune    response, we created an immune-compromised non-obese diabetic/SCID/IL2rg(null) strain (NSG) with homozygous expression of HLA class I heavy chain and light chain (NSG-HLA-A2/HHD). Transplantation of purified Lin-CD34+CD38- human hematopoietic    stem cells into NSG-HLA-A2/HHD newborns resulted in the development of human CD4+ and CD8+ TCR alphabeta+ T cells and CD4-CD8- and CD8+ TCR gammadelta+ cells in recipient bone marrow and spleen. Human cytotoxic T lymphocytes (CTLs) become    functionally mature, as evidenced by the production of granzyme corresponding to phenotypic transition from naive to effector memory CTLs. In these recipients, human Th17 cells developed along with Th1 and Th2 cells. Epstein-Barr virus (EBV)    infection in the humanized NSG-HLA-A2/HHD recipients resulted in the formation of lymphoproliferative lesions consisting mainly of human B cells with scattered human T cells. Human CTLs developing in the recipients recognized EBV-derived peptides    in an HLA-restricted manner and exerted HLA-restricted cytotoxicity against EBV-infected human B cells. The HLA-expressing humanized mouse with functional HLA-restricted T cells and consistent representation of rare T-cell subsets overcomes a    major constraint in human immunology, and serves as a useful model for investigation of human immune responses against pathogens and for the development of therapeutic strategies against human diseases.</p>

	]]>
</description>

<author>L D. Shultz et al.</author>


</item>


<item>
<title>The R109H variant of fascin-2, a developmentally regulated actin crosslinker in hair-cell stereocilia, underlies early-onset hearing loss of DBA/2J mice.</title>
<link>http://mouseion.jax.org/stfb2010/90</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/90</guid>
<pubDate>Tue, 08 May 2012 10:55:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>The quantitative trait locus ahl8 is a key contributor to the early-onset, age-related hearing loss of DBA/2J mice. A nonsynonymous nucleotide substitution in the mouse fascin-2 gene (Fscn2) is responsible for this phenotype,    confirmed by wild-type BAC transgene rescue of hearing loss in DBA/2J mice. In chickens and mice, FSCN2 protein is abundant in hair-cell stereocilia, the actin-rich structures comprising the mechanically sensitive hair bundle, and is concentrated    toward stereocilia tips of the bundle's longest stereocilia. FSCN2 expression increases when these stereocilia differentially elongate, suggesting that FSCN2 controls filament growth, stiffens exposed stereocilia, or both. Because ahl8    accelerates hearing loss only in the presence of mutant cadherin 23, a component of hair-cell tip links, mechanotransduction and actin crosslinking must be functionally interrelated.</p>

	]]>
</description>

<author>J B. Shin et al.</author>


</item>


<item>
<title>Photoreceptor degeneration, azoospermia, leukoencephalopathy, and abnormal RPE cell function in mice expressing an early stop mutation in CLCN2.</title>
<link>http://mouseion.jax.org/stfb2010/89</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/89</guid>
<pubDate>Tue, 08 May 2012 10:55:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: To determine the molecular basis and the pathologic consequences of a chemically induced mutation in a mouse model of photoreceptor degeneration, nmf240. METHODS: Mice from a G3 N-ethyl-N-nitrosourea mutagenesis program    were screened by indirect ophthalmoscopy for abnormal fundi. A chromosomal position for the recessive nmf240 mutation was determined by a genome-wide linkage analysis by use of simple sequence length polymorphic markers in an F2 intercross. The    critical region was refined, and candidate genes were screened by direct sequencing. The nmf240 phenotype was characterized by histologic analysis of the retina, brain, and male reproductive organs and by electroretinogram (ERG)-based studies of    the retina and retinal pigment epithelium (RPE). RESULTS: Clinically, homozygous nmf240 mutants exhibit a grainy retina that progresses to panretinal patches of depigmentation. The mutation was localized to a region on chromosome 16 containing    Clcn2, a gene associated with retinal degeneration.  Sequencing identified a missense C-T mutation at nucleotide 1063 in Clcn2 that converts a glutamine to a stop codon. Mice homozygous for the Clcn2(nmf240) mutation experience a severe loss of    photoreceptor cells at 14 days of age that is preceded by an elongation of RPE apical microvilli. Homozygous mutants also experience leukoencephalopathy in multiple brain areas and male sterility.  Despite a normal retinal histology in nmf240    heterozygotes, the ERG light peak, generated by the RPE, is reduced. CONCLUSIONS: The nmf240 phenotype closely resembles that reported for Clcn2 knockout mice. The observation that heterozygous nmf240 mice present with a reduced ERG light peak    component suggests that CLCN2 is necessary for the generation of this response component.</p>

	]]>
</description>

<author>M M. Edwards et al.</author>


</item>


<item>
<title>The mouse model of Down syndrome Ts65Dn presents visual deficits as assessed by pattern visual evoked potentials.</title>
<link>http://mouseion.jax.org/stfb2010/88</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/88</guid>
<pubDate>Tue, 08 May 2012 10:55:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: The Ts65Dn mouse is the most complete widely available animal model of Down syndrome (DS). Quantitative information was generated about visual function in the Ts65Dn mouse by investigating their visual capabilities by means    of electroretinography (ERG) and patterned visual evoked potentials (pVEPs).  METHODS: pVEPs were recorded directly from specific regions of the binocular visual cortex of anesthetized mice in response to horizontal sinusoidal gratings of    different spatial frequency, contrast, and luminance generated by a specialized video card and presented on a 21-in. computer display suitably linearized by gamma correction. RESULTS: ERG assessments indicated no significant deficit in retinal    physiology in Ts65Dn mice compared with euploid control mice.  The Ts65Dn mice were found to exhibit deficits in luminance threshold, spatial resolution, and contrast threshold, compared with the euploid control mice. The behavioral counterparts    of these parameters are luminance sensitivity, visual acuity, and the inverse of contrast sensitivity, respectively. CONCLUSIONS: DS includes various phenotypes associated with the visual system, including deficits in visual acuity,    accommodation, and contrast sensitivity. The present study provides electrophysiological evidence of visual deficits in Ts65Dn mice that are similar to those reported in persons with DS. These findings strengthen the role of the Ts65Dn mouse as a    model for DS. Also, given the historical assumption of integrity of the visual system in most behavioral assessments of Ts65Dn mice, such as the hidden-platform component of the Morris water maze, the visual deficits described herein may    represent a significant confounding factor in the interpretation of results from such experiments.</p>

	]]>
</description>

<author>McKean J. Scott et al.</author>


</item>


<item>
<title>Mesenchymal cell remodeling during mouse secondary palate reorientation.</title>
<link>http://mouseion.jax.org/stfb2010/87</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/87</guid>
<pubDate>Tue, 08 May 2012 10:55:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>The formation of mammalian secondary palate requires a series of developmental events such as growth, elevation, and fusion. Despite recent advances in the field of palate development, the process of palate elevation remains poorly    understood. The current consensus on palate elevation is that the distal end of the vertical palatal shelf corresponds to the medial edge of the elevated horizontal palatal shelf. We provide evidence suggesting that the prospective medial edge of    the vertical palate is located toward the interior side (the side adjacent to the tongue), instead of the distal end, of the vertical palatal shelf and that the horizontal palatal axis is generated through palatal outgrowth from the side of the    vertical palatal shelf rather than rotating the pre-existing vertical axis orthogonally. Because palate elevation represents a classic example of embryonic tissue re-orientation, our findings here may also shed light on the process of tissue    re-orientation in general.</p>

	]]>
</description>

<author>J Z. Jin et al.</author>


</item>


<item>
<title>Human immune system development and rejection of human islet allografts in spontaneously diabetic NOD-Rag1null IL2rgammanull Ins2Akita mice.</title>
<link>http://mouseion.jax.org/stfb2010/86</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/86</guid>
<pubDate>Tue, 08 May 2012 10:55:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: To create an immunodeficient mouse model that spontaneously develops hyperglycemia to serve as a diabetic host for human islets and stem cell-derived beta-cells in the absence or presence of a functional human immune    system.  RESEARCH DESIGN AND METHODS: We backcrossed the Ins2(Akita) mutation onto the NOD-Rag1(null) IL2rgamma(null) strain and determined 1) the spontaneous development of hyperglycemia, 2) the ability of human islets, mouse islets, and    dissociated mouse islet cells to restore euglycemia, 3) the generation of a human immune system following engraftment of human hematopoietic stem cells, and 4) the ability of the humanized mice to reject human islet allografts. RESULTS: We    confirmed the defects in innate and adaptive immunity and the spontaneous development of hyperglycemia conferred by the IL2rgamma(null), Rag1(null), and Ins2(Akita) genes in NOD-Rag1(null) IL2rgamma(null) Ins2(Akita) (NRG-Akita) mice.  Mouse and    human islets restored NRG-Akita mice to normoglycemia. Insulin-positive cells in dissociated mouse islets, required to restore euglycemia in chemically diabetic NOD-scid IL2rgamma(null) and spontaneously diabetic NRG-Akita mice, were quantified    following transplantation via the intrapancreatic and subrenal routes.  Engraftment of human hematopoietic stem cells in newborn NRG-Akita and NRG mice resulted in equivalent human immune system development in a normoglycemic or chronically    hyperglycemic environment, with >50% of engrafted NRG-Akita mice capable of rejecting human islet allografts. CONCLUSIONS: NRG-Akita mice provide a model system for validation of the function of human islets and human adult stem cell, embryonic    stem cell, or induced pluripotent stem cell-derived beta-cells in the absence or presence of an alloreactive human immune system.</p>

	]]>
</description>

<author>M A. Brehm et al.</author>


</item>


<item>
<title>BMPs and FGFs target Notch signalling via jagged 2 to regulate tooth morphogenesis and cytodifferentiation.</title>
<link>http://mouseion.jax.org/stfb2010/85</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/85</guid>
<pubDate>Tue, 08 May 2012 10:54:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Notch signalling pathway is an evolutionarily conserved intercellular signalling mechanism that is essential for cell fate specification and proper embryonic development. We have analysed the expression, regulation and function    of the jagged 2 (Jag2) gene, which encodes a ligand for the Notch family of receptors, in developing mouse teeth. Jag2 is expressed in epithelial cells that give rise to the enamel-producing ameloblasts from the earliest stages of tooth    development. Tissue recombination experiments showed that its expression in epithelium is regulated by mesenchyme-derived signals. In dental explants cultured in vitro, the local application of fibroblast growth factors upregulated Jag2    expression, whereas bone morphogenetic proteins provoked the opposite effect. Mice homozygous for a deletion in the Notch-interaction domain of Jag2 presented a variety of severe dental abnormalities. In molars, the crown morphology was    misshapen, with additional cusps being formed. This was due to alterations in the enamel knot, an epithelial signalling structure involved in molar crown morphogenesis, in which Bmp4 expression and apoptosis were altered.  In incisors,    cytodifferentiation and enamel matrix deposition were inhibited. The expression of Tbx1 in ameloblast progenitors, which is a hallmark for ameloblast differentiation and enamel formation, was dramatically reduced in Jag2(-/-) teeth. Together,    these results demonstrate that Notch signalling mediated by Jag2 is indispensable for normal tooth development.</p>

	]]>
</description>

<author>T A. Mitsiadis et al.</author>


</item>


<item>
<title>MeCP2 is required for normal development of GABAergic circuits in the thalamus.</title>
<link>http://mouseion.jax.org/stfb2010/84</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/84</guid>
<pubDate>Tue, 08 May 2012 10:54:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Methyl-CpG binding protein 2 (MeCP2) is highly expressed in neurons in the vertebrate brain, and mutations of the gene encoding MeCP2 cause the neurodevelopmental disorder Rett syndrome. This study examines the role of MeCP2 in the    development and function of thalamic GABAergic circuits. Whole cell recordings were carried out in excitatory neurons of the ventrobasal complex (VB) of the thalamus and in inhibitory neurons of the reticular thalamic nucleus (RTN) in acute brain    slices from mice aged P6 through P23. At P14-P16, the number of quantal GABAergic events was decreased in VB neurons but increased in RTN neurons of Mecp2-null mice, without any change in the amplitude or kinetics of quantal events. There was no    difference between mutant and wild-type mice in paired-pulse ratios of evoked GABAergic responses in the VB or the RTN. On the other hand, unitary responses evoked by minimal stimulation were decreased in the VB but increased in the RTN of    mutants. Similar changes in the frequency of quantal events were observed at P21-P23 in both the VB and RTN. At P6, however, quantal GABAergic transmission was altered only in the VB not the RTN. Immunostaining of vesicular GABA transporter    showed opposite changes in the number of GABAergic synaptic terminals in the VB and RTN of Mecp2-null mice at P18-P20. The loss of MeCP2 had no significant effect on intrinsic properties of RTN neurons recorded at P15-P17. Our findings suggest    that MeCP2 differentially regulates the development of GABAergic synapses in excitatory and inhibitory neurons in the thalamus.</p>

	]]>
</description>

<author>Z W. Zhang et al.</author>


</item>


<item>
<title>A mouse model of generalized non-Herlitz junctional epidermolysis bullosa.</title>
<link>http://mouseion.jax.org/stfb2010/83</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/83</guid>
<pubDate>Tue, 08 May 2012 10:54:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Epidermolysis bullosa (EB) is a class of intractable, rare, genetic disorders characterized by fragile skin and blister formation as a result of dermal-epidermal mechanical instability. EB presents with considerable clinical and    molecular heterogeneity. Viable animal models of junctional EB (JEB), that both mimic the human disease and survive beyond the neonatal period, are needed.  We identified a spontaneous, autosomal recessive mutation (Lamc2(jeb)) due to a murine    leukemia virus long terminal repeat insertion in Lamc2 (laminin gamma2 gene) that results in a hypomorphic allele with reduced levels of LAMC2 protein.  These mutant mice develop a progressive blistering disease validated at the gross and    microscopic levels to closely resemble generalized non-Herlitz JEB. The Lamc2(jeb) mice display additional extracutaneous features such as loss of bone mineralization and abnormal teeth, as well as a respiratory phenotype that is recognized but    not as well characterized in humans. This model faithfully recapitulates human JEB and provides an important preclinical tool to test therapeutic approaches.</p>

	]]>
</description>

<author>J A. Bubier et al.</author>


</item>


<item>
<title>Is the filaggrin-histidine-urocanic acid pathway essential for stratum corneum acidification?</title>
<link>http://mouseion.jax.org/stfb2010/82</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/82</guid>
<pubDate>Tue, 08 May 2012 10:54:40 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J W. Fluhr et al.</author>


</item>


<item>
<title>Mouse oocytes enable LH-induced maturation of the cumulus-oocyte complex via promoting EGF receptor-dependent signaling.</title>
<link>http://mouseion.jax.org/stfb2010/81</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/81</guid>
<pubDate>Tue, 08 May 2012 10:54:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>LH triggers the maturation of the cumulus-oocyte complex (COC), which is followed by ovulation. These ovarian follicular responses to LH are mediated by epidermal growth factor (EGF)-like growth factors produced by granulosa cells    and require the participation of oocyte-derived paracrine factors. However, it is not clear how oocytes coordinate with the EGF receptor (EGFR) signaling to achieve COC maturation. The aim of the present study was to test the hypothesis that    oocytes promote the expression of EGFR by cumulus cells, thus enabling them to respond to the LH-induced EGF-like peptides. Egfr mRNA and protein expression were dramatically reduced in cumulus cells of mutant mice deficient in the production of    the oocyte-derived paracrine factors growth differentiation factor 9 (GDF9) and bone morphogenetic protein 15 (BMP15). Moreover, microsurgical removal of oocytes from wild-type COCs dramatically reduced expression of Egfr mRNA and protein, and    these levels were restored by either coculture with oocytes or treatment with recombinant GDF9 or GDF9 plus recombinant BMP15. Blocking Sma- and Mad-related protein (SMAD)2/3 phosphorylation in vitro inhibited Egfr expression in wild-type COCs    and in GDF9-treated wild-type cumulus cells, and conditional deletion of Smad2 and Smad3 genes in granulosa cells in vivo resulted in the reduction of Egfr mRNA in cumulus cells. These results indicate that oocytes promote expression of Egfr in    cumulus cells, and a SMAD2/3-dependent pathway is involved in this process. At least two oocyte-derived growth factors, GDF9 and BMP15, are required for EGFR expression by cumulus cells.</p>

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</description>

<author>Y Q. Su et al.</author>


</item>


<item>
<title>Mutation of Eif4g3, encoding a eukaryotic translation initiation factor, causes male infertility and meiotic arrest of mouse spermatocytes.</title>
<link>http://mouseion.jax.org/stfb2010/80</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/80</guid>
<pubDate>Tue, 08 May 2012 10:54:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ENU-induced repro8 mutation was identified in a screen to uncover genes that control mouse gametogenesis. repro8 causes male-limited infertility, with failure of spermatocytes to exit meiotic prophase via the G2/MI transition.    The repro8 mutation is in the Eif4g3 gene, encoding eukaryotic translation initiation factor 4, gamma 3. Mutant germ cells appear to execute events of meiotic prophase normally, and many proteins characteristic of the prophase-to-metaphase    transition are not obviously depleted. However, activity of CDC2A (CDK1) kinase is dramatically reduced in mutant spermatocytes. Strikingly, HSPA2, a chaperone protein for CDC2A kinase, is absent in mutant spermatocytes in spite of the presence    of Hspa2 transcript, consistent with the observation that the repro8 phenotype is markedly similar to the phenotype of the Hspa2 knockout. Thus, EIF4G3 is required for HSPA2 translation in spermatocytes, a finding that provides the first genetic    evidence for selective translational control of meiotic exit in mammalian spermatocytes.</p>

	]]>
</description>

<author>F Sun et al.</author>


</item>


<item>
<title>Cdcs1 a major colitis susceptibility locus in mice; subcongenic analysis reveals genetic complexity.</title>
<link>http://mouseion.jax.org/stfb2010/79</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/79</guid>
<pubDate>Tue, 08 May 2012 10:54:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: The cytokine-deficiency-induced colitis susceptibility (Cdcs)1 locus is a major modifier of murine inflammatory bowel disease (IBD) and was originally identified in experimental crosses of interleukin-10-deficient    (Il10(-/-)) mice.  Congenic mice, in which this locus was reciprocally transferred between IBD-susceptible C3H/HeJBir-Il10(-/-) and resistant C57BL/6J-Il10(-/-) mice, revealed that this locus likely acts by inducing innate hypo- and adaptive    hyperresponsiveness, associated with impaired NF-kappaB responses of macrophages.  The aim of the present study was to dissect the complexity of Cdcs1 by further development and characterization of reciprocal Cdcs1 congenic strains and to    identify potential candidate genes in the congenic interval. METHODS: In total, 15 reciprocal congenic strains were generated from Il10(-/-) mice of either C3H/HeJBir or C57BL/6J genetic backgrounds by 10 cycles of backcrossing. Colitis activity    was monitored by histological grading. Candidate genes were identified by fine mapping of congenic intervals, sequencing, microarray analysis, and a high-throughput real-time reverse-transcription polymerase chain reaction (RT-PCR) approach using    bone marrow-derived macrophages. RESULTS: Within the originally identified Cdcs1-interval, 3 independent regions were detected that likely contain susceptibility-determining genetic factors (Cdcs1.1, Cdcs1.2, and Cdcs1.3). Combining results of    candidate gene approaches revealed Fcgr1, Cnn3, Larp7, and Alpk1 as highly attractive candidate genes with polymorphisms in coding or regulatory regions and expression differences between susceptible and resistant mouse strains. CONCLUSIONS:    Subcongenic analysis of the major susceptibility locus Cdcs1 on mouse chromosome 3 revealed a complex genetic structure. Candidate gene approaches revealed attractive genes within the identified regions.</p>

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</description>

<author>A Bleich et al.</author>


</item>


<item>
<title>Effects of alcohol on skeletal response to growth hormone in hypophysectomized rats.</title>
<link>http://mouseion.jax.org/stfb2010/78</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/78</guid>
<pubDate>Tue, 08 May 2012 10:54:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chronic alcohol abuse is an established risk factor for osteoporosis. However, the precise mechanisms for the bone loss are largely unknown. Alcohol decreases skeletal expression of insulin-like growth factor-I (IGF-I), an important    growth hormone (GH)-regulated skeletal growth factor. Therefore, we investigated the effects of alcohol on the skeletal response to GH in male Sprague-Dawley rats made GH-deficient by hypophysectomy (HYPOX). Four groups of sexually mature    (3-month-old) rats were studied: pituitary-intact (control), HYPOX, HYPOX + GH, and HYPOX + alcohol + GH. All animals were transferred to a liquid diet 6 days following surgery. The alcohol-fed group was adapted to a graded increase in alcohol    beginning 11 days following surgery. GH or vehicle was administered during the final 8 days of study and all animals were sacrificed 25 days following surgery. HYPOX resulted in cessation of body weight gain and tibial growth. Compared to    controls, longitudinal bone growth and cancellous bone formation were lower following HYPOX. The latter was associated with lower mineralizing perimeter/bone perimeter. Bone marrow adiposity was higher following HYPOX. Compared to HYPOX, GH    treatment increased body weight gain and bone formation rate, and decreased bone marrow adiposity. In contrast to the effects of GH treatment without alcohol, bone marrow adiposity did not differ between HYPOX and alcohol-fed GH-treated HYPOX    rats. Alcohol did not alter GH-induced weight gain or increases in serum IGF-I levels, but significantly impaired the effects of GH on tibial growth and cancellous bone formation. We conclude that the detrimental skeletal effects of alcohol abuse    observed in this experiment are mediated, at least in part, by skeletal resistance to GH.</p>

	]]>
</description>

<author>R T. Turner et al.</author>


</item>


<item>
<title>Peripherin-reactive antibodies in mouse, rabbit, and human blood.</title>
<link>http://mouseion.jax.org/stfb2010/77</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/77</guid>
<pubDate>Tue, 08 May 2012 10:54:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Type 1 diabetes (T1D) is an autoimmune disorder that results from the destruction of insulin-producing beta-cells in the islets of Langerhans. To date, autoimmune T-cell response and antibody reactivity to more than 20 autoantigens    have been linked to this disease. Some studies have described the intermediate filament protein peripherin (PRPH) as an autoantigen associated with T1D in non-obese diabetic (NOD) mice. We evaluated immune reactivity of mouse and rabbit sera and    human plasma to a 58 kDa protein expressed in RIN-m5F rat insulinoma cells. The protein was isolated using 2-DE and identified by mass spectrometry as PRPH.  Antibodies from healthy humans and T1D patients, CD-1 mice, C57BL/6 mice, NOR (non-obese    diabetes resistant) mice, and NOD mice reacted with PRPH on Western blots. However, antibody response to PRPH was stronger in NOD than non-autoimmune prone C57BL/6 mice. We conclude that immune reactivity to PRPH is not exclusively associated    with NOD mice or human patients with T1D. Furthermore, the frequent occurrence of PRPH-reactive antibodies in mouse and human blood suggests that binding may be non-specific or could reflect the presence of natural autoantibodies against PRPH.    These findings point to the need for a re-evaluation of PRPH as a T1D autoantigen in NOD mice and raise the question of the physiological relevance of such widespread immune reactivity against this peripheral nervous system    protein.</p>

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</description>

<author>A Strom et al.</author>


</item>


<item>
<title>High-fat diet leads to tissue-specific changes reflecting risk factors for diseases in DBA/2J mice.</title>
<link>http://mouseion.jax.org/stfb2010/76</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/76</guid>
<pubDate>Tue, 08 May 2012 10:54:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The aim of this study was to characterize the responses of individual tissues to high-fat feeding as a function of mass, fat composition, and transcript abundance. We examined a panel of eight tissues [5 white adipose tissues (WAT),    brown adipose tissue (BAT), liver, muscle] obtained from DBA/2J mice on either a standard breeding diet (SBD) or a high-fat diet (HFD). HFD led to weight gain, decreased insulin sensitivity, and tissue-specific responses, including inflammation,    in these mice. The dietary fatty acids were partially metabolized and converted in both liver and fat tissues. Saturated fatty acids (SFA) were converted in the liver to monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA),    and oleic acid (C18:1) was the preferred MUFA for storage of excess energy in all tissues of HFD-fed mice. Transcriptional changes largely reflected the tissue-specific fat deposition. SFA were negatively correlated with genes in the collagen    family and processes involving the extracellular matrix. We propose a novel role of the tryptophan hydroxylase 2 (Tph2) gene in adipose tissues of diet-induced obesity. Tissue-specific responses to HFD were identified. Liver steatosis was evident    in HFD-fed mice. Gonadal, retroperitoneal and subcutaneous adipose tissue and BAT exhibited severe inflammatory and immune responses. Mesenteric adipose tissue was the most metabolically active adipose tissue. Gluteal adipose tissue had the    highest mass gain but was sluggish in its metabolism. In HFD conditions, BAT functioned largely like WAT in its role as a depot for excess energy, whereas WAT played a role in thermogenesis.</p>

	]]>
</description>

<author>R S. Hageman et al.</author>


</item>


<item>
<title>Male mice not alone in research.</title>
<link>http://mouseion.jax.org/stfb2010/75</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/75</guid>
<pubDate>Tue, 08 May 2012 10:54:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>B Bolon et al.</author>


</item>


<item>
<title>Molecular and phenotypic reassessment of an infrequently used mouse model for spinal muscular atrophy.</title>
<link>http://mouseion.jax.org/stfb2010/74</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/74</guid>
<pubDate>Tue, 08 May 2012 10:53:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Proximal spinal muscular atrophy (SMA) results from loss of the survival motor neuron 1 (SMN1) gene, with retention of its nearly identical homolog, SMN2. There is a direct correlation between disease severity and SMN2 copy number.    Mice do not have a Smn2 gene, and thus cannot naturally replicate the disorder. However, two murine models of SMA have been generated using SMN2-BAC transgenic mice bred onto a mutant Smn background. In these instances mice die shortly after    birth, have variable phenotypes within the same litter, or completely correct the SMA phenotype. Both models have been imported to The Jackson Laboratory for distribution to the research community. To ensure that similar results are obtained    after importation to The Jackson Laboratory to what was originally reported in the literature, we have begun a molecular and phenotypic evaluation of these mouse models. Here we report our findings for the SMA mouse model that has been deposited    by the Li group from Taiwan. These mice, JAX stock number TJL-005058, are homozygous for the SMN2 transgene, Tg(SMN2)2Hung, and a targeted Smn allele that lacks exon 7, Smn1(tm1Hung). Our findings are consistent with those reported originally for    this line and clarify some of the original data. In addition, we have cloned and mapped the integration site for Tg(SMN2)2Hung to Chromosome 4, and provide a simple genotyping assay that is specific to the junction fragment. Finally, based upon    the survival data from our genetic crosses, we suggest that this underused SMA model may be a useful compliment or alternative to the more commonly used "delta7" SMA mouse. We provide breeding schemes in which two genotypes of mice can be    generated so that 50% of the litter will be SMA-like pups while 50% will be controls.</p>

	]]>
</description>

<author>R G. Gogliotti et al.</author>


</item>


<item>
<title>Segregation analysis of a sex ratio distortion locus in congenic mice.</title>
<link>http://mouseion.jax.org/stfb2010/73</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/73</guid>
<pubDate>Tue, 08 May 2012 10:53:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>The congenic HG.CAST-(D17Mit196-D17Mit190) (HQ17(hg/hg)) mouse strain showed a significant departure on the expected 50%/50% offspring sex ratio in more than 2400 progeny (55.7% females). The entire pedigree file included data from    13 nonoverlapping purebred generations and an F(2) cross with the C57BL/6J inbred strain. Offspring sex ratio data were analyzed on the basis of 40 purebred HQ17(hg)(/hg) sires and 29 F(1) HQ17(hg)(/hg) x B6 sires under a Bayesian Binomial    segregation model accounting for 4 different autosomal inheritance models of gene action (i.e., additive, dominance, recessive, and overdominance) and X-linked and Y-linked loci. For each model, the segregation effect was evaluated as a single    regression coefficient for all sires or assuming 2 independent regression coefficients accounting for offspring sex ratio departures in purebred and F(1) sires, respectively. The deviance information criterion clearly favored the autosomal    dominance model with different regression coefficients for the 2 groups of sires. Under this model, the dominance effect increased the percentage of female offspring by 4.3% (HQ17(hg)(/hg) purebred sires) and 8.2% (F(1) sires) with the highest    posterior density regions ranging from 0.5% to 10.6% and from 1.3% to 14.4%, respectively. This article provides significant evidence of genetic determinism for sex ratio distortion in the HQ17(hg)(/hg) strain and develops new analytical tools to    perform segregation studies on dichotomous traits.</p>

	]]>
</description>

<author>J Casellas et al.</author>


</item>


<item>
<title>Retrospective study of spontaneous osteosarcomas in the nonobese diabetic strain and nonobese diabetic-derived substrains of mice.</title>
<link>http://mouseion.jax.org/stfb2010/72</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/72</guid>
<pubDate>Tue, 08 May 2012 10:53:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this retrospective study, spontaneous osteosarcomas were found in 85 of 1,202 (7.1%) nonobese diabetic (NOD) and NOD-derived mice. Gross tumors were evident at an average age of 155.8 days in male mice and 151.4 days in female    mice. Compared with male mice, female mice had a statistically insignificant higher incidence: 56 cases (8.3% of 672) versus 28 cases (6.1% of 458). NOD/ShiLtJ mice had the highest incidence, with 39 cases among all the strains and substrains    represented (3.2% of 1,202 necropsies), whereas NOD.SCID substrains had the highest incidence, with 16 cases among the various NOD-derived substrains (1.3% of 1,202 necropsies). There was a statistically significant difference in tumor incidence    between NOD/ShiLtJ and NOD.SCID mice. Tumors were more frequent in the appendicular skeleton (55.7%) than in the axial skeleton (44.3%) and most often arose from the femurs. Histologically, osteoblastic osteosarcoma was the most common tumor    type, with 79 cases (94%), followed by mixed osteosarcoma, with 5 cases (6%). Metastases were rare, with only 2 cases (2.3%).</p>

	]]>
</description>

<author>A M. Kavirayani et al.</author>


</item>


<item>
<title>The importance of open-source integrative genomics to drug discovery.</title>
<link>http://mouseion.jax.org/stfb2010/71</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/71</guid>
<pubDate>Tue, 08 May 2012 10:53:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Researchers investigating many areas of disease recognize the value of integrating large-scale genomic experiments across species and experimental methods. Analysis methods have been developed to make use of the breadth and depth of    data from new technologies. Current paradigms of data storage, sharing and analysis are not yet ideal for these purposes. Open-access and analysis-enabled repositories are critical to progress, as they put the global integration of genomic data    within reach of individual expert investigators.  Current analytic approaches use the full scale and scope of data, but require data sharing, interoperability and community recognition of the value of shared information.</p>

	]]>
</description>

<author>E J. Chesler et al.</author>


</item>


<item>
<title>Effective targeting of quiescent chronic myelogenous leukemia stem cells by histone deacetylase inhibitors in combination with imatinib mesylate.</title>
<link>http://mouseion.jax.org/stfb2010/70</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/70</guid>
<pubDate>Tue, 08 May 2012 10:53:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Imatinib mesylate (IM) induces remission in chronic myelogenous leukemia (CML) patients but does not eliminate leukemia stem cells (LSCs), which remain a potential source of relapse. Here we investigated the ability of HDAC    inhibitors (HDACis) to target CML stem cells. Treatment with HDACis combined with IM effectively induced apoptosis in quiescent CML progenitors resistant to elimination by IM alone, and eliminated CML stem cells capable of engrafting    immunodeficient mice. In vivo administration of HDACis with IM markedly diminished LSCs in a transgenic mouse model of CML. The interaction of IM and HDACis inhibited genes regulating hematopoietic stem cell maintenance and survival. HDACi    treatment represents an effective strategy to target LSCs in CML patients receiving tyrosine kinase inhibitors.</p>

	]]>
</description>

<author>B Zhang et al.</author>


</item>


<item>
<title>Anti-IL5 decreases the number of eosinophils but not the severity of dermatitis in Sharpin-deficient mice.</title>
<link>http://mouseion.jax.org/stfb2010/69</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/69</guid>
<pubDate>Tue, 08 May 2012 10:53:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sharpin-deficient (Sharpin(cpdm)) mutant mice develop a chronic eosinophilic dermatitis. To determine the efficacy of eosinophil-depletion in chronic inflammation, Sharpin(cpdm) mice were treated with anti-IL5 antibodies. Mice    treated with anti-IL5 had a 90% reduction of circulating eosinophils and a 50% decrease in cutaneous eosinophils after 10 days compared with sham-treated littermates. Reducing the number of eosinophils resulted in increased severity of alopecia    and erythema and a significant increase in epidermal thickness. Skin homogenates from mice treated with anti-IL5 had decreased mRNA expression of arylsulfatase B (Arsb), diamine oxidase (amiloride-binding protein 1, also called histaminase; Abp1)    and Il10, which are mediators that eosinophils may release to quench inflammation. Skin homogenates from mice treated with anti-IL5 also had decreased mRNA expression of Il4, Il5, Ccl11, kit ligand (Kitl) and Tgfa; and increased mRNA expression    of Tgfb1, Mmp12 and tenascin C (Tnc). In order to further decrease the accumulation of eosinophils, Sharpin(cpdm) mice were crossed with IL5 null mice. Il5(-/-), Sharpin(cpdm)/Sharpin(cpdm) mice had a 98% reduction of circulating eosinophils and    a 95% decrease in cutaneous eosinophils compared with IL5-sufficient Sharpin(cpdm) mice. The severity of the lesions was similar between IL5-sufficient and IL5-deficient mice. Double mutant mice had a significant decrease in Abp1, and a    significant increase in Tgfb1, Mmp12 and Tnc mRNA compared with controls. These data indicate that eosinophils are not essential for the development of dermatitis in Sharpin(cpdm) mice and suggest that eosinophils have both pro-inflammatory and    anti-inflammatory roles in the skin of these mice.</p>

	]]>
</description>

<author>M L. Renninger et al.</author>


</item>


<item>
<title>JAX Colony Management System (JCMS): an extensible colony and phenotype data management system.</title>
<link>http://mouseion.jax.org/stfb2010/68</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/68</guid>
<pubDate>Tue, 08 May 2012 10:53:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Jackson Laboratory Colony Management System (JCMS) is a software application for managing data and information related to research mouse colonies, associated biospecimens, and experimental protocols. JCMS runs directly on    computers that run one of the PC Windows operating systems, but can be accessed via web browser interfaces from any computer running a Windows, Macintosh, or Linux operating system. JCMS can be configured for a single user or multiple users in    small- to medium-size work groups. The target audience for JCMS includes laboratory technicians, animal colony managers, and principal investigators. The application provides operational support for colony management and experimental workflows,    sample and data tracking through transaction-based data entry forms, and date-driven work reports. Flexible query forms allow researchers to retrieve database records based on user-defined criteria. Recent advances in handheld computers with    integrated barcode readers, middleware technologies, web browsers, and wireless networks add to the utility of JCMS by allowing real-time access to the database from any networked computer.</p>

	]]>
</description>

<author>C J. Donnelly et al.</author>


</item>


<item>
<title>Induction of cell cycle entry eliminates human leukemia stem cells in a mouse model of AML.</title>
<link>http://mouseion.jax.org/stfb2010/67</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/67</guid>
<pubDate>Tue, 08 May 2012 10:53:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cancer stem cells have been proposed to be important for initiation, maintenance and recurrence of various malignancies, including acute myeloid leukemia (AML).  We have previously reported that CD34+CD38- human primary AML stem    cells residing in the endosteal region of the bone marrow are relatively chemotherapy resistant.  Using a NOD/SCID/IL2rgamma(null) mouse model of human AML, we now show that the AML stem cells in the endosteal region are cell cycle quiescent and    that these stem cells can be induced to enter the cell cycle by treatment with granulocyte colony-stimulating factor (G-CSF). In combination with cell cycle-dependent chemotherapy, G-CSF treatment significantly enhances induction of apoptosis and    elimination of human primary AML stem cells in vivo. The combination therapy leads to significantly increased survival of secondary recipients after transplantation of leukemia cells compared with chemotherapy alone.</p>

	]]>
</description>

<author>Y Saito et al.</author>


</item>


<item>
<title>Quantitative lymphatic vessel trait analysis suggests Vcam1 as candidate modifier gene of inflammatory bowel disease.</title>
<link>http://mouseion.jax.org/stfb2010/66</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/66</guid>
<pubDate>Tue, 08 May 2012 10:53:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inflammatory bowel disease (IBD) is a chronic debilitating disease resulting from a complex interaction of multiple genetic factors with the environment. To identify modifier genes of IBD, we used an F2 intercross of IBD-resistant    C57BL/6J-Il10(-/-) mice and IBD-susceptible C3H/HeJBir-Il10(-/-) (C3Bir-Il10(-/-)) mice. We found a prominent involvement of lymphatic vessels in IBD and applied a scoring system to quantify lymphatic vascular changes.  Quantitative trait locus    (QTL) analyses revealed a large-effect QTL on chromosome 3, mapping to an interval of 43.6 Mbp. This candidate interval was narrowed by fine mapping to 22 Mbp, and candidate genes were analyzed by a systems genetics approach that included    quantitative gene expression profiling, search for functional polymorphisms, and haplotype block analysis. We identified vascular adhesion molecule 1 (Vcam1) as a candidate modifier gene in the interleukin 10-deficient mouse model of IBD.    Importantly, VCAM1 protein levels were increased in susceptible C3H/HeJ mice, compared with C57BL/6J mice; systemic blockade of VCAM1 in C3Bir-Il10(-/-) mice reduced their inflammatory lymphatic vessel changes. These results indicate that    genetically determined expression differences of VCAM1 are associated with susceptibility to colon inflammation, which is accompanied by extensive lymphatic vessel changes. VCAM1 is, therefore, a promising therapeutic target for    IBD.</p>

	]]>
</description>

<author>G Jurisic et al.</author>


</item>


<item>
<title>Phenotype ontologies for mouse and man: bridging the semantic gap.</title>
<link>http://mouseion.jax.org/stfb2010/65</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/65</guid>
<pubDate>Tue, 08 May 2012 10:53:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>A major challenge of the post-genomic era is coding phenotype data from humans and model organisms such as the mouse, to permit the meaningful translation of phenotype descriptions between species. This ability is essential if we    are to facilitate phenotype-driven gene function discovery and empower comparative pathobiology. Here, we review the current state of the art for phenotype and disease description in mice and humans, and discuss ways in which the semantic gap    between coding systems might be bridged to facilitate the discovery and exploitation of new mouse models of human diseases.</p>

	]]>
</description>

<author>P N. Schofield et al.</author>


</item>


<item>
<title>A Comparative-Qualitative Research Analysis of Character Education in the Christian School and Home Education Milieu</title>
<link>http://digitalcommons.cedarville.edu/education_theses/12</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/12</guid>
<pubDate>Tue, 08 May 2012 10:53:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>This qualitative study provides a phenomenological perspective and comparative analysis of character education within the Christian school and home education milieu. The study is based on semi-structured interviews of fifty-two individuals (N = 52) representative of a sampling of Christian educators from four private, evangelical Christian Schools (n = 26) and area home educating families (n = 26). The intent of the researcher was to bring attention to the importance for Christian educators to come to terms with the worldview from which the desire to educate Christian youth in a separate moral community originates. Although the purpose and intent of both sets of educators were in many instances similar, significant deviations in methodology and application were found. The results of this study are defined in four similarities and six differences, suggesting that character education and the juxtaposition of that goal along with the transference of faith was a major contributor to the obvious commitment and calling felt by Christian educators.</p>

	]]>
</description>

<author>Gretchen M. Wilhelm</author>


</item>


<item>
<title>A recombinant heavy chain antibody approach blocks ART2 mediated deletion of an iNKT cell population that upon activation inhibits autoimmune diabetes.</title>
<link>http://mouseion.jax.org/stfb2010/64</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/64</guid>
<pubDate>Tue, 08 May 2012 10:52:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>The ectoenzyme ADP-ribosyltransferase 2.2 (ART2.2) can apoptotically delete various T-cell subsets. Depending on the involved apoptotic T-cell subset, enhanced ART2.2 activity could result in immunosuppression or autoimmunity.     Diminished activity of the CD38 ectoenzyme that normally represents a counter-regulatory competitor for the NAD substrate represents one mechanism enhancing ART2.2 activity. Hence, it would be desirable to develop an agent that efficiently blocks    ART2.2 activity in vivo. While the llama derived recombinant s+16 single domain antibody overcame the difficulty of specifically targeting the ART2.2 catalytic site potential therapeutic use of this reagent is limited due to short in vivo    persistence. Thus, we tested if a modified version of s+16 incorporating the murine IgG1 Fc tail (s+16Fc) mediated long-term efficient in vivo suppression of ART2.2. We reasoned an ideal model to test the s+16Fc reagent were NOD mice in which    genetic ablation of CD38 results in an ART2.2 mediated reduction in already sub-normal numbers of immunoregulatory natural killer T-(NKT) cells to a level that no longer allows them when activated by the super-agonist alpha-galactosylceramide    (alpha-GalCer) to elicit effects inhibiting autoimmune type 1 diabetes (T1D) development. Treatment with s+16Fc efficiently mediated long-term in vivo inhibition of ART2.2 activity in NOD.CD38(null) mice, restoring their iNKT cell numbers to    levels that upon alpha-GalCer activation were capable of inhibiting T1D development.</p>

	]]>
</description>

<author>F Scheuplein et al.</author>


</item>


<item>
<title>alpha- and beta-Adducin polymorphisms affect podocyte proteins and proteinuria in rodents and decline of renal function in human IgA nephropathy.</title>
<link>http://mouseion.jax.org/stfb2010/63</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/63</guid>
<pubDate>Tue, 08 May 2012 10:52:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Adducins are cytoskeletal actin-binding proteins (alpha, beta, gamma) that function as heterodimers and heterotetramers and are encoded by distinct genes.  Experimental and clinical evidence implicates alpha- and beta-adducin    variants in hypertension and renal dysfunction. Here, we have addressed the role of alpha- and beta-adducin on glomerular function and disease using beta-adducin null mice, congenic substrains for alpha- and beta-adducin from the Milan    hypertensive (MHS) and Milan normotensive (MNS) rats and patients with IgA nephropathy. Targeted deletion of beta-adducin in mice reduced urinary protein excretion, preceded by an increase of podocyte protein expression (phospho-nephrin,    synaptopodin, alpha-actinin, ZO-1, Fyn). The introgression of polymorphic MHS beta-adducin locus into MNS (Add2, 529R) rats was associated with an early reduction of podocyte protein expression (nephrin, synaptopodin, alpha-actinin, ZO-1,    podocin, Fyn), followed by severe glomerular and interstitial lesions and increased urinary protein excretion. These alterations were markedly attenuated when the polymorphic MHS alpha-adducin locus was also present (Add1, 316Y). In patients with    IgA nephropathy, the rate of decline of renal function over time was associated to polymorphic beta-adducin (ADD2, 1797T, rs4984) with a significant interaction with alpha-adducin (ADD1, 460W, rs4961). These findings suggest that adducin genetic    variants participate in the development of glomerular lesions by modulating the expression of specific podocyte proteins.</p>

	]]>
</description>

<author>M Ferrandi et al.</author>


</item>


<item>
<title>Notch1 activation in mice causes arteriovenous malformations phenocopied by ephrinB2 and EphB4 mutants.</title>
<link>http://mouseion.jax.org/stfb2010/62</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/62</guid>
<pubDate>Tue, 08 May 2012 10:52:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Notch signaling is essential for embryonic vascular development in mammals and other vertebrates. Here we show that mouse embryos with conditional activation of the Notch1 gene in endothelial cells (Notch1 gain of function embryos)    exhibit defects in vascular remodeling increased diameter of the dorsal aortae, and form arteriovenous malformations. Conversely, embryos with either constitutive or endothelial cell-specific Notch1 gene deletion also have vascular defects, but    exhibit decreased diameter of the dorsal aortae and form arteriovenous malformations distinctly different from the Notch1 gain of function mutants.  Surprisingly, embryos homozygous for mutations of the ephrinB/EphB pathway genes Efnb2 and Ephb4    exhibit vascular defects and arteriovenous malformations that phenocopy the Notch1 gain of function mutants. These results suggest that formation of arteriovenous malformations in Notch1 gain of function mutants and ephrinB/EphB pathway loss of    function mutant embryos occurs by different mechanisms.</p>

	]]>
</description>

<author>L T. Krebs et al.</author>


</item>


<item>
<title>Assessing the prospects of genome-wide association studies performed in inbred mice.</title>
<link>http://mouseion.jax.org/stfb2010/61</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/61</guid>
<pubDate>Tue, 08 May 2012 10:52:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The remarkable success in mapping genes linked to a number of disease traits using genome-wide association studies (GWAS) in human cohorts has renewed interest in applying this same technique in model organisms such as inbred    laboratory mice. Unlike humans, however, the limited genetic diversity in the ancestry of laboratory mice combined with selection pressure over the past decades have yielded an intricate population genetic structure that can complicate the    results obtained from association studies. This problem is further exacerbated by the small number of strains typically used in such studies where multiple spurious associations arise as a result of random chance. We sought to empirically assess    the viability of GWAS in inbred mice using hundreds of expression traits for which the true location of the expression quantitative trait locus was known a priori. We then measured transcript abundance levels for these expression traits in 16    classical and 3 wild-derived inbred strains and carried out a genome-wide association scan, demonstrating the low statistical power of such studies and empirically estimating the large extent to which allelic association of transcripts gives rise    to spurious associations. We provide evidence illustrating that in a large fraction of cases, the marker with the most significant p values fails to map to the location of the true eQTL.  Finally, we provide experimental support for hundreds of    traits, and that combining linkage analysis with association mapping provides significant increases in statistical power over a stand-alone GWAS as well as significantly higher mapping resolution than either study alone.</p>

	]]>
</description>

<author>W L. Su et al.</author>


</item>


<item>
<title>Congenic and bioinformatics analyses resolved a major-effect Fob3b QTL on mouse Chr 15 into two closely linked loci.</title>
<link>http://mouseion.jax.org/stfb2010/60</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/60</guid>
<pubDate>Tue, 08 May 2012 10:52:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>We previously identified a Chr 15 quantitative trait locus (QTL) Fob3b in lines of mice selected for high (Fat line) and low (Lean line) body fat content that represent a unique model of polygenic obesity. Here we genetically    dissected the Fob3b interval by analyzing the phenotypes of eight overlapping congenic lines and four F(2) congenic intercrosses and prioritized candidates by bioinformatics approaches. Analyses revealed that the Fob3b QTL consists of at least    two separate linked QTLs Fob3b1 and Fob3b2. They exhibit additive inheritance and are linked in coupling with alleles originating from the Lean line, decreasing obesity-related traits. In further analyses, we focused on Fob3b1 because it had a    larger effect on obesity-related traits than Fob3b2, e.g., the difference between homozygotes for adiposity index (ADI) percentage was 1.22 and 0.77% for Fob3b1 and Fob3b2, respectively. A set of bioinformatics tools was used to narrow down    positional candidates from 85 to 4 high-priority Fob3b1 candidates. A previous single Fob3b QTL was therefore resolved into another two closely linked QTLs, confirming the fractal nature of QTLs mapped at low resolution. The interval of the    original Fob3b QTL was narrowed from 22.39 to 4.98 Mbp for Fob3b1 and to 7.68 Mbp for Fob3b2, which excluded the previously assigned candidate squalene epoxidase (Sqle) as the causal gene because it maps proximal to refined Fob3b1 and Fob3b2    intervals. A high-resolution map along with prioritization of Fob3b1 candidates by bioinformatics represents an important step forward to final identification of the Chr 15 obesity QTL.</p>

	]]>
</description>

<author>Z Prevorsek et al.</author>


</item>


<item>
<title>High-throughput behavioral phenotyping in the expanded panel of BXD recombinant inbred strains.</title>
<link>http://mouseion.jax.org/stfb2010/59</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/59</guid>
<pubDate>Tue, 08 May 2012 10:52:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Genetic reference populations, particularly the BXD recombinant inbred (BXD RI) strains derived from C57BL/6J and DBA/2J mice, are a valuable resource for the discovery of the bio-molecular substrates and genetic drivers responsible    for trait variation and covariation. This approach can be profitably applied in the analysis of susceptibility and mechanisms of drug and alcohol use disorders for which many predisposing behaviors may predict the occurrence and manifestation of    increased preference for these substances. Many of these traits are modeled by common mouse behavioral assays, facilitating the detection of patterns and sources of genetic coregulation of predisposing phenotypes and substance consumption.    Members of the Tennessee Mouse Genome Consortium (TMGC) have obtained phenotype data from over 250 measures related to multiple behavioral assays across several batteries: response to, and withdrawal from cocaine,    3,4-methylenedioxymethamphetamine; "ecstasy" (MDMA), morphine and alcohol; novelty seeking; behavioral despair and related neurological phenomena; pain sensitivity; stress sensitivity; anxiety; hyperactivity and sleep/wake cycles.  All traits    have been measured in both sexes in approximately 70 strains of the recently expanded panel of BXD RI strains. Sex differences and heritability estimates were obtained for each trait, and a comparison of early (N = 32) and recent (N = 37) BXD RI    lines was performed. Primary data are publicly available for heritability, sex difference and genetic analyses using the MouseTrack database, and are also available in GeneNetwork.org for quantitative trait locus (QTL) detection and genetic    analysis of gene expression. Together with the results of related studies, these data form a public resource for integrative systems genetic analysis of neurobehavioral traits.</p>

	]]>
</description>

<author>V M. Philip et al.</author>


</item>


<item>
<title>Effects of a high-frequency augmented acoustic environment on parvalbumin immunolabeling in the anteroventral cochlear nucleus of DBA/2J and C57BL/6J mice.</title>
<link>http://mouseion.jax.org/stfb2010/58</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/58</guid>
<pubDate>Tue, 08 May 2012 10:52:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Neurons in the anteroventral cochlear nucleus (AVCN) of DBA/2J (D2) and C57BL/6J (B6) mice were immunohistochemically labeled for the calcium binding protein parvalbumin (PV). Prior to this, mice were treated for 12h nightly with a    "high-frequency" augmented acoustic environment (HAAE: repetitive bursts of a 70 dB sound pressure level, half-octave noise band centered at 20 kHz). This was done during the period that hearing loss occurs: pre-weaning to 55 days in D2 mice and    weaning to 9 months in B6 mice. After HAAE treatment in D2 mice, high-frequency hearing loss was ameliorated and fewer PV-labeled neurons were found in the AVCN compared to untreated controls. HAAE treatment in B6 mice exacerbated high-frequency    hearing loss, yet the number of PV-labeled AVCN neurons in treated mice did not differ significantly from that of control mice.  The findings suggest that HAAE treatment provides relief from physiological stress caused by deprivation of auditory    input from the impaired cochlea.</p>

	]]>
</description>

<author>J F. Willott et al.</author>


</item>


<item>
<title>Humanized mouse models to study human diseases.</title>
<link>http://mouseion.jax.org/stfb2010/57</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/57</guid>
<pubDate>Tue, 08 May 2012 10:52:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE OF REVIEW: Update on humanized mouse models and their use in biomedical research. RECENT FINDINGS: The recent description of immunodeficient mice bearing a mutated IL-2 receptor gamma chain (IL2rgamma) facilitated greatly    the engraftment and function of human hematolymphoid cells and other cells and tissues. These mice permit the development of human immune systems, including functional T and B cells, following engraftment of hematopoietic stem cells (HSCs). The    engrafted functional human immune systems are capable of T and B cell-dependent immune responses, antibody production, antiviral responses, and allograft rejection. Immunodeficient IL2rgamma(null) mice also support heightened engraftment of    primary human cancers and malignant progenitor cells, permitting in-vivo investigation of pathogenesis and function. In addition, human-specific infectious agents for which animal models were previously unavailable can now be studied in vivo    using these new-generation humanized mice. SUMMARY: Immunodeficient mice bearing an IL2rgamma(null) mutated gene can be engrafted with functional human cells and tissues, including human immune systems, following engraftment with human    hematolymphoid cells. These mice are now used as in-vivo models to study human hematopoiesis, immunity, regeneration, stem cell function, cancer, and human-specific infectious agents without putting patients at risk.</p>

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</description>

<author>M A. Brehm et al.</author>


</item>


<item>
<title>Ush1c gene expression levels in the ear and eye suggest different roles for Ush1c in neurosensory organs in a new Ush1c knockout mouse.</title>
<link>http://mouseion.jax.org/stfb2010/56</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/56</guid>
<pubDate>Tue, 08 May 2012 10:52:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Usher syndrome (USH) is the most common form of deaf-blindness in humans.  Molecular characterization revealed that the USH gene products form a macromolecular protein network in hair cells of the inner ear and in photoreceptor    cells of the retina via binding to PDZ domains in the scaffold protein harmonin encoded by the Ush1c gene in mice and humans. Although several mouse mutants for the Ush1c gene have been described, we generated a targeted null mutation Ush1c mouse    model in which the first four exons of the Ush1c gene were replaced with a reporter gene. Here, we assessed the expression pattern of the reporter gene under control of Ush1c regulatory elements and characterized the phenotype of mice defective    for Ush1c. These Ush1 knockout mice are deaf but do not recapitulate vision defects before 10 months of age. Our data show LacZ expression in multiple layers of the retina but in neither outer nor inner segments of the photoreceptor layers in    mice bearing the knockout construct at 1-5 months of age. The fact that Ush1c expression is much higher in the ear than in the eye suggests a different role for Ush1c in ear function than in the eye and may explain why Ush1c mutant mice do not    recapitulate vision defects.</p>

	]]>
</description>

<author>C Tian et al.</author>


</item>


<item>
<title>Identification of therapeutic targets for quiescent, chemotherapy-resistant human leukemia stem cells.</title>
<link>http://mouseion.jax.org/stfb2010/55</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/55</guid>
<pubDate>Tue, 08 May 2012 10:52:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human acute myeloid leukemia (AML) originates from rare leukemia stem cells (LSCs). Because these chemotherapy-resistant LSCs are thought to underlie disease relapse, effective therapeutic strategies specifically targeting these    cells may be beneficial. Here, we report identification of a primary human LSC gene signature and functional characterization of human LSC-specific molecules in vivo in a mouse xenotransplantation model. In 32 of 61 (53%) patients with AML,    either CD32 or CD25 or both were highly expressed in LSCs. CD32- or CD25-positive LSCs could initiate AML and were cell cycle-quiescent and chemotherapy-resistant in vivo. Normal human hematopoietic stem cells depleted of CD32- and CD25-positive    cells maintained long-term multilineage hematopoietic reconstitution capacity in vivo, indicating the potential safety of treatments targeting these molecules. In addition to CD32 and CD25, quiescent LSCs within the bone marrow niche also    expressed the transcription factor WT1 and the kinase HCK. These molecules are also promising targets for LSC-specific therapy.</p>

	]]>
</description>

<author>Y Saito et al.</author>


</item>


<item>
<title>An Msh2 conditional knockout mouse for studying intestinal cancer and testing anticancer agents.</title>
<link>http://mouseion.jax.org/stfb2010/54</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/54</guid>
<pubDate>Tue, 08 May 2012 10:52:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND & AIMS: Mutations in the DNA mismatch repair (MMR) gene MSH2 cause Lynch syndromes I and II and sporadic colorectal cancers. Msh2(null) mice predominantly develop lymphoma and do not accurately recapitulate the colorectal    cancer phenotype. METHODS: We generated and examined mice with a conditional Msh2 disruption (Msh2(LoxP)), permitting tissue-specific gene inactivation.  ECMsh2(LoxP/LoxP) mice carried an EIIa-Cre transgene, and VCMsh2(LoxP/LoxP) mice carried a    Villin-Cre transgene. We combined the VCMsh2(LoxP) allele with either Msh2(Delta7null) (VCMsh2(LoxP/null)) or Msh2(G674D) mutations (VCMsh2(LoxP/G674D)) to create allelic phase mutants. These mice were given cisplatin or 5-fluorouracil/leucovorin    and oxaliplatin (FOLFOX), and their tumors were measured by magnetic resonance imaging. RESULTS: Embryonic fibroblasts from ECMsh2(LoxP/LoxP) mice do not express MSH2 and are MMR deficient. Reverse transcription, polymerase chain reaction, and    immunohistochemistry from VCMsh2(LoxP/LoxP) mice demonstrated specific loss of Msh2 messenger RNA and protein from epithelial cells of the intestinal tract. Microsatellite instability was observed in all VCMsh2 strains and limited to the    intestinal mucosa.  Resulting adenomas and adenocarcinomas had somatic truncation mutations to the adenomatous polyposis coli (Apc) gene. VCMsh2(LoxP/LoxP) mice did not develop lymphoma. Comparison of allelic phase tumors revealed significant    differences in multiplicity and size. When treated with cisplatin or FOLFOX, tumor size was reduced in VCMsh2(LoxP/G674D) but not VCMsh2(LoxP/null) tumors. The apoptotic response to FOLFOX was partially sustained in the intestinal mucosa of    VCMsh2(LoxP/G674D) animals. CONCLUSIONS: Msh2(LoxP/LoxP) mice in combination with appropriate Cre recombinase transgenes have excellent potential for preclinical modeling of Lynch syndrome, MMR-deficient tumors of other tissue types, and use in    drug development.</p>

	]]>
</description>

<author>M H. Kucherlapati et al.</author>


</item>


<item>
<title>Integrating human and rodent data to identify the genetic factors involved in chronic kidney disease.</title>
<link>http://mouseion.jax.org/stfb2010/53</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/53</guid>
<pubDate>Tue, 08 May 2012 10:51:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The increasing numbers of patients with chronic kidney disease combined with no satisfying interventions for preventing or curing the disease emphasize the need to better understand the genes involved in the initiation and    progression of complex renal diseases, their interactions with other host genes, and the environment. Linkage and association studies in human, rat, and mouse have been successful in identifying genetic loci for various disease-related phenotypes    but have thus far not been very successful identifying underlying genes. The purpose of this review is to summarize the progress in human, rat, and mouse genetic studies to show the concordance between the loci among the different species. The    collective utilization of human and nonhuman mammalian datasets and resources can lead to a more rapid narrowing of disease loci and the subsequent identification of candidate genes. In addition, genes identified through these methods can be    further characterized and investigated for interactions using animal models, which is not possible in humans.</p>

	]]>
</description>

<author>M R. Garrett et al.</author>


</item>


<item>
<title>A MOD(ern) perspective on literature curation.</title>
<link>http://mouseion.jax.org/stfb2010/52</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/52</guid>
<pubDate>Tue, 08 May 2012 10:51:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Curation of biological data is a multi-faceted task whose goal is to create a structured, comprehensive, integrated, and accurate resource of current biological knowledge. These structured data facilitate the work of the scientific    community by providing knowledge about genes or genomes and by generating validated connections between the data that yield new information and stimulate new research approaches. For the model organism databases (MODs), an important source of    data is research publications. Every published paper containing experimental information about a particular model organism is a candidate for curation. All such papers are examined carefully by curators for relevant information. Here, four    curators from different MODs describe the literature curation process and highlight approaches taken by the four MODs to address: (1) the decision process by which papers are selected, and (2) the identification and prioritization of the data    contained in the paper. We will highlight some of the challenges that MOD biocurators face, and point to ways in which researchers and publishers can support the work of biocurators and the value of such support.</p>

	]]>
</description>

<author>J Hirschman et al.</author>


</item>


<item>
<title>Targeted deletion of betaIII spectrin impairs synaptogenesis and generates ataxic and seizure phenotypes.</title>
<link>http://mouseion.jax.org/stfb2010/51</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/51</guid>
<pubDate>Tue, 08 May 2012 10:51:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The spectrin membrane skeleton controls the disposition of selected membrane channels, receptors, and transporters. In the brain betaIII spectrin binds directly to the excitatory amino acid transporter (EAAT4), the glutamate    receptor delta, and other proteins. Mutations in betaIII spectrin link strongly to human spinocerebellar ataxia type 5 (SCA5), correlating with alterations in EAAT4. We have explored the mechanistic basis of this phenotype by targeted gene    disruption of Spnb3. Mice lacking intact betaIII spectrin develop normally. By 6 months they display a mild nonprogressive ataxia. By 1 year most Spnb3(-/-) animals develop a myoclonic seizure disorder with significant reductions of EAAT4, EAAT1,    GluRdelta, IP3R, and NCAM140. Other synaptic proteins are normal. The cerebellum displays increased dark Purkinje cells (PC), a thin molecular layer, fewer synapses, a loss of dendritic spines, and a 2-fold expansion of the PC dendrite diameter.    Membrane and expanded Golgi profiles fill the PC dendrite and soma, and both regions accumulate EAAT4. Correlating with the seizure disorder are enhanced hippocampal levels of neuropeptide Y and EAAT3 and increased calpain proteolysis of alphaII    spectrin. It appears that betaIII spectrin disruption impairs synaptogenesis by disturbing the intracellular pathways selectively regulating protein trafficking to the synapse. The mislocalization of these proteins secondarily disrupts glutamate    transport dynamics, leading to seizures, neuronal damage, and compensatory changes in EAAT3 and neuropeptide Y.</p>

	]]>
</description>

<author>M C. Stankewich et al.</author>


</item>


<item>
<title>Nocturnin: a circadian target of Pparg-induced adipogenesis.</title>
<link>http://mouseion.jax.org/stfb2010/50</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/50</guid>
<pubDate>Tue, 08 May 2012 10:51:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nuclear receptors (NRs) control cell fate and regulate tissue function. Some of the NRs are expressed in a circadian and tissue-specific manner. Clock genes are part of the circadian network and fine-tune gene expression in adipose    and skeletal tissues. Pparg, a master transcription factor that determines adipogenesis, exhibits a circadian expression pattern in white adipose tissue and liver. Here we report the finding that the message and protein for a peripheral clock    gene, nocturnin, is markedly upregulated with Pparg activation in adipocytes and bone marrow stromal cells. Nocturnin is also expressed in relatively high amounts in other tissues that may have physiologic relevance for bone, including the brain    and hypothalamus. Of importance, we found polymorphic strain differences in bone marrow nocturnin expression that relate to phenotypic determinants of skeletal acquisition. Defining the function of nocturnin in peripheral tissues should provide    new insights into lineage allocation and the intimate relationship between nuclear receptors and physiologic timekeeping.</p>

	]]>
</description>

<author>M Kawai et al.</author>


</item>


<item>
<title>Regulation of selenoproteins and methionine sulfoxide reductases A and B1 by age, calorie restriction, and dietary selenium in mice.</title>
<link>http://mouseion.jax.org/stfb2010/49</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/49</guid>
<pubDate>Tue, 08 May 2012 10:51:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Methionine residues are susceptible to oxidation, but this damage may be reversed by methionine sulfoxide reductases MsrA and MsrB. Mammals contain one MsrA and three MsrBs, including a selenoprotein MsrB1. Here, we show that MsrB1    is the major methionine sulfoxide reductase in liver of mice and it is among the proteins that are most easily regulated by dietary selenium. MsrB1, but not MsrA activities, were reduced with age, and the selenium regulation of MsrB1 was    preserved in the aging liver, suggesting that MsrB1 could account for the impaired methionine sulfoxide reduction in aging animals. We also examined regulation of Msr and selenoprotein expression by a combination of dietary selenium and calorie    restriction and found that, under calorie restriction conditions, selenium regulation was preserved. In addition, mice overexpressing a mutant form of selenocysteine tRNA reduced MsrB1 activity to the level observed in selenium deficiency,    whereas MsrA activity was elevated in these animals.  Finally, we show that selenium regulation in inbred mouse strains is preserved in an outbred aging model. Taken together, these findings better define dietary regulation of methionine    sulfoxide reduction and selenoprotein expression in mice with regard to age, calorie restriction, dietary Se, and a combination of these factors.</p>

	]]>
</description>

<author>S V. Novoselov et al.</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 18, no. 1</title>
<link>http://collected.jcu.edu/carrollquarterly/54</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/54</guid>
<pubDate>Tue, 08 May 2012 10:51:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 18, no. 3</title>
<link>http://collected.jcu.edu/carrollquarterly/53</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/53</guid>
<pubDate>Tue, 08 May 2012 10:51:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>Representing ontogeny through ontology: a developmental biologist&apos;s guide to the gene ontology.</title>
<link>http://mouseion.jax.org/stfb2010/48</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/48</guid>
<pubDate>Tue, 08 May 2012 10:51:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Developmental biology, like many other areas of biology, has undergone a dramatic shift in the perspective from which developmental processes are viewed. Instead of focusing on the actions of a handful of genes or functional RNAs,    we now consider the interactions of large functional gene networks and study how these complex systems orchestrate the unfolding of an organism, from gametes to adult.  Developmental biologists are beginning to realize that understanding ontogeny    on this scale requires the utilization of computational methods to capture, store and represent the knowledge we have about the underlying processes. Here we review the use of the Gene Ontology (GO) to study developmental biology. We describe the    organization and structure of the GO and illustrate some of the ways we use it to capture the current understanding of many common developmental processes. We also discuss ways in which gene product annotations using the GO have been used to ask    and answer developmental questions in a variety of model developmental systems. We provide suggestions as to how the GO might be used in more powerful ways to address questions about development. Our goal is to provide developmental biologists    with enough background about the GO that they can begin to think about how they might use the ontology efficiently and in the most powerful ways possible.</p>

	]]>
</description>

<author>D P. Hill et al.</author>


</item>


<item>
<title>Novel sequence feature variant type analysis of the HLA genetic association in systemic sclerosis.</title>
<link>http://mouseion.jax.org/stfb2010/47</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/47</guid>
<pubDate>Tue, 08 May 2012 10:51:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>We describe a novel approach to genetic association analyses with proteins sub-divided into biologically relevant smaller sequence features (SFs), and their variant types (VTs). SFVT analyses are particularly informative for study    of highly polymorphic proteins such as the human leukocyte antigen (HLA), given the nature of its genetic variation: the high level of polymorphism, the pattern of amino acid variability, and that most HLA variation occurs at functionally    important sites, as well as its known role in organ transplant rejection, autoimmune disease development and response to infection. Further, combinations of variable amino acid sites shared by several HLA alleles (shared epitopes) are most likely    better descriptors of the actual causative genetic variants. In a cohort of systemic sclerosis patients/controls, SFVT analysis shows that a combination of SFs implicating specific amino acid residues in peptide binding pockets 4 and 7 of    HLA-DRB1 explains much of the molecular determinant of risk.</p>

	]]>
</description>

<author>D R. Karp et al.</author>


</item>


<item>
<title>The major locus for mouse adenovirus susceptibility maps to genes of the hematopoietic cell surface-expressed LY6 family.</title>
<link>http://mouseion.jax.org/stfb2010/46</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/46</guid>
<pubDate>Tue, 08 May 2012 10:51:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Susceptibility to mouse adenovirus type 1 is associated with the major quantitative trait locus Msq1. Msq1 was originally mapped to a 13-Mb region of mouse chromosome (Chr) 15 in crosses between SJL/J and BALB/cJ inbred mice. We    have now narrowed Msq1 to a 0.75-Mb interval from 74.68 to 75.43 Mb, defined by two anonymous markers, rs8259436 and D15Spn14, using data from 1396 backcross mice. The critical interval includes 14 Ly6 or Ly6-related genes, including Ly6a    (encoding Sca-1/TAP), Ly6e (Sca-2/Tsa1), Ly6g (Gr-1), and gpihbp1 (GPI-anchored high-density lipoprotein-binding protein 1), as well as the gene encoding an aldosterone synthase (Cyp11b2). The Ly6 family members are attractive candidates for    virus susceptibility genes because their products are GPI-anchored membrane proteins expressed on lymphoid and myeloid cells, with proposed functions in cell adhesion and cell signaling. To determine interstrain variation in susceptibility and    produce additional resources for cloning Msq1, we assayed the susceptibility phenotype of four previously untested inbred mouse strains. Susceptibility of strain 129S6/SvEvTac was subsequently localized to the Ly6 complex region, using    polymorphic genetic markers on Chr 15 in a population of 271 (129S6/SvEvTac x BALB/cJ)F(1) x BALB/cJ backcross mice. We identified a major 129S6/SvEvTac susceptibility allele, Msq1(129S6), on Chr 15 in the same region as Msq1(SJL).  The results    indicate that a major host factor in mouse adenovirus type 1 susceptibility is likely to be a member of the Ly6 gene family.</p>

	]]>
</description>

<author>K R. Spindler et al.</author>


</item>


<item>
<title>Visualization of omics data for systems biology.</title>
<link>http://mouseion.jax.org/stfb2010/45</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/45</guid>
<pubDate>Tue, 08 May 2012 10:51:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>High-throughput studies of biological systems are rapidly accumulating a wealth of 'omics'-scale data. Visualization is a key aspect of both the analysis and understanding of these data, and users now have many visualization methods    and tools to choose from. The challenge is to create clear, meaningful and integrated visualizations that give biological insight, without being overwhelmed by the intrinsic complexity of the data. In this review, we discuss how visualization    tools are being used to help interpret protein interaction, gene expression and metabolic profile data, and we highlight emerging new directions.</p>

	]]>
</description>

<author>N Gehlenborg et al.</author>


</item>


<item>
<title>The insulin-like growth factor-1 binding protein acid-labile subunit alters mesenchymal stromal cell fate.</title>
<link>http://mouseion.jax.org/stfb2010/44</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/44</guid>
<pubDate>Tue, 08 May 2012 10:51:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Age-related osteoporosis is accompanied by an increase in marrow adiposity and a reduction in serum insulin-like growth factor-1 (IGF-1) and the binding proteins that stabilize IGF-1. To determine the relationship between these    proteins and bone marrow adiposity, we evaluated the adipogenic potential of marrow-derived mesenchymal stromal cells (MSCs) from mice with decreased serum IGF-1 due to knockdown of IGF-1 production by the liver or knock-out of the binding    proteins.  We employed 10-16-week-old, liver-specific IGF-1-deficient, IGFBP-3 knock-out (BP3KO) and acid-labile subunit knock-out (ALSKO) mice. We found that expression of the late adipocyte differentiation marker peroxisome    proliferator-activated receptor gamma was increased in marrow isolated from ALSKO mice. When induced with adipogenic media, MSC cultures from ALSKO mice revealed a significantly greater number of differentiated adipocytes compared with controls.    MSCs from ALSKO mice also exhibited decreased alkaline-phosphatase positive colony size in cultures that were stimulated with osteoblast differentiation media. These osteoblast-like cells from ALSKO mice failed to induce osteoclastogenesis of    control cells in co-culture assays, indicating that impairment of IGF-1 complex formation with ALS in bone marrow alters cell fate, leading to increased adipogenesis.</p>

	]]>
</description>

<author>J C. Fritton et al.</author>


</item>


<item>
<title>Protein 4.2 binds to the carboxyl-terminal EF-hands of erythroid alpha-spectrin in a calcium- and calmodulin-dependent manner.</title>
<link>http://mouseion.jax.org/stfb2010/43</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/43</guid>
<pubDate>Tue, 08 May 2012 10:50:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Spectrin and protein 4.1 cross-link F-actin protofilaments into a network called the membrane skeleton. Actin and 4.1 bind to one end of beta-spectrin. The adjacent end of alpha-spectrin, called the EF-domain, is calmodulin-like,    with calcium-dependent and calcium-independent EF-hands. It has no known function.  However, the sph(1J)/sph(1J) mouse has very fragile red cells and lacks the last 13 amino acids in the EF-domain, suggesting the domain is critical for skeletal    integrity. Using pulldown binding assays, we find the alpha-spectrin EF-domain either alone or incorporated into a mini-spectrin binds native and recombinant protein 4.2 at a previously identified region of 4.2 (G(3) peptide). Native 4.2 binds    with an affinity comparable with other membrane skeletal interactions (K(d) = 0.30 microM). EF-domains bearing the sph(1J) mutation are inactive. Binding of protein 4.2 to band 3 (K(d) = 0.45 microM) does not interfere with the spectrin-4.2    interaction. Spectrin-4.2 binding is amplified by micromolar concentrations of Ca(2+) (but not Mg(2+)) by three to five times. Calmodulin also binds to the EF-domain (K(d) = 17 microM), and Ca(2+)-calmodulin blocks Ca(2+)-dependent binding of    protein 4.2 but not Ca(2+)-independent binding. The data suggest that protein 4.2 is located near protein 4.1 at the spectrin-actin junctions. Because proteins 4.1 and 4.2 also bind to band 3, the erythrocyte anion channel, we suggest that one or    both of these proteins cause a portion of band 3 to localize near the spectrin-actin junctions and provide another point of attachment between the membrane skeleton and the lipid bilayer.</p>

	]]>
</description>

<author>C Korsgren et al.</author>


</item>


<item>
<title>Mutations in Lama1 disrupt retinal vascular development and inner limiting membrane formation.</title>
<link>http://mouseion.jax.org/stfb2010/42</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/42</guid>
<pubDate>Tue, 08 May 2012 10:50:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Neuromutagenesis Facility at the Jackson Laboratory generated a mouse model of retinal vasculopathy, nmf223, which is characterized clinically by vitreal fibroplasia and vessel tortuosity. nmf223 homozygotes also have reduced    electroretinogram responses, which are coupled histologically with a thinning of the inner nuclear layer. The nmf223 locus was mapped to chromosome 17, and a missense mutation was identified in Lama1 that leads to the substitution of cysteine for    a tyrosine at amino acid 265 of laminin alpha1, a basement membrane protein. Despite normal localization of laminin alpha1 and other components of the inner limiting membrane, a reduced integrity of this structure was suggested by ectopic cells    and blood vessels within the vitreous. Immunohistochemical characterization of nmf223 homozygous retinas demonstrated the abnormal migration of retinal astrocytes into the vitreous along with the persistence of hyaloid vasculature. The Y265C    mutation significantly reduced laminin N-terminal domain (LN) interactions in a bacterial two-hybrid system. Therefore, this mutation could affect interactions between laminin alpha1 and other laminin chains. To expand upon these findings, a    Lama1 null mutant, Lama1(tm1.1Olf), was generated that exhibits a similar but more severe retinal phenotype than that seen in nmf223 homozygotes. The increased severity of the Lama1 null mutant phenotype is probably due to the complete loss of    the inner limiting membrane in these mice.  This first report of viable Lama1 mouse mutants emphasizes the importance of this gene in retinal development. The data presented herein suggest that hypomorphic mutations in human LAMA1 could lead to    retinal disease.</p>

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</description>

<author>M M. Edwards et al.</author>


</item>


<item>
<title>Enhanced antibody half-life improves in vivo activity.</title>
<link>http://mouseion.jax.org/stfb2010/41</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/41</guid>
<pubDate>Tue, 08 May 2012 10:50:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Improved affinity for the neonatal Fc receptor (FcRn) is known to extend antibody half-life in vivo. However, this has never been linked with enhanced therapeutic efficacy. We tested whether antibodies with half-lives extended up to    fivefold in human (h)FcRn transgenic mice and threefold in cynomolgus monkeys retain efficacy at longer dosing intervals. We observed that prolonged exposure due to FcRn-mediated enhancement of half-life improved antitumor activity of    Fc-engineered antibodies in an hFcRn/Rag1(-/-) mouse model. This bridges the demand for dosing convenience with the clinical necessity of maintaining efficacy.</p>

	]]>
</description>

<author>J Zalevsky et al.</author>


</item>


<item>
<title>Ontology engineering.</title>
<link>http://mouseion.jax.org/stfb2010/40</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/40</guid>
<pubDate>Tue, 08 May 2012 10:50:36 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>G Alterovitz et al.</author>


</item>


<item>
<title>Genetic dependence of central corneal thickness among inbred strains of mice.</title>
<link>http://mouseion.jax.org/stfb2010/39</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/39</guid>
<pubDate>Tue, 08 May 2012 10:50:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>PURPOSE: Central corneal thickness (CCT) exhibits broad variability. For unknown reasons, CCT also associates with diseases not typically considered corneal, particularly glaucoma. The purpose of this study was to test the strain    dependence of CCT variability among inbred mice and identify cellular and molecular factors associated with differing CCT. METHODS: Methodology for measuring murine CCT with ultrasound pachymetry was developed and used to measure CCT among 17    strains of mice. Corneas from three strains with nonoverlapping differences in CCT (C57BLKS/J, C57BL/6J, and SJL/J) were compared by histology, transmission electron microscopy, and expression profiling with gene microarrays.  RESULTS: CCT in    mice was highly strain dependent. CCT exhibited continuous variation from 89.2 microm in C57BLKS/J to 123.8 microm in SJL/J. Stromal thickness was the major determinant of the varying murine CCT, with epithelial thickness also contributing.    Corneal expression levels of many genes differed between strains with differing CCT, but most of these changes did not correlate with the changes observed in previously studied corneal diseases nor did they correlate with genes encoding major    structural proteins of the cornea.  CONCLUSIONS: Murine CCT has been measured with a variety of different techniques, but only among a limited number of different strains. Here, pachymetry was established as an additional tool and used to conduct    a broad survey of different strains of inbred mice. These results demonstrated that murine CCT was highly influenced by genetic background and established a baseline for future genetic approaches to further elucidate mechanisms regulating CCT and    its disease associations.</p>

	]]>
</description>

<author>G D. Lively et al.</author>


</item>


<item>
<title>Genetic analysis of albuminuria in aging mice and concordance with loci for human diabetic nephropathy found in a genome-wide association scan.</title>
<link>http://mouseion.jax.org/stfb2010/38</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/38</guid>
<pubDate>Tue, 08 May 2012 10:50:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Aging in the kidney can cause albuminuria, and discovering molecular mechanisms responsible for this might offer a new perspective on the etiology of this abnormality. Haplotype association mapping in the mouse is a novel approach    which uses the haplotypes of the relatively closely related mouse inbred strains and the phenotypic variation among these strains to find associations between haplotypes and phenotype. The albumin-to-creatinine ratios, a measure of urinary    albumin excretion, were determined in 30 inbred mouse strains at 12, 18, and 24 months of age. Mapping was performed for males and females separately at all three time points using a high density set of 63,222 single-nucleotide polymorphisms to    determine genetic loci involved in albuminuria. One significant and eight suggestive loci were found, some of which map to previously identified loci for traits associated with kidney damage in the mouse, but with a much higher resolution thus    narrowing their chromosomal location. These nine loci were then compared with genome-wide association scans for diabetic nephropathy (DN) in human type I diabetes. Our study found that two of the nine mouse loci for age-related albuminuria were    significantly associated with DN and consistent across male and female strata. This suggests common underlying genes predispose to kidney disease in mice and humans.</p>

	]]>
</description>

<author>S W. Tsaih et al.</author>


</item>


<item>
<title>Model based precision structural measurements on barely resolved objects.</title>
<link>http://mouseion.jax.org/stfb2010/37</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/37</guid>
<pubDate>Tue, 08 May 2012 10:50:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>A model based method for the accurate quantification of the 3D structure of fluorescently labelled cellular objects similar in size to the optical resolution limit is presented. This method is applied to both simulated confocal    images of chromatin structures and to real confocal data obtained on a Fluorescence in situ Hybridization (FISH) labelled gene domain. The model assumes that the object is composed of a small number of discrete points which are convolved with the    microscope point spread function to give the image. Fitting this model to image data results in a method to assess object structure which is accurate, shows a low bias, and does not require user intervention or the potentially subjective setting    of a threshold.</p>

	]]>
</description>

<author>D Baddeley et al.</author>


</item>


<item>
<title>Bone: adiposity and bone accrual-still an established paradigm?</title>
<link>http://mouseion.jax.org/stfb2010/36</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/36</guid>
<pubDate>Tue, 08 May 2012 10:50:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>The paradigm that obesity at any age is protective against skeletal failure has been ingrained in clinical practice for several decades. A new study published in the Journal of Bone and Mineral Research challenges the basic    framework of that tenet.</p>

	]]>
</description>

<author>M Kawai et al.</author>


</item>


<item>
<title>ZFP191 is required by oligodendrocytes for CNS myelination.</title>
<link>http://mouseion.jax.org/stfb2010/35</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/35</guid>
<pubDate>Tue, 08 May 2012 10:50:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The controlling factors that prompt mature oligodendrocytes to myelinate axons are largely undetermined. In this study, we used a forward genetics approach to identify a mutant mouse strain characterized by the absence of CNS myelin    despite the presence of abundant numbers of late-stage, process-extending oligodendrocytes. Through linkage mapping and complementation testing, we identified the mutation as a single nucleotide insertion in the gene encoding zinc finger protein    191 (Zfp191), which is a widely expressed, nuclear-localized protein that belongs to a family whose members contain both DNA-binding zinc finger domains and protein-protein-interacting SCAN domains. Zfp191 mutants express an array of    myelin-related genes at significantly reduced levels, and our in vitro and in vivo data indicate that mutant ZFP191 acts in a cell-autonomous fashion to disrupt oligodendrocyte function. Therefore, this study demonstrates that ZFP191 is required    for the myelinating function of differentiated oligodendrocytes.</p>

	]]>
</description>

<author>S Y. Howng et al.</author>


</item>


<item>
<title>NOD-scid IL2rgamma(null) mouse model of human skin transplantation and allograft rejection.</title>
<link>http://mouseion.jax.org/stfb2010/34</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/34</guid>
<pubDate>Tue, 08 May 2012 10:49:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>BACKGROUND: Transplantation of human skin on immunodeficient mice that support engraftment with functional human immune systems would be an invaluable tool for investigating mechanisms involved in wound healing and transplantation.    Nonobese diabetic (NOD)-scid interleukin-2 gamma chain receptor (NSG) readily engraft with human immune systems, but human skin graft integrity is poor. In contrast, human skin graft integrity is excellent on CB17-scid bg (SCID.bg) mice, but they    engraft poorly with human immune systems. METHODS: Human skin grafts transplanted onto immunodeficient NSG, SCID.bg, and other immunodeficient strains were evaluated for graft integrity, preservation of graft endothelium, and their ability to be    rejected after engraftment of allogeneic peripheral blood mononuclear cells. RESULTS: Human skin transplanted onto NSG mice develops an inflammatory infiltrate, consisting predominately of host Gr1(+) cells, that is detrimental to the survival of    human endothelium in the graft. Treatment of graft recipients with anti-Gr1 antibody reduces this cellular infiltrate, preserves graft endothelium, and promotes wound healing, tissue development, and graft remodeling. Excellent graft integrity of    the transplanted skin includes multilayered stratified human epidermis, well-developed human vasculature, human fibroblasts, and passenger leukocytes. Injection of unfractionated, CD4 or CD8 allogeneic human peripheral blood mononuclear cell    induces a rapid destruction of the transplanted skin graft. CONCLUSIONS: NSG mice treated with anti-Gr1 antibody provide a model optimized for both human skin graft integrity and engraftment of a functional human immune system. This model    provides the opportunity to investigate mechanisms orchestrating inflammation, wound healing, revascularization, tissue remodeling, and allograft rejection and can provide guidance for improving outcomes after clinical    transplantation.</p>

	]]>
</description>

<author>W J. Racki et al.</author>


</item>


<item>
<title>A survey of airway responsiveness in 36 inbred mouse strains facilitates gene mapping studies and identification of quantitative trait loci.</title>
<link>http://mouseion.jax.org/stfb2010/33</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/33</guid>
<pubDate>Tue, 08 May 2012 10:49:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Airway hyper-responsiveness (AHR) is a critical phenotype of human asthma and animal models of asthma. Other studies have measured AHR in nine mouse strains, but only six strains have been used to identify genetic loci underlying    AHR. Our goals were to increase the genetic diversity of available strains by surveying 27 additional strains, to apply haplotype association mapping to the 36-strain survey, and to identify new genetic determinants for AHR. We derived AHR from    the increase in airway resistance in females subjected to increasing levels of methacholine concentrations. We used haplotype association mapping to identify associations between AHR and haplotypes on chromosomes 3, 5, 8, 12, 13, and 14.  And we    used bioinformatics techniques to narrow the identified region on chromosome 13, reducing the region to 29 candidate genes, with 11 of considerable interest. Our combined use of haplotype association mapping with bioinformatics tools is the first    study of its kind for AHR on these 36 strains of mice. Our analyses have narrowed the possible QTL genes and will facilitate the discovery of novel genes that regulate AHR in mice.</p>

	]]>
</description>

<author>A S. Leme et al.</author>


</item>


<item>
<title>Altered metabolism and lipodystrophy in the early B-cell factor 1-deficient mouse.</title>
<link>http://mouseion.jax.org/stfb2010/32</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/32</guid>
<pubDate>Tue, 08 May 2012 10:49:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>We previously reported that mice deficient for the transcription factor early B-cell factor (Ebf1) exhibit markedly increased numbers of osteoblasts, bone formation rate, and serum osteocalcin, but the bone marrow of Ebf1(-/-) mice    is also striking in its increased marrow adiposity. The purpose of this work was to analyze the metabolic phenotype that accompanies the altered bone morphology of Ebf1(-/-) mice. Whereas marrow adiposity was increased, deposition of white    adipose tissue in other regions of the body was severely reduced (sc 40-50%, abdominally 80-85%). Brown adipose exhibited decreased lipid deposition.  Subcutaneous and perigonadal white adipose tissue showed a decrease in mRNA transcripts for    peroxisomal proliferator-activated receptor-gamma2 and CCAAT/enhancer-binding protein-beta in Ebf1(-/-) tissue compared with wild type.  Circulating levels of leptin were decreased in Ebf1(-/-) animals compared with their littermate controls    (down 65-95%), whereas adiponectin remained comparable after 2 wk of age. Serum analysis also found the Ebf1(-/-) animals were hypoglycemic and hypotriglyceridemic. After ip injection of insulin, the serum glucose levels in Ebf1(-/-) mice took    longer to recover, and after a glucose challenge the Ebf1(-/-) animals reached serum glucose levels almost twice that of their wild-type counterparts. Measurement of circulating pancreatic hormones revealed normal or reduced insulin levels in the    Ebf1(-/-) mice, whereas glucagon was significantly increased (up 1.7- to 8.5-fold). Metabolically the Ebf1(-/-) mice had increased O(2) consumption, CO(2) production, food and water intake, and activity. Markers for gluconeogenesis, however, were    decreased in the Ebf1(-/-) mice compared with controls. In conclusion, the Ebf1-deficient animals exhibit defects in adipose tissue deposition with increased marrow adiposity and impaired glucose mobilization.</p>

	]]>
</description>

<author>J A. Fretz et al.</author>


</item>


<item>
<title>Functional hierarchy and reversibility within the murine spermatogenic stem cell compartment.</title>
<link>http://mouseion.jax.org/stfb2010/31</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/31</guid>
<pubDate>Tue, 08 May 2012 10:49:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Stem cells support tissue maintenance by balancing self-renewal and differentiation. In mice, it is believed that a homogeneous stem cell population of single spermatogonia supports spermatogenesis, and that differentiation, which    is accompanied by the formation of connected cells (cysts) of increasing length, is linear and nonreversible. We evaluated this model with the use of lineage analysis and live imaging, and found that this putative stem cell population is not    homogeneous. Instead, the stem cell pool that supports steady-state spermatogenesis is contained within a subpopulation of single spermatogonia. We also found that cysts are not committed to differentiation and appear to recover stem cell    potential by fragmentation, and that the fate of individual spermatogonial populations was markedly altered during regeneration after damage.  Thus, there are multiple and reversible paths from stem cells to differentiation, and these may also    occur in other systems.</p>

	]]>
</description>

<author>T Nakagawa et al.</author>


</item>


<item>
<title>In vivo selection of human embryonic stem cell-derived cells expressing methotrexate-resistant dihydrofolate reductase.</title>
<link>http://mouseion.jax.org/stfb2010/30</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/30</guid>
<pubDate>Tue, 08 May 2012 10:49:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Human embryonic stem cells (hESCs) provide a novel source of hematopoietic and other cell populations suitable for gene therapy applications. Preclinical studies to evaluate engraftment of hESC-derived hematopoietic cells    transplanted into immunodeficient mice demonstrate only limited repopulation. Expression of a drug-resistance gene, such as Tyr22-dihydrofolate reductase (Tyr22-DHFR), coupled to methotrexate (MTX) chemotherapy has the potential to selectively    increase the engraftment of gene-modified, hESC-derived cells in mouse xenografts. Here, we describe the generation of Tyr22-DHFR-GFP-expressing hESCs that maintain pluripotency, produce teratomas and can differentiate into    MTXr-hemato-endothelial cells. We demonstrate that MTX administered to nonobese diabetic/severe combined immunodeficient/IL-2Rgammac(null) (NSG) mice after injection of Tyr22-DHFR-hESC-derived cells significantly increases human CD34(+) and    CD45(+) cell engraftment in the bone marrow (BM) and peripheral blood of transplanted MTX-treated mice. These results demonstrate that MTX treatment supports selective, long-term engraftment of Tyr22-DHFR cells in vivo, and provides a novel    approach for combined human cell and gene therapy.</p>

	]]>
</description>

<author>J L. Gori et al.</author>


</item>


<item>
<title>New candidate genes identified for controlling mouse gonadal sex determination and the early stages of granulosa and Sertoli cell differentiation.</title>
<link>http://mouseion.jax.org/stfb2010/29</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/29</guid>
<pubDate>Tue, 08 May 2012 10:49:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mammalian gonadal sex-determining (GSD) genes are expressed in a unique population of somatic cells that differentiate into granulosa cells in XX gonads or Sertoli cells in XY gonads. The ability to efficiently isolate these somatic    support cells (SSCs) during the earliest stages of gonad development would facilitate identifying 1) new candidate GSD genes that may be involved in cases of unexplained abnormal gonad development and 2) genes involved in the earliest stages of    granulosa and Sertoli cell differentiation. We report the development of a unique mouse carrying two transgenes that allow XX and XY mice to be distinguished as early as Embryonic Day 11.5 (E11.5) and allow SSCs to be isolated from    undifferentiated (E11.5) and early differentiated (E12.5) fetal gonads. The Mouse Genome 430v2.0 GeneChip (Affymetrix) was used to identify transcripts exhibiting a sexual dimorphic expression pattern in XX and XY isolated SSCs. The analysis    revealed previously unidentified sexually dimorphic transcripts, including low-level expressed genes such as Sry, a gene not identified in other microarray studies. Multigene real-time PCR analysis of 57 genes verified that 53 were expressed in    fetal gonads in a sexually dimorphic pattern, and whole-mount in situ hybridization analysis verified 4930563E18Rik, Pld1, and Sprr2d are expressed in XX gonads, and Fbln2, Ppargc1a, and Scrn1 are expressed in XY gonads. Taken together, the data    provide a comprehensive resource for the spatial-temporal expression pattern of genes that are part of the genetic network underlying the early stages of mammalian fetal gonadal development, including the development of granulosa and Sertoli    cells.</p>

	]]>
</description>

<author>G J. Bouma et al.</author>


</item>


<item>
<title>Differential expression of choline kinase isoforms in skeletal muscle explains the phenotypic variability in the rostrocaudal muscular dystrophy mouse.</title>
<link>http://mouseion.jax.org/stfb2010/28</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/28</guid>
<pubDate>Tue, 08 May 2012 10:49:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Choline kinase in mammals is encoded by two genes, Chka and Chkb. Disruption of murine Chka leads to embryonic lethality, whereas a spontaneous genomic deletion in murine Chkb results in neonatal forelimb bone deformity and hindlimb    muscular dystrophy. Surprisingly, muscular dystrophy isn't significantly developed in the forelimb. We have investigated the mechanism by which a lack of choline kinase beta, encoded by Chkb, results in minimal muscular dystrophy in forelimbs. We    have found that choline kinase beta is the major isoform in hindlimb muscle and contributes more to choline kinase activity, while choline kinase alpha is predominant in forelimb muscle and contributes more to choline kinase activity.  Although    choline kinase activity is decreased in forelimb muscles of Chkb(-/-) mice, the activity of CTP:phosphocholine cytidylyltransferase is increased, resulting in enhanced phosphatidylcholine biosynthesis. The activity of phosphatidylcholine    phospholipase C is up-regulated while the activity of phospholipase A(2) in forelimb muscle is not altered. Regeneration of forelimb muscles of Chkb(-/-) mice is normal when challenged with cardiotoxin. In contrast to hindlimb muscle,    mega-mitochondria are not significantly formed in forelimb muscle of Chkb(-/-) mice. We conclude that the relative lack of muscle degeneration in forelimbs of Chkb(-/-) mice is due to abundant choline kinase alpha and the stable homeostasis of    phosphatidylcholine.</p>

	]]>
</description>

<author>G Wu et al.</author>


</item>


<item>
<title>Analysis of novel sph (spherocytosis) alleles in mice reveals allele-specific loss of band 3 and adducin in alpha-spectrin-deficient red cells.</title>
<link>http://mouseion.jax.org/stfb2010/27</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/27</guid>
<pubDate>Tue, 08 May 2012 10:49:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Five spontaneous, allelic mutations in the alpha-spectrin gene, Spna1, have been identified in mice (spherocytosis [sph], sph(1J), sph(2J), sph(2BC), sph(Dem)).  All cause severe hemolytic anemia. Here, analysis of 3 new alleles    reveals previously unknown consequences of red blood cell (RBC) spectrin deficiency. In sph(3J), a missense mutation (H2012Y) in repeat 19 introduces a cryptic splice site resulting in premature termination of translation. In sph(Ihj), a    premature stop codon occurs (Q1853Stop) in repeat 18. Both mutations result in markedly reduced RBC membrane spectrin content, decreased band 3, and absent beta-adducin.  Reevaluation of available, previously described sph alleles reveals band 3    and adducin deficiency as well. In sph(4J), a missense mutation occurs in the C-terminal EF hand domain (C2384Y). Notably, an equally severe hemolytic anemia occurs despite minimally decreased membrane spectrin with normal band 3 levels and    present, although reduced, beta-adducin. The severity of anemia in sph(4J) indicates that the highly conserved cysteine residue at the C-terminus of alpha-spectrin participates in interactions critical to membrane stability. The data reinforce    the notion that a membrane bridge in addition to the classic protein 4.1-p55-glycophorin C linkage exists at the RBC junctional complex that involves interactions between spectrin, adducin, and band 3.</p>

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</description>

<author>R F. Robledo et al.</author>


</item>


<item>
<title>The Experiences of Women Who Live with an Implantable Cardioverter-Defibrillator (lCD)</title>
<link>http://digitalcommons.unf.edu/etd/198</link>
<guid isPermaLink="true">http://digitalcommons.unf.edu/etd/198</guid>
<pubDate>Tue, 08 May 2012 10:49:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>The implantable cardioverter defibrillator (lCD) is the most effective treatment available for terminating potentially life-threatening ventricular fibrillation and ventricular tachycardia. The lCD detects and attempts to correct these arrhythmias by pacing, cardioversion, and defibrillation thereby providing lifesaving therapy to patients at risk for sudden cardiac death. Currently, 150,000 Americans receive ICDs each year. Although most lCD recipients are men, more women are now qualifying for insertion (Stutts, Cross, Conti, & Sears, 2007). <br><br>Despite its established health benefits, lCD implantation is accompanied by psychological factors which merit research attention. This study investigated the experiences of women who live an lCD. The homogenous, purposeful sample consisted of 15 women who had an lCD that was implanted within the last three years and were receiving follow-up treatment at the same north Florida clinic. Data collection was accomplished through a semi-structured interview specific to the areas of pre-implantation, immediate post-implantation, and discharge home. Results were transcribed verbatim and then analyzed. Five core themes emerged from the transcripts along with multiple subcategories. The main themes included: Psychological Reactions, Physical Comfort, Procedural Issues, Body Image, and Feelings Regarding a Shock. Information obtained from this research is beneficial to nurses providing care to women with ICDs and to primary care advanced nurse practitioners in order to improve the overall health outcome and ongoing care of these women.</p>

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</description>

<author>Jenea Mary Smith</author>


</item>


<item>
<title>Parameters for establishing humanized mouse models to study human immunity: analysis of human hematopoietic stem cell engraftment in three immunodeficient strains of mice bearing the IL2rgamma(null) mutation.</title>
<link>http://mouseion.jax.org/stfb2010/26</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/26</guid>
<pubDate>Tue, 08 May 2012 10:49:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>"Humanized" mouse models created by engraftment of immunodeficient mice with human hematolymphoid cells or tissues are an emerging technology with broad appeal across multiple biomedical disciplines. However, investigators wishing    to utilize humanized mice with engrafted functional human immune systems are faced with a myriad of variables to consider. In this study, we analyze HSC engraftment methodologies using three immunodeficient mouse strains harboring the    IL2rgamma(null) mutation; NOD-scid IL2rgamma(null), NOD-Rag1(null) IL2rgamma(null), and BALB/c-Rag1(null) IL2rgamma(null) mice. Strategies compared engraftment of human HSC derived from umbilical cord blood following intravenous injection into    adult mice and intracardiac and intrahepatic injection into newborn mice. We observed that newborn recipients exhibited enhanced engraftment as compared to adult recipients. Irrespective of the protocol or age of recipient, both immunodeficient    NOD strains support enhanced hematopoietic cell engraftment as compared to the BALB/c strain. Our data define key parameters for establishing humanized mouse models to study human immunity.</p>

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</description>

<author>M A. Brehm et al.</author>


</item>


<item>
<title>Human FcRn transgenic mice for pharmacokinetic evaluation of therapeutic antibodies.</title>
<link>http://mouseion.jax.org/stfb2010/25</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/25</guid>
<pubDate>Tue, 08 May 2012 10:49:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Therapeutic monoclonal antibodies are widely recognized to be a most promising means to treat an increasing number of human diseases, including cancers and autoimmunity. To a large extent, the efficacy of monoclonal antibody    treatment is because IgG antibodies have greatly extended persistence in vivo. However, conventional rodent models do not mirror human antibody pharmacokinetics. The key molecule responsible for the extended persistence antibodies is the major    histocompatibility complex class I family Fc receptor, FcRn. We describe human FcRn transgenic mouse models and how they can be exploited productively for the preclinical pharmacokinetic evaluation of therapeutic antibodies.</p>

	]]>
</description>

<author>D C. Roopenian et al.</author>


</item>


<item>
<title>Prdm9 controls activation of mammalian recombination hotspots.</title>
<link>http://mouseion.jax.org/stfb2010/24</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/24</guid>
<pubDate>Tue, 08 May 2012 10:48:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mammalian meiotic recombination, which preferentially occurs at specialized sites called hotspots, ensures the orderly segregation of meiotic chromosomes and creates genetic variation among offspring. A locus on mouse chromosome 17,    which controls activation of recombination at multiple distant hotspots, has been mapped within a 181-kilobase interval, three of whose genes can be eliminated as candidates. The remaining gene, Prdm9, codes for a zinc finger containing histone    H3K4 trimethylase that is expressed in early meiosis and whose deficiency results in sterility in both sexes. Mus musculus exhibits five alleles of Prdm9; human populations exhibit two predominant alleles and multiple minor alleles. The    identification of Prdm9 as a protein regulating mammalian recombination hotspots initiates molecular studies of this important biological control system.</p>

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</description>

<author>E D. Parvanov et al.</author>


</item>


<item>
<title>Genetics of mammalian meiosis: regulation, dynamics and impact on fertility.</title>
<link>http://mouseion.jax.org/stfb2010/23</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/23</guid>
<pubDate>Tue, 08 May 2012 10:48:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Meiosis is an essential stage in gamete formation in all sexually reproducing organisms. Studies of mutations in model organisms and of human haplotype patterns are leading to a clearer understanding of how meiosis has adapted from    yeast to humans, the genes that control the dynamics of chromosomes during meiosis, and how meiosis is tied to gametic success. Genetic disruptions and meiotic errors have important roles in infertility and the aetiology of developmental defects,    especially aneuploidy. An understanding of the regulation of meiosis, coupled with advances in genomics, may ultimately allow us to diagnose the causes of meiosis-based infertilities, more wisely apply assisted reproductive technologies, and    derive functional germ cells.</p>

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</description>

<author>M A. Handel et al.</author>


</item>


<item>
<title>Molecular basis for hair loss in mice carrying a novel nonsense mutation (Hrrh-R ) in the hairless gene (Hr).</title>
<link>http://mouseion.jax.org/stfb2010/22</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/22</guid>
<pubDate>Tue, 08 May 2012 10:48:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Animal models carrying mutations in the hairless (Hr) gene provide a rich resource for study of hair follicle biology. A spontaneous mouse mutant with a phenotype strikingly similar to rhino mutants of Hr arose spontaneously in the    mouse facility at Oak Ridge National Laboratory. Sequence analysis of Hr in these mutants uncovered a nonsense mutation in exon 12, designated as Hr(rh-R) (rhino, Oak Ridge). The mutation led to significant reduction in Hr mRNA levels, predicted    to be due to nonsense-mediated decay. Histological analysis indicated dilated hair follicle infundibula at 14 days of age that rapidly became filled with cornified material. Microarray analyses revealed that expression levels of many genes    involved in keratinocyte differentiation, epidermal regeneration, and wound healing were significantly upregulated before morphological detection of the phenotype, suggesting their role in onset of the Hr(rh-R) phenotype.  Identification of this    new Hr allele and the underlying molecular alterations allows further understanding of the role of Hr in hair follicle biology.</p>

	]]>
</description>

<author>Y Liu et al.</author>


</item>


<item>
<title>Mutations in Grxcr1 are the basis for inner ear dysfunction in the pirouette mouse.</title>
<link>http://mouseion.jax.org/stfb2010/21</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/21</guid>
<pubDate>Tue, 08 May 2012 10:48:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recessive mutations at the mouse pirouette (pi) locus result in hearing loss and vestibular dysfunction due to neuroepithelial defects in the inner ear. Using a positional cloning strategy, we have identified mutations in the gene    Grxcr1 (glutaredoxin cysteine-rich 1) in five independent allelic strains of pirouette mice. We also provide sequence data of GRXCR1 from humans with profound hearing loss suggesting that pirouette is a model for studying the mechanism of    nonsyndromic deafness DFNB25. Grxcr1 encodes a 290 amino acid protein that contains a region of similarity to glutaredoxin proteins and a cysteine-rich region at its C terminus. Grxcr1 is expressed in sensory epithelia of the inner ear, and its    encoded protein is localized along the length of stereocilia, the actin-filament-rich mechanosensory structures at the apical surface of auditory and vestibular hair cells. The precise architecture of hair cell stereocilia is essential for normal    hearing. Loss of function of Grxcr1 in homozygous pirouette mice results in abnormally thin and slightly shortened stereocilia. When overexpressed in transfected cells, GRXCR1 localizes along the length of actin-filament-rich structures at the    dorsal-apical surface and induces structures with greater actin filament content and/or increased lengths in a subset of cells. Our results suggest that deafness in pirouette mutants is associated with loss of GRXCR1 function in modulating actin    cytoskeletal architecture in the developing stereocilia of sensory hair cells.</p>

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</description>

<author>H Odeh et al.</author>


</item>


<item>
<title>Alteration of the unfolded protein response modifies neurodegeneration in a mouse model of Marinesco-Sjogren syndrome.</title>
<link>http://mouseion.jax.org/stfb2010/20</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/20</guid>
<pubDate>Tue, 08 May 2012 10:48:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Endoplasmic reticulum (ER) stress has been linked to the onset and progression of many diseases. SIL1 is an adenine nucleotide exchange factor of the essential ER lumen chaperone HSPA5/BiP that senses ER stress and is involved in    protein folding. Mutations in the Sil1 gene have been associated with Marinesco-Sjogren syndrome, hallmarks of which include ataxia and cerebellar atrophy. We have previously shown that loss of SIL1 function in mouse results in ER stress,    ubiquitylated protein inclusions, and degeneration of specific Purkinje cells in the cerebellum. Here, we report that overexpression of HYOU1/ORP150, an exchange factor that works in parallel to SIL1, prevents ER stress and rescues    neurodegeneration in Sil1(-/-) mice, whereas decreasing expression of HYOU1 exacerbates these phenotypes. In addition, loss of DNAJC3/p58(IPK), a co-chaperone that promotes ATP hydrolysis by BiP, ameliorates ER stress and neurodegeneration in    Sil1(-/-) mice. These findings suggest that alterations in the nucleotide exchange cycle of BiP cause ER stress and neurodegeneration in Sil1-deficient mice. Our results present the first evidence of important genetic modifiers of    Marinesco-Sjogren syndrome, and provide additional pathways for therapeutic intervention for this, and other ER stress-induced, diseases.</p>

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</description>

<author>L Zhao et al.</author>


</item>


<item>
<title>MDA5 and MAVS mediate type I interferon responses to coxsackie B virus.</title>
<link>http://mouseion.jax.org/stfb2010/19</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/19</guid>
<pubDate>Tue, 08 May 2012 10:48:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Coxsackie B viruses (CVB) are enteroviruses that have been associated with a variety of human diseases, including myocarditis. In the present study, we found that MDA5 and its adaptor molecule MAVS are critical for type I interferon    responses to CVB, since the absence of either MAVS or MDA5 leads to deficient type I interferon production and early mortality in mice infected with CVB.  Pancreatic and hepatic necrosis were observed on histopathological examination of MAVS and    MDA5 knockout mice infected with CVB. Inflammatory cytokine production in response to systemic CVB infection was independent of MAVS. Surprisingly, virus titers were not elevated in MAVS-deficient mice, despite significant reductions in type I    interferon levels. These data highlight the importance of type I interferon in host defense and provide insight on the mechanisms of innate immune responses following coxsackievirus infection.</p>

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</description>

<author>J P. Wang et al.</author>


</item>


<item>
<title>Preadipocyte factor-1 is associated with marrow adiposity and bone mineral density in women with anorexia nervosa.</title>
<link>http://mouseion.jax.org/stfb2010/18</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/18</guid>
<pubDate>Tue, 08 May 2012 10:48:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>CONTEXT: Despite having low visceral and sc fat depots, women with anorexia nervosa (AN) have elevated marrow fat mass, which is inversely associated with bone mineral density (BMD). Adipocytes and osteoblasts differentiate from a    common progenitor cell, the human mesenchymal stem cell. Therefore, understanding factors that regulate this differentiation process may provide insight into bone loss in AN. OBJECTIVE: The objective of the study was to investigate the    relationship between preadipocyte factor-1 (Pref-1), a member of the epidermal growth factor-like family of proteins and regulator of adipocyte and osteoblast differentiation, and fat depots and BMD in AN. Design: This was a cross-sectional    study. SETTING: The study was conducted at a clinical research center. PATIENTS: Patients included 20 women with AN (26.8 +/- 1.5 yr) and 10 normal-weight controls (29.2 +/- 1.7 yr). INTERVENTIONS: There were no interventions. MAIN OUTCOMES    MEASURE: Pref-1, leptin, IGF-I, IGF binding protein (IGF-BP)-2 and estradiol levels were measured. BMD of the spine and hip was measured by dual-energy x-ray absorptiometry. Marrow fat content of the L4 vertebra and femur was measured by    (1)H-magnetic resonance spectroscopy. RESULTS: Pref-1 levels were significantly higher in AN compared with controls (P = 0.01). There was a positive correlation between Pref-1 and marrow fat of the proximal femoral metaphysis (R = 0.50, P = 0.01)    and an inverse association between leptin and L4 marrow fat (R = -0.45, P < 0.05). There was an inverse association between Pref-1 and BMD of both the anteroposterior spine and lateral spine (R = -0.54, P = 0.003; R = -0.44, P = 0.02,    respectively). CONCLUSIONS: Pref-1 is elevated in AN.  Pref-1, IGF-I, IGF-BP2 and leptin are associated with marrow adiposity and BMD.</p>

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</description>

<author>P K. Fazeli et al.</author>


</item>


<item>
<title>Lunatic Fringe-mediated Notch signaling is required for lung alveogenesis.</title>
<link>http://mouseion.jax.org/stfb2010/17</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/17</guid>
<pubDate>Tue, 08 May 2012 10:48:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Distal lung development occurs through coordinated induction of myofibroblasts, epithelial cells, and capillaries. Lunatic Fringe (Lfng) is a beta(1-3) N-acetylglucosamine transferase that modifies Notch receptors to facilitate    their activation by Delta-like (Dll1/4) ligands. Lfng is expressed in the distal lung during saccular development, and deletion of this gene impairs myofibroblast differentiation and alveogenesis in this context. A similar defect was observed in    Notch2(beta-geo/+)Notch3(beta-geo/beta-geo) compound mutant mice but not in Notch2(beta-geo/+) or Notch3(beta-geo/beta-geo) single mutants. Finally, to directly test for the role of Notch signaling in myofibroblast differentiation in vivo, we    used ROSA26-rtTA(/+);tetO-CRE(/+);RBPJkappa(flox/flox) inducible mutant mice to show that disruption of canonical Notch signaling during late embryonic development prevents induction of smooth muscle actin in mesenchymal cells of the distal lung.    In sum, these results demonstrate that Lfng functions to enhance Notch signaling in myofibroblast precursor cells and thereby to coordinate differentiation and mobilization of myofibroblasts required for alveolar septation.</p>

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</description>

<author>K Xu et al.</author>


</item>


<item>
<title>Targeted delivery of small interfering RNA to human dendritic cells to suppress dengue virus infection and associated proinflammatory cytokine production.</title>
<link>http://mouseion.jax.org/stfb2010/16</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/16</guid>
<pubDate>Tue, 08 May 2012 10:48:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dengue is a common arthropod-borne flaviviral infection in the tropics, for which there is no vaccine or specific antiviral drug. The infection is often associated with serious complications such as dengue hemorrhagic fever (DHF) or    dengue shock syndrome (DSS), in which both viral and host factors have been implicated. RNA interference (RNAi) is a potent antiviral strategy and a potential therapeutic option for dengue if a feasible strategy can be developed for delivery of    small interfering RNA (siRNA) to dendritic cells (DCs) and macrophages, the major in vivo targets of the virus and also the source of proinflammatory cytokines. Here we show that a dendritic cell-targeting 12-mer peptide (DC3) fused to    nona-D-arginine (9dR) residues (DC3-9dR) delivers siRNA and knocks down endogenous gene expression in heterogenous DC subsets, (monocyte-derived DCs [MDDCs], CD34(+) hematopoietic stem cell [HSC])-derived Langerhans DCs, and peripheral blood    DCs). Moreover, DC3-9dR-mediated delivery of siRNA targeting a highly conserved sequence in the dengue virus envelope gene (siFvE(D)) effectively suppressed dengue virus replication in MDDCs and macrophages. In addition, DC-specific delivery of    siRNA targeting the acute-phase cytokine tumor necrosis factor alpha (TNF-alpha), which plays a major role in dengue pathogenesis, either alone or in combination with an antiviral siRNA, significantly reduced virus-induced production of the    cytokine in MDDCs. Finally to validate the strategy in vivo, we tested the ability of the peptide to target human DCs in the NOD/SCID/IL-2Rgamma(-/-) mouse model engrafted with human CD34(+) hematopoietic stem cells (HuHSC mice). Treatment of    mice by intravenous (i.v.)  injection of DC3-9dR-complexed siRNA targeting TNF-alpha effectively suppressed poly(I:C)-induced TNF-alpha production by DCs. Thus, DC3-9dR can deliver siRNA to DCs both in vitro and in vivo, and this delivery    approach holds promise as a therapeutic strategy to simultaneously suppress virus replication and curb virus-induced detrimental host immune responses in dengue infection.</p>

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</description>

<author>S Subramanya et al.</author>


</item>


<item>
<title>The mouse mutation &quot;thrombocytopenia and cardiomyopathy&quot; (trac) disrupts Abcg5: a spontaneous single gene model for human hereditary phytosterolemia/sitosterolemia.</title>
<link>http://mouseion.jax.org/stfb2010/15</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/15</guid>
<pubDate>Tue, 08 May 2012 10:47:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>The spontaneous mouse mutation "thrombocytopenia and cardiomyopathy" (trac) causes macrothrombocytopenia, prolonged bleeding times, anemia, leukopenia, infertility, cardiomyopathy, and shortened life span. Homozygotes show a 20-fold    decrease in platelet numbers and a 3-fold increase in platelet size with structural alterations and functional impairments in activation and aggregation.  Megakaryocytes in trac/trac mice are present in increased numbers, have poorly developed    demarcation membrane systems, and have decreased polyploidy. The thrombocytopenia is not intrinsic to defects at the level of hematopoietic progenitor cells but is associated with a microenvironmental abnormality. The trac mutation maps to mouse    chromosome 17, syntenic with human chromosome 2p21-22. A G to A mutation in exon 10 of the adenosine triphosphate (ATP)-binding cassette subfamily G, member 5 (Abcg5) gene, alters a tryptophan codon (UGG) to a premature stop codon (UAG). Crosses    with mice doubly transgenic for the human ABCG5 and ABCG8 genes rescued platelet counts and volumes. ABCG5 and ABCG8 form a functional complex that limits dietary phytosterol accumulation. Phytosterolemia in trac/trac mice confirmed a functional    defect in the ABCG5/ABCG8 transport system. The trac mutation provides a new clinically significant animal model for human phytosterolemia and provides a new means for studying the role of phytosterols in hematologic diseases and testing    therapeutic interventions.</p>

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</description>

<author>T H. Chase et al.</author>


</item>


<item>
<title>The Mouse Genome Database: enhancements and updates.</title>
<link>http://mouseion.jax.org/stfb2010/14</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/14</guid>
<pubDate>Tue, 08 May 2012 10:47:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Mouse Genome Database (MGD) is a major component of the Mouse Genome Informatics (MGI, http://www.informatics.jax.org/) database resource and serves as the primary community model organism database for the laboratory mouse. MGD    is the authoritative source for mouse gene, allele and strain nomenclature and for phenotype and functional annotations of mouse genes. MGD contains comprehensive data and information related to mouse genes and their functions, standardized    descriptions of mouse phenotypes, extensive integration of DNA and protein sequence data, normalized representation of genome and genome variant information including comparative data on mammalian genes. Data for MGD are obtained from diverse    sources including manual curation of the biomedical literature and direct contributions from individual investigator's laboratories and major informatics resource centers, such as Ensembl, UniProt and NCBI. MGD collaborates with the    bioinformatics community on the development and use of biomedical ontologies such as the Gene Ontology and the Mammalian Phenotype Ontology. Recent improvements in MGD described here includes integration of mouse gene trap allele and sequence    data, integration of gene targeting information from the International Knockout Mouse Consortium, deployment of an MGI Biomart, and enhancements to our batch query capability for customized data access and retrieval.</p>

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</description>

<author>C J. Bult et al.</author>


</item>


<item>
<title>The Role of Traf2 in Zebrafish</title>
<link>http://digitalcommons.library.umaine.edu/honors/22</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/honors/22</guid>
<pubDate>Tue, 08 May 2012 10:47:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Tumor necrosis factor (TNF) receptor associated factor 2 (Traf2) is suspected to be involved in the anti-apoptotic pathways of the innate immune system in the zebrafish. The expression of three different forms of Traf2, 2a1, 2a2, and 2b, was knocked down in pairs using antisense morpholino oligonucleotides in zebrafish embryos. A rescue was attempted by knocking down a potential receptor for the Traf2 to pathway. After infection with snakehead rhabdovirus (SHRV), mortality was quantified and the apoptotic effects of each of the Traf2 genes was assessed. Cell death was quantified using the TUNEL technique. The findings indicated that at least two zebrafish Traf2 proteins were necessary for function. Increased mortality due to infection was not caused by an increased amount of virus in the Traf2 morphants or increased amount of apoptosis.</p>

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</description>

<author>Bradie N. Manion</author>


</item>


<item>
<title>The Gene Ontology in 2010: extensions and refinements.</title>
<link>http://mouseion.jax.org/stfb2010/13</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/13</guid>
<pubDate>Tue, 08 May 2012 10:47:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Gene Ontology (GO) Consortium (http://www.geneontology.org) (GOC) continues to develop, maintain and use a set of structured, controlled vocabularies for the annotation of genes, gene products and sequences. The GO ontologies    are expanding both in content and in structure. Several new relationship types have been introduced and used, along with existing relationships, to create links between and within the GO domains. These improve the representation of biology,    facilitate querying, and allow GO developers to systematically check for and correct inconsistencies within the GO. Gene product annotation using GO continues to increase both in the number of total annotations and in species coverage. GO tools,    such as OBO-Edit, an ontology-editing tool, and AmiGO, the GOC ontology browser, have seen major improvements in functionality, speed and ease of use.</p>

	]]>
</description>

<author>Ontology Consortium Gene</author>


</item>


<item>
<title>A novel spontaneous mutation of Irs1 in mice results in hyperinsulinemia, reduced growth, low bone mass and impaired adipogenesis.</title>
<link>http://mouseion.jax.org/stfb2010/12</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/12</guid>
<pubDate>Tue, 08 May 2012 10:47:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>A spontaneous mouse mutant, designated 'small' (sml), was recognized by reduced body size suggesting a defect in the IGF1/GH axis. The mutation was mapped to the chromosome 1 region containing Irs1, a viable candidate gene whose    sequence revealed a single nucleotide deletion resulting in a premature stop codon.  Despite normal mRNA levels in mutant and control littermate livers, western blot analysis revealed no detectable protein in mutant liver lysates. When compared    with the control littermates, Irs1(sml)/Irs1(sml) (Irs1(sml/sml)) mice were small, lean, hearing impaired; had 20% less serum IGF1; were hyperinsulinemic; and were mildly insulin resistant. Irs1(sml/sml) mice had low bone mineral density, reduced    trabecular and cortical thicknesses, and low bone formation rates, while osteoblast and osteoclast numbers were increased in the females but not different in the males compared with the Irs1(+/+) controls. In vitro, Irs1(sml/sml) bone marrow    stromal cell cultures showed decreased alkaline phosphatase-positive colony forming units (pre-osteoblasts; CFU-AP+) and normal numbers of tartrate-resistant acid phosphatase-positive osteoclasts.  Irs1(sml/sml) stromal cells treated with IGF1    exhibited a 50% decrease in AKT phosphorylation, indicative of defective downstream signaling. Similarities between engineered knockouts and the spontaneous mutation of Irs1(sml) were identified as well as significant differences with respect to    heterozygosity and gender. In sum, we have identified a spontaneous mutation in the Irs1 gene associated with a major skeletal phenotype. Changes in the heterozygous Irs1(+)(/sml) mice raise the possibility that similar mutations in humans are    associated with short stature or osteoporosis.</p>

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</description>

<author>V E. DeMambro et al.</author>


</item>


<item>
<title>Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatment.</title>
<link>http://mouseion.jax.org/stfb2010/11</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/11</guid>
<pubDate>Tue, 08 May 2012 10:47:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Most genetically engineered mouse (GEM) models for colon cancer are based on tissuewide or germline gene modification, resulting in tumors predominantly of the small intestine. Several of these models involve modification of the    adenomatous polyposis coli (Apc) gene and are excellent models for familial cancer predisposition syndromes. We have developed a stochastic somatic mutation model for sporadic colon cancer that presents with isolated primary tumors in the distal    colon and recapitulates the entire adenoma-carcinoma-metastasis axis seen in human colon cancer. Using this model, we have analyzed tumors that are either solely mutant in the Apc gene or in combination with another colon cancer-associated mutant    gene, the Kras G12D allele. Because of the restricted location in the distal colon, the natural history of the tumors can be analyzed by serial colonoscopy. As the mammalian target of rapamycin (mTOR) pathway is a critical component of the    complex signaling network in colon cancer, we used this model to assess the efficacy of mTOR blockade through rapamycin treatment of mice with established tumors. After treatment, Apc mutant tumors were more than 80% smaller than control tumors.    However, tumors that possessed both Apc and Kras mutations did not respond to rapamycin treatment. These studies suggest that mTOR inhibitors should be further explored as potential colorectal cancer therapies in patients whose tumors do not have    activating mutations in KRAS.</p>

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</description>

<author>K E. Hung et al.</author>


</item>


<item>
<title>Measurement of replication structures at the nanometer scale using super-resolution light microscopy.</title>
<link>http://mouseion.jax.org/stfb2010/10</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/10</guid>
<pubDate>Tue, 08 May 2012 10:47:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>DNA replication, similar to other cellular processes, occurs within dynamic macromolecular structures. Any comprehensive understanding ultimately requires quantitative data to establish and test models of genome duplication. We used    two different super-resolution light microscopy techniques to directly measure and compare the size and numbers of replication foci in mammalian cells. This analysis showed that replication foci vary in size from 210 nm down to 40 nm.     Remarkably, spatially modulated illumination (SMI) and 3D-structured illumination microscopy (3D-SIM) both showed an average size of 125 nm that was conserved throughout S-phase and independent of the labeling method, suggesting a basic unit of    genome duplication. Interestingly, the improved optical 3D resolution identified 3- to 5-fold more distinct replication foci than previously reported.  These results show that optical nanoscopy techniques enable accurate measurements of cellular    structures at a level previously achieved only by electron microscopy and highlight the possibility of high-throughput, multispectral 3D analyses.</p>

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</description>

<author>D Baddeley et al.</author>


</item>


<item>
<title>Hydrologic Variability and the Application of Index of Biotic Integrity Metrics to Wetlands: A Great Lakes Evaluation</title>
<link>http://digitalcommons.brockport.edu/env_facpub/52</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/52</guid>
<pubDate>Tue, 08 May 2012 10:47:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Interest by land-management and regulatory agencies in using biological indicators to detect wetland degradation, coupled with ongoing use of this approach to assess water quality in streams, led to the desire to develop and evaluate an Index of Biotic Integrity (IBI) for wetlands that could be used to categorize the level of degradation. We undertook this challenge with data from coastal wetlands of the Great Lakes, which have been degraded by a variety of human disturbances. We studied six barrier beach wetlands in western Lake Superior, six drowned-river-mouth wetlands along the eastern shore of Lake Michigan, and six open shoreline wetlands in Saginaw Bay of Lake Huron. Plant, fish, and invertebrate communities were sampled in each wetland. The resulting data were assessed in various forms against gradients of human disturbance to identify potential metrics that could be used in IBI development. Our results suggested that the metrics proposed as potential components of an IBI for barrier beach wetlands of Lake Superior held promise. The metrics for Lake Michigan drowned-river-mouth wetlands were inconsistent in identifying gradients of disturbance; those for Lake Huron open embayment wetlands were yet more inconsistent. Despite the potential displayed by the Lake Superior results within the year sampled, we concluded that an IBI for use in Great Lakes wetlands would not be valid unless separate scoring ranges were derived for each of several sequences of water-level histories. Variability in lake levels from year to year can produce variability in data and affect the reproducibility of data collected, primarily due to extreme changes in plant communities and the faunal habitat they provide. Substantially different results could be obtained in the same wetland in different years as a result of the response to lake-level change, with no change in the level of human disturbance. Additional problems included limited numbers of comparable sites, potential lack of undisturbed reference sites, and variable effects of different disturbance types. We also evaluated our conclusions with respect to hydrologic variability and other major natural disturbances affecting wetlands in other regions. We concluded that after segregation of wetland types by geographic, geomorphic, and hydrologic features, a functional IBI may be possible for wetlands with relatively stable hydrology. However, an IBI for wetlands with unpredictable yet recurring influences of climate-induced, long-term high water periods, droughts, or drought-related fires or weather-related catastrophic floods or high winds (hurricanes) would also require differing scales of measurement for years that differ in the length of time since the last major natural disturbance. A site-specific, detailed ecological analysis of biological indicators may indeed be of value in determining the quality or status of wetlands, but we recommend that IBI scores not be used unless the scoring ranges are calibrated for the specific hydrologic history pre-dating any sampling year.</p>

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</description>

<author>Douglas A. Wilcox et al.</author>


</item>


<item>
<title>Invariant natural killer T-cell control of type 1 diabetes: a dendritic cell genetic decision of a silver bullet or Russian roulette.</title>
<link>http://mouseion.jax.org/stfb2010/9</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/9</guid>
<pubDate>Tue, 08 May 2012 10:47:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>OBJECTIVE: In part, activation of invariant natural killer T (iNKT)-cells with the superagonist alpha-galactosylceramide (alpha-GalCer) inhibits the development of T-cell-mediated autoimmune type 1 diabetes in NOD mice by inducing    the downstream differentiation of antigen-presenting dendritic cells (DCs) to an immunotolerogenic state. However, in other systems iNKT-cell activation has an adjuvant-like effect that enhances rather than suppresses various immunological    responses. Thus, we tested whether in some circumstances genetic variation would enable activated iNKT-cells to support rather than inhibit type 1 diabetes development. RESEARCH DESIGN AND METHODS: We tested whether iNKT-conditioned DCs in NOD    mice and a major histocompatibility complex-matched C57BL/6 (B6) background congenic stock differed in capacity to inhibit type 1 diabetes induced by the adoptive transfer of pathogenic AI4 CD8 T-cells. RESULTS: Unlike those of NOD origin,    iNKT-conditioned DCs in the B6 background stock matured to a state that actually supported rather than inhibited AI4 T-cell-induced type 1 diabetes.  The induction of a differing activity pattern of T-cell costimulatory molecules varying in    capacity to override programmed death-ligand-1 inhibitory effects contributes to the respective ability of iNKT-conditioned DCs in NOD and B6 background mice to inhibit or support type 1 diabetes development. Genetic differences inherent to both    iNKT-cells and DCs contribute to their varying interactions in NOD and B6.H2(g7) mice. CONCLUSIONS: This great variability in the interactions between iNKT-cells and DCs in two inbred mouse strains should raise a cautionary note about considering    manipulation of this axis as a potential type 1 diabetes prevention therapy in genetically heterogeneous humans.</p>

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</description>

<author>J P. Driver et al.</author>


</item>


<item>
<title>Nephroblastoma overexpressed (Nov) inactivation sensitizes osteoblasts to bone morphogenetic protein-2, but nov is dispensable for skeletal homeostasis.</title>
<link>http://mouseion.jax.org/stfb2010/8</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/8</guid>
<pubDate>Tue, 08 May 2012 10:47:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Overexpression of nephroblastoma overexpressed (Nov), a member of the Cyr 61, connective tissue growth factor, Nov family of proteins, inhibits osteoblastogenesis and causes osteopenia. The consequences of Nov inactivation on    osteoblastogenesis and the postnatal skeleton are not known. To study the function of Nov, we inactivated Nov by homologous recombination. Nov null mice were maintained in a C57BL/6 genetic background after the removal of the neomycin selection    cassette and compared with wild-type controls of identical genetic composition. Nov null mice were identified by genotyping and absent Nov mRNA in calvarial extracts and osteoblast cultures. Nov null mice did not exhibit developmental skeletal    abnormalities or postnatal changes in weight, femoral length, body fat, or bone mineral density and appeared normal. Bone volume and trabecular number were decreased only in 1-month-old female mice. In older mice, after 7 months of age,    osteoblast surface and bone formation were increased in females, and osteoclast and eroded surfaces were increased in male Nov null mice.  Calvarial osteoblasts from Nov null mice displayed enhanced alkaline phosphatase activity, alkaline    phosphatase mRNA, and transactivation of a bone morphogenetic protein (BMP)/phosphorylated mothers against decapentaplegic reporter construct in response to BMP-2. Similar results were obtained after the down-regulation of Nov by RNA interference    in ST-2 stromal and MC3T3 cells. Osteoclast number was increased in marrow stromal cell cultures from Nov null mice. Surface plasmon resonance demonstrated direct interactions between Nov and BMP-2. In conclusion, Nov sensitizes osteoblasts to    BMP-2, but Nov is dispensable for the maintenance of bone mass.</p>

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</description>

<author>E Canalis et al.</author>


</item>


<item>
<title>The sophisticated mouse: protecting a precious reagent.</title>
<link>http://mouseion.jax.org/stfb2010/7</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/7</guid>
<pubDate>Tue, 08 May 2012 10:47:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Definable, genetically and environmentally, the humble mouse has become a reagent with which to probe the human condition. The information thus gained is leading to a greater understanding of inter-individual variation in drug    responses and disease processes and is forming the basis for personalized medicine. Inbred mice are the tool of choice as each strain is essentially clonal in nature creating a defined, uniform setting where the effects of genetic background and    modifications can be evaluated coherently. However, the creation and characterization of novel mouse strains remain expensive and time consuming.  Further, the continual maintenance of these valuable animals as live colonies is financially    draining and carries continual potential risks, including disastrous loss due to fire, flood, disease, etc. There are also other more insidious disasters including genetic contamination and genetic drift, either of which can go undiscovered until    their effects ruin experiments. With this in mind, we strongly recommend that all mouse strains be cryopreserved as a matter of standard mouse management. Cryopreservation is a powerful colony management tool, assuring strains are available upon    demand, for example, for regulatory requirements, re-initiation of projects, collaborations, re-evaluation of data etc. However, it is essential that any cryopreservation approach be cost-effective for both strain closure and strain recovery. In    this chapter, we describe the variables which can afflict an inbred mouse's genetic background (and hence phenotype), options to consider for strain archiving, and describe how to economically store and recover strains by sperm    cryopreservation.</p>

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</description>

<author>M V. Wiles et al.</author>


</item>


<item>
<title>Development of novel major histocompatibility complex class I and class II-deficient NOD-SCID IL2R gamma chain knockout mice for modeling human xenogeneic graft-versus-host disease.</title>
<link>http://mouseion.jax.org/stfb2010/6</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/6</guid>
<pubDate>Tue, 08 May 2012 10:47:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Immunodeficient mice have been used as recipients of human peripheral blood mononuclear cells (PBMC) for in vivo analyses of human xeno-graft-versus-host disease (GVHD). This xeno-GVHD model system in many ways mimics the human    disease. The model system is established by intravenous or intraperitoneal injection of human PBMC or spleen cells into unconditioned or irradiated immunodeficient recipient mice. Recently, the development of several stocks of immunodeficient    Prkdc ( scid ) (scid) and recombination activating 1 or 2 gene (Rag1 or Rag2) knockout mice bearing a targeted mutation in the gene encoding the IL2 receptor gamma chain (IL2rgamma) have been reported. The addition of the mutated IL2rgamma gene    onto an immunodeficient mouse stock facilitates heightened engraftment with human PBMC. Stocks of mice with mutations in the IL2rgamma gene have been studied in several laboratories on NOD-scid, NOD-Rag1 ( null ), BALB/c-Rag1 ( null ),    BALB/c-Rag2 ( null ), and Stock-H2(d)-Rag2 ( null ) strain backgrounds. Parameters to induce human xeno-GVHD in H2(d)-Rag2 ( null ) IL2rgamma ( null ) mice have been published, but variability in the frequency of disease and kinetics of GVHD were    observed. The availability of the NOD-scid IL2rgamma ( null ) stock that engrafts more readily with human PBMC than does the Stock-H2(d)-Rag2 ( null ) IL2rgamma ( null ) stock should lead to a more reproducible humanized mouse model of GVHD and    for the use in drug evaluation and validation. Furthermore, GVHD in human PBMC-engrafted scid mice has been postulated to result predominately from a human anti-mouse major histocompatibility complex (MHC) class II reactivity. Our recent    development of NOD-scid IL2rgamma ( null ) beta2m ( null ) and NOD-scid IL2rgamma ( null ) Ab ( null ) stocks of mice now make it possible to investigate directly the role of host MHC class I and class II in the pathogenesis of GVHD in humanized    mice using NOD-scid IL2rgamma ( null ) stocks that engraft at high levels with human PBMC and are deficient in murine MHC class I, class II, or both classes of MHC molecules.</p>

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</description>

<author>S Pino et al.</author>


</item>


<item>
<title>Bridging mice to men: using HLA transgenic mice to enhance the future prediction and prevention of autoimmune type 1 diabetes in humans.</title>
<link>http://mouseion.jax.org/stfb2010/5</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/5</guid>
<pubDate>Tue, 08 May 2012 10:47:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Similar to the vast majority of cases in humans, the development of type 1 diabetes (T1D) in the NOD mouse model is due to T-cell mediated autoimmune destruction of insulin-producing pancreatic beta cells. Particular major    histocompatibility complex (MHC) haplotypes (designated HLA in humans and H2 in mice) provide the primary genetic risk factor for T1D development. It has long been appreciated that within the MHC, particular unusual class II genes contribute to    the development of T1D in both humans and NOD mice by allowing for the development and functional activation of beta-cell autoreactive CD4 T cells.  However, studies in NOD mice have revealed that through interactions with other background    susceptibility genes, the quite common class I variants (K(d), D(b)) characterizing this strain's H2 ( g7 ) MHC haplotype aberrantly acquire an ability to support the development of beta cell autoreactive CD8 T-cell responses also essential to    T1D development. Similarly, recent studies indicate that in the proper genetic context some quite common HLA class I variants also aberrantly contribute to T1D development in humans. This chapter will focus on how "humanized" HLA transgenic NOD    mice can be created and used to identify class I-dependent beta cell autoreactive CD8 T-cell populations of clinical relevance to T1D development. There is also discussion on how HLA transgenic NOD mice can be used to develop protocols that may    ultimately be useful for the prevention of T1D in humans by attenuating autoreactive CD8 T-cell responses against pancreatic beta cells.</p>

	]]>
</description>

<author>D V. Serreze et al.</author>


</item>


<item>
<title>Skin diseases in laboratory mice: approaches to drug target identification and efficacy screening.</title>
<link>http://mouseion.jax.org/stfb2010/4</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/4</guid>
<pubDate>Tue, 08 May 2012 10:46:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>A large variety of mouse models for human skin and adnexa diseases are readily available from investigators and vendors worldwide. While the skin is an obvious organ to observe lesions and their response to therapy, actually    treating and monitoring progress in mice can be challenging. This chapter provides an overview on how to use the laboratory mouse as a preclinical tool to evaluate efficacy of a new compound or test potential new uses for a compound approved for    use for treating an unrelated disease. Basic approaches to handling mice, applying compounds, and quantifying effects of the treatment are presented.</p>

	]]>
</description>

<author>J P. Sundberg et al.</author>


</item>


<item>
<title>p53 controls radiation-induced gastrointestinal syndrome in mice independent of apoptosis.</title>
<link>http://mouseion.jax.org/stfb2010/3</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/3</guid>
<pubDate>Tue, 08 May 2012 10:46:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Acute exposure to ionizing radiation can cause lethal damage to the gastrointestinal (GI) tract, a condition called the GI syndrome. Whether the target cells affected by radiation to cause the GI syndrome are derived from the    epithelium or endothelium and whether the target cells die by apoptosis or other mechanisms are controversial issues. Studying mouse models, we found that selective deletion of the proapoptotic genes Bak1 and Bax from the GI epithelium or from    endothelial cells did not protect mice from developing the GI syndrome after sub-total-body gamma irradiation. In contrast, selective deletion of p53 from the GI epithelium, but not from endothelial cells, sensitized irradiated mice to the GI    syndrome. Transgenic mice overexpressing p53 in all tissues were protected from the GI syndrome after irradiation. These results suggest that the GI syndrome is caused by the death of GI epithelial cells and that these epithelial cells die by a    mechanism that is regulated by p53 but independent of apoptosis.</p>

	]]>
</description>

<author>D G. Kirsch et al.</author>


</item>


<item>
<title>Neuromuscular disease models and analysis.</title>
<link>http://mouseion.jax.org/stfb2010/2</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/2</guid>
<pubDate>Tue, 08 May 2012 10:46:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Neuromuscular diseases can affect the survival of peripheral neurons, their axons extending to peripheral targets, their synaptic connections onto those targets, or the targets themselves. Examples include motor neuron diseases such    as amyotrophic lateral sclerosis, peripheral neuropathies, such as Charcot-Marie-Tooth diseases, myasthenias, and muscular dystrophies.  Characterizing these phenotypes in mouse models requires an integrated approach, examining both the nerve and    the muscle histologically, anatomically, and functionally by electrophysiology. Defects observed at these levels can be related back to onset, severity, and progression, as assessed by "quality-of-life measures" including tests of gross motor    performance such as gait or grip strength. This chapter describes methods for assessing neuromuscular disease models in mice, and how interpretation of these tests can be complicated by the inter-relatedness of the phenotypes.</p>

	]]>
</description>

<author>R W. Burgess et al.</author>


</item>


<item>
<title>Behavioral validation of the Ts65Dn mouse model for Down syndrome of a genetic background free of the retinal degeneration mutation Pde6b(rd1).</title>
<link>http://mouseion.jax.org/stfb2010/1</link>
<guid isPermaLink="true">http://mouseion.jax.org/stfb2010/1</guid>
<pubDate>Tue, 08 May 2012 10:46:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Ts65Dn mouse is the most studied and complete aneuploid model of Down syndrome (DS) widely available. As a model for human trisomy 21, these mice display many attractive features, including performance deficits in different    behavioral tasks, alterations in synaptic plasticity and adult neurogenesis, motor dysfunction, and age-dependent cholinergic neurodegeneration. Currently, Ts65Dn mice are maintained on a genetic background that leads to blindness in about 25% of    their offspring, because it segregates for the retinal degeneration 1 (Pde6b(rd1)) mutation of C3H/HeSnJ. This means that 25% of the mice have to be discarded in most experiments involving these animals, which is particularly problematic because    the Ts65Dn stock has low reproductive performance. To circumvent this problem, we have bred the Ts65Dn extra chromosome many generations into a closely related genetic background that does not carry the Pde6b(rd1) mutation. Although the new    genetic background is expected to be nearly identical to the original, differences in genetic background have the potential to alter mouse performance in certain behavioral tests. Therefore, we designed the present study primarily as a behavioral    validation of Ts65Dn mice of the new background. We compared side-by-side their performance with that of Ts65Dn mice of the original background on the following set of assessments: (1) body length and weight; (2) 24-h locomotor activity; (3) the    Morris water maze; (4) fear conditioning; and (5) grip strength. Except for very subtle differences on water maze performance, we found no significant differences between Ts65Dn mice on the two backgrounds in the measures assessed.</p>

	]]>
</description>

<author>A C. Costa et al.</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 07</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/48</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/48</guid>
<pubDate>Tue, 08 May 2012 10:44:05 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p>The pyre located in the top portion of the sculpture was added shortly before the burn, with the intent of helping to direct the flames up through the top of the sculpture.</p>

	]]>
</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 06</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/47</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/47</guid>
<pubDate>Tue, 08 May 2012 10:44:03 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012, it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>
<p><em><strong>Photographer's Notes</strong></em></p>
<p>A crowd gathers prior to the celebration and ceremonial burning.</p>

	]]>
</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 05</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/46</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/46</guid>
<pubDate>Tue, 08 May 2012 10:44:01 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012 it was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

	]]>
</description>

<author>Kathleen Spring</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 04</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/45</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/45</guid>
<pubDate>Tue, 08 May 2012 10:43:59 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012, the sculpture was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

	]]>
</description>

<author>Jean Caspers</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 03</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/44</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/44</guid>
<pubDate>Tue, 08 May 2012 10:43:57 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012, the sculpture was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

	]]>
</description>

<author>Jean Caspers</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 02</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/43</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/43</guid>
<pubDate>Tue, 08 May 2012 10:43:55 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012, the sculpture was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

	]]>
</description>

<author>Jean Caspers</author>


</item>


<item>
<title>Temple of Inner Fire Collaborative Burn Sculpture 01</title>
<link>http://digitalcommons.linfield.edu/avcstud_collab/42</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/avcstud_collab/42</guid>
<pubDate>Tue, 08 May 2012 10:43:53 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Temple of Inner Fire</em> is the collaborative sculpture built by the <em>Introduction to Studio</em> class at Linfield College during the 2012 January term. On April 20, 2012, the sculpture was burned to the ground in a celebration to complete the cycle of collaboration and creation. The <em>Introduction to Studio</em> class included students Michael K. Carrillo, Nicholas Fairhart, Abe Harder-Cattell, Sherilyn Harrington, Bryce Hayunga, Cameron Howser, Marina Jablonski, Ashley Kimi, Tim Marl, Joey Paysinger, Cole Perry, Chloe Shields, Kate Straube, Addison Wisthoff, and Dawn Wyruchowski.</p>

	]]>
</description>

<author>Jean Caspers</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 17, no. 1</title>
<link>http://collected.jcu.edu/carrollquarterly/52</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/52</guid>
<pubDate>Tue, 08 May 2012 10:43:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 17, no. 2</title>
<link>http://collected.jcu.edu/carrollquarterly/51</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/51</guid>
<pubDate>Tue, 08 May 2012 10:43:50 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 17, no. 3</title>
<link>http://collected.jcu.edu/carrollquarterly/50</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/50</guid>
<pubDate>Tue, 08 May 2012 10:43:49 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 17, no. 4</title>
<link>http://collected.jcu.edu/carrollquarterly/49</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/49</guid>
<pubDate>Tue, 08 May 2012 10:43:48 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>Altered Behavior in Bats Affected by White-Nose Syndrome</title>
<link>http://digitalcommons.bucknell.edu/masters_theses/75</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/masters_theses/75</guid>
<pubDate>Tue, 08 May 2012 10:43:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>WNS-affected bats did so over similar time frames as WNSunaffected bats. The behaviors of bats with WNS did not change as drastically as expected. Thereseems to be little to no effect on their ability to fly/forage  until much later stages of the disease  when they are likely near death. WNS-affected bats are grooming more  which could be altering the way they use energy reserves during hibernation  possibly leading tostarvation and eventually death. The decreased likelihood of arousals in response to external cues may be the result of spending more energy during previous and increasingly frequent arousals. While it is clear that WNS does result in changes in behavior  whether these changes are directly in response to fungal skin infection or to some other component of the syndrome  such as decreased energy availability or loss of homeostasis is unknown.     bat behavior, white-nose syndrome, behavior, video surveillance, arousal patterns White-Nose Syndrome (WNS) is a disease of hibernating bats caused by the fungal pathogen Geomyces destructans. The fungus, which was first noted in 2006, invades bats wings and other exposed membranes, eventually resulting in death. Researchers have yet to understand many aspects of this disease, including basic etiology and epidemiology. There is also a lack of information on how fungal infection may change the behavior of healthy bats during hibernation or how changes in behavior may influence disease progression. Based upon the physiological changes that are known to occur in affected bats, and upon anecdotal observations of aberrant behavior in these bats, I hypothesized that WNS would significantly change the behavior of the little brown myotis (Myotis lucifugus). My research examined the behavior of hibernating bats during arousals from torpor. I compared WNS-affected and unaffected bats, in the field and incaptivity, using motion-sensitive infrared cameras. Flight maneuverability and echolocation were also tested between WNS-affected and unaffected bats during arousalsfrom hibernation to detect changes in the bats' ability to perform basic locomotion or potentially catch insect prey. Lastly, hibernating bats were artificially disturbed and theirarousal patterns were monitored to examine changes in the response to external stimuli between WNS-affected and unaffected bats.Bats with WNS groomed for longer periods of time after arousing from torpor, both in the field and in captivity. They also engaged in longer periods of any sort of activity during these arousals. There were no changes in acoustical signaling during flight tests and changes in flight maneuverability were only found in bats were seen staging" near the entrance of the mine  which is itself a unique behavior exhibited by affected bats. At this point  these bats were likely near death and could barely fly at all. In response toexternal stimuli  bats with WNS were less likely to arouse than unaffected bats. However  when they did arouse  WNS-affected bats did so over similar time frames as WNSunaffected bats. The behaviors of bats with WNS did not change as drastically as expected. Thereseems to be little to no effect on their ability to fly/forage  until much later stages of the disease  when they are likely near death. WNS-affected bats are grooming more  which could be altering the way they use energy reserves during hibernation  possibly leading tostarvation and eventually death. The decreased likelihood of arousals in response to external cues may be the result of spending more energy during previous and increasingly frequent arousals. While it is clear that WNS does result in changes in behavior  whetherthese changes are directly in response to fungal skin infection or to some other component of the syndrome  such as decreased energy availability or loss of homeostasis is unknown."</p>

	]]>
</description>

<author>Sarah Brownlee</author>


</item>


<item>
<title>Identification of persistent defects in insulin receptor structure and function in capillary endothelial cells from diabetic rats</title>
<link>http://jdc.jefferson.edu/medfp/77</link>
<guid isPermaLink="true">http://jdc.jefferson.edu/medfp/77</guid>
<pubDate>Tue, 08 May 2012 10:40:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Insulin actions and receptors were studied in capillary endothelial cells cultured from diabetic BB rats and their nondiabetic colony mates. The endothelial cells from diabetic rats of 2 mo duration had persistent biological and biochemical defects in culture. Compared with normal rats, endothelial cells from diabetic rats grew 44% more slowly. Binding studies of insulin and insulin-like growth factor I (IGF-I) showed that cells from diabetic rats had 50% decrease of insulin receptor binding (nondiabetic: 4.6 +/- 0.7; diabetic: 2.6 +/- 0.4% per milligram protein, P < 0.01), which was caused by a 50% decrease in the number of binding sites per milligram protein, whereas IGF-I binding was not changed. Insulin stimulation of 2-deoxy-glucose uptake and alpha-aminoisobutyric acid uptake were also severely impaired with a 80-90% decrease in maximal stimulation, in parallel with a 62% decrease in insulin-stimulated autophosphorylation (P < 0.05). <sup>125</sup>I-insulin cross-linking revealed an 140-kD alpha subunit of the insulin receptor similar to that in cells from nondiabetic rats, although bands at > 200 kD were also detected. The molecular weight of the insulin receptor beta subunit (by SDS-PAGE) was smaller in cells from diabetic than from normal rats (88-90 vs. 95 kD). Neuraminadase treatment of the partially purified insulin receptors decreased the molecular weight of the insulin receptors from nondiabetic rats to a greater degree than its diabetic counterpart. In contrast, Northern blot analysis of insulin receptor mRNAs using human cDNA probes revealed two species of 9.4 and 7.2 kb with no difference in mRNA abundance between cells from diabetic and nondiabetic rats. We conclude that the exposure of capillary endothelial cells to a diabetic milieu in vivo can cause specific and persistent changes in the insulin receptor and insulin action.</p>

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</description>

<author>Ching Fai Kwok et al.</author>


</item>


<item>
<title>Search for the Other: National Geographic&apos;s Search of the Afghan Girl as Neocolonial Discourse</title>
<link>http://digitalcommons.library.umaine.edu/etd/1025</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1025</guid>
<pubDate>Tue, 08 May 2012 10:39:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the past twenty years, documentary productions as journalistic endeavors have dramatically increased while not being held to the same ethical standards as journalism. One ethical issue is that colonial and neocolonial discourses are inherent in Western documentary productions. Neocolonial discourses are ideologies that are shared in a dominant nation justifying indirect intervention and imposition of a foreign nation. In this thesis, I argue National Geographic's Search for the Afghan Girl (2003) engages in neocolonial discourse through the process of Othering (a process of reducing a person to an object rather than as a self-thinking, co-existing human being capable of equal interaction). The Search provides a case study example to examine the subtle language of Othering in documentary productions that advocate for humanitarian assistance. Other post-9/11 documentary productions posit similar stories and advocacies such as Born into Brothels: Calcutta's Red Light Kids (Briski & Kauffman, 2004) and The Beauty Academy of Kabul (Mermin, 2004). Each production situates an American going to a third-world or developing country and producing a documentary about a marginalized subject in that country. Each production advocates the role of education for the marginalized as the redeeming factor for the documentarians' intervention. Moreover, each production lacks a degree of transparency about the producer's role in engaging these particular subjects and the role these stories play in the larger discourse of neocolonialism. Transparency is one of the fundamental principles of journalistic ethics because of conflicts of interests. The Search is an excellent example of problematic documentary ethics because it is produced by one of the world's largest and oldest scientific and education institutions, the National Geographic Society. Furthermore, National Geographic has a history of engaging in colonial and neocolonial discourses through their magazines and their co-construction of the Other via the focus of their productions. Therefore, the Search, as a case study, is exemplary for examining the role of documentary productions in post-9/11 neocolonial discourse.</p>

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</description>

<author>Shane Perry</author>


</item>


<item>
<title>It&apos;s 33 A.D. Again!</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/382</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/382</guid>
<pubDate>Tue, 08 May 2012 10:37:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bob Stamps</author>


</item>


<item>
<title>Cdo patterns the musculature of the esophagus and is required for esophageal motility in mice</title>
<link>http://jdc.jefferson.edu/medfp/78</link>
<guid isPermaLink="true">http://jdc.jefferson.edu/medfp/78</guid>
<pubDate>Tue, 08 May 2012 10:36:27 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Introduction:</strong></p>
<p>Cdo is a multifunctional cell surface co-receptor that promotes Hedgehog signaling during rostroventral midline development and cadherin-mediated signaling during skeletal myogenesis. We report here novel roles for Cdo in patterning of the murine esophageal musculature and esophageal motility disorders such as achalasia.</p>

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</description>

<author>Anthony I. Romera et al.</author>


</item>


<item>
<title>Hydrogeomorphic Factors and Ecosystem Responses in Coastal Wetlands of the Great Lakes</title>
<link>http://digitalcommons.brockport.edu/env_facpub/51</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/51</guid>
<pubDate>Tue, 08 May 2012 10:33:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gauging the impact of manipulative activities, such as rehabilitation or management, on wetlands requires having a notion of the unmanipulated condition as a reference. An understanding of the reference condition requires knowledge of dominant factors influencing ecosystem processes and biological communities. In this paper, we focus on natural physical factors (conditions and processes) that drive coastal wetland ecosystems of the Laurentian Great Lakes. Great Lakes coastal wetlands develop under conditions of largelake hydrology and disturbance imposed at a hierarchy of spatial and temporal scales and contain biotic communities adapted to unstable and unpredictable conditions. Coastal wetlands are configured along a continuum of hydrogeomorphic types: open coastal wetlands, drowned river mouth and Hooded delta wetlands, and protected wetlands, each developing distinct ecosystem properties and biotic communities. Hydrogeomorphic factors associated with the lake and watershed operate at a hierarchy of scales: a) local and short-term (seiches and ice action), b) watershed /lakewide /annual (seasonal water- level change), and c) larger or year-to-year and longer (regional and/or greater than one-year). Other physical factors include the unique water quality features of each lake. The aim of this paper is to provide scientists and managers with a framework for considering regional and site-specific geomorphometry and a hierarchy of physical processes in planning management and conservation projects.</p>

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</description>

<author>Janet R. Keough et al.</author>


</item>


<item>
<title>Florida: Worth Avenue in Palm Beach</title>
<link>http://digitalcommons.ric.edu/smolski_images/833</link>
<guid isPermaLink="true">http://digitalcommons.ric.edu/smolski_images/833</guid>
<pubDate>Tue, 08 May 2012 10:31:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Worth Avenue is viewed as one of the most famous shopping districts in the state of Florida. The area first gained retail insight when The Everglades Club was built on this road in 1918. This club held weekly fashion shows showing the latest trends and designs around the world. In 1938, the Worth Avenue Association formed, which still governs the general look and upkeep of this famous area. In present days, the avenue has over 200 shops that offer retail ranging from high fashion designs to antique paintings.</p>

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</description>

<author>Chet Smolski</author>


</item>


<item>
<title>Centennial Library E-News, January/February 2012</title>
<link>http://digitalcommons.cedarville.edu/library_enews/1</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/library_enews/1</guid>
<pubDate>Tue, 08 May 2012 10:31:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Articles in this issue: Centennial Library 25th year, Staff member earns degree, On-line tutorials developed, Gallery opens exhibit, LibQUAL survey planned, University faculty in print, University alumni in print, Spring break hours</p>

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</description>

<author>Centennial Library</author>


</item>


<item>
<title>Framing a Killing: The Stuart Murder Hoax, the Boston News Media, and the Politics of Modern Racism</title>
<link>http://digitalcommons.library.umaine.edu/etd/1024</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1024</guid>
<pubDate>Tue, 08 May 2012 10:29:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>In October, 1989, Charles Stuart murdered his wife in inner-city Boston by staging a robbery-homicide, which he would blame on a nondescript black man. News of the suburban white couple's alleged attack sent shock waves throughout Boston and made national headlines, resulting in an outpouring of sympathy for the Stuarts and condemnation for the alleged attacker. Accepting Stuart's claim at face value, the Boston media would devote over two months of coverage to the alleged incident, before the hoax was revealed. This research carries out a framing analysis of news coverage during the hoax period, as reported in The Boston Globe and Boston Herald, and demonstrates that such reportage should not be surprising, as it is based on prevailing crime discourse that is the product of expectations and stereotypes of race, class, violent crime, and notions of who ought to be protected from such crime. Prior to the framing analysis, I will provide some background on shifting white racial perceptions and how a prevailing violent crime news narrative has developed and become accepted by the mainstream media, the political class, and the public. After the framing analysis, I will examine the discourse of Boston's African American newspaper, The Bay State Banner, during the hoax period of the Stuart case, in an effort to have a sense of its alternative framing and what implications this alternative framing might have for the broader public sphere. I will conclude this thesis with some thoughts on what the 21-year-old murder case might reveal about our current media and political landscape.</p>

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</description>

<author>Brian Lepine</author>


</item>


<item>
<title>Performance Characteristics of Beamline 6.3.1 from 200 eV to 2000 eV at the Advanced Light Source</title>
<link>http://digitalcommons.library.unlv.edu/chem_fac_articles/82</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/chem_fac_articles/82</guid>
<pubDate>Tue, 08 May 2012 10:28:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bend magnet beamline 6.3.1 at the Advanced Light Source operates from 200 eV to 2000 eV, primarily used for x-ray absorption fine structure investigations. The beamline optics consist of a compact, entrance-slitless, Hettrick-Underwood type variable-line-spacing plane-grating monochromator and refocusing mirrors to provide a 25 μm × 500 μm spot at the focal point in the reflectometer end station. Wavelength is scanned by the simple rotation of the grating and illuminates a fixed exit slit. The LabView based beamline control and data acquisition computer code has been implemented to provide a convenient interface to the user. The dedicated end station is a reflectometer that is isolated from the beamline by a differential ion pump. The reflectometer can position samples to within 4 μm with an angular position of 0.002°, has total electron and fluorescence yield detectors, and pumps down in about 30 minutes. External end stations can be mounted downstream of the reflectometer as well. The versatility and simplicity of beamline 6.3.1 have made it useful for a wide range of applications such as the characterization of optical components, reflective coatings, and the investigation of a diverse range of materials in both the solid state and in solution.</p>

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</description>

<author>Ponnusamy Nachimuthu et al.</author>


</item>


<item>
<title>Identifying Effective Behavior Management in the Early Childhood Classroom</title>
<link>http://digitalcommons.cedarville.edu/education_theses/11</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/11</guid>
<pubDate>Tue, 08 May 2012 10:24:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Every educator has a dream to maintain a classroom free from disruptions; one in which each child is being molded, shaped, and corrected in a loving and caring environment that inspires appropriate behavior. The purpose of this research project was to determine how to create an effective behavior management plan and effectively teach classroom management techniques. Students involved in this project were preschoolers age three and four from a local Young Men Christian Association in Akron, OH.</p>

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</description>

<author>Kelly R. Victor</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 16, no. 1</title>
<link>http://collected.jcu.edu/carrollquarterly/48</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/48</guid>
<pubDate>Tue, 08 May 2012 10:21:40 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 16, no. 2</title>
<link>http://collected.jcu.edu/carrollquarterly/47</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/47</guid>
<pubDate>Tue, 08 May 2012 10:21:39 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 16, no. 3</title>
<link>http://collected.jcu.edu/carrollquarterly/46</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/46</guid>
<pubDate>Tue, 08 May 2012 10:21:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 16, no. 4</title>
<link>http://collected.jcu.edu/carrollquarterly/45</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/45</guid>
<pubDate>Tue, 08 May 2012 10:21:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>Health and Foreign Policy</title>
<link>http://www.repository.law.indiana.edu/facpub/526</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/526</guid>
<pubDate>Tue, 08 May 2012 10:21:06 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>David P. Fidler et al.</author>


</item>


<item>
<title>Health as Foreign Policy: Between Principle and Power</title>
<link>http://www.repository.law.indiana.edu/facpub/525</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/525</guid>
<pubDate>Tue, 08 May 2012 10:21:03 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>David P. Fidler</author>


</item>


<item>
<title>1,3-Bis(9-ethyl­carbazol-3-yl)propane</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/5</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/5</guid>
<pubDate>Tue, 08 May 2012 10:21:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the title compund, C<sub>31</sub>H<sub>30</sub>N<sub>2</sub>, π–π  overlap is absent in the region where carbazole groups of two adjacent  mol­ecules are inclined toward each other. The eth­yl groups which  protrude from the plane of the carbazole groups and the alkyl­ene chain  connecting the two carbazole groups are responsible for the poor  mol­ecular stacking.</p>

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</description>

<author>Erol Asker et al.</author>


</item>


<item>
<title>The Problem of Statutory Detail in National Park Establishment Legislation and its Relationship to Pollution Control Law</title>
<link>http://www.repository.law.indiana.edu/facpub/524</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/524</guid>
<pubDate>Tue, 08 May 2012 10:20:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Robert L. Fischman</author>


</item>


<item>
<title>Administrative Appeal Reform: The Case of the Forest Service</title>
<link>http://www.repository.law.indiana.edu/facpub/523</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/523</guid>
<pubDate>Tue, 08 May 2012 10:20:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Robert L. Fischman et al.</author>


</item>


<item>
<title>[Re]Doing Christianity: An Ideological and Rhetorical Critique of &lt;em&gt;The 700 Club&lt;/em&gt; and &lt;em&gt;God&apos;s Politics&lt;/em&gt;</title>
<link>http://digitalcommons.library.umaine.edu/etd/1023</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1023</guid>
<pubDate>Tue, 08 May 2012 10:20:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Among the many and diverse Christian movements that exist in the contemporary U.S. are two opposed groups: Conservative Christianity and Progressive Christianity. Individuals from various evangelical denominations comprise these movements which thus cut across specific church affiliations. Both movements have the stated goal of promoting authentic Christian lives pursuing God. Both movements make use of the Christian Bible as the authoritative text in determining what exactly the "authentic Christian life" is. That said, there are marked irreconcilable differences. The similarities of and differences between these movements provide an interesting site of critical analysis. Through close textual analysis and ideological criticism of two Christian texts, The 700 Club and God's Politics (Wallis, 2005), this thesis explores how the Conservative Christian movement and Progressive Christian movement both enact hegemonic masculine ideology, albeit in different ways. In addition, this thesis attempts to understand how God's Politics (Wallis, 2005) as a Progressive Christian text, positions itself in response to Conservative Christianity. I examine how the text subverts and/or affirms the ideology of Conservative Christianity. Approaching this study from a critical perspective, I argue that The 700 Club seeks to erase the fractured nature of the U.S. Christian church and enacts white hegemonic masculinity by constructing Pat Robertson as a prophetic spiritual authority. Second, I argue that God's Politics embraces the fissured and diverse nature of the Christian church in the U.S. and attempts to subvert the ideology of the Christian Right. Wallis does so by rearticulating a Christian political agenda and refocusing on issues such as poverty and social justice. While God's Politics does this, it also reiterates hegemonic tropes present within Conservative Christianity. Falling into ideological traps of Conservative Christianity undermines Wallis's stated goal of transcending partisan politics and bad theology.</p>

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</description>

<author>Sarita Joyce Field</author>


</item>


<item>
<title>Index</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/40</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/40</guid>
<pubDate>Tue, 08 May 2012 10:19:58 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Tables</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/39</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/39</guid>
<pubDate>Tue, 08 May 2012 10:19:57 PDT</pubDate>
<description>
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Chapter 34: Administration of Justice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/38</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/38</guid>
<pubDate>Tue, 08 May 2012 10:19:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan J. Dimond</author>


</item>


<item>
<title>Chapter 33: Evidence</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/37</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/37</guid>
<pubDate>Tue, 08 May 2012 10:19:55 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frederick A. McDermott</author>


</item>


<item>
<title>Chapter 32: Civil Procedure and Practice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/36</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/36</guid>
<pubDate>Tue, 08 May 2012 10:19:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Wendell F. Grimes</author>


</item>


<item>
<title>Chapter 31: Food and Drug, Health, and Welfare Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/35</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/35</guid>
<pubDate>Tue, 08 May 2012 10:19:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William J. Curran</author>


</item>


<item>
<title>Chapter 30: Workmen&apos;s Compensation</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/34</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/34</guid>
<pubDate>Tue, 08 May 2012 10:19:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph Bear et al.</author>


</item>


<item>
<title>Chapter 29: State and Municipal Government</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/33</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/33</guid>
<pubDate>Tue, 08 May 2012 10:19:50 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph C. Duggan</author>


</item>


<item>
<title>Chapter 28: Insurance</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/32</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/32</guid>
<pubDate>Tue, 08 May 2012 10:19:49 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J. Marshall Leydon</author>


</item>


<item>
<title>Chapter 27: State Taxation</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/31</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/31</guid>
<pubDate>Tue, 08 May 2012 10:19:48 PDT</pubDate>
<description>
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</description>

<author>David Flower Jr.</author>


</item>


<item>
<title>Chapter 26: Public Utilities</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/30</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/30</guid>
<pubDate>Tue, 08 May 2012 10:19:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Hirsh Freed et al.</author>


</item>


<item>
<title>Chapter 25: Labor Relations</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/29</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/29</guid>
<pubDate>Tue, 08 May 2012 10:19:45 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Robert M. Segal</author>


</item>


<item>
<title>Chapter 24: Administrative Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/28</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/28</guid>
<pubDate>Tue, 08 May 2012 10:19:44 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Albert M. Sacks</author>


</item>


<item>
<title>Chapter 23: Criminal Law, Procedure, and Administration</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/27</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/27</guid>
<pubDate>Tue, 08 May 2012 10:19:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>J. Edward Collins</author>


</item>


<item>
<title>Chapter 22: Constitutional Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/26</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/26</guid>
<pubDate>Tue, 08 May 2012 10:19:42 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John D. O&apos;Reilly Jr.</author>


</item>


<item>
<title>Chapter 21: Conflict of Laws</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/25</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/25</guid>
<pubDate>Tue, 08 May 2012 10:19:41 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Monroe Inker</author>


</item>


<item>
<title>Chapter 20: Security and Mortgages</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/24</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/24</guid>
<pubDate>Tue, 08 May 2012 10:19:40 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Austin T. Stickells</author>


</item>


<item>
<title>Chapter 19: Domestic Relations and Persons</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/23</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/23</guid>
<pubDate>Tue, 08 May 2012 10:19:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William J. Greenler Jr.</author>


</item>


<item>
<title>Chapter 18: Commercial Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/22</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/22</guid>
<pubDate>Tue, 08 May 2012 10:19:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kenneth B. Hughes</author>


</item>


<item>
<title>Chapter 17: Agency</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/21</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/21</guid>
<pubDate>Tue, 08 May 2012 10:19:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Austin T. Stickells</author>


</item>


<item>
<title>Chapter 16: Corporations</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/20</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/20</guid>
<pubDate>Tue, 08 May 2012 10:19:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bertram H. Loewenberg</author>


</item>


<item>
<title>Chapter 15: Equity and Equity Practice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/19</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/19</guid>
<pubDate>Tue, 08 May 2012 10:19:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Harry Zarrow</author>


</item>


<item>
<title>Chapter 14: Contracts</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/18</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/18</guid>
<pubDate>Tue, 08 May 2012 10:19:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Richard G. Huber</author>


</item>


<item>
<title>Chapter 13: Torts</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/17</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/17</guid>
<pubDate>Tue, 08 May 2012 10:19:31 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Warren A. Seavey</author>


</item>


<item>
<title>Chapter 12: Trusts and Estates</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/16</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/16</guid>
<pubDate>Tue, 08 May 2012 10:19:30 PDT</pubDate>
<description>
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</description>

<author>Emil Slizewski</author>


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<item>
<title>Chapter 11: Property and Conveyancing</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/15</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/15</guid>
<pubDate>Tue, 08 May 2012 10:19:29 PDT</pubDate>
<description>
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</description>

<author>Cornelius J. Moynihan</author>


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<item>
<title>Chapter 10: Article Nine: Secured Transactions</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/14</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/14</guid>
<pubDate>Tue, 08 May 2012 10:19:27 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Peter F. Coogan et al.</author>


</item>


<item>
<title>Chapter 9: Article Eight: Investment Securities</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/13</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/13</guid>
<pubDate>Tue, 08 May 2012 10:19:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Fred B. Lund et al.</author>


</item>


<item>
<title>Chapter 8: Article Seven: Documents of Title</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/12</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/12</guid>
<pubDate>Tue, 08 May 2012 10:19:25 PDT</pubDate>
<description>
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</description>

<author>Robert Braucher</author>


</item>


<item>
<title>Chapter 7: Article Six: Bulk Transfers</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/11</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/11</guid>
<pubDate>Tue, 08 May 2012 10:19:24 PDT</pubDate>
<description>
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</description>

<author>Harold Horvitz et al.</author>


</item>


<item>
<title>Chapter 6: Article Five: Letters of Credit</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/10</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/10</guid>
<pubDate>Tue, 08 May 2012 10:19:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Austin S. Ashley</author>


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<item>
<title>Chapter 5: Article Four: Bank Deposits and Collections</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/9</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/9</guid>
<pubDate>Tue, 08 May 2012 10:19:21 PDT</pubDate>
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</description>

<author>Arthur E. Sutherland</author>


</item>


<item>
<title>Chapter 4: Article Three: Commercial Paper</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/8</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/8</guid>
<pubDate>Tue, 08 May 2012 10:19:20 PDT</pubDate>
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</description>

<author>Arthur E. Sutherland</author>


</item>


<item>
<title>Chapter 3: Article Two: Sales</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/7</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/7</guid>
<pubDate>Tue, 08 May 2012 10:19:19 PDT</pubDate>
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</description>

<author>William E. Hogan</author>


</item>


<item>
<title>Chapter 2: Article One: General Provisions</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/6</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/6</guid>
<pubDate>Tue, 08 May 2012 10:19:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Robert Braucher</author>


</item>


<item>
<title>Chapter 1: General Statement</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/5</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/5</guid>
<pubDate>Tue, 08 May 2012 10:19:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Walter D. Malcolm</author>


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<item>
<title>Table of Contents</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/4</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/4</guid>
<pubDate>Tue, 08 May 2012 10:19:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Summary of Contents</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/3</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/3</guid>
<pubDate>Tue, 08 May 2012 10:19:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Foreword</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/2</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/2</guid>
<pubDate>Tue, 08 May 2012 10:19:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Raymond S. Wilkins</author>


</item>


<item>
<title>Masthead</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/1</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1957/iss1/1</guid>
<pubDate>Tue, 08 May 2012 10:19:12 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Hydrogeomorphic Classification for Great Lakes Coastal Wetlands</title>
<link>http://digitalcommons.brockport.edu/env_facpub/50</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/50</guid>
<pubDate>Tue, 08 May 2012 10:15:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>A hydrogeomorphic classification scheme for Great Lakes coastal wetlands is presented. The classification is hierarchical and first divides the wetlands into three broad hydrogeomorphic systems, lacustrine, riverine, and barrier-protected, each with unique hydrologic flow characteristics and residence time. These systems are further subdivided into finer geomorphic types based on physical features and shoreline processes. Each hydrogeomorphic wetland type has associated plant and animal communities and specific physical attributes related to sediment type, wave energy, water quality, and hydrology.</p>

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</description>

<author>Dennis A. Albert et al.</author>


</item>


<item>
<title>The Indigent Defense Crisis</title>
<link>http://digitalcommons.tourolaw.edu/scholarlyworks/424</link>
<guid isPermaLink="true">http://digitalcommons.tourolaw.edu/scholarlyworks/424</guid>
<pubDate>Tue, 08 May 2012 10:14:52 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Richard Klein et al.</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 15, no. 1</title>
<link>http://collected.jcu.edu/carrollquarterly/44</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/44</guid>
<pubDate>Tue, 08 May 2012 10:10:39 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 15, no. 2</title>
<link>http://collected.jcu.edu/carrollquarterly/43</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/43</guid>
<pubDate>Tue, 08 May 2012 10:10:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 15, no. 3</title>
<link>http://collected.jcu.edu/carrollquarterly/42</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/42</guid>
<pubDate>Tue, 08 May 2012 10:10:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 15, no. 4</title>
<link>http://collected.jcu.edu/carrollquarterly/41</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/41</guid>
<pubDate>Tue, 08 May 2012 10:10:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>Nitrogen Fertilizer Rate and Weather Dictate
Nutritive Value of Fall Stockpiled Bermudagrass</title>
<link>http://digitalcommons.unl.edu/agronomyfacpub/554</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/agronomyfacpub/554</guid>
<pubDate>Tue, 08 May 2012 10:09:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Stockpiled bermudagrass [<em>Cynodon dactylon </em>(L.) Pers. ‘Midland’] as a standing forage may meet nutritional needs of beef cows during winter. Our objective was to evaluate accumulation and nutritive value of fall stockpiled bermudagrass in response to N fertilization rate, N application date, and harvest date. Research was conducted near Burneyville, OK from 2000 to 2003. Fertilization rates included 0, 50, 100, and 150 lb N per acre applied on 15 August, 1 September, 15 September, 1 October, and 15 October. Forage accumulation was measured 10 days after the first killing frost; thereafter, crude protein (CP), acid detergent fiber (ADF), neutral detergent fiber (NDF), and total digestible nutrients (TDN) were assessed biweekly from 6 December to 20 February. An exceptionally hot and dry summer resulted in negligible forage production and unrepresentative forage quality in 2000. Forage accumulated linearly in 2001 and 2002 and quadratically in 2003 with N fertilization rate (<em>P </em>≤ 0.05). The dry matter averaged 56% TDN and 6.0, 6.9, 7.9, and 8.7% CP when N was applied at 0, 50, 100, and 150 lb/acre, respectively. The fertilized bermudagrass stands would have met CP and TDN requirements of mid-gestation beef cows had they been maintained on this forage.</p>

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</description>

<author>John A. Guretzky et al.</author>


</item>


<item>
<title>Georgia: The Westin Peachtree Plaza, Atlanta</title>
<link>http://digitalcommons.ric.edu/smolski_images/832</link>
<guid isPermaLink="true">http://digitalcommons.ric.edu/smolski_images/832</guid>
<pubDate>Tue, 08 May 2012 10:03:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Built in 1976, the Westin Peachtree Plaza Hotel stood 73 stories tall as Atlanta’s tallest building. This changed in 1983 when 191 Peachtree Center was built even taller. The hotel was built in a cylindrical shape with reflective glass so as to reflect the skyline downtown. Alongside the building is another cylindrical piece of architecture that houses 2 elevators for the hotel. At the very top of the building rests the Sun Dial Restaurant and Bar, a very popular establishment that features a revolving floor.</p>

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</description>

<author>Chet Smolski</author>


</item>


<item>
<title>Geomorphic and Sedimentologic Evidence for the Separation of Lake Superior from Lake Michigan and Huron</title>
<link>http://digitalcommons.brockport.edu/env_facpub/49</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/49</guid>
<pubDate>Tue, 08 May 2012 10:03:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>A common break was recognized in four Lake Superior strandplain sequences using geomorphic and sedimentologic characteristics. Strandplains were divided into lakeward and landward sets of beach ridges using aerial photographs and topographic surveys to identify similar surficial features and core data to identify similar subsurface features. Cross-strandplain, elevation trend changes from a lowering towards the lake in the landward set of beach ridges to a rise or reduction of slope towards the lake in the lakeward set of beach ridges indicates that the break is associated with an outlet change for Lake Superior. Correlation of this break between study sites and age model results for the strandplain sequences suggest that the outlet change occurred sometime after about 2,400 calendar years ago (after the Algoma phase). Age model results from one site (Grand Traverse Bay) suggest an alternate age closer to about 1,200 calendar years ago but age models need to be investigated further. The landward part of the strandplain was deposited when water levels were common in all three upper Great Lakes basins (Superior, Huron, and Michigan) and drained through the Port Huron/Sarnia outlet. The lakeward part was deposited after the Sault outlet started to help regulate water levels in the Lake Superior basin. The landward beach ridges are commonly better defined and continuous across the embayments, more numerous, larger in relief, wider, have greater vegetation density, and intervening swales contain more standing water and peat than the lakeward set. Changes in drainage patterns, foreshore sediment thickness and grain size help in identifying the break between sets in the strandplain sequences. Investigation of these breaks may help identify possible gaps in the record or missing ridges in strandplain sequences that may not be apparent when viewing age distributions and may justify the need for multiple age and glacial isostatic adjustment models.</p>

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</description>

<author>John W. Johnston et al.</author>


</item>


<item>
<title>ckn520310p1a4</title>
<link>http://place.asburyseminary.edu/ecommonsfacultylectures/8</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsfacultylectures/8</guid>
<pubDate>Tue, 08 May 2012 10:03:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>ATS</author>


</item>


<item>
<title>For Health Reform Success, Context Matters Most</title>
<link>http://jdc.jefferson.edu/pehc/vol1/iss15/6</link>
<guid isPermaLink="true">http://jdc.jefferson.edu/pehc/vol1/iss15/6</guid>
<pubDate>Tue, 08 May 2012 10:00:41 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bonnie L. Zell MD, MPH</author>


</item>


<item>
<title>Health Care Innovation in Medicare Advantage: The Humana Experience</title>
<link>http://jdc.jefferson.edu/pehc/vol1/iss15/5</link>
<guid isPermaLink="true">http://jdc.jefferson.edu/pehc/vol1/iss15/5</guid>
<pubDate>Tue, 08 May 2012 10:00:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Tom James MD</author>


</item>


<item>
<title>Health Care Reform: &quot;Uhhh, Do We Have to Include the Patients?&quot;</title>
<link>http://jdc.jefferson.edu/pehc/vol1/iss15/4</link>
<guid isPermaLink="true">http://jdc.jefferson.edu/pehc/vol1/iss15/4</guid>
<pubDate>Tue, 08 May 2012 10:00:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Samuel Lin MD</author>


</item>


<item>
<title>A Message from Lilly: Health Literacy Matters</title>
<link>http://jdc.jefferson.edu/pehc/vol1/iss15/3</link>
<guid isPermaLink="true">http://jdc.jefferson.edu/pehc/vol1/iss15/3</guid>
<pubDate>Tue, 08 May 2012 10:00:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jack Harris MD</author>


</item>


<item>
<title>Understanding the Patient&apos;s Role in Health Care Reform</title>
<link>http://jdc.jefferson.edu/pehc/vol1/iss15/2</link>
<guid isPermaLink="true">http://jdc.jefferson.edu/pehc/vol1/iss15/2</guid>
<pubDate>Tue, 08 May 2012 10:00:30 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>David B. Nash MD, MBA</author>


</item>


<item>
<title>Prescriptions for Excellence in Health Care Spring 2012 Download Full PDF</title>
<link>http://jdc.jefferson.edu/pehc/vol1/iss15/1</link>
<guid isPermaLink="true">http://jdc.jefferson.edu/pehc/vol1/iss15/1</guid>
<pubDate>Tue, 08 May 2012 10:00:28 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>


</item>


<item>
<title>An Exposition of Augustine&apos;s Theodicy: From Its Influences to Its Modern Application</title>
<link>http://digitalcommons.providence.edu/philosophy_students/1</link>
<guid isPermaLink="true">http://digitalcommons.providence.edu/philosophy_students/1</guid>
<pubDate>Tue, 08 May 2012 09:57:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper delineates the thrust of Augustine's theodicy against the broader background of his Christian Neoplatonic outlook. We examine Augustine's initial Manichean influences and see how these beliefs carry over to his mature thought, which is evident in the seventh book of the <em>Confessions</em>. After Augustine's time with the Manicheans, we look at how he was so influenced by the books of the Platonists (<em>libri platonicorum</em>). Although Augustine's position regarding the problem of evil shifts, his idea of the primacy of the soul is still evident in his thought process. To wit, Augustine posits that evil must be considered a privation of the Good, so much so as to reach the point of complete nonentity. Human beings' ability to be corrupted by evils rests in their position as being created <em>ex-nihilo</em> by God. With this creation also comes an inherent mutability. Due to human mutability, Augustine believes that God is not responsible for such evil actions.</p>
<p>This paper also contrasts this belief with modern empiricist David Hume's idea regarding God's responsibility for human actions. Hume argues that the volition of all human actions rests in God as Creator of the world. As creator, Hume claims that God places human beings in a position to act. If humans are predisposed to perform evil actions, they cannot be faulted. Augustine would counter that argument by claiming that evil is not a substance. Not being a substance, evil is there not ascribable to God. Ultimately, Augustine's theodicy is based upon the goodness of God.</p>

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</description>

<author>Kevin J. Gray</author>


<category>Philosophy</category>

<category>Theology</category>

</item>


<item>
<title>A Best-Evidence Synthesis of The Relationship of Multiple Intelligence Instructional Approaches and Student Achievement Indicators In Secondary School Classrooms</title>
<link>http://digitalcommons.cedarville.edu/education_theses/10</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/10</guid>
<pubDate>Tue, 08 May 2012 09:55:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to synthesize the literature in order to assess and quantify (if possible) the relationship between MI instructional approaches and student achievement indicators in secondary school classrooms (grades 6-12). This study employed the best-evidence synthesis methodology devised by Robert Slavin. Criteria for study inclusio n included germaneness, minimization of bias, and validity. This study allows for several conclusions: (1) a very limited amount of research focusing on the relationship of MI instructional approaches and student achievement indicators in secondary school classrooms exists, (2) instances of MI instructional approaches vary widely in methodology and implementation but demonstrate a fairly consistent philosophical approach, and (3) the studies included in this research synthesis failed to prove causation in the relationship of MI instructional approaches and student achievement indicators in secondary school classrooms. However, substantial evidence exists showing that multiple intelligences theory contributes positively to student learning and development. Further research is needed to quantify the relationship between MI instructional approaches and academic achievement indicators in secondary classrooms.</p>

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</description>

<author>Ethan E. Hodge</author>


</item>


<item>
<title>Fogler Favorites - Underfoot in Show Business</title>
<link>http://digitalcommons.library.umaine.edu/faves/16</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/16</guid>
<pubDate>Tue, 08 May 2012 09:55:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series. Hansie Grignon’s Fogler Favorite is Underfoot in Show Business.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Fogler Favorites - The Watchman</title>
<link>http://digitalcommons.library.umaine.edu/faves/15</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/15</guid>
<pubDate>Tue, 08 May 2012 09:55:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series. Martin Wallace’s Fogler Favorite is The Watchman.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Race and the Doctrine of Self Defense:  The Role of Race in Determining the Proper Use of Force to Protect Oneself</title>
<link>http://digitalcommons.tourolaw.edu/scholarlyworks/423</link>
<guid isPermaLink="true">http://digitalcommons.tourolaw.edu/scholarlyworks/423</guid>
<pubDate>Tue, 08 May 2012 09:54:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Richard Klein</author>


</item>


<item>
<title>Fogler Favorites - Seven Days in May</title>
<link>http://digitalcommons.library.umaine.edu/faves/14</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/14</guid>
<pubDate>Tue, 08 May 2012 09:48:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series.  Gretchen Gfeller’s Fogler Favorite is Seven Days in May.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Fogler Favorites - The Structure of Scientific Revolutions</title>
<link>http://digitalcommons.library.umaine.edu/faves/13</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/13</guid>
<pubDate>Tue, 08 May 2012 09:48:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series.  Charlie Slavin’s Fogler Favorite is The Structure of Scientific Revolutions.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Fogler Favorites - Titus Andronicus</title>
<link>http://digitalcommons.library.umaine.edu/faves/12</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/12</guid>
<pubDate>Tue, 08 May 2012 09:48:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series.  Brad Finch’s Fogler Favorite is Titus Andronicus.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>The umuD gene products are molecular adaptors in the regulation of DNA damage tolerance</title>
<link>http://iris.lib.neu.edu/chemistry_diss/40</link>
<guid isPermaLink="true">http://iris.lib.neu.edu/chemistry_diss/40</guid>
<pubDate>Tue, 08 May 2012 09:48:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>The homodimeric umuD gene products play key roles in regulating the cellular response to DNA damage in Escherichia coli. UmuD is composed of 139-amino acid subunits and is upregulated as part of the SOS DNA damage response. Subsequently, damage-induced RecA:ssDNA nucleoprotein filaments mediate the slow autocleavage of the N-terminal 24-amino acid arms of UmuD yielding UmuD'. It was previously proposed that UmuD cleaves only in the trans conformation, in which the arm of one monomer utilizes that active site of the adjacent monomer for cleavage. Cleavage in trans would therefore require dimerization. However, isoenergetic models of UmuD suggested that the arms may adopt cis (intramolecular) or trans (intermolecular) conformations, and may be unbound from or bound to the globular C-terminal domain. The dynamic nature of the N-terminal arms may explain how a number of distinct protein-protein contacts that prevent and facilitate mutagenic translesion synthesis (TLS) are made. The overall goal of my research is to determine the conformation and dynamics of the UmuD proteins in order to understand its regulatory role in response to DNA damage. Chapter 1 presents the relevant background and details of structure, function and interactions of UmuD with proteins involved in DNA replication and DNA damage repair.</p>
<p>In an effort to learn more about the structural dynamics and functions of UmuD proteins, we designed a UmuD protein variant that is defective in dimerization. Such a variant would not only answer the question as to whether UmuD is active in the cis conformation, but also address the possibility that UmuD may be functionally active as a monomer. Although models of UmuD with the arms in the cis conformation have been proposed, evidence that this conformation is physiologically relevant has been lacking. Wild-type UmuD and UmuD' form exceptionally tight dimers in solution; however, in chapter 2 we show that the single amino-acid change N41D generates stable, active UmuD and UmuD' monomers that functionally mimic the dimeric wild-type proteins. The UmuD N41D monomer is proficient for cleavage and interacts physically with DNA polymerase IV (DinB). Furthermore, the N41D variants facilitate UV-induced mutagenesis and promote overall cell viability. Taken together, these observations show that a monomeric form of UmuD retains substantial function in vivo and in vitro.</p>
<p>UmuD and UmuD' can display differential interactions with their partner proteins which can lead to dramatically different cellular outcomes. These key differences may be due to the dynamics of the N-terminal arms of UmuD. Previous biochemical evidence supported a model in which the arms of UmuD are stably bound to its globular domain. However, recent experiments suggest that the N-terminal arms of UmuD are somewhat dynamic. Chapter 3 describes the use of Electron Paramagnetic Resonance (EPR) spectroscopy to probe the conformational dynamics of the N-terminal arms of the umuD gene products and variants. We determined that the arms of UmuD display a large degree of motion, are largely unbound from the globular C-terminal domain, and that the free energy of dissociation is +2.1 kJ/mol.</p>
<p>In chapter 4, we discuss the dimer exchange and conformation-dependent cleavage of the UmuD proteins. To further understand the dynamic regulatory roles of the umuD gene products, we monitored the kinetics of exchange and cleavage of the UmuD and UmuD' homodimers as well as of the UmuDD'; heterodimer under equilibrium conditions. We found that the heterodimer is the preferred but not exclusive dimeric protein form, and that both the heterodimer and homodimers exhibit slow exchange kinetics. In addition, the heterodimer efficiently cleaves to form UmuD'. Together, this work reveals an intricate UmuD lifecycle that involves dimer exchange and cleavage in the regulation of the DNA damage response.</p>
<p>Chapter 5 discusses the use of UmuD N-terminal truncations, UmuD 8 and UmuD 18, in accessing the role of the arms in regulating protein-protein interactions. Extensive characterization reveals that the loss of even the N-terminal seven amino acids results in a notable change in domain conformation, binding affinity to DinB as detected by tryptophan fluorescence, and the facilitation of UV-induced mutagenesis and UV survival. Additionally, we have also discovered a smaller version of UmuD that is also UV-inducible. Given the information above, it is plausible that this smaller UmuD may be involved in yet another level of DNA damage and repair regulation.</p>

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</description>

<author>Jaylene N. Ollivierre</author>


</item>


<item>
<title>Formation of Alewife Concretions in Polluted Onondaga Lake</title>
<link>http://digitalcommons.brockport.edu/env_facpub/48</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/48</guid>
<pubDate>Tue, 08 May 2012 09:46:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The previously reported finding of alewife concretions along the shores of Onondaga Lake in Upstate New York prompted investigation of the field conditions necessary for their formation and laboratory simulation of these conditions to induce concretion formation. Onondaga Lake is shown to be calcium-polluted and continuously supersaturated with respect to CaC03• Anaerobic conditions exist in the hypolimnion in approximately eight months of every year. In controlled laboratory experiments, formation of structure-retaining alewife concretions was successful under anaerobic conditions, and was enhanced by elevated calcium concentrations. Additional chemical analyses of fresh alewives, natural concretions and laboratory-formed concretions were performed. A previously proposed mechanism for concretion formation is evaluated with respect to the presented results. The common occurrence of alewife concretions in Onondaga Lake is a manifestation of the unique polluted state of the ecosystem, combined with the invasion of the lipid-rich alewife.</p>

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</description>

<author>Douglas A. Wilcox et al.</author>


</item>


<item>
<title>New Orleans: Bourbon Street at Mardi Gras</title>
<link>http://digitalcommons.ric.edu/smolski_images/831</link>
<guid isPermaLink="true">http://digitalcommons.ric.edu/smolski_images/831</guid>
<pubDate>Tue, 08 May 2012 09:44:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bourbon Street is one of the most celebrated areas of Mardi Gras in New Orleans. The street is most known for its burlesque clubs and lively night life. Some of the major attractions include: The Royal Sonesta Hotel, Jean Lafitte’s Blacksmith Shop, and the Old Absinthe House. All of the buildings on this street reflect the folklore and beauty of the 1700s. The major event that takes place on this street is called The Bourbon Street Awards. Up until 1980, the awards were hosted by Cafe-Lafitte-In-Exile, the oldest gay bar in the country. Since the event has gained huge crowds, it has recently moved to the corner or Bourbon Street and St. Ann Street. This corner is commonly known as the “Gay Mardi Gras.”</p>

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</description>

<author>Chet Smolski</author>


</item>


<item>
<title>Dante Gabriel Rossetti and the Romance of Loss</title>
<link>http://scholarship.rollins.edu/mls/27</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/27</guid>
<pubDate>Tue, 08 May 2012 09:41:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Through paired poems and paintings, Dante Gabriel Rossetti explored the nature of Love—both physical and spiritual—as made evident by distance or absence.  Influenced early by his familiarity with Dante Alighieri and a confluence of changing social and artistic attitudes, Rossetti transformed the dialogue around him to a more personal internal conversation, revealed by pen and brush.  This paper examines the dynamic of that pervasive thread in Rossetti’s work through a discussion of the influences upon the artist, the artist’s effect upon important figures of mid- to late nineteenth century England, and the important relationships that shaped his discourse.  In addition, commentaries on a number of Rossetti’s paired works delineate the interplay between his written and painted “words” as they reveal the progression of his thoughts.</p>

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</description>

<author>Jane N. Cooper</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 14, no. 1</title>
<link>http://collected.jcu.edu/carrollquarterly/40</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/40</guid>
<pubDate>Tue, 08 May 2012 09:37:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 14, no. 2</title>
<link>http://collected.jcu.edu/carrollquarterly/39</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/39</guid>
<pubDate>Tue, 08 May 2012 09:36:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 14, no. 3</title>
<link>http://collected.jcu.edu/carrollquarterly/38</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/38</guid>
<pubDate>Tue, 08 May 2012 09:36:58 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 14, no. 4</title>
<link>http://collected.jcu.edu/carrollquarterly/37</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/37</guid>
<pubDate>Tue, 08 May 2012 09:36:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>Constitutional Concerns About Capital Punishment:  The Death Penalty Statute in New York State</title>
<link>http://digitalcommons.tourolaw.edu/scholarlyworks/422</link>
<guid isPermaLink="true">http://digitalcommons.tourolaw.edu/scholarlyworks/422</guid>
<pubDate>Tue, 08 May 2012 09:34:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Richard Klein</author>


</item>


<item>
<title>Perfecting holiness</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/381</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/381</guid>
<pubDate>Tue, 08 May 2012 09:31:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Timothy C. Tennent</author>


</item>


<item>
<title>The Roman North American Macella: Their Chronology, Typology, Urban Placement and Patronage</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6932</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6932</guid>
<pubDate>Tue, 08 May 2012 09:31:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>From the first to the fifth centuries A.D., the inhabitants of many Roman North African towns went to a <em>macellum</em> to buy food for their dinner banquets. The typical <em>macellum</em> plan consists of an enclosed structure with a peristyle court lined with shops. The archaeological evidence suggests that the Roman North African <em>macella</em> were often bold and innovative variations from the Italian <em>macella</em>.</p>
<p>Since many of the Roman North African <em>macella</em> were excavated in the early 1900s, there have been relatively few recent publications and excavations undertaken on these significant buildings. One exception is C. De Ruyt's book, Macellum. Marché alimentaire des Romains (1983). De Ruyt, catalogued the remains of eighty-three <em>macella</em> found in Sicily, Italy, Greece, Turkey, Hungary, England, Spain and North Africa. Additionally, De Ruyt's book includes a detailed study of the origins of the <em>macellum</em> type, information about the market's urban and historical context, and evidence for the varieties of foods sold.</p>
<p>This thesis, using De Ruyt's book as the starting point for research on the <em>macellum</em>, focuses specifically on the Roman North African <em>macella</em>, since there are still problems to be resolved concerning these buildings. For example, was there a <em>macellum</em> which was essentially Roman North African in design? Did the market-type in North Africa simply imitate the plans of earlier Italian <em>macella</em>? What does the placement of the <em>macellum</em> within an urban setting tell us about its importance and function? What was the role of patrons in the construction and restoration of these markets?</p>
<p>The thesis on Roman North African <em>macella</em> is divided into four chapters: Chronology, Typology, Urban placement and Patronage (euergetism). Archaeological and epigraphical evidence is included for Roman North African <em>macella</em> not listed in De Ruyt's catalogue.</p>

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</description>

<author>Alexis Mary Young</author>


</item>


<item>
<title>Linking Ecosystem Processes with Wetland Management Goals: Charting a Course for a Sustainable Future</title>
<link>http://digitalcommons.brockport.edu/env_facpub/47</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/47</guid>
<pubDate>Tue, 08 May 2012 09:30:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Wetland management in the United States has never been as challenging as in today’s highly modified landscape. Initially, wetland science and management emerged as professions in response to widespread conversion of wetlands to other uses and concerns over negative impacts on wildlife populations, especially migratory birds. Consequently, wetland management was focused on wildlife, and the initial management technique was simply to protect wetlands. However, extensive conversion of lands for agricultural and urban expansion over the past 60 years has modified ecosystem processes at the landscape scale sufficiently to compromise wetland management activities on adjacent lands dedicated to conservation. Moreover, society now expects a broad suite of ecosystem services to be delivered. As a result, many previously used wetland management techniques are no longer appropriate because they do not take into account influences of adjacent land uses or other ecosystem services, such as ground-water recharge. Other early management approaches may have been ineffective because they were based on an incomplete understanding of wetland processes or social influences. Meanwhile, wetland losses continued, as well as loss of services provided by the remaining managed wetlands. Regulation starting in the 1970s and subsequent research attention on wetland functioning has led to new knowledge and a broader understanding of wetland processes and recognition of the full suite of services (e.g., water storage, water quality improvement, aquifer maintenance, climate mitigation). To be effective in today’s highly modified landscape, knowledge of social choices, political influences, and dynamic wetland processes is required to meet wetland management objectives for a range of ecosystem services. We argue that adopting a process-based perspective is critical to develop strategies to optimize a suite of wetland services, including providing traditional wildlife habitat.</p>

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</description>

<author>Ned H. Euliss Jr. et al.</author>


</item>


<item>
<title>A Model of Data Structures Commonly Used in Programming Languages and Data Base Management Systems</title>
<link>http://ecommons.luc.edu/cs_facpubs/61</link>
<guid isPermaLink="true">http://ecommons.luc.edu/cs_facpubs/61</guid>
<pubDate>Tue, 08 May 2012 09:30:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis claims that contemporary data structures can be understood and studied with an intelligible model which captures their essential differences and similarities and, further, that such a model is an appropriate basis for a top-down description method for data structures. To define the scope of the model, the data structures included in 21 programming languages and data base management systems have been tabulated. Each individual data structure is illustrated with an example drawn from a published paper or a working computer program. This mélange of data structures is divided into three classes (aggregates, associations , and files) and each class is modeled with a set of questions . Each question delineates one significant characteristic of the data structure and can be viewed as one axis of a n-dimensional universe of data structures. To demonstrate the clarity and generality of the model numerous existing examples, including several CODASYL Data Base Task Group and Feature Analysis data organizations, are described with the model. Additionally, a “completeness” exercise demonstrates that the model can represent all of the data structures identified in the survey of 21 programming languages and data base management systems.</p>
<p>The top-down data structure design method is based upon the model and is particularly suited to both the design and documentation of large data bases. Two special features, restatement and redefinition, allow the designs to remain intellectually manageable throughout a large number of conceptual levels. To show the utility of these methods a practical data base design for a software development system is presented. The requirements for this data base are drawn from the typical situation in which a number of individual programmers cooperate to create a software system which is used and modified over a long time period. This design proffers a general solution to a common programming problem and is thus a “software engineering" approach to data base design.</p>
<p>In order to compare and contrast the model of this thesis with existing work, 11 other data structure models are surveyed and divided into four groups: semantic, prototype, analysis, and information models. The data structure model of this thesis is an analysis model; such models provide a compilation of all possible variations among a collection of data structures. To aid the comparison, a common example is expressed in terms of each data structure model.</p>

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</description>

<author>William L. Honig</author>


</item>


<item>
<title>Fogler Favorites - European Local Color Literature</title>
<link>http://digitalcommons.library.umaine.edu/faves/11</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/11</guid>
<pubDate>Tue, 08 May 2012 09:23:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series.  Deborah Roger’s Fogler Favorite is European Local Color Literature.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Fogler Favorites - Interlibrary Loan</title>
<link>http://digitalcommons.library.umaine.edu/faves/10</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/10</guid>
<pubDate>Tue, 08 May 2012 09:23:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series.  Jeffrey St. John’s Fogler Favorite is the Interlibrary Loan Department.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>The CADRE Project: A Retention Study</title>
<link>http://digitalcommons.unomaha.edu/tedfacpub/23</link>
<guid isPermaLink="true">http://digitalcommons.unomaha.edu/tedfacpub/23</guid>
<pubDate>Tue, 08 May 2012 09:20:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>I his article describes the findings of a study of leachcr retention and the effectiveness of one induction program, the Career Advancement and Development for Recruits and Experienced teachers (CADRE) Project, in helping teachers remain in the profession. National statistics report teacher attrition rate to be 40 percent over five years. CADRE participants have a retention rule ol 89 percent over five years.</p>

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</description>

<author>Sheryl McGlamery et al.</author>


</item>


<item>
<title>An Analysis and Synthesis of Research on Classroom Peer Tutoring Methods that Benefit Intermediate Math Students</title>
<link>http://digitalcommons.cedarville.edu/education_theses/9</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/9</guid>
<pubDate>Tue, 08 May 2012 09:20:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>What are the benefits of peer tutoring? What do productive peer tutoring sessions include? This study occurred in fourth and fifth grade classrooms at a private school in a rural community. The researcher conducted an experiment to determine if students benefited from the opportunity to have their fellow students tutor them and elaborate on their method of problems solving during math class. In light of the inconsistent results, the author believes no assumptions can be made based on the data from this research. The fourth grade results showed definite progress according to the standardized test, but there was some inconsistency in the achievement shown in the classroom tests. The fifth grade results did not show a significant growth from fourth to fifth grade on the math portion of the achievement test. There is also inconsistency in the significance of the growth in learning shown in the fifth grade classroom tests. However, the researcher hopes this study will encourage further exploration in the study of beneficial peer tutoring methods.</p>

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</description>

<author>Shelley R. Grimm</author>


</item>


<item>
<title>Modeling Wetland Plant Community Response to Assess Water-Level Regulation Scenarios in the Lake Ontario – St. Lawrence River Basin</title>
<link>http://digitalcommons.brockport.edu/env_facpub/46</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/46</guid>
<pubDate>Tue, 08 May 2012 09:18:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>The International Joint Commission has recently completed a five-year study (2000– 2005) to review the operation of structures controlling the flows and levels of the Lake Ontario – St. Lawrence River system. In addition to addressing the multitude of stakeholder interests, the regulation plan review also considers environmental sustainability and integrity of wetlands and various ecosystem components. The present paper outlines the general approach, scientific methodology and applied management considerations of studies quantifying the relationships between hydrology and wetland plant assemblages (% occurrence, surface area) in Lake Ontario and the Upper and Lower St. Lawrence River. Although similar study designs were used across the study region, different methodologies were required that were specifically adapted to suit the important regional differences between the lake and river systems, range in water-level variations, and confounding factors (geomorphic types, exposure, sediment characteristics, downstream gradient of water quality, origin of water masses in the Lower River). Performance indicators (metrics), such as total area of wetland in meadow marsh vegetation type, that link wetland response to water levels will be used to assess the effects of different regulation plans under current and future (climate change) water-supply scenarios.</p>

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</description>

<author>Christiane Hudon et al.</author>


</item>


<item>
<title>Sailing into the wind: Exploring the relationships among ambidexterity, vacillation, and organizational performance</title>
<link>http://digitalcommons.hope.edu/faculty_publications/433</link>
<guid isPermaLink="true">http://digitalcommons.hope.edu/faculty_publications/433</guid>
<pubDate>Tue, 08 May 2012 09:17:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>While sustainable high performance requires the capacity to simultaneously explore and exploit, the management literature is divided on the most feasible and efficient route toward this end. We review two proposed approaches for achieving simultaneously high levels of exploration and exploitation: organizational ambidexterity and organizational vacillation. To facilitate comparison, we map these approaches onto a common performance landscape, making precise the empirical question of which delivers superior long run performance. We then analyze canonical cases from both literatures, examining patterns of decision making and corresponding performance over time. These cases suggest that vacillation may offer higher long run performance than ambidexterity, while ambidexterity enhances performance on the margin when utilized within larger epochs of vacillation. We conclude that ambidexterity and vacillation are complements with respect to performance, albeit through different mechanisms. Copyright (c) 2012 John Wiley & Sons, Ltd.</p>

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</description>

<author>Peter A. Boumgarden et al.</author>


</item>


<item>
<title>Yoga and Art as Creative Bridges for Autism</title>
<link>http://digitalcommons.lasalle.edu/asd/2012/2012/11</link>
<guid isPermaLink="true">http://digitalcommons.lasalle.edu/asd/2012/2012/11</guid>
<pubDate>Fri, 04 May 2012 13:30:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>As we seek to support and enhance the quality of life for persons and families living with Autism, research and experience demonstrate the usefulness of creative expression and fitness as ways to tend to the whole person. Art and movement are wonderful holistic strategies complementing other interventions.</p>
<p><strong>This program is designed to help you:</strong></p>
<p>1. Learn simple breathing techniques for stress reduction</p>
<p>2. Observe and experience easy yoga movements useful in various settings</p>
<p>3. Explore how mindfulness improves focus and attention</p>
<p>4. Discover Art as a powerful way to integrate and advance educational & therapeutic interventions</p>
<p>5. Promote the beauty and uniqueness of our Spectrum persons through creative expression.</p>

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</description>

<author>Robin Schwoyer</author>


</item>


<item>
<title>The Subculture of Rugby Players: A Form of Resistance and Incorporation</title>
<link>http://digitalcommons.mcmaster.ca/opendissertations/6931</link>
<guid isPermaLink="true">http://digitalcommons.mcmaster.ca/opendissertations/6931</guid>
<pubDate>Tue, 08 May 2012 09:12:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>The genesis of rugby football is to be found in the unique all-male environment of the nlneteenth century British public schools. The game was initially introduced by masters as an agent of social control - to restrain the usually unruly behaviour of boys. Outside the confines of the public schools (and particularly at university), old Boys formed Rugby clubs in which clusters of cultural characteristics based principally around amateurism and specific non-game features came to be developed into a subculture of rugby players, and although certain changes have taken place, this subculture is still intact today in the United Kingdom.</p>
<p>Rugby, in its embryonic form, was introduced in North America in the mid-nineteenth century by garrison soldiers and British immigrants. For a short while it enjoyed some popularity but the war years took their toll and the sport dwindled. However, it sprang up with renewed vigour in the late 1950's and early 1960's replete with all the cultural features that had come to characterize the British game, but these features had taken on different meanings.</p>
<p>In order to examine the subculture and public image of rugby players, the redevelopment of rugby as an increasingly popular sport in North America and this apparent transformation of meaning of various cultural elements, data were collected during one season of participant-observation with a canadian university rugby team and supplemented with extensive informal observations of and lnterviews with players and members of the subculture in the United Klngdom and North America.</p>
<p>It is hypothesized here that on a continent preoccupied with professlonal sport and a win-at-all-cost philosophy in sport, the amateur game of Rugby Union exists as a type of 'resistance' to the dominant sporting forms in North America (particularly football), and for Britons as a resistance to assimilation.</p>

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</description>

<author>Kevin Mark Young</author>


</item>


<item>
<title>Legislative Mandates Concerning Truancy Effects on Attendance Rates</title>
<link>http://mds.marshall.edu/etd/217</link>
<guid isPermaLink="true">http://mds.marshall.edu/etd/217</guid>
<pubDate>Tue, 08 May 2012 09:08:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>The correlation between truancy and dropping out of school is high, prompting school districts and the state legislature to attempt to intervene (Sparks, 2010). The purpose of this study is to determine the effectiveness of the West Virginia Code 18-8-4 that requires mandatory legal compulsory attendance (CA2) meetings to be held at the county level when a student obtains five days of unexcused absences. In the summer of 2010, the WV state legislature changed the CA2 meeting requirements from 10 days of unexcused absences to five. Barbour County Schools began to intervene in truancy using a multidisciplinary approach in 2007. Attendance data between 2007 through 2012 were analyzed. Results indicated that there were significant improvements in attendance between 2007-2009 when the collaboration with the court system began. However, when comparing attendance rates before and after the 2010 legislative mandates there were no significant changes; in fact, there was a slight decrease in attendance the following year.</p>

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</description>

<author>Felicia Corley</author>


<category>&lt;p&gt;School attendance - West Virginia.&lt;/p&gt;
&lt;p&gt;School attendance - Law and Legislation.&lt;/p&gt;</category>

</item>


<item>
<title>Fogler Favorites - Einstein&apos;s Dreams</title>
<link>http://digitalcommons.library.umaine.edu/faves/9</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/9</guid>
<pubDate>Tue, 08 May 2012 09:06:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series.  Kjerste Christensen’s Fogler Favorite is Einstein's Dreams.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Fogler Favorites - Emerald Fulltext</title>
<link>http://digitalcommons.library.umaine.edu/faves/8</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/8</guid>
<pubDate>Tue, 08 May 2012 09:06:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series.  Terry Porter’s Fogler Favorite is Emerald Fulltext.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 13, no. 1</title>
<link>http://collected.jcu.edu/carrollquarterly/36</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/36</guid>
<pubDate>Tue, 08 May 2012 09:06:29 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 13, no. 2</title>
<link>http://collected.jcu.edu/carrollquarterly/35</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/35</guid>
<pubDate>Tue, 08 May 2012 09:06:27 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 13, no. 3 and no. 4</title>
<link>http://collected.jcu.edu/carrollquarterly/34</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/34</guid>
<pubDate>Tue, 08 May 2012 09:06:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>Effects Of Coal Fly-Ash Disposal On Water Chemistry in an Intradunal Wetland at Indiana Dunes</title>
<link>http://digitalcommons.brockport.edu/env_facpub/45</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/45</guid>
<pubDate>Tue, 08 May 2012 09:06:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>An intradunal wetland within the Indiana Dunes National Lakeshore on the south shore of Lake Michigan was flooded for 15 years by seepage from fly-ash settling ponds located adjacent to the park. Studies were undertaken to determine the effects of the seepage on water chemistry in the flooded wetlands. These water chemistry conditions have been correlated to ongoing studies of soil contamination and secondary succession in the wetland basin following cessation of seepage. The seepage increased the concentrations of calcium, potassium, sulfate, aluminum, boron, iron, manganese, molybdenum, nickel, strontium, and zinc in ground water and surface water downgradient from the settling ponds. Chemical interactions with aquifer materials, particularly organic matter, significantly limit the transport of aluminum, iron, nickel, and zinc in this system. The organic soils of the dewatered wetland basin now contain elevated concentrations of aluminum, boron, manganese, and zinc that are potentially phytotoxic under the low pH (<4) conditions that exist. Plant growth and secondary succession were affected by the soil chemistry of the dewatered wetlands.</p>

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</description>

<author>Douglas A. Wilcox et al.</author>


</item>


<item>
<title>Where Stories Collide : Montage and the Short Story Cycle</title>
<link>http://digitalcommons.bucknell.edu/masters_theses/74</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/masters_theses/74</guid>
<pubDate>Tue, 08 May 2012 09:05:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis uses Sergei Eisenstein’s filmic theories of montage to examine the modernist American short story cycle, a genre of independent short stories that work together to create a larger and interrelated whole. Similar to the shot-by-shot editing process of montage, the story cycle builds its intertextual meaning story-by-story from an aggregate of abrupt narrative transitions and juxtapositions. Eisenstein famously felt that montage, the editing together of film fragments, was not a process of linkage, but of collision –each radically different shot in a film should crash into the next shot, until audience members were intellectually provoked into synthesizing these collisions through dialectical processes. I offer montage as an interpretive strategy for negotiating the narrative collisions in story cycles such as Sherwood Anderson’s Winesburg, Ohio, William Faulkner’s Go Down, Moses, and Eudora Welty’s The Golden Apples. For Go Down, Moses, I argue that Eisenstein’s politically rendered “montage of attractions” provides a template for investigating the shock tactics behind Faulkner’s chronologically and racially entangled stories of whites and African Americans. For The Golden Apples, I consider the opposites and doubles in Welty’s fiction with Eisenstein’s similar belief in the “opposing passions” of the world. Not only, then, do I suggest that the modernist story cycle bears a cinematic influence, but I also offer Eisenstein’s theories of montage and collision as a heuristic for formal, thematic, and even political patterns in a genre infamous for its resistance to definition and classification.</p>

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</description>

<author>Jacob Agner</author>


</item>


<item>
<title>A Chandra Observation of the Diffuse Emission in the Face-on Spiral NGC 6946</title>
<link>http://digitalcommons.olin.edu/facpub_2003/4</link>
<guid isPermaLink="true">http://digitalcommons.olin.edu/facpub_2003/4</guid>
<pubDate>Tue, 08 May 2012 08:57:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper describes the Chandra observation of the diffuse emission in the face-on spiral NGC 6946. Overlaid on optical and Halpha images, the diffuse emission follows the spiral structure of the galaxy. An overlay on a 6 cm polarized radio intensity map confirms the phase offset of the polarized emission. We then extract and fit the spectrum of the unresolved emission with several spectral models. All model fits show a consistent continuum thermal temperature with a mean value of 0.25 +/- 0..03 keV. Additional degrees of freedom are required to obtain a good fit, and any of several models satisfy that need; one model uses a second continuum component with a temperature of 0.70 +/- 0.10 keV. An abundance measure of 3(-1.90)(+1.95) for Si differs from the solar value at the 90% confidence level; the net diffuse spectrum shows that the line lies above the instrumental Si feature. For Fe the abundance measure of 0.67 +/- 0.13 is significant at 99%. Multiple Gaussians also provide a good fit. Two of the fitted Gaussians capture the O VII and O VIII emission; the fitted emission is consistent with an XMM-Newton RGS spectrum of diffuse gas in M81. The ratio of the two lines is less than 0.6-0.7 and suggests the possibility of nonequilibrium ionization conditions existing in the interstellar medium of NGC 6946. An extrapolation of the point-source luminosity distribution shows that the diffuse component is not the sum of unresolved point sources; their contribution is at most 25%.</p>

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</description>

<author>Eric M. Schlegel et al.</author>


</item>


<item>
<title>The determinants and measurement of a country brand: the country brand strength index</title>
<link>http://scholarship.rollins.edu/as_facpub/38</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/as_facpub/38</guid>
<pubDate>Tue, 08 May 2012 08:53:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Purpose: A strong country brand can stimulate exports, attract tourism, investments, and immigration. The purpose of this paper is to construct and present a country brand strength index (CBSI) which assesses the strength of a country brand based on objective secondary data.</p>
<p>Design/methodology/approach: By applying a company-based brand equity approach, we present a standardized country brand strength index.</p>
<p>Findings: Our results show that the countries with the strongest country brand are smaller, developed countries in Europe. Our proposed index leads to results similar to the widely used Anholt GfK Roper Nation Brand Index (NBI), which measures perceptions of a country brand based on subjective survey data. Countries that are perceived positively (based on the NBI) have a stronger country brand (CBSI) and countries perceived negatively (based on NBI) have a weak country brand (CBSI). The two indexes are highly and significantly correlated, indicating they measure the same phenomena, although they use different approaches, methodologies and data, suggesting that the indexes are complementary and inter-dependent.</p>
<p>Practical Implications: To stay competitive in the global economy, countries need to understand how to assess their country brand in order to manage it. With the proposed index, a country can identify its position compared to others. This can assist public and private organizations to develop a more powerful country brand strategy.</p>
<p>Originality/value: The proposed index is original in operationalizing the strength of a country brand based on objective secondary data. The proposed index represents an alternative measurement to existing subjective survey-based measurement indexes.</p>

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</description>

<author>Marc Fetscherin</author>


</item>


<item>
<title>The Chief Prosecutor is Sacked</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/380</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/380</guid>
<pubDate>Tue, 08 May 2012 08:52:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Timothy C. Tennent</author>


</item>


<item>
<title>Clam Digger</title>
<link>http://escholar.salve.edu/monumenta-images/8</link>
<guid isPermaLink="true">http://escholar.salve.edu/monumenta-images/8</guid>
<pubDate>Tue, 08 May 2012 08:52:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bronze, 57 inches high.  Featured in Monumenta art exhibit, 1974, where it was installed at Chateau-sur-Mer. Lent by Fourcade, Droll, Inc., New York</p>
<p><strong>Publisher:</strong> Salve Regina University Archives and Special Collections.</p>
<p><strong>Source:</strong> Digital reproduction of photograph of work of art. Digitization specifications: Adobe Photoshop 7.0, 240 dpi, RGB, 24-bit.</p>
<p><strong>Rights:</strong> This content is provided for educational research and personal use only. While the photographs in this collection are held in the Salve Regina University Archives and Special Collections, copyright for the artwork still resides with the artists. See <a href="http://library.salve.edu/archives/archives_copyright.html" >http://library.salve.edu/archives/archives_copyright.html</a>.</p>

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</description>

<author>Willem De Kooning</author>


</item>


<item>
<title>Vol. 15, No. 01 (September 2004)</title>
<link>http://www.repository.law.indiana.edu/resipsa/55</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/resipsa/55</guid>
<pubDate>Tue, 08 May 2012 08:49:18 PDT</pubDate>
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<item>
<title>Vol. 15, No. 02 (October 2004)</title>
<link>http://www.repository.law.indiana.edu/resipsa/54</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/resipsa/54</guid>
<pubDate>Tue, 08 May 2012 08:49:17 PDT</pubDate>
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</description>


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<item>
<title>Vol. 15, No. 03 (November 2004)</title>
<link>http://www.repository.law.indiana.edu/resipsa/53</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/resipsa/53</guid>
<pubDate>Tue, 08 May 2012 08:49:15 PDT</pubDate>
<description>
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</description>


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<item>
<title>Vol. 15, No. 04 (December 2004)</title>
<link>http://www.repository.law.indiana.edu/resipsa/52</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/resipsa/52</guid>
<pubDate>Tue, 08 May 2012 08:49:14 PDT</pubDate>
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</description>


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<item>
<title>Vol. 15, No. 05-06 (February/March 2005)</title>
<link>http://www.repository.law.indiana.edu/resipsa/51</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/resipsa/51</guid>
<pubDate>Tue, 08 May 2012 08:49:12 PDT</pubDate>
<description>
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</description>


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<item>
<title>Vol. 15, No. 07 (April 2005)</title>
<link>http://www.repository.law.indiana.edu/resipsa/50</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/resipsa/50</guid>
<pubDate>Tue, 08 May 2012 08:49:11 PDT</pubDate>
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</description>


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<item>
<title>Vol. 15, No. 08 (May 2005)</title>
<link>http://www.repository.law.indiana.edu/resipsa/49</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/resipsa/49</guid>
<pubDate>Tue, 08 May 2012 08:49:09 PDT</pubDate>
<description>
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</description>


</item>


<item>
<title>Using Ground Penetrating Radar Signal Reflection to Model a Highly Transmissive Bedrock Aquifer</title>
<link>http://digitalcommons.uconn.edu/gs_theses/242</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/242</guid>
<pubDate>Tue, 08 May 2012 08:45:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>The use of numerical modeling software to characterize groundwater contaminant fate and transport requires an understanding of the distribution of hydraulic properties of the aquifer. As the complexity of this distribution increases, a more sophisticated understanding is required. Modeling contaminant transport in bedrock aquifers requires that the spatial distributions of highly conductive geologic features are characterized along with the hydraulic transmissivities of those features (Shapiro, 2003). The goal of this research is to refine the numerical model of a highly transmissive crystalline aquifer by characterizing the spatial variability of the hydraulic transmissivity using the attenuation of the ground penetrating radar (GPR) signal.</p>
<p>Slug tests were performed in ten bedrock wells, located within and surrounding a highly conductive zone. The transmissivities measured in these wells ranged from 1.5 E-1 ft<sup>2</sup>/day to 4.2 E+2 ft<sup>2</sup>/day; values greater than 100 ft<sup>2</sup>/day were measured in four of the bedrock wells. A GPR survey was conducted over the well network and five transects were selected for further analysis. The location of the ten wells were projected onto the nearest GPR transects and the GPR data from each location were isolated for further analysis. A visual inspection GPR signal data indicates that the signal reflection increases at locations where high transmissivity values were measured. This relationship was attributed to an increased volume of fluid present within the fractures; a characteristic previously used to identify productive bedrock aquifers at multiple sites (e.g., Porsani, 2005, Halihan, 2008).</p>
<p>The correlation between the transmissivities and the analyzed signal was evaluated at the four locations where higher transmissivities were measured. No correlation was observed when all four points were included. When the data collected from well BW-18 were excluded from the analysis, a near perfect correlation was observed for the remaining three points. The transmissivity measured in BW-18 was the highest value measured onsite. This suggests that the aperture thickness, a characteristic which is not identified using GPR, may play a significant role in the distribution of transmissivities at this location.</p>
<p>The remaining GPR data were transformed to the corresponding hydraulic conductivity using a linear regression fitted to the three correlating points. The values calculated were used as the conductivity values for the model layer corresponding to the shallow bedrock. The resulting model was no more accurate than an identical model created using only the measured transmissivities.</p>
<p>Consistent with previous findings, this investigation determined that GPR data collected by surficial geophysical methods is capable of characterizing highly transmissive regions. Since the spatial variations in the aperture thickness are not identified using this method, it is not appropriate for sites where significant variation is expected. The high correlation suggests that it may be possible to relate signal attenuation to transmissivity over relatively small scales; however an attempt to demonstrate the method’s ability to improve modeling at this site has not been successful. <strong></strong></p>

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</description>

<author>Daniel J. Brockmeyer Mr.</author>


</item>


<item>
<title>X-ray Studies of the Pulsar Wind Nebula Around PSR B0540-69</title>
<link>http://digitalcommons.olin.edu/facpub_2004/10</link>
<guid isPermaLink="true">http://digitalcommons.olin.edu/facpub_2004/10</guid>
<pubDate>Tue, 08 May 2012 08:44:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>The pulsar wind nebula (PWN) surrounding the 50-ms pulsar B0540-69 in the Large Magellanic Cloud shares many properties with the Crab Nebula, the canonical Galactic PWN. We have used the ACIS instrument on the Chandra X-ray Observatory to perform spatially resolved spectroscopy of the PWN. The spectrum of the inner 10" is characterized by a simple power law, with a spectral index that steepens strongly with radius. Outside the central 10" the spectra also require a thermal component. This diameter corresponds to a shell detected in [0 111], suggesting that this shell represents a skin around the PWN, in analogy to the Crab. We infer the value of several key PWN parameters, including sigma, the average ratio of electromagnetic to particle flux.</p>

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</description>

<author>R Petre et al.</author>


</item>


<item>
<title>Martinez v. Long Island Jewish Hillside Medical Center, Emotional Distress Compensation Without a Physical Manifiestation of the Harm: Has New York Gone Too Far?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss1/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss1/5</guid>
<pubDate>Tue, 08 May 2012 08:43:58 PDT</pubDate>
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</description>

<author>Edward M. Pinter</author>


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<item>
<title>The Successorship Doctrine Revisited: Fall River Dyeing &amp; Finishing Corp. v. NLRB</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss1/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss1/4</guid>
<pubDate>Tue, 08 May 2012 08:43:57 PDT</pubDate>
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</description>

<author>Dana M. Schear</author>


</item>


<item>
<title>Booth v. Maryland: Silencing the Victim in the Sentencing Proceeding</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss1/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss1/3</guid>
<pubDate>Tue, 08 May 2012 08:43:56 PDT</pubDate>
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</description>

<author>Jean Marie Schieler</author>


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<item>
<title>Takings Clause Interpretation: The Tradition of Inconsistency Continues</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss1/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss1/2</guid>
<pubDate>Tue, 08 May 2012 08:43:55 PDT</pubDate>
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</description>

<author>Christopher P. Belisle et al.</author>


</item>


<item>
<title>The Pattern Requirement of Civil RICO: &quot;Enterprise&quot; as a Means to End the Confusion</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol3/iss1/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol3/iss1/1</guid>
<pubDate>Tue, 08 May 2012 08:43:54 PDT</pubDate>
<description>
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</description>

<author>Aaron M. Oser</author>


</item>


<item>
<title>A Re-examination of the Liberty of Press and Media Shield Laws After Knight-Ridder Broadcasting, Inc. v. Greenberg</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol2/iss2/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol2/iss2/5</guid>
<pubDate>Tue, 08 May 2012 08:43:46 PDT</pubDate>
<description>
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</description>

<author>Stephen G. Mason</author>


</item>


<item>
<title>The Tax Consequences of Wraparound Mortgages</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol2/iss2/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol2/iss2/4</guid>
<pubDate>Tue, 08 May 2012 08:43:45 PDT</pubDate>
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</description>

<author>Robert Liquerman et al.</author>


</item>


<item>
<title>A Three Prong Approach to the Admissability of Expert Testimony on Child Sexual Abuse Syndrome</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol2/iss2/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol2/iss2/3</guid>
<pubDate>Tue, 08 May 2012 08:43:44 PDT</pubDate>
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</description>

<author>Elizabeth MacEwen et al.</author>


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<item>
<title>Reliability of Codefendant Confessions and the Confrontation Clause: Lee v. Illinois</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol2/iss2/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol2/iss2/2</guid>
<pubDate>Tue, 08 May 2012 08:43:42 PDT</pubDate>
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</description>

<author>John T. Gallagher</author>


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<item>
<title>Surrogate Motherhood at a Legal Crossroad: An Analysis of Proposed Legislation in New York</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol2/iss2/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol2/iss2/1</guid>
<pubDate>Tue, 08 May 2012 08:43:41 PDT</pubDate>
<description>
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</description>

<author>Diana Greco Attner et al.</author>


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<item>
<title>Arbitration and the Securities Exchange Act of 1934: The Prospect of Extending Wilko v. Swan</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol2/iss1/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol2/iss1/5</guid>
<pubDate>Tue, 08 May 2012 08:43:35 PDT</pubDate>
<description>
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</description>

<author>Roslyn A. Quarto et al.</author>


</item>


<item>
<title>Delegation and the Deficit: The Gramm-Rudman Act</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol2/iss1/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol2/iss1/4</guid>
<pubDate>Tue, 08 May 2012 08:43:34 PDT</pubDate>
<description>
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</description>

<author>John D. Beling</author>


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<item>
<title>The Tender Offer Pinch: A Constitutional Analysis of the New York Security Takeover Disclosure Act</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol2/iss1/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol2/iss1/3</guid>
<pubDate>Tue, 08 May 2012 08:43:32 PDT</pubDate>
<description>
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</description>

<author>Eric Steinberg et al.</author>


</item>


<item>
<title>A Return to Technical Pleadings?--Schiavone v. Fortune</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol2/iss1/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol2/iss1/2</guid>
<pubDate>Tue, 08 May 2012 08:43:31 PDT</pubDate>
<description>
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</description>

<author>Ken C. Chin</author>


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<item>
<title>Drug Testing and the Fourth Amendment</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol2/iss1/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol2/iss1/1</guid>
<pubDate>Tue, 08 May 2012 08:43:29 PDT</pubDate>
<description>
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</description>

<author>Leslie A. Harasym</author>


</item>


<item>
<title>The One-Man Corporation and the Fifth Amendment Privilege Agains Self-Incrimination</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss2/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss2/5</guid>
<pubDate>Tue, 08 May 2012 08:43:22 PDT</pubDate>
<description>
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</description>

<author>Anthony M. Battisti</author>


</item>


<item>
<title>Resolution of Primary Residency Status in New York City</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss2/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss2/4</guid>
<pubDate>Tue, 08 May 2012 08:43:21 PDT</pubDate>
<description>
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</description>

<author>Louise G. Conway</author>


</item>


<item>
<title>The New York State Gains Tax--A Constitutional Analysis</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss2/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss2/3</guid>
<pubDate>Tue, 08 May 2012 08:43:20 PDT</pubDate>
<description>
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</description>

<author>Joan Ellsworth</author>


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<item>
<title>Ramifications of Phillips Petroleum Co. v. Shutts on Multistate Plaintiff Class Actions</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss2/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss2/2</guid>
<pubDate>Tue, 08 May 2012 08:43:19 PDT</pubDate>
<description>
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</description>

<author>Mario M. Gazzola</author>


</item>


<item>
<title>Attorney-Client Privilege--Requiring A Preliminary Showing of Relevancy and Need in Grand Jury Proceedings</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss2/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss2/1</guid>
<pubDate>Tue, 08 May 2012 08:43:18 PDT</pubDate>
<description>
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</description>

<author>Daniel J. O&apos;Donnell</author>


</item>


<item>
<title>Aerial Searches of Business Premises: A Bird&apos;s Eye View of the Fourth Amendment</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss1/6</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss1/6</guid>
<pubDate>Tue, 08 May 2012 08:43:12 PDT</pubDate>
<description>
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</description>

<author>Nancy Cifone</author>


</item>


<item>
<title>The Medical Malpractice &quot;Crisis&quot;: The Constitutionality of Damage Limitations</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss1/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss1/5</guid>
<pubDate>Tue, 08 May 2012 08:43:11 PDT</pubDate>
<description>
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</description>

<author>Andrea Palazzolo</author>


</item>


<item>
<title>The Fairness Doctrine: A Principle Under Attack</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss1/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss1/4</guid>
<pubDate>Tue, 08 May 2012 08:43:09 PDT</pubDate>
<description>
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</description>

<author>Richard Halpern</author>


</item>


<item>
<title>Recent Developments in the Weingarten Doctrine: The NLRB Shifts to the Right</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss1/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss1/3</guid>
<pubDate>Tue, 08 May 2012 08:43:08 PDT</pubDate>
<description>
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</description>

<author>Thomas V. Walsh</author>


</item>


<item>
<title>The Longarm Reaches Too Far--Burger King Corp. v. Rudzewicz</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss1/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss1/2</guid>
<pubDate>Tue, 08 May 2012 08:43:07 PDT</pubDate>
<description>
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</description>

<author>Louis M. Lagalante</author>


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<item>
<title>AIDS--A Legal Emergency</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol1/iss1/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol1/iss1/1</guid>
<pubDate>Tue, 08 May 2012 08:43:06 PDT</pubDate>
<description>
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</description>

<author>Geoffrey R. Mazel</author>


</item>


<item>
<title>Iron and Nickel Line Diagnostics for the Galactic Center Diffuse Emission</title>
<link>http://digitalcommons.olin.edu/facpub_2007/24</link>
<guid isPermaLink="true">http://digitalcommons.olin.edu/facpub_2007/24</guid>
<pubDate>Tue, 08 May 2012 08:42:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>We have observed the diffuse X-ray emission from the Galactic Center (GC) using the X-ray Imaging Spectrometer (XIS) on Suzaku. The high-energy resolution and the low-background orbit provided excellent spectra of the GC diffuse X-rays (GCDX). The XIS found many emission lines in the GCDX near the energy of K-shell transitions of iron and nickel. The most pronounced features are Fe I K alpha at 6.4 keV and K-shell absorption edge at 7.1 keV, which are from neutral and/or low ionization states of iron, and the K-shell lines at 6.7 keV and 6.9 keV from He-like (Fe XXV K alpha) and hydrogenic (Fe XXVI Ly alpha) ions of iron. In addition, K alpha lines from neutral or low ionization nickel (Ni I K alpha) and He-like nickel (Ni XXVII K alpha), Fe I K beta, Fe XXV K beta, Fe XXVI Ly beta, Fe XXV K gamma, and Fe XXVI Ly gamma were detected for the first time. The line center energies and widths of Fe XXV K alpha and Fe XXVI Ly alpha favor a collisional excitation plasma for the origin of the GCDX. The electron temperature determined from the line flux ratio of Fe XXV K alpha/Fe XXV K beta is similar to the ionization temperature determined from that of Fe XXV K alpha/Fe XXVI Ly alpha. Thus it would appear that the GCDX plasma is close to ionization equilibrium. The 6.7 keV flux and temperature distribution to the galactic longitude is smooth and monotonic, in contrast to the integrated point source flux distribution. These facts support the hypothesis that the GCDX is truly diffuse emission rather than the integration of the outputs of a large number of unresolved point sources. In addition, our results demonstrate that the chemical composition of Fe in the interstellar gas near the GC is constrained to be about 3.5 times solar abundance.</p>

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</description>

<author>Katsuji Koyama et al.</author>


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<item>
<title>Transactional Support in MapReduce for Speculative Parallelism</title>
<link>http://docs.lib.purdue.edu/cstech/1737</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1737</guid>
<pubDate>Tue, 08 May 2012 08:41:47 PDT</pubDate>
<description>
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</description>

<author>Naresh Rapolu et al.</author>


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<item>
<title>Lightweight Task Graph Inference for Distributed Applications</title>
<link>http://docs.lib.purdue.edu/cstech/1736</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1736</guid>
<pubDate>Tue, 08 May 2012 08:41:39 PDT</pubDate>
<description>
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</description>

<author>Bin Xin et al.</author>


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<item>
<title>vSnoop: Improving TCP Throughput in Virtualized Environments via Acknowledgement Offload</title>
<link>http://docs.lib.purdue.edu/cstech/1735</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1735</guid>
<pubDate>Tue, 08 May 2012 08:41:31 PDT</pubDate>
<description>
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</description>

<author>Ardalan Kangarlou et al.</author>


</item>


<item>
<title>Analyzing Concurrency Bugs Using Dual Slicing</title>
<link>http://docs.lib.purdue.edu/cstech/1734</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1734</guid>
<pubDate>Tue, 08 May 2012 08:41:23 PDT</pubDate>
<description>
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</description>

<author>Dasarath Weeratunge et al.</author>


</item>


<item>
<title>One Stack to Run Them All Reducing Concurrent Analysis to Sequential Analysis Under Priority Scheduling</title>
<link>http://docs.lib.purdue.edu/cstech/1733</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1733</guid>
<pubDate>Tue, 08 May 2012 08:41:15 PDT</pubDate>
<description>
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</description>

<author>Nicholas Kidd et al.</author>


</item>


<item>
<title>Path-Sensitive Analysis Using Edge Strings</title>
<link>http://docs.lib.purdue.edu/cstech/1732</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1732</guid>
<pubDate>Tue, 08 May 2012 08:41:08 PDT</pubDate>
<description>
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</description>

<author>Armand Navabi et al.</author>


</item>


<item>
<title>Isolates: Serializability Enforcement for Concurrent ML</title>
<link>http://docs.lib.purdue.edu/cstech/1731</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1731</guid>
<pubDate>Tue, 08 May 2012 08:41:00 PDT</pubDate>
<description>
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</description>

<author>Lukasz Ziarek et al.</author>


</item>


<item>
<title>Composable Asynchronous Events</title>
<link>http://docs.lib.purdue.edu/cstech/1730</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1730</guid>
<pubDate>Tue, 08 May 2012 08:40:52 PDT</pubDate>
<description>
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</description>

<author>Lukasz Ziarek et al.</author>


</item>


<item>
<title>The Impact of Content Courses on Pre-service Elementary Teachers’ Mathematical Content Knowledge</title>
<link>http://digitalcommons.unomaha.edu/tedfacpub/22</link>
<guid isPermaLink="true">http://digitalcommons.unomaha.edu/tedfacpub/22</guid>
<pubDate>Tue, 08 May 2012 08:40:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>In response to research documenting the mathematical deficiencies of pre-service elementary teachers, many teacher preparation programs are requiring mathematical content courses specifically focusing on the mathematics taught at the elementary level. This study considers what impact two such courses (one course focusing on Arithmetic, and the other course focusing on Geometry and Measurement) had on the mathematical content knowledge and attitude towards mathematics by comparing a group of pre-service elementary teachers who took these courses to a group of pre-service elementary teachers who took only a more general mathematics course (such as College Algebra). Results indicated that those teachers who took the specialized content courses had significantly higher mathematical content knowledge compared to those pre-service elementary teachers who took more general mathematics courses, but not significantly better attitudes towards mathematics.</p>

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</description>

<author>Michael Matthews et al.</author>


</item>


<item>
<title>FineComb: Measuring Microscopic Latencies and Losses in the Presence of Reordering</title>
<link>http://docs.lib.purdue.edu/cstech/1729</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1729</guid>
<pubDate>Tue, 08 May 2012 08:40:44 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Myungjin Lee et al.</author>


</item>


<item>
<title>Memory Indexing and its Use in Automated Debugging</title>
<link>http://docs.lib.purdue.edu/cstech/1728</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1728</guid>
<pubDate>Tue, 08 May 2012 08:40:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William Summer et al.</author>


</item>


<item>
<title>Revisiting Overlay Multicasting for the Cloud</title>
<link>http://docs.lib.purdue.edu/cstech/1727</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1727</guid>
<pubDate>Tue, 08 May 2012 08:40:28 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Karthik Nagaraj et al.</author>


</item>


<item>
<title>Correcting Bias in Statistical Tests for Network Classifier Evaluation</title>
<link>http://docs.lib.purdue.edu/cstech/1726</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1726</guid>
<pubDate>Tue, 08 May 2012 08:40:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jennifer Neville et al.</author>


</item>


<item>
<title>Generalizations with Probability Distributions for Data Anonymization</title>
<link>http://docs.lib.purdue.edu/cstech/1725</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/cstech/1725</guid>
<pubDate>Tue, 08 May 2012 08:40:12 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mehmet Ercan Nergiz et al.</author>


</item>


<item>
<title>Modeling Cardiac Muscle Mechanics</title>
<link>http://digitalrepository.trincoll.edu/theses/213</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/213</guid>
<pubDate>Tue, 08 May 2012 08:37:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The heart is a complex electro-mechanical system which is intrinsically and intimately linked to physiology and pathology. Cardiac muscle tissue underlies the dynamics of the heart; understanding cardiac muscle tissue allows insight into the working of the heart at a fundamental level. Indeed, models allow a theoretical understanding of systems which necessarily exceeds that of experiment. Here, we describe a novel mathematical model of cardiac muscle mechanics based on functional relations.</p>

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</description>

<author>Lorenzo Sewanan</author>


</item>


<item>
<title>Implementation of a Simultaneous Localization and Mapping Algorithm in an Autonomous Robot</title>
<link>http://digitalrepository.trincoll.edu/theses/212</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/212</guid>
<pubDate>Tue, 08 May 2012 08:37:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>A robot was built and programmed to implement a Simultaneous Localization and Mapping (SLAM) Algorithm. Traditional robotic mapping suffers from compounding sensor error, thus resulting in maps that become highly erroneous over time. SLAM combats this problem by taking a probabilistic approach to mapping. By combining odometry data with sensor measurements of surrounding landmarks through a Kalman Filter, the robot was able to accurately map its surrounding environment, and localize itself within that environment.</p>

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</description>

<author>Adam T. Norton et al.</author>


</item>


<item>
<title>The Benevolent Game: Soccer, a Tool for Community-Building in the Israeli-Palestinian Conflict</title>
<link>http://digitalrepository.trincoll.edu/theses/211</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/211</guid>
<pubDate>Tue, 08 May 2012 08:37:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Soccer, and other sports, has provided and will continue to be a tool for community building and peace making in the Israeli-Palestinian Conflict. This thesis will analyze the local, national and international efforts striving to provide the next generation living in conflict zones, specifically Israel, with the tools, skills and abilities needed to achieve the United Nations Millennium Development Goals of global development and peace. In order to understand these efforts, the reader will be provided with Israel’s recent history as well as the current status of the Israeli-Palestinian Conflict. This history and status will provide the context needed to help the reader appreciate how the Sport for Development and Peace Movement can positively effect the existing situation in Israel and the complex and problematic relationship between the Israelis and Palestinians.</p>
<p>Three case studies of Israeli grassroots organizations, the Peres Center for Peace, Mifalot and Football4Peace, shape the discussion surrounding the effectiveness of using soccer as a powerful tool to build a peaceful resolution to the Israeli-Palestinian Conflict. This thesis concludes with a discussion of the continued role soccer initiatives and other grassroots organizations must play in Israel to achieve a peaceful, co-existent society. The conclusions drawn in this thesis help the reader understand the usage of soccer as a tool and powerful division of the global “Sport for Development and Peace” movement at the local, national and international levels, in the hopes of supporting and furthering the efforts of the many grassroots soccer organizations and programs around the world.</p>

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</description>

<author>Lily F. Pepper</author>


</item>


<item>
<title>From Divestment to a Student Revolution: Trinity College and the Anti-Apartheid Movement</title>
<link>http://digitalrepository.trincoll.edu/theses/210</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/210</guid>
<pubDate>Tue, 08 May 2012 08:37:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>A few passionate students started what would become Trinity’s largest campus movement since the anti-Vietnam War protests in the late 1960’s and early 1970’s.<a title="">[1]</a> When I interviewed former students and professors, their memories of the anti-apartheid era flooded back. Some even recalled these moments as the most pivotal moments in their lives. In this paper, I will retract the claim that no students were involved at this monumental time and prove that Trinity students had always been engaged. In fact, the students of Trinity led the anti-apartheid movement at the college.</p>
<p>John F. Kennedy said “In giving rights to others which belong to them, we give rights to ourselves and our country.”<a title="">[2]</a> The fight against apartheid in South Africa was part of a global struggle against racism that emerged from the Civil Rights Movement. The students at Trinity fought for change in South Africa and simultaneously looked inward at racism in their own community. The Anti-Apartheid Committee (AAC) at Trinity made a significant contribution to the struggle for freedom and justice not only in South Africa but also in Hartford, Connecticut. The anti-apartheid struggle addressed issues of race in South Africa and structural racism in the United States. The student movement at Trinity was not solely for South Africa, but understanding and identifying Trinity’s relationship with the city of Hartford and transforming the student body. It was this activism that helped improve Trinity’s role in the greater Hartford community and alter the perceptions of students at Trinity.</p>
<p><a title="">[1]</a> Barry A. Freedman, “To Learn, To Remember,” <em>Trinity Tripod, </em>29 April 1986, 7.</p>
<p><a title="">[2]</a> Anthony St. Peter, <em>The Greatest Quotations of All-Time</em> (Anthony St. Peter, 2010), 128.</p>

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</description>

<author>Molly E. Cohen</author>


</item>


<item>
<title>Science diplomacy with swissnex China: A Swiss nation brand initiative</title>
<link>http://scholarship.rollins.edu/as_facpub/37</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/as_facpub/37</guid>
<pubDate>Tue, 08 May 2012 08:37:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Switzerland has a long tradition of expertise in the fields of science, research and education, with “science diplomacy” (SD) now assuming an important role for innovation economies. Past experience shows that international scientific cooperation can have valuable outcomes for the involved countries and complements traditional foreign policy and diplomacy. In Switzerland, a worldwide network of science and technology outposts under the auspices of the Swiss State Secretariat for Education and Research (SER) in cooperation with the Federal Department of Foreign Affairs (FDFA) was established in 2000. The very swissnex network around the world defines one of those established science diplomacy instruments.</p>
<p>In this article, we discuss the swissnex office in China, which acts both as a physical and virtual environment to foster closer ties between Switzerland and China in science and technology, innovation and culture. This case study examines the history and mission of swissnex China, its role and organizational structure, and reviews other nations’ comparable branding initiatives. The paper analyzes clients and partners as well as the main challenges for swissnex China during its three years of operation.</p>

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</description>

<author>Flavia Schlegel et al.</author>


</item>


<item>
<title>HIGH-RESOLUTION CORRELATION OF THE UPPER CRETACEOUS STRATIGRAPHY BETWEEN THE BOOK CLIFFS AND WESTERN HENRY MOUNTAINS SYNCLINE, UTAH, U.S.A.</title>
<link>http://digitalcommons.unl.edu/embargotheses/26</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/embargotheses/26</guid>
<pubDate>Tue, 08 May 2012 08:33:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study presents high-resolution correlations of the Upper Cretaceous stratigraphy between the Book Cliffs and the western Henry Mountains Syncline in Utah. The objective of this study is to understand changes in patterns of regional sediment dispersal during the Late Cretaceous on the western margin of the Cretaceous Western Interior Seaway. The intensely studied Book Cliffs consist of formations deposited in terrestrial, marginal-marine, and open-marine environments. A composite section was logged at Coal Canyon near Green River, UT. The western Henry Mountains Syncline is located in south-central Utah ~135 km S-SW of Coal Canyon. A composite section was logged at Blind Trail. High-resolution correlation between the Book Cliffs and Henry Mountains is not straightforward because the correlative interval in the Henry Mountains succession is highly condensed (~1015m) relative to the Book Cliffs succession (>1750m). This is in part due to their proximal vs. distal locations from the Sevier thrust front and unequal rates of accommodation creation caused by spatially variable subsidence and uplift patterns. Correlating at high-resolution from Coal Canyon to the Henry Mountains section poses similar challenges as correlating from the eastern Book Cliffs to the Wasatch Plateau because key stratigraphic surfaces in shallow-marine successions cannot necessarily be carried into coeval coastal plain strata up-depositional dip. Radiogenic isotope ages and biostratigraphic data provide age constraints on correlations between the Coal Canyon and Blind Trail sections. Correlations are based on vertical facies and depositional environmental stacking patterns, and changes in sediment dispersal directions at discrete stratigraphic horizons derived from 745 paleocurrent measurements. Recognition of these patterns suggest that the Muley Canyon Sst., Muley Canyon Coal Zone at the base of the Masuk Fm., and the Masuk Fm. correlate to the Star Point Fm., basal Blackhawk transgressive coal zones, and the Blackhawk Fm., respectively, in the Wasatch Plateau. These interpretations provide the means to then correlate the Henry Mountains and Book Cliffs sections as well as allowing pinning points that constrain correlations both up- and down-stratigraphic section.</p>
<p>Adviser: Christopher R. Fielding</p>

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</description>

<author>Drew L. Seymour</author>


</item>


<item>
<title>The Grinning Wall: History, Exhibition, and Application of the Hyrtl Skull Collection at the Mutter Museum</title>
<link>http://scholarship.shu.edu/theses/212</link>
<guid isPermaLink="true">http://scholarship.shu.edu/theses/212</guid>
<pubDate>Tue, 08 May 2012 08:31:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sara K. Keckeisen</author>


</item>


<item>
<title>Suzaku Observations of Diffuse X-ray Emission From the Carina Nebula</title>
<link>http://digitalcommons.olin.edu/facpub_2007/23</link>
<guid isPermaLink="true">http://digitalcommons.olin.edu/facpub_2007/23</guid>
<pubDate>Tue, 08 May 2012 08:30:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>We studied extended X-ray emission from the Carina Nebula taken with the Suzaku CCD camera XIS on 2005 August 29. The X-ray morphology, plasma temperature, and absorption to the plasma are consistent with the earlier Einstein results. The Suzaku spectra newly revealed emission lines from various species, including oxygen, but not from nitrogen. This result restricts the N/O ratio to be significantly low, compared with evolved massive stellar winds, suggesting that the diffuse emission originated in an old supernova remnant or a super shell produced by multiple supernova remnants. The X-ray spectra from the north and south of eta Car showed distinct differences between 0.3-2 keV. The south spectrum shows strong L-shell lines of iron ions and K-shell lines of silicon ions, while the north spectrum shows them weak in intensity. This means that the silicon and iron abundances are a factor of 2-4 higher in the south region than in the north region. The abundance variation may be produced by an SNR ejecta, or related to dust formation around the star-forming core.</p>

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</description>

<author>Kenji Hamaguchi et al.</author>


</item>


<item>
<title>Fogler Favorites - Communication and Mass Media Complete</title>
<link>http://digitalcommons.library.umaine.edu/faves/7</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/7</guid>
<pubDate>Tue, 08 May 2012 08:28:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series. Laura Lindenfeld’s Fogler Favorite is Communication and Mass Media Complete.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Journal Toolkit</title>
<link>http://fordham.bepress.com/lib_resources/4</link>
<guid isPermaLink="true">http://fordham.bepress.com/lib_resources/4</guid>
<pubDate>Tue, 08 May 2012 08:23:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jeremy Watson</author>


</item>


<item>
<title>Chandra Spatially Resolved Spectroscopic Study and Multiwavelength Imaging of the Supernova Remnant 3C 397 (G41.1-0.3)</title>
<link>http://digitalcommons.olin.edu/facpub_2005/18</link>
<guid isPermaLink="true">http://digitalcommons.olin.edu/facpub_2005/18</guid>
<pubDate>Tue, 08 May 2012 08:23:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present a Chandra observation of the supernova remnant (SNR) 3C 397 (G41.1-0.3) obtained with the Advanced CCD Imaging Spectrometer (ACIS-S). Previous studies of this SNR have shown that the remnant harbors a central X-ray "hot spot'' suggestive of a compact object associated with 3C 397. With the Chandra data, we can rule out the nature of the hot spot as a pulsar or a pulsar wind nebula and put an upper limit on the flux of a hidden compact object of F-X(0.5-10 keV) similar to6 x 10(13) ergs cm(-2) s(-1). We found two point sources in the observed Chandra field. We argue that neither of them is associated with 3C 397 and that the hard source, CXO J190741.2+070650, which is characterized by a heavily absorbed spectrum with a strong Fe line, is a newly discovered active galactic nucleus. The Chandra image reveals arcsecond-scale clumps and knots that are strongly correlated with the radio VLA image, except for the X-ray hot spot. Our Chandra spatially resolved spectroscopic study shows that one-component models are inadequate and that at least two nonequilibrium ionization thermal components are needed to fit the spectra of each selected region. The derived average spectral parameters are consistent with the previous global ASCA fits performed by Safi-Harb and coworkers. However, the hard component requires a high abundance of Fe indicating the presence of hot Fe ejecta. When comparing the eastern with the western lobe, we find that the column density, the brightness, and the ionization timescales are generally higher for the western side. This result, combined with our study of the 3C 397 environs at millimeter wavelengths, indicates a denser medium to the west of the SNR. Our multiwavelength imaging and spectral study favors the scenario in which 3C 397 is a similar to5300 year old SNR expanding in a medium with a marked density gradient and is likely to be encountering a molecular cloud on the western side. We propose that 3C 397 will evolve into a mixed-morphology SNR.</p>

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</description>

<author>S Safi-Harb et al.</author>


</item>


<item>
<title>The New Techie: The Times They Are A-Changing, and Techies Along with Them</title>
<link>http://digitalcommons.unomaha.edu/tedfacpub/21</link>
<guid isPermaLink="true">http://digitalcommons.unomaha.edu/tedfacpub/21</guid>
<pubDate>Tue, 08 May 2012 08:22:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>It’s great to be a former English teacher working in the world of technology — although it hasn’t always been pretty. When I first started working in technology (in the late 1980s), techies greeted me with wary disdain. I didn’t know the lingo, I didn’t live to be the first to know about the next hardware release, and my idea of a good time on Saturday night was to spend time with a warm, breathing being, not a keyboard and a screen. Furthermore, I was much too verbal, too in-your-face. I lacked that certain je ne c’est quoi, that cool detachment so apparent in most techies with whom I worked at the beginning of this adventure.</p>

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</description>

<author>Melodee Landis</author>


</item>


<item>
<title>Evaluating the Efficacy of Training Programs for Community Health Workers in Rural Uganda</title>
<link>http://escholarship.umassmed.edu/ssp/127</link>
<guid isPermaLink="true">http://escholarship.umassmed.edu/ssp/127</guid>
<pubDate>Tue, 08 May 2012 08:22:20 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Background: </strong>The Ministry of Health and Omnimed, a non-profit U.S.-based organization that works with international communities to provide basic health education, have partnered to provide health training to community health workers (henceforth referred to as village health workers or VHWs) in rural villages in Uganda. The training is provided via an intensive five-day long session that introduces a wide variety of themes in basic health education taught by experts in the respective fields. The participants are selected by the local government based on their age, reliability, level of education and availability. On the first day, the participants are given a pre-test that evaluates their level of knowledge about the subjects that will be taught during the training session, and are given the same questions as a post-test on the last day of training. This is done to evaluate how much information the participants learned about basic health during the training. The participants are followed after this training by quarterly meetings, focus groups and further, more specific, training sessions. We analyzed data from the pre- and post-tests to evaluate the amount of information learned through the training sessions and we also evaluated feedback from the focus groups to determine how trainees thought the program was affecting their community and to analyze the challenges facing the VHWs.</p>
<p><strong>Objectives: </strong>The objective of this project was two-fold: 1) to evaluate the amount of information about basic health retained by VHWs who participated in a week-long training session; and 2) to follow-up with VHWs to see what changes they noticed in their communities and determine what challenges they face in disseminating health information in their villages.</p>
<p><strong>Methods: </strong>The study sample consisted of 110 participants who were asked to complete the pre- and post-tests. The pre- and post-training test consisted of 49 multiple choice questions, written in Luganda, with a total possible score of 105. The pre-test was distributed to the participants on the first day of the training session. Participants were administered post-tests on the last day of the training session. The questions and the delivery of the exams were the same at both points in time. The grading of the tests was as follows: each correct answer received one point, incorrect answers received no points, and questions with more than one answer received no points. We compared the percentage of correct answers of the pre- and post-tests to determine any changes in knowledge as a result of the training session.</p>
<p>A total of 99 trainees were recruited to participate in focus groups. Focus groups were conducted three and six months after the original training session and involved five to ten VHWs per session. Questionnaires were distributed to the groups and questions were read aloud with discussion about each topic. We asked the VHWs: 1) Have you noticed healthy changes in your community?; 2) What changes have you noticed; 3) How does the community view a VHW?; and 4) What support could you use as a VHW?</p>
<p><strong>Results: </strong>The VHWs selected from the communities were aged 25-40, were more likely to be female than male, and generally had a non-health related occupation. One hundred and two participants completed both the pre- and post-tests. The average difference between test scores at the two points in time was an improvement of 20.25 points, or 19.3%. The range of differences between the scores was -5 to +61. Given that the VHWs were not previously educated about basic health, this was viewed a marginal improvement. However, the data from the focus groups indicates that the VHWs were enacting changes in their community. The participants in the focus group were also aged 25-40 and 43 were males and 56 were females.</p>
<p>The focus groups demonstrated that 86% of the VHWs noticed positive changes in the community; including the creation of latrines (34%), more drying racks (16%), more hand-washing (11%), increased usage of boiled water (9%) and the newfound creation and usage of “tippy-taps” (8%). When asked if the community viewed the VHWs as a positive asset, 81% answered yes. Lastly, when queried as to what support VHWs could use to facilitate their work, the majority answered some type of transport (51%); while other popular answers were gumboots and raingear, more training, cell phones or a stipend to compensate them for their work.</p>
<p><strong>Conclusion: </strong>The increased mean score of the post-tests indicates that the VHWs did learn basic health information during the training session. However, the improvement in score was not as notable as one would expect given the intense nature of the trainings and the baseline level of knowledge being somewhat low. The data from the focus groups, however, indicated that VHWs are creating positive change in their communities. This could mean that the simple act of appointing one person to educate their community imbues in them a responsibility to spread the knowledge that they do possess; however basic it may be. It also could indicate that the VHWs learned more at the training sessions than the test scores reveal. This could be due to a multitude of factors, including difficulty with reading, the advanced nature of the test questions, difficulty with multiple choice questions, or difficulty applying knowledge to the test, especially considering that most of the VHWs were adults many years out of school. In light of this information, one could consider a different method of evaluation, and more focus on the follow-up to assess what the VHWs are actually able to do in their communities. Moving forward, it would be ideal to evaluate the villages themselves via a system of door-to-door surveys that ask the villagers about changes they have or have not made and if they have seen any improvement in their health. This information will provide further evidence as to whether VHWs are an ideal model in the field of health education.</p>

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</description>

<author>Elizabeth Butler et al.</author>


<category>Community Health Workers</category>

<category>Health Education</category>

<category>Inservice Training</category>

<category>Uganda</category>

</item>


<item>
<title>Gestational Weight Gain Prior to Glucola and Risk of Gestational Diabetes Mellitus</title>
<link>http://escholarship.umassmed.edu/ssp/126</link>
<guid isPermaLink="true">http://escholarship.umassmed.edu/ssp/126</guid>
<pubDate>Tue, 08 May 2012 08:22:18 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Background</strong>: Gestational diabetes mellitus (GDM) complicates 4–7% of U.S. pregnancies. Diabetes and obesity rates are consistently higher in Hispanics compared to non-Hispanic whites. Early-to-mid gestational weight gain (GWG) has been thought to be associated with GDM risk; however, the Institute of Medicine (IOM) found insufficient evidence when re-examining GWG guidelines in 2009.</p>
<p><strong>Objective</strong>: To investigate associations of GWG adherence per 2009 IOM guidelines prior to 1-hr 50g Glucose Tolerance Test (GTT), or glucola, with GDM diagnoses in Latinas.</p>
<p><strong>Methods</strong>: The study is a retrospective chart review of all Hispanic women delivered by UMass Memorial faculty between 4/1/06-3/31/11 and received prenatal care at faculty-resident practices (n=1163). Pre-pregnancy weight and height, weight and gestational age (GA) most proximate to glucola and 100g GTT where appropriate, lab results and relevant demographics were abstracted. Weight gain was categorized as inadequate, appropriate or excessive according to 2009 IOM Guidelines with adjustment for gestational age. Mean and standard deviation (SD) and frequency measures reported for continuous and categorical variables, respectively. Comparisons were evaluated with chi-squared tests with statistical significance set at p<0.05.</p>
<p><strong>Results</strong>: Data for 1115 subjects was analyzed. Preliminary cohort was mean age 25.3 years (sd±6.0), mean gravidity 2.8 (sd±1.8) and 72.1% English and 26.4% Spanish-speaking. Eleven subjects excluded for pregestational diabetes. BMI calculable for 858 subjects (5.4% underweight, 40.3% normal, 26.0% overweight and 28.3% obese); 70 subjects missing GWG prior to glucola. Seven hundred eighty-eight subjects had complete data, on which remainder of analyses were performed. By 2009 IOM guidelines, 174 (22.1%), 193 (24.5%) and 421 (53.4%) gained inadequately, appropriately and excessively as per BMI criteria, respectively. Overall, 86 of 788 diagnosed with GDM (10.9%). According to weight gain adherence, 14 of 174 (8.0%) inadequate-gainers, 20 of 193 (10.4%) appropriate-gainers and 52 of 421 (12.4%) excessive-gainers were diagnosed with GDM. Of subjects with GDM diagnosis (n=86), 16.3%, 23.3% and 60.5% were inadequate, appropriate and excessive-gainers, respectively. Compared to appropriate gainers, the crude odds ratio and 95% CI for GDM diagnosis was 1.22 (0.71-2.11) for excessive-gainers and 0.76 (0.37-1.55) for inadequate-gainers. No statistically significant association between pre-glucola GWG and GDM detected (p=0.3).</p>
<p><strong>Conclusion</strong>: The rate of GDM in this cohort of Latina women is almost double that of the general population. Though no statistically significant association was identified, the majority of patients diagnosed with GDM were classified as excessive-gainers as per pre-glucola GWG adherence. The trend warrants further evaluation of this population at increased risk for GDM as well as analysis within high-risk subgroups.</p>

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</description>

<author>Anna BuAbbud et al.</author>


<category>Pregnancy Complications</category>

<category>Diabetes, Gestational</category>

<category>Weight Gain</category>

<category>Glucose Tolerance Test</category>

<category>Hispanic Americans</category>

</item>


<item>
<title>New Nurse Residency - An Evidence Based Approach</title>
<link>http://digitalcommons.unf.edu/etd/197</link>
<guid isPermaLink="true">http://digitalcommons.unf.edu/etd/197</guid>
<pubDate>Tue, 08 May 2012 08:19:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nurse educators believe that their graduates are well-prepared for entry level positions in nursing. In the acute healthcare setting, new graduates are placed on virtually every type of nursing unit, including critical care. Employers have developed formal orientations to familiarize new graduate nurses new with the institution and its policies and procedures and to teach the things employers believe new RNs need to know but do not, either because they were never taught the material or they have not retained it.</p>
<p>The purposes of this project were to (a) examine the evidence relative to a disconnect between nursing education and nursing practice, (b) design a formal residency program for new graduates based on the evidence, and (c) implement and evaluate the residency program. Based on the evidence, a 16-week new nurse residency was developed in which Residents were each assigned both a Preceptor and Mentor to assist their progress. Weekly educational offerings were targeted at specific competency deficits identified by Residents, Preceptors and Mentors at the beginning of the residency program.</p>
<p>Seven out of the original 10 Residents completed the Residency. Pre-residency, the Residents were very confident of their clinical skills and abilities and this was unchanged post-residency. The Preceptors and Mentors were much less confident of the clinical skills and abilities of the Residents pre-residency. Post-residency, the confidence level of the Preceptors and Mentors was improved, but significantly so only for the Mentors.</p>
<p>It is imperative that nursing administrators be aware of the discrepancy between the confidence new nurses have in their own skills and the perceptions of the nurses who work side by side with them on a daily basis. Residencies for new graduate nurses are costly. Nursing administrators must make the determination if the benefits outweigh the costs. They may find the results of not having a residency are far more costly.</p>

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</description>

<author>Alice M. Nied</author>


</item>


<item>
<title>Leprosy Flees Him</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/379</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/379</guid>
<pubDate>Tue, 08 May 2012 08:19:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Timothy C. Tennent</author>


</item>


<item>
<title>Education and Training of Future Wetland Scientists</title>
<link>http://digitalcommons.brockport.edu/env_facpub/44</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/44</guid>
<pubDate>Tue, 08 May 2012 08:17:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Wetland science emerged as a distinct discipline in the 1980s. In response, courses addressing various aspects of wetland science and management were developed by universities, government agencies, and private firms. Professional certification of wetland scientists began in the mid-1990s to provide confirmation of the quality of education and experience of persons involved in regulatory, management, restoration/construction, and research involving wetland resources. The education requirements for certification and the need for persons with specific wetland training to fill an increasing number of wetland-related positions identified a critical need to develop curriculum guidelines for an undergraduate wetland science and management major for potential accreditation by the Society of Wetland Scientists. That proposed major contains options directed toward either wetland science or management. Both options include required basic courses to meet the general education requirements of many universities, required upper-level specialized courses that address critical aspects of physical and biological sciences applicable to wetlands, and a minimum of four additional upper-level specialized courses that can be used to tailor a degree to students’ interests. The program would be administered by an independent review board that would develop guidelines and evaluate university applications for accreditation. Students that complete the required coursework will fulfill the education requirements for professional wetland scientist certification and possess qualifications that make them attractive candidates for graduate school or entry level positions in wetland science or management. Universities that offer this degree program could gain an advantage in recruiting highly qualified students with an interest in natural resources. Alternative means of educating established wetland scientists are likewise important, especially to provide specialized knowledge and experience or updates related to new management discoveries, policies, and regulations.</p>

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</description>

<author>Douglas A. Wilcox</author>


</item>


<item>
<title>The Investigation of Uniform, Monodisperse Crystalline Particles via the Evaporation of Small Droplets</title>
<link>http://digitalcommons.bucknell.edu/masters_theses/73</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/masters_theses/73</guid>
<pubDate>Tue, 08 May 2012 08:16:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many industrial solids processes require the production of disperse particles. In industries such as food, personal care, and pharmaceuticals, particle formation is widely used to produce solid products or to separate substances in intermediate process steps. The most important characteristics known to impact the effectiveness of a solid product are purity, size, internal structure, and morphology. These characteristics are essential to maintain optimal operation of subsequent process steps and for obtaining the desired high quality product. This thesis aims to aid in the advancement of particle production technology by (1) investigating the use of a vibrating orifice aerosol generator (VOAG) for collecting data to predict particle attributes including morphology, size, and internal structure as a function of processing parameters such as solvent, solution concentration, air flow rate, and initial droplet size, as well as to (2) determine the extent to which uniform droplet evaporation can be a tool to achieve novel particle morphologies, controlled sizes, or internal structures (crystallinity and crystal form). Experimental results for succinic acid, L-serine, and L-glutamic acid suggest that particles of controlled characteristics can indeed be produced by this method. Analysis by scanning electron microscopy (SEM), nanoindentation, and X-ray diffraction (XRD) shows that various sizes, internal structures, and morphologies can be obtained using the VOAG. Furthermore, unique morphologies and unexpected internal structures were able to be achieved for succinic acid, providing an added benefit to particle formation by this method.</p>

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</description>

<author>Kelly M. Carver</author>


</item>


<item>
<title>You have full text access to this content (E)-9,10-Dihydro-9-methyl-9-nitro-10-(trinitro­meth­yl)anthracene</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/4</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/4</guid>
<pubDate>Tue, 08 May 2012 08:13:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The title compound, C<sub>16</sub>H<sub>12</sub>N<sub>4</sub>O<sub>8</sub>,  was prepared by the photochemical reaction of 9-methyl­anthracene and  tetra­nitro­methane in dichloromethane. Intermolecula face-to-face π–π  stacking inter­actions are present along the <em>a</em> axis.</p>

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</description>

<author>Mustafa Arslan et al.</author>


</item>


<item>
<title>Fat is a Feminist Issue, but it is Complicated: Commentary on Fikkan and Rothblum</title>
<link>http://digitalcommons.hope.edu/faculty_publications/432</link>
<guid isPermaLink="true">http://digitalcommons.hope.edu/faculty_publications/432</guid>
<pubDate>Tue, 08 May 2012 08:13:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Fikkan and Rothblum (2011) review the literature on discrimination and bias against overweight and obese (fat) women. They provide convincing evidence that fat women face discrimination in the workplace, are treated disparately in medical, mental health, and educational settings, are at a disadvantage in social and romantic situations, and are either absent or portrayed negatively in the media. They conclude with the observation that feminists have largely ignored this issue that disproportionately affects women. While I agree that fat is a feminist issue, I also argue that the issue of gender differences in the experience of weight discrimination is more complicated than suggested in the Fikkan and Rothblum review. The commentary concludes with some possible explanations for why feminists have neglected this issue, emphasizing the historical changes in the feminist movement which have taken the focus off of issues primarily related to White middle-class women.</p>

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</description>

<author>Patricia V. Roehling</author>


</item>


<item>
<title>International Service-Learning and the Development of Civic Identity: Understanding the Role of Short-Term International Service-Learning and its Influence on the Development of Civic Identity in College Students Using a Mixed Methodological Approach</title>
<link>http://digitalcommons.bucknell.edu/masters_theses/72</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/masters_theses/72</guid>
<pubDate>Tue, 08 May 2012 08:12:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Higher education has a responsibility to educate a democratic citizenry and recent research indicates civic engagement is on the decline in the United States. Through a mixed methodological approach, I demonstrate that the potential exists for well structured short-term international service-learning programming to develop college students’ civic identities. Quantitative analysis of questionnaire data, collected from American college students immediately prior to their participation in a short-term service-learning experience in Northern Ireland and again upon their return to the United States, revealed increases in civic accountability, political efficacy, justice oriented citizenship, and service-learning. Subsequent qualitative analysis of interview transcripts, student journals, and field notes suggested that facilitated critical reflection before, during, and after the experience promoted transformational learning. Emergent themes included: (a) responsibilities to others, (b) the value of international service-learning, (c) crosspollination of ideas, (d) stepping outside the daily routine to facilitate divergent thinking, and (e) the necessity of precursory thinking for sustaining transformations in thinking. The first theme, responsibilities to others, was further divided into subthemes of thinking beyond oneself, raising awareness of responsibility to others, and voting responsibly.</p>

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</description>

<author>Jennifer B. Lassahn</author>


</item>


<item>
<title>A Method for Assessing the Sustainability of Design in Developing World Projects</title>
<link>http://digitalcommons.bucknell.edu/masters_theses/71</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/masters_theses/71</guid>
<pubDate>Tue, 08 May 2012 08:12:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Projects for the developing world usually find themselves at the bottom of an engineer’s priority list. There is often very little engineering effort placed on creating new products for the poorest people in the world. This trend is beginning to change now as people begin to recognize the potential for these projects. Engineers are beginning to try and solve some of the direst issues in the developing world and many are having positive impacts. However, the conditions needed to support these projects can only be maintained in the short term. There is now a need for greater sustainability.</p>
<p>Sustainability has a wide variety of definitions in both business and engineering. These concepts are analyzed and synthesized to develop a broad meaning of sustainability in the developing world. This primarily stems from the “triple bottom line” concept of economic, social, and environmental sustainability. Using this model and several international standards, this thesis develops a metric for guiding and evaluating the sustainability of engineering projects. The metric contains qualitative questions that investigate the sustainability of a project. It is used to assess several existing projects in order to determine flaws. Specifically, three projects seeking to deliver eyeglasses are analyzed for weaknesses to help define a new design approach for achieving better results.</p>
<p>Using the metric as a guiding tool, teams designed two pieces of optometry equipment: one to cut lenses for eyeglasses and the other to diagnose refractive error, or prescription. These designs are created and prototyped in the developed and developing worlds in order to determine general feasibility. Although there is a recognized need for eventual design iterations, the whole project is evaluated using the developed metric and compared to the existing projects. Overall, the success demonstrates the improvements made to the long-term sustainability of the project resulting from the use of the sustainability metric.</p>

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</description>

<author>Adam Andersen</author>


</item>


<item>
<title>Analyzing an Urban University&apos;s Diversity Dilemma</title>
<link>http://digitalcommons.unomaha.edu/tedfacpub/20</link>
<guid isPermaLink="true">http://digitalcommons.unomaha.edu/tedfacpub/20</guid>
<pubDate>Tue, 08 May 2012 08:12:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lack of diversity in the teaching force is proving to be a grievous problem for our country. Across the nation the percentage of teachers of color in our schools remains stagnant as the percentage of students of color increases (Gay, Dingus & Jackson, 2003; Gordon, 2000; Gursky, 1999). Councils have been convened and conferences held to confront the issue (National Collaborative on Diversity in the Teaching Force, 2004). This disparity between the supply and demand for a diverse teaching force not only violates our standards of equity, it also appears to have a deleterious effect on achievement of students, particularly those of color (Gay, Dingus & Jackson, 2003; Hurtado, 1996). Growing awareness of this problem is strengthening the resolve of many educators to find ways to recruit persons of color to the teaching force in their region or community. The problem proves to be more complex than meets the eye, however. The causes are deeply rooted, requiring careful analysis of the cultural character of each specific community (Gordon, 2000). An additional complication stems from the fact that the majority of the United States teachers and administrators are of European descent, and may have little insight into the reasons young people of color don't select teaching as a career. Without that understanding, it is difficult for them to create successful programs to recruit people of color.</p>

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</description>

<author>Melodee Landis et al.</author>


</item>


<item>
<title>Eurotech Students in Germany: Preparation, Experience and Outcome</title>
<link>http://digitalcommons.uconn.edu/gs_theses/241</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/241</guid>
<pubDate>Tue, 08 May 2012 08:10:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Higher education study abroad programs for U.S. students are on the rise. A variety of undergraduate disciplines are being coupled with international components to bring U.S. students to a higher level of global awareness to meet the demands of today’s economy. The University of Connecticut’s Eurotech Program is an example of this trend. Its students earn degrees in both German and engineering in a five year program. They are given practical training through study and internships in Germany under the auspices of the Baden-Württemberg Exchange Program. One of the Eurotech Program’s major goals is to enhance job opportunities for its graduates by giving them the linguistic and cultural skills to interact with German engineers in the U.S. and Germany and thereby making them more attractive to employers. The study includes an overview of the Eurotech Program, a survey of literature concerning study abroad goals and the collection and analysis of data from former and current participants of the program through their responses on questionnaires. The study highlights the achievements of the program’s goals as the Eurotech students see them.</p>

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</description>

<author>Daisy A. Michaels</author>


</item>


<item>
<title>Suzaku Observations of Tycho&apos;s Supernova Remnant</title>
<link>http://digitalcommons.olin.edu/facpub_2009/18</link>
<guid isPermaLink="true">http://digitalcommons.olin.edu/facpub_2009/18</guid>
<pubDate>Tue, 08 May 2012 08:08:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Tycho's supernova remnant was observed by the XIS and HXD instruments onboard the Suzaku satellite on 2006 June 26-29 for 92 ks. The spectrum up to 30 keV was well fitted with a two-component model, consisting of a power-law with a photon index of 2.7 and a thermal bremsstrahlung model with a temperature of 4.7 keV. The former component can alternatively be modeled as synchrotron emission from a population of relativistic electrons with an estimated roll-off energy of around 1 keV. In the XIS spectra, in addition to the prominent Fe K alpha line (6.445 keV), we observed for the first time significant K alpha line emission from trace species Cr and Mn at energies of 5.48 keV and 5.95 keV, respectively. Faint K beta lines from Ca (4.56 keV) and Fe (7.11 keV) were also seen. The ionization states of Cr and Mn, based on their line centroids, Lire estimated to be similar to that of Fe K alpha (Fe XV or XVI).</p>

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</description>

<author>Toru Tamagawa et al.</author>


</item>


<item>
<title>The Impact of Gender and Pedagogy on the Development of Self-Regulated Learning Strategies in Undergraduate Engineering Classrooms</title>
<link>http://digitalcommons.bucknell.edu/masters_theses/70</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/masters_theses/70</guid>
<pubDate>Tue, 08 May 2012 08:07:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this paper is to examine ways in which pedagogy and gender of instructor impact the development of self-regulated learning strategies as assessed by the Motivated Strategies for Learning Questionnaire (MSLQ) in male and female undergraduate engineering students. Pedagogy was operationalized as two general formats: lecture plus active learning techniques or problem-base/project-based learning. One hundred seventy-six students from four universities participated in the study. Within-group analyses found significant differences with regard to pedagogy, instructors’ gender, and student gender on the learning strategies and motivation subscales as operationalized by the MSLQ. Male and females students reported significant post-test differences with regard to the gender of instructor and the style of pedagogy. The results of this study showed a pattern where more positive responses for students of both genders were found with the same-gendered instructor. The results also suggested that male students responded more positively to project and problem-based courses with changes evidenced in motivation strategies and resource management. Female students showed decreases in resource management in these two types of courses. Further, female students reported increases in the lecture with active learning courses.</p>

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</description>

<author>Jennifer Walter</author>


</item>


<item>
<title>Gatekeepers of legal information: evaluating and integrating free internet legal resources into the classroom</title>
<link>http://iris.lib.neu.edu/slaw_fac_pubs/92</link>
<guid isPermaLink="true">http://iris.lib.neu.edu/slaw_fac_pubs/92</guid>
<pubDate>Tue, 08 May 2012 08:05:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>This Article provides a new analytical tool for legal researchers and practitioners to evaluate free or low-cost Internet resources. Since the global financial crisis has discouraged legal researchers and practitioners from accessing high-cost databases and has encouraged increased reliance on free or low-cost Internet resources, it is important now to establish appropriate evaluation standards for free or low-cost Internet resources. The author believes that evaluation standards based on authority, accuracy, currency, coverage, and usability are necessary for legal instructors in order to safely introduce these resources into their classrooms. <br><br></p>

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</description>

<author>Jootaek Lee</author>


</item>


<item>
<title>Writing the Unspeakable: an Ethical Approach to a Traumatized Narrative</title>
<link>http://digitalcommons.bucknell.edu/masters_theses/69</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/masters_theses/69</guid>
<pubDate>Tue, 08 May 2012 08:02:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>This project uses the works of contemporary author Tim O’Brien, whose fiction often performs the trauma of the Vietnam War, to explore new ways of encountering the traumatized text. Informed by Emmanuel Levinas’s ethics of the face, and Sigmund Freud’s and Dominick LaCapra’s work on the narratology of the melancholic and the mourner, I consider the different ways we respond to the suffering Other and explore the paradox that through reading a traumatized narrative empathically we may come face-toface, as it were, with the suffering Other. If this is indeed the case, I reason, then the obligations that are due to the Other are also due to the text itself.</p>

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</description>

<author>Catrina Joos</author>


</item>


<item>
<title>Systemic Functional Linguistic Discourse Features in the Personal Essay</title>
<link>http://mds.marshall.edu/etd/216</link>
<guid isPermaLink="true">http://mds.marshall.edu/etd/216</guid>
<pubDate>Tue, 08 May 2012 08:01:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this thesis is to look at published and student-produced creative writing, more specifically, personal essays, through the lens of discourse analysis theories in Systemic Functional Linguistics (SFL). From the analysis of these personal essays, this thesis provides pedagogical insight concerning the linguistic features that are prevalent in published and student personal essays. Although research has been conducted looking at academic student writing through the lens of SFL, little research has been conducted looking specifically at the elements that make up pieces of creative writing. In fact, Blythe and Sweet (2008), with over seventy years of experience teaching creative writing, question whether or not good creative writing can even be explicitly taught. Although creative writing is, by its nature, creative, and therefore artful, the effective (or ineffective) use of language in a text can be analyzed through the lens of SFL. This thesis examines a model personal essay and student-produced personal essays through the lens of four discourse analysis theories in SFL: appraisal, identification, ideation, and conjunction. These theories are then paired with common global issues cited as problematic in creative texts—focus, flow, and voice—in order to demonstrate that issues that seemingly deal with content can be analyzed in the grammar of a text.</p>

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</description>

<author>Anna Jones Rollins</author>


<category>&lt;p&gt;Creative writing (Higher education)&lt;/p&gt;</category>

</item>


<item>
<title>9-Ethyl-3-Methyl-1, 6-Dinitrocarbazole</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/3</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/3</guid>
<pubDate>Tue, 08 May 2012 08:01:41 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Erol Asker et al.</author>


</item>


<item>
<title>Development and Evaluation of a Mouse Neocortical Cells Neurodevelopment Assay to Assess the Effects of Pyrethroids</title>
<link>http://escholar.salve.edu/pell_theses/80</link>
<guid isPermaLink="true">http://escholar.salve.edu/pell_theses/80</guid>
<pubDate>Tue, 08 May 2012 08:00:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pyrethroid insecticides have been used for more than 40 years and account for 25% of the global insecticide market with household, agricultural and public health applications. With increasing use of pyrethroids over recent years, human exposure to these chemicals is likely. The acute toxicity of pyrethroids to mammalian adults has been documented as moderately toxic by the U.S. Environmental Protection Agency. However, little evidence is available regarding the potential toxicological effects of pyrethroids on mammalian neurodevelopment. In this study, a neurodevelopment assay was developed for future investigation of potential pyrethroid effects on the neuronal development of Mus musculus neocortical cells.</p>

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</description>

<author>Stephanie I. Savino</author>


</item>


<item>
<title>The Suzaku High Resolution X-ray Spectrometer</title>
<link>http://digitalcommons.olin.edu/facpub_2007/22</link>
<guid isPermaLink="true">http://digitalcommons.olin.edu/facpub_2007/22</guid>
<pubDate>Tue, 08 May 2012 08:00:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>The X-Ray Spectrometer (XRS) has been designed to provide the Suzaku Observatory with non-dispersive, high-resolution X-ray spectroscopy. As designed, the instrument covers the energy range 0.3 to 12 keV, which encompasses the most diagnostically rich part of the X-ray band. The sensor consists of a 32-channel array of X-ray microcalorimeters, each with an energy resolution of about 6 eV. The very low temperature required for operation of the array (60 mK) is provided by a four-stage cooling system containing a single-stage adiabatic demagnetization refrigerator, a superfluid-helium cryostat, a solid-neon dewar, and a single-stage, Stirling-cycle cooler. The Suzaku/XRS is the first orbiting X-ray microcalorimeter spectrometer and was designed to last more than three years in orbit. The early verification phase of the mission demonstrated that the instrument worked properly and that the cryogen consumption rate was low enough to ensure a mission lifetime exceeding 3 years. However, the liquid-He cryogen was completely vaporized two weeks after opening the dewar guard vacuum vent. The problem has been traced to inadequate venting of the dewar He and Ne gases out of the spacecraft and into space. In this paper we present the design and ground testing of the XRS instrument, and then describe the in-flight performance. An energy resolution of 6 eV was achieved during pre-launch tests and a resolution of 7 eV was obtained in orbit. The slight degradation is due to the effects of cosmic rays.</p>

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</description>

<author>Richard L. Kelley et al.</author>


</item>


<item>
<title>The X-ray Observatory Suzaku</title>
<link>http://digitalcommons.olin.edu/facpub_2007/21</link>
<guid isPermaLink="true">http://digitalcommons.olin.edu/facpub_2007/21</guid>
<pubDate>Tue, 08 May 2012 08:00:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>High-sensitivity wide-band X-ray spectroscopy is the key feature of the Suzaku X-ray observatory, launched on 2005 July 10. This paper summarizes the spacecraft, in-orbit performance, operations, and data processing that are related to observations. The scientific instruments, the high-throughput X-ray telescopes, X-ray CCD cameras, non-imaging hard X-ray detector are also described.</p>

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</description>

<author>Kazuhisa Mitsuda et al.</author>


</item>


<item>
<title>Microwave-Assisted Phospha-Michael Reactions with Internal Alkenes</title>
<link>http://digitalcommons.bucknell.edu/masters_theses/68</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/masters_theses/68</guid>
<pubDate>Tue, 08 May 2012 07:58:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The atom efficient phospha-Michael reaction between bis 4-methylphenyl phosphine oxide and several activated internal alkenes has been shown to occur under microwave irradiation without added solvent or catalyst. The alkenes used for this study were ethyl 4-nitrocinnamate, two chalcones ((E)-3-(4-methoxy-phenyl)-1-(4- nitrophenyl)-prop-2-en-1-one and (E)-1-(4-methoxyphenyl)-3-(3-nitro-phenyl)-prop-2- en-1-one), and 2-phenylmethylene-propanedinitrile. In the case of ethyl 4-nitrocinnamate, reaction with bis 4-methylphenyl phosphine oxide for sixty minutes at 130 °C yielded the desired phospha-Michael product in a 55% yield after purification. Varying the location of the nitro group on the phenyl rings of the chalcones did not seem to have a large effect on their reactivity. By NMR, both chalcones seemed to react to the same extent when the reaction times and temperatures were held constant. Interestingly, a phospha-Michael reaction was observed at a reaction temperature of 65°C for experiments involving 2- phenyl-methylene-propanedinitrile while the other substrates required a reaction temperature of 130 °C. Similar experiments were carried out with bis mesityl phosphine oxide and two internal alkenes: 2-phenylmethylene-propanedinitrile and ethyl-2-cyano-3- methyl-2-butenoate. These experiments did not yield any of the predicted phospha- Michael products, which suggest steric limitations to the Michael donor for this reaction.</p>

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</description>

<author>Timothy Bergeron</author>


</item>


<item>
<title>Nature, Poetry, and Liminality in the Poetry of Robert Frost</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/108</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/108</guid>
<pubDate>Tue, 08 May 2012 07:57:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Explores how Frost examines and configures the divide between life’s imperfections and its rewards. I am particularly interested in how Frost positions both the non-human natural world and poetry itself as intermediary (or liminal) realms that might help us live simultaneously in the worlds of reality and the imagination, or truth and beauty, or heaven and earth.</p>

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</description>

<author>Elizabeth M. Yale</author>


</item>


<item>
<title>A Failing Correctional System: State Prison Overcrowding in the United States</title>
<link>http://escholar.salve.edu/pell_theses/79</link>
<guid isPermaLink="true">http://escholar.salve.edu/pell_theses/79</guid>
<pubDate>Tue, 08 May 2012 07:54:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>State prison overcrowding has grown into a detrimental problem within our American penal system, such that after decades of being ignored by politicians, media outlets, and the lower court system, it has resulted in an ineffective and overcrowded correctional system that craves reformation.</p>

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</description>

<author>Susan M. Campers</author>


</item>


<item>
<title>Managing Knowledge in Project Environments</title>
<link>http://digitalcommons.ilr.cornell.edu/intl/218</link>
<guid isPermaLink="true">http://digitalcommons.ilr.cornell.edu/intl/218</guid>
<pubDate>Tue, 08 May 2012 07:52:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Projects ought to be vehicles for both practical benefits and organizational learning. However, if an organization is designed for the long term, a project exists only for its duration. Project-based organizations face an awkward dilemma: the project-centric nature of their work makes knowledge management, hence learning, difficult.</p>

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</description>

<author>Olivier Serrat</author>


</item>


<item>
<title>The importance of historical Tang dynasty for place branding the contemporary city Xi&apos;an</title>
<link>http://scholarship.rollins.edu/as_facpub/36</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/as_facpub/36</guid>
<pubDate>Tue, 08 May 2012 07:51:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Purpose – The purpose of this paper is to discuss the opportunity of utilizing Tang dynasty history, heritage, buildings and names in the effort to place brand the contemporary city Xi'an.</p>
<p>Design/methodology/approach – The paper presents a conceptual framework for place branding cities consisting of two main dimensions. The first describes the continuum of functional versus emotional values within a city; the second measures the degree to which the image of a place is historical or contemporary. The paper then employs historical analysis to examine the meaning and construction of a Tang dynasty brand for place branding twenty-first century Xi'an.</p>
<p>Findings – While Xi'an may possess an illustrious historical identity, the contemporary city is still searching for an image. Xi'an's glorious heritage attracts considerable tourism, but has not yet drawn substantial business, foreign direct investment or talents to contribute to and support economic development of the metropolitan region.</p>
<p>Research limitations/implications – Historical analysis of a city can allow a reconstruction of identity in the modern context. Since this is a case study of one key Chinese city, additional cases are needed for other historically important cities to see their influence on business and marketing development.</p>
<p>Practical implications – Cities that are attempting to grow should consider their historical legacy. Building on images of the past, they can leapfrog development and establish a brand identity. Modernization was often thought of as a practical developmental tool. Building on the history of a region, modernization can take unique characteristics and differentiated developmental patterns.</p>
<p>Originality/value – Few, if any, studies examined the historical antecedents of a remaking and a re-branding of a city. Destination marketing is an emerging area of research. Xi'an was a great, pivotal city in the past. This paper explores how one region built on the greatness of the past can re-emerge in modern society.</p>

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</description>

<author>Norman Harry Rothschild et al.</author>


</item>


<item>
<title>Sean Kinsella</title>
<link>http://arrow.dit.ie/scthebk/25</link>
<guid isPermaLink="true">http://arrow.dit.ie/scthebk/25</guid>
<pubDate>Tue, 08 May 2012 07:50:18 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sean Kinsella</author>


</item>


<item>
<title>Dietary Protein and Vitamin D Intake and Risk of Falls: A Secondary Analysis of Postmenopausal Women from the Study of Osteoporotic Fractures</title>
<link>http://digitalcommons.uconn.edu/gs_theses/240</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/240</guid>
<pubDate>Tue, 08 May 2012 07:49:46 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Background: </strong>Falling is a major concern with 90% of hip fractures in older Americans resulting from a fall. Inadequate intake of dietary protein and vitamin D are common in older adults and diets low in either could contribute to the loss of muscle mass and strength, coordination, in turn increasing the risk of falling. Published data on vitamin D intake and falls are conflicting; data on protein intake and falls are limited.<strong></strong></p>
<p><strong>Objective: </strong>Evaluate the relationship between protein and vitamin D intake with the occurrence of falls in older women in the SOF (Study of Osteoporotic Fracture) study.</p>
<p><strong>Design: </strong>Prospective cohort study of 4,369 postmenopausal women participating in SOF from the 6<sup>th</sup> visit (1/1997- 9/1998). Fall occurrence (yes/no) was recorded 1-yr after their clinical visit. Protein and vitamin D’s associations with a reported fall were estimated with logistic regression, adjusted for fall related covariates and energy.</p>
<p><strong>Results</strong>: 1,429 women reported a fall one-year post visit 6 (V6). In separate, unadjusted models dietary protein and vitamin D significantly increased the odds of falling (OR 1.35 95% CI 1.15-1.59, OR 1.11 95% CI 1.03-1.19, respectively). Protein and vitamin D were modeled separately because they were highly correlated (rho= 0.55, p < 0.001). Once fall-related covariates were added to each model, dietary protein and vitamin D were noncontributory to falls. <strong></strong></p>
<p><strong>Conclusion: </strong>After accounting for<strong> </strong>established risk factors of falling, protein and vitamin D intake had no association with falls.</p>

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</description>

<author>Sarah C. Brown</author>


</item>


<item>
<title>9-Phenyl-3,4,4a,9a-Tetrahydrotriptycene and 9-Phenyl-1,2,3,4,4a,9a-Hexahydrotriptycene</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/2</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/2</guid>
<pubDate>Tue, 08 May 2012 07:47:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>The structure of 9-phenyl-3,4,4a,9a-tetrahydrotriptycene, C26H22, (I), exhibits regiochemistry consistent with a stepwise mechanism for its formation from photocycloaddition of 1,3- cyclohexadiene and 9-phenylanthracene. Bond distances involving the bridgehead C atoms are similar in (I) and the hydrogenated derivative, 9-phenyl-1,2,3,4,4a,9a-hexahydrotriptycene, C26H24, (II), with bonds to the quaternary-C atoms exhibiting significant elongation [1.581 (2) A Ê in (I) and 1.585 (2) A Ê in (II)]. The molecular geometry precludes significant  overlap between the phenyl groups and the interannular bonds in both compounds, indicating that the origin of the bond lengthening is steric in nature.</p>

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</description>

<author>John Masnovi et al.</author>


</item>


<item>
<title>Ogawa Mimei&apos;s Children&apos;s Stories:  A Case Study of the Rise of Childhood in the Context of Westernization and Japanese Modernization</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/107</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/107</guid>
<pubDate>Tue, 08 May 2012 07:47:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this thesis, I examine the influences of westernization, the tension between Japanese modernity and tradition, and the stories of Hans Christian Andersen on Ogawa Mimei’s children’s stories. I begin the body of my thesis with a brief historical background of Japan, beginning with the start of the Meiji period in 1868. Within the historical section, I focus on societal and cultural elements and changes that pertain to my thesis. I also include the introduction of Hans Christian Andersen in Japan. I wrap up the historical section by a description of Ogawa’s involvement in the Japanese proletarian literature movement and the rise of the Japanese proletarian children’s literature movement. Then, I launch into an analysis of Ogawa’s works categorized by thematic elements. These elements include westernization, class conflict, nature and civilization, religion and morals, and children and childhood. When relevant, I also compare and contrast Ogawa’s stories with Andersen’s. In the westernization section, I show how some of Ogawa’s stories demonstrate contact between Japan and the West. In the Class Conflict section, I discuss how Ogawa views class through a socialist lens, whereas Andersen does not dispute class distinctions, but encourages his readers to attempt an upward social climb. In the nature and civilization section, I show how Ogawa and Andersen share common opinions on the impact of civilization on nature. In the religion and morals section, I show how Ogawa incorporates religion, including Christianity, into vii his works. Andersen utilizes religion in a more overt manner in order to convey morals to his audience. Both authors address religious topics like the concept of the afterlife. Finally, in children and childhood, I demonstrate how both Ogawa and Andersen treat their child protagonists and use them and their situations to instruct their readers. Through this case study, I show how westernization and the tensions between Japanese modernization and tradition led to the rise of the proletarian children’s literature movement, which is exemplified by Ogawa’s stories. The emergence of the proletarian children’s literature movement is an indication of the establishment of a new concept of childhood in Japan. Writers like Ogawa Mimei attempted to write children’s stories that represented the new Japanese culture that was a result of adapting Western ideals to fit Japanese society. Some of Ogawa’s stories are a direct commentary on his opinion of Japanese interaction with the West. By comparing Ogawa’s and Andersen’s stories, I demonstrate how Ogawa borrows certain Western elements and possibly responds directly to Andersen. Ogawa also addresses some of the same topics as Andersen, yet their reactions are not always the same. What I find in my analysis supports my thesis that Ogawa is able to maintain Japanese tradition while infusing his children’s stories with Western and modern elements. In doing so, he reflects a largely popular social and cultural practice of his time.</p>

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</description>

<author>Alexandra E. Kint</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 12, no. 1</title>
<link>http://collected.jcu.edu/carrollquarterly/33</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/33</guid>
<pubDate>Tue, 08 May 2012 07:46:52 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 12, no. 2</title>
<link>http://collected.jcu.edu/carrollquarterly/32</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/32</guid>
<pubDate>Tue, 08 May 2012 07:46:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 12, no. 3</title>
<link>http://collected.jcu.edu/carrollquarterly/31</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/31</guid>
<pubDate>Tue, 08 May 2012 07:46:50 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 12, no. 4</title>
<link>http://collected.jcu.edu/carrollquarterly/30</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/30</guid>
<pubDate>Tue, 08 May 2012 07:46:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Kentucky Law Survey: Evidence</title>
<link>http://uknowledge.uky.edu/law_facpub/165</link>
<guid isPermaLink="true">http://uknowledge.uky.edu/law_facpub/165</guid>
<pubDate>Tue, 08 May 2012 07:46:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>This Article is a survey of recent developments in evidence law. It focuses on specific issues, including statements for medical treatment or diagnosis, tape recordings, "probativeness" versus "prejudice," and others.</p>

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</description>

<author>Robert G. Lawson</author>


</item>


<item>
<title>The Past and Future of Kentucky&apos;s Fraudulent Transfer and Preference Laws</title>
<link>http://uknowledge.uky.edu/law_facpub/164</link>
<guid isPermaLink="true">http://uknowledge.uky.edu/law_facpub/164</guid>
<pubDate>Tue, 08 May 2012 07:46:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>An important part of the law of creditors' remedies is the ability of creditors to recover property formerly held by the debtor, but transferred to others under circumstances that are considered to be unfair or inequitable. There are two principal ways a creditor can seek to have a debtor's transfer characterized as unfair in order to recover it. First, a transfer to another creditor or a third party can be fraudulent as to one or all of the remaining creditors, or may be deemed to be fraudulent because of the circumstances surrounding the transfer, such as a transfer made by an insolvent debtor for less than fair value. Second, even a transfer to another creditor for full value can be considered "preferential" to that creditor. Recovery of a preferential transfer to one creditor, in theory, makes all of the debtor's property available for an orderly distribution to all creditors. Fraudulent transfers and preferences are recoverable in state law collective actions such as assignments for the benefit of creditors, or in a proceeding under the federal Bankruptcy Code.</p>
<p>Kentucky has a unique and antique collection of laws governing fraudulent transfers and preferences. Both the singularity and age of these laws are easily established with a few examples. The most recent of these laws were written 140 years ago. Kentucky is one of only eight states that have not adopted one of two uniform laws offered on the subjects in the past ninety years. In addition, Kentucky is one of only three states allowing creditors to set aside preferences, a power reserved otherwise for bankruptcy or other insolvency proceedings. Indeed, most other states have declared their policy to permit preferences, almost as a fundamental right of debtors to pay any debts they might have at any time, regardless of the effect on other creditors.</p>
<p>This background suggests that Kentucky's singularity is perhaps not a good thing, but rather evidence of old laws left to languish long past their time. In Part I of this article, I review the development of modem fraudulent transfer and preference law. Part II contrasts that development with the existing law in Kentucky and other non-uniform states. Part III reviews the need and prospects for reform of Kentucky's laws. I conclude that in most respects improvement and modernization is overdue, but should proceed carefully with due regard taken of the effect of broadly written fraudulent transfer statutes on commercial transactions.</p>

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</description>

<author>Douglas C. Michael</author>


</item>


<item>
<title>The Kentucky Law Survey: Taxation</title>
<link>http://uknowledge.uky.edu/law_facpub/163</link>
<guid isPermaLink="true">http://uknowledge.uky.edu/law_facpub/163</guid>
<pubDate>Tue, 08 May 2012 07:46:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Certainly the most publicized development in Kentucky tax law during the last five years was the series of decisions in <em>St. Ledger v. Kentucky Revenue Cabinet</em>, striking down two of Kentucky's intangibles taxes. The <em>St. Ledger </em>decisions, however, were not the only tax law development to receive attention.</p>
<p>There were a number of legislative developments of some significance. Specifically, Governor Brereton Jones formed a Tax Policy Commission that comprehensively reviewed Kentucky's tax structure. Although the 1996 General Assembly did not fully embrace the Commission's recommendations over the last five years, the General Assembly did enact some significant legislation. For example, the General Assembly enacted legislation permitting affiliated corporations to choose between filing their income tax returns on a separate or consolidated basis. In addition, it replaced Kentucky's century-old bank shares tax with a franchise-based tax. Finally, the General Assembly enacted legislation phasing out much of the inheritance tax.</p>
<p>On the judicial side, a number of unreported decisions also received a good deal of attention. For example, in a decision that has yet to become final, the Supreme Court of Kentucky upheld the constitutionality of the Revenue Cabinet's interim method of assessing unmined coal for tax years 1989 through 1991. In an unpublished opinion that subsequently was withdrawn, the Kentucky Court of Appeals denied a foreign holding company a remedy for unconstitutional discrimination imposed by a preferential license tax scheme.</p>
<p>This Article discusses the legislative and judicial developments described above. In addition, it discusses a few other developments that may be of interest to tax practitioners.</p>

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</description>

<author>Kathryn L. Moore</author>


</item>


<item>
<title>Genetics, Genetic Testing, and the Specter of Discrimination: A Discussion Using Hypothetical Cases</title>
<link>http://uknowledge.uky.edu/law_facpub/162</link>
<guid isPermaLink="true">http://uknowledge.uky.edu/law_facpub/162</guid>
<pubDate>Tue, 08 May 2012 07:46:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>A "genetic revolution" is upon us. Techniques for genetic testing have increased in sophistication, and an international effort to map and sequence human DNA—The Human Genome Project ("HGP")—is now well under way. We are beginning to exploit our new found genetic knowledge. Recognition of the relationship between developments in genetic science, law, and public policy, is creeping into the "literature" and into the law school curriculum. Even the popular <em>60 Minutes</em> television "news magazine" recently did a program on the perils of genetic testing. Still, for lawyers and policymakers at least, the material is not all that accessible.</p>
<p>The following Problems were developed by the faculty of the College of Medicine of the University of Kentucky and were used in a panel presentation for medical students. The discussion that follows each hypothetical is far from exhaustive, and is offered as a starting point. Readers desiring more information are directed to the Sele<em>cted Bibliography</em>.</p>
<p>These Problems present a rather thorough survey of the "issues." They give the reader some notion of the state-of-the-art in genetic research and its applications; the Problems also suggest possible implications for confidentiality, tort liability for disclosure, lawsuits for "wrongful birth" and "wrongful life," and so on; and they allude to the newsworthy Americans with Disabilities Act ("ADA"). Finally, the Problems may motivate the reader to reflect on other topics, such as euthanasia and eugenics, from another perspective.</p>

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</description>

<author>Richard H. Underwood et al.</author>


</item>


<item>
<title>Ecology and Management Potential for Purple Loosestrife (Lythrum salicaria)</title>
<link>http://digitalcommons.brockport.edu/env_facpub/43</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/43</guid>
<pubDate>Tue, 08 May 2012 07:46:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Purple loosestrife (Lythrum salicaria), an exotic wetland plant from Eurasia, has become widespread in the northeast and northcentral regions of the U.S. and Canada. When it becomes established in a wetland, it crowds out most native plant species, and can form dense stands either in standing water or on moist soil. This results in decreased plant diversity and the loss of food and cover species valuable to wildlife. Some attempted control methods, such as controlled burning and water-level manipulation have proven to be unsuccessful. Other control measures, including mechanical cutting, replacement, and cattail competition, have shown encouraging, but inconclusive, results. This study was therefore initiated to further explore the possibility of controlling purple loosestrife through competition with cattails (Typha angustifolia) in mixed stands. A competitive edge was given to Typha by cutting Lythrum and selectively fertilizing Typha. First-year results of the study showed a significant decrease in Lythrum biomass as a result of cutting treatments. Cutting did not significantly reduce resprouting Lythrum stems, as Lythrum resprouted in greater numbers than Typha, but Typha sprouts grew faster and increased in biomass more quickly than Lythrum sprouts. With carbohydrate replenishment to the roots reduced, it is expected that Lythrum biomass will be reduced in subsequent years. The stress caused by cutting, and increased shade by the Typha canopy, may help to control purple loosestrife spread.</p>

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</description>

<author>Douglas A. Wilcox et al.</author>


</item>


<item>
<title>A Comparison of Interaction in AV-Based and Internet-Based Distance Courses</title>
<link>http://digitalcommons.unomaha.edu/tedfacpub/19</link>
<guid isPermaLink="true">http://digitalcommons.unomaha.edu/tedfacpub/19</guid>
<pubDate>Tue, 08 May 2012 07:45:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>At the center of the debate over the viability of distance education is whether the newer electronic technologies can offer enough interaction to maintain quality learner outcomes and critical mass. Two of the most commonly used forms of distance education are 1) two-way, fully interactive audio-video classrooms and 2) on-line instruction through the Internet or Worldwide Web. This study used qualitative methods to compare and contrast the interaction that occurred in distance learning courses offered via each medium. The research process confirmed findings that there were fundamental differences in the interaction that occurred in the two environments. On-line interaction is so profoundly different than interaction in the traditional and AV-based class room that it appears instructors and students will need a substantial period of adjustment to feel comfortable with it and to fully appreciate its value. It appears that, as distance teaching and learning moves to a “mixed media” approach to teaching and learning, how interaction is handled with each of the media may be important to the success of a distance program.</p>

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</description>

<author>Melodee Landis</author>


</item>


<item>
<title>Matt</title>
<link>http://lux.lawrence.edu/artgallery_se2012/3</link>
<guid isPermaLink="true">http://lux.lawrence.edu/artgallery_se2012/3</guid>
<pubDate>Tue, 08 May 2012 07:43:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Materials: Gelatin Silver Print</p>
<p>Dimensions: 16" x 20"</p>
<p>Advisor: Julie Lindemann and John Shimon</p>
<p>Graduating Class: 2012</p>

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</description>

<author>Sara L. Sheldon-Rosson</author>


</item>


<item>
<title>Amanda</title>
<link>http://lux.lawrence.edu/artgallery_se2012/2</link>
<guid isPermaLink="true">http://lux.lawrence.edu/artgallery_se2012/2</guid>
<pubDate>Tue, 08 May 2012 07:41:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Materials: Gelatin Silver Print</p>
<p>Dimensions: 16" x 20"</p>
<p>Advisor: Julie Lindemann and John Shimon</p>
<p>Graduating Class: 2012</p>

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</description>

<author>Sara L. Sheldon-Rosson</author>


</item>


<item>
<title>Entrepreneurial Leadership and Familiness as Resources For Strategic Entrepreneurship</title>
<link>http://digitalknowledge.babson.edu/stepdatapw/21</link>
<guid isPermaLink="true">http://digitalknowledge.babson.edu/stepdatapw/21</guid>
<pubDate>Tue, 08 May 2012 07:38:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Juha Kansikas et al.</author>


</item>


<item>
<title>The Bucknell Community College Scholarship Program: a Documentary as a Performative Social Science</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/106</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/106</guid>
<pubDate>Tue, 08 May 2012 07:38:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Reviews Bucknell participation with the Jack Kent Cooke Foundation (a non-profit foundation with a mission to “help under-resourced students of exceptional promise reach their full potential through education".</p>

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</description>

<author>Sean D. Fortney</author>


</item>


<item>
<title>Sedimentology, Depositional Age, and Provenance of Sedimentary and Volcanic Rocks  Exposed Along Willow Creek, Eastern Susitna Basin, South-Central Alaska: Implications for Modification of a Forearc Basin by Spreading Ridge Subduction</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/105</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/105</guid>
<pubDate>Tue, 08 May 2012 07:38:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>This is the first detailed study of the westernmost portion of the outcrop belt, which extends along the western flank of the Talkeetna Mountains and includes thick, well-exposed outcrops along Willow Creek in the eastern Susitna basin. New sedimentologic, compositional, and geochronologic data were obtained from stratigraphic sections within Arkose Ridge Formation strata at Willow Creek. This data combined with new geologic mapping and geochronologic data from Willow Bench and Kashwitna River Bluff (north of Willow Creek), and from the Government Peak area (east of Willow Creek), help constrain depositional processes and source terranes that provided detritus to the westernmost Arkose Ridge Formation strata.</p>

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</description>

<author>Erin E. Donaghy</author>


</item>


<item>
<title>A Workman That Needeth Not to Be Ashamed</title>
<link>http://place.asburyseminary.edu/firstfruitsheritagematerial/10</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/firstfruitsheritagematerial/10</guid>
<pubDate>Tue, 08 May 2012 07:36:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Grank Bateman Stanger</author>


</item>


<item>
<title>In the Classroom: Using Children&apos;s Literature (Oct. &apos;89)</title>
<link>http://digitalcommons.unomaha.edu/tedfacpub/18</link>
<guid isPermaLink="true">http://digitalcommons.unomaha.edu/tedfacpub/18</guid>
<pubDate>Tue, 08 May 2012 07:35:29 PDT</pubDate>
<description>
	<![CDATA[
	<p><dl id="x-x-citationFields"><dd>Lists children's literature in reading instruction. "Children's Literature in the Reading Program"; "Literature-based Reading Programs at Work"; "Children's Choices: Teaching With Books Children Like"; "Transitions: From Literature to Literacy".</dd></dl></p>

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</description>

<author>Michael P. French et al.</author>


</item>


<item>
<title>The Development and Validation of the Diversity Dispositions Index</title>
<link>http://digitalcommons.unomaha.edu/tedfacpub/17</link>
<guid isPermaLink="true">http://digitalcommons.unomaha.edu/tedfacpub/17</guid>
<pubDate>Tue, 08 May 2012 07:35:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The population of the U.S. is becoming increasingly more diverse. Yet, administrators and teachers in the U.S. are predominantly "European Americans from middle-class backgrounds who speak only English. Many of their students are racial and ethnic minorities, live in poverty, and speak a first language other than English" (Banks et aI., 2005, p. 237). The "No Child Left Behind Act" signed into law in2002 requires school districts to hire highly qualified teachers who possess the necessary dispositions to ensure that all children learn (Center on Education Policy, 2002). School administrators and teachers must understand students' backgrounds and experiences, and they must possess the necessary dispositions to work with students from diverse backgrounds (Villegas & Lucas, 2007).</p>

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</description>

<author>Laura E. Schulte et al.</author>


</item>


<item>
<title>Milestone 1998</title>
<link>http://digitalcommons.hope.edu/milestone/10</link>
<guid isPermaLink="true">http://digitalcommons.hope.edu/milestone/10</guid>
<pubDate>Tue, 08 May 2012 07:33:36 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Milestone</em>, the Hope College yearbook, is an annual publication of Hope College. The first yearbook was published in 1905 as a single edition and was titled <em>The Hope College Annual</em>. The yearbooks became an annual publication in 1916, which was also when it was titled <em>Milestone. </em></p>

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</description>

<author>Hope College</author>


</item>


<item>
<title>Milestone 1999</title>
<link>http://digitalcommons.hope.edu/milestone/9</link>
<guid isPermaLink="true">http://digitalcommons.hope.edu/milestone/9</guid>
<pubDate>Tue, 08 May 2012 07:33:35 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Milestone</em>, the Hope College yearbook, is an annual publication of Hope College. The first yearbook was published in 1905 as a single edition and was titled <em>The Hope College Annual</em>. The yearbooks became an annual publication in 1916, which was also when it was titled <em>Milestone. </em></p>

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</description>

<author>Hope College</author>


</item>


<item>
<title>Feasibility of Farming Nile Tilapia, Oreochromis niloticus (L.), in Suboptimal Water Temperature</title>
<link>http://opus.ipfw.edu/biology_facpubs/194</link>
<guid isPermaLink="true">http://opus.ipfw.edu/biology_facpubs/194</guid>
<pubDate>Tue, 08 May 2012 07:29:28 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ahmed Mustafa Dr. et al.</author>


</item>


<item>
<title>Improving Cognitive/Academic Language Proficiency (CALP) of Low-achieving Sixth Grade Students: A Catalyst For Improving Proficiency Scores?</title>
<link>http://digitalcommons.cedarville.edu/education_theses/8</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/8</guid>
<pubDate>Tue, 08 May 2012 07:26:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cognitive/Academic Language Proficiency (CALP) is a construct developed by linguists that distinguishes everyday conversational language and language used in literature and on academic tests. The “No Child Left Behind Act” has created impetus for scientifically researched pedagogy that serves to increase academic achievement of groups who have been historically marginalized. Lack of CALP was identified as one factor that may prevent academic advancement among certain populations. An experiment was performed to demonstrate a causal relationship between increased CALP and improved Ohio Proficiency Test Scores. Twenty-three low-achieving sixth grade students, six of whom had IEPs, received an eight-week treatment program to improve their cognitive/academic language. Pre- and post-tests assessed changes in proficiency test scores. Differences in scores were statistically analyzed. Scores showed a significant positive treatment effect for students not on IEPs. The development of cognitive/academic language shows promise as a method for improving the proficiency test scores of low-achieving students.</p>

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</description>

<author>Margaret Grigorenko</author>


</item>


<item>
<title>Recombinant DNA Technology -- A Patent Case in the House of Lords</title>
<link>http://www.repository.law.indiana.edu/facpub/522</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/522</guid>
<pubDate>Tue, 08 May 2012 07:23:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Yvonne Cripps</author>


</item>


<item>
<title>Family Gatherings and a Dirty Little Secret of the Law and Society Association</title>
<link>http://www.repository.law.indiana.edu/facpub/521</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/521</guid>
<pubDate>Tue, 08 May 2012 07:23:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>This article discusses the irony of the longstanding suspicion of economic approaches within the law and society movement, despite the fact that some of the movement's greatest scholars have not so surreptitiously used economic theory in their work. Although economists are generally treated as the "black sheep" of the law and society family, economic principles have been employed in the work of several well respected law and society scholars, including Willard Hurst and Marc Galanter. Galanter's seminal law and society article Why the 'Haves' Come Out Ahead is discussed at length. The author concludes that the dirty little secret of the law and society movement is that a very good argument can be made that the progressive wing of the law and economics movement owes its paternity to law and society scholars such as Hurst and Galanter.</p>

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</description>

<author>Kenneth G. Dau-Schmidt</author>


</item>


<item>
<title>The Fruits of Our Labors: An Empirical Study of the Distribution of Income and Job Satisfaction Across the Legal Profession</title>
<link>http://www.repository.law.indiana.edu/facpub/520</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/520</guid>
<pubDate>Tue, 08 May 2012 07:23:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this study we undertake a simple empirical analysis to examine the distribution of pecuniary and nonpecuniary benefits across the legal profession. Using the University of Michigan alumni data set, we conduct a series of regressions to examine how the participants' self-reported income and job satisfaction vary across the legal profession according to type of practice, gender, and whether the respondent is black or Hispanic. Regression analysis allows us to undertake this analysis while correcting for the effects of several other variables, including years of practice, hours worked, law school grades, satisfaction with family life, and population of the respondent's city of residence. We conduct the analysis on two separate subsamples of respondents - one for respondents who were surveyed five years after graduation and another for respondents surveyed fifteen years after graduation. Separate analysis of these subsamples allows us to obtain snapshots of the distribution of rewards across the profession at two distinct stages in lawyer careers. With the exception of certain tests that are performed on coefficients for minority status, the University of Michigan alumni data set is large enough and rich enough to allow a very interesting and detailed analysis of how the benefits of legal practice are distributed across the legal profession.</p>

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</description>

<author>Kenneth G. Dau-Schmidt et al.</author>


</item>


<item>
<title>[2,3:5,6]Dibenzo[2.2.2]octa-2,5,7-triene (C2/c) and [2,3:5,6]dibenzo[2.2.2]octa-2,5-diene</title>
<link>http://engagedscholarship.csuohio.edu/scichem_facpub/1</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scichem_facpub/1</guid>
<pubDate>Tue, 08 May 2012 07:22:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Two barrelene homologs are reported. Strain in the bicyclic framework of [2,3:5,6]dibenzo[2.2.2]octa-2,5,7- triene, (I) (C16H12), which is manifest in the deviations from ideality of the bond angles in the central bicyclic ringoSyStem and compression of the double bond [1.312 (3)A], is reduced in the more saturated derivative, [2,3:5,6]dibenzo[2.2.2]octa-2,5-diene, (II) (CI6H14), with the corresponding single bond being 1.5380 (19)A. The formation of isomorphs of (I) in both chiral (C2) and achiral (C2/c) space groups has implications for asymmetric syntheses involving solid (I) which rely on a non-centrosymmetric space group.</p>

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</description>

<author>Lary Burrows et al.</author>


</item>


<item>
<title>Mesoproterozoic Deposition, Regional Metamorphism and Deformation in North-Central New Mexico: Evidence from Metamorphic Monazite and Detrital Zircon Geochronology in the Picuris Mountains</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/104</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/104</guid>
<pubDate>Tue, 08 May 2012 07:21:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Detrital zircon and metamorphic monazite ages from the Picuris Mountains, north central New Mexico, were used to confirm the depositional age of the Marquenas Formation, to document the depositional age of the Vadito Group, and to constrain the timing of metamorphism and deformation in the region.</p>
<p>Detrital zircon 207Pb/206Pb ages were obtained with the LA-MC-ICPMS from quartzites collected from the type locality of the Marquenas Formation exposed at Cerro de las Marquenas, and from the lower Vadito Group in the southern and eastern Picuris Mountains. The Marquenas Formation sample yields 113 concordant ages including a Mesoproterozoic age population with four grains ca. 1470 Ga, a broad Paleoproterozoic age peak at 1695 Ma, and minor Archean age populations. Data confirm recent findings of Mesoproterozoic detrital zircons reported by Jones et al. (2011), and show that the Marquenas Formation is the youngest lithostratigraphic unit in the Picuris Mountains. Paleoproterozoic and Archean detrital grains in the Marquenas Formation are likely derived from local recycled Vadito Group rocks and ca. 1.75 Ga plutonic complexes, and ca. 1.46 detrital zircons were most likely derived from exposed Mesoproterozoic plutons south of the Picuris. Ninety-five concordant grains from each of two Vadito Group quartzites yield relatively identical unimodal Paleoproterozoic age distributions, with peaks at 1713-1707 Ma. Eastern exposures of quartzite mapped as Marquenas Formation yield detrital zircon age patterns and metamorphic mineral assemblages that are nearly identical to the Vadito Group. On this basis, I tentatively assigned the easternmost quartzite to the Vadito Group. Zircon grains in all samples show low U/Th ratios, welldeveloped concentric zoning, and no evidence of metamorphic overgrowth events, consistent with an igneous origin. North-directed paleocurrent indicators, such as tangential crossbeds (Soegaard & Eriksson, 1986) and other primary sedimentary structures, are preserved in the Marquenas Formation quartzite. Together with pebble-toboulder metaconglomerates in the Marquenas, these observations suggest that this formation was deposited in a braided alluvial plain environment in response to syntectonic uplift to the south of the Picuris Mountains.</p>
<p>Metamorphic monazite from two Vadito Group quartzite samples were analyzed with an electron microprobe (EMP). Elemental compositional variation with respect to Th and Y define core and rim domains in monazite grains, and show lower concentrations of Th (1.46-1.52 wt%) and Y (0.67 wt%) in the cores, and higher concentrations of Th (1.98 wt%) and Y (1.06 wt%) in the rims. Results show that Mesoproterozoic core and rim ages from five grains overlap within uncertainty, ranging from 1395-1469 Ma with an average age of 1444 Ma. This 1.44 Ga average age is the dominant timing of metamorphic monazite growth in the region, and represents the timing of metamorphism experienced by the region. An older 1630 Ma core observed in sample CD10-12 may be interpreted as a result of low temperature metamorphism in lower Vadito Group rocks due to heat from ca. 1.65 Ga granitic intrusions. Core ages ca. 1.5 Ga are likely due to a mixing age of two different age domains during analyses. Confirmed sedimentation at 1.48-1.45 Ga and documented mid-crustal regional metamorphism in northern New Mexico ca. 1.44-1.40 are likely associated with a Mesoproterozoic orogenic event.</p>

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</description>

<author>Lily S. Pfeifer</author>


</item>


<item>
<title>Nationalism in Cyprus: the effects of institutionalization on nationalist mobilizations and political conflicts as reflected in Turkish Cypriot nationalism and Greek Cypriot nationalism</title>
<link>http://mds.marshall.edu/etd/215</link>
<guid isPermaLink="true">http://mds.marshall.edu/etd/215</guid>
<pubDate>Tue, 08 May 2012 07:21:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Historical events in Cyprus have played a very important role in the institutionalization of nationalist movements and political conflict between the Turkish Cypriot and Greek Cypriot nationalist movements on the island of Cyprus. In order to make the case of the “Cyprus problem” understandable, the sociological elements of the Turkish Cypriot and Greek Cypriot nationalism of the island were analyzed in this study in relation to some fundamental elements of the conflict. Internal and external elements including nationalism, the role of outsiders, modernization, and some other cultural factors, such as the educational and religious systems and colonial policies, played an important role in the creation of these rival nationalisms. Different ethno-national identities on the island caused ethnic and geographical partitions among the Turkish and Greek Cypriot communities. In this analysis, the effects of nationalist mobilizations and political conflicts in Cyprus as reflections of both Turkish Cypriot and Greek Cypriot nationalisms will be the main elements for demonstrating the rise and fall of both Cypriot nationalist movements that caused the failure of the civic nation state in 1960.</p>

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</description>

<author>Nicel Masarogullari</author>


<category>&lt;p&gt;Nationalism - Cyprus.&lt;/p&gt;
&lt;p&gt;Cyprus - Politics and government.&lt;/p&gt;</category>

</item>


<item>
<title>Myrtle Allen</title>
<link>http://arrow.dit.ie/scthebk/24</link>
<guid isPermaLink="true">http://arrow.dit.ie/scthebk/24</guid>
<pubDate>Tue, 08 May 2012 07:20:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Myrtle Allen</author>


</item>


<item>
<title>Political Change through Narrative</title>
<link>http://scarab.bates.edu/honorstheses/52</link>
<guid isPermaLink="true">http://scarab.bates.edu/honorstheses/52</guid>
<pubDate>Tue, 08 May 2012 07:17:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>When faced with well-organized opposition, political organizations often incorporate new strategies into their campaigns. Some progressive organizations situate their work within overarching frameworks or perspectives called narratives, which are designed to shift the terms of public discourse to favor particular social and political goals. Despite the theoretical significance of narratives, actual efforts to connect everyday change-making activities to narrative development are often complicated by practical and theoretical obstacles. I address this dilemma in collaboration with Maine People’s Alliance (MPA), a progressive community action group with 32,000 members throughout Maine. We ask how an organization such as MPA can pursue the abstract goal of a “narrative” while remaining committed to more concrete change-making activities that measure an organization’s success. To answer this question and the three tensions of power, practicality, and perceptions that it spawns, we build on the work of community organizers, social movement framing theorists, scholars who study political myth, narrative analysts, and policy analysts. We explore a new integration of narratives and policymaking that simultaneously develops an alternative perspective and accomplishes measurable political change. This investigation uncovers the two tiers of narrative: organizational narratives and public worldviews. By focusing on organizational narratives, we explore various methods of story collection and evaluation to develop a model of narrative development that accommodates the varied realities and complexities of MPA, MPA membership, and the current political environment.</p>

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</description>

<author>Catherine Elliott</author>


</item>


<item>
<title>Roger Williams Park Edible Forest Garden</title>
<link>http://digitalcommons.uri.edu/srhonorsprog/275</link>
<guid isPermaLink="true">http://digitalcommons.uri.edu/srhonorsprog/275</guid>
<pubDate>Tue, 08 May 2012 07:15:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>An edible forest garden is a low-maintenance system that uses edible native and regionally-adapted plants arranged in beneficial relationships to meet human, wildlife and ecosystem needs. The forest garden in Roger Williams Park will transform underutilized urban land into a highly productive parcel producing market-viable fruits, nuts, vegetables, medicine and fiber. Forest gardens mimic natural forest systems in architecture and complexity. The design follows ecological principles to create a system that promotes biodiversity and enhances the surrounding ecosystem. This project also demonstrates the potential to grow food and create land-based livelihoods in the city.</p>
<p>Located on the edge of a USDA-designated "food desert" in Providence's lower south side, the Edible Forest Garden will supplement produce grown in the adjacent Roger Williams Park Community Garden. This increases the volume of fresh, locally produced food available to city-dwellers living in food insecure areas. The Edible Forest Garden will also serve as a living laboratory for environmental education opportunities. Through a partnership with URI Master Gardeners and community gardeners, residents will have the opportunity to actively participate in harvests and garden maintenance through a mentor program.</p>
<p>The Edible Forest Garden design will draw upon sustainable land use practices rooted in generations of indigenous culture, coupled with the latest scientific data concerning agriculture, forestry and ecology. This union of time-tested methods and peer-reviewed inquiry is the foundation for the planning, design and implementation of the Roger Williams Park Edible Forest Garden. Simply put, an edible forest garden is our best attempt at designing an ecosystem based on the complexities and layers found in natural systems, only we choose the course of ecological succession.</p>

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</description>

<author>Mark S. Scialla</author>


</item>


<item>
<title>Disturbance Effects on Aquatic Vegetation in Regulated and Unregulated Lakes in Northern Minnesota</title>
<link>http://digitalcommons.brockport.edu/env_facpub/42</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/42</guid>
<pubDate>Tue, 08 May 2012 07:15:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>The effects of water-level regulation on aquatic macrophyte communities were investigated by comparing two regulated lakes in northern Minnesota with a nearby unregQlated lake. Natural annual fluctuations of about 1.8 m were replaced with fluctuations of 1.1 m and 2. 7 m in the regulated lakes, and the timing of water-level changes was also altered. Quadrats were sampled along transects that followed depth contours representing different plant habitats in the unregulated lake. Ordinations showed that the macrophyte communities at all sampled depths of the regulated lakes differed from those in the unregulated lake. The unregulated lake supported structurally diverse plant communities at all depths. In the lake with reduced fluctuations, only four taxa were present along transects that were never dewatered; all were erect aquatics that extended through the entire water column. In the lake with increased fluctuations, rosette and mat-forming species dominated transects where drawdown occurred in early winter and disturbance resulted from ice formation in the sediments. The natural hydrologic regime at the unregulated lake resulted in intermediate disturbance and high diversity. There was either too little or too much disturbance from water-level fluctuations in the regulated lakes, both resulting in reduced structural diversity.</p>

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</description>

<author>Douglas A. Wilcox et al.</author>


</item>


<item>
<title>A Qualitative Examination of Middle Grade Practices in Christian Schools: Could They Become Models for Middle Level Reform?</title>
<link>http://digitalcommons.cedarville.edu/education_theses/7</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/7</guid>
<pubDate>Tue, 08 May 2012 07:13:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>There has been much debate concerning the educational structures best suited for the teaching of students during the pivotal years from ages ten to fifteen. Many researchers and educators believe that the educational experiences for this age group need to be tailored to the unique qualities of this time in the life of a student. One purpose of this thesis is to examine the best practices for educating children during this time period. Another purpose of the study is to compare and contrast the practices in private Christian day schools to similar studies done of public school settings. The study found that although Christian schools are strong in areas like dedicated teachers, communication with parents, and ease of transition to the middle grades, they are not strong in things like teaming, heterogeneous grouping, and being task oriented.</p>

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</description>

<author>Teresea Baumann</author>


</item>


<item>
<title>Survey of antibiotic resistant bacteria in fish gut collected from selected sites.</title>
<link>http://opus.ipfw.edu/biology_facpres/74</link>
<guid isPermaLink="true">http://opus.ipfw.edu/biology_facpres/74</guid>
<pubDate>Tue, 08 May 2012 07:10:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ahmed Mustafa Dr. et al.</author>


</item>


<item>
<title>Government Influence and the Failure of Fannie Mae and Freddie Mac</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/103</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/103</guid>
<pubDate>Tue, 08 May 2012 07:09:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>In 2008 two government-sponsored enterprises, Fannie Mae and Freddie Mac, were placed into conservatorship due to insolvency. The financial bailout of the two publically traded corporations came at the expense of the American tax payer. This study investigates the relationship between direct and indirect government influence and the increasing risk taking of Fannie Mae and Freddie Mac from the late 1990’s through their conservatorship in 2008. As government-sponsored enterprises Fannie Mae and Freddie Mac have many special advantages that other publically traded companies did not possess. These advantages allowed Fannie Mae and Freddie Mac to increase their profitability. Theoretical literature regarding Congress and the bureaucracy suggests that the actions of bureaucrats can be linked to the preferences of Congressional members because bureaucrats are responsive to potential threats or perceived threats from the legislature. This theory is applicable to Fannie Mae and Freddie Mac, and is used to explain why the government was able to directly and indirectly influence the government-sponsored enterprises. Overall this investigation has determined that the United States government pursued a clear mission that determined to increase the availability of housing to all Americans, specifically to low-income and under-served individuals, through the use of the government-sponsored enterprises. Despite this link there is no conclusive data to show that the pursuit of this housing mission led Fannie Mae and Freddie Mac to operate in riskier business segments. This study has also found that motivation regarding profit-seeking and compensation structure provide a more plausible explanation for why the government-sponsored enterprises began to engage in riskier business practices that led to their insolvency.</p>

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</description>

<author>Aravind Mohan</author>


</item>


<item>
<title>April 16, 2012</title>
<link>http://digitalcommons.iwu.edu/spbc/93</link>
<guid isPermaLink="true">http://digitalcommons.iwu.edu/spbc/93</guid>
<pubDate>Tue, 08 May 2012 07:06:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>SPBC, Illinois Wesleyan University</author>


</item>


<item>
<title>April 2, 2012</title>
<link>http://digitalcommons.iwu.edu/spbc/92</link>
<guid isPermaLink="true">http://digitalcommons.iwu.edu/spbc/92</guid>
<pubDate>Tue, 08 May 2012 07:05:41 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>SPBC, Illinois Wesleyan University</author>


</item>


<item>
<title>Discoloration of Polyvinyl Chloride (PVC) Tape as a Proxy for Water-Table Depth in Peatlands: Validation and Assessment of Seasonal Variability</title>
<link>http://digitalcommons.brockport.edu/env_facpub/41</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/41</guid>
<pubDate>Tue, 08 May 2012 07:02:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Summary</p>
<p>1. Discoloration of polyvinyl chloride (PVC) tape has been used in peatland ecological and hydrological studies as an inexpensive way to monitor changes in water-table depth and reducing conditions.</p>
<p>2. We investigated the relationship between depth of PVC tape discoloration and measured water-table depth at monthly time steps during the growing season within nine kettle peatlands of northern Wisconsin. Our specific objectives were to: (1) determine if PVC discoloration is an accurate method of inferring water-table depth in Sphagnum -dominated kettle peatlands of the region; (2) assess seasonal variability in the accuracy of the method; and (3) determine if systematic differences in accuracy occurred among microhabitats, PVC tape colour and peatlands.</p>
<p>3. Our results indicated that PVC tape discoloration can be used to describe gradients of water-table depth in kettle peatlands. However, accuracy differed among the peatlands studied, and was systematically biased in early spring and late summer/autumn. Regardless of the month when the tape was installed, the highest elevations of PVC tape discoloration showed the strongest correlation with midsummer (around July) water-table depth and average water-table depth during the growing season.</p>
<p>4. The PVC tape discoloration method should be used cautiously when precise estimates are needed of seasonal changes in the water-table.</p>

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</description>

<author>Robert K. Booth et al.</author>


</item>


<item>
<title>Transnationalism and Identity: the Concept of Community in Ghanaian Literature and Contemporary Ghanaian Culture</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/102</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/102</guid>
<pubDate>Tue, 08 May 2012 07:01:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>In my thesis, I use anthropology, literature, and adinkra, an indigenous art, to study Ghanaian concepts of community from an interactive standpoint. While each of these disciplines has individually been used to study the concept of community, the three have not previously been discussed in relation to one another. I explore the major findings of each field—mainly that in anthropology, transnational informants find communities upheld; in literature, transnational characters find the opposite; and in adinkra, there are elements of both continuity and dissolution—to discuss Ghanaian constructs of community in the transnational world. Throughout time, there have always been transnational individuals and concepts, but as globalization continues, transnationalism has become an ever-more vital topic, and combined with the common anthropological discussion of tradition and modernity, its influence on developing countries, like Ghana, is significant. Therefore, in my thesis, I explore how differing conceptions of community present themselves in each discipline, and how those divergences create a new understanding of place and identity.</p>

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</description>

<author>Devin M. Geary</author>


</item>


<item>
<title>Wrapped Cove at King’s Beach, Newport, 1974</title>
<link>http://escholar.salve.edu/monumenta-images/7</link>
<guid isPermaLink="true">http://escholar.salve.edu/monumenta-images/7</guid>
<pubDate>Tue, 08 May 2012 06:58:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Width, 420 feet; depth, 320 feet; 14,800 square yards of woven polypropylene fabric floating on the ocean and attached inland to 40 anchors.  Featured in Monumenta art exhibit, 1974, where it was installed at King's Beach. Lent by the artist.</p>
<p><strong>Publisher:</strong> Salve Regina University Archives and Special Collections.</p>
<p><strong>Source:</strong> Digital reproduction of photograph of work of art. Digitization specifications: Adobe Photoshop 7.0, 240 dpi, RGB, 24-bit.</p>
<p><strong>Rights:</strong> This content is provided for educational research and personal use only. While the photographs in this collection are held in the Salve Regina University Archives and Special Collections, copyright for the artwork still resides with the artists. See <a href="http://library.salve.edu/archives/archives_copyright.html" >http://library.salve.edu/archives/archives_copyright.html</a>.</p>

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</description>

<author>Christo</author>


</item>


<item>
<title>Learning by Gaming: Supply Chain Management</title>
<link>http://arrow.dit.ie/buschmarcon/79</link>
<guid isPermaLink="true">http://arrow.dit.ie/buschmarcon/79</guid>
<pubDate>Tue, 08 May 2012 06:53:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Today's third level students are of a virtual generation, where online interactive multi-player games, virtual reality and simulations are a part of everyday life, making gaming and simulation a very important catalyst in the learning process. Teaching methods have to be more innovative to help students understand the complexity of decisions within dynamic supply chain environment. Interactive simulation games have the potential to be an efficient and enjoyable means of learning. A serious interactive business game, Automobile Supply Chain Management Game (AUSUM), has been introduced in this paper. Using theories learnt in class as a knowledge base, participants have to develop effective supply chain partnership strategy to enhance their supply chain networks. Deploying the game over the web encourages student interaction and group work. Most importantly the game will enable students to fundamentally grasp the impact of strategic decisions on other parts and players of the supply chain network.</p>

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</description>

<author>Amr Arisha et al.</author>


</item>


<item>
<title>A Union Of Negatives: Ayatollah Khomeini and the Mobilization of Dissent in the Iranian Revolution of 1979</title>
<link>http://digitalcommons.providence.edu/history_students/4</link>
<guid isPermaLink="true">http://digitalcommons.providence.edu/history_students/4</guid>
<pubDate>Tue, 08 May 2012 06:51:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Islamic Revolution of 1979 eradicated half a century of Westernization in Iran and installed Ayatollah Khomeini as the leader of Iran’s new Islamic Republic. However, the revolutionary forces were not strongly unified under Khomeini’s radical Islamic vision. Indeed, many facets of the opposition simply desired moderate political reforms to increase democratic participation in the government and opposed the imposition of a government directed under the auspices of Islam. By the late 1970s, though, these various moderate revolutionaries realized that the only legitimate means to overthrow the reign of the American-supported Shah, Mohammad Reza Pahlavi, would be to join the Ayatollah and his network of radical Islamic mullahs. Acting as a cunning politician, Khomeini kept his plans for post-revolutionary Iran purposefully vague in order to galvanize the maximum amount of support for his cause. Khomeini unified the various opposition groups and directed their anger towards overthrowing the Shah, blinding them to his true motives for the future. A complex relationship between economic crises, the effects of the Shah’s brutal police-state, and the mobilization of average Iranians by the intelligentsia and the Ayatollah’s organized network of radical mullahs all contributed to the Shah’s eventual downfall and the subsequent imposition of the first Islamic Republic. The well-being of the average Iranian citizen did not improve after the revolution. Khomeini’s government continued to utilize the repressive political tactics employed by the Shah, including the execution of political opponents, to safeguard the regime. The failures of the Iranian Revolution offers a cautionary tale to today’s current revolutionary fighters in the uprisings throughout the Middle East, collectively known as the “Arab Spring.”</p>

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</description>

<author>Nicholas G. Sumski</author>


<category>History</category>

</item>


<item>
<title>Assessment of Self-Reported Studying Habits in a High-Risk Business Calculus Course</title>
<link>http://digitalcommons.uri.edu/srhonorsprog/274</link>
<guid isPermaLink="true">http://digitalcommons.uri.edu/srhonorsprog/274</guid>
<pubDate>Tue, 08 May 2012 06:51:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The University of Rhode Island offers a number of undergraduate courses that are considered high-risk, which is constituted by a high failure rate. BUS 111: Business Calculus has been identified as a high-risk course that focuses on basic concepts in calculus and is typically taken by freshman students. There are a multitude of potential factors that increase the likelihood of students struggling in BUS 111, such as prior math knowledge, class attendance, lack of resources, and ineffective studying strategies. However, the most salient factors for determining performance in BUS 111 have not been identified. Therefore, I sought to examine what studying techniques undergraduate students employed in BUS 111 and which techniques contributed to successful performance on examinations.</p>
<p>In order to gather data on studying habits, I constructed two surveys that were distributed to approximately 200 students enrolled in BUS 111 during the Fall 2010 semester. The surveys included information that assessed demographics, studying techniques and duration, use of social media and examination performance. In addition, I conducted interviews with faculty, and spoke with other universities to determine whether they offered high-risk undergraduate math courses. Following this, I examined the survey responses to attempt to determine what factors contributed to successful performance on examinations.</p>
<p>I was able to identify factors that contributed to successful performance on BUS 111 examinations. As a result of the findings, I have made some suggestions for studying habits and additional approaches to this class that may improve the likelihood of successful performance in BUS 111. This project has helped me develop skills to conduct a basic research study and communicate findings to an audience regarding a certain problem. Ultimately, these recommendations may help future undergraduate students perform successfully in BUS 111.</p>

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</description>

<author>Stephanie Allen</author>


</item>


<item>
<title>Improving the Quality of Life of a Homeless Person Using Co-Design and Paul Polak&apos;s 12 Steps to Practical Problem Solving</title>
<link>http://digitalcommons.uri.edu/srhonorsprog/273</link>
<guid isPermaLink="true">http://digitalcommons.uri.edu/srhonorsprog/273</guid>
<pubDate>Tue, 08 May 2012 06:51:05 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Improving the Quality of Life of Homeless Persons using Co-Design and Paul Polack’s </strong></p>
<p><strong>12 Steps for Practical Problem Solving</strong><strong></strong></p>
<p>Nana Ofei-Tenkorang</p>
<p>Sponsor: Vinka Oyanedel-Craver, Civil and Environmental Engineering</p>
<p>The Stewart B. McKinney Act (1994) defines a homeless person as one who lacks a fixed, regular, and adequate night-time residence; and has a primary night time residency that is (A) either a publicly or privately supervised operated shelter designed to provide temporary living accommodations, (B) a public or private place not designed for, or ordinarily used as, a regular sleeping accommodation for human beings and, (C) an institution that provides a temporary residence or service for individuals intended to be institutionalized. This definition includes those people who are on the streets or in shelters and people who face eviction from private dwellings or institutions and who have no residence or resource to obtain housing.</p>
<p>There are two major reasons why people become homeless in Rhode Island: (A) lack of affordable housing and, (B) lack of adequate income. A diverse group of people experience homelessness – namely, children, the elderly, individuals and families in both rural communities and in the cities. The number of homeless people has been on the increase over the past few years. For example there were 484 more homeless people in 2011 than in 2007 who visited shelters in the State which accounts for a 12% increase.</p>
<p>Considering the increase in numbers of affected people, I have tried to develop some practices that improve the quality of life of a homeless person. In this study I try to answer the following question, <em>Is it possible for a homeless person to have access to a better life? </em>One of the best strategies to obtain an answer to this question is to go out and talk to them. This is where <em>co-design </em>comes in. The term <em>co-design </em>simply means developing or improving a service or device together with the user and customers.</p>
<p>To address the root causes of homelessness with the aim to improve the quality of many lives, I utilized Paul Polak’s 12 steps to practical problem solving. He has successfully used this approach to develop alternative solutions to eradicate poverty in developing countries. These steps not only apply to global poverty alleviation, but can also be used to solve problems found in many disciplines.</p>
<p>The goal of this study is to develop a prototype that solves a common problem faced by a person who is homeless. To do this I selected a group of 18 Rhode Island residents who are homeless or on the edge of homelessness and asked them to complete a 13-question survey which I developed. Results of the survey showed that resources such as service providers, labor services, and transportation are not easily accessible. Using co-design, a prototype will be developed to solve these common problems faced by the homeless.</p>
<p>Keywords:</p>
<p>Co-Design, Practical Problem solving, a homeless person, Paul Polak, Poverty</p>

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</description>

<author>Nana Ama Ofei-Tenkorang</author>


</item>


<item>
<title>Transitional Justice and the Truth Commission in Nepal</title>
<link>http://digitalcommons.uri.edu/srhonorsprog/272</link>
<guid isPermaLink="true">http://digitalcommons.uri.edu/srhonorsprog/272</guid>
<pubDate>Tue, 08 May 2012 06:51:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this project is to explore the role of transitional justice mechanisms in directing the peace process, constitution making, and power sharing in Nepal.  For more than ten years Nepal experienced violent conflict between the national army and an insurgent political movement led by the Communist Party of Nepal-Maoist.  The conflict claimed more than 13,000 lives and was characterized by widespread cases of disappearance.  The families of those who were abducted or killed without a trace remain without answers, and the call for a Truth and Reconciliation Commission to document past injustices is strong.</p>
<p>In March 2012, I travelled to Nepal with URI’s Center for Nonviolence and Peace Studies to participate in a cross-cultural nonviolence training with Nepali human rights advocates, social workers and graduate students.  I conducted interviews with the participants and administered a survey to discern the underlying social causes of the violence that occurred from 1996-2006 and to identify the social institutions that allowed the violence to continue for so long.  The survey aimed to evaluate the role of the international community and to answer the question of how to confront the violent events of the past without threatening national unity.</p>
<p>Here I present a report on the results of this survey, critically evaluate the strengths and limitations of Nepal’s Truth and Reconciliation Commission proposed framework, and attempt to answer how a Truth and Reconciliation Commission will move Nepal towards a more democratic, peaceful, just and equitable nation.</p>

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</description>

<author>Andrea Russell</author>


</item>


<item>
<title>The Effects of Interstate Speed Limit Increases: Fatality Rates and Traffic Diversion Versus Speed Spillover</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/101</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/101</guid>
<pubDate>Tue, 08 May 2012 06:50:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis examines two panel data sets of 48 states from 1981 to 2009 and utilizes ordinary least squares (OLS) and fixed effects models to explore the relationship between rural Interstate speed limits and fatality rates and whether rural Interstate speed limits affect non-Interstate safety. Models provide evidence that rural Interstate speed limits higher than 55 MPH lead to higher fatality rates on rural Interstates though this effect is somewhat tempered by reductions in fatality rates for roads other than rural Interstates. These results provide some but not unanimous support for the traffic diversion hypothesis that rural Interstate speed limit increases lead to decreases in fatality rates of other roads. To the author’s knowledge, this paper is the first econometric study to differentiate between the effects of 70 MPH speed limits and speed limits above 70 MPH on fatality rates using a multi-state data set. Considering both rural Interstates and other roads, rural Interstate speed limit increases above 55 MPH are responsible for 39,700 net fatalities, 4.1 percent of total fatalities from 1987, the year limits were first raised, to 2009.</p>

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</description>

<author>Daniel L. Dillon</author>


</item>


<item>
<title>Differentiating Climatic And Successional Influences On Long-Term Development Of A Marsh</title>
<link>http://digitalcommons.brockport.edu/env_facpub/40</link>
<guid isPermaLink="true">http://digitalcommons.brockport.edu/env_facpub/40</guid>
<pubDate>Tue, 08 May 2012 06:50:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Comparison of long-term records of local wetland vegetation dynamics with regional, climate-forced terrestrial vegetation changes can be used to differentiate the rates and effects of autogenic successional processes and allogenic environmental change on wetland vegetation dynamics. We studied Holocene plant macrofossil and pollen sequences from Portage Marsh, a shallow, 18-ha marsh in northeastern Indiana. Between 10 000 and 5700 yr BP the basin was occupied by a shallow, open lake, while upland vegetation consisted of mesic forests of Pinus, Quercus, Ulmus, and Carya. At 5700 yr BP the open lake was replaced rapidly by a shallow marsh, while simultaneously Quercus savanna developed on the surrounding uplands. The marsh was characterized by periodic drawdowns, and the uplands by periodic fires. Species composition of the marsh underwent further changes between 3000 and 2000 yr BP. Upland pollen spectra at Portage Marsh and other sites in the region shifted towards more mesic vegetation during that period. The consistency and temporal correspondence between the changes in upland vegetation and marsh vegetation indicate that the major vegetational changes in the marsh during the Holocene resulted from hydrologic changes forced by regional climate change. Progressive shallowing of the basin by autogenic accumulation of organic sediment constrained vegetational responses to climate change but did not serve as the direct mechanism of change.</p>

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</description>

<author>Darren K. Singer et al.</author>


</item>


<item>
<title>Ocean Front Project for Covering the Cove at King’s Beach, Newport, July, 1974</title>
<link>http://escholar.salve.edu/monumenta-images/6</link>
<guid isPermaLink="true">http://escholar.salve.edu/monumenta-images/6</guid>
<pubDate>Tue, 08 May 2012 06:49:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Charcoal on paper, 36 x 50 inches.  Study for art installation for Monumenta art exhibit, 1974. Lent by the artist.</p>
<p><strong>Publisher:</strong> Salve Regina University Archives and Special Collections.</p>
<p><strong>Source:</strong> Digital reproduction of photograph of work of art. Digitization specifications: Adobe Photoshop 7.0, 600 dpi, 8-bit.</p>
<p><strong>Rights:</strong> This content is provided for educational research and personal use only. While the photographs in this collection are held in the Salve Regina University Archives and Special Collections, copyright for the artwork still resides with the artists. See <a href="http://library.salve.edu/archives/archives_copyright.html" >http://library.salve.edu/archives/archives_copyright.html</a>.</p>

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</description>

<author>Christo</author>


</item>


<item>
<title>No Adequate Remedy at Law: Equity in Massachusetts 1692-1877</title>
<link>http://digitalcommons.law.yale.edu/student_legal_history_papers/2</link>
<guid isPermaLink="true">http://digitalcommons.law.yale.edu/student_legal_history_papers/2</guid>
<pubDate>Tue, 08 May 2012 06:49:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although Massachusetts became the leading jurisdiction for trust law in the United States across the nineteenth century, it never established a separate court resembling the High Court of Chancery in England. This Article asks how the judicial system of Massachusetts functioned without a separate court of chancery. The Article explains that Massachusetts managed by gradually integrating the distinctive elements of English equity into its common law courts. Beginning in the 1690s, the legislature passed laws authorizing components of equity for use in the common law courts. By 1836 the commonwealth's Supreme Judicial Court could oversee discovery, entertain cases with multiple parties, and grant injunctions and- specific performance. The court could also administer certain areas of substantive law, including trust, guardianship, and settlement of estates, that in England belonged to the jurisdiction of the Court of Chancery. Thus, the Supreme Judicial Court had concurrent jurisdictions in law and equity early in the nineteenth century. In this respect the court resembled the federal courts before the merger of law and equity in the Federal Rules of Civil Procedure in 1938. The long process of adding the powers and substantive law of equity to the common law courts of Massachusetts ended in 1877, when the legislature granted the Supreme Judicial Court general equity jurisdiction.</p>

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</description>

<author>Phyllis Maloney Johnson</author>


</item>


<item>
<title>UA45/6 Commencement Program</title>
<link>http://digitalcommons.wku.edu/dlsc_ua_records/1061</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_ua_records/1061</guid>
<pubDate>Tue, 08 May 2012 06:47:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Commencement program listing graduates.</p>

	]]>
</description>

<author>WKU Registrar</author>


</item>


<item>
<title>UA45/6 Commencement Program</title>
<link>http://digitalcommons.wku.edu/dlsc_ua_records/1060</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_ua_records/1060</guid>
<pubDate>Tue, 08 May 2012 06:43:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Commencement program listing graduates.</p>

	]]>
</description>

<author>WKU Registrar</author>


</item>


<item>
<title>Ocean Front Project for Covering the Cove at King’s Beach, Newport, July, 1974</title>
<link>http://escholar.salve.edu/monumenta-images/5</link>
<guid isPermaLink="true">http://escholar.salve.edu/monumenta-images/5</guid>
<pubDate>Tue, 08 May 2012 06:41:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>White cardboard, fabric, charcoal, colored pencil and pencil, 28 x 22 inches.  Study for art installation for Monumenta art exhibit, 1974. Lent by the artist.</p>
<p><strong>Publisher:</strong> Salve Regina University Archives and Special Collections.</p>
<p><strong>Source:</strong> Digital reproduction of photograph of work of art. Digitization specifications: Adobe Photoshop 7.0, 600 dpi, 8-bit.</p>
<p><strong>Rights:</strong> This content is provided for educational research and personal use only. While the photographs in this collection are held in the Salve Regina University Archives and Special Collections, copyright for the artwork still resides with the artists. See <a href="http://library.salve.edu/archives/archives_copyright.html" >http://library.salve.edu/archives/archives_copyright.html</a>.</p>

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</description>

<author>Christo</author>


</item>


<item>
<title>The Evolution of Media Coverage of Historical Sports Controversies</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/100</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/100</guid>
<pubDate>Tue, 08 May 2012 06:41:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis will cover sports controversies throughout the 20th Century in the context of the media’s newspaper coverage of the events. The 1919 Black Sox Scandal, the debate over American participation in the 1936 Olympics, and Muhammad Ali’s conversion to the Nation of Islam, standing as a notorious public figure, and conscientious objection to the Vietnam War will represent the three sports controversies. The media’s adherence to cultural norms is clear in all three cases. The consistent devotion to the cultural and racial atmosphere of their respective eras was constant and helped to perpetuate accepted, mainstream cultural attitudes. Cultural and racial norms were followed in the coverage of the three discussed controversies. The anti-Semitism and racially intolerant sentiments in America during great waves of immigration in the early 1900s allowed for journalists to freely vilify Jews as corrupters of baseball and the ballplayers who were rumored to have thrown the 1919 World Series. The white ballplayers were supported in the press, who protected their own and blamed outsiders. Jim Crow and the Americanization movement forced African American and Jewish newspapers to limit their journalistic bias on both sides of the debate over American participation in the 1936 Berlin Olympics. The white, mainstream press was void of bias as the spirit of isolationism in America triumphed over journalist’s leanings in the Olympic debate. The racial tension created by the Civil Rights movement of the 1960s created an atmosphere that allowed mainstream journalists to heap endless criticism on Muhammad Ali as he gained fame. By portraying him as a villain of society as both a religious radical and traitor to America, journalists created a common enemy in the minds of white America. In all three cases, a pattern of journalists expressing the state of cultural and racial norms of the era is present and significant.</p>

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</description>

<author>Stuart Marsh Dezenhall</author>


</item>


<item>
<title>Free Exercise, Federalism, and the States as Laboratories</title>
<link>http://www.repository.law.indiana.edu/facpub/519</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/519</guid>
<pubDate>Tue, 08 May 2012 06:39:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Daniel O. Conkle</author>


</item>


<item>
<title>Professing Professionals: Christian Pilots on the River of Law</title>
<link>http://www.repository.law.indiana.edu/facpub/518</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/518</guid>
<pubDate>Tue, 08 May 2012 06:39:55 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Daniel O. Conkle</author>


</item>


<item>
<title>Some Problems with &quot;Origins&quot;</title>
<link>http://www.repository.law.indiana.edu/facpub/517</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/517</guid>
<pubDate>Tue, 08 May 2012 06:39:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Stephen A. Conrad</author>


</item>


<item>
<title>Book Review. Conceptual Change and the Constitution</title>
<link>http://www.repository.law.indiana.edu/facpub/516</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/516</guid>
<pubDate>Tue, 08 May 2012 06:39:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Stephen A. Conrad</author>


</item>


<item>
<title>UA45/6 Commencement Program</title>
<link>http://digitalcommons.wku.edu/dlsc_ua_records/1059</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_ua_records/1059</guid>
<pubDate>Tue, 08 May 2012 06:38:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Commencement program listing graduates.</p>

	]]>
</description>

<author>WKU Registrar</author>


</item>


<item>
<title>UA45/6 Commencement Program</title>
<link>http://digitalcommons.wku.edu/dlsc_ua_records/1058</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_ua_records/1058</guid>
<pubDate>Tue, 08 May 2012 06:35:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Commencement program listing graduates.</p>

	]]>
</description>

<author>WKU Registrar</author>


</item>


<item>
<title>UA45/6 Commencement Program</title>
<link>http://digitalcommons.wku.edu/dlsc_ua_records/1057</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_ua_records/1057</guid>
<pubDate>Tue, 08 May 2012 06:32:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Commencement program listing graduates.</p>

	]]>
</description>

<author>WKU Registrar</author>


</item>


<item>
<title>Viper&apos;s Bugloss</title>
<link>http://escholar.salve.edu/monumenta-images/4</link>
<guid isPermaLink="true">http://escholar.salve.edu/monumenta-images/4</guid>
<pubDate>Tue, 08 May 2012 06:31:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Crushed aluminum foil with acrylic lacquer resin, 49 x 68 x 76 inches. Featured in Monumenta art exhibit, 1974, where it was installed at Chateau-sur-Mer. Lent by the Leo Castelli Gallery, New York.</p>
<p><strong>Publisher:</strong> Salve Regina University Archives and Special Collections.</p>
<p><strong>Source:</strong> Digital reproduction of photograph of work of art. Digitization specifications: Adobe Photoshop 7.0, 240 dpi, RGB, 24-bit.</p>
<p><strong>Rights:</strong> This content is provided for educational research and personal use only. While the photographs in this collection are held in the Salve Regina University Archives and Special Collections, copyright for the artwork still resides with the artists. See <a href="http://library.salve.edu/archives/archives_copyright.html" >http://library.salve.edu/archives/archives_copyright.html</a>.</p>

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</description>

<author>John Chamberlain</author>


</item>


<item>
<title>Examining Different School Structures&apos; Effect on Reducing the Achievement Gap Between African-American and White Students</title>
<link>http://digitalcommons.cedarville.edu/education_theses/6</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/6</guid>
<pubDate>Tue, 08 May 2012 06:25:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>The fact that an achievement gap between White and African- American students exists is undisputed. The reasons for this gap are many and complex. Evidence does exist, though, that this gap can be narrowed and potentially eliminated. Evidence also exists that demonstrates that when the gap in academic achievement becomes equal African-Americans are more likely to complete college and earn nearly the same income as Whites. Educators must understand the many reasons for the achievement gap and find ways to narrow the gap and further ensure the future success of all students. It is the purpose for this thesis to explore the reasons for the achievement gap and some possible solutions for narrowing the gap. Specifically, the paper will show one possible solution – the Academy structure.</p>

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</description>

<author>Eric Reini</author>


</item>


<item>
<title>Customer Management Analysis of Irish Plumbing &amp; Heating Distribution System: A Simulation Study</title>
<link>http://arrow.dit.ie/buschmarcon/78</link>
<guid isPermaLink="true">http://arrow.dit.ie/buschmarcon/78</guid>
<pubDate>Tue, 08 May 2012 06:24:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>The sudden burst of the property bubble, coupled with current global economic conditions has resulted in a huge decrease in demand for plumbing and heating fixtures in the Irish construction industry. Moreover, inefficient supply chain management policies have imposed further pressures on companies resulting in more system bottlenecks and unnecessary costs. Inventory management is seen as a functional area that can ease such bottlenecks and in turn increase supply chain efficiency, decrease costs and increase customer satisfaction. The challenge is to predict the balance of on-hand inventory and order quantity to optimise customer satisfaction and minimise inventory cost. It is also essential that managers clearly understand the cost effect stock-outs have on different groups of customer, i.e. customer segmentation policy. Traditional inventory mathematical techniques are inadequate in investigating the influence of customer segmentation policy on performance. To investigate this further, conceptual modelling using flowcharts and data flow diagrams in conjunction with simulation modelling and design of experiments have been developed to characterise the inventory management process of a plumbing and heating distribution centre. Significant process parameters where identified and examined with and without segmented customer management policies, aiming to achieve a high level of customer satisfaction rate at the lowest possible total cost.</p>

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</description>

<author>Amr Arisha et al.</author>


</item>


<item>
<title>Vespers</title>
<link>http://escholar.salve.edu/monumenta-images/3</link>
<guid isPermaLink="true">http://escholar.salve.edu/monumenta-images/3</guid>
<pubDate>Tue, 08 May 2012 06:24:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Steel, 120 x 135 x 40 inches. Featured in Monumenta art exhibit, 1974, where it was installed at Bleak House, Ocean Drive. Lent by the André Emmerich Gallery, New York.</p>
<p><strong>Publisher:</strong> Salve Regina University Archives and Special Collections.</p>
<p><strong>Source:</strong> Digital reproduction of photograph of work of art. Digitization specifications: Adobe Photoshop 7.0, 240 dpi, RGB, 24-bit.</p>
<p><strong>Rights:</strong> This content is provided for educational research and personal use only. While the photographs in this collection are held in the Salve Regina University Archives and Special Collections, copyright for the artwork still resides with the artists. See <a href="http://library.salve.edu/archives/archives_copyright.html" >http://library.salve.edu/archives/archives_copyright.html</a>.</p>

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</description>

<author>Anthony Caro</author>


</item>


<item>
<title>The Synthesis of Macrocyclic Polystyrene by Sequential Atom Transfer Radical Reactions</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/99</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/99</guid>
<pubDate>Tue, 08 May 2012 06:23:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>A method for the production of macrocyclic polystyrene via ring closing of a linear !,"-dibrominated polystyrene by an Atom Transfer Radical Coupling (ATRC) reaction is described. The dibrominated polystyrene chain was produced from two simultaneous atom transfer radical polymerizations (ATRPs) originating from a dibrominated benzal bromide initiator. To ensure the retention of the halogen end groups polymerization was allowed to proceed to less than 50% conversion. Using this precursor in an intramolecular ATRC (ring closing) reaction was found to yield in excess of 90% cyclic product based on refractive index-gel permeation chromatography (GPC) analysis. The cyclic architecture of the polymer was verified by GPC, Nuclear Magnetic Resonance (NMR), and mass spectrometry analysis. The utility of this method has been expanded by the addition of 2-methyl-2-nitrosopropane to the coupling reaction, which allows for the coupling to proceed at a faster rate and to yield macrocycles with incorporated alkoxyamine functionality. The alkoxyamine functionality allows for degradation of the cycles at high temperatures (>125° C) and we hypothesize that it may allow the macrocycles to act as a macroinitiator for a ring expansion polymerization in future studies.</p>

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</description>

<author>Andrew F. Voter</author>


</item>


<item>
<title>Verifying Harder&apos;s Conjecture for Classical and Siegel Modular Forms</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/98</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/98</guid>
<pubDate>Tue, 08 May 2012 06:23:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>A conjecture by Harder shows a surprising congruence between the coefficients of “classical” modular forms and the Hecke eigenvalues of corresponding Siegel modular forms, contigent upon “large primes” dividing the critical values of the given classical modular form.</p>
<p>Harder’s Conjecture has already been verified for one-dimensional spaces of classical and Siegel modular forms (along with some two-dimensional cases), and for primes p 37. We verify the conjecture for higher-dimensional spaces, and up to a comparable prime p.</p>

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</description>

<author>David Sulon</author>


</item>


<item>
<title>Intelligent Simulation-based Lot Scheduling of Photolithography Toolsets in a Wafer Fabrication Facility</title>
<link>http://arrow.dit.ie/buschmarcon/77</link>
<guid isPermaLink="true">http://arrow.dit.ie/buschmarcon/77</guid>
<pubDate>Tue, 08 May 2012 06:20:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Scheduling of a semiconductor manufacturing facility is one of the most complex tasks encountered. Confronted with a high technology product market, semiconductor manufacturing is increasingly more dynamic and competitive in the introduction of new products in shorter time intervals. Photolithography, being one of the processes repeated often, is a fabrication bottleneck. Lot scheduling within photolithography is a challenging activity where substantial improvements in factory performance can be made. The proposed scheduling methodology integrates two common approaches, simulation and artificial intelligence. Using detailed simulation modeling within a structured modeling method, a comprehensive model to characterize the photolithography process was developed. An artificial intelligence scheduler was then developed and integrated with the model with the goal of reducing work-in-process (WIP), setup time, and throughput time. The results have shown a significant improvement in lot cycle time as well as tool utilization, improved the throughput time by an average of 15% and is currently in use for scheduling the photolithography process.</p>

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</description>

<author>Amr Arisha et al.</author>


</item>


<item>
<title>Lightening</title>
<link>http://escholar.salve.edu/monumenta-images/2</link>
<guid isPermaLink="true">http://escholar.salve.edu/monumenta-images/2</guid>
<pubDate>Tue, 08 May 2012 06:17:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sheet metal, painted red, 144 x 180 inches. Featured in Monumenta art exhibit, 1974, where it was installed at Bleak House, Ocean Drive. Lent by Pens Galleries, New York.</p>
<p><strong>Publisher:</strong> Salve Regina University Archives and Special Collections.</p>
<p><strong>Source:</strong> Digital reproduction of photograph of work of art. Digitization specifications: Adobe Photoshop 7.0, 240 dpi, RGB, 24-bit.</p>
<p><strong>Rights:</strong> This content is provided for educational research and personal use only. While the photographs in this collection are held in the Salve Regina University Archives and Special Collections, copyright for the artwork still resides with the artists. See <a href="http://library.salve.edu/archives/archives_copyright.html" >http://library.salve.edu/archives/archives_copyright.html</a>.</p>

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</description>

<author>Alexander Calder</author>


</item>


<item>
<title>Ray Wilson</title>
<link>http://digitalcommons.iwu.edu/oralhistory_gallery/74</link>
<guid isPermaLink="true">http://digitalcommons.iwu.edu/oralhistory_gallery/74</guid>
<pubDate>Tue, 08 May 2012 06:17:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Interview located at <br><a href="http://europa.iwu.edu:8080/ramgen/reserves/bpress/wilson_edited.ra" target="_blank" >http://europa.iwu.edu:8080/ramgen/reserves/bpress/wilson_edited.ra</a></p>

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</description>

<author>Wesleyana, Illinois Wesleyan University</author>


</item>


<item>
<title>Utilization of Probabilistic Models in Short Read Assembly from Second-Generation Sequencing</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/97</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/97</guid>
<pubDate>Tue, 08 May 2012 06:16:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>With the advent of cheaper and faster DNA sequencing technologies, assembly methods have greatly changed. Instead of outputting reads that are thousands of base pairs long, new sequencers parallelize the task by producing read lengths between 35 and 400 base pairs. Reconstructing an organism’s genome from these millions of reads is a computationally expensive task. Our algorithm solves this problem by organizing and indexing the reads using n-grams, which are short, fixed-length DNA sequences of length n. These n-grams are used to efficiently locate putative read joins, thereby eliminating the need to perform an exhaustive search over all possible read pairs. Our goal was develop a novel n-gram method for the assembly of genomes from next-generation sequencers. Specifically, a probabilistic, iterative approach was utilized to determine the most likely reads to join through development of a new metric that models the probability of any two arbitrary reads being joined together. Tests were run using simulated short read data based on randomly created genomes ranging in lengths from 10,000 to 100,000 nucleotides with 16 to 20x coverage. We were able to successfully re-assemble entire genomes up to 100,000 nucleotides in length.</p>

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</description>

<author>Matthew W. Segar</author>


</item>


<item>
<title>The Impact of Education and Gender on Perceptions of Borderline Personality Disorder</title>
<link>http://scholarship.shu.edu/theses/211</link>
<guid isPermaLink="true">http://scholarship.shu.edu/theses/211</guid>
<pubDate>Tue, 08 May 2012 06:16:44 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jennifer J. Noonan</author>


</item>


<item>
<title>Simulation Model to Investigate Flexible Workload Management for Healthcare and Servicescape Environment</title>
<link>http://arrow.dit.ie/buschmarcon/76</link>
<guid isPermaLink="true">http://arrow.dit.ie/buschmarcon/76</guid>
<pubDate>Tue, 08 May 2012 06:16:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>High demand and poor staffing conditions cause avoidable pressure and stress among healthcare personnel which results in burnout symptoms and unplanned absenteeism which are hidden cost drivers. The work environment within an emergency department is commonly arranged in a flexible workload which is highly dynamic and complex for the outside observer. Using detailed simulation modeling within structured modeling methods, a comprehensive model to characterize the nurses' time utilization in such flexible dynamic workload environment was investigated. The results have been used to derive a generalized analytic expression that describes certain settings that lead to an instable queuing system with serious consequences for the healthcare facility. Thus decision makers are hence equipped with a tool which allows identifying and preventing such conditions that affect service quality level.</p>

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</description>

<author>Amr Arisha et al.</author>


</item>


<item>
<title>A Teacher&apos;s Approach: Integrating Technology Appropriately Into a First Grade Classroom</title>
<link>http://digitalcommons.cedarville.edu/education_theses/5</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/5</guid>
<pubDate>Tue, 08 May 2012 06:14:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>How are first grade classrooms using technology? How are children using technology at home? Does the use of technology really improve academic achievement? An experiment was conducted to determine the effectiveness of using technology to teach a unit in Social Studies to first grade students. The study occurred in a Christian school in Lancaster, Ohio using thirty-seven first grade students. One class comprised the control group with Social Studies instruction taught in a traditional manner. The other class was the experimental group, which used technology such as the Internet, PowerPoint Presentations, and video and audio recordings to provide the instruction. One Social Studies unit was used in the six-week study with an assessment taken each week. Independent-Samples T-Tests were done on the six assessments. Only one of the assessments showed a significant difference in scores in favor of the experimental group. The other five assessments did not show a significant difference. Due to the experimental group having one of the assessments showing a statistically significant difference, and to the fact that the means were higher on four of the other tests, although not significantly, the researcher is encouraged that technology does provide a difference in student achievement. When combined with the increase in interest and enjoyment of the students using technology, technology appears to be a positive motivation for student achievement.</p>

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</description>

<author>Loretta J. Phalen</author>


</item>


<item>
<title>Ray Wilson</title>
<link>http://digitalcommons.iwu.edu/oralhistory_gallery/73</link>
<guid isPermaLink="true">http://digitalcommons.iwu.edu/oralhistory_gallery/73</guid>
<pubDate>Tue, 08 May 2012 06:13:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Interview located at <br><a href="http://europa.iwu.edu:8080/ramgen/reserves/bpress/wilson_edited.ra" target="_blank" >http://europa.iwu.edu:8080/ramgen/reserves/bpress/wilson_edited.ra</a></p>

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</description>

<author>Daniel Maurer 2012</author>


</item>


<item>
<title>Integrating Balanced Scorecard and Simulation Modelling to Improve Emergency Department Performance in Irish Hospitals</title>
<link>http://arrow.dit.ie/buschmarcon/75</link>
<guid isPermaLink="true">http://arrow.dit.ie/buschmarcon/75</guid>
<pubDate>Tue, 08 May 2012 06:11:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the healthcare sector, there is a requirement for innovative solutions in managing the high levels of complexity and uncertainty within Emergency Departments (EDs). Simulation modeling is currently seen as a competent means of analyzing EDs, which allows changes effects to be understood and predicted more easily. The Balanced Scorecard (BSC), well-known performance management concept, has become a steering method in approaching new improvement cycles. This paper presents a methodology that integrates BSC and simulation modeling to improve the performance of ED in a University Hospital in North Dublin. BSC design began with understanding patient's needs, ED activities, as well as training and development programs. Then a detailed simulation model was developed and integrated with the BSC to provide a comprehensive decision support system. This integrated model can be used for evaluation of various decisions in emergency area. The developed integrated model is also a tool for improvement.</p>

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</description>

<author>Amr Arisha et al.</author>


</item>


<item>
<title>Frank Corr</title>
<link>http://arrow.dit.ie/scthebk/23</link>
<guid isPermaLink="true">http://arrow.dit.ie/scthebk/23</guid>
<pubDate>Tue, 08 May 2012 06:10:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank Corr</author>


</item>


<item>
<title>Americans&apos; Unwillingness to Pay Taxes Before the American Revolution: An Uncomfortable Legacy</title>
<link>http://uknowledge.uky.edu/law_facpub/161</link>
<guid isPermaLink="true">http://uknowledge.uky.edu/law_facpub/161</guid>
<pubDate>Tue, 08 May 2012 06:09:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>When one reflects on the sorry condition of America’s finances one has to wonder why there is such resistance to fiscal discipline. Is it merely because there is an obstreperous group in the US Congress who cannot abide any tax? Has the public been subtly lobbied into believing that American taxes are high, pointless and intolerable or is there some gene in the America’s body politic that has always been there that expresses itself from time to time in a pernicious cheapness? Perhaps all those things are true, or perhaps none. Nevertheless, a glance backward at Colonial days can stimulate a sense of déjà-vu. This article explores the history of America’s relationship to taxes prior to the American Revolution.</p>

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</description>

<author>Richard A. Westin</author>


</item>


<item>
<title>Runoff Water Quality and Pollutant Mass Loads From Extensive Green Roofs</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/96</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/96</guid>
<pubDate>Tue, 08 May 2012 06:09:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Green roof mitigation of volume and peak flow-rate of stormwater runoff has been studied extensively. However, due to the common practice of green roof fertilization, there is the potential for introduction of nutrients into local bodies of water. Therefore, this study compares green roof runoff quality with the water quality of precipitation and runoff from a bare shingle roof. The runoff from a demonstration-scale extensive green roof was analyzed during the summer of 2011 for its effect on runoff volume and analyzed during eleven storm events in the fall and winter for concentrations of copper, cadmium, zinc, lead, nitrogen species, total nitrogen, total organic carbon, sulfate, orthophosphate, and other monovalent and divalent ions. The green roof reduced the overall volume of runoff and served as a sink for NO3 - and NH4 +. However, the green roof was also a source for the pollutants PO4 3-, SO4 2-, TOC, cations, and total nitrogen. Metals such as zinc and lead showed trends of higher mass loads in the bare roof runoff than in precipitation and green roof runoff, although results were not statistically significant. The green roof also showed trends, although also not statistically significant, of retaining cadmium and copper. With the green roof serving as a source of phosphorous species and a sink for nitrogen species, and appearing to a retain metals and total volume, the life cycle impact analysis shows minimum impacts from the green roof, when compared with precipitation and bare roof runoff, in all but fresh water eutrophication. Therefore, the best environments to install a green roof may be in coastal environments.</p>

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</description>

<author>Rebecca H. Shopiro</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 11, no. 1</title>
<link>http://collected.jcu.edu/carrollquarterly/29</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/29</guid>
<pubDate>Tue, 08 May 2012 06:08:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 11, no. 2</title>
<link>http://collected.jcu.edu/carrollquarterly/28</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/28</guid>
<pubDate>Tue, 08 May 2012 06:08:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 11, no. 3</title>
<link>http://collected.jcu.edu/carrollquarterly/27</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/27</guid>
<pubDate>Tue, 08 May 2012 06:08:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Carroll Quarterly, vol. 11, no. 4</title>
<link>http://collected.jcu.edu/carrollquarterly/26</link>
<guid isPermaLink="true">http://collected.jcu.edu/carrollquarterly/26</guid>
<pubDate>Tue, 08 May 2012 06:08:19 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Carroll University</author>


</item>


<item>
<title>The Implementation of a Visco-hyperelastic Numerical Material Model for Simulating the Behaviour of Polymer Foam Materials</title>
<link>http://arrow.dit.ie/cerart/10</link>
<guid isPermaLink="true">http://arrow.dit.ie/cerart/10</guid>
<pubDate>Tue, 08 May 2012 06:02:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Polyurethane foam has been in use for some time in wheelchair seating systems as it offers good pressure relieving capabilities in most cases. However, little characterisation work has gone into seating foam materials by comparison with conventional elastomeric materials. Accurate material models could allow better prediction of foam in-service behaviour, which could potentially improve seating design practises. The objective of this work was to develop an approach for the validation of hyperelastic and viscoelastic material model parameters used to simulate polyurethane foam behaviour. Material parameters were identified from relevant test procedures and implemented in a Finite Element simulation of an ISO foam indentation procedure. Physical test results were compared to results predicted using the identified material parameters. Simulations suggest a good overall agreement between test and model results.</p>

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</description>

<author>Conor Briody et al.</author>


</item>


<item>
<title>A study of visual puffery in fragrance advertising: Is the message sent stronger than the actual scent?</title>
<link>http://scholarship.rollins.edu/as_facpub/35</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/as_facpub/35</guid>
<pubDate>Tue, 08 May 2012 06:02:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Purpose - This paper investigates visual exaggerations of fragrance advertisements by comparing subjects’ expectations resulting from print ads to their subsequent product evaluations. It then considers whether the actual scents fall short, meet or exceed these expectations.</p>
<p>Design/methodology/approach - By means of a semiotic analysis we capture the corresponding literary attributes of the ads to develop adjective pairs describing the meaning of the ads. Interviews are conducted to assess the meaning that consumers draw from the fragrance ads and we supplement these findings by performing a blind olfactory product evaluation of the fragrances. Paired sample t-tests are used to compare subjects’ ad expectations to their subsequent product evaluation of the actual scent.</p>
<p>Findings - Our results show that the visual cues and imagery in the fragrance ads appear, under certain conditions, to result in product expectations that exceed actual product evaluations, suggesting the existence of visual puffery. We also found that the more abstract descriptors of the ad resulted in significantly higher expectations, while the more concrete descriptors resulted in significantly lower expectations than the actual product evaluation.</p>
<p>Research limitations/implications - A small sample size of homogenous consumers limits the generalizability of the results. No measures of attitude effectiveness were taken.</p>
<p>Practical implications - Visual puffery may be effective and help marketers, even in countries where verbal puffery is illegal, to use another means to reach consumers.</p>
<p>Originality/value - This paper investigates an under-researched area in advertising. A multi-method approach and primary data are used to assess subjects’ ad expectations of a fragrance and the actual product evaluation and demonstrates the existence of visual puffery.</p>

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</description>

<author>Mark Toncar et al.</author>


</item>


<item>
<title>A Test of Absolute Numerousness Judgments in Lion-Tailed Macaques (Macaca Silenus)</title>
<link>http://digitalcommons.bucknell.edu/honors_theses/95</link>
<guid isPermaLink="true">http://digitalcommons.bucknell.edu/honors_theses/95</guid>
<pubDate>Tue, 08 May 2012 06:01:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Numerous studies have shown that animals have a sense of quantity and can distinguish between relative amounts. The concepts of relative numerousness, estimation, and subitizing are well established in species as diverse as chimpanzees and salamanders. Mobile animals have practical use for an understanding of number in common situations such as predation, mating, and competition. However, the ability to identify discrete quantities has only been firmly established in humans. The purpose of this study was to test for such “absolute numerousness” judgments in three lion-tailed macaques (Macaca silenus), a non-human primate.</p>
<p>The three macaques tested had previously been trained on a computerized matchto- sample (MTS) task using geometric shapes. In this study, they were introduced to a MTS task containing a numerical cue, which required the monkeys to match stimuli containing either one or two items for rewards. If monkeys were successful at the initial matching task, they were tested with stimuli in which the position of the items and then the surface area of the items was controlled. If the monkeys could match successfully without using these non-numerical cues, they would demonstrate the capability to make absolute numerousness judgments.</p>
<p>None of the monkeys matched successfully using the numerical cue, so no evidence of absolute numerosity was found. Each macaque progressed through the experiment in an individualized manner, attempting a variety of strategies to obtain rewards. These included side preferences and an alternating-side strategy that were unrelated to the numerical cues in the stimuli. When it became clear that the monkeys were not matching based on a stimulus-based cue, they were tested again on matching geometric shapes. All three macaques stopped using their alternate strategies and were able to match shapes successfully, demonstrating that they were still capable of completing the matching task. The data suggest that the monkeys could not transfer this ability to the numerical stimuli. This indicates that the macaques lack a sense of exact quantity, or that they could not recognize the numerical cues in the stimuli as being relevant to the task.</p>

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</description>

<author>Allison S. Fox</author>


</item>


<item>
<title>Mental Illness, Advocacy &amp; Recovery: Ready or Not?</title>
<link>http://escholarship.umassmed.edu/pib/vol9/iss4/1</link>
<guid isPermaLink="true">http://escholarship.umassmed.edu/pib/vol9/iss4/1</guid>
<pubDate>Tue, 08 May 2012 05:58:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Mental health advocates in America have been in existence since the opening of the first public asylum – Eastern State Hospital in Williamsburg, Virginia – in 1772. Advocacy and the role of advocates still continues today, 240 years later, as the mental health community lobbies for the rights and concerns of individuals living with mental illness. Advocacy efforts focus on various issues such as comprehensive health insurance coverage (e.g., the federal Patient Protection and Affordable Care Act), the implementation of advance directives, and the need for specialized services for children with mental health conditions and their families. This Psychiatry Issue Brief explores the history of recovery and advocacy, barriers and strategies to the advocacy movement, and potential pitfalls of advocates not working together toward shared goals.</p>

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</description>

<author>Jeffrey L. Geller</author>


<category>Legal Issues</category>

<category>Policy</category>

<category>Rehabilitation/Recovery</category>

</item>


<item>
<title>The Origins of the Oral Deposition in the Federal Rules: Who’s in Charge?</title>
<link>http://digitalcommons.law.yale.edu/student_legal_history_papers/1</link>
<guid isPermaLink="true">http://digitalcommons.law.yale.edu/student_legal_history_papers/1</guid>
<pubDate>Tue, 08 May 2012 05:58:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper traces the origins of the oral deposition in the Federal Rules of Civil Procedure (“Federal Rules”) with an emphasis on the role of the officer in charge of the deposition. In Parts II and III, I document the origins of the deposition, drawing on published sources. In Parts IV and V, I draw upon unpublished sources regarding the 1930s Advisory Committee’s decision not to provide for a judicial officer who would have the authority to rule on the admissibility of evidence during the deposition. That decision was an important, yet overlooked, element in the shaping of modern American civil procedure, including the displacement of civil trial by pretrial discovery. A striking attribute of the modern American deposition is that opposing counsel conduct the questioning in the absence of a judicial officer. The Advisory Committee that drafted the 1938 Federal Rules considered a proposal to provide deponents (both party witnesses and non-party witnesses) with the option of requesting a master to rule on the admissibility of evidence at the pretrial examination. According to archival sources, members of the Advisory Committee concluded that the systemic disadvantages of that proposal outweighed the advantages. I describe the historical origins of three salient features of the deposition: the near-absence of the rules of evidence; the presence of an “officer in charge” who has no power the rule on the admissibility of evidence; and the breadth of the permitted scope of inquiry. I discuss why the term “officer” is misleading: the examination is conducted entirely by adverse parties in the absence of a judge or a judge-like figure. The officer in charge is simply a stenographer or notary public who swears in the deponent and records the testimony; he or she exercises no adjudicatory function.</p>

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</description>

<author>Ezra Siller</author>


</item>


<item>
<title>Media Convergence of Newspapers: A Content Analysis of the Houston Chronicle&apos;s Print- and Web-based Content</title>
<link>http://digitalcommons.liberty.edu/masters/238</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/masters/238</guid>
<pubDate>Tue, 08 May 2012 05:58:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The channels of news media have changed. The traditional route of receiving news via a newspaper has evolved into a more digital path, leaving many to question the future of the print publication.  This study evaluates the print- and Web-based content of the Houston Chronicle. The researcher adds to the field of research on news media by analyzing the online and print content of the publication, creating a new way to categorize and evaluate the subject matter by placing it into four categories: repetition, adaptation, representation, and unique. The researcher seeks to answer three research questions, discovering how each medium exemplifies elements of media convergence.</p>

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</description>

<author>Amanda Sullivan</author>


<category>Journalism</category>

<category>Mass Communications</category>

<category>Information Science</category>

</item>


<item>
<title>Federalism, Education, and Citizenship in an Era of Democratic Deliberation</title>
<link>http://opus.ipfw.edu/dpea_facpubs/129</link>
<guid isPermaLink="true">http://opus.ipfw.edu/dpea_facpubs/129</guid>
<pubDate>Tue, 08 May 2012 05:58:03 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Brian L. Fife</author>


</item>


<item>
<title>Public Pension Crisis and Investment Risk Taking: Underfunding, Fiscal Constraints, Public Accounting, and Policy Implications</title>
<link>http://research.upjohn.org/up_policypapers/13</link>
<guid isPermaLink="true">http://research.upjohn.org/up_policypapers/13</guid>
<pubDate>Tue, 08 May 2012 05:55:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Public pension funds that cover retirement benefits for almost 20 million active or retired employees have been significantly underfunded. An important, though largely overlooked, issue related to pension underfunding is the excessive investment risk levels assumed by public plans. Our analysis suggests government accounting standards strongly affect public fund investment risk, as higher return assumptions (used to discount pension liabilities) are associated with higher investment risk. Public funds undertake more risk if they are underfunded and have lower investment returns in previous years, consistent with the risk transfer hypothesis. Furthermore, pension funds in states facing fiscal constraints allocate more assets to equity and have higher betas. There also appears to be a herding effect in that a change in CalPERS portfolio beta or equity allocation is mimicked by other pension funds. Solutions to excessive investment risk include use of more realistic discount rates such as a Treasury rate or a municipal bond yield to estimate liabilities and regulations or practices that reduce the ability of a plan to shift an underfunding burden to future generations.</p>

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</description>

<author>Nancy Mohan et al.</author>


<category>EMPLOYMENT and COMPENSATION</category>

<category>Retirement and pensions</category>

<category>Pensions</category>

</item>


<item>
<title>The Effects of Technology Instruction on the Academic Achievement of Fifth Grade Students</title>
<link>http://digitalcommons.liberty.edu/doctoral/556</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/doctoral/556</guid>
<pubDate>Tue, 08 May 2012 05:51:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>A digital native is an individual born between 1981 and 2001, and children born after 2001 are called millennials. Educators are expected to meet the needs of today's technologically savvy students. Some researchers assert that an academic `moral panic' is taking place that lacks the empirical and theoretical knowledge to support the claims that education needs to change to meet the needs of digital natives and millennials. The problem is that considering that the majority of students today are digital natives are educators meeting the learning needs of their students. This research study focused on the use of instructional technology and how it effects student achievement for fifth grade science and math instruction. Using the 2010 and 2011 math and science CRCT test scores, the SPSS statistical software was employed to run an independent sample t test to measure the mean difference between the experimental and control groups. The results found that the use of technological instruction in this instance did not increase student academic achievement.</p>

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</description>

<author>Karen Davis</author>


<category>Education, General</category>

<category>Education, Technology</category>

<category>Education, Curriculum and Instruction</category>

<category>Education, Elementary</category>

<category>Education, Teacher Training</category>

<category>Education, Tests and Measurements</category>

</item>


<item>
<title>The Effects of Single-Gender Classes on Students&apos; Physical Fitness Test Performances and Attitudes</title>
<link>http://digitalcommons.liberty.edu/doctoral/555</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/doctoral/555</guid>
<pubDate>Tue, 08 May 2012 05:51:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this pretest-posttest control group study was to test the Social Cognitive Theory by comparing the effects of class type, coeducational or single-gender, on physical fitness test performance and attitudes, controlling for previous fitness levels, among sixth-grade male and female physical education students at a Northwest Georgia Middle School.  A total of 277 students participated in the newly state-mandated FitnessGram physical fitness test as part of their regular physical education class. The groups then participated in standard physical education lessons for four weeks.  Then, in each of the two sixth-grade physical education periods, students were divided among the teachers according to gender, resulting in a female-only group, a male-only group, and a typical coeducational group.  Students again participated in the FitnessGram with their newly formed groups.  Afterwards, students were given the Physical Fitness Attitudinal Scale to determine their attitudes about physical education and fitness.  The data collected were then analyzed by ANCOVA and MANOVA to determine the effect of gender-grouped classes on physical fitness test performance and student attitudes.  The data revealed statistically significant differences between participant groups' performances on some but not all parts of the FitnessGram physical fitness assessment. The data did not show a statistically significant difference between student attitudes toward physical fitness with and without single-gender grouping on the Physical Fitness Attitudinal Scale.</p>

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</description>

<author>Zachary Wilson</author>


<category>Education, General</category>

<category>Education, Physical</category>

<category>Education, Tests and Measurements</category>

<category>Education, Educational Psychology</category>

<category>Education, Secondary</category>

<category>Education, Health</category>

<category>Health Sciences, General</category>

</item>


<item>
<title>Relational Leadership: A Study of Organizational Health and Clergy within the Wesleyan Church</title>
<link>http://place.asburyseminary.edu/ecommonsatsdissertations/14</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatsdissertations/14</guid>
<pubDate>Tue, 08 May 2012 05:47:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>In many large churches (over one thousand in weekend worship attendance) today, a vast relational disconnect exists between senior pastors and pastoral staff team members. As a result, many staff pastors feel unsatisfied in their team roles and relationships as well as feeling devalued as leader. This relational deficiency frequently results in a lack of communication, trust, and belief in and with the senior leader. The staff pastor’s productivity decreases and the church ceases to be what God designed it to be—a place of relational and social connection.</p>
<p>The purpose of this study was to determine characteristics of relational leadership and utilize these traits to assess the relational and leadership health of the top twenty flagship churches of the Wesleyan Church of North America. The assessment was completed using two instruments: the Organizational Leadership Assessment (OLA) and the Relational Support Scale (RSS). The OLA measured the organizational health of the churches using six servant leadership characteristics. The RSS measured church health in regards to four relational leadership characteristics. Semi-structured senior pastor interviews were also utilized as a supplementary measure.</p>
<p>This explanatory, non-experimental, mixed-design study used standardized, Web-based surveys, phone calls, and e-mails to gather the necessary data.</p>
<p>An analysis of the findings suggests that senior pastors tend to view their relational leadership performance and ability in a more positive manner than do their pastoral staff members or key lay leaders.</p>

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</description>

<author>Brian Voyght Bradford</author>


</item>


<item>
<title>A Project Designed to Examine the Effects that Collaborative Peer Interactions Have on the Professional Development of Teachers</title>
<link>http://digitalcommons.cedarville.edu/education_theses/4</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/4</guid>
<pubDate>Tue, 08 May 2012 05:46:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>﻿﻿Much research links collaborative experiences to the professional development of teachers. The author of this study designed a project, called the Buddy System, which provided opportunities for teachers to observe one another in the classroom and to interact with one another collaboratively. The goal was to determine if these activities provided a means of professional development. After the implementation of this sixteen-week project, the author collected data from a variety of sources which indicated that professional development had taken place.</p>

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</description>

<author>Van Holloway</author>


</item>


<item>
<title>A retrospective study to evaluate the efficacy of trimethoprim/sulfamethoxazole (TMP/SMX) compared to daptomycin or linezolid for the treatment of infections due to methicillin-resistant staphylococcus aureus (MRSA)</title>
<link>http://commons.emich.edu/theses/387</link>
<guid isPermaLink="true">http://commons.emich.edu/theses/387</guid>
<pubDate>Tue, 08 May 2012 05:45:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Aparna Lakshmi Murari</author>


</item>


<item>
<title>Effective Technology Integration: A Plan for Professional Development</title>
<link>http://digitalcommons.cedarville.edu/education_theses/3</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/3</guid>
<pubDate>Tue, 08 May 2012 05:34:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Is educational technology effective in increasing student learning? If technology is an effective tool in the classroom, how can teachers best be trained to use it appropriately? An experiment was conducted to determine the effectiveness of a constructivist math class utilizing computer technology as well as other tools. The study occurred in a Christian school in Northern Kentucky using fifty-one sixth grade students. One class comprised the control group, with math instruction that differed little from the traditional background of the school. The other class was the experimental group, which used the Internet, spread sheets, word processors, and measuring devices to learn in a hands-on environment. Two math units were used in the six-week study. A one-way ANOVA test showed no significant difference in the first unit scores. The one-way ANOVA test of the second unit showed a significant difference in favor of the control group. Despite these results, the researcher was not discouraged, primarily because chi-square tests of a survey given to students in the experimental group overwhelmingly showed positive motivation in math during the study.</p>

	]]>
</description>

<author>Craig G. Dunlap</author>


</item>


<item>
<title>Effects of Divorce on Children and Ways Schools Can Offer Support</title>
<link>http://digitalcommons.cedarville.edu/education_theses/2</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/2</guid>
<pubDate>Tue, 08 May 2012 05:34:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>From 1990 to 1999, almost 15 million children in the United States experienced the divorce of their parents. Children experience varied effects from the divorce process, and they carry these effects with them into the classroom. By knowing what possible effects may occur, educators can be better equipped to effectively teach the children from divorced families who are in their care. It is the purpose of this thesis to explore both the possible effects of parental separation and divorce on children and to discover ways schools can provide support to help the children thrive. A unique characteristic of this study was its setting in a Christian school of approximately 700 students.</p>

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</description>

<author>Cheryl Ellington</author>


</item>


<item>
<title>Woodwinds Performance at Wagon Wheel Theatre&apos;s production of MIRACLE ON 34th STREET</title>
<link>http://opus.ipfw.edu/music_facperform/176</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/176</guid>
<pubDate>Tue, 08 May 2012 05:19:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Performed as a pit orchestra player for the musical MIRACLE ON 34th STREET at the Wagon Wheel Theatre. The run was between Nov. 23 - Dec. 18.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Alto saxophone Performance with the Jim Petty Big Band</title>
<link>http://opus.ipfw.edu/music_facperform/175</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/175</guid>
<pubDate>Tue, 08 May 2012 05:19:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Performed lead alto with the Jim Petty Big Band from Texas. This was for a fundraiser for Defiance College.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Presented the FORGOTTEN SAXOPHONE concert for the Defiance, Ohio Cultural Council Concert Series</title>
<link>http://opus.ipfw.edu/music_facperform/174</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/174</guid>
<pubDate>Tue, 08 May 2012 05:19:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Presented a two hour concert of music all featuring the En Sopranino Saxophone with IPFW professors Laura Lydy (guitar) and Steven Walley (piano).</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Woodwinds Performance at Civic Theatre&apos;s production of CHICAGO</title>
<link>http://opus.ipfw.edu/music_facperform/173</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/173</guid>
<pubDate>Tue, 08 May 2012 05:19:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Performed as a pit orchestra member for the Civic's production of CHICAGO. Played Reed 1 for the run of the show between October 24-November 12.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Faculty Artists Recital at ACPL featuring music from CONVERGENCE in CD</title>
<link>http://opus.ipfw.edu/music_facperform/172</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/172</guid>
<pubDate>Tue, 08 May 2012 05:19:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>This recital featured new works from my upcoming 3rd solo sopranino saxophone CD. It was presented at ACPL to fulfill a requirement by the Indiana Arts Commission for a grant I received to assist in producing this CD.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Release of 2nd Solo Sopranino Saxophone CD entitled HIGH NOTES: MORE NEW MUSIC FOR THE SOPRANINO SAXOPHONE on the Centaur label.</title>
<link>http://opus.ipfw.edu/music_facperform/171</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/171</guid>
<pubDate>Tue, 08 May 2012 05:19:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The official release of the 2nd solo CD project for sopranino saxophone by Centaur Record label, Baton Rouge, Louisiana.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Recorded a Saxophone Quartet CD with the Sempre Saxophone Quartet</title>
<link>http://opus.ipfw.edu/music_facperform/170</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/170</guid>
<pubDate>Tue, 08 May 2012 05:16:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Record an entire saxophone quartet CD project at Sweetwater with the Sempre Saxophone Quartet. It was recorded between July 25-29. The CD will be produced by Centaur Records and will be released in 2013. The CD is entitled THE MUSIC OF WILLIAM SCHMIDT.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Woodwinds Performance at Civic Theatre&apos;s production of HAIRSPRAY</title>
<link>http://opus.ipfw.edu/music_facperform/169</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/169</guid>
<pubDate>Tue, 08 May 2012 05:16:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Performed as a pit orchestra player on woodwinds for the production of HAIRSPRAY at the  Fort Wayne Civic Theater. The run was from July 18- August 7.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Woodwinds Performance at Wagon Wheel Theatre&apos;s production of STATE FAIR</title>
<link>http://opus.ipfw.edu/music_facperform/168</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/168</guid>
<pubDate>Tue, 08 May 2012 05:16:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Performed as a pit orchestra player on woodwinds for the production of STATE FAIR at the Wagon Wheel Theater. The run was from July 3-16</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Woodwinds Performance at Wagon Wheel Theatre&apos;s production of HAIRSPRAY</title>
<link>http://opus.ipfw.edu/music_facperform/167</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/167</guid>
<pubDate>Tue, 08 May 2012 05:16:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Performed as a pit orchestra player on woodwinds for the production of HAIRSPRAY at the Wagon Wheel Theater. The run was from June 19 - July 2.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Woodwinds Performance at Wagon Wheel Theatre&apos;s production of TARZAN</title>
<link>http://opus.ipfw.edu/music_facperform/166</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/166</guid>
<pubDate>Tue, 08 May 2012 05:16:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Performed as a pit orchestra player on woodwinds for the production of TARZAN at the Wagon Wheel Theater. The run was from June 1-18</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Guest Artist for Huntington North High School&apos;s Jazz Explosion concert</title>
<link>http://opus.ipfw.edu/music_facperform/165</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/165</guid>
<pubDate>Tue, 08 May 2012 05:16:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Presented two days of clinics with the Huntington North High School Jazz Bands and was the featured guest artist on their JAZZ EXPLOSION concert.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Sempre Saxophone Quartet signed at Recording Contract with Centaur Records to record CD</title>
<link>http://opus.ipfw.edu/music_facpubs/29</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facpubs/29</guid>
<pubDate>Tue, 08 May 2012 05:16:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Victor Sachse, owner of Centaur Records, listened to our recordings and signed the Sempre Saxophone Quartet to produce our first CD. The CD features the saxophone quartets by William Schmidt and will be entitled: SEMPRE SAXOPHONE QUARTET - THE MUSIC OF WILLIAM SCHMIDT. It will b released in 2013.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Judged the Barry Ashton Jazz Festival</title>
<link>http://opus.ipfw.edu/music_facperform/164</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/164</guid>
<pubDate>Tue, 08 May 2012 05:16:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Judged the competitive high school jazz bands for the Barry Ashton Jazz Festival at Northrop High School.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Performed Woodwinds for Musical Production &quot;Curtains&quot; at Grace College</title>
<link>http://opus.ipfw.edu/music_facperform/163</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/163</guid>
<pubDate>Tue, 08 May 2012 05:16:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Played woodwinds for the production of CURTAINS presented by Grace College's Theater department. The run went from April 2-10.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Tenor Saxophone Performance with the MVCJO at the Barry Ashton Jazz Festival at Northrop High School</title>
<link>http://opus.ipfw.edu/music_facperform/162</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/162</guid>
<pubDate>Tue, 08 May 2012 05:15:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Played first tenor with the Mark Van Cleave Jazz Orchestra as the featured guest artist for the Barry Ashton Jazz Festival.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Sopranino Saxophone Performance at North American Saxophone Alliance</title>
<link>http://opus.ipfw.edu/music_facperform/161</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/161</guid>
<pubDate>Tue, 08 May 2012 05:12:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Performed Mpingo for Eb Sopranino Saxophone and CD; and Fantasy for Eb Sopranino Saxophone and Piano on the culminating evening concert for the Region V North American Saxophone Alliance conference. The performance was held at Eastern Illinois University in Chicago, Illinois.</p>

	]]>
</description>

<author>James F. Vernon DA</author>


</item>


<item>
<title>Indiana Music Educator&apos;s Association Jazz Combo Conductor</title>
<link>http://opus.ipfw.edu/music_facperform/160</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/160</guid>
<pubDate>Tue, 08 May 2012 05:12:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Conducted the All-State Indiana Music Educator's Association Jazz Combo. Chose the music, rehearsed the charts with the combo for two days and presented a concert for the IMEA state conference in Fort Wayne, IN.</p>

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</description>

<author>James Farrell Vernon DA</author>


</item>


<item>
<title>IPFW Faculty Jazz Ensemble</title>
<link>http://opus.ipfw.edu/music_facperform/159</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facperform/159</guid>
<pubDate>Tue, 08 May 2012 05:12:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Concert of original music in various jazz styles, composed and performed by IPFW faculty Dr. Farrell Vernon (saxes), Dr. Kenneth Johnson (guitar), Dr. Chris Rutkowski (piano), Prof. Erik Schweikert (percussion), Prof. Phil Schurgerv (guitar), and Brad Kuhns (bass), and Akira Muritani (trumpet) . The latter two are members of the Fort Wayne Philharmonc. These concerts are ongoing concerts of original music, began in 2006 by Drs. Vernon and Johnson for the purpose of presenting original jazz compositions as part of a Fort Wayne jazz collective of musicians and composers.</p>

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</description>

<author>Kenneth Johnson Dr.</author>


</item>


<item>
<title>Sean Hogan</title>
<link>http://arrow.dit.ie/scthebk/22</link>
<guid isPermaLink="true">http://arrow.dit.ie/scthebk/22</guid>
<pubDate>Tue, 08 May 2012 04:43:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Sean Hogan</author>


</item>


<item>
<title>Bill Kavanagh</title>
<link>http://arrow.dit.ie/scthebk/21</link>
<guid isPermaLink="true">http://arrow.dit.ie/scthebk/21</guid>
<pubDate>Tue, 08 May 2012 02:43:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bill Kavanagh</author>


</item>


<item>
<title>Simulation Optimisation Methods in Supply Chain Applications: A Review</title>
<link>http://arrow.dit.ie/buschmarart/108</link>
<guid isPermaLink="true">http://arrow.dit.ie/buschmarart/108</guid>
<pubDate>Tue, 08 May 2012 02:18:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>The competitiveness and dynamic nature of today’s marketplace is due to rapid advances in information technology, short product life cycles and the continuing trend in global outsourcing. Managing the resulting supply chain networks effectively is challenged by high levels of uncertainty in supply and demand, confl ict objectives, vagueness of information, numerous decision variables and constraints. With such levels of complexity, supply chain optimisation has the potential to make a signifi cant contribution in resolving these challenges. In this paper, a literature review – based on more than 100 peer-reviewed articles – of state-of-the-art simulation-based optimisation techniques in the context of supply chain management is presented. A classifi cation of supply chain problems that apply simulation–optimisation techniques is proposed. The main criteria for selecting supply chain optimisers are also identifi ed, which are then used to develop a map of optimisation techniques. Such a map provides guidance for researchers and practitioners for a proper selection of optimisation techniques.</p>

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</description>

<author>Amr Arisha et al.</author>


</item>


<item>
<title>An Investigation in Culinary Life and Professional Identity in Practice during Internship</title>
<link>http://arrow.dit.ie/tourrcart/1</link>
<guid isPermaLink="true">http://arrow.dit.ie/tourrcart/1</guid>
<pubDate>Tue, 08 May 2012 02:05:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The primary objective of this research was to investigate the selection process used by consumers when choosing a restaurant to dine. This study examined literature on consumer behavior, restaurant selection, and decision-making, underpinning the contention that service quality is linked to the consumer’s selection of a restaurant. It supports the utility theories that consumers buy bundles of attributes that simultaneously combined represent a certain level of service quality at a certain price. The findings of the research displayed a preference by Dublin consumers for Italian and Chinese styled restaurants and identified quality of the food, type of food, cleanliness of the restaurant, location and the reputation of the restaurant as the key decision variables/attributes used by consumers to select restaurants. The study also established that the importance of the attributes changed, depending on the consumer’s age, prior experience, their</p>

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</description>

<author>Frank Cullen</author>


</item>


<item>
<title>Nanozeolites Doped Photopolymer Layers with Reduced Shrinkage</title>
<link>http://arrow.dit.ie/cieoart/74</link>
<guid isPermaLink="true">http://arrow.dit.ie/cieoart/74</guid>
<pubDate>Tue, 08 May 2012 02:02:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>An acrylamide based photopolymer doped with pure silica MFI-type zeolite (silicalite-1) nanoparticles has been characterized for holographic recording purposes. The concentrations of the silicalite-1 nanoparticles in the photopolymer layers were 1, 2.5, 5 and 7.5 wt.%. The inclusion of silicalite-1 nanoparticle in the photopolymer has resulted in an increase of the diffraction efficiency by up to 40%, and decrease of the shrinkage from 1.32% to 0.57%. The best results were obtained in layers doped with 5 wt.% silicalite-1 nanoparticles.</p>

	]]>
</description>

<author>Mohesh Moothanchery et al.</author>


</item>


<item>
<title>Johnny Opperman</title>
<link>http://arrow.dit.ie/scthebk/20</link>
<guid isPermaLink="true">http://arrow.dit.ie/scthebk/20</guid>
<pubDate>Tue, 08 May 2012 01:48:14 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Johnny Opperman</author>


</item>


<item>
<title>Women are the Dominant Decision Makers when Selecting Restaurants to Dine</title>
<link>http://arrow.dit.ie/tfschafart/118</link>
<guid isPermaLink="true">http://arrow.dit.ie/tfschafart/118</guid>
<pubDate>Tue, 08 May 2012 01:46:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>The primary objective of this research was to investigate the selection process used by consumers when choosing a restaurant to dine. The findings of the research displayed a preference by Dublin consumers for Italian and Chinese styled restaurants and identified quality of the food, type of food, cleanliness of the restaurant, its location and reputation were the key decision variables/attributes used by consumers to select restaurants. The study also established that the importance of the attributes changed, depending on the consumers age, prior experience, their mood and the occasion involved.</p>

	]]>
</description>

<author>Frank Cullen</author>


</item>


<item>
<title>International Study Abroad in Engineering/Industrial Technology: Through the Eyes of Students</title>
<link>http://arrow.dit.ie/engineduccon/13</link>
<guid isPermaLink="true">http://arrow.dit.ie/engineduccon/13</guid>
<pubDate>Tue, 08 May 2012 01:35:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Faculty and programs in engineering/industrial technology often promote international exchange and study abroad as a desirable component of a university experience— particularly in this increasingly globalized world. But, what do students who have actually had such experiences perceive? How do they view such experiences, before, during and after the event? The following paper evolved from the experiences of four universities collaborating on an EU-FIPSE funded Atlantis project called DETECT that consist of the partnerships of four Engineering/Technology Educational institutions; Hochschule Darmstadt in Germany, Dublin Institute of Technology in Ireland, and Pennsylvania State University & Purdue University from the USA.</p>

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</description>

<author>Michael Dyrenfurth et al.</author>


</item>


<item>
<title>The Truth Behind Echols v. State: How an Alford Guilty Plea Saved the West Memphis Three</title>
<link>http://digitalcommons.lmu.edu/llr/vol45/iss3/9</link>
<guid isPermaLink="true">http://digitalcommons.lmu.edu/llr/vol45/iss3/9</guid>
<pubDate>Mon, 07 May 2012 23:18:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>After they spent eighteen years in prison for the notorious 1993 murders of three young boys, the West Memphis Three were released on August 19, 2011, after they entered Alford pleas. Under an Alford plea, a defendant can voluntarily, knowingly, and understandingly plead guilty while he simultaneously proclaims his innocence. But with little evidence linking the West Memphis Three to the crime and with recent DNA evidence likely establishing their innocence, was it appropriate for the Circuit Court of Craighead County, Arkansas, to allow the men to even plead guilty? This Comment argues that the circuit court in <i>Echols v. State</i> took a step in the wrong direction when it allowed the West Memphis Three to enter Alford pleas. This Comment discusses the background of Alford pleas and examines the inherent problems with their application, particularly in cases that involve DNA evidence. Finally, this Comment suggests a method of judicial reform that urges judges to proceed with caution and conduct a stricter factual-basis inquiry in order to prevent the injustice that arises when they allow innocent defendants to plead guilty.</p>

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</description>

<author>Kaytee Vota</author>


</item>


<item>
<title>New Media and the News Media: Too Much Media, LLC v. Hale and the Reporter&apos;s Privilege in the Digital Age</title>
<link>http://digitalcommons.lmu.edu/llr/vol45/iss3/7</link>
<guid isPermaLink="true">http://digitalcommons.lmu.edu/llr/vol45/iss3/7</guid>
<pubDate>Mon, 07 May 2012 23:18:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Rooted in the U.S. Constitution and state statutes known as shield laws, the reporter’s privilege has long guarded news gatherers who wish to keep their sources secret. The majority of states have codified shield laws. These statutes support the First Amendment, whose free-press provision allows journalists to act without government control. But the boundaries of the reporter’s privilege have become blurred. Who, in this electronic era of citizen journalism, qualifies as a reporter for the purposes of shield-law protection? Can a blogger enjoy the same benefits that a typical print, radio, or television journalist receives? This Comment examines the case of <i>Too Much Media, LLC v. Hale</i>, in which the Supreme Court of New Jersey took an early step toward answering those questions. In holding that the state’s shield law did not protect a woman who posted her reporting on an Internet message board, the court was among the first to apply the reporter’s privilege in cyberspace. But it should have done more in order to preserve the vitality of shield laws—and of the democratic values that underpin the First Amendment—in the age of new media.</p>

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</description>

<author>Joshua Rich</author>


</item>


<item>
<title>Connecting the Dots: The Ninth Circuit&apos;s Refusal to Find Probable Cause in Dougherty v. City of Covina</title>
<link>http://digitalcommons.lmu.edu/llr/vol45/iss3/8</link>
<guid isPermaLink="true">http://digitalcommons.lmu.edu/llr/vol45/iss3/8</guid>
<pubDate>Mon, 07 May 2012 23:18:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>The relationship between molesting children and possessing child pornography is significant, and the U.S. Supreme Court’s decision in <i>Illinois v. Gates</i> sets a low threshold requirement for probable cause in justifying search warrants. Nonetheless, federal circuit courts disagree as to whether evidence of child molestation is sufficient in itself to establish probable cause for a search warrant for child pornography. In <i>Dougherty v. City of Covina</i>, the Ninth Circuit furthered this circuit split by siding with the Second and Sixth Circuits in determining that such evidence is insufficient to establish probable cause justifying a search warrant. This Comment examines the Ninth Circuit’s ruling in <i>Dougherty</i> and argues that the court incorrectly refused to find probable cause justifying the search warrant and set a dangerous precedent in doing so.</p>

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</description>

<author>Carmelo Tringali</author>


</item>


<item>
<title>The Descent of Responsible Procreation: A Genealogy of an Ideology</title>
<link>http://digitalcommons.lmu.edu/llr/vol45/iss3/4</link>
<guid isPermaLink="true">http://digitalcommons.lmu.edu/llr/vol45/iss3/4</guid>
<pubDate>Mon, 07 May 2012 23:18:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Just as societal practices related to marriage and procreation have changed remarkably during the past several decades, the amount of litigation regarding same-sex marriage has increased substantially. Over time, defenders of state bans on same-sex marriage have primarily leaned on the responsible-procreation defense, which surmises that same-sex couples already procreate responsibly and that the rights and responsibilities of marriage should be limited to furthering the goal of encouraging more responsible procreation by heterosexuals.</p>
<p>This Article traces the genealogy of responsible procreation. Rooted in religion, the defense was once rejected as a justification for limiting heterosexuals’ constitutional rights. Later, it appeared as a justification of the federal Defense of Marriage Act. Soon, courts split on its constitutionality: the high court of Massachusetts found it to be “unpersuasive” while other state appellate courts used it as a justification for their rejections of challenges to same-sex-marriage bans. Finally, with the first federal trial and subsequent Ninth Circuit decision on the constitutionality of California’s Proposition 8, the responsible-procreation defense succumbed to the overwhelming weight of evidence against its logic.</p>
<p>As a result, the emerging trend is that both executive officials and courts are rejecting the defense and concluding that same-sex-marriage bans are drawn not to further proper legislative ends but to make same-sex couples and their children unequal to everyone else.</p>

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</description>

<author>Julie A. Nice</author>


</item>


<item>
<title>Health Care Issues Affecting People with an Intersex Condition or DSD: Sex or Disability Discrimination?</title>
<link>http://digitalcommons.lmu.edu/llr/vol45/iss3/5</link>
<guid isPermaLink="true">http://digitalcommons.lmu.edu/llr/vol45/iss3/5</guid>
<pubDate>Mon, 07 May 2012 23:18:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>People with an intersex condition or a Difference of Sex Development (DSD) depend on health care professionals for critical medical treatment. Many intersex activists assert that some current medical practices are not in the best interests of patients with an intersex condition. They contend that greater safeguards should be adopted to ensure that the rights to liberty and autonomy of people with a DSD are respected.</p>
<p>Thus far, intersex advocacy has focused on extralegal strategies. The movement is at a point, however, where legal challenges to current medical protocols could provide an additional tool to improve life-altering health care practices. This Article examines whether the intersex movement could effectively use legal frameworks developed by feminists, the LGBT movement, and disability activists to advance its goal of modifying current medical procedures that are based on sex, gender, sexual orientation, and disability stereotypes.</p>

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</description>

<author>Julie A. Greenberg</author>


</item>


<item>
<title>HIV Discrimination in Dental Care: Results of a Testing Study in Los Angeles County</title>
<link>http://digitalcommons.lmu.edu/llr/vol45/iss3/6</link>
<guid isPermaLink="true">http://digitalcommons.lmu.edu/llr/vol45/iss3/6</guid>
<pubDate>Mon, 07 May 2012 23:18:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Thirty years after HIV was first identified, for the majority of those infected in the United States, effective combination therapies to combat HIV have turned the disease into a manageable chronic condition. But HIV discrimination has still proven intractable in the field of health care. For example, a series of studies has revealed that 46 percent of skilled nursing facilities, 55 percent of OB/GYNs, and 26 percent of plastic surgeons in Los Angeles County refuse to provide services to any HIV-positive patient, in violation of state and federal law.</p>
<p>This Study examines HIV discrimination among dentists in Los Angeles County. For people living with HIV/AIDS (PLWHA), dental care is particularly important because problems in the mouth may be the first symptoms of an HIV infection and can also signify disease progression; routine, proper dental care can have a significant impact on oral and general health. This Study reveals that 5 percent of dentists in Los Angeles County have a blanket policy of refusing to accept any HIV-positive patient, which is substantially lower than the finding for other health care providers. However, this Study also suggests that PLWHA who are poor and the most vulnerable, including women and people of color, face higher rates of discrimination. This Study goes on to explain that dentists can effectively and safely treat PLWHA, and it identifies why they are legally and ethically obligated to provide such care. After reviewing prior social science research on HIV discrimination by dentists, this Study presents its methodology and findings. Finally, it concludes by exploring potential reasons for why the documented discrimination rate is lower for dentists than it is for other health care providers in Los Angeles County, and it argues that future enforcement and education efforts should be targeted toward specific categories of dentists.</p>

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</description>

<author>Brad Sears et al.</author>


</item>


<item>
<title>LGBT Identity: A Demographer&apos;s Perspective</title>
<link>http://digitalcommons.lmu.edu/llr/vol45/iss3/2</link>
<guid isPermaLink="true">http://digitalcommons.lmu.edu/llr/vol45/iss3/2</guid>
<pubDate>Mon, 07 May 2012 23:18:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>In a recent study, the Author of this Article estimated that the self-identified lesbian, gay, bisexual, and transgender (LGBT) community makes up 3.8 percent of the American population. The Author’s estimate was far lower than many scholars and activists had contended, and it included a relatively high proportion of persons self-identifying as bisexuals. This Article responds to two of the central criticisms that arose in the controversy that followed. First, in response to claims that his estimate did not account for people who are in the closet, the Author describes how demographers might measure the size of the closet. Second, in response to those who either ignored the reported large incidence of bisexuality or misconstrued the meaning of that incidence, the Author considers how varying frameworks for conceptualizing sexual orientation might alter the ratio of lesbian or gay individuals to bisexuals. This Article goes on to offer observations about the challenges and implications that are associated with the varying estimates of the size of the LGBT population. And it concludes by arguing that, today, the size of the LGBT community is less important than understanding the struggles of its members and informing crucial policy debates with facts rather than stereotype and anecdote.</p>

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</description>

<author>Gary J. Gates</author>


</item>


<item>
<title>Evidence of Persistent and Pervasive Workplace Discrimination Against LGBT People: The Need for Federal Legislation Prohibiting Discrimination and Providing for Equal Employment Benefits</title>
<link>http://digitalcommons.lmu.edu/llr/vol45/iss3/3</link>
<guid isPermaLink="true">http://digitalcommons.lmu.edu/llr/vol45/iss3/3</guid>
<pubDate>Mon, 07 May 2012 23:18:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lesbian, gay, bisexual, and transgender (LGBT) people have experienced a long and pervasive history of employment discrimination. Today, more than eight million people in the American workforce identify as LGBT, but there still is no federal law that explicitly prohibits sexual orientation and gender identity discrimination against them.</p>
<p>This Article begins by surveying the social science research and other evidence illustrating the nature and scope of the discrimination against LGBT workers and the harmful effects of this discrimination on both employees and employers. It then analyzes the existing legal protections against this discrimination, which include constitutional protections for public sector workers, court interpretations of Title VII’s ban on sex discrimination, state and local antidiscrimination laws, and corporate policies. This Article determines that, while these laws and policies provide important protection, the current system is incomplete, confusing, and inadequate. This Article next considers empirical research showing that employers do not offer employees with a same-sex spouse or partner the same access to family benefits that they offer to employees with a different-sex spouse, and it examines court decisions finding that a denial of equal benefits is unlawful employment discrimination.</p>
<p>Based on this research and legal analysis, the Article concludes that a federal law like the Employment Non-Discrimination Act (ENDA), a bill pending in Congress that would prohibit sexual orientation and gender identity employment discrimination, is needed. To serve its purpose consistently, however, the bill’s current exemption of employee benefits should be removed. To be sure, ending all forms of unequal treatment based on sexual orientation or gender identity is warranted and feasible, and doing so will have positive effects for both employees and employers.</p>

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</description>

<author>Jennifer C. Pizer et al.</author>


</item>


<item>
<title>Introduction: Talking Around Marriage</title>
<link>http://digitalcommons.lmu.edu/llr/vol45/iss3/1</link>
<guid isPermaLink="true">http://digitalcommons.lmu.edu/llr/vol45/iss3/1</guid>
<pubDate>Mon, 07 May 2012 23:18:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Douglas NeJaime</author>


</item>


<item>
<title>Mountain Movement: The Design, Implementation, &amp; Evaluation of a Youth Yoga Program</title>
<link>http://digitalcollections.sit.edu/capstones/2520</link>
<guid isPermaLink="true">http://digitalcollections.sit.edu/capstones/2520</guid>
<pubDate>Mon, 07 May 2012 21:26:33 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Abigail Ann Long – PIM 70</strong></p>
<p><strong>Mountain Movement: The Design, Implementation, & Evaluation </strong></p>
<p><strong>of a Youth Yoga Program</strong></p>
<p><strong>May 2012</strong></p>
<p>Mountain Movement is a youth yoga program designed to introduce children to the sustainable practice of yoga as well as convey the ability to recognize stress and utilize relaxation techniques. Children face a number of challenges throughout their daily lives. These challenges, ranging from academic pressures to bullying, can create stresses with negative impacts. Yoga is an activity that can provide children with tools and methods to better deal with and cope with these challenges. Mountain Movement has demonstrated that a youth yoga program can favorable impact children while remaining simple to implement and requiring minimal logistic support.</p>

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</description>

<author>Abigail A. Long</author>


</item>


<item>
<title>A SAT-based algorithm for reparameterization in symbolic simulation</title>
<link>http://repository.cmu.edu/compsci/2213</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2213</guid>
<pubDate>Mon, 07 May 2012 21:25:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Parametric representations used for symbolic simulation of circuits usually use BDDs. After a few steps of symbolic simulation, state set representation is converted from one parametric representation to another smaller representation, in a process called reparameterization. For large circuits, the reparameterization step often results in a blowup of BDDs and is expensive due to a large number of quantifications of input variables involved. Efficient SAT solvers have been applied successfully for many verification problems. This paper presents a novel SAT-based reparameterization algorithm that is largely immune to the large number of input variables that need to be quantified. We show experimental results on large industrial circuits and compare our new algorithm to both SAT-based Bounded Model Checking and BDD-based symbolic simulation. We were able to achieve on average 3x improvement in time and space over BMC and able to complete many examples that BDD-based approach could not even finish."</p>

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</description>

<author>Pankaj Chauhan et al.</author>


</item>


<item>
<title>Adaptive memoization</title>
<link>http://repository.cmu.edu/compsci/2212</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2212</guid>
<pubDate>Mon, 07 May 2012 21:25:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We combine adaptivity and memoization to obtain an incremental computation technique that dramatically improves performance over adaptivity and memoization alone. The key contribution is adaptive memoization, which enables result re-use by matching any subset of the function arguments to a previous function call and updating the result to satisfy the unmatched arguments via adaptivity. We study the technique in the context of a purely functional language, called IFL, and as an ML library. The library provides an efficient implementation of our techniques with constant overhead. As examples, we consider Quicksort and Insertion Sort. We show that Quicksort handles insertions or deletions at random positions in the input list in O(log n) expected time. For insertion sort, we show that insertions and deletions anywhere in the list take O(n) time."</p>

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</description>

<author>Umut A. Acar et al.</author>


</item>


<item>
<title>Improving hash join performance through prefetching</title>
<link>http://repository.cmu.edu/compsci/2211</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2211</guid>
<pubDate>Mon, 07 May 2012 21:24:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Hash join algorithms suffer from extensive CPU cache stalls. This paper shows that the standard hash join algorithm for disk-oriented databases (i.e. GRACE) spends over 73% of its user time stalled on CPU cache misses, and explores the use of prefetching to improve its cache performance. Applying prefetching to hash joins is complicated by the data dependencies, multiple code paths, and inherent randomness of hashing. We present two techniques, group prefetching and software-pipelined prefetching, that overcome these complications. These schemes achieve 2.0-2.9X speedups for the join phase and 1.4-2.6X speedups for the partition phase over GRACE and simple prefetching approaches. Compared with previous cache-aware approaches (i.e. cache partitioning), the schemes are at least 50% faster on large relations and do not require exclusive use of the CPU cache to be effective."</p>

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</description>

<author>Shimin Chen</author>


</item>


<item>
<title>Evolutionary dynamics with large aggregate shocks</title>
<link>http://repository.cmu.edu/compsci/2210</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2210</guid>
<pubDate>Mon, 07 May 2012 21:24:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This paper examines a class of evolutionary models in which large shocks cause frequent movement between short-term 'stable' equilibria. Mutations are rare in our model, but their effects are magnified by a 'spread process' which causes a finite proportion of the population to initially adopt the entering strategy before the short-term selection dynamics takes effect. We examine the long run invariant distribution for a variety of games, under several different spread processes: most interestingly, we find that cooperative strategies prevail in the long run in the Finitely Repeated Prisoner's Dilemma game, contrary to the backward induction solution. We also study equilibrium selection in 2x2 and NxN coordination games, establishing conditions under which the risk-dominant equilibrium is selected, and demonstrate rapid convergence to the long run invariant distribution."</p>

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</description>

<author>Daniel B. Neill</author>


</item>


<item>
<title>Convergence testing in term-level bounded model checking</title>
<link>http://repository.cmu.edu/compsci/2209</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2209</guid>
<pubDate>Mon, 07 May 2012 21:24:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We consider the problem of bounded model checking of systems expressed in a decidable fragment of first-order logic. While model checking is not guaranteed to terminate for an arbitrary system, it converges for many practical examples, including pipelined processors. We give a new formal definition of convergence that generalizes previously stated criteria. We also give a sound semi-decision procedure to check this criterion based on a translation to quantified separation logic. Preliminary results on simple pipeline processor models are presented."</p>

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</description>

<author>Randal Bryant et al.</author>


</item>


<item>
<title>Learning to identify TV news monologues by style and context</title>
<link>http://repository.cmu.edu/compsci/2208</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2208</guid>
<pubDate>Mon, 07 May 2012 21:24:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We focus on the problem of learning semantics from multimedia data associated with broadcast video documents. In this paper we propose to learn semantic concepts from multimodal sources based on style and context detectors, in combination with statistical classifier ensembles. As a case study we present our method for detecting the concept of news subject monologues. This approach had the best average precision performance amongst 26 submissions in the 2003 video track of the Text Retrieval Conference benchmark. Experiments were conducted with respect to individual detector contribution, ensemble size, and ranking mechanism. It was found that the combination of detectors is decisive for the final result, although some detectors might appear useless in isolation. Moreover, by using a probabilistic ranking, in combination with a large classifier ensemble, results can be improved even further."</p>

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</description>

<author>Cees G. M. Snoek et al.</author>


</item>


<item>
<title>Location-based node IDs : enabling explicit locality in DHTs</title>
<link>http://repository.cmu.edu/compsci/2207</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2207</guid>
<pubDate>Mon, 07 May 2012 21:24:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Current peer-to-peer systems based on DHTs struggle with routing locality and content locality because of random node ID assignment. To address these issues, we promote the use of location-based node IDs to encode physical topology and improve routing. This gives applications explicit knowledge about and control over data locality at a coarse-grain. Applications can place content in particular regions or route towards a close replica. Schemes to address the difficulties that ensue, particularly load imbalance, are discussed."</p>

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</description>

<author>Shuheng Zhou et al.</author>


</item>


<item>
<title>On the language inclusion problem for timed automata : closing a decidability gap</title>
<link>http://repository.cmu.edu/compsci/2206</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2206</guid>
<pubDate>Mon, 07 May 2012 21:24:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We consider the language inclusion problem for timed automata: given two timed automata A and B, are all the timed traces accepted by B also accepted by A? While this problem is known to be undecidable, we show here that it becomes decidable if A is restricted to having at most one clock. This is somewhat surprising, since it is well-known that there exist timed automata with a single clock that cannot be complemented. The crux of our proof consists in reducing the language inclusion problem to a reachability question on an infinite graph; we then construct a suitable well-quasi-order on the nodes of this graph, which ensures the termination of our search algorithm. We also show that the language inclusion problem is decidable if the only constant appearing among the clock constraints of A is zero. Moreover, these two cases are essentially the only decidable instances of language inclusion, in terms of restricting the various resources of timed automata."</p>

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</description>

<author>Joe╠êl Ouaknine et al.</author>


</item>


<item>
<title>Simple bounds on SMART scheduling</title>
<link>http://repository.cmu.edu/compsci/2205</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2205</guid>
<pubDate>Mon, 07 May 2012 21:24:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We define the class of SMART scheduling policies. These are policies that bias towards jobs with short remaining service times, jobs with small original sizes, or both, with the motivation of minimizing mean response time and/or mean slowdown. Examples of SMART policies include PSJF, SRPT, and hybrid policies such as RS (which biases according to the product of the response time and size of a job. For many policies in the SMART class, the mean response time and mean slowdown are not known or have complex representations involving multiple nested integrals, making evaluation difficult. In this work, we prove three main results. First, for all policies in the SMART class, we prove simple upper and lower bounds on mean response time. In particular, we focus on the SRPT and PSJF policies and prove even tighter bounds in these cases. Second, we show that all policies in the SMART class, surprisingly, have very similar mean response times. Third, we show that the response times of SMART policies are largely invariant to the variability of the job size distribution."</p>

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</description>

<author>Adam Wierman et al.</author>


</item>


<item>
<title>How many servers are best in a dual-priority FCFS system?</title>
<link>http://repository.cmu.edu/compsci/2204</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2204</guid>
<pubDate>Mon, 07 May 2012 21:23:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We ask the question, 'for minimizing mean response time, which is preferable: one fast server of speed 1, or k slow servers each of speed 1/k?' Our setting is the M/GI/k system with two priority classes of customers, high priority and low priority, where G is a phase-type distribution. We find that multiple slow servers are often preferable -- and we demonstrate exactly how many servers are preferable as a function of load and G. In addition, we find that the optimal number of servers with respect to the high priority jobs may be very different from that preferred by low priority jobs, and we characterize these preferences. We also evaluate the optimal number of servers with respect to overall mean response time, averaged over high and low priority jobs. Lastly, we ascertain the effect of the variability of high priority jobs on low priority jobs. This paper is the first to analyze an M/GI/k system with two priority classes and a general phase-type distribution. Prior analyses of the M/GI/k with two priority classes either require that G be exponential, or are approximations that work well when G is exponential, but are less reliable for more variable G. Our analytical method is very different from the prior literature: it combines the technique of dimensionality reduction (see [9]) with Neuts' technique for determining busy periods in multiserver systems [22]. Our analysis is approximate, but can be made as accurate as desired, and is verified via simulation."</p>

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</description>

<author>Takayuki Osogami</author>


</item>


<item>
<title>Bounds on a fair policy with near optimal performance</title>
<link>http://repository.cmu.edu/compsci/2203</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2203</guid>
<pubDate>Mon, 07 May 2012 21:23:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Providing fairness and providing good response times are often viewed as conflicting goals in scheduling. Scheduling policies that provide low response times, such as Shortest Running Processing Time (SRPT), are sometimes not fair, while fair policies like Processor Sharing (PS) provide response times far worse than SRPT. This seemingly inevitable tension between providing fairness and providing good response times was eliminated at last year's ACM Sigmetrics conference with the introduction of a new scheduling policy, Fair Sojourn Protocol (FSP), that appears to provide both [9]. The FSP policy is provably fair, as seen directly from its definition, and simulations show that FSP has a very low mean response time, close to that of SRPT in many cases [9]. Unfortunately, analyzing the mean response time of the FSP policy has proven to be difficult, and thus the queueing performance of FSP has only be [sic] assessed via simulation. In this work, we present the first queueing analysis of FSP. This analysis yields close upper and lower bounds on the mean response time and mean slowdown of the M/GI/1/FSP queue. Our upper bound shows that the improvement of FSP over PS is substantial: for all job size distributions, the mean response time and mean slowdown under FSP are a fraction (1 - [rho]/2) of that under PS, where [rho] is the system load. For distributions with decreasing failure rate the improvement is even greater. We also prove that the mean response time of SRPT and FSP are quite close. Lastly, our bounds reveal that FSP has yet another desirable property: similarly to PS, the FSP policy is largely insensitive to the variability of the job size distribution."</p>

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</description>

<author>Adam Wierman et al.</author>


</item>


<item>
<title>Multi-modal network protocols : adapting to highly variable operating conditions</title>
<link>http://repository.cmu.edu/compsci/2202</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2202</guid>
<pubDate>Mon, 07 May 2012 21:23:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Most network protocols are uni-modal: they employ a single set of algorithms that allows them to cope well only within a narrow range of operating conditions. This rigid design renders these protocols inefficient in the face of widely varying operating environments or in conditions different from the ones for which they are optimized. Such uni-modal protocols have great difficulty in the mobile computing world where the operating conditions, including number of nodes, computational capabilities and rate of mobility, are not fixed. Consider, for example, routing in a network of ad-hoc nodes. Solutions like DSDV work well when the number of nodes is small. Unfortunately, such schemes scale poorly to larger population sizes. In such situations, more scalable algorithms that impose a structure on the network of ad-hoc nodes, in a manner similar to routing protocols in the Internet, provides better results. However, these scalable algorithms tend to incur high overheads in situations that DSDV handles well. Clearly, no single routing solution handles all situations that a node may encounter. Motivated by such examples, this paper attempts to answer the following question: Is it possible to redesign the traditional protocols to take on very different operating modes when faced with different environments? We present a case for such multi-modal protocols in our paper. Specifically, we discuss multi-modal reliability and routing. We show the feasibility of designing multi-modal protocols by describing how these protocols can make operating mode decisions and switch modes without additional overhead."</p>

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</description>

<author>Aditya Akella</author>


</item>


<item>
<title>A monadic analysis of information flow security with mutable state</title>
<link>http://repository.cmu.edu/compsci/2201</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2201</guid>
<pubDate>Mon, 07 May 2012 21:23:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We explore the logical underpinnings of higher-order, security-typed languages with mutable state. Our analysis is based on a logic of information flow derived from lax logic and the monadic metalanguage. Thus, our logic deals with mutation explicitly, with impurity reflected in the types, in contrast to most higher-order security typed languages, which deal with mutation implicitly via side-effects. More importantly, we also take a store-oriented view of security, wherein security levels are associated with regions of the mutable store. In contrast, most other accounts are value-oriented, in that security levels are associated with individual values. Our store-oriented viewpoint allows us to address information flow security while still using a largely conventional logic, but we show that it does not lessen the expressive power of the logic. An interesting feature of our analysis lies in its treatment of upcalls (low-security computations that include high-security ones), employing an 'informativeness' judgement indicating under what circumstances a type carries useful information."</p>

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</description>

<author>Karl Crary et al.</author>


</item>


<item>
<title>Protein similarity from knot theory and geometric convolution</title>
<link>http://repository.cmu.edu/compsci/2200</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2200</guid>
<pubDate>Mon, 07 May 2012 21:23:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michael Andreas. Erdmann</author>


</item>


<item>
<title>Self-* storage : brick-based storage with automated administration</title>
<link>http://repository.cmu.edu/compsci/2199</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2199</guid>
<pubDate>Mon, 07 May 2012 21:23:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This white paper describes a new project exploring the design and implementation of 'self-* storage systems:' self-organizing, self-configuring, self-tuning, self-healing, self-managing systems of storage bricks. Borrowing organizational ideas from corporate structure and automation technologies from AI and control systems, we hope to dramatically reduce the administrative burden currently faced by data center administrators. Further, compositions of lower cost components can be utilized, with available resources collectively used to achieve high levels of reliability, availability, and performance."</p>

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</description>

<author>Gregory R. Ganger et al.</author>


</item>


<item>
<title>Predicate abstraction of ANSI-C programs using SAT</title>
<link>http://repository.cmu.edu/compsci/2198</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2198</guid>
<pubDate>Mon, 07 May 2012 21:23:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Predicate abstraction is a major method for verification of software. However, the generation of the abstract Boolean program from the set of predicates and the original program suffers from an exponential number of theorem prover calls as well as from soundness issues. This paper presents a novel technique that uses an efficient SAT solver for generating the abstract transition relation of ANSI-C programs. The SAT-based approach computes a more precise and safe abstraction compared to existing predicate abstraction techniques."</p>

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</description>

<author>E. M. Clarke</author>


</item>


<item>
<title>Using SAT based image computation for reachability analysis</title>
<link>http://repository.cmu.edu/compsci/2197</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2197</guid>
<pubDate>Mon, 07 May 2012 21:23:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Satisfiability procedures have shown significant promise for symbolic simulation of large circuits, hence they have been used in many formal verification techniques, including automated abstraction refinement, ATPG etc. We show how to use modern SAT solvers like Chaff and GRASP to compute images of sets of states and how to efficiently detect fixed point of the sets of states during reachability analysis. Our method is completely SAT based, and does not use BDDs at all. The sets of states and transition relation are represented in clausal form, which can be processed by SAT checkers. The SAT checker subsequently generates the set of newly reached states in clausal form as well. At the heart of our engine lie two efficient algorithms. The first algorithm shortens the cubes that the SAT checker generates by a static-analysis algorithm, which significantly reduces the number of cubes the SAT checker needs to enumerate. The second algorithm reduces the space required to store sets of states as a set of cubes by a recursive cube-merging procedure. We demonstrate the effectiveness of our procedure on ISCAS sequential benchmarks for reachability. In particular, our algorithm does not have BDD size explosion surprises and deteriorates in a predictable manner."</p>

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</description>

<author>Pankaj Chauhan et al.</author>


</item>


<item>
<title>Planning for communication resources</title>
<link>http://repository.cmu.edu/compsci/2196</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2196</guid>
<pubDate>Mon, 07 May 2012 21:22:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "For many human team activities, ranging from military operations through to emergency rescue or large entertainment events, communications resources must be assigned to different teams or team members. These assignments must reflect the capabilities of the available communication devices and avoid conflicting use of communications channels already in use in the local environment. In general, finding and assigning available communication channels for short-term use is a task performed manually by human operators. Operators, using generic tools, such as spreadsheets and database manipulation programs, access government databases to obtain information on frequency usage and then manually attempt to locate suitable unused channels. This process is time intensive, prone to error, and 'mechanistic' in nature. In this paper, we describe the CommPlanner, a new fully implemented system developed to automate this assignment procedure and thereby speed up and make more reliable the process. We describe the algorithms used by the CommPlanner, and the underlying issues that, while not always obvious, must be addressed in the processes of assigning frequency usage."</p>

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</description>

<author>Brett Browning et al.</author>


</item>


<item>
<title>The Aura software architecture : an infrastructure for ubiquitous computing</title>
<link>http://repository.cmu.edu/compsci/2195</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2195</guid>
<pubDate>Mon, 07 May 2012 21:22:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Computing environments of the future should enable mobile users to take full advantage of the computing capabilities available at each location, while allowing them to focus on their real tasks, rather than being distracted by dealing with the configuration and reconfiguration of computer systems to support those tasks. The Aura infrastructure performs automatic configuration and reconfiguration of Ubicomp environments, according to the user's task and intent. This report describes the software architecture of the Aura infrastructure, and discusses the underlying rational. It describes the architecture from a layered perspective, detailing the partition of responsibility and shared assumptions, as well as from a component-connector perspective, detailing the protocols of interaction between the components (APIs and sequencing). The contents and format of the exchanged messages is extensively discussed, as well as the details pertaining [sic] service interconnection and decomposition. This report proposes a utility-based approach for modeling user preferences, and details how such models can be exploited for both coarse-grain automatic (re)configuration, and fine-grain adaptation to resource change."</p>

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</description>

<author>Joa╠âo Pedro. Sousa et al.</author>


</item>


<item>
<title>An examination of remote access help desk cases</title>
<link>http://repository.cmu.edu/compsci/2194</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2194</guid>
<pubDate>Mon, 07 May 2012 21:22:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "As a precursor to explorations on future network interoperability problem resolution methods and tools, it is necessary to obtain an understanding of problems in the present day. The remote network access application area was chosen as a case study due to rich sources of information, frequent problems, and considerable detrimental impact on user efficiency. To this end, existing remote network access help desk data was acquired and analyzed. The data was used to characterize remote network access interoperability problems and identify key issues. For the data examined, the two largest problems specific to remote end users were obtaining modem phone numbers for their location and adequate user rights upon connection. Potential for better knowledge re-use and dissemination of solutions to common problems to the general population was also observed."</p>

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</description>

<author>Aaron Steinfeld</author>


</item>


<item>
<title>The inverse method for intuitionistic linear logic : (the propositional fragment)</title>
<link>http://repository.cmu.edu/compsci/2193</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2193</guid>
<pubDate>Mon, 07 May 2012 21:22:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We present a forward sequent calculus for intuitionistic propositional linear logic ([circle with x], 1, &, T, -o, [circle with plus], 0, !) and a corresponding inverse-method search strategy. Our approach centres around resource management, inspired by similar approaches for backward-directed calculi such as top-down linear logic programming. Surprisingly, the resource management problems for the forward direction turn out to have a different character to those of the backward direction, arising for different connectives. Our approach identifies conditions for which we may relax linearity to allowing (implicit) weakening. We characterize two such classes of affine behaviour -- as a form of weak sequent designed to handle T-weakening lazily, and as affine contexts to control the multiplicative unit 1 using a general matching framework."</p>

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</description>

<author>Kaustuv Chaudhuri</author>


</item>


<item>
<title>AutoPart : automating schema design for large scientific databases using data partitioning</title>
<link>http://repository.cmu.edu/compsci/2192</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2192</guid>
<pubDate>Mon, 07 May 2012 21:22:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Database applications that use multi-terabyte datasets are becoming increasingly important for scientific fields such as astronomy and biology. To improve query execution performance, modern DBMS build indexes and materialized views on the wide tables that store experimental data. The replication of data in indexes and views, however, implies large amounts of additional storage space, and incurs high update costs as new experiments add or change large volumes of data. In this paper we explore automatic data partitioning as a tool to redesign the relational tables in a database for faster sequential access before creating indexes and views. We present AutoPart, a vertical partitioning tool that uses the optimizer's hints to determine optimal partitions for a given workload. According to our experiments, the schemas recommended by AutoPart (a) improve query execution by 12%-44% when compared to the original schema without indexes, (b) execute queries up to 37% faster and updates almost twice as fast compared to the original after indexing. Furthermore, they require half the space for indexes. Finally, we show that a form of categorical partitioning can further improve query performance up to 29%-62% without any indexes and up to 54% with indexes, while update performance improves up to 60%. AutoPart can be used with any commercial database system. Our experimental results are based on the Sloan Digital Sky Survey (SDSS) database, a real-world astronomical database, running on Microsoft's SQL Server 2000."</p>

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</description>

<author>Efstratios Papadomanolakis et al.</author>


</item>


<item>
<title>Robust subspace computation using L1 norm</title>
<link>http://repository.cmu.edu/compsci/2191</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2191</guid>
<pubDate>Mon, 07 May 2012 21:22:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Linear subspace has many important applications in computer vision, such as structure from motion, motion estimation, layer extraction, object recognition, and object tracking. Singular Value Decomposition (SVD) algorithm is a standard technique to compute the subspace from the input data. The SVD algorithm, however, is sensitive to outliers as it uses L2 norm metric, and it can not handle missing data either. In this paper, we propose using L1 norm metric to compute the subspace. We show that it is robust to outliers and can handle missing data. We present two algorithms to optimize the L1 norm metric: the weighted median algorithm and the quadratic programming algorithm."</p>

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</description>

<author>Qifa Ke et al.</author>


</item>


<item>
<title>The etree library : a system for manipulating large octrees on disk</title>
<link>http://repository.cmu.edu/compsci/2190</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2190</guid>
<pubDate>Mon, 07 May 2012 21:22:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This report describes a library, called the etree library, that allows C programmers to manipulate large octrees stored on disk. Octrees are stored as a sequence of fixed sized octant records sorted by a locational code order that is equivalent to a preorder traversal of the tree and a Z-order traversal through the domain. The sorted records are indexed by a conventional file-resident B-tree index and queried using fixed-length locational code keys. A schema can be defined to make an etree portable across different platforms. The etree library provides functions for creating, modifying, and searching octrees, including efficient mechanisms for appending octants and iterating over octants in Z-order. The library is the foundation for a larger research effort aimed at enabling scientists and engineers to solve large physical simulations on their desktop systems by recasting the simulation process to work directly on large etrees stored on disk."</p>

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</description>

<author>Tiankai Tu et al.</author>


</item>


<item>
<title>An integrated contextual information service for pervasive computing applications</title>
<link>http://repository.cmu.edu/compsci/2189</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2189</guid>
<pubDate>Mon, 07 May 2012 21:21:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Pervasive computing applications are increasingly leveraging contextual information from several sources to provide users with behavior appropriate to the environment in which they reside. If these sources of contextual information are used and deployed in an ad hoc manner, however, they may provide overlapping functionality, fail to provide needed functionality, and require the use of inconsistent interfaces by applications. To overcome these problems, we introduce a Contextual Information Service that provides applications with contextual information via a virtual database. Unlike previous efforts, our service provides applications a consistent, lightweight, and powerful mechanism for obtaining contextual information, and includes explicit support for the on demand computation of contextual information. We show, using a Contextual Information Service prototype and example applications that we have implemented, how this approach can be used by proactive applications to adapt their behavior to match a user's current environment."</p>

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</description>

<author>Glenn Judd et al.</author>


</item>


<item>
<title>Acquiring domain-specific planners by example</title>
<link>http://repository.cmu.edu/compsci/2188</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2188</guid>
<pubDate>Mon, 07 May 2012 21:21:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Intelligent problem solving requires the ability to select actions autonomously from a specific state to reach objectives. Planning algorithms provide approaches to look ahead and select a complete sequence of actions. Given a domain description consisting of preconditions and effects of the actions the planner can take, an initial state, and a goal, a planning program returns a sequence of actions to transform the initial state into a state in which the goal is satisfied. Classical planning research has addressed this problem in a domain-independent manner -- the same algorithm generates a complete plan for any domain specification. This feature comes at a cost which domain-independent planners incur either in high search efforts or in tedious hand-coded domain knowledge. Previous approaches to efficient general-purpose planning have focused on reducing the search involved in an existing general-purpose planning algorithm. An interesting alternative is to use example plans in a particular domain to demonstrate how to solve problems in that domain and to use that information to solve new problems independently of a domain-independent planner. Others have used example plans for case-based planning, but the retrieval and adaptation mechanisms were still domain-independent and efficiency issues were still a concern. In my thesis, I propose to introduce algorithms to extract complex, repeating processes, in the form of domain-specific planning programs, from example plans. I will investigate the application of these learned programs to modelling agent preferences and choices. I will also investigate how the programs can be used, extended, and repaired dynamically as an agent encounters new problems and acquires new experience. Finally, I will compare the template-based planning paradigm to existing general-purpose and domain-specific planning programs with a full evaluation on new and existing planning domains. I expect the core contribution of this thesis to be a new planning paradigm in which domain-specific planners are learned by example."</p>

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</description>

<author>Elly Winner et al.</author>


</item>


<item>
<title>Advances in counterexample-guided abstraction refinement</title>
<link>http://repository.cmu.edu/compsci/2187</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2187</guid>
<pubDate>Mon, 07 May 2012 21:21:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This report is a collection of six articles on model checking in the abstraction/refinement framework. This framework is used by various techniques for tackling the state-space explosion problem that is frequently encountered in model checking."</p>

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</description>

<author>E. M. Clarke et al.</author>


</item>


<item>
<title>Protecting privacy in key-value search systems</title>
<link>http://repository.cmu.edu/compsci/2186</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2186</guid>
<pubDate>Mon, 07 May 2012 21:21:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This paper investigates the general problem of performing key-value search at untrusted servers without loss of user privacy. Specifically, given key-value pairs from multiple owners that are stored across untrusted servers, how can a client search these pairs such that no server, on its own, can reconstruct any of them? We propose a protocol, called Peekaboo, that is applicable to any type of key-value search while protecting both the data owner privacy and the client privacy. The main idea is to separate the key-value pairs and store them on different servers based on an important observation that key-value pairs release information only if they are together. Supported by access control and user authentication, Peekaboo allows search to be performed only by authorized clients without reducing the levels of user privacy."</p>

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</description>

<author>Yinglian Xie et al.</author>


</item>


<item>
<title>Meeting the software engineering challenges of adaptive mobile applications</title>
<link>http://repository.cmu.edu/compsci/2185</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2185</guid>
<pubDate>Mon, 07 May 2012 21:21:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "A critical factor for the commercial success of mobile and task-specific devices is the fast turnaround time of software development. However, developing software for mobile devices is especially hard since applications need to be aware of and adapt to changing resources such as bandwidth and battery. In this paper we validate that the idea of stub generation can successfully address the complexity introduced by resource adaptation. Our approach is based on factoring generic resource-adaptation mechanisms out of the applications and into operating system extensions. Rather than having to deal with system-specific details, an application writer provides a high-level description of the adaptation needs for each application. The generation of code stubs bridges such high-level descriptions to the adaptation mechanisms specific to each platform. We validated this approach against three representative applications: a video streaming application, a natural language translator and an augmented reality application. In all three cases, the effort for the application writer was reduced by orders of magnitude. The cost of writing the operating system extensions and the stub generator is amortized over the many applications that can share the generic resource-adaptation mechanisms."</p>

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</description>

<author>Rajesh Krishna. Balan et al.</author>


</item>


<item>
<title>A Bezier-based approach to unstructured moving meshes</title>
<link>http://repository.cmu.edu/compsci/2184</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2184</guid>
<pubDate>Mon, 07 May 2012 21:21:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We present in this report a new framework for maintaining good quality of two dimensional triangular moving meshes. The use of curved elements is the key idea that allows us to avoid excessive refinement and still obtain good quality meshes consisting of a low number of well shaped elements. We use B-splines curves to model object boundaries and objects are meshed with second order Be╠üzier triangles. As the mesh evolves according to a non-uniform flow velocity field, we keep track of object boundaries and, if needed, carefully modify the mesh to keep it well shaped by applying a combination of vertex insertion and deletion, edge flipping, and curve smoothing operations at each time step. Our algorithms for these tasks are extensions of known algorithms for meshes build [sic] of straight-sided elements and are designed for any fixed-order Be╠üzier elements and B-splines. We discuss a calculus of geometric primitives for Be╠üzier curves and triangles that we employ to implement such operations. Although in this work we have concentrated on quadratic elements, most of the operations are valid for elements of any order and they generalize well to higher dimensions. We present results of our scheme for a set of objects mimicking red blood cells subject to a a priori computed flow velocity field. As a pure geometric exploration, our method does not account for neither refinement nor coarsening dictated by the simulation results."</p>

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</description>

<author>David Cardoze</author>


</item>


<item>
<title>Semi-supervised learning : from Gaussian fields to Gaussian processes</title>
<link>http://repository.cmu.edu/compsci/2183</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2183</guid>
<pubDate>Mon, 07 May 2012 21:21:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We show that the Gaussian random fields and harmonic energy minimizing function framework for semi-supervised learning can be viewed in terms of Gaussian processes, with covariance matrices derived from the graph Laplacian. We derive hyperparameter learning with evidence maximization, and give an empirical study of various ways to parameterize the graph weights."</p>

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</description>

<author>Xiaojin Zhu et al.</author>


</item>


<item>
<title>女性主義文學論 ── 蕭紅作品研究</title>
<link>http://commons.ln.edu.hk/chi_diss/19</link>
<guid isPermaLink="true">http://commons.ln.edu.hk/chi_diss/19</guid>
<pubDate>Mon, 07 May 2012 21:06:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>蕭紅(1911-1942)生於東北呼蘭城中的地主家庭，年幼的她，已飽受冷漠的對待，家中各人對她並不友善，父親對她更是殘暴，遏止其戀愛的自由，終於導致她和家庭決裂，出走私奔。在她生命中，每次的戀愛皆不如意，亦受到很大的壓力和痛苦。她為追求自由戀愛而出走，結果是換來獨自面對懷孕、無處棲身的悲哀。及後與蕭軍的一段婚姻，也受盡他的打罵而弄致分手收場。這些愛情的創傷，使蕭紅對男性和當時社會有更深刻的感受。</p>
<p>三十年代的中國，隨著不少女性作家的湧況，她們均描寫父權社會下種種不合理的現象，出生在哈爾濱的蕭紅，在純樸的環境中成長，培養樸實的筆法，加上其命運的坎河、戀愛希望的幻滅，還有飽受男性及社會之壓迫，都給予她源源不絕的寫作靈感。蕭紅的經歷使她的作品風格有別一般女性作家;在其眾多作品中，有大量描寫女性受壓迫的題材，如《生死場》、《呼蘭河傳》、《玉阿嫂的死》等，當中大部分的故事均以女性為主人公，講述農村婦女所受的逼迫，而且蕭紅亦將自身遭遇投射於故事的女角中，如《生死場》中金枝未婚懷孕正是作者的寫照。另外，除了描寫女性的壓迫外，蕭紅亦於小說中創作具反抗意味的角色，如《小城三月》、《看風箏》、《生死場》等篇，其中翠姨對戀愛的追求、農婦對壓迫的反抗，均表現小說強烈的女權意識。故本論文將採用英國女性主義的壓迫觀點，配合小說中女角的不同遭遇和反抗，作者於寫作上的語言運用等詳加分析，在蕭紅作品中找尋一條結構的脈絡。</p>

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</description>

<author>李 永燊</author>


</item>


<item>
<title>從李漁的戲劇理論看《風箏誤》</title>
<link>http://commons.ln.edu.hk/chi_diss/18</link>
<guid isPermaLink="true">http://commons.ln.edu.hk/chi_diss/18</guid>
<pubDate>Mon, 07 May 2012 20:39:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>李漁的劇作，因他的不良性格而遭後人非議，以致文學史家也不為他立傅，在一些較詳細的戲曲史上亦只渺渺數頁，直到近人吳梅才得到肯定。反之在日本和 歐洲，李漁的文學地位，早就得到很高的評價。一八九七年，日本學者笹川種郎(Sasagawa Taneo)在《支那小說戲曲小史》(Shina Shosetsu gikyoku shoshi)一書裡，將李漁與曹雪芹(1719-1764)、金聖嘆(1610?-1661)及孔尚任(1648-1718)並稱，同年更完成李漁的生 平研究<sup>1</sup>。可見笠翁的文學地位，確是與眾不同的。</p>
<p>近數十年來，國內外學者均重新評價李漁，如吳梅、 朱東潤、黃麗貞、杜書瀛、孫楷第、許金榜及胡天成等；日人除上述的笹川種郎外，還有目加田誠(Mekada Makoto)、松田靜枝(Matsuda Shizue)等；美國就有韓南(Patrick Hanan)；德國就有馬漢茂(Helmut Martin)，可見研究之盛。</p>
<p>在眾多研究文獻裡，大多以他的生平、小說、戲曲及評論作總體分析，鮮見對某一傳奇或小說作深入探討。有見及此，本文就以《風箏誤》傳奇為例，探討它與其戲曲理論《間情偶寄》〈詞曲部〉及〈演習部〉的一致性。</p>
<p>本文共分以下幾個部份：分析前人對李漁的評價、分析《風箏誤》與劇論的一致性、探討《風箏誤》的喜劇元素、說明《風箏誤》的缺點及笠翁重視喜劇的原因。</p>

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</description>

<author>黃 杰華</author>


</item>


<item>
<title>從權力與情慾鬥爭看潘金蓮的變態心理</title>
<link>http://commons.ln.edu.hk/chi_diss/17</link>
<guid isPermaLink="true">http://commons.ln.edu.hk/chi_diss/17</guid>
<pubDate>Mon, 07 May 2012 20:39:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>歷來都有人考究《金瓶梅》這本小說，例如考究它的版本、成書年代等；但是最為人議論的莫過於書中的性慾描寫。因此，一談到性便使人聯想到《金瓶 梅》。 雖然文中有些性慾描寫史使人 "慘不忍睹" 但是性是人類生理上正常的需要，所謂 "食、色，性也。" 只是宋明理學 "存天理，滅人慾" 的觀念影響了我們對這本小說的看法。其實《金瓶梅》在其他方面也有它的意義，例如它反映了明代的社會和政治狀況、富貴人家的生活、佛教、道教對人們的影 響、商人的形象等。在藝術方面亦有它的價值，例如人物描寫鮮明、生活的描寫細膩和真實、文中的詞曲優美等。可是人們的著眼點只在它的性描寫， 因此忽略了其他值得談論的地方。 女主角潘金蓮，更是從古到今受人非議的人物，與那些 "三從四德" 堅守貞潔的婦女比較，她的行為真是十分矚目。但其實她的所作所為是受到家庭和社會環境影響，使她感到自卑、焦慮和失去安全感。所以她在西門家常生事故，搬 弄是非。一方面是自衛 (self defense)，一方面是引起西門慶的注意，希望他尊愛、關懷自己，因為這樣才使她感到安全、消除她的自卑感和焦慮情緒。正如荷妮(Karen Horney)說：</p>
<p>卻彷彿是他們的存在，幸福及安全，都有賴於受人歡迎似的。</p>
<p>此外她的行為就是對抗這個道德的社會，希望突破父權的約束。</p>
<p>除了潘金蓮外，故事中其他人物都有他(她)獨特的心理和性格，所以無論我們從甚麼角度、方法去看《金瓶梅》也可以在這塊肥泛的土地裏發掘到它的意義。</p>
<p>從古到今，大部分論者都認為潘金蓮是萬惡淫為首的代表人物。對於她殺死親夫式大，改嫁西門慶，並自願被他虐待，又經常勾搭男人的放蕩行為，甚是噁心。但是， 我們只是罵她不守婦道、傷風敗德，我們又是否了解她的內心世界?明白她是基於甚麼心理有這些異常的行為呢?其實一個人的異常行為和心理，與他身處的環境有 很大的關係。同樣，潘金蓮的不平衡心理和不正常的行為，都與她的身份地位和社會環境有關。正如張竹坡說：</p>
<p>今看其一腔機詐，喪廉寡恥，若云本自天生， 則良心為不可必，而性善為不可據也。吾知其二、三歲時，未必便如此涅蕩也。(二十三回評2)</p>
<p>可見環境對潘金蓮影響之大。</p>
<p>在小說裏，潘金蓮自出娘胎使標誌她在這個男尊女卑的父權社會的次等身份。由出生至嫁入西門家，她都沒有人身自由。壓逼的生活，使她感到自卑和缺乏安全感，形成她焦慮的情緒。因此引起了她要出人頭地的念頭，只有出人頭地，她才能重建自己的人格尊嚴，提高自己的地位，以及增加安全感。潘金蓮爭權、爭利、爭寵、爭愛就是一種自我保護的方法。但是，這種鬥爭生活，卻影響了她的心理，也導致她行為失常。</p>
<p>這篇文章裏的主題是希望透過她的遭遇、身份和身處的環境去了解她的變態心理和她種種行為的動機，並希望能為讀者提供微薄的見解和一個新角度去了解潘金蓮，而不是片面去評價她。</p>
<p>此外，我會從權力和情慾兩方面，以宗法制度、婚姻制度、女性主義及心理學四個理論，去探討和分析潘金蓮的受虐被虐心理、補償和報復心理及變態的嫉妒心理。</p>

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</description>

<author>劉 可欣</author>


</item>


<item>
<title>Psoriasis patients are enriched for genetic variants that protect against HIV-1 disease</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1028</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1028</guid>
<pubDate>Mon, 07 May 2012 19:08:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Haoyan Chen et al.</author>


</item>


<item>
<title>Species-specific differences among KCNMB3 BK β3 auxiliary subunits: Some β3 n-terminal variants may be primate-specific subunits</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1027</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1027</guid>
<pubDate>Mon, 07 May 2012 19:08:29 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Xuhui Zeng et al.</author>


</item>


<item>
<title>GST and residential premises - which intention is relevant?</title>
<link>http://epublications.bond.edu.au/rlj/vol21/iss1/6</link>
<guid isPermaLink="true">http://epublications.bond.edu.au/rlj/vol21/iss1/6</guid>
<pubDate>Mon, 07 May 2012 18:38:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sale of ‘residences’ normally do not attract capital gains tax, unless the sale is part of an enterprise. Australian courts have been inconsistent in interpreting the expression ‘intended to be occupied and is capable of being occupied as a residence’ in the GST legislation. This article explores whether a consistent approach has now emerged.</p>

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</description>

<author>John Tretola et al.</author>


</item>


<item>
<title>Zur Geschichte der internationalen und freiwilligen Krankenpflege im Kriege</title>
<link>http://digitalcommons.law.scu.edu/monographs/1</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/monographs/1</guid>
<pubDate>Mon, 07 May 2012 17:53:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ernst Julius Gurlt</author>


</item>


<item>
<title>Proposed mechanistic basis of cellular decision making</title>
<link>http://digitalcommons.library.unlv.edu/cs_urop/2011/aug9/34</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/cs_urop/2011/aug9/34</guid>
<pubDate>Tue, 09 Aug 2011 10:15:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Max Olsen et al.</author>


</item>


<item>
<title>Illness Perceptions of Hemodialysis (HD) Patients with Type 2 Diabetes Mellitus (DM) and their Association with Empowerment</title>
<link>http://scholarship.shu.edu/dissertations/1799</link>
<guid isPermaLink="true">http://scholarship.shu.edu/dissertations/1799</guid>
<pubDate>Mon, 07 May 2012 17:13:18 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jaime L. Pula</author>


</item>


<item>
<title>A Proposal for Comprehensive and Specific Essential Mental Health and Substance Use Disorder Benefits</title>
<link>http://scholars.law.unlv.edu/facpub/695</link>
<guid isPermaLink="true">http://scholars.law.unlv.edu/facpub/695</guid>
<pubDate>Mon, 07 May 2012 16:34:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>This Article analyzes the initial efforts of the Federal Department of Health and Human Services to implement the essential mental health and substance use disorder services benefit required by section 1302(b)(1)(E) of the Affordable Care Act and proposes the adoption of a comprehensive and specific essential mental health and substance use disorder benefit set. At a minimum, the benefit set should cover medically necessary and evidence-based inpatient and outpatient mental healthcare services, inpatient substance abuse detoxification services, inpatient and outpatient substance abuse rehabilitation services, emergency mental healthcare services, prescription drugs for mental health conditions, participation in psychiatric disease management programs, and community-based mental healthcare services.</p>

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</description>

<author>Stacey A. Tovino</author>


</item>


<item>
<title>The Chinese Socio-Cultural Influence on the Legal System of the People’s Republic of China and Its Implications for Foreign Investment: A Critical Analysis</title>
<link>http://ro.uow.edu.au/theses/3484</link>
<guid isPermaLink="true">http://ro.uow.edu.au/theses/3484</guid>
<pubDate>Mon, 07 May 2012 16:25:55 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ying Lin</author>


</item>


<item>
<title>Analyzing the University of Tennessee and Its Peer Institutions for Structural Support of Queer Individuals</title>
<link>http://trace.tennessee.edu/utk_chanhonoproj/1502</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_chanhonoproj/1502</guid>
<pubDate>Mon, 07 May 2012 15:57:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Rick A. Mula</author>


</item>


<item>
<title>April 25, 2012 Cal Poly Report</title>
<link>http://digitalcommons.calpoly.edu/pao_rpt/330</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/pao_rpt/330</guid>
<pubDate>Mon, 07 May 2012 15:49:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Public Affairs Office</author>


</item>


<item>
<title>April 18, 2012 Cal Poly Report</title>
<link>http://digitalcommons.calpoly.edu/pao_rpt/329</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/pao_rpt/329</guid>
<pubDate>Mon, 07 May 2012 15:49:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Public Affairs Office</author>


</item>


<item>
<title>April 11, 2012 Cal Poly Report</title>
<link>http://digitalcommons.calpoly.edu/pao_rpt/328</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/pao_rpt/328</guid>
<pubDate>Mon, 07 May 2012 15:49:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Public Affairs Office</author>


</item>


<item>
<title>April 4, 2012 Cal Poly Report</title>
<link>http://digitalcommons.calpoly.edu/pao_rpt/327</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/pao_rpt/327</guid>
<pubDate>Mon, 07 May 2012 15:49:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Public Affairs Office</author>


</item>


<item>
<title>IL-10R blockade during chronic schistosomiasis mansoni results in the loss of B cells from the liver and the development of severe pulmonary disease</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1026</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1026</guid>
<pubDate>Mon, 07 May 2012 15:37:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Keke C. Fairfax et al.</author>


</item>


<item>
<title>Lack of evidence from studies of soluble protein fragments that Knops blood group polymorphisms in complement receptor-type 1 are driven by malaria</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1025</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1025</guid>
<pubDate>Mon, 07 May 2012 15:36:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Patience B. Tetteh-Quarcoo et al.</author>


</item>


<item>
<title>Leishmania amazonensis arginase compartmentalization in the glycosome is important for parasite infectivity</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1024</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1024</guid>
<pubDate>Mon, 07 May 2012 15:36:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Maria Fernanda Laranjeira da Silva et al.</author>


</item>


<item>
<title>Ligand-induced movements of inner transmembrane helices of Glut1 revealed by chemical cross-linking of di-cysteine mutants</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1023</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1023</guid>
<pubDate>Mon, 07 May 2012 15:36:48 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mike Mueckler et al.</author>


</item>


<item>
<title>Listeriolysin O is strongly immunogenic independently of its cytotoxic activity</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1022</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1022</guid>
<pubDate>Mon, 07 May 2012 15:36:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Javier A. Carrero et al.</author>


</item>


<item>
<title>A multicenter study of Clostridium difficile infection-related colectomy, 2000-2006</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1021</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1021</guid>
<pubDate>Mon, 07 May 2012 15:36:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Amelia M. Kasper et al.</author>


</item>


<item>
<title>Physiological notch signaling maintains bone homeostasis via RBPjk and Hey upstream of NFATc1</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1020</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1020</guid>
<pubDate>Mon, 07 May 2012 15:36:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Xiaolin Tu et al.</author>


</item>


<item>
<title>Semi-quadratic variational problems for multiphase equilibria</title>
<link>http://repository.cmu.edu/math/462</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/462</guid>
<pubDate>Mon, 07 May 2012 15:35:31 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Eliot Fried et al.</author>


</item>


<item>
<title>Thermomechanics and the formulation of the Stefan problem for fully faceted interfaces</title>
<link>http://repository.cmu.edu/math/461</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/461</guid>
<pubDate>Mon, 07 May 2012 15:35:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This paper develops a thermomechanics of two-phase heat conductors in which the interface between phases is fully faceted. The theory is based on balance of forces, balance of energy, and growth of entropy in conjunction with constitutive equations for the interface; and the chief result is a free-boundary problem of Stefan type in which the classical interface condition u = O is replaced by a condition relating the integral of u over each facet to the normal velocity of that facet."</p>

	]]>
</description>

<author>Morton E. Gurtin et al.</author>


</item>


<item>
<title>Dynamic solid-solid transitions with phase characterized by an order parameter</title>
<link>http://repository.cmu.edu/math/460</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/460</guid>
<pubDate>Mon, 07 May 2012 15:35:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We develop a thermodynamically consistent continuum theory for the study of solid-solid phase transitions where deformation dominates heat and mass transfer. We use an order parameter to characterize the notion of phase and identify phase interfaces with thin transition zones within which the strain and order parameter exhibit large gradients. To model the growth of one phase at the expense of another we introduce configurational forces, subject to their own balance, that work against changes in the order parameter. By studying traveling waves and the asymptotics of a transition layer, we establish connections between our theory and more standard approaches that identify phase interfaces with surfaces of strain discontinuity."</p>

	]]>
</description>

<author>Eliot Fried et al.</author>


</item>


<item>
<title>Geometric singularities for solutions of single conservation laws</title>
<link>http://repository.cmu.edu/math/459</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/459</guid>
<pubDate>Mon, 07 May 2012 15:35:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "In this paper we describe the geometric framework for the study of generation and propagation of shock waves in R[superscript n] appearing in weak solutions of scalar conservation laws. We first define the notion of geometric solutions for scalar conservation laws in the framework of one-parameter unfoldings of immersions. The geometric solutions are, in general, multi-valued and they are constructed by the method of characteristics. We use singularity theory techniques to classify the generic types of multi-valuedness of the geometric solutions. Such a classification is used to construct the unique entropy solution of the scalar conservation law by selecting the proper single-valued discontinuous branch of the geometric solution satisfying the entropy condition across the discontinuity."</p>

	]]>
</description>

<author>Shyuichi Izumiya et al.</author>


</item>


<item>
<title>Understanding Scaffolding and the ZPD in Educational Research</title>
<link>http://ro.uow.edu.au/edupapers/381</link>
<guid isPermaLink="true">http://ro.uow.edu.au/edupapers/381</guid>
<pubDate>Mon, 07 May 2012 15:35:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Marcia (pseudonyms have been used for the students and teachers mentioned in this paper), a third year early childhood student, was undertaking her teaching practice in a Kindergarten classroom. At the Faculty of Education reflection day Marcia approached me in tears. The reflection day is held half way though the practicum in order to give students an opportunity to share their classroom experiences with peers and lecturers. She was not happy with her supervising teacher, Annette, who would not allow her to scaffold the pupils reading comprehension in her classroom. Annette demanded of Marcia that books be read to the children without comments or questions. The teacher's concern was that Marcia would impose her own understanding of the story on her students which might suppress their spontaneity and freedom in interpreting the text and take away their ability to think for themselves. Mostly, Annette was concerned with Marcia's questions on "story prediction". She didn't think that asking specific questions such as, "Do you think the Duck will come back?" was appropriate. To support her claim, Annette, an educator of the older generation, referred to the theory of Piaget which she studied in her undergraduate degree. Marcia was very disappointed with her supervising teacher, as she believed in scaffolding as one of the most advanced teaching technique to date. She also felt that to her, scaffolding was a natural way of sharing reading with young children. As an educator, she felt somewhat constrained and restricted by not being able to talk to children and ask questions while reading to them</p>

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</description>

<author>Irina Verenikina</author>


</item>


<item>
<title>On the kinematics of incoherent phase transitions</title>
<link>http://repository.cmu.edu/math/458</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/458</guid>
<pubDate>Mon, 07 May 2012 15:35:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Incoherent phase transitions are far more difficult to treat than their coherent counterparts. The interface, which appears as a single surface in the deformed configuration, is represented in its undeformed state by a separate surface in each phase. This leads to a rich but detailed kinematics, one in which defects such as vacancies and dislocations are generated by the moving interface. We introduce an incoherency tensor that measures the stretching and twisting of one phase relative to the other. We show that incoherency is completely characterized by the incoherency tensor, the vacancy production, and the slip between phases."</p>

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</description>

<author>Paolo Cermelli et al.</author>


</item>


<item>
<title>Maxwell equations in a nonlinear Kerr medium</title>
<link>http://repository.cmu.edu/math/457</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/457</guid>
<pubDate>Mon, 07 May 2012 15:34:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "In this paper we present an exact calculation of the transfer function associated with the nonlinear Fabry-Perot resonator. While our exact result cannot be evaluated in terms of elementary functions, it does permit us to obtain a number of simple approximate expressions of various orders of accuracy. In addition, our derivation yields criteria of validity for the approximate formulae. Our approach is to be compared with others in which approximations are introduced in the model itself, either through the equations or through the boundary conditions. Our lowest order approximate formula turns out to be identical, interestingly, with the result obtained from the slowly varying envelope approximation (SVEA). Thus, our validity criteria apply to the SVEA result, and predict well its domain of validity and its breakdown for short wavelengths and for very high intensities and nonlinearities. The simple higher order formulae we present provide improved estimations in such regimes."</p>

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</description>

<author>Oscar P. Bruno et al.</author>


</item>


<item>
<title>Quasiconvex integrands and lower semicontinuity in L1</title>
<link>http://repository.cmu.edu/math/456</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/456</guid>
<pubDate>Mon, 07 May 2012 15:34:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Irene Fonseca et al.</author>


</item>


<item>
<title>A local translation of untyped [lambda] calculus into simply typed [lambda] calculus</title>
<link>http://repository.cmu.edu/math/455</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/455</guid>
<pubDate>Mon, 07 May 2012 15:34:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Richard Statman</author>


</item>


<item>
<title>There is no hyperrecurrent S,K combinator</title>
<link>http://repository.cmu.edu/math/454</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/454</guid>
<pubDate>Mon, 07 May 2012 15:34:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Richard Statman</author>


</item>


<item>
<title>Decidable discriminator varieties with lattice stalks</title>
<link>http://repository.cmu.edu/math/453</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/453</guid>
<pubDate>Mon, 07 May 2012 15:34:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We determine those universal classes of lattices which generate a decidable discriminator variety when augmented by a ternary discriminator term. They are the locally finite universal classes whose finite members are almost homogeneous."</p>

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</description>

<author>Ross Willard</author>


</item>


<item>
<title>A Neumann problem with critical Sobolev exponent</title>
<link>http://repository.cmu.edu/math/452</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/452</guid>
<pubDate>Mon, 07 May 2012 15:34:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Myriam Comte et al.</author>


</item>


<item>
<title>Hamilton cycles in a class of random directed graphs</title>
<link>http://repository.cmu.edu/math/451</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/451</guid>
<pubDate>Mon, 07 May 2012 15:34:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We prove that almost every 5-in, 5-out digraph is Hamiltonian."</p>

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</description>

<author>Colin Cooper et al.</author>


</item>


<item>
<title>A sufficient condition for finite decidability</title>
<link>http://repository.cmu.edu/math/450</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/450</guid>
<pubDate>Mon, 07 May 2012 15:34:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We prove that a locally finite, finitely generated, congruence modular variety V whose subdirectly irreducible algebras are all either abelian or linear type 3 above the monolith is finitely decidable if and only if the theory of the finite abelian algebras in V is decidable."</p>

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</description>

<author>Michael H. Albert</author>


</item>


<item>
<title>Some properties of finitely decidable varieties</title>
<link>http://repository.cmu.edu/math/449</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/449</guid>
<pubDate>Mon, 07 May 2012 15:34:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Let V be a variety whose class of finite members has a decidable first-order theory. We prove that each finite member A of V satisfies the (3,1) and (3,2) transfer principles, and that the minimal sets of prime quotients of type 2 or 3 in A must have empty tails. The first result has already been used by J. Jeong [9] in characterizing the finite subdirectly irreducible members of V with nonabelian monolith. The second result implies that if V is also locally finite and omits type 1, then V is congruence modular."</p>

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</description>

<author>Matthew Valeriote</author>


</item>


<item>
<title>Counting the number of Hamilton cycles in random digraphs</title>
<link>http://repository.cmu.edu/math/448</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/448</guid>
<pubDate>Mon, 07 May 2012 15:34:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We show that there exists a a [sic] fully polynomial randomized approximation scheme for counting the number of Hamilton cycles in almost all directed graphs."</p>

	]]>
</description>

<author>Frieze et al.</author>


</item>


<item>
<title>Solving equations in free nilpotent groups</title>
<link>http://repository.cmu.edu/math/447</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/447</guid>
<pubDate>Mon, 07 May 2012 15:33:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "In this paper we show that any system of equations over a free nilpotent group of class c is either unitary or nullary. In fact, such a system either has a most general solution (akin to the most general solution of a system of linear diophantine equations), or every solution has a proper generalization. In principle we provide an algorithm for determining whether or not a most general solution exists, and exhibiting it if it does. This requires solving a system of linear diophantine equations for approximately c(k over c) different right hand sides, where k is the number of parameters which occur in a most general solution of the system in the variety of abelian groups."</p>

	]]>
</description>

<author>Michael H. Albert et al.</author>


</item>


<item>
<title>Discriminating varieties</title>
<link>http://repository.cmu.edu/math/446</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/446</guid>
<pubDate>Mon, 07 May 2012 15:33:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "In this paper we determine those locally finite varieties that generate decidable discriminator varieties when argumented by a ternary discriminator term."</p>

	]]>
</description>

<author>Matthew Valeriote et al.</author>


</item>


<item>
<title>Approximation of dissipative hereditary systems</title>
<link>http://repository.cmu.edu/math/445</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/445</guid>
<pubDate>Mon, 07 May 2012 15:33:41 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Richard C. MacCamy</author>


</item>


<item>
<title>Polychromatic Hamilton cycles</title>
<link>http://repository.cmu.edu/math/444</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/444</guid>
<pubDate>Mon, 07 May 2012 15:33:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "The edges of the complete graph K[subscript n] are coloured so that no colour appears no more than k times, k = [n/A 1n n], for some sufficiently large A. We show that there is always a Hamiltonian cycle in which each edge is a different colour. The proof technique is probabilistic."</p>

	]]>
</description>

<author>Frieze et al.</author>


</item>


<item>
<title>On the expected performance of a parallel algorithm for finding maximal independent subsets of a random graph</title>
<link>http://repository.cmu.edu/math/443</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/443</guid>
<pubDate>Mon, 07 May 2012 15:33:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We consider the parallel greedy algorithm of Coppersmith, Raghavan and Tompa [CRT] for finding the lexicographically first maximal independent set of a graph. We prove an [omega](log n) bound on the expected number if [sic] iterations for most edge densities. This complements the O(log n) bound proved in Calkin and Frieze [CF]."</p>

	]]>
</description>

<author>Neil J. Calkin et al.</author>


</item>


<item>
<title>Computing the volume of convex bodies : a case where randomness provably helps</title>
<link>http://repository.cmu.edu/math/442</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/442</guid>
<pubDate>Mon, 07 May 2012 15:33:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We discuss the problem of computing the volume of a convex body K in R[superscript n]. We review worst-case results which show that it is hard to deterministically approximate vol[subscript n]K and randomised approximation algorithms which show that with randomisation one can approximate very nicely. We then provide some applications of this latter result."</p>

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</description>

<author>Martin Dyer et al.</author>


</item>


<item>
<title>On the fundamental eigenfunctions of a clamped punctured disk</title>
<link>http://repository.cmu.edu/math/441</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/441</guid>
<pubDate>Mon, 07 May 2012 15:33:14 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. V.(Charles Vernon) Coffman et al.</author>


</item>


<item>
<title>Lyapunov exponents and stochastic flows of linear and affine hereditary systems : a survey</title>
<link>http://repository.cmu.edu/math/440</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/440</guid>
<pubDate>Mon, 07 May 2012 15:33:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Salah-Eldin A. Mohammed</author>


</item>


<item>
<title>Equilibrium models with singular asset prices</title>
<link>http://repository.cmu.edu/math/439</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/439</guid>
<pubDate>Mon, 07 May 2012 15:32:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "General equilibrium models in which economic agents have finite marginal utility from consumption at the origin lead to financial assets whose prices are continuous but exhibit singular components. In particular, there is no bona-fide 'interest rate' in such models, although asset prices can be determined by equilibrium considerations (and uniquely, up to the formation of mutual funds). The singularly continuous processes in question charge precisely the set of time-points at which some agent 'drops out' of the economy, or 'comes back' into it, between intervals of zero-consumption. Not surprisingly, these processes are governed by local time."</p>

	]]>
</description>

<author>Ioannis Karatzas et al.</author>


</item>


<item>
<title>Equivalent martingale measures and optimal market completions</title>
<link>http://repository.cmu.edu/math/438</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/438</guid>
<pubDate>Mon, 07 May 2012 15:32:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Optimal fictitious completions of an incomplete financial market are shown to be associated with exponential martingales (not just local martingales) and, therefore, to 'an optimal equivalent martingale measure'. Results of independent interest, in the theory of continuous-time martingales, are derived as well."</p>

	]]>
</description>

<author>Ioannis Karatzas et al.</author>


</item>


<item>
<title>Decidable discriminator varieties from unary classes</title>
<link>http://repository.cmu.edu/math/437</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/437</guid>
<pubDate>Mon, 07 May 2012 15:32:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Let K be a class of (universal) algebras of fixed type. K[superscript t] denotes the class obtained by augmenting each member of K by the ternary discriminator function (t(x,y,z) = x if x [does not equal] y, t(x,x,z) = z), while V(K[superscript t]) is the closure of K[superscript t] under the formulation of subalgebras, homomorphic images, and arbitrary Cartesian products. For example, the class of Boolean algebras is definitionally equivalent to V(K[superscript t]) where K consists of a two-element algebra whose only operations are the two constants. Any equationally defined class (that is, variety) of algebras which is equivalent to some V(K[superscript t]) is known as a discriminator variety. Building on recent work of S. Burris, R. McKenzie and M. Valeriote, we characterize these locally finite universal classes K of unary algebras of finite type for which the first-order theory of V(K[superscript t]) is decideable."</p>

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</description>

<author>Ross Willard</author>


</item>


<item>
<title>On perfect matchings in random bipartite graphs with minimum degree at least two</title>
<link>http://repository.cmu.edu/math/436</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/436</guid>
<pubDate>Mon, 07 May 2012 15:32:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frieze</author>


</item>


<item>
<title>Weakly Lipschitzian mappings and restricted uniqueness of solutions of ordinary differential equations</title>
<link>http://repository.cmu.edu/math/435</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/435</guid>
<pubDate>Mon, 07 May 2012 15:32:32 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>David R. Owen et al.</author>


</item>


<item>
<title>A free boundary problem related to singular stochastic control</title>
<link>http://repository.cmu.edu/math/434</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/434</guid>
<pubDate>Mon, 07 May 2012 15:32:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "It is desired to control a multi-dimensional Brownian motion by adding a (possibly singularly) continuous process to its n[superscript th] components so as to minimize an expected infinite-horizon discounted running cost. The Hamilton-Jacobi-Bellman characterization of the value function is a variational inequality which has a unique twice continuously differentiable solution. The optimal process is constructed by solving the Skorokhod problem of reflecting the Brownian motion along a free boundary in the (0,0,..., -1) direction."</p>

	]]>
</description>

<author>Steven E. Shreve et al.</author>


</item>


<item>
<title>Symmetric finite element and boundary integral coupling methods for fluid-solid interaction</title>
<link>http://repository.cmu.edu/math/433</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/433</guid>
<pubDate>Mon, 07 May 2012 15:32:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This paper presents a coupled finite element and boundary integral method for solving the time-periodic oscillation and scattering problem of an inhomogeneous elastic body immersed in a compressible, inviscid, homogeneous fluid. By using integral representations for the solution in the infinite exterior region occupied by the fluid, the problem is reduced to one defined only over the finite region occupied by the solid, with associated non-local boundary conditions. This problem is then given a family of variational formulations, including a symmetric one, which are used to derive finite dimensional Galerkin approximations. The validity of the method is established explicitly, and results of an error analysis are discussed, showing optimal convergence to a classical solution."</p>

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</description>

<author>Jacobo Bielak et al.</author>


</item>


<item>
<title>DET = DET : a remark on the distributional determinant</title>
<link>http://repository.cmu.edu/math/432</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/432</guid>
<pubDate>Mon, 07 May 2012 15:32:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "A proof of a conjecture of J.M. Ball concerning the distributional determinant is given and an application to nonlinear elasticity is indicated."</p>

	]]>
</description>

<author>Stefan Mu╠êller</author>


</item>


<item>
<title>Randomized greedy matching</title>
<link>http://repository.cmu.edu/math/431</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/431</guid>
<pubDate>Mon, 07 May 2012 15:32:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We consider a randomized version of the usual greedy algorithm for finding a large matching in a graph. We assume that the next edge is randomly chosen from those remaining at any stage. We analyse the expected performance of this algorithm when the input graph is fixed. We show that there are graphs for which this Randomized Greedy Algorithm (RGA) usually only obtains a matching close in size to that guaranteed by worst-case analysis (i.e. half the size of the maximum). For some classes of sparse graphs (e.g. planar graphs and forests) we prove that randomization does produce an improvement over the worst-case, the ratios to maximum being at least 6/11 and 0.76┬╖┬╖┬╖ respectively."</p>

	]]>
</description>

<author>Martin Dyer et al.</author>


</item>


<item>
<title>On the length of the longest monotone subsequence in a random permutation</title>
<link>http://repository.cmu.edu/math/430</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/430</guid>
<pubDate>Mon, 07 May 2012 15:31:57 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Frieze</author>


</item>


<item>
<title>Spanning maximal planar subgraphs of random graphs</title>
<link>http://repository.cmu.edu/math/429</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/429</guid>
<pubDate>Mon, 07 May 2012 15:31:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We study the threshold for the existence of a spanning maximal planar subgraph in the random graph G[subscript n,p]. We show that it is very near p = 1[over][subscript n]1/3. We also discuss the threshold for the existence of a spanning maximal outerplanar subgraph. This is very near p = 1[over][subscript n]1/2."</p>

	]]>
</description>

<author>Be╠üla Bolloba╠üs et al.</author>


</item>


<item>
<title>A hyperbolic theory for the evolution of plane curves</title>
<link>http://repository.cmu.edu/math/428</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/428</guid>
<pubDate>Mon, 07 May 2012 15:31:44 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Morton E. Gurtin et al.</author>


</item>


<item>
<title>Planar motion of an anisotropic interface</title>
<link>http://repository.cmu.edu/math/427</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/427</guid>
<pubDate>Mon, 07 May 2012 15:31:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Morton E. Gurtin</author>


</item>


<item>
<title>A nonlinear elliptic equation arising from gauge field theory and cosmology</title>
<link>http://repository.cmu.edu/math/426</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/426</guid>
<pubDate>Mon, 07 May 2012 15:31:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We study radially symmetric solutions of a nonlinear elliptic partial differential equation in R┬▓ with critical Sobolev growth, i.e., the nonlinearity is of exponential type. This problem arises from a wide variety of important areas in theoretical physics including superconductivity and cosmology. Our results lead to many interesting implications for the physical problems considered. For example, for the self-dual Chern-Simons theory, we are able to conclude that the electric charge, magnetic flux, or energy of a non-topological N-vortex solution may assume any prescribed value above an explicit lower bound. For the Einstein-matter-gauge equations, we find a necessary and sufficient condition for the existence of a self-dual cosmic string solution. Such a condition imposes an obstruction for the winding number of a string in terms of the universal gravitational constant."</p>

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</description>

<author>X Chen</author>


</item>


<item>
<title>Finite element methods for the time-dependent Ginzburg-Landau model of superconductivity</title>
<link>http://repository.cmu.edu/math/425</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/425</guid>
<pubDate>Mon, 07 May 2012 15:31:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "The initial-boundary value problem for the time-dependent Ginzburg-Landau equations that model the macroscopic behavior of superconductors is considered. The convergence of finite-dimensional, semi-discrete Galerkin approximations is studied as is a fully-discrete scheme. The results of some computational experiments are presented."</p>

	]]>
</description>

<author>Qiang Du</author>


</item>


<item>
<title>Semi-local classification of geometric singularities for Hamilton-Jacobi equations</title>
<link>http://repository.cmu.edu/math/424</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/424</guid>
<pubDate>Mon, 07 May 2012 15:31:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Shyuichi Izumiya et al.</author>


</item>


<item>
<title>Relaxation in BV x L[infinity] of functionals depending on strain and composition</title>
<link>http://repository.cmu.edu/math/423</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/423</guid>
<pubDate>Mon, 07 May 2012 15:31:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "</p>

	]]>
</description>

<author>Irene Fonseca et al.</author>


</item>


<item>
<title>On algorithms for non-convex optimization</title>
<link>http://repository.cmu.edu/math/422</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/422</guid>
<pubDate>Mon, 07 May 2012 15:31:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "A simple algorithm for the computation of local minima of non-convex problems in one dimension is proposed. This algorithm avoids certain well known local minima which are distant from the global minimum, and can be used to improve the minima obtained using classical descent methods. The calculated minima have mesh scale oscillations typical of weakly converging sequences. It is shown that these local minima converge weakly to the correct limit for certain simple problems; however, numerical evidence suggests that the gradients may not converge to the correct weak limits, and this is verified using asymptotic expansions. Extensions to multiple dimensions and some numerical examples in two dimensions are considered."</p>

	]]>
</description>

<author>Ling Ma et al.</author>


</item>


<item>
<title>Spurious oscillations in computing microstructures</title>
<link>http://repository.cmu.edu/math/421</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/421</guid>
<pubDate>Mon, 07 May 2012 15:30:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>David Kinderlehrer et al.</author>


</item>


<item>
<title>Mathematical approaches to the study of smart materials</title>
<link>http://repository.cmu.edu/math/420</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/420</guid>
<pubDate>Mon, 07 May 2012 15:30:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Richard D. James et al.</author>


</item>


<item>
<title>Computation of magnetostrictive materials</title>
<link>http://repository.cmu.edu/math/419</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/419</guid>
<pubDate>Mon, 07 May 2012 15:30:45 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Ling Ma</author>


</item>


<item>
<title>On the Lavrentiev phenomenon for autonomous second order integrands</title>
<link>http://repository.cmu.edu/math/418</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/418</guid>
<pubDate>Mon, 07 May 2012 15:30:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Chih-Wen Cheng et al.</author>


</item>


<item>
<title>Structured deformations of continua</title>
<link>http://repository.cmu.edu/math/417</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/417</guid>
<pubDate>Mon, 07 May 2012 15:30:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>G Del Piero et al.</author>


</item>


<item>
<title>Theory of magnetostriction with applications to TbxDy1-xFe2</title>
<link>http://repository.cmu.edu/math/416</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/416</guid>
<pubDate>Mon, 07 May 2012 15:30:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We present a new approach to magnetostriction that is formulated to describe materials with large magnetostriction. The main idea of the theory is to derive precisely from lattice considerations the potential wells of the anisotropy energy. The theory exhibits frustration in the sense explored by the authors in the rigid case (James and Kinderlehrer [1990]), with fine domains modeled by minimizing sequences. The theory is applied to the material Tb[subscript x]Dy[subscript 1-x]FeΓéé. The theory predicts accurately the domain structures observed by Lord [1990] in growth twinned crystals, and suggests a mechanism of magnetostriction involving a switch from a coarse domain structure to a different finer domain structure."</p>

	]]>
</description>

<author>Richard D. James et al.</author>


</item>


<item>
<title>Numerical solution of diffraction problems : a method of variation of boundaries.</title>
<link>http://repository.cmu.edu/math/415</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/415</guid>
<pubDate>Mon, 07 May 2012 15:30:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We present a new numerical method for the solution of the problem of diffraction of light by a doubly periodic surface. This method is based on a high order rigorous perturbative technique, whose application to singly periodic gratings was treated in the first two papers of this series. We briefly discuss the theoretical basis of our algorithm, namely, the property of analyticity of the diffracted fields with respect to variations of the interfaces. While the algebraic derivation of some basic recursive formulae is somewhat involved, it results in expressions which are easy to implement numerically. We present a variety of numerical examples (for bi-sinusoidal gratings), in order to demonstrate the accuracy exhibited by our method as well as its limited requirements in terms of computing power. Generalization of our computer code to crossed gratings other than bi-sinusoidal is in principle immediate, but the full domain of applicability of our algorithm remains to be explored. Comparison with results presented previously for actual experimental configurations shows a substantial improvement in the resolution of our numerics over that given by other methods introduced in the past."</p>

	]]>
</description>

<author>Oscar P. Bruno et al.</author>


</item>


<item>
<title>The elementary defects of the Oseen-Frank energy for a liquid crystal</title>
<link>http://repository.cmu.edu/math/414</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/414</guid>
<pubDate>Mon, 07 May 2012 15:30:04 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>David Kinderlehrer et al.</author>


</item>


<item>
<title>On distribution functions of the derivatives of weakly differentiable mappings</title>
<link>http://repository.cmu.edu/math/413</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/413</guid>
<pubDate>Mon, 07 May 2012 15:29:56 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Victor J. Mizel</author>


</item>


<item>
<title>Numerical solution of diffraction problems : a method of variation of boundaries.</title>
<link>http://repository.cmu.edu/math/412</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/412</guid>
<pubDate>Mon, 07 May 2012 15:29:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We have recently introduced a method of variation of boundaries for the solution of diffraction problems. This method, which is based on a theorem of analyticity of the electromagnetic field with respect to variations of the interfaces, has been successfully applied in problems of diffraction of light by perfectly conducting gratings. In this paper we continue our investigation of diffraction problems. Using our previous results on analytic dependence with respect to the grating groove-depth, we present a new numerical algorithm which applies to dielectric gratings. We also incorporate Pade╠ü approximation in our numerics. This addition enlarges the domain of applicability of our methods, and it results in computer codes which can predict more accurately the response of diffraction gratings in the resonance region. In many cases, results are obtained which are several orders of magnitude more accurate than those given by other methods available at present, such as the integral or differential formalisms. We present a variety of numerical applications, including examples for several types of grating profiles and for wavelengths of light ranging from microwaves to ultraviolet, and we compare our results with experimental data. We also use Pade╠ü approximants to gain insight on the analytic structure and the spectrum of singularities of the fields as functions of the groove-depth. Finally, we discuss some connections between Pade╠ü approximation and another summation mechanism, enhanced convergence, which we introduced earlier. It is argued that, provided certain numerical difficulties can be overcome, the performance of our algorithms could be further improved by a combination of these summation methods."</p>

	]]>
</description>

<author>Oscar P. Bruno et al.</author>


</item>


<item>
<title>The dynamics of solid-solid phase transitions.</title>
<link>http://repository.cmu.edu/math/411</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/411</guid>
<pubDate>Mon, 07 May 2012 15:29:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Morton E. Gurtin</author>


</item>


<item>
<title>Constitutive laws for pseudo-elastic materials</title>
<link>http://repository.cmu.edu/math/410</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/410</guid>
<pubDate>Mon, 07 May 2012 15:29:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "In this paper a new model of pseudo-elastic materials based on experimental observations of one-dimensional motions of SMA materials is introduced. The model incorporates phase fractions as an internal variable and allows for both reversible (elastic) and irreversible (plastic) modes inside the hysteresis loop. As such, the model accounts for a wider range of physical phenomena than the traditional plasticity theories. The constitutive equations predict transitions between elastic and plastic modes through a dependence on the time history of strain and phase fractions. These history effects are included in a way that allows for easy computation."</p>

	]]>
</description>

<author>Deborah Brandon et al.</author>


</item>


<item>
<title>On the thermodynamics of viscoelastic materials of single-integral type</title>
<link>http://repository.cmu.edu/math/409</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/409</guid>
<pubDate>Mon, 07 May 2012 15:29:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Morton E. Gurtin et al.</author>


</item>


<item>
<title>A mechanical theory for crystallization of a rigid solid in a liquid melt : melting-freezing waves</title>
<link>http://repository.cmu.edu/math/408</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/408</guid>
<pubDate>Mon, 07 May 2012 15:29:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Morton E. Gurtin</author>


</item>


<item>
<title>A duality method for optimal consumption and investment under short-selling prohibition</title>
<link>http://repository.cmu.edu/math/407</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/407</guid>
<pubDate>Mon, 07 May 2012 15:29:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "A continuous-time, consumption/investment problem on a finite horizon is considered for an agent seeking to maximize expected utility from consumption plus expected utility from terminal wealth. The agent is prohibited from selling stocks short, so the usual martingale methods for solving this problem do not directly apply. A dual problem is posed and solved, and the solution to the dual problem provides information about the existence and nature of the solution to the original problem. When the market coefficients are constant, the value functions for both problems are provided in terms of solutions to linear, second-order, partial differential equations. If, furthermore, the utility functions are of the power form, the solutions to these equations take a particularly simple form, as do the formulas for the optimal consumption and investment processes."</p>

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</description>

<author>Gan-Lin Xu et al.</author>


</item>


<item>
<title>On the continuum mechanics of the motion of a phase interface</title>
<link>http://repository.cmu.edu/math/406</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/406</guid>
<pubDate>Mon, 07 May 2012 15:29:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "A recent series of papers [G, AG, GS] began an investigation whose goal is a thermomechanics of two-phase continua based on Gibbs's [sic] notion of a sharp phase-interface endowed with thermomechanical structure. In [G] a new balance law, balance of capillary forces, was introduced and then applied in conjunction with suitable statements of the first two laws of thermodynamics; the chief results are thermodynamic restrictions on constitutive equations, exact and approximate free-boundary conditions at the interface, and a hierarchy of free-boundary problems. [AG] applied this theory to perfect conductors, in which the underlying equations reduce to a single evolution equation for the interface. [G] and [AG] were limited to rigid systems; [GS] extends the theory to include bodies that deform as they solidify or melt. These theories involve several new concepts, examples being: the creation of new material points; work intrinsic to a moving interface; the formulation of conservation laws for a moving interface. Here I shall discuss some of the new ideas involved in [GS]."</p>

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</description>

<author>Morton E. Gurtin</author>


</item>


<item>
<title>On small subgraphs of random graphs</title>
<link>http://repository.cmu.edu/math/405</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/405</guid>
<pubDate>Mon, 07 May 2012 15:29:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Alan Frieze</author>


</item>


<item>
<title>Multiphase thermomechanics with interfacial structure.</title>
<link>http://repository.cmu.edu/math/404</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/404</guid>
<pubDate>Mon, 07 May 2012 15:28:53 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Morton E. Gurtin et al.</author>


</item>


<item>
<title>Lower semicontinuity of surface energies</title>
<link>http://repository.cmu.edu/math/403</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/403</guid>
<pubDate>Mon, 07 May 2012 15:28:46 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Irene Fonseca</author>


</item>


<item>
<title>Probabilistic analysis of a parallel algorithm for finding maximal independent sets</title>
<link>http://repository.cmu.edu/math/402</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/402</guid>
<pubDate>Mon, 07 May 2012 15:28:40 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Neil J. Calkin et al.</author>


</item>


<item>
<title>Strong convergence of numerical solutions to degenerate variational problems</title>
<link>http://repository.cmu.edu/math/401</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/401</guid>
<pubDate>Mon, 07 May 2012 15:28:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Numerical approximations of strongly degenerate variational problems of the form J(u) = F ΓéÇ┬╣ F(u)╠ü + u-f)┬▓ are considered, where F is assumed convex but may have intervals where F" = 0. It is shown that, in spite of the degeneracy, natural numerical approximations still converge in W[superscript 1,p]. Rates in weaker norms and the connection with non-convex variational problems are also considered."</p>

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</description>

<author>Roy A. Nicolaides et al.</author>


</item>


<item>
<title>Energy minimization and the formation of microstructure in dynamic anti-plane shear</title>
<link>http://repository.cmu.edu/math/400</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/400</guid>
<pubDate>Mon, 07 May 2012 15:28:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Pieter J. Swart et al.</author>


</item>


<item>
<title>Approximation of analytic functions : a method of enhanced convergence</title>
<link>http://repository.cmu.edu/math/399</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/399</guid>
<pubDate>Mon, 07 May 2012 15:28:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We present a method of enhanced convergence for the approximation of analytic functions. This method introduces conformal transformations in the approximation problems in order to help extract the values of a given analytic function from its Taylor expansion. We show that conformal transformations can extend the radius of convergence of a power series far into infinity, enhance substantially its convergence rates inside the circle of convergence, and can produce a rather dramatic improvement in the conditioning of Pade╠ü approximation. This improvement, which we discuss theoretically for Stieltjes type functions, is most notorious in cases of very poorly conditioned Pade╠ü problems. In some instances, an application of enhanced convergence leads to results which are many orders of magnitude more accurate than those obtained by clasical approximants."</p>

	]]>
</description>

<author>Oscar P. Bruno et al.</author>


</item>


<item>
<title>Multiplicity results for an inhomogeneous Neumann problem with critical exponent</title>
<link>http://repository.cmu.edu/math/398</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/398</guid>
<pubDate>Mon, 07 May 2012 15:28:11 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Gabriella Tarantello</author>


</item>


<item>
<title>On the propagation of singularities of semi-convex functions</title>
<link>http://repository.cmu.edu/math/397</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/397</guid>
<pubDate>Mon, 07 May 2012 15:28:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "The paper deals with the propagation of singularities of semi-convex functions. We obtain lower bounds on the degree of the singularities and on the size of the singular set in a neighborhood of a singular point. These results apply to viscosity solutions of Hamilton-Jacobi-Bellman equations. In particular, they provide sufficient conditions for the propagation of singularities, depending only on the geometry of the superdifferential at the singular point."</p>

	]]>
</description>

<author>I Ambrosio et al.</author>


</item>


<item>
<title>A dynamic programming approach to nonlinear boundary control problems of parabolic type</title>
<link>http://repository.cmu.edu/math/396</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/396</guid>
<pubDate>Mon, 07 May 2012 15:27:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "In this paper we study a Hamilton-Jacobi equation related to the boundary control of a parabolic equation with Neumann boundary conditions. The state space of this problem is a Hilbert space and the equation is defined classically only on a dense subset of the state space. Moreover the Hamiltonian appearing in the equation contains fractional powers of an unbounded operator. These facts render the problem difficult. In this paper we give a revised definition of a viscosity solution to accommodate the unboundedness of the Hamiltonian. We then obtain existence and uniqueness results for viscosity solutions. In particular we show that under suitable assumptions the value function of the boundary control problem is the unique viscosity solution of the related Hamilton-Jacobi equation."</p>

	]]>
</description>

<author>Piermarco Cannarsa et al.</author>


</item>


<item>
<title>On three-phase boundary motion and the singular limit of a vector-valued Ginzburg-Landau equation</title>
<link>http://repository.cmu.edu/math/395</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/395</guid>
<pubDate>Mon, 07 May 2012 15:27:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We present a formal asymptotic analysis which suggests a model for three-phase boundary motion as a singular limit of a vector-valued Ginzburg-Landau equation. We prove short-time existence and uniqueness of solutions for this model, that is, for a system of three-phase boundaries undergoing curvature motion with assigned angle conditions at the meeting point. Such models pertain to grain boundary motion in alloys. The method we use, based on linearization about the initial conditions, applies to a wide class of parabolic systems. We illustrate this further by its application to an eutectic solidification problem."</p>

	]]>
</description>

<author>Lia Bronsard et al.</author>


</item>


<item>
<title>Front propagation and phase field theory</title>
<link>http://repository.cmu.edu/math/394</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/394</guid>
<pubDate>Mon, 07 May 2012 15:27:37 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Guy Barles et al.</author>


</item>


<item>
<title>Deformations and stresses with and without microslip</title>
<link>http://repository.cmu.edu/math/393</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/393</guid>
<pubDate>Mon, 07 May 2012 15:27:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Kinematical definitions of deformations with and without microslip are presented. Transformation properties for such deformations are shown to follow directly from their definitions, and Burgers vector is related to the deformation without microslip. A limit procedure provides a concept of stress without microslip and leads to a natural concept of elastic response. Various decompositions of local deformation into elastic and plastic parts proposed in the literature are shown to be compatible with this kinematical setting."</p>

	]]>
</description>

<author>David R. Owen</author>


</item>


<item>
<title>On semilinear elliptic equations with indefinite nonlinearities</title>
<link>http://repository.cmu.edu/math/392</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/392</guid>
<pubDate>Mon, 07 May 2012 15:27:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This paper concerns semilinear elliptic equations whose nonlinear term has the form W(x)f(u) where W changes sign. We study the existence of positive solutions and their multiplicity. The important role played by the negative part of W is contained in a condition which is shown to be necessary for homogeneous f. More general existence questions are also discussed."</p>

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</description>

<author>Stanley Alama et al.</author>


</item>


<item>
<title>Self duality of the gauge field equations and the cosmological constant</title>
<link>http://repository.cmu.edu/math/391</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/391</guid>
<pubDate>Mon, 07 May 2012 15:27:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This paper considers the Einstein equations coupled with the nonabelian gauge and Higgs fields. It is shown that, when cosmic string solutions are sought in the Einstein-Georgi-Glashow system and the Einstein-Weinberg-Salam system governing the gravitational-electromagnetic weak interaction forces, the self duality conditions lead to positive values of the cosmological constant which can be expressed by some fundamental parameters in particle physics."</p>

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</description>

<author>Yisong Yang</author>


</item>


<item>
<title>Generalized motion by mean curvature with Neumann conditions and the Allen-Cahn model for phase transitions</title>
<link>http://repository.cmu.edu/math/390</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/390</guid>
<pubDate>Mon, 07 May 2012 15:27:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We study a sharp-interface model for phase transitions that incorporates the interaction of the phase-boundaries with the walls of a container [omega]. In this model the interfaces move by their mean curvature and are normal to [delta omega]. We first establish local-in-time existence and uniqueness of smooth solutions for the mean curvature equation with a normal contact angle condition. We then discuss global solutions by interpreting the equation and the boundary condition in a weak (viscosity) sense. Finally, we investigate the relation of the aforementioned model with a transition-layer model. We prove that if [omega] is convex, the transition-layer solutions converge to the sharp-interface solutions as the thickness of the layer tends to zero. We conclude with a discussion of the difficulties that arise in establishing this result in non-convex domains."</p>

	]]>
</description>

<author>Markos Katsoulakis et al.</author>


</item>


<item>
<title>Cosmic string solutions of the Einstein-matter-gauge equations</title>
<link>http://repository.cmu.edu/math/389</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/389</guid>
<pubDate>Mon, 07 May 2012 15:26:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This paper establishes the existence of string-like static solutions of the coupled Einstein-matter-gage equations. Such solutions have important implications in cosmology and quantum physics. It is shown that for a prescribed string location, the system possesses a continuous family of distinct finite energy solution configurations. The proof relies on a two-side shooting method. Power-type decay estimates at spatial infinity are also obtained."</p>

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</description>

<author>Joel Spruck et al.</author>


</item>


<item>
<title>What Shapes Perceptions of the Federal Court System?</title>
<link>http://scholarship.law.cornell.edu/facpub/366</link>
<guid isPermaLink="true">http://scholarship.law.cornell.edu/facpub/366</guid>
<pubDate>Mon, 07 May 2012 15:26:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Two hundred years is a long time. It is too long after formation of a court system to ask such basic questions as (1) what cases occupy the system, and (2) whether even informed professionals have a reasonable picture of what goes on within the system. Nonetheless, continuing debate about the volume and makeup of litigation in general and of federal court litigation in particular requires legal scholars to address these questions. Professor Marc Galanter's work on the litigation explosion questions central assumptions about the nature and growth of the federal docket. Our prior work undermines widely held views about constitutional tort litigation, the effect of the civil rights fee-shifting statute, and prisoner constitutional tort litigation. Yet observers continue to note the many constitutional tort actions, describing them as "an ever more powerful tool" for challenging official action and noting an "explosion" in new uses of section 1983. The section is "swamping the federal courts" and expediting the financial decay facing many local governments. And respected judges and commentators fervently argue that the caseload is smothering the courts. Judge Harry Edwards and some of his judicial colleagues have "the feeling that our friends in the law schools [do] not really understand the problems facing the judiciary ....”</p>
<p>Plainly, interested observers of the system have radically different views of litigation reality. This article explores why this might be so. For example, why is it that we cannot identify a civil rights explosion when judges and others perceive one? How can a Supreme Court Justice announce a geometric increase in civil rights litigation after enactment of a fee-shifting statute at a time when there was little support for even arithmetic growth? Why is it that some observers suspect that constitutional tort litigation is highly successful when, by most tangible measures, it is one of the less successful classes of federal litigation?</p>

	]]>
</description>

<author>Theodore Eisenberg et al.</author>


</item>


<item>
<title>The geometry of contact, separation and reformation of continuous bodies</title>
<link>http://repository.cmu.edu/math/388</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/388</guid>
<pubDate>Mon, 07 May 2012 15:26:48 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>W Noll</author>


</item>


<item>
<title>An equivalence theorem for string solutions of the Einstein-matter-gauge equations</title>
<link>http://repository.cmu.edu/math/387</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/387</guid>
<pubDate>Mon, 07 May 2012 15:26:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "String-like static solutions of the Einstein-matter-gauge equations have interesting implications in cosmology. It has been shown recently that, at a critical coupling phase, this system of equations allows a reduction into a coupled Einstein-Bogomol'nyi system. In this paper, we prove that, in the important case where the underlying two-dimensional Riemannian manifold is either compact or asymptotically Euclidean, the two systems are actually equivalent. Moreover, we show that the standard assumption that the strings reside in a conformally Euclidean surface will give us a metric which fails to be asymptotically Euclidean. In particular, in the radially symmetric case, we establish under the finite energy condition the boundary behavior of the metric. These results may indicate that a string solution will inevitably lead to nonflatness of the space at infinity even on the cross section."</p>

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</description>

<author>Yisong Yang</author>


</item>


<item>
<title>On the weak lower semicontinuity of energies with polyconvex integrands</title>
<link>http://repository.cmu.edu/math/386</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/386</guid>
<pubDate>Mon, 07 May 2012 15:26:32 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Wilfrid Gangbo</author>


</item>


<item>
<title>Some methods of analysis in the study of microstructure</title>
<link>http://repository.cmu.edu/math/385</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/385</guid>
<pubDate>Mon, 07 May 2012 15:26:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>David Kinderlehrer</author>


</item>


<item>
<title>A coercive bilinear form for Maxwell&apos;s equations</title>
<link>http://repository.cmu.edu/math/384</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/384</guid>
<pubDate>Mon, 07 May 2012 15:26:16 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Costabel</author>


</item>


<item>
<title>A remark on the regularity of solutions of Maxwell&apos;s equations on Lipshitz domains</title>
<link>http://repository.cmu.edu/math/383</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/383</guid>
<pubDate>Mon, 07 May 2012 15:26:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Costabel</author>


</item>


<item>
<title>Rich models</title>
<link>http://repository.cmu.edu/math/382</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/382</guid>
<pubDate>Mon, 07 May 2012 15:25:59 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michael H. Albert et al.</author>


</item>


<item>
<title>Indiscernible sequences in stable models</title>
<link>http://repository.cmu.edu/math/381</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/381</guid>
<pubDate>Mon, 07 May 2012 15:25:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rami Grossberg</author>


</item>


<item>
<title>Characterizing stability and superstability by unions of chains and saturated models</title>
<link>http://repository.cmu.edu/math/380</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/380</guid>
<pubDate>Mon, 07 May 2012 15:25:45 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michael H. Albert et al.</author>


</item>


<item>
<title>An approximation result for strongly positive kernels</title>
<link>http://repository.cmu.edu/math/379</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/379</guid>
<pubDate>Mon, 07 May 2012 15:25:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Stig-Olof Londen</author>


</item>


<item>
<title>A transport theorem for moving interfaces</title>
<link>http://repository.cmu.edu/math/378</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/378</guid>
<pubDate>Mon, 07 May 2012 15:25:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Morton E. Gurtin et al.</author>


</item>


<item>
<title>Necessary and sufficient conditions for a sum-free set of positive integers to be ultimately periodic</title>
<link>http://repository.cmu.edu/math/377</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/377</guid>
<pubDate>Mon, 07 May 2012 15:25:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Neil J. Calkin</author>


</item>


<item>
<title>The strong perfect graph conjecture holds for diamonded odd cycle-free graphs</title>
<link>http://repository.cmu.edu/math/376</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/376</guid>
<pubDate>Mon, 07 May 2012 15:25:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Olivia M. Carducci</author>


</item>


<item>
<title>On chains of relatively saturated submodels of a stable model</title>
<link>http://repository.cmu.edu/math/375</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/375</guid>
<pubDate>Mon, 07 May 2012 15:25:06 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Rami Grossberg</author>


</item>


<item>
<title>COMPARING THE DEMOGRAPHICS OF TWO STEELHEAD POPULATIONS AND THEIR HABITAT CHARACTERISTICS</title>
<link>http://digitalcommons.calpoly.edu/theses/719</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/theses/719</guid>
<pubDate>Mon, 07 May 2012 15:02:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Currently, little is known about the demographics of the <em>Oncorhynchus mykiss irideus</em>, or steelhead trout, populations in San Luis Obispo County.  Specifically, demographic information including length, age, and condition when first leaving a watershed for the open ocean is lacking.  This thesis takes a closer look at a biological and environmental data collected by the California Department of Fish and Game Central Coast Steelhead and Coho Salmon project under the direction of Associate Biologist Jennifer Nelson.  The main goal of this thesis is to analyze demographic and habitat data from the steelhead populations of two northern San Luis Obispo county coastal streams, San Simeon and Santa Rosa Creeks.</p>
<p>Habitat mapping surveys were conducted on each stream in order to identify suitable habitat for various steelhead life stages.  The data generated from the habitat mapping surveys was compared between the two creeks over the two different survey years (1993 and 2005).  The results of these surveys showed that habitat types have changed on San Simeon Creek between survey years while Santa Rosa Creek appeared to remain the same.</p>
<p>Biological inventory methods were conducted on the populations of <em>O. m. irideus </em>in San Simeon and Santa Rosa Creeks during the years of 1993 and 2005.   There were very few observations of steelhead moving downstream on both survey creeks in 1993.  During the 2005 out-migrant trapping season, the data revealed that non-smolting fish are moving downstream in the watershed in addition to smolting fish.  There is evidence that age 1+ and 2+ fish make up the majority of downstream migrants.  Older, larger fish tend to migrate downstream earlier in the trapping season.  Fork length – weight relationships are not significant between steelhead sampled from out-migrant traps, while those sampled throughout the watersheds by means of electrofishing were different between creeks.   Percent frequency distribution of electrofished steelhead reveal that steelhead sampled in 2005 have a similar distribution of total lengths between creeks, where as those sampled in 1993 have a slightly different distribution from each other.</p>
<p>Further analysis of steelhead scales sampled from the populations on San Simeon and Santa Rosa Creeks in 2005 gave greater insight into the growth of these fish.   In most cases, steelhead from Santa Rosa Creek have greater growth increments and higher circuli counts per annuli than those surveyed from San Simeon Creek.  The majority of scale samples analyzed showed growth since the last annuli mark suggesting an increase in growth over the winter months.  The average number of circuli to the first annuli is significantly different between watersheds, as is the relationship between fork length and scale radius.</p>
<p>Analyzing steelhead demographics is important to understanding the life history pattern of steelhead in the South Central California Coast Distinct Population Segment (DPS).  Surveys that monitor environmental conditions and habitat help to identify potential limiting factors and risks to steelhead populations.  The results of this thesis present such data in hopes to promote continued research and efficient management practices of steelhead trout populations in San Luis Obispo County.</p>

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</description>

<author>Eileen Ann Baglivio</author>


</item>


<item>
<title>Occupy Chicago Oral History Project</title>
<link>http://ecommons.luc.edu/history_facpubs/1</link>
<guid isPermaLink="true">http://ecommons.luc.edu/history_facpubs/1</guid>
<pubDate>Mon, 07 May 2012 15:00:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>This public website exhibits the oral history interviews compiled by students in the Fall 2011 History Graduate Seminar at Loyola University Chicago under the supervision of Professor Michelle Nickerson, M.A. student Zachary Weber transcribed the interviews and produced the site as part of a Spring 2012 Independent Study under Professor Nickerson's direction.</p>

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</description>

<author>Michelle Nickerson et al.</author>


</item>


<item>
<title>Risk maps for targeting exotic plant pest detection programs in the
United States</title>
<link>http://digitalcommons.unl.edu/usdafsfacpub/152</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/usdafsfacpub/152</guid>
<pubDate>Mon, 07 May 2012 14:54:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the United States, pest risk maps are used by the Cooperative Agricultural Pest Survey for spatial and temporal targeting of exotic plant pest detection programs. Methods are described to create standardized host distribution, climate and pathway risk maps for the top nationally ranked exotic pest targets. Two examples are provided to illustrate the risk mapping process: late wilt of corn (<em>Harpophora-maydis</em>) and the giant African land snail (<em>Achatina fulica</em>). Host risk maps were made from county-level crop census and USDA Forest Inventory and Analysis data, respectively. Climate risk maps were made using the North Carolina State University–USDA APHIS Plant Pest Forecasting System (NAPPFAST), which uses a web-based graphical user interface to link climatic and geographic databases with interactive templates for biological modelling. Pathway risk maps were madeusing freight flow allocation data sets to move commodities from 7 world regions to 3162 US urba areas. A new aggregation technique based on the Pareto dominance principle was used to integrate maps of host abundance, climate and pathway risks into a single decision support product. The maps are publicly available online (http://www.nappfast.org). Key recommendations to improve the risk maps and their delivery systems are discussed.</p>

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</description>

<author>R Magarey et al.</author>


</item>


<item>
<title>Authentic Pedagogy and the Novice Teacher: Acculturating Teachers into a Reflective Practice</title>
<link>http://scholarworks.boisestate.edu/literacy_facpubs/68</link>
<guid isPermaLink="true">http://scholarworks.boisestate.edu/literacy_facpubs/68</guid>
<pubDate>Mon, 07 May 2012 14:52:09 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jonathan L. Brendefur et al.</author>


</item>


<item>
<title>Ranking viruses: Measures of positional importance within
networks define core viruses for rational polyvalent vaccine
development</title>
<link>http://digitalcommons.unl.edu/virologypub/222</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/virologypub/222</guid>
<pubDate>Mon, 07 May 2012 14:51:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Motivation: The extraordinary genetic and antigenic variability of RNA viruses is arguably the greatest challenge to the development of broadly effective vaccines. No single viral variant can induce sufficiently broad immunity, and incorporating all known naturally circulating variants into one multivalent vaccine is not feasible. Further, no objective strategies currently exist to select actual viral variants that should be included or excluded in polyvalent vaccines.</p>
<p>Results: To address this problem, we demonstrate a method based upon graph theory that quantifies the relative importance of viral variants. We demonstrate our method through application to the envelope glycoprotein gene of a particularly diverse RNA virus of pigs: porcine reproductive and respiratory syndrome virus (PRRSV). Using distance matrices derived from sequence nucleotide difference, amino acid difference, and evolutionary distance we constructed viral networks and used common network statistics to assign each sequence an objective ranking of relative “importance.” To validate our approach, we use an independent published algorithm to score our top-ranked wild-type variants for coverage of putative T-cell epitopes across the 9383 sequences in our dataset. Top-ranked viruses achieve significantly higher coverage than lower-ranked viruses, and top-ranked viruses achieve nearly equal coverage as a synthetic mosaic protein constructed in silico from the same set of 9383 sequences.</p>
<p>Conclusion: Our approach relies on the network structure of PRRSV, but applies to any diverse RNA virus because it identifies subsets of viral variants that are the most important to overall viral diversity. We suggest that this method, through the objective quantification of variant importance, provides criteria for choosing viral variants for further characterization, diagnostics, surveillance, and ultimately polyvalent vaccine development.</p>
<p>3 files of supplementary information are attached (below).</p>

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</description>

<author>Tavis K. Anderson et al.</author>


</item>


<item>
<title>Evolution in coyotes (Canis latrans) in response to the
megafaunal extinctions</title>
<link>http://digitalcommons.unl.edu/natlpark/44</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/natlpark/44</guid>
<pubDate>Mon, 07 May 2012 14:51:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Living coyotes modify their behavior in the presence of larger carnivores, such as wolves. However, little is known about the effects of competitor presence or absence on morphological change in coyotes or wolves over long periods of time. We examined the evolution of coyotes and wolves through time from the late Pleistocene, during which many large carnivorous species coexisted as predators and competitors, to the Recent; this allowed us to investigate evolutionary changes in these species in response to climate change and megafaunal extinctions at the end of the Pleistocene. We measured postcranial skeletal morphologies of wolves (<em>Canis lupus</em>) and coyotes (<em>C. latrans</em>) from Pleistocene-aged tar deposits, as well as early, mid, and recent Holocene populations of both. We found few morphological differences between Pleistocene and Holocene wolf populations. Conversely, we found many differences in coyotes: Pleistocene coyotes were larger and more robust than Holocene populations. However, within 1,000 y of the megafaunal extinctions, coyotes are morphologically indistinguishable from modern populations. We cannot attribute these differences directly to climate change because modern coyotes do not follow Bergmann’s rule, which states body size increases with decreasing temperature. Instead, we suggest that Pleistocene coyotes may have been larger and more robust in response to larger competitors and a larger-bodied prey base. Although we cannot separate competition from predator-prey interactions, this study indicates that the effects of biotic interactions can be detected in the fossil record.</p>

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</description>

<author>Julie Meachen et al.</author>


</item>


<item>
<title>The Blackwood Creek Reach 6 Restoration Project&apos;s Influence on Reach Scale Sediment Scour and Storage Characteristics</title>
<link>http://digitalcommons.usu.edu/gradreports/118</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/118</guid>
<pubDate>Mon, 07 May 2012 14:49:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Stream restoration activities in Reach 6 of Blackwood Creek involved constructing a new stream channel in a reach that had been eroding and adjusting to historic land uses since the 1960s. In 2010, the spring after restoration work was completed, the project had a 2.3-year recurrence peak flow of 12.3 m3/s. This post-project assessment looks at the impacts of restoration work in Reach 6 in the short time since the project was completed. Project objectives for restoration work were to: increase the extent of floodplain inundation for seasonal flooding, reduce the rate of bank erosion, and to encourage sediment deposition, particularly fine sediment, on the floodplain. Using HEC-RAS, a one dimensional hydrologic model, I predict that the extent of flooding over a wide range of recurrences will increase as a result of restoration work, with the largest proportional increase for small magnitude, high recurrence floods. To assess the impact restoration activities will have on stream channel erosion, the average predicted shear stress was compared between pre-restoration and post-restoration conditions. This work indicates that there will be a decrease in average shear stress for all floods, with a 39% decrease for the 1.5-year recurrence flow and a 48% decrease for a 20-year recurrence flow. In 2010, areas of deposition iii and scour were mapped in Reach 6 to assess whether the project reach was accumulating sediment on the floodplain. I found that 1,129 m3 of sediment had been deposited and 142 m3 of sediment has been scoured. Of the 1,541 Mg of sediment deposited within Reach 6, 40% was gravel and coarser sizes, 50% was sand, 7% was silt, and 2% was clay.</p>

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</description>

<author>David Raymond Immeker</author>


</item>


<item>
<title>Civic Engagement and Internet Use in Cache Valley</title>
<link>http://digitalcommons.usu.edu/gradreports/117</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/117</guid>
<pubDate>Mon, 07 May 2012 14:49:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Internet technology has provided tools for communication only dreamed of decades ago. This technology, coupled with civic engagement, has the power to influence local legislation in powerful ways. In this project, I conducted interviews and focus groups to find out how citizens of Cache County, Utah, are using the Internet to engage in civic affairs affecting local legislation. Interviewees were also asked what aspects of a community website would likely enhance their civic activity. It was found that people primarily use the Internet to access information and send email. Suggestions for enhancing engagement included more creative, and interactive ways of using the Internet. The project culminated in a rudimentary website implementing the information gleaned from interviews.</p>

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</description>

<author>Dave Wind</author>


</item>


<item>
<title>Finding the Soul in the Soil: How Welfare Farms of the Church of Jesus Christ of Latter-Day Saints Create Spiritual Communities</title>
<link>http://digitalcommons.usu.edu/gradreports/116</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/gradreports/116</guid>
<pubDate>Mon, 07 May 2012 14:49:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Church of Jesus Christ of Latter-day Saints was founded by Joseph Smith in 1830, but its connection with agrarian themes is found in all of LDS canonized scripture, implying a sense of antiquity from the time of Adam in the Garden of Eden. Scriptural examples and teachings of LDS leaders build the foundation of the Latter-day Saint agrarian theology. Valuing this connection to the land remained constant during the Church’s early development, but diminished in theological focus years before the Great Depression. During the Depression, the Church proactively created a Church Security Plan (later renamed the Church Welfare Plan) to aid Church members’ temporal and spiritual needs. Welfare projects provided relief through Mormonism’s concepts of independence, self-reliance, stewardship, and welfare. The application of the Church Welfare Program encouraged the development of these doctrinal principles, and resulted in the creation of spiritual communities on Church welfare farms as the needs of the community were met, both LDS and non-LDS. Welfare farms, created during the Great Depression, establish an environment for the application of the agrarian theology that has existed within Mormonism since its beginnings, and acts as an ideal setting for the creation of spiritual communities.</p>

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</description>

<author>Matthew L. Maughan</author>


</item>


<item>
<title>What is mission critical in the hotel guest room: Examining in-room guest empowerment technologies</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1288</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1288</guid>
<pubDate>Mon, 07 May 2012 14:47:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study examined 18 in-room technologies and identified the ones perceived to be mission critical for the hotel guests. It also determined the differences in guest empowerment technology preferences and expectations across generations, purpose of travel, and travel frequency. Moreover, it investigated whether the quality of in-room technologies impacts guests' decision in choosing a hotel.</p>
<p>The data were collected through an online survey. A total of 508 people responded to the survey. An importance and performance analysis was utilized to identify the mission critical in-room technologies for the hotels. The analysis indicated that in-room movie on demand services, in-room wireless high speed internet service, high definition television content, in-room electronic temperature control, in-room electronic safe, connectivity panels, and all in one guest room control unit were perceived as being mission critical in-room technologies for hotel guests. The utilization of ANOVA and subsequent post-hoc tests showed that there were significant technology preference differences across the generations and travel frequency. Another important finding of this study was that a majority of respondents reported that the availability of new guest-room technologies would favorably impact their decision to select a hotel. The overall findings of this study provide information that would help hotel managers and owners to understand guests' perceptions of and expectations for in-room technologies. These findings may possibly provide guidance for strategic purchasing, upgrading or implementing in-room technologies.</p>

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</description>

<author>Pelin Nasoz</author>


</item>


<item>
<title>An examination of the preparation, experiences, and attitudes of effective school leaders of students with disabilities: Voices from the field</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1287</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1287</guid>
<pubDate>Mon, 07 May 2012 14:47:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Research reflecting the preparation, experiences, and attitudes of effective school leaders of students with disabilities is scarce despite the fervent federal requirements changing special education over the past four decades. Although there is extensive literature on perspectives and contexts of disability, the legislative journey toward special education, inclusion and educational leadership, the expanding role of the principalship, principal attitudes on inclusion, and preparing educational leaders for inclusive education, a review of the related literature revealed an absence of the skill-set and disposition needed by school leaders who are improving academic achievement for students with disabilities.</p>
<p>This qualitative dissertation study documents and examines the preparation, experiences, and attitudes of two elementary school principals that have demonstrated success at improving student achievement among their special education population. The questions guiding this study are: (1) In what way does a school leader's leadership preparation program impact the education of students with disabilities? (2) In what way does a school leader's leadership experience impact the education of students with disabilities? (3) In what ways do a school leader's attitudes and perceptions impact the education of students with disabilities?</p>
<p>Using a qualitative research methodology and narrative inquiry research methods, this study aims to capture the lived experiences and perspectives of such leaders. In-depth interviews, field notes, site observations, and reflexive journaling were used to illustrate and examine the dispositions of the school leaders.</p>
<p>This study is important because it will provide insight to those concerned about what is essential to make an education for students with disabilities not only an accessible one, but a quality one. It will also guide educational leadership programs in developing curricula for future school leaders as they face the challenges of implementing state and federal policy. It also adds to the growing literature in the fields of educational leadership and special education.</p>

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</description>

<author>Patricia Ann Schultz</author>


</item>


<item>
<title>Effects of high-impedance-contrast boundary upon multi-modal seismic surface wave data</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1286</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1286</guid>
<pubDate>Mon, 07 May 2012 14:47:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Synthetic studies and analyses of an experimental dataset were conducted to address the use of Rayleigh-type surface waves for estimation of shear wave velocity (VS) profiles of shallow bedrock sites. The shallow bedrock presents a high impedance contrast boundary which causes surface wave energy to be partitioned to higher modes. Idealized studies of hypothetical datasets and root-mean-squared calculations of error surfaces showed that if reliable dispersion data are available over a broad frequency spectrum, the VS profile can be recovered using the fundamental mode alone. However, when dispersion data are limited to a relatively narrow frequency band representing what might be commonly sampled in practice, the fundamental mode alone is insufficient to resolve the VS profile, but joint consideration of higher modes along with the fundamental mode will be successful in some cases. Outcomes of similar tests on experimental data from a shallow bedrock site were instructive but less definitive. Tests repeatedly demonstrated that a good quality starting model is necessary to converge upon a reasonable solution. To improve the starting model, the dispersion dataset can be scrutinized to estimate depth to bedrock. Dispersion curves for the shallow bedrock case are particularly susceptible to misinterpretation. Tests revealed that the consequences of a likely form of misinterpretation are strong velocity fluctuations and overestimation of VS of the bedrock.</p>

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</description>

<author>Prajwol Tamrakar</author>


</item>


<item>
<title>Retrospective investigation of course content evaluation by students: A survey of domestic violence education and experience among current UNLV-SDM dental students</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1285</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1285</guid>
<pubDate>Mon, 07 May 2012 14:47:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>The overall purpose of this research project is to survey experience and education of current dental students regarding domestic violence. Domestic violence has been recognized as one of our nation's most serious public health issues. Domestic violence can result in physical injury, psychological trauma, and sometimes death. Dentists can act as one of the first lines of intervention in recognizing common dental and facial trauma which may be associated with domestic violence victims including: broken teeth, facial bruising, and jaw fractures.</p>
<p>Current data suggest that education about domestic violence can help the dental professional in overcoming some of the barriers they face in intervening to help domestic violence victims. A UNLV Office of Research Integrity - Human Subjects Exemption (1103-3752M - Retrospective Investigation of Course Content Evaluation by Students: A Survey of Domestic Violence Education and Experience among Current UNLV-SDM Dental Students) was filed and approved June 7, 2011 to facilitate the use of an existing survey administered at UNLV-SDM, before and after a domestic violence education seminar. Although there is growing evidence of domestic violence education and instruction in medical education, few studies have evaluated the need for this type of education or the results of this instruction in dental schools specifically.</p>

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</description>

<author>Rhonda J. Everett</author>


</item>


<item>
<title>Optimizing heart dose reduction for deep inspiration left breast radiotherapy</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1284</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1284</guid>
<pubDate>Mon, 07 May 2012 14:47:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Multiple studies have shown that an increased risk of late injury cardiac abnormalities including congestive heart failure (CHF), ischemia, and coronary artery disease (CAD) can be associated with common left breast radiation therapy (RT) techniques. Many radiation therapy clinics have adopted the Deep Inspiration Breath Hold (DIBH) technique for the treatment of the left breast with external beam therapy based on studies showing a decrease in the dose received by the heart. A common technology used to monitor inhalation during DIBH is the Real-Time Position Management (RPM) system (Varian Medical Systems, Palo Alto, CA). This study analyzes if there is an optimal setup protocol for the use of the RPM system in order to minimize heart dose during DIBH RT of the left breast.</p>

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</description>

<author>Ronald James Harder</author>


</item>


<item>
<title>Effects of Chainring Type (Circular vs. Rotor Q-Ring) on 1km Time Trial Performance Over Six Weeks in Competitive Cyclists and Triathletes</title>
<link>http://digitalcommons.calpoly.edu/kine_fac/102</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/kine_fac/102</guid>
<pubDate>Mon, 07 May 2012 14:46:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to examine the effects of chainring type (circular vs. the non- circular Rotor Q-Ring) on performance during a 1km time trial and physiological responses over a six week period. Eight competitive male cyclists and triathletes were pre-tested using the original circular chainring. Graded submaximal exercise tests were followed by the 1km time trial with subjects using their own racing bicycle. The circular chainrings were then removed and replaced with Rotor Q-Rings during the intervention period. Subjects trained and raced with this alteration to their bicycles and repeated the submaximal and 1km performance tests for the next four weeks. Post-testing occurred with the original circular chainrings for the final week of testing. Oxygen consumption, carbon dioxide output, heart rate, ventilation, respiratory exchange ratio, and perceived exertion were continuously measured during the submaximal tests. Blood lactate concentration was measured during the last 30 s of each three minute stage. The main findings were: 1) Significant increases in performance in the 1km time trial with Rotor Q-Rings compared to circular chainrings. Subjects completed the time trial on average 1.6 seconds faster (p < 0.05), increased average speed approximately 0.7 kph (p < 0.05), and increased average power approximately 26 watts (p < 0.05). 2) During submaximal testing, oxygen consumption during weeks 2-4 and heart rate during weeks 1-3 were significantly lower (p < 0.05) with Rotor Q-Rings compared to circular chainrings. Furthermore, 1km time trial improvements occurred after just one week employing the Rotor Q-Rings and results were consistent over subsequent 1km time trials with the Rotor Q-Rings. Performance levels returned to initial values during final testing with the circular chainrings. The maximal oxygen consumption results from the Pre-test and week 5 Post-test further demonstrated that positive performance effects were only evident with the Rotor Q- Rings. While it appears from this study that there may also be positive long term effects as noted by the significant reduction in submaximal oxygen consumption and heart rate during the intervention period (i.e., cycling with Rotor Q-Rings), the majority of the physiological measures we examined do not equivocally support the notion that an adaptation period is necessary for this increased 1km time trial performance.</p>

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</description>

<author>Christiane R. O&apos;Hara et al.</author>


</item>


<item>
<title>Dielectric function spectra and critical-point energies of Cu2ZnSnSe4
from 0.5 to 9.0 eV</title>
<link>http://digitalcommons.unl.edu/usdoepub/102</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/usdoepub/102</guid>
<pubDate>Mon, 07 May 2012 14:46:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present dielectric function e=e<sub>1</sub>+ie<sub>2</sub>spectra and critical-point energies of Cu<sub>2</sub>ZnSnSe<sub>4 </sub>determined by spectroscopic ellipsometry from 0.5 to 9.0 eV. We reduce artifacts from surface overlayers to the maximum extent possible by performing chemical-mechanical polishing and wet-chemical etching of the surface of a Cu<sub>2</sub>ZnSnSe<sub>4</sub> thin film. Ellipsometric data are analyzed by the multilayer model and the e spectra are extracted. The data exhibit numerous spectral features associated with critical points, whose energies are obtained by fitting standard lineshapes to second energy derivatives of the data. The experimental results are in good agreement with the e spectra calculated within the <em>GW </em>quasi-particle approximation, and possible origins of the pronounced critical-point structures are identified.</p>

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</description>

<author>S. . G. Choi et al.</author>


</item>


<item>
<title>Finding Lips in Unconstrained Imagery for Improved Automatic Speech Recognition</title>
<link>http://digitalcommons.calpoly.edu/eeng_fac/312</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/eeng_fac/312</guid>
<pubDate>Mon, 07 May 2012 14:44:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lip movement of a speaker conveys important visual speech information and can be exploited for Automatic Speech Recognition. While previous research demonstrated that visual modality is a viable tool for identifying speech, the visual information has yet to become utilized in mainstream ASR systems. One obstacle is the difficulty in building a robust visual front end that tracks lips accurately in a real-world condition. In this paper we present our current progress in addressing the issue. We examine the use of color information in detecting the lip region and report our results on the statistical analysis and modeling of lip hue images by examining hundreds of manually extracted lip images obtained from several databases. In addition to hue color, we also explore spatial and edge information derived from intensity and saturation images to improve the robustness of the lip detection. Successful application of this algorithm is demonstrated over imagery collected in visually challenging environments.</p>

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</description>

<author>Jane Zhang et al.</author>


</item>


<item>
<title>Face and Lip Localization in Unconstrained Imagery</title>
<link>http://digitalcommons.calpoly.edu/eeng_fac/311</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/eeng_fac/311</guid>
<pubDate>Mon, 07 May 2012 14:44:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>When combined with acoustical speech information, visual speech information (lip movement) significantly improves Automatic Speech Recognition (ASR) in acoustically noisy environments. Previous research has demonstrated that visual modality is a viable tool for identifying speech. However, the visual information has yet to become utilized in mainstream ASR systems due to the difficulty in accurately tracking lips in real-world conditions. This paper presents our current progress in addressing this issue. We derive several algorithms based on a modified HSI color space to successfully locate the face, eyes, and lips. These algorithms are then tested over imagery collected in visually challenging environments.</p>

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</description>

<author>Brandon Crow et al.</author>


</item>


<item>
<title>Face and Lip Tracking in Unconstrained Imagery for Improved Automatic Speech Recognition</title>
<link>http://digitalcommons.calpoly.edu/eeng_fac/310</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/eeng_fac/310</guid>
<pubDate>Mon, 07 May 2012 14:44:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>When combined with acoustical speech information, visual speech information (lip movement) significantly improves Automatic Speech Recognition (ASR) in acoustically noisy environments. Previous research has demonstrated that visual modality is a viable tool for identifying speech. However, the visual information has yet to become utilized in mainstream ASR systems due to the difficulty in accurately tracking lips in real-world conditions. This paper presents our current progress in tracking face and lips in visually challenging environments. Findings suggest the mean shift algorithm performs poorly for small regions, in this case the lips, but it achieves near 80% accuracy for facial tracking.</p>

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</description>

<author>Brandon Crow et al.</author>


</item>


<item>
<title>2D Motion Detection Bounded Hand 3D Trajectory Tracking and Gesture Recognition under Complex Background</title>
<link>http://digitalcommons.calpoly.edu/eeng_fac/309</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/eeng_fac/309</guid>
<pubDate>Mon, 07 May 2012 14:44:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this paper, a 2D motion detection bounded hand 3D trajectory tracking and gesture recognition system is proposed for virtual reality interactions. First, the Bayes decision rule for classification of background and foreground is utilized to automatically locate the hand that bounded within a rectangle, and then the trajectory of the hand in 3D space is tracked by mean shift particle filter and stereo imaging. The skin color feature is exploited for image matting that effectively segment the hand contour in video sequence automatically. Finally the hand gesture is recognized by the connected component analysis and line approximation.</p>

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</description>

<author>Shuangqing Wu et al.</author>


</item>


<item>
<title>Real-Time 3D Markerless Multiple Hand Detection and Tracking for Human Computer Interaction Applications</title>
<link>http://digitalcommons.calpoly.edu/eeng_fac/308</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/eeng_fac/308</guid>
<pubDate>Mon, 07 May 2012 14:44:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this paper we present a purely vision based implementation of markerless hand detection and tracking system which effectively detects and tracks the hand positions irrespective of hand orientation. A shape based detection algorithm using a new line approximation technique followed by an adaptive minimum distance classifier based tracking technique is implemented. The technique is very generic and can be practically used in all types of immersive and semi-immersive environments like simulations, three-dimensional (3D) games, visually assisted medical surgery and other humancomputer interactive applications.</p>

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</description>

<author>Soumita Ghosh et al.</author>


</item>


<item>
<title>Building a Visual Front-end for Audio-Visual Automatic Speech Recognition in Vehicle Environments</title>
<link>http://digitalcommons.calpoly.edu/eeng_fac/307</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/eeng_fac/307</guid>
<pubDate>Mon, 07 May 2012 14:44:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Automatic speech recognition (ASR) holds the promise of providing a natural, efficient, and safer means for communication between humans and computers and can profoundly change the way we live. Since its invention in the 1950s, ASR has witnessed considerable research activities and in recent years is finding its way into practical applications as evidenced by more and more consumer devices such as PDAs and mobile phones adding ASR features. While mainstream ASR has focused almost exclusively on the acoustic signal, the performance of these systems degrades considerably in the real-world in the presence of noise. One way to overcome this limitation is to supplement the acoustic speech with a visual signal that remains unaffected in an audibly noisy environment, yielding what is known as audio-visual automatic speech recognition (AVASR).</p>

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</description>

<author>Robert Hursig et al.</author>


</item>


<item>
<title>Lip Localization Algorithm Using Gabor Filters</title>
<link>http://digitalcommons.calpoly.edu/eeng_fac/306</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/eeng_fac/306</guid>
<pubDate>Mon, 07 May 2012 14:43:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper describes a lip localization algorithm within a still image frame for subsequent tracking and audiovisual speech recognition processing. A Gabor filter-based feature space is promoted as a means to localize lips within an image based off of shape. This filtered space is shown to effectively differentiate facial features, including lips, from their backgrounds and to bound the full extent of the lips within a face-classified region of interest. Extensive training and test sets are used to justify design decisions and performance.</p>

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</description>

<author>Robert E. Hursig et al.</author>


</item>


<item>
<title>Anaheim Advanced Traffic Control System Field Operational Test: Technical Evaluation of SCOOT</title>
<link>http://digitalcommons.calpoly.edu/eeng_fac/305</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/eeng_fac/305</guid>
<pubDate>Mon, 07 May 2012 14:43:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>This article provides a technical evaluation of the traffic control element of the Anaheim Advanced Traffic Control System Field Operations Test (FOT), sponsored by the US Department of Transportation. The primary objective for this test was the evaluation of adaptive traffic signal control technologies, including the Split Cycle and Offset Optimization Technique (SCOOT) for intersection signal control. The SCOOT evaluation was defined relative to existing, first generation Urban Traffic Control System (UTCS)-based control using standard US field detectorization. This US geometry is not the detector configuration normally used with SCOOT. SCOOT was implemented with some degree of success, though technical problems limited its performance. Anaheim's existing communication and controller systems contributed major deployment limitations since they were less adequate than anticipated. SCOOT remains in use in selected areas, with plans for system expansion.</p>

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</description>

<author>James E. Moore II et al.</author>


</item>


<item>
<title>Making is Thinking: Emphasizing Inquiry Through Technique in the Beginning Design Studio</title>
<link>http://digitalcommons.calpoly.edu/arch_fac/66</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/arch_fac/66</guid>
<pubDate>Mon, 07 May 2012 14:41:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Mark Cabrinha et al.</author>


</item>


<item>
<title>Life Size: Environmental Knowing Through Full-Scale Installations</title>
<link>http://digitalcommons.calpoly.edu/arch_fac/65</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/arch_fac/65</guid>
<pubDate>Mon, 07 May 2012 14:41:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Mark Cabrinha</author>


</item>


<item>
<title>Crossing the Digital Divide Through Digital Dexterity</title>
<link>http://digitalcommons.calpoly.edu/arch_fac/64</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/arch_fac/64</guid>
<pubDate>Mon, 07 May 2012 14:41:08 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Mark Cabrinha</author>


</item>


<item>
<title>Ray Wilson</title>
<link>http://digitalcommons.iwu.edu/oral_hist/40</link>
<guid isPermaLink="true">http://digitalcommons.iwu.edu/oral_hist/40</guid>
<pubDate>Mon, 07 May 2012 14:39:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Professor in Physics Department 1962-1997. Continues to teach May Term through the present (as of 2012).</p>

	]]>
</description>

<author>Ray Wilson et al.</author>


</item>


<item>
<title>Focusing of longitudinal ultrasonic waves in air with an
aperiodic flat lens</title>
<link>http://digitalcommons.unl.edu/usafresearch/35</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/usafresearch/35</guid>
<pubDate>Mon, 07 May 2012 14:39:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Modeling and experimental results of an ultrasonic aperiodic flat lens for use in air are presented. Predictive modeling of the lens is performed using a hybrid genetic-greedy algorithm constrained to a linear structure. The optimized design parameters are used to fabricate a lens. A method combining a fiber-disk arrangement and scanning laser vibrometer measurements is developed to characterize the acoustic field distribution generated by the lens. The focal spot size is determined to be 0.88 of the incident wavelength of 8090 kHz at a distance of 2.5 mm from the lens. Theoretically computed field distributions, optimized frequency of operation, and spatial resolution focal length are compared with experimental measurements. The differences between experimental measurements and the theoretical computations are analyzed. The theoretical calculation of the focal spot diameter is 1.7 mm which is 48% of the experimental measurement at a frequency of 80–90 kHz. This work illustrates the capabilities of a hybrid algorithm approach to design of flat acoustic lenses to operate in air with a resolution of greater than the incident wavelength and the challenges of characterizing acoustic field distribution in air.</p>

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</description>

<author>John T. Welter et al.</author>


</item>


<item>
<title>Estimating Minimum Effective Dose in Dose Response Studies</title>
<link>http://digitalcommons.library.umaine.edu/etd/1018</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1018</guid>
<pubDate>Mon, 07 May 2012 14:37:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>The proper understanding and characterization of the dose-response relationship for a new compound is a fundamental step in the clinical development process of any medicinal drug. A major goal of dose-finding studies is to estimate target doses of interest. Among the many target doses that can be estimated the minimum effective dose (MED) is of particular interest. Here the MED is defined as the smallest dose that produces a practically relevant response. Thus, any dose smaller than the MED can be discarded for future studies or for potential release in the market. In this thesis, we will study various optimal designs for estimating the MED. More specifically, we will study designs that minimize the asymptotic variance of the MED estimator under a particular dose response model.</p>

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</description>

<author>Zezheng Li</author>


</item>


<item>
<title>Computing Galois Groups over Q</title>
<link>http://digitalcommons.library.umaine.edu/etd/1017</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1017</guid>
<pubDate>Mon, 07 May 2012 14:36:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Galois theory is an area of modern algebra which provides a framework for transforming problems involving fields into more manageable problems involving groups. The fundamental theorem of Galois theory asserts that there exists a one-to-one correspondence between certain subfields of a splitting field of a polynomial and the subgroups of its Galois group. This realization provides an elegant answer to the question of whether a polynomial equation over a base field is solvable by radicals. In fact, a polynomial is solvable by radicals if its Galois group is a solvable group. In general, the determination of the Galois group of a polynomial is not itself a trivial task, thus the determination of Galois groups provides a basis for the content of this thesis. More specifically, this thesis is concerned with the determination of Galois groups using resolvent polynomials from theory to implementation.</p>

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</description>

<author>Christian L. Wilson</author>


</item>


<item>
<title>A Variation on Geometric Constructions</title>
<link>http://digitalcommons.library.umaine.edu/etd/1016</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1016</guid>
<pubDate>Mon, 07 May 2012 14:36:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Since the time of the Greeks straightedge and compass constructions have been studied extensively. These constructions represent geometry in its purist form and have been taught to students of mathematics since. As elegant as these constructions are they have very real limitations. The Greeks suspected these limitations and modern algebra fully exposed them. In spite of these limitations innovative tools have found their way into mathematical literature and have enabled us to construct cube roots and trisect any angle. Some of these tools have been fully characterized while some have not. This thesis investigates marked straightedge and compass constructions through an intriguing analog tool set that is coined as q-construction. It is known that taking cube roots and finding an arbitrary angle trisection is possible with marked straightedge and compass. At least one construction that is unknown is the taking of fifth roots. We show that it is possible to take fifth roots using q-construction. This non-trivial result suggests that it is possible to take fifth roots using a marked ruler and compass.</p>

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</description>

<author>James Robertson</author>


</item>


<item>
<title>Spluttered Birds</title>
<link>http://digitalcommons.library.umaine.edu/etd/1015</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1015</guid>
<pubDate>Mon, 07 May 2012 14:36:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The following manuscript is a collection of original poetry written by Rachel Perry, a candidate for the M.A. in English at the University of Maine. These poems investigate and explore a range of themes, including art, linguistics, nature, human relationships, illusion and landscape, and draw influence from a mix of the poet's experiences and her imagination.</p>

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</description>

<author>Rachel Perry</author>


</item>


<item>
<title>Formation of 2-chlorobenzylidenemalononitrile (CS riot control
agent) thermal degradation products at elevated temperatures</title>
<link>http://digitalcommons.unl.edu/usarmyresearch/163</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/usarmyresearch/163</guid>
<pubDate>Mon, 07 May 2012 14:33:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>2-Chlorobenzylidenemalononitrile (CS riot control agent) has been shown to produce a number of thermal degradation products when dispersed at high temperature.We hypothesized that these CS-derived compounds are formed by energy input from heating during the dispersion process. Here we identified organic CS-derived compounds formed from purified CS subjected to temperatures ranging from 300 to 900 degrees C in an inert atmosphere with analysis of tube furnace effluent by gas chromatography and mass spectrometry. We conclude that the production of many CS-derived compounds previously observed during high-temperature dispersion is likely to be heat related.</p>

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</description>

<author>Timothy A. Kluchinsky et al.</author>


</item>


<item>
<title>Trust Development in
Swift Starting Action
Teams: A Multilevel
Framework</title>
<link>http://digitalcommons.unl.edu/usarmyresearch/162</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/usarmyresearch/162</guid>
<pubDate>Mon, 07 May 2012 14:29:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Swift starting action teams (STATs) are increasingly prevalent in organizations, and the development of trust is often a critical issue for their effectiveness. However, current theory and research do not provide a clear picture regarding how trust toward the team (i.e., the team as the target) is developed in these settings. The primary contribution of this article is to present a theoretical framework describing how individual-level trust <em>toward one’s team </em>is developed in STAT contexts. This article integrates several existing trust theories into one comprehensive context-specific multilevel theory of how trust develops in STATs from cognitive, affective, behavioral, and contextual perspectives. This framework furthers our understanding of the unique antecedents of initial trust in STATs, how trust attitudes are adjusted over the short amount of time the team interacts, and how the team context influences this developmental process.</p>

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</description>

<author>Jessica Wildman et al.</author>


</item>


<item>
<title>American Indian Studies and the Politics of Educational Colonialism</title>
<link>http://digitalcommons.calpoly.edu/eth_fac/22</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/eth_fac/22</guid>
<pubDate>Mon, 07 May 2012 14:28:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The politics of higher education at universities pose challenges for Native and Indigenous students that impact equity and equality, and the teaching and learning process. The most recent challenge: Native Studies Departments are no longer necessary as an academic discipline. This paper calls into question the right to education and future success and achievement in scholarship that increases knowledge for all peoples in the future. However, higher education institutions are still “working on deconstructing colonialism” with less attention to the enduring marginalization of disempowered peoples as campuses continue struggle with issues of inclusion, budgetary crises, and the minimizing of scholarship. Included is an examination of the current status of five (5) “critical points” identified by Robert E. Powless (2002) as important for the future of American Indian Studies, faculty and students.</p>

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</description>

<author>Kathleen J. Martin et al.</author>


</item>


<item>
<title>Short List of Candidates for Supreme Court, 1981</title>
<link>http://digitalcommons.law.scu.edu/historical/60</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/historical/60</guid>
<pubDate>Mon, 07 May 2012 14:24:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Anonymous</author>


</item>


<item>
<title>In the Classroom: Poetry in Motion (May &apos;91)</title>
<link>http://digitalcommons.unomaha.edu/tedfacpub/16</link>
<guid isPermaLink="true">http://digitalcommons.unomaha.edu/tedfacpub/16</guid>
<pubDate>Mon, 07 May 2012 14:22:17 PDT</pubDate>
<description>
	<![CDATA[
	<p><dl id="x-x-citationFields"><dd>Presents a look at several special projects designed by various teachers to foster learning in young children. Includes using a body movement to respond to poetry, creating a `Book-a-Mania' week of instructional and entertaining events, and using logos and street signs to teach reading awareness.</dd></dl></p>

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</description>

<author>Michael P. French et al.</author>


</item>


<item>
<title>In the Classroom: Reading and Writing in the Content Areas (Dec. &apos;89)</title>
<link>http://digitalcommons.unomaha.edu/tedfacpub/15</link>
<guid isPermaLink="true">http://digitalcommons.unomaha.edu/tedfacpub/15</guid>
<pubDate>Mon, 07 May 2012 14:22:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Students comprehend content material by reading, discussing, writing, questioning, investigating, exploring, and organizing. Reading and writing in the content areas relates prior knowledge, classroom interaction, cooperative learning, vocabulary instruction, and questioning techniques. Children practice research skills by organizing information in a meaningful and practical manner. This month's In the Classroom column presents ways in which teachers can enhance their students' comprehension of content area topics by involving them in various classroom activities. Additional resources for content area reading and writing activities follow :</p>
<p>Dupuis, M.M. (1983). Reading in the content areas: Research for teachers. Newark, DE: International Reading Association.</p>
<p>Graves, D.H. (1989). Investigate nonfiction. Portsmouth, NH: Heinemann.</p>
<p>Heimlich, J.E. and Pittelman, S.D. (1986). Semnntic mapping: Classroom applications. Newark, DE: International Reading Association.</p>
<p>Marzano, R.J, and Marzano, J.S. (1988). A cluster approach to elementary vocabulary instruction. Newark, DE: International Reading Association.</p>
<p>Thelen, J.N. (1984). Improving reading in science. Newark, DE: International Reading Association.</p>

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</description>

<author>Michael P. French et al.</author>


</item>


<item>
<title>A Cancer and Leukemia Group B multi-center study of DA-EPOCH-rituximab
in untreated diffuse large B-cell lymphoma with analysis of outcome
by molecular subtype</title>
<link>http://digitalcommons.unl.edu/publichealthresources/157</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/157</guid>
<pubDate>Mon, 07 May 2012 14:21:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Background</p>
<p>A phase II trial of dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin and rituximab (DA-EPOCH-R) from the National Cancer Institute showed promising activity in untreated diffuse large B-cell lymphoma. The Cancer and Leukemia Group B conducted a study to determine if these results could be reproduced in a multi-institutional setting.</p>
<p>Design and Methods</p>
<p>The study included 69 patients with untreated diffuse large B-cell lymphoma at least 18 years of age and at least stage II. Radiaton therapy was not permitted on study. Median age was 58 years (range 23-83) and 40% had high-intermediate or high International Prognostic Index risk. Immunohistochemical biomarkers for cell of origin and proliferation were performed.</p>
<p>Results</p>
<p>With a median follow up of 62 months, time to progression and overall survival were 81% and 84%, respectively, and time to progression was 87%, 92% and 54% for low/low-intermediate, high-intermediate and high International Prognostic Index risk groups, respectively, at 5-years and beyond. The time to progression and event-free survival of germinal center B-cell lymphoma were 100% and 94%, respectively, and non-germinal center B-cell GCB diffuse large Bcell lymphoma were 67% and 58%, respectively, at 62 months (germinal center <em><em>vs</em></em>. non-germinal center B cell <em><em>P</em></em>=0.008). DA-EPOCH-R was tolerated without significant grade 4 non-hematologic toxicities.</p>
<p>Conclusions</p>
<p>These results provide the first confirmation by a multi-institutional group that DA-EPOCH-R provides high durable remissions in diffuse large B-cell lymphoma and is effective in both germinal center and non-germinal center B-cell subtypes. <em>The trial was registered at ClinicalTrials.Gov </em>(NCT00032019)</p>

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</description>

<author>Wyndham Wilson et al.</author>


</item>


<item>
<title>Was Arthur Andersen Different? An Empirical Examination of Major Accounting Firm Audits of Large Clients</title>
<link>http://scholarship.law.cornell.edu/facpub/365</link>
<guid isPermaLink="true">http://scholarship.law.cornell.edu/facpub/365</guid>
<pubDate>Mon, 07 May 2012 14:20:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Enron and other corporate financial scandals focused attention on the accounting industry in general and on Arthur Andersen in particular. Part of the policy response to Enron, the criminal prosecution of Andersen eliminated one of the few major audit firms capable of auditing many large public corporations. This article explores whether Andersen’s performance, as measured by frequency of financial restatements, measurably differed from that of other large auditors. Financial restatements trigger significant negative market reactions and their frequency can be viewed as a measure of accounting performance. We analyze the financial restatement activity of approximately 1,000 large public firms from 1997 through 2001. After controlling for client size, region, time, and industry, we find no evidence that Andersen’s performance significantly differed from that of other large accounting firms.</p>

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</description>

<author>Theodore Eisenberg et al.</author>


</item>


<item>
<title>Empirical Methods and the Law</title>
<link>http://scholarship.law.cornell.edu/facpub/364</link>
<guid isPermaLink="true">http://scholarship.law.cornell.edu/facpub/364</guid>
<pubDate>Mon, 07 May 2012 14:20:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>One can divide empirical analysis of legal issues into three major branches: (1) the use of scientific empirical analysis by litigants to attempt to prevail in individual cases, (2) the use of <em>social </em>scientific empirical analysis in individual cases, and (3) the use of the empirical methods to describe the legal system’s operation. The first two uses present difficulties that reflect a fundamental limitation on using statistical methods in law: the difference between establishing statistical association and establishing actual causation in an individual case filtered through our adversary legal system. The third use encounters no such obstacle and can aid understanding of how the legal system operates and inform policymakers. Accurate description of the legal system’s operation can in turn influence the outcome of specific cases. More important accurate description of the legal system can supply the information necessary for sound policymaking; for example, a substantial body of evidence suggests that our civil justice system performs quite well.</p>

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</description>

<author>Theodore Eisenberg</author>


</item>


<item>
<title>Understanding Early Writing and Instructional Opportunities in the Inclusive Classroom</title>
<link>http://scholarworks.boisestate.edu/literacy_facpubs/67</link>
<guid isPermaLink="true">http://scholarworks.boisestate.edu/literacy_facpubs/67</guid>
<pubDate>Mon, 07 May 2012 14:18:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Most children enter schools believing they are writers. They have the expectation that print, especially the print that they make and use, will be meaningful (Harste, Woodward, & Burke, 1984). This understanding is commonly observed when they question the adults around them about their writing, saying things like, "What did I write?" or "What does this say?"</p>
<p>Children in these instances are creating and constructing meaning, and they are communicating these meanings through their explorations with print. Writing for these early literates is not about conforming to adult models of correctness, but is rather a process of experimentation. As they engage with print, initially using scribbles and soon marks that look something like letters, then writing strings of letters; they are hypothesizing and checking their hypotheses on what print is and how it can and does function in their lives.</p>
<p>It is the role of the teacher to confirm when their hypotheses about print are correct and to support these young writers in this process. But how does a teacher of young children do this? This chapter offers some explanation of this early process and provides some instructional strategies that you might use to scaffold the writing of young children.</p>

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</description>

<author>Anne E. Gregory et al.</author>


</item>


<item>
<title>Solitude Mountain Resort Master Development Plan Update: Final Environmental Impact Statement</title>
<link>http://digitalcommons.usu.edu/elusive_docs/96</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/elusive_docs/96</guid>
<pubDate>Mon, 07 May 2012 14:13:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>USDA Forest Service</author>


</item>


<item>
<title>Solitude Mountain Resort Master Development Plan Update: Final Environmental Impact Statement- Volume II: Response to Comments</title>
<link>http://digitalcommons.usu.edu/elusive_docs/95</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/elusive_docs/95</guid>
<pubDate>Mon, 07 May 2012 14:13:08 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>USDA Forest Service</author>


</item>


<item>
<title>Granting the Consent of Congress to the Amended Bear River Compact Between the States of Utah, Wyoming and Idaho</title>
<link>http://digitalcommons.usu.edu/elusive_docs/94</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/elusive_docs/94</guid>
<pubDate>Mon, 07 May 2012 14:13:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Mr. Bayh et al.</author>


</item>


<item>
<title>Three Steps Forward, Two Steps Back: Tobacco Policy Making in Nebraska</title>
<link>http://digitalcommons.unl.edu/publichealthresources/156</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/156</guid>
<pubDate>Mon, 07 May 2012 14:13:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>EXECUTIVE SUMMARY</p>
<p>• In 2002, 22.7% of Nebraskans over the age of 18 were current smokers, accounting for</p>
<p>approximately 389,000 smokers.</p>
<p>• Since 1995, the prevalence of adult tobacco use in Nebraska has remained about 1 percentage</p>
<p>point below the national average, but per capita tobacco consumption in Nebraska has been falling</p>
<p>more slowly than the Unites States as whole.</p>
<p>• The tobacco industry has directly been a major political force in Nebraska through lobbying and</p>
<p>campaign contributions. The tobacco industry spent over $1,027,000 on lobbying from 1997-2002.</p>
<p>The tobacco industry made direct campaign contributions to the members of the 2003- 2004</p>
<p>Nebraska Legislature totaling almost $93,000 over the course of their legislative careers.</p>
<p>• Only 20 of the 49 members of the 2003-2004 Legislature have never accepted money from the</p>
<p>tobacco industry.</p>
<p>• The tobacco industry has also worked to increase its political influence in Nebraska by</p>
<p>recruiting, often through financial contributions, third-party allies such as the Nebraska Restaurant</p>
<p>Association, the Nebraska Chamber of Commerce, the Nebraska Retail Grocers Association,</p>
<p>the Nebraska Petroleum Marketers and Convenience Store Association, the Nebraska Retail</p>
<p>Federation, the Nebraska Association of Tobacco and Candy Distributors and the Nebraska</p>
<p>Licensed Beverage Association.</p>
<p>• Despite opposition from the tobacco industry and its allies and the lack of a well-established</p>
<p>grassroots tobacco control community, Nebraska was an early leader in passing statewide clean</p>
<p>indoor air laws. Due largely to the efforts of state Senator Shirley Marsh, the Nebraska Legislature</p>
<p>passed its first clean indoor air law in 1974, only one year after Arizona passed the first law in the</p>
<p>nation that required smoking restrictions in some public places.</p>
<p>• In 1979, the Nebraska Legislature passed the Nebraska Clean Indoor Air Act, which was</p>
<p>sponsored by state Senator Larry Stoney. The Nebraska Clean Indoor Air Act was stronger than</p>
<p>similar legislation that was proposed in New York, Connecticut and Massachusetts at the same</p>
<p>time. The tobacco industry and its allies responded by mobilizing against the implementing rules</p>
<p>and regulations for the Act and succeeded in weakened these regulations.</p>
<p>• The Nebraska Clean Indoor Air Act was not strengthened for 20 years until 1999 when the</p>
<p>Legislature passed a bill that required that almost all state buildings and vehicles become</p>
<p>smokefree.</p>
<p>• From 2000 -2003, the Legislature also strengthened the Nebraska Clean Indoor Air Act</p>
<p>by requiring that commercial daycare facilities be smokefree and extending its enforcement</p>
<p>provisions to include business owners. • From 1999-2004, the Nebraska Legislature has rejected</p>
<p>three different attempts by state Senator Nancy Thompson to make restaurants throughout</p>
<p>Nebraska smokefree. • Using tobacco settlement money, in 2000, the Nebraska Legislature</p>
<p>approved $7 million per year for three years to increase funding for a preexisting state tobacco</p>
<p>control program, Tobacco Free Nebraska.</p>
<p>• Due to pressure from tobacco control advocates, the Nebraska Legislature approved a $0.30</p>
<p>cigarette excise tax increase in 2002, but the Legislature was only willing to pass this increase</p>
<p>during a budget crisis and no earmark was provided for tobacco control.</p>
<p>• Citing budget concerns in 2003, the Legislature cut funding for Tobacco Free Nebraska from $7</p>
<p>million per year to $405,000, despite several different options for continuing funding for tobacco</p>
<p>control.</p>
<p>• In 2003, the Lincoln-Lancaster County Health Department led the push to pass Nebraska first</p>
<p>comprehensive smokefree workplaces ordinances, but due to pressure from the tobacco industry</p>
<p>and its allies, the Lincoln City Council passed a weakened and confusing ordinance that exempted</p>
<p>bars and allowed separately ventilated “smoking rooms.”</p>
<p>• Tobacco control advocates have made progress in Nebraska, but they have not yet mobilized</p>
<p>the political resources necessary to avoid suffering significant defeats at the hands of the tobacco</p>
<p>industry.</p>

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</description>

<author>Andrew Wessel et al.</author>


</item>


<item>
<title>Rule 11 Sanctions: The Supreme Court Gives Rule 11 a Stronger Bite and a Longer Leash</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss2/10</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss2/10</guid>
<pubDate>Mon, 07 May 2012 14:12:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Monica M. Bartow</author>


</item>


<item>
<title>Securities Attorneys Face Liability For Wrongs of Their Corporate Clients</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss2/9</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss2/9</guid>
<pubDate>Mon, 07 May 2012 14:12:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Colleen Graham</author>


</item>


<item>
<title>&quot;. . . And Justice For All&quot;?--The Bar, the Indigent and Mandatory Pro Bono</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss2/8</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss2/8</guid>
<pubDate>Mon, 07 May 2012 14:12:33 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Timothy R. Couch et al.</author>


</item>


<item>
<title>Cohen v. Lord, Day &amp; Lord: A Partnership Agreement&apos;s Impermissable Restriction on the Practice of Law</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss2/7</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss2/7</guid>
<pubDate>Mon, 07 May 2012 14:12:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Christine Ardita</author>


</item>


<item>
<title>Adversary Proceedings: Does 28 U.S.C. § 1109(b) Confer an Absolute Right of Intervention?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss2/6</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss2/6</guid>
<pubDate>Mon, 07 May 2012 14:12:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Stacey A. Fabrizio et al.</author>


</item>


<item>
<title>Joint Trials: Judicial Inefficiency?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss2/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss2/5</guid>
<pubDate>Mon, 07 May 2012 14:12:28 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Lewis Popovski et al.</author>


</item>


<item>
<title>Jury Trials in Bankruptcy Court: Are There Any Constitutional, Statutory or Practical Limitations?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss2/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss2/4</guid>
<pubDate>Mon, 07 May 2012 14:12:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Anthony G. Bianchi et al.</author>


</item>


<item>
<title>Qualified Immunity for Private Party Defendants in Section 1983 Civil Rights Cases</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss2/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss2/3</guid>
<pubDate>Mon, 07 May 2012 14:12:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Catherine D. Glover et al.</author>


</item>


<item>
<title>Begging: Free Speech or Poor Conduct?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss2/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss2/2</guid>
<pubDate>Mon, 07 May 2012 14:12:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Patrick B. Gonzalez et al.</author>


</item>


<item>
<title>Will the Empire State Strike Back at Commercial Polluters? A Proposal For A Transaction-Triggered Hazardous Waste Cleanup Statute in New York</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss2/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss2/1</guid>
<pubDate>Mon, 07 May 2012 14:12:21 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Nancy G. Feeney et al.</author>


</item>


<item>
<title>The Business Judgment Rule and Unocal: Twin Barriers to Shareholder Welfare</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss1/9</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss1/9</guid>
<pubDate>Mon, 07 May 2012 14:12:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frank Cara et al.</author>


</item>


<item>
<title>SEC v. Levine: Determining the Fate of Disgorged Assets Obtained in Settlement</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss1/8</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss1/8</guid>
<pubDate>Mon, 07 May 2012 14:12:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Maria Credle et al.</author>


</item>


<item>
<title>Town of Islip v. Caviglia: &quot;Secondary Effects&quot;--Censorship in Disguise</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss1/7</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss1/7</guid>
<pubDate>Mon, 07 May 2012 14:12:08 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William C. Kelly et al.</author>


</item>


<item>
<title>The Criminal Provisions of RCRA: Should Strict Liability Be Applied to its Permit Requirement?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss1/6</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss1/6</guid>
<pubDate>Mon, 07 May 2012 14:12:06 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James S. Lynch</author>


</item>


<item>
<title>Rethinking the Physical Takings Test: An Expanded Notion of Property Rights--Seawall Assoc. v. City of New York</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss1/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss1/5</guid>
<pubDate>Mon, 07 May 2012 14:12:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Karen L. Lynch et al.</author>


</item>


<item>
<title>Pendent-Party Jurisdiction Under the FTCA: Finley v. United States</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss1/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss1/4</guid>
<pubDate>Mon, 07 May 2012 14:12:02 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Maria E. Lozano et al.</author>


</item>


<item>
<title>Complicating the Copyright Law&apos;s &quot;Work Made for Hire Provisions:&quot; Community for Creative Non-violence v. Reid</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss1/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss1/3</guid>
<pubDate>Mon, 07 May 2012 14:12:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Douglas W. Hammond</author>


</item>


<item>
<title>The Breadth of Section 514 of ERISA and the Preemptibility of State Antisubrogation Laws</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss1/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss1/2</guid>
<pubDate>Mon, 07 May 2012 14:11:58 PDT</pubDate>
<description>
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</description>

<author>Christopher R. Carroll et al.</author>


</item>


<item>
<title>The Drug War in the Workplace: Employee Drug Testing Under Collective Bargaining Agreements</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol5/iss1/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol5/iss1/1</guid>
<pubDate>Mon, 07 May 2012 14:11:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Philip K. Davidoff et al.</author>


</item>


<item>
<title>Judicial Immunity in Bar Admissions</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss2/9</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss2/9</guid>
<pubDate>Mon, 07 May 2012 14:11:43 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Katherine Ann Wopat</author>


</item>


<item>
<title>Privity Requirement for Attorney Liability to Non-clients</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss2/8</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss2/8</guid>
<pubDate>Mon, 07 May 2012 14:11:41 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Melinda R. Katz</author>


</item>


<item>
<title>United States v. Long: When May a Criminal Defense Attorney Disclose His Client&apos;s Future Perjurious Testimony?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss2/7</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss2/7</guid>
<pubDate>Mon, 07 May 2012 14:11:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Anthony P. Giustino</author>


</item>


<item>
<title>New York State Warranties on Sales of New Homes Act: From Caveat Emptor to Statutory Warranty Protection</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss2/6</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss2/6</guid>
<pubDate>Mon, 07 May 2012 14:11:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Nancy B. Burlingame</author>


</item>


<item>
<title>The Right to Succeed: The Validity of the Succession Provisions in the 1987 Rent Stabilization Code</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss2/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss2/5</guid>
<pubDate>Mon, 07 May 2012 14:11:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>James A. Prestiano</author>


</item>


<item>
<title>Contractual Protection: An Existing Remedy for Bondholder Distress</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss2/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss2/4</guid>
<pubDate>Mon, 07 May 2012 14:11:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Thomas E. Stagg et al.</author>


</item>


<item>
<title>Gains and Losses From Foreign Currency Hedges After Arkansas Best Corp. v. Commissioner</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss2/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss2/3</guid>
<pubDate>Mon, 07 May 2012 14:11:30 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Ferretti</author>


</item>


<item>
<title>Your Sound or Mine?: The Digital Sampling Dilemma</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss2/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss2/2</guid>
<pubDate>Mon, 07 May 2012 14:11:28 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Lori D. Fishman</author>


</item>


<item>
<title>DNA Fingerprinting: Dick Tracy of the &apos;90s</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss2/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss2/1</guid>
<pubDate>Mon, 07 May 2012 14:11:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Nancy Slater</author>


</item>


<item>
<title>Landowner Liability Under CERCLA: Is Innocence a Defense?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss1/7</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss1/7</guid>
<pubDate>Mon, 07 May 2012 14:11:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ginamarie Alvino</author>


</item>


<item>
<title>Calendar Marketing Agreements: How Much Longer Till the Soda Spills?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss1/6</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss1/6</guid>
<pubDate>Mon, 07 May 2012 14:11:15 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joyce M. Bowers et al.</author>


</item>


<item>
<title>Separate Prosecutions for Continuous Criminal Possession of a Weapon In New York--Twice in Jeopardy? People v. Okafore</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss1/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss1/5</guid>
<pubDate>Mon, 07 May 2012 14:11:13 PDT</pubDate>
<description>
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</description>

<author>Patricia A. LaFroscia</author>


</item>


<item>
<title>Notice is Preempted for Civil Rights Actions: Felder v. Casey</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss1/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss1/4</guid>
<pubDate>Mon, 07 May 2012 14:11:11 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Robin Singer</author>


</item>


<item>
<title>The Right Against Self-Incrimination and the Production of Corporate Papers: Braswell v. United States</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss1/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss1/3</guid>
<pubDate>Mon, 07 May 2012 14:11:09 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Catherine A. Collins</author>


</item>


<item>
<title>Computer Software Piracy: The Need for Integration of Statutory and Technological Protections of Intellectual Property</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss1/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss1/2</guid>
<pubDate>Mon, 07 May 2012 14:11:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Christopher G. Dorman et al.</author>


</item>


<item>
<title>United States v. Starrett City Associates and United States v. Yonkers Board of Education: Can More Be Done to Remedy Housing Discrimination?</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol4/iss1/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol4/iss1/1</guid>
<pubDate>Mon, 07 May 2012 14:11:06 PDT</pubDate>
<description>
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</description>

<author>Edward J. Hansen et al.</author>


</item>


<item>
<title>Of Griots and Grace: The Art of Oral History and The History of African American Religion</title>
<link>http://engagedscholarship.csuohio.edu/clhist_facpub/29</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/clhist_facpub/29</guid>
<pubDate>Mon, 07 May 2012 14:10:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>The article discusses the history of African  American religion which was expressed in oral histories and in the music  known as spirituals and how it survived in the centuries of slavery.  Despite racism in American Christianity, the African worship tradition  evidently remained in America as women in church wear African-inspired  headwraps or hats to symbolize possession by the spirit in a ringshout.</p>

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</description>

<author>Regennia N. Williams</author>


</item>


<item>
<title>Replicating Adenovirus-Simian Immunodeficiency Virus (SIV) Vectors
Efficiently Prime SIV-Specific Systemic and Mucosal Immune
Responses by Targeting Myeloid Dendritic Cells and Persisting in
Rectal Macrophages, Regardless of Immunization Route</title>
<link>http://digitalcommons.unl.edu/publichealthresources/155</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/155</guid>
<pubDate>Mon, 07 May 2012 14:08:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although priming with replicating adenovirus type 5 host range mutant (Ad5hr)-human immunodeficiency virus (HIV)/simian immunodeficiency virus (SIV) recombinants, followed by HIV/SIV envelope boosting, has proven highly immunogenic, resulting in protection from SIV/simian-human immunodeficiency virus (SHIV) challenges, Ad5hr recombinant distribution, replication, and persistence have not been examined comprehensively in nonhuman primates. We utilized Ad5hr-green fluorescent protein and Ad5hr-SIV recombinants to track biodistribution and immunogenicity following mucosal priming of rhesus macaques by the intranasal/intratracheal, sublingual, vaginal, or rectal route. Ad recombinants administered by all routes initially targeted macrophages in bronchoalveolar lavage (BAL) fluid and rectal tissue, later extending to myeloid dendritic cells in BAL fluid with persistent expression in rectal mucosa 25 weeks after the last Ad immunization. Comparable SIV-specific immunity, including cellular responses, serum binding antibody, and mucosal secretory IgA, was elicited among all groups. The ability of the vector to replicate in multiple mucosal sites irrespective of delivery route, together with the targeting of macrophages and professional antigen-presenting cells, which provide potent immunogenicity at localized sites of virus entry, warrants continued use of replicating Ad vectors.</p>

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</description>

<author>L. Jean Patterson et al.</author>


</item>


<item>
<title>Clinical Research and Development of
Tuberculosis Diagnostics: Moving From Silos to
Synergy</title>
<link>http://digitalcommons.unl.edu/publichealthresources/154</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/154</guid>
<pubDate>Mon, 07 May 2012 14:05:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The development, evaluation, and implementation of new and improved diagnostics have been identified as critical needs by human immunodeficiency virus (HIV) and tuberculosis researchers and clinicians alike. These needs exist in international and domestic settings and in adult and pediatric populations. Experts in tuberculosis and HIV care, researchers, healthcare providers, public health experts, and industry representatives, as well as representatives of pertinent US federal agencies (Centers for Disease Control and Prevention, Food and Drug Administration, National Institutes of Health, United States Agency for International Development) assembled at a workshop proposed by the Diagnostics Working Group of the Federal Tuberculosis Taskforce to review the state of tuberculosis diagnostics development in adult and pediatric populations.</p>

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</description>

<author>Payam Nahid et al.</author>


</item>


<item>
<title>Fault diagnosis with adaptive kalman filters and CMG design for picosatellite ACS</title>
<link>http://digitalcommons.ryerson.ca/dissertations/655</link>
<guid isPermaLink="true">http://digitalcommons.ryerson.ca/dissertations/655</guid>
<pubDate>Mon, 07 May 2012 14:03:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Picosatellites have only recently become a viable research topic thanks to the creation of the cubesat standard in 1999 and improvements in technology. However they are still limited in application because there are no high performance active actuators available in the market that can satisfy the mass/power/budget constraints of a picosatellite. Space and power are limited in these satellites which means that hardware redundancy is not very practical. If actuator faults occur, analytical redundancy techniques should be employed to determine if, where, and how the fault(s) occurred. This thesis focuses on enhancing picosatellite actuator tehnologies, as well as presenting an alogrithm for fault detection, isolation, and identification of ACS actuators.</p>
<p>A CMG cluster design is proposed to demonstrate the feasibility of using CMGs in picosatellites to enhance their performance. The proposed CMG cluster design weighs less than 100g, occupies less than 25% of a cubesat's volume, and theoretically consumes less than 1.5W and 1W of peak and average power respectively. Furthermore, it is capable of providing sufficient torque and momentum storage for picosatellite attitude control in LEO. Next a novel adaptive Kalman filter algorithm is presented that can be implemented with the EKF and UKF for linear and non-linear systems respectively. The algorithm performs parameter estimation with sequential adaptive estimation and fading memory mechanisms that allow it to track changes in faulty parameters even in the presence of high levels of measurement noise. Furthermore, it is capable of tracking continuously varying and instantaneous changes in parameters. Numerical simulations are carried out to verify the performance of the propsed CMG cluster design as well as the fault diagnosis algorithm. The capabilities of the filter are further demonstrated via its application to a systems identification problem for a nonosatellite RW prototype being developed at SSDC group.</p>

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</description>

<author>Noel Abreu</author>


</item>


<item>
<title>The fourier spectral element method for vibration analysis of general dynamic structures</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/490</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/490</guid>
<pubDate>Mon, 07 May 2012 14:02:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Fourier Spectral Element Method (FSEM) was proposed by Wen Li on the vibration of simple beams (Li, 1999), and was extended to the vibration of rectangular plates (Li, 2004). This dissertation proposes a revised formulation on the vibration of rectangular plates with general boundary conditions, and extends the FSEM on the vibration of general triangular plates with elastic boundary supports. 3-D coupling formulation among the plates and beams is further developed. A general dynamic structure is then analyzed by dividing the structure into coupled triangular plates, rectangular plates, and beams. The accuracy and fast convergence of FSEM method is repeatedly benchmarked by analytical, experimental, and numerical results from the literature, Laboratory test, and commercial software.</p>
<p>The Key feature of FSEM method is that the approximation solution satisfies both the governing equation and the boundary conditions of the beam (plates) vibration in an exact sense. The displacement function composes a standard Fourier cosine series plus several supplementary functions to ensure the convergence to the exact solution including displacement, bending moment, and shear forces, etc. All the formulation is transformed into standard form and a set of stored matrices ensure fast assembly of the studied structure matrix. Since the matrix size of the FSEM method is substantially smaller than the FEA method, FSEM method has the potential to reduce the calculation time, and tackle the unsolved Mid-frequency problem.</p>

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</description>

<author>Xuefeng Zhang</author>


</item>


<item>
<title>Molecular mechanisms of strain-stimulated intestinal epithelial cell differentiation and migration</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/489</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/489</guid>
<pubDate>Mon, 07 May 2012 14:01:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The intestinal epithelium is subjected to repetitive deformation during normal gut function by peristalsis and villous motility. In vitro, cyclic strain promotes intestinal epithelial proliferation and induces an absorptive phenotype characterized by increased dipeptidyl dipeptidase (DPPIV) expression. Schlafen 3 is a novel gene recently associated with cellular differentiation. We sought to evaluate whether Schlafen 3 mediates the effects of strain on the differentiation of IEC-6 intestinal epithelial cells in the absence or presence of cyclic strain. Strain increased Schlafen 3 mRNA and protein. In cells transfected with a control non-targeting siRNA, strain increased DPPIV specific activity. However, Schlafen</p>
<p>3 reduction by siRNA decreased basal DPPIV and prevented any stimulation of DPPIV activity by strain. Schlafen 3 reduction also prevented DPPIV induction by sodium butyrate (1mM) or TGF-â (0.1ng/ml), two unrelated differentiating stimuli. However, Shlafen-3 reduction by siRNA did not prevent the mitogenic effect of strain or that of EGF. Blocking Src and PI-3-kinase prevented strain induction of Schlafen 3, but Schlafen 3 induction required activation of p38 but not ERK. These results suggest that cyclic strain induces an absorptive phenotype characterized by increased DPPIV activity via Src-, p38-, and PI-3-kinasedependent induction of Schlafen 3 in rat intestinal epithelial IEC-6 cells on collagen, while Schlafen 3 may also be a key factor in the induction of intestinal epithelial differentiation by other stimuli such as sodium butyrate or TGF-â. The induction of Schlafen 3 or its human homologues may modulate intestinal epithelial differentiation and preserve the gut mucosa during normal gut function.</p>
<p>Repetitive strain promotes intestinal epithelial migration across fibronectin in vitro, but signaling mediators for this are poorly understood. We hypothesized that integrin linked kinase (ILK) mediates strain-stimulated migration in intestinal epithelial cells cultured on fibronectin. ILK kinase activity increased rapidly five minutes after strain induction in both Caco-2 and IEC-6 cells. Wound closure in response to strain was reduced in ILK siRNA transfected Caco-2 cell monolayers compared to control siRNA transfected Caco-2 cells. Pharmacologic blockade of PI3K or Src or reducing Src by siRNA prevented strain activation of ILK. ILK coimmunoprecipitated with FAK, and this association was decreased by mutation of FAK Tyr925 but not FAK Tyr397. Strain induction of FAK Tyr925 phosphorylation but not FAK Tyr397 or FAK Tyr576 phosphorylation was blocked in ILK siRNA transfected cells. ILK-Src association was stimulated by strain and was blocked by the Src inhibitor PP2. Finally, ILK reduction by siRNA inhibited strain-induced phosphorylation of myosin light chain and Akt. These results suggest a strain-dependent signaling pathway in which ILK association with FAK and Src mediates the subsequent downstream strain-induced motogenic response, and suggest that ILK induction by repetitive deformation may contribute to recovery from mucosal injury and restoration of the mucosal barrier in patients with prolonged ileus. ILK may therefore be an important target for intervention to maintain the mucosa in such patients.</p>

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</description>

<author>Lisi Yuan</author>


</item>


<item>
<title>Faith and (un)certainty in the writing of stowe, hawthorne, and dickinson: the intersecting language of theology and feminism</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/488</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/488</guid>
<pubDate>Mon, 07 May 2012 14:01:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>This research considers how Hawthorne's, Dickinson's, and Stowe's writing express the prevailing culture's attitudes toward the operation of meaning in religion.  It poses the question: Is a crisis of meaning threatening to the religious sensibility?  Looking at Hawthorne's <i>The Scarlet Letter</i> and specific poems of Dickinson, I show how their writing gestures to a kind of religious sensibility that is not threatened by such a crisis, but suggests, rather, that it is essential to a genuine openness to otherness, and ultimately to the Divine.  The fiction and poetry of these two authors express this both negatively, as an attack on conventional religion as well as particular nineteenth-century trends in religion, but also positively by expressing themes of possibility and hope in a posture of uncertainty.  It is also expressed through their particular use of associative language and metaphor.  By emphasizing the ever-shifting mechanism of signification, their writing emphasizes the contingency of language and of subjectivity.  This contingency is experienced in the chaos of physical desire and suggests that it is not antithetical to religious belief but the very foundation of it, challenging the common religious binary of the spirit and the flesh.</p>
<p>The historical conflation of the material realm with women leads this discussion in areas of feminist thought and theory, in particular,  <i>l'é;criture fé;minine</i>, due to the emphasis on language materiality.</p>
<p>Stowe's writing in <i>Uncle Tom's Cabin</i> supports another stream of religious thought that relies more on discreet boundaries and assurances of belief.  By appealing to common Christian principles in the novel, Stowe relies on and reinforces universal religious and ethical constructs.  Her use of sentimental rhetoric is based on assumptions that clearly delineate between right and wrong, male and female, and even black and white.</p>
<p>All writing around the same time, Hawthorne's, Dickinson's, and Stowe's texts express attitudes toward religion that would later burgeon within American culture and are still prominent today.</p>

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</description>

<author>Denise Yezbick</author>


</item>


<item>
<title>Conceptual change and science achievement related to a lesson sequence on acids and bases among african american alternative high school students&apos;: ateacher&apos;s practical arguments and the voice of the &quot;other&quot;</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/487</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/487</guid>
<pubDate>Mon, 07 May 2012 14:00:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>The study of teaching and learning during the period of translating ideals of reform into classroom practice enables us to understand student-teacher-researcher symbiotic learning. In line with this assumption, the purpose of this study is threefold:(1) observe effects of the Common Knowledge Construction Model (CKCM), a conceptual change inquiry model of teaching and learning, on African American students' conceptual change and achievement; (2) observe the shift in teacher's practical arguments; and (3) narrate the voice of "the Other" about teacher professional learning.</p>
<p>This study uses retrospective data from a mixed-method approach consisting of Phenomenography, practical arguments and story-telling. Data sources include audio-recordings of a chemistry teacher's individual interviews of her students' prior- and post-intervention conceptions of acids and bases; results of Acid-Base Achievement Test (ABA-T); video-recordings of a chemistry teacher's enactment of CKCM acid-base lesson sequence; audio-recordings of teacher-researcher reflective discourse using classroom video-clips; teacher interviews; and teacher and researcher personal reflective journals.</p>
<p>Students' conceptual changes reflect change in the number of categories of description; shift in language use from everyday talk to chemical talk; and development of a hierarchy of chemical knowledge. ABA-T results indicated 17 students in the experimental group achieved significantly higher scores than 22 students in the control group taught by traditional teaching methods. The teacher-researcher reflective discourse about enactment of the CKCM acid-base lesson sequence reveals three major shifts in teacher practical arguments: teacher inadequate preparedness to adequate preparedness; lack of confidence to gain in confidence; and surface learning to deep learning. The developing story uncovers several aspects about teaching and learning of African American students: teacher caring for the uncared; cultivating student and teacher confidence; converting dependence on teacher and self to peer interdependence.</p>
<p>The study outlines six implications: caring conceptual change inquiry model for the often unreached mind; developing simple chemical talk into coherent chemical explanation; using CKCM for alternative high school students' conceptual change and achievement; engaging teachers in elicitation and appraisal of practical arguments for reconstruction of beliefs; overcoming challenges in teacher practical argument research; and "storytelling" as a way of unpacking teacher transformation amidst complexities of classroom teaching and learning.</p>

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</description>

<author>Lynda Charese Wood</author>


</item>


<item>
<title>Cultural enrichment: connecting african american elementary children to academic achievement</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/486</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/486</guid>
<pubDate>Mon, 07 May 2012 14:00:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>A large, growing number of mis-educated American citizens are being produced by America's public schools. Many of these students are being funneled into the penal system shortly after dropping out of high school. This phenomenon is especially prevalent among African American male students, many of whom have withdrawn academically years prior to permanently dropping out of school. Additionally, to further underscore the importance of successfully educating African American students are the debilitating effects brought about after incarceration. About 4 million people in the United States, including 1.4 million Black men (13 percent of the adult male Black population) have currently or permanently lost their right to vote as a result of a felony conviction. In essence, more than a million poorly educated Black male individuals have lost their fundamental American right - the right of "one person, one vote". The denial of the right to vote subjects this population to a powerless status. They exist in society, but are politically powerless to influence their lives or the lives of their families. Consequently, the future of America's economic, political and social fabric is weakened as the number of well educated, self-actualized individuals diminishes.</p>

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</description>

<author>Deborah L. Winston</author>


</item>


<item>
<title>Biofuels production from hydrotreating of vegetable oil using supported noble metals, and transition metal carbide and nitride</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/485</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/485</guid>
<pubDate>Mon, 07 May 2012 14:00:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>The focus of this research is to prepare non-sulfided hydrotreating catalysts, supported noble metal and transition metal carbide/ nitride, and evaluate their hydrocracking activities and selectivities by using soybean oil as the feedstock. For comparison study, catalytic cracking of soybean oil over a commercialized ZSM-5 was investigated. However, steady state could not be reached because significant amounts of tar and coke were generated during the reaction though a high yield (21%) of jet fuel was obtained from the process. Compared to the catalytic cracking process, less tar and coke were formed during the hydrocracking process and stable continuous flow reaction was obtained by using the bifunctional Ru/ZSM-5 catalyst. 16% yield of jet fuel, which is comparable to yields over commercialized sulfided NiMo catalysts while at a much lower pressure of 650 psi was produced. A 20 - 29% diesel yield was also obtained during the process. But coke was the issue with this noble metal catalyst.</p>
<p>In the following stage, novel bi-functional catalysts, NiMo carbide or nitride supported on ZSM-5, zeolite â, USY, ã-alumina oxide, and Al-SBA-15 were prepared by the temperature-programmed reaction method and the effects of process parameters on catalytic hydrocracking of soybean oil were investigated. 100% conversion of soybean oil was attained under the 650 psi and 360-450 oC reaction conditions. Among them, three zeolite supported carbide catalysts showed high selectivity to green gasoline (about 15-40%) due to the high cracking activities. ã-alumina and Al-SBA-15 supported catalysts mainly produced green diesel fuels. Especially Al-SBA-15 supported NiMo carbide catalyst gave the highest yield of organic liquid product (96%) and highest selectivity (97%) to hydrocarbons in the boiling range of the diesel fraction. The study of carbide and nitride catalysts provides a promising approach for preparing drop-in fuels from renewable resources under a lower pressure without sulfurization reagents involved in the process. NiMoC/Al-SBA-15 showed the greatest potential for producing green diesel from renewable feedstock.</p>

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</description>

<author>Huali Wang</author>


</item>


<item>
<title>Drug resistance mechanisms and drug design strategies for human immunodeficiency virus and hepatitis c virus proteases</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/484</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/484</guid>
<pubDate>Mon, 07 May 2012 13:59:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>The antiviral drug development has improved steadily to treat the infections of human immunodeficiency virus (HIV) and hepatitis C virus (HCV) which represent heavy public health burdens. The viral protease plays an indispensable role in viral maturation and therefore becomes one of the most important targets for drug design. Nine HIV-1 protease inhibitors and two HCV protease inhibitors have been developed and approved by the U.S. Food and Drug Administration. However, mutations in the protease decrease reduce the efficacy the drugs. In this study, the enzyme assays indicate that darunavir and tipranavir exhibit the most potent inhibition against the multi-drug resistant (MDR) HIV-1 protease, which is supported by the co-crystal structures of the MDR protease-darunavir complex and the MDR protease-tipranavir complex. The MDR HIV-1 protease not only decreases the susceptibility to drugs but also impedes the formation of protease-substrate complex. Molecular dynamics simulation results show that the MDR HIV-1 protease needs to conquer a higher desolvation energy barrier to bind the substrate. Besides the study of drug resistance mechanisms, two drug discovery methods have been carried out in the study. One method is the modification of a current drug, lopinavir. The potency of the lopinavir analog against the MDR HIV-1 protease increases. The other method is the identification of a novel HIV-1 protease inhibitor scaffold to increase the structural diversity of inhibitors. In the HCV section, the study focuses on an HCV NS3/4A protease inhibitor, telaprevir, which is approved for the treatment of patients infected with the HCV genotype 1. The enzyme assays and molecular dynamic studies suggest that telaprevir may retain sufficient potency to treat the non-genotype 1 HCV strains.</p>

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</description>

<author>Yong Wang</author>


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<item>
<title>Examining the factors of a technology professional development intervention</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/483</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/483</guid>
<pubDate>Mon, 07 May 2012 13:59:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>In response to the ever increasing demand to compete in a global economy, the United States needs to prepare its students with the appropriate technical knowledge and communication skills to be competitive in the 21st century (Watson, 2007). Students must begin utilizing current technology tools during their K-12 educational experience and online learning can assist students with developing these skills. Teachers with online technology skills and equipped with effective pedagogical strategies for teaching in an online environment are the keys to achieving this goal. To ensure teachers are keeping pace with changing teaching and learning environments, and effectively utilizing new technologies, teacher technology professional development (PD) is a major initiative throughout K-12 education (Lawless & Pellegrino, 2007). In turn, it is the responsibility of school districts to prepare our nation's teachers to model and teach the use of these tools. Funding initiatives and federal and state programs have been put in place to assist school districts with preparing their teachers to teach with new technologies. While there are government mandates requiring teachers to become knowledgeable in online teaching, many teachers and school districts are not meeting these mandates, and often barriers, such as lack of funding, time, and accessibility to experts, impact the quality of PD provided (Reeves & Pedulla, 2011). One way to gain more knowledge for providing quality PD is to examine the factors of a technology professional development intervention (TPDI) to establish best practices for designing quality technology PD for teachers.</p>
<p>The purpose of this qualitative multiple-case research study was to examine secondary education teachers' perceptions of a technology professional development intervention (TPDI). This study was designed to provide a deeper understanding of which factors teachers' perceived to be beneficial to the quality of technology professional development (PD) they received. An extensive review of literature surrounding technology integration within K-12 educational settings, demonstrated important factors to be incorporated into a TPDI to increase its quality and effectiveness. These factors aligned with the TPACK (Technological Pedagogical Content Knowledge) theoretical framework, so it was used to for designing, developing, and implementing the TPDI for this study. The instructional goal of the TPDI was to assist teachers in meeting two Entry-Level Standards for Michigan teachers related to designing and facilitating learning in the online environment. A learning technology by design approach (Koehler & Mishra, 2005; Mishra & Koehler, 2003) was the basis for the TPDI. This hands on approach exposed teachers to Google Applications while designing instruction and instructional materials to use in their teaching practice. The instructional design of the TPDI was evaluated by a panel of subject matter experts to increase content validity, and was modified based on feedback. The TPDI was implemented in an online learning environment.</p>
<p>The quality of PD can be influenced by a variety of factors, but Guskey and Sparks (1996) suggest that the factors with the most direct influence can be grouped into content, processes, and contextual factors. To investigate the complex relationship between the TPDI factors and teacher practice, I used the first piece of the Guskey and Sparks (1996)  Model of the Relationship between Professional Development and Improvements on Student Learning, as a conceptual framework for collecting and analyzing data to address the research questions. The data was analyzed using a content analysis methodology to examine the factors of the TPDI that the teachers perceived to be most beneficial for transferring the knowledge and skills taught during the TPDI to teaching practice.  Studying teachers' perceptions of these factors during the TPDI provided insight into which factors teachers believed were most beneficial to their learning. Comparing teachers' perceptions of the same factors after they began applying the knowledge and skills from the TPDI with their students, provided insight about which factors were most beneficial for teacher practice.</p>
<p>The results of this study demonstrated seven beneficial factors to narrow the transfer gap between technology PD and practice. These factors include: relevant, learning, access, reactions, interactions, clear and easy, and instructor. This suggest that instructional designers should incorporate relevant learning by doing activities that are structured to impact learners' perceptions of how their knowledge can be expanded by creating their own learning path in a situated contextual environment. While this study examined a specific TPDI designed for secondary education teachers at a high school in Michigan, the design of the TPDI incorporated factors that are rooted in constructivist design principles, making the implications of the findings from this study relevant to instructional design. These recommendations could be used to guide instructional designers when designing environments for other technology training and adoption initiatives for employees.</p>

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</description>

<author>Kelly L. Unger</author>


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<item>
<title>Review of Zora Neale Hurston &amp; a History of Southern Life</title>
<link>http://engagedscholarship.csuohio.edu/clhist_facpub/28</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/clhist_facpub/28</guid>
<pubDate>Mon, 07 May 2012 13:59:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The article reviews the book "Zora Neale Hurston and a History of Southern Life," by Tiffany Ruby Patterson.</p>

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</description>

<author>Regennia N. Williams</author>


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<item>
<title>Throughput analysis and bottleneck management of production lines</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/482</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/482</guid>
<pubDate>Mon, 07 May 2012 13:59:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Companies are increasing their manufacturing excellence in order to stay competitive in the globalizing market. Plants are becoming more complex year by year due to increasing product classes, hardware complexity, etc... The design and operation of manufacturing systems is of greater importance today than it was in the past. Many studies have been carried out on the design and operation of manufacturing systems by academicians and practitioners over the years, however, there is still no agreement on how to best predict and improve the factory performance (Gershwin, 2000). The studies are based on either analytical approaches or simulation-based approaches. Success stories from some companies, for instance General Motors, which applied these techniques in combination, motivate our study.</p>
<p>In the dissertation, our main focus area is the automotive industry. Maintenance, being the most critical component of the automotive industry, has a direct impact on the improvement of the overall production performance. Therefore, we introduce an anticipative plant level maintenance decision support system (APMDSS), which gives guidance on the corrective and the preventive maintenance priorities, and the times for doing preventive maintenance tasks based on the bottleneck ranks with an objective of improving the throughput of a plant which consists deteriorating machinery. Unlike the previous bottleneck management approaches, APMDSS anticipates the system dynamics (i.e., bottlenecks, hourly buffer levels, and machine health) of the upcoming shift by using initial state information such as machine ages, operational status of machines, buffer levels, and model mix. In order to make a more realistic and detailed analysis, we model the factory dynamics using a simulation model.</p>
<p>We also propose two analytic models for throughput evaluation. First one is an exact formula for a deteriorating two-machine system. In the model, the machines degrade with usage and the reliability behavior of each machine changes depending on the machine's health condition. The model considers both perfect and imperfect repairs simultaneously.</p>
<p>The second one is hybrid aggregation-decomposition algorithm that approximates the throughput of longer production lines. The algorithm selectively aggregates the parts of the line based on the location of the bottlenecks. In this model, we engage the existing aggregation and decomposition methods. The basic idea of making a hybrid of these two throughput evaluation approaches is to benefit from the speed of the aggregation method and the accuracy of the decomposition method.</p>
<p>We obtained promising results in the experiments that we tested our models using real data from a major automotive company. We also used synthetic data in the experiments to investigate different scenarios.</p>

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</description>

<author>Hatice Ucar</author>


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<item>
<title>Roots</title>
<link>http://digitalcommons.calpoly.edu/roots/vol5/iss1/1</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/roots/vol5/iss1/1</guid>
<pubDate>Mon, 07 May 2012 13:59:02 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>


</item>


<item>
<title>Social movement theory and far right organizations</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/481</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/481</guid>
<pubDate>Mon, 07 May 2012 13:59:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>This research examines the organized far right movement and interviews members of four right wing organizations to understand their goals and operations.  This study compares the utility of two social movement theories, Resource Mobilization Theory (RMT) and New Social Movement Theory (NSMT) to explain the functioning of the four organizations.  Resource Mobilization Theory contends that change is done politically in the sphere of institutional power, while New Social Movement Theory argues that change occurs in civil society.</p>
<p>The study was qualitative in nature and involved in-depth interviews with 97 members of four far right organizations across two Midwest states.  The research hypothesis for this study is that RMT will better explain the nature of all four right organizations than NMST.</p>
<p>Three of the four organizations were better explained by RMT. They had highly sophisticated and hierarchical organizational structures with limited membership, aggressive forms of resource attainment through membership dues, and varying levels of political and/or legal mobilization such as lobbying, involvement with local, state, and federal political campaigns, running candidates for school board or political office, and legal challenges through the courts.</p>
<p>One of the four organizations tended to be better explained by RMT, but up to one-third of its members answered questions in manner consistent with NSMT.  This finding was explained by the fact that the organization was an affiliate of a head branch, and therefore had limited autonomy.  It relied significantly on the chief branch to direct its policies, and several of its members appeared to have less experience or knowledge of political and legal issues.</p>

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</description>

<author>Frank Tridico</author>


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<item>
<title>The mental model comparison of expert and novice performance improvement practitioners</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/480</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/480</guid>
<pubDate>Mon, 07 May 2012 13:58:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The primary purpose of this study was to reveal performance improvement practitioner expert and novice mental models and identify differences and similarities between these models. The secondary purpose was to analyze the potential relationships of the professional profile characteristics of performance improvement practitioners with their mental model of expertise derived from Pathfinder scaling algorithm. The study was stemmed from one of the critical research trends in the field of Human Performance Technology (HPT).</p>
<p>There are two phases of the study. In the first round of the first phase, experts, who were selected based on several criteria, were contacted to identify the most critical concepts related the HPT. The Online Ranking Questionnaire was utilized. 23 experts were responded, and 11 of 30 concepts were selected. In the second round of the first phase, the experts who responded to the first round were contacted again to share their professional profile characteristics and ratings about the concept-pairs generated from the 11 concepts. These ratings provided the proximity data necessary to generate the common mental models of expert (the expert referent model) in the KNOT using the Pathfinder algorithm. The Professional Profile Characteristics and The Concept-Pairs Comparison online questionnaires were used. 16 experts responded in this round. In the second phase of the study, practitioners in the field were invited to participate in the study via International Society for Performance Improvement (ISPI) newsletters, The American Society for Training and Development (ASTD) discussion forums, and Association for Educational Communications and Technologies (AECT) mailing list. Moreover, professional social networking sites, e.g., Linked-In, and the researcher personal contact list were used as well to increase return-rate. Practitioners were asked to complete the same online questionnaires completed by the experts in the second round of the first phase. 335 practitioners started the questionnaires; 272 completed the Professional Profile Characteristics questionnaire; 242 completed both the Professional Profile Characteristics and the Concept-Pairs Comparison questionnaires. 33 practitioners of 242 were identified as novices who were selected based on the criteria used to select experts. In contrast to the experts, the novices were chosen as those who do not meet all of the criteria. The proximity data of those 33 novices were used to create the common mental model of novices.</p>
<p>The common mental model of experts demonstrated more coherent and hierarchical structure. However, the common mental model of novices was in more linear structure. The models were also compared, and the experts' model was different from the novices' model. The expert model had deep structure of practical knowledge; whereas, the novice model contained step-by-step and textbook style structure. The professional profile characteristics of the practitioners and the experts were also presented. Several relationships found between the professional profile characteristics and the mental model of expertise, which was generated from three Pathfinder measures: relatedness, coherence, and similarity. The mental model of expertise was positively associated with the number of organizations worked, the number of completed projects, the diversity of project types, the number of the HPT related courses taught; whereas, it was negatively associated with the total years spent to earn degrees.</p>
<p>There were several implications of the current study. The first is either informal or formal approaches for the development of expertise. This study may enlighten the mentoring novices while progressing to expertise in the field. Colleges, universities and other types of institutions providing education or training for performance improvement practitioners may take advantage of the results of this study by improving their course or curriculum designs with additional experiences. Moreover, the professional organizations, such as ISPI and ASTD, may be informed with this study for their certification and designation programs. They may include new rationale and criteria for assessment and evaluation processes. This study also may provide additional information from the expertise perspective to the efforts related to the development of competencies in the performance improvement field.</p>
<p>Finally, future studies were recommended. The first recommendation was the replication of the current study with different sample characteristics and sizes. The future studies regarding expertise in HPT may consider different using different research design and knowledge elicitation techniques. Since the current study utilized stand-alone concepts, the studies examining groups of stand-alone concepts with common characteristics may provide more meaningful and overarching interpretations. There were numerous either demographic, e.g., age, or professional, e.g., years of experience, deliberate practice, and so forth, factors influencing in expertise in either general or more specific to performance improvement field. These factors needed to be analyzed to reveal the relationships with the progression to expertise.</p>

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</description>

<author>Sacip Toker</author>


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<item>
<title>A framework for personalized dynamic cross-selling in e-commerce retailing</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/479</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/479</guid>
<pubDate>Mon, 07 May 2012 13:58:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Cross-selling and product bundling are prevalent strategies in the retail sector. Instead of static bundling offers, i.e. giving the same offer to everyone, personalized dynamic cross-selling generates targeted bundle offers and can help maximize revenues and profits. In resolving the two basic problems of dynamic cross-selling, which involves selecting the right complementary products and optimizing the discount, the issue of computational complexity becomes central as the customer base and length of the product list grows. Traditional recommender systems are built upon simple collaborative filtering techniques, which exploit the informational cues gained from users in the form of product ratings and rating differences across users. The retail setting differs in that there are only records of transactions (in period X, customer Y purchased product Z). Instead of a range of explicit rating scores, transactions form binary datasets; 1-purchased and 0-not-purchased. This makes it a one-class collaborative filtering (OCCF) problem. Notwithstanding the existence of wider application domains of such an OCCF problem, very little work has been done in the retail setting. This research addresses this gap by developing an effective framework for dynamic cross-selling for online retailing.</p>
<p>In the first part of the research, we propose an effective yet intuitive approach to integrate temporal information regarding a product's lifecycle (i.e., the non-stationary nature of the sales history) in the form of a weight component into latent-factor-based OCCF models, improving the quality of personalized product recommendations. To improve the scalability of large product catalogs with transaction sparsity typical in online retailing, the approach relies on product catalog hierarchy and segments (rather than individual SKUs) for collaborative filtering. In the second part of the work, we propose effective bundle discount policies, which estimate a specific customer's interest in potential cross-selling products (identified using the proposed OCCF methods) and calibrate the discount to strike an effective balance between the probability of the offer acceptance and the size of the discount. We also developed a highly effective simulation platform for generation of e-retailer transactions under various settings and test and validate the proposed methods.</p>
<p>To the best of our knowledge, this is the first study to address the topic of real-time personalized dynamic cross-selling with discounting. The proposed techniques are applicable to cross-selling, up-selling, and personalized and targeted selling within the e-retail business domain. Through extensive analysis of various market scenario setups, we also provide a number of managerial insights on the performance of cross-selling strategies.</p>

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</description>

<author>Arun K. Timalsina</author>


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<item>
<title>A model of student engagement and academic achievement: the role of teacher-student relationships and teacher expectations</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/478</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/478</guid>
<pubDate>Mon, 07 May 2012 13:58:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>A MODEL OF STUDENT ENGAGEMENT AND ACADEMIC ACHIEVEMENT: THE ROLE OF TEACHER-STUDENT RELATIONSHIPS AND TEACHER EXPECTATIONS</p>
<p>by</p>
<p>AJA C. TEMPLE</p>
<p>MAY 2012</p>
<p>Advisor:	        Dr. Jina Yoon</p>
<p>Major:		Educational Psychology</p>
<p>Degree: 		Doctor of Philosophy</p>
<p>The purpose of this study was to examine patterns of academic achievement among minority students and investigate teacher-student relationships, teachers' classroom and future educational expectations for students, and students' levels of classroom engagement in order to better understand their patterns of academic achievement. Participants (n=522) were students in grades four through six from a suburban district in Michigan. Student achievement varied according to both gender and ethnicity in this study. Teacher expectations did not differ as a function of gender or ethnicity. Perceptions of the teacher-student relationship differed significantly for Hispanic students, with males reporting more clarity of expectations, consistency of response, adjustment of teaching strategies, and instrumental help from their teachers. Engagement did not mediate the relation between teacher-student relationships and student achievement in this study, but was associated with student rule compliance. Student compliance was related to perceptions of the relationship. A separate model testing the associations between teacher-student relationships, teacher expectations, and student achievement was significant for both the full sample and African American subgroup. Perceiving higher teacher expectations predicted perceptions of more involvement, structure, and autonomy support from teachers. Perceived relationship was negatively associated with overall GPA. Higher achievement outcomes were associated with both teacher expectations and teacher-student relationships. A moderating effect of gender was supported in this study, showing the model as most relevant to the achievement of African American males.</p>

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</description>

<author>Aja C. Temple</author>


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<item>
<title>An ethnographic analysis of adolescent sexual minority website usage: exploring notions of information seeking and sexual identity development</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/477</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/477</guid>
<pubDate>Mon, 07 May 2012 13:57:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation explores the website usage of adolescent sexual minorities, examining notions of information seeking and sexual identity development. Sexual information seeking is an important element within human information behavior and is uniquely problematic for young sexual minorities. Utilizing a contemporary gay teen website, this five-year virtual ethnography of GLBT (Gay, Lesbian, Bisexual, Transgender) youth demonstrates an understanding of the function of the Internet as an invaluable tool for exploring social and psychological needs while providing anonymity and keeping information-seeking behavior relatively unknown. The use of Chatman's (1996) Information Impoverished Theory and Cass's (1979) Model of Gay and Lesbian Identity Formation aids the analysis of this particular culture's information- seeking behavior and sexual orientation identity formation. As a result, a number of salient themes are revealed, including exploration of and experimentation with sexuality; struggles with identity; ascertaining a social network; the "coming out" process; sexual identity confusion; and negative effects associated with homosexuality, such as low self-esteem, suicide, and conflict surrounding religious ideology. In addition, the findings suggest that sexual prejudice is a pervasive issue for this community and that the use of a gay teen chat forum is an effective means of ethnographic data collection. This dissertation concludes by identifying limitations and offering insights for further inquiry into the communication behavior of adolescent sexual minorities.</p>

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</description>

<author>Rocky M. Sulfridge</author>


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<item>
<title>Buried Treasure: A Business Librarian’s Insights on Finding the Evidence</title>
<link>http://repository.cmu.edu/lib_science/86</link>
<guid isPermaLink="true">http://repository.cmu.edu/lib_science/86</guid>
<pubDate>Mon, 07 May 2012 13:57:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>This chapter offers my perspective as a professional librarian and former manager on accessing the research evidence in the business and management fields. I describe the barriers faced by managers, students, and scholars in locating and reading the peer-reviewed literature: its scattered placement, varying formats, controlled access, and swiftly changing environment. I explore how those roadblocks are being overcome, and I offer practical recommendations for both managers and researchers on what they can do today to bring that evidence to light.</p>

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</description>

<author>Roye Werner</author>


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<item>
<title>Making mathematics matter: professional development improving outcomes in high-poverty environments</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/476</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/476</guid>
<pubDate>Mon, 07 May 2012 13:57:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>This research study is a mixed – methods quantitative and qualitative study that analyzed data from an intensive, long – term professional development project named,  " Project : Making Mathematics Matter. (PM<sup>3</sup>) " carried out in two low – performing, high – poverty districts. Two of the districts served as treatment districts and ALL teachers (general education, special education, ELL) who taught mathematics to students in grades 4-8 participated in a four-year PM<sup>3</sup> mathematical intervention.</p>
<p>Three elements identified in the research as effective components in mathematics professional development served as foundational for this project. They were: teachers attended monthly institutes focused on deepening the pedagogical, content knowledge for teaching mathematics; teachers received on-site coaching from an experienced mathematics educator to support implementation of new instructional strategies; and teachers participated in monthly, collegial, grade band meetings facilitated by their coach.</p>
<p>This studys analyses focused around three areas: 1. increased pedagogical knowledge for teaching mathematics as measured by the "Learning Mathematics for Teaching" (LMT) assessment (Hill, Schilling, & Ball, 2004); 2. improved mathematics instructional quality as measured by the SAMPI Classroom Observational Protocol; 3. increased mathematics performance of students as measured on the state-wide MEAP test.</p>
<p>Research findings were: 1. LMT data collected at the beginning, middle, and end of PM<sup>3</sup> showed treatment teachers significantly increased their pedagogical, content knowledge for teaching mathematics over their matched-comparison teachers; 2. Analyses of SAMPI data demonstrated  teachers significantly improved the quality of their classroom instruction; 3. Analyzing sets of MEAP student scale scores by grade and year, there was a significant interaction between district of the student and the year, during and following treatment teachers  participation in PM<sup>3</sup>. Where in 2005, all sets of treatment scale scores were significantly different and lower than comparison scores, as the years of treatment teacher participation in PM<sup>3</sup> increased many sets of compared sets of MEAP scores were no longer significantly different.</p>
<p>This study suggests a connection between the increased content knowledge of teachers, the improved quality of classroom instruction, and the increased mathematics achievement of their students in high – poverty, low ndash performing districts.</p>

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</description>

<author>Carolyn A. Siebers</author>


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<item>
<title>Modes and mechanisms of hfq mediated stress regulation in bacteria</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/475</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/475</guid>
<pubDate>Mon, 07 May 2012 13:57:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>To survive bacteria must be able to respond to its ever-changing environmental conditions. sRNAs have been implicated in a variety of stress-response pathways that help bacterial systems modulate gene expression. The RNA binding protein Hfq facilities this process by, helping sRNA to base pair with its target mRNAs to initiate gene regulation. A common feature of Hfq-mediated gene regulation is the network-based organization where a single sRNA can control multiple messages to promote integrated response to stress. Current mechanistic models that are present to describe Hfq functions cannot explain the complexity at which Hfq performs gene regulation. In this work we have used a variety of biophysical, biochemical and biological approaches to understand the nature of Hfq interactions with target mRNAs.</p>

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</description>

<author>Nilshad Nilam Salim</author>


</item>


<item>
<title>Oscillator strength measurements in singly-ionized, doubly-ionized and neutral lanthanides and transition elements (sm, nd, pr, gd, cu, and fe) using laser-induced breakdown spectroscopy.</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/474</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/474</guid>
<pubDate>Mon, 07 May 2012 13:56:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Models for stellar nucleosynthesis, age determinations for stars in the Milky Way's galactic halo, and stellar chemical abundance determinations are dependent upon accurate atomic spectroscopic data to allow the correct interpretation of stellar absorption and emission spectra. It is well known that calculations of many astrophysically important atomic parameters are limited due to line blending, insufficient spectral resolution of some key spectral lines, and also the complicated electronic structure of the important heavy elements. Astrophysicists have therefore looked to laboratory astrophysics experiments to provide accurate atomic data to help resolve these limiting issues. In this dissertation, laser-induced breakdown spectroscopy (LIBS) has been employed for the first time on a large scale as a spectroscopic technique for the rapid and convenient production of atomic and ionic plasmas as sources of atomic emission in order to determine radiative properties in astrophysically relevant lanthanides (Gd, Nd, Pr and Sm) and transition metals (Cu and Fe).</p>
<p>Nanosecond laser pulses incident on pure elemental targets in a rarified argon environment were used to create high-temperature plasmas. The resulting spontaneous emission from the high-temperature micro-plasmas was dispersed in a spectrally-corrected high-resolution broadband Échelle spectrometer, and detected with a high-sensitivity intensified CCD camera which allowed the simultaneous determination of the relative intensities of thousands of decay branches from hundreds of excited energy levels and multiple ionization states. These experimentally measured relative emission intensities were combined with previously obtained atomic lifetimes to calculate transition probabiliites and oscillator strengths.</p>
<p>In two transition metals, emission intensities have been measured for 192 transitions from 108 excited states in neutral copper and 27 emission lines from 108 excited states in singly-ionized copper as well as 776 emission lines from 108 excited states in neutral iron and 1453 emission lines from 108 excited states in singly-ionized iron.</p>
<p>In four important lanthanide elements, emission intensities have been measured for 587 lines of 113 excited states in neutral gadolinium, 480 lines from 43 excited states of singly-ionized gadolinium, and 40 lines in 6 states of doubly-ionized gadolinium; 121 emission lines from 93 excited states in neutral neodymium, 368 lines from 46 excited states in singly-ionized neodymium, and two lines from a single excited level of doubly-ionized neodymium; 19 lines from 19 excited levels of neutral praseodymium, 367 lines from 41 excited states in singly-ionized praseodymium, and 359 lines from 7 excited levels of doubly-ionized praseodymium; 137 lines from 70 excited states in neutral samarium, 713 lines from 115 excited states in singly-ionized samarium, and 49 lines from 17 excited levels of doubly-ionized samarium. The degree of uncertainty for strong emission lines is 9.3%, for moderate lines 10.3%, and 23.3% for weak transitions. This degree of uncertainty is typical for such laboratory astrophysics work and is usually an improvement upon available calculations.</p>

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</description>

<author>Caleb Ryder</author>


</item>


<item>
<title>This fact which is not one: differential poetics in transatlantic american modernism</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/473</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/473</guid>
<pubDate>Mon, 07 May 2012 13:56:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation proposes that the literary fact, first discussed by Jurij Tynajnov in his 1924 essay "The Literary Fact," and later in "On Literary Evolution" (1929), names an intersection of literary formalism and social representation central to experimental modernist texts in the twentieth century. The poetics of literary fact that I propose finds its basis in Russian Formalist and Frankfurt School theory and reflects several important twentieth century social moments to illustrate how historical and social facts seek poetic form. In my use of the term, "fact" is the materiality of history as it moves from the social world, carrying with it the index of its own production, through to literary form. Radical form thus becomes a mode of social rethinking for conditions like gender, race, queerness, and nationality as they relate to historical context and individual authorship. In turn, the literary fact helps us to see how experimental texts are not purely self-conscious formalist gestures but are, instead, crucially connected to the social and historical periods that produced them. I propose that form follows fact, and thus that a study of the literary fact can open even the most radically anti-realist texts to socially based readings.</p>
<p>Gertrude Stein's Geography and Plays incorporates into its form the facts of World War One, its ruptures and transformations, and joins them with sociality as Stein has experienced it to create a way of knowing the war that is both a model of relating to history and a language to bring forward into future social and textual investments. Likewise, Langston Hughes's Montage of a Dream Deferred produces not simply an illustration of black modernity with a bebop soundtrack, but a record of the emergence of modern blackness freed from American capitalist narratives of progress to tell modernity in its own terms. Jack Spicer's practice of dictation becomes more than alien transmissions reaching a poet fatally estranged from the pre-Stonewall, Cold War social world; Heads of the Town up to the Aether documents spaces outside of language that Spicer called "love" in the facts this text makes literary. Spicer's devotion to the idea of (queer) love implored poets to create a world that they would not be consumed by. Finally, Nan Goldin's photographs cease to be simple snapshots of a now mythologized bohemia; beyond their transformation into documents of the loss of that bohemia to the early days of AIDS, we can see how these images disclose the facts of the collective production of both a community's history and its possible future. Thus, experimental forms transform both documentary evidence and material language into facts that accumulate, creating new knowledges.</p>

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</description>

<author>Sarah Ruddy</author>


</item>


<item>
<title>Motion(less) pictures: the cinema of stasis</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/472</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/472</guid>
<pubDate>Mon, 07 May 2012 13:56:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Since cinema's inception, there has been much disagreement among film theorists about the role of movement in cinema's ontology. For example, while Rudolf Arnheim has argued that motion is a <i> sine qua non </i> of cinema, Roland Barthes has insisted that motion is not as central to cinema's ontology as duration, an experiential "unfolding." In this dissertation, I argue--following Barthes--that movement is merely a contingent, not a necessary, condition of cinema. I further suggest that the very enterprise of prescribing necessary conditions of cinema is myopic, reductive, and reactionary.</p>
<p>In supporting these claims, I interrogate the cinema of stasis, a modality of avant-garde films which feature little or no movement. By foregrounding stillness, these films often blur the lines between cinema and other art forms, including photography, painting, and literature. Giving especially close attention to films by Andy Warhol, Fluxus, Michael Snow, and Derek Jarman, I explore the aesthetic and affective valences of cinematic stasis, while drawing attention to the numerous ways that static films broaden our conception of what films can be and do.</p>

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</description>

<author>Justin Remeselnik</author>


</item>


<item>
<title>Processing random signals in neuroscience, electrical engineering and operations research</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/471</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/471</guid>
<pubDate>Mon, 07 May 2012 13:56:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The topic of this dissertation is the study of noise in electrical engineering, neuroscience, biomedical engineering, and operations research through mathematical models that describe, explain, predict and control dynamic phenomena.  Noise is modeled through Brownian Motion and the research problems are mathematically addressed by different versions of a generalized Langevin equation.  Our mathematical models utilize stochastic differential equations (SDEs) and stochastic optimal control, both of which were born in the soil of electrical engineering.  Central to this dissertation is a brain-physics based model of cerebrospinal fluid (CSF) dynamics, whose structure is fundamentally determined by an electrical circuit analogy.  Our general Langevin framework encompasses many of the existing equations used in electrical engineering, neuroscience, biomedical engineering and operations research.</p>
<p>The generalized SDE for CSF dynamics extends a fundamental model in the field to discover new clinical insights and tools, provides the basis for a nonlinear controller, and suggests a new way to resolve an ongoing controversy regarding CSF dynamics in neuroscience.  The natural generalization of the SDE for CSF dynamics is a SDE with polynomial drift.  We develop a new analytical algorithm to solve SDEs with polynomial drift, thereby contributing to the electrical engineering literature on signal processing models, many of which are special cases of SDEs with polynomial drift.  We make new contributions to the operations research literature on marketing communication models by unifying different types of dynamically optimal trajectories of spending in the framework of a classic model of market response, in which these different temporal patterns arise as a consequence of different boundary conditions.</p>
<p>The methodologies developed in this dissertation provide an analytical foundation for the solution of fundamental problems in gas discharge lamp dynamics in power engineering, degradation dynamics of ultra-thin metal oxides in MOS capacitors, and molecular motors in nanotechnology, thereby establishing a rich agenda for future research.</p>

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</description>

<author>Kalyan Raman</author>


</item>


<item>
<title>Stabilization and classification of poincare duality embeddings</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/470</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/470</guid>
<pubDate>Mon, 07 May 2012 13:56:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>We define a space E(K,X) of Poincare Duality embeddings and show that such spaces admit a highly connected stabilization map.</p>
<p>This serves as a tool for classifying Poincare Duality embeddings in terms of the homotopy types of their complements. In</p>
<p>particular, a Poincare embedding gives rise to a fiberwise duality</p>
<p>map in the category of retractive spaces over X. We use this construction to obtain a highly connected classification map with target a moduli space of unstable complements for Poincare embeddings. As consequences, we obtain stabilization and classication results for</p>
<p>smooth embeddings.</p>

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</description>

<author>John Whitson Peter</author>


</item>


<item>
<title>Prediction of Clinical Outcomes in Primary Biliary
Cirrhosis by Serum Enhanced Liver Fibrosis Assay</title>
<link>http://digitalcommons.unl.edu/publichealthresources/153</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/153</guid>
<pubDate>Mon, 07 May 2012 13:55:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Primary biliary cirrhosis (PBC) is sometimes diagnosed based on a positive antimitochondrial antibody in the appropriate clinical setting without a liver biopsy. Although a liver biopsy can assess the extent of liver fibrosis and provide prognostic information, serum fibrosis markers avoid biopsy complications and sampling error and provide results as a continuous variable, which may be more precise than categorical histological stages. The current study was undertaken to evaluate serum fibrosis markers as predictors of clinical progression in a large cohort of PBCpatients. Serial liver biopsy specimens and serum samples were collected every 2 years in 161 PBC subjects for a median of 7.3 years. Clinical progression was defined as development of one or more of the following events: varices, variceal bleed, ascites, encephalopathy, liver transplantation, or liver-related death. Serum hyaluronic acid, tissue inhibitor of metalloproteinase 1, and procollagen III aminopeptide were measured and entered into the previously validated enhanced liver fibrosis (ELF) algorithm. The ability of ELF, histological fibrosis, bilirubin, Model for End-Stage Liver Disease (MELD), and Mayo Risk Score to differentiate between individuals who would experience a clinical event from those who would not was evaluated at different time points. Event-free survival was significantly lower in those with high baseline ELF. Each 1-point increase in ELF was associated with a threefold increase in future complications. The prognostic performance of all tests was similar when performed close to the time of the first event. However, at earlier times in the disease process (4 and 6 years before the first event), the prognostic performance of ELF was significantly better than MELD or Mayo R score. Conclusion: The ELF algorithm is a highly accurate noninvasive measure of PBC disease severity that provides useful long-term prognostic information. (HEPATOLOGY 2008;48:1549-1557.)</p>

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</description>

<author>Marlyn J. Mayo et al.</author>


</item>


<item>
<title>Itch occurring with chronic wounds</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/469</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/469</guid>
<pubDate>Mon, 07 May 2012 13:55:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract</p>

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</description>

<author>Julia Claire Paul</author>


</item>


<item>
<title>Metal chalcogenide nanoparticle gel networks: their formation mechanism and application for novel material generation and heavy metal remediation via cation exchange reactions</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/468</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/468</guid>
<pubDate>Mon, 07 May 2012 13:55:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>METAL CHALCOGENIDE NANOPARTICLE GEL NETWORKS: THEIR FROMATION MECHANISM AND APPLICATION FOR NOVEL MATERIAL GENERATION AND HEAVY METAL REMEDIATION VIA CATION EXCHANGE REACTIONS</p>
<p>by</p>
<p>IRINA R. PALA</p>
<p>February 2012</p>
<p>Advisor:     Dr. Stephanie L. Brock</p>
<p>Major:        Chemistry</p>
<p>Degree:       Doctor of Philosophy</p>
<p>The dissertation research is focused on (1) uncovering the mechanism of metal chalcogenide nanoparticle gel formation; (2) extending the cation exchange reaction protocol to zinc sulfide gel networks, with the goal of accessing new aerogel chemistries and understanding the factors that drive the process; and (3) conducting a quantitative analysis of the ability of ZnS aerogels to remove heavy metal ions from aqueous solutions.</p>
<p>The mechanism of metal chalcogenide nanoparticle gel formation was investigated using Raman spectroscopy and X-ray Photoelectron Spectroscopy to probe the chemical changes that occur during the gelation process. These techniques suggest that the bonding between the particles in the CdSe nanoparticle gels is due to the oxidation of surface selenide species, forming covalent Se-Se bonds. Treating the gel networks with a suitable reducing agent, such as a thiol, breaks the covalent bond and disperses the gel network. The addition of sodium borohydride, a "pure" reducing agent, also breaks down the gel network, strengthening the hypothesis that the reducing character of the thiols, not their ligation ability, is responsible for the gel network breakdown. UV-Vis spectroscopy, Transmission Electron Microscopy and Powder X-ray Diffraction were used to analyze the particles after successive gelation-dispersion cycles. The primary particle size decreases after repeated oxidation-reduction cycles, due to nanoparticle surface etching. This trend is observed for CdSe and CdS gel networks, allowing for the proposition that the oxidative-reductive mechanism responsible for the formation-dispersion of the gels is general, applying to other metal chalcogenide nanocrystals as well.</p>
<p>The cation exchange reaction previously demonstrated for CdSe gels was extended to ZnS gel networks. The exchange occurs under mild reaction conditions (room temperature, methanol solvent) with exchanging ions of different size, charge and mobility (Ag<sup>+</sup>, Pb<sup>2+</sup>, Cd<sup>2+</sup>,  Cu<sup>2+</sup>). The overall reaction is kinetically controlled, since systems with similar solubility, and thus similar thermodynamic driving force (e.g. PbS and CdS) exchange at very different rates. A correlation exists between the speed of the reaction and the difference between the reduction potential of the incoming cation and that of Zn<sup>2+</sup>; the larger the difference, the faster the exchange. At the same time, the porosity of the aerogels and the surfactant-free surfaces hold great importance for the exchange reactions, allowing for exchange between cations of similar size and charge (i.e. Pb<sup>2+</sup> for Zn<sup>2+</sup>), a phenomenon that was previously reported as impossible in ligand-capped metal chalcogenide nanoparticles. These observations allowed for a better understanding of the factors governing the cation exchange reaction in nanoscale metal chalcogenides. Quaternary ZnS-CuInS<sub>2</sub> gels were obtained by cation exchange with Cu<sup>+</sup> and In<sup>3+</sup>, but the pure CuInS<sub>2</sub> phase was not obtained under the mild reaction conditions used, probably due to the very different mobility of the two exchanging cations.</p>
<p>The kinetically fast cation exchange process and the propensity of the soft chalcogenide gel networks to bind heavy metal ions selectively, suggest that these materials could also be suitable for the removal of heavy metal ions from the environment. The dissertation research studied the capacity of ZnS aerogels to sequester heavy metal ions such as Pb<sup>2+</sup> and Hg<sup>2+</sup> from water. The materials are efficient in removing the heavy metal ions from aqueous solutions with a wide range of initial concentrations. For initial concentrations that mimic an environmental spill (i.e. 100 ppb Pb<sup>2+</sup>), the treatment with the aerogel affords a final concentration lower than the 15 ppm action level recommended by the EPA. Under thermodynamically forcing conditions, the water remediation capacity of the ZnS nanoparticle aerogels was determined to be 14.2 mmol Pb<sup>2+</sup> / g ZnS aerogel, which is the highest value reported to date.</p>

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</description>

<author>Irina Ramona Pala</author>


</item>


<item>
<title>Modelling surface evolution in abrasive jet micromachining using level set methods</title>
<link>http://digitalcommons.ryerson.ca/dissertations/654</link>
<guid isPermaLink="true">http://digitalcommons.ryerson.ca/dissertations/654</guid>
<pubDate>Mon, 07 May 2012 13:55:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>The time dependent surface evolution in abrasive jet micromachining (AJM) is described by a partial differential equation which is difficult to solve using analytical or traditional numerical techniques. These techniques can yield incorrect predicted profile evolution or fail altogether under certain conditions. More recently developed particle tracking cellular automaton simulations can address some of these limitations but are difficult to implement and are computationally expensive.</p>
<p>In this work, level set methods (LSM) were introduced to develop novel surface evolution models to predict resulting feature shapes in AJM. Initially, a LSM-based numerical model was developed to predict the surface evolution of unmasked channels machined at normal and oblique jet impact angles (incidence), as well as masked micro-channels and micro-holes at normal incidence, in both brittle and ductile targets.</p>
<p>This model was then extended to allow the prediction of: surface evolution of inclined masked micro-channels made using AJM at oblique incidence, where the developing profiles rapidly become multi-valued necessitating a more complex formulation; mask erosive wear by permitting surface evolution of both the mask and target micro-channels simultaneously at any jet incidence; and surface damage due to secondary particle strikes in brittle target micro-channels resulting from particle mask-to-target and target-to-target ricochets at any jet incidence. For all the models, a general ‘masking’ function</p>
<p>was developed by applying previous concepts to model the adjustment to abrasive mass flux incident to the target or mask surfaces to reflect the range of particle sizes that are ‘visible’ to these surfaces. The models were also optimized for computational efficiency using an adaptive Narrow Band LSM scheme.</p>
<p>All models were experimentally verified and, where possible, compared against existing models. Generally, good predictive capabilities and improvements over previous attempts in terms of feature prediction or execution time, were observed.</p>
<p>The proposed LSM-based models can be practical assistive tools during the micro-fabrication of complex MEMS and microfluidic devices using AJM.</p>

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</description>

<author>Tom Burzynski</author>


</item>


<item>
<title>Effects of sex, free testosterone, and androgen receptor cag repeat number on spatial cognition and virtual navigation performance</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/467</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/467</guid>
<pubDate>Mon, 07 May 2012 13:55:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The male advantage typically found on some measures of spatial cognition (e.g., mental rotations) has been approached for three decades from the perspective  that androgens contribute to this sex difference. To date, evidence to support the notion that androgens affect spatial cognition in healthy young individuals is balanced by evidence to the contrary. The present study sought to clarify the association between androgens and spatial performance by extending our measurements of androgenicity to include both a measure of circulating testosterone as well as a receptor-specific marker.</p>
<p>The aims of this dissertation were to assess the effects of sex, testosterone, and androgen receptor CAG repeat number on spatial performance and experience in a group of healthy young men and women. The hypothesis that men would outperform women on measures of spatial skills was largely supported, with some caveats.  Predictions that testosterone would relate directly to spatial performance were not confirmed; however, results indicate that number of CAG repeats may have a direct impact on cognition, and may modify the relationship between testosterone and spatial cognition within sex. Future research with larger samples of men and women is needed to clarify the significance of the patterns reported from these initial observations.</p>

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</description>

<author>Nicole Therese Nowak</author>


</item>


<item>
<title>The development and validation of a conditional reasoning test of withdrawal</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/466</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/466</guid>
<pubDate>Mon, 07 May 2012 13:55:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study developed and evaluated a measure of implicit dispositional tendencies associated with lateness, absenteeism, and permanent withdrawal behaviors.  The conditional reasoning framework developed by Lawrence James and colleagues was adopted.  Novel cognitive biases or justification mechanisms associated with withdrawal were proposed, drawing on research and theory from the attribution (marginalization of withdrawal), commitment (revocable commitment), and fairness/equity (social injustice bias) domains.  As part of the empirical validation design, college students enrolled in an Introductory Psychology course completed the conditional reasoning measure, and corresponding behavioral withdrawal criteria were collected unobtrusively throughout the 16-week course.  Results of scale development analyses pointed to a subset of items (13 of 25) with positive evidence of predictive validity and indicated that the items assess largely heterogeneous content, possessing low internal consistency.  Results of hypothesis testing revealed positive and statistically significant predictive relationships for revocable commitment and social injustice (i.e., higher scores on the conditional reasoning items associated with higher frequencies of the withdrawal behaviors), but not for marginalization of withdrawal.  Taken together, these results provide initial evidence for the role of implicit dispositional tendencies in the withdrawal process and underscore potential avenues for further development of a conditional reasoning test of withdrawal.</p>

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</description>

<author>Levi Ryan gust Nieminen</author>


</item>


<item>
<title>Multi-component ab2 metal hydride alloys for nickel metal hydride battery applications</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/465</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/465</guid>
<pubDate>Mon, 07 May 2012 13:55:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Compared to the mish metal-based AB<sub>5</sub> MH alloy commonly used in Ni/MH batteries, the transition metal-based AB<sub>2</sub> MH alloy not only reduces the rare earth dependency, it also has higher specific energy.  In order to further improve the performance of AB<sub>2</sub> MH alloy, it's crucial to full understand its multi-phase nature, which includes the main C14/C15 Laves phases and the secondary non-Laves phases.</p>
<p>In order to optimize the gaseous phase and electrochemical advantages of both the C14 and C15 Laves phases, a study was established to recognize the factors that affect the C14/C15 phase abundance.  Average electron density (<i>e</i>/<i>a</i>) was proven to be an influential parameter in determining the C14/C15 phase abundance: as <i>e</i>/<i>a</i> increased, C14/C15 became less/more dominant, respectively.  However, with different A-site composition, a shift in <i>e</i>/<i>a</i> was observed in the C14/C15 phase abundance vs. <i>e</i>/<i>a</i> relationship.  The average chemical potential for electronic charge of A atoms (<i>Φ</i>             <sup>*</sup>             <sub>A</sub>) was found to show a nearly perfect linear correlation to the C14/C15 threshold with various selections of A-site elements.  The combination of e/a and <i>Φ</i>             <sup>*</sup>             <sub>A</sub> can be used to predict the C14/C15 phase abundance and assist future AB<sub>2</sub> MH alloy design process.</p>
<p>Four non-Laves phase alloys, Zr<sub>8</sub>Ni<sub>21</sub>, Zr<sub>7</sub>Ni<sub>10</sub>, Zr<sub>9</sub>Ni<sub>11</sub>, and ZrNi, commonly seen in AB<sub>2</sub> MH alloys were studied.  Annealing treatment was adopted on each alloy to change the abundances of various phases.  Annealing suppressed secondary phases except for the case of Zr<sub>9</sub>Ni<sub>11</sub>, where its secondary ZrNi phase increased.  As the Zr/Ni ratio increased, the maximum gaseous phase hydrogen storage capacity increased but maximized at Zr : Ni = 9 : 11.  Comparing the properties before and after annealing, it was clear that the natures of constituent phases influenced the gaseous phase storage.  The highest full discharge capacity was obtained at Zr : Ni = 7 : 10, which is a compromise between the hydrogen desorption rate and the theoretical maximum gaseous phase hydrogen storage.  As the Zr/Ni ratio increased, the amount of metallic Ni in the surface oxide decreased, therefore the high-rate dischargeablity decreased.  Among all alloys, the unannealed Zr<sub>7</sub>Ni<sub>10</sub> demonstrated the best gaseous phase hydrogen storage and electrochemical capacities, and the unannealed Zr<sub>8</sub>Ni<sub>21</sub> showed excellent HRD and activation.</p>
<p>Zr<sub>8</sub>Ni<sub>21</sub> alloy was then chosen based on its promising performance to be further modified for the purpose of developing alternative MH alloys for Ni/MH batteries.  Zr<sub>8</sub>Ni<sub>19</sub>             <i>X</i>             <sub>2</sub> alloys (<i>X</i> = Ni, Mg, Al, Sc, V, Mn, Co, Sn, La, and Hf) were prepared and studied.  The effect of annealing on these alloys was also investigated.  Only the main phase of the annealed Sn-substitution remained Zr<sub>8</sub>Ni<sub>21</sub>-structured while those of other substitutions turned into Zr<sub>7</sub>Ni<sub>10</sub> or Zr<sub>2</sub>Ni<sub>7</sub>.  Annealing generally suppressed secondary phases except for the case of Zr<sub>8</sub>Ni<sub>19</sub>Sn<sub>2</sub>, where the major phase transformed from Zr<sub>2</sub>Ni<sub>7</sub> to Zr<sub>8</sub>Ni<sub>21</sub>.  Both the maximum gaseous phase hydrogen storage and electrochemical full discharge capacities followed the increasing order of B/A ratio of the main phase.  After annealing, all alloys except for the Sn-substituion showed degradation in full discharge capacity due to the reduction in number and abundance of the catalytic secondary phases.  Among all alloys, the as-cast Hf-substituted Zr<sub>8</sub>Ni<sub>21</sub> alloy demonstrated the best overall gaseous phase hydrogen storage and electrochemical properties.</p>

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</description>

<author>Jean Nei</author>


</item>


<item>
<title>Immigrant integration into host societies: the case of yemeni immigrant communities in metro detroit</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/464</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/464</guid>
<pubDate>Mon, 07 May 2012 13:54:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study is intended to extend our understanding of immigrant political integration by analyzing Yemeni immigrants' attitudes toward integration into North American society, exploring the case of Yemeni-Americans, a group reputedly resistant to integration, in both Dearborn and Hamtramck, Michigan, and comparatively assessing those data with already published data on Lebanese-Americans, retrieved from the U.S. Census Bureau and the Detroit Arab American Study (DAAS).  Relying on an existing theoretical framework on immigrant integration based on sociological and cognitive approaches and my own theoretical model on transnational dimensions related to political, economic, and cultural integration, I will examine a series of hypotheses against the quantitative data from DAAS with the extracted subpopulations of Yemeni and Lebanese populations in Dearborn and Hamtramck. Specifically, I hypothesize that Yemeni-Americans overall will be less integrated than their Lebanese-American counterparts. The reasons for these differences are likely to be explained by cultural and economic differences ranging from ethnic orientations to the country of origin, social demographics, language orientation, to political stances.</p>
<p>For the data collection, I will use the following approach:  I will utilize the data from the DAAS to explore the general attitudes on key dimensions of integration, focusing especially on political participation, as well as factors associated with reluctance toward integration. Yemeni data will be compared to Lebanese counterpart data to highlight reasons for varied patterns and degrees of integration among segments of the Arab-American "community."</p>
<p>I expect to find that Yemeni-Americans overall are less integrated than their Lebanese-American counterparts. The reasons for these differences are likely to relate to a series of variables which include income and educational levels, length of stay in the Detroit area, and extent of US language and degree of continued attachment to the country of origin. The implications from the proposed research will address how and at what rates Yemeni immigrants in comparison to Lebanese  immigrants, at various economic levels, adjust and participate politically and culturally most readily in their new host societies. This analysis will afford insight into expected variations in immigrant integration among specific cultures such as Arabs.</p>

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</description>

<author>Samra Abdulla Nasser</author>


</item>


<item>
<title>Linear and non-linear deformations of a wind turbine blade considering warping and all aeroelastic load couplings</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/463</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/463</guid>
<pubDate>Mon, 07 May 2012 13:54:38 PDT</pubDate>
<description>
	<![CDATA[
	<p><i>The structural dynamics behavior of the blade of a horizontal axis wind turbine that reacts to the different components of the aerodynamic loading were studied by many researchers using different approaches and assumptions.  In the present research, the author considered all the extensional, torsional and flexural loadings acting on the blade with their couplings, variable airfoil cross sections with warping effects, shear deflection, rotary inertia and with or without blade's pretwist for both the linear small deformation case and the nonlinear large deformation case.  To the best knowledge of the author the simultaneous inclusion of all these factors has not been done before.  The "assumed modes method" was used, in which displacements are assumed to be an expansion of products of time-step dependent constants and polynomial functions of x (where x is the coordinate along the length of the blade) that satisfy the boundary conditions at the fixed end where x=0 (hub of the blade) and at the free end where x=L (tip of the blade).  The mass matrix, linear and nonlinear stiffness matrices and the load vector (function of time step) of the dynamic equations of motion are deduced from the Lagrange equations of motion that were derived step by step.  The steps of the linear and nonlinear Newmark implicit iteration schemes used for solving the linear and nonlinear dynamic equations of motion respectively were explained in detail.  Numerical implementation examples for both linear and nonlinear cases were demonstrated for a 14m long blade with and without pretwisting that has specific material and geometrical properties and a decreasing NACA4415 airfoil cross section from hub to tip.  For both of the linear and nonlinear examples, the aerodynamic loadings (lift, drag and pitch moment) and the nonlinear stiffness matrices were computed at each time step utilizing a time dependent set of parameters such as angle of attack, material and air density, wind and blade speed, flow angle, yaw and  pitch angles.  Then the unknown displacements u,v and w  in the directions of x, y and z axes respectively, the bending rotations Θ<sub> 1</sub> and Θ<sub> 2</sub> about the y and z axes respectively and the torsional rotation Φ about the x axis, were solved using the linear and nonlinear Newmark  implicit iteration schemes.  The linear case displacement result plots are shown to agree with the work of Younsi et al.  The nonlinear case displacement result plots are shown to agree with the Ls-Dyna code.</i></p>

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</description>

<author>Fouad Mohammad Mohammad</author>


</item>


<item>
<title>Queer adolescent girls use of out-of school literacy events to semiotically express</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/462</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/462</guid>
<pubDate>Mon, 07 May 2012 13:54:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>This qualitative study focused on the use of multiliteracies (reading, writing, viewing, visually representing, talking, and listening) by four low-income African American LBT (lesbian, bisexual, transgender) adolescents in an out-of-school setting. Data collection methods over a three-month period included transcribed field notes, interviews, questionnaires, participants' writer's notebooks, college workbooks and identity facemasks.</p>
<p>The study focused on critical literacy to understand how the girls used multiliteracies to understand the social practices and socially ascribed identities, which construct them as lesbian, bisexual or transgender and to critique this social construction thereby contributing to their ability to reconstruct identities and beliefs that have the potential to lead to human agency.</p>
<p>The girls engaged with a variety of literacy activities during the weekly sessions such as reading, discussion, writing, drawing, and visual artifacts. Through a mulititeracies pedagogy, the girls developed the critical engagement with literacy required for them to be (come) agents in their own lives.</p>
<p>The things learned because of this study are identifying the features that contribute to the effectiveness of out-of-school literacies for African American LBT adolescents while assisting educators and stakeholders in creating strategies and literacy space to support the identity development and growth of African American LBT adolescents in secondary school settings. It is the hope that such work will aid in extending the boundaries of educational spaces, such as schools, for the purposes of promoting democratic reform and social transformation to achieve societal balance.</p>

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</description>

<author>Candice Marie Moench</author>


</item>


<item>
<title>Becoming a functioning member of the collegiate culture: how cellphone communication affects first-year college students&apos; self and identity in college transition.</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/461</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/461</guid>
<pubDate>Mon, 07 May 2012 13:54:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>This longitudinal ethnographically-oriented study explores the meanings of cellphones and cellphone communication of first-year college students during their college transition and how such newly populated human communicative conducts affect their sense of self and identity during this life period. The findings from this study suggest that participants' perceptions about appropriate cellphone communication are closely tied with a growing sense of emerging adulthood that college students develop in conjunction with their college transition. Cellphone communication creates social situations where participants engage in identity exploration and strategic impression management by switching their social roles in order to properly present their self as a more independent, mature, and responsible member of a new community. Thus they continue to making efforts to become a functioning member of a collegiate culture. Participants in this study also handle varied degrees of relational dynamics by managing the vicinity of friendship and the vicinity of parenting in order to maintain their sense of functioning self during college transition. Corresponding to the lack of literature regarding cellphone communication in the American context, the current study contributes to the understanding of cellphone communication among young people. Also, the findings of this study contribute to the theoretical development of symbolic interactionism that has long explored the concepts of self and identity based predominantly upon face-to-face contexts.</p>

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</description>

<author>Arata Miyazaki</author>


</item>


<item>
<title>A ritual investigation of sudden death events in an urban united states emergency department</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/460</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/460</guid>
<pubDate>Mon, 07 May 2012 13:54:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study investigated sudden death as a social act and a ritual process (Hertz, 1960) in an urban hospital emergency department (ED) in the United States.  An analytical auto ethnographic approach was utilized by the author who is a nurse-anthropologist and a bereaved parent. In sudden and a more "prepared for" death, the dying person goes through a rite of passage van Gennep (1960[1909]) and enters into an area of liminality Turner (1967). A key transition from life to death occurs and crossing a threshold where the dying person cannot cross back. The aims of the study were to: 1) Identify and describe the meaning of social rituals to families and healthcare staff involved in sudden death events, 2) Discover the organizational culture and power structure involved with the formal and informal rituals in a sudden death and 3) Analyze the data collected regarding the social rituals and organizational culture in sudden events in an urban ED in the U.S. to contribute to the anthropological literature on death and dying and ritual processes. In a yearlong ethnographic study, these research activities were conducted: 1) extensive participation observation in the ED setting, 2) twenty in-depth face-to-face interviews with staff members who worked with families experiencing sudden death events and 3) ten in-depth face-to-face interviews with eleven family members who experienced a sudden death event. All interviews were audiotaped, transcribed and analyzed for themes. Findings included identification of ritualized activity by hospital staff in sudden death events despite the lack of official policy in this area. Staff and families' stories about the ritual process as the sudden death event progressed in the ED were analyzed in terms of six key properties of secular rituals (Moore & Myerhoff 1977). The stages of the ritual process analyzed in detail included gathering in the ED and coming together for the death ritual, the transitional social time of becoming dead in the ED, leaving the ED and re-entering society as a mourner and final rituals. It was concluded that the ritual process overall gave structure and meaning to staff and families involved in sudden death events.</p>

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</description>

<author>Mary Eleanor Mitsch</author>


</item>


<item>
<title>The effects of motivational interviewing on marital and pain adjustment in chronic pain patients and their spouses</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/459</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/459</guid>
<pubDate>Mon, 07 May 2012 13:53:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Chronic pain is a costly health condition that is estimated to affect 150 million Americans. Numerous studies have shown that chronic pain affects a variety of aspects of life including mood, daily activities, and relationships. Not only does the individual with chronic pain suffer, spouses often do as well. The purpose of this study was to develop and test an intervention that utilized motivational interviewing techniques while providing tailored feedback to couples who are affected by chronic pain. This study examined which changes arose following the intervention and explored potential reasons for why these changes occurred.</p>
<p>Participants consisted of 47 couples in which at least one member had a chronic pain condition. Each couple completed questionnaires, participated in an interview about the history of their relationship and pain, and engaged in an interaction about coping with pain. Then the couples were randomly assigned to either the intervention group or control group. The couples in the intervention group received oral and written feedback, utilizing motivational interviewing techniques, regarding strengths and weaknesses of their relationship and pain coping. The couples in the control group received oral and written educational feedback about the Gate Control Theory.</p>
<p>The motivational interviewing intervention in this study provided several benefits for couples facing chronic pain. Specifically, the intervention produced greater marital satisfaction, lower pain ratings, greater positive mood, and lower negative mood for both patients and spouses in the intervention group compared to those in the control group. In addition, there were benefits on some of the secondary outcome variables. The patients in the intervention group had lower personal distress than the controls following the intervention and the spouses had greater empathy and mindfulness. This study also found that some of the changes in secondary variables were associated with changes in the primary variables, suggesting that these could be mechanisms of change within the intervention.</p>
<p>This study is a promising step to enhancing current treatments for couples facing chronic pain as well as other chronic illnesses. By including aspects of this intervention in future treatments, it is possible that existing treatments can become more effective.</p>

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</description>

<author>Lisa Miller</author>


</item>


<item>
<title>Sex differences in the cardiac beta-adrenergic receptor contractile response</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/458</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/458</guid>
<pubDate>Mon, 07 May 2012 13:53:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Premenopausal females are at a reduced risk for developing cardiovascular disease as compared to males; this sex difference is not present following menopause.  &beta-adrenergic receptors are pharmaceutical targets in the treatment of cardiovascular disease, and sex differences in &beta-adrenergic responsiveness have been demonstrated.  However, limited studies have addressed the mechanism(s) underlying these differences.  To investigate these sex differences, studies were performed using isolated perfused hearts from male, intact female and ovariectomized female mice, as well as male and female ventricular myocytes.  Female hearts exhibited blunted contractile responses to the &beta-adrenergic receptor agonist isoproterenol (ISO) compared to males but not ovariectomized females.  The role of the A1 adenosine receptor (A<sub>1</sub>AR) in antagonizing the &beta-adrenergic contractile response was investigated using the A<sub>1</sub>AR agonist CCPA and A<sub>1</sub>AR knockout (KO) mice.  Intact females showed an enhanced A1AR anti-adrenergic effect compared to males and ovariectomized females.  The &beta-adrenergic contractile response was potentiated in male and female A<sub>1</sub>ARKO hearts, with sex differences no longer present. Forskolin (FSK), IBMX and CPT-cAMP dose response studies were performed in the isolated heart to investigate the role of adenylyl cyclase, phosphodiesterase and the cAMP signaling cascade, respectively, in generating sex differences in the &beta-adrenergic contractile response. There were essentially no sex differences in the contractile responses to FSK, IBMX or CPT-cAMP.  There were no sex differences in the expression of the &beta1R, &beta2R, or A<sub>1</sub>AR gene in ventricular myocytes, nor were there differences in the expression of G<sub>s</sub>á protein, G<sub>i-2</sub>á protein, PDE4D, PP1 or PP2A as determined with western blotting.  Adenylyl cyclase V/VI was expressed in significantly higher levels in female myocytes.  Females showed enhanced cAMP accumulation upon ISO treatment with and without PDE4 inhibition.  No sex differences were present in troponin I phosphorylation at 10 or 100 nM ISO, while females displayed enhanced phospholamban phosphorylation only at 100 nM ISO.  Females appear to show compensatory increases in adenylyl cyclase expression, cAMP accumulation and phospholamban phosphorylation.  The mechanism(s) for the reduced &beta-adrenergic contractile response in female hearts remains unresolved.</p>

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</description>

<author>Victoria Mcintosh</author>


</item>


<item>
<title>Spray characterization of flex-fuel gasoline di injectors and spray interaction with charge motion in a variable valve actuation engine</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/457</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/457</guid>
<pubDate>Mon, 07 May 2012 13:53:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>The objective of this study is to understand the characteristics of GDI sprays and behavior of in-cylinder charge motion in a GDI engine which is equipped with variable valve actuation. High speed spray visualization in a spray chamber was conducted for a study of spray development. By Schlieren visualization technique, the effect of different conditions including ambient conditions (temperature, pressure) and injection conditions (fuel type, fuel temperature, nozzle design) on spray formation was discussed in both qualitative and quantitative methods. High-speed visualization of the in-cylinder charge motion was carried out as well using an optical accessible engine. The testing was conducted for the conventional valve strategy with the production cam, and for the advanced valve strategies with the prototype cams. Multi-dimensional CFD was carried out to support the optical engine work.</p>
<p>By the experiments, Schlieren visualization was found to be very effective method to observe the vapor phase of the fuel spray, and the 2-stage thresholding image processing method was developed to process Schlieren images. Evaluation of the spray images revealed that the effect of flash boiling could change the spray shape drastically by plume collapse. Significance of flash boiling depended not only on ambient condition, but on injection condition and a combination of other effects including fuel properties and nozzle design. The optical engine testing revealed that the interaction of spray and in-cylinder flow, especially contradiction of the direction of spray momentum and tumble rotation, was a key factor for mixture formation. Stronger inlet air flow by low-lift cam resulted in higher turbulent energy and enhanced vaporization rate which was proven in both experiment and simulation. Deactivation of one of the intake valves produced swirl charge motion in the cylinder which was mixed with tumble. Soot emission caused by piston impingement of the early injection could be reduced by valve deactivation. The use of high-lift long-duration cam promoted more vigorous charge motion, but dynamic ratios of low-lift short-duration cam developed faster.</p>

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</description>

<author>Atsushi Matsumoto</author>


</item>


<item>
<title>Hallowed ground: literature and the encounter with god in post-reformtion england, c. 1550 - 1704</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/456</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/456</guid>
<pubDate>Mon, 07 May 2012 13:53:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation  examines the ways in which the encounter with God is figured in post-Reformation English writing between the years 1550 and 1704. The introduction contextualizes the ways in which individuals might encounter God within cultural and historical circumstances of the period: the gradual disappearance of the tradition of spiritual direction that accompanied the suppression of Catholicism in England during the period and the growing influence of more purely "scientific" modes of inquiry, especially after Descartes. Because of these changes, the ways the encounter with God could be experienced were also changing. The introduction also shows how developments in religious studies deriving from Continental philosophy can offer a fresh perspective when considering the phenomena of religious experience. Chapter one, "John Dee: Mysticism, Technology, Idolatry," considers the career of early modern polymath John Dee  and his conversations with angels as a kind of "mysticism" compromised by the technology of magic and early modern science. In chapter two, "A Glass Darkly: John Donne's Negative Approach to God," I explore the Anglican priest and preacher John Donne's reimagination of negative and mystical theologies as both his way of approaching God and as a tool for the cura animarum, the care of souls. Chapter three, "Love's Alchemist: Science and Resurrection in the Writing of Sir Kenelm Digby," considers Digby's scientific researches into palingenesis, the attempt to raise a plant or animal phoenix-like from its ashes, as a kind of unconscious religious experience. In chapter four, "The Rosicrucian Mysticism of Henry and Thomas Vaughan," I trace the influence of Rosicrucianism in the writing of the poet Henry Vaughan and his twin brother, the alchemist and priest Thomas Vaughan, as a symbiosis disclosing a kind of mysticism more consciously informed by scientific inquiry. Chapter five, "The Pauline Mission of Jane Lead," argues that the seventeenth-century mystic Jane Lead, founder of the Philadelphian Society, deliberately modeled her career on that of St. Paul. It explores the way she follows Paul as one remaining true to the religious experience that initiated his conversion while she deviates when necessary from some traditional and Pauline teachings that do not cohere with her religious vision, much as Paul did in his own historical context.</p>

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</description>

<author>Michael Thomas Martin</author>


</item>


<item>
<title>&quot;treating the whole person:&quot; an ethnographic study of an integrative medicine pain clinic</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/455</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/455</guid>
<pubDate>Mon, 07 May 2012 13:53:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although chronic pain has been increasingly recognized as a critical health issue in the U.S., solely biomedical approaches to pain management are often less effective than comprehensive ones in addressing this condition (Crowley-Matoka, et al. 2009; Good 1994; Greenhalgh 2001; Institute of Medicine 2011; Kleinman 1988; National Center for Health Statistics-Centers for Disease Control and Prevention 2006).  This ethnographic study describes in-depth how a Detroit metropolitan area multidisciplinary pain clinic specifically applies an integrative medicine (IM) approach to the treatment and management of chronic pain.  The aims of this study included: 1) identifying the history of this IM clinic and the development of their treatment approach, 2) describing the roles of the clinic's practitioners and staff, 3) documenting patients' experiences with integrative medicine and pain treatment through the collection of narratives and 4) recording the co-created integrative medicine clinical encounter and examining how pain treatment approaches are enacted and perceived.  This study took place between August 2008-August 2009, and utilized ethnographic methods that included participant-observation of the daily workings of the clinic, direct observation of the co-created clinical encounters (N=40), and formal interviews with clinic staff (N=8) and patients (N=11).  Findings describe a three part process that comprises the clinic's "treating the whole person" approach: 1) identifying the cause of the patient's pain, 2) developing the patient's integrative treatment plan, and 3) customizing this treatment plan to meet the patient's life circumstances.  A series of eight narratives describe how the clinic's patients engaged with their approach.  These narratives reveal how the real work of healing at this clinic resides not in the integration of treatment modalities, but in the social relationships that develop between practitioners and patients.  While variability exists as to whether patients chose to embrace the clinic's approach either fully or in part, the patients concur that the clinic's approach appears to at least be doing something for their pain.  By working with patients' current life circumstances, the clinic provides some hope that while patients' futures may not be completely pain-free, they can at least start working towards restoring some semblance of order to their lives.</p>

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</description>

<author>Lindsey Ann Martin</author>


</item>


<item>
<title>Engineering Advantage, Spring 2012</title>
<link>http://digitalcommons.calpoly.edu/ceng_news/13</link>
<guid isPermaLink="true">http://digitalcommons.calpoly.edu/ceng_news/13</guid>
<pubDate>Mon, 07 May 2012 13:53:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>College of Engineering</author>


</item>


<item>
<title>Postsecondary developmental education and its impact on student learning and academic success</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/454</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/454</guid>
<pubDate>Mon, 07 May 2012 13:52:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>ABSTRACT</p>
<p>POSTSECONDARY DEVELOPMENTAL EDUCATION AND ITS IMPACT ON STUDENT LEARNING AND ACADEMIC SUCCESS</p>
<p>by</p>
<p>KIM NOREEN LUTZ</p>
<p>March 2012</p>
<p>Advisor:	Dr. Gerald Oglan</p>
<p>Major: 		Curriculum and Instruction</p>
<p>Degree:	Doctor of Education</p>
<p>This study explores the affective characteristics of students taking developmental education courses at the postsecondary level. It is widely acknowledged in research that affective issues still remain at the forefront of impeding the success of developmental education students. This is one step in examining the types of interventions which may aid in the academic success of students. This study focuses on an ethnographic approach as it relates to learning and the academic success of developmental education students. Through an interview process, the study encourages students to explore and reflect upon their college experience, their experiences as a college student, specific course experiences, and the developmental education experience. Along with studying the potential academic conflicts a student may encounter, both personal and institutional conflicts will be examines. In addition, this study may contribute to the research on how a college can best support developmental students, both in and outside of the classroom.</p>
<p>In this study, a qualitative design methodology is utilized through an ethnographic approach which is supported by a case study format. Data collection in the natural setting is used to develop a narrative of the experiences of three developmental education students over a period of one quarter. Data sets include transcribed interviews, field notes from classroom observation, reflective journal entries of each participant, and transcribed member checking. Data collection authentically documents and represents each participant's experiences while taking developmental education courses. Constant comparative analysis of the data identifies meaning and patterns across categories.</p>
<p>This study focuses on the participants' reflections of their own college experiences, being a college student, specific course experiences, and developmental education experiences. Key findings emerged that support current research in how affective characteristics impact the academic success of a student, setting academic goals and focusing on the future helps to move a student forward to meeting those goals, support from the developmental education program can aid in student academic success, success in developmental courses can help a student succeed in other courses. Significant and worthwhile personal changes occur with implication for all areas in student learning and academic success.</p>

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</description>

<author>Kim Noreen Lutz</author>


</item>


<item>
<title>Neighborhood risk and protective factors for teenage childbearing and fathering</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/453</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/453</guid>
<pubDate>Mon, 07 May 2012 13:52:44 PDT</pubDate>
<description>
	<![CDATA[
	<p><b>Background and Purpose:</b></p>
<p>Informed by ecological systems theory, social disorganization theory and social capital theory, this study investigates the neighborhood contexts associated with teenage childbearing and fathering for Latino and Black adolescents who resided in Denver public housing for a substantial period of time during their childhood. Specifically, I examine the extent to which teenage childbearing/fathering (between the ages of 15 and 19) are statistically related to various conditions in the neighborhoods in which these youth were raised. The purpose of this study is to examine how neighborhood effects may vary according to the timing and duration of neighborhood exposure.</p>
<p><b>Methods:</b></p>
<p>Methods</p>
<p>This study utilized a secondary data source, the Denver Child Study, a large-scale, mixed-methods study of current and former residents of the Denver (CO) Housing Authority (DHA). Quasi-random assignment to neighborhoods offers a natural experiment for overcoming selection bias in the measurement of neighborhood effects. Data include (1) survey data from parent/caregivers; and (2) administrative data from the U.S.Census Bureau and the Piton</p>
<p>192</p>
<p>Foundation. Data gathered from parent/caregivers were geocoded for each year of their child(ren)'s life thereby providing a rare opportunity to comprehensively examine neighborhood exposure. The study sample (N=781) is approximately half Latino and half Black, and nearly one fifth of the sample birthed or fathered a child between the ages 15 and 19.</p>
<p><b>Results:</b></p>
<p>Using a two-level random effects logit model to account for clustering at the family level, I found that neighbborhoods with higher fractions of foreign born residents protected Black and Latino youth from teenage childbearing andfathering. This was true for contemporaneous, lagged, and cumulative models. In the cumulative model of neighborhood exposure, percentage of foreing born in the neighborhood evinced a larger effect on teenage childbearing/fathering than in separate developmental stages suggesting that neighborhood conditions across the lifecourse were magnified.</p>
<p><b>Conclusions and Implications:</b></p>
<p>Study findings are discussed in terms of their contributions to the literature regarding the magnitude of cumulative neighborhood effects and the existence of lagged and/or developmental stage specific effects of immigrant concentration on teenage childbearing/fathering for low-income Latino and Black youth. Study findings also are discussed in the context of expanding current policy and intervention efforts for teenage childbearing/fathering from focusing only on changing individual behavior to focusing on changeable social aspects of neighborhood. Finally recommendations for future research are made.</p>

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</description>

<author>Jessica Lee Lucero</author>


</item>


<item>
<title>Sustainable design of complex industrial and energy systems under uncertainty</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/452</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/452</guid>
<pubDate>Mon, 07 May 2012 13:52:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Depletion of natural resources, environmental pressure, economic globalization, etc., demand seriously industrial organizations to ensure that their manufacturing be sustainable.  On the other hand, the efforts of pursing sustainability also give raise to potential opportunities for improvements and collaborations among various types of industries.</p>
<p>Owing to inherent complexity and uncertainty, however, sustainability problems of industrial and energy systems are always very difficult to deal with, which has made industrial practice mostly experience based.  For existing research efforts on the study of industrial sustainability, although systems approaches have been applied in dealing with the challenge of system complexity, most of them are still lack in the ability of handling inherent uncertainty.  To overcome this limit, there is a research need to develop a new generation of systems approaches by integrating techniques and methods for handling various types of uncertainties.</p>
<p>To achieve this objective, this research introduced series of holistic methodologies for sustainable design and decision-making of industrial and energy systems.  The introduced methodologies are developed in a systems point of view with the functional components involved in, namely, modeling, assessment, analysis, and decision-making.  For different methodologies, the interval-parameter-based, fuzzy-logic-based, and Monte Carlo based methods are selected and applied respectively for handling various types of uncertainties involved, and the optimality of solutions is guaranteed by thorough search or system optimization.  The proposed methods are generally applicable for any types of industrial systems, and their efficacy had been successfully demonstrated by the given case studies.</p>
<p>Beyond that, a computational tool was designed, which provides functions on the industrial sustainability assessment and decision-making through several convenient and interactive steps of computer operation.  This computational tool should be able to greatly facilitate the academic and industrial practices on the study of sustainability problems, and it is the first one available to the public.</p>

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</description>

<author>Zheng Liu</author>


</item>


<item>
<title>Synthesis, spectroscopic, and electrochemical properties of 3d metal and ruthenium complexes with phenolate and catecholate ligands</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/451</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/451</guid>
<pubDate>Mon, 07 May 2012 13:52:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>The integration of amphiphilic properties into transition metal coordination systems is a pertinent step toward the development of candidate metallosurfactant precursors for the formation of responsive monolayer films. This concept is intended to preserve the solution-observed redox, spectroscopic, and magnetic responses onto solid surfaces for potential application. Selected metal ions and various ligand designs are investigated to address the effect of coordination and protonation preferences on amphiphilic behavior, the aspects of new modular approaches for Langmuir film precursors of differentiated topologies to extend amphiphilicity and redox behavior, and the introduction of photosensitizing properties into electroactive metallosurfactant precursors. In an attempt to enhance the redox response of our current phenolato-based ligand scaffolds, rich multielectronic ligand-centered redox reactivity is established with the amino-catecholate functionality and will be incorporated into prospective ligand schemes. A concerted effort merges the comprehensive synthetic, electrochemical, spectroscopic, and photophysical evidence, film formation methods, and computational techniques.</p>

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</description>

<author>Frank Donald Lesh</author>


</item>


<item>
<title>Cellular plasticity in white adipose tissue: in vivo identification of bipotent adipocyte progenitors in adult white adipose tissue</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/450</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/450</guid>
<pubDate>Mon, 07 May 2012 13:52:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nutritional and pharmacological stimuli can dramatically alter the cellular composition and phenotype of white adipose tissue (WAT). Nonetheless, the identity of progenitors that contribute to this cellular plasticity in vivo remains poorly understood. Utilizing genetic lineage tracing techniques in combination with in situ imunohistochemical analysis, we demonstrate that brown adipocytes (BA) that are induced by beta3-adrenergic receptor activation (ADRB3) in WAT arise from the proliferation and differentiation of cells that express platelet-derived growth factor receptor alpha (PDGFRA), CD34 and Sca1 (PDGFRA+ cells). PDGFRA+ cells have a unique morphology in which extended processes contact multiple cells in the tissue microenvironment. Surprisingly, these cells also give rise to white adipocytes (WA) that can comprise up to 25% of total fat cells in abdominal fat pads following 8 weeks of high fat feeding. PDGFRA+ cells isolated by fluorescence-activated cell sorting differentiated into both BA and WA in vitro, and generated WA after transplantation in vivo, confirming dual potential. Studies on the interplay of progenitors with niche components demonstrated that ADRB3 activation recruited M2 macrophage to form crown-like structures in epididymal WAT and M2 macrophages released OPN and PDGFC to induce progenitor migration and proliferation. Progenitor activation was dependent on PDGF signaling and attenuated by pharmacologic inhibition of the receptor tyrosine kinase. Together, we identified a novel population of adipocyte progenitors with in vivo dual adipogenic potential that respond to pharmacologic stimulation and nutritional modification and their interaction with adipose tissue macrophages. These finding provides new information on adipose lineage specification and have clinical implication for diabetes therapy and restorative medicine.</p>

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</description>

<author>Yun-hee Lee</author>


</item>


<item>
<title>Development of a cargo delivery system and inhibition studies focused on clostridium difficile toxin a</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/449</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/449</guid>
<pubDate>Mon, 07 May 2012 13:51:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Virulence factors of pathogenic bacteria are to be blamed for life-threatening infections such as diphtheria, anthrax, botulism, and tentanus.  In the case of enzymatic exotoxins, disease arises from cytotoxic proteins, and cytotoxicity is acheived only after cell entry.  This intrinsic mechanism for cell entry is intriguing from research and medical views.  Along with a review on existing cargo delivery systems utilizing protein toxins and the usefulness of such a system, here is described the first reported Clostridium difficile toxin A fusion protein, luciferase-TcdA, and evidence of the successful transport of an active enzyme, luciferase, into the cytosol of vero cells.  A feature that makes our system so attractive, is the auto-proteolytic event that releases the cargo protein after internalization.  In addition to protein delivery, the exciting success of a peptide-based inhibitor is described.  Almost complete inhibition of toxin A was observed in cellulo by a peptide, identified to reversibly bind to the active site, HQSPWHHGGGC, that was functionalized with an epoxy group, HQSPGepoxyHHGGGC.  Placement of the functional group is crucial for toxin inhibition.  Through studying protein toxins we not only gain insight necessary for defending against deadly diseases, but we can also learn to harness their distinctive properties for the development of novel biotechnology tools, such as a protein translocation system.</p>

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</description>

<author>Stephanie Marie Kern</author>


</item>


<item>
<title>A family affair: the effects of familial relations on offender recidivism</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/448</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/448</guid>
<pubDate>Mon, 07 May 2012 13:51:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Prisoner recidivism has and continues to impact families and communities.  Traditional methods aimed at reducing this phenomenon have had little success in curtailing this problem.  One obvious but often overlooked tool that may play a significant role in dealing with this issue is the importance of family relationships.  This dissertation quantitatively examines offender's perceptions of the importance of family relations, specifically the relationships with the offender's children, spouse or significant other.  These relationships are analyzed to determine their level of impact on prison misconduct and parole recidivism.</p>
<p>Response data from 102 male ex-offenders from the years of 2009 to 2010 are used to test the originating question of this dissertation:  To what extent are the relationships between offenders and their families related to prison misconduct or recidivism?  Variations in perceptions towards familial importance are ascertained via sub-group analyses.  These subgroups analyses use demographic/personal factors (age, race, marital status, educational attainment prior to incarceration, educational attainment during incarceration), and family background/structural factors (residence of children before incarceration and during parole supervision, strength of bond with children and spouse or significant other prior to and during incarceration, and while under parole supervision).</p>
<p>This analysis found that differences in prison misconducts does exist between offenders who had children prior to incarceration, or were married or in a relationship during incarceration and those offenders who did not have children or were not in a relationship during this time period.  The results show that offender's who have children, are married or in a relationship are less likely to engage in prison misconduct.  However, these relationships are not significant predictors of recidivism.</p>
<p>Some linear regression models indicate that factors or variables such as age, educational attainment prior to prison, composite measures of the quality of the relationship with spouse or significant other help predict prison misconduct, but only the variable of educational attainment during incarceration helps to predict parole recidivism.</p>

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</description>

<author>Kenneth Tarez Kelso</author>


</item>


<item>
<title>Use of visual representations and drawings in writing for arabic high school english language learners</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/447</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/447</guid>
<pubDate>Mon, 07 May 2012 13:51:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>bold</p>

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</description>

<author>Iman Ali Ismail</author>


</item>


<item>
<title>The relationship of rehabilitation counselors&apos; knowledge of the americans with disabilities act 1990, attitudes toward reasonable accommodation, and job development efficacy</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/446</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/446</guid>
<pubDate>Mon, 07 May 2012 13:51:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this research was to evaluate the relationship between the rehabilitation counselors' level of knowledge, attitudes towards reasonable accommodations and job development efficacy. The more knowledgeable rehabilitation counselors are about ADA, reasonable accommodations, and their attitude toward job development, the less likely their attitudes will be expected to fluctuate. In addition, there has been very little research in terms of evaluating rehabilitation counselor's level of job placement efficacy. A survey-based design was utilized to create both a quantitative description of knowledge of the ADA, beliefs about reasonable accommodations and job placement efficacy and qualitative information concerning the barriers to job placement outcomes and enhancements needed to assist rehabilitation counselors in working with employers. The self-report survey instruments were e-mailed to 1,000 rehabilitation counselors listed on a national database maintained by the Commission for Rehabilitation Counselor Certification (CRCC®). A statistically significant negative correlation was obtained for the ADA Knowledge Survey (N = 114) and Disability Questionnaire (N = 113) which can be described as a subtle but detectable correlation. This negative correlation indicated increases in the respondents' knowledge of the ADA were associated with less reasonable attitudes toward reasonable accommodation. The study found Licensure/Certification to be a significant predictor of respondents' knowledge of the ADA and attitudes toward reasonable accommodation. The research found no statistically significant difference in gender and attitudes toward reasonable accommodation and no specific demographic characteristic was found to make statistically significant contribution to predicting respondents' job development efficacy. Counselor Preparation (36.8%) was the largest percentage theme for enhancements to increase rehabilitation counselors comfort level in assisting employers with job placement, Partnering between Stakeholders (33.3%) was second, and the least was Education and Skill Enhancement (1.7%). Interpretations and generalizations should be made with caution. Despite the statistical and non-statistical findings, future research to determine rehabilitation counselors' knowledge of ADA, attitudes toward reasonable accommodation, and job development efficacy is warranted as the number of persons with disabilities increases.</p>

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</description>

<author>Joy Elizabeth Inniss-johnson</author>


</item>


<item>
<title>An examination of the role of school climate in adolescent test anxiety</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/445</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/445</guid>
<pubDate>Mon, 07 May 2012 13:51:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to examine intrapersonal and contextual variables in relation to test anxiety among adolescents.  Participants (n=298) were students in grades seven and eight from a middle school in a suburb in southeastern Michigan.  Academic self-concept was found to fully mediate the relation between academic performance (as measured by GPA) and test anxiety.  The intrapersonal variables of perceived threat of tests, effortful control, and academic self-concept significantly predicted test anxiety.  The contextual variables were unrealistic parental expectations and school climate.  Unrealistic parental expectations was a predictor of test anxiety in a regression model including only those two contextual variables, but was no longer a significant predictor when all study variables were included.  School climate was not found to significantly predict test anxiety, nor did it serve the hypothesized role of moderating the relation of effortful control and test anxiety.  The study provides support for the importance of intrapersonal variables in predicting test anxiety among adolescents.</p>

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</description>

<author>Lea Ann Imasa</author>


</item>


<item>
<title>Remote software upload techniques in future vehicles and their performance analysis</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/444</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/444</guid>
<pubDate>Mon, 07 May 2012 13:50:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Updating software in vehicle Electronic Control Units (ECUs) will become a mandatory requirement for a variety of reasons, for examples, to update/fix functionality of an existing system, add new functionality, remove software bugs and to cope up with ITS infrastructure.  Software modules of advanced vehicles can be updated using Remote Software Upload (RSU) technique. The RSU employs infrastructure-based wireless communication technique where the software supplier sends the software to the targeted vehicle via a roadside Base Station (BS). However, security is critically important in RSU to avoid any disasters due to malfunctions of the vehicle or to protect the proprietary algorithms from hackers, competitors or people with malicious intent. In this thesis, a mechanism of secure software upload in advanced vehicles is presented which employs mutual authentication of the software provider and the vehicle using a pre-shared authentication key before sending the software. The software packets are sent encrypted with a secret key along with the Message Digest (MD). In order to increase the security level, it is proposed the vehicle to receive more than one copy of the software along with the MD in each copy. The vehicle will install the new software only when it receives more than one identical copies of the software. In order to validate the proposition, analytical expressions of average number of packet transmissions for successful software update is determined.  Different cases are investigated depending on the vehicle's buffer size and verification methods. The analytical and simulation results show that it is sufficient to send two copies of the software to the vehicle to thwart any security attack while uploading the software.</p>
<p>The above mentioned unicast method for RSU is suitable when software needs to be uploaded to a single vehicle.  Since multicasting is the most efficient method of group communication, updating software in an ECU of a large number of vehicles could benefit from it.  However, like the unicast RSU, the security requirements of multicast communication, i.e., authenticity, confidentiality and integrity of the software transmitted and access control of the group members is challenging. In this thesis, an infrastructure-based mobile multicasting for RSU in vehicle ECUs is proposed where an ECU receives the software from a remote software distribution center using the road side BSs as gateways. The Vehicular Software Distribution Network (VSDN) is divided into small regions administered by a Regional Group Manager (RGM). Two multicast Group Key Management (GKM) techniques are proposed based on the degree of trust on the BSs named Fully-trusted (FT) and Semi-trusted (ST) systems. Analytical models are developed to find the multicast session establishment latency and handover latency for these two protocols. The average latency to perform mutual authentication of the software vendor and a vehicle, and to send the multicast session key by the software provider during multicast session initialization, and the handoff latency during multicast session is calculated. Analytical and simulation results show that the link establishment latency per vehicle of our proposed schemes is in the range of few seconds and the ST system requires few ms higher time than the FT system. The handoff latency is also in the range of few seconds and in some cases ST system requires less handoff time than the FT system. Thus, it is possible to build an efficient GKM protocol without putting too much trust on the BSs.</p>

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</description>

<author>Irina Hossain</author>


</item>


<item>
<title>African-centered education in middle schools: the decision-making process in a parental engagement model</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/443</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/443</guid>
<pubDate>Mon, 07 May 2012 13:50:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>ABSTRACT</p>
<p>AFRICAN-CENTERED   EDUCATION IN MIDDLE SCHOOLS: THE DECISION-MAKING PROCESS IN A PARENTAL ENGAGEMENT MODEL</p>
<p>by</p>
<p>LATRICE N. HICKS DUNN</p>
<p>May 2012</p>
<p>Advisor: 	Dr. David Whitin</p>
<p>Major:	Curriculum and Instruction</p>
<p>Degree:	Doctor of Education</p>
<p>The ways in which key stakeholders influencing decision-making processes in African-centered   schools in urban areas are qualitatively different from that of parental involvement in mainstream schools; these perceived differences influence decision-making in various ways. The purpose of this research is to investigate ways in which parents, teachers and administrators of African American middle-school student's talk about the decision-making aspect of parental engagement in African-centered   school settings. Parental involvement significantly impacts student achievement. Therefore, identifying beliefs about parental roles at the school and home level provides some insight into ways in which parents are a part of the decision-making process in curriculum and instruction. Increasing parents' ability to negotiate the education of their children is the goal of this research. An ethnographic research approach was utilized in this study. This pragmatic approach was chosen because of the interest in understanding the effect of the actual role of parents and perceptions about the role of parents in the decision-making process. Three data sources were established for this study; they included interviews of parents, teachers, and administrators. The findings of this study suggests that the ways in which the parents, teachers, and administrators interviewed talk about parent participation in African-centered   schools include forms of traditional parental involvement and parental engagement as defined by the research; the extent of parent decision-making varies and is not an isolated form of participation but rather exists at all levels on the continuum from involvement to engagement.</p>

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</description>

<author>Latrice Nichol Hicks</author>


</item>


<item>
<title>Reliability and effect of partially restrained wood shear walls</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/442</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/442</guid>
<pubDate>Mon, 07 May 2012 13:50:35 PDT</pubDate>
<description>
	<![CDATA[
	<p><b>ABSTRACT</b></p>
<p>RELIABILITY AND EFFECT OF PARTIALLY RESTRAINED WOOD SHEAR WALLS</p>
<p>by</p>
<p>JOHN J. GRUBER</p>
<p>MARCH 2012</p>
<p>Advisor:	Dr. Gongkang Fu</p>
<p>Major:		Civil Engineering</p>
<p>Degree:	Doctor or Philosophy</p>
<p>The prescriptive design of the most widely used residential building code in the United States, the IRC, allows the use of partially restrained wood shear walls to resist wind and seismic loads.  Wind load is the most common controlling lateral design load for these structures.  In contrast, the complimenting building code, the IBC, requires either a restraining dead load or a mechanical hold down device to resist overturning.  To prescribe a safe structure, it is important to know the effect of partial restraint on the overturning resistance of wood shear walls constructed in accordance with the IRC and equally important whether the partially restrained wood shear walls provide the same level of reliability as fully restrained wood shear walls for wind load.  This is the focus of this research.</p>
<p>Twenty five Monotonic tests were conducted of 4' x 8' wood shear walls with five varying restraining methods (wall types). There were five sets of five wall types.  One of the sets had only an anchor bolt, three sets had different dead loads with one anchor bolt, and one set had a mechanical hold down.  The results of the test program were used to determine the partial restraint effect, create a nonlinear finite element model, and to determine the statistical data required to perform a Monte Carlo simulation of the wall behavior.</p>
<p>The Monte Carlo simulation result was used to calibrate a nonlinear partial restraint factor to a target reliability index of 3.25.  The calibration was performed for both ASD and LRFD load combinations as required by the IBC.  The research concludes with a closed-form solution, including the calibrated nonlinear partial restraint factor developed, to determine the unit shear capacity of a partially restrained or fully restrained (with dead load or mechanical hold down) wood shear wall constructed in accordance with the IRC by utilizing the fully restrained nominal unit shear values of AF&PA's Special Design Provisions for Wind and Seismic.</p>

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</description>

<author>John Joseph Gruber</author>


</item>


<item>
<title>It&apos;s a birth not a procedure: an ethnographic study of intrauterine fetal death in a labor and delivery unit of an american hospital setting</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/441</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/441</guid>
<pubDate>Mon, 07 May 2012 13:50:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>Life transitions such as birth and death constitute a significant area within anthropological studies of ritual.  It is important to investigate how individuals, groups, and communities organize around these events.  Birth and death can be considered as <i>rites of passage</i> that mark key life transitions (van Gennep 1909/1960).  Thus birth and death related rituals need to be investigated within the social and cultural context of American hospital settings to better understand the social organization of life, death, and personhood.  In the American hospital setting, a reproductive loss at any gestational age receives the medical diagnostic label of an intrauterine fetal death (IUFD).  An IUFD is consequently both a physical and social process that is medically managed in a labor and delivery unit.  There is a need to more meaningfully understand how life, death, and personhood issues are handled during this difficult event for women, their families, and the health care staff.  The pregnancy loss (IUFD) process, staff caring practices, and meaning making can be anthropologically viewed as a ritualistic process.  An IUFD is a unique rite of passage that is a juxtaposition of a birth and a death.  Ten women and their families, and 20 health care staff participated in this yearlong ethnographic study.  Qualitative ethnographic methods included engaging in participant observation and conducting in-depth and follow-up interviews.  Two exemplar case studies are discussed in detail.  Data was coded and analyzed.  Findings suggest that women and their families experience an IUFD as a birth rather than a procedure and recognize their non-viable fetus as a person.  Women and their families assign personhood to a fetus during post-birth rituals such as naming, receiving a memory box with mementos, and having unrestricted time with the baby.  The findings contribute to a better understanding of how the categories of life, death, and personhood are culturally made in the labor and delivery unit of an American hospital setting.</p>

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</description>

<author>Catherine Mcleod Griffin</author>


</item>


<item>
<title>School improvements and student achievement: teachers&apos; conceptions and practices in an urban school community</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/440</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/440</guid>
<pubDate>Mon, 07 May 2012 13:50:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>SCHOOL IMPROVEMENTS AND STUDENT ACHIEVEMENT:</p>
<p>TEACHERS' CONCEPTIONS AND PRACTICES IN AN URBAN SCHOOL COMMUNITY</p>
<p>by</p>
<p>JENDAYI JOHARI GARDNER</p>
<p>May 2012</p>
<p>Advisor: Dr. Jazlin Ebenezer</p>
<p>Major: Curriculum & Instruction</p>
<p>Degree: Doctor of Philosophy</p>
<p>This mixed-methods study is represented by three articles that examine student achievement. The articles were developed based on the following purposes: (1) to examine teachers' conceptions about student achievement; (2) to examine teacher practices for school improvement that reflects elements of a reform model; and (3) to examine teachers' conceptions about school improvement challenges. Individual interviews were administered to examine teachers' conceptions about student achievement and school improvement challenges. The conceptions were then converted to excerpts that were grouped into common categories. Common descriptive categories were developed using the methodological framework, phenomenography. To examine teacher practices that reflect elements of a reform model, the researcher used classroom observations. The classroom observations were analyzed using a Classroom Observation Protocol that determined the frequency of teacher practices that reflect elements of the 90/90/90 Model. The study also examined MEAP test scores using the chi-squared goodness-of-fit test to compare the 2009 and 2010 results.</p>
<p>To address the first purpose of the study, three descriptive categories were revealed based on the data. The three categories were: (1) analyzing student achievement data to develop interventions; (2) a model to decrease disruptive behavior; and (3) parent involvement to support children's learning. To address the second purpose of the study, the results revealed that of the five elements, teacher practice displayed three elements:  (1) the focus on academic achievement; (2) the choice of curriculum; and (3) the frequent use of multiple assessments. The third purpose of the study was addressed by the emergence of three descriptive categories from the data. The three categories are as follows: (1) student transiency throughout the school year; (2) staff restructure and transfers to different schools; and (3) lack of parent involvement in school and at home. In addition, the results of the chi-squared test revealed a significant difference between the observed (2010) and expected (2009) MEAP Test scores.</p>
<p>The following implications emerged from the results of the study: (1) a practical reform model for school improvement that is anchored in a theory of curriculum can be used as a lens to view student achievement; (2) school districts that incorporate teachers' conceptions about student achievement are able to make effective curriculum-based decisions; (3) school districts that identify the intra-and inter-variations of teacher conceptions enable schools to address challenges with a common mindset; (4) in order for schools to improve student achievement, all five elements of the reform model should be practiced by teachers; and (5)  teachers' conceptions of school improvement challenges should be considered by educational leaders during the decision-making process.</p>

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</description>

<author>Jendayi Johari Gardner</author>


</item>


<item>
<title>Index</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/29</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/29</guid>
<pubDate>Mon, 07 May 2012 13:49:56 PDT</pubDate>
<description>
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>A higher education case: millennial experience toward learning through a virtual world designed as an authentic learning environment</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/439</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/439</guid>
<pubDate>Mon, 07 May 2012 13:49:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Current educational initiatives encourage the use of authentic learning environments to realistically prepare students for jobs in a constantly changing world.  Many students of the Millennial generation may be social media savvy.  However, what can be said about learning conditions and student readiness for active, reflective and collaborative learning and media literacy within their discipline?  Virtual worlds such as Second Life (SL) represent future hybridized work environments which can support authentic learning.  With their immersive and interaction affordances, virtual worlds may be designed to incorporate real-world team projects for both online and blended courses.</p>
<p>This qualitative single embedded case study sought to understand learner experiences regarding the authentic learning environment instructional design which was provided through Second Life.  The study took place in a higher education game development course facilitated through SL during the fall 2009 semester.  The goals of the student project were to work in simulated real-world teams to design and co-create a game, test the game by role-play as non player characters with a random student player, experience game development requirements, and reflect upon lessons learned.  The research study took place at a mid-size private university in a Midwest metropolitan suburb.  Participants included eighteen Millennial generation students who had never used SL in a formal learning setting. The majority of the students were white male gamers majoring in STEM disciplines. Data collection included participant observation over a three month period, 75 student journal entries, 12 in-depth interviews, and four student focus groups.  Data analysis included domain, taxonomic, componential, vignette, and theme analyses and trustworthiness methods.  The case study was presented through abstract models of learner processes, rich thick detailed descriptions, theme analysis matrices, and in-world snapshots.</p>
<p>The case study scene was parsed into three components representing learner needs in an authentic learning multi-user virtual environment (ALMUVE): 1) support of authentic active, reflective and collaborative learning, 2) design of authentic activities and assessment, and 3) creation of an authentic learning environment and community.  Students exhibited active learning over a range of learning domains and problem types through the team project.  Chances of sustained learning engagement increased when class sessions were choreographed and activities were varied.  Both peer-reflective and self-reflective learning were facilitated and categorized into five types, ranging from low to high levels of self-reflection.  Students were not comfortable with reflective writing and they requested more structure.  For virtual world collaborative learning, participation and synthesis were observed rather than division of labor found with other tools.  Though team behaviors mirrored face-to-face ones, there was a need for increased transparency and communication.</p>
<p>Authentic activities need to be progressively staged with a variety of perspectives and tasks to construct a real-world team project.  Co-creation and role-play activities were conducive for ALMUVE engagement.  Authentic assessment mirrored authentic activities and included opportunities for assessing individual and team efforts.  The study showed a need for more authentic assessment methods for virtual world team projects.  Team projects were successful, with each team developing and enacting an innovative game with their own interpretation of game narrative, characters, environment, player choices, goals and rewards, and methods of interaction.  Though a rich environment could be created, the locus of class activities as well as resources and tools competed for student attention.  There was a need for additional technology, instructional design, and 3-D development support as well as a need to match the instructor's use of technology to that required of students.  Embedding multiple perspectives in activities created opportunities for immersion and interactivity.  More team role rotation and accountability, modeling and coaching strategies may enhance engagement. Students desired more `learning by doing' to take advantage of virtual world attributes.</p>
<p>Millennial learner types of the game development course were identified in terms of their perspectives toward virtual learning.  Gamers who played mostly first-person shooter games exhibited a bias toward learning in SL, viewing SL in terms of the games they play.  It was difficult for them to visualize how game development could be taught using SL.  They may also have viewed the virtual world building subculture in contrast to their own gaming subcultures.  Gamers, who were engaged team leaders, demonstrated comfort with ambiguity, creativity, collaboration, self-confidence, and an inclination toward lifelong learning. These characteristics aligned to class challenges with ALMUVE engagement.</p>
<p>Virtual world media effects were explored regarding evolution of communication practices, student-development of the 3-D environment, and progression of collaboration on the project.  Communication was found to be short, frequent and transmitted through various tools.  There were inferred differences between affordances and cultures of a virtual world, an MMORPG, and uses of an application.  As the communication became easier and more expressive, a more authentic 3-D environment developed.  Likewise, team collaboration increased with co-created 3-D environments and role-play.</p>
<p>This case study has implications for instructional designers and faculty interested in creating real-world learning experiences using virtual worlds.  The findings illuminate instructional design considerations when creating virtual world learning environments for Millennial students and for the gamer subculture in particular.  The study is also applicable to instructional design constructivist studies, studies related to learning through virtual worlds, studies involving Millennial subcultures, and studies using virtual research methodologies.</p>

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</description>

<author>Marija Franetovic</author>


</item>


<item>
<title>Tables</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/28</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/28</guid>
<pubDate>Mon, 07 May 2012 13:49:55 PDT</pubDate>
<description>
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


</item>


<item>
<title>Chapter 23: Administration of Justice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/27</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/27</guid>
<pubDate>Mon, 07 May 2012 13:49:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan J. Dimond</author>


</item>


<item>
<title>Chapter 22: Evidence</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/26</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/26</guid>
<pubDate>Mon, 07 May 2012 13:49:52 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frederick A. McDermott</author>


</item>


<item>
<title>Chapter 21: Civil Procedure and Practice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/25</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/25</guid>
<pubDate>Mon, 07 May 2012 13:49:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph G. Crane</author>


</item>


<item>
<title>Chapter 20: Food and Drug, Health, and Welfare Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/24</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/24</guid>
<pubDate>Mon, 07 May 2012 13:49:50 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William J. Curran et al.</author>


</item>


<item>
<title>Chapter 19: Workmen&apos;s Compensation</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/23</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/23</guid>
<pubDate>Mon, 07 May 2012 13:49:49 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph Bear et al.</author>


</item>


<item>
<title>Chapter 18: State and Municipal Government</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/22</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/22</guid>
<pubDate>Mon, 07 May 2012 13:49:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph C. Duggan</author>


</item>


<item>
<title>Chapter 17: Insurance</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/21</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/21</guid>
<pubDate>Mon, 07 May 2012 13:49:46 PDT</pubDate>
<description>
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</description>

<author>J. Marshall Leydon</author>


</item>


<item>
<title>Chapter 16: State and Local Taxation</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/20</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/20</guid>
<pubDate>Mon, 07 May 2012 13:49:45 PDT</pubDate>
<description>
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</description>

<author>David Flower Jr.</author>


</item>


<item>
<title>Chapter 15: Public Utilities</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/19</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/19</guid>
<pubDate>Mon, 07 May 2012 13:49:44 PDT</pubDate>
<description>
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</description>

<author>Edward N. Gadsby</author>


</item>


<item>
<title>Effective semantic-based keyword search over relational databases for knowledge discovery</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/438</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/438</guid>
<pubDate>Mon, 07 May 2012 13:49:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Keyword-based search has been popularized by Internet web search engines such as Google which is the most commonly used search engine to locate the information on the web. On the other hand while traditional database management systems offer powerful query languages such as SQL, they do not provide keyword-based search similar to the one provided by web search engines. The current amount of text data in relational databases is massive and is growing fast. This increases the importance and need for non-technical users to be able to search for such information using simple keyword search just as how they would search for text documents on the web. Keyword search over relational databases (KSRDBs) enables ordinary users to query relational databases by simply submitting keywords without having to know any SQL or having any knowledge of the underlying structure of the data. In this research work our primary focus is to enhance the effectiveness of the keyword search over relational databases using semantic web technologies. We have also addressed some the issues with the effectiveness of the current keyword search over relational databases. In particular we are addressing the followings:</p>
<p>We have improved (gained significantly higher precision/recall curve) the existing state-of-the-art ranking functions by incorporating the query keywords' proximity and query keywords' quadgrams of the text attributes with long string into the scoring function.</p>
<p>We have adapted a novel approach in making keyword search recommendations based on the text attributes in which the search terms were found without relying on the user's past search criteria. A proof of concept (POC) prototype system called TupleRecommender has been implemented based on this approach.</p>
<p>We have designed and implemented a proof of concept (POC) prototype system called database semantic search explorer (DBSemSXplorer) which can answer the traditional keyword search over relational databases in a more effective way with a better presentation of search results. This system is based on semantic web technologies and is equipped with faceted search and inference capability of the Semantic Web to ease the task of knowledge discovery for the end user.</p>

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</description>

<author>Sina Fakhraee</author>


</item>


<item>
<title>Chapter 14: Labor Relations</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/18</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/18</guid>
<pubDate>Mon, 07 May 2012 13:49:43 PDT</pubDate>
<description>
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</description>

<author>Lawrence M. Kearns</author>


</item>


<item>
<title>Chapter 13: Administrative Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/17</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/17</guid>
<pubDate>Mon, 07 May 2012 13:49:42 PDT</pubDate>
<description>
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<author>William J. Curran</author>


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<title>Chapter 12: Criminal Law, Procedure, and Administration</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/16</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/16</guid>
<pubDate>Mon, 07 May 2012 13:49:40 PDT</pubDate>
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<author>Wilbur G. Hollingsworth</author>


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<title>Chapter 11: Constitutional Law</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/15</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/15</guid>
<pubDate>Mon, 07 May 2012 13:49:39 PDT</pubDate>
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<author>Henry Parkman et al.</author>


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<title>Chapter 10: Conflict of Laws</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/14</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/14</guid>
<pubDate>Mon, 07 May 2012 13:49:38 PDT</pubDate>
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<author>Monroe Inker</author>


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<title>Chapter 9: Domestic Relations and Persons</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/13</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/13</guid>
<pubDate>Mon, 07 May 2012 13:49:37 PDT</pubDate>
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<author>William J. Greenler Jr. et al.</author>


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<item>
<title>Chapter 8: Security and Mortgages</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/12</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/12</guid>
<pubDate>Mon, 07 May 2012 13:49:35 PDT</pubDate>
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<author>John D. O&apos;Reilly Jr.</author>


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<item>
<title>Chapter 7: Commercial Law and Banking</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/11</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/11</guid>
<pubDate>Mon, 07 May 2012 13:49:34 PDT</pubDate>
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<author>William E. Hogan et al.</author>


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<item>
<title>Exploring the relationship between pre service school counselor&apos;s academic training and reported levels of multicultural competence as predictors of attitudes toward inclusion</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/437</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/437</guid>
<pubDate>Mon, 07 May 2012 13:49:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>The principal aim of this study was to explore the relationships between preservice school counselors' academic training and their self-reported levels of multicultural competence as predictors of attitudes toward inclusion. Variances in demographic data also were examined as predictors of attitudes regarding inclusion. A nonexperimental, correlational research design was used. Pearson product moment correlations were used to test the relationships between preservice school counselors' level of academic training and their attitudes toward inclusions. No statistically significant correlations were obtained on these analyses, indicating that academic training does not predict attitudes toward inclusion. . Pearson product moment correlations were used to test the relationships between preservice school counselors' perceived level of multicultural competence and their attitudes toward inclusions. The results of these analyses were not statistically significant, Preservice school counselors self-reported level of multicultural competence could not be used to predict their attitudes toward inclusion. Selected demographic variables (age, gender, ethnicity, having a disability, having a family member with a disability, higher degree, counseling major, type of credential or endorsement, and consider students with disabilities as a distinct culture) were used as the independent variables in these analyses. None of the independent variables entered the stepwise multiple linear regression equations, indicating they were not statistically significant predictors of the four subscales (physical, academic, behavioral, social) or the total score for attitudes toward inclusion. In addition to the research questions, Pearson product moment correlations were used to determine the strength and direction of the relationships between practical experiences with students with disabilities and their attitudes toward inclusion and multicultural competencies. Three statistically significant correlations were obtained on these analyses. Students who reported they felt better prepared to provide services to students with disabilities were more likely to have higher scores for the academic subscale measuring attitudes toward inclusion. In addition, the knowledge subscale on multicultural competence was significantly related to having a greater number of practical experiences with students with disabilities and practical experiences with students from diverse cultures. The remaining correlations were not statistically significant. Recommendations for future research were offered.</p>

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<author>Rachael Annette Evans</author>


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<item>
<title>Chapter 6: Corporations</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/10</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/10</guid>
<pubDate>Mon, 07 May 2012 13:49:33 PDT</pubDate>
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<author>Bertram H. Loewenberg</author>


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<title>Chapter 5: Equity and Equity Practice</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/9</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/9</guid>
<pubDate>Mon, 07 May 2012 13:49:32 PDT</pubDate>
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<author>Harry Zarrow</author>


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<title>Chapter 4: Contracts and Agency</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/8</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/8</guid>
<pubDate>Mon, 07 May 2012 13:49:30 PDT</pubDate>
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<author>Paul M. Siskind</author>


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<item>
<title>Chapter 3: Torts</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/7</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/7</guid>
<pubDate>Mon, 07 May 2012 13:49:29 PDT</pubDate>
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<author>Joseph Schneider</author>


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<item>
<title>Chapter 2: Trusts and Estates</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/6</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/6</guid>
<pubDate>Mon, 07 May 2012 13:49:27 PDT</pubDate>
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<author>Emil Slizewski</author>


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<item>
<title>Chapter 1: Property and Conveyancing</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/5</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/5</guid>
<pubDate>Mon, 07 May 2012 13:49:26 PDT</pubDate>
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<author>Cornelius J. Moynihan</author>


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<item>
<title>Table of Contents</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/4</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/4</guid>
<pubDate>Mon, 07 May 2012 13:49:25 PDT</pubDate>
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<author>Boston College Annual Survey of Massachusetts Law</author>


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<title>Summary of Contents</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/3</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/3</guid>
<pubDate>Mon, 07 May 2012 13:49:24 PDT</pubDate>
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</description>

<author>Boston College Annual Survey of Massachusetts Law</author>


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<item>
<title>Foreword</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/2</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/2</guid>
<pubDate>Mon, 07 May 2012 13:49:23 PDT</pubDate>
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<author>Paul C. Reardon</author>


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<item>
<title>Studying the glial cell response to biomaterials and surface topography for improving the neural electrode interface</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/436</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/436</guid>
<pubDate>Mon, 07 May 2012 13:49:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Neural electrode devices hold great promise to help people with the restoration of lost functions, however, research is lacking in the biomaterial design of a stable, long-term device.  Current devices lack long term functionality, most have been found unable to record neural activity within weeks after implantation due to the development of glial scar tissue (Polikov et al., 2006; Zhong and Bellamkonda, 2008).  The long-term effect of chronically implanted electrodes is the formation of a glial scar made up of reactive astrocytes and the matrix proteins they generate (Polikov et al., 2005; Seil and Webster, 2008).  Scarring is initiated when a device is inserted into brain tissue and is associated with an inflammatory response.  Activated astrocytes are hypertrophic, hyperplastic, have an upregulation of intermediate filaments GFAP and vimentin expression, and filament formation (Buffo et al., 2010; Gervasi et al., 2008).</p>
<p>Current approaches towards inhibiting the initiation of glial scarring range from altering the geometry, roughness, size, shape and materials of the device (Grill et al., 2009; Kotov et al., 2009; Kotzar et al., 2002; Szarowski et al., 2003).    Literature has shown that surface topography modifications can alter cell alignment, adhesion, proliferation, migration, and gene expression (Agnew et al., 1983; Cogan et al., 2005; Cogan et al., 2006; Merrill et al., 2005).  Thus, the goals of the presented work are to study the cellular response to biomaterials used in neural electrode fabrication and assess surface topography effects on minimizing astrogliosis.</p>
<p>Initially, to examine astrocyte response to various materials used in neural electrode fabrication, astrocytes were cultured on platinum, silicon, PMMA, and SU-8 surfaces, with polystyrene as the control surface.  Cell proliferation, viability, morphology and gene expression was measured for seven days in vitro.  Results determined the cellular characteristics, reactions and growth rates of astrocytes grown on PMMA resembled closely to that of cells grown on the control surface, thus confirming the biocompatibility of PMMA.  Additionally, the astrocyte GFAP gene expressions of cells grown on PMMA were lower than the control, signifying a lack of astrocyte reactivity.</p>
<p>Based on the findings from the biomaterials study, it was decided to optimize PMMA by changing the surface characteristic of the material.  Through the process of hot embossing, nanopatterns were placed on the surface in order to test the hypothesis that nanopattterning can improve the cellular response to the material.  Results of this study agreed with current literature showing that topography effects protein and cell behavior.  It was concluded that for the use in neural electrode fabrication and design, the 3600mm/gratings pattern feature sizes were optimal.  The 3600 mm/gratings pattern depicted cell alignment along the nanopattern, less protein adsorption, less cell adhesion, proliferation and viability, inhibition of GFAP and MAP2k1 compared to all other substrates tested.</p>
<p>Results from the initial biomaterials study also indicated platinum was negatively affected the cells and may not be a suitable material for neural electrodes.  This lead to pursuing studies with iridium oxide and platinum alloy wires for the glial scar assay.  Iridium oxide advantages of lower impedance and higher charge injection capacity would appear to make iridium oxide more favorable for neural electrode fabrication. However, results of this study demonstrate iridium oxide wires exhibited a more significant reactive response as compared to platinum alloy wires.  Astrocytes cultured with platinum alloy wires had less GFAP gene expression, lower average GFAP intensity, and smaller glial scar thickness.</p>
<p>Results from the nanopatterning PMMA study prompted a more thorough investigation of the nanopatterning effects using an organotypic brain slice model.  PDMS was utilized as the substrate due to its optimal physical properties.  Confocal and SEM imaging illustrated cells from the brain tissue slices were aligned along the nanopattern on the PDMS pins.  Decreases in several inflammatory markers (GFAP, TNFα, IL-1β) determined from gene expression analysis, was shown with the nanopatterned PDMS pins.  Results of this study confirm nanopatterning not only influences cell morphology, but alters molecular cascades within the cells as well.</p>
<p>The results of these studies provide essential information for the neural electrode research community.  There is a lack of information available in the scientific community on acceptable and effective materials for neural electrode fabrication.  The results of the presented studies provide more information which could lead to classifying guidelines to create biocompatible neural electrode materials.</p>
<p>This research project was partially supported by the Wayne State University President's Translational Enhancement Award and by the Kales Scholarship for Biomedical Engineering students.</p>

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</description>

<author>Evon S. Ereifej</author>


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<item>
<title>Masthead</title>
<link>http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/1</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/asml/vol1956/iss1/1</guid>
<pubDate>Mon, 07 May 2012 13:49:21 PDT</pubDate>
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<author>Boston College Annual Survey of Massachusetts Law</author>


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<item>
<title>The effects of two group counseling interventions on arab-american high school students&apos; perceptions of their primary relationships (parent, teacher, peer)</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/435</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/435</guid>
<pubDate>Mon, 07 May 2012 13:49:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study specifically investigated the effects of two group counseling interventions on Arab-American high school students' perceptions of the strength of their primary relationships (parent, teachers, and peers). It was designed to help high school students increase their acceptance of the culture of their host society and develop a sense of comfort so they can retain some of their own culture and Arab identity without feeling they will totally lose them. One approach was Choice group theory grounded in the reality of making choices concerning thoughts and behaviors. Choice Theory is described as the idea that people have mental images of their needs and behave accordingly; thus individuals are ultimately self-determining (i.e., their life choices). The Psychoeducational approach's primary purpose is to educate or instruct participants in regards to certain relationships or areas pertinent to their lives (e.g., child education group). Arab American high school students were recruited from two high schools in a large urban metropolitan school district in the Midwest. Initially, there were a total of 54 high school students who volunteered to participate in this study. However, four participants failed to complete the study. Therefore, data was analyzed for 50 participants. The participants were randomly assigned to one of the two treatment conditions. There were a total of six counseling groups of approximately 8-12 high school students in each group. The Parent, Teacher and Peers subscale scores on the Clinical Assessments of Interpersonal Relationships were used to determine the pre-and-post levels in Arab American high school students' perceptions of the strength of their relationships in three primary contexts. The results indicated there was no statistically significant level of difference in any of the three primary contexts. Based on the statistically non-significant findings on the differential group changes in perceptions Arab-American high school students have of their primary relationships pre-to-post, the null hypotheses were retained. A summary and discussion of the results pertinent to each research hypothesis and recommendations for future research are presented.</p>

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</description>

<author>Nuzmeya Bader Elder</author>


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<item>
<title>New adaptations of analytical tools for the study of dynamic interactions of lanthanide-based catalysis in aqueous media</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/434</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/434</guid>
<pubDate>Mon, 07 May 2012 13:48:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lewis acid catalyzed carbon-carbon bond-forming reactions are of great interest in organic synthesis.  However, many conventional Lewis acids, and almost all enantioselective Lewis acid catalysts, must be used under strictly anhydrous conditions to avoid hydrolysis and the difficulties associated with recovery and reuse of the catalysts. Due to these drawbacks of conventional Lewis acids, there is a growing desire to perform many organic transformations using more environmentally friendly aqueous-stable catalysts. The advantages of using aqueous-stable catalysts include the ability to use unprotected functional groups, ease of product separation and catalyst recovery, and avoidance of costly solvent drying procedures. Lanthanide trifluoronmethanesulfonates (triflates), Ln(OTf)3, address this goal because they are water-tolerant Lewis acid precatalysts that can catalyze a wide range of important carbon-carbon and carbon-heteroatom bond-forming reactions such as the aldol, nitro-aldol, Mannich, Diels-Alder, Michael, Mukaiyama aldol, and Friedal-Crafts reactions due to their hard, electrophilic, and hydrolysis-stable character.</p>
<p>Despite their favorable properties, the use of lanthanide triflates in asymmetric carbon-carbon bond formation under aqueous conditions has been limited due to lack of mechanistic understanding of these precatalysts in aqueous solution: the influence of counter ion coordination, the effect of solvent coordination, and the identification of intermediates in the catalytic cycle. Further, identification of the rate-determining step and product-dissociation rate of aqueous lanthanide triflate-based catalysis is of fundamental importance for developing more efficient catalysts.</p>
<p>I adapted luminescence-decay measurements to enable the study of the mechanism of lanthanide-based precatalysts in aqueous systems. Because the number of water molecules coordinated to the lanthanide ion is critical to more thoroughly understanding the nature and the reactivity of lanthanide-based precatalysts, I used luminescence-decay studies to measure the dynamics of water molecules coordinated to lanthanide-ions throughout the catalytic cycle of a selected Mukaiyama aldol reaction. Using these luminescence-decay measurements, I determined equilibrium constants as well as structural and mechanistic information regarding lanthanide-based chiral catalytic systems in aqueous medium. Furthermore, I used this analytical tool to study the influence of the coordination environment of europium-based precatalysts including europium nitrates, chlorides, and acetates on reaction rate and yield. I also empirically derived equations that enable fast and accurate determination of the water-coordination number of lanthanides in binary solvent systems. In summary, I adapted luminescence-decay measurements to probe the coordination environment of europium-based precatalysts in aqueous media and the details of my efforts are described in this thesis.</p>
<p>The other analytical tool described in this thesis involves the use of 17O NMR spectroscopy with variable temperature for the determination of important exchange rates in lanthanide-catalyzed reactions. The results described in this thesis demonstrate the utility of these two powerful analytical tools to study aqueous, lanthanide-catalyzed bond-forming reactions.</p>

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<author>Prabani Lakmanthi Dissanayake</author>


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<item>
<title>Sex differences in marital satisfaction and happiness: the contribrution of children, attractiveness, and financial status</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/433</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/433</guid>
<pubDate>Mon, 07 May 2012 13:48:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Though numerous studies in the evolutionary psychology literature have investigated how humans select mates in order to successfully reproduce and raise progeny to reproductive maturity, few have examined if factors involved in mate selection matter in marital satisfaction and individual happiness. Being youthful and attractive are indices of reproductive viability and are traits preferred by men universally while women are most known to prefer a mate of high financial status (Buss, 1989), thus underscoring the importance of a male's ability to offer financial investment to potential mates. In addition, women are more likely to evaluate the parental ability of potential long-term mates (Kruger & Fisher, 2003). If reproduction is the unconscious end goal, positive aspects of child quality should be important to parents because children represent the reproductive success individuals have been able to achieve, though the presence and number of children have documented detrimental effects on marital satisfaction (Twenge, Campbell, & Foster, 2003). The present study sought to analyze how information related to child quality, their happiness, spousal attractiveness, and financial status affect individual happiness and marital satisfaction based on the premise that if individuals have made choices that positively affect reproduction, there ought to be a measurable psychological benefit. While the expected sex differences between husbands and wives were apparent when comparing responses on attractiveness, financial status, and children, finding sex differences in how these variables impacted happiness and marital satisfaction were not as clear. The regression models showed that individual happiness and marital satisfaction can be predicted for both husbands and wives from these variables, though financial status and contributing less of the joint income is more important in the marital satisfaction of wives. The findings are discussed in an evolutionary framework with respect to how future work can benefit from extending the application of evolutionary principles of mating to the entire human lifespan.</p>

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<author>Lisa Marie Dillon</author>


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<item>
<title>Changing the Culture of Teaching</title>
<link>http://scholarworks.boisestate.edu/literacy_facpubs/66</link>
<guid isPermaLink="true">http://scholarworks.boisestate.edu/literacy_facpubs/66</guid>
<pubDate>Mon, 07 May 2012 13:48:39 PDT</pubDate>
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<author>Anne E. Gregory et al.</author>


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<item>
<title>An examination of the impact of early retirement incentives on school district financial health</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/432</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/432</guid>
<pubDate>Mon, 07 May 2012 13:48:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The combination of state controlled school funding in Michigan, rising employee costs and shrinking school enrollments have caused school districts to seek a variety of cost control measures.  One of the measures frequently supported by both school districts and employee unions is the use of Early Retirement Incentives (ERI) to incentivize teachers to separate from the school district via a cash payment.</p>
<p>The purpose of this study was to analyze how offering or not-offering an ERI impacted on the financial health of a school districts in the State of Michigan.  Selected school districts in Michigan were surveyed regarding any ERI's they may have offered during the 2003-04 to 2007-08 school years.  If the district offered an ERI, various descriptive aspects of the offered ERI including ERI amount, number of participants in the ERI and replacement percentage of separating teachers was tabulated.  The data points collected to determine the financial health of the school district included school district bond rating, the school district fund equity percentage and change in general fund expenditures of school districts.</p>
<p>This study used both t-tests and multiple regression analysis to determine if offering an ERI had any effect on the financial health of the school district as measured by fund equity percentage and changes in general fund expenditures.  Additionally, a multiple regression analysis was used to determine which various descriptor factors of an ERI might have the most significant impact on school district financial health.</p>
<p>This study found that no significant relationship existed between offering an ERI and the financial health of the school district as measured by either fund equity percentage or changes in general fund expenditure.  Additionally, this study found that other independent variables including changes in student enrollment were more impactful on changes in general fund expenditures than offering an ERI.  While bond ratings of school districts were originally designed to be used as a metric of school district financial health, they were discarded from the final analysis due to their relatively infrequent nature.</p>

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<author>Michael Jon Dean</author>


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<item>
<title>Writing the self: feminist experiment and cultural identity</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/431</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/431</guid>
<pubDate>Mon, 07 May 2012 13:48:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation examines how twentieth-century experimental women writers construct non/narrative texts whose text-subjects mediate identity and call for increased possibilities for subject-identification in the world. The use of innovative formal strategies and experiment with narrative, combined with the content of identity critique, make these texts political projects that variously explore gender, sexuality, race, and ethnicity in relation to contemporary American culture. In this project I bring discussions of identity into the theorization of formally innovative writing. I work to move away from the kinds of essentializing practices of identity politics--in which subjects are fit into specific identity categories--and toward more complicated, contextualized, and historical understandings of identity formation. I begin with the notion that identity categories, or markers, play out in different contexts and are, at different moments: simultaneous, fluctuating, overlapping, and spatial (instead of hierarchical). I then continue toward readings of literary texts that function as new models of identification for spatially contextualized subjects. This project is significant for the way in which it brings together a diverse selection of non/narrative writing by women in the twentieth-century, and combines textual and cultural analysis to think through identity issues in relation to contemporary social subjects.</p>
<p>This project is grounded in literary modernism and moves into work by contemporary American women writers at the end of the twentieth century. I begin by pairing the work of Gertrude Stein and Lyn Hejinian in chapter 1, and that of H.D. and Beverly Dahlen in chapter 2. As modernists, Stein and H.D. are key figures who negotiate identity and non/narrative writing, and are important influences for Hejinian and Dahlen. The paring of modern and contemporary authors in the first two chapters illustrates a correlation between writing styles and practices as well as how these diverge from the early to late part of the century. Hejinian's body of work, beginning in the 1970s, can be read as coming out of Stein and thinking avant-garde practice through her own contemporary politics as a Language poet. Dahlen seems to pick up H.D.'s Freudian project, and additionally incorporates deconstruction and feminist criticism of the 1970s and 80s in her work. Hejinian and Dahlen also serve as intermediaries between the modernists and later contemporary writers--many of whom have been influenced by modernists such as Stein and H.D., as well as subsequent avant-garde authors and practices. Chapters 3 and 4 focus on contemporary prose and hybrid works by Pamela Lu, Renee Gladman, Claudia Rankine, Juliana Spahr, Gloria Anzaldua, and Theresa Hak Kyung Cha. These writers, to different degrees, use a variety of formal strategies and problematize narrative autobiographical writing to simultaneously focus on language as instrumental to subjectivity and to represent "experience" as cultural content. They negotiate practices of avant-garde experimentation and writing that explores identity-as-process through examinations of gender, sexual orientation, race, ethnicity, and history. Their text-subjects become witnesses to the discrepancies in culturally inscribed norms, and call for expanded possibilities for narrative and social representation; their texts become new models for representing contemporary subjectivity. Reading the primary texts through theorists including Julia Kristeva, Judith Butler, Susan Stanford Friedman, Rachel Blau DuPlessis, and Kelly Oliver, among others, offers me ways to show how textual practice and cultural critique in this literature lend toward theorizing expanded possibilities for personal and social subject identification--how subjects identify--in the world. This project is invested in continuing to open spaces of possibility for textual practice and social subjectivity, as well as the feminist political impulse to dissolve margins and bring those "marginalized" voices into spaces with greater potential for personal and social identifications and politics.</p>

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<author>Jill Darling</author>


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<item>
<title>The structural requirements of histone deacetylase (hdac) inhibitors: suberoylanilide hydroxamic acid (saha) analogues modified at c3, c6, and c7 positions enhance selectivity</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/430</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/430</guid>
<pubDate>Mon, 07 May 2012 13:48:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Histone deacetylase (HDAC) proteins are targets for drug design towards the treatment of cancers since overexpression of HDAC is linked to cancer. Several HDAC inhibitors, including the FDA approved drug suberoylanilide hydroxamic acid (SAHA, Vorinostat), have cleared clinical trials and emerged as anti-cancer drugs. However, SAHA inhibits all of the 11 metal ion-dependent HDAC proteins. Therefore, we synthesized several libraries of small molecule HDAC inhibitors based on SAHA to help understand the structural requirements of inhibitory potency and isoform selectivity.</p>
<p>In previous work, SAHA analogues functionalized at the C2 position (C2-SAHA analogues) near the metal binding hydroxamic acid displayed decreased inhibitory activity compared to the parent compound, SAHA. The lack of potency of the C2 library indicated that limited flexibility exists in the HDAC active site near the hydroxamic acid. Therefore, we theorized the substituents on the C3, C4, C5, C6, and C7 positions would display more potent inhibition compared to the C2-SAHA library due to the solvent exposed location. Interestingly, while the C2-SAHA analogues containing any substituents were poor potent, the C3-SAHA analogue with a methyl substituent displayed potency, . The potency of the remaining analogues decreased with increasing size of the C3 substituents. Moreover, the C6-SAHA phenyl analogue even displayed potency in the submicromolar range. Finally, most of the C7-SAHA analogues displayed equal or greater potency compared to SAHA. The results indicate that more flexibility in the HDAC active site exists closer to the capping group region near the C6 and C7 position, while only modest flexibility exists in the bottom of the active site near the C2 and C3 position.</p>
<p>After analyzing the potency of SAHA analogues, isoform selective inhibition of the individual compounds was evaluated. Seven of the SAHA analogues demonstrated selectivity. The C3-SAHA ethyl-substituted analogue showed preference for HDAC6 over HDAC1 and HDAC3 even though it displayed decreased potency. The C6-SAHA analogues displayed diverse selectivity; the C6-SAHA methyl variant displayed preference for class I, t-butyl variant showed a dual-HDAC1 and HDAC6 selectivity, and 2-ethylhexyl variant showed HDAC3-selectivity. The C7-SAHA analogues displayed selective inhibition as well; the C7-SAHA pyridylmethyl and anthracenylmethyl variants displayed a dual-HDAC1 and HDAC6 selectivity, and naphthylmethyl variant showed HDAC3-selectivity. The interesting potency and selectivity of linker-modified SAHA analogues suggest that the linker region substituents can be exploited in the design of new anti-cancer drugs.</p>

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</description>

<author>Sun ea Choi</author>


</item>


<item>
<title>The impact of spirituality on the self-reported recovery of adults who experienced childhood trauma</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/429</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/429</guid>
<pubDate>Mon, 07 May 2012 13:48:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Objective: To examine whether adults who had experienced childhood trauma, and who had a higher sense of personal meaning or spirituality, would have improved mental health and lower trauma symptoms such as depression, lower self-esteem, anxiety, dissociative disabilities, PTSD, and the like.</p>
<p>Method: 115 participants were randomly selected from five mental health centers in the southeast of the State of Michigan of the United States. Each participant had an experience of one or multiple childhood abuses, namely: physical abuse, sexual abuse, verbal/emotional abuse, child neglect or cumulative trauma. They had also been to treatment, and were between 18 and 60 years old. A demographic questionnaire, Personal Meaning Profile (PMP) and Trauma Symptom Checklist-40 (TSC-40) surveys were used as clinical measures. A multinomial logistic regression statistic was used for data analyses.</p>
<p>Results: Each set of the hypotheses for PMP-and-Group and TSC-40-and-Group models were assessed for their overall significance using chi-square and goodness-of-fit tests, and both were statistically significant (p<0.05) in both tests, respectively.</p>
<p>Conclusion: The results suggest that adults who had experienced childhood trauma, and who had a higher sense of personal meaning or spirituality, would have better mental, physical and general health conditions, and lower trauma symptoms. Many research studies also indicate that this treatment option powerfully restores mental, physical and overall health conditions of the affected adults, and that the cost is usually inexpensive.</p>

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</description>

<author>Chijioke Alphonsus Chigbo</author>


</item>


<item>
<title>The role of cad,flash and fam129b in cancer cell survial and apoptosis</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/428</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/428</guid>
<pubDate>Mon, 07 May 2012 13:47:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Apoptosis is a normal process in the human body. However, apoptosis is desregulated in cancer cells.  Most cancer cells gain resistance to apoptosis, leading to uncontrolled proliferation.  In this dissertation, we identified three proteins, associated with apoptosis pathway. 1) CAD, a large multifunctional complex that is invariably elevated in tumor cells, 2) FLASH, a large protein with multiple growth related functions and 3) FAM129B.  We demonstrate that CAD could interact with FLASH by using yeast two hybrid, co-immunopreciptation and fluorescence microscopy.  In addition, functional analysis using siRNA technology further indicated that CAD could co-operate with FLASH and play roles in multiple cellular processes such as cell mitosis, S phase progression and apoptosis.  Moreover, we identified FAM129B, a newly discovered protein that has been implicated in metastasis of melanoma cells.  My study was focused on identification of this protein in apoptosis pathway. We first demonstrated that this protein is a novel cell cell junction associated protein.  Knockdown of this protein could sensitize cells to apoptotic stimuli and induce rapid apoptosis. Consistent with previous studies, we also provided evidence to show that FAM129B plays important roles in breast cancer metastasis.</p>

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</description>

<author>Song Chen</author>


</item>


<item>
<title>Phylogenetic utility of mitochondrial and nuclear genes: a case study in the diptera (true flies)</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/427</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/427</guid>
<pubDate>Mon, 07 May 2012 13:47:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The value of mitochondrial versus nuclear gene sequence data in phylogenetic analysis has received much attention without yielding definitive conclusions. Theoretical arguments and empirical data suggest a lower phylogenetic utility than equivalent nuclear gene sequences, but there are also many examples of important progress made using mitochondrial sequences. We therefore undertook a systematic performance analysis of mitochondrial and nuclear sequence partitions taken from a representative sample of dipteran species. For phylogenetic tree reconstruction, mitochondrial genes performed generally inferior to nuclear genes. However, the mitochondrial genes resolved branches for which nuclear genes failed.  Moreover, the combined use of mitochondrial and nuclear sequences produced superior results without artifacts for nodes where mitochondrial and nuclear gene data sets on their own generated conflicting topologies.  These findings strongly advocate the inclusion of mitochondrial sequences even in deep phylogeny reconstruction. The comparison of tree support between our and previous analyses identified robustly supported high confidence clades in the Diptera but also a number of problematic groupings in need of further analysis.  For divergence time estimation, we show widespread convergence of clade age estimates from both mitochondrial and nuclear gene sources under a wide variety of data preparation and model paradigms.  Our results indicate slightly superior performance of nuclear gene derived ages for nodes for several clades in the tree ranging in age from approximately 30 to 160 myo.  We further find that third codon position inclusion negatively affects our ability to resolve ages under many circumstances.  Increasing model complexity and granularity of data partitioning offered little benefit in terms of final results while increasing the computational complexity.  Finally, we produce high confidence age estimates for cyclorrhaphan divergences in agreement with previous literature, and provide the first timeline for major divergences within the calyptrate flies.</p>

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</description>

<author>Jason Caravas</author>


</item>


<item>
<title>Polymeric nanocarriers for the regional and systemic delivery of therapeutics to and through the lungs</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/426</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/426</guid>
<pubDate>Mon, 07 May 2012 13:47:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>The lungs are considered as one of the fastest portals of entry to the bloodstream and oral inhalation (OI) has long been accepted as the preferred mode of administration of therapeutics to the respiratory tract.  However, despite its advantages, the lungs have been largely underutilized to target ailments not only of systemic relevance but also several other grave conditions including lung cancer and tuberculosis.  Polymeric nanocarriers (PNCs) have several advantages over other drug delivery vehicles including sustained release of moieties, ease of cellular internalization and improved targeting, and hence hold the promise to greatly augment the potential of OI therapies.  The surface chemistry, architecture, and size of PNCs may be potentially altered in order to modulate their interaction with the extra and intracellular barriers present in the lung epithelia, and thus their transport, overcoming challenges observed when delivering free drug molecules. They can be utilized to enhance the residence time of drugs required to exert prolonged therapeutic effect in the airspace (regional therapy), and conversely speed up the transport of drug molecules that would traverse sluggishly to the bloodstream (systemic therapy).  In this work, we report the preparation, characterization of a series of PNCs ranging from polymeric nanoparticles (PNPs) to surface modified dendrimer nanocarriers (DNCs) and we studied their interaction with in vitro and in vivo models of the lung epithelium.  We observed that transport and cellular uptake can be efficiently modulated as the surface characteristics of the PNCs is varied, suggesting that OI strategies incorporating such nanoscopic entities may potentially be employed for targeting regional diseases and also the systemic circulation.  Finally, we also discuss the formulation, dispersion stability and aerosol characteristics of the aforementioned PNCs in portable, inexpensive pressurized metered dose inhalers (pMDIs).</p>

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</description>

<author>Balaji Bharatwaj</author>


</item>


<item>
<title>Man with Flowers</title>
<link>http://escholar.salve.edu/monumenta-images/1</link>
<guid isPermaLink="true">http://escholar.salve.edu/monumenta-images/1</guid>
<pubDate>Mon, 07 May 2012 13:47:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Polychromed enamel and aluminum, 98.5 x 72 x 48 inches. Featured in Monumenta art exhibit, 1974, where it was installed at Bowen's Wharf. Lent by the Martha Jackson Gallery, New York.</p>
<p><strong>Publisher:</strong> Salve Regina University Archives and Special Collections.</p>
<p><strong>Source:</strong> Digital reproduction of photograph of work of art. Digitization specifications: Adobe Photoshop 7.0, 240 dpi, RGB, 24-bit.</p>
<p><strong>Rights:</strong> This content is provided for educational research and personal use only. While the photographs in this collection are held in the Salve Regina University Archives and Special Collections, copyright for the artwork still resides with the artists.  See <a href="http://library.salve.edu/archives/archives_copyright.html" >http://library.salve.edu/archives/archives_copyright.html</a>.</p>

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</description>

<author>Karel Appel</author>


</item>


<item>
<title>Reliability model for ductile hybrid frp rebar using randomly dispersed chopped fibers</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/425</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/425</guid>
<pubDate>Mon, 07 May 2012 13:47:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>RELIABILITY MODEL FOR DUCTILE HYBRID FRP REBAR USING RANDOMLY DISPERSED CHOPPED FIBERS</p>
<p>Fiber reinforced polymer composites or simply FRP composites have become more attractive to civil engineers in the last two decades due to their unique mechanical properties. However, there are many obstacles such as low elasticity modulus, non-ductile behavior, high cost of the fibers, high manufacturing costs, and absence of rigorous characterization of the uncertainties of the mechanical properties that restrict the use of these composites. However, when FRP composites are used to develop reinforcing rebars in concrete structural members to replace the conventional steel, a huge benefit can be achieved since FRP materials don't corrode.</p>
<p>Two FRP rebar models are proposed that make use of multiple types of fibers to achieve ductility, and chopped fibers are used to reduce the manufacturing costs. In order to reach the most optimum fractional volume of each type of fiber, to minimize the cost of the proposed rebars, and to achieve a safe design by considering uncertainties in the materials and geometry of sections, appropriate material resistance factors have been developed, and a Reliability Based Design Optimization (RBDO), has been conducted for the proposed schemes.</p>

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</description>

<author>Bashar Ramzi Behnam</author>


</item>


<item>
<title>Gene duplication and the evolution of the higher diptera</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/424</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/424</guid>
<pubDate>Mon, 07 May 2012 13:47:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gene duplication is an important source of evolutionary innovation. Using the publicly available genomic information, I studied lineage-specific gene duplications in <i>Drosophila melanogaster</i> (fruit fly), <i>Anopheles gambiae</i> (mosquito), <i>Tribolium castaneum</i> (red flour beetle), and <i>Apis mellifera</i> (honey bee) at three scales: eye-specific genes, developmental genes, and genome-wide. All three studies consistently show that the <i>Drosophila</i> genome contains an exceptionally high number of lineage-specific yet ancient gene duplicates, the majority of which must have originated during the early diversification of the higher Diptera (Brachycera) at least 100 million years ago. Genetic data suggest that gene duplication played an important role in the evolution of visual performance in the fast flying higher Diptera by spatial or intracellular subfunctionalization. Developmental gene duplications, by contrast, in many cases retained overlapping expression patterns and preserved partial to complete redundancy consistent with a role in boosting developmental robustness. Genes involved in metabolic process constantly occupy approximately 50% of all the conserved protein-coding gene families in the insect genomes, both in different species and at various evolutionary time periods, suggesting that the fraction of metabolic genes is maintained over the long term. Further, gene ontology analysis suggests that energy metabolism-related genes are significantly enriched in Brachycera-specific duplicates. My work leads to the conclusion that the early evolution of the higher Diptera was exceptionally impacted by gene duplication. This mutational mechanism apparently fueled the genetic underpinnings of energy metabolism related pathways coinciding with the emergence of the exceptionally fast flight capacities, which characterize most members of the Brachycera clade. I further propose that the retention of duplicated genes spiked during the early diversification of the higher Diptera due to an extended period of effective population size reduction.</p>

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</description>

<author>Riyue Bao</author>


</item>


<item>
<title>Bankruptcy and politics: a framework for bankruptcy policymaking in the united states congress and courts</title>
<link>http://digitalcommons.wayne.edu/oa_dissertations/423</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_dissertations/423</guid>
<pubDate>Mon, 07 May 2012 13:46:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Bankruptcy Abuse Prevention and Consumer Protection Act of 2005 was enacted amid much controversy and was considered by many observers to mark a major change in the direction of U.S. bankruptcy policy.  The dissertation uses the law's passage as a vehicle to develop an explicit model of the integrated role of Congress, issue networks, and the courts in making policy.  Following Baumgartner and Jones (1993), Sabatier (1988), and others, the dissertation tracks bankruptcy policymaking and implementation over a seventy-five year period to demonstrate that policy is made in three distinct venues: Congress; a policy community made up of lawyers, bankruptcy judges, and members of academia; and the courts.  Agenda setting theory explains why policymaking authority shifts between traditionally understood venues like Congress to non-traditional ones like the courts and the policy community. The community monopolized bankruptcy policymaking from the 1930s until the mid-1990s.  Its hold on policymaking was broken when pro-creditor forces successfully characterized proposed reforms as fitting within a broader congressional agenda of retrenchment in social welfare policy in favor of laws promoting particular notions of personal responsibility.</p>
<p>The dissertation identifies the key role of bankruptcy judges in the three-part structure: they make policy not only in their traditional juridical capacities, but also as active entrepreneurs and advocates for legislative reforms as part of the policy community.  The inclusion of courts in the model places the dissertation squarely in the emerging area of interbranch scholarship.  Moreover, it extends existing studies in that field through its application of agenda setting and policy implementation scholarship.  The model suggests the differing policy image increases the likelihood that the new laws will not be faithfully implemented.  The dissertation includes a proposal for testing its hypothesis.</p>

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</description>

<author>Kevin Mandell Ball</author>


</item>


<item>
<title>The Messiah Revealed</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/378</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/378</guid>
<pubDate>Mon, 07 May 2012 13:46:01 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Timothy C. Tennent</author>


</item>


<item>
<title>Influence of Religious Coping on the Substance Use and HIV Risk Behaviors of Recent Latino Immigrants</title>
<link>http://digitalcommons.fiu.edu/etd/603</link>
<guid isPermaLink="true">http://digitalcommons.fiu.edu/etd/603</guid>
<pubDate>Mon, 07 May 2012 13:44:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study examines the influence of acculturative stress on substance use and HIV risk behaviors among recent Latino immigrants. The central hypothesis of the study is that specific religious coping mechanisms influence the relationship that acculturative stress has on the substance use and HIV-risk behaviors of recent Latino immigrants. Within the Latino culture religiosity is a pervasive force, guiding attitudes, behaviors, and even social interactions. When controlling for education and socioeconomic status, Latinos have been found to use religious coping mechanisms more frequently than their Non-Latino White counterparts. In addition, less acculturated Latinos use religious coping strategies more frequently than those with higher levels of acculturation. Given its prominent role in Latino culture, it appears probable that this mechanism may prove to be influential during difficult life transitions, such as those experienced during the immigration process. This study examines the moderating influence of specific religious coping mechanisms on the relationship between acculturative stress and substance use/HIV risk behaviors of recent Latino immigrants. Analyses for the present study were conducted with wave 2 data from an ongoing longitudinal study investigating associations between pre-immigration factors and health behavior trajectories of recent Latino immigrants. Structural equation and zero-inflated Poisson modeling were implemented to test the specified models and examine the nature of the relationship among the variables. Moderating effects were found for negative religious coping. Higher levels of negative religious coping strengthened an inverse relationship between acculturative stress and substance use. Results also indicated direct relationships between religious coping mechanisms and substance use. External and positive religious coping were inversely related to substance use. Negative religious coping was positively related to substance use. This study aims to contribute knowledge of how religious coping influence’s the adaptation process of recent Latino immigrants. Expanding scientific understanding as to the function and effect of these coping mechanisms could lead to enhanced culturally relevant approaches in service delivery among Latino populations. Furthermore this knowledge could inform research about specific cognitions and behaviors that need to be targeted in prevention and treatment programs with this population.</p>

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</description>

<author>Mariana Sanchez</author>


</item>


<item>
<title>VHITS: Vertical Handoff Initiation and Target Selection in a Heterogeneous Wireless Network</title>
<link>http://digitalcommons.fiu.edu/etd/602</link>
<guid isPermaLink="true">http://digitalcommons.fiu.edu/etd/602</guid>
<pubDate>Mon, 07 May 2012 13:43:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Global connectivity, for anyone, at anyplace, at anytime, to provide high-speed, high-quality, and reliable communication channels for mobile devices, is now becoming a reality. The credit mainly goes to the recent technological advances in wireless communications comprised of a wide range of technologies, services, and applications to fulfill the particular needs of end-users in different deployment scenarios (Wi-Fi, WiMAX, and 3G/4G cellular systems). In such a heterogeneous wireless environment, one of the key ingredients to provide efficient ubiquitous computing with guaranteed quality and continuity of service is the design of intelligent handoff algorithms.</p>
<p>Traditional single-metric handoff decision algorithms, such as Received Signal Strength (RSS) based, are not efficient and intelligent enough to minimize the number of unnecessary handoffs, decision delays, and call-dropping and/or blocking probabilities.</p>
<p>This research presented a novel approach for the design and implementation of a multi-criteria vertical handoff algorithm for heterogeneous wireless networks. Several parallel Fuzzy Logic Controllers were utilized in combination with different types of ranking algorithms and metric weighting schemes to implement two major modules: the first module estimated the necessity of handoff, and the other module was developed to select the best network as the target of handoff.</p>
<p>Simulations based on different traffic classes, utilizing various types of wireless networks were carried out by implementing a wireless test-bed inspired by the concept of Rudimentary Network Emulator (RUNE).</p>
<p>Simulation results indicated that the proposed scheme provided better performance in terms of minimizing the unnecessary handoffs, call dropping, and call blocking and handoff blocking probabilities. When subjected to Conversational traffic and compared against the RSS-based reference algorithm, the proposed scheme, utilizing the FTOPSIS ranking algorithm, was able to reduce the average outage probability of MSs moving with high speeds by 17%, new call blocking probability by 22%, the handoff blocking probability by 16%, and the average handoff rate by 40%. The significant reduction in the resulted handoff rate provides MS with efficient power consumption, and more available battery life. These percentages indicated a higher probability of guaranteed session continuity and quality of the currently utilized service, resulting in higher user satisfaction levels.</p>

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</description>

<author>Faisal Kaleem</author>


</item>


<item>
<title>History Education and the Construction of National Identity in Iran</title>
<link>http://digitalcommons.fiu.edu/etd/601</link>
<guid isPermaLink="true">http://digitalcommons.fiu.edu/etd/601</guid>
<pubDate>Mon, 07 May 2012 13:43:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study examined the representation of national and religious dimensions of Iranian history and identity in Iranian middle school history textbooks. Furthermore, through a qualitative case study in a school in the capital city of Tehran, teachers’ use of textbooks in classrooms, students’ response, their perceptions of the country’s past, and their definitions of national identity is studied. The study follows a critical discourse analysis framework by focusing on the subjectivity of the text and examining how specific concepts, in this case collective identities, are constructed through historical narratives and how social actors, in this case students, interact with , and make sense of, the process. My definition of national identity is based on the ethnosymbolism paradigm (Smith, 2003) that accommodates both pre-modern cultural roots of a nation and the development and trajectory of modern political institutions.</p>
<p>Two qualitative approaches of discourse analysis and case study were employed. The textbooks selected were those published by the Ministry of Education; universally used in all middle schools across the country in 2009. The case study was conducted in a girls’ school in Tehran. The students who participated in the study were ninth grade students who were in their first year of high school and had just finished a complete course of Iranian history in middle school. Observations were done in history classes in all three grades of the middle school.</p>
<p>The study findings show that textbooks present a generally negative discourse of Iran’s long history as being dominated by foreign invasions and incompetent kings. At the same time, the role of Islam and Muslim clergy gradually elevates in salvaging the country from its despair throughout history, becomes prominent in modern times, and finally culminates in the Islamic Revolution as the ultimate point of victory for the Iranian people. Throughout this representation, Islam becomes increasingly dominant in the textbooks’ narrative of Iranian identity and by the time of the Islamic Revolution morphs into its single most prominent element. On the other hand, the students have created their own image of Iran’s history and Iranian identity that diverges from that of the textbooks especially in their recollection of modern times. They have internalized the generally negative narrative of textbooks, but have not accepted the positive role of Islam and Muslim clergy. Their notion of Iranian identity is dominated by feelings of defeat and failure, anecdotal elements of pride in the very ancient history, and a sense of passivity and helplessness.</p>

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</description>

<author>Maryam Soltan Zadeh</author>


</item>


<item>
<title>Global scale climate–crop yield
relationships and the impacts of recent
warming</title>
<link>http://digitalcommons.unl.edu/publichealthresources/152</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/152</guid>
<pubDate>Mon, 07 May 2012 13:39:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Changes in the global production of major crops are important drivers of food prices, food security and land use decisions. Average global yields for these commodities are determined by the performance of crops in millions of fields distributed across a range of management, soil and climate regimes. Despite the complexity of global food supply, here we show that simple measures of growing season temperatures and precipitation—spatial averages based on the locations of each crop—explain ∼30% or more of year-to-year variations in global average yields for the world’s six most widely grown crops. For wheat, maize and barley, there is a clearly negative response of global yields to increased temperatures. Based on these sensitivities and observed climate trends, we estimate that warming since 1981 has resulted in annual combined losses of these three crops representing roughly 40 Mt or $5 billion per year, as of 2002. While these impacts are small relative to the technological yield gains over the same period, the results demonstrate already occurring negative impacts of climate trends on crop yields at the global scale.</p>

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</description>

<author>David Lobell et al.</author>


</item>


<item>
<title>Cleveland, Ohio</title>
<link>http://engagedscholarship.csuohio.edu/scholbks/130</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/scholbks/130</guid>
<pubDate>Mon, 07 May 2012 13:37:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Featuring over 200 striking photographs from the 1920s through 1980,  Black America: Cleveland, Ohio celebrates the rich history of this great  city's African-American community. Its neighborhoods, churches, civil,  religious, business and cultural leaders, musical icons, and sports  heroes are all brought to life here through the archives of local  newspapers and historical societies, as well as the private collections  of many Cleveland residents.</p>

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</description>

<author>Regennia N. Williams</author>


</item>


<item>
<title>A brief content analysis of attachment and sexual relationships in sex therapy and research journals</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1283</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1283</guid>
<pubDate>Mon, 07 May 2012 13:37:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>A surge of scholarly publications on attachment within couple relationships prompted this content analysis of attachment articles published in six sex therapy and sex research journals. This study investigates the extent to which these journals attend to attachment in the context of adult sexual relationships. The researcher found 2257 articles published within these journals; 64 of which attend to attachment and 9 of which attend to attachment and sex. Implications for couples therapy in the field of sex therapy and future directions are discussed.</p>

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</description>

<author>Kathryn Zambrano Devis</author>


</item>


<item>
<title>A comparative study of indicator bacteria present in ice and soda from Las Vegas food establishments</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1282</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1282</guid>
<pubDate>Mon, 07 May 2012 13:37:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Microbial analysis has long been used as an indicator of water quality. Since the passing of the Safe Drinking Water Act in 1974, microbial standards have been strictly set by the Environmental Protection Agency (EPA) to ensure that the public health is protected from bacterial pathogens. The bacteriological quality of water generally deteriorates as it travels from water treatment facilities through the main distribution system and into private plumbing and distribution systems. For example, Heterotrophic Plate Count (HPC) values typically increase once the water has entered plumbing devices such as beverage vending machines. Upon reaching a private facility, the opportunity for bacterial growth and human contamination is present.</p>
<p>In this study used the EPA water quality standards were used as a reference to analyze ice and soda samples collected from local food establishments for the presence of heterotrophic and coliform bacteria. The samples were evaluated with respect to the U.S. drinking water standards as indicators of the quality of the ice and soda. The study provided important information regarding the quality of the ice and soda dispensed in Las Vegas food establishments. Of the samples analyzed in this study, 33.3% of ice samples and 55.6% of soda samples exceeded the EPA limits set for heterotrophic bacteria concentration for drinking water. Of the ice samples collected, 72.2% were positive for presumptive coliform bacteria presence, and 88.9% of the soda samples were positive for presumptive coliform presence. No statistical significance was observed between the concentration of heterotrophic bacteria in ice samples (median = 202 CFU/ml) and soda samples (median = 775 CFU/ml). However, the presumptive coliform bacteria data did show that the soda samples (median = 139 CFU/ml) had a significantly higher concentration when compared to the ice samples (median = 3 CFU/ml). The type of food establishment from which the samples were collected did not have a significant influence on the bacteriological quality of the ice and soda. The findings of this study provide important evidence that could have public health implications and may influence future studies related to bacterial contamination of beverages sold in the Las Vegas Valley.</p>

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</description>

<author>Kimberly Jo Hertin</author>


</item>


<item>
<title>Analysis of the morbidity and mortality of severe influenza infection in Clark County, Nevada for the 2010--2011 influenza season</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1281</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1281</guid>
<pubDate>Mon, 07 May 2012 13:37:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Influenza circulates in the community in a fairly predictable manner each year; however, throughout the duration of any influenza season, influenza strains have the ability to evolve through antigenic mutations, viral reassortment, development of anti-viral resistance, and alterations in virulence. These changes are likely to cause illness among the unimmunized and can result in severe illness or death. Therefore, it is especially important to closely monitor severe influenza-associated hospitalizations and deaths. The University of Nevada, Las Vegas in collaboration with the Southern Nevada Health District (SNHD), Office of Epidemiology (OOE) analyzed data from the severe hospitalized influenza morbidity and mortality surveillance project for all residents of Clark County from October 1, 2010 through May 31, 2011. These data were analyzed using a descriptive approach to illustrate the epidemiology of severe influenza-associated hospitalizations and deaths, and an analytical approach to identify any associations between the variables of interest and the incidence of severe influenza-associated deaths. Among the study population (N= 158), the influenza strain type was found to be significantly associated with deaths (n= 25). Of the 36 cases diagnosed with influenza A (H1N1), 30.6% resulted in death; patients diagnosed with influenza B demonstrated a similar proportion of deaths at 29.6%; and influenza A (no subtype) was the most commonly diagnosed influenza strain (n= 94) in Clark County, but it had the lowest proportion of deaths at 6.4%. Vaccine status was not found to be significantly associated with death among hospitalized patients. The majority of deaths (n= 14) had an unknown vaccine status; therefore, these results are inconclusive. The length of stay distribution for influenza-associated hospitalizations and deaths was non-normal because the majority of patients (70.4%) were admitted for ≤ 7 days. Transformed data showed that there was no statistically significant difference in the mean length of stay based on the influenza strain type. It is expected that the results of this study will help inform policy makers, hospitals, public health agencies, and other community partners in Clark County of the impact of influenza-associated hospitalizations and deaths.</p>

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</description>

<author>Kindra Maureen St. Jacques</author>


</item>


<item>
<title>Bacterial adherence of Streptococcus mutans and Lactobacillus acidophilus on poly-methyl methacrylate and thermoplastic polypropene used in orthodontic retention</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1280</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1280</guid>
<pubDate>Mon, 07 May 2012 13:37:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>Retention is required in the majority of orthodontic patients throughout the remainder of their life. The two primary removable appliances are known as the traditional Hawley retainer or the vacuum formed retainer. These appliances were developed to maintain the position of the dentition without sacrificing oral health. The orthodontic population is at a higher risk for caries due to plaque accumulation from poor diet, suboptimal oral hygiene and often lack of motivation. These two retainers occupy different niches and are comprised of different materials; therefore the retainers' effect on oral health could be very different. An understanding of which bacteria and to what extent the bacteria adhere to these two retention appliance materials could ultimately provide clinicians with another factor to consider when choosing a specific retainer.</p>
<p>Two common caries bacteria, <em>Streptococcus mutans</em> and <em> Lactobacillus acidophilus</em> , were chosen to study their adherence properties on two common retention materials; polymethyl methacrylate in the traditional Hawley retainer and a thermoplastic polymer made of polypropene in the vacuum formed retainer. Bacterial adhesion tests on both materials were run either with or without prior coating in saliva and the number of adhered bacteria was determined by both directly counting colony-forming units of bacteria swabbed from the materials and by inference from total metabolic activity of the adhered bacteria as determined by incubation with the tetrazolium dye,sodium2,3,-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino)-carbonyl]-2H-tetrazolium inner salt)(XTT) reagent.</p>
<p>Culture analysis from adhesion testing determined through colony forming units, showed an increased adherence of both bacteria to polymethyl methacrylate compared to Polypropene. This was reflected in a 3-fold increase for <em> Lactobacillus acidophilus</em> and 7-fold increase for <em>Streptococcus mutans</em> on the polymethyl methacrylate. Bacterial adhesion testing performed using the metabolic XTT proliferation assay also demonstrated increased adhesion on polymethyl methacrylate. Bacterial adhesion to polypropene was decreased by 30% for <em>Lactobacillus acidophilus</em> and 27% for <em> Streptococcus mutans</em> compared to polymethyl methacrylate. XTT assay also indicated that prior coating of materials to saliva had little effect on the extent of bacterial adhesion.</p>
<p>In conclusion, bacterial adherence is increased for polymethyl methacrylate when compared to polypropene, regardless of the assay technique used to determine the number of adhered bacteria. Further research needs to be conducted to determine if increased adherence to polymethyl methacrylate is significant enough to influence choices for orthodontic retention.</p>

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</description>

<author>Lindsay Ann Pfepper</author>


</item>


<item>
<title>Association between childhood demographics and blood lead screening---Nevada Kindergarten Health Survey 2010</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1279</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1279</guid>
<pubDate>Mon, 07 May 2012 13:37:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lead, as a toxic substance, invades the human body, and gradually damages the organs. Oftentimes, elevated blood lead levels are not recognized until serious health issues are found. In the United States, approximately 250,000 children aged 1-5 years have elevated blood lead levels greater than 10 micrograms of lead per deciliter of blood (Centers for Disease Control and Prevention, 2004).</p>
<p>However, there is no effective treatment for lead poisoning. Chelation can merely decrease the blood lead levels but cannot reverse the existing damage. To prevent and control childhood lead poisoning, many studies have been conducted to investigate the sources of lead and analyze effective prevention strategies. Blood lead screening tests, as preventive methods for childhood lead poisoning, have been implemented by several states for years. However, some still question the effectiveness of blood lead screening tests, and the cost of these tests creates another barrier. These factors largely hinder the progress of eliminating childhood lead poisoning. To institute blood lead screening tests among different populations, some crucial factors must be considered, such as the children's demographic information and the barriers of accessing health care.</p>
<p>The data used in this study was provided by the Nevada Kindergarten Health Survey conducted in 2010. This study aims to analyze the association between the likelihood of obtaining blood lead screening tests and childhood demographic characteristics, namely annual household income, race/ethnicity, home zip code, and barriers to accessing to healthcare. The study results signal the barriers for children's blood lead screening tests and provide recommendations for public health professionals and policy makers to implement effective preventive methods for childhood lead poisoning.</p>

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</description>

<author>Lina Zhang</author>


</item>


<item>
<title>Gingival crevicular fluid (GCF) levels of interleukin-6 (IL-6), soluble glycoprotein 130 (sgp130), and soluble interleukin-6 receptor (sIL-6R) during orthodontic tooth movement</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1278</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1278</guid>
<pubDate>Mon, 07 May 2012 13:37:09 PDT</pubDate>
<description>
	<![CDATA[
	<p><em>Introduction</em> . Orthodontic tooth movement requires the precise coordination of a multitude of biological factors in order for proper bone remodeling to occur. Cytokines, such as Interleukin-6 (IL-6), play a critical role in the communication necessary for both bone resorption and bone apposition. IL-6 reacts with receptor proteins, such as soluble IL-6 receptor (sIL-6R), on target cells in order to transmit signals important to both osteoclast and osteoblast activities. Soluble glycoprotein 130 (sgp130), on the other hand, acts as a natural inhibitor to IL-6 activity. The purpose of this investigation was to evaluate the levels of IL-6, sIL-6R, and sgp130 in the gingival crevicular fluid (GCF) of human teeth undergoing orthodontic forces on both the tension and compression sides in the initial stages of orthodontic tooth movement. <em>Methods</em> . GCF samples were obtained from 9 healthy orthodontic patients [5 males, 4 females, age range 11 to 31 years (mean 17.445 years)] just prior to initial wire placement (0.012 or 0.014 Nickel Titanium archwire) with fixed orthodontic appliances. GCF samples were then collected 1, 6, and 24 hours after orthodontic force application. Patients returned in 5-7 weeks for a 2 <sup>nd</sup> visit and orthodontic re-activation. GCF samples were again collected immediately before orthodontic activation, as well as 1, 6, and 24 hours after force application. Sampling sites included the mesiobuccal and distolingual of an experimental tooth, as well as the mesiobuccal of a control. GCF volumes were assessed with a Periotron 6000 (OraFlow, Smithtown, New York), while a Bradford assay was performed to obtain protein levels. Processing was carried out with a multiplex bead-based Luminex assay to detect IL-6, sgp130, and sIL-6R levels in the GCF samples. <em>Results</em> . GCF volumes were significantly higher in the experimental samples at both the initial (p=0.009) and recall visits (p=0.055). The greatest difference between GCF volumes for the experimental and control sites was after 6 hours of orthodontic activation (p=0.02). Relative to the control site, GCF IL-6 levels were significantly elevated for the mesiobuccal experimental site at 6 (p=0.001) and 24 hours (p=0.004) post-activation, whereas the IL-6 levels for the distobuccal experimental site were only elevated at 24 hours post-activation (p=0.034). GCF sgp130 levels were elevated for the mesiobuccal experimental site at 1, 6, and 24 hours post-activation relative to both the distobuccal experimental site (p=0.005, p=0.012, p=0.001) and the control site (p=0.005, p=0.001, p=0.000). Similarly, GCF sIL-6R levels were also elevated for the mesiobuccal experimental site at 1, 6, and 24 hours post-activation relative to both the distobuccal experimental site (p=0.035, p=0.029, p=0.001) and the control site (p=0.037, p=0.006, p=0.006). <em> Conclusions</em> . GCF volumes increase in a time-dependent fashion after orthodontic forces are applied to a tooth. Meanwhile, IL-6 levels in the GCF of orthodontically treated teeth increase earlier than previously reported. In the present study, IL-6 levels peaked at approximately 6 hours post-activation. Additionally, sgp130 and sIL-6R levels in the GCF are elevated throughout the first 24-hour post-activation period in orthodontic tooth movement. While there was a definitive difference in protein levels between opposing sides of the experimental teeth, further research is needed to differentiate the levels of IL-6, sgp130, and sIL-6R on the compression and tension sides during orthodontic tooth movement.</p>

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</description>

<author>Mathue Gene Faulkner</author>


</item>


<item>
<title>Impact of home hospital program on empowerment and professional practice behaviors</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1277</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1277</guid>
<pubDate>Mon, 07 May 2012 13:37:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to evaluate the impact of a Home Hospital Clinical Placement program on professional behaviors of nursing staff within the Home Hospital and professional behaviors of baccalaureate nursing students enrolled in the Home Hospital Clinical Placement program. The study used a conceptual model developed and tested by Manojlovich (2003).</p>
<p>The study was a non-experimental, cross-sectional design to compare selected attributes between students enrolled in a Home Hospital Clinical Placement and students enrolled in a traditional clinical placement and between registered nurses with high levels of teaching interaction with home hospital students and registered nurses with low levels of teaching interaction with home hospital students. The specific attributes were those included in the Manojlovich model (2003) depicting the relationships among structural empowerment, self-efficacy, and professional behaviors.</p>
<p>There were no significant differences noted in overall structural empowerment ratings between home hospital and non-home hospital students. However, there was a significant difference in one structural empowerment subscale. Home hospital students reported higher ratings of formal and informal power. There were no significant differences between home hospital and non-home hospital students in ratings of self-efficacy, professional autonomy, and observed leadership behaviors of clinical faculty. Additionally, no significant differences were noted between home hospital students and non-home hospital students when controlling for clinical level.</p>
<p>In the registered nurse (RN) sample, there was no significant difference noted in overall structural empowerment between nurses with high levels of teaching interaction and nurses with low levels of teaching interaction. However, there was a significant difference on one structural empowerment subscale of opportunity. Registered nurses with a high level of teaching interaction reported higher ratings of access to opportunity. There were no significant differences noted within the registered nurse sample in ratings of self-efficacy and professional autonomy based on level of teaching interaction. There was a significant difference in one subscale of observed leadership behaviors, Challenge the Process. Registered nurses with a high level of teaching interaction reported higher ratings of observed clinical faculty leadership behaviors on the subscale.</p>
<p>In both samples, nursing student and registered nurse, a significant positive relationship was noted between structural empowerment and professional practice behaviors and structural empowerment and observed clinical faculty leadership behaviors. In the nursing student sample, a significant positive relationship was also noted between structural empowerment and ratings of self-efficacy. In both samples there was a significant positive relationship between professional practice behaviors and self-efficacy. In the RN sample, there was a significant positive relationship between professional practice behaviors and observed clinical faculty leadership. In the nursing student sample there was a significant positive relationship noted between observed faculty leadership and self-efficacy.</p>
<p>The relationship among the study attributes of structural empowerment, selfefficacy, and professional behaviors confirmed previous findings (Manojlovich, 2003). In this study, a significant positive relationship was noted in the nursing student sample between observed faculty leadership and self-efficacy. This finding has not been previously reported. Additionally, in the registered nurse sample, the significant positive relationship between clinical faculty leadership behaviors and professional practice behaviors has not been previously reported.</p>
<p>In conclusion, this study revealed that the home hospital model can be an effective intervention to provide clinical instruction for nursing students. These findings demonstrated that a non-traditional approach to employing clinical faculty can be effective. Additionally, the findings of this study expand knowledge on unique characteristics of the work environment that impact the quality of a registered nurse's professional life. High levels of teaching interaction were significantly related to increased ratings of structural empowerment as it related to access to opportunity. Ratings of faculty leadership were noted to have a positive relationship to professional practice behaviors of registered nurses. This supports the premise that clinical placement models should not only be evaluated for their impact on students but also the impact on the practice environment.</p>

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</description>

<author>Marcille Jo Jorgenson</author>


</item>


<item>
<title>Evaluation of the pilot program, Pediatric Early Warning Sentinel Surveillance Program (PEWSS), and its efficacy in monitoring pediatric illness in Clark County, Nevada</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1276</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1276</guid>
<pubDate>Mon, 07 May 2012 13:36:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>The influenza outbreak that occurred during 2009 stimulated the formation of several surveillance programs throughout the country. The majority monitor only influenza; however, there are several other circulating respiratory pathogens, especially within the pediatric community. These other respiratory pathogens cause a variety of illnesses, such as bronchitis, pneumonia, croup, etc. Prior research has provided the medical community with valuable information about respiratory illnesses, especially those which afflict pediatric patients. Areas of knowledge including seasonality, demographics, signs and symptoms, prevention measures, and pathogenicity, have been greatly expanded over the years. This information has been of tremendous help to the medical community in identifying respiratory illness. Coupled with surveillance, this can further help to expand the knowledge of illnesses that are circulating, especially for local public health communities.</p>
<p>In May 2009, the Southern Nevada Health District (SNHD) and the Southern Nevada Public Health Laboratory (SNPHL) collaborated to create a new pilot surveillance program, the Enhanced Pediatric Influenza Surveillance project (EPIS). It began like most others and monitored only influenza. Evolution of the program took place and ultimately developed into a more enhanced monitoring program, the Pediatric Early Warning Sentinel Surveillance program (PEWSS). This became a one of a kind program that went above and beyond traditional surveillance, to include more than just the reportable respiratory pathogens. The objective of the PEWSS program is to relay the knowledge of circulating viruses to the community to increase public health awareness and prevention, along with developing seasonal baselines for each virus.</p>
<p>Once a public health program is in place, an evaluation should be conducted to determine the efficacy and usefulness of the system. Evaluations can help streamline the goals and objectives, along with improving the manner in which the program operates. In July 2001, the CDC published guidelines that are used as the basis to evaluate any public health surveillance system. These CDC guidelines were the foundation for the evaluation of the PEWSS program.</p>
<p>The goal of this project was to evaluate the efficiency and effectiveness of the PEWSS program by determining the strengths and weaknesses of the program. In addition, an analysis of the data already collected by the EPIS and PEWSS programs was performed. The PEWSS data were compared to similar local and national data sources. Comparison of data between the PEWSS program and the outside sources showed similar seasons among the different respiratory pathogens, which substantiated the effectiveness of the program. The conclusion of the evaluation and data analysis showed that the PEWSS program is an efficient and effective system that can monitor respiratory illness, and trends, and also provide pertinent circulating respiratory pathogen information to the community.</p>

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</description>

<author>Michelle Lee Lutman</author>


</item>


<item>
<title>A diffusion tensor imaging software comparison and between control subjects and subjects with known anatomical diagnosis</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1275</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1275</guid>
<pubDate>Mon, 07 May 2012 13:36:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Diffusion weighted imaging (DWI) is a magnetic resonance imaging (MRI) method that produces in vivo images of biological tissues weighted with the local micro-structural characteristics of water diffusion. Diffusion tensor imaging (DTI), a form of DWI, is useful when a tissue, such as the neural axons of white matter in the brain, has an internal fibrous structure that allows water to diffuse more rapidly in alignment with the fibers. Changes in the water diffusion pattern indicate changes in the fiber structure which can result from damage to the fibers. Measurements of the water diffusion patterns include overall diffusivity, Apparent Diffusion Coefficient (ADC), and the linear component of the ADC known as the Fractional Anisotropy (FA). The purpose of this study is three fold: (1) to evaluate the reproducibility of ADC and FA values obtained from the same dataset between two Diffusion Tensor Imaging analysis software packages (Analyze 10.0 and Philips PRIDE), (2) to use the results of the Analyze 10.0 software analysis to characterize the corpus callosum (CC) and anatomical regions of the CC from a dataset of control subjects with no known anatomical abnormalities obtained via 3.0 Tesla (3T) MRI, and (3) to identify and characterize patterns present in ADC and FA values of subjects with known anatomical abnormalities by comparing the results to the control datasets. In this DTI software analysis study, Analyze 10.0 produced significantly different results for mean ADC and mean FA when compared to the PRIDE software package. Pearson correlation values show that Analyze 10.0 provides reliably similar mean ADC and mean FA values. Regardless of the software package, gender and age of the subjects did not provide significantly different values for mean ADC and mean FA. Using results from Analyze 10.0 on the control group, provides a baseline of comparison for subjects with CO, MS, or TBI diagnosis. Comparisons of seven anatomical and physiological regions of the CC between control and non-control subjects show that medial regions of the CC (AMB, PMB, Isthmus 1 and Isthmus 2) are most likely to show significant differences in mean ADC and FA; while the genu and splenium regions are less likely to show significant differences.</p>

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</description>

<author>Michael C. Moore</author>


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<item>
<title>Analysis of 200 food items for benzo[a]pyrene and
estimation of its intake ίη an epidemiologic study</title>
<link>http://digitalcommons.unl.edu/publichealthresources/151</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/151</guid>
<pubDate>Mon, 07 May 2012 13:36:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Animal stιιdies have shown that dietary intake of benzo[α]pyrene (BaP), a polycyclic aromatic hydrocarbon (ΡΑΗ), causes increased levels of tumors at several sites, particιιlarly ίη the upper gastrointestinal tract. However, the role of dietary intake of BaP and cancer ίη humans is not clear. We CIeated a BaP database of selected food products that could be lίnl(ed to Food Frequency Qnestionnaires (FFQs) to estimate BaP intake. BaP levels were measnred for each food line-item (composite samples) which consisted of a variety of foods ίη a FFQ. Composite sample parts were derived from the Second National Health and Nutrition Examination Survey (NHANES II) which represents the most common food items consumed by the general popιιlation. Meat samples were cooked by different techniqnes ίn controlled conditions, and by varions restanrants and fast-food chains. Non-meat products were purchased from the major national supermarket chains. The qnantities of BaP were measnred using a thin-layer chromatography (TLC)/spectrofluorometer technique and were highly coaelated with both BaP (radius = 0.99) and sum of carcinogenic ΡΑΗ (<em>r</em>=0.98) measured by HPLC technique. We linked our database to the results from a FFQ and estimated the daily BaP intake of various foods is 228 subjects ίn the Washington, DC metropolitan area. The highest levels of BaP (up to abont 4ng BaP/g of cooked meat) were found in grilled/barbecued very well done steaks and hamburgers and in grilled/barbecued well done chicken with skin. BaP concentrations were lower in meats that were grilled/barbecued to medium done and ίη all broiled or pan-fried meat samples regardless of doneness level. The BaP levels in non-meat items were generally low. However, certain cereals and greens (e.g. kale, collard greens) had levels up to 0.5 ng/g. In our population, the bread/cereal/grain, and grilled/barbecued meat, respectively, contributed 29 and 21 Ρeιτent to the mean daily intal(e of BaP. This database may be helpful in initial attempts to assess dietary BaP exposures ίn stιιdies of cancer etiology.</p>

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</description>

<author>Ν. Kazerouni et al.</author>


</item>


<item>
<title>The role of metrical structure in tonal knowledge acquisition</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1274</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1274</guid>
<pubDate>Mon, 07 May 2012 13:36:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Experienced listeners possess a working knowledge of pitch structure in Western music, such as scale, key, harmony, and tonality, which develops gradually throughout childhood. It is commonly assumed that tonal representations are acquired through exposure to the statistics of music, but few studies have investigated potential learning mechanisms directly. In Western tonal music, tonally stable pitches not only have a higher overall frequency of occurrence, but they may occur more frequently at strong than weak metrical positions, providing two potential avenues for tonal learning. Two experiments employed an artificial grammar learning paradigm to examine tonal learning mechanisms. During a familiarization phase, we exposed nonmusician adult listeners to a long (whole tone scale) sequence with certain distributional properties. In a subsequent test phase we examined listeners' learning using grammaticality or probe tone judgments. In the grammaticality task, participants indicated which of two short test sequences conformed to the familiarization sequence. In the probe tone task, participants provided fit ratings for individual probe tones following short "reminder" sequences. Experiment 1 examined learning from overall frequency of occurrence. Grammaticality judgments were significantly above chance (Exp. 1a), and probe tone ratings were predicted by frequency of occurrence (Exp. 1b). In Experiment 2 we presented a familiarization sequence containing one sub-set of pitches that occurred more frequently on strong than on weak metrical positions and another sub-set that did the opposite. Overall frequency of occurrence was balanced between both sub-sets. Grammaticality judgments were again above chance (Exp. 2a) and probe tone ratings were higher for pitches occurring on strong metrical positions (Exp. 2b). These findings implicate metrical structure in tonal knowledge acquisition.</p>

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</description>

<author>Matthew Rosenthal</author>


</item>


<item>
<title>Adolphe Nourrit, Gilbert Duprez, and the high C: The influences of operatic plots, culture, language, theater design, and growth of orchestral forces on the development of the operatic tenor vocal production</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1273</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1273</guid>
<pubDate>Mon, 07 May 2012 13:36:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>The operatic tenor voice has evolved from a variety of influences. This document identifies four influences involved in the development of the operatic tenor voice and describes their impact on performance practices including the chest voice high C (C5). Modern tenors’ performance practices originate in the nineteenth century ascendance of an Italian singing technique. This particular singing technique achieved popularity when Gilbert Duprez sang the role of Arnold in Rossini’s Guillaume Tell with a do di petto (i.e. from-the-chest) production of sound rather than the mix of falsetto and head voice that was traditional at the time. The role of Arnold was written for this type of vocal production and was traditional at the time. It was in this role in which the performance of the aria “Asil héréditaire” that Duprez sang the first do di petto C5 as was noted by critics. This feat shocked and impressed the Parisian public (who were predisposed to view Duprez unfavorably), which then thunderously applauded their approval of Duprez’ performance.</p>
<p>In 1837, after a combined ten years in Italy among Italian singers, Duprez performed for the Parisian public, his do di petto high C. The ability and skill to perform iv this well grew to be an in indicator of consummate vocal ability among tenors.</p>
<p>When Duprez performed the first do di petto high C, he created a shift in vocal technique and tenor performance practice. Italy and France were the dominant cultures in opera at this time. The two aforementioned cultures valued different qualities in vocal performance. The French culture of restrained passion highlighted the already singing quality of the language itself. According to Richard Miller, sung French corresponded to the spoken French more than any other European language. This necessary equivalence of spoken and sung French tended to limit its musical expressivity. This limitation had effects on the vocal technique of the tenor, which as a result tended to favor a traditional head voice and falsetto mix that had its origins in the vocal technique and acoustic properties of the castrato. The Italian culture, on the other hand, valued a more fiery and passionate approach to unleashing the power of an operatic performance and the expressive power of the voice. For the Italians, the sound of the voice should come first in importance while the declamation of the language should come second in importance. Miller observed that this was due in large part to the relative simplicity of the Italian language that is centered on pure vowels as compared to the French language, which is centered on a balance of nasal vowels and soft consonants.</p>
<p>The approach this document takes in discussion of these influences on the changes in technique and performance practices of the tenor is one that looks through the lens of the culturally emblematic lives of two of the most famous French tenors of the early nineteenth century: Adolphe Nourrit (1802–39) and Gilbert Duprez (1806–96). Both were involved in this sensational and decisive event: Duprez’ debut at the Paris Opéra as Arnold in Rossini’ Guillaume Tell, in which he sang most, if not all of the notes v above A4 in a full voiced—from the chest—production of sound. This event and Nourrit’s distaste for and inability to accept any comparison or competition between the two tenors led him to attempt the same journey to Italy in hopes of acquiring the technique that gave Duprez his success. Unfortunately, Nourrit’s attempt at acquiring an Italian technique was mostly unsuccessful. In order to gain facility in the technique embodied by Duprez he lost the French singing skills that were the keys to his fame and success. His subsequent failure to acquire an Italian technique of singing left him without a musical home. This along with chronic illness drove him mad to the point where he took his life at the age of thirty-seven. However, the question remains, why was Nourrit unable to find a suitable teacher in France to help him discover the do di petto vocal technique, which appeared to be such a success for Duprez?</p>
<p>There has been little research done to determine the influences on the change in vocal technique, performance practice, and audience expectations of what created this masculine tenor sound. John Potter’s Tenor: History of a Voice speaks in general terms of the history of the tenor voice. He notes changes and contemporaneous states of tenor vocal production and differences in timbre, but does not identify the causes for the changes. There are a small number of doctoral dissertations and documents that tangibly addresses this evolution in performance practice, but do not identify the reasons and causes for the change. Therefore, this document proposes answers to the following questions: was the adoption of Italian vocal technique (that remains the standard today) a result of the necessities of physical and vocal demands of the tenor roles and repertoire being composed over time? Was it a result of changes in audience tastes for a natural tenor sound to embody the heroic roles? Did the interaction of the French and Italian vi language and culture play a part in this technical change? Could it simply have resulted from advances in vocal technique and pedagogical expertise that occurred as a result of a more scientific approach to vocal technique in the early nineteenth century? Finally, were there economic concerns that influenced choices in the design of operatic venues resulting in acoustical adversity for the tenor? And consequently, did the diverse acoustic qualities of theaters—notably in France and Italy— affect the tenor vocal production. I propose that it was a combination of all of these factors.</p>

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</description>

<author>Michael Lee Smith Jr.</author>


</item>


<item>
<title>Being outside learning about science is amazing: A mixed methods study</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1272</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1272</guid>
<pubDate>Mon, 07 May 2012 13:36:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study used a convergent parallel mixed methods design to examine teachers' environmental attitudes and concerns about an outdoor educational field trip. Converging both quantitative data (Environmental Attitudes Scale and teacher demographics) and qualitative data (Open-Ended Statements of Concern and interviews) facilitated interpretation. Research has shown that adults' attitudes toward the environment strongly influence children's attitudes regarding the environment. Science teachers' attitudes toward nature and attitudes toward children's field experiences influence the number and types of field trips teachers take. Measuring teacher attitudes is a way to assess teacher beliefs.</p>
<p>The one day outdoor field trip had significant outcomes for teachers. Quantitative results showed that practicing teachers' environmental attitudes changed following the Forever Earth outdoor field trip intervention. Teacher demographics showed no significance. Interviews provided a more in-depth understanding of teachers' perspectives relating to the field trip and environmental education. Four major themes emerged from the interviews: 1) environmental attitudes, 2) field trip program, 3) integrating environmental education, and 4) concerns. Teachers' major concern, addressed prior to the field trip through the Open-Ended Statements of Concern, was focused on students (i.e., behavior, safety, content knowledge) and was alleviated following the field trip. Interpretation of the results from integrating the quantitative and qualitative results shows that teachers' personal and professional attitudes toward the environment influence their decision to integrate environmental education in classroom instruction.</p>
<p>Since the Forever Earth field trip had a positive influence on teachers' environmental attitudes, further research is suggested to observe if teachers integrate environmental education in the classroom to reach the overall goal of increasing environmental literacy.</p>

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</description>

<author>Michelle L. Weibel</author>


</item>


<item>
<title>The long-term impact of a loyalty program: An evaluation from a Las Vegas casino hotel</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1271</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1271</guid>
<pubDate>Mon, 07 May 2012 13:36:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Loyalty programs are popular marketing strategies intended to attract, maintain, and enhance customer relationships. Despite the widespread usage of loyalty programs across various businesses, its effectiveness has not been well validated. Few empirical studies attempted to evaluate the value of loyalty programs but the findings have been conflicting with each other. Given the competitive climate of such a highly saturated competitive market of the hospitality industry, it is meaningful for hospitality marketers to evaluate the effectiveness of loyalty programs to increase customer retention and profitability. Therefore, the main purpose of this study was to examine the effectiveness of a hospitality loyalty program from a longitudinal perspective.</p>
<p>The literature review is separated in four sections. The first section is the theory building section, which examined social exchange theory, equity theory, and the relationship marketing theory to understand the development of customer loyalty. The second section describes the definition of loyalty and the factors that affect customer loyalty. It gives an understanding about loyalty marketing from a general perspective. The third section describes the purpose of loyalty programs, and finally the last section summarized the investigation of loyalty programs from previous studies. Overall, the literature review section suggested that despite the prevailing usage and attention on loyalty programs, the effectiveness from the customers' behavioral standpoint has not been well understood. For this reason, this study aims to find out the effectiveness of loyalty programs from a longitudinal perspective and study hypotheses were advanced.</p>
<p>This study obtained secondary data from a Las Vegas casino hotel and performed time series ARIMA modeling to test the study hypotheses. Results of this study supported the research hypotheses and indicated that loyalty programs do have a positive impact on customers' behavioral loyalty. The findings are expected to provide valuable insights for casino marketers to understand the impact of loyalty programs and develop marketing tactics to maintain loyal customers and maximize profitability as well.</p>
<p>Key Words: Consumer Behavior, Loyalty Marketing, Loyalty Programs, Rewards Program, Marketing Strategy, Time Series Analysis</p>

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</description>

<author>Myongjee Yoo</author>


</item>


<item>
<title>Change is learning: Metacognition to resolve concerns during the third year of the implementation of a technological innovation</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1270</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1270</guid>
<pubDate>Mon, 07 May 2012 13:36:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>"We are living in a time of change. Rather than viewing change as a painful course of action, let's develop an understanding of how it works, how to facilitate the process, and how to learn from our experiences" (Hall & Hord, 2011, p. 18).</p>
<p>This study used a snapshot of a private Kindergarten-12<sup>th</sup> grade school during the third year of the implementation of a technological innovation (RenWeb) to investigate teacher concerns during the process of change and gain insights into individuals' use of metacognition to resolve those concerns. Two primary research instruments were used, the Stages of Concern Questionnaire (George, Hall, & Stiegelbauer, 2006) and the Learning Combination Inventory (Johnston, 1996). Although both instruments have been used extensively for research studies, they have not been used together in the same study.</p>
<p>The researcher used Johnston's (2010) description of "metacognition [which] is the internal talk that goes on in your mind among your team of Learning Processes" (p. 60). The interaction of these four Learning Processes; Sequence, Precision, Technical Reasoning, and Confluence combine to create an individual's learning combination.</p>
<p>Research data were collected through the self-administered Web-based Stages of Concern Questionnaire (SoCQ) and Learning Combination Inventory (LCI). After grouping SoCQ profiles based on their relative distance across the Implementation Bridge (Hall & Hord, 2011), and the LCI reports based on similarity of patterns, 11 randomly selected interviewees were chosen to provide more in-depth data.</p>
<p>One part of the research provided teachers with information about their learning patterns by completing the LCI online, which included a personal report and a website to obtain more information. The researcher thought this would stimulate conversations about how people learn, however that was not the case. The data revealed in this research suggest that people need more time and support to use knowledge of their learning patterns in order to increase communication about learning. Even though teachers did not engage in any further research about Let Me Learn <sup>©</sup> or participate in conversations about the process many people thought knowledge of learning patterns might influence the way they approach learning about RenWeb in the future.</p>
<p>The second part of the research explored the SoCQ and LCI groups in a variety of ways to search for a relationship between an individual's Stages of Concern profile and learning pattern. Although the data comparing individuals' Stages of Concern and approach to learning provided a rich description of both research instruments, there was no clear relationship between them. However, there were some similarities between them in the larger SoCQ and LCI groups. Based on the data, using the SoCQ along with knowledge of learning patterns and how they interact (metacognition) may provide a change facilitator with adequate information to address the concerns of participants with appropriate support and training to increase the effectiveness of implementing an innovation.</p>
<p>Finally, Friedman (2005) challenges "being adaptable in a flat world, knowing how to 'learn how to learn', will be one of the most important assets any worker can have, because job churn will come faster, because innovation will happen faster" (p. 239). Johnston (2010) believes metacognition answers the challenge because "the mind remains the most vital technology for communication with others and ... navigating the world of the 21 <sup>st</sup> century requires high-speed learning and communicating" (p.134).</p>

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</description>

<author>Nola Allen-Raffail</author>


</item>


<item>
<title>Improving Outpatient Diabetes Care</title>
<link>http://digitalcommons.unl.edu/publichealthresources/150</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/150</guid>
<pubDate>Mon, 07 May 2012 13:32:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>More than 20% of patients in the Veterans Health Administration (VHA) have diabetes; therefore, disseminating “best practices” in outpatient diabetes care is paramount. The authors’ goal was to identify such practices and the factors associated with their development. First, a national VHA diabetes registry with 2008 data identified clinical performance based on the percentage of patients with an A1c >9%. Facilities (n = 140) and community-based outpatient clinics (n = 582) were included and stratified into high, mid, and low performers. Semistructured telephone interviews (31) and site visits (5) were conducted. Low performers cited lack of teamwork between physicians and nurses and inadequate time to prepare. Better performing sites reported supportive clinical teams sharing work, time for non-face-to-face care, and innovative practices to address local needs. A knowledge management model informed our process. Notable differences between performance levels exist. “Best practices” will be disseminated across the VHA as the VHA Patient-Centered Medical Home model is implemented.</p>

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</description>

<author>Susan Kirsh et al.</author>


</item>


<item>
<title>Introduction, The Sesquicentennial of the 1848 Seneca Falls Women&apos;s Rights Convention: American Women&apos;s Unfinished Quest for Legal, Economic, Political, and Social Equality</title>
<link>http://uknowledge.uky.edu/law_facpub/160</link>
<guid isPermaLink="true">http://uknowledge.uky.edu/law_facpub/160</guid>
<pubDate>Mon, 07 May 2012 13:32:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>On July 19, 1998, America celebrated the 150th anniversary of the Seneca Falls Convention. Almost three hundred women and men including Lucretia Mott, Elizabeth Cady Stanton, and Frederick Douglass met on that July date in 1848 at Seneca Falls, New York, for a two-day discussion of the "social, civil and religious rights of woman." At the conclusion of the meeting, sixty-eight women and thirty-two men signed their names to a Declaration of Sentiments and this country's organized women's rights movement began. The Declaration of Sentiments was the earliest, systematic, public articulation in the United States of the ideas that fuel the quest for women's economic, political, social, and legal equality to this day. In recognition of the enduring importance of this conference to women <em>qua</em> women, a group of researchers at the University of Kentucky came together to discuss an appropriate and meaningful way to celebrate the sesquicentennial of the Seneca Falls Conference. As direct beneficiaries of the women's rights movement, these researchers wanted to make their own contribution to that centuries long struggle. They decided to create a symposium issue for the Kentucky Law Journal that examines contemporary aspects of problems that were first identified in the Seneca Falls Declaration of Sentiments.</p>

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</description>

<author>Carolyn S. Bratt</author>


</item>


<item>
<title>A Positive Analysis of the Common Law of Corporate Fiduciary Duties</title>
<link>http://uknowledge.uky.edu/law_facpub/159</link>
<guid isPermaLink="true">http://uknowledge.uky.edu/law_facpub/159</guid>
<pubDate>Mon, 07 May 2012 13:32:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this Article is to offer a positive analysis of the common law of corporate managers' fiduciary duties. The Article attempts to explain the present shape of these corporate fiduciary duties by reference to Pareto criteria.</p>
<p>A particular state of affairs ("state B") is considered to be Pareto superior to another state of affairs ("state A") if at least one person in state B is better off than he or she is in state A and no one in state B is worse off than he or she is in state A. Since in a move from state A to state B, no one loses and at least one person gains, state B is considered superior to state A. Any state is Pareto efficient if no further move to a Pareto superior state is possible.</p>
<p>This Article proposes that corporate managers' fiduciary duties as developed through the common law are best understood as mandates from courts for corporate managers to take all actions that move corporate shareholders to Pareto superior states. This Article suggests that such an analysis enables one to discover a general consistency in the spate of seemingly confusing cases interpreting managers' fiduciary duties in such diverse matters as lock-ups, managers' freedom (or perhaps obligation) to promote the interests of constituencies other than stockholders, freeze-outs, and the meaning and applicability of the so called <em>Revlon</em> duties.</p>
<p>The Article offers not only explanations of the major cases in the area of corporate fiduciary duties but also examples of cases in which courts have varied from the requirement that managers pursue Pareto superior states. Such deviations have wrought confusion and problematic outcomes. Accordingly, in connection with the positive analysis, this Article at times offers prescriptions for rules of law that are inconsistent with managers' obligations to pursue Pareto superiority on behalf of corporate stockholders.</p>
<p>While all of this admittedly sounds esoteric, in fact the analysis is intended to be intensely practical by providing courts and corporate planners with clear principles that can be applied in a fashion that promotes consistency and reduces the deadweight costs of uncertainty. To assist in this practical side of the Article, references to Pareto criteria, which seem more suited to the lexicons of moral theorists and economists, are translated in Part I of the Article into the most usual and traditional corporate law language.</p>

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</description>

<author>Rutheford B. Campbell Jr.</author>


</item>


<item>
<title>The Kentucky Law Survey: Professional Responsibility</title>
<link>http://uknowledge.uky.edu/law_facpub/158</link>
<guid isPermaLink="true">http://uknowledge.uky.edu/law_facpub/158</guid>
<pubDate>Mon, 07 May 2012 13:32:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>This article is a survey of recent Kentucky ethics cases and Kentucky Bar Association ethics opinions. The cases and opinions selected are those of general application but special interest.</p>

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</description>

<author>William H. Fortune</author>


</item>


<item>
<title>The Kentucky Law Survey: Family Law</title>
<link>http://uknowledge.uky.edu/law_facpub/157</link>
<guid isPermaLink="true">http://uknowledge.uky.edu/law_facpub/157</guid>
<pubDate>Mon, 07 May 2012 13:32:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>This Article addresses some of the family law developments occurring since the Kentucky Law Journal last published a Kentucky law survey. Space limitations preclude discussion of every post-1985 change. Instead, this Article focuses on general trends, significant cases, and legislative developments.</p>
<p>Inquiry into family law developments in Kentucky is timely, not only because of the social importance of family relations, but also because of other contemporaneous efforts at family law reform. The American Law Institute ("ALl") is currently considering a final draft of principles governing family dissolution. That draft, and the discussions that surround its ultimate acceptance or rejection by the ALI, undoubtedly will be the focus of national concern. Kentucky courts, the General Assembly, and Kentucky lawyers will need to determine to what extent the Restatement's positions should prompt changes in this state's law.</p>
<p>Emerging controversies have marked other areas of family law. Grandparent visitation and third-party custody rights may overlap as more child custody cases involve intergenerational disputes between parents and grandparents. Rights of unwed fathers also have figured prominently in custody-related decisions. Finally, Kentucky courts have addressed international custody disputes, a new trend that involves interpretation of federal law.</p>
<p>Child support enforcement continues to raise numerous issues. The Uniform Interstate Family Support Act became effective January 1, 1998. Interpretation of the Act will affect this state's ability to serve as a forum for child support disputes as well as this state's duty to enforce child support orders from other states.</p>
<p>Other developments involving the family center on the parent-child relationship rather than marriage dissolution. New concerns about the right of children to permanent, safe homes may alter state practice regarding termination of parental rights.</p>

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</description>

<author>Louise Everett Graham</author>


</item>


<item>
<title>Honorable Intentions: An Explanation of No Child Left Behind</title>
<link>http://scholarworks.boisestate.edu/literacy_facpubs/65</link>
<guid isPermaLink="true">http://scholarworks.boisestate.edu/literacy_facpubs/65</guid>
<pubDate>Mon, 07 May 2012 13:29:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mary Ann Rawley et al.</author>


</item>


<item>
<title>United States Registered
Nurse Workforce Report Card
and Shortage Forecast</title>
<link>http://digitalcommons.unl.edu/publichealthresources/149</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/149</guid>
<pubDate>Mon, 07 May 2012 13:21:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Registered nurses (RNs) play a critical role in health care delivery. With an aging US population, health care demand</p>
<p>is growing at an unprecedented pace. Using projected changes in population size and age, the authors developed</p>
<p>demand and supply models to forecast the RN job shortage in each of the 50 states. Letter grades were assigned</p>
<p>based on projected RN job shortage ratios. The number of states receiving a grade of “D” or “F” for their RN</p>
<p>shortage ratio will increase from 5 in 2009 to 30 by 2030, for a total national deficit of 918 232 (725 619 - 1 112 112)</p>
<p>RN jobs. There will be significant RN workforce shortages throughout the country in 2030; the western region will</p>
<p>have the largest shortage ratio of 389 RN jobs per 100 000. Increased efforts to understand shortage dynamics are</p>
<p>warranted.</p>

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</description>

<author>Stephen P. Juraschek et al.</author>


</item>


<item>
<title>The Impact of an Early Literacy Intervention: Where Are the Children Now?</title>
<link>http://scholarworks.boisestate.edu/literacy_facpubs/64</link>
<guid isPermaLink="true">http://scholarworks.boisestate.edu/literacy_facpubs/64</guid>
<pubDate>Mon, 07 May 2012 13:20:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to contribute to and strengthen previous work that examined the long-lasting effects of Reading Recovery in statewide efforts aimed at bolstering early literacy achievement and reducing early learning difficulties. Specifically, the study explored the literacy achievement of Reading Recovery participants whose series of lessons had been successfully discontinued during their first-grade year at points 1, 2, and 3 years beyond receiving the intervention in Indiana—providing a picture in time for where the children are now.</p>
<p>The participants included randomly selected children who had either successfully completed Reading Recovery or who had not participated in the intervention (i.e., cohort sample) from the three grade levels in 253 schools in Indiana. The two assessment instruments used to gauge literacy performance included the running record of oral text reading (Clay, 1993) and the comprehension and vocabulary subtests of the Gates-MacGinitie Reading Tests and the score for <em>total test</em>. The fourth-grade former Reading Recovery children’s results on the state achievement test taken in third grade were collected from their school records to establish their achievement distribution 2 years beyond the intervention.</p>
<p>Results indicate a considerable majority of the former successful Reading Recovery children were reading text at or above their grade level and that 1, 2, and 3 years beyond the intervention, Reading Recovery children were performing roughly as well as or better than their cohort sample peers on the task of oral text reading.</p>
<p>Analysis of the Gates-MacGinitie Reading Test data indicated the vast majority of the previously successful Reading Recovery children performed within the calculated average bands of the cohort sample groups at each grade level, indicating the formerly struggling learners were continuing to progress with their peers in literacy. In addition, the former Reading Recovery fourth graders achieved a normal curve distribution with a mean of the 45th percentile on the Indiana State Test of Education Progress (ISTEP), a considerably different pattern from their first-grade 15–20% achievement range.</p>

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</description>

<author>Maribeth Cassidy Schmitt et al.</author>


</item>


<item>
<title>Population Dynamics and Ecology of White-Tailed Deer in Illinois</title>
<link>http://opensiuc.lib.siu.edu/cwrl_fr/1</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/cwrl_fr/1</guid>
<pubDate>Mon, 07 May 2012 13:20:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alan Woolf et al.</author>


</item>


<item>
<title>Genome-wide MicroRNA profiling of mantle cell lymphoma reveal a distinct subgroup with poor prognosis</title>
<link>http://digitalcommons.unl.edu/publichealthresources/148</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/148</guid>
<pubDate>Mon, 07 May 2012 13:17:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>MicroRNA (miRNA) deregulation has been implicated in the pathogenesis of mantle cell lymphoma (MCL). Using a high-throughput quantitative real-time PCR platform, we performed miRNA profiling on cyclin D1- positive MCL (n=30) and cyclin D1-negative MCL (n=7) and compared them with small lymphocytic leukemia/lymphoma (SLL, n=12), aggressive B-cell lymphomas (n=138), normal B-cell subsets and stromal cells. We identified a 19-miRNA classifier which included six upregulated miRNAs (miR-135a, miR-708, miR-150, miR-363, miR-184, miR-342-5p) and 13 downregulated miRNAs, that was able to distinguish MCL from other aggressive lymphomas with >90% probability. Some of these upregulated miRNAs are highly expressed in naïve B-cells. MicroRNA classifier showed consistent results in FFPE tissues and was able to distinguish cyclin D1-negative MCL from other lymphomas. A 26-miRNA classifier could distinguish MCL from SLL, dominated by 23 upregulated miRNAs in MCL. Unsupervised hierarchical clustering of MCL cases demonstrated a cluster characterized by high expression of miRNAs from polycistronic miR17~92 cluster and its paralogs miR-106a-363 and miR-106b-25, which was distinct from the other clusters showing enrichment of stroma associated miRNAs. The corresponding gene-expressionprofiling (GEP) data showed that the former cluster of MCL had significantly higher proliferation genesignature (PS), while the other subsets had higher expression of stroma associated genes. Clinical outcome analysis suggests that miRNAs can serve as prognosticators.</p>

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</description>

<author>Javeed Iqbal et al.</author>


</item>


<item>
<title>Olanzapine and risperidone disrupt conditioned avoidance
responding by selectively weakening motivational salience
of conditioned stimulus: Further evidence</title>
<link>http://digitalcommons.unl.edu/psychfacpub/565</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/psychfacpub/565</guid>
<pubDate>Mon, 07 May 2012 13:17:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Suppression of conditioned avoidance response is a preclinical behavioral index of antipsychotic activity. Previous work shows that olanzapine and risperidone disrupt avoidance response elicited by a less salient conditioned stimulus (CS2) to a greater extent than avoidance elicited by a more salient stimulus (CS1), suggesting that antipsychotic drugs may have a weakening action on motivational salience of stimuli. In the present study, we further examined this mechanism of antipsychotic action, focusing on the possible impact of baseline difference of CS1 and CS2 response rates on the avoidance-disruptive effect of olanzapine and risperidone. Rats were first trained to acquire avoidance responding in a procedure in which the number of CS2 trials (i.e. 20) was twice the number of CS1 trials (i.e. 10), but the percentage of CS2-shock pairing was set at 25% lower (15 trials out of 20) than the percentage of CS1- shock pairing (20 trials out of 20). They were then tested daily under olanzapine (0.5 and 1.0 mg/kg, sc) or risperidone (0.33 and 1.0 mg/kg, sc) for 5 consecutive days. Repeated olanzapine and risperidone treatment dose-dependently disrupted avoidance responding to both CS1 and CS2. Both drugs at the high dose disrupted the CS2 avoidance to a greater extent than the CS1 avoidance. In the final challenge test, rats previously treated with olanzapine were tested under risperidone (0.33 mg/kg), whereas rats previously treated with risperidone were tested under olanzapine (0.5 mg/kg). Results show that rats previously treated with risperidone 1.0 mg/kg group made significantly fewer avoidance responses than the vehicles under olanzapine at 0.5 mg/kg. These findings confirm that olanzapine and risperidone disrupt avoidance response primarily by selectively attenuating the motivational salience of the CS. The present study also suggests that there is a generality of antipsychotic drug experience that is mediated by a shared interoceptive drug state mechanism.</p>

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</description>

<author>Chen Zhang et al.</author>


</item>


<item>
<title>Control of mesenchymal lineage progression by microRNAs targeting the skeletal gene regulators Trps1 and Runx2</title>
<link>http://escholarship.umassmed.edu/stein/257</link>
<guid isPermaLink="true">http://escholarship.umassmed.edu/stein/257</guid>
<pubDate>Mon, 07 May 2012 13:11:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Multiple microRNAs (miRNAs) that target the osteogenic Runt-related transcription factor 2 (RUNX2) define an interrelated network of miRNAs that control osteoblastogenesis. We addressed whether these miRNAs have functional targets beyond RUNX2 that co-regulate skeletal development. Here, we find that seven RUNX2-targeting miRNAs (miR-23a, miR-30c, miR-34c, miR-133a, miR-135a, miR-205 and miR-217) also regulate the chondrogenic GATA transcription factor Tricho-Rhino-Phalangeal Syndrome I (TRPS1). While the efficacy of each miRNA to target RUNX2 or TRPS1 differs in osteoblasts and chondrocytes, each effectively blocks maturation of pre-committed osteoblasts and chondrocytes. Furthermore, these miRNAs can redirect mesenchymal stem cells into adipogenic cell fate with concomitant up-regulation of key lineage specific transcription factors. Thus, a program of multiple miRNAs controls mesenchymal lineage progression by selectively blocking differentiation of osteoblasts and chondrocytes to control skeletal development.</p>

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</description>

<author>Ying Zhang et al.</author>


<category>MicroRNAs</category>

<category>Osteoblasts</category>

<category>Chondrocytes</category>

<category>DNA-Binding Proteins</category>

<category>Transcription Factors</category>

<category>Core Binding Factor Alpha 1 Subunit</category>

<category>Mesenchymal Stem Cells</category>

<category>Musculoskeletal Development</category>

</item>


<item>
<title>Textual Importations Following a Modified Dialogic Reading Approach</title>
<link>http://scholarworks.boisestate.edu/literacy_facpubs/63</link>
<guid isPermaLink="true">http://scholarworks.boisestate.edu/literacy_facpubs/63</guid>
<pubDate>Mon, 07 May 2012 13:10:16 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Anne E. Gregory et al.</author>


</item>


<item>
<title>Notebook - October-December 1984</title>
<link>http://scholarcommons.sc.edu/notebook/56</link>
<guid isPermaLink="true">http://scholarcommons.sc.edu/notebook/56</guid>
<pubDate>Mon, 07 May 2012 13:09:26 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Contents:</strong></p>
<p>Table of Contents.....p. i<br> The Camden Jail and Market Site: A Report on Preliminary Investigations.....p. iii</p>

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</description>

<author>South Carolina Institute of Archaeology and Anthropology--University of South Carolina</author>


</item>


<item>
<title>Most Physicians Were Eligible
For Federal Incentives In 2011,
But Few Had EHR Systems
That Met Meaningful-Use Criteria</title>
<link>http://digitalcommons.unl.edu/publichealthresources/147</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/147</guid>
<pubDate>Mon, 07 May 2012 13:09:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>As more physicians adopt electronic health record systems in their practices, policy interest is focusing on whether physicians are ready to meet the federal “meaningful use” criteria—a vital threshold to qualify for financial incentives. In our analysis of a 2011 nationally representative survey of office-based physicians, we found that 91 percent of physicians were eligible for Medicare or Medicaid meaningful-use incentives. About half of all physicians intended to apply. However, only 11 percent both intended to apply for the incentives and had electronic health record systems with the capabilities to support even two-thirds of the stage 1 core objectives required for meaningful use. Although the federal Medicare incentives will be available through 2016, and Medicaid incentives through 2021, widespread gaps in readiness throughout the states illustrate the challenges physicians face in meeting the federal schedule for the incentive programs.</p>

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</description>

<author>Chun-Ju Hsiao et al.</author>


</item>


<item>
<title>On a Diophantine Equation That Generates All Integral Apollonian Gaskets</title>
<link>http://opensiuc.lib.siu.edu/math_articles/111</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/math_articles/111</guid>
<pubDate>Mon, 07 May 2012 13:08:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>A remarkably simple Diophantine quadratic equation is known to generate all, Apollonian integral gaskets disk packings. A new derivation of this formula is presented here based on inversive geometry. Also, occurrence of Pythagorean triples in such gaskets is discussed.</p>

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</description>

<author>Jerzy Kocik</author>


</item>


<item>
<title>Family level phylogenies reveal modes of
macroevolution in RNA viruses</title>
<link>http://digitalcommons.unl.edu/publichealthresources/146</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/146</guid>
<pubDate>Mon, 07 May 2012 13:06:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite advances in understanding the patterns and processes of microevolution in RNA viruses, little is known about the determinants of viral diversification at the macroevolutionary scale. In particular, the processes by which viral lineages assigned as different “species” are generated remain largely uncharacterized. To address this issue, we use a robust phylogenetic approach to analyze patterns of lineage diversification in five representative families of RNA viruses. We ask whether the process of lineage diversification primarily occurs when viruses infect new host species, either through cross-species transmission or codivergence, and which are defined here as analogous to allopatric speciation in animals, or by acquiring new niches within the same host species, analogous to sympatric speciation. By mapping probable primary host species onto family level viral phylogenies, we reveal a strong clustering among viral lineages that infect groups of closely related host species. Although this is consistent with lineage diversification within individual hosts, we argue that this pattern more likely represents strong biases in our knowledge of viral biodiversity, because we also find that better-sampled human viruses rarely cluster together. Hence, although closely related viruses tend to infect related host species, it is unlikely that they often infect the same host species, such that evolutionary constraints hinder lineage diversification within individual host species. We conclude that the colonization of new but related host species may represent the principle mode of macroevolution in RNA viruses.</p>

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</description>

<author>Andrew Kitchen et al.</author>


</item>


<item>
<title>Ecological Literacy: Global Planetary Stewardship is Everyone’s Responsibility</title>
<link>http://scholarship.rollins.edu/mls/26</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/26</guid>
<pubDate>Mon, 07 May 2012 13:05:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>No longer can nature simply be defined as ‘essences unchanged by man’ as Ralph Waldo Emerson once claimed. Technology, the result of applied science, has produced accomplishments that have made the quality of human life better in terms of health care and transportation. These advancements, however, have come at a great ecological cost as is evident everywhere in nature today. Humans need to acquire Ecological Literacy, the knowledge to lead a sustainable life.  This entails meeting current needs without preventing future generations and species from doing the same. Since the days of the Industrial Revolution, the health of our planet has been in a decline because of man’s urge to dominate. Overuse of fossil fuels and industrial farming to feed the nihilistic human race has proven toxic to Gaia.  Global warming is a direct result of this irresponsibility and these effects have become visible at a sobering rate.  According to the Population Reference Bureau, the number of human beings now living in an urban setting is equal to those in rural areas; a shocking fact considering that only three percent of the world’s population lived in urban areas in 1800. Planetary health is a moral imperative for Homo sapiens as the seven billion residents of Earth continue to multiply. We are in dire need of change to become what David Orr calls a ‘planet-broken’ race. Effective change can only be made through both community and academic education and the acquisition of Ecological Literacy.  This study looks at the literary, scientific, ethical, and educational aspects that are necessary to evolve sustainably into this century.  Through the use of survey data, literature, hands-on educational activities, and scholarly sources this study examines the process of changing each human beings’ worldview to include a zero impact lifestyle.</p>

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</description>

<author>Eileen Bobeck-Thoresen</author>


</item>


<item>
<title>Dignity in Race Jurisprudence</title>
<link>http://scholarship.law.gwu.edu/faculty_publications/8</link>
<guid isPermaLink="true">http://scholarship.law.gwu.edu/faculty_publications/8</guid>
<pubDate>Mon, 07 May 2012 13:04:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Racial justice demands dignity; the acknowledgment and affirmation of the equal humanity of people of color. Denying dignity on the basis of color creates racial subordination, which triggers dignitary harms such as individual acts of racism and communal exclusion leading to diminished health, wealth, income, employment and social status. The legal recognition of dignity is therefore a prerequisite to political and social equality.  For Americans of African descent, dignity was long denied by the legal endorsement of slavery and the degrading policies of segregation. The struggle to be treated equally human eventually found success in landmark cases such as Brown v. Board of Education where the Supreme Court enshrined the rights of people color in the name of a collective sense of justice and dignity. But negative racial stereotypes and presumptions of cultural inferiority continue to pervade today’s social network, housing patterns, and racially disparate law enforcement policies.  This paper suggests that the Supreme Court has recently shifted its focus away from the idea of dignity and is therefore unable to address the contemporary racial problems of racial stereotypes, subtle racism, and societal discrimination. Instead, the Court is placing too much emphasis on the concept of colorblindness, ignoring the hallmarks of dignity and justice set forth in the civil rights era cases.  I propose that the Supreme Court return to a discussion of dignity in contemporary race jurisprudence, and to do so, need only look to the Court’s recent affirmation of gay rights and the dignity of the homosexual lifestyle in Lawrence v. Texas. Second, I offer what a renewed emphasis on dignity night look like in the equally contentious field of race relations. An emphasis on dignity may provide the Court with an anchor for its future race-based decision making designed to address the true nature of racial injustice. Racial justice demands dignity; the acknowledgment and affirmation of the equal humanity of people of color. Denying dignity on the basis of color creates racial subordination, which triggers dignitary harms such as individual acts of racism and communal exclusion leading to diminished health, wealth, income, employment and social status. The legal recognition of dignity is therefore a prerequisite to political and social equality.  For Americans of African descent, dignity was long denied by the legal endorsement of slavery and the degrading policies of segregation. The struggle to be treated equally human eventually found success in landmark cases such as Brown v. Board of Education where the Supreme Court enshrined the rights of people color in the name of a collective sense of justice and dignity. But negative racial stereotypes and presumptions of cultural inferiority continue to pervade today’s social network, housing patterns, and racially disparate law enforcement policies.  This paper suggests that the Supreme Court has recently shifted its focus away from the idea of dignity and is therefore unable to address the contemporary racial problems of racial stereotypes, subtle racism, and societal discrimination. Instead, the Court is placing too much emphasis on the concept of colorblindness, ignoring the hallmarks of dignity and justice set forth in the civil rights era cases.  I propose that the Supreme Court return to a discussion of dignity in contemporary race jurisprudence, and to do so, need only look to the Court’s recent affirmation of gay rights and the dignity of the homosexual lifestyle in Lawrence v. Texas. Second, I offer what a renewed emphasis on dignity night look like in the equally contentious field of race relations. An emphasis on dignity may provide the Court with an anchor for its future race-based decision making designed to address the true nature of racial injustice.</p>

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</description>

<author>Christopher A. Bracey</author>


</item>


<item>
<title>Getting Back to Basics: Some Thoughts on Dignity, Materialism, and a Culture of Racial Equality</title>
<link>http://scholarship.law.gwu.edu/faculty_publications/7</link>
<guid isPermaLink="true">http://scholarship.law.gwu.edu/faculty_publications/7</guid>
<pubDate>Mon, 07 May 2012 13:04:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dignity is the most compelling value in racial reform. Racial inequality is expressed as an ongoing attempt to deny minorities dignity. Dignity requires that to truly have freedom and equality, each of us has equal ability to exercise our fundamental freedoms. In order to ensure that this is possible, persons must possess the material wherewithal to exercise that freedom. The government, in order to combat racial inequality, must ensure that persons have the capability to live a “safe, well-nourished, productive, educated, social, and politically and culturally participatory life of normal length.” This approach requires structural changes in the obligations of the state, and promotes a culture of racial equality that traditional race jurisprudence is unable to realize. This article presents a dignity centered model of racial empowerment, and explores and critiques its viability.</p>

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</description>

<author>Christopher A. Bracey</author>


</item>


<item>
<title>Louis Brandeis and the Race Question</title>
<link>http://scholarship.law.gwu.edu/faculty_publications/6</link>
<guid isPermaLink="true">http://scholarship.law.gwu.edu/faculty_publications/6</guid>
<pubDate>Mon, 07 May 2012 13:04:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>We live in a culture enamored by our heroes. They are celebrated for their extraordinary accomplishments, and canonized by histories that rarely reflect the true texture of their lives. Legal academics share in these tendencies and, as a result, heroes in the law are often viewed with the same rose-colored glasses accorded to their counterparts in popular culture.  The late Louis Brandeis was an Associate Justice on the Supreme Court of the United States from 1916 to 1939. Born to Jewish immigrant parents, he graduated from Harvard Law School, and gained a reputation as America’s “People’s Attorney.” He pioneered an approach to lawyering and legal analysis that would help defeat segregation as a national policy. While serving on the Supreme Court, Brandeis advocated that judges should make decisions grounded in social and economic realities, and wrote insightful opinions that many historians and commentators have deemed prophetic. As a result, he is considered a revered paragon in American law of the public-spirited lawyer and jurist, and a champion of the rights of all men.  This paper delves beyond this heroic image to critique Brandeis’ conspicuous, though historically overlooked, evasion of issues affecting African-Americans at a time when such avoidance bolstered a segregationist regime. This study will encompass Brandeis’ familiarity with such issues, what Brandeis did or did not do for inter-ethnic relations both as a practitioner and as a jurist, and finally, why the “People’s Attorney” may have chosen to ignore public issues affecting the rights of African-Americans.</p>

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</description>

<author>Christopher A. Bracey</author>


</item>


<item>
<title>The Color of Our Future: The Pitfalls and Possibilities of the Race Card in American Culture</title>
<link>http://scholarship.law.gwu.edu/faculty_publications/5</link>
<guid isPermaLink="true">http://scholarship.law.gwu.edu/faculty_publications/5</guid>
<pubDate>Mon, 07 May 2012 13:04:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>We live in a country haunted by a past of slavery, segregation, racism, and violence. Though many systemic corrections have been attempted, a large percentage of African-Americans continue to fall behind their White counterparts in nearly every index of socio-economic well-being. The debate rages on as to why this situation exists and persists, and people on both sides of the color divide have become increasingly sensitive to perceptions and accusations of racial injustice.  In his book, The Race Card: How Bluffing About Bias Makes Race Relations Worse, Richard Thompson Ford explores the phenomenon called “the race card,” wherein individuals play on the public’s sensitivity by deliberately invoking racial paranoia, suspicion, or sympathy in order to secure some personal or professional windfall. Ford points out that the use of the rhetoric and legacy of racism and racial injustice in this way is not only dishonest, but has serious discursive and material consequences beyond any personal gain that can be achieved. Each use of the race card effectively drains the reservoir of public sympathy, which can create a problematic situation for true victims of racial injustice. Instead, he advocates for an approach he terms “coolheaded pragmatism.”  In this essay, I want to explore the idea of the race card more deeply, as well as discuss Ford’s idea of “coolheaded pragmatism.” Though deeply moved by the spirit of Ford’s book, I believe he looks only at a modern variant of the race card. In the first part of my essay, I will explore an alternative take on the history of the race card. Second, I will discuss some key differences between the true “classic form” of the race card and what I call the “neoclassical” race card, showing the neoclassical race card as a tool that can be used to promote social justice when used responsibly. Finally, I will offer a short critique of Ford’s “coolheaded pragmatism” and discuss how this alternative to the race card, while admirable, is normatively problematic.</p>

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</description>

<author>Christopher A. Bracey</author>


</item>


<item>
<title>Adjudication, Antisubordination, and the Jazz Connection</title>
<link>http://scholarship.law.gwu.edu/faculty_publications/4</link>
<guid isPermaLink="true">http://scholarship.law.gwu.edu/faculty_publications/4</guid>
<pubDate>Mon, 07 May 2012 13:04:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>We live in the midst of a pervasive and sustained democratic crisis. Our society expresses a deep commitment to core notions of freedom, justice, and equality for all citizens. Yet, it is equally clear that our democracy tolerates a great deal of social and economic inequality. Membership in a socially disfavored group can (and often does) profoundly distort one's life chances and opportunities. Our constitutional democracy acknowledges this tension, providing for both majority rule and the protection of minority rights and interests.  Although we seek to safeguard minority rights and interest through express legal prohibitions on the subordination of socially disfavored groups, our society nevertheless retains informal structures and networks that have the effect of perpetuating social inequality among groups - social inequality that was once secured by formal law. Confronted with entrenched and destructive patterns of social and economic stratification, what more can law do to realize democracy for members of subordinated groups?  This paper offers some preliminary thoughts on how law should respond, and in particular, what we might ask of judges and the Constitution that they interpret and uphold. The paper presents a normative and descriptive account of "successful" judging in constitutional civil rights cases in a democratic society. By "successful," I mean to describe a style of judging that is self-consciously engaged in the constructive enterprise of giving full meaning and content to minority rights in a manner consistent with the best of the American democratic tradition of freedom and majority rule. Successful judging, then, is judging deliberately styled to realize democracy for subordinated groups in American society.  I seek to accomplish three main tasks in this paper. First, I argue for a particular understanding of the judicial role within our constitutional democracy in the contentious area of race relations. Second, I argue that judges committed to realizing democracy for members of socially disfavored groups should embrace an antisubordination interpretation of the Fourteenth Amendment and the Court's equality jurisprudence as a guiding principle of adjudication for constitutional cases that pit the rights and interests of socially disfavored and minority groups against majority rule. Third, I provide a functionalist account for how this idealized style of adjudication works. Drawing upon the insights and impressions of free jazz movement and musician Ornette Coleman in particular, I argue that the hallmarks of Coleman's work - freedom, improvisation, reimagination, and courage - serve as useful points of departure for deepening our understanding of what judges committed to realizing democracy for members of subordinated groups do or ought to do.</p>

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</description>

<author>Christopher A. Bracey</author>


</item>


<item>
<title>Thinking Race, Making Nation (reviewing Glenn C. Loury, The Anatomy of Racial Inequality)</title>
<link>http://scholarship.law.gwu.edu/faculty_publications/3</link>
<guid isPermaLink="true">http://scholarship.law.gwu.edu/faculty_publications/3</guid>
<pubDate>Mon, 07 May 2012 13:04:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>We live in a race-conscious culture. As Americans, we are a nation of people who self-consciously chose to adopt a vision of society that embraced lofty ideals of individual freedom and democracy for all along with powerful mechanisms for devastating racial oppression. Our history is replete with instances of differential treatment on account of race - slavery being only the most egregious example - that achieved the desired effect of generating remarkable disparities in socioeconomic well-being among individuals and between different racial groups. Such disparities are not simply historical artifacts. They are facts of the contemporary American racial landscape as well. Racial disparity in socioeconomic well-being has always been, and continues to be, a central feature of American life.  Of course, we each choose how we come to terms with racial inequality, how we rationalize, compartmentalize, or explain this phenomenon, and how we integrate our "raced" existence into our personal view of the world. For nearly three generations, we have undertaken a largely sustained collective effort to eliminate racial discrimination in American society. For some, the persistence of chronic racial inequality in the face of sustained efforts to ameliorate racial discrimination provides subtle confirmation of deeply held suspicions regarding the intellectual, cultural, or economic capacity of African Americans. For others, the persistence of racial disparity highlights the limits of the prevailing approach to antidiscrimination law and makes the case for greater intervention.  Professor Glenn C. Loury's "The Anatomy of Racial Inequality" is a thoroughgoing attempt to ascertain the root causes of racial inequality and provide insight into the thought process that causes us to view racial disparity with complacency and indifference. However, Loury's project is not merely descriptive. His structural account of racial inequality provides the staging ground from which he launches a deep critique of prevailing views on American race relations. Racial inequity is not the product of some inherent deficiency in the minds and hearts of African Americans. Rather, it is a social pathology "deeply rooted in American history" - a pathology that "evolved in tandem with American political and economic institutions, and with cultural practices that supported and legitimated those institutions . . . that were often deeply biased against blacks." Loury therefore rejects the conservative policy of indifference toward racial disparities, and declares emphatically that racial inequality is "an American tragedy [and] a national, not merely a communal disgrace."  In a very real sense, Loury's free and extended meditation on racial inequality and the prospects of racial reform provides us with an insightful theoretical and discursive structure through which we can engage the struggle for racial justice anew. In this review essay, I offer an extended examination and critique of the major arguments presented in the book. In the course of connecting Loury's work with historic and contemporary literature on racial disparities in American life, I offer some thoughts on the impact his project may have upon the shape of American race relations to come.</p>

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</description>

<author>Christopher A. Bracey</author>


</item>


<item>
<title>Notebook - April-September 1984</title>
<link>http://scholarcommons.sc.edu/notebook/55</link>
<guid isPermaLink="true">http://scholarcommons.sc.edu/notebook/55</guid>
<pubDate>Mon, 07 May 2012 13:01:08 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Contents:</strong></p>
<p>Table of Contents.....p. i<br> Woodland Occupation in the Upper Coastal Plain of South Carolina: An Archeological Reconnaissance of the Carolina Power and Light Company's Lake Robinson to Sumter 230 kV Transmission Line corridor.....p. iii</p>

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</description>

<author>South Carolina Institute of Archaeology and Anthropology--University of South Carolina</author>


</item>


<item>
<title>Molecular distinctions between pediatric and adult mature B-cell non-Hodgkin
lymphomas identified through genomic profiling</title>
<link>http://digitalcommons.unl.edu/publichealthresources/145</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/145</guid>
<pubDate>Mon, 07 May 2012 12:59:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Burkitt lymphoma (BL) predominates in pediatric patients, whereas diffuse large B-cell lymphoma (DLBCL) is uncommon. In contrast to adults, BL and DLBCL are treated similarly in children and both entities have superior outcomes in children compared with adults. Gene expression profiling (GEP) and miRNA expression profiling clearly differentiated pediatric DLBCL from BL, forming distinct clusters regardless of patient age. However, pathway analysis of GEP data identified minor differences between corresponding pediatric and adult tumors. Predominance (6:1) of the germinal center B-cell subtype to activated B-cell subtype was found among pediatric DLBCL. Two cases were molecularly classified as primary mediastinal B-cell lymphoma. We observed frequent abnormalities in 8q24 in pediatric DLBCL, including MYC rearrangement in 31% (5 of 16) and gain or amplification in 50% (6 of 12) nonrearranged cases. MYC rearrangement was present in 96% (23 of 24) BL cases. Array-based CGH analysis identified abnormalities that are shared between adult and pediatric DLBCL (+12q15, +19q13, -6q), and abnormalities unique to the pediatric cases (-4p14, -19q13.32, +16p11.2), suggesting distinct pathogenetic mechanisms relative to age. Elucidation of the underlying target genes may provide insight into factors that modulate outcome and could provide potential novel therapeutic targets with less toxicity for pediatric patients with B-cell non-Hodgkin lymphoma.</p>

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</description>

<author>Karen Deffenbacher et al.</author>


</item>


<item>
<title>Data Mining in Health-Care: Issues and a Research Agenda</title>
<link>http://epublications.marquette.edu/mgmt_fac/125</link>
<guid isPermaLink="true">http://epublications.marquette.edu/mgmt_fac/125</guid>
<pubDate>Mon, 07 May 2012 12:56:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>While data mining has become a much-lauded tool in business and related fields, its role in the healthcare arena is still being explored. Currently, most applications of data mining in healthcare can be categorized into two areas: decision support for clinical practice, and policy planning/decision making. However, it is challenging to find empirical literature in this area since a substantial amount of existing work in data mining for health care is conceptual in nature. In this paper, we review the challenges that limit the progress made in this area and present considerations for the future of data mining in healthcare.</p>

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</description>

<author>Monica Adya</author>


</item>


<item>
<title>Effect of Operating Conditions on Gearbox Noise</title>
<link>http://engagedscholarship.csuohio.edu/enme_facpub/6</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/enme_facpub/6</guid>
<pubDate>Mon, 07 May 2012 12:56:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Low-contact-ratio spur gears were tested in the NASA gear noise rig to study the noise radiated from the top of the gearbox. The measured sound power from the gearbox top was obtained from a near-field acoustic intensity scan taken at 63 nodes just above the surface. The sound power was measured at a matrix of 45 operating speeds and torque levels. Results are presented in the form of a spectral speed map and as plots of sound power versus torque (at constant speed) and as sound power versus speed (at constant torque) Because of the presence of vibration modes, operating speed was found to have more impact on noise generation than torque level. A NASA gear dynamics code was used to compute the gear tooth dynamic overload at the same 45 operating conditions used for the experiment. Similar trends were found between the analytical results for dynamic tooth overload and experimental results for sound power. Dynamic analysis may be used to design high-quality gears with profile relief optimized for minimum dynamic load and noise.</p>

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</description>

<author>Fred B. Oswald et al.</author>


</item>


<item>
<title>Contributions of neuroanatomical and cognitive factors to age-related differences in navigational skill</title>
<link>http://digitalcommons.wayne.edu/oa_theses/167</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/167</guid>
<pubDate>Mon, 07 May 2012 12:54:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Aging is associated with declines in spatial navigation skills. In this study, I used structural equation modeling (SEM) to explore the contributions of variances in regional brain volume (prefrontal cortices, basal ganglia, and medial temporal lobe), processing speed, working memory and episodic memory to age-related differences in spatial navigation. As expected, advanced age was associated with smaller regional brain volumes and reduced cognitive performance. Once cognitive factors were taken into account, the direct effects of age on navigational skill was no longer significant. Thus, age-related difference in spatial navigation skill could be explained by individual differences in the cognitive factors. More specifically, age-related slowing of processing and reduction in episodic memory accounted for the age-related difference in spatial navigational skill. However, the variance in regional volumes did not mediate age-related difference in navigational skill.</p>

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</description>

<author>Peng Yuan</author>


</item>


<item>
<title>Patient trust: predicting university students&apos; trust in their physicians and the health care system</title>
<link>http://digitalcommons.wayne.edu/oa_theses/166</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/166</guid>
<pubDate>Mon, 07 May 2012 12:54:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this thesis was to determine if sociodemographic characteristics of University students predict their level of trust with their physicians and their level of trust with the health care system.  This study used the Primary Care Assessment Survey (PCAS) trust subscale to measure physician trust and the Medical Mistrust Index to measure health care system trust through a self-administered survey (N=186) using convenience sampling. A principle components analysis was conducted to avoid issues of multicollinearity and examine underlying constructs. Bivariate correlations, and regression analyses were conducted to examine the relationship between patient trust in his/her physician and patient trust in the health care system. Physician trust and system trust were significantly correlated. How one chose his/her physician, marital status, education, and age significantly predicted trust in one's physician. How one chose his/her physician, race, education, gender and age significantly predicted trust in the health care system.</p>

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</description>

<author>Lisa Elizabeth Stack</author>


</item>


<item>
<title>Applications of lindenmayer systems to quantum computation and quantum information</title>
<link>http://digitalcommons.wayne.edu/oa_theses/165</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/165</guid>
<pubDate>Mon, 07 May 2012 12:54:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Due to their compactness, robustness, and conciseness, Lindenmayer systems (L-systems) have served as a popular tool for modeling numerous types of systems. Quantum systems, algorithms, and processes maintain a certain regularity to which L-systems are proficient at modeling. In this thesis we explore how one may formulate L-systems in terms of quantum computational areas and the benefits incurred from doing so. This new approach is oriented toward a further extension in the field of L-systems, allowing us to model behavior of quantum computational aspect and more expressively describe quantum processes and phenomena. A particular implementation strategy of how one may invoke an L-system to model these constituents are presented and evaluated.</p>

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</description>

<author>Vincent Paul Russo</author>


</item>


<item>
<title>Flexural analysis of balsa core sandwich composite: failure mechanisms, core grain orientation and padding effect</title>
<link>http://digitalcommons.wayne.edu/oa_theses/164</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/164</guid>
<pubDate>Mon, 07 May 2012 12:54:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>A comprehensive investigation was undertaken to study failure mechanisms of sandwich composites and their influence on flexural behavior (load-displacement curve). Sandwich composite panels were cured from compression thermoforming of E-glass/epoxy skins and a low density balsa wood core. Balsa core grain orientation is found to have major effect on flexural response and failure modes. Flexural behavior, failure mode and its sequence varies with different core grain orientations. Indentation, skin failure, core shear failure were dominant failure modes observed for various cases. Skin-core interface adhesion was reasonably good, as delamination was not the first failure mode in sandwich beam with balsa core. Indentation of skin is a major concern under localized loading, as the skin failure is premature as compared to its normal compressive strength. Hence, the effect of padding on sandwich beam with soft core was also completed as part of this work. Finite element analysis for modeling this type of sandwich composite beam is conducted using LS-Dyna. Several material parameters required for finite element analysis were determined from extensive testing and data from literature. Composite failure model and wood material model available in LS-Dyna were applied for skin and core of sandwich beam. At the skin-core interface, nodes were merged as delamination was not a prominent failure mode. Flexural analysis response from FEA shows good correlation with experimental behavior.</p>

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</description>

<author>Avinash S. Phadatare</author>


</item>


<item>
<title>Study of two particle correlations in the ampt model</title>
<link>http://digitalcommons.wayne.edu/oa_theses/163</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/163</guid>
<pubDate>Mon, 07 May 2012 12:54:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>We look for and find evidence of radial flow in two particle momentum correlations in Multi Phase Transport (AMPT) simulated collisions.  The feature of interest is identified as a flattening of the away side () correlation vs. azimuthal angle curve, with an increase in the nearside peak.</p>

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</description>

<author>Robert Ward Pearce</author>


</item>


<item>
<title>Development and validation of a 3d fe model of advanced combat helmet and biomechanical analysis of human head and helmet response to primary blast insult</title>
<link>http://digitalcommons.wayne.edu/oa_theses/162</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/162</guid>
<pubDate>Mon, 07 May 2012 12:54:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Blast-induced traumatic brain injury (bTBI) has emerged as a "signature injury" in combat casualty care. Present combat helmets are designed primarily to protect against ballistic and blunt impacts, but the current issue with helmets is protection from primary blast effects.  In order to delineate wave interaction and propagation with the combat helmet and human head, a detailed finite element (FE) model of Advanced Combat Helmet (ACH) was developed and validated. A series of finite element analyses was undertaken to evaluate blast wave attenuating capability of the ACH by comparing the head/brain responses against blast loadings between the validated FE human head models with and without helmet.</p>
<p>The integrated FE helmet/head model was subjected to blast insults at various overpressures (0.27-0.66 MPa) according to Bowen's lung iso damage threshold curves. Effectiveness of the helmet with respect to various head orientations was also investigated. The resulting biomechanical responses of the brain to blast threats were compared for the human head with and without the helmet.</p>
<p>For all Bowen's cases, the peak intracranial pressures sustained by the head without helmet ranged from 0.68-1.8 MPa in the coup cortical region. ACH was found to mitigate intracranial pressures in the head by 10-35%. The helmeted head resulted in average 30% lower peak brain strains and product of strain and strain rate. Among three blast-loading directions with ACH in use, the highest reduction in peak intracranial pressure (44%) was from backward blast, whereas the lowest reduction in peak intracranial pressures and brain strains was due to forward blast (27%).  The biomechanical responses of a human head to primary blast insult exhibited directional sensitivity owing to the different geometric contours and coverage of the helmet construction and asymmetric anatomy of the human head. Thus, direction-specific tolerances for bTBI are needed in helmet design in order to offer omni-directional protection for the human head.</p>
<p>A series of FE analyses was also conducted to evaluate the effects of blast overpressure on the brain of a new blast anatomical headform model constructed with the actual human head geometry and simulant materials for skull and brain. Biomechanical parameters within the intracranial cavity of the blast headform model were compared to those from the human head model. Results suggested that differences in mechanical properties between the simulant materials and human skull/brain tissue properties influenced shock propagation through the head.</p>

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</description>

<author>Rahul Makwana</author>


</item>


<item>
<title>In vitro study of breast cancer progression</title>
<link>http://digitalcommons.wayne.edu/oa_theses/161</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/161</guid>
<pubDate>Mon, 07 May 2012 12:54:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Breast cancer is the most common form of cancer in woman in the United States.  Current imaging techniques have increased detection rates of breast cancer, specifically ductal carcinoma <i>in situ</i>.  However, these imaging techniques are unable to provide information at the molecular level, which is essential in understanding the underlying causes of cancer, the pathogenesis of local recurrence, inter- and intra- cellular changes, and treatment efficacy.  Most information on cellular behavior has been based off of fixed samples at specific time points, and thus dynamic processes that occur in between those time points are likely to be missed, especially the subtle changes that occur in the progression of normal breast cells to cancer.  We aim to address these issues by combining visual observation and molecular characterization techniques.</p>
<p>A custom built live cell imaging system is used to visually observe normal, pre-malignant, and malignant breast cells growing in real-time for a period of 2.5 days.  Cells were grown in three-dimensional cultures to depict true mammary structure.  Characterization techniques, such as Raman spectroscopy and X-ray photoelectron spectroscopy (XPS) will be used to detect the subtle dynamic changes that occur as cancer progresses, as well characterize the differences in order to understand the history and aggressive nature of cancerous cells.  A trypsinized single cell suspension in phenol free media was used for preliminary Raman and XPS studies.</p>
<p>Preliminary research was also performed to study proteomic changes with Raman spectroscopy.  Matrix metalloproteinases are known to play a role in the invasiveness and metastasis of cancer.  This may be due in part to its cleavage of α-1-antitrypsin (AAT).  This is the first attempt to dynamically visualize proteomic changes that occur in cells.</p>
<p>All three modalities were able to show characteristic differences between normal and cancerous breast cells.  Future work will be performed to (a) integrate Raman spectroscopy and live cell imaging for long term real-time characterization of cancer progression and (b) further study of the atomic composition and chemistry of cell with XPS to understand the changes of elemental composition of normal versus cancer.</p>

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</description>

<author>Krystle Laja</author>


</item>


<item>
<title>Subacute effect of olfactory mucosal stem cells in the treatment of traumatic brain injury</title>
<link>http://digitalcommons.wayne.edu/oa_theses/160</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/160</guid>
<pubDate>Mon, 07 May 2012 12:54:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Worldwide, traumatic brain injury (TBI) is a major cause of death and disabilities. In United States, TBI is a serious public health problem since it contributes a third of all injury-related deaths. Despite a large number of clinical trials, no treatment exists for TBI so additional preclinical studies are needed to evaluate new therapies. In this study, an injury model developed by Marmarou and colleagues was used, that mimics a particular type of traumatic brain injury called diffuse axonal injury (Marmarou et al., 1994). The effectiveness of olfactory mucosal stem cells in the treatment of subacute traumatic brain injury was examined using a series of functional tests and analyses of brain sections. Inbred Lewis strains of rats were used so that cellular transplants are not rejected (Coyne et al., 2006). Behavioral results showed significant difference between the cell treated group and vehicle (saline) treated group in cognitive function and the qualitative histological analyses suggested lessened injury between the groups. Further investigation is required to understand the complete mechanisms behind the differences and the mode of action of stem cells.</p>

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</description>

<author>Saravanan Kumaran</author>


</item>


<item>
<title>Clinical and kinematic characteristics of cursive handwriting in elementary age children</title>
<link>http://digitalcommons.wayne.edu/oa_theses/159</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/159</guid>
<pubDate>Mon, 07 May 2012 12:53:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this research was to study the clinical and kinematic characteristics of cursive handwriting in healthy third and fifth grade children. One hundred-nine children participated in this study; 53 were in grade three and 56 were in grade five. Five commonly used clinical assessments were selected addressing strength, sensorimotor and coordination characteristics specific to handwriting. Two handwriting assessments, the Evaluation Tool of Children's Handwriting–Cursive, and the writing subtest of the Jebsen Test of Hand Function, assessed speed and/or legibility of handwriting. A simple cursive writing task was also produced on a digitized tablet and analyzed for kinematic features. Multiple T–Tests were used to determine significant gender differences and the effects of maturation on handwriting. Logistic regression analysis was used to determine if clinical or kinematic characteristics were predictors of legibility in cursive handwriting. Multiple linear regression analyses were used to determine if clinical or kinematic characteristics of handwriting contributed to handwriting speed and legibility. Results of this study indicate that in all groups, boys had less legible handwriting than girls. With maturation, healthy children in the third and fifth grades improve in their ability to smoothly write in the up and down direction, which is complemented by improved hand steadiness and coordination. The strong association between the grooved pegboard and legibility suggest that improving a child's in-hand manipulation skills may contribute to improvement in handwriting skills. The Jebsen and grooved pegboard contributed to handwriting speed and legibility. The findings of this study will guide Occupational Therapists in improving their understanding of the clinical and kinematic mechanisms underlying handwriting, which are critical to the development of appropriate intervention paradigms.</p>

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</description>

<author>Penelope Nikolakakis Ikonomakis</author>


</item>


<item>
<title>v. 74, issue 16, April 6, 2007</title>
<link>http://digitalcommons.bryant.edu/archway/887</link>
<guid isPermaLink="true">http://digitalcommons.bryant.edu/archway/887</guid>
<pubDate>Mon, 07 May 2012 12:53:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


<category>Higher education</category>

</item>


<item>
<title>Urban soil genesis, weathering of waste building materials, and bioavailability of lead in a chronosequence at former demolition sites, detroit, michigan</title>
<link>http://digitalcommons.wayne.edu/oa_theses/158</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/158</guid>
<pubDate>Mon, 07 May 2012 12:53:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>An urban soil chronosequence in downtown Detroit, MI spanning 95 years of weathering was studied to determine the effects of time on soil genesis, artifact weathering, and Pb geochemistry. The results show that ^A- and ^Ck-horizons can develop within a few decades, whereas B-horizon development occurs on a scale of centuries.  Melanization of ^A-horizons was enhanced by airborne deposition of soot and flyash, and ^Ck horizons have formed by weathering of calcareous artifacts.  Hence, urban soil genesis has been significantly affected by anthropogenic activities.  Plaster and mortar artifacts may weather away completely within a few decades.  Corrosion of iron-artifacts begins shortly after burial, and is enhanced by deicing salts and solution of gypsic artifacts.  However, iron artifacts have survived 95 years of weathering.  Weathering of iron artifacts has resulted in pedocementation and mobilization of Fe.  This is attributed to fluctuating redox conditions (ferrolysis) produced by seasonal wet-dry and freeze-thaw cycles, and waterlogging caused by reduced permeability associated with densic horizons. All of the demolition site soils are contaminated with Pb, but total Pb concentrations are below the EPA trigger level of 400 mg kg-1.  Soot and other carbonaceous microparticles appear to be controlling the bioavailability of Pb in ^A-horizons.  Organically bound-Pb is being leached from ^A-horizons, and accumulating in ^Ck-horizons where it is sorbed by pedogenic calcite, corroded iron-artifacts and ferruginous microparticles. Pedogenic calcite and ferrihydrite, generated by weathering of calcareous and ferruginous building materials, are potential immobilizing agents for Pb and thus may have ameliorating effects on urban soils.  Sand-sized microparticles related to coal combustion are locally abundant in the soils studied.  They represent a previously unrecognized sink for heavy metals, but more study is needed because most of this material is likely found in finer size fractions which were not studied.  More study is also needed of earthworms in urban soils because levels of bioaccessible Pb were found to be lower in the rhizosphere and earthworm casts than in the bulk ^A-horizons.  Hence, earthworms may be significantly reducing the amount of bioavailable-Pb in the rhizosphere through bio-uptake and their extensive casting activity.  If so, earthworms could be used as a natural remediation tool for reducing the hazard associated with resuspension of contaminated urban soil.  ^A-horizon</p>

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</description>

<author>Brian Robert Dubay</author>


</item>


<item>
<title>Antioxidant properties of gooseberry affected by in vitro digestion</title>
<link>http://digitalcommons.wayne.edu/oa_theses/157</link>
<guid isPermaLink="true">http://digitalcommons.wayne.edu/oa_theses/157</guid>
<pubDate>Mon, 07 May 2012 12:53:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The health benefits of antioxidants have been supported for decades. Dietary acquisition of these compounds is common and berries are especially rich in antioxidants. Due to the roles they play in protecting the human body from oxidative odamage, studies of the bioaccessibility of antioxidant absorption are on the rise. In this study, the stability of antioxidant capacity via in vitro digestion of gooseberries was investigated. Digested and undigested samples of two species of gooseberry, Tixia (T, bright red) and Invicta (I, pale green), were tested for antioxidant capacity via total phenolic content (TPC) assay, DPPH radical scavenging assay, and oxygen radical absorbance capacity (ORAC) assay. Results from this study implied that digestion enhances the availability of antioxidants in these fruits, where the digested batches showed a higher antioxidant content and ability, with p<0.01 (T & I), p<0.05 (T & I) and p<0.05 (I only) as computed from TPC, DPPH and ORAC, respectively. Another remarkable finding noted that Tixia species possess higher antioxidant ability than Invicta species, according to TPC, DPPH, and ORAC with p<0.001, p<0.001 and p<0.01, respectively. In addition to determining the total antioxidant content and capacity through the aforementioned assays, high performance liquid chromatography (HPLC) profiling enabled us to identify 8 of the antioxidants found in Tixia and Invicta, using 23 standard antioxidants as reference. The profiling revealed that only quercetin hydrate was significantly higher in digested samples (p<0.05). It is important to note that digestion may also modify the chemical characteristics of antioxidants thus altering their identification but not necessarily their function. In conclusion, antioxidants of gooseberry (Tixia and Invicta) may have an enhanced bioaccessibility after in vitro digestion but compounds contributing to the antioxidant capacity of these fruits require further investigation.</p>

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</description>

<author>Chia-jung Chiang</author>


</item>


<item>
<title>Notebook - January-March 1984</title>
<link>http://scholarcommons.sc.edu/notebook/54</link>
<guid isPermaLink="true">http://scholarcommons.sc.edu/notebook/54</guid>
<pubDate>Mon, 07 May 2012 12:51:17 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Contents:</strong></p>
<p>Table of Contents.....p. i<br> Archeological Field Reconnaissance of Proposed City of Denmark Waste Treatment Project.....p. iii</p>

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</description>

<author>South Carolina Institute of Archaeology and Anthropology--University of South Carolina</author>


</item>


<item>
<title>Administration of clozapine to a mother rat potentiates
pup ultrasonic vocalization in response to separation
and re-separation: Contrast with haloperidol</title>
<link>http://digitalcommons.unl.edu/psychfacpub/564</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/psychfacpub/564</guid>
<pubDate>Mon, 07 May 2012 12:47:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The present study examined how haloperidol (typical) and clozapine (atypical) treatment to mother rats affected their pups’ ultrasonic vocalization (USV) response to maternal separation and re-separation (termed “maternal potentiation”). Clozapine (10 mg/kg, sc) but not haloperidol (0.2 mg/kg, sc) significantly enhanced the maternal potentiation of 40 kHz USVs in pups that were briefly reunited with their dams. This novel paradigm provides an indirect way of assessing the impact of antipsychotic treatment on the quality of maternal care. It may also be useful in examining the impact of antipsychotic treatment on social bonding between infants and mothers.</p>

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</description>

<author>Ming Li et al.</author>


</item>


<item>
<title>The Emergence of Feminism During the Late Eighteenth and Nineteenth Centuries by Female Artists and Authors</title>
<link>http://scholarship.rollins.edu/mls/25</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/25</guid>
<pubDate>Mon, 07 May 2012 12:45:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis paper identifies the ways in which the painters Elisabeth Vigée-Lebrun and Mary Cassatt and the writers Charlotte Brontë and Elizabeth Barrett Browning challenged the limitations of their sex by engaging in professions outside of the domestic sphere during the late eighteenth and nineteenth centuries. This essay first focuses on the negative effects that a separation between the private and public spheres had on women, how these changes came about, the expectations society imposed on women, and how many women learned to cope and step forward into the public sphere. The emphasis shifts to an examination of the lives of Vigée-Lebrun, Cassatt, Brontë, and Barrett Browning and the career paths they pursued as women living in a patriarchal society. By providing a detailed analysis of their works, this essay reveals how each woman maintained her idealized feminine image while she pursued a profession outside of the domestic realm. All four women expressed their creative minds to the public eye and challenged the patriarchal theory that women could not and should not pursue creative ambitions. Their works, both visual and literary, sought out awareness and solicited a reexamination of women’s values, roles, and duties in the Victorian era.</p>

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</description>

<author>Tracy S. Koubek</author>


</item>


<item>
<title>Creating Change Through Documentary Film:  An Examination of Select Films</title>
<link>http://scholarship.rollins.edu/mls/24</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/24</guid>
<pubDate>Mon, 07 May 2012 12:45:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Radically altering or expanding the worldview of an individual or the collective of society requires the interacting media to engage and invoke an emotional response. In many instances, film, educates and elucidates—thus facilitating a shift of perspective. By challenging the status quo and creating a definitive alteration in perception when circumstances and information prove the former viewpoint or worldview is no longer valid. Documentaries that are related to causes can be part of this process is that it holds the potential to provoke action and evoke an emotional response. The foundation for building a new framework through an application of knowledge is shaped as visual connections are created by the documentary on the viewer. Shifting an individual’s fixed perspective requires an alteration in thinking. Through film, a collective shift in worldview can be activated when enough individuals throughout society know and understand that change is imminent and necessary.  Deliberate activation of this process is the goal of the cause related documentarian.  Film and media are instrumental in creating and implementing shifts in viewpoints that foster change within the individual and the collective of society.</p>

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</description>

<author>Elizabeth C. Faulcon</author>


</item>


<item>
<title>Subsidiarity and Self-Interest: Federalism at the European Court of Justice</title>
<link>http://scholarship.law.gwu.edu/faculty_publications/2</link>
<guid isPermaLink="true">http://scholarship.law.gwu.edu/faculty_publications/2</guid>
<pubDate>Mon, 07 May 2012 12:45:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Subsidiarity is the principle which the European Community has begun applying to consider whether federal legislation is necessary, or whether action by the Member States will suffice. This article considers whether subsidiarity should constrain the Court of Justice's jurisprudence as well. It begins by analyzing the federalism problems posed by the Court's case law concerning remedies for the violation of Community law, in particular the doctrine holding Member States liable in damages for failing properly to implement Community directives. After concluding that the Court is required to review this jurisprudence for consistency with the subsidiarity principle, and that the Court's existing compensation and rights-centered rationale is largely insufficient, the article develops a two-fold argument for sustaining Member State liability even under the subsidiarity principle: such liability is essential to deterring Member State cheating on implementation, and encourages the development of directives that delegate rather than precisely prescribe regulatory content. The article concludes by describing possible modifications to prevailing liability doctrine in order to render it more consistent with the subsidiarity and proportionality principles.</p>

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</description>

<author>Edward T. Swaine</author>


</item>


<item>
<title>Evaluation of Pneumonia Virus of Mice as a Possible Human
Pathogen</title>
<link>http://digitalcommons.unl.edu/publichealthresources/144</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/144</guid>
<pubDate>Mon, 07 May 2012 12:43:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pneumonia virus of mice (PVM), a relative of human respiratory syncytial virus (RSV), causes respiratory disease in mice. There is serologic evidence suggesting widespread exposure of humans to PVM. To investigate replication in primates, African green monkeys (AGM) and rhesus macaques (<em>n=</em>4) were inoculated with PVM by the respiratory route. Virus was shed intermittently at low levels by a subset of animals, suggesting poor permissiveness. PVM efficiently replicated in cultured human cells and inhibited the type I interferon (IFN) response in these cells. This suggests that poor replication in nonhuman primates was not due to a general nonpermissiveness of primate cells or poor control of the IFN response. Seroprevalence in humans was examined by screening sera from 30 adults and 17 young children for PVM-neutralizing activity. Sera from a single child (6%) and 40% of adults had low neutralizing activity against PVM, which could be consistent with increasing incidence of exposure following early childhood. There was no cross-reaction of human or AGM sera between RSV and PVM and no cross-protection in the mouse model. In native Western blots, human sera reacted with RSV but not PVM proteins under conditions in which AGM immune sera reacted strongly. Serum reactivity was further evaluated by flow cytometry using unfixed Vero cells infected with PVM or RSV expressing green fluorescent protein (GFP) as a measure of viral gene expression. The reactivity of human sera against RSV-infected cells correlated with GFP expression, whereas reactivity against PVM-infected cells was low and uncorrelated with GFP expression. Thus, PVM specificity was not evident. Our results indicate that the PVM-neutralizing activity of human sera is not due to RSV- or PVM-specific antibodies but may be due to low-affinity, polyreactive natural antibodies of the IgG subclass. The absence of PVM-specific antibodies and restriction in nonhuman primates makes PVM unlikely to be a human pathogen.</p>

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</description>

<author>Linda G. Brock et al.</author>


</item>


<item>
<title>An Examination of Gender Differences in Today&apos;s Mathematics Classrooms</title>
<link>http://digitalcommons.cedarville.edu/education_theses/1</link>
<guid isPermaLink="true">http://digitalcommons.cedarville.edu/education_theses/1</guid>
<pubDate>Mon, 07 May 2012 12:42:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Much research identifies a gender gap in mathematics, and some research points to single-gender math classrooms as a solution to the math gender divide. The author conducted a seven week study in which she divided fifty fifth grade students into singlegender mathematics classes. She wanted to examine if single-gender math classes affected the math achievement and attitudes of her female students. Upon completion of the study the author found there was no statistical significance in the girls’ achievement between a single-gender classroom and a coeducational classroom. There was a significant difference in the girls’ perceptions as to how they best learn math.</p>

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</description>

<author>Celeste E. Dunlap</author>


</item>


<item>
<title>Comparison of Analysis and Experiment for Gearbox Noise</title>
<link>http://engagedscholarship.csuohio.edu/enme_facpub/5</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/enme_facpub/5</guid>
<pubDate>Mon, 07 May 2012 12:42:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Low-contact-ratio spur gears were tested in the NASA gearnoise rig to study the noise radiated from the top of the gearbox. Experimental results were compared with a NASA acoustics code to validate the code for predicting transmission noise. The analytical code is based on the boundary element method (BEM) which models the gearbox top as a plate in an infinite baffle. Narrow-band vibration spectra measured at 63 nodes on the gearbox top were used to produce input data for the BEM model. The BEM code predicted the total sound power based on this measured vibration. The measured sound power was obtained from an acoustic intensity scan taken near the surface of the gearbox at the same 63 nodes used for vibration measurements. Analytical and experimental results were compared at four different speeds for sound power at each of the narrow-band frequencies over the range of 400 to 3200 Hz. Results are also compared for the sound power level at meshing frequency plus three sideband pairs and at selected gearbox resonant frequencies. The difference between predicted and measured sound power is typically less than 3 dB with the predicted value generally less than the measured value.</p>

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</description>

<author>Fred B. Oswald et al.</author>


</item>


<item>
<title>The genealogical construction of the Kyrgyz Republic: kinship, state, and “tribalism” by David Gullette [book review]</title>
<link>http://opus.ipfw.edu/anthro_facpubs/105</link>
<guid isPermaLink="true">http://opus.ipfw.edu/anthro_facpubs/105</guid>
<pubDate>Mon, 07 May 2012 12:40:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Noor O&apos;Neill Borbieva</author>


</item>


<item>
<title>Regulation of the OTC Derivatives Market: a Regulatory Proposal of CDS</title>
<link>http://digitalcommons.sacredheart.edu/wcob_sp/2</link>
<guid isPermaLink="true">http://digitalcommons.sacredheart.edu/wcob_sp/2</guid>
<pubDate>Mon, 07 May 2012 12:40:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>According to many commentators the credit derivatives and especially CDS have been a leading cause to the development of the current financial crisis. During the last year, policy makers, regulators, and other commentators around the world have therefore focused their attention on how to regulate OTC derivatives and especially CDS.</p>
<p>The purpose of this paper is to analyze some of the proposed regulatory responses to OTC derivatives and especially CDS from an economic point of view. The paper proposes a twofold regulatory response. First it proposes that we return to the old common law rule of "rule against difference contracts". The second part of the proposal, which relates especially to CDS, is to simultaneously assist the market participants establish central counterparty trading. This would include collateral requirements, daily mark to market, standardization of CDS, etc.</p>
<p>Building upon the misunderstandings of derivatives and the urge by policy makers to act, it’s easy that the regulatory debate goes out of hand and that misunderstanding about derivatives leads to miss regulation of the same. The risk is therefore apparent that policy makers will overact and over regulate OTC derivatives. This would destroy the undoubtedly positive effect OTC derivatives play for sound risk management in many corporations. The challenge is to find the right balance between over and under regulation. The policy proposal in this paper is a way to strike this tradeoff.</p>
<p>Submitted as a requirement for FN699 "Current Issues in Finance: Financial Crisis and Risk Management", taught by Dr. Lucjan T. Orlowski, Sacred Heart University John F. Welch College of Business, Luxembourg Campus</p>

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</description>

<author>Erik Welin</author>


</item>


<item>
<title>Automated Acoustic Intensity Measurements and the Effect of Gear Tooth Profile on Noise</title>
<link>http://engagedscholarship.csuohio.edu/enme_facpub/4</link>
<guid isPermaLink="true">http://engagedscholarship.csuohio.edu/enme_facpub/4</guid>
<pubDate>Mon, 07 May 2012 12:39:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Acoustic intensity measurements were made at NASA Lewis Research Center on a spur gear test apparatus. The measurements were obtained with the Robotic Acoustic Intensity Measurement System developed by Cleveland State University. This system provided dense spatial positioning, and was calibrated against a high quality acoustic intensity system. The measured gear noise compared gearsets having two different tooth profiles. The tests evaluated the sound field of the different gears for two speeds and three loads. The experimental results showed that gear tooth profile had a major effect on measured noise. Load and speed were found to have an effect on noise also.</p>

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</description>

<author>William J. Atherton et al.</author>


</item>


<item>
<title>Lorentzian isothermic surfaces in R-j(n)</title>
<link>http://repository.wellesley.edu/mathematicsfaculty/5</link>
<guid isPermaLink="true">http://repository.wellesley.edu/mathematicsfaculty/5</guid>
<pubDate>Mon, 07 May 2012 12:37:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>If a time-like surface in R-j(n) is isothermic then there is another, uniquely determined surface which is either anti-conformal or conformal and sign-reversing with the same Gauss map. The choice of mapping depends on whether the shape operator is diagonalizable over R or C.</p>

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</description>

<author>Martin A. Magid</author>


</item>


<item>
<title>Lorentzian Isothermic Surfaces and Bonnet Pairs</title>
<link>http://repository.wellesley.edu/mathematicsfaculty/4</link>
<guid isPermaLink="true">http://repository.wellesley.edu/mathematicsfaculty/4</guid>
<pubDate>Mon, 07 May 2012 12:37:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lorentzian surfaces in Lorentz three-space are studied using an indefinite version of the quaternions. A classification theorem for Bonnet pairs in Lorentz three-space is obtained.</p>

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</description>

<author>Martin A. Magid</author>


</item>


<item>
<title>Association between Acculturation and Breastfeeding among Hispanic Women: Data from the Pregnancy Risk Assessment and Monitoring System</title>
<link>http://digitalcommons.unl.edu/publichealthresources/143</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/publichealthresources/143</guid>
<pubDate>Mon, 07 May 2012 12:36:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Background: Breastfeeding rates are typically higher among Hispanic women; however, they vary by acculturation status in that those more acculturated are less likely to breastfeed than those who are less acculturated. This study examined the association between acculturation and breastfeeding behaviors using population-based data.</p>
<p>Methods: Data (N = 8942) from the Pregnancy Risk Assessment Monitoring System (PRAMS) were used for analysis. Acculturation status was determined using self-reported Hispanic ethnicity and the language in which the women responded to the PRAMS survey, either English or Spanish. Hispanic women who responded to the survey in Spanish were categorized as less acculturated than those who responded in English. Breastfeeding indicators used were: initiation, duration to ≥ 10 weeks, and exclusive breastfeeding to ≥ 10 weeks.</p>
<p>Results: The prevalence rates of breastfeeding initiation, duration, and exclusive breastfeeding to ≥ 10 weeks were significantly higher among less acculturated than among highly acculturated. More acculturated were less likely to initiate breastfeeding (prevalence ratio [PR] = 0.88; 95% CI, 0.86-0.90), less likely to breastfeed ≥ 10 weeks (PR = 0.77; 95% CI, 0.72-0.82), and less likely to report exclusive breastfeeding to ≥ 10 weeks (PR =,0.70; 95% CI, 0.58-0.85). The relationship between breastfeeding continuation and acculturation persisted after adjusting for covariates in that more acculturated were less likely to breastfeed to ≥ 10 weeks (adjusted prevalence ratio [APR] = 0.81; 95% CI, 0.75-0.87), as did the relationship between exclusivity and acculturation; more acculturated were less likely to report exclusive breastfeeding (APR = 0.69; 95% CI, 0.55-0.87).</p>
<p>Conclusions: Breastfeeding promotion efforts must include culturally/linguistically supportive services to assure that women are able to make optimal infant feeding decisions.</p>

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</description>

<author>Indu B. Ahluwalia et al.</author>


</item>


<item>
<title>Assessing Patient-Provider Collaboration in Subjects with Type 2 Diabetes in Jamaica and Effects on Glycemic Control</title>
<link>http://escholarship.umassmed.edu/ssp/125</link>
<guid isPermaLink="true">http://escholarship.umassmed.edu/ssp/125</guid>
<pubDate>Mon, 07 May 2012 12:31:46 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Background: </strong>Type 2 Diabetes Mellitus is a growing health problem worldwide that places patients at increased risk of morbidity and mortality from microvascular and macrovascular complications. Research suggests that a patient-centered approach which focuses on patient-physician communication and collaboration in the management of chronic diseases such as diabetes may improve clinical outcomes in a glycemic parameter such as HbA1c. We measured the degree of this patient-centered approach in a sample population of subjects with Type 2 Diabetes in Jamaica with the use of the Patient Assessment of Care for Chronic Illness (PACIC) questionnaire and assessed the relationship between patient-centered care and glycemic control.</p>
<p><strong>Purpose: </strong>To compare PACIC scores to hemoglobin A1C values in subjects with Type 2 Diabetes and to determine the correlation between patient-physician collaboration and glycemic control.</p>
<p><strong>Methods: </strong>Participants were selected from the Diabetes Clinic at the University Hospital of the West Indies in Kingston, Jamaica, in August 2011. A total of 40 patients were screened, but only 19 met eligibility requirements and agreed to participate in the study. Informed consent was obtained. The patients were assigned a study number and then self-administered the Patient Assessment of Care for Chronic Illness (PACIC) questionnaire in a private examination room. The PACIC is a validated instrument consisting of a total of 20 multiple choice questions. It measures five subjective categories: 1) Patient activation; 2) Delivery system design and decision support; 3) Goal setting; 4) Problem solving/contextual counseling; and 5) Follow-up/ coordination. Each category can be averaged individually with scores ranging from 1-5. The overall PACIC score measures patient-physician collaboration with a score ranging from a low of 1.0 to a high of 5.0. Additional study data was collected by one of the authors (PD) for both characterization of the study population and for analysis of potential confounders. These additional independent variables included: patient age, type of treatment (i.e., lifestyle modification), and years diagnosed with diabetes mellitus.</p>
<p><strong>Results: </strong>There were 19 subjects who were eligible for study and completed the PACIC questionnaire. There were more women than men (78.9%, 15 women and 4 men). The age range was 33-78 years with a mean age of 55. The range for years diagnosed with diabetes was 0.03 – 32 years with a mean of 14 years. Eight of the subjects (42.1%) were on combination therapy with insulin and oral hypoglycemic agents. Hemoglobin A1c values ranged from 5.4% – 15.5% with a mean of 10.8%. The PACIC scores ranged from 1.85 – 4.80 with a mean of 3.15. No statistically significant correlations were found between PACIC scores and HbA1c (r=.184). HbA1c did not significantly correlate with patient age (r=-.408), nor with years diagnosed with diabetes (r=-.244). Further statistical analysis using non-parametric correlation coefficients to take small sample sizes into account did not reveal any significant relationship either.</p>
<p><strong>Conclusion: </strong>There was no statistically significant trends between our main variables of the patient-physician collaboration (PACIC score) and glycemic control (HbA1c). Analysis of potential confounders also failed to elicit any correlations with HbA1c. The major limitation in this study is the small sample size. An important next step would be to repeat this study with a larger clinic sample.</p>

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</description>

<author>Paul E. Daniel Jr. et al.</author>


<category>Diabetes Mellitus, Type 2</category>

<category>Patient-Centered Care</category>

<category>Physician-Patient Relations</category>

<category>Blood Glucose</category>

<category>Hemoglobin A, Glycosylated</category>

</item>


<item>
<title>Admission Hyperglycemia in Setting of Acute Heart Failure is Associated with Increased In-hospital Mortality Among Patients without Diabetes</title>
<link>http://escholarship.umassmed.edu/ssp/124</link>
<guid isPermaLink="true">http://escholarship.umassmed.edu/ssp/124</guid>
<pubDate>Mon, 07 May 2012 12:31:44 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Background: </strong>Heart Failure (HF) in the setting of comorbid diabetes mellitus (DM) has been extensively examined and is associated with increased mortality. More recently, hyperglycemia independent of DM status during critical illness admissions has become recognized as an indicator of poor outcomes. Despite evolving understanding of DM in the setting of acute HF, hyperglycemia at time of admission for acute HF has not been examined with regard to in-hospital treatment and patient outcomes.</p>
<p><strong>Objective: </strong>The goal of this study is to examine differences in in-hospital treatment and outcomes of patients hospitalized for acute HF according to glycemic status.</p>
<p><strong>Methods: </strong>The sample consisted of 9,748 residents of the Worcester (MA) metropolitan area hospitalized at all 11 greater Worcester medical centers for acute decompensated HF during the years 1995 - 2004 with data available on diabetic status and admission glucose measurements. Patients were stratified into three groups based on history of DM and admission hyperglycemia defined by glucose ≥200 mg/dL: 1) nondiabetic, normoglycemic (NDNG); 2) non-diabetic, hyperglycemic (NDHG); and 3) diabetic (DM).</p>
<p><strong>Results: </strong>Non-diabetic, normoglycemic patients were similar to NDHG patients with respect to age and medical history and were significantly older and less likely to have a history of various comorbid conditions such as hypertension, stroke and renal disease when compared to diabetics (p-values</p>
<p><strong>Conclusions: </strong>The results of our population-based investigation suggest that non-diabetic patients hospitalized for acute HF who are hyperglycemic at the time of admission represent a vulnerable group of patients at risk for increased mortality during hospitalization. Hyperglycemia ≥200 mg/dL during acute HF hospitalization should be taken into account when providing in-hospital management for HF with additional consideration given to ascertainment of diabetic status and glycemic control.</p>

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</description>

<author>Nicholas J. Maselli et al.</author>


<category>Hyperglycemia</category>

<category>Heart Failure</category>

<category>Diabetes Mellitus</category>

<category>Hospitalization</category>

</item>


<item>
<title>Diagnostic Patterns and Immunohistochemical Stain Usage in Extended Core Prostate Biopsies: Comparisons Between Genitourinary and Non-Genitourinary Pathologists</title>
<link>http://escholarship.umassmed.edu/ssp/123</link>
<guid isPermaLink="true">http://escholarship.umassmed.edu/ssp/123</guid>
<pubDate>Mon, 07 May 2012 12:31:41 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Background</strong>: Ancillary immunohistochemical (IPOX) stains are useful in clarifying diagnostically challenging pathologic specimens. In diagnostic workup of prostate needle biopsies, stains for basal cells and α-methylacyl coenzyme A racemase are routinely used to support or refute the diagnosis of prostate cancer. Although useful, these stains add cost and must be used judiciously. There is a lack of firm guidelines establishing the proper utilization of IPOX studies in prostate pathology. Therefore, differences in patterns of stain use and diagnoses may exist, related to expertise of the pathologist.</p>
<p><strong>Objectives</strong>: The purpose of this study was to compare patterns of diagnoses and IPOX stain use in extended core prostate biopsies between genitourinary (GU) and non-genitourinary (NGU) pathologists in the University of Massachusetts Medical Center Pathology department.</p>
<p><strong>Methods</strong>: By computer search of medical records, consecutive extended core prostate biopsies (6+ cores) from years 2006-2011 were identified. Using Current Procedural Terminology (CPT) billing data, the number of cores and number of IPOX stains were retrieved. Diagnoses were recorded. Pathologists were divided into two groups based on expertise: genitourinary and non-genitourinary. Differences in the patterns of IPOX use and diagnoses between the two groups were analyzed.</p>
<p><strong>Results</strong>: GU pathologists diagnose significantly higher rates of prostate cancer (43.8% vs. 35.8%, p</p>
<p><strong>Conclusion</strong>: Significant differences exist in patterns of IPOX usage between GU and NGU pathologists in extended core prostate biopsy in this single institution study. This suggests the need for guidelines and continuing education focused on this issue to standardize practice, an intervention likely to improve quality of diagnoses and to reduce unnecessary costs.</p>

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</description>

<author>Anna Plourde et al.</author>


<category>Prostate</category>

<category>Biopsy, Needle</category>

<category>Pathology, Clinical</category>

<category>Staining and Labeling</category>

<category>Immunohistochemistry</category>

</item>


<item>
<title>Codon Optimization for Alpha 1-Antitrypsin Disease</title>
<link>http://escholarship.umassmed.edu/ssp/122</link>
<guid isPermaLink="true">http://escholarship.umassmed.edu/ssp/122</guid>
<pubDate>Mon, 07 May 2012 12:31:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Alpha 1-antitrypsin deficiency is a genetic disorder caused by defective production of alpha 1-antitrypsin (AAT).  Gene therapy approaches have been conducted in patients with AAT deficiency with successful AAT expression, but not to the therapeutic levels required to reduce the risk of emphysema.  Codon optimization, a somewhat new and evolving technique, is used by many scientists to maximize protein expression in living organisms by altering translational and transcriptional efficiency as well as protein refolding.  The purpose of this study was to develop single stranded and double stranded AAT gene constructs, test their protein expression in vitro, and compare with those levels expressed by the AAT construct that is currently in clinical trials.  Three constructs were to be developed, yet only one construct was successfully cloned.  This clone, optimized ds-CB-AAT, illustrated increased AAT protein expression as the transfection time increased.  However, protein levels were appreciably lower in the optimized construct compared to the single stranded (long intron) AAT construct that is currently being administered in clinical trials. The data did not suggest that the optimized AAT construct does in fact express more AAT protein in vitro as expected.  In order to achieve data that can be reproduced, the 2 remaining constructs need to be cloned and all of the isolated plasmid DNA should be prepared on the same scale to minimize any additional confounding variables.</p>

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</description>

<author>Timothy Menz et al.</author>


<category>alpha 1-Antitrypsin Deficiency</category>

<category>alpha 1-Antitrypsin</category>

<category>Gene Therapy</category>

<category>Codon</category>

</item>


<item>
<title>Are Our Students Teachers?</title>
<link>http://escholarship.umassmed.edu/ssp/121</link>
<guid isPermaLink="true">http://escholarship.umassmed.edu/ssp/121</guid>
<pubDate>Mon, 07 May 2012 12:31:37 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Background: </strong>Though the practical and philosophical importance of teaching educational skills to students of medicine has been widely acknowledged, the principle accrediting bodies of resident and medical student training in the U.S. do not require medical schools to offer formal training in how to teach. Both recognize resident teaching in their competencies: the Accreditation Council for Graduate Medical Education (ACGME) requires all residencies to have a formal program in teaching; the Liaison Committee on Medical Education (LCME) mandates that all residents and faculty charged with teaching medical students “be prepared for their roles in teaching and assessment.” But many medical students begin to teach their peers and junior students during medical school. In a 2008 poll of 130 accredited, M.D.-granting US medical schools, all 99 responding institutions reported using their students as teachers, though less than half offered formal curriculum in teaching, and among them, the majority of curricula reached only a fraction of graduating students, usually toward the end of their final year. In addition, students teach patients from early in their training, and formal teaching skills may support this activity and thus enhance patient care. Despite favorable argument for the value and efficacy of such programs in the literature of the past three decades, U.S. medical education has largely deferred the formal instruction of educational skills to the postgraduate level.</p>
<p>UMMS offers its students a patchwork of peer and patient educational opportunities without presently offering formal background in evidence-based teaching skills. While this type of scattered elective experience can be immensely valuable to students, further formalization may better prepare UMMS students to satisfy the institutional competency of “assuming the role of teacher when appropriate.” The introduction and refinement of teaching skills may in turn benefit the quality of the educational program, the wider institutional and interprofessional learning environment, and patient care and health education across the Commonwealth. Many UMMS students stay on to become teaching residents and faculty, and remain – or later return – to the state to practice and teach. In a demanding era of expanding biomedical complexity, reduced resident duty hours, collaborative health care delivery, and patient-centered decision-making, offering or requiring relevant educational training to our clinicians early in their development may provide substantial benefit to our health care system and patients.</p>
<p><strong>Objectives: </strong>The objectives of this project were: 1) Quantify the existence of peer and patient teaching opportunities within and outside the formal UMMS educational program at all levels of the curriculum; 2) Describe the receptiveness of faculty and students toward institution of a formal program preparing all UMMS students to teach both peers and patients in a variety of settings common to residency and clinical practice in any field; 3) Report arguments for and against such a program from the vantage of faculty and students, including barriers specific to UMMS; and 4) Propose a blueprint for such a program based on the opportunities already offered, new ideas from faculty and students, and models culled both from the educational literature and from other institutions.</p>
<p><strong>Methods: </strong>Short online surveys were sent to course-directing faculty and to all currently enrolled UMMS students in years 1-4 of the curriculum using a combination of Likert-scale and open response items. Per the IRB, the survey did not require a formal approval or exemption process.</p>
<p><strong>Results: </strong>FACULTY: 58% of all course and clerkship faculty responded; 48% stated that their courses already offer some opportunity in peer and patient teaching, though only in select cases do students receive formal training in educational methodology and thorough feedback on their performance as educators. Often, these programs do not apply to all students. 50% of faculty were most (4-5 on a 5-point scale) “interested in incorporating a formal student teaching component into [their] course,” and when asked whether they had particular “ideas for how students might practice their peer education or patient teaching skills within [their] course?” 67% answered “yes,” posing a variety of possibilities for peer and patient education, both familiar and innovative.</p>
<p><strong>Students: </strong>143 responses (28%) were received from currently enrolled students, constituting 17.6% of MS1, 25.4% of MS2, 26.9% of MS3, and 39.6% of MS4 and extending students. Self-reported comfort as a peer and patient educator increased modestly over class years, when expressed as an average of responses on a 1-5 Likert scale (Peer: MS1 3.00, MS2 3.13, MS3 3.13, MS4 3.47, MS4 extended 3.57; Patient: MS1 3.32, MS2 3.75, MS3 3.88, MS4 3.95, MS4 extended 4.21). 30.8% of students identified some opportunity to teach within the formal curriculum; outside the formal curriculum, 28.7% of students listed no opportunity, while the rest listed different amounts and frequencies ranging from daily to once a year, depending on how they defined teaching. 75.6% of responding students emphasized the value of “learn[ing] formal teaching skills - small group, lecture, bedside - in medical school” and 77.7% emphasized the value of opportunities to “practice formal teaching skills” (4-5 on a 5-point scale). 41.3% indicated that they would “actively create time to learn, practice, and refine these skills prior to residency if it were not included in the formal academic program.”</p>
<p><strong>Conclusion: </strong>Though teaching opportunities exist at UMMS, most are not formalized, and those offered reach less than a third of students. While comfort with peer and patient teaching increases across the educational continuum from first to fourth year, the increase remains modest. 84% of graduates report that they felt prepared to teach as interns based on their 2011 AAMC graduation questionnaire responses, but given the importance of teaching in many aspects of medicine, we see room for improvement. Overall, there is a strong call both from both faculty and students at UMMS for formally incorporating educational training into the curriculum, with a particular focus on teaching practice. Free-response items emphasized dramatic differences in student and faculty understanding and recognition of teaching as a professional role among both peers and patients. These discrepancies highlight a need for increased awareness of the teaching responsibilities of medical students, and of the possibilities that are open to them during medical school. A structured approach to medical student teaching skills across the continuum of undergraduate medical education is the first step in this process.</p>

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</description>

<author>Joel Bradley et al.</author>


<category>Education, Medical, Undergraduate</category>

<category>Teaching</category>

<category>Students, Medical</category>

<category>Patient Education as Topic</category>

</item>


<item>
<title>Maeve and the Lost King</title>
<link>http://scholarship.rollins.edu/mls/23</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/23</guid>
<pubDate>Mon, 07 May 2012 12:28:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Maeve and the Lost King is a fantasy adventure novel. This is a story that takes place in a long-ago time in a totally fictitious Celtic land. It is a story of two young people, Maeve and Sé, living a simple existence, falling in love, getting married and then discovering through two magic torcs that they are the lost King and Queen of Tór-roisín. They set out on a journey with old friends, new friends, fairies and two elves to reclaim Sé's family's home, Castle Muireach, in the town of Tór-roisín.</p>

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</description>

<author>Sunshine Guilkey Schulenberg</author>


</item>


<item>
<title>Search for Dark Matter Satellites Using &lt;em&gt;FERMI&lt;/em&gt;-LAT</title>
<link>http://scholarworks.boisestate.edu/physics_facpubs/100</link>
<guid isPermaLink="true">http://scholarworks.boisestate.edu/physics_facpubs/100</guid>
<pubDate>Mon, 07 May 2012 12:24:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Numerical simulations based on the ΛCDM model of cosmology predict a large number of as yet unobserved Galactic dark matter satellites.We report the results of a Large Area Telescope (LAT) search for these satellites via the <em>γ</em>-ray emission expected from the annihilation of weakly interacting massive particle (WIMP) dark matter. Some dark matter satellites are expected to have hard <em>γ</em>-ray spectra, finite angular extents, and a lack of counterparts at other wavelengths. We sought to identify LAT sources with these characteristics, focusing on <em>γ</em>-ray spectra consistent with WIMP annihilation through the <em>b¯b</em> channel. We found no viable dark matter satellite candidates using one year of data, and we present a framework for interpreting this result in the context of numerical simulations to constrain the velocity-averaged annihilation cross section for a conventional 100 GeVWIMP annihilating through the <em>b¯b</em> channel.</p>

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</description>

<author>Jay Norris</author>


</item>


<item>
<title>Beck, Louis Marvin (FA 76)</title>
<link>http://digitalcommons.wku.edu/dlsc_fa_fin_aid/577</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_fa_fin_aid/577</guid>
<pubDate>Mon, 07 May 2012 12:24:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Finding aid only for Folklife Archives Project 76. Interview with Ophelia Ellen Johnson Hanna about her family and education growing up as an African American in Warren County, Kentucky.  Includes taped interview and index.</p>

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</description>

<author>Manuscripts &amp; Folklife Archives</author>


</item>


<item>
<title>Anderson, Linda Allen (FA 77)</title>
<link>http://digitalcommons.wku.edu/dlsc_fa_fin_aid/576</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_fa_fin_aid/576</guid>
<pubDate>Mon, 07 May 2012 12:24:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Finding aid only for Folklife Archives Project 77.  “Stone Masons and Their Craft in the Bluegrass Area of Kentucky,” interpretive paper and interviews executed for a folk studies class at Western Kentucky University in 1986.  Collection includes photographs of stone cutting and stonework in the Bluegrass region.</p>

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</description>

<author>Manuscripts &amp; Folklife Archives</author>


</item>


<item>
<title>Barefoot, Jeffrey Allen (FA 78)</title>
<link>http://digitalcommons.wku.edu/dlsc_fa_fin_aid/575</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_fa_fin_aid/575</guid>
<pubDate>Mon, 07 May 2012 12:24:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Finding aid only for Foklifle Archives Project 78.  “The Middle Bridge Ghost” interpretive paper and videotaped interviews executed for a folk studies class at Western Kentucky University.</p>

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</description>

<author>Manuscripts &amp; Folklife Archives</author>


</item>


<item>
<title>Cox, Carolyn Ann (Helm) (FA 79)</title>
<link>http://digitalcommons.wku.edu/dlsc_fa_fin_aid/574</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_fa_fin_aid/574</guid>
<pubDate>Mon, 07 May 2012 12:24:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Finding aid only for Folklife Archives Project 79.  “1920-1930 Logan CountyFurnishings: The Felts House,” oral history project executed for a folk studies class at Western Kentucky University.  Interviews were recorded on cassette tape and are indexed.</p>

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</description>

<author>Manuscripts &amp; Folklife Archives</author>


</item>


<item>
<title>Gipson, Kenneth Todd (FA 80)</title>
<link>http://digitalcommons.wku.edu/dlsc_fa_fin_aid/573</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_fa_fin_aid/573</guid>
<pubDate>Mon, 07 May 2012 12:23:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>Finding aid only for Folklife Archives Project 80. “Occupational Folklore of Monument Makers.”  Interviews with Carroll Monument Company employees regarding their occupation and related stories.  Includes one summary and one transcript.</p>

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</description>

<author>Manuscripts &amp; Folklife Archives</author>


</item>


<item>
<title>Good News from the Bible for Tough Economic Times</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/377</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/377</guid>
<pubDate>Mon, 07 May 2012 12:23:42 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mark Allen Powell</author>


</item>


<item>
<title>A Game Changer? The Complexities of Cultural Heritage in the Debate Over the Elgin Marbles</title>
<link>http://digitalwindow.vassar.edu/senior_capstone/67</link>
<guid isPermaLink="true">http://digitalwindow.vassar.edu/senior_capstone/67</guid>
<pubDate>Mon, 07 May 2012 12:22:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Alexandra Zeman</author>


</item>


<item>
<title>Promoting and Preserving Scholarly and Creative Work at Parkland College</title>
<link>http://digitalcommons.bepress.com/webinars/23</link>
<guid isPermaLink="true">http://digitalcommons.bepress.com/webinars/23</guid>
<pubDate>Mon, 07 May 2012 12:21:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>What is the role of scholarship at a community college? The process of identifying, sharing, showcasing, and using the scholarly and creative work of a community college can lay the groundwork for cross-curricular collaborations and encourage students to demonstrate learning at a higher level. At Parkland College, the institutional repository (SPARK) has played a key role in this process.</p>
<p>In this webinar, Erika Hackman and Sherry Cmiel share their experiences creating and developing Parkland's repository. They talk about how SPARK evolved to meet institutional needs, as well as discuss funding, generating buy-in, forming partnerships, the benefits of focusing on faculty-sponsored student work, and how this can be replicated at other community colleges.</p>

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</description>

<author>Sherry Cmiel et al.</author>


</item>


<item>
<title>Making Spaces to Learn.</title>
<link>http://repository.brynmawr.edu/edu_pubs/4</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/edu_pubs/4</guid>
<pubDate>Mon, 07 May 2012 12:20:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>An essay review of <em>What the Best College Teachers Do</em> (Bain, Ken. Cambridge, MA: Harvard University Press, 2004).</p>

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</description>

<author>Alison Cook-Sather</author>


</item>


<item>
<title>Chris</title>
<link>http://lux.lawrence.edu/artgallery_se2012/1</link>
<guid isPermaLink="true">http://lux.lawrence.edu/artgallery_se2012/1</guid>
<pubDate>Mon, 07 May 2012 12:19:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Materials: Gelatin Silver Print</p>
<p>Dimensions: 16" x 20"</p>
<p>Advisor: Julie Lindemann and John Shimon</p>
<p>Graduating Class: 2012</p>

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</description>

<author>Sara L. Sheldon-Rosson</author>


</item>


<item>
<title>Guided data repair</title>
<link>http://docs.lib.purdue.edu/ccpubs/451</link>
<guid isPermaLink="true">http://docs.lib.purdue.edu/ccpubs/451</guid>
<pubDate>Mon, 07 May 2012 12:17:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this paper we present GDR, a Guided Data Repair framework that incorporates user feedback in the cleaning process to enhance and accelerate existing automatic repair techniques while minimizing user involvement. GDR consults the user on the updates that are most likely to be beneficial in improving data quality. GDR also uses machine learning methods to identify and apply the correct updates directly to the database without the actual involvement of the user on these specific updates. To rank potential updates for consultation by the user, we first group these repairs and quantify the utility of each group using the decision-theory concept of value of information (VOI). We then apply active learning to order updates within a group based on their ability to improve the learned model. User feedback is used to repair the database and to adaptively refine the training set for the model. We empirically evaluate GDR on a real-world dataset and show significant improvement in data quality using our user guided repairing process. We also, assess the trade-off between the user efforts and the resulting data quality.</p>

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</description>

<author>Ahmed Elmagarmid et al.</author>


</item>


<item>
<title>What Is and What Can Be: How a Liminal Position Can Change: Learning and Teaching in Higher Education</title>
<link>http://repository.brynmawr.edu/edu_pubs/3</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/edu_pubs/3</guid>
<pubDate>Mon, 07 May 2012 12:16:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this article we analyze what happens when undergraduate students are positioned as pedagogical consultants in a faculty development program. Drawing on their spoken and written perspectives, and using the classical anthropological concept of liminality, we illustrate how these student consultants revise their relationships with their teachers and their responsibilities within their learning. These revisions have the potential to transform deep-seated societal understandings of education based on traditional hierarchies and teacher/student distinctions.</p>

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</description>

<author>Alison Cook-Sather et al.</author>


</item>


<item>
<title>Plague and Violence in Saint-Louis-du-Sénégal, 1917-1920</title>
<link>http://repository.brynmawr.edu/history_pubs/9</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/history_pubs/9</guid>
<pubDate>Mon, 07 May 2012 12:16:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this article I will examine the impact of the plague epidemics that hit the urban colonial society in Saint-Louis between 1917 and 1920.   This research shows that because the poor, who lived in appalling hygienic conditions, were the most affected, the measures taken against the plague soon became discriminatory.   The refusal by the medical authorities to find a compromise between what was necessary to prevent further contagion and the cultural and religious practices of the poor, especially funeral rites, provoked anger amongst the poor and resulted in a disobedience campaign which lasted several months.   This crisis revealed a deep gap between the medical authorities who advocated the use of force against the rebels on the one side, and the political authorities on the other.   Although well-know figures such as Carrera and Blaise Diagne intervened with the inhabitants of the contaminated areas, they failed to reconcile the two sides.   The frightening idea of seeing the epidemics reach the better-off classes pushed the authorities to declare a state of emergency, force the recalcitrants to go to the lazaret, and set fire to the contaminated areas. The evacuated remained homeless until the day when the decision was made to rebuild Guet-Ndar.</p>

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</description>

<author>Kalala J. Ngalamulume</author>


</item>


<item>
<title>Bryn Mawr Alumnae Quarterly, 1907-1909</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/30</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/30</guid>
<pubDate>Mon, 07 May 2012 12:14:39 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bryn Mawr College, Alumni Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Quarterly, 1909-1911</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/29</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/29</guid>
<pubDate>Mon, 07 May 2012 12:14:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College, Alumni Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Quarterly, 1911-1913</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/28</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/28</guid>
<pubDate>Mon, 07 May 2012 12:13:10 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bryn Mawr College, Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Quarterly, 1913-1915</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/27</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/27</guid>
<pubDate>Mon, 07 May 2012 12:13:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College, Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Quarterly, 1915-1917</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/26</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/26</guid>
<pubDate>Mon, 07 May 2012 12:11:04 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College, Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Quarterly, 1917-1919</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/25</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/25</guid>
<pubDate>Mon, 07 May 2012 12:05:12 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Quarterly, 1919-1921</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/24</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/24</guid>
<pubDate>Mon, 07 May 2012 12:05:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College, Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1921</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/23</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/23</guid>
<pubDate>Mon, 07 May 2012 12:03:12 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1922</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/22</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/22</guid>
<pubDate>Mon, 07 May 2012 12:03:10 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1923</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/21</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/21</guid>
<pubDate>Mon, 07 May 2012 12:03:08 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1924</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/20</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/20</guid>
<pubDate>Mon, 07 May 2012 12:01:16 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1925</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/19</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/19</guid>
<pubDate>Mon, 07 May 2012 12:01:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>The following copyrighted material has been removed from this volume: Vol. 5, No. 9, pp. 5-14: Edwin Arlington Robinson's Treatment of the Arthurian Legend by Charles Cester of the Sorbonne; "The article which we have the privilege of printing below in the third of a series of six lectures on Edwin Arlington Robinson which were delivered at Bryn Mawr in the first art of November. The six lectures are later to be published in book form."</p>

	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1926</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/18</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/18</guid>
<pubDate>Mon, 07 May 2012 11:59:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1927</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/17</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/17</guid>
<pubDate>Mon, 07 May 2012 11:59:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>The following material has been removed from this volume: Vol. 7, no. 7, p. 6: The Women's Colleges reprinted by special permission from The Saturday Evening Post, copyright, 1927, by The Curtis Publishing Company; Vol. 7, no. 8, p. 7: Fair Play for Women's Colleges, reprinted by permission from The New York Times</p>

	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1928</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/16</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/16</guid>
<pubDate>Mon, 07 May 2012 11:59:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1929</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/15</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/15</guid>
<pubDate>Mon, 07 May 2012 11:57:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>The following material has been removed from this volume: Vol. 9, no. 8, p. 14: Syria by Kate Chambers Seeyle, BMC Class of 1911, reprinted from the Christian Herald.</p>

	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1930</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/14</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/14</guid>
<pubDate>Mon, 07 May 2012 11:56:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>The following material has been removed from this volume: Vol. 10, no. 8., pp. 8-10: Financing a College Education by Margaret Gilman, Chairman, Scholarship and Loan Committee, Bryn Mawr College, appeared in Savings Bank Journal of March, 1930.</p>

	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1931</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/13</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/13</guid>
<pubDate>Mon, 07 May 2012 11:56:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The following material has been removed from this volume: Vol. 12, no. 6, p. 4: Impressions of May Day, John Mason Brown, Dramatic Critic, Praises Revels, New York Evening Post, May 9, 1932; Vol. 12, no. 8, pp.6-7, In Memorial Anne Crosby Emery Allinson, 1892, Editorial from The Providence Journal, August 18, 1932.</p>

	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Approximate String Matching With Dynamic Programming and Suffix Trees</title>
<link>http://digitalcommons.unf.edu/etd/196</link>
<guid isPermaLink="true">http://digitalcommons.unf.edu/etd/196</guid>
<pubDate>Mon, 07 May 2012 11:56:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>The importance and the contribution of string matching algorithms to the modern society cannot be overstated. From basic search algorithms such as spell checking and data querying, to advanced algorithms such as DNA sequencing, trend analysis and signal processing, string matching algorithms form the foundation of many aspects in computing that have been pivotal in technological advancement.</p>
<p>In general, string matching algorithms can be divided into the categories of exact string matching and approximate string matching. We study each area and examine some of the well known algorithms. We probe into one of the most intriguing data structure in string algorithms, the suffix tree. The lowest common ancestor extension of the suffix tree is the key to many advanced string matching algorithms. With these tools, we are able to solve string problems that were, until recently, thought intractable by many. Another interesting and relatively new data structure in string algorithms is the suffix array, which has significant breakthroughs in its linear time construction in recent years.</p>
<p>Primarily, this thesis focuses on approximate string matching using dynamic programming and hybrid dynamic programming with suffix tree. We study both approaches in detail and see how the merger of exact string matching and approximate string matching algorithms can yield synergistic results in our experiments.</p>

	]]>
</description>

<author>Leng Hui Keng</author>


</item>


<item>
<title>Focus</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/376</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/376</guid>
<pubDate>Mon, 07 May 2012 11:55:57 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Al Gwinn</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1932</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/12</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/12</guid>
<pubDate>Mon, 07 May 2012 11:55:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1933</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/11</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/11</guid>
<pubDate>Mon, 07 May 2012 11:54:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The following material has been removed from this volume: Vol. 14, no. 4, pp. 22-23: Doings of Alumnae: Sylvia Bowditch, 1933, tells of her work as a courier with the frontier nursing service, reprinted in part from the Boston Sunday Herald</p>

	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1934</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/10</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/10</guid>
<pubDate>Mon, 07 May 2012 11:54:41 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1935</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/9</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/9</guid>
<pubDate>Mon, 07 May 2012 11:54:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>The following material has been removed from this volume: Vol. 16, no. 6, p. 9: The Late Emmy Noether, Professor (Albert) Einsten writes in apprciation of a fellow-mathematician, New York Times, Friday, May 3rd.</p>

	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1936</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/8</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/8</guid>
<pubDate>Mon, 07 May 2012 11:53:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Constructing Critical Literacy: Self-Reflexive Ways for Curriculum and Pedagogy</title>
<link>http://scholarworks.boisestate.edu/literacy_facpubs/62</link>
<guid isPermaLink="true">http://scholarworks.boisestate.edu/literacy_facpubs/62</guid>
<pubDate>Mon, 07 May 2012 11:48:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Schools have the potential to be places where students can come to understand how and why knowledge and power are constructed (Aronowitz & Giroux, 1993). This paper provides an overview of critical literacy from a critical theory/Freirian perspective. Within it, critical literacy is posited as a necessary component of all classroom practices, one that is elemental to Dewey’s (1916) view of democracy, social justice, and what it means to be literate. Features of a critical literacy approach to instruction are provided along with rationales for the necessity of its inclusion in a democratic society.</p>

	]]>
</description>

<author>Anne Gregory et al.</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1937</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/7</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/7</guid>
<pubDate>Mon, 07 May 2012 11:44:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Influence of hydrologic linkages on fluvial ecosystem structure and
function</title>
<link>http://digitalcommons.usu.edu/biology_facpub/181</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/181</guid>
<pubDate>Mon, 07 May 2012 11:43:44 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1938</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/6</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/6</guid>
<pubDate>Mon, 07 May 2012 11:43:40 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Influence de l’hydrodynamique sur la structure et le fonctionnement
des écosystèmes fluviaux: des ruisseaux aux grand cours d’eau</title>
<link>http://digitalcommons.usu.edu/biology_facpub/180</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/180</guid>
<pubDate>Mon, 07 May 2012 11:43:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Role of hydrologic linkages in fluvial ecosystem structure and
function</title>
<link>http://digitalcommons.usu.edu/biology_facpub/179</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/179</guid>
<pubDate>Mon, 07 May 2012 11:43:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Organic carbon retention and metabolism in near-stream
groundwater</title>
<link>http://digitalcommons.usu.edu/biology_facpub/178</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/178</guid>
<pubDate>Mon, 07 May 2012 11:43:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>How to begin teaching a course for the first time beginning with
nothing…filling the void</title>
<link>http://digitalcommons.usu.edu/biology_facpub/177</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/177</guid>
<pubDate>Mon, 07 May 2012 11:43:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Beyond the riparian zone: Aquatic-terrestrial linkages in watersheds</title>
<link>http://digitalcommons.usu.edu/biology_facpub/176</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/176</guid>
<pubDate>Mon, 07 May 2012 11:43:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Organic matter dynamics at the groundwater -
surface water interface of a mountain stream</title>
<link>http://digitalcommons.usu.edu/biology_facpub/175</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/175</guid>
<pubDate>Mon, 07 May 2012 11:43:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. N. Dahm et al.</author>


</item>


<item>
<title>Dissolved organic carbon dynamics and the
groundwater and surface water interface</title>
<link>http://digitalcommons.usu.edu/biology_facpub/174</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/174</guid>
<pubDate>Mon, 07 May 2012 11:43:12 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. N. Dahm et al.</author>


</item>


<item>
<title>Tricks of the trade: how to succeed in graduate school</title>
<link>http://digitalcommons.usu.edu/biology_facpub/173</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/173</guid>
<pubDate>Mon, 07 May 2012 11:43:08 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Hydrologic linkages and ecosystem function</title>
<link>http://digitalcommons.usu.edu/biology_facpub/172</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/172</guid>
<pubDate>Mon, 07 May 2012 11:43:04 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Ceci n’est pas une pipe– Understanding nutrient uptake and flux in
stream ecosystems</title>
<link>http://digitalcommons.usu.edu/biology_facpub/171</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/171</guid>
<pubDate>Mon, 07 May 2012 11:43:00 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Fluvial discontinua- influence on flowpaths and ecosystem processes</title>
<link>http://digitalcommons.usu.edu/biology_facpub/170</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/170</guid>
<pubDate>Mon, 07 May 2012 11:42:55 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Ecological basis for site-specific TMDL targets in Utah</title>
<link>http://digitalcommons.usu.edu/biology_facpub/169</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/169</guid>
<pubDate>Mon, 07 May 2012 11:42:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Nutrient processes in aquatic ecosystems</title>
<link>http://digitalcommons.usu.edu/biology_facpub/168</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/168</guid>
<pubDate>Mon, 07 May 2012 11:42:48 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Biochemical oxygen demand in rivers</title>
<link>http://digitalcommons.usu.edu/biology_facpub/167</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/167</guid>
<pubDate>Mon, 07 May 2012 11:42:44 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Nutrient dynamics in streams: known knowns, known unknowns, and
why you should care</title>
<link>http://digitalcommons.usu.edu/biology_facpub/166</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/166</guid>
<pubDate>Mon, 07 May 2012 11:42:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Understanding hydrologic transport and biogeochemical reaction
(HTBR) in streams and lakes: challenges and opportunities</title>
<link>http://digitalcommons.usu.edu/biology_facpub/165</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/165</guid>
<pubDate>Mon, 07 May 2012 11:42:36 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Rivulets to rivers: a journey down the continuum with atom Y</title>
<link>http://digitalcommons.usu.edu/biology_facpub/164</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/164</guid>
<pubDate>Mon, 07 May 2012 11:42:32 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Air and water quality concerns along the Wasatch Front: Science for
sustainability</title>
<link>http://digitalcommons.usu.edu/biology_facpub/163</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/163</guid>
<pubDate>Mon, 07 May 2012 11:42:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Ceci n’est pas une pipe: understanding nutrient transport and
removal processes in rivers</title>
<link>http://digitalcommons.usu.edu/biology_facpub/162</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/162</guid>
<pubDate>Mon, 07 May 2012 11:42:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Ecology readings from the University of Wisconsin</title>
<link>http://digitalcommons.usu.edu/biology_facpub/161</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/161</guid>
<pubDate>Mon, 07 May 2012 11:42:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Natural
Ecosystems II- Aquatic Ecosystems</title>
<link>http://digitalcommons.usu.edu/biology_facpub/160</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/160</guid>
<pubDate>Mon, 07 May 2012 11:42:14 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>A. P. Covich et al.</author>


</item>


<item>
<title>Improving quantitative understanding using spreadsheet models</title>
<link>http://digitalcommons.usu.edu/biology_facpub/159</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/159</guid>
<pubDate>Mon, 07 May 2012 11:42:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker</author>


</item>


<item>
<title>Research to inform nutrient
endpoints in East Canyon Creek, Utah</title>
<link>http://digitalcommons.usu.edu/biology_facpub/158</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/158</guid>
<pubDate>Mon, 07 May 2012 11:42:04 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker et al.</author>


</item>


<item>
<title>Final Report: research to inform
nutrient endpoints in Spring Creek, Utah</title>
<link>http://digitalcommons.usu.edu/biology_facpub/157</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/157</guid>
<pubDate>Mon, 07 May 2012 11:41:59 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker et al.</author>


</item>


<item>
<title>Epilogue: United Nations sponsored
1992 Earth Summit in Rio de Janeiro- where do we go from here?</title>
<link>http://digitalcommons.usu.edu/biology_facpub/156</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/156</guid>
<pubDate>Mon, 07 May 2012 11:41:55 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>E. W. Miller et al.</author>


</item>


<item>
<title>Simulation of stream-groundwater exchange and near-stream flow
paths of two first order mountain streams using MODFLOW</title>
<link>http://digitalcommons.usu.edu/biology_facpub/155</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/155</guid>
<pubDate>Mon, 07 May 2012 11:41:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>G. J. Wroblicky et al.</author>


</item>


<item>
<title>Implications of pollutants on diversity
of aquatic bacteria and fungi</title>
<link>http://digitalcommons.usu.edu/biology_facpub/154</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/154</guid>
<pubDate>Mon, 07 May 2012 11:41:47 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker et al.</author>


</item>


<item>
<title>Spatial and temporal variation in methane distribution at the ground
water- surface water interface in headwater catchments</title>
<link>http://digitalcommons.usu.edu/biology_facpub/153</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/153</guid>
<pubDate>Mon, 07 May 2012 11:41:42 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker et al.</author>


</item>


<item>
<title>Anoxia, anaerobic metabolism
biogeochemistry of the stream water- ground water interface</title>
<link>http://digitalcommons.usu.edu/biology_facpub/152</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/152</guid>
<pubDate>Mon, 07 May 2012 11:41:37 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker et al.</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1939</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/5</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/5</guid>
<pubDate>Mon, 07 May 2012 11:41:36 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Bryn Mawr Alumnae Bulletin, 1940</title>
<link>http://repository.brynmawr.edu/bmc_alumnae/4</link>
<guid isPermaLink="true">http://repository.brynmawr.edu/bmc_alumnae/4</guid>
<pubDate>Mon, 07 May 2012 11:41:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Bryn Mawr College. Alumnae Association</author>


</item>


<item>
<title>Genotoxic effects of gossypol acetic acid on cultured murine erythroleukemia
cells</title>
<link>http://digitalcommons.usu.edu/biology_facpub/151</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/151</guid>
<pubDate>Mon, 07 May 2012 11:41:32 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>S. K. Majumdar et al.</author>


</item>


<item>
<title>In vitro cytotoxicity of carboplatin on human breast adenocarcinoma and
normal fetal lung cells</title>
<link>http://digitalcommons.usu.edu/biology_facpub/150</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/150</guid>
<pubDate>Mon, 07 May 2012 11:41:27 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>B. D. Bobrin et al.</author>


</item>


<item>
<title>Heterotrophic bacteria and fungi
associated with decomposing leaves submerged in a lake in Pennsylvania, USA</title>
<link>http://digitalcommons.usu.edu/biology_facpub/149</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/149</guid>
<pubDate>Mon, 07 May 2012 11:41:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker et al.</author>


</item>


<item>
<title>Elemental processing in
leaf litter and sediments in an aquatic system: effects of anthropogenic
pollution</title>
<link>http://digitalcommons.usu.edu/biology_facpub/148</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/148</guid>
<pubDate>Mon, 07 May 2012 11:41:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. C. Daehler et al.</author>


</item>


<item>
<title>Hydrologic influences on groundwater-surface water ecotones:
heterogeneity in nutrient composition and retention</title>
<link>http://digitalcommons.usu.edu/biology_facpub/147</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/147</guid>
<pubDate>Mon, 07 May 2012 11:41:12 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H. M. Valett et al.</author>


</item>


<item>
<title>Acetate retention and metabolism in the
hyporheic zone of a mountain stream</title>
<link>http://digitalcommons.usu.edu/biology_facpub/146</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/146</guid>
<pubDate>Mon, 07 May 2012 11:41:07 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker et al.</author>


</item>


<item>
<title>Organic carbon supply and metabolism
in a near-stream groundwater ecosystem</title>
<link>http://digitalcommons.usu.edu/biology_facpub/145</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/145</guid>
<pubDate>Mon, 07 May 2012 11:41:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker et al.</author>


</item>


<item>
<title>Biodegredation of
dissolved free simple carbohydrates in surface, hyporheic and riparian waters of
a large river</title>
<link>http://digitalcommons.usu.edu/biology_facpub/144</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/144</guid>
<pubDate>Mon, 07 May 2012 11:40:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>P. Vervier et al.</author>


</item>


<item>
<title>Biogeochemistry of
surface waters and alluvial ground waters in streams and rivers during drought</title>
<link>http://digitalcommons.usu.edu/biology_facpub/143</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/143</guid>
<pubDate>Mon, 07 May 2012 11:40:53 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. N. Dahm et al.</author>


</item>


<item>
<title>Hydrologic variability, organic matter supply, and
denitrification in the Garonne River ecosystem</title>
<link>http://digitalcommons.usu.edu/biology_facpub/142</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/142</guid>
<pubDate>Mon, 07 May 2012 11:40:48 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker et al.</author>


</item>


<item>
<title>The flood pulse in a semi-arid riparian forest:
metabolic and biogeochemical responses to inter-flood interval</title>
<link>http://digitalcommons.usu.edu/biology_facpub/141</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/141</guid>
<pubDate>Mon, 07 May 2012 11:40:44 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H. M. Valett et al.</author>


</item>


<item>
<title>Amphibian chytridomycosis in Guatemala: Decline of a
cloud-forest frog fauna</title>
<link>http://digitalcommons.usu.edu/biology_facpub/140</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/140</guid>
<pubDate>Mon, 07 May 2012 11:40:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J. R. Mendelson III et al.</author>


</item>


<item>
<title>Stream geomorphology in a
mountain lake district: Sediment links, lake-modified hydraulics, and
downstream lake effects</title>
<link>http://digitalcommons.usu.edu/biology_facpub/139</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/139</guid>
<pubDate>Mon, 07 May 2012 11:40:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. D. Arp et al.</author>


</item>


<item>
<title>Discontinuities in stream nutrient uptake below lakes
in mountain drainage networks</title>
<link>http://digitalcommons.usu.edu/biology_facpub/138</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/138</guid>
<pubDate>Mon, 07 May 2012 11:40:30 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. D. Arp et al.</author>


</item>


<item>
<title>Poor growth of rainbow trout (Oncorhynus mykiss)
fed New Zealand mud snails (Potamopyrgus antipodarum)</title>
<link>http://digitalcommons.usu.edu/biology_facpub/137</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/137</guid>
<pubDate>Mon, 07 May 2012 11:40:25 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M. R. Vinson et al.</author>


</item>


<item>
<title>Are rivers just big
streams? Using a pulse method to measure nitrogen demand in a large river</title>
<link>http://digitalcommons.usu.edu/biology_facpub/136</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/136</guid>
<pubDate>Mon, 07 May 2012 11:40:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J. L. Tank et al.</author>


</item>


<item>
<title>Effects of periphyton
stoichiometry on mayfly excretion rates and nutrient ratios</title>
<link>http://digitalcommons.usu.edu/biology_facpub/135</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/135</guid>
<pubDate>Mon, 07 May 2012 11:40:15 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J. D. Rothlisberger et al.</author>


</item>


<item>
<title>Informing a stream
transient storage model with two-storage zones to discriminate in-channel dead
zones and hyporheic exchange</title>
<link>http://digitalcommons.usu.edu/biology_facpub/134</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/134</guid>
<pubDate>Mon, 07 May 2012 11:40:09 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>M. A. Biggs et al.</author>


</item>


<item>
<title>Differences in nitrate uptake
among benthic algal assemblages in a mountain stream</title>
<link>http://digitalcommons.usu.edu/biology_facpub/133</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/133</guid>
<pubDate>Mon, 07 May 2012 11:40:03 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michelle A. Baker et al.</author>


</item>


<item>
<title>Hydrologic control of nitrogen
removal, storage and export in a mountain stream</title>
<link>http://digitalcommons.usu.edu/biology_facpub/132</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/132</guid>
<pubDate>Mon, 07 May 2012 11:39:58 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R. O. Hall Jr. et al.</author>


</item>


<item>
<title>Species and genotype diversity drive community and ecosystem properties
in experimental microcosms</title>
<link>http://digitalcommons.usu.edu/biology_facpub/131</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/131</guid>
<pubDate>Mon, 07 May 2012 11:39:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>L. C. Latta IV et al.</author>


</item>


<item>
<title>Separating physical and biological
nutrient retention and quantifying uptake kinetics from ambient to saturation in
successive mountain stream reaches</title>
<link>http://digitalcommons.usu.edu/biology_facpub/130</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/130</guid>
<pubDate>Mon, 07 May 2012 11:39:47 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. Covino et al.</author>


</item>


<item>
<title>Dynamics of
nitrate production and removal as a function of residence time in the hyporheic
zone: a 15N tracer study</title>
<link>http://digitalcommons.usu.edu/biology_facpub/129</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/129</guid>
<pubDate>Mon, 07 May 2012 11:39:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J. P. Zarnetske et al.</author>


</item>


<item>
<title>Dissimilatory nitrate reduction
pathways in an oligotrophic aquatic ecosystem: spatial and temporal trends</title>
<link>http://digitalcommons.usu.edu/biology_facpub/128</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/128</guid>
<pubDate>Mon, 07 May 2012 11:39:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>I. J. Washbourne et al.</author>


</item>


<item>
<title>Labile dissolved
organic carbon supply limits hyporheic denitrification</title>
<link>http://digitalcommons.usu.edu/biology_facpub/127</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/biology_facpub/127</guid>
<pubDate>Mon, 07 May 2012 11:39:33 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>J. P. Zarnetske et al.</author>


</item>


<item>
<title>Characterization of Focused Ion Beam Milled Lines</title>
<link>http://digitalcommons.linfield.edu/studsymp_sci/2012/all/43</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/studsymp_sci/2012/all/43</guid>
<pubDate>Fri, 11 May 2012 15:00:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>As the nanotechnology is becoming an important aspect of science research and development, the application of the focused ion beam (FIB) technique is getting more attention. The focused ion beam is a tool for milling tiny objects. This research explored the characterization of FIB by relating milled line widths with their milling time. The scanning electron microscope (SEM) is used to image the milled lines and ImageJ to analyze the images. We found that the through-lens-detector (TLD) provides the best SEM image by reducing the shadowing effect which interfered with the data analysis. A logarithmic relation between the milled line width and milling time was determined. These presented results can help scientists design a FIB milling experiment in the future.</p>

	]]>
</description>

<author>Yingshi Guo</author>


<category>Physics (general)</category>

</item>


<item>
<title>Making Sense of Medicaid Reform</title>
<link>http://digitalcommons.providence.edu/health_policy_fac/2</link>
<guid isPermaLink="true">http://digitalcommons.providence.edu/health_policy_fac/2</guid>
<pubDate>Mon, 07 May 2012 11:22:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Robert B. Hackey</author>


<category>Health care policy</category>

</item>


<item>
<title>U.S. Radio in the 21st Century: Staying the Course in Unknown Territory</title>
<link>http://digitalcommons.linfield.edu/mscmfac_pubs/9</link>
<guid isPermaLink="true">http://digitalcommons.linfield.edu/mscmfac_pubs/9</guid>
<pubDate>Mon, 07 May 2012 11:21:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>This essay examines the development of the radio industry in the United States as it makes its way into the 21<sup>st</sup> century. Issues of regulation, technology, commerce, and culture are addressed.</p>

	]]>
</description>

<author>Michael Huntsberger</author>


</item>


<item>
<title>Our Mission To Theologically Educate</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/375</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/375</guid>
<pubDate>Mon, 07 May 2012 11:09:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Timothy C. Tennent</author>


</item>


<item>
<title>What Defines Our Community</title>
<link>http://place.asburyseminary.edu/ecommonsatschapelservices/374</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsatschapelservices/374</guid>
<pubDate>Mon, 07 May 2012 10:53:49 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Maxie D. Dunnam</author>


</item>


<item>
<title>State Dependent Neurophysiology: Depression</title>
<link>http://trace.tennessee.edu/utk_psycpubs/1</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_psycpubs/1</guid>
<pubDate>Mon, 07 May 2012 10:47:55 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Introduction:</strong> The DSM-IV-TR proposes that patients suffering from MDD will display state-dependent irregularities during examination by electroencephalogram (EEG) and other experimental methods. This study sought to capture this state dependency by utilizing topographical EEG and connectivity and LORETA current source density in the alpha frequency domain would differ between groups as would pre-post task salivary cortisol levels.</p>
<p><strong>Methods:</strong> This study was conducted with 23 (13 depressed) participants, 16 female, with a mean age of 20 ± 2.45. Depressed individuals had received a diagnosis of depression within the past year. We administered the SCID-R to depressed group. We collected salivary cortisol prior to any experimental conditions. Participants then provided 4 minute eyes-closed and eyes-opened baseline EEG recordings (ECB and EOB, respectively). The participants then completed the Beck Depression Inventory while EEG was continuously recorded. Items were presented for 8s in power point and responses were marked within the EEG record. These segments were extrapolated and compared for significance within and between groups. Post session cortisol was collected and analyzed. Although numerous differences may be expected, this study focuses on power, connectivity and LORETA current source density differences in the alpha frequency domain (8-12Hz) given its prominence in the depression literature.</p>
<p><strong>Results:</strong> Minimal differences are seen between depressed and non-clinical groups for topographical absolute and relative power. Significant differences were found in asymmetry, coherence and phase measures between groups. Current source density in alpha differs between groups with depressed showing specific regional increases in right prefrontal regions. Notably, cortisol decreased relative to the BDI task in all subjects, with differences still evident between groups.</p>
<p><strong>Discussion:</strong> As with many other studies, topographical power differences are sparse. Connectivity and LORETA current source density measures do reveal significant differences between groups and may provide a more accurate method for differential diagnosis of depressive disorder. Several studies have reported blunted cortisol responsivity in depression relative to stressors and our data appear to follow these results. Diagnostic, research, and clinical implications are discussed.</p>

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</description>

<author>Kelley G. Callaway et al.</author>


</item>


<item>
<title>Nesting ecology and cuticular microbial loads in dampwood (Zootermopsis angusticollis) and drywood termites (Incisitermes minor, I. schwarzi, Cryptotermes cavifrons)</title>
<link>http://iris.lib.neu.edu/biology_fac_pubs/20</link>
<guid isPermaLink="true">http://iris.lib.neu.edu/biology_fac_pubs/20</guid>
<pubDate>Mon, 07 May 2012 10:42:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Termites form one-piece nests in wood that can vary in their moisture content and degree of decomposition, and thus microbial richness. To estimate the microbial load of nests and the potential risk they pose for colony members, we quantified the number of microbes in the nest and on the cuticle of the dampwood termite, Zootermopsis angusticollis, and three drywood termites, Incisitermes minor, I. schwarzi, and Cryptotermes cavifrons. The number of colony forming units (CFUs) cultured from nest material samples and washes of the cuticle of larvae and nymphs were determined. CFUs recorded from nest material was low (fewer than 60 CFUs/g) in the drywood termites and comparatively high in the dampwood species, as more than 800 bacterial and fungal CFUs/g were cultured from the nest material of Z. angusticollis. Similarly, cuticular microbial loads were negligible in the drywood termites sampled, ranging from 0.5 to fewer than 16 CFUs/cm<sup>2</sup>, whereas approximately 200 CFUs/cm<sup>2</sup> were cultured from Z. angusticollis. The nesting and feeding habits of these basal species likely influence colony microbial load and the degree of pathogen exposure, which in turn could favor adaptations to resist disease that vary with termite nesting biology.</p>

	]]>
</description>

<author>Rebeca B. Rosengaus et al.</author>


</item>


<item>
<title>Disease resistance in the drywood termite, Incisitermes schwarzi: does nesting ecology affect immunocompetence?</title>
<link>http://iris.lib.neu.edu/biology_fac_pubs/19</link>
<guid isPermaLink="true">http://iris.lib.neu.edu/biology_fac_pubs/19</guid>
<pubDate>Mon, 07 May 2012 10:41:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Termites live in nests that can differ in microbial load and thus vary in degree of disease risk. It was hypothesized that termite investment in immune response would differ in species living in nest environments that vary in the richness and abundance of microbes. Using the drywood termite, <em>Incisitermes schwarzi</em> Banks (Isoptera: Kalotermitidae), as a model for species having low nest and cuticular microbial loads, the susceptibility of individuals and groups to conidia of the entomopathogenic fungus, <em>Metarhizium anisopliae</em> Sorokin (Hypocreales: Clavicipitaceae), was examined. The survivorship of I. schwarzi was compared to that of the dampwood termite, <em>Zootermopsis angusticollis</em> Hagen (Termopsidae), a species with comparatively high microbial loads. The results indicated that <em>I. schwarzi</em> derives similar benefits from group living as <em>Z. angusticollis</em>: isolated termites had 5.5 times the hazard ratio of death relative to termites nesting in groups of 25 while termites in groups of 10 did not differ significantly from the groups of 25. The results also indicated, after controlling for the influence of group size and conidia exposure on survivorship, that <em>Z. angusticollis</em> was significantly more susceptible to fungal infection than <em>I. schwarzi</em>, the former having 1.6 times the hazard ratio of death relative to drywood termites. Thus, disease susceptibility and individual investment in immunocompetence may not be dependent on interspecific variation in microbial pressures. The data validate prior studies indicating that sociality has benefits in infection control and suggest that social mechanisms of disease resistance, rather than individual physiological and immunological adaptations, may have been the principle target of selection related to variation in infection risk from microbes in the nest environment of different termite species.</p>

	]]>
</description>

<author>Daniel V. Calleri II et al.</author>


</item>


<item>
<title>2012 Chartbook: Table of Contents</title>
<link>http://scholarworks.umass.edu/cranchart/156</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/156</guid>
<pubDate>Mon, 07 May 2012 10:38:04 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>UMass Amherst Cranberry Exp Station</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Cautions</title>
<link>http://scholarworks.umass.edu/cranchart/155</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/155</guid>
<pubDate>Mon, 07 May 2012 10:38:03 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>UMass Amherst Cranberry Exp Station</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Resistance Management</title>
<link>http://scholarworks.umass.edu/cranchart/154</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/154</guid>
<pubDate>Mon, 07 May 2012 10:38:02 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Sylvia, Martha</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Warnings</title>
<link>http://scholarworks.umass.edu/cranchart/153</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/153</guid>
<pubDate>Mon, 07 May 2012 10:38:01 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>UMass Amherst Cranberry Exp Station</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Diseases</title>
<link>http://scholarworks.umass.edu/cranchart/152</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/152</guid>
<pubDate>Mon, 07 May 2012 10:38:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Caruso, Frank</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Weeds</title>
<link>http://scholarworks.umass.edu/cranchart/151</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/151</guid>
<pubDate>Mon, 07 May 2012 10:37:58 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sandler, H. A.</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Nutrition</title>
<link>http://scholarworks.umass.edu/cranchart/150</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/150</guid>
<pubDate>Mon, 07 May 2012 10:37:57 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>DeMoranville, Carolyn</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Irrigation Water Management</title>
<link>http://scholarworks.umass.edu/cranchart/149</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/149</guid>
<pubDate>Mon, 07 May 2012 10:37:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jeranyama, Peter</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Late Water</title>
<link>http://scholarworks.umass.edu/cranchart/148</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/148</guid>
<pubDate>Mon, 07 May 2012 10:37:55 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>DeMoranville, Carolyn J. et al.</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Winter Management</title>
<link>http://scholarworks.umass.edu/cranchart/147</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/147</guid>
<pubDate>Mon, 07 May 2012 10:37:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>DeMoranville, Carolyn</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Groundwater Protection Regulations &amp; Zone II</title>
<link>http://scholarworks.umass.edu/cranchart/146</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/146</guid>
<pubDate>Mon, 07 May 2012 10:37:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sylvia, Martha</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Measures and Conversions/Pesticide Storage</title>
<link>http://scholarworks.umass.edu/cranchart/145</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/145</guid>
<pubDate>Mon, 07 May 2012 10:37:52 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sandler, Hilary</author>

<source></source>

</item>


<item>
<title>2012 Chartbook: Index</title>
<link>http://scholarworks.umass.edu/cranchart/144</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/144</guid>
<pubDate>Mon, 07 May 2012 10:37:50 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>UMass Amherst Cranberry Exp Station</author>

<source></source>

</item>


<item>
<title>Clearing the Air: Four Propositions About Property Rights and Environmental Protection</title>
<link>http://www.repository.law.indiana.edu/facpub/515</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/515</guid>
<pubDate>Mon, 07 May 2012 10:35:33 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Daniel H. Cole</author>


</item>


<item>
<title>Book Review. From Renaissance Poland to Poland&apos;s Renaissance</title>
<link>http://www.repository.law.indiana.edu/facpub/514</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/514</guid>
<pubDate>Mon, 07 May 2012 10:35:29 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Daniel H. Cole</author>


</item>


<item>
<title>The Evocation of the Physical, Metaphysical, and Sonic Landscapes in Samuel Beckett&apos;s Short Dramatic Works</title>
<link>http://digitalrepository.trincoll.edu/theses/209</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/209</guid>
<pubDate>Mon, 07 May 2012 10:32:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>A historical analysis of the playwright’s theatrical spaces including the concept of temporality, which is central to the subsequent elements within the physical, metaphysical and sonic landscapes. The choice to focus on the philosophy of phenomenology centers on the notion that these short dramatic works present the theatrical landscape as the conscious character perceives it to be. The perceptual experience is explained by Maurice Merleau-Ponty as the relationship between the body and the world and the way as to which the self-limited interior space of the mind interacts with the limitless exterior space that surrounds it.</p>

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</description>

<author>Theresa A. Incampo</author>


</item>


<item>
<title>The Paradox within Modernity: How the Enlightenment has enabled a better quality of life while eroding the means by which life is given meaning</title>
<link>http://digitalrepository.trincoll.edu/theses/208</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/208</guid>
<pubDate>Mon, 07 May 2012 10:32:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>The modern order stands upon an intellectual paradox, with far reaching implications both at the level of the individual and on the global stage. Throughout most of human history, people have lived within distinct cultures. These cultures provided the individuals within them with a place within a larger whole, a moral system by which to direct their lives, and an answer to those pervasive existential doubts that plague us finite creatures with an awareness of infinity; in short, with a means of living fulfilling human lives. Societies as wholes were characterized by their cultures, forging and maintaining a cohesive identity based on a shared moral order and the myths that upheld it. However, the Enlightenment sparked a radical change in human perception, and from the new vantage point of reason much that was vital to the maintenance of culture is discredited. The philosophers of the Enlightenment promised a world made better by the light of reason, where objective means to finding truth would engender natural sciences with immeasurable potential to better the human condition and a new political science that would free men from the shackles of arbitrary and oppressive rule. And to an amazing extent, the Enlightenment philosophers have delivered. Yet there are vital human needs that cultures have satisfied, and which reason cannot. In a world of medicine, technology and political freedom, there is a pervasive awareness that something is missing, that some existential longings go unsatisfied in the modern order. In eroding the grounds for culture without being able to undertake its functions, the Enlightenment has enabled enormous advances in quality of life while eroding the means by which life is given meaning. I explore the causes of this paradox, tracing a history of religion and philosophy from pre-Enlightenment times until modernity, and the manifestations of this paradox in the modern world, including nihilism and the rise of fundamentalist religion. I conclude with a suggestion for a possible resolution.</p>

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</description>

<author>Alberto Martinez</author>


</item>


<item>
<title>Scavenger Interactions in a Human-Influenced Environment: The Foraging Behavior of the Red-Shouldered Hawk (Buteo lineatus) at Residential Compost Piles</title>
<link>http://digitalrepository.trincoll.edu/theses/207</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/207</guid>
<pubDate>Mon, 07 May 2012 10:32:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Residential composting has increased in popularity in recent years, along with the untested claim that the addition of animal-based kitchen scraps will increase the number of scavenging wildlife visitors. This study represents the first experimental test of that claim. Using three compost piles consisting respectively of no kitchen scraps (CON), a mix of animal and vegetable scraps (MIX), or only vegetable scraps (VEG) that were monitored with heat-in-motion sensitive cameras, we studied the visitation pattern of attracted wildlife. Of the 29 species identified thus far at the compost piles, I chose to focus on the red-shouldered hawk (<em>Buteo lineatus</em>), the most common raptor species, and the American crow (<em>Corvus brachyrhynchos</em>), by far the most common diurnal species. The red-shouldered hawk had a preference for the MIX pile, which was consistent with the overall trend of increased visitation to the MIX pile by all wildlife visitors, and frequented the piles more often in the winter/spring season. These two avian scavengers showed a distinct association at the compost piles, which appears to be due to the red-shouldered hawk attraction by American crows, perhaps to enhance their foraging.</p>
<p>In addition, I noted a novel behavior of the strictly carnivorous red-shouldered hawk: ingestion of vegetable matter at the VEG pile. As a possible explanation of this aberrant behavior, I investigated the presence of small mammals at the compost piles and a nearby location to determine whether the red-shouldered hawk was attracted to the VEG pile primarily because of these prey and not to forage on the vegetable material itself. I found that small mammal activity was significantly higher at the non-pile location. This finding, coupled with related observations, suggested that small mammals were not likely to be the primary cause of red-shouldered hawk foraging at the VEG pile.</p>

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</description>

<author>Eleanor Lucadamo</author>


</item>


<item>
<title>Traffic Flow Model and Simulation at Near Maximum Density</title>
<link>http://digitalrepository.trincoll.edu/theses/206</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/206</guid>
<pubDate>Mon, 07 May 2012 10:32:04 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Todor Mitev</author>


</item>


<item>
<title>The Conflicts of Euro-Islam: The issues of immigration and integration of Muslims into European Society</title>
<link>http://digitalrepository.trincoll.edu/theses/205</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/205</guid>
<pubDate>Mon, 07 May 2012 10:32:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Islamophobia is on the rise and is now a sentiment that has transcended almost every European country. In the aftermath of 9/11 and the subsequent bombings in Madrid and London, anxiety and fear of the “other” has been heightened. This fear has been harnessed by political parties in many European countries, most notably Denmark, Sweden, the Netherlands, Switzerland, and France. These countries all have supported political parties that have formed an anti-Muslim platform. The main claim is that the “Islamic identity” is incompatible with the “European identity”. Despite these xenophobic attitudes, the immigration population still inhabits European countries and continues to grow. An intense debate has ensued about the immigration and integration polices within many European countries. Immigration policies in general are being reexamined in the rise of this discourse.</p>
<p>My thesis examines the issues and questions surrounding the conflict of foreigners in Europe. Through my research I have found that the issue of Muslim immigrants in Europe is particularly problematic and complex. My paper seeks to outline the immigration and integration policies in Europe and to compare the difference in circumstances in Southern and Northern Europe. I have focused on Spain as a sample country for Southern Europe, and Denmark as a sample country for Northern Europe. While my findings and conclusions are by no means true for all Southern or Northern European countries, there is evidence of general trends for each region. My thesis is framed by this comparison but what it really analyzes is why countries have such a challenge with the successful integration of immigrants. I look towards historical imperial legacies, 20<sup>th</sup> century migration trends, geographical location, the legal systems, and the construction of national identities.</p>

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</description>

<author>Shayla B. Campbell</author>


</item>


<item>
<title>Fogler Favorites - Circulation/Reserve Department</title>
<link>http://digitalcommons.library.umaine.edu/faves/6</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/6</guid>
<pubDate>Mon, 07 May 2012 10:31:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series.  John Mahon’s Fogler Favorite is the Circulation/Reserve Department.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Fogler Favorites - Possession</title>
<link>http://digitalcommons.library.umaine.edu/faves/5</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/5</guid>
<pubDate>Mon, 07 May 2012 10:31:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series. Sharon Quinn Fitzgerald’s Fogler Favorite is Posession.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Las Trans: Negotiating Gender, Personhood, and Citizenship in Chile</title>
<link>http://scarab.bates.edu/honorstheses/51</link>
<guid isPermaLink="true">http://scarab.bates.edu/honorstheses/51</guid>
<pubDate>Mon, 07 May 2012 10:31:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>“Las Trans,” a group of male-to-female transgender residents living in Arica, Chile, challenge the strict dual-sex, dual-gender system of Chile’s family-oriented society. Chile presents an especially interesting case when analyzing the social position of sexual minorities due to the country’s historically strong ties to the Catholic Church, and, on a political level, the experience of 17 years of dictatorship during a crucial period of time in world history. Drawing on ethnographic fieldwork conducted with las Trans, I consider how gender identity and gender expression affect to what extent an individual can achieve full personhood and full citizenship in this South American country. Because of las Trans’ gender identities, they are unable to take advantage of many opportunities that are, in theory, guaranteed as basic human rights. Specifically, they are unable to attain legitimate jobs and are instead forced to earn a living through sex work, putting them at a heightened risk of being assaulted and contracting STDs. Additionally, las Trans experience numerous barriers in effectively accessing government-sponsored institutions, like healthcare, which are allegedly free and accessible for all citizens. This thesis argues that such discriminatory and exclusionary practices, rooted in social discrimination and reinforced through government legislation and religious discourse, further marginalize those who fail to conform to culturally prescribed gender categories and norms.</p>

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</description>

<author>Sydney A. Hare</author>


</item>


<item>
<title>Wireless Channel Equalization in Digital Communication Systems</title>
<link>http://scholarship.claremont.edu/cgu_etd/42</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/42</guid>
<pubDate>Mon, 07 May 2012 10:28:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Our modern society has transformed to an information-demanding system, seeking voice, video, and data in quantities that could not be imagined even a decade ago. The mobility of communicators has added more challenges. One of the new challenges is to conceive highly reliable and fast communication system unaffected by the problems caused in the multipath fading wireless channels. Our quest is to remove one of the obstacles in the way of achieving ultimately fast and reliable wireless digital communication, namely Inter-Symbol Interference (ISI), the intensity of which makes the channel noise inconsequential.</p>
<p>The theoretical background for wireless channels modeling and adaptive signal processing are covered in first two chapters of dissertation.</p>
<p>The approach of this thesis is not based on one methodology but several algorithms and configurations that are proposed and examined to fight the ISI problem. There are two main categories of channel equalization techniques, supervised (training) and blind unsupervised (blind) modes. We have studied the application of a new and specially modified neural network requiring very short training period for the proper channel equalization in supervised mode. The promising performance in the graphs for this network is presented in chapter 4.</p>
<p>For blind modes two distinctive methodologies are presented and studied. Chapter 3 covers the concept of multiple "cooperative" algorithms for the cases of two and three cooperative algorithms. The "select absolutely larger equalized signal" and "majority vote" methods have been used in 2-and 3-algoirithm systems respectively. Many of the demonstrated results are encouraging for further research.</p>
<p>Chapter 5 involves the application of general concept of simulated annealing in blind mode equalization. A limited strategy of constant annealing noise is experimented for testing the simple algorithms used in multiple systems. Convergence to local stationary points of the cost function in parameter space is clearly demonstrated and that justifies the use of additional noise. The capability of the adding the random noise to release the algorithm from the local traps is established in several cases.</p>

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</description>

<author>Sammuel Jalali</author>


</item>


<item>
<title>Developing Teachers&apos; Capacities to Create Caring Relationships with Students: A Case Study of a Gandhi-Inspired Private School in India</title>
<link>http://scholarship.claremont.edu/cgu_etd/41</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/41</guid>
<pubDate>Mon, 07 May 2012 10:28:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Research indicates that many factors may impede teachers' ability to develop caring relationships with students such as the school environment (Schaps, 2009), lack of cultural understanding (Thompson, 1998), the teacher's beliefs and attitudes about care (Goldstein, 2002), and personal experience of being cared for (Noddings, 1984). Yet, little research exists on how schools can address these and other potential limiting factors in order to help teachers cultivate caring relationships with students. The purpose of this study was to examine how one school in India, which claims to emphasize the importance of the teacher-student relationship, develops and supports teachers' capacities to create caring relationships with students. The hope was that the outcomes might provide insight for policy-makers, school administrators, and teachers about what is needed to best support teachers in their relationships with students.</p>
<p>The research site for this study was a pre-Kindergarten through 12th grade private school in India. The choice of India as a cultural context stemmed from the historical precedence of the importance of the teacher-student relationship. A mixed-methods descriptive case study served as the design for this study. Qualitative methods included interviews of teachers, administrators, and students, classroom and event observations, and document analysis. Quantitative methods included surveys of teachers and students. The qualitative data were analyzed using Noddings' (1984) four methods for teaching care (modeling, dialogue, practice, and confirmation) with other themes added as needed. Descriptive statistics and factor analyses of both surveys were used to triangulate and expand upon the qualitative data.</p>
<p>Findings indicated that schools can support teachers' capacity to care for students through a strong commitment to the teacher-student relationship, deliberate fostering of relationships between students, teachers, and parents, and through the modeling by and direct receipt of care from administrators. Other factors that may help teachers to care for students include cultural respect for the teaching profession and acknowledgement of care from both students and parents. However, teachers' efforts to care may be impeded by intense testing environments. Recommendations were made for the implementation of resources and support needed by teachers to create caring relationships with students.</p>

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</description>

<author>Victoria S. Zakrzewski</author>


</item>


<item>
<title>Fogler Favorites - America: History and Life</title>
<link>http://digitalcommons.library.umaine.edu/faves/4</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/4</guid>
<pubDate>Mon, 07 May 2012 10:21:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series. Katherine O'Flaherty’s Fogler Favorite is America: History and Life.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Fogler Favorites - Blueberries for Sal</title>
<link>http://digitalcommons.library.umaine.edu/faves/3</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/3</guid>
<pubDate>Mon, 07 May 2012 10:21:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series. Elaine Smith’s Fogler Favorite is Blueberries for Sal.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Fogler Favorites - Business Plans Handbook</title>
<link>http://digitalcommons.library.umaine.edu/faves/2</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/2</guid>
<pubDate>Mon, 07 May 2012 10:20:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series. James McConnon’s Fogler Favorite is Business Plans Handbook.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>Fogler Favorites - Cider House Rules</title>
<link>http://digitalcommons.library.umaine.edu/faves/1</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/faves/1</guid>
<pubDate>Mon, 07 May 2012 10:20:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poster is part of the “Fogler Favorites” series.  Thomas Jones’ Fogler Favorite is Cider House Rules.</p>

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</description>

<author>Jerry Lund et al.</author>


</item>


<item>
<title>ckn520310p1b2</title>
<link>http://place.asburyseminary.edu/ecommonsfacultylectures/5</link>
<guid isPermaLink="true">http://place.asburyseminary.edu/ecommonsfacultylectures/5</guid>
<pubDate>Mon, 07 May 2012 10:20:49 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>ATS</author>


</item>


<item>
<title>Protistan species and their diversity from a molecular perspective</title>
<link>http://iris.lib.neu.edu/biology_diss/26</link>
<guid isPermaLink="true">http://iris.lib.neu.edu/biology_diss/26</guid>
<pubDate>Mon, 07 May 2012 10:20:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Traditionally protists have been described based on their morphology using what is often referred to as alpha taxonomy approaches. However, today it is all but certain that these approaches have not revealed the real scale of protistan diversity. The two main reasons are the current uncultivability of most of microbial eukaryotes, which often makes direct observations impossible, and the lack of a comprehensive concept of species. Today, the molecular based (beta) taxonomy of comparisons of DNA sequences is increasingly used to bypass the limitations of the alpha taxonomy. The challenge is that the two approaches are typically used separately, and with different units of diversity. For example, it is not known to what extent the genetic distance between two taxa corresponds to morphological differences between them, and it is not clear if morphologically defined species do or do not cluster as phylogenetically distinct genetic groups of rRNA gene sequences (Operational Taxonomic Units, or OTUs). In the end, there is little understanding whether traditionally defined species vs OTUs combine identical, similar, or entirely different populations. Since traditional morphology and molecular taxonomy will likely both be used for the foreseeable future, it is important to understand what a morphologically defined species means in terms of gene sequence variability among cells composing this species. Here we use marine ciliates as model representatives of protists to investigate the level of intra&ndash and interspecies heterogeneity in the most widely used genetic marker, the 18S rRNA gene. Using single&ndashcell analysis and molecular cloning, we show that OTUs comprising 18S rRNA gene sequences that share &ge99% homology correspond well to species as defined by alpha taxonomy. Therefore, at least in ciliates, there appears to be a level of genetic variability in 18S rRNA gene sequences that could be used as a proxy for morphologically defined species. Merging alpha and beta taxonomy is very convenient for protistan diversity studies as this opens a way to assess this diversity faster and more objectively. Capitalizing on this, we surveyed ciliate diversity in several marine habitats, and statistically estimated the total ciliate richness in these habitats. The resulting throughput compares favorably to, and at times exceeds, what would have been achieved by more traditional alpha taxonomy approaches.</p>

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</description>

<author>Angela Schena</author>


</item>


<item>
<title>&quot;Been Hazed and Fused for So Long it&apos;s Not True&quot; - Drugs and Television in Thomas Pynchon&apos;s Inherent Vice</title>
<link>http://digitalrepository.trincoll.edu/theses/204</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/204</guid>
<pubDate>Mon, 07 May 2012 10:18:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>By analyzing the concurrent presences of television and drug use within Thomas Pynchon's <em>Inherent Vice,</em> I will argue that the book presents 1970 as a time when the counterculture was facing a losing battle to authority and to its own hedonistic impulses. Why and how are these elements so pervasive, and what does their effect have on the characters? Television and drugs are both pacifying by being all-consuming, and create an altered sense of time and place. They are modes of consumption that consume the characters in the novel (best categorized as “hippies,” those that attempted to revolt against the status quo through a denial of its conventions), and distract them from the social unrest and political changes going on in the background of the United States at the time. These elements are related to the vague sense of nostalgia in the novel (the text itself is in the form of nostalgic pastiche), as the characters implicitly and explicitly long for a different time and a place.</p>

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</description>

<author>William F. Moffett Jr.</author>


</item>


<item>
<title>Calling The Shots:  An Examination of the  Vaccination Debate in American Politics</title>
<link>http://digitalrepository.trincoll.edu/theses/203</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/203</guid>
<pubDate>Mon, 07 May 2012 10:18:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Inspired by the claim that vaccines cause autism, this thesis explores the many facets of the debate surrounding immunizations in our country. My research questions are: (1) <em>How has vaccination policy evolved in America and how has it influenced U.S. Health Policy?; </em>and<em> (2) What effect has the anti-vaccination movement had on the American public?</em><strong> </strong>The development of vaccinations is commonly accepted as one of the most significant scientific developments of all time. Vaccination policy in American politics plays a significant role in the individual’s greater perception of general health care policy in our country. Additionally, because of the unique timing and influential role immunizations play in the lives of young children, many citizens who are also parents use vaccination policy as a baseline for voting patterns and political views. The intensity of the anti-vaccination movement contrasted with the immense scientific research and funding directed toward advancing immunization technology provokes political dialogue, and influences fierce social movements.</p>
<p>Health care is at the center of American politics today and the health of our country’s children is at the forefront of the minds of schoolteachers, parents and politicians. Beginning with an examination of the historical path of vaccination policy in America, this paper will shed light on the decision-making process of political leaders with regard to the costs and benefits of immunization policy at both the societal and individual level. Furthermore, in cases where a child is not vaccinated, I plan to understand the role government plays as the ultimate guarantor of health in this country. I will look into several controversies that have rocked American politics such as the introduction of the small pox vaccine, the alleged connection that autism is caused by vaccines and the recent debate about the Human Papillomavirus (HPV) vaccine, specifically the examination of the issues surrounding the requirement that all young women in Texas be given the vaccination as a prerequisite for school entry. I also plan to examine the role government plays in cases where families cannot afford immunizations. I find this topic to be engaging because of its many facets: the implications on the American family, politics, voting patterns, and its connection to sensationalized journalistic tendencies. While the dimensions of this debate remain intriguing, it is most significant on the political stage because of its role in the timeless debate concerning the balance between an individual’s right to refuse a vaccine with the right of the public to be protected from disease.</p>

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</description>

<author>Nicole E. Lustig</author>


</item>


<item>
<title>The Theology of William Porcher DuBose: Life, Movement, and Being</title>
<link>http://epublications.marquette.edu/theo_fac/125</link>
<guid isPermaLink="true">http://epublications.marquette.edu/theo_fac/125</guid>
<pubDate>Mon, 07 May 2012 10:17:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Recognized and appreciated as one of the most original and creative theologians in the Episcopal Church's history, William Porcher DuBose (1836–1918) published seven books of theological importance, including an autobiographical work, and his life is commemorated in a "lesser feast" of the Episcopal Calendar of the Church Year. Despite making significant contributions to Anglicanism, DuBose's works are, according to Robert Boak Slocum, more widely honored than understood or applied to questions facing theologians and lay people today. To fill the gap of knowledge and understanding, Slocum's study of DuBose draws parallels between essential experiences in his life and major themes in his published theology.</p>
<p>Slocum chronicles the theologian's life—including childhood on a plantation near Columbia, South Carolina; education at The Citadel and the University of Virginia; years as an adjutant and then as a chaplain in the Civil War; and a distinguished career as a chaplain, professor, and dean at the University of the South at Sewanee, Tennessee. Here, Slocum brings out the impact of conversion, suffering, discovery, and transformation on the development of DuBose's theology and also investigates how in DuBose's own thinking, theology is deeply connected with the experience of the Christian life as lived, especially in the context of the life of the church.</p>
<p>In considering DuBose's theological system, Slocum finds an understanding of salvation that culminates in DuBose's theology of the Church, a pneumatology that serves as a point of synthesis for DuBose's work, and an ecclesiology that is preeminently ecumenical. Out of this he constructs an account of the relevance of DuBose's theological vision for the life and unity of the church today.</p>

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</description>

<author>Robert Boak Slocum</author>


</item>


<item>
<title>2012 Chartbook</title>
<link>http://scholarworks.umass.edu/cranchart/143</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranchart/143</guid>
<pubDate>Mon, 07 May 2012 10:15:18 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>UMass Amherst Cranberry Exp Station</author>

<source></source>

</item>


<item>
<title>The Changing Face of Privacy Protection in the European Union and the United States</title>
<link>http://www.repository.law.indiana.edu/facpub/513</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/513</guid>
<pubDate>Mon, 07 May 2012 10:08:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Among the wide variety of national and multinational legal regimes for protecting privacy, two dominant models have emerged, reflecting two very different approaches to the control of information. The European Union has enacted a sweeping data protection directive that imposes significant restrictions on most data collection, processing, dissemination, and storage activities, not only within Europe, but throughout the world if the data originates in a member state. The United States has taken a very different approach that extensively regulates government processing of data, while facilitating private, market-based initiatives to address private sector data processing.</p>
<p>Under the EU data protection directive, information privacy is a basic human right; the failure of the U.S. legal system to treat it as such offends European values and has led the EU to threaten to suspend information flows to the United States. This threat is understandable in light of the directive's treatment of privacy as a human right, and necessary if the privacy of European nationals is to be protected effectively in a global information economy. In the United States, however, the government is constitutionally prohibited under the First Amendment from interfering with the flow of information, except in the most compelling circumstances. The EU data protection directive is plainly contrary to that constitutional maxim, and the suggestion that the directive should be extended to the United States exacerbates that conflict, as well as threatens U.S. leadership in information technologies and services.</p>
<p>This Article examines the expanding conflict and emerging compromises between the European Union and the United States over data protection. After describing each of the legal regimes and the principles that undergird them, the article concludes by addressing the conflict between those principles, current political efforts to minimize that conflict, and the inadequacies of both systems in the context of the Internet.</p>

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</description>

<author>Fred H. Cate</author>


</item>


<item>
<title>Privacy and Telecommunications</title>
<link>http://www.repository.law.indiana.edu/facpub/512</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/512</guid>
<pubDate>Mon, 07 May 2012 10:08:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>This article explores the differences in privacy protection between the European Union and the United States, and examines the emerging conflict over data protection. Professor Cate analyzes the European data protection Directive, with particular emphasis on the Directive's extraterritorial provisions. He then examines privacy protection under United States laws and the extent to which that protection satisfies the requirements of the Directive. Finally, Professor Cate focuses on privacy issues involved in telecommunications, an area significantly regulated by United States and European laws, and therefore one area in which some commonality among privacy protection might be anticipated. Even in this highly regulated area, Professor Cate concludes, United States privacy protection for telecommunications-related information fails to meet the standard required by the Directive. However, he argues, the most effective protections for privacy are not legal regulations, but rather individual responsibility, limited governmental oversight, and competition among telecommunication service providers.</p>

	]]>
</description>

<author>Fred H. Cate</author>


</item>


<item>
<title>Pesticide Safety 2012 - Pesticide Safety Review</title>
<link>http://scholarworks.umass.edu/cranberry_extension/144</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranberry_extension/144</guid>
<pubDate>Mon, 07 May 2012 10:07:56 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Sylvia, Martha</author>

<source></source>

</item>


<item>
<title>Melton Family Papers (SC 2523)</title>
<link>http://digitalcommons.wku.edu/dlsc_mss_fin_aid/2074</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_mss_fin_aid/2074</guid>
<pubDate>Mon, 07 May 2012 10:00:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>Finding aid only for Manuscripts Small Collection 2523.  Genealogical records, correspondence, and receipts for various members of the Melton family of Webster County, Kentucky.  Also includes genealogical information about the Lively and Norvell families.</p>

	]]>
</description>

<author>Manuscripts &amp; Folklife Archives</author>


</item>


<item>
<title>Eclectic Book Club (MSS 407)</title>
<link>http://digitalcommons.wku.edu/dlsc_mss_fin_aid/2073</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_mss_fin_aid/2073</guid>
<pubDate>Mon, 07 May 2012 10:00:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Finding aid only for Manuscripts Collection 407.  Minute book, yearbooks, and financial data of the Eclectic Book Club, a women's literary club in Bowling Green, Kentucky.</p>

	]]>
</description>

<author>Manuscripts &amp; Folklife Archives</author>


</item>


<item>
<title>Pond, Alonzo William, 1894-1986</title>
<link>http://digitalcommons.wku.edu/dlsc_mss_fin_aid/2072</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_mss_fin_aid/2072</guid>
<pubDate>Mon, 07 May 2012 10:00:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Finding aid only for Manuscripts Small Collection 278.  Report, 25 June 1935, of Alonzo W. Pond, National Park Service archaeologist, on a discovery of prehistoric human remains in Mammoth Cave, Kentucky.  Includes photographs of the discovery.</p>

	]]>
</description>

<author>Manuscripts &amp; Folklife Archives</author>


</item>


<item>
<title>Wood, Arthur Fox, 1829-1878 (SC 2524)</title>
<link>http://digitalcommons.wku.edu/dlsc_mss_fin_aid/2071</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_mss_fin_aid/2071</guid>
<pubDate>Mon, 07 May 2012 10:00:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Finding aid only for Manuscripts Small Collection 2524. Letter, 14 July 1851, from Arthur Fox Wood, Philadelphia, Pennsylvania, to “Tom” in Mason County, Kentucky. He compares Philadelphia (and its women) unfavorably to Mason County, reports on his medical studies, deplores abolitionism in the North, and asks about family and friends.</p>

	]]>
</description>

<author>Manuscripts &amp; Folklife Archives</author>


</item>


<item>
<title>Cherry, Ariel Clarence, 1878-1961 (SC 2525)</title>
<link>http://digitalcommons.wku.edu/dlsc_mss_fin_aid/2070</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/dlsc_mss_fin_aid/2070</guid>
<pubDate>Mon, 07 May 2012 10:00:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Finding aid only for Manuscripts Small Collection 2525. Letter from Ariel Clarence Cherry, Yakima, Washington, to his sisters, relating memories of their recently deceased mother, Leona Celeste (White) Cherry, of Warren County, Kentucky. Includes a note from a sister, Elizabeth (Cherry) McCallum, commenting on the wartime shortage of granite for grave markers.</p>

	]]>
</description>

<author>Manuscripts &amp; Folklife Archives</author>


</item>


<item>
<title>Overcoming Educational Stratification: Effect of Athletic Status and Race on Odds of Graduating at Western Kentucky University</title>
<link>http://digitalcommons.wku.edu/theses/1142</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/theses/1142</guid>
<pubDate>Mon, 07 May 2012 09:56:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study examines the effect of stratification on graduation at Western Kentucky University, a master’s level regional Division I Football Bowl Subdivision university in the South. The study begins by examining the historical basis of stratification in sport and higher education, and hypothesizes that becoming an intercollegiate athlete can eliminate the effect of being African American on graduation, which is generally negative and can be seen in lower graduation rates for African Americans compared to other populations. Using a data set that included 18,966 students, logistic regression was used to assess: 1) the effect of race on sport profile and 2) the effect of race and athletic status on graduation, controlling for sex, high school GPA, pre-collegiate standardized test scores, and department of academic major. Results indicate that African American students have 771 percent greater odds of participating in high profile sports compared to low profile sports, which supports the literature that sport is stratified in such a way that African Americans are more likely to bear a disproportionate load in revenue-producing sports. Even so, when interacting sport profile, athlete, and race, the penalty on graduation for being African American is eliminated, and African American athletes have the same odds of graduating as white non-athletes.</p>

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</description>

<author>Justin Schilke</author>


</item>


<item>
<title>Rāmāyaṇa</title>
<link>http://digitalrepository.trincoll.edu/theses/202</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/202</guid>
<pubDate>Mon, 07 May 2012 09:48:40 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Parth Sharma</author>


</item>


<item>
<title>Efficiency and Power Density Improvement of Grid-Connected Hybrid Renewable Energy Systems utilizing High Frequency-Based Power Converters</title>
<link>http://digitalcommons.fiu.edu/etd/600</link>
<guid isPermaLink="true">http://digitalcommons.fiu.edu/etd/600</guid>
<pubDate>Mon, 07 May 2012 09:44:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>High efficiency of power converters placed between renewable energy sources and the utility grid is required to maximize the utilization of these sources. Power quality is another aspect that requires large passive elements (inductors, capacitors) to be placed between these sources and the grid. The main objective is to develop higher-level high frequency-based power converter system (HFPCS) that optimizes the use of hybrid renewable power injected into the power grid. The HFPCS provides high efficiency, reduced size of passive components, higher levels of power density realization, lower harmonic distortion, higher reliability, and lower cost.</p>
<p>The dynamic modeling for each part in this system is developed, simulated and tested. The steady-state performance of the grid-connected hybrid power system with battery storage is analyzed. Various types of simulations were performed and a number of algorithms were developed and tested to verify the effectiveness of the power conversion topologies. A modified hysteresis-control strategy for the rectifier and the battery charging/discharging system was developed and implemented. A voltage oriented control (VOC) scheme was developed to control the energy injected into the grid. The developed HFPCS was compared experimentally with other currently available power converters. The developed HFPCS was employed inside a microgrid system infrastructure, connecting it to the power grid to verify its power transfer capabilities and grid connectivity. Grid connectivity tests verified these power transfer capabilities of the developed converter in addition to its ability of serving the load in a shared manner.</p>
<p>In order to investigate the performance of the developed system, an experimental setup for the HF-based hybrid generation system was constructed. We designed a board containing a digital signal processor chip on which the developed control system was embedded. The board was fabricated and experimentally tested. The system’s high precision requirements were verified. Each component of the system was built and tested separately, and then the whole system was connected and tested. The simulation and experimental results confirm the effectiveness of the developed converter system for grid-connected hybrid renewable energy systems as well as for hybrid electric vehicles and other industrial applications.</p>

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</description>

<author>mahmoud amin</author>


</item>


<item>
<title>The Moderating Mediation Effects of Maternal Psychological Control and Maternal Acceptance on the Relation Between Maternal Acculturation and Youth Anxiety</title>
<link>http://digitalcommons.fiu.edu/etd/599</link>
<guid isPermaLink="true">http://digitalcommons.fiu.edu/etd/599</guid>
<pubDate>Mon, 07 May 2012 09:44:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The present study examined the relations among maternal psychological control, maternal acceptance, maternal acculturation and youth anxiety within the framework of a (partially) moderated mediation model. The sample consisted of 535 Hispanic-Latino youth (46% girls; <em>M</em> = 9.79 years) and their mothers. The study’s data were analyzed using structural equation modeling in the MPlus statistical software program.</p>
<p>Results indicated that maternal psychological control and youth anxiety are significantly and positively related. Results also indicated that more acculturated mothers were more psychologically controlling than less acculturated mothers. Results further provided evidence for a partial mediational role of maternal psychological control on the relation between maternal acculturation and youth anxiety symptoms. In addition, there was a direct, positive relation between maternal acculturation and youth anxiety symptoms. No significant findings were observed regarding the moderating role of maternal acceptance on the relation between maternal psychological control and youth anxiety. The findings’ theoretical and clinical implications are further discussed.</p>

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</description>

<author>Ileana Hernandez</author>


</item>


<item>
<title>Pesticide Safety 2012 - What to do when your pesticide application goes wrong?</title>
<link>http://scholarworks.umass.edu/cranberry_extension/143</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranberry_extension/143</guid>
<pubDate>Mon, 07 May 2012 09:43:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Letourneau, Linda</author>

<source></source>

</item>


<item>
<title>Pesticide Safety 2012 - Zone II, New Website, and NPDES in Cranberry</title>
<link>http://scholarworks.umass.edu/cranberry_extension/142</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranberry_extension/142</guid>
<pubDate>Mon, 07 May 2012 09:43:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Wick, Brian</author>

<source></source>

</item>


<item>
<title>Pesticide Safety 2012 - Label Review and Resistance Management</title>
<link>http://scholarworks.umass.edu/cranberry_extension/141</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranberry_extension/141</guid>
<pubDate>Mon, 07 May 2012 09:43:24 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Sylvia, Martha</author>

<source></source>

</item>


<item>
<title>Pesticide Safety 2012 - Disease Predictions</title>
<link>http://scholarworks.umass.edu/cranberry_extension/140</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranberry_extension/140</guid>
<pubDate>Mon, 07 May 2012 09:43:22 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Caruso, Frank</author>

<source></source>

</item>


<item>
<title>Pesticide Safety 2012 - MRL Review and Frost</title>
<link>http://scholarworks.umass.edu/cranberry_extension/139</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranberry_extension/139</guid>
<pubDate>Mon, 07 May 2012 09:43:21 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>DeMoranville, Carolyn</author>

<source></source>

</item>


<item>
<title>Pesticide Safety 2012 -Herbicide Update</title>
<link>http://scholarworks.umass.edu/cranberry_extension/138</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranberry_extension/138</guid>
<pubDate>Mon, 07 May 2012 09:43:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Sandler, Hilary</author>

<source></source>

</item>


<item>
<title>Pesticide Safety 2012 - Mix This, Not That...Tank Mixing</title>
<link>http://scholarworks.umass.edu/cranberry_extension/137</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranberry_extension/137</guid>
<pubDate>Mon, 07 May 2012 09:43:17 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Sandler, Hilary</author>

<source></source>

</item>


<item>
<title>Pesticide Safety 2012 - Insect Review, Bee Toxicity, and Management Decisions</title>
<link>http://scholarworks.umass.edu/cranberry_extension/136</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranberry_extension/136</guid>
<pubDate>Mon, 07 May 2012 09:43:16 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Averill, Anne L.</author>

<source></source>

</item>


<item>
<title>Pesticide Safety 2012 - Chemigation Review</title>
<link>http://scholarworks.umass.edu/cranberry_extension/135</link>
<guid isPermaLink="true">http://scholarworks.umass.edu/cranberry_extension/135</guid>
<pubDate>Mon, 07 May 2012 09:43:14 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Beaton, Matt</author>

<source></source>

</item>


<item>
<title>100 Years of Service History of the Martha M. Brown and Lois H. Daniel Memorial Library 1912-2012</title>
<link>http://digitalscholarship.tnstate.edu/lib/13</link>
<guid isPermaLink="true">http://digitalscholarship.tnstate.edu/lib/13</guid>
<pubDate>Mon, 07 May 2012 09:40:19 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Dr.Yildiz B. Binkley</author>


</item>


<item>
<title>Transcriptome Analysis Reveals Strain-Specific and Conserved Stemness Genes in Schmidtea Mediterranea</title>
<link>http://digitalcommons.uconn.edu/uchcres_articles/87</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/uchcres_articles/87</guid>
<pubDate>Mon, 07 May 2012 09:38:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The planarian <em>Schmidtea mediterranea</em> is a powerful model  organism for studying stem cell biology due to its extraordinary  regenerative ability mediated by neoblasts, a population of adult  somatic stem cells. Elucidation of the <em>S. mediterranea</em> transcriptome and the dynamics of transcript expression will increase  our understanding of the gene regulatory programs that regulate stem  cell function and differentiation. Here, we have used RNA-Seq to  characterize the <em>S. mediterranea</em> transcriptome in sexual and  asexual animals and in purified neoblast and differentiated cell  populations. Our analysis identified many uncharacterized genes,  transcripts, and alternatively spliced isoforms that are differentially  expressed in a strain or cell type-specific manner. Transcriptome  profiling of purified neoblasts and differentiated cells identified  neoblast-enriched transcripts, many of which likely play important roles  in regeneration and stem cell function. Strikingly, many of the  neoblast-enriched genes are orthologs of genes whose expression is  enriched in human embryonic stem cells, suggesting that a core set of  genes that regulate stem cell function are conserved across metazoan  species.</p>

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</description>

<author>Alissa M. Resch et al.</author>


</item>


<item>
<title>Employment and Social Developments in Europe 2011</title>
<link>http://digitalcommons.ilr.cornell.edu/intl/217</link>
<guid isPermaLink="true">http://digitalcommons.ilr.cornell.edu/intl/217</guid>
<pubDate>Mon, 07 May 2012 09:34:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>[Excerpt] This annual review on Employment and Social Developments in Europe (ESDE) brings together for the first time a comprehensive analysis of challenges facing the EU in the areas of both employment and social policy. Replacing two previous reports - Employment in Europe and the Social Situation Report, the ESDE becomes the European Commission’s flagship analytical review on employment and social issues. It builds on the Quarterly Reviews of the EU Employment and Social Situation which the Commission has started producing in 2011 and provides detailed analysis of key structural developments. The 2011 edition focuses on changes in Europe’s job structure, recent increases in income inequalities, the varying patterns of poverty and social exclusion, the problem of in-work poverty, challenges and measures in the area of active ageing, and provides an updated analysis of intra-EU labour mobility.</p>
<p>The integrated approach which the Commission has applied in preparation of the review corresponds to the Europe 2020 strategy. This is a long-term development strategy which sees social inclusion, the fight against poverty, greater labour market participation, employment and job quality as essential elements for Europe’s prosperity. Europe 2020 emphasizes that the objectives of smart, sustainable, and inclusive growth are mutually reinforcing and sets economic, employment and social policies on an equal footing. This approach also underpins the Europe 2020 Integrated Guidelines and the country-specific recommendations adopted by the European Council in June 2011. Nearly all social challenges have a strong labour market dimension, for example the problem of in-work poverty. At the same time, social policy plays a very important role in improving employment outcomes, e.g. as regards the inclusion of disadvantaged people or active ageing.</p>

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</description>

<author>European Commission</author>


</item>


<item>
<title>Investigation of the rheology, cure kinetics, and thermo-mechanical properties of GRC-A loaded with zeolites</title>
<link>http://digitalcommons.auctr.edu/dissertations/256</link>
<guid isPermaLink="true">http://digitalcommons.auctr.edu/dissertations/256</guid>
<pubDate>Mon, 07 May 2012 09:33:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Phenylethynyl terminated imides (PETI) are high temperature, high performance matrix resins that can be processed into composites by various methods including resin transfer molding (RTM) arid vacuum assisted resin transfer molding (VARTM). PETI resins have experienced extremely rapid development in recent years, with major emphasis placed on engineering applications that take advantage of their high cured TgS,high thermooxidative stability, high strength to weight ratio, outstanding mechanical properties, and compatibility with RTM and VARTM processing. In recent years the addition of nanoparticles to resin systems has been shown to further enhance the mechanical properties and thermooxidative stability. In this study, we incorporated nanoporous aluminosilicate materials, otherwise known as zeolites, into PETI resin GRC-A, and investigated the effect the zeolites have on the viscosity, cure kinetics, thermooxidative stability and other thermomechanical properties of GRC-A. Rheological and differential scanning calorimetry studies conducted on the GRC-Alzeolite mixtures showed that zeolite L acts like a filler and retards the curing of the phenylethynyl end-groups, while zeolite Y catalyzes the curing process. Additionally, cure kinetic studies via melt rheology and DSC confirmed that the activation energies for GRC-A/zeolite Y mixtures as lower than for neat GRC-A and GRC-A/zeolite L mixtures, further supporting zeolite L acts as a filler while zeolite Y serves as a catalyst during the cure process. While the cured Tgs, from the DMA and TMA studies showed that in spite of the catalytic properties of zeolite Y; it did not afford additional properties over GRC-A and zeolite L mixtures. However, the catalytic properties of zeolite Y allows PETI resins to be cured at a lower temperatures, which could lead to lower energy costs in the production of composite parts from PETI resins.</p>

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</description>

<author>Trancy Brown</author>


</item>


<item>
<title>Hidden Wheel</title>
<link>http://digitalcommons.library.umaine.edu/etd/1014</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1014</guid>
<pubDate>Mon, 07 May 2012 09:33:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>A trust fund kid, posing as a drug dealer to maintain street cred, opens an art gallery designed to fail. A self-employed drummer sells sperm to raise funds for a new kit before his band embarks on their first-ever tour. A former chess prodigy-turned- dominatrix paints sixty words a day on a giant canvas to stave off the coming Singularity. A hipster blogs about his fictional tagger alter ego and bumbles into quick fame with a series of paintings on CD covers. Hidden Wheel is an unflinching reflection of the growing complexities of navigating art, commerce, and the internet. Its use of intersecting plotlines illustrates the confusion and potential of the early 21st century and the evolving ways in which its inhabitants try to make a mark in the specter of financial ruin and shifting technologies. Hidden Wheel's narrative frame is the scholarship from a 24 century scholar attempting to reconstruct 21st century history using only paper documents remaining after a solar flare erases the world's digital media storage in 2308. By distancing the narrator from the story he reconstructs, space is created for observations of both our time period and the notion of artistic ownership.</p>

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</description>

<author>Michael T. Fournier</author>


</item>


<item>
<title>6AMUGH</title>
<link>http://digitalcommons.library.umaine.edu/etd/1013</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1013</guid>
<pubDate>Mon, 07 May 2012 09:33:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>6AMUGH is a novel about the crew of a classic rock radio station morning show in Boston during October and November of 2001. The novel begins on the day Barry Babcock, the show's host, Mike, the producer, Chuck the Sports Nut, the sports reporter, and Jennifer Friendly, aka the Traffic Bunny, the traffic reporter, move from the afternoon spot they've been in for 3 years to the higher-profile morning spot. A few things are different about the morning timeslot: they now have to get to work by 5 a.m., the writer, Lenny, quit, retired rather than wake up so early, and he's being replaced by his nephew, Louis. And everyone keeps calling up and asking for Jimbo Russell, who retired after decades on the air, leaving behind a big pair of shoes they're going to try to fill. On Day One the show is interrupted by the station manager's wife who announces that she's discovered her husband's been having an affair with the Traffic Bunny, and that she's getting her revenge by appointing herself the new station manager and adding a co-host to the show, a professor of Women's Studies from UMass Amherst, Gloria Ramone. The two hosts clash, and just as the show hits its stride, the station manager's wife cancels the show, sending the staff into a variety of quandaries, pondering their own existences, and possibly ending the golden age of radio.</p>

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</description>

<author>Peter Dutton</author>


</item>


<item>
<title>Creating the World of the Táin through the Remscéla: Prologemena to Reading</title>
<link>http://digitalcommons.library.umaine.edu/etd/1012</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1012</guid>
<pubDate>Mon, 07 May 2012 09:32:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation argues that the great twelfth-century Irish Epic Táin Bó Cuailnge (Cattle Raid of Cooley) cannot be read with understanding without first addressing the remscela, or foretales, that set the context for the Táin itself. The remscela create a rationale for the actions depicted in the Táin. They also serve to establish the fact that the Táin action is the result of Other World involvement in human affairs. This dissertation uses the 1969 English translation by Thomas Kinsella and challenges his omission of some of the remscéla. Kinsella's decision to present a battle of the sexes story allowed for a popularization of the text, but it failed to address the sacred nature of the story.</p>

	]]>
</description>

<author>Kay Lynn Retzlaff</author>


</item>


<item>
<title>Prime Modulo and Pascals Triangle as Seen with Fractal Geometry</title>
<link>http://digitalcommons.library.umaine.edu/etd/1011</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1011</guid>
<pubDate>Mon, 07 May 2012 09:32:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Looking at Pascal's Triangle there are many patterns that arise and phenomena that happen. Considering the elements of the triangle under a given modulus there are clear triangular patterns that can be mathematically described. The patterns in this structure can be described well with the aid of fractal geometry. Fractal geometry characterizes and describes many fascinating and intricate patterns in nature by comparing sections of an object to other sections. Taking certain values or sets of values from Pascal's triangle, and under certain conditions (such as taking the modulus) the entire triangle can be recreated or values can be predicted directly from values that are in a given relative position. There are patterns of vertical and horizontal symmetry as well as entire sets that contain the pattern that depict the infinitely large and complete Pascal's triangle. With the concept of fractals in mind, such patterns and symmetries are used to find fractal dimension under given conditions like modulo 2, modulo p, for p prime and to look ahead to what a modulo p to a power n might look like. This would show patterns of divisibility by any such numbers and also patterns in the residues they leave behind. This is used to compare the triangle under various moduli and to describe many interesting properties that any related modulo might share.</p>

	]]>
</description>

<author>Matthew Potter</author>


</item>


<item>
<title>Gauss Composition and Bhargava&apos;s Cube Law</title>
<link>http://digitalcommons.library.umaine.edu/etd/1010</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1010</guid>
<pubDate>Mon, 07 May 2012 09:32:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>A basic question in mathematics asks "Which primes are of the form x²+ y²where x and y are integers?" The answer was known to Fermat in 1640 and is easy to state: a prime p is a sum of two squares if and only if p = 2 or p = 1mod4. To generalize this basic question, one might ask "Which primes are of the form x²+ ny²where x, n, and y are integers?" It turns out that this question is much more difficult to answer and yet the solution is still easy to state. The study of x²+ ny²naturally leads to the study of quadratic forms, which are expressions of the form f(x,y) = ax²+ bxy + cy², a, b, c eZ. In 1801, a group law on equivalence classes of quadratic forms was published by Gauss in which the class of x²+ ny² is the identity element. In his 2001 Princeton PhD thesis, Manjul Bhargava developed a series of far-reaching generalizations of Gauss composition that give new information about class groups in number fields of degree < 6. The first of these generalizations is a composition law based on geometric cubes with an integer assigned to each corner. This thesis outlines Gauss composition and introduces the first generalization developed by Bhargava. Using this generalization, a theory of composition of binary cubic forms is introduced.</p>

	]]>
</description>

<author>Adam Barker-Hoyt</author>


</item>


<item>
<title>The Bicycle in Western Literature: Transformations on Two Wheels</title>
<link>http://scholarship.rollins.edu/mls/22</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/22</guid>
<pubDate>Mon, 07 May 2012 09:24:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Since the invention of the modern bicycle in the 1880s, bicycles have played an integral role in western culture.  As a reflection of its cultural significance and impact on individuals, many novelists have incorporated bicycles into their works in both realistic and symbolic ways.  This paper focuses on the use of bicycles in western literature from the bicycle boom decade of the 1890s to the mid-twentieth century and includes works of H. G. Wells, Émile Zola, Arthur Conan Doyle, Dorothy Richardson, D. H. Lawrence, Ernest Hemingway, F. Scott Fitzgerald, Simone de Beauvoir, Samuel Becket, Luigi Bartolini and L. P. Hartley.   These novelists used bicycles not merely as a means to transport characters, but as catalysts for or symbols of social and personal transformation.    Novels written around the turn of the twentieth century reflect the significant positive role bicycles played in the cultural changes and personal freedom of this era.  Later, after the first World War and the advent of the automobile, bicycles remained literary devices, but their symbolic use changed.  While in the post-World War I era bicycles are still capable of transforming characters, their transformational potential is often unrealized or is tempered by skepticism or pessimism.</p>

	]]>
</description>

<author>Nanci J. Adler</author>


</item>


<item>
<title>Aspectos ecológicos de Phyllomedusa rohdei
em uma lagoa permanente de Nova Venécia, Espírito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/22</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/22</guid>
<pubDate>Mon, 07 May 2012 09:20:57 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Análise preliminar da Anurofauna de um
tanque permanente sobre influência antrópica na regiao serrana do Espirito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/21</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/21</guid>
<pubDate>Mon, 07 May 2012 09:20:55 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Anatomia foliar de
Crataeva tapia</title>
<link>http://digitalcommons.usu.edu/eco_pres/20</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/20</guid>
<pubDate>Mon, 07 May 2012 09:20:54 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Aspectos da Ecologia e Biologia Trofica de
Scinax alter em região de montanha do Espirito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/19</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/19</guid>
<pubDate>Mon, 07 May 2012 09:20:52 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Ocorrência e dieta de Sphaenorhynchus
planicola de uma lagoa costeira em Anchieta, Espirito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/18</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/18</guid>
<pubDate>Mon, 07 May 2012 09:20:51 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Dieta de jovens da perereca de capacete,
Aparasphenodon brunoi de um fragmento de mata atlantica em Linhares, Espirito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/17</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/17</guid>
<pubDate>Mon, 07 May 2012 09:20:50 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Dieta de Hyla faber em uma lagoa artificial
em Anchieta, Espirito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/16</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/16</guid>
<pubDate>Mon, 07 May 2012 09:20:48 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Aspectos reprodutivos e variação ontogenética
em Leptodactylus natalensis Lutz, 1930 (Anura, Leptodactylidae) do sudeste do Brasil</title>
<link>http://digitalcommons.usu.edu/eco_pres/15</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/15</guid>
<pubDate>Mon, 07 May 2012 09:20:47 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Análise da anurofauna de dois tanques
permanentes sobre influência antrópica em Marechal Floriano, região serrana do Espírito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/14</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/14</guid>
<pubDate>Mon, 07 May 2012 09:20:45 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>O hábito alimentar de Bufo crucifer (Anura,
Bufonidae) em uma lagoa artificial no sudeste do Brasil</title>
<link>http://digitalcommons.usu.edu/eco_pres/13</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/13</guid>
<pubDate>Mon, 07 May 2012 09:20:43 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Distribuição Espacial e Temporal da anurofauna na Universidade Federal do
Espírito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/12</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/12</guid>
<pubDate>Mon, 07 May 2012 09:20:42 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira</author>


</item>


<item>
<title>Diversity and abundance variations
of anurans at a permanent pond in Suruaca&apos;s Valley, Linhares, Espírito Santo, Southeastern
Brazil</title>
<link>http://digitalcommons.usu.edu/eco_pres/11</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/11</guid>
<pubDate>Mon, 07 May 2012 09:20:41 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>R. L. Teixeira et al.</author>


</item>


<item>
<title>Herpetofauna da Universidade Federal do Espírito Santo,
sudeste do Brasil</title>
<link>http://digitalcommons.usu.edu/eco_pres/10</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/10</guid>
<pubDate>Mon, 07 May 2012 09:20:40 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Aspectos Ecológicos de Leptodactylus ocellatus (Anura;
Leptodactylidae) na Universidade Federal do Espírito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/9</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/9</guid>
<pubDate>Mon, 07 May 2012 09:20:38 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H. R. Rangel et al.</author>


</item>


<item>
<title>Diversidade de Anfíbios Anuros no
Entorno da Reserva Biológica Augusto Ruschi, sudeste do Brasil</title>
<link>http://digitalcommons.usu.edu/eco_pres/8</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/8</guid>
<pubDate>Mon, 07 May 2012 09:20:36 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Serpentes Atropeladas no Parque Estadual da
Fonte Grande, Vitória, Sudeste do Brasil</title>
<link>http://digitalcommons.usu.edu/eco_pres/7</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/7</guid>
<pubDate>Mon, 07 May 2012 09:20:35 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Mormon cricket
(Anabrus simplex) Laboratory colony development</title>
<link>http://digitalcommons.usu.edu/eco_pres/6</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/6</guid>
<pubDate>Mon, 07 May 2012 09:20:34 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Rodrigo B. Ferreira et al.</author>


</item>


<item>
<title>Anuros do Corredor
Florestal Parque Estadual de Forno Grande e Parque Estadual do Forno Grande, sudeste do
Brasil</title>
<link>http://digitalcommons.usu.edu/eco_pres/5</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/5</guid>
<pubDate>Mon, 07 May 2012 09:20:32 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>P. V. Scherrer et al.</author>


</item>


<item>
<title>Description of tadpole of the hylid
frog Scinax belloni (Anura: Hylidae)</title>
<link>http://digitalcommons.usu.edu/eco_pres/4</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/4</guid>
<pubDate>Mon, 07 May 2012 09:20:31 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>T. Silva-Soares et al.</author>


</item>


<item>
<title>Anurofauna na
Reserva Particular do Patrimonio Natural Oiutrem, Regiao de Montanha do Espirito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/3</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/3</guid>
<pubDate>Mon, 07 May 2012 09:20:29 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. Mattedi et al.</author>


</item>


<item>
<title>Distribuicao Geografica de Eclpeopus
gaudichaudii no Espirito Santo, Sudeste do Brasil</title>
<link>http://digitalcommons.usu.edu/eco_pres/2</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/2</guid>
<pubDate>Mon, 07 May 2012 09:20:28 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>P. V. Scherrer et al.</author>


</item>


<item>
<title>Padrao de
sazonalidade e aspectos reprodutivos de anuros em Unidade de Conservacao na região de
montanha no Espirito Santo</title>
<link>http://digitalcommons.usu.edu/eco_pres/1</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/eco_pres/1</guid>
<pubDate>Mon, 07 May 2012 09:20:26 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>C. Mattedi et al.</author>


</item>


<item>
<title>Cutting the Red Tape: Direct Engagement with the University and College Campus Student Body for Outreach and Programming Needs</title>
<link>http://scholar.valpo.edu/ccls_fac_presentations/2</link>
<guid isPermaLink="true">http://scholar.valpo.edu/ccls_fac_presentations/2</guid>
<pubDate>Mon, 07 May 2012 09:15:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>This workshop discusses various ways to directly engage student patrons for outreach and programming purposes, while eliminating post-secondary administration red-tape that could hinder establishment of this programming. The presenters illustrate ways to delegate to certain students creation and promotion of library-related content for consumption by the rest of the campus community. The presenters show that engaging directly with this group of creative students, not only gives this student project experience and confidence, but frees the outreach and programming staff’s time commitment to explore additional ways to connect with the campus’ community. Going to the students directly and not relying on the academic administration to facilitate programming, can show the student body that the library staff is committed to their needs and is willing to have one-on-one interactions in relation to their library-related needs. This also allows the library staff to directly assess emerging student needs and personalize future initiatives to those needs. We specifically discuss embedded librarianship and non-curricular based initiatives for student affinity groups and library media projects undertaken at Valparaiso University in the past year.</p>

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</description>

<author>Rachael Muszkiewicz et al.</author>


</item>


<item>
<title>Open Access at Valparaiso University: Two Perspectives - The User and the Publisher</title>
<link>http://scholar.valpo.edu/ccls_fac_presentations/1</link>
<guid isPermaLink="true">http://scholar.valpo.edu/ccls_fac_presentations/1</guid>
<pubDate>Mon, 07 May 2012 09:15:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>This is part 2 of 2 of the presentation, "Open Access: Resources of tomorrow or Resources of a lower-quality?" which was presented at the Indiana Library Federation (District 1) conference on May 1, 2012. In this presentation, I discuss current Open Access initiatives at Valparaiso University as well as the Valpo user experience in relation to Open Access resources. Part 1 of 2 was "Open Access: The Basics," presented by Joseph Coates, Reference Coordinator at Calumet College of St. Joseph.</p>

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</description>

<author>Jonathan Bull</author>


</item>


<item>
<title>El Conflicto Armado en Colombia: Análisis Regional de los Impactos de la Política de  Seguridad Democrática</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/756</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/756</guid>
<pubDate>Mon, 07 May 2012 09:11:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation examines the politics of political violence in contemporary Colombia. Levels of violent contestation declined significantly in Colombia after 2003, during the implementation of the so-called Democratic Security Policy (DSP). Notwithstanding this general diminution of violence, the results of the DSP varied significantly across the different regions of the country. While the level of violent contestation of state authority by non-state actors has decreased in some regions, in others violence actually increased or remained basically unchanged. What explains these variations in political violence? The argument explored in this dissertation is that distinctive regional configurations or combinations of economic, social, political, institutional, cultural and geographic factors crucially shape the effectiveness of state security policies. Employing Boolean algebra and comparative case study analysis the dissertation examines seven variables in order to identify these regional configurations: poverty and inequality; presence of lootable resources (coca, oil and gold); institutional presence; political inclusion; number of insurgent groups; social density and geography.  Although the implementation of the DSP produced significant changes in the level of contestation at a national scale, empirical analysis of the 1995-2011 period leads to the conclusion that the particular characteristics of each regional configuration are ultimately fundamental in determining variations in violent conflict at the subnational level.</p>

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</description>

<author>Lilian Yaffe</author>


</item>


<item>
<title>The Unbought Grace of Life: Chivalry in Western Literature</title>
<link>http://scholarship.rollins.edu/mls/21</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/21</guid>
<pubDate>Mon, 07 May 2012 09:07:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The code of chivalry has a rich literary history.  From the violence and misogyny of pre-chivalric ancient Greece and Rome, the chivalric code was constructed in a deliberate effort to curb and improve the most violent aspects of male behavior.  The chivalric male ideal was built upon the tripartite foundation of the ancient archaic virtues, the gallantry of Germanic barbarians, and the Christian beatitudes.  Chivalry sought a male ideal which brought raw strength and power under the concept of legitimate authority.  By casting the literary male ideal – the knight – into the role of the defender of the weak and defenseless, chivalric literature served as an exemplar for actual male behavior.  This system of control, which came to be known as the chivalric code, had a turbulent history in the course of Western civilization with certain eras and cultures becoming enthusiastic proponents and others becoming skeptical or even hostile to the ideals of chivalry.  From the Middle Ages to the Renaissance, the Enlightenment and up to Modernity, the literature of these epochs provide a fascinating window into society’s acceptance or rejection of chivalric ideals.</p>

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</description>

<author>Richard N. Boggs</author>


</item>


<item>
<title>Westerners</title>
<link>http://diginole.lib.fsu.edu/etd/4598</link>
<guid isPermaLink="true">http://diginole.lib.fsu.edu/etd/4598</guid>
<pubDate>Mon, 07 May 2012 09:02:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>Westerners is a collection of eleven stories, mostly about people struggling to connect in this time of so-called “globalization.” Two stories set in the 19th century aim to enhance the meanings found in some of the contemporary stories. Exploring uneasy times, many of these tales are also about how simple and similar our desires really are. Set in places like Thailand, China, India, Canada and the U.S., my characters search to belong somewhere in our world today.</p>

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</description>

<author>Jocelyn Cullity</author>


</item>


<item>
<title>Luther and Hitler: A Linear Connection between Martin Luther and Adolf Hitler’s Anti-Semitism with a Nationalistic Foundation</title>
<link>http://scholarship.rollins.edu/mls/20</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/20</guid>
<pubDate>Mon, 07 May 2012 08:57:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Two of the most notoriously unshakable Anti-Semitics were the Protestant reformer Martin Luther and German Chancellor-turned dictator Adolf Hitler.  But who exactly were Martin Luther and Adolf Hitler?  Although four centuries apart, both Martin Luther and Adolf Hitler had a remarkable impact on both Germany and the world.  Luther is renowned still today as the initiator and leader of the Protestant Reformation.  Centuries later, Lutherans and Germans alike admire and honor him for his bold and daring actions against the Catholic Church in the 1500s.  Hitler remains one of the most hated men in history.  The similarities shared between Luther and Hitler were not limited to their hatred for anything Jewish, however.  Both men were led by a strong sense of German nationalism and a yearning for unity among their fellow Germans.</p>
<p>What exactly was it about these two men that allowed them to start a rebellion and garner support from their fellow Germans?  More importantly, what led them to live a life filled with rage and hatred, and why was it directed toward the Jews?  Was there something about the German people in particular that allowed them to be susceptible to the leadership of Luther and Hitler?  Martin Luther and Adolf Hitler are inseparably linked with their extreme anti-Semitism and nationalism. It is impossible to assume that Luther did not have any influence on Hitler and his views, for it cannot be mere coincidence that Hitler’s anti-Jewish sentiment of the 1930s and 1940s mirrors that of Luther’s anti-Semitism of the 1500s.  This paper will explore the connection between Luther and Hitler; it will attempt to illustrate the similarities between their German nationalism and anti-Semitism, and explain how Luther laid the foundation for Hitler’s holocaust.</p>

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</description>

<author>Daphne M. Olsen</author>


</item>


<item>
<title>Is the Doctor Really In?</title>
<link>http://jdc.jefferson.edu/jmbcim_lectures/50</link>
<guid isPermaLink="true">http://jdc.jefferson.edu/jmbcim_lectures/50</guid>
<pubDate>Mon, 07 May 2012 08:45:22 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Overall Goals and Objectives: </strong></p>
<p>1. Identify recent advances in integrative medical care and discuss their application to clinical practice.</p>
<p>2. Describe the latest data on complementary and alternative medical therapies that could improve patient outcomes.</p>
<p>3. Discuss core integrative medicine topics that patients frequently ask physicians about.</p>

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</description>

<author>Susan Marcel, DO, ABPN</author>


</item>


<item>
<title>The Cul De Sac of Race Preference Discourse</title>
<link>http://scholarship.law.gwu.edu/faculty_publications/1</link>
<guid isPermaLink="true">http://scholarship.law.gwu.edu/faculty_publications/1</guid>
<pubDate>Mon, 07 May 2012 08:44:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>Affirmative action policy remains a contentious issue in public debate despite public endorsement by America’s leading institutions and validation by the United States Supreme Court. But the decades old disagreement is mired in an unproductive rhetorical stalemate marked by entrenched ideology rather than healthy dialogue. Instead of evolving, racial dialogue about the relevance of race in university admissions and hiring decisions is trapped in a cycle of resentment.</p>
<p>In this article, I argue that the stagnation of race preference discourse arises because the basic rhetorical themes advanced by opponents have evolved little over 150 years since the racial reform efforts following the Civil War. Nineteenth-century opponents to the Freedmen’s Bureau, Negro citizenship, and Reconstruction era proposals deployed a host of arguments that bear a striking family resemblance to the modern arguments against race preferences. Rhetorical themes advanced by opponents in modern race preference discourse therefore generate resentment and skepticism among proponents because of this odious nineteenth-century pedigree, leading to a conversational impasse.</p>
<p>A deepened understanding of this rhetorical pedigree is crucial to restoring public conversation on race preferences. Opponents of race preferences must understand that this pedigree taints the underlying merit of their arguments. Concurrently, proponents must recognize that the advancement of these themes does not automatically signal agreement with nineteenth-century conservative racial norms. Through acknowledgement and understanding, we can stop the retreat into traditional ideologies and meet in the middle for a renewed and meaningful discussion of race preferences.</p>
<p>This article begins by discussing four dominant rhetorical themes deployed by opponents in the modern race preference debate, and compares and contrasts those modern arguments with their nineteenth-century counterparts. Next, I discuss the effects of the prevailing modern theme and motivations driving modern policy positions. Finally, I argue that racial progress demands continued dialogue and offer how public conversation on race preferences ought to proceed in the wake of these revelations.</p>

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</description>

<author>Christopher A. Bracey</author>


</item>


<item>
<title>Dante&apos;s Pilgrimage on Infernal Sadism</title>
<link>http://scholarship.shu.edu/theses/210</link>
<guid isPermaLink="true">http://scholarship.shu.edu/theses/210</guid>
<pubDate>Mon, 07 May 2012 08:43:36 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>P.Theodore M. Hart</author>


</item>


<item>
<title>Movie and Television Fathers: A Positive Reflection of Positive Changes</title>
<link>http://scholarship.rollins.edu/mls/19</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/19</guid>
<pubDate>Mon, 07 May 2012 08:42:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Certain films and television programs depicting fathers have both enduring popularity and have reflected the advances in the institution of fatherhood. This has happened because of a symbiosis that has delivered positive results: popular films and television shows that earn money for producers and advertisers have depicted fathers who have changed to reflect the popular example. These depictions have contributed in their way to mending the family dynamic, specifically related to the father’s essential role in the family. Such family-oriented films and television shows have effectively showed fathers (and men that would become fathers) that they could be much more than a stereotype. These pages will show how these films and television programs have reflected how the institution of fatherhood has changed over time in America and how these shows and films have modeled, instructed, and encouraged fathers and future fathers to be more, deliver more and influence their children in a more positive direction. The changes in the institution of fatherhood that arose through these years from 1950 to 1980 have been reflected back to the public through these movie and television fathers. Such “reflection” has solidified and helped institutionalize the advancements in the role of the American father to its present model of a nurturer who sees great value in being responsible, accessible, and engaged with his children.</p>

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</description>

<author>George J. McGowan</author>


</item>


<item>
<title>Book Review. Making Civil Rights Law: Thurgood Marshall and the Supreme Court, 1936-1961</title>
<link>http://www.repository.law.indiana.edu/facpub/511</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/511</guid>
<pubDate>Mon, 07 May 2012 08:41:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kevin D. Brown</author>


</item>


<item>
<title>The Implications of the Equal Protection Clause for the Mandatory Integration of Public School Students</title>
<link>http://www.repository.law.indiana.edu/facpub/510</link>
<guid isPermaLink="true">http://www.repository.law.indiana.edu/facpub/510</guid>
<pubDate>Mon, 07 May 2012 08:41:14 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kevin D. Brown</author>


</item>


<item>
<title>Physical Activity in the High School Curricula</title>
<link>http://scholar.valpo.edu/sarp/13</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/13</guid>
<pubDate>Mon, 07 May 2012 08:40:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>My research is based on the student athletes in my classroom, who also are on the basketball team that I help coach. With my research, I plan to monitor my students’ grades while they are in season and interview them about the hard work they put into their sports and schoolwork. With this interview, I will be asking my students how much time they spend doing homework, how fatigued they are during school, how much time they spend playing their sport, and why they think their grades slip during season. Also, I plan on interviewing some of the girls on my basketball team to get their opinions on their motivation on schoolwork during their season.</p>

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</description>

<author>Katy Foster</author>


</item>


<item>
<title>Reading Muscles: Preparation for Standardized Testing in High School Students</title>
<link>http://scholar.valpo.edu/sarp/12</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/12</guid>
<pubDate>Mon, 07 May 2012 08:40:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>As educators, it is our responsibility to help students in their journey to academic growth and discovery. Being such, many teachers find themselves struggling for that perfect balance between making students more comfortable and pushing them outside of their comfort zones. Many Language Arts teachers, if asked, would likely state that when they hold test preparation activities, the class is run in a relatively similar manner as it might be on any other given day. Yes, the reading material and subsequent questions might have been acquired from a test preparation booklet appropriate to the students’ grade level, but most other circumstances remain stable, unchanged. Students are often only expected to complete one reading and one coinciding set of questions with minimal limitations on where and from whom they might attain assistance when a problem occurs. The material is test preparation-worthy but the situation is not. <strong></strong></p>

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</description>

<author>Katie Genereux</author>


</item>


<item>
<title>The Problem with Group Work: Engagement of all Students in Group Assignments</title>
<link>http://scholar.valpo.edu/sarp/11</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/11</guid>
<pubDate>Mon, 07 May 2012 08:40:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>The premise of this research project was to attempt to finds solutions to eradicate the problem of disengagement in the classroom when conducting group work and employing the use of group assignments in order to assess student learning. I wanted to propose a way teachers can strive to ensure all students within the group contribute to the groups’ success and learning without having some students disengage from the situation and rely on others to do the work of the group. The problem with group projects is too often the division of work becomes unfair, and only some members of the group are actually engaged in learning. The accountability for learning and progress forward shifts from the individual to the group, and this too often results in only part of the group making any learning contributions while the other part of the group has checked out and become disengaged from the learning.</p>

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</description>

<author>Samantha Glasgow</author>


</item>


<item>
<title>Varying Curricula to Meet Physics Students Learning Styles</title>
<link>http://scholar.valpo.edu/sarp/10</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/10</guid>
<pubDate>Mon, 07 May 2012 08:40:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Through differentiation of physics curriculum, teachers are able to meet various students’ learning styles. Educators are able to differentiate the curriculum so that it builds on students’ strengths and addresses their weaknesses. An inventory can be administered to assess the students’ abilities with certain concepts, and this inventory could be compiled from various assessment questions. Once teachers assess areas of weakness, they are able to make adjustments to curriculum and lesson plans to address these issues. Teaching techniques found in <em> Just-in-time Teaching: Blending Active Learning with Web Technology</em> will be used in the lesson planning and instruction of the course taught in this research. After the curriculum and lesson plans have been implemented and completed by students, educators can then administer to their students the inventory again, now post instruction, to assess the effectiveness of their teaching techniques.</p>

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</description>

<author>Gavin Grillo</author>


</item>


<item>
<title>Time to Learn: When Classroom Engagement is at Its Peak</title>
<link>http://scholar.valpo.edu/sarp/9</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/9</guid>
<pubDate>Mon, 07 May 2012 08:40:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>"The purpose of the study was to investigate how the time of day affects the ability of students to focus and remain attentive in the math classroom and the level of engagement during the class period. The math classes that were included in this study included Honors Algebra 2, Precalculus, and Algebra 1. These classes had students from grades 9 through 12. The study took place over the course of three months. Students were asked to fill out a survey about how the time of day affects their own attention level and their own sense of engagement and observations of the teacher were recorded daily. The research showed that students and teachers feel as if the time of day greatly affects students' ability to concentrate and the 'Time to Learn' seems to be in the mid-morning.'</p>

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</description>

<author>Caleb Grim</author>


</item>


<item>
<title>Health Curriculum in the Middle School Classroom: Assignment Completion vs. Academic Success</title>
<link>http://scholar.valpo.edu/sarp/8</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/8</guid>
<pubDate>Mon, 07 May 2012 08:40:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>In order for teachers to most effectively help their students retain knowledge, instructors must be aware of the achievement students are attaining from their homework assignments. Assignments are used as tools by teachers to guide students on their learning paths. If the assignments are not structured properly or if students do not turn them in, the gain of students towards academic achievement is lessened. This research looks at the effect that assignment completion can have on academic success in the middle school classroom. Completion percentages and test scores will be looked at on a unit basis for two separate health units. The literature reviewed revolves around student work in relation to overall achievement in school. Overall, the results correlated positively between student assignment completion percentage and high achievement tests.</p>

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</description>

<author>Chris Hovan</author>


</item>


<item>
<title>Can we motivate student behavior in a first grade classroom? Reward System vs. Conventional Teaching Discipline Plan</title>
<link>http://scholar.valpo.edu/sarp/7</link>
<guid isPermaLink="true">http://scholar.valpo.edu/sarp/7</guid>
<pubDate>Mon, 07 May 2012 08:40:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>What effect does a reward system have on first grade student behavior? Is there any way to have students behave better than they are currently? There is plenty of research conducted on different types of distracting behavior as well as different types of systems and programs that try to influence behavior. Three first grade classes were selected, observed, and data were recorded on any disruptive or unwanted behavior for three consecutive weeks. Post the first three weeks, a reward system was implanted for each class. Each class was given the opportunity to earn a “free day” in physical education class by decreasing their disruptive behavior during class. Only two of the classes were able to earn their free day.</p>

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</description>

<author>Nicholas Strzelecki</author>


</item>


<item>
<title>User Task Scenarios for Map-Based Decision Support in Community Health Planning</title>
<link>http://digitalcommons.ryerson.ca/geography/37</link>
<guid isPermaLink="true">http://digitalcommons.ryerson.ca/geography/37</guid>
<pubDate>Mon, 07 May 2012 08:27:19 PDT</pubDate>
<description>
	<![CDATA[
	<p>Health outcomes are affected by the socio-demographic and physical-environmental characteristics of the places where people live. Therefore, epidemiologists have been interested in the use of maps to explore spatial patterns of disease for a long time. Geographic Information Systems (GIS) are not only useful when visualizing complex spatial datasets but also when mapping the results of analytical processes. One such process is multi-criteria evaluation (MCE), which can be used to generate composite measures of public health based on individual, medical and non-medical factors.</p>
<p>The objective of this study was to determine if geovisual MCE can be an effective tool in community health planning. We provided highly interactive thematic maps coupled with MCE tools to planners at a community health centre and evaluated their use for community health planning and decision-making. User task scenarios were designed in a way to compare the usefulness of different representation methods for a number of tasks.</p>
<p>The pilot user test with two expert participants included interviews, questionnaires, and user task scenarios with think-aloud audio and screen video recording. We assessed the easiness of completing the tasks using completion rates and times and could identify a number of specific usability issues with the tool at hand.</p>

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</description>

<author>Brian Kelsey et al.</author>


</item>


<item>
<title>Litter, Color Variation, and Sex Effects on Feeding and Anti-Predator Behavior in Individual Thamnophis sirtalis</title>
<link>http://trace.tennessee.edu/utk_ecolpubs/12</link>
<guid isPermaLink="true">http://trace.tennessee.edu/utk_ecolpubs/12</guid>
<pubDate>Mon, 07 May 2012 08:25:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>There are stark coloration differences within single populations of <em>Thamnophis sirtalis</em> such as the Isle Royale population. While these red color patterns cause the snakes to stand out, it is unsure if it is for some defensive purpose such as aposematic coloring. To see if this or other genetic factors, sex, and relatedness with litters, could influence behavior anti-predator and feeding tests were performed on 38 captive-born neonate T. sirtalis. The feeding experiment recorded the latency of feeding from placement of the piece of night crawler to food capture. The anti-predator experiment recorded reactions to a probe touching each snake 20 times with three seconds in between. The feeding results indicated that there is a connection between that behavior and litter but not coloration or sex. This held true for the anti-predator behaviors of directional reversals and freezing but none of the groups showed any connection to total active anti-predator behaviors. There were also no correlations between the anti-predator and feeding behaviors. Litter seems to be the strongest indicator of behavior.</p>

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</description>

<author>Jennifer F. Porter et al.</author>


</item>


<item>
<title>El deber de sostener la equidad</title>
<link>http://pub.bsalut.net/risai/vol4/iss1/8</link>
<guid isPermaLink="true">http://pub.bsalut.net/risai/vol4/iss1/8</guid>
<pubDate>Mon, 07 May 2012 08:25:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>Es difícil en estos momentos de crisis abordar ninguna cuestión ética que no esté relacionada con el sistema económico. Todos los problemas tradicionales de la bioética, referidos hasta ahora a principios como la autonomía del paciente y la beneficencia, se desvanecen ante la prioridad de la justicia. La redistribución de los bienes básicos, entre los que tienen especial relieve los relativos a la sanidad, empieza a tambalearse y, a la vista del panorama, todos reclaman un sistema sanitario sostenible. No nos confundamos con el concepto de sostenibilidad. Desde un punto de vista ético, lo primero que debemos preguntarnos es qué hay que sostener. ¿Un sistema sanitario minimizado por los recortes? ¿Un sistema sanitario menos universal que el que tenemos? Evidentemente, no. Lo que hay que sostener es la equidad del sistema sanitario. Si tenemos que repensar cómo hacerlo y empezar a hacer reformas, hagámoslo, pero sin perder de vista que lo que hay que preservar por encima de todo es la equidad.</p>

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</description>

<author>Victoria Camps</author>


</item>


<item>
<title>Whistleblower Tug-of-War: Corporate Attempts to Secure Internal Reporting Procedures in the Face of External Monetary Incentives Provided by the Dodd-Frank Act</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/7</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/7</guid>
<pubDate>Mon, 07 May 2012 08:20:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Shannon Kay Quigley</author>


</item>


<item>
<title>Eradicating Elder Abuse in California Nursing Homes</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/6</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/6</guid>
<pubDate>Mon, 07 May 2012 08:20:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Linda K. Chen</author>


</item>


<item>
<title>More than Words: Rethinking the Role of Modern Demonstrative Evidence</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/4</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/4</guid>
<pubDate>Mon, 07 May 2012 08:19:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>David S. Santee</author>


</item>


<item>
<title>Proportionality&apos;s Cultural Foundation</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/5</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/5</guid>
<pubDate>Mon, 07 May 2012 08:19:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jordan M. Singer</author>


</item>


<item>
<title>Delaware&apos;s Expanding Duty of Loyalty and Illegal Conduct: A Step Towards Corporate Social Responsibility</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/3</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/3</guid>
<pubDate>Mon, 07 May 2012 08:19:58 PDT</pubDate>
<description>
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</description>

<author>David Rosenberg</author>


</item>


<item>
<title>Infancy Doctrine Inquiries</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/2</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/2</guid>
<pubDate>Mon, 07 May 2012 08:19:57 PDT</pubDate>
<description>
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</description>

<author>Cheryl B. Preston et al.</author>


</item>


<item>
<title>Takings by Regulation: How Should Courts Weigh the Balancing Factors</title>
<link>http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/1</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/lawreview/vol52/iss1/1</guid>
<pubDate>Mon, 07 May 2012 08:19:56 PDT</pubDate>
<description>
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</description>

<author>David Crump</author>


</item>


<item>
<title>AIDS Stigma and Discrimination in Public Schools: A Case Study of HIV-Positive Children in Kenya</title>
<link>http://ir.lib.uwo.ca/etd/518</link>
<guid isPermaLink="true">http://ir.lib.uwo.ca/etd/518</guid>
<pubDate>Mon, 30 Apr 2012 14:30:00 PDT</pubDate>
<description>
	<![CDATA[<br>
	</br>
	<p><h1>ABSTRACT</h1></p>
<p>The advancement of the antiretroviral therapy (ARV) has extended life expectancy for children born with HIV, allowing them to live longer, healthier lives and to attend school. Conversely, medical evidence indicates that it is unlikely for HIV transmission to occur during social interactions, and therefore exclusion of HIV-positive children (CLWHA) from school is unwarranted. Kenya’s education policy guarantees every child the right to education and protection from all forms of discrimination. However, due to social misconstructions about HIV/AIDS, CLWHA’s continue to face various forms of stigmatization. Therefore, the aim of this study was to examine the manifestation and experiences of AIDS stigma and discrimination in Kenyan public schools. It specifically explored how these experiences affected social interactions and learning of CLWHA.</p>
<p>This ethnographic qualitative case study utilized social stigma theories (Goffman, 1963) to illuminate the educational realities of CLWHA and divulge relevant implications. The study utilized purposeful criteria sampling to select 22 participants. Data were collected using qualitative in-depth interviews, participant observation and document analysis. Emerging data from the interviews and observations were analyzed into themes. Owing to the participants’ vulnerability and the sensitive nature of this study, confidentiality was maintained at all levels and pseudonyms were assigned to all the participants and institutions.</p>
<p>The results indicated that stigma and discrimination were visible in the school milieu and negatively impacted the social interactions and learning of CLWHA. Lack of empowerment and inadequate resources suggested that CLWHA received limited support and stigma and discrimination were poorly addressed. The study however demonstrated that support was critical in enhancing learning and social integration of CLWHA into public schools. Based on the study findings, collaborative efforts and policies are necessary to enhance effective interventions aimed at reducing S& D in schools, and for directing government and school-based policies and practices towards improving CLWHA’s right to education, empowerment and support.</p>
<p><strong>Key words</strong>: AIDS stigma and discrimination, HIV-positive children, empowerment and support, social interactions and learning</p>

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</description>

<author>Maryanne N. Kamau</author>


<program>Education</program>
<degree>Doctor of Philosophy</degree>
</item>


<item>
<title>The Palestinian-Israeli Conflcit: The Way Forward</title>
<link>http://digitalrepository.trincoll.edu/theses/201</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/201</guid>
<pubDate>Mon, 07 May 2012 08:13:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Looking back at the major peace negotiations of the past twenty years, since the collapse of the Soviet Union and the end of the Cold War, The Madrid Conference and Oslo Accords, the Camp David negotiations, the Roadmap to Peace, and the more recent attempts at negotiation have failed to produce any lasting peace agreement between the Israelis and the Palestinians. At the moment, the two sides are so polarized that they have locked in a stale mate. Many politicians and pundits have become as cynical as to preach that the only way out of the stale mate is through a full scale war. Similar to the Cold War, this cannot be the outcome. Another war has the potential to assure the mutual destruction of Israel and the Palestinians. In order to get both the Israelis and the Palestinians to the negotiating table, we must look to the failures of the past to plan for the future.</p>

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</description>

<author>Michael P. Levy</author>


</item>


<item>
<title>Kalirin, a Key Player in Synapse Formation, Is Implicated in Human Diseases</title>
<link>http://digitalcommons.uconn.edu/uchcres_articles/86</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/uchcres_articles/86</guid>
<pubDate>Mon, 07 May 2012 08:04:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>Synapse formation is considered to be crucial for learning and memory.  Understanding the underlying molecular mechanisms of synapse formation  is a key to understanding learning and memory. Kalirin-7, a major  isoform of Kalirin in adult rodent brain, is an essential component of  mature excitatory synapses. Kalirin-7 interacts with multiple  PDZ-domain-containing proteins including PSD95, spinophilin, and GluR1  through its PDZ-binding motif. In cultured hippocampal/cortical neurons,  overexpression of Kalirin-7 increases spine density and spine size  whereas reduction of endogenous Kalirin-7 expression decreases synapse  number, and spine density. In Kalirin-7 knockout mice, spine length,  synapse number, and postsynaptic density (PSD) size are decreased in  hippocampal CA1 pyramidal neurons; these morphological alterations are  accompanied by a deficiency in long-term potentiation (LTP) and a  decreased spontaneous excitatory postsynaptic current (sEPSC) frequency.  Human Kalirin-7, also known as Duo or Huntingtin-associated  protein-interacting protein (HAPIP), is equivalent to rat Kalirin-7.  Recent studies show that Kalirin is relevant to many human diseases such  as Huntington's Disease, Alzheimer's Disease, ischemic stroke,  schizophrenia, depression, and cocaine addiction. This paper summarizes  our recent understanding of Kalirin function.</p>

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</description>

<author>Prashant Mandela et al.</author>


</item>


<item>
<title>An Overview of Physics Education Research on Problem Solving</title>
<link>http://opus.ipfw.edu/physics_facpubs/49</link>
<guid isPermaLink="true">http://opus.ipfw.edu/physics_facpubs/49</guid>
<pubDate>Mon, 07 May 2012 08:04:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>As the title states this is a review of the physics education research on students problem solving efforts.  This was part of the Getting Started in PER volumes edited by C. Henderson and K. A. Harper published on the Compadre website</p>

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</description>

<author>David P. Maloney</author>


</item>


<item>
<title>Newtonian Tasks Inspired by Physics Education Research: nTIPERs</title>
<link>http://opus.ipfw.edu/physics_facpubs/48</link>
<guid isPermaLink="true">http://opus.ipfw.edu/physics_facpubs/48</guid>
<pubDate>Mon, 07 May 2012 08:04:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>This volume is a collection of paper and pencil tasks in ten different formats designed to help students make sense of basic Newtonian physics.  The formats and/or concepts/issues in the tasks are inspired by the results of physics education research into students learning introductory physics.</p>

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</description>

<author>David P. Maloney et al.</author>


</item>


<item>
<title>Richard Upjohn and Richard Morris Hunt: The Evolution of Newport Domestic Architecture</title>
<link>http://digitalrepository.trincoll.edu/theses/200</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/200</guid>
<pubDate>Mon, 07 May 2012 07:59:46 PDT</pubDate>
<description>
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</description>

<author>Caroline L. Peck</author>


</item>


<item>
<title>Do Gender and Relationship Composition Affect College Students’ Perceptions of Intimate Partner Violence Severity?</title>
<link>http://digitalrepository.trincoll.edu/theses/199</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/199</guid>
<pubDate>Mon, 07 May 2012 07:59:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Previous research has examined college students’ opinions about the severity of physical abuse in heterosexual, lesbian, and gay couples, but not their opinions regarding the severity of psychological and sexual abuse in the context of these relationships. The main aims of this study were to examine whether participant gender and relationship composition (i.e., heterosexual, lesbian, and gay couples) affected college students’ opinions about the severity of physical, psychological, and sexual intimate partner violence (IPV), if abuse in opposite-sex relationships was perceived as more severe than abuse in same-sex relationships, and if prior exposure to IPV was associated with lower IPV severity ratings. Seventy-two undergraduates enrolled in psychology courses at a small, private college in the Northeastern United States were recruited in order to examine these research questions. They read three short vignettes that varied the gender of the victims and perpetrators and then rated the severity of the violence and assigned a blame rating to the victim and perpetrator. Results were consistent with previous research, in that participants rated psychological abuse as the least severe form of abuse. Contrary to previous research, however, male participants in this study did not assign less blame to male perpetrators, nor did the participants view the violence in opposite-sex relationships as more severe than the violence in same-sex couples. Also prior exposure to IPV did not seem to have a large effect on participants’ perceptions of IPV severity.</p>

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</description>

<author>Jasmine Owarish-Gross</author>


</item>


<item>
<title>Truth and Being: Heidegger&apos;s Turn to Poetry</title>
<link>http://digitalrepository.trincoll.edu/theses/198</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/198</guid>
<pubDate>Mon, 07 May 2012 07:55:04 PDT</pubDate>
<description>
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</description>

<author>Alexandra J. Pell</author>


</item>


<item>
<title>Reason, Happiness, and the Divine Spark: A Global Perspective on HIV and Bioethics</title>
<link>http://digitalrepository.trincoll.edu/theses/197</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/197</guid>
<pubDate>Mon, 07 May 2012 07:55:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Much of the international effort to prevent and treat HIV involves testing products and techniques on members of highly-infected populations in places such as sub-Saharan Africa. All of the ethical principles guiding and structuring this research are rooted in prominent Western ethical systems, and most research projects are conducted by Western or Westernized institutions. In a global culture that tends to reject ethical cultural relativism, the international community regularly touts these Western ideals as universally acceptable and applicable, often coming dangerously close to paternalism. While institutions and researchers are fundamentally well-intentioned, often the study set-up and procedures conflict with the values and ideals local to the area on some level. To illuminate the difficulties and complexities of modern, global, bioethical guidelines and research practices, this thesis analyzes two related HIV-prevention case studies from both traditional, Western and local, non-Western perspectives. It reveals the difficulties and strengths of both Kantian ethics and John Stuart Mill’s Utilitarianism before moving on to develop an ethic based upon the concept of <em>ubuntu</em> found in the region of Africa where the two studies take place. From these discussions arises the possibility for a universal ethic rooted in the common valuation of humanity that transcends all cultural differences and is common to all cultures and societies. This universal commonality opens up a much-needed space for discourse on global bioethics across cultural boundaries, allowing for mutual respect and providing a promising possibility for a universal, yet culturally sensitive, standard for global bioethics.</p>

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</description>

<author>Anna K. Grindy</author>


</item>


<item>
<title>Steel Pan&apos;s Heart</title>
<link>http://digitalrepository.trincoll.edu/theses/196</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/196</guid>
<pubDate>Mon, 07 May 2012 07:55:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Even though mostly Afro-Trinidadians play pan, the Steel Pan instills national identity and pride because Pan has become internationally popular and the proliferation of so many steel drum events before carnival, including Panorama-the world largest Steel Pan competition.The purpose of this paper looks the hybridization and Creolization of the music culture of the nation, in regards to the major ethnic groups, especially Indo-Trinidadian.</p>

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</description>

<author>Chioma Viola Ozuzu</author>


</item>


<item>
<title>Leading, learning, practicing and reflecting: Insights from an overseas  Practicum</title>
<link>http://opus.ipfw.edu/english_facpres/76</link>
<guid isPermaLink="true">http://opus.ipfw.edu/english_facpres/76</guid>
<pubDate>Mon, 07 May 2012 07:51:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Drawing on students’ experience and perspectives, this presentation discusses a curriculum innovation of a practicum offered overseas and the benefits students gained through learning, leading, practicing and reflecting in an international setting, a rare educational opportunity combining curriculum requirements, professional growth and experience of living in a new culture.</p>

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</description>

<author>Hao Sun</author>


</item>


<item>
<title>Scholarly Resistance: Appalachians Re-Reading the Academy</title>
<link>http://opus.ipfw.edu/english_facpres/75</link>
<guid isPermaLink="true">http://opus.ipfw.edu/english_facpres/75</guid>
<pubDate>Mon, 07 May 2012 07:51:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sara Webb-Sunderhaus</author>


</item>


<item>
<title>Foreigners from the Same Country</title>
<link>http://digitalrepository.trincoll.edu/theses/195</link>
<guid isPermaLink="true">http://digitalrepository.trincoll.edu/theses/195</guid>
<pubDate>Mon, 07 May 2012 07:50:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>My thesis aims to dissect the confounding factors that lead to the build up of social tension between the Hong Kong and Mainland Chinese population. The three main causes of this tension are the major increase in the wealthy population within China, Hong Kong’s “autonomous” political status, and Hong Kong’s resource constraints. My thesis also aims to provide suitable solutions to diminish or extinguish the tension and give a logical prediction of Hong Kong’s economic, political and social outlook in the upcoming years.</p>

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</description>

<author>Adrian J. Lo</author>


</item>


<item>
<title>Latino/Latin American Muralism and Social Change:  A Reflection on the Social Significance of the Cold Spring Mural</title>
<link>http://digitalcommons.csbsju.edu/art_students/1</link>
<guid isPermaLink="true">http://digitalcommons.csbsju.edu/art_students/1</guid>
<pubDate>Mon, 07 May 2012 07:43:51 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Shannon McEvoy</author>


</item>


<item>
<title>My Dear Watson: A Musical Interpretation of Sherlock Holmes’s Friendship with Dr. John Watson</title>
<link>http://scholarship.rollins.edu/mls/18</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/18</guid>
<pubDate>Mon, 07 May 2012 07:43:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>The relationship between Sherlock Holmes and John Watson is complicated and certainly untraditional.  Some theorize that Holmes is merely using Watson while Watson desperately seeks his affection.  Others theorize that they have an unrequited homosexual relationship.  However, it is Holmes’ unemotional nature paired with Watson’s fierce loyalty and admiration that creates a new and unique type of relationship.  Many would define friendship as an emotional bond, but with Holmes, this is impossible.  That does not mean, however, that he is incapable of deeply caring for Watson.  It means that the relationship looks different than the traditional friendship.  Watson and Holmes’ friendship is the depiction of a genuine intimate friendship with an unemotional man. My Dear Watson is a full-length musical including 15 original songs plus overture, entr’acte, and instrumental interludes orchestrated for a 12-piece orchestra that explores the complexity, eccentricity, and beauty of Holmes’s and Watson’s friendship. The plot is based mainly on A Study in Scarlet, The Valley of Fear, and “The Final Problem,” though other stories are also incorporated, and much of the dialogue is original.  In addition to this dramatic work, I have also written a scholarly essay entitled “Sherlock and John: A Redefined Friendship,” which explores Sir Arthur Conan Doyle’s stories and utilizes them to redefine the very nature of friendship through the lens of this unusual friendship with an unemotional man.  Use of the Sherlock Holmes characters created by the late Sir Arthur Conan Doyle is by permission of the rights owner, Conan Doyle Estate, Ltd.</p>

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</description>

<author>Jami-Leigh C. Bartschi</author>


</item>


<item>
<title>Supreme Court Institute Annual Report, 2010-2011</title>
<link>http://scholarship.law.georgetown.edu/sci_papers/2</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/sci_papers/2</guid>
<pubDate>Mon, 07 May 2012 07:43:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>During the 2010-2011 academic year--corresponding to the U.S. Supreme Court’s October Term (OT) 2010--the Supreme Court Institute (SCI) provided moot courts for advocates in over 93% of the cases heard by the Court this Term; sponsored a range of programming related to the Supreme Court; and hosted delegations of lawyers and judges visiting from Britain, Rwanda, Kosovo, Korea, China, and Germany. A list of all SCI moot courts held in OT 2010, listed by sitting and date of moot and including the name and affiliation of each advocate and the number of student observers, follows the narrative portion of this report.</p>

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</description>

<author>Georgetown University Law Center, Supreme Court Institute</author>


</item>


<item>
<title>Supreme Court Institute Annual Report, 2011-2012</title>
<link>http://scholarship.law.georgetown.edu/sci_papers/1</link>
<guid isPermaLink="true">http://scholarship.law.georgetown.edu/sci_papers/1</guid>
<pubDate>Mon, 07 May 2012 07:43:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>During the 2011-2012 academic year--corresponding to the U.S. Supreme Court’s October Term (OT) 2011--the Supreme Court Institute (SCI) provided moot courts for advocates in over 94% of the cases heard by the Court this Term and offered over a dozen programs related to the Supreme Court. All SCI moot courts held in OT 2011, listed by sitting and date of moot, and including the name and affiliation of each advocate and the number of student observers, follows the narrative portion of this report.</p>

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</description>

<author>Georgetown University Law Center, Supreme Court Institute</author>


</item>


<item>
<title>Religion and Architecture in Downtown Orlando</title>
<link>http://scholarship.rollins.edu/mls/17</link>
<guid isPermaLink="true">http://scholarship.rollins.edu/mls/17</guid>
<pubDate>Mon, 07 May 2012 07:42:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Since the onset of Western civilization, religion has continuously influenced architectural and urban forms. These material echoes of religion are often unrecognized in the modern city. This work identifies, analyzes and classifies such influences, and illustrates their manifestation with the example of downtown Orlando. Religious influences can be observed in the locations of the cities, in their urban planning, and in many constructive and architectural elements and styles developed for religious purposes. One principal group of architectural elements that that carries a religious connotation is the elements of classical antiquity, which reflect their pagan origins. The other group is the religion-related elements of Christian architecture. Major contributors to the preservation of these influences are constant trends of copying historical styles. The thesis develops a taxonomy of religious influences that can be identified in the architecture of a modern Western city. The accompanying photographic monograph of downtown Orlando presents three predominant groups of buildings that either intentionally or unconsciously suggest the presence of religion in the city. Those are secular structures that incorporate various religious elements and styles, buildings with predominantly secular architecture that display the sign of the cross and church buildings designed in traditional styles characteristic to ecclesiastical structures. Accenting the mix of traditional and modern, as well as religious and secular forms in downtown Orlando, the monograph points to the often-disregarded echoes of religion and demonstrates the points developed in the theoretical part.</p>

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</description>

<author>Djordje Jovanović</author>


</item>


<item>
<title>Performance Changes During a Weeklong High Altitude Training Camp in Lowlander Youth Athletes</title>
<link>http://digitalcommons.uconn.edu/gs_theses/239</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/239</guid>
<pubDate>Mon, 07 May 2012 07:37:41 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jay R. Hydren</author>


</item>


<item>
<title>Understanding the Importance of the Zinc Binding Domain in CESA Protein Interaction: Some Assembly Required</title>
<link>http://digitalcommons.uri.edu/srhonorsprog/271</link>
<guid isPermaLink="true">http://digitalcommons.uri.edu/srhonorsprog/271</guid>
<pubDate>Mon, 07 May 2012 07:24:14 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Understanding the Importance of the zinc binding domain in the cellulose synthase complex: Some Assembly Required</strong></p>
<p>Alfred Schupp</p>
<p>Sponsor: Alison Roberts, Biological Sciences</p>
<p>Cellulose microfibrils are vital components of the cell wall. A microfibril is made up of multiple strands of glucose chains, and these cellulose microfibrils are produced by protein complexes in the plasma membrane called cellulose synthase complexes, or CSCs for short. Each complex is made up of 36 subunits called Cellulose Synthase proteins, or CESAs. Each CESA produces a glucose polymer made from beta-1,4 glucan linkages. It is known that CESA proteins aggregate to form CSCs, and that different CESA proteins come together to make the primary or secondary cell wall, but exactly how the proteins associate is unknown.</p>
<p>Previous studies in cotton suggest that the beginning of the CESA protein contains a zinc binding motif with specific amino acid residues that form strong covalent bonds following oxidation. This senior project explores what would happen if this motif were completely deleted and not simply mutagenized as previous studies have done. I looked at CESA5, which is required for the formation of leafy gametophores in the moss <em>Physcomitrella patens</em>. If DNA encoding a zinc binding domain deficient CESA5 cannot rescue a CESA5 knockout, it suggests that this motif is essential for proper protein association in the CSCs involved in the formation of leafy shoots. It does not explain which CESAs specifically interact, but it would show the importance of the zinc binding domain for protein interaction.</p>
<p>If a CESA5 knockout could not be rescued, I wanted to know if a coiled-coil, another type of protein association, could restore the normal phenotype in the zinc binding domain deficient CESA5.</p>
<p>The project was carried out using PCR, restriction digestion and ligation enzymes to produce the gene with the deleted zinc binding motif, and transformation techniques to introduce the altered gene into the moss plant.</p>
<p>Keywords: Cellulose, Moss, Molecular, Zinc, CESA,</p>

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</description>

<author>Alfred Schupp III</author>


</item>


<item>
<title>A Doubling Method for the Generalized Lambda Distribution</title>
<link>http://opensiuc.lib.siu.edu/epse_pubs/8</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/epse_pubs/8</guid>
<pubDate>Mon, 07 May 2012 07:03:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper introduces a new family of generalized lambda distributions GLDs based on a method of <em>doubling</em> symmetric GLDs. The focus of the development is in the context of <em>L</em>-moments and <em>L</em>-correlation theory. As such, included is the development of a procedure for specifying double GLDs with controlled degrees of <em>L</em>-skew, <em>L</em>-kurtosis, and <em>L</em>-correlations. The procedure can be applied in a variety of settings such as modeling events and Monte Carlo or simulation studies. Further, it is demonstrated that estimates of <em>L</em>-skew, <em>L</em>-kurtosis, and <em>L</em>-correlation are substantially superior to conventional product-moment estimates of skew, kurtosis, and Pearson correlation in terms of both relative bias and efficiency when heavy tailed distributions are of concern.</p>

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</description>

<author>Todd C. Headrick et al.</author>


</item>


<item>
<title>Benchmarking the CM-5 for Image Processing Applications</title>
<link>http://surface.syr.edu/eecs_techreports/180</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/180</guid>
<pubDate>Mon, 07 May 2012 07:01:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper presents benchmarking results for image processing algorithms on the Connection Machine model CM-5 and compares them with the results from the CM-2 and the Sun-4. Image processing algorithms with varying communication and computational requirements were implemented, tested and timed. The performance and the scalabilty of the CM-5 were analyzed and compared with that of the CM-2.</p>

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</description>

<author>Ravi V. Shankar et al.</author>


</item>


<item>
<title>Conceptual Background for Symbolic Computation</title>
<link>http://surface.syr.edu/eecs_techreports/179</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/179</guid>
<pubDate>Mon, 07 May 2012 07:01:14 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper is a tutorial which examines the three major models of computation--the Turing Machine, Combinators, and Lambda Calculus--with respect to their usefulness to practical engineering of computing machines. While the classical von Neumann architecture can be deduced from the Turing Machine model, and Combinator machines have been built on an experimental basis, no serious attempts have been made to construct a Lambda Calculus machine. This paper gives a basic outline of how to incorporate a Lambda Calculus capability into a von Neumann type architecture, maintaining full backward compatibility and at the same time making optimal use of its advantages and technological maturity for the Lambda Calculus capability.</p>

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</description>

<author>Klaus Berkling</author>


</item>


<item>
<title>A Declarative Foundation of λProlog with Equality</title>
<link>http://surface.syr.edu/eecs_techreports/178</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/178</guid>
<pubDate>Mon, 07 May 2012 07:01:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>We build general model-theoretic semantics for higher-order logic programming languages. Usual semantics for first-order logic is two-level: i.e., at a lower level we define a domain of individuals, and then, we define satisfaction of formulas with respect to this domain. In a higher-order logic which includes the propositional type in its primitive set of types, the definition of satisfaction of formulas is mutually recursive with the process of evaluation of terms. As result of this in higher-order logic it is extremely difficult to define an effective semantics. For example to define T p operator for logic program P, we need a fixed domain without regard to interpretations. In usual semantics for higher-order logic, domain is dependent on interpretations. We overcome this problem and argue that our semantics provides a more suitable declarative basis for higher-order logic programming than the usual general model semantics. We develop a fix point semantics based on our model. We also show that a quotient of the domain of our model can be the domain of a model for higher-order logic programs with equality.</p>

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</description>

<author>Mino Bai</author>


</item>


<item>
<title>Fault-Detection in Networks</title>
<link>http://surface.syr.edu/eecs_techreports/177</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/177</guid>
<pubDate>Mon, 07 May 2012 07:01:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>To find broken links in networks we use the cut-set space. Information on which nodes can talk, or not, to which other nodes allows reduction of the problem to that of decoding the cut-set code of a graph. Special classes of such codes are known to have polynomial-time decoding algorithms. We present a simple algorithm to achieve the reduction and apply it in two examples.</p>

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</description>

<author>H. F. Mattson Jr</author>


</item>


<item>
<title>A Non-Deterministric Parallel Sorting Algorithm</title>
<link>http://surface.syr.edu/eecs_techreports/176</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/176</guid>
<pubDate>Mon, 07 May 2012 07:01:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>A miniswap Si,1 ≤ i < n, compares two adjacent keys Пi, Пi+1 in the sequence (П1, ... , Пn), and transposes them if they are out of order. A full sweep is any composition of all n - 1 possible miniswaps. We prove that the composition of any n- 1 full sweeps is a sorting function.</p>

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</description>

<author>Xue Shirley Li et al.</author>


</item>


<item>
<title>Embedding Data Mappers with Distributed Memory Machine Compilers</title>
<link>http://surface.syr.edu/eecs_techreports/175</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/175</guid>
<pubDate>Mon, 07 May 2012 07:01:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>In scalable multiprocessor systems, high performance demands that computational load be balanced evenly among processors and that interprocessor communication be limited as much as possible.  Compilation techniques for achieving these goals have been explored extensively in recent years [3, 9, 11, 13, 17, 18]. This research has produced a variety of useful techniques, but most of it has assumed that the programmer specifies the distribution of large data structures among processor memories. A few projects have attempted to automatically derive data distributions for regular problems [12, 10, 8, 1]. In this paper, we study the more challenging problem of automatically choosing data distributions for irregular problems.</p>

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</description>

<author>Ravi Ponnusamy et al.</author>


</item>


<item>
<title>A Probabilistic Analysis of a Locality Maintaining Load Balancing Algorithm</title>
<link>http://surface.syr.edu/eecs_techreports/174</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/174</guid>
<pubDate>Mon, 07 May 2012 07:01:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper presents a simple load balancing algorithm and its probabilistic analysis. Unlike most of the previous load balancing algorithms, this algorithm maintains locality. We show that the cost of this load balancing algorithm is small for practical situations and discuss some interesting applications for data remapping.</p>

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</description>

<author>Kishan G. Mehrotra et al.</author>


</item>


<item>
<title>General Model Theoretic Semantics for Higher-Order Horn Logic Programming</title>
<link>http://surface.syr.edu/eecs_techreports/173</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/173</guid>
<pubDate>Mon, 07 May 2012 07:01:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>We introduce model-theoretic semantics [6] for Higher-Order Horn logic programming language. One advantage of logic programs over conventional non-logic programs has been that the least fixpoint is equal to the least model, therefore it is associated to logical consequence and has a meaningful declarative interpretation. In simple theory of types [9] on which Higher-Order Horn logic programming language is based, domain is dependent on interpretation [10]. To define T p operator for a logic program P, we need a fixed domain without regard to interpretation which is usually taken to be a set of atomic propositions. We build a semantics where we can fix a domain while changing interpretations. We also develop a fixpoint semantics based on our model, and show that we can get the least fixpoint which is the least model. Using this fixpoint we prove the completeness of the interpreter of our language in [14].</p>

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</description>

<author>Mino Bai et al.</author>


</item>


<item>
<title>Designing Efficient Maximum-Likelihood Soft-Decision Decoding Algorithms for Linear Block Codes Using Algorithm A*</title>
<link>http://surface.syr.edu/eecs_techreports/172</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/172</guid>
<pubDate>Mon, 07 May 2012 07:01:02 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this report we present a class of efficient maximum-likelihood soft-decision decoding algorithms for linear block codes. The approach used here is to convert the decoding problem into a search problem through a graph which is a trellis for an equivalent code of the transmitted code. Algorithm A*, which uses a priority-first search strategy, is employed to search through this graph. This search is guided by an evaluation function f defined to take advantage of the information provided by the received vector and the inherent properties of the transmitted code. This function f is used to drastically reduce the search space and to make the decoding efforts of this decoding algorithm adaptable to the noise level. For example, simulation results for the (128,64) binary extended BCH code indicate that for most real channels the proposed decoding algorithm is at least fifteen orders of magnitude more efficient in time and in space than that proposed by Wolf. Simulation results for the (104, 52) binary extended quadratic residue code are also given. These simulation results indicate that the use of Algorithm A* for decoding has resulted not only in an efficient soft-decision decoding algorithm for hitherto intractable linear block codes, but an algorithm which is in fact optimal as well.</p>

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</description>

<author>Yunghsiang S. Han et al.</author>


</item>


<item>
<title>Parallel Monte Carlo Trials</title>
<link>http://surface.syr.edu/eecs_techreports/171</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/171</guid>
<pubDate>Mon, 07 May 2012 07:01:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>The best results of Monte Carlo methods are generally obtained by performing the same computation many times with different random numbers. We develop a generic algorithm for parallel execution of Monte Carlo trials on a multicomputer. The generic algorithm has been adapted for simulated annealing and primality testing by simple substitutions of data types and procedures. The performance of the parallel algorithms was measured on a Computing Surface.</p>

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</description>

<author>Per Brinch Hansen</author>


</item>


<item>
<title>Simulated Annealing</title>
<link>http://surface.syr.edu/eecs_techreports/170</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/170</guid>
<pubDate>Mon, 07 May 2012 07:00:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>This tutorial describes simulated annealing, an optimization method based on the principles of statistical mechanics. Simulated annealing finds near-optimal solutions to optimization problems that cannot be solved exactly because they are NP-complete. The method is illustrated by a Pascal algorithm for the traveling salesperson problem. The performance of the algorithm was measured on a Computing Surface.</p>

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</description>

<author>Per Brinch Hansen</author>


</item>


<item>
<title>Primality Testing</title>
<link>http://surface.syr.edu/eecs_techreports/169</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/169</guid>
<pubDate>Mon, 07 May 2012 07:00:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>This tutorial describes the Miller-Rabin method for testing the primality of large integers. The method is illustrated by a Pascal algorithm. The performance of the algorithm was measured on a Computing Surface.</p>

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</description>

<author>Per Brinch Hansen</author>


</item>


<item>
<title>Numerical Solution of Laplace&apos;s Equation</title>
<link>http://surface.syr.edu/eecs_techreports/168</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/168</guid>
<pubDate>Mon, 07 May 2012 07:00:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>This tutorial discusses Laplace's equation for steady state heat flow in a two-dimensional region with fixed temperatures on the boundaries. The equilibrium temperatures are computed for a square grid using successive overrelaxation with parity ordering of the grid elements. The numerical method is illustrated by a Pascal algorithm. We assume that the reader is familiar with elementary calculus.</p>

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</description>

<author>Per Brinch Hansen</author>


</item>


<item>
<title>Parallel Cellular Automata: A Model Program for Computational Science</title>
<link>http://surface.syr.edu/eecs_techreports/167</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/167</guid>
<pubDate>Mon, 07 May 2012 07:00:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>We develop a model program for parallel execution of cellular automata on a multicomputer. The model program is then adapted for simulation of forest fires and numerical solution of Laplace's equation for stationary heat flow. The performance of the parallel program is analyzed and measured on a Computing Surface configured as a matrix of transputers with distributed memory.</p>

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</description>

<author>Per Brinch Hansen</author>


</item>


<item>
<title>Multiple-Length Division Revisited: A Tour of the Minefield</title>
<link>http://surface.syr.edu/eecs_techreports/166</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/166</guid>
<pubDate>Mon, 07 May 2012 07:00:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Long division of natural numbers plays a crucial role in Cobol arithmetic, cryptography, and primality testing. Only a handful of textbooks discuss the theory and practice of long division, and none of them do it satisfactorily. This tutorial attempts to fill this surprising gap in the literature on computer algorithms. We illustrate the subtleties of long division by examples, define the problem concisely, summarize the theory, and develop a complete Pascal algorithm using a consistent terminology.</p>

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</description>

<author>Per Brinch Hansen</author>


</item>


<item>
<title>All-to-Many Communication Avoiding Node Contention</title>
<link>http://surface.syr.edu/eecs_techreports/165</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/165</guid>
<pubDate>Mon, 07 May 2012 07:00:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this paper we present several algorithms for all-too-many personalized communications which avoid node contention.</p>

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</description>

<author>Sanjay Ranka et al.</author>


</item>


<item>
<title>Genetic Algorithms for Stochastic Flow Shop No Wait Scheduling</title>
<link>http://surface.syr.edu/eecs_techreports/164</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/164</guid>
<pubDate>Mon, 07 May 2012 07:00:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>ln this paper we present Genetic Algorithms - evolutionary algorithms based on an analogy with natural selection and survival of the fittest - applied to an NP Complete combinatorial optimization problem: minimizing the makespan of a Stochastic Flow Shop No Wait (FSNW) schedule. This is an important optimization criteria in real-world situations and the problem itself is of practical significance. We restrict our applications to the three machine flow shop no wait problem which is known to be NP complete. The stochastic hypothesis is that the processing times of jobs are described by normally distributed random variables. We discuss how this problem may be translated into a TSP problem by using the start interval concept.  Genetic algorithms, both sequential and parallel are then applied to search the solution space and we present the algorithms and empirical results.</p>

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</description>

<author>Harpal Maini et al.</author>


</item>


<item>
<title>Binary Resolution in Surface Reasoning</title>
<link>http://surface.syr.edu/eecs_techreports/163</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/163</guid>
<pubDate>Mon, 07 May 2012 07:00:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Intuition suggests the hypothesis that everyday human reasoning is conducted in the written or spoken natural language, rather than in some disparate representation into which the surface language is translated. An examination of human reasoning reveals patterns of inference that parallel binary resolution. But any standard implementation of resolution requires Skolemization. Skolemization would seem an unlikely component of human reasoning. This appears to contradict the hypothesis that human reasoning takes place at the surface.  To reconcile these observations, this paper develops a new rule of inference, which operates on surface expressions directly. This rule is shown to produce results which exactly parallel those produced by Skolemization and resolution. It extends the notion of 'surface reasoning' that was defined in previous papers. Several examples are given to illustrate its use in surface reasoning.</p>

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</description>

<author>William C. Purdy</author>


</item>


<item>
<title>The Effect of Season on Hoof Growth and Travel Patterns of Domestic Horses</title>
<link>http://digitalcommons.uconn.edu/gs_theses/238</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/238</guid>
<pubDate>Mon, 07 May 2012 07:00:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hoof and paddock management are two of the most important facets of domestic horse care. Understanding hoof growth and shoeing needs as well as managing turnout to match behavior patterns may benefit equine well-being. The objective of this study was to determine the effect of season on hoof growth rate and travel patterns in turnout. Nine Morgan horses were used in this study. Each horse's turnout travel patterns were measured four times in each season using a Garmin Edge® GPS tracking device. Additionally, hoof and body measurements were taken to determine change over a one month period in each season. Season was found to have a significant effect on hoof growth as well as body condition score and waist size. Season and weather had no significant effect on distance traveled in overnight turnout. A direction for future research may be to determine an average growth rate for each season, which would allow horse owners and farriers to create a more specific shoeing and trimming schedule. The data from GPS tracking provides horse owners with a better understanding of equine behavior in turnout, allowing them to create more efficient management schedules.</p>

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</description>

<author>Caitlin E. Lewis</author>


</item>


<item>
<title>A Generalization of the Trie Data Structure</title>
<link>http://surface.syr.edu/eecs_techreports/162</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/162</guid>
<pubDate>Mon, 07 May 2012 07:00:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Tries, a form of string-indexed look-up structure, are generalized to permit indexing by terms built according to an arbitrary signature. The construction is parametric with respect to the type of data to be stored as values; this is essential, because the recursion which defines tries appeals from one value type to others. "Trie" (for any fixed signature) is then a functor, and the corresponding look-up function is a natural isomorphism. The trie functor is in principle definable by the "initial fixed point" semantics of Smyth and Plotkin. We simplify the construction, however, by introducing the "category-cpo", a class of category within which calculations can retain some domain-theoretic flavor. Our construction of tries  extends easily to many-sorted signatures.</p>

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</description>

<author>Richard H. Connelly et al.</author>


</item>


<item>
<title>Genetic Algorithms for Soft Decision Decoding of Linear Block Codes</title>
<link>http://surface.syr.edu/eecs_techreports/161</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/161</guid>
<pubDate>Mon, 07 May 2012 07:00:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Soft-decision decoding is an NP-hard problem of great interest to developers of communication systems. We show that this problem is equivalent to the problem of optimizing Walsh polynomials. We present genetic algorithms for soft-decision decoding of binary linear block codes and compare the performance with various other decoding algorithms. Simulation results show that our algorithms achieve bit-error-probabilities as low as 0.00183 for a [104, 52] code with a low signal-to-noise ratio of 2.5 dB, exploring only 30,000 codewords, whereas the search space contains 4.5 x 1015 codewords. We define a new crossover operator that exploits domain-specific information and compare it with uniform and two point crossover. We also give a schema theorem for our genetic algorithm, showing that high reliability, low order codewords are the building blocks for the evolutionary process.</p>

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</description>

<author>Harpal Maini et al.</author>


</item>


<item>
<title>On Inverse Sigmoid Functions</title>
<link>http://surface.syr.edu/eecs_techreports/160</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/160</guid>
<pubDate>Mon, 07 May 2012 07:00:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Networks with sigmoid node functions have been shown to be universal approximators, and can use straightforward implementations of learning algorithms. Mathematically, what is common to different sigmoid functions used by different researchers? We establish a common representation of inverse sigmoid functions in terms of the Guass Hypergeometric function, generalizing different node function formulations. We also show that the continuous Hopfield network equation can be transformed into a Legendre differential equation, without assuming the specific form of the node function; this establishes a link between Hopfield nets and the method of function approximation using Legendre polynomials</p>

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</description>

<author>Anil Ravindran Menon et al.</author>


</item>


<item>
<title>Putting Humpty-Dumpty together again: Reconstructing functions from their projections.</title>
<link>http://surface.syr.edu/eecs_techreports/159</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/159</guid>
<pubDate>Mon, 07 May 2012 07:00:39 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present a problem decomposition approach to reduce neural net training times. The basic idea is to train neural nets in parallel on marginal distributions obtained from the original distribution (via projection), and then reconstruct the original table from the marginals (via a procedure similar to the join operator in database theory). A function is said to be reconstructible, if it may be recovered without error from its projections. Most distributions are non-reconstructible. The main result of this paper is the Reconstruction theorem, which enables non-reconstructible functions to be expressed in terms of reconstructible ones, and thus facilitates the application of decomposition methods.</p>

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</description>

<author>Anil Ravindran Menon et al.</author>


</item>


<item>
<title>Parametricity and Local Variables</title>
<link>http://surface.syr.edu/eecs_techreports/158</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/158</guid>
<pubDate>Mon, 07 May 2012 07:00:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>We propose that the phenomenon of local state may be understood in terms of Strachey's concept of parametric (i.e., uniform) polymorphism. The intuitive basis for our proposal is the following analogy: a non-local procedure is independent of locally-declared variables in the same way that a parametrically polymorphic function is independent of types to which it is instantiated. A connection between parametricity and representational abstraction was first suggested by J. C. Reynolds. Reynolds used logical relations to formalize this connection in languages with type variables and user-defined types. We use relational parametricity to construct a model for an Algol-like language in which interactions between local and non-local entities satisfy certain relational criteria. Reasoning about local variables essentially involves proving properties of polymorphic functions. The new model supports straightforward validations of all the test equivalences that have been proposed in the literature for local-variable semantics, and encompasses standard methods of reasoning about data representations. It is not known whether our techniques yield fully abstract semantics. A model based on partial equivalence relations on the natural numbers is also briefly examined.</p>

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</description>

<author>P. W. O&apos;Hearn et al.</author>


</item>


<item>
<title>Knowledge-Based Nonuniform Crossover</title>
<link>http://surface.syr.edu/eecs_techreports/157</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/157</guid>
<pubDate>Mon, 07 May 2012 07:00:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present a new "knowledge-based non-uniform crossover" (KNUX) operator for genetic algorithms (GA's) that generalizes uniform crossover. We extend this to "Dynamic KNUX" (DKNUX), which  constantly updates the knowledge extracted so far from the environment's feedback on previously generated chromosomes. KNUX can improve on good solutions previously obtained by using other algorithms. The modifications made by KNUX are orthogonal to other changes in parameters of GA's, and can be pursued together with any other proposed improvements. Whereas most genetic search methods focus on improving the move-selection procedures, after having chosen a fixed move-generation mechanism, KNUX and DKNUX make the move-generation process itself time-dependent. The same parents may give rise to different offspring at different moments in the evolutionary process, based on the past experience of the species. Simulation results show orders of magnitude improvement of KNUX over two-point and uniform crossover, on three NP optimization problems: graph partitioning, soft-decision decoding of linear block codes, and the traveling salesperson problem. KNUX has been applied to variants of the graph partitioning problem that cannot be solved easily using non-GA approaches, and to improve quality of solutions obtained using non-GA methods. DKNUX opens up the field of applying GA's to Incremental Optimization problems, characterized by a slow change in problem structure with time. DKNUX also achieves some of the goals of diploid representations with adaptive dominance, with smaller computational requirements.</p>

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</description>

<author>Harpal Maini et al.</author>


</item>


<item>
<title>Analysis of Myoelectrical Signals for Building a Dextrous Hand</title>
<link>http://surface.syr.edu/eecs_techreports/156</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/156</guid>
<pubDate>Mon, 07 May 2012 07:00:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>We analyze techniques for myoelectrical signals classification for the purpose of designing a multifunctional prosthetic device for human amputees. The main advantage of our system over existing models is that it is more robust, easier to work with, more general, and efficient enough to run in real time. We achieve this with the help of "Supervised Growing Cell Structures." an artificial neural network model designed by Fritzke [10]. The current paper focuses on the flexion of the index, middle and ring fingers, as these are the most difficult movements to tackle.</p>

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</description>

<author>Christopher T. Creel et al.</author>


</item>


<item>
<title>Decoding Linear Block Codes Using a Priority-First Search: Performance Analysis and Suboptimal Version</title>
<link>http://surface.syr.edu/eecs_techreports/155</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/155</guid>
<pubDate>Mon, 07 May 2012 07:00:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>An efficient maximum-likelihood soft-decision decoding algorithm for linear block codes using a generalized Dijkstra's Algorithm was proposed by Han, Hartmann, and Chen. In this report we prove that this algorithm is efficient for most practical communication systems where the probability of error is less than 10-3 by finding an upper bound of the computation performance of the algorithm. A suboptimal decoding algorithm is also proposed. The performance of this suboptimal decoding algorithm is within 0.25 dB and 0.5 dB of the performance of an optimal decoding algorithm for the (104, 52) binary extended quadratic residue code and the (128, 64) binary extended BCH code, respectively.</p>

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</description>

<author>Yunghsiang S. Han et al.</author>


</item>


<item>
<title>Fluted Formulas and the Limits of Decidability</title>
<link>http://surface.syr.edu/eecs_techreports/154</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/154</guid>
<pubDate>Mon, 07 May 2012 07:00:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>In the predicate calculus, variables provide a flexible indexing service that selects the actual arguments to a predicate letter from among possible arguments that precede the predicate letter (in the parse of the formula). In the process of selection, the possible arguments can be permuted, repeated (used more than once), and skipped. If this service is withheld, so that arguments must be the immediately preceding  ones, taken in the order in which they occur, the formula is said to be fluted. Quine showed that if a fluted formula contains only homogeneous conjunction (conjoins only subformulas of equal arity), then the satisfiability of the formula is decidable. It remained an open question whether the satisfiability of a fluted formula without this restriction is decidable. This paper answers that question.</p>

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</description>

<author>William C. Purdy</author>


</item>


<item>
<title>A Domain-Specific Parallel Programming System I: Design and Application to Ecological Modelling</title>
<link>http://surface.syr.edu/eecs_techreports/153</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/153</guid>
<pubDate>Mon, 07 May 2012 07:00:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>The goal of the εm project is to make parallel programming easily accessible to a broad community of scientists. Previous approaches such as the use of general parallel programming languages and parallelizing compilers for sequential languages have fallen short in this respect. The approach is to design a special purpose programming language which is oriented towards a specific area of application. The result is a specialized and effective scientific tool.  εm is a high-level programming system which puts parallelism into the hands of scientists who are not sophisticated programmers. By restricting and simplifying the programming interface, εm eases both the conceptual task of the programmer and the analytical task of the compiler. The model of success is the financial spreadsheet, a specialized tool which makes programmers out of relatively naive end-users and makes computer technology broadly accessible to business. Here the initial prototype is described, motivated by practical ecological modelling problems.</p>

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</description>

<author>Elaine Wenderholm et al.</author>


</item>


<item>
<title>Characterization of a Class of Sigmoid Functions with Applications to Neural Networks</title>
<link>http://surface.syr.edu/eecs_techreports/152</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/152</guid>
<pubDate>Mon, 07 May 2012 07:00:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Sigmoid functions, whose graphs are "S-shaped" curves, appear in a great variety of contexts, such as the transfer functions in many neural networks. Their ubiquity is no accident; these curves are the among the simplest non-linear curves, striking a graceful balance between linear and non-linear behavior.</p>

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</description>

<author>Anil Ravindran Menon et al.</author>


</item>


<item>
<title>Multiprocessor Document Allocation: a Neural Network Approach</title>
<link>http://surface.syr.edu/eecs_techreports/151</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/151</guid>
<pubDate>Mon, 07 May 2012 07:00:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>We consider the problem of distributing the documents to a given set of processors so that the load on each processor is as equal as possible and the amount of communication is as small as possible. This is an NP-Complete problem. We apply continuous as well as discrete Hopfield neural networks to obtain suboptimal solutions for the problem. These networks perform better than a genetic algorithm for this task proposed by Frieder et al. [4]; in particular, the continuous Hopfield network performs extremely well.</p>

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</description>

<author>Abdulaziz Sultan Al-Sehibani et al.</author>


</item>


<item>
<title>Covering Radius 1985-1994</title>
<link>http://surface.syr.edu/eecs_techreports/150</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/150</guid>
<pubDate>Mon, 07 May 2012 07:00:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>We survey important developments in the theory of covering radius during the period 1985-1994. We present lower bounds, constructions and upper bounds, the linear and nonlinear cases, density and asymptotic results, normality, specific classes of codes, covering radius and dual distance, tables, and open problems.</p>

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</description>

<author>G. D. Cohen et al.</author>


</item>


<item>
<title>Semantics vs. Syntax vs. Computations Machine Models for Type-2 Polynomial-Time Bounded Functionals (Preliminary Draft)</title>
<link>http://surface.syr.edu/eecs_techreports/149</link>
<guid isPermaLink="true">http://surface.syr.edu/eecs_techreports/149</guid>
<pubDate>Mon, 07 May 2012 07:00:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper investigates analogs of the Kreisel-Lacombe-Shoenfield Theorem in the context of the type-2 basic feasible functionals, a.k.a. the Mehlhorn-Cook class of type-2 polynomial-time functionals. We develop a direct, polynomial-time analog of effective operation, where the time bound on  computations is modeled after Kapron and Cook's scheme for their basic polynomial-time functionals. We show that (i) if P = NP, these polynomial-time effective operations are strictly more powerful on R  (the class of recursive functions) than the basic feasible functions, and (ii) there is an oracle relative to which these polynomial-time effective operations and the basic feasible functionals have the same power on R. We also consider a weaker notion of polynomial-time effective operation where the machines computing these functionals have access to the computations of their "functional" parameter, but not to its program text. For this version of polynomial-time effective operation, the analog of the Kreisel-Lacombe-Shoenfield is shown to hold-their power matches that of the basic feasible functionals on R.</p>

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</description>

<author>James S. Royer</author>


</item>


<item>
<title>Behavioral Ecology of Parental Care in a Dendrobatid Frog (Oophaga pumilio)</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/755</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/755</guid>
<pubDate>Mon, 07 May 2012 07:00:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Parental care is essential to the success of both parents and offspring in many species, and plays an important role in the evolution of animal mating systems and life histories. The mechanisms that regulate the intensity and form of parental care in a species are determined by many factors and are highly variable across taxa. However, our understanding of the behavioral ecology of parental care is built on research that is highly taxonomically biased to birds, with some studies also in mammals, arthropods, and fish. Amphibians display an impressive diversity of form in parental care, yet few studies of parental care have explained the mechanisms behind parental behaviors in this vertebrate class. Accordingly, the research in this dissertation tested four hypotheses about parental care in a species of dendrobatid frog that displays complex parental behavior, the strawberry poison frog (Oophaga pumilio). In this species, father frogs guard egg clutches in the leaf litter for approximately one week. When eggs hatch into tadpoles, mother frogs return to transport tadpoles individually to small terrestrial water pools such as those in the axils of a bromeliad plant. For approximately six weeks, mother frogs continue to visit tadpoles. When mother frogs visit, tadpoles display a vibration behavior. Then, mother frogs supply unfertilized eggs to their tadpoles as their principal source of food.    To develop a thorough understanding of the behavioral mechanisms at play between mother and offspring O. pumilio, this dissertation tests hypotheses related to offspring discrimination, the use of multimodal sensory cues, honest signaling, and provisioning of potential chemical defenses. Studies mostly made use of behavioral tests and observations in the laboratory and in the field at the La Selva Biological Station in the lowland wet forest of Costa Rica. To facilitate observation of the interactions between mothers and tadpoles in a natural setting as well as easy access to large quantities of tadpoles, an extensive setup of 1000 artificial tadpole-rearing sites (“cups”) was installed on the trees in abandoned plantations adjacent to primary forest. Mother frogs used cups to deposit and feed tadpoles just as they would the natural phytotelmata in their habitat. Furthermore, motion-activated IR video cameras were installed at the site to permit 24-hour observation of mother-offspring interactions. Findings demonstrated that mother frogs use indirect recognition to locate tadpoles, and rely on honest signals of hunger from tadpoles to allocate nutritive eggs. Tadpole begging signals are likely reliable because of a significant cost of signal production via reduction in growth and as a result of a differential benefit of maternal eggs. Tadpoles use visual and tactile cues to discriminate between mother frogs and other visitors such as other species of frogs and potential predators when deciding whether to signal their level of need or to avoid predation. The eggs that mother frogs provide tadpoles as nourishment may also be provisioned with alkaloids that could provide chemical defenses for offspring. Thus, the behavioral mechanisms described in this research explain how mother O. pumilio determine who, when, and how much to feed, as well as how both tadpoles and mothers contribute to reducing the risk of predation to offspring.</p>

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</description>

<author>Jennifer L. Stynoski</author>


</item>


<item>
<title>Ex Parte Communications with Employees of a Business Enterprise: The Need for a Bright Line Test</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss2/8</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss2/8</guid>
<pubDate>Mon, 07 May 2012 06:56:03 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph Christian Sekula et al.</author>


</item>


<item>
<title>Admission? Yes; Practice? No: New York&apos;s Inconsistent Treatment of Nonresident Attorneys</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss2/7</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss2/7</guid>
<pubDate>Mon, 07 May 2012 06:56:03 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Brian N. Corrigan et al.</author>


</item>


<item>
<title>People v. Keta: The Search for Stolen Auto Parts--Warrantless Searches of Chop Shops in New York</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss2/6</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss2/6</guid>
<pubDate>Mon, 07 May 2012 06:56:02 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Paul R. Walsh et al.</author>


</item>


<item>
<title>International Society for Krishna Consciousness, Inc. v. Lee: Public Forum Analysis of Airport Restrictions on Speech</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss2/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss2/5</guid>
<pubDate>Mon, 07 May 2012 06:56:02 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Jennifer A. Giaimo et al.</author>


</item>


<item>
<title>The Supreme Court&apos;s Unsuccessful Attempt to Clarify when School Boards Have Complied with Desegregation Decrees: Board of Education of Oklahoma City v. Dowell</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss2/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss2/4</guid>
<pubDate>Mon, 07 May 2012 06:56:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Kevin P. Fitzpatrick et al.</author>


</item>


<item>
<title>Clearing the Air of Environmental Sovereign Immunity: Ohio v. United States Department of Energy</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss2/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss2/3</guid>
<pubDate>Mon, 07 May 2012 06:56:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Louise M. Gleason et al.</author>


</item>


<item>
<title>Justice Scalia&apos;s Due Process Model: A History Lesson in Constitutional Interpretation</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss2/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss2/2</guid>
<pubDate>Mon, 07 May 2012 06:56:00 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Bethany A. Cook et al.</author>


</item>


<item>
<title>Warning: New Jersey Supreme Court has Determined that Compliance with the Federal Cigarette Labeling and Advertising Act May Be Hazardous to the Tobacco Industry</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss2/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss2/1</guid>
<pubDate>Mon, 07 May 2012 06:55:59 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph M. Nador et al.</author>


</item>


<item>
<title>Dietrick v. Kemper Insurance Co.--The First Step Toward Limiting Workers&apos; Compensation Liens on Third-Party Tort Recoveries</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss1/8</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss1/8</guid>
<pubDate>Mon, 07 May 2012 06:55:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mark Keller et al.</author>


</item>


<item>
<title>Copyright Misuse . . . Getting Defensive: Lasercomb America, Inc. v. Reynolds</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss1/7</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss1/7</guid>
<pubDate>Mon, 07 May 2012 06:55:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Christina Ambrosio et al.</author>


</item>


<item>
<title>Guilty Until Proven Innocent? Protections for Innocent Owners in Civil Forfeiture Cases Under 21 U.S.C. § 881(a) and New York&apos;s CPLR Article 13-A</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss1/6</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss1/6</guid>
<pubDate>Mon, 07 May 2012 06:55:55 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joseph A. Brintle et al.</author>


</item>


<item>
<title>The Free Exercise Clause: Employment Division v. Smith&apos;s Inexplicable Departure from the Strict Scrutiny Standard</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss1/5</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss1/5</guid>
<pubDate>Mon, 07 May 2012 06:55:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Janet V. Rugg et al.</author>


</item>


<item>
<title>Confusion Surrounding the Good Faith Doubt Evidentiary Standard Goes Unchecked: NLRB v. Curtin Matheson Scientific, Inc.</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss1/4</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss1/4</guid>
<pubDate>Mon, 07 May 2012 06:55:54 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Diane Bruce et al.</author>


</item>


<item>
<title>Unjust Elections of State Judges Under Section 2 of the Voting Rights Act: League of United Latin American Citizens Council No. 4434 v. Clements</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss1/3</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss1/3</guid>
<pubDate>Mon, 07 May 2012 06:55:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Eileen Campbell et al.</author>


</item>


<item>
<title>Federal Superlien: An Alternative to Lender Liability Under CERCLA</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss1/2</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss1/2</guid>
<pubDate>Mon, 07 May 2012 06:55:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John Andrew Maher et al.</author>


</item>


<item>
<title>Acquired Immunodeficiency Syndrome: The Case for Anonymous Limited Discovery</title>
<link>http://scholarship.law.stjohns.edu/jcred/vol6/iss1/1</link>
<guid isPermaLink="true">http://scholarship.law.stjohns.edu/jcred/vol6/iss1/1</guid>
<pubDate>Mon, 07 May 2012 06:55:52 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Mark G. Pedretti et al.</author>


</item>


<item>
<title>Library Focus - Spring 2012</title>
<link>http://aquila.usm.edu/libraryfocus/1</link>
<guid isPermaLink="true">http://aquila.usm.edu/libraryfocus/1</guid>
<pubDate>Mon, 07 May 2012 06:53:12 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>University Libraries</author>


</item>


<item>
<title>BUT WHAT IS IT &lt;i&gt;SAYING&lt;/i&gt;? TRANSLATING THE MUSICAL LANGUAGE OF STRAVINSKY’S &lt;i&gt;THREE PIECES FOR CLARINET SOLO&lt;/i&gt;</title>
<link>http://opensiuc.lib.siu.edu/music_gradworks/5</link>
<guid isPermaLink="true">http://opensiuc.lib.siu.edu/music_gradworks/5</guid>
<pubDate>Mon, 07 May 2012 06:53:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>In response to questions of interpretation of his music, Igor Stravinsky has said simply to let the notes speak for themselves. In this paper I will translate the language of Stravinsky’s music in his <em>Three Pieces for Clarinet Solo</em>. I will demonstrate the following: how Stravinsky was able to derive a harmonic structure out of melodic content, thereby creating a two-dimensional space; the formal structure of each of the three <em>Pieces</em>; and relationships between <em>Three Pieces</em> and another of Stravinsky’s works, <em>L’Histoire du Soldat</em>. This analysis will serve as my translation of Stravinsky’s musical language, which will then be compared to scholarly research conducted regarding the <em>Three Pieces</em>.</p>

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</description>

<author>Derek Emch</author>


</item>


<item>
<title>Application of 3D-Fluorescence and PARAFAC Modeling in Marine DOM Investigations</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/753</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/753</guid>
<pubDate>Mon, 07 May 2012 06:52:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Dissolved organic matter (DOM) plays a crucial role in the nutrient and carbon cycling in the coastal-shelf-ocean boundary.  It is a major reservoir of reduced carbon and carries important information on how the sea and landscape have been modified.  Due to the complexity of the biogeochemical processes in this boundary, its distribution is not well understood. This study evaluated the Excitation Emission Matrix (EEM) fluorescence method combined with Parallel Factorial Analysis (PARAFAC) modeling to resolve DOM fluorescence components, and their distribution from near-shore to off-shore. Results of this study demonstrated several advances in monitoring the temporal distribution of DOM on the continental shelf of Florida using EEM and PARAFAC, including the methods application in harmful algal bloom and oil spill studies.  This study employed PARAFAC models that were able to:  1) resolve sources of individual components of the bulk DOM from nearshore to the continental margins of southwest Florida; 2) provide insight into the biological, chemical, and physical processes that control the DOM variabilities of each of the resolved DOM components on the Shelf; 3) develop and test the hypothesis that the protein-like fluorescence component supported the October 2011 K. brevis bloom; 4) observe relationship of brevetoxin incorporation in marine sediments enriched with terrestrial DOM; and, 5) simultaneously discriminate residues of the Macondo crude oil components, the  dispersants, and dissociate signal related to CDOM in the water column after the Deepwater Horizon oil spill in the Gulf of Mexico.</p>

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</description>

<author>Wilson G. Mendoza</author>


</item>


<item>
<title>Prescription Opioid Abuse Etiology: Pathways to Initiation</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/752</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/752</guid>
<pubDate>Mon, 07 May 2012 06:52:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although studies on the initiation of substance abuse abound, the body of literature on prescription opioid abuse (POA) etiology is quite small. Little is known about why and how the onset of POA occurs, especially among high risk drug using populations. The present study aims to fill this important knowledge gap by exploring the POA initiation experiences of 90 prescription opioid abusers currently in treatment and their narrative accounts of the circumstances surrounding their POA onset. Audiotapes of in-depth interviews were transcribed, coded, and thematically analyzed using the NVivo software program. This research was conducted within a storylines framework, which operates on the premise that the path to drug abuse represents a biography, or a process, rather than a static condition. Analysis revealed the presence of four trajectories leading to POA. The first pathway to POA, the South Florida Effect, highlighted the role that the local “pill culture” can play in influencing the formation of POA, while the second focused on females who initiate their POA through the help of an abusing male. The third, or the Cocaine Context, describes an entryway into POA via the world of cocaine. The final POA trajectory, Prescribed Addiction, reveals how users who are prescribed opioids can fall into problems with POA. This study adds to the dearth of research on POA etiology by not only illuminating the psycho-social factors that contribute to POA onset, but also by situating initiation experiences within broader life processes. While some of these findings support previous research, others alter the manner in which POA etiology should be viewed. This study expands current notions of POA initiation by providing clear and detailed descriptions of the circumstances and events that can lead to POA. These findings provide crucial insights to policymakers and interventionists in identifying who is at risk for POA, and more importantly when and how to intervene most efficaciously.</p>

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</description>

<author>Khary Rigg</author>


</item>


<item>
<title>Detection of SK2 Channels on Hippocampal Neurons</title>
<link>http://digitalcommons.uconn.edu/gs_theses/237</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/237</guid>
<pubDate>Mon, 07 May 2012 06:35:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Calcium-activated small conductance potassium channels (SK) are crucial for synaptic plasticity, sleep, and learning and memory (Hammond, Bond et al. 2006; Cueni, Canepari et al. 2008; Lin, Lujan et al. 2008). Despite the recent progress on SK channel physiology, the precise spatial organization of SK channels in neurons has remained unknown. Such knowledge is critical as the subcellular distribution of SK channels is an important determinant of neuronal excitability. Currently, there are no techniques to image ion channel distribution quantitatively at the nanometer scale in living cells. Here, it is demonstrated that integration of natural toxins with single molecule atomic force microscopy (AFM) allows for the mapping of native SK channels in living cells. By measuring the adhesive forces between cell surface expressed SK channels and apamin, a toxin that specifically binds to SK channels, it was found that SK channels are spatially organized in nanodomains of one to three channels. It is also shown that SK channel distribution in pyramidal neurons is polarized, increasing by 40 fold between the soma and dendrites. Additionally, the SK channel dendritic maps are dynamic under the control of the cAMP second messenger cascade. Together, our study demonstrates that integration of pharmacology with single molecule AFM allows to quantitatively reveal ion channel distribution in living cells thus providing a new tool for the study of ion channels and receptors in cell physiology.</p>

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</description>

<author>Jamie L. Maciaszek</author>


</item>


<item>
<title>Supportive Housing for Families in Child Welfare: Client Characteristics and Risk Factors at Intake</title>
<link>http://digitalcommons.uconn.edu/gs_theses/236</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/gs_theses/236</guid>
<pubDate>Mon, 07 May 2012 06:26:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many families involved in the child welfare system also face housing difficulties. Housing problems can disrupt family preservation efforts and delay reunifications from foster care. Supportive housing programs work with families who have dual vulnerabilities in housing and child welfare to integrate services and improve outcomes. Families in these programs might face barriers in addition to their housing and child welfare needs, but little is known about other risk factors in this population. This study uses a sample of 80 clients referred to a supportive housing for families program in order to examine the rate and prevalence of other risk factors: mental health needs, parenting stress, and substance abuse. Overall, 34.2% of clients had mental health needs, 46.0% showed elevated levels of parenting stress in at least one dimension, and 31.3% were identified as being at a moderate to high risk for substance abuse. For many of these clients, these risks were co-occurring. Additionally, after meeting with clients, Assessment Specialists completed a comprehensive measure of family functioning; high levels of barriers were reflected for families across multiple domains. A better understanding of risk at intake can help inform case management, match services to client needs, and guide the use of limited program resources more effectively.</p>

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</description>

<author>Kellie G. Randall</author>


</item>


<item>
<title>Pinkberry Business Plan</title>
<link>http://scholarsarchive.jwu.edu/ac_symposium/20</link>
<guid isPermaLink="true">http://scholarsarchive.jwu.edu/ac_symposium/20</guid>
<pubDate>Mon, 07 May 2012 06:21:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>The following business plan details a franchising plan of a frozen yogurt shop to be constructed, developed, and operated in a very popular shopping mall in Rhode Island. The shop will be a franchise of Pinkberry brand. Pinkberry is an upscale frozen dessert brand that serves as an alternative to ice cream. Pinkberry anticipates continued success due to its location, high quality product, and strong brand name.</p>

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</description>

<author>Adriana Briones et al.</author>


</item>


<item>
<title>Humor Me to Heaven: Humor&apos;s Redemptive Role in the Works of Eudora Welty, Flannery O&apos;Connor, and Marilynne Robinson</title>
<link>http://digitalcommons.liberty.edu/masters/237</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/masters/237</guid>
<pubDate>Mon, 07 May 2012 06:10:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>Humor is the topic of many psychological, social, and cultural studies, but this project examines humor under a new lens. Humor's unique qualities explored in this study prove that humor is capable of more than just causing laughter; the nature of humor allows it to unveil truths about humanity, both spiritual and physical, through exposing man's flaws. This quality is especially important to consider when analyzing humor in the context of literature, in which humor also works as an aesthetic element. This study searches several short stories by Eudora Welty and Flannery O'Connor along with Marilynne Robinson's Gilead to reveal that each author implements in her works the element of humor in her own style, making humor an integral component in her fiction. Considering the unique qualities of humor and recognizing humor as an aesthetic element in the selected works show that these authors use humor as more than a mere literary element; their uses of humor, though they vary in form, work to convey significant themes of redemption throughout their stories. The term redemption defined in this thesis refers to a new and truthful perspective that humor creates for the characters, audience, or both. Since this new perspective ultimately points to spiritual truths about man's nature, this discovery lends more credit to humor than other scholars have previously offered.</p>

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</description>

<author>Stephanie Johnson</author>


<category>Literature, American</category>

<category>Literature, General</category>

<category>Women&apos;s Studies</category>

<category>Psychology, General</category>

</item>


<item>
<title>School Change: Adolescents Transitioning from Conventional Schooling to Home-Based Online Education</title>
<link>http://digitalcommons.liberty.edu/doctoral/554</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/doctoral/554</guid>
<pubDate>Mon, 07 May 2012 06:04:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>This hermeneutic phenomenological research explored the lived experiences of six recently graduated adolescents to extrapolate the valued essence of their transitional encounters in changing from conventional school to home-based online schooling.  The homeschool research shifted the emphasis from the outcome-based academic achievement studies prevalent during the past 20 years to a focus on internal and external factors impacting student learning within this technological instructional process.  Findings produced from analysis and interpretation of reflective adolescent lived experiences revealed rich truth regarding the internal emotions, environmental adaptations, academic ramifications, and social adaptations encountered when changing from conventional schooling to home-based online school.  Cognitive, maturational, and social skills showed reported gains in the move from conventional school to home-based online school.  Gender differences were not reported as major contributing adjustment factors.  The greatest transitional ramifications were noted by participants who made a geographic move while simultaneously enrolling in home-based online school.  The magnitude of the loss in social capital was accentuated by the geographic move.  Adolescent attitude in acceptance of the move was a defining element, leading to successful re-establishment of new social capital or resulting in social and psychological withdrawal.</p>

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</description>

<author>Harvey Klamm</author>


<category>Education, General</category>

<category>Education, Philosophy of</category>

<category>Education, Sociology of</category>

<category>Education, Technology</category>

<category>Education, Administration</category>

</item>


<item>
<title>Teachers and Hand-Held Graphing Technology: An Examination of Concerns</title>
<link>http://digitalcommons.liberty.edu/doctoral/553</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/doctoral/553</guid>
<pubDate>Mon, 07 May 2012 06:04:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this nonexperimental causal-comparative study was to examine the concerns of teachers in reference to the graphing calculator, as measured by the Stages of Concern Questionnaire (SoCQ) and compare the results to a combination of levels of concerns between groups. The study participants were high school teachers of mathematics in Northwest Georgia and Southeast Tennessee (n = 128). This study utilized a two-way multivariate analysis of variance (MANOVA) to determine the effect of two independent variables, formal training and experience teaching with a graphing calculator, on seven dependent variables, teachers' Stages of Concern (stages 0-6). Also, a one-way MANOVA was conducted to determine if there was a statistically significant difference in means between the dependent variables, teachers Stages of Concern (stages 0-6), and the independent variable, the state where a teacher was employed (Georgia or Tennessee). The results for the two-way MANOVA were statistically significant for the teaching experience main effect. The one-way MANOVA was found to be significant at stage 0.</p>

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</description>

<author>Edward Helton</author>


<category>Education, Teacher Training</category>

<category>Education, General</category>

<category>Education, Mathematics</category>

<category>Education, Secondary</category>

<category>Education, Technology</category>

</item>


<item>
<title>She&apos;s Sold: Persuading American Women Through Advertising</title>
<link>http://digitalcommons.liberty.edu/honors/311</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/honors/311</guid>
<pubDate>Mon, 07 May 2012 05:58:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study attempted to analyze the effects of an advertising campaign on American women in to illustrate that these women are vastly unaware of just how influential advertising is on their thoughts and actions. It aimed to make women more aware of the presence of advertising in their lives by giving a brief history of the subject, by outlining some current claims in the field, and by introducing a new concept known as shared gender culture. To follow up on secondary research, this study also conducted an experiment on thirty-four women ages eighteen to fifty-five to discover their reactions to a new, never seen advertising campaign for beef. The study attempted to persuade and analyze the effects of persuasion. The study was conducted by survey and asked women their thoughts on and uses of beef before and after revealing the entire print campaign to them. Results showed that half of the participants were not persuaded by the campaign at all through their first and only viewing of it; 26.5% of the women consider themselves entirely invulnerable to advertising persuasion at all. Many women showed great distrust for claims in advertisements, calling them false. Those who did admit to persuasion did so out of a desire to be sexy, happy, healthy, and nurturing to others.</p>

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</description>

<author>Bethany L. Keef</author>


</item>


<item>
<title>Our Covenant Constitution: The Covenantal Nature of the United States Constitution</title>
<link>http://digitalcommons.liberty.edu/honors/310</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/honors/310</guid>
<pubDate>Mon, 07 May 2012 05:58:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>The problem with the national government and politics in the United States today is that citizens and politicians have both forgotten, ignored, and undermined the nature and significance of the U.S. Constitution as a civil covenant based on civil and religious liberty and limited government. This thesis proposes to analyze the nature of the Constitution as a civil covenant and how a proper interpretation and application of it as such can solve many of today’s most pressing political problems. It will discuss the nature and history of civil covenants, examine the mechanics of the Constitution in the creation of a Federal Republic, briefly trace the breakdown of this system through sundry events and policies in American history, and delineate a few possible solutions.</p>

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</description>

<author>William T. Crabtree</author>


<category>Political Science, General</category>

</item>


<item>
<title>Pornography and Human Trafficking: The Beliefs of the Effects of Personal Pornography Use</title>
<link>http://digitalcommons.liberty.edu/honors/309</link>
<guid isPermaLink="true">http://digitalcommons.liberty.edu/honors/309</guid>
<pubDate>Mon, 07 May 2012 05:58:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Each individual has different beliefs about the effects of pornography use in relation to the self, a romantic relationship, the family, and society as a whole.  There is research that shows pornography tends to negatively affect these areas of life and there is also evidence for some human trafficking occurring within the pornography industry. Thus, the ultimate goal of this thesis is to not only assess what people believe about those involved in the pornography industry, but to test whether information about the pornography industry might change people’s beliefs about their personal pornography use.  Human nature tends to not equate one’s personal actions with effects, especially negative results. If there were no users of pornography, then there would be no demand. Therefore, one’s actions do affect the pornography industry and human trafficking.</p>
<p>A survey was created that assessed beliefs about the effects of one’s personal pornography use. Then, these beliefs were assessed again after information about the pornography industry was presented.  The research question was whether the information would change one’s beliefs about pornography use in relation to the family and society, with an emphasis on the negative aspects of pornography such as human trafficking.  The 100 participants were recruited from Amazon’s Mechanical Turk through an online format. After being presented with statistics about sex trafficking and the pornography industry, participants did change their beliefs about personal pornography use.</p>

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</description>

<author>Chelsea M. Thompson</author>


<category>Psychology, Experimental</category>

</item>


<item>
<title>Dams over Nukes:  Explaining Indian Water Treaties</title>
<link>http://scarab.bates.edu/honorstheses/50</link>
<guid isPermaLink="true">http://scarab.bates.edu/honorstheses/50</guid>
<pubDate>Mon, 07 May 2012 05:36:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>In 1947 India and Pakistan, sworn enemies on all fronts, managed to settle a water dispute on the Indus Basin eventually signing one of the most successful treaties that have since existed on the water front. I investigate this puzzle of cooperation in my thesis. Ultimately I show that the Indus Waters Treaty succeeded due to the intervention of an epistemic community which managed to depoliticize the dispute and establish an equitable treaty between the two sides. Without the contribution of the epistemic community the outcome of cooperation would most likely have been unsuccessful. I specify also that the initial impetus for cooperation came in the form of an international idea on dam construction which “convinced” India and (epiphenomenally) Pakistan that the dispute on the Indus needed to be resolved urgently and cooperatively.This is only part of the explanation however; the research conducted in this thesis leads to the conclusion that the distribution of bargaining capabilities between the signatories played a central role in determining the empowerment of the epistemic community, which then intervened to ensure a successful outcome of cooperation.</p>

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</description>

<author>Romina Istratii</author>


</item>


<item>
<title>&quot;The Vindication of Spinsters: Winifred Holtby&apos;s Case for Female Satisfaction&quot;</title>
<link>http://scarab.bates.edu/honorstheses/49</link>
<guid isPermaLink="true">http://scarab.bates.edu/honorstheses/49</guid>
<pubDate>Mon, 07 May 2012 05:36:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Winifred Holtby, the British interwar feminist, was one of the most talented and insightful writers of her time, yet sadly never achieved the status of household name. In a society where marriage was assumed to correlate directly with female happiness and satisfaction, the single woman was an object of pity. Never married herself, Holtby was passionate about promoting singleness as a viable alternative to marriage and even one that might bring about more satisfaction to a woman. Chapter 1 of this thesis deals with the portrayal of women and singleness in an earlier novel, <em>The Crowded Street</em> (1924), and Chapter 3, with her last and perhaps most famous novel, <em>South Riding</em> (1936). In Chapter 2 I look at her nonfiction work, <em>Women and a Changing Civilization</em> (1935), in order to examine her account of female history, the feminist movement, and her thoughts on the direction in which women are going. Holtby, in her own words, claims women can find satisfaction outside of marriage or living in relation to men, but these themes do not always manifest themselves so cleanly in her novels. I observe her handling of female characters, the choices they make in regard to men, and whether or not those choices result in satisfaction.</p>

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</description>

<author>Katherine Ann Wiryaman</author>


</item>


<item>
<title>The Unbending Pillars of John Adams&apos;s Political Philosophy</title>
<link>http://scarab.bates.edu/honorstheses/48</link>
<guid isPermaLink="true">http://scarab.bates.edu/honorstheses/48</guid>
<pubDate>Mon, 07 May 2012 05:36:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Though John Adams is rightly seen as one of the most active proponents of the American drive towards independence in the 1770s, he was also a staunch <em>opponent</em><strong> </strong>of another revolutionary movement: the French Revolution of the 1790s.  It has been difficult for scholars to reconcile the “radical” Adams of the 1760s with the apparently “conservative” and wary Adams of the 1790s. Historians have generally taken one of two approaches. Some argue that he underwent a deep and fundamental shift in political philosophy in the 1780s in reaction to a number of political developments in Europe and America. These trends, they argue, led to a wariness of popular control and an abandoned faith in the wisdom of the general will.  Others contend that he did not change significantly during this period but maintained his previous positions, but they have tended to provide little support for this position with examples from Adams’s own writing. Reading a varied selection of Adams’s writings—some published, such as his well-known <em>Thoughts on Government, </em>others virtually unheard of, such as his extended marginalia in Mary Wollstonecraft’s 1794 book on the French Revolution—we see that Adams did not undergo a major shift in political thought. He held a consistent set of political beliefs, deeply rooted in the Puritan tradition, and which informed his reaction to many of the events in his lifetime, including the independence movement in America and the Revolution in France two decades later.</p>

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</description>

<author>Anna Kane Wallman</author>


</item>


<item>
<title>Redefining community for first-year music education majors.</title>
<link>http://opus.ipfw.edu/music_facpres/55</link>
<guid isPermaLink="true">http://opus.ipfw.edu/music_facpres/55</guid>
<pubDate>Mon, 07 May 2012 05:36:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although a goal of most first-year seminars is developing a community of learners, music majors often bring to college pre-existing perceptions of community, narrowly defined by the kinships formed and nurtured in their high school music programs. This presentation offers a model of a first-year seminar for music education majors that broadens students’ perception of community to embrace the breadth of the university experience, civic engagement, and identification with the teaching profession.</p>

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</description>

<author>Barbara J. Resch</author>


</item>


<item>
<title>The Evolution of Chivalric Values in the Order of the Garter: Edward III to Elizabeth I</title>
<link>http://scarab.bates.edu/honorstheses/47</link>
<guid isPermaLink="true">http://scarab.bates.edu/honorstheses/47</guid>
<pubDate>Mon, 07 May 2012 05:36:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis examines the evolution of chivalric values embodied in the Order of the Garter through historically conscious readings of the fourteenth-century romance <em>Sir Gawain and the Green Knight</em> and Book I of Edmund Spenser’s <em>Faerie Queene</em>. These texts each reference the Order of the Garter to prescribe an ideal of chivalric knighthood—<em>Sir Gawain</em> through the story of the green girdle (reminiscent of the garter symbol) and its acceptance by the court as a symbol of honor, and the <em>Faerie Queene</em> through the narrative of the Redcrosse Knight, who is in fact St. George, patron saint of the Order. Examining these texts through the lens of the Order illuminates the chivalric values of their times and illustrates the evolution of chivalry from the Edwardian to Elizabethan periods. Providing historical background on the Order of the Garter—England’s first chivalric knightly Order founded in 1348 by Edward III—and close reading of the texts in light of this context, I argue that chivalry in the medieval period was in a period of transition, characterized by conflicts between the military, courtly, and religious ideals of the time. By the time of Elizabeth I, these diverse elements had been united to create a hegemonic chivalric ideology emphasizing the elevated status of the courtly lady. This ideology was used as a political tool to support Elizabeth’s rule. The Order embodied the combination of chivalric elements, and provides one example of Elizabeth’s manipulation of chivalry as a means of justification of female rule.</p>

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</description>

<author>Sarah Joy Vigne Ms.</author>


</item>


<item>
<title>A &apos;Snap Shot&apos; of the Health of Homeless People in Inner Sydney: St Vincent&apos;s Hospital</title>
<link>http://researchonline.nd.edu.au/med_article/567</link>
<guid isPermaLink="true">http://researchonline.nd.edu.au/med_article/567</guid>
<pubDate>Sun, 06 May 2012 23:42:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Objectives: The poor health profile of people who are homeless results in a disproportionate use of health resources by these people. An in-hospital count of demographic and health data of homeless patients was conducted on two occasions at St Vincent’s Hospital in Sydney as an indicator of health resource utilisation for the Sydney region.</p>
<p>Methods: Two in-hospital counts were conducted of homeless patients within the boundaries of St Vincent’s Hospital to coincide with the inaugural City of Sydney homeless street counts in winter 2008 and summer 2009. Data collected included level of homelessness, principal diagnosis, triage category, bed occupancy and linkages to services post hospital discharge.</p>
<p>Results: Homeless patients at St Vincent’s utilised over four times the number of acute ward beds when compared with the state average. This corresponds to a high burden of mental health, substance use and physical health comorbidities in homeless people. There was high utilisation of mental health and drug and alcohol services by homeless people, and high levels of linkages with these services post-discharge. There were relatively low rates of linkage with general practitioner and ambulatory care services.</p>
<p>Conclusion: Increasing knowledge of the health needs of the homeless community will assist in future planning and allocation of health services.</p>

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</description>

<author>Caroline N. Chin et al.</author>


</item>


<item>
<title>Production of a prototype online leadership learning tool and system for Australian universities</title>
<link>http://research.acer.edu.au/higher_education/29</link>
<guid isPermaLink="true">http://research.acer.edu.au/higher_education/29</guid>
<pubDate>Sun, 06 May 2012 23:25:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>This ALTC project has involved more than 600 experienced leaders in higher education within and beyond Australia in the production of a comprehensive Online Leadership Learning System (OLLS) for our universities. The report outlines the project's outcomes, approach and methodology; indicates its contribution to the field; identifies key factors assisting and constraining success; summarises its achievements in terms of dissemination and linkages; and evaluates its quality and impact.</p>

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</description>

<author>Geoff Scott et al.</author>


</item>


<item>
<title>Comparison of 3MP medical-grade to 1MP office-grade LCD monitors in mammographic diagnostic and perceptual performance</title>
<link>http://researchonline.nd.edu.au/med_article/566</link>
<guid isPermaLink="true">http://researchonline.nd.edu.au/med_article/566</guid>
<pubDate>Sun, 06 May 2012 20:13:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>Introduction: Picture archiving and communication systems images designed to be viewed on high-resolution medical-grade monitors are routinely viewed on office-grade monitors on the wards or at home. This study aimed to determine whether a statistically significant difference in diagnostic (cancer detection) and perceptual (microcalcification detection) performance exists between 3MP grade and 1MP office-grade monitors.</p>
<p>Methods: 3MP Dome medical-grade liquid crystal display (LCD) monitors (Planar, Beaverton, OR, USA) were compared to 1MP Dell office-grade LCD monitors (Dell Inc, Round Rock, TX, USA). Eight radiologists (reader experience 8–30 years) read the same set of 100 mammograms (23/100 with proven cancers and 52/100 with microcalcifications) presented in random order on three occasions separated by two time intervals of 12 weeks. Reads 1 and 3 utilised 3MP monitors and formed the baseline read. Read 2 utilised 1MP monitors and constituted the experimental read. Reading conditions were standardised. Readers were aware of which monitors they were using. Multivariate logistic regression analysis (to account for reader variability and monitor impact) was performed to assess for statistical significance.</p>
<p>Results: At α = 5%, confidence intervals analysis comparing the measured parameters between 1MP to 3MP monitors demonstrated no statistically significant difference in diagnostic and perceptual performance for the reader group. In cancer detection (the diagnostic task), reader accuracy remained high irrespective of monitor type. Regression analysis comparing performance with 1MP against 3MP monitors found P values of 0.693 and 0.324 for diagnostic and perceptual performance, respectively.</p>
<p>Conclusion: There were no statistically and clinically significant differences between 3MP and 1MP monitors in mammographic diagnostic and perceptual performance. Comparable performance may be due to compensatory behaviour by readers.</p>

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</description>

<author>Aaron H J Ong et al.</author>


</item>


<item>
<title>Determining standard criteria for endotracheal suctioning in the paediatric intensive care patient: An exploratory study</title>
<link>http://researchonline.nd.edu.au/nursing_article/58</link>
<guid isPermaLink="true">http://researchonline.nd.edu.au/nursing_article/58</guid>
<pubDate>Sun, 06 May 2012 19:30:33 PDT</pubDate>
<description>
	<![CDATA[
	<p><p id="x-x-spar0005">This four-phase mixed method study developed an evidence based “Endotracheal Suction Assessment Tool” (ESAT) as a guide for nurses undertaking “endotracheal tube” (ETT) suction within “Paediatric Intensive Care” (PIC). Phase 1 involved a comprehensive literature review to determine the most commonly used criteria for assessing the need for ETT suction. In Phase 2 an “Endotracheal Suction Questionnaire” (ESQ) was developed to survey experienced PIC nurses in Australia and New Zealand regarding their ETT suction decision making process and validity testing of the ESQ. In Phase 3, the ESQ was administered to target group (<em>n</em> = 104). In Phase 4, the empirical evidence generated from this study, based upon the criteria rated by nurses in this study as being most clinically important and essential during the decision making process, determined the ESAT design. Analyses of quantitative results showed a positive correlation between the perceived frequency of use of a criterion and the appropriateness of the assessment. Where a criterion was used less frequently as a clinical indicator for the requirement for ETT suction, participants had a lower regard for this when rating the criterion as a specific single indicator to perform suction. Findings from qualitative data identified six criteria not previously documented within the literature.  <p id="x-x-spar0010">Further testing and validation of the tool within the PIC setting will determine the clinical viability of the ESAT.</p>

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</description>

<author>Kylie Davies et al.</author>


</item>


<item>
<title>Anatomical landmark localization in breast dynamic contrast-enhanced MR imaging</title>
<link>http://researchonline.nd.edu.au/med_article/565</link>
<guid isPermaLink="true">http://researchonline.nd.edu.au/med_article/565</guid>
<pubDate>Sun, 06 May 2012 18:29:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this article, we present a novel approach to localize anatomical features—breast costal cartilage—in dynamic contrast-enhanced MRI using level sets. Current breast MRI diagnosis involves magnetic-resonance compatible needles for localization [12]. However, if the breast costal cartilage structure can be used as an alternative to the MR needle, this will not only assist in avoiding invasive procedures, but will also facilitate monitoring of the movement of breasts caused by cardiac and respiratory motion. This article represents a novel algorithm for achieving reliable detection and extraction of costal cartilage structures, which can be used for the analysis of motion artifacts, with possible shape variations of the structure caused by uptake of contrast agent, as well as a potential for the registration of breast. The algorithm represented in this article is to extract volume features from post-contrast MR images at three different time slices for the analysis of motion artifacts, and we validate the current algorithm according to the anatomic structure. This utilizes the level-set method [18] for the size selection of the region of interest. The variable shape of contours acquired from a level-set-based segment image actually determines the feature region of interest, which is used as a guide to achieve initial masks for feature extraction. Following this, the algorithm uses a <em>K</em>-means method for classification of the feature regions from other types of tissue and morphological operations with a choice of an appropriate structuring element to achieve reliable masks and extraction of features. The segments of features can be therefore obtained with the application of extracted masks for subsequent motion analysis of breast and for potential registration purposes.</p>

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</description>

<author>X X. Yin et al.</author>


</item>


<item>
<title>Crawl Space</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/325</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/325</guid>
<pubDate>Sun, 06 May 2012 16:25:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>The looming figure of God, at times metaphorical, at times literal, is both present and absent throughout the body of Crawl Space. It’s through this representation of the ineffable that the thesis attempts to cast light on memories both tragic and redemptive, these moments that come to shape identity. Death, intimacy, displacement, and violence permeate the text, which seeks to find beauty in the dark and commonplace, humor in the strange, and crawl in that dank space beneath the surface where, sometimes, the work must be done.</p>

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</description>

<author>William Joyner</author>


</item>


<item>
<title>Individual Adequacy of Immersed Music Program Participants</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/326</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/326</guid>
<pubDate>Sun, 06 May 2012 16:25:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to examine individual adequacy of immersed music program participants. Participants (N = 485) of summer music camps and drum and bugle corps, ages 15 to 21, completed an online questionnaire that measured individual adequacy in general and immersed music settings. The questionnaire contained two scales. The Individual Adequacy Measure examined participants’ self-reported individual adequacy in general settings and the Program Experience Measure examined individual adequacy within the context of summer music camp and drum and bugle corps experiences. Results revealed non-significant differences between summer music camp and drum and bugle corps participants’ self-reported individual adequacy in general and immersed music settings. Additionally, the sample’s self-reported individual adequacy in general settings was positively correlated with their self-reported individual adequacy in immersed music settings. Furthermore, demographic and participation characteristics (age, gender, school attendance, employment status, program type, instrument played, years completed, and leadership roles) did not correlate with participants’ self-reported individual adequacy.</p>

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</description>

<author>Sandra M. Sanchez</author>


</item>


<item>
<title>The Impact of Teacher Intensity on Student Motivation in the 4th and 5th Grade Music Classroom: A Case Study</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/324</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/324</guid>
<pubDate>Sun, 06 May 2012 16:19:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to examine the impact of teacher intensity on student motivation in the 4th and 5th grade music classroom through a case study of a private K-12 Lutheran school. Students of two 4th (N=21) and two 5th grade classes (N=37) were given the Asmus (1989) Magnitude of Motivation Measure.  The music teacher was videotaped and observed by the researcher on four, separate occasions. To determine the teacher’s (N=1) level of intensity and frequency of body language/gesture occurrences, videotaped excerpts of each class were viewed and evaluated by two independent observers. Lastly, I took copious notes and informally interviewed the teacher following each classroom visit. Results of this study cannot be generalized, however several conclusions were made from this particular case: (1) the teacher was aware of her nonverbal behaviors, but not her level of teacher intensity; (2) the teacher was influenced by her background and school setting; (3) lesson content was correct, but lesson delivery lacked pacing, enthusiasm, and feedback; and (4) the motivation of the students reflected the teacher’s behaviors.</p>

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</description>

<author>Monica J. Kurtz</author>


</item>


<item>
<title>Maximón: The Shape Shifting Trickster Provides Hope for Some of The Disenfranchised in the Highlands of Guatemala</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/323</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/323</guid>
<pubDate>Sun, 06 May 2012 16:11:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Scholars often refer to Maximón, the modern Mayan deity, as a trickster.  To date, there has been little research to support this title.  The author of this thesis surveys existing research on Maximón's history and roles, along with scholarly literature on the nature of the trickster character, to test whether he is, in fact, a trickster.  It is determined that Maximón is a descendent of the ancient Mayan gods, actively worshipped today by some in the highlands of Guatemala as part of a blended "Folk Catholicism," a trickster who has survived the religion of the conquering Spanish by shift shaping, and a hero in the tradition of Hunahpu and Xbalanque.  These roles culminate during Semana Santa, when Maximón plays Judas Iscariot in the Passion of Christ.  The findings of this research will help future scholars understand Maximón's purpose in Guatemalan Highland culture and religion, as both he and they face life on a shrinking planet.</p>

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</description>

<author>Franklin D. Clark</author>


</item>


<item>
<title>Impact of Group Voice Climate on Team Performance Through Team Creativity and Team Reflexivity</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/322</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/322</guid>
<pubDate>Sun, 06 May 2012 16:08:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study was designed to investigate whether or not group voice climate contributes to team performance. And, if so, how it contributes. Specifically, it was hypothesized that one kind of team emergent states, group voice climate, defined as the extent to which team members feel safe and effective to speak up, exerts a positive influence on team performance. Furthermore, team creativity and team reflexivity, generally arise during team member interactions, were presumed to be team process mediators bridging the relationship between group voice climate and team performance. Team creativity allows team to find ways to improve working procedures and methods, while team reflexivity enables teams to both reevaluate past activities and plan for the future. A cross-sectional survey of 265 employees from 84 engineer teams at three high-tech companies in China was used to test the three hypotheses. The results demonstrated that group voice climate contributed to team performance. Moreover, team reflexivity fully mediated the relationship between group voice climate and team performance, while the mediating role of team creativity was not supported empirically. Theoretical and practical implications are discussed as well.</p>

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</description>

<author>Mengqi Zhan</author>


</item>


<item>
<title>Parent-teen communication about dating behaviors and its relationship to teenage dating behaviors: From the teen’s perspective.</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2008/iss1/5</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2008/iss1/5</guid>
<pubDate>Sun, 06 May 2012 15:58:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Research on parent-teen communication and teen sexual behavior has found that differing levels of parent-teen communication play a role in shaping their teens subsequent behaviors.  This study examined teen reported parent-teen communication about dating behaviors and its relationship to the teen’s own dating behaviors.  The differences and relationships among communication between mother and father and male and female participants is reported. 1st year college students were invited by e-mail to take an on-line survey about parent communication topics and different dating behaviors. The college student-based sample consisted 90 teens aged 18-19. Results present correlations and differences between the teen reported frequencies of topics of parent-teen communication between teen girls and boys and the frequencies of dating behaviors presented correlations and differences between themselves and the communication topics.</p>

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</description>

<author>Kimberly S. Reeb</author>


</item>


<item>
<title>&quot;Because I Said So&quot; and Other Notions of Authority: An Advanced Course on Communication and Power</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2008/iss1/4</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2008/iss1/4</guid>
<pubDate>Sun, 06 May 2012 15:58:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Many college students have inconsistent knowledge of historic and policy contexts where communication and power have played a key role. As Anton Ego, <em>Ratatouille</em>food critic would say, “What we need is some perspective.”<strong> </strong>We have found one avenue for the development of such perspective is an advanced course for the consideration of power or, more accurately, the examination of powerlessness and how communication can be brought to bear for both the manifestation and limitation of power. By examining those factors that render one less powerful and historic instances that are glaring in this regard, the student can better understand communication as a valuable tool and better prepare themselves to use their communication skills to improve the world. This paper will describe our 400 level seminar course on the subject of power and communication.</p>

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</description>

<author>Maureen M. Louis</author>


</item>


<item>
<title>The link (or lack thereof) among communication networks, organizational commitment, and job satisfaction: A case study</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2008/iss1/3</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2008/iss1/3</guid>
<pubDate>Sun, 06 May 2012 15:58:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this paper is to determine whether and to what extent one’s communication networks (both social and task) come to influence commitment to, and satisfaction with, one’s organization. Using Social Identity Theory as the theoretical framework, the main argument is that employees will have similar levels of organizational commitment and satisfaction as compared to those considered part of their socially constructed networks. After conducting a social network analysis of an organization involved in the creation, production, and distribution of foot care products, and conducting multivariate statistical tests, results indicate that neither commitment, nor satisfaction, is predicted by network membership. As such, although communication networks are predictive of certain organizational variables, this study forces one to reconsider whether social relations, manifested in network ties, result in psychological “sameness” or homophily.</p>

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</description>

<author>Corey Jay Liberman</author>


</item>


<item>
<title>Public Relations: A role for women?</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2008/iss1/2</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2008/iss1/2</guid>
<pubDate>Sun, 06 May 2012 15:58:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>In an effort to seek coherence, continuity and connection in the communication discipline, this paper explores the issue of gender and culture within the field of public relations. This paper examines how gender affects the disciplinary detachment of public relations from the many communication disciplines. Secondary research that has emerged over the last 25 years is analyzed by discussing the feminization and perspectives of gender’s influence in the discipline of public relations. Future opportunities for both universities and the industry are explored, in order to help bridge the gap of detachment of public relations to that of similar disciplines.</p>

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</description>

<author>Victoria Geyer</author>


</item>


<item>
<title>The Loss of Culture: The Changing Role of Communication</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2008/iss1/1</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2008/iss1/1</guid>
<pubDate>Sun, 06 May 2012 15:58:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Although, tradition serves as a core common ground for a culture’s identity, today, technology has been instrumental in breaking down cultural tradition into specialized areas within the communication discipline. When examining various contexts of media and technology, we see the role of tradition begin to fragment. However, this same media and technology also presents future possibilities of coherence and continuity for the discipline of communication. Through examining differing contexts of technology’s affect on tradition in culture, we can explore tradition(s) lost and found; traditions that may limit, integrate, or even establish a new found structure to help promote the common ground of tradition in the communication discipline.</p>

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</description>

<author>Suzanne N. Berman</author>


</item>


<item>
<title>Keeping the Balance: The Role of the Serotonin Subtype 1A Receptor in Regulating Cortisol Secretion in the Gulf Toadfish (Opsanus beta)</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/751</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/751</guid>
<pubDate>Sun, 06 May 2012 15:53:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>It is well established that serotonin (5-HT; 5-hydroxytryptamine) plays a role in regulating the mammalian hypothalamic-pituitary-adrenal (HPA) axis via the 5-HT receptor subtype 1A (5-HT1A).  To date, there has not been a comprehensive investigation of the molecular, pharmacological and physiological aspects of the 5-HT1A receptor and its role in the activation of the hypothalamic-pituitary-interrenal (HPI) axis in a single species of teleost fish.  The Gulf toadfish (Opsanus beta) 5-HT1A receptor was cloned and sequenced, showing 67.5% amino acid similarity to the human homologue.  The 5-HT1A receptor was distributed throughout the brain, with the midbrain/diencephalon region containing significantly higher transcript levels than any other brain region.  Substantial levels of transcript were also found in the pituitary, while very low levels were found in the kidney, which contains the interrenal cells.  Xenopus oocyte binding experiments demonstrated that the pharmacology of the Gulf toadfish 5-HT1A receptor is similar to the mammalian form.  Confirming these molecular and pharmacological findings, intravenous injection of 8-OH-DPAT, a mammalian 5-HT1A receptor agonist, stimulated the HPI axis to cause a 2-fold increase in circulating levels of cortisol.  As the pharmacology and functionality of the toadfish 5-HT1A receptor is similar to the mammalian 5-HT1A receptor, it seemed likely that regulation of the receptor would also be subject to the negative feedback loop that exists in mammals whereby increased circulating levels of cortisol inhibit 5-HT1A receptor activity.  To investigate the possibility of such a feedback mechanism in teleosts, plasma cortisol levels in Gulf toadfish (Opsanus beta) were manipulated and the role of cortisol and glucocorticoid receptors (GRs) in the control of 5-HT1A was evaluated.  Initial investigations revealed that chronic elevation of plasma cortisol mediates changes in brain 5-HT1A receptor mRNA and protein levels via the GR; however, there appears to be a disconnect between brain levels of the receptor and activation of cortisol release from the interrenal tissue.  Targeted investigations confirmed that the release of both corticotropin-releasing factor (CRF) and adrenocorticotropic hormone (ACTH) can be stimulated by activation of centrally located 5-HT1A receptors.  Additionally, it was discovered that 8-OH-DPAT-stimulated release of CRF and ACTH was attenuated by crowding stress, and that treatment with RU486 returned secretion rates to control levels.  However, while it appears that the GR is responsible for mediating the negative feedback of cortisol on 5-HT1A receptors located in the central nervous system, it does not appear to be responsible for mediating attenuation of cortisol secretion from the interrenal cells.  In vitro experiments using isolated kidney tissue suggest that chronically elevated plasma cortisol attenuates ACTH- and 5-HT-stimulated cortisol secretion from the interrenal cells of toadfish.  Furthermore, the 5-HT1A receptor is not a mediator of cortisol release at the level of the interrenal cells, explaining in part the disconnect between brain 5-HT1A levels and HPI axis function. The series of investigations outlined in this dissertation have provided key information about the functional aspects of the 5-HT1A receptor in a single species, providing a comprehensive examination of the role it plays in both activating and attenuating the stress response in the Gulf toadfish (Opsanus beta).  These findings, combined with the fact that cortisol is the predominant corticosteroid in both humans and fish, provide support for considering the Gulf toadfish as a model for the human 5-HT1A receptor.</p>

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</description>

<author>Lea R. Medeiros</author>


</item>


<item>
<title>Comparison of Workplace Protection Factors for Different Biological Contaminants</title>
<link>http://digitalcommons.wku.edu/nurs_fac_pub/56</link>
<guid isPermaLink="true">http://digitalcommons.wku.edu/nurs_fac_pub/56</guid>
<pubDate>Sun, 06 May 2012 15:53:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study compared workplace protection factors (WPFs) for five different contaminants (endotoxin, fungal spores, (1→3)-β-D-glucan, total particle mass, and total particle number) provided by an N95 elastomeric respirator (ER) and an N95 filtering facepiece respirator (FFR). We previously reported size-selective WPFs for total particle numbers for the ER and FFR, whereas the current article is focused on WPFs for bioaerosols and total particle mass. Farm workers (n = 25) wore the ER and FFR while performing activities at eight locations representing horse farms, pig barns, and grain handling facilities. For the determination of WPFs, particles were collected on filters simultaneously inside and outside the respirator during the first and last 15 min of a 60-min experiment. One field blank per subject was collected without actual sampling. A reporting limit (RL) was established for each contaminant based on geometric means (GMs) of the field blanks as the lowest possible measurable values. Depending on the contaminant type, 38–48% of data points were below the RL. Therefore, a censored regression model was used to estimate WPFs (WPFcensored). The WPFcensored provided by the two types of respirators were not significantly different. In contrast, significant differences were found in the WPFcensored for different types of contaminants. GMs WPFscensored for the two types of respirators combined were 154, 29, 18, 19, and 176 for endotoxin, fungal spore count, (1→3)-β-D-glucan, total particle mass, and total particle number, respectively. The WPFcensored was more strongly associated with concentrations measured outside the respirator for endotoxin, fungal spores, and total particle mass except for total particle number. However, when only data points with outside concentrations higher than 176×RL were included, the WPFs increased, and the association between the outside concentrations and the WPFs became weaker. Results indicate that difference in WPFs observed between different contaminants may be attributed to differences in the sensitivity of analytical methods to detect low inside concentrations, rather than the nature of particles (biological or non-biololgical).</p>

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</description>

<author>Kyungmin Jacob Cho et al.</author>


</item>


<item>
<title>MRI Simulation by the EFNMR System and MatLab for Medical Imaging Teaching</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/321</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/321</guid>
<pubDate>Sun, 06 May 2012 15:39:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Magnetic Resonance Imaging (MRI) is a fast growing medical imaging technique. Biomedical engineers will find more and more opportunities in this field. There is a growing demand of an effective teaching system for training engineering students to learn principle knowledge and have hands on experience for MRI. The objective of this research project is to cast a MRI teaching demonstration system in the laboratory environment and assist student to learn MRI through interactive simulations in the Internet accessible learning environment. The first part of the work is to customize the newly installed EFNMR (Earth Field Nuclear Magnetic Resonance) system in the Bioimaging Lab to demonstrate nuclear magnetic resonance (NMR) phenomenon, NMR relaxation and T1/T2 weighted contrast mechanisms under laboratory environment. This demo is performed in the Earth’s magnetic field with a low field coil probe. Procedures to acquire and optimize MRI signal, estimate/calculate T1 and T2 values are presented. Relaxation time T1/T2 weighted images are also presented. The second part is to build two graphical user interface (GUI) platforms to simulate the magnetic resonance imaging reconstruction process. Assuming an ideal noiseless condition is setup and the Magnetic Resonance signal intensity is proportional to the image pixel intensity. The GUI-based simulation provides students online demonstrations of combined resonance signal, K-space construction, and FFT used to decompose signal from frequency domain back to spatial domain in an interactive fashion.</p>

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</description>

<author>Zhuang Nie</author>


</item>


<item>
<title>Dispelling Rape Myths through Prison Theatre</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/6</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/6</guid>
<pubDate>Sun, 06 May 2012 15:29:35 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Lorraine F. Moller</author>


</item>


<item>
<title>Behaviors That Eliminate Health Disparities for Racial and Ethnic Minorities: A Narrative Systematic Review</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/5</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/5</guid>
<pubDate>Sun, 06 May 2012 15:29:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Within the health care provider-health care recipient relationship the communication must be culturally competent to eliminate barriers to equitable health care for all Americans. This assertion has conceptual grounding in Public Law 106-129 (the Health Care Research and Quality Act of 1999) and Public Law 106-525 (the Minority Health and Health Disparities Research and Education Act of 2000). This narrative systematic review examines this assertion by using selection and exclusion criteria to gather interventions, assessments, and testimonies conducted from 2000-2007. Reports that were not eliminated via these criteria were analyzed to determine the effect of specific practices that were undertaken in interventions, assessments, and testimonies. Which practices does research propose as indispensable to efforts to eliminate health disparities for racial and ethnic minority health care recipients? Findings indicate that culturally competent behaviors by providers and recipients promote effective intercultural communication that eliminates health care disparities, and removes obstacles to care.</p>

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</description>

<author>Truman Ryan Keys</author>


</item>


<item>
<title>An Analysis of College-aged Women’s Personal Relations</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/4</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/4</guid>
<pubDate>Sun, 06 May 2012 15:29:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Current communication literature regarding personal relations is limited by its focus on romantic, friendship and friends with benefits relations. To better understand the types of relations college-aged women practice, this study sought to explore (a) the types of cross-sex relations college-aged women practice (b) the reasons they give for practicing the relations and (c) the identities they construct by practicing the relations. Results indicated a myriad of relational types. Types were categorized under three supra-categories and were explored in terms of their description, initiation, maintenance and communication rules, as well as their benefits and drawbacks. Identities associated with the relations were also examined, along with relational fluidity, commitment and intimacy.</p>

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</description>

<author>Amanda E. Hamilton</author>


</item>


<item>
<title>Roundtable Discussion Examining Ritual, Technology, and Community in Urban Communication</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/3</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/3</guid>
<pubDate>Sun, 06 May 2012 15:29:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>Pervasive technologies that now exist in the urban setting have greatly improved the ability to connect on a macro-level, but have minimized the intimate shared experience of community on a micro level. This paper explores how technology has changed rituals within the global community and has contributed new methods to the process of human interaction. Technology’s influence on civic engagement, business meetings, shopping and socializing are examined to assess the impact technology has on human connections.</p>

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</description>

<author>Victoria Geyer et al.</author>


</item>


<item>
<title>Understanding space and time through the exploration of a cafe as a workplace</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/2</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/2</guid>
<pubDate>Sun, 06 May 2012 15:29:34 PDT</pubDate>
<description>
	<![CDATA[
	<p>This paper examines a café as a workplace. The position adopted is the constitutive view, whereby patrons of the café were observed as they worked. Data was obtained from thirteen ethnographic participant-observations, two hours each in length, conducted over a two-month period. It is argued that the environment provides a “sense of place” that normalizes patrons’ use of space and time, resulting in the typology of a leisure time-space worker. Themes include: patrons’ use of space to work, type of work done, and lastly, that the multi-functional work-leisure context allows for patrons’different use of time to work. This project contributes to existing research by showing how, in subtle ways, people behave in public spaces, and thereby informing our understanding of the norms underlying social behavior in public settings.</p>

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</description>

<author>Erin Christie</author>


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<item>
<title>KEYNOTE ADDRESS: On the Binding Biases of Time</title>
<link>http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/1</link>
<guid isPermaLink="true">http://docs.rwu.edu/nycsaproceedings/vol2009/iss1/1</guid>
<pubDate>Sun, 06 May 2012 15:29:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lance Strate is Professor of Communication and Media Studies at Fordham University, and Executive Director of the Institute of General Semantics. He is a Past President of the New York State Communication Association, and a recipient of NYSCA's John F. Wilson Award. He is a founder and Past President of the Media Ecology Association, and author of <em>Echoes and Reflections: On Media Ecology as a Field of Study</em>. This is the text of his Keynote Address presented at the 67th Annual Conference of the New York State Communication Association, Ellenville, NY, October 23-25, 2009.</p>

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</description>

<author>Lance A. Strate</author>


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<item>
<title>Mangroves on the Move: Predictions of Storm Surge Effects on Coastal Vegetation</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/750</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/750</guid>
<pubDate>Sun, 06 May 2012 15:26:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>The landward coastal zones of the low-lying habitats are characterized by sharp ecotones between salinity-tolerant (halophytic) vegetation types, such as mangroves, and salinity-intolerant (glycophytic) vegetation types, such as freshwater marsh and hardwood hammocks. Empirical studies show a gradual landward migration of these ecotones in some areas, due to sea level rise (SLR), and evidence in some areas of rapid change from glycophytic to halophytic vegetation, possibly as regime shifts resulting from salinity overwash from storm surges. In this dissertation work, the plausibility of storm surge related regime shifts of glycophytic vegetation was  investigated using  a coupled hydrological and ecological simulation model, and the resilience of the ecotone was  studied using a mathematical model. In view of potential effects of storm surge associate with SLR on Everglades ecosystems, particularly the consequences these pose for the Comprehensive Everglades Restoration Plan, both empirical and modeling studies on coastal vegetation are underway. In this dissertation work, the Spatially Explicit Hammock/Mangrove (SEHM) computer simulation model of the ecotone between those vegetation types was used to show the influence of both abiotic (elevation gradient, groundwater salinity, tidal amplitude, precipitation, freshwater flow) and biotic factors (plant physiology, competitive abilities, dispersal, positive feedbacks between plants and soil salinity) on the mechanisms of ecotone formation.  The model simulation results indicate that an environmental gradient of salinity, caused by tidal flux, is the key factor separating vegetation communities, while positive feedback involving the interactions of vegetation types with the vadose zone salinity increases the sharpness of boundaries, and maintains the ecological resilience of mangrove/ hammock ecotones against minor disturbances. The model also shows that the dry season, with its low precipitation, has a strong effect on the position of the mangrove/hammock ecotone.  Using a mathematical model of an ecotone vulnerable to possible future changes, I estimated the resilience of the ecotone to disturbances. The specific ecotone is that between two different vegetation types, salinity-tolerant and salinity-intolerant, along a gradient in groundwater salinity. In the case studied, each vegetation type, through soil feedback loops, promoted local soil salinity levels that favor itself in competition with the other type. Alternative stable equilibria, one for salinity-tolerant and one for salinity intolerant vegetation, were shown to exist over a region of the groundwater salinity gradient, bounded by two bifurcation points. This region was shown to depend sensitively on parameters such as the rate of upward infiltration of salinity from groundwater into the soil due to evaporation.  I showed also that increasing diffusion rates of vegetation can lead to shrinkage of the range between the two bifurcation points. Sharp ecotones are typical of salt-tolerant vegetation (mangroves) near the coastline and salt-intolerant vegetation inland, even though the underlying elevation and groundwater salinity change very gradually.  A disturbance such as an input of salinity to the soil from a storm surge could upset this stable boundary, leading to a regime shift of salinity-tolerant vegetation inland.  I showed, however, that, for my model as least, a simple pulse disturbance would not be sufficient; the salinity would have to be held at a high level, as a ‘press,’ for some time.  The approach used here should be generalizable to study the resilience of a variety of ecotones to disturbances. The SEHM model has been modified to simulate the mangrove-freshwater marsh ecotone.  This model is based on intensive field studies by USGS across a mangrove-marsh ecotone on the Harney River in Everglades National Park. The model indicates that two factors are closely related to storm surge effect on vegetation. One of these is salinity intrusion, which has been proposed as a major disturbance to freshwater wetlands. The other is invasion of mangrove seedlings, which have rarely been reported as drivers for ecotone position changes. The model simulation results indicate that, at least for the cases studied, the regime shift of vegetation from freshwater marsh to mangroves was more sensitive to the density of mangrove seedlings passively transported by the storm surge than to the magnitudes of the salinity intrusion. The observed high salinities after regime shifts in the model are the result of more than simply the salinity overwash from the storm surge. Once mangrove prapagules establish successfully, high salinity can be maintained via evapotranspiration of the invading halophytic vegetation, which leaves salt in the soil. While initial salinity intrusion helps mangrove prapagules compete with dense freshwater marsh, the mangroves, once established, continue to hold the concentration of soil salinity high.</p>

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</description>

<author>Jiang Jiang</author>


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<item>
<title>Applying the Ševčík Approach to Selected Excerpts from the First Movement of the Brahms Viola Sonata in F Minor</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/749</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/749</guid>
<pubDate>Sun, 06 May 2012 15:20:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>Originally for clarinet, the Brahms Viola Sonata in F Minor Op. 120 no. 1 is famous amongst violists for its technical challenges. This doctoral lecture recital essay is an archival version of a live lecture recital given in April 2012 about how one can apply renowned violin pedagogue Otakar Ševčík’s method of creating original exercises designed to conquer the technical and musical challenges of this Brahms sonata. This document includes the lecture recital script, DeBardelaben’s original exercises, which serve as a catalyst for learning correlating passages of the Brahms, and DeBardelaben’s edited viola part with his bowings and fingerings for the first movement of the sonata.</p>

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</description>

<author>Ross A. DeBardelaben</author>


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<item>
<title>Public Education in an Era of Privatization: A Spatial Examination of the Relationship Between Charter School Clusters and Gentrification in Washington, D.C. and Brooklyn, NY</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/320</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/320</guid>
<pubDate>Sun, 06 May 2012 15:08:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Over the past decade, American public education has undergone a major transformation. Today, corporations, philanthropists, and the federal government promote and fund the charter school movement, which effectively diminishes the role of public education. Although charter schools in the United States were created with the intention of serving underprivileged students, several studies by geographers and education policy specialists have found that some of these schools have become institutions of gentrification and, in turn, establishments that reproduce social class distinctions. This thesis examines the distribution of charter schools in Washington, D.C. and New York’s borough of Brooklyn and compares charter school clusters to local spatial trends in gentrification. The methodology combines spatial, quantitative, and qualitative analyses, specifically a spatial statistical analysis of charter school clustering; a quantitative analysis of census data since 1990; and a qualitative assessment of the literature on gentrification and charter schools as it applies to these study areas. The findings indicate a growing trend in school choice and gentrification as a state-sponsored method of social exclusion, dissolving public systems, and further advancing the neoliberal urban agenda.</p>

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</description>

<author>Stacey Kerr</author>


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<item>
<title>Synthesis and Characterization of Transition Metal Complexes with Bulky Tin Ligands for Application in Small Molecule Activation</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/748</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/748</guid>
<pubDate>Sun, 06 May 2012 15:04:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>The role of bulky tin ligands in the stabilization of transition metal complexes with electronic unsaturation has been studied to understand the mode of binding of small molecules at an unsaturated metal center.  We were able to isolate electronically unsaturated Pt-Sn bimetallic complexes effective in the reversible activation of small molecules including CO, H2, C2H4, and NH3 at room temperature.  We have examined the effect of the modification of ligands in Pt-Sn bimetallic complexes for the activation of small molecules and have observed that the Pt(SnBut3)2(CNBut)2 bimetallic complex reversibly activates hydrogen at room temperature both in the solid state and in solution. Similarly, we have also prepared bimetallic Pt-Sn complexes with an NHC carbine ligand which were also shown to activate hydrogen and alkenes reversibly. A bimetallic Fe-Sn cluster complex, Fe2 (µ-SnBut2)2(CO)8, was synthesized from the reaction of But3SnH with the Fe2(CO)9 and shown to be selective at activating the benzylic C-H bond of alkylaromatic solvent  molecules.  The new complexes containing tin have been characterized spectroscopically to gain an insight into the reaction mechanism involved in small molecule activation.</p>

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</description>

<author>Veeranna Yempally</author>


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<item>
<title>Predictors of Classroom Management Challenges and Practices of Secondary Choral Music Educators</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/747</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/747</guid>
<pubDate>Sun, 06 May 2012 14:54:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Data were collected from secondary choral music educators (N = 593) from across the United States using the Choral Classroom Management Inventory.  The use of classroom management practices and occurrences of classroom management challenges were evaluated and relationships between teacher background variables, context variables, and classroom management practices and challenges were calculated. Variables with significant correlations were included in the multiple regression analyses to determine predictors of use of classroom management practices and occurrences of classroom management challenges.  Results showed that teacher background and context variables accounted for 40% of the variance in use of classroom management practices, and included the teacher background variables of teacher gender, teaching area emphasis, overall teaching experience, classroom management support and music-specific training, and overall classroom management self-efficacy, as well as the context variable of ability (ensemble selectivity). Significant predictors accounted for 22% of variance in classroom management challenges, and included teacher background variables of teacher gender, overall teaching experience, and overall classroom management self-efficacy, as well as the context variable of ability (primary level and ensemble selectivity).  Implications for practice and recommendations for future research were provided.</p>

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</description>

<author>Kathryn L. Simon</author>


</item>


<item>
<title>Langerhans cell histiocytosis of the spine in children: Long-term follow-up</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1019</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1019</guid>
<pubDate>Sun, 06 May 2012 14:52:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sumeet Garg et al.</author>


</item>


<item>
<title>Location and initiation of degenerative rotator cuff tears: An analysis of three hundred and sixty shoulders</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1018</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1018</guid>
<pubDate>Sun, 06 May 2012 14:52:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>H. Mike Kim et al.</author>


</item>


<item>
<title>The Structure of Sensory Imagination</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/746</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/746</guid>
<pubDate>Sun, 06 May 2012 14:49:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>My dissertation concerns sensory imagining: experiences like imagining a colorful parrot, or imagining its squawk. Just as with perception, there are three sorts of question to be asked about imagination. First, what is it like, phenomenologically, to imagine? Second, what can we do by imagining? Third, what is the essential nature of the experience? There are many theories about perception's nature, which explain its phenomenology and capacities. By contrast, there is some work on imagination's phenomenology, and a lot of work about its putative capacities, but very few theories of its nature. In the dissertation, I give a theory of imagination's nature, taking as explananda facts about its phenomenology and some of its capacities. The most striking facts about imagination's phenomenology concern its quasi-perceptual nature: ways in which it is like and unlike perception. Imagining is like perceiving, in that it is sensory, perspectival, and presentational: objects seem to appear to one. But it is unlike perceiving, in that the objects of imagination seem to be dependent on the subject, and in that investigation of the objects will not reveal anything more about their nature. These observations are sufficient to rule out three simple views of imagination. According to denialism, there is not really any such thing as sensory imagining. According to the perceptual model, imagining is very much like perceiving, differing only in vivacity. According to the pictorial model, imagining is like seeing an internal picture. None of these models adequately accounts for the phenomenology of imagining. For example, unlike when we perceive, our visual field need not be replete when we imagine. And unlike when we see a picture, we can't attend to both the object and the vehicle of a mental image.  The challenge is to improve on these models. To do so, I first examine the sensory nature of imagination. I argue that the Humean intuition that you can first experience a color by imagining it amounts to the claim that you can secure de re reference to sensible properties by imagining them. This in turn means that dependency views, like M.G.F. Martin's, on which imagining constitutively depends on perceiving, are false. I also argue that this de re capacity of imagination cannot be explained by content views, on which to imagine is to stand in an attitude-like relation to a propositional content. I argue that a relational view of experience of sensible properties is the best way to explain this capacity. Since imagining involves a relation to sensible properties, it might also involve a relation to an extraordinary object which has sensible properties. I consider three such proposals regarding imagination: sense-data, Meinongian, and sensible profile views. I argue that none of these proposals is adequate. Each recapitulates problems with the simple perceptual and pictorial models.  I argue that instead of a relational view, we should adopt a view on which sensible properties are structured by intentional content intrinsic to imaginative experiences. Starting from A.D. Smith's account of the nature of perceptual intentionality, I argue that the subjectivity of imagined objects can be explained by adopting Sartre's notion of positing, and the idea that sensible properties are predicated of posited objects. This intentional view faces two problems. The first is that it makes what might seem a dubious appeal to intentional objects. The second is that it seems to be a theory of how we imagine appearances, rather than objects. I argue that the first problem is not pressing; talk of intentional objects is not ontologically pernicious. The second problem is more serious. To address it, I argue that all the views of imagination thus far discussed are variants of the additive view, on which to imagine is to apply conceptual content to an ambiguous mental image. However, additive views are bound to fail as views of imagination. The root of their problems is the idea that imagining involves multiple intentional experiences which are somehow amalgamated. I propose instead an approach to imagination which draws on Gestalt psychology. Imaginative experiences consist of a range of parts, which are seamlessly synthesized into a whole experience. The whole experiences are intentional, but the parts are not; they inherit their intentionality from the whole. It is not the case that one generates an image and then applies intentional content to it; rather, the image, the intentionality, and the rest of the content come combined. I argue that this approach not only helps to explain how imaginative experiences can be about particulars, but also promises to be fruitful in explaining features of imagination, in part via the Gestalt idea of Prägnanz.</p>

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</description>

<author>Nicholas Wiltsher</author>


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<item>
<title>The 1943 Bryant Yearbook, &quot;The Bryant Ledger&quot;</title>
<link>http://digitalcommons.bryant.edu/yearbooks/4</link>
<guid isPermaLink="true">http://digitalcommons.bryant.edu/yearbooks/4</guid>
<pubDate>Sun, 06 May 2012 14:48:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Co-Editors........Clair A. Gilfix</p>
<p>......................Julia H. Scott</p>
<p>Art Director........Mary Ann Steiner</p>

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</description>


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<item>
<title>Testing a Model of Jazz Rhythm: Validating a Microstructural Swing Paradigm</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/745</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/745</guid>
<pubDate>Sun, 06 May 2012 14:18:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to create and test two hypothesized models for swing in jazz performance. In order to estimate the hypothesized fully latent variable Swing model, eighth note samples (N = 815) from five improvised solos by Chris Potter were analyzed. Three first order factors were identified and examined that were hypothesized to define swing: eighth note duration, beat placement, and note dynamics. These three factors were measured with accuracy beyond a thousandth of a millisecond. Nine second order factors were identified and grouped into soloist-controlled variables and non-soloist controlled variables: metrical beat placement, melodic character, intervals, articulation, range, underlying harmony, tempo, bass beat placement, and drummer beat placement. The methodology of the measurement system and data collection procedures prescribed in this research study was found to contain limitations that prevented the administration of a proper statistical analysis for an estimation of the proposed models. Results of the simultaneous multiple regression analysis revealed that metrical beat placement, melodic character preceding, melodic character succeeding, interval preceding, interval succeeding, articulation, range, underlying harmony, and tempo combined to account for 6.7% of the variance in eighth note duration (N = 394), with interval preceding and interval succeeding having a statistically significant effect. Metrical beat placement, melodic character preceding, melodic character succeeding, interval preceding, interval succeeding, articulation, range, underlying harmony, and tempo combined to account for 22.3% of the variance in note dynamics (N = 231) with tempo having a statistically significant effect on note dynamics. The omnibus test for beat placement (N = 99) was found to be statistically insignificant.</p>

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</description>

<author>Brian C. Wesolowski</author>


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<item>
<title>Goldie and Che: Blueprint for a Sand Castle</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/319</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/319</guid>
<pubDate>Sun, 06 May 2012 14:11:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>This poetry book depicts the complexities of the individual in society and the relevance of unique, personal and creative expression.  Essentially, the project illuminates the following themes: the role of the individual in the context of society and culture, the servitude to gender roles, the exploitation of the body and the natural environment, and the diktat of popular culture.  This project intends to dissect as well as radiate the effects of assigning identity according to gender by honestly illustrating human existence through memory and private contemplation.  Exploitations of the environment and the body are portrayed by way of recollection, imagination and passion.  The current wrecking of ocean waters aligns with and scaffolds the wrecking/utilization of the physical body.  Corruption of the natural environment mirrors the corruption of the mortal self.  Like gender roles assign identity, pop culture assigns identity and community via mass deliverance.  Pop culture acts as a fountain of detail and context that cascades the concerns of the project.  In order for the collection to emit these themes, intimacy with and exploration of the private self is significant and indispensable.  Personal experience, agenda, taste and topic fixation function as tools of communication and campaign for the abovementioned matters.  The collection engages closely with the reader and germinates reader empathy to raise awareness toward social injustice while simultaneously endorsing the use of personal imagination.</p>

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</description>

<author>Nicole Hospital-Medina</author>


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<item>
<title>Leptin as a Novel Predictor of Somatic Depressive Symptoms in Hispanics with the Metabolic Syndrome</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/318</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/318</guid>
<pubDate>Sun, 06 May 2012 14:11:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The association between depression and the Metabolic Syndrome (MetS) has been extensively investigated, and inflammation has been identified as an underlying link. Recent reports, however, indicate a possible role of leptin in modulating the immune response, yielding increases in inflammatory markers. The literature suggests this hormone may not only explain the metabolic abnormalities associated with depression but may also act as a biomarker of depression itself. This study aimed to determine the association between circulating leptin and total depressive symptoms and depressive symptom dimensions (cognitive and somatic) after controlling for important confounding factors such as age, gender, insulin resistance, body mass index (BMI) and inflammation. We studied 119 Hispanic participants, 60 women and 59 men, recruited for the Community Health and Risk-reduction for the Metabolic Syndrome (CHARMS) study. Depression was measured using the Beck Depression Inventory (BDI). Somatic and Cognitive subscale scores were calculated. Leptin was measured using a leptin-specific enzyme immunoassay. Inflammation was assessed using C-reactive protein (CRP) measured with a high-sensitivity assay. Participants with CRP levels greater than 10 mg/L were excluded from analysis. CRP and leptin levels were log transformed to achieve a normal distribution. Median BDI total score, BDI cognitive score and BDI somatic score were 8, 3 and 5, respectively. Median circulating leptin levels were 30.6 ng/ml. In univariate regression, leptin levels were significantly associated with total (β =0.36, P=.000), cognitive (β =0.24, P=.011) and somatic depressive symptoms (β =0.48, P=.000). After controlling for age, gender, insulin resistance, BMI and inflammation, circulating leptin levels remained significantly associated with somatic depressive symptoms only (β =.41, P=.004). Another important predictor of somatic depressive symptoms was age (β=0.23; P=0.004). The model accounted for 31% of the variance in somatic depression scores. Leptin is significantly associated with somatic depressive symptoms in Hispanics with the MetS. This association was independent of important confounding factors such as gender, age, BMI, insulin resistance and inflammation. Further research is needed to elucidate the complex pathways linking depression and the MetS while incorporating the potential role of leptin.</p>

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</description>

<author>Diana A. Chirinos</author>


</item>


<item>
<title>The Creation of Context-Specific Exercises Related to Advanced Solo Flute Literature: A Pedagogical Approach</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/744</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/744</guid>
<pubDate>Sun, 06 May 2012 14:05:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study is to create a comprehensive collection of some of the most important and difficult excerpts from the standard advanced solo flute literature and to provide a set of context-specific exercises with suggested practice methods.  In order to determine results, a survey was administered to expert collegiate level flute teachers (N = 230). The first five chapters of this essay detail the need for the study, a review of literature, the method of the study, the results of the study and a summary/conclusions section which includes implications for further research.  The last chapter of this essay includes excerpts from the standard advanced solo flute literature and associated context-specific exercises that can be used as a resource for students and teachers.  The excerpts and exercises are listed in alphabetical order, according to the composer's last name.  They are also organized in the appendix by area of difficulty including: technique, articulation, rhythm, phrasing, style, ensemble and intonation.</p>

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</description>

<author>Cassandra A. Rondinelli</author>


</item>


<item>
<title>The Implications of Centering in a Three-Level Multilevel Model</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/743</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/743</guid>
<pubDate>Sun, 06 May 2012 13:41:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>Hierarchical data are becoming increasingly complex, often involving more than two levels.  This study investigated the implications of centering within context (CWC) and grand mean centering (CGM) in three distinct three-level models.  The goals were to (1) determine equivalencies in the means and variances across the centering options, (2) identify the algebraic relationships between the three-level contextual models, and (3) clarify the interpretation of the estimated parameters.  Artificial datasets were used for illustration.  Centering decisions in multilevel models are closely tied to substantive hypotheses and require researchers to be clear and cautious about their choices.  This work is designed to assist the researcher in making centering decisions for analysis of three-level hierarchical data.</p>

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</description>

<author>Ahnalee Brincks</author>


</item>


<item>
<title>Pediatric Voice: Delineating the Voice Science and Investigating Child Training Methods Toward Pedagogical Application</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/742</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/742</guid>
<pubDate>Sun, 06 May 2012 13:33:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study investigates the synergistic relationship between voice science and voice pedagogy to inform the practices of voice teachers, music educators, and voice trainers.  Furthermore, it is an effort to augment existing knowledge of the anatomy and physiology of the pediatric voice so voice professionals may design targeted curricula in pediatric pedagogy. The most current materials in voice science and voice pedagogy were reviewed and relevant findings connecting both fields of study delineated. In the field of voice science, research concerning the progression of the vocal mechanism from fetus through adolescence was evaluated to clarify physiological findings potentially relevant to voice teaching. Similarly, the practices of voice pedagogues were reviewed in order to ascertain whether those practices were research-based, observational, or suppositional. The results found in the amassed literature provided context for current thought in both fields. New technological modalities provided the most current and authentic depiction of the pediatric laryngeal structure. These depictions applied pedagogically provide a point of justification for the anatomical scrutiny of the pediatric larynx. Research findings also contextualize the observational assessments of voice pedagogues, which in turn substantiates the practical application voice science has in teaching. Additionally, studies have not only found that pediatric vocal mechanism is resilient, but also that it is suited to the vocal demands of childhood and adolescence. Finally, the physical act of singing is somatic to the normal pediatric vocal mechanism. However, tangential issues in the process of singing, physiological growth and developmental factors, impact ability and capability in the developing singer. The identification of synergistic connections provides both clarification of the anatomical development of the pediatric voice and contextualization of the resultant findings toward pedagogical application.</p>

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</description>

<author>Maria Fenty Denison</author>


</item>


<item>
<title>Haitian-Dominican Relations in Times of Cholera: Migration, Public Health and Human Security on the Border</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/317</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/317</guid>
<pubDate>Sun, 06 May 2012 13:25:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to examine how the cholera outbreak in the Dominican Republic has affected the human security of both Haitians and Dominicans living in the Dominican Republic. Additionally, it explores whether the policies implemented to control the spread of cholera on the border with Haiti have been effective or have detrimentally affected the human security of the population of Dajabón. An ethnographic study was conducted in Dajabón, Dominican Republic from September 15, 2011 until October 21, 2011. Data was collected through observation, ethnographic mapping and semi-structured, open-ended interviews with residents, public officials and healthcare workers in Dajabón. This thesis establishes that current border control policies implemented on the Dominican border with Haiti in the province of Dajabón are ineffective in preventing the cross-border spread of cholera, detrimental to human security and public health, and have stigmatized the Haitian population. This thesis argues that real progress in controlling cholera can only be made through increased cooperation and solidarity between the Dominican Republic and Haiti in the area of public health.</p>

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</description>

<author>Erin C. Coldsmith</author>


</item>


<item>
<title>Risk Factors for Future Cardiac Diseases in Childhood Cancer Survivors</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/741</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/741</guid>
<pubDate>Sun, 06 May 2012 13:22:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Background: With 12,000 children diagnosed with cancer annually in the United States and survival rates approaching 80%, the long-term health of childhood cancer survivors is an increasingly important concern. This is especially true given that over 70% of survivors develop a chronic health condition by 30 years after their original diagnosis. Cardiovascular diseases (CVD) are the most common non-cancer related complications. Although some risk factors for therapy-induced cardiovascular damage  have been identified, their influence on longitudinal CVD risk is not well described, and therefore, their clinical utility is limited. While guidelines exist for protecting the long-term cardiovascular health of survivors, they are generalized from general population recommendations, placing a strong reliance on healthy lifestyle habits such as diet. By failing to consider the clinical heterogeneity of survivors, these recommendations may miss those survivors with the greatest need for risk management and ignore the possibility that survivors require unique strategies for effective CVD prevention. It is also unclear how a history of childhood cancer affects diet, how diet in-turn affects the development of traditional CVD risk factors among survivors, and what the combined effects of these traditional CVD risk factors imply for the long-term health of survivors. Methods: This dissertation presents results from 3 investigations related to the long-term cardiovascular health of survivors using data from the Cardiac Risk Factors in Pediatric Cancer Survivors Study. This study included 201 survivors, a median of 11 years from cancer diagnosis, and 76 of their siblings who were assessed during day-long study visits including echocardiography, patient histories, and laboratory tests conducted from 1999 to 2003. Cancer treatment records were reviewed and 3-day food records collected. First, the associations between cranial irradiation and cardiac abnormalities associated with anthracycline chemotherapy were examined. Associations with insulin-like growth factor 1 (IGF-1), a marker of growth hormone, were also examined. Second, diet records were used to estimate daily caloric intake relative to recommended levels and dietary quality using the Healthy Eating Index-2005 (HEI). The diets of survivors and siblings were compared and associations with cancer types and treatments investigated. The association between dietary quality and adiposity among survivors was also examined. Third, future CVD risk due to traditional CVD risk factors was examined using Pathobiological Determinants of Atherosclerosis in Youth (PDAY) scores and the Framingham Risk Calculator (FRC), both expressed as ratios relative to an individual of similar age and sex without modifiable risk factors. The PDAY odds ratio represents the increased odds of currently having an advanced coronary artery lesion. The FRC risk ratio represents the increased risk of a myocardial infarction, stroke, or coronary death in the next 30 years. Survivor and sibling risk estimates were compared and associations with cancer diagnoses and treatments as well as physical inactivity examined. Results: Survivors exposed to cranial radiation had an additional 12% decrease in LV mass compared to unexposed survivors (P<.01), and an additional 3.6% decrease in LV dimension (P=.03). Survivors exposed to cranial radiation also had a greater decrease in IGF-1 relative to normal levels than unexposed survivors (30.8% vs. 10.5% decrease, P<.01). There were no differences between survivors and siblings in daily caloric intake (97 vs. 105% of recommended caloric intake) or the HEI total score (55.5 vs. 53.3), respectively. Survivors exposed to cranial radiation had lower total HEI scores (-6.4, P=.01). Among survivors, increasing dietary quality was associated with decreasing percent body fat (β=-.19, P=.04). The median PDAY odds ratio for survivors was 2.2 (interquartile range, 1.3-3.3). The median FRC risk ratio was 1.7 (interquartile range, 1.0-2.0). Survivors and siblings had similar mean PDAY odds ratios (2.33 vs. 2.29, P=.86) and FRC risk ratios (1.72 vs. 1.53, P=.24). Cancer type and treatments were not associated with the CVD risk estimated from traditional metabolic CVD risk factors, cardiometabolic health. There was a suggested association of physical inactivity with PDAY odds ratios (r=0.17, P=.10) and FRC risk ratios (r = 0.19, P=.12). Discussion: Among anthracycline-treated survivors, those with cranial radiation exposure had significantly greater decreases in LV mass and dimension. Because cranial irradiation was also associated with decreased IGF-1, it is possible that GH deficiencies mediated this effect suggesting that GH replacement therapy may help prevent the development of cardiotoxicity. Survivors consumed diets similar in quality to their siblings though both groups were only moderately adherent to guidelines. Dietary quality was associated with increased body fat in survivors suggesting interventions focused on diet quality may help reduce their adiposity. Cardiometabolic health was poor in survivors but not different than that of their siblings, highlighting the importance of managing traditional CVD risk factors and considering novel exposures in survivors.</p>

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</description>

<author>David C. Landy</author>


</item>


<item>
<title>High Fidelity Simulation of Non-Synchronous Vibration for Aircraft Engine Fan/Compressor</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/740</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/740</guid>
<pubDate>Sun, 06 May 2012 13:22:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>The objectives of this research are to develop a high fidelity simulation methodology for turbomachinery aeromechanical problems and to investigate the mechanism of non-synchronous vibration (NSV) of an aircraft engine axial compressor. A fully conservative rotor/stator sliding technique is developed to accurately capture the unsteadiness and interaction between adjacent blade rows. Phase lag boundary conditions (BC) based on the time shift (direct store) method and the Fourier series phase lag BC are implemented to take into account the effect of phase difference for a sector of annulus simulation. To resolve the nonlinear interaction between flow and vibrating blade structure, a fully coupled fluid-structure interaction (FSI) procedure that solves the structural modal equations and time accurate Navier-Stokes equations simultaneously is adopted. An advanced mesh deformation method that generates the blade tip block mesh moving with the blade displacement  is developed to ensure the mesh quality. An efficient and low diffusion E-CUSP (LDE) scheme as a Riemann solver designed to minimize numerical dissipation is used with an improved hybrid RANS/LES turbulence strategy, delayed detached eddy simulation (DDES). High order accuracy (3rd and 5th order) weighted essentially non-oscillatory (WENO) schemes for inviscid flux and a conservative 2nd and 4th order viscous flux differencing are employed.  Extensive validations are conducted to demonstrate high accuracy and robustness of the high fidelity FSI simulation methodology. The validated cases include: 1) DDES of NACA 0012 airfoil at high angle of attack with massive separation. The DDES accurately predicts the drag whereas the URANS model significantly over predicts the drag. 2) The AGARD Wing 445.6 flutter boundary is accurately predicted including the point at supersonic incoming flow. 3) NASA Rotor 67 validation for steady state speed line and radial profiles at peak efficiency point and near stall point. The calculated results agree excellently with the experiment. 4) NASA Stage 35 speed line and radial profiles to validate the steady state mixing plane BC for multistage computation. Excellent agreement is obtained between the computation and experiment. 5) NASA Rotor 67 full annulus and single passage FSI simulation at near peak condition to validate phase lag BC. The time shifted phase lag BC accurately predicts blade vibration responses that agrees better with the full annulus FSI simulation. The DDES methodology is used to investigate the stall inception of NASA Rotor 67. The stall process begins with spike inception and develops to full stall. The whole process is simulated with full annulus of the rotor. The fully coupled FSI is then used to simulate the stall flutter of NASA Rotor 67. The multistage simulations of a GE aircraft engine high pressure compressor (HPC) reveal for the first time that the travelling tornado vortex formed on the rotor blade tip region is the root cause for the NSV of the compressor. The rotor blades under NSV have large torsional vibration due to the tornado vortex propagation in the opposite to the rotor rotation. The tornado vortex frequency passing the suction surface of each blade in the tip region agrees with the NSV frequency. The predicted NSV frequency based on URANS model with rigid blades  agrees very well with the experimental measurement with only  3.3% under-predicted. The NSV prediction using FSI with vibrating blades also obtain the same frequency as the rigid blades. This is because that the NSV is primarily caused by the flow vortex instability and the no resonance occurs. The blade structures respond passively and the small amplitudes of the blade vibration do not have significant effect on the flow. The predicted frequency using DDES with rigid blades is more deviated from the experiment and is 14.7% lower. The reason is that the DDES tends to predict the rotor stall earlier than the URANS and the NSV can be achieved only at higher mass flow rate, which generates a lower frequency. The possible reason for the DDES to predict the rotor stall early may be because DDES is more sensitive to wave reflection and a non-reflective boundary condition may be necessary. Overall, the high fidelity FSI methodology developed in this thesis for aircraft engine fan/compressor aeromechanics simulation is demonstrated to be very successful and has advanced the forefront of the state of the art. Future work to continue to improve the accuracy and efficiency is discussed at the end of the thesis.</p>

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</description>

<author>Hong-Sik Im</author>


</item>


<item>
<title>On Becoming and Being a Homeless Youth Activist</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/739</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/739</guid>
<pubDate>Sun, 06 May 2012 06:19:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Despite decades of interventions to address the immediate needs of homeless youth, America still suffers with youth homelessness. This study suggests that real solutions have come, and will continue to come, from individuals using collective action to redistribute sociopolitical power and resources. The study aimed to understand (1) why people become activists on behalf of this population, and (2) what qualities and characteristics allow them to remain in this work despite its challenges. A review of the literature uncovered more than twenty situational and developmental factors for activists of numerous causes but none examined homeless youth activists and very few integrated factors from multiple disciplines. Some factors spoke to the essence of ‘being’ an activist whereas others spoke to developmental processes of ‘becoming’ one. I used a critical qualitative orientation (Carspecken, 1996) blending phenomenology and grounded theory to explore the development and prolonged engagement of collective action in 13 adult participants (six males, seven females, with a combined experience of over 175 years of collective action). Six participants held advocacy or policy positions and seven held administrative roles in organizations that served youth. Participants were recruited by snowball sampling methods and completed surveys of activism identity, commitment and behavior, as well as semi-structured individual interviews touching on themes identified in the literature. The data revealed that homeless youth activists tend to identify themselves more as advocates and describe their work as advocacy instead of activism. Moreover, participants described five developmental categories containing 20 factors and two situational categories containing ten factors which supported and expanded the extant literature. On “becoming” advocates, participants (1) received foundations of community involvement, (2) experienced privilege or marginalization, (3) started careers foreshadowing homeless youth advocacy, (4) chose to advocate for homeless youth in their careers, and (5) possessed self and world-view promoting advocacy. On “being” advocates, participants (6) felt validated and supported in their roles, and (7) possessed or articulated necessary qualities of being an enduring advocate. This study provides an illustrated application of various factors at work on individuals sharing similar passion and commitment for homeless youth. It demonstrates a bidirectional relationship between individual actors and the micro, meso, and macro sites they inhabit. It is one of the first syntheses of a set of broad and diverse factors and one of only a few critical examinations of privilege and marginalization in participants who address privilege and marginalization in others. Implications for theory, research, training, and the researcher-participant are discussed.</p>

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</description>

<author>Edward Ameen</author>


</item>


<item>
<title>Aristotle&apos;s Lanterns</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/316</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/316</guid>
<pubDate>Sun, 06 May 2012 06:07:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Aristotle’s Lanterns is a collection of poems that explores the spaces of convergence among memory, music, and the natural world. These poems attempt to create an aural landscape which draws on the linguistic musicality inherent in both lyrical free verse and received forms to explore the intersections of natural, emotional, and spiritual topographies.</p>

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</description>

<author>Leah Silvieus Silvieus</author>


</item>


<item>
<title>The Election of a Lesbian Mayor in a Religiously Conservative City: The Case of Houston, Texas</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/315</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/315</guid>
<pubDate>Sun, 06 May 2012 06:00:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>The American South in general remains a pocket of predominantly conservative, Baptist and Evangelical Christian hegemony; however, metropolitan areas of the South display more diversity and pluralism as a result of foreign and domestic migration into the region, changes in religious affiliation, an increasing population choosing no religious affiliation, and the growing influence of popular culture on religious participation. These forces act within a paradigm of neosecularization in which personal conscience exerts more influence than religious authority. Houston, Texas, within the context of the South, serves as the case study that demonstrates the temporal and spatial changes to Houston’s religious and political landscape and the manner in which these changes influence voter behavior. In 2009, Houston, home to a large, active Christian community, became the first major U.S. city to elect an openly homosexual mayor. The changes in Houston’s religious landscape, changes in attitudes toward gays and lesbians, and the varying degrees of voter participation among religious groups across the city, illustrate the unpredictability of religion as an influence on voter behavior in local elections.</p>

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</description>

<author>Nancy S. Morris</author>


</item>


<item>
<title>Public Performance: Free People of Color Fashioning Identities in Mid-Nineteenth-Century Cuba</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/738</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/738</guid>
<pubDate>Sun, 06 May 2012 05:44:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Free people of color held an ambiguous place in Caribbean slave societies. On the one hand they were nominally free, but the reality of their daily lives was often something less than free. This work examines how free people of color, or libres de color, in nineteenth-century Cuba attempted to carve out lives for themselves in the face of social, economic, and political constraints imposed on them by white Cubans and Spaniards living in the island. It focuses on how through different Afro-Cuban associations some libres de color used public music and dance performances to self-fashion identities on their own terms. The images they constructed were in direct contrast to those in circulation in the emerging Cuban public sphere and reveal that free blacks did not acquiesce to the constraints being levied against them and the negative stereotyping of their community, but rather attempted to self-define their identities.</p>

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</description>

<author>Jacqueline C. Grant</author>


</item>


<item>
<title>Notes on a Foundation Crumbling</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/314</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/314</guid>
<pubDate>Sun, 06 May 2012 05:36:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Notes on a Foundation Crumbling takes place in a fishing village in contemporary coastal New England. Paul Mallory is a veteran who falls in love with and marries a young painter, Emma Moore. Emma’s childhood home has been condemned to be demolished. In an effort to prove his love, Mallory uproots the house, tows it by water to the village harbor, and works to replant it. As Mallory works to renovate the house, Emma reconnects with a former lover, Liam Flynn, who is now raising his five-year-old brother Danny (who is sick with pneumonia). For a time the four characters form a close-knit albeit unlikely family. The house provides the novel with its underlying structure; its motion, construction, and problems coincide with those of the group dynamic. As the situation deteriorates and the project fails, Emma leaves with Danny, but the emblem of obsession lingers and burns. At the heart of this story are the obsessions that determine what characters do and how tragedies unfold. It is a story about the compulsion to try to know and to own someone, and the impossibility of doing just that. It is a story about the seductive danger and inevitability of the narratives that we construct around ourselves and around those we love.</p>

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</description>

<author>Justin Engles</author>


</item>


<item>
<title>Improving Search In Genetic Algorithms Through Instinct-Based Mating Strategies</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/737</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/737</guid>
<pubDate>Sun, 06 May 2012 05:29:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Genetic Algorithm (GA) is a popular approach to search and optimization that has been applied to hundreds of real-world optimization problems across numerous domains of science. The GA describes an iterative search process that seeks to improve the quality of an initially random set of solutions with respect to some user-defined optimization criteria. The components of this iterative search process mimic Darwinian biological evolutionary processes such as mating, recombination, mutation, and survival of the fittest. Over the years, researchers have attempted to improve various components of the GA search process. However, the impact of the mating strategy, which determines how existing solutions to a problem are paired during the genetic search process to generate new and better solutions, has so far been neglected in the rich and vast GA literature. In this work, five novel mating strategies inspired from the Darwinian evolutionary principle of "opposites-attract" are proposed to speed up the GA search process. The impact of the proposed mating strategies on the GA’s performance is tested on two well-established and complex testbed optimization problems from the domain of supervised classification: 1) the 1-NN Tuning problems, and 2) the Optimal Decision Forests problem. The results from rigorous experiments with various UCI data sets reveal that the proposed mating strategies both accelerate the GA search and lead to the discovery of better solutions. Moreover, these improvements come at the cost of only negligible additional computational overhead.</p>

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</description>

<author>Thiago S. Quirino</author>


</item>


<item>
<title>Impulsivity and Performance on a Music-Based Cognitive Rehabilitation Protocol in Persons with Alcohol Dependence</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/313</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/313</guid>
<pubDate>Sun, 06 May 2012 04:57:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this study was to examine the performance of individuals with alcohol dependence on a music-based cognitive rehabilitation protocol (MBCR), and to examine the relationship between degree of impulsivity and performance on the MBCR. Twenty adults with a primary diagnosis of alcohol dependence or polysubstance dependence participated in the study. Each participant first completed a 14-minute computerized assessment of impulsivity and then took part in one, 25-minute individual music session during which they completed four different MBCR exercises. Included in the MBCR were a Five-Finger exercise, Bordun exercise, Rhythm Repetition exercise, and Song Playing exercise. Participants’ performances on each of the MBCR exercises were scored using a rubric which included 1 (poor), 2 (fair), 3 (good), or 4 (excellent), for a total possible score of 16. Results indicated that participants’ impulsivity, as measured by Perseverations and Hit Reaction Time (Hit RT) on the Continuous Performance Test (Conners, 2007) as well as a Total Impulsivity composite score, was significantly greater than a normative group. In regards to performance on the MBCR, participants scored the highest on the Song Playing exercise, and performed most poorly on the Bordun exercise. A repeated measures ANOVA revealed that participants’ performance on the Song Playing exercise was significantly better than on the Five-Finger, Bordun, and Rhythm Repetition exercises. Bivariate correlation was used to examine relationships between scores of CPT impulsivity measures, Total Impulsivity, the rubric scores for the four MBCR exercises, and a composite Total Rubric score. Significantly negative correlations were found between Hit RT and Commission Errors, Perseverations and Total Impulsivity, Perseverations and the Rhythm Repetition exercise, and Total Impulsivity and the Rhythm Repetition exercise. Significantly positive correlations were found between Hit RT and the Song Playing exercise, Commission Errors and the Bordun exercise, the Five-finger exercise and Total Rubric, and the Rhythm Repetition exercise and Total Rubric score. Because all of the MBCR exercises required different types of attentional control, analysis of the relationships between participants’ impulsivity (as measured by Hit RT, Commission Errors, Perseverations, and Total Impulsivity) and performance on the MBCR implicate attention deficits as being related to impulsivity in individuals with alcohol dependence. Despite the presence of attention deficits, all participants were able to complete the entire MBCR protocol with scores of 2, 3, or 4 on all exercises. Therefore, music may be able to prime attention in individuals with alcohol dependence, which may be useful in addressing impulsivity in therapeutic treatment environments.</p>

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</description>

<author>Carolyn D. Dachinger</author>


</item>


<item>
<title>Estrogen Hydraulics</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/312</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/312</guid>
<pubDate>Sun, 06 May 2012 04:52:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Just as its name implies, Estrogen Hydraulics is a collection of poems and a short play that seeks to manhandle the reader’s preconceived notions about identity and its interface with the modern world. The collection churns memory and knowledge in a supersonic stereotype tumbler, and what emerges is not antithesis but rather synthesis of thought—a fusion of viewpoint with human emotion, humor, and consequence. Using pop culture as a lens that zooms in and out of focus on acceptance, self-awareness, and witness, Estrogen Hydraulics sees its role as both colorful commentary and historical documentation of what it means to be a child of the ’80s.</p>

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</description>

<author>Meredith Camel</author>


</item>


<item>
<title>Train Country</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/311</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/311</guid>
<pubDate>Sun, 06 May 2012 04:49:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>After a backyard boxing match results in the death of his older brother, Billy Salmonet impulsively hops a train out of town, bearing the blame for a murder he did not commit and leaving behind a web of secrets, rumor and conjecture. Miles from home, he constructs a new identity as a civil engineer in Ohio only to be discovered years later by Effie Cheever, a young girl from his hometown and the only one who knows his true identity. Effie’s compassion for the man she supposes to be a murderer, her wild fantasies, and her desire to forgive spiral her into a hasty romance with secrets at its core.  This novel considers the narratives we compose for those we love, the choices that come to define us, and the necessary fractures when the real meets the imagined.</p>

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</description>

<author>Lindsey Griffin</author>


</item>


<item>
<title>Predator-Specificity of Multimodal Alarm Signals in the Eastern Gray Squirrel (Sciurus carolinensis)</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/736</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/736</guid>
<pubDate>Sun, 06 May 2012 04:18:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Communication is a fundamental biological phenomenon, necessary in many species for successful reproduction, social interactions, and predator avoidance. Understanding animal communication systems is therefore vital to our understanding of biology. One of the core attributes of any signaling system is the information contained in each signal. In this dissertation I first review the literature on the information contained in sciurid alarm calls, and note the dearth of knowledge about the presence or absence of predator-specific alarm calls in arboreal squirrels. Arboreal squirrels are closely related to ground squirrels, which have a variety of alarm calling systems, but seek refuge in trees like many primates that have been shown to use predator-specific calls. I then examine the alarm-signaling system of the eastern gray squirrel. Using field experiments I show that some, but not all, of their alarm signals contain information about predator type, specifically, whether a predator is approaching from the air or approaching on the ground. Unlike most studies of alarm signaling, which consider only alarm calls, I considered two signaling modalities, vocal signals and tail signals. When examining the entire alarm-signaling bout, the use of vocal and tail signals is associated with threat type. Of the three vocal alarms (kuks, quaas, and moans), only moans show predator specificity, being highly associated with aerial threats. Of the two tail signals used as alarms, twitches and flicks, only flicks show predator specificity, being associated with terrestrial threats. This is a unique case of two modalities being used to specify two threat types. When gray squirrels use alarm vocalizations, their alarm calling bouts can consist of kuks, quaas, and moans. Each calling bout could consist of one, two or all three vocal alarms. To examine the information contained in alarm calls about whether a threat is approaching aerially or terrestrially, I tested alarm calling bouts for an association of each signal type with threat type (aerial or terrestrial). If alarm calls function to communicate with conspecifics, the initial period of calling should be most relevant to squirrels seeking safety, so I focused on the initial 60s of calling. In this initial period the presence of kuks is associated with terrestrial threats, as is the presence of quaas. Moans are exclusively used in response to aerial threats. Initial rates of kuks, moans, and calls in general are also associated with threat type, but rate of quaas is not. Kuks and quaas are usually mixed within calling bouts and are both associated with terrestrial threats. I then examined squirrels’ responses to playbacks of modified calling bouts to test whether kuks and quaas elicit different degrees of antipredator behavior. Kuks and quaas appear to have a similar effect on conspecific behavior, although rate of calling may have a strong impact on response. Additionally, white noise bursts of equal duration to alarm vocalizations appear to be functionally equivalent to kuks or quaas; any sudden, broadband noise may be sufficient to increase alert behavior. This broad acoustic criterion for eliciting a response may facilitate eavesdropping on heterospecific alarm calls, which are often abrupt, broadband sounds. In combination, this work demonstrates an alarm-signaling system in which signalers use varimodal (either unimodal or multimodal) signals, with the amount of information about predator type contained in their signal varying from general alarms to highly specific alarms. This study is the first to test for predator specificity in multiple signaling modalities; the differential use of tail signals as terrestrial threat alarms and vocal signals as aerial threat alarms highlights the importance of examining multiple signaling modalities in other species.</p>

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</description>

<author>Thaddeus R. McRae</author>


</item>


<item>
<title>Role of Deimination for Protein Synthesis in Neuronal Cells</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/735</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/735</guid>
<pubDate>Sun, 06 May 2012 04:09:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Deimination refers to conversion of protein-bound arginine into citrulline. In contrast to global hyper-deimination in the brain and eyes, we have found local hypo-deimination in the retinal ganglion cell layer of patients and in a transgenic mouse model of multiple sclerosis. REF, an RNA and export binding protein, was specifically found to undergo loss of deimination in multiple sclerosis, resulting in functional changes in RNA binding.  mRNAs for SNARE complex and mitochondrial ATPase complex are enriched by deiminated REF. We confirmed the presence of REF in dendritic site and mitochondrial surface. Only the deiminated form of REF interacts with the eIF4F complex in both cytosolic and mitochondrial surface. Down-regulation of deimination or REF results in decreased neurite outgrowth and reduced the mitochondrial ATP synthase activity compared to the control. Restoration of deimination in the optic nerve results in dramatic improvement in visual function and elongation of neurite length in isolated neurons.  Together, these findings support a key role for protein deimination in dendritic protein synthesis and mitochondrial mRNA transport and identify a potential new pathway for early events in the pathogenesis of multiple sclerosis and possibly other neurodegenerative diseases.</p>

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</description>

<author>Di Ding</author>


</item>


<item>
<title>Concerto Blue, for Classical Guitar</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/734</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/734</guid>
<pubDate>Sun, 06 May 2012 04:02:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>Concerto Blue is a three-movement concerto for classical guitar and medium-sized orchestra. Aesthetic considerations of this piece involve taking essential ingredients that define the blues and de-contextualizing them into an artful collage. The work celebrates the blues guitar by utilizing elements and phrasing that span the tradition of the blues from its acoustic foundation in the Mississippi Delta to the formation and expansion of rock music. The concerto is scored for an amplified classical guitar that can compete sonically with the orchestra as they are often pitted against each other for an affect reminiscent of a concerto grosso within the Baroque tradition as well as an old fashion duel often found in the blues tradition. A loop pedal for the guitar is called for in the score to create textures that rival the orchestra in volume and density. The entire work in three movements can be seen as a sonata form while a traditional blues progression is used as a basis for tonal polarity. Near the end of the third movement, the guitar is given a highly technical cadenza. The orchestra then merges with the guitar at the end of the cadenza to create a sentimental conclusion. The live loop effect and extended techniques offer a contribution to the evolution of the guitar concerto genre.</p>

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</description>

<author>Bruce H. Johnston</author>


</item>


<item>
<title>Comparison of Near Surface and Column-Integrated Atmospheric Aerosol Optical Properties</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/733</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/733</guid>
<pubDate>Sun, 06 May 2012 03:56:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Optical and chemical properties of size-resolved aerosols in near-surface air at Tudor Hill, Bermuda were measured between July 2006 and June 2009. Vertical distributions of aerosol backscattering and column-averaged aerosol optical properties were characterized with a Micro-pulse lidar (MPL) and a CIMEL automated sun-sky radiometer. The chemical species in size-segregated aerosols in marine air were compared with the surface level aerosol optical properties. The aerosol concentration, along with chemical components, was compared with the surface level wind speed and showed a significant correlation with the sea salt components. The non-sea salt components such as non-sea salt sulfate and ammonium did not show a correlation with the surface level wind speed. A comparison between scattering data at surface level with the extinction coefficient at the lowest altitude bin (75m) from the lidar inversion shows a consistent correlation but is quantitatively different. This quantitative discrepancy was explained based on the hygroscopic growth due to differences in relative humidity in measurement conditions.  Aerosol optical properties measured near the surface were often significantly correlated with those averaged over the column.  These include scattering by near-surface bulk aerosol at 530 nm versus column aerosol optical depth (AOD), near-surface sub-µm scattering fraction versus column averaged sub-µm scattering fraction, and the average angstrom exponent over column and lidar ratio derived using column integrated size distribution and complex refractive index. We also found that the single scattering albedo (ωo) measured at the surface by combining daily averages of the aerosol absorption and aerosol light scattering were in the same range as the instantaneous ωo retrieved for the column. The relative contribution of submicron aerosol light scattering to total aerosol light scattering is slightly higher in the column relative to the surface. Surface level wind speed was found to have a more important affect on bulk aerosol light scattering at the surface than in column.</p>

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</description>

<author>Rudra P. Aryal</author>


</item>


<item>
<title>A Conductor&apos;s Guide to André Campra&apos;s Messe de Requiem</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/732</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/732</guid>
<pubDate>Sun, 06 May 2012 03:56:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>André Campra (1660-1744) lived and worked in France during the transitional period between Jean-Baptiste Lully (1632-1687) and Jean-Philippe Rameau (1683-1764). He earned a reputation as one of France’s most accomplished composers through his sacred and secular works, including twenty-six major works for Paris Opera, three masses, fifty-three grands motets, and sixty solo motets. The Messe de Requiem’s twentieth-century discovery renewed interest in the Frenchman’s oeuvre. European musicians have embraced André Campra’s Requiem in recent decades, but American ensembles have been slow to engage in performances of Campra’s work. This document attempts to make this masterwork more accessible to modern musicians. It provides biographical information on the composer; a history of the Messe de Requiem; a structural overview; an analysis of each movement; performance practice suggestions; a French-Latin pronunciation guide; an instrumental and vocal usage chart; and a new performance edition for SATBB chorus and orchestra that makes the work more practical for the use of the performer.</p>

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</description>

<author>Jeb Mueller</author>


</item>


<item>
<title>The Flute Music of Franco Donatoni: A Performance Guide</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/731</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/731</guid>
<pubDate>Sat, 05 May 2012 14:46:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this doctoral essay is to create a performer’s guide for two pieces by Italian composer Franco Donatoni: Fili for Flute and Piano (1981) and Midi: due pezzi per flauto (1989). Despite being one of the most prolific composers of music in the mid- to late-twentieth century, Franco Donatoni has been largely overlooked by both scholars and performers. This is especially true in the United States, where Donatoni’s flute music is not well known. This doctoral essay includes a brief biography of Franco Donatoni as well as detailed analysis and performance suggestions for Fili and Midi. Theoretical, technical, as well as stylistic issues are addressed in depth. Through this essay, Donatoni’s flute music will become more accessible to the performer, leading to more performances of these works.</p>

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</description>

<author>Farah Zolghadr</author>


</item>


<item>
<title>The Index Bundle for a Family of Dirac-Ramond Operators</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/730</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/730</guid>
<pubDate>Sat, 05 May 2012 14:45:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>String theoretic considerations imply the existence of a Dirac-like operator, known as the Dirac-Ramond operator, on the free loop space of a closed string manifold.  We study the index bundle of the Dirac-Ramond operator associated with a family π : Z → X of closed spin manifolds.  We work instead with a formal version of the operator, the usual Dirac operator twisted by a certain formal q-series of vector bundles.  Its index bundle is an element of K(X)[[q]]. In the case where the total space Z is a string manifold, we show that the Chern character of this index bundle has certain modular properties.  We then use the modularity to derive some explicit formulas for the Chern character of this index bundle. We also show that these formulas identify the index bundle with an L(E₈) bundle in a special case.</p>

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</description>

<author>Christopher L. Harris</author>


</item>


<item>
<title>The Comparison of Body Composition, Eating Habits, Exercise Habits, and High Risk Behaviors in a Tri-Racial Group of Division I Collegiate Female Athletes</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/729</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/729</guid>
<pubDate>Sat, 05 May 2012 14:37:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Given the increased participation in competitive sports and athletics among women, there is a greater number of issues related to body weight concerns, eating and exercise habits, as well as high risk behaviors, which are particularly evident in female athletes.  There are also many more minority women participating in competitive sports, presenting a greater need to examine these issues among a more diverse population of competitive female athletes.  Hispanic American (HA) athletes in particular, represent a growing segment of the athletic population that is in need of more information regarding their exercise-related behaviors.  The aim of this study was to compare and examine body composition, eating habits, exercise habits, and high risk behavior patterns in a tri-racial group of Caucasian American (CA), African American (AA), and HA athletes.  Methods:  A total of 168 female collegiate athletes were recruited for study which included 82 CA athletes, 35 AA athletes, and 51 HA athletes.  Physical characteristics including body mass index (BMI), waist circumference (WAIST), and percent body fat were examined in all athletes.  In addition, all athletes completed a self-administered modified Youth Risk Behavior Survey and Eating Attitudes Test – 26 (EAT-26).   Logistic regression analyses was used to determine the influence of BMI and race on categorical variables related to body weight concerns, eating and exercise habits, and high risk behaviors.  Results:  BMI significantly contributed to the variance in categorical variables related to body weight concerns (p<0.01 for all), eating habits (p<0.05), scores on the EAT-26 (p<0.001), and high- risk behaviors (p<0.05 for all).  Race significantly contributed to the variance in physical characteristics (p<0.01 for all) and categorical variables related to body weight concerns (p<0.05 for all), eating habits (p<0.05 for all), exercise habits (p<0.05 for all), and high risk behaviors (p<0.05 for all).  BMI and race together contributed significantly to the variance in categorical variables related to body weight concerns (p<0.01 for all), eating habits (p<0.01), exercise habits (p<0.01), and high risk behaviors (p<0.05 for all).   Conclusion:  Our study demonstrated that BMI significantly contributed to behavioral characteristics associated with body weight concerns, eating and exercise habits, as well as high- risk behaviors.  This is similar to what has been found in non-athletic adolescent girls and young adult women.  Specifically, HA female athletes demonstrated significantly different behavior characteristics than CA and AA female athletes.  Our study reinforces the need for more research in this growing segment of minority athletes.</p>

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</description>

<author>Yi-Tzu Kuo</author>


</item>


<item>
<title>Structural Violence and Vulnerable Populations: Health and Health Care Utilization among Black, Female, Sex Workers in Miami, Florida</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/728</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/728</guid>
<pubDate>Sat, 05 May 2012 14:27:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>Vulnerable populations are affected by social ills resulting from unjust social, political, and economic systems.  The consequences of these structural inequalities may affect health care utilization patterns. I examined the health needs, barriers, and utilization of health care services among a sample of Black, female street-based sex workers in Miami, Florida, while exploring the impact of violence, both physical and structural, on utilization of health care services.  To do this, both quantitative and qualitative methods were applied.  I used focus group data and a grounded theory approach to illuminate health care experiences and the relationship between structural violence and health care utilization for this group of women.  For the quantitative portion, I used Andersen’s Behavioral Model for Vulnerable Populations to test which variables were most efficient in predicting utilization, as well as to test the effect of victimization on utilization.  Overall, results indicated that having a consistent and meaningful link or resource for accessing health care facilitates utilization for this group of women and determines future utilization behaviors. Vulnerable and traditional domains in Andersen’s model contributed to predicting health care utilization behaviors, particularly enabling and need variables; however, victimization had no effect on utilization.  From the qualitative data, the Experiential Model of Health and Health Care Utilization was constructed linking health definitions, goals, and experiences of seeking health care at one level, all of these to structural violence at a more abstract level and the general ideology that maintains a repressive system.  Recommendations for future research are included.</p>

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</description>

<author>Leah M. Varga</author>


</item>


<item>
<title>Social Media as a Relationship Strategy: Twitter’s Impact on Enhancing Brand Loyalty</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/310</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/310</guid>
<pubDate>Sat, 05 May 2012 14:17:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study looked into Twitter usage as represented by top U.S. retail corporations in a quantitative way. A content analysis was conducted comparing two groups of retail corporations — one came from the “top 100 customer loyalty brand leaders” as identified by Brand Keys (2011a), and the other came from the Fortune 500 retailers, but excluded from the top-100 loyalty leaders list.  This study aimed to find out the dominant purpose of Twitter usage by major U.S. retail industry companies, and to what extent the relationship maintenance strategies were incorporated in Twitter. In addition, the study aimed to test a proposed model that delineates relationship as a precursor of brand loyalty. The study results indicated Twitter as an important channel for corporate communication and relationship maintenance. It was found that for the retail industry, Twitter was mainly used for consumer relations. Access was the most widely used strategy (91.6%), followed by assurance (36.4%) and positivity (28.2%). In addition, the retailers in the brand loyalty leader group were discovered more inclined to use Twitter in a two-way communication manner, while the Fortune 500 group were more one-way oriented.  Meanwhile, two relationship maintenance strategies were found significantly more frequent in use in the brand loyalty leader group than the Fortune 500 group – positivity and assurance. Further more, evidence was found to support that the retail companies in the brand loyalty leader group utilized Twitter to a greater level as a communication tool than the Fortune 500 group.</p>

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</description>

<author>Zongchao Li</author>


</item>


<item>
<title>Impact of Accelerometry and Spirography Data Analysis of Essential Tremor on BOLD-fMRI Data Interpretation</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/309</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/309</guid>
<pubDate>Sat, 05 May 2012 14:11:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Essential Tremor (ET) is the most common neurological movement disorder, with slowly progressive symptoms that impact the patient's quality of life and ability to perform activities of daily living. Tremors in ET occur during kinetic, with two subtypes: postural tremors and kinetic tremors. Postural tremors appear when the arms are topically maintained in a position against gravity, whereas kinetic tremors appear during sustained voluntary movements such as writing or drawing. The underlying mechanisms of either tremor type are not known, and further work is needed to determine whether they are two manifestations of the same brain dysfunction, or consequences of different underlying causes. To further understand these disease manifestations, we employed functional magnetic resonance imaging (fMRI) in conjunction with quantitative tremor measures (accelerometry and spirography).</p>

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</description>

<author>Saman Sargolzaei</author>


</item>


<item>
<title>Band Music, A Handbook. A Comprehensive Catalog of Band Music Written Since 1995.</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/727</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/727</guid>
<pubDate>Sat, 05 May 2012 13:25:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this essay is to present wind band conductors with a comprehensive catalog of music written for the medium since the year 1995. This study provides new information and research that, to this date, only existed for orchestral, choral, and pop(s) music. For each work listed, this document provides its date of origin, duration, exact instrumentation, and publisher. There are a number of appendices that further classify the repertoire by composer, title, and duration. The document concludes with a detailed publisher listing, a catalog of numerous compositions about which information is not readily available, and a directory of composers for future study, consideration, and inclusion in this project. The data for this study are collected through three different methods. The primary method of gathering composition information is through viewing and reading specific composers’ and their publishers’ websites. The second method includes searching for specific music scores through numerous band libraries across the country. The third method is through correspondence with the actual composer with regard to specific pieces where information is not available through the initial two methods.  It is my intention to present band directors and their ensembles of varying abilities a valuable tool when selecting appropriate repertoire written in the last sixteen years.</p>

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</description>

<author>Christopher M. Cicconi</author>


</item>


<item>
<title>A Defense of Two-Level Ethical Theory</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/726</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/726</guid>
<pubDate>Sat, 05 May 2012 13:09:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation argues that the nature of love gives us reasons to accept a two-level ethical theory.  A two-level ethical theory recommends a view of the world that conflicts with the view of the theory itself.  Two-level theories face influential objections; the dissertation argues that changes in point of view over a life contain the basis of a reply to these objections.  The dissertation focuses in particular on changes in love and supports a defense of a two-level approach to ethics by developing and defending an original view of love.  Later chapters offer arguments about (1) the impact changes in love have on our well-being, and (2) recent disputes over whether specific theoretical approaches to ethics, such as virtue ethics and consequentialism, are two-level in objectionable ways.</p>

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</description>

<author>Daniel L. Cohen</author>


</item>


<item>
<title>The University of Miami Frost Wind Ensemble 1993-2012: Repertoire, Commissions, and Premieres</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/725</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/725</guid>
<pubDate>Sat, 05 May 2012 13:02:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>The scope and focus of this essay is the repertoire performed, commissioned, and premiered by the Frost Wind Ensemble during Gary Green’s tenure as Director of Bands at the University of Miami Frost School of Music, 1993 – present (2012). It includes a detailed catalog of all repertoire performed by the Frost Wind Ensemble in three different formats: by composer, by title, and also as a rendering of the actual concert programs. In addition to the chapters containing the various sorted repertoire catalogs, the essay devotes two chapters to chronological lists of works that have been commissioned (individually or through a consortium) or premiered by Mr. Green and the University of Miami Frost Wind Ensemble. This essay is a much-needed addition to wind-ensemble research regarding the University of Miami Frost Wind Ensemble’s influence and role in encouraging a significant and lasting repertoire for the medium. It is my hope that conductors, performers, and other interested parties will find this a useful resource not simply for information about pieces this ensemble has performed or commissioned, but as an account of how the University of Miami Frost Wind Ensemble serves as a model for others in approaching this work with passion, dedication, and commitment to only the best in music.</p>

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</description>

<author>Douglas L. Phillips</author>


</item>


<item>
<title>The Effect of Differential Item Functioning on Population Invariance of Item Response Theory True Score Equating</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/724</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/724</guid>
<pubDate>Sat, 05 May 2012 12:45:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>Population invariance in equating exists when the relationship between two scales is the same for two or more subpopulations of examinees and hence the function used to equate the scales is not dependent on subpopulations. A lack of equating invariance (i.e., equating dependence) leads to a situation whereby examinees having the same score on one scale, but belonging to different subpopulations, have different expected test scores on the corresponding equated scale. This situation results in an expected advantage for one or more subpopulations of examinees and hence is a concern for fairness in assessment and disaggregated accountability. Little is known about the causes of equating dependence, and the purpose of this study is to locate a source of this problem. It is hypothesized that differential item functioning manifested in the anchor items of an assessment will have an effect on population invariance of equating. Findings show that when differential item functioning varies across forms in a differential manner across subpopulations, population invariance of equating can be compromised. Under these conditions, an increase in equating dependence is associated with increases in magnitudes of the differential item functioning and, to a lesser degree, increases in the frequency of anchor items with differential item functioning. These effects can be problematic in conditions of both unidirectional and bidirectional differential item functioning, and can pose problems for subpopulations that have equal or different mean ability levels.</p>

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</description>

<author>Anne C. Huggins</author>


</item>


<item>
<title>Hierarchical Multi-Label Classification: Going Beyond Generalization Trees</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/723</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/723</guid>
<pubDate>Sat, 05 May 2012 12:38:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Traditional approach to automated classification assumes that each object should be assigned to only one out of two or more classes. However, some real-world applications digress from this generic scenario in two important ways. First, each example can belong to several classes simultaneously (multi-label classification). Second, the classes can be hierarchically ordered in the sense that some are more specific versions of others (hierarchical classification). Seeking to address both of these issues, the presented work deals with “hierarchical multi-label classification”. In non-hierarchical multi-label classification, literature survey indicates that good performance is achieved when a Support Vector Machine (SVM) is used to induce each class separately. This said, some experiments suggest that further improvement can be achieved by explicitly dealing with the problem of imbalanced training sets. The author proposes a solution in terms of a technique referred to as R-SVM; the idea is to re-adjust the SVM-hyperplane offset accordingly. Experiments in the first part of this dissertation rely on data from domains of text-categorization. More important, however, is then the second part that focuses on hierarchical multi-label classification. Here, the author proposes a new technique, HR-SVM, which constitutes a hierarchical extension of R-SVM proceeding in a top-down fashion with a new mechanism to correct errors propagated from classifiers at higher levels of the hierarchy. The system has been subjected to experiments with data from the field of gene function prediction. The results show that the new technique compares favorably with other existing approaches along various performance criteria.</p>

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</description>

<author>Peerapon Vateekul</author>


</item>


<item>
<title>Professional Socialization: Transition from the Classroom Setting to the Clinical Environment</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/722</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/722</guid>
<pubDate>Sat, 05 May 2012 12:38:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Background and Purpose.  Entry-level physical therapy students go through a distinct period of professional socialization in which they acquire the specialized knowledge, psychomotor skills and professional behaviors essential for effective and efficient patient care. Physical therapists practitioners agree that professionalism is an essential component of this process of socialization to the successful practice of physical therapy in the 21st century. Academic faculty and clinical instructors agree that appropriate affective skills are more difficult to promote, assess and model than cognitive or psychomotor skills. Evidence suggests that underdevelopment of professional behaviors is often the reason why students struggle with the transition from the classroom setting to the clinical environment and that engaging students in affective learning experiences is one of the most challenging experiences academicians and clinical instructors face. This qualitative study explored the professional socialization process from the perspective of academic faculty, clinical faculty and the entry-level doctor of physical therapy (DPT) students and the teachings fostering the development of professional behaviors in entry-level physical therapy professional education.  This qualitative study also explores the appropriateness of the Weidman, Twale, and Stein (2001) Socialization Framework conceptualizing the graduate and professional student socialization process as it applies to entry-level graduate physical therapy students. Subjects. The participants were eight academic faculty and nine clinical faculty associated with the academic and clinical programs of the University of Miami Physical Therapy Department, as well as 12 entry-level DPT students enrolled in this educational program. Methods. Using a phenomenology approach, the investigator conducted single case study interviews with 3 participants and focus groups with the other participants. This consisted of asking questions to explore the current perceptions about the process of professional socialization and development of professional behaviors in entry-level DPT students, and the appropriateness of the Weidman et al framework to conceptualize the socialization process as it applies to physical therapy. The behavioral constructs of professional responsibility, interpersonal skills and communication skills were used as benchmarks of professionalism. Interviews and focus group sessions were audiotaped and transcribed by a professional transcriptionist. Each participant completed a survey to gather demographic data. Qualitative and quantitative methods were used to analyze the data. Triangulation of the data and other research strategies ensured trustworthiness of the data. Results. Quantitative data was used to describe the participants. Qualitative data analysis led to the emergence of 8 themes: 1) professional behaviors develop over time, 2) knowledge acquisition develops over time, 3) skills in the affective domain encompass qualities that are critical in primary care physical therapy, 4) from implicit to explicit approach to Physical therapy education, 5) professional appearance, 6) socialization is a developmental process based on overlapping stages of identity and commitment: anticipatory stage (background), academic stage (formal and informal) and personal stage (outcome), 7) internalization of professional role into one’s identity happens over time, and 8) personal, academic and clinical experiences play an important role in the process of professional socialization. Discussion and Conclusion. The findings indicate that the process of professional socialization is vital for individuals pursuing physical therapy as a profession. The themes that emerged indicate that entry-level DPT students develop knowledge and professional behaviors over time. Engaging the entry-level DPT students in affective learning experiences focused around a set of expected skills and competencies is essential for effective patient care and the ability to practice as autonomous primary care practitioners. An explicit approach to education in the affective domain is essential when teaching today’s millennial students, and the modeling and teachings about professional appearance is an important aspect of professional practice.  In addition, entry-level graduate DPT students go through a process of socialization parallel to the Weidman, Twale and Stein (2001) Socialization Framework conceptualizing graduate and professional student socialization in higher education and this model can be applied to facilitate physical therapist professional education and entry-level graduates’ preparedness for the professional working life.</p>

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</description>

<author>Anna Katerina Tischenko-Osorno</author>


</item>


<item>
<title>The Effect of Verbal Versus Nonverbal Parent Cues on Children&apos;s Listening Skills</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/308</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/308</guid>
<pubDate>Sat, 05 May 2012 12:36:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>This research sought to find a relationship between parental verbal and nonverbal cues and children's focused listening skill. The data collection took place in February 2012 with children participating in the University of Miami MusicTime 3 program who were four to six years of age. Seventy-four children and parents participated in the study. A review of the literature established the basis for the theory that various types of parental cues and time enrolled in this music program could positively effect a child's focused listening skill. A child's focused listening checklist and verbal vs. nonverbal parental cue scale were devised to rate each child and parent videotaped during a MusicTime duple meter pattern activity.  Results showed that neither, parental cues, teacher cues or time enrolled in the program showed an effect on children's focused listening skills.</p>

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</description>

<author>Alaina J. Galliford Lorenzo</author>


</item>


<item>
<title>Assembly and Function of the Yersinia pestis YscKLQ Complex</title>
<link>http://scholarlyrepository.miami.edu/oa_theses/307</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_theses/307</guid>
<pubDate>Sat, 05 May 2012 12:36:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Yersinia pestis, the ethological agent of plague, uses the type III secretion system (T3SS) to inject effector proteins into eukaryotic cells.  Effector proteins termed Yersinia outer proteins (Yops) cause cytotoxicity in host cells and apoptosis in macrophages.  The T3S apparatus is a complex injectisome composed of 21 essential Yesinia secretion (Ysc) proteins.  T3S substrates are targeted for secretion by secretion signals and/or chaperone binding domains.  How these substrates interact with the T3S apparatus is not known.  In a recent study in Salmonella they found a “sorting platform” composed of the homologs to YscQ, YscK, and YscL in Y. pestis targets substrate/chaperone complexes to the T3S apparatus for orderly secretion.  We hypothesize that a similar sorting complex exists in Y. pestis and is composed of a YscKLQ complex and possibly the YscN ATPase and interacts with the N-terminal portion of YscD to deliver substrate/chaperone complexes to the T3S apparatus for secretion.  In this study, I investigate the YscKLQ complex and its interactions with the N-terminal portion of YscD and substrate/chaperone complexes.  We found that the N-terminal portion of YscD interacts directly or indirectly with YscQ and YscK and that YscK interacts with the components of the sorting complex, YscQ and YscL, along with T3S substrates.  Since the needle type substrate, YscF in Y. pestis, was not looked at in the Salmonella study, I decided to further investigate YscF and its two chaperones YscE and YscG.  We found that the YscE/YscG chaperone is not only important for the stabilization of YscF but also for the secretion of YscF.</p>

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</description>

<author>Kristian L. Richards</author>


</item>


<item>
<title>Molecular Ecology and Evolution of Reef Corals and their Algal Symbionts</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/720</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/720</guid>
<pubDate>Sat, 05 May 2012 12:28:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>Molecular approaches to the fields of taxonomy, systematics and population genetics are imperative in order to better understand the evolutionary history and ecological interactions among organisms. This dissertation utilized genetic techniques to address evolutionary and ecological questions in corals and octocorals at different levels of resolution, from ancient phylogenetic relationships to the relatively recent population dynamics of individuals within species in both the coral host and its algal endosymbionts (genus Symbiodinium). Collectively, this work: (1) demonstrates a novel use of genes involved in the calcification process to test hypotheses of morphological convergence in scleractinian corals; (2) helps reconcile contrasting morphological and molecular phylogenetic perspectives among closely related species of a gorgonian octocoral; and (3) elucidates the genetic connectivity, dispersal potential, host acquisition, and specificity between a reef coral and its algal symbionts. Results show that the phylogenetic history of two genes involved in calcification in scleractinian corals is complex and consists of species-specific gene duplications and losses. However, in at least some cases, these calcification gene phylogenies agreed with taxonomic hypotheses based on morphology, in contrast to standard molecular phylogenies of neutral genes not involved in calcification. Second, molecular data support calyx morphology as a valid systematic character among species within the gorgonian octocoral genus Pterogorgia, but do not corroborate branch morphology as a useful systematic character. In addition, hybridization and/or morphological plasticity likely play important roles in shaping the morphological species described within this genus. Finally, populations of the gorgonian octocoral Plexaura flexuosa and its algal symbiont, Symbiodinium B1, showed different genetic structure across the Florida reef tract and Caribbean. P. flexuosa displayed high genetic connectivity over distances up to ~1900 km, while Symbiodinium B1 showed clear population subdivisions among sites separated by <100 >km, as well as within sites (<100 >m). Despite this structure, local environmental pools of Symbiodinium B1 are genetically diverse, and there is evidence for limited dispersal of Symbiodinium vectored by the larval stage of their coral hosts over ecological timescales. Together, data from the host (P. flexuosa) and its symbiont suggest high resilience potential, mediated by a passive process of stochastic host acquisition and dispersal. Additionally, in contrast to the very high specificity previously reported for gorgonian octocorals and Symbiodinium, genotypic clones (and genetically similar genotypes) of P. flexuosa did not show specificity to particular genotypes of Symbiodinium B1, and vice versa. Future work should continue to further integrate molecular techniques to establish a more comprehensive understanding of the ecology and evolution of these important organisms and the ecosystems they build.</p>

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</description>

<author>Herman H. Wirshing</author>


</item>


<item>
<title>The Mighty Casey: A Study of the Performances and Editions of William Schuman&apos;s One-Act Opera</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/721</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/721</guid>
<pubDate>Sat, 05 May 2012 12:28:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>On May 4, 1953, William Schuman’s first opera The Mighty Casey, based on the Ernest Thayer poem Casey at the Bat, premiered at the Hartt School of Music in Hartford, Connecticut. While this debut performance and a subsequent portrayal of the work on the television program Omnibus in 1955 were critically unpopular, Schuman remained invested in the work’s success for decades to come. The composer consistently worked with individuals at G. Schirmer (the publisher of Casey), arrangers, editors, and conductors to rework the opera into: a four-hand piano arrangement of choral excerpts; a two-piano arrangement of the entire work; and a more critically successful cantata version of the opera (renamed Casey at the Bat), scored for symphonic instrumental forces. After discussing the relevant literature on The Mighty Casey, this essay examines the published editions, along with the work’s important premieres and recordings, and focuses on the unique aspects of each publication and performance. The document concludes with a discussion of suggested performance considerations for successful future productions. Ultimately, this paper aims to foster further study of the editions of The Mighty Casey, and to promote future performances of William Schuman’s unique composition.</p>

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</description>

<author>Jeffrey S. Stern</author>


</item>


<item>
<title>French Orientalism in Reynaldo Hahn&apos;s Series &quot;Orient&quot; from Le Rossignol Eperdu</title>
<link>http://scholarlyrepository.miami.edu/oa_dissertations/719</link>
<guid isPermaLink="true">http://scholarlyrepository.miami.edu/oa_dissertations/719</guid>
<pubDate>Sat, 05 May 2012 12:28:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Reynaldo Hahn, a Venezuelan-born French composer, is growing in popularity for his vocal repertoires in the American academia.  His piano works have been practically unknown on this continent until the late American pianist Earl Wild recorded a series of his piano works, Le Rossignol Eperdu, containing 53 solo piano compositions. Le Rossignol Eperdu is divided into four series, and the second suite entitled “Orient” drew particular attention from disc reviewers. Currently, there is no publication or dissertation written about Reynaldo Hahn’s solo piano compositions in English, which limits accessibility to Reynaldo Hahn’s piano music. The purpose of this research is to promote understanding of the highlighted piano pieces by Hahn, “Orient” from Le Rossignol Eperdu, by tracing the history of French Orientalism in music and by providing compositional analysis of each piece in his “Orient” series. I would like to add that my study of Orientalism in this essay is purely for academic purpose, and, by no means do I support the French imperialism in the past. This essay is not political, and it is meant to further both musical and aesthetic understanding of the selected piano pieces.</p>

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</description>

<author>Norito Irei</author>


</item>


<item>
<title>Synthesis and Characterisation of Poly(L-Lysine) for Directed Transfection of siRNA</title>
<link>http://epubs.rcsi.ie/mscrestheses/8</link>
<guid isPermaLink="true">http://epubs.rcsi.ie/mscrestheses/8</guid>
<pubDate>Sat, 05 May 2012 05:00:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>This work focuses primarily on the synthesis of the cell penetrating peptide poly(L-lysine). This 30mer peptide (K³º) has been shown to be extremely useful in delivery of genetic material to the cell for gene therapy. So far it has shown transgene expression of up to twelve weeks, using DNA, which was delivered to the brain.[l] Lung cells have also been success full transfected by ths method.[2,3]</p>
<p>In this research we aim to use a polymer conjugate of K³º for the delivery of small interfering RNA (siRNA), a new exciting alternative to gene therapy, which operates downstream in the transcription pathway, through modulation of mRNA to produce gene silencing. Once optirnised, it is hoped that PEGylated K³º can be used as a universal delivery agent for any number of siRNA therapeutics in vivo.</p>
<p>K³º can be classified as a 'difficult peptide sequence'. This so-called terminology is used in the literature to describe any peptide which cannot be synthesised by classical means, involving rvutine automated peptide synthesis.[4-7] Generally, automated synthesis is reliable to a length of approxiinately twenty residues[8], so it is not surprising that K³º has been difficult to make by these means.</p>
<p>Various methods were attempted towards the synthesis of K³º, including (i) modification of the standard automated procedure with double coupling from a PEG-polystyrene composite resin, (ii) stepwise synthesis of two unprotected fragments to be ligated orthogonal to amide bond chemistry, and (iii) the synthesis of protected fragments to be coupled in solution to form the amide bond. [8]</p>
<p>In the end, monitoring of the sequence assembly was used to overcome the limitations associated with the solid phase synthesis of this peptide and the polylyshe sequence was successfully elongated by this approach.</p>
<p>After a certain point, about 18 residues, the peptide begins to aggregate on the solid support, preventing the reagents from reaching and reacting with the N-terminal of the peptide. To overcome this aggregation, a resin with a high hydrophilic content and <strong><em></em></strong>a low substitution was chosen. The hydrophilicity of this resin repels the growing hydrophobic, protected chain. Furthermore the sparsity of linkers reduces the contact between adjacent chains. This NovaPEG Low Loading resin, combined with double coupling chemistry yielded the peptide K³º.</p>
<p>Other work included synthesis of host defence and cell penetrating peptide P17, peptide PEGylation by thiol-maleimide ligation and azo-modified amino acids for use in Click chemistry with alkynyl PEG.</p>

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</description>

<author>Sarah McCarthy</author>


</item>


<item>
<title>Prevalence of Psychiatric Morbidity and Behavioural Problems in 22q11.2DS: An Irish Population Study</title>
<link>http://epubs.rcsi.ie/mdtheses/22</link>
<guid isPermaLink="true">http://epubs.rcsi.ie/mdtheses/22</guid>
<pubDate>Sat, 05 May 2012 02:57:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>Introduction:</p>
<p>This population study examines the prevalence of psychiatric morbidity, behavioural difficulties, autistic and schizotypal features in a sample of individuals with 22q11.2DS and in their sibling controls.</p>
<p>Methods:</p>
<p>Forty-five individuals with 22q11.2DS and their 27 siblings were recruited and studied. Psychiatric morbidity was assessed by using the parent Diagnostic Interview Schedule for Children (DISC-P), Kiddie SADS-Present and Lifetime Version (K-SADPL) (psychotic supplement), Comprehensive Assessment of the At Risk Mental State (CAARMS), Schedule for Clinical Assessment in Neuropsychiatry (SCAN) and the parent Conners' rating scale. Behavioural difficulties were measured by the Strengths and Difficulties Questionnaire (SDQ) and the Child Behaviour Checklist (CBCL). The Social Responsiveness Scale (SRS) and the Social Communication Questionnaire (SCQ) were used to measure symptoms of autism. The Schizotypal Personality Questionnaire (SPQ) was used to measure for schizotypal features.</p>
<p>Results:</p>
<p>Children and adolescents with 22q11.2DS were found to have more internalising and externalising behaviour compared to their siblings; 25% of children and adolescents with 22q11.2DS had social problems within the clinical range. Individuals with (see Figure 1,2,3,4,5 & 6)</p>

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</description>

<author>Sarah E. Prasad</author>


</item>


<item>
<title>The studnt production system : a study of encoding knowledge in production systems</title>
<link>http://repository.cmu.edu/compsci/2182</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2182</guid>
<pubDate>Fri, 04 May 2012 20:12:14 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>Michael D. Rychener</author>


</item>


<item>
<title>A robotically-augmented walker for older adults</title>
<link>http://repository.cmu.edu/compsci/2181</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2181</guid>
<pubDate>Fri, 04 May 2012 20:12:06 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Many older adults use walkers to improve their stability and safety while walking. We have developed a robotically augmented walker to reduce fall risk and confusion, and to increase walker convenience and enjoyment. Using a modified version of the CARMEN navigation software suite [11], the walker is capable of parking itself and returning to the user when signaled by remote control. The system also supports navigation in large indoor environments by providing simple directions to target locations such as a cafeteria. The walker received positive reviews during informal testing with residents of a Pennsylvania residence facility for older adults."</p>

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</description>

<author>Jared Glover</author>


</item>


<item>
<title>An evolutionary resolution to the finitely repeated prisoner&apos;s dilemma paradox</title>
<link>http://repository.cmu.edu/compsci/2180</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2180</guid>
<pubDate>Fri, 04 May 2012 20:11:58 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Argument by backward induction forces us to conclude that two 'rational' players will defect on every turn of the Finitely Repeated Prisoner's Dilemma (FRPD) game, thus performing significantly worse than agents with imperfect rationality. When this game is treated from an evolutionary perspective, using the standard evolutionary model, we encounter a similar paradox: a population which cooperates through turn k can be invaded by a strategy which cooperates through turn k - 1, and this process continues until the population is dominated by defectors. However, though the strategy of continual defection is evolutionarily stable, it is inferior to nearly all other FRPD strategies: a bistable equilibrium occurs, in which a very small proportion of the other strategy can take over the population. Thus we propose and defend an alternative evolutionary model, a random invasion model in which 'evolutionary dominance' is used instead of Maynard Smith's invasion criteria. This model combines the Lamarckian spread of ideas through a population with Darwinian natural selection of the organisms adopting those ideas, and thus is a more reasonable model of communicating populations. When the new evolutionary model is applied to the Finitely Repeated Prisoner's Dilemma, we find that defectors dominate the population for very short FRPD games, but as game length increases, it becomes more and more certain that successful strategies will cooperate until near the end of the game. Defining rationality based on evolutionary fitness (or fictitious evolutionary play) using this model, we achieve a resolution to the Finitely Repeated Prisoner's Dilemma paradox. Additionally, the model can be generalized and applied to many other decision situations, and thus it serves as a possible standard for rational decision-making under uncertainty."</p>

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</description>

<author>Daniel B. Neill</author>


</item>


<item>
<title>Navigating computer science research through waves of privacy concerns : discussions among computer scientists at Carnegie Mellon University</title>
<link>http://repository.cmu.edu/compsci/2179</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2179</guid>
<pubDate>Fri, 04 May 2012 20:11:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Computer Science research and practice are raising growing privacy concerns among the public and government. Computer technology's increasing ability to capture, organize, interpret and share data about individuals raises questions about what privacy practices computer science researchers should adopt, if any. These issues are already very real in ongoing research projects in the School of Computer Science (SCS) at Carnegie Mellon University, from mining databases of individual transactions, to studying how people use the web, to mounting cameras in lounges, to building hallway robots that capture data about passers by, to building intelligent workstation assistants that learn user habits. This paper introduces the nature of privacy concerns often related to computer science research, explains potential benefits and risks (especially of abuse and misuse) and examines traditional and innovative methods for providing privacy assurances in research. Examples are provided from projects at Carnegie Mellon's School of Computer Science."</p>

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</description>

<author>Latanya Sweeney</author>


</item>


<item>
<title>A type system for well-founded recursion</title>
<link>http://repository.cmu.edu/compsci/2178</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2178</guid>
<pubDate>Fri, 04 May 2012 20:11:41 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "In the interest of designing a recursive module extension to ML that is as simple and general as possible, we propose a novel type system for general recursion over effectful expressions. The presence of effects seems to necessitate a backpatching semantics for recursion based on Scheme's. Our type system ensures statically that recursion is well-founded (that the body of a recursive expression will evaluate without attempting to access the undefined recursive variable), which avoids some unnecessary run-time costs associated with backpatching. To ensure well-founded recursion in the presence of multiple recursive variables and separate compilation, we track the usage of individual recursive variables, represented statically by 'names'. So that our type system may eventually be integrated smoothly into ML's, reasoning involving names is only required inside code that uses our recursive construct and does not need to infect existing ML code."</p>

	]]>
</description>

<author>Derek R. Dreyer et al.</author>


</item>


<item>
<title>That&apos;s AI? : a history and critique of the field</title>
<link>http://repository.cmu.edu/compsci/2177</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2177</guid>
<pubDate>Fri, 04 May 2012 20:11:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "What many AI researchers do when they say they are doing AI contradicts what some AI researchers say is AI. Surveys of leading AI textbooks demonstrate a lack of a generally accepted historical record. These surveys also show AI researchers as primarily concerned with prescribing ideal mathematical behaviors into computers -- accounting for 987 of 996 (or 99%) of the AI references surveyed. The most common expectation of AI concerns constructing machines that behave like humans, yet only 27 of 996, (or 2%) of the AI references surveyed were directly consistent with this description. Both approaches have shortcomings -- prescribing superior behavior into machines fails to scale to multiple tasks easily, while on the other hand, modeling human behaviors in machines can give results that are not always correct or fast. The discrepancy between the kind of work conducted in AI and the kind of work expected from AI cripples the ability to measure progress in the field."</p>

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</description>

<author>Latanya Sweeney</author>


</item>


<item>
<title>Simultaneous source location</title>
<link>http://repository.cmu.edu/compsci/2176</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2176</guid>
<pubDate>Fri, 04 May 2012 20:11:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We consider the problem of Simultaneous Source Location -- selecting locations for sources in a capacitated graph such that a given set of demands can be satisfied. We give an exact algorithm for trees and show how this can be combined with a result of Ra╠êcke to give a solution that exceeds edge capacities by at most O(log n log log n), where n is the number of nodes. On graphs of bounded treewidth, we show the problem is still NP-Hard, but we are able to give a PTAS with at most O(1 + [epsilon]) violation of the capacities, or a (k + 1)-approximation with exact capacities, where k is the treewidth and [epsilon] can be made arbitrarily small."</p>

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</description>

<author>Konstantin Andreev</author>


</item>


<item>
<title>A fast multi-resolution method for detection of significant spatial overdensities</title>
<link>http://repository.cmu.edu/compsci/2175</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2175</guid>
<pubDate>Fri, 04 May 2012 20:11:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Given an N x N grid of squares, where each square s[subscript ij] has a count c[subscript ij] and an underlying population p[subscript ij], our goal is to find the square region S with the highest density, and to calculate the significance of this region by Monte Carlo testing. Any density measure D, which depends on the total count and total population of the region, can be used. For example, if each count c[subscript ij] represents the number of disease cases occurring in that square, we can use Kulldorff's spatial scan statistic D[subscript K] to find the most significant spatial disease cluster. A naive approach to finding the region of maximum density would be to calculate the density measure for every square region: this requires O(RN┬│) calculations, where R is the number of Monte Carlo replications, and hence is generally computationally infeasible. We present a novel multi-resolution algorithm which partitions the grid into overlapping regions, bounds the maximum score of subregions contained in each region, and prunes regions which cannot contain the maximum density region. For sufficiently dense regions, this method finds the maximum density region in optimal O(RN┬▓) time, and in practice it results in significant (10-200x) speedups as compared to the naive approach."</p>

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</description>

<author>Daniel B. Neill et al.</author>


</item>


<item>
<title>ARA : formal analysis</title>
<link>http://repository.cmu.edu/compsci/2174</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2174</guid>
<pubDate>Fri, 04 May 2012 20:11:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "In real world problems, time for deliberation is often limited. Anytime algorithms are beneficial in these conditions as they usually find a first, possibly highly suboptimal, solution very fast and then continually work on improving the solution until allocated time expires. While anytime algorithms are popular, existing anytme search methods are unable to provide a measure of goodness of their results. In this paper we propose the ARA* algorithm. ARA* is an anytime heuristic search which tunes its performance bound based on available search time. It starts by finding a suboptimal solution quickly using a loose bound, then tightens the bound progressively as time allows. Given enough time it finds a provably optimal solution. In addition to the theoretical analysis we demonstrate the practical utility of ARA* with experiments on a simulated robot kinematic arm and dynamic path planning problem for an outdoor rover."</p>

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</description>

<author>Maxim Likhachev et al.</author>


</item>


<item>
<title>The eXtreme programming (XP) metaphor and software architecture</title>
<link>http://repository.cmu.edu/compsci/2173</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2173</guid>
<pubDate>Fri, 04 May 2012 20:11:00 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "The Metaphor is intended to contribute to the Agile Programming value of communication. Previously, some of the author [sic] studied the Metaphor as a means of communication among team members and between them and clients. This paper examines the Metaphor's contribution to the software architecture. Both experiments seem to reveal that the Metaphor has poor effectiveness."</p>

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</description>

<author>James Herbsleb et al.</author>


</item>


<item>
<title>Finding lists of people on the Web</title>
<link>http://repository.cmu.edu/compsci/2172</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2172</guid>
<pubDate>Fri, 04 May 2012 20:10:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Among the vast amounts of personal information published on the World Wide Web ('Web') and indexed by search engines are lists of names of people. Examples include employees at companies, students enrolled in universities, officers in the military, law enforcement personnel, members of social organizations, and lists of acquaintances. Knowing who works where, attends what, or affiliates with whom provides strategic knowledge to competitors, marketers, and government surveillance efforts. However, finding online rosters of people does not lend itself to keyword lookup on search engines because the keywords tend to be common expressions such as 'employees' or 'students.' A typical search often retrieves hundreds of Web pages requiring many hours of human inspection to locate a page containing a list of names. As a result, people may falsely believe online rosters provide more privacy than they do. This paper presents RosterFinder, a set of simple algorithms for locating Web pages that consist predominately of a list of names. The specific names are not known beforehand. RosterFinder works by identifying rosters from candidate Web pages based on the ratio of distinct known names to distinct words appearing in the page. Accurate classification by RosterFinder depends on the set of names used. Results are reported on real Web pages using: (1) dictionary lookup employing a limited set of known names; and, (2) dictionary lookup on utilizing an extensive set of known names. Privacy implications are discussed using the example of FERPA and online student rosters."</p>

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</description>

<author>Latanya Sweeney</author>


</item>


<item>
<title>A subspace approach to layer extraction, patch-based SFM, and video compression</title>
<link>http://repository.cmu.edu/compsci/2171</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2171</guid>
<pubDate>Fri, 04 May 2012 20:10:43 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Representing videos with layers has important applications such as video compression, motion analysis, 3D modeling and rendering. This thesis proposes a subspace approach to extracting layers from video by taking advantages of the fact that homographies induced by planar patches in the scene form a low dimensional linear subspace. In the subspace, layers in the input images are mapped onto well-defined clusters, and can be reliably identified by a standard clustering algorithm (e.g., mean-shift). Global optimality is achieved since both spatial and temporal redundancy are simultaneously taken into account, and noise can be effectively reduced by enforcing the subspace constraint. The existence of subspace also enables outlier detection, making the subspace computation robust. Based on the subspace constraint, we propose a patch-based scheme for affine structure from motion (SFM), which recovers the plane equation of each planar patch in the scene, as well as the camera epipolar geometry. We propose two approaches to patch-based SFM: (1) factorization approach; and (2) layer based approach. Patch-based SFM provides a compact video representation that can be used to construct a high quality texture map for each layer. We plan to apply our approach to generating Video Object Planes (VOPs) defined by MPEG-4 standard. VOP generation is a critical but unspecified step in MPEG-4 standard. Our motion model for each VOP consists of a global planar motion and localized deformations, which has a closed-form solution. Our goals are: (1) combining different low level cues to model VOPs; and (2) extracting VOPs that undergo more complicated motion (non-planar or non-rigid)."</p>

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</description>

<author>Qifa Ke et al.</author>


</item>


<item>
<title>A modal calculus for effect handling</title>
<link>http://repository.cmu.edu/compsci/2170</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2170</guid>
<pubDate>Fri, 04 May 2012 20:10:35 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "In their purest formulation, monads are used in functional programming for two purposes: (1) to hygienically propagate effects, and (2) to globalize the effect scope -- once an effect occurs, the purity of the surrounding computation cannot be restored. As a consequence, monadic typing does not provide very naturally for the practically important ability to handle effects, and there is a number of previous works directed toward remedying this deficiency. It is mostly based on extending the monadic framework with further extra-logical constructs to support handling. In this paper we adopt a different approach, founded on the observation of Pfenning and Davies that an abstract monad can be decomposed in terms of modal operators for possibility [diamond] and necessity [square]. Our idea is to use the [square] modality (which is a comonad) for hygienic propagation of effects, and leave the globalization of effect scope to [diamond]. Then the effects which admit a natural notion of handling can be encoded using [square]; since they are not global, there is no need to push them under [diamond]. Based on this idea, we develop a general framework for effect handling systems, and obtain novel calculi for exceptions, catch-and-throw and composable continuations as specific instantiations."</p>

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</description>

<author>Aleksandar Nanevski</author>


</item>


<item>
<title>A Markov model for the acquisition of morphological structure</title>
<link>http://repository.cmu.edu/compsci/2169</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2169</guid>
<pubDate>Fri, 04 May 2012 20:10:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We describe a new formalism for word morphology. Our model views word generation as a random walk on a trellis of units where each unit is a set of (short) strings. The model naturally incorporates segmentation of words into morphemes. We capture the statistics of unit generation using a probabilistic suffix tree (PST) which is a variant of variable length Markov models. We present an efficient algorithm that learns a PST over the units whose output is a compact stochastic representation of morphological structure. We demonstrate the applicability of our approach by using the model in an allomorphy decision problem."</p>

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</description>

<author>Leonid Kontorovich et al.</author>


</item>


<item>
<title>Maximal lattice overlap in example-based machine translation</title>
<link>http://repository.cmu.edu/compsci/2168</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2168</guid>
<pubDate>Fri, 04 May 2012 20:10:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Example-based Machine Translation (EBMT) retrieves pre-translated phrases from a sentence-aligned bilingual training corpus to translate new input sentences. EBMT uses long pre-translated phrases effectively but is subject to disfluencies at phrasal translation boundaries. We address this problem by introducing a novel method that exploits overlapping phrasal translations and the increased confidence in translation accuracy they imply. We specify an efficient algorithm for producing translations using overlap. Finally, our empirical analysis indicates that this approach produces higher quality translations than the standard method of EMBT in a peak-to-peak comparison."</p>

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</description>

<author>Rebecca Hutchinson</author>


</item>


<item>
<title>Efficient consistency for erasure-coded data via versioning servers</title>
<link>http://repository.cmu.edu/compsci/2167</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2167</guid>
<pubDate>Fri, 04 May 2012 20:10:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This paper describes the design, implementation and performance of a family of protocols for survivable, decentralized data storage. These protocols exploit storage-node versioning to efficiently achieve strong consistency semantics. These protocols allow erasure-codes to be used that achieve network and storage efficiency (and optionally data confidentiality in the face of server compromise). The protocol family is general in that its parameters accommodate a wide range of fault and timing assumptions, up to asynchrony and Byzantine faults of both storage-nodes and clients, with no changes to server implementation or client-server interface. Measurements of a prototype storage system using these protocols show that the protocol performs well under various system model assumptions, numbers of failures tolerated, and degrees of reader-writer concurrency."</p>

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</description>

<author>Garth R. Goodson</author>


</item>


<item>
<title>Exposing and exploiting internal parallelism in MEMS-based storage</title>
<link>http://repository.cmu.edu/compsci/2166</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2166</guid>
<pubDate>Fri, 04 May 2012 20:10:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "MEMS-based storage has interesting access parallelism features. Specifically, subsets of a MEMStore's thousands of tips can be used in parallel, and the particular subset can be dynamically chosen. This paper describes how such access parallelism can be exposed to system software, with minimal changes to system interfaces, and utilized cleanly for two classes of applications. First, background tasks can utilize unused parallelism to access media locations with no impact on foreground activity. Second, two-dimensional data structures, such as dense matrices and relational database tables, can be accessed in both row order and column order with maximum eficiency. With proper table layout, unwanted portions of a table can be skipped while scanning at full speed. Using simulation, we explore performance features of using this device parallelism for an example application from each class."</p>

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</description>

<author>Steven W. Schlosser</author>


</item>


<item>
<title>Lachesis : robust database storage management based on device-specific performance characteristics</title>
<link>http://repository.cmu.edu/compsci/2165</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2165</guid>
<pubDate>Fri, 04 May 2012 20:09:53 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Database systems work hard to tune I/O performance, but they do not always achieve the full performance potential of modern disk drives. Their abstracted view of storage components hides useful device-specific characteristics, such as disk track boundaries and advanced built-in firmware algorithms. This paper presents a new storage manager architecture, called Lachesis, that exploits a few observable device-specific characteristics to achieve more robust performance. Most notably, it enables efficiency nearly equivalent to sequential streaming even in the presence of competing I/O traffic. With automatic adaptation to device characteristics, Lachesis simplifies manual configuration and restores optimizer assumptions about the relative costs of different access patterns expressed in query plans. Based on expriments with both IBM DB2 and an implementation inside the Shore storage manager, Lachesis improves performance of TPC-H queries on average by 10% when running on dedicated hardware. More importantly, it speeds up TPC-H by up to 3X when running concurrently with an OLTP workload, which is simultaneously improved by 7%."</p>

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</description>

<author>Jiri Schindler et al.</author>


</item>


<item>
<title>Selecting the right data distribution scheme for a survivable storage system</title>
<link>http://repository.cmu.edu/compsci/2164</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2164</guid>
<pubDate>Fri, 04 May 2012 20:09:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Survivable storage system design has become a popular research topic. This paper tackles the difficult problem of reasoning about the engineering trade-offs inherent in data distribution scheme selection. The choice of an encoding algorithm and its parameters positions a system at a particular point in a complex trade-off space between performance, availabilty, and security. We demonstrate that no choice is right for all systems, and we present an approach to codifying and visualizing this trade-off space. Using this approach, we explore the sensitivity of the space to system characteristics, workload, and desired levels of security and availability."</p>

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</description>

<author>Jay J. Wylie</author>


</item>


<item>
<title>Computing the volume element of a family of metrics on the multinomial simplex</title>
<link>http://repository.cmu.edu/compsci/2163</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2163</guid>
<pubDate>Fri, 04 May 2012 20:09:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We compute the differential volume element of a family of metrics on the multinomial simplex. The metric family is composed of pull-backs of the Fisher information metric through a continuous group of transformations. This note complements the paper by Lebanon [3] that describes a metric learning framework and applies the results below to text classification."</p>

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</description>

<author>Guy Lebanon</author>


</item>


<item>
<title>Scaling properties of the internet graph</title>
<link>http://repository.cmu.edu/compsci/2162</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2162</guid>
<pubDate>Fri, 04 May 2012 20:09:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "As the Internet grows in size, it becomes crucial to understand how the speeds of links in the network must improve in order to sustain the pressure of new end-nodes being added each day. Although the speeds of links in the core and at the edges roughly improve according to Moore's law, this improvement alone might not be enough. Indeed, the structure of the Internet graph and routing in the network might necessitate much faster improvements in the speeds of key links in the network. In this paper, using a combination of analysis and extensive simulations, we show that the worst congestion in the Internet in fact scales poorly with the network size (n[superscript 1+[omega](1)], where n is the number of nodes), when shortest-path routing is used. We also show, somewhat surprisingly, that policy-based routing does not exacerbate the maximum congestion when compared to shortest-path routing. Our results show that it is crucial to identify ways to alleviate this congestion to avoid some links from being perpetually congested. To this end, we show that the congestion scaling properties of the Internet graph can be improved dramatically by introducing moderate amounts of redundancy in the graph in terms of parallel edges between pairs of adjacent nodes."</p>

	]]>
</description>

<author>Aditya Akella</author>


</item>


<item>
<title>Minmax payoffs of a location game</title>
<link>http://repository.cmu.edu/compsci/2161</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2161</guid>
<pubDate>Fri, 04 May 2012 20:09:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We consider a two-player, sequential location game, with n stages. At each stage, players 1 and 2 choose locations from a feasible set in sequence. After all moves are made, consumers each purchase one unit of the good from the closest location. Since player 1 has a natural first-mover disadvantage here (player 2 can obtain a payoff of 1/2 just by replicating player 1's moves), we examine her minmax payoff. When the number of stages is known to both players we show that (i) if the feasible locations form a finite set in R[superscript d], player 1 must obtain at least 1/d+1 in the single-move game (ii) in the original Hotelling game (uniformly distributed consumers on the unit interval), player 1 obtains 1/2 even in the multiple stage game. However, player 1's minmax payoff suffers if she does not know the number of moves, but player 2 does. In the Hotelling game, where the number of stages is either 1 or 2, player 1's payoff falls to 5/12. If she has no information at all about n, we provide a lower bound for her minmax payoff: it must at least equal half the payoff of the single-stage game."</p>

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</description>

<author>Shuchi Chawla</author>


</item>


<item>
<title>Lowering the barriers to programming : a survey of programming environments and languages for novice programmers</title>
<link>http://repository.cmu.edu/compsci/2160</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2160</guid>
<pubDate>Fri, 04 May 2012 20:09:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Since the early 1960's, researchers have built a number of programming languages and environments with the intention of making programming accessible to a larger number of people. This paper presents a taxonomy of languages and environments designed to make programming more accessible to novice programmers of all ages. The systems are organized by their primary goal, either to teach programming or to use programming to empower their users, and then by the authors' approach to making learning to program easier for novice programmers. The paper explains all categories in the taxonomy, provides a brief description of the systems in each category, and suggests some avenues for future work in novice programming environments and languages."</p>

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</description>

<author>Caitlin Kelleher et al.</author>


</item>


<item>
<title>A two-tiered software architecture for automated tuning of disk layouts</title>
<link>http://repository.cmu.edu/compsci/2159</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2159</guid>
<pubDate>Fri, 04 May 2012 20:09:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Many heuristics have been developed for adapting on-disk data layouts to expected and observed workload characteristics. This paper describes a two-tiered software architecture for cleanly and extensibly combining such heuristics. In this architecture, each heuristic is implemented independently and an adaptive combiner merges their suggestions based on how well they work in the given environment. The result is a simpler and more robust system for automated tuning of disk layouts, and a useful blueprint for other complex tuning problems such as cache management, scheduling, data migration, and so forth."</p>

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</description>

<author>Brandon Salmon</author>


</item>


<item>
<title>A human organization analogy for self-* systems</title>
<link>http://repository.cmu.edu/compsci/2158</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2158</guid>
<pubDate>Fri, 04 May 2012 20:08:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "The structure and operation of human organizations, such as corporations, offer useful insights to designers of self-* systems (a.k.a. self-managing or automatic). This paper explores the analogy, and describes the design of a self-* storage system that borrows from it."</p>

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</description>

<author>John D. Strunk et al.</author>


</item>


<item>
<title>Behavioral consistency of C and Verilog programs using bounded model checking</title>
<link>http://repository.cmu.edu/compsci/2157</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2157</guid>
<pubDate>Fri, 04 May 2012 20:08:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We present an algorithm that checks behavioral consistency between an ANSI-C program and a circuit given in Verilog using Bounded Model Checking. Both the circuit and the program are unwound and translated into a formula that is satisfiable if and only if the circuit and the code disagree. The formula is then checked using a SAT solver. We are able to translate C programs that make use of side effects, pointers, dynamic memory allocation, and loops with conditions that cannot be evaluated statically. We describe experimental results on various reactive circuits and programs, including a small processor given in Verilog and its Instruction Set Architecture given in ANSI-C."</p>

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</description>

<author>Edmund Clarke et al.</author>


</item>


<item>
<title>A Boolean approach to unbounded, fully symbolic model checking of timed automata</title>
<link>http://repository.cmu.edu/compsci/2156</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2156</guid>
<pubDate>Fri, 04 May 2012 20:08:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We present a new approach to unbounded, fully symbolic model checking of timed automata that is based on an efficient translation of quantified separation logic to quantified Boolean logic. Our technique preserves the interpretation of clocks over the reals and can check any property expressed in the timed [mu] calculus. The core operations of eliminating quantifiers over real variables and deciding separation logic are respectively translated to eliminating quantifiers on Boolean variables and checking Boolean satisfiability (SAT). We can thus leverage well-known techniques for Boolean formulas, including Binary Decision Diagrams (BDDs) and recent advances in SAT and SAT-based quantifier elimination. We present preliminary empirical results for a BDD-based implementation of our method."</p>

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</description>

<author>Sanjit A. Seshia et al.</author>


</item>


<item>
<title>Towards higher disk head utilization : extracting &quot;free&quot; bandwidth from busy disk drives</title>
<link>http://repository.cmu.edu/compsci/2155</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2155</guid>
<pubDate>Fri, 04 May 2012 20:08:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Freeblock scheduling is a new approach to utilizing more of disks' potential media bandwidths. By filling rotational latency periods with useful media transfers, 20[50% [sic] of a never-idle disk's bandwidth can often be provided to background applications with no effect on foreground response times. This paper describes freeblock scheduling and demonstrates its value with two concrete applications: free segment cleaning and free data mining. Free segment cleaning often allows an LFS file system to maintain its ideal write performance when cleaning overheads would otherwise cause up to factor of 3 performance decreases. Free data mining can achieve 45 - 70 full disk scans per day on an active transaction processing system, with no effect on transaction performance."</p>

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</description>

<author>Christopher R. Lumb</author>


</item>


<item>
<title>FastCARS : fast, correlation-aware sampling for network data mining</title>
<link>http://repository.cmu.edu/compsci/2154</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2154</guid>
<pubDate>Fri, 04 May 2012 20:08:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Measuring traffic on routers is vital for finding patterns, traffic modeling, and anomaly detection. Unfortunately, technology trends are making it more and more difficult to observe and record the large amount of data generated by high speed links. Traffic sampling techniques provide a simple alternative that reduces the volume of data collected. Real world data is seldom temporally independent and data observed at one time is likely to have important correlations with data observed at close-by instants in time. A good sampling method should be able to give measurements that take this correlation into account. Unfortunately, existing sampling techniques largely hide any temporal relationship in the recorded data. Our proposed method, 'FastCARS', naturally captures statistics for packets that are 1, 2 or more steps away. It has the following properties: (a) provides accurate measurements of full trace's statistics, (b) is simple and scalable for implementation, (c) captures correlations between successive packets, as well as packets that are further apart, (d) evenly separate [sic] sampling efforts over time, and (e) generalizes previously proposed sampling methods and includes them as special cases. We also propose several new tools for network data mining and demonstrate the good quality of the information provided by FastCARS. These tools include: (a) The n-step histograms which give correlated statistics at different levels of temporal correlation, (b) the convolution test which could be used to examine the dependence level betwen packet arrivals. (c) the n-step packet-size/delay graph which provides accurate bandwidth estimation and load monitoring, and (d) the n-step flow graph which effectively visualizes flow patterns hidden in a trace. The experimental results on multiple, real-world datasets (479Mb in total), show that the proposed FastCARS sampling method and these new data mining tools are effective. With these tools, we show that the independence assumption of packet arrival is not correct, and that packet trains may not be the only cause of dependence among arrivals. The provided tools may be useful in applications such as monitoring link load and traffic flows."</p>

	]]>
</description>

<author>Jia-Yu Pan et al.</author>


</item>


<item>
<title>Eliminating machine duplicity in traceroute-based Internet topology measurements</title>
<link>http://repository.cmu.edu/compsci/2153</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2153</guid>
<pubDate>Fri, 04 May 2012 20:08:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "One of the hurdles faced by Internet topology measurements is machines appearing within the induced topology many times, each time with a different IP address, sometimes many hops apart. Most topology measurements are based on traceroute, which may reult in a machine responding with different IP addresses in different traceroutes. There are three major techniques known for finding or detecting pairs of IP addresses belonging to the same machine. However, two of the three techniques naively require quadratic packets in the number of IP addresses to test. This paper presents practical, scaleable algorithms for each technique, using three novel methods to divide the input set to make the quadratic techniques practical on large sets. For each technique, the error is analyzed, looking at both the source and amount of error the technique exhibits, as well as looking at how responsive machines on the Internet are to the technique."</p>

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</description>

<author>Hal Burch</author>


</item>


<item>
<title>Enabling dynamic security management of networked systems via device-embedded security</title>
<link>http://repository.cmu.edu/compsci/2152</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2152</guid>
<pubDate>Fri, 04 May 2012 20:08:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "This report contains the technical content of a recent funding proposal. In it, we propose a new approach to network security in which each individual device erects its own security perimeter and defends its own critical resources. Together with conventional border defenses (e.g., firewalls and OS kernels), such self-securing devices could provide a flexible infrastructure for dynamic prevention, detection, diagnosis, isolation, and repair of successful breaches in borders and device security perimeters. Managing network security is difficult in current systems, because a small number of border protections are used to protect a large number of resources. We plan to explore the fundamental principles and practical costs/benefits of embedding security functionality into infrastructural devices, such as network interface cards (NICs), network-attached storage (NAS) devices, video surveillance equipment, and network switches and routers. The report offers several examples of how different devices might be extended with embedded security functionality and outlines some challenge [sic] of designing and managing self-securing devices."</p>

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</description>

<author>Gregory R. Ganger et al.</author>


</item>


<item>
<title>Two case studies in using cognitive walkthrough for interface evaluation</title>
<link>http://repository.cmu.edu/compsci/2151</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2151</guid>
<pubDate>Fri, 04 May 2012 20:07:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Previous HCI-studies have compared usability evaluation methods quantitatively without supplementing these data with detailed qualitative data about how analysts actually learn and use methods. In contrast, we present two diary-based case studies that describe the processes of two novice analysts who learned about and applied the Cognitive Walkthrough (CW; Lewis, et al., 1990) to the specification of a multimedia authoring system. Results show that the two analysts easily learned to use CW but also that they found the technique tedious to use. Moreover, CW was neither reliable when comparing the two analysts' processes and outcomes to each other, nor accurate when comparing the analysts' problem predictions to results from usability tests applied to a running system. We examine these data in detail, searching for possible causes of the observed reliability and accuracy. Based on these analyses, we suggest three changes to CW method to improve its accuracy and two changes to improve its reliability. Further, we recommend developing a tool to reduce the tedium and integrate our suggested improvements to CW."</p>

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</description>

<author>Niels Ebbe. Jacobsen et al.</author>


</item>


<item>
<title>Design and implementation of a self-securing storage device</title>
<link>http://repository.cmu.edu/compsci/2150</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2150</guid>
<pubDate>Fri, 04 May 2012 20:07:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Self-securing storage prevents intruders from undetectably tampering with or permanently deleting stored data. To accomplish this, self-securing storage devices internally audit all requests and keep all versions of all data for a window of time, regardless of the commands received from potentially compromised host operating systems. Within the window, system administrators are guaranteed to have this valuable information for intrusion diagnosis and recovery. The S4 implementation combines log-structuring with novel metadata journaling and data replication techniques to minimize the performance costs of comprehensive versioning. Experiments show that self-securing storage devices can deliver performance that is comparable with conventional storage. Further, analyses indicate that several weeks worth of all versions can reasonably be kept on state-of-the-art disks, especially when differencing and compression technologies are employed."</p>

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</description>

<author>John D. Strunk</author>


</item>


<item>
<title>Finding and containing enemies within the walls with self-securing network interfaces</title>
<link>http://repository.cmu.edu/compsci/2149</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2149</guid>
<pubDate>Fri, 04 May 2012 20:07:37 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Self-securing network interfaces (NIs) examine the packets that they move between network links and host software, looking for and potentially blocking malicious network activity. This paper describes how self-securing network interfaces can help administrators to identify and contain compromised machines within their intranet. By shadowing host state, self-securing NIs can better identify suspicious traffic originating from that host, including many explicitly designed to defeat network intrusion detection systems. With normalization and detection-triggered throttling, self-securing NIs can reduce the ability of compromised hosts to launch attacks on other systems inside (or outside) the intranet. We describe a prototype self-securing NI and example scanners for detecting such things as TTL abuse, fragmentation abuse, 'SYN bomb' attacks, and random-propagation worms like Code-Red."</p>

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</description>

<author>Gregory R. Ganger et al.</author>


</item>


<item>
<title>Uniquely decodable n-gram embeddings</title>
<link>http://repository.cmu.edu/compsci/2148</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2148</guid>
<pubDate>Fri, 04 May 2012 20:07:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We define the family of n-gram embeddings from strings over a finite alphabet into the semimodule N[superscript K]. We classify all [xi] [element of] N[superscript K] that are valid images of strings under such embeddings, as well as all [xi] whose inverse image consists of exactly 1 string (we call such [xi] uniquely decodable). We prove that for a fixed alphabet, the set of all strings whose image is uniquely decodable is a regular language."</p>

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</description>

<author>Leonid Kontorovich</author>


</item>


<item>
<title>A unified framework for modeling TCP-Vegas, TCP-SACK, and TCP-Reno</title>
<link>http://repository.cmu.edu/compsci/2147</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2147</guid>
<pubDate>Fri, 04 May 2012 20:07:20 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We present a general analytical framework for the modeling and analysis of TCP variations. The framework is quite comprehensive and allows the modeling of multiple variations of TCP, i.e. TCP-Vegas, TCP-SACK, and TCP-Reno, under very general network situations. In particular, the framework allows us to propose the first analytical model of TCP-Vegas under on-off traffic -- all existing analytical models of TCP-Vegas assume bulk transfer only. All TCP models are validated against event driven simulations (ns-2) and existing state-of-the-art analytical models. Finally, the analysis provided by our framework leads to many interesting observations with respect to both the behavior of bottleneck links that are shared by TCP sources and the effectiveness of the design decisions in TCP-SACK and TCP-Vegas."</p>

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</description>

<author>Adam Wierman et al.</author>


</item>


<item>
<title>StackPi : a new defense mechanism against IP spoofing and DDoS attacks</title>
<link>http://repository.cmu.edu/compsci/2146</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2146</guid>
<pubDate>Fri, 04 May 2012 20:07:12 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Today's Internet hosts are threatened by IP spoofing attacks and large scale Distributed Denial-of-Service (DDoS) attacks. We propose a new defense mechanism, StackPi, which unlike previous approaches, allows the host being attacked, or its upstream ISP, to filter out attack packets and to detect spoofed source IP addresses, on a per-packet basis. In StackPi, a packet is marked deterministically by routers along its path towards the destination. Packets traveling along the same path will have the same marking so that an attack victim need only identify the StackPi marks of attack packets to filter out all further attack packets with the same marking. In addition, the victim can associate StackPi marks with source IP addresses to detect source IP address spoofing by changes in the corresponding StackPi mark. StackPi filtering can thus defend against not only DDoS attacks, but also many IP spoofing attacks -- such as TCP hijacking, and multicast source spoofing attacks. Because each complete mark fits within a single packet, the StackPi defense responds quickly to attacks and can be effective after the first attack packet in a IP spoofing attack, or after a small number of attack packets in the case of a DDoS attack. StackPi also supports incremental deployment, such that significant benefits are realized even if only one third of Internet routers implement StackPi marking. We show these results through analysis and simulations based on several real Internet topologies."</p>

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</description>

<author>Adrian Perrig et al.</author>


</item>


<item>
<title>Systolic algorithms for the CMU warp processor</title>
<link>http://repository.cmu.edu/compsci/2145</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2145</guid>
<pubDate>Fri, 04 May 2012 20:07:03 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>H. T. Kung</author>


</item>


<item>
<title>Production system conflict resolution strategies</title>
<link>http://repository.cmu.edu/compsci/2144</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2144</guid>
<pubDate>Fri, 04 May 2012 20:06:55 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>McDermott et al.</author>


</item>


<item>
<title>Design and use of dynamic modeling in ASCEND IV</title>
<link>http://repository.cmu.edu/compsci/2143</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2143</guid>
<pubDate>Fri, 04 May 2012 20:06:46 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "We present an alternative design for communicating information between an interactive, equation-based modeling environment user and an intial value problem (IVP) solver. The design is practically demonstrated by connecting the widely available integrator LSODE and the freely available plotting program Xgraph to the ASCEND IV modeling environment. In contrast to the ASCEND III integrator interface, this new design allows an order of magnitude improvement in the ease of developing an understanding of a dynamic model's behavior. The improvement is in part achieved by allowing the user to interactively define what time varying quantities should be recorded for postprocessing by graphics packages or other tools without requiring that a new ASCEND model be compiled, thus making visualization easy. The more significant improvement, however, is the new ability to select any part of the complete dynamic model and solve it, thus making exploration of component dynamic behaviors easy. Finally, the user may interactively change a variable between algebraic and dynamic (state or derivative) roles. This makes it possible to negotiate a solution to the index problems which frequently arise in chemical engineering."</p>

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</description>

<author>Jennifer L. Perry et al.</author>


</item>


<item>
<title>Proposal for a Center for the Study of Information Processing : submitted by Carnegie Institute of Technology to the Advanced Research Projects Agency of the Department of Defense</title>
<link>http://repository.cmu.edu/compsci/2142</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2142</guid>
<pubDate>Fri, 04 May 2012 20:06:38 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Allen Newell et al.</author>


</item>


<item>
<title>Asynchronous teams : cooperation schemes for autonomous, computer-based agents</title>
<link>http://repository.cmu.edu/compsci/2141</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2141</guid>
<pubDate>Fri, 04 May 2012 20:06:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "An asynchronous team (A-Team) is a strongly cyclic network of autonomous agents (workers) and memories (workplaces). Results (trial solutions to computational problems) circulate continually through this network. Agents work in parallel and cooperate by modifying one another's results. We have accumulated a good deal of experience in making the circulating results converge to better solutions of optimization and constraint satisfaction problems than the agents can find when working independently. This paper does three things. First, it distills our experiences with A-Teams into a protocol for designing them. Second, it points out that a sufficient condition for the circulating results to converge is that the skills of the agents that construct new results be complementary to the skills of the agents that destroy old results. Third, it argues that this complemantarity [sic] is relatively easy to achieve. The practical implications are: a) the quality of solutions obtained by any problem-solving-algorithm, even the best one available, can invariably be improved by combining it with other available algorithms into an A-Team, b) the quality of solutions obtained by any A-Team can invariably be improved by expanding its size, and C) expansions are relatively easy to make."</p>

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</description>

<author>Sarosh Talukdar</author>


</item>


<item>
<title>All algebraic functions can be computed fast</title>
<link>http://repository.cmu.edu/compsci/2140</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2140</guid>
<pubDate>Fri, 04 May 2012 20:06:20 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>

<author>H. T. Kung et al.</author>


</item>


<item>
<title>Using an issue-based model in a team-based software engineering course</title>
<link>http://repository.cmu.edu/compsci/2139</link>
<guid isPermaLink="true">http://repository.cmu.edu/compsci/2139</guid>
<pubDate>Fri, 04 May 2012 20:06:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "Communication in software engineering projects becomes a bottleneck as the number of participants increases. As today's software systems grow in complexity and size, teaching effective communication skills in software engineering courses becomes a critical issue. This paper is an experience report on the use of a [sic] issue-based model for teaching meeting procedures in a team-based software engineering project course (7 teams, 25 students). We observed that, when carefully introduced in the classroom, the use of an issue-based model provided significant benefits, even with such limited tool support as a word processor template. More specifically, we observed that students conducted meetings more efficiently, that they maintained a more complete record of the issues under discussion, and that intra-team communication was significantly improved."</p>

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</description>

<author>Allen Dutoit et al.</author>


</item>


<item>
<title>January 2001 (No.1)</title>
<link>http://commons.ln.edu.hk/lnc/1</link>
<guid isPermaLink="true">http://commons.ln.edu.hk/lnc/1</guid>
<pubDate>Fri, 04 May 2012 19:11:47 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Hong Kong Institute of Business Studies</author>


</item>


<item>
<title>The Effect of Mainstream Media on Body Image and Stress Reactivity in Latina Females</title>
<link>http://scholarship.claremont.edu/pitzer_theses/23</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/pitzer_theses/23</guid>
<pubDate>Fri, 04 May 2012 19:06:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The role of mainstream media in women’s views of female beauty and body image has been well documented. However, few published studies have observed ethnic differences in physiological stress reactivity that may occur from pressures to comply with a particular image of beauty. This study examined whether the exposure to the mainstream ideal body image would negatively affect Latina women’s physiological and psychological functioning, and how their responses differed in comparison to their White counterparts. Participants included college-aged female students from Pitzer College who self-identified as Latina or Caucasian. Participants completed questionnaires assessing, body esteem (MSBRQ-AS; SATAQ; CDFRS), ethnic identity (SEE), state anxiety (STAI-State) and affect (PANAS) prior to and following exposure to Victoria’s Secret or Chrysler automobile commercials. Physiological stress reactivity was assessed through changes in systolic and diastolic blood pressure, as well as salivary cortisol. 3-way ANOVA tests indicated a significant 2-way interaction between condition and time on participants’ levels of diastolic blood pressure, F(1, 27) = 4.266, MSe = 29.803, p =.049, η2 =.136, as well as ratings of appearance evaluation, F(1,36) = 5.733, MSe = 3.692, p =.022, η2 =.137, and body satisfaction F(1,36) = 4.27, MSe = 4.747, p = .046, η2 =.106. Women who viewed the Victoria’s Secret commercials demonstrated increased levels of diastolic blood pressure and reported lower ratings of body esteem in comparison to women who viewed the Chevy Sonic commercials. Potential trends in anxiety reactivity and the internalization of mainstream female beauty in Latina women following exposure to the stimuli are further discussed.</p>

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</description>

<author>Madison L. Noble</author>


</item>


<item>
<title>Spectroscopic methods of process monitoring for safeguards of used nuclear fuel separations</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1269</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1269</guid>
<pubDate>Fri, 04 May 2012 18:10:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>To support the demonstration of a more proliferation-resistant nuclear fuel processing plant, techniques and instrumentation to allow the real-time, online determination of special nuclear material concentrations in-process must be developed. An ideal materials accountability technique for proliferation resistance should provide nondestructive, realtime, on-line information of metal and ligand concentrations in separations streams without perturbing the process. UV-Visible spectroscopy can be adapted for this precise purpose in solvent extraction-based separations.</p>
<p>The primary goal of this project is to understand fundamental URanium EXtraction (UREX) and Plutonium-URanium EXtraction (PUREX) reprocessing chemistry and corresponding UV-Visible spectroscopy for application in process monitoring for safeguards. By evaluating the impact of process conditions, such as acid concentration, metal concentration and flow rate, on the sensitivity of the UV-Visible detection system, the process-monitoring concept is developed from an advanced application of fundamental spectroscopy. Systematic benchtop-scale studies investigated the system relevant to UREX or PUREX type reprocessing systems, encompassing 0.01-1.26 M U and 0.01-8 M HNO <sub>3</sub> . A laboratory-scale TRansUranic Extraction (TRUEX) demonstration was performed and used both to analyze for potential online monitoring opportunities in the TRUEX process, and to provide the foundation for building and demonstrating a laboratory-scale UREX demonstration.</p>
<p>The secondary goal of the project is to simulate a diversion scenario in UREX and successfully detect changes in metal concentration and solution chemistry in a counter current contactor system with a UV-Visible spectroscopic process monitor. UREX uses the same basic solvent extraction flowsheet as PUREX, but has a lower acid concentration throughout and adds acetohydroxamic acid (AHA) as a complexant/reductant to the feed solution to prevent the extraction of Pu. By examining UV-Visible spectra gathered in real time, the objective is to detect the conversion from the UREX process, which does not separate Pu, to the PUREX process, which yields a purified Pu product. The change in process chemistry can be detected in the feed solution, aqueous product or in the raffinate stream by identifying the acid concentration, metal distribution and the presence or absence of AHA. A fiber optic dip probe for UV-Visible spectroscopy was integrated into a bank of three counter-current centrifugal contactors to demonstrate the online process monitoring concept. Nd, Fe and Zr were added to the uranyl nitrate system to explore spectroscopic interferences and identify additional species as candidates for online monitoring. This milestone is a demonstration of the potential of this technique, which lies in the ability to simultaneously and directly monitor the chemical process conditions in a reprocessing plant, providing inspectors with another tool to detect nuclear material diversion attempts.</p>
<p>Lastly, dry processing of used nuclear fuel is often used as a head-end step before solvent extraction-based separations such as UREX or TRUEX. A non-aqueous process, used fuel treatment by dry processing generally includes chopping of used fuel rods followed by repeated oxidation-reduction cycles and physical separation of the used fuel from the cladding. Thus, dry processing techniques are investigated and opportunities for online monitoring are proposed for continuation of this work in future studies.</p>

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</description>

<author>Jamie Lee Warburton</author>


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<item>
<title>School counselor assignment in secondary schools: Replication and extension</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1268</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1268</guid>
<pubDate>Fri, 04 May 2012 18:10:04 PDT</pubDate>
<description>
	<![CDATA[
	<p>Before school counselors can carry out the duties and responsibilities outlined as part of a comprehensive school counseling program, they must know which students they are responsible for helping. The topic of assigning students to school counselors has only recently been seen in the educational research arena in a study by Akos, Schuldt, and Walendin (2009). The current study attempts to replicate and extend the findings of Akos, Schuldt, and Walendin by addressing the questions of how secondary school counselors are assigned and what are their perceptions of their assignment. In addition, the study attempts to determine whether a particular type of school counselor assignment is more effective in enhancing student achievement in a large school district. A review of literature relevant to this study includes: the history of school counseling; the role of the school counselor; student achievement as defined by NCLB (2001); school counselor interventions in the areas of standardized-test scores, attendance, and graduation rates; and school counselor assignment.</p>
<p>The study was conducted in two parts. Part one of the study was conducted using a survey questionnaire--School Counselor Assignment Questionnaire, SCAQ (Akos, Schuldt, and Walendin, 2009). A total of 213 secondary school counselors from Clark County School District participated in the survey. The results found that the breakdown of school counselor assignment used in participating secondary schools was similar to that found by Akos, Schuldt, and Walendin (2009) with a majority of middle schools using a grade level looping method and a majority of high schools using an alphabetical method. Also evident in the findings of this study was that school counselors using methods of school counselor assignment in which they keep the same students from year to year, had more positive perceptions of their method than those who were using a mixed method.</p>
<p>Part two of the study is an analysis of student achievement data from schools using different school counselor assignment methods. Results of this analysis show no significant difference between school counselor assignment and the student achievement variables--percentage of students who meet or exceed standards on the standards-based reading test, percentage of students who meet or exceed standards on the standards-based math test, and student daily average attendance. At the middle school level there was a difference related to method of assignment in the student achievement variables, but extended analysis suggested this was an artifact of extraneous variables.</p>
<p>Although the findings of this study do not identify a relationship between school counselor assignment and the three NCLB variables representing student achievement, it does further the findings of the original study by showing statistically significant differences in counselor perceptions of several aspects of their school counselor assignment method. These findings appear to warrant consideration when discussing school counselor assignment with school counseling students, when school counseling departments are developing their comprehensive guidance program, or when working to create better guidelines for determining school counselor assignment.</p>

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<author>Jennifer L. Williamson</author>


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<item>
<title>Hydroclimatic forecasting in the western United States using paleoclimate reconstructions and data-driven models</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1267</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1267</guid>
<pubDate>Fri, 04 May 2012 17:47:55 PDT</pubDate>
<description>
	<![CDATA[
	<p>This thesis investigated climate variability and their associated hydrologic responses in the western United States. The western United States faces the problem of water scarcity, where the management and mitigation of available water supplies are further complicated by climate variability. Climate variability associated with the phases of oceanic-atmospheric oscillations has been shown to influence streamflow and precipitation, where predictive relationships have led to the possibility of producing long-range forecasts. Based on literature review, four oceanic-atmospheric oscillation indices were identified in having the most prominent influence over the western United States including the El Niño - Southern Oscillation (ENSO), Pacific Decadal Oscillation (PDO), Atlantic Multidecadal Oscillation (AMO), and North Atlantic Oscillation (NAO). However, these hydroclimatic processes are not fully understood and are difficult to describe in physically-based models. A viable alternative to generating forecasts is through data-driven models, which extract relationships in a dataset of oscillation inputs and hydrologic outputs to build a structured forecasting model.</p>
<p>One of the limitations to using oceanic-atmospheric oscillations in a data-driven model is a short instrumental record from which the model can train on. Data-driven models often perform better when they are subjected to a larger training dataset. Reconstructions have the potential to extend the period of record by several centuries, which may aid in identifying important hydroclimatological relationships and improving the quality of forecasts.</p>
<p>With this motivation, this study focused on increasing the forecast lead time through the use of reconstructions of oceanic-atmospheric oscillations in the western United States. First, reconstructions of oscillations were investigated to increase the forecast lead time of four streamflow gages in the Upper Colorado River Basin (UCRB) by using the KStar and M5P data-driven models. Secondly, an expanded spatial examination was performed over the western United States for 21 streamflow gages to increase the forecast lead time using the KStar model. Thirdly, different combinations of oceanic-atmospheric oscillations were tested for precipitation forecasts for 20 climate divisions throughout the western United States. Finally, a support vector machine (SVM) was used to increase the streamflow forecast lead time for 21 gages in the western United States.</p>
<p>In order to accomplish this task, a collection of annual time series, processing techniques, testing procedures, and performance measures were used. Reconstructions were available for oscillation indices, streamflow volumes, and climate division precipitation was developed with a common timeframe available as far back as 1658. The instrumental records used ranged from 1900 to 2007 Noise was removed from the dataset using a 3-year, 5-year, and 10-year moving average filter. A 10-fold cross-validation technique was used as opposed to splitting the dataset into training and testing periods so that the entire dataset could be tested and to better capture the non-stationarity of the dataset. The performance of the models were evaluated through a series of independent measures which include the root mean squared error (RMSE), mean absolute error (MAE), RMSE-standard deviation ratio (RSR), Pearson's correlation coefficient (R), Nash-Sutcliffe coefficient of efficiency (NSE), and linear error in probability space (LEPS) skill score (SK). In addition, all of the models were compared with a multiple linear regression (MLR) model.</p>
<p>The results indicated that the lead time for streamflow forecasts in the Upper Colorado River Basin were increased up to 5 years with the KStar model. In addition, 1-year and 2-year lead-time forecasts with the KStar model were achieved for 21 streamflow gages in the western United States. A 1-year precipitation forecast was also made for 20 climate divisions with the KStar model throughout the western United States and found that the forecasts deteriorated when any of the four oscillations were dropped as predictors. Finally, the SVM model produced streamflow forecasts in the western United States using the raw data at the 1-year and 5-year lead time. In addition, the results indicated that the use of all four oceanic-atmospheric oscillation indices (i.e. ENSO, PDO, AMO, and NAO) provided the best forecasts, and dropping any of the indices yielded inferior results. It was also found that noise removal increased the performance of the model, by aiding in the identification of the oscillation phases.</p>
<p>The contributions made from this research include an extension of the lead-time for streamflow and precipitation forecasts and a better understanding of the effects of climate variability. This study was the first to use reconstructions in a data-driven forecasting model for streamflow and precipitation. Other studies have incorporated reconstructions for use in determining hydroclimatic behaviors and relationships in comparison to the observed record; however, there have been no previous attempts to use reconstructions with data-driven techniques for forecasting purposes. Overall, this research provided a better understanding of climate variability and their hydrologic responses in the western United States. The forecasting models produced through this research are expected to aid water managers in the long-term planning and management of water resources in the western United States.</p>

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</description>

<author>Christopher Allen Carrier</author>


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<item>
<title>Job stress, mentoring, psychological empowerment, and job satisfaction among nursing faculty</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1266</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1266</guid>
<pubDate>Fri, 04 May 2012 17:47:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>The National League for Nursing (NLN) endorses mentoring throughout the nursing faculty career trajectory as the method to recruit nurses into academia and improve retention of nursing faculty within the academy (NLN, 2006). One way mentoring assists faculty is by easing socialization to the culture of the employing institution and decreasing faculty stress (Lewallen, Crane, Letvak, Jones, & Hu, 2003). Mentoring can also be a facilitating factor of an individual's psychological empowerment. Academia is an environment able to foster psychological empowerment, a state in which faculty may be self-directed, highly productive, confident, and find a meaningful connection to their work (Spreitzer, 1995a).</p>
<p>This research study was a descriptive cross-sectional quantitative design, conducted via online survey administered by Survey Monkey. A nationwide sample of 959 Commission on Collegiate Nursing Education (CCNE) accredited full-time nursing faculty completed the study. The survey was comprised of a researcher-created demographic questionnaire plus several psychometrically tested instruments: Dreher's mentoring scale, Gmelch's faculty stress index, Spreitzer's psychological empowerment scale, and the National Survey for Postsecondary Faculty's (NSOPF) job satisfaction scale.</p>
<p>The average subject (<em>N</em> = 959) is female, 53 years old, Caucasian, married, and is not presently supporting dependent children. Professionally the average subject was doctorally prepared, and does not hold additional employment to their full-time faculty job. In addition, the following were the most commonly occurring career characteristics of the sample; less than 10 years of experience as a full-time faculty member, less than 10 years of employment at the current institution, rank of assistant professor or clinical assistant professor, untenured, and an annual salary of $70,000 to $79,999.</p>
<p>Results showed that 40% of the sample had a current work mentor. Variables showed significant relationships to job satisfaction (<em>p</em> < .01): mentoring quality (.229), job stress (-.568), and psychological empowerment (.482). Multiple regression results indicated that job satisfaction was significantly influenced (<em>p</em> < .01) by the presence of a mentoring relationship (β = .110, <em>t</em> = 3.477, <em>p</em> < .001), salary (β = .171, <em>t</em> = 4.582, <em>p</em> < .0005), tenure status (β = -.094, <em>t</em> = -2.722, <em> p</em> < .007), psychological empowerment (β = .305, <em> t</em> = 8.860, <em>p</em> < .0005), and job stress (β = -.426, <em>t</em> = -12.851, <em>p</em> < .0005). The regression model explained 47% of the variance in job satisfaction for the sample.</p>

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</description>

<author>Catherine Emily Ebersole Chung</author>


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<item>
<title>A study of a novel modular variable geometry frame arranged as a robotic surface</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1265</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1265</guid>
<pubDate>Fri, 04 May 2012 17:47:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>The novel concept of a "variable geometry frame" is introduced and explored through a three-dimensional robotic surface which is devised and implemented using triangular modules. The link design is optimized using surplus motor dimensions as firm constraints, and round numbers for further arbitrary constraints. Each module is connected by a passive six-bar mechanism that mimics the constraints of a spherical joint at each triangle intersection. A three dimensional inkjet printer is used to create a six-module prototype designed around surplus stepper motors powered by an old computer power supply as a proof-of-concept example.</p>
<p>The finite element method is applied to the static and dynamic loading of this device using linear three dimensional (6 degrees of freedom per node) beam elements to calculate the cartesian displacement and force and the angular displacement and torque at each joint. In this way, the traditional methods of finding joint forces and torques are completely bypassed. An efficient algorithm is developed to linearly combine local stiffness matrices into a full structural stiffness matrix for the easy application of loads. This is then decomposed back into the local matrices to easily obtain joint variables used in the design and open-loop control of the surface.</p>
<p>Arbitrary equation driven surfaces are approximated ensuring that they are within the joints limits. Moving shapes are then calculated by considering the initial position of the surface, the desired position of the surface, and intermediate shapes at discrete times along the desired path.</p>
<p>There are no sensors on the prototype, but feedback models and state estimators are developed for future use. These models include shape sampling methods derived from existing meshing algorithms, trajectory planning using sinusoidal acceleration profiles, spline-based path approximation to allow lower curvature paths able to be traversed more quickly and/or able to be travelled with a constant velocity and optimized by iteratively calculating actuator saturation with no discontinuities, and the optimal tracking of a desired path (modeled with a time-varying ricatti equation).</p>

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</description>

<author>Christopher James Salisbury</author>


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<item>
<title>The Watchmaker Series</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1264</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1264</guid>
<pubDate>Fri, 04 May 2012 17:47:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Watchmaker Series celebrates and inquires into time as a biproduct of consciousness and practices the application of this notion in poetry. The series begins with the numeral poems, all of which relate directly to the theoretical and polemical aspects. Along the way, other poems with individual titles are interspersed to reflect or redirect the abstract considerations to more concrete subjects. Gradually, as the series progresses, the interacting and recurring associations meld theory and practice into a compositional whole.</p>
<p>The central notion that contemporary poetry is not a machine made of words but rather, like the watch that gives itself as evidence of the existence of a watchmaker, each poem is a watchmaker presents the poet as a watchmaker who makes watchmakers instead of watches, having dispensed with the utility of language in favor of its creative impulse.</p>

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</description>

<author>Christopher Michael Seelie</author>


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<item>
<title>The utilization and effectiveness of the HESI E(square) exit exam as a graduation requirement toward increasing NCLEX-RNRTM pass rates in baccalaureate nursing programs</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1263</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1263</guid>
<pubDate>Fri, 04 May 2012 17:47:32 PDT</pubDate>
<description>
	<![CDATA[
	<p>Due to a desire to better prepare BSN students for the Nurse Council Licensure Examination for Registered Nurses (NCLEX-RN<sup>®</sup> ) and to increase first-time pass rates, nursing programs across the US are using predictive testing to implement policies that require students to pass a standardized exit exam to graduate (National League for Nursing, 2010). Evolve Learning Systems owned by Elsevier, Inc. offers such an exit exam named the HESI E <sup>2</sup> , which recommends a benchmark score to predict success on the NCLEX-RN<sup>®</sup> . To offset an expected decrease in NCLEX-RN<sup>®</sup> pass rates due to recent changes in the passing standard, BSN program faculty may consider implementing a graduation requirement using predictive exams such as the HESI E<sup>2</sup> , to motivate students to better prepare for NCLEX-RN<sup>®</sup> . From a student's perspective, a requirement to pass a single exam to graduate may seem unfair, after spending time and money for an education. A single high stakes exam can cause pronounced individual student personal and social stress (Spurlock & Hunt, 2008).</p>
<p>Adult Education Theory and Classical Test Theory were used as a conceptual framework to design this quasi-experimental retrospective study. A large sample of BSN student graduates and potential graduates from nursing programs across the US that may or may not incorporate the HESI E <sup>2</sup> exit exam as part of their curriculum were examined. The sampling of this study is hierarchical in that graduate BSN students were sampled within graduation periods of BSN programs and BSN programs were sampled within the population of BSN programs in the United States.</p>
<p>The purpose of the study was threefold. The first purpose compared the NCLEX-RN<sup>®</sup> first-time pass rates of BSN students in nursing programs that use the HESI E<sup>2</sup> exit exam with other computerized exit exams, and those using no exit exam. NCLEX-RN<sup>®</sup> first-time pass rates for students taking HESI E<sup>2</sup> did not show a statistically significant increase compared to students that took no exit exam. The results would suggest that the education acquired in nursing school prepares students adequately for the NCLEX-RN<sup>®</sup> without the use of a standardized exit exam. It may also be that the assessment results provided by the HESI E<sup>2</sup> are not being utilized by the BSN students to better prepare for NCLEX-RN<sup>®</sup> .</p>
<p>A second purpose, compared NCLEX-RN<sup>®</sup> first-time pass rates of BSN students in nursing programs utilizing the E<sup>2</sup> that require a minimum benchmark score as a graduation requirement with those BSN students that use HESI E<sup>2</sup> but are not subjected to this requirement. The results from this study did show a statistically significant increase in NCLEX-RN<sup>®</sup> first-time pass rates for students in BSN programs in the South and West, regions of the US that used the E<sup> 2</sup> minimum benchmark score as a graduation requirement. The third purpose was to determine an estimated percentage of BSN students that would have actually failed NCLEX-RN<sup>®</sup> among students that failed to graduate because of a failure to meet an E<sup>2</sup> minimum benchmark score. Application of an algorithm, designed by the author, revealed that E<sup> 2</sup> predicted failure on NCLEX-RN<sup>®</sup> 73% of the time. This finding did not agree with a previous study by Spurlock and Hanks (2004), which stated that E<sup>2</sup> was good at predicting success on NCLEX-RN<sup> ®</sup> but was not able to predict failure 81% of the time. In other words, 81% students that failed to pass E<sup>2</sup> went on to pass NCLEX-RN<sup>®</sup> . Their study did not consider the motivator of a graduation requirement, and when this was included in this study, the result was very different: only 27% of the students that failed E<sup>2</sup> would have passed NCLEX-RN<sup>®</sup> and 73% would have failed NCLEX-RN<sup> ®</sup> .</p>
<p>Lauchner et al.(2006), Morrison et al. ( 2002), Newman et al.(2000) Nibert & Young (2001), and Nibert et al. (2002) offer evidence that HESI E<sup> 2</sup> exit exam has predictive value in predicting success on NCLEX-RN<sup> ®</sup> . The results of this study agree with their assertion and offers new information in that the HESI E<sup>2</sup> exit exam has value in predicting failure on NCLEX-RN<sup>®</sup> when a motivator such as a graduation requirement is in place. Although this study did reveal that HESI E<sup>2</sup> exit exam was accurate at predicting failure, nursing faculty are advised to consider the profound impact of a "high stakes" exam on a student's livelihood. Recommendations from this study suggest that the use of the predictive value of HESI E <sup>2</sup> exit exam in nursing programs be only part of a constellation of evaluation criteria to assist BSN students to prepare to pass NCLEX-RN<sup>®</sup> .</p>

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<author>Debra Henline Sullivan</author>


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<item>
<title>Boundary Element Method (BEM) and Method of Fundamental Solutions (MFS) for the boundary value problems of the 2-D Laplace&apos;s equation</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1262</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1262</guid>
<pubDate>Fri, 04 May 2012 17:47:26 PDT</pubDate>
<description>
	<![CDATA[
	<p>In this thesis we study the solution of the two dimensional Laplace equation by the boundary Element method (BEM) and the method of fundamental solutions (MFS). Both the BEM and MFS used to solve boundary value problems involving the Laplace equation 2-D settings. Both methods rely on the use of fundamental solution of the Laplace's equation (the solution of Laplace's equation in the distributional sense). We will contrast and compare the results we get using the BEM with results we get using the MFS.</p>

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<author>Ermes Anthony Salgado-Ibarra</author>


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<title>Bryoecology in the American southwest: Patterns of biodiversity and responses to global change</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1261</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1261</guid>
<pubDate>Fri, 04 May 2012 17:47:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation combines investigation of the large-scale responses of bryophyte species diversity and distribution with small-scale physiological adaptations to global change. These two areas of inquiry are linked because one way to predict plant species responses to global change is to examine their distribution across current ecological gradients produced by factors such as latitude and elevation. By examining these biogeographic patterns one can identify those species that have a narrow tolerance and therefore are most sensitive to change. Selected bryophytes might then be used as indicator species in long-term monitoring programs. Where historical data exist, these can be used to reconstruct the past and continuing range shifts of bryophytes in response to decades of global change.</p>
<p>In chapter 2 a checklist of the 310 bryophyte taxa (two hornworts, 46 liverworts and 262 mosses) reported to occur within the political boundaries of the state of Nevada is presented. 238 new county records are also listed. Notes are provided for species with complex synonymies, taxonomic difficulties or interesting histories. This checklist is intended to improve efforts towards a complete bryophyte flora of the state by identifying those species, habitats and geographic regions that have been neglected or poorly sampled. Chapter 4 describes a baseline assessment of the bryophyte diversity on the Grand Canyon-Parashant National Monument. Collecting locations were selected in order to maximize the number of species collected and to cover the monument both geographically and ecologically. Forty-seven sites were visited and 679 voucher specimens were collected. A checklist, flora and photographic guide were prepared for the 110 species identified from among these collections.</p>
<p>Finally, chapter 3 describes an experiment where intact Mojave desert scrub and associated biological soil crust were exposed over multiple years to experimental treatments designed to simulate predicted global change. Field treatments included a FACE (Free Air Carbon dioxide Enrichment) site where plants were exposed to experimentally elevated atmospheric CO <sub>2</sub> (550 ppm). In order to determine the responses of the bryophyte component of the soil crust to elevated CO<sub>2</sub> concentrations, patches of the dominant Mojave Desert moss <em>Syntrichia caninervis</em> Mitt. were sampled from the FACE treatments. Shoots grown under elevated CO<sub>2</sub> expressed sex more frequently and tolerated repeated cycles of desiccation better than their ambient counterparts. In a follow-up experiment, plants were grown at both elevated and ambient CO<sub>2</sub> concentrations in the laboratory. All plants grown at elevated CO<sub>2</sub> under laboratory conditions exhibited greater regenerational vigor than plants grown at ambient CO<sub> 2</sub> ; however there were interaction effects between the laboratory and field treatments that suggest photosynthetic down-regulation is occurring. It appears that while they are capable of harnessing additional CO<sub>2</sub> for growth, in the harsh conditions of their native environment these plants preferentially allocate those added resources to sexual reproduction and stress tolerance. Biological soil crusts perform several valuable ecosystem functions in arid regions so it is important that we understand their responses under various scenarios of global change.</p>

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</description>

<author>John Carroll Brinda</author>


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<item>
<title>Evaluating a social skills training protocol in a private setting: Outcomes and issues</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1260</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1260</guid>
<pubDate>Fri, 04 May 2012 17:47:15 PDT</pubDate>
<description>
	<![CDATA[
	<p>Society is dealing with a trend of aggressive and destructive behavior among children and adolescence. Children with social, emotional, and conduct problems are at high risk for academic failure, peer rejection, conduct disorder, school dropout, delinquency, and drug and alcohol problems (Webster-Stratton, Reid, & Stoollmiller, 2008). A high priority for the United States public health and crime prevention is the prevention of aggressive and delinquent behavior during childhood and adolescence (Taylor, Eddy, & Biglan 1999).</p>
<p>Social skills trainings aim to increase the performance of key social behaviors that are important for children to succeed in social situations. Solutions may be provided with social skills trainings for the increasing trend of aggressive and destructive behavior among children and adolescence. Various studies of social skills trainings have shown effectiveness in improving children's levels of social interaction and cognitive problem- solving (Erwin, 1994), declining aggression and bullying behavior, (DeRosier, 2004), and reducing disruptive, off-task behaviors in children with ADHD (DuPaul & Weyandt, 2006).</p>
<p>The purpose of this study is to evaluate the effectiveness of a particular social skills treatment protocol. The study also explores issues related to conducting research in real-life settings. Additionally, the challenges in using various rating scales to evaluate the program's effectiveness are explored.</p>
<p>Four measures were used in the analysis of the study. The findings indicate that one of the four measures, the Program Evaluation Form (PEF) showed statistical significance for seven of the eight program modules evaluated. The other three measures, the Bar-On Emotional Quotient Inventory: Youth Version (EQ-SF), the Child Feeling Scale (CFS), and the Presenting Problem Rating Scale (PPRS), all indicated little or no significant change.</p>
<p>Conducting research in a real-life setting had various challenges. The small sample size proved to be problematic. Consistent data collection from parents was difficult to manage, as well as managing data collection from the children within the context of the group. Additionally, it was questionable whether the Rapid Assessment Instruments (RAI) used were effective in the evaluation of the program.</p>

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<author>Judi Davis</author>


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<title>Retrospective evaluation of microbial presence in existing saliva repository: A PCR based molecular survey of oral microbial populations from existing saliva samples</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1259</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1259</guid>
<pubDate>Fri, 04 May 2012 17:47:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>The overall purpose of this research project is to explore the link between oral health and disease in the University of Nevada, Las Vegas - School of Dental Medicine (UNLV-SDM) clinic patient population. More specifically, the population of interest is the UNLV-SDM orthodontic clinic patient population, which is mostly composed of adults, females, and minorities. The University of Nevada, Las Vegas, School of Dental Medicine, with more than 70,000 active patients and a post-graduate specialty program in Orthodontics is uniquely positioned to perform this type of oral health epidemiology survey, as well as targeted oral microbial testing among populations within the clinic and the local community.</p>
<p>A UNLV Office of Research Integrity - Human Subjects Exemption (OPRS#1104-3801M - <em>Retrospective Evaluation of Microbial Presence in Existing Saliva Repository: A PCR-Based Molecular Survey of Oral Microbial Populations from Existing Saliva Samples</em> ) was filed and approved May 10, 2011 to facilitate the use of an existing saliva database of more than one hundred clinical samples that have already been collected from adult patients in the UNLV-SDM clinic, including patients from the orthodontic clinic. These saliva samples contain DNA representative of the host (human), as well as any endogenous microbial flora (bacteria, viruses). Analysis of these samples to test for microbial presence, as well as quantitative analysis of microbial burden will provide UNLV-SDM clinicians with information about the types of public health interventions that may be needed to serve the local population.</p>
<p>This project will attempt to determine if there are oral microbial burden differences within the patient population that could positively or negatively influence their orthodontic needs. Variables to be assessed will include: gender, age, and ethnicity. No previous survey of this population has been attempted; therefore, this study will be among the first to report on the oral microbial burden within this patient pool.</p>

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<author>Jay Ericksen Davis</author>


</item>


<item>
<title>Automating construction and selection of a neural network using stochastic optimization</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1258</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1258</guid>
<pubDate>Fri, 04 May 2012 17:47:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>An artificial neural network can be used to solve various statistical problems by approximating a function that provides a mapping from input to output data. No universal method exists for architecting an optimal neural network. Training one with a low error rate is often a manual process requiring the programmer to have specialized knowledge of the domain for the problem at hand.</p>
<p>A distributed architecture is proposed and implemented for generating a neural network capable of solving a particular problem without specialized knowledge of the problem domain. The only knowledge the application needs is a training set that the network will be trained with. The application uses a master-slave architecture to generate and select a neural network capable of solving a given problem.</p>

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</description>

<author>Jason Lee Hurt</author>


</item>


<item>
<title>The information battlefield: Al-Qaeda&apos;s use of advanced media technologies for framed messaging</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1257</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1257</guid>
<pubDate>Fri, 04 May 2012 17:46:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>Through a descriptive and qualitative content analysis of Al-Qaeda videos from 2001 to 2010, this thesis describes how the organization's video production has undergone a surge in production quality by using modern technology and skilled recruits. This thesis also provides background on the Islamic culture and the history of Al-Qaeda in order to put into perspective the goals of the organization's framed messages that are incorporated into their videos. The study also draws on parallels of propaganda use throughout history to highlight how regimes from all over the world understand the importance of communication during a time of war.</p>

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</description>

<author>Jessica Marie Martin</author>


</item>


<item>
<title>Strike Out Across the Shoreless Ocean</title>
<link>http://digitalcommons.library.unlv.edu/thesesdissertations/1256</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/thesesdissertations/1256</guid>
<pubDate>Fri, 04 May 2012 17:46:52 PDT</pubDate>
<description>
	<![CDATA[
	<p>What happens between a reader and a poem is none of my business. The world has always been yours; find your own way.</p>
<p>(1) Every choice is correct.</p>
<p>(2) Everything is true.</p>
<p>(3) What is anything, unless so far as it is enjoyed?</p>
<p>All you have to do is see the course, and when you see it, go.</p>

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</description>

<author>Julia Claire Paajanen</author>


</item>


<item>
<title>Should Our Genes Be Part of the Patent Bargain?: Maximizing Access to Medical Diagnostic Advances While Ensuring Research Remains Profitable</title>
<link>http://digitalcommons.law.scu.edu/chtlj/vol28/iss2/5</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/chtlj/vol28/iss2/5</guid>
<pubDate>Fri, 04 May 2012 17:35:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Johanna Jacob</author>


</item>


<item>
<title>The Unitary Progress Clause: District of Columbia v. Heller and the Structural Interpretation of the Progress Clause</title>
<link>http://digitalcommons.law.scu.edu/chtlj/vol28/iss2/3</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/chtlj/vol28/iss2/3</guid>
<pubDate>Fri, 04 May 2012 17:35:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Joshua I. Miller</author>


</item>


<item>
<title>Qualifying Intellectual Property II: A New Innovation Index for Pharmaceutical Patents &amp; Products</title>
<link>http://digitalcommons.law.scu.edu/chtlj/vol28/iss2/4</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/chtlj/vol28/iss2/4</guid>
<pubDate>Fri, 04 May 2012 17:35:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ron A. Bouchard</author>


</item>


<item>
<title>Auspicium Melioris Aevi: A Token Of A Better Age</title>
<link>http://digitalcommons.law.scu.edu/chtlj/vol28/iss2/1</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/chtlj/vol28/iss2/1</guid>
<pubDate>Fri, 04 May 2012 17:35:23 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Michael VanAuker</author>


</item>


<item>
<title>The Inequitable Conduct Defense In Patent Litigation: Where We Are, Where We Have Been, and Where We Should Go From Here</title>
<link>http://digitalcommons.law.scu.edu/chtlj/vol28/iss2/2</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/chtlj/vol28/iss2/2</guid>
<pubDate>Fri, 04 May 2012 17:35:23 PDT</pubDate>
<description>
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</description>

<author>Brett Ira Johnson</author>


</item>


<item>
<title>Seeing Stars: Emotional Trauma in Athlete Retirement: Contexts, Intersections, and Explorations</title>
<link>http://scholarship.claremont.edu/cgu_etd/40</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/40</guid>
<pubDate>Fri, 04 May 2012 16:42:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Few areas of modern sport are as misunderstood in popular and academic literature as that of retired professional and elite athletes. While the subject has been studied, the case of the retiring athlete has yet to be fully explored in a detailed, qualitative, and interdisciplinary study focusing on nuanced contexts affecting the quality of an athlete's exit from sport. Utilizing 3 participant groups--29 elite athletes (16 sports, 18 males, 11 females), 9 professional sport administrators, and 8 sport media journalists--over an 18-month period, extensive semi-structured interviews resulted in 1,436 raw data themes that constituted 13 direct, 3 indirect, and 3 emerging philosophical contexts. Significant direct contexts emerged including health, social support/influence, and preretirement counseling. Unexplored indirect contexts include athlete's relationship with media narratives, corporate sport structures, and consumers. Emerging philosophical contexts included issues of fear, mortality, bodily awareness, and shifting identities. Positive ideology, appreciation, and predisposed conditions such as having realistic perspective, and a knowledge of self were noted. Participant group responses and all 19 contexts were noted for their interdependency. Hypotheses included that socially-constructed and cultural ideas exist about retired athletes and are embedded in perceptions of fame and fortune associated with the role of professional athlete. Results indicated that considerations of micro and macro social processes of athlete commodification (especially immediacy in production/consumption by the corporate sport and media/fan nexus) contributed to the quality of their transition. Cultural narratives and mythologies about athletes-as-heroes--including ways in which the athletes themselves internalize these popular ideas--produce a system in which elite athletes are often unprepared for life after sport. Analysis of the data suggested that role residue and mortality themes were present. A longitudinal portion confirmed the significant affecting contexts and corroborated self-identity factors. However, identity-as-project was aligned with extended transitions and eventual return to emotional satisfaction. Suggestions for reconsideration of retired elite athlete's sociocultural and economic roles were included as ambiguity in responsibility remained prevalent. Significant contributions of the study include application of data that offers behavioral, social, and cultural scientist insight to the transcendent challenges that constitute fluid and emerging human conditions when individuals move from one life condition to another. Additional contributions suggest social costs for disposing of transitioning athletes.</p>

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</description>

<author>Scott P. Tinley</author>


</item>


<item>
<title>Technology Use in Higher Education Instruction</title>
<link>http://scholarship.claremont.edu/cgu_etd/39</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/39</guid>
<pubDate>Fri, 04 May 2012 16:42:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>The significance of integrating technology use in higher education instruction is undeniable. The benefits include those related to access to instruction by underserved populations, adequately preparing students for future careers, capitalizing on best instructional practices, developing higher order thinking activities, and engaging students whose relationships with technology are increasingly native, among others. The significance of the current study is based on the fact that few prior studies focused on the factors that support, or inhibit, the use of educational technology by faculty in schools of education. The data collection instrument was a survey designed by the principal investigator based on review of the literature and professional experience. Five constructs were addressed by the survey: institutional policies, belief in the learning benefits, efficacy with integrating technology with content, barriers to technology use, and personal uses of technology. The survey was administered online and targeted 379 full and part time faculty in schools of education throughout the U.S. A total of 203 faculty members responded which was a response rate of 53%. Several path analyses were conducted to determine the variables that most related with the dependent variable, rate of technology adoption for professional instructional purposes. The variable that had the strongest relationship with the adoption rate for professional use was the adoption rate for personal use. This held true for all subgroups except part-time and older faculty. Suggestions for future research include the use of additional data sources to measure the variables described here. Study of the role of institutional policies in technology adoption should consider administrator perspectives in addition to those of faculty. Study of learning benefits should consider students' views in addition to those of faculty. Finally, efficacy variables should consider perspectives of college leaders and administrators.</p>

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</description>

<author>Sammy Elzarka</author>


</item>


<item>
<title>Timelessly Present, Compassionately Impassible: A Defense of Two Classical Divine Attributes</title>
<link>http://scholarship.claremont.edu/cgu_etd/38</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/38</guid>
<pubDate>Fri, 04 May 2012 16:42:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study articulates a God-concept in the tradition of classical Christian theism, contending with calls to modify significantly or revise classical constructions. Attention falls upon two closely related divine attributes that have, especially in recent decades, come under philosophical and theological attack – God’s timelessness and impassibility (inability to suffer). Is the “classical” Lord truly Immanuel, i.e. with us? This general question motivates the study.</p>
<p>The opening three chapters analyze aspects of the God-concepts put forth by Augustine, Aquinas, and Calvin. Apparent tensions between a timeless transcendence and an affirming union of the Trinity with creation are countenanced, with an eye to doing justice to both doctrines. Chapter One examines the idea of divine timelessness and corresponding thoughts about temporal reality found in the <em>Confessions</em>, supplementing Augustinian transcendence with the creational and eschatological insights of two other Church Fathers. Chapter Two documents Aquinas’s affirmation of both God’s strong immutability and the non-necessity of creation, while questioning whether he affirms these in a logically consistent way. Chapter Three then follows the contours of Calvin’s Trinitarianism and Christology, reflecting on the Triune Creator’s gracious “wedding” of himself to the whole work of creation.</p>
<p>The final three chapters operate within the fields of philosophy and philosophical theology. Chapter Four commends a tenseless (or <em>B</em>) theory of time, highlighting several problems surrounding tensed (or <em>A</em>) theories of time. But this former view implies that there is no “official present,” leaving no apparent room for the presence of the timeless God with times and temporally located agents. Thus Chapter Five seeks to address classical eternalism’s “present problem.” The conclusion is reached that the temporally absent God’s “present problem” can be resolved by embracing a “risk-free” understanding of divine providence, best understood in terms of a “Reformed decree” that strongly actualizes all non-divine entities and events. Chapter Six begins by wrestling with what implications the timelessness doctrine might have for “responsive” divine compassion and ends by proposing that the infinite God “embraces” the finite world not by way of a panentheistic inclusion but in some ways more akin to a husband’s attentive care for his wife.</p>

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</description>

<author>Philip R. Olsson</author>


</item>


<item>
<title>Family Support Factors in African American Families That Promote Academic Achievement for Male Middle-School Students</title>
<link>http://scholarship.claremont.edu/cgu_etd/37</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/37</guid>
<pubDate>Fri, 04 May 2012 16:42:28 PDT</pubDate>
<description>
	<![CDATA[
	<p>One of the most consistently reported challenges in the education literature is the underachievement of African American males at all levels of the education pipeline - from elementary and secondary schools through to postsecondary education. African American boys are falling behind and they are falling behind early. This research focuses on resources within the home environment that are available to support the educational achievement of African American boys. There are a number of mechanisms through which parental involvement in the home and at school may promote academic success that are being examined: parental involvement in school activities, expectations that parents share with their sons and for which they hold them accountable, and parental trust and support for both their sons and their sons' schools.</p>
<p>This research sampled families of African American boys in the eighth grade attending Middle Schools in the North Long Beach area of Southern California. It employed a mixed methods approach in using both questionnaires and surveys for collecting data. Thirty two parents were selected at random and completed questionnaires about attitudes and behaviors related to the home environment that impact their sons' educations. An additional group of randomly selected parents were personally interviewed to gain more in-depth responses.</p>
<p>The sample was then divided into two groups according to the STAR Math scores attained by eighth grade boys in the families responding. This measure was used as an indicator of academic success because the STAR test score determines the Math class level for children in the local school district - with those scoring above 325 advancing to Geometry and those scoring below 325 taking lower level classes. The results of the questionnaires and interviews indicate an overall relationship in both groups showing trust and high expectations as being very important in fostering academic success in African American boys in the eighth grade. The consistency of positive home structural factors contributed to the academic success of boys in the families studied in spite of negative factors such as economic deprivation, parental unemployment, previous parental incarceration and lack of transportation.</p>

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</description>

<author>Osie Leon Wood Jr.</author>


</item>


<item>
<title>How One Writes, Makes, Markets a Movie and How an Audience Reads the Movie: Two Biographical Films of Hitler as a Case Study</title>
<link>http://scholarship.claremont.edu/cgu_etd/36</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/36</guid>
<pubDate>Fri, 04 May 2012 16:42:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>According to John Lukacs, German people's views on Hitler and Nazism once got examined right after the fall the Third Reich in the 1950s but this subject has lost its appeal since then. How do Germans nowadays, specifically those young ones raised in the "New Germany" after the fall of the Berlin Wall, think of Hitler and their country's Nazi legacy? This dissertation is to explore how six young Germans growing up in the new "unified Germany" interpret two films' representations of Hitler and Nazism.</p>

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</description>

<author>Nick (Chi-Shu) J. Yeh</author>


</item>


<item>
<title>County of Santa Clara Office of Women&apos;s Policy: An Outcome Evaluation</title>
<link>http://scholarworks.sjsu.edu/etd_projects/219</link>
<guid isPermaLink="true">http://scholarworks.sjsu.edu/etd_projects/219</guid>
<pubDate>Fri, 04 May 2012 16:42:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Julie Ramirez</author>


</item>


<item>
<title>Mortgage Default in Southern California: Examining Distressed Borrower&apos;s Decision Making and Market Contagion</title>
<link>http://scholarship.claremont.edu/cgu_etd/35</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/35</guid>
<pubDate>Fri, 04 May 2012 16:42:25 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation focuses on mortgage defaults in Southern California during the housing bubble of the 2000s. The rapid decline in the housing market that precipitated the current recession has been accompanied by an unprecedented number of loan defaults and foreclosures. Recent studies have identified two major theories of default--the "double trigger" hypothesis, where negative equity and an income shock are necessary conditions for default--and "strategic default" where negative equity is a sufficient condition for default. This paper adds to the default literature by adding short sale as another possible outcome of mortgage default.</p>
<p>The primary goal is to analyze the determinants of mortgage default to assist in understanding the conditions under which strategic behavior of home sales is most likely to occur. Data from Los Angeles County was analyzed from 2007 to 2010 for every closed sale, then coded into three possible sales outcomes: 1) Organic 2) Short Sale 3) Real Estate Owned (REO). A multinomial probit model was used to model homeowner decision-making based on the sale outcome. The model rejected the "double trigger" hypothesis, as it was found that income shocks do no have a significant effect on impacting the predicted probability for distressed sales. Education levels, the sales price of homes, credit card debt, and market price reductions were found to be significant variables in determining distressed sales outcomes, thereby confirming the strategic default hypothesis.</p>
<p>The next section studied spatial association of short sales and REO to see if any contagion effects were present. It was found that both short sales and REO form into clusters of hot and cold spots. Social stigma is believed to impact consumer behavior, the theory was confirmed through the findings of contagion and spatial lag. The final section constructed a hedonic price model to capture the price effects that distressed sales have on neighborhood pricing. Foreclosures were found to have three times the negative impact on neighborhood pricing compared to short sales.</p>

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</description>

<author>Michael Wilkerson</author>


</item>


<item>
<title>On the Economic Effects of Policy Responsiveness: The Role of Candidate Selection for General Elections</title>
<link>http://scholarship.claremont.edu/cgu_etd/34</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/34</guid>
<pubDate>Fri, 04 May 2012 16:42:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>development: Institutions that make governments more inclusive favor economic progress and factors that make governments more exclusive inhibit prosperity. Growth-enhancing policies likely to please the citizenry include policies that ensure the prevalence of the rule of law, policies that protect property and intellectual rights, and policies that foster competition, access and the perfection of markets. In contrast, growth-retarding policies likely to initiate from the representation efforts of politicians advancing narrow concerns include infringement on property rights, diffuse patent legislation, regulation to rise some price or wage, regulation blocking the entry into specific markets, official protection to monopolistic markets and adoption of legal barriers against international competition.</p>
<p>If policy responsiveness to the interests of the whole favors economic affluence, what political institutions matter for the advancement of wide-encompassing interests through the policy making process? This dissertation examines the idea that the incentives provided by the intra-party candidate selection methods are crucial in order to understand the politicians' representation efforts. Expressly, increasing participation and democratization of the intra-party nomination process increase the incumbent's propensity to represent wide-encompassing interests and adopt policies that favor economic affluence. In contrast, elite-centered nomination methods decrease the incumbent's incentive to be politically responsive to the interests of the whole in favor of the representation of narrow concerns that often demand policies that benefit the group at the expense of overall economic growth.</p>
<p>Empirically, the idea that aspirants to party tickets must first respond to the demands of those with the power to add their names to the electoral ballot finds robust support. In the developed world, candidate nomination appears largely informed by inclusive and democratic practices. Quite the opposite, in the less-developed world events of intraparty participatory politics are for the most part absent, with nomination decisions often monopolized by national party leaders and local party bosses.</p>

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</description>

<author>Marco Alejandro Perez-Mares</author>


</item>


<item>
<title>The Problem of Coming to Terms with the Past: A Post-Holocaust Theology of Remembrance</title>
<link>http://scholarship.claremont.edu/cgu_etd/33</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/33</guid>
<pubDate>Fri, 04 May 2012 16:42:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>This dissertation examines the problem of coming to terms with the past in post-World War II Germany in the wake of the Holocaust by examining the philosophical critiques of Theodor Adorno and Eric Voegelin. It then extends these critiques into the ongoing discussion of post-Holocaust philosophy and theology, while introducing the speculative philosophy of Alfred North Whitehead as a helpful and appropriate means for continuing metaphysical reflection and perceiving the influence of the past upon the present and future in post-Holocaust discourse. This dissertation suggests, alongside Adorno and Voegelin, that finally coming to terms with the past proves much more dangerous than helpful. Instead, the focus should remain on remembering and reflecting critically upon the deleterious past of the Holocaust in order to avoid forgetfulness or effacement of the past. Whitehead's philosophy provides a metaphysical means for considering how the past remains with us in the present and into the future. Out of this injunction to remember comes a theology of remembrance, which draws heavily from Walter Benjamin's writing on weak messianism and inverse theology. The final focus of the dissertation is the development of a Christian theology of remembrance that requires Christians to rethink theology in light of the Holocaust.</p>

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</description>

<author>Jeremy D. Fackenthal</author>


</item>


<item>
<title>Overcoming Cognitive and Motivational Barriers to Media Literacy: A Dual-Process Approach</title>
<link>http://scholarship.claremont.edu/cgu_etd/32</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/32</guid>
<pubDate>Fri, 04 May 2012 16:42:21 PDT</pubDate>
<description>
	<![CDATA[
	<p>In today's fast-paced, hyper-mediated society, the ability to balance accuracy and efficiency is essential. Media literacy educational programs have arisen to meet this need and proliferated in recent years. Although the practice of media literacy is thriving, its underlying mechanisms are poorly understood and evidence of effectiveness is mixed (e.g., Bergsma & Carney, 2008). A social psychological perspective has the potential to illuminate previously overlooked variables and inform research and practice in this growing field. In particular, whereas media literacy efforts typically emphasize thorough processing of media messages, dual-process theories of persuasion (e.g., Eagly & Chaiken, 1993; Petty & Cacioppo, 1986) suggest this is not always realistic. When motivation or ability is compromised, individuals default to a low-effort processing mode, relying on peripheral cues or heuristics rather than carefully evaluating message arguments. In this mode, media messages can persuade unconsciously.</p>
<p>Using a dual-process approach, the present research investigated how specific barriers to motivation (perceptions of personal invulnerability) and processing ability (emotion-based advertising, environmental distractions) influence the processes of media literacy. Participants (N = 882) were randomly assigned to 16 conditions in a 2 [vulnerability: demonstrated, control] x 2 [distractions: present, absent] x 2(2) [ad type: informational, emotional; two replicates of each type] between-subjects nested design. The vulnerability manipulation increased distrust in the target ads and reduced their persuasiveness, not through the hypothesized mechanism of heightened perceptions of vulnerability, but mediated by increased counterarguing. Relative to informational ads, emotional ads were judged more persuasive, attractive, similar to personal experience, and elicited greater identification. However, they were also rated less trustworthy than informational ads, suggesting emotional advertising largely bypasses logical decision-making processes. Distraction reduced counterarguing only among those who found the ad relatively unpersuasive.</p>
<p>The results of this research highlight the central role of trust in media literacy processes. Although individuals recognize and distrust emotional forms of advertising, they are nonetheless persuaded by such appeals. Given the sophistication of contemporary advertising techniques and the ubiquity of distractions, the present research suggests new approaches to media literacy are needed, specifically tailored to decision-making under these more realistic media-use conditions.</p>

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</description>

<author>Erica Lynn Rosenthal</author>


</item>


<item>
<title>Intervening with urinary tract infections using anti-adhesives based on the crystal structure of the FimH–oligomannose-3 complex</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1017</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1017</guid>
<pubDate>Fri, 04 May 2012 16:36:58 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Adinda Wellens et al.</author>


</item>


<item>
<title>Documents Relating to Courtesy Calls Made by Supreme Court Nominee Sandra Day O&apos;Connor</title>
<link>http://digitalcommons.law.scu.edu/historical/59</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/historical/59</guid>
<pubDate>Fri, 04 May 2012 16:36:29 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Anonymous</author>


</item>


<item>
<title>List of Potential Supreme Court Nominees, 1981</title>
<link>http://digitalcommons.law.scu.edu/historical/58</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/historical/58</guid>
<pubDate>Fri, 04 May 2012 16:36:27 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Anonymous</author>


</item>


<item>
<title>Memorandum re Selection of Sandra Day O&apos;Connor as Supreme Court Nominee</title>
<link>http://digitalcommons.law.scu.edu/historical/57</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/historical/57</guid>
<pubDate>Fri, 04 May 2012 16:36:25 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>William French Smith</author>


</item>


<item>
<title>Biographical Information re: Anthony Kennedy from White House Supreme Court Nominee Binder</title>
<link>http://digitalcommons.law.scu.edu/historical/56</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/historical/56</guid>
<pubDate>Fri, 04 May 2012 16:36:22 PDT</pubDate>
<description>
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</description>

<author>Anonymous</author>


</item>


<item>
<title>Say It Loud: An Action Research Project Examining the Afrivisual and Africology, Looking for Alternative African American Community College Teaching Strategies</title>
<link>http://scholarship.claremont.edu/cgu_etd/31</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/31</guid>
<pubDate>Fri, 04 May 2012 16:25:11 PDT</pubDate>
<description>
	<![CDATA[
	<p>For this study, the researcher sought to implement a visual arts-based Afrivisual to help inspire, motivate and empower African American students in gaining a culturally relevant education in Euro-American-centered schools. Using the Afrivisual in this work as an action-oriented tool the researcher sought to expose African American students to an African historical context.</p>
<p>This research project utilized three African-centered theoretical frameworks: (1) Afrocentricity, (2) Africana Philosophy, and (3) Africana Critical Theory. The problem this work addresses is found in four areas, (1) American history is Eurocentric, (2) African history has been distorted, (3) Africa’s contribution to world civilization has been ignored, and (4) African American students have suffered from identity issues.</p>
<p>The primary purpose of the study was to show how African American students may react to culturally relevant exposure to African history and to investigate if exposure to African history is culturally relevant for them. The researcher also hoped to present an effective strategy for Black students from an African-centered point of view. The central questions of this study were, “How do native-born African American community college students respond to a culturally relevant visual tool? What experiences have they had with history? How has their exposure to history affected them?”</p>
<p>Both quantitative and qualitative phases of this study were based on data and interviews with African American community college students. Descriptive statistics, including frequency percentages shown in tables were used to present the questionnaire data. Qualitative coding techniques were used to present the focus group data. The qualitative phase of the study highlighted the introduction of the Afrivisual, a visual arts-based and culturally relevant educational tool.</p>
<p>There were similarities between the survey sample and the interview sample. The quantitative and qualitative data combined to show the strong desire African American students have to study African history, African civilizations, and to learn about their African ancestors. The triangulation of the data revealed that African American students who were found to be proud to be Black, vowed to be vigilant in future history classes about what they’re being taught, and to present questions about African history. The students also expressed a tremendous need to share what they’ve learned about African history with other African Americans.</p>
<p>The significance of this study is that the Afrivisual can be a potentially effective teaching strategy. Also additional researchers may be able to build upon the findings of this inquiry by using another media form of the Afrivisual. Lastly, it exposed weaknesses in the self-hatred thesis as it applies to African American adults, and called for the groundbreaking theoretical framework to be revisited.</p>

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</description>

<author>Daniel E. Mitchell</author>


</item>


<item>
<title>Gossip and the Group: A Self-Categorization Perspective</title>
<link>http://scholarship.claremont.edu/cgu_etd/30</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/30</guid>
<pubDate>Fri, 04 May 2012 16:25:09 PDT</pubDate>
<description>
	<![CDATA[
	<p>Gossip is a little studied topic and even fewer studies have examined gossip from the perspective of social identity and self categorization theories. However, many of the functions of gossip have significant implications for group processes, including bonding, norm transmission and reinforcement, marginalization of deviants, and social influence. Particularly for those on the margins of the group, gossip may be used as a tool to gain acceptance in the group, as gossip is an effective way to express group loyalty and adherence to group norms. Study One investigated the extent to which being a prototypical member of one's group was predictive of likelihood to spread gossip. Using sororities as the group, members were presented with a hypothetical piece of gossip and asked the extent to which the member who gossiped is prototypical, how likely they would be to share the gossip with other group members, and how prototypical they perceive themselves to be of the sorority. It was predicted that peripheral group members would be more likely to spread gossip than central group members, particularly about other peripheral group members, and particularly when the information was not highly negative. Study Two was conducted in parallel, using the same methodology, but with a piece of gossip about a celebrity instead of a fellow sorority member. It was predicted that the results would mirror those of Study One and that peripheral members would be most likely to spread the gossip. While none of the stated hypotheses were supported, there were several unanticipated interactions. In both Study One and Study Two, there was a significant three-way interaction, in that a highly uncertain respondent, a prototypical target, and relatively mildly negative gossip was associated with anticipated transmission to the highest number of sorority members. While the results were unanticipated, they are not inexplicable and the implications for research in the areas of gossip, celebrity, and self categorization theory are discussed.</p>

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</description>

<author>Dana Turcotte</author>


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<item>
<title>Africa&apos;s Unresponsive Democratization: the Relationship between Regime Type and the Quality of Life in Africa</title>
<link>http://scholarship.claremont.edu/cgu_etd/29</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/29</guid>
<pubDate>Fri, 04 May 2012 16:25:07 PDT</pubDate>
<description>
	<![CDATA[
	<p>Scholars and policy makers alike argue that leaders of democracies should find it in their interest to provide high levels of social services due to a fear of being voted out of office. Yet, I find that Africa's newer democracies provide levels of social services strikingly similar to what the continent's existing non-democracies supply. This dissertation seeks to explain why this is the case.</p>
<p>I start by exploring the determinants of Africa's most recent wave of democratization, and find that much of Africa's 1990s democratic wave can be attributed to changes in foreign circumstances rather than from pressures from domestic democratic movements. I argue democratization has become disassociated with social services on the continent because of this exogenous nature of political liberalization. Rather than institutionalizing electoral incentives to provide social services, leadership of exogenously derived democracies become principally accountable to the foreign actors for whom political change was meant to appease. However, foreign actors are effectively unable and unwilling to demand political reforms that will institutionalize a more responsive democracy. This dynamic threatens any electoral incentive a ruling party might have to produce higher levels of social services. I test this argument quantitatively and find support for the notion that exogeneity of political change has dampened the impact that democratization has had on social service delivery in Africa.</p>
<p>Additionally, through in-country, qualitative fieldwork I examine how citizens demand social services and how the government responds to such demands in Zambia, a country whose democratization was heavily influenced by foreign pressure. There, I found that while there were important initial strides made by Zambia's post-transition government to institutionalize a higher level of responsiveness in social services, later erosions in Zambia's checks and balances undermined these gains. Finally, using Afrobarometer's cross-national survey data, I explore what impact foreign influenced democratization has on citizens' attachment to and satisfaction with democracy. I find that exogenously derived democratization has a small negative impact on people's attachment to democracy and satisfaction with the way democracy works in their country. I conclude by discussing some of the policy implications of these findings.</p>

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</description>

<author>Caryn Anne Peiffer</author>


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<item>
<title>Authoring Authority: The Apostle Paul and the Prophet Joseph Smith--A Critical Comparison of Texts and Power in the Generation of Religious Community</title>
<link>http://scholarship.claremont.edu/cgu_etd/28</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/28</guid>
<pubDate>Fri, 04 May 2012 16:25:05 PDT</pubDate>
<description>
	<![CDATA[
	<p>. . . believe in God, believe also in me . . . --John 14.1</p>
<p>"Authoring Authority" analyzes the ways texts function to generate social cohesion while at the same time advancing the power interests of their authors. The study is a comparative, critical, and interdisciplinary/transdisciplinary excavation of the religion-making efforts of the first-century Christian Apostle Paul and the nineteenth-century Mormon Prophet Joseph Smith.</p>
<p>This comparison defamiliarizes and recharacterizes the heroes and origin-stories of the dominant (and my own) tradition to force important questions about scholarly perspectives, interests and deferences (protection, exceptionalization), self-reflexivity, and politics. The project's critical orientation deploys insights and models from a range of disciplines to "read" these texts, not for exegetical purposes, but for what they signify and how they function in nascent social formations. The texts of these men were presented as if their contents were other than the products of embedded social actors (e.g. "it really is God's word" 1 Thes 2.13) contending for limited resources such as discursive authority and social power. These charismatic narrators harnessed the authority of pre-existing texts and traditions and integrated them with contemporary perspectives and sentiment. Their texts and performances offered a contingent construal of reality as ultimate reality--which served the power needs of their authors and the existential needs of their communities of subscribers.</p>
<p>The dissertation begins with the articulation of an analytical framework appropriate for the critical and comparative academic study of religion. Chapter two contextualizes the lives of these men within cultural settings that provided motivation, made available vocational training and, ultimately provisioned social opportunities for them as adept charismatics. Chapter three directly illuminates the range of techniques embedded in texts, both implicit and explicit, of claiming power and developing a following. The final chapter wrestles with the functional role of deception in social formation and human life.</p>

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</description>

<author>Alonzo Huntsman</author>


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<item>
<title>Toward Understanding the Nature of Leadership in Alleviating State Fragility</title>
<link>http://scholarship.claremont.edu/cgu_etd/27</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/27</guid>
<pubDate>Fri, 04 May 2012 16:25:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Approximately sixty countries have been designated `Fragile States' by international development agencies. Home to two billion of the world's poorest people, these fragile states are characterized by violence, weak institutions and shattered economies. Not only do they pose a challenge to regional security, they often become the breeding grounds for terrorism.</p>
<p>Donor agencies pour billions of dollars annually into these countries - through policy advice and conditional loans - to alleviate fragility and promote development. Development, however it is defined, involves economic, social and political transformation. Such a transformation is shaped by ideas, engages multiple interests, and proceeds within rules and norms set by political institutions. Since the structure of political institutions is influenced by human agency, leadership becomes important to study. Leadership is crucial particularly in fragile states, where institutions are weak or have been destroyed by conflict; however, a systematic effort to examine the role of leaders and coalitions in fragile states is lacking.</p>
<p>This dissertation seeks to create a methodology to improve understanding of the role of different leadership strategies in bringing about transitions in and out of fragility. To make the scope manageable, the study focuses on: (i) leadership at the national level; and (ii) fragile states in Africa. It does so by examining: (i) evidence from country level panel data on leadership (regime) change and fragility; and (ii) in-depth analytical case studies of transitions in and out of fragility in four countries: Zimbabwe, Uganda, Rwanda, and South Africa.</p>
<p>The analysis looks at the relationship between the change agent's leadership strategy (the independent variable: political participation and inclusion, economic growth and inclusion, and security and justice) and fragility outcomes (dependent variable: conflict and security indicators, economic indicators, and the approach to political inclusion). The results of the regression analysis exhibit a robust association between leadership change and fragility. Furthermore, the country cases show how different types of leadership strategies lead to varying trajectories of fragile states' post-transition. The case studies reveal different approaches to sequencing of political inclusion and the role of leadership exit in transitions from fragility.</p>

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</description>

<author>Ajay Tejasvi Narasimhan</author>


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<title>Fearing the Uncertain: A Causal Exploration of Self-Esteem, Self-Uncertainty, and Mortality Salience</title>
<link>http://scholarship.claremont.edu/cgu_etd/26</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/26</guid>
<pubDate>Fri, 04 May 2012 16:25:01 PDT</pubDate>
<description>
	<![CDATA[
	<p>Social identity theory (Tajfel & Turner, 1979) is one of the most influential social psychological theories of group behavior and intergroup relations. Early social identity research focused on many different group processes; however, the motivation behind group identification was not fully explored. Researchers have proposed a variety of accounts for why people join and identify with groups. This dissertation unravels the relationship between, on the one hand, mortality salience, self-related uncertainty and self-esteem, and on the other group identification and ingroup defense. The general hypothesis derived from uncertainty-identity theory (Hogg, 2010) is that uncertainty and not fear of death or pursuit of self-esteem motivate people to identify with and defend their groups, and that identification mediates the relationship between uncertainty and defense of the group. Experiment 1 (<em>N</em> = 112) tested the relationship between uncertainty and self-esteem on defense of the ingroup, with the additional test of the mediating effects of identification with the group between uncertainty and ingroup defense. Results showed that uncertainty and not self-esteem motivate people to identify with a group, to defend their group, and that group defense is mediated by identification. Experiment 2 (<em>N</em> = 112) provided a replication of the typical TMT study, which suggests that self-esteem will buffer the effects of mortality salience on ingroup defense, with the additional test of the mediating effects of identification between mortality salience and defense of one's group. As predicted, mortality salience only increased identification and defense of the group when self-esteem was not enhanced, as well, the interactive effects of mortality salience and self-esteem on defense was mediated by identification. Experiment 3 (<em>N</em> = 294) was a combination of both Experiments 1 and 2 and tested the hypothesis that uncertainty would moderate the relationship between self-esteem and mortality salience on group identification and ingroup defense. Exactly as predicted, only under high uncertainty the typical TMT results are demonstrated. Results across these three experiments demonstrate that self-uncertainty plays a significant role in reactions to mortality salience, and support uncertainty-identity theory's analysis of the role of self-uncertainty in ideological conviction and group behavior.</p>

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</description>

<author>Zachary P. Hohman</author>


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<item>
<title>Framing a Blaxicana Identity: A Cultural Ethnography of Family, Race and Community in the Valley Homes, Lincoln Heights, Ohio, 1955-1960</title>
<link>http://scholarship.claremont.edu/cgu_etd/25</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/25</guid>
<pubDate>Fri, 04 May 2012 16:24:59 PDT</pubDate>
<description>
	<![CDATA[
	<p>Framing a Blaxicana Identity: A Cultural Ethnography of Family, Race and Community in the Valley Homes, Lincoln Heights, Ohio, 1955-1960 (Blaxicana Identity) is set within the construct of identity formation, against a backdrop of color and culture clash, and the social construction of race. The author's narrative will constitute contextual introductions to discussion topics and iterate direct correlations of her lived experience to larger community and cultural accounts that helped to shape aspects of her <em>Blaxicana</em> identity. The individual and community perceptions of what it means and what it feels like to grow up Negro, Mexican and female in an all black town will determine the scope and complexity of the identity formation factors that may be brought forth in <em>Blaxicana Identity</em>. Geographically situated in the Valley Homes housing projects located in Lincoln Heights, Ohio, just north of Cincinnati, this ethnography will engage the area's background, environment and residents in a dialogue with the larger arenas of race and racism, history, migration, critical race theory, interracial marriage, cultural studies and black towns as they inform the aspects involved in the creation of the author's <em>Blaxicana</em> identity. This multi-perspective engagement will produce a cultural ethnographic portrayal of the Valley Homes, its residents and the author and comprise the ways in which the social and cultural phenomenon of mixed-race identity may be constructed, observed and understood - a depiction that may differ from the historical concepts of identity formation based on color and race. This research will draw its conclusions regarding the construction of a <em>Blaxicana</em> identity by using a critical, self-reflexive method of inquiry that incorporates the author's memories, impressions and artifacts from the 1950's. The author's interracial family experience, defined by an African American father from Nashville, Tennessee and a Mexican mother from Hermosillo, Sonora, Mexico, presents the opportunity to examine what was then, considering the time and place, an uncommon combination.</p>

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</description>

<author>Ana Viola Thorne</author>


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<item>
<title>An Assessment of United States Ethanol Policy</title>
<link>http://scholarship.claremont.edu/cgu_etd/24</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/24</guid>
<pubDate>Fri, 04 May 2012 16:24:57 PDT</pubDate>
<description>
	<![CDATA[
	<p>From 1978 on there have been a series of legislative acts that have placed substantial protectionist burdens on the American taxpayer to provide incentives, credits and mandates for the production and use of ethanol under the rationale of reducing U.S. dependence on foreign sources of oil while purporting to economically benefit the American economy and strengthening American security. While there has been much discussion about the economic benefits of ethanol policy, there is growing literature suggesting that in addition to being neither economically nor environmentally beneficial, ethanol policy may not be achieving its intended goals. Connection between political contributions, policy formation, and the actual outcomes of the enacted policies does not appear to have been addressed. Throughout the course of ethanol policy development the narrow interests of some stakeholders may have been met at the expense of others. Given the very large economic and social costs of ongoing ethanol subsidies and mandates an exploration of such a nexus would be illuminating and valuable.</p>
<p>Hence the question of this research will be:</p>
<p>Has the ethanol energy policy of the United States, as outlined in legislative actions, requiring subsidies and mandates from taxpayers, been  reflective of a <em>deliberative</em> democratic process that after taking into account the input and influence of various competing viewpoints has resulted in a beneficial national policy? Consequently have the policy outcomes of the legislative stakeholders matched the stated intentions of those involved in the <em>deliberative</em> debate that enacted it or, where have those objectives not been met?</p>
<p>Research that can increase understanding of how such an important policy may have failed can inform policy deliberation in such diverse areas as agriculture, national security and energy policy while illuminating how and why such public policy was made.  Examination of a policy created and continuing which may have failed the most basic cost benefit analysis and does very little to enhance national energy security could demonstrate how a distortion of the legislative process resulted in outcomes that differ markedly from the stated intentions of those who enacted the policy.</p>

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</description>

<author>Mark Chapin Johnson</author>


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<item>
<title>Historical Accuracy and the IRA Over 70 Years of Cinema</title>
<link>http://scholarship.claremont.edu/cgu_etd/23</link>
<guid isPermaLink="true">http://scholarship.claremont.edu/cgu_etd/23</guid>
<pubDate>Fri, 04 May 2012 16:24:56 PDT</pubDate>
<description>
	<![CDATA[
	<p>The purpose of this research is to examine how the Irish Republican Army has been represented in theatrical cinema since the 1930s. The goal is to demonstrate the necessity for historical accuracy in movies produced for public entertainment, which often neglect historical facts and circumstances in portraying an organization as controversial and complex as the IRA. This has been done by examining five movies produced for wide-distribution and comparing each to the detailed historical record. Upon analysis of these movies, it becomes clear that the films which are the most historically relevant are also the most powerful cinematic productions, both through emotional power and overall entertainment.</p>

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</description>

<author>Eric Scott Elliott</author>


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<title>Memo from John Roberts to Fred Fielding re S. 383</title>
<link>http://digitalcommons.law.scu.edu/historical/55</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/historical/55</guid>
<pubDate>Fri, 04 May 2012 15:59:06 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>John G. Roberts</author>


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<title>Dynamical relativistic effects in photoionization: Spin-orbit-resolved angular distributions of xenon 4d photoelectrons near the Cooper minimum</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/27</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/27</guid>
<pubDate>Fri, 04 May 2012 15:43:29 PDT</pubDate>
<description>
	<![CDATA[
	<p>Two decades ago, it was predicted [Y. S. Kim et al., Phys. Rev. Lett. 46, 1326 (1981)] that relativistic effects should alter the dynamics of the photoionization process in the vicinity of Cooper minima. The present experimental and theoretical study of the angular distributions of Xe 4d<sub>3/2</sub> and 4d<sub>5/2</sub> photoelectrons demonstrates this effect for the first time. The results clearly imply that relativistic effects are likely to be important for intermediate- Z atoms at most energies.</p>

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</description>

<author>H. Wang et al.</author>


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<item>
<title>C.A.C. Lookout, Volume 5, Number 5, November 1900</title>
<link>http://digitalcommons.uconn.edu/dcamp/41</link>
<guid isPermaLink="true">http://digitalcommons.uconn.edu/dcamp/41</guid>
<pubDate>Fri, 04 May 2012 15:37:50 PDT</pubDate>
<description>
	<![CDATA[
	<p>In 1896, the students of the Storrs Agricultural College established a student newspaper, The Lookout. Published every month, The Lookout had a small, unpaid staff who laid out the pages by hand using tiny metal slugs with embossed letters from a printer's California job case. By 1914, the paper had changed its name to The Connecticut Campus, reflecting the growth of the institution that had become the Connecticut Agricultural School in 1899 and the student newspaper increased its publication schedule to twice a month. The paper continued to grow along with the campus in Storrs, CT, and in 1953 the The Connecticut Campus, which had moved from being published monthly, to weekly and then to a three days a week publication schedule made its last transition to becoming a daily newspaper. In 1955, the renamed Connecticut Daily Campus becomes a morning paper that is printed on newsprint. In the 1970s, the University of Connecticut Board of Trustees granted the Connecticut Daily Campus its independence from the Associated Student Government. Currently, Daily Campus is the largest daily college newspaper in the state of Connecticut and employs more than 120 students during the academic year. Published Monday through Friday during the academic year, 10,000 copies are delivered to over 80 locations both on- and off-campus.<br><br></p>

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</description>

<author>T. F. Downing</author>


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<title>Large Nondipole Effects in the Angular Distributions of K-Shell Photoelectrons from Molecular Nitrogen</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/26</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/26</guid>
<pubDate>Fri, 04 May 2012 15:25:54 PDT</pubDate>
<description>
	<![CDATA[
	<p>Measurements of angular distributions of K-shell electrons photoejected from molecular nitrogen are reported which reveal large deviations at relatively low photon energies ( ħω≤500eV) from emission patterns anticipated from the dipole approximation to interactions between radiation and matter. A concomitant theoretical analysis incorporating the effects of electromagnetic retardation attributes the observed large nondipole behaviors in N<sub>2</sub> to bond-length-dependent terms in the E1⊗(E2,M1) photoelectron emission amplitudes which are indicative of a potentially universal nondipole behavior in molecular photoionization.</p>

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</description>

<author>Oliver Hemmers et al.</author>


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<item>
<title>Open Access Funding Pilot Program</title>
<link>http://digitalcommons.usu.edu/oadc/2</link>
<guid isPermaLink="true">http://digitalcommons.usu.edu/oadc/2</guid>
<pubDate>Fri, 04 May 2012 15:22:35 PDT</pubDate>
<description>
	<![CDATA[
	<p><strong>Utah State University Libraries Pilot Program to Support Open-Access Publishing Opportunities for Faculty: Fall 2011</strong></p>
<p>In the spirit of the Compact for Open-Access Publishing (COPE), Utah State University Libraries recognizes “the crucial value of the services provided by scholarly publishers, the desirability of open access to the scholarly literature, and the need for a stable source of funding for publishers who choose to provide open access to their journals’ contents.” To concretely support open-access (OA) publishers that require a steady funding source to continue to provide their essential functions, the USU Libraries has committed to seeding a pilot project underwriting the reasonable journal processing fees of USU authors who choose to publish their research articles in peer-reviewed, open-access journals, or, on a case-by-case basis, openly available hybrid open-access journals.</p>
<p>Fully open-access journals, which make their publication fee schedule publicly available and are members of the Open Access Scholarly Publishers Association, are helping change the landscape of scholarly communication. USU Libraries is committed to supporting this effort. Examples of open-access journals can be found in the <a href="http://www.doaj.org/" >Directory of Open Access Journals</a>.</p>
<p>Faculty and graduate students are encouraged to apply for these funds by emailing Scholarly Communications and Institutional Repository Librarian Andrew Wesolek at Andrew.wesolek@usu.edu. Conditions of awards include:  <ul> <li>Funds will be available on a first-come-first-served basis during the pilot phase.</li> <li>USU tenured and tenure-track faculty as well as graduate students in all disciplines are eligible to apply.</li> <li>Funding Preference will be given to: <ul> <li>Those who are able to demonstrate matching funds from their department, college, or an outside granting agency. Without a match, full funding is not guaranteed.</li> <li>Those who publish in fully open access journals</li> </ul> </li> <li>In some cases funding for hybrid open-access journals may be considered, but strictly on a case-by-case basis</li> <li>Application for funding may be completed at the time of submission or immediately upon an article’s acceptance for publication.</li> <li>Authors must deposit a copy of the funded article in the USU DigitalCommons.</li> </ul></p>
<p><em> This policy has been drafted based on the Compact for Open-Access Publishing Equity: http://www.oacompact.org/</em></p>

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<author>Scholarly Communications Office</author>


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<item>
<title>An Application of Landscape Design to Student Academic Success</title>
<link>http://digitalcommons.library.umaine.edu/etd/1009</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1009</guid>
<pubDate>Fri, 04 May 2012 15:18:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study is an assessment of a use in a higher education setting of an organizational design technique developed in industrial settings. This technique called landscape design is an application of principles of complexity theory. The technique involves influencing localized decisions by altering the setting in which localized decisions are made (Levinthal & Warglien, 1999). This study assesses an application of landscape design principles to student academic success in a higher educational setting. A small, rural campus of a state university system used a first-year-experience course to increase new student, academic performance. This study compares the aggregate performance, as measured by average grade point average and retention rate of incoming classes of new students who were subjected to a first-year-experience course that incorporated landscape design principles, to the aggregate performance of classes of students who were subjected to an earlier non-landscape-design version of first-year-experience</p>

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</description>

<author>Roger A. Roy</author>


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<item>
<title>The Role of Email in Faculty-Student Relationships Toward Understanding Engagement and Retention</title>
<link>http://digitalcommons.library.umaine.edu/etd/1008</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1008</guid>
<pubDate>Fri, 04 May 2012 15:18:31 PDT</pubDate>
<description>
	<![CDATA[
	<p>Contact between students and their faculty is one of the most important factors in student motivation and their continuation in college. Faculty can encourage students to be engaged in their courses, motivated to learn, and ultimately more capable of completing a four-year degree. This dissertation study sought to address a dearth in the information regarding the impact of email communication, despite its widespread use, on student-faculty relationships and the impact that the fostered relationship may have on engagement and ultimate college persistence. A survey was administered to a class of students in their second year of college at a small private college in the northeast, seeking perceptions about their first year experiences. Follow-up interviews were conducted to illustrate the responses of 15 students. Survey and interview data determined that students prefer to contact their faculty members via email, especially in the first year of college. A preference to email faculty differed from a preference to connect with friends and family face-to-face. Interview data indicated that the student preference for email contact with faculty was a result of feeling intimidated during face-to-face contacts. Survey data found that gender impacted the faculty-student email relationship as well. Female students were more likely to email female professors, and male students were more likely to email male professors. Students indicated in survey and interview data that their trust in faculty members increased as a result of email correspondence. Responses from the survey were also compared to data collected from the same pool of students in the National Survey of Student Engagement (NSSE) and considered for improving a retention prediction model adapted by the researcher for use at the study location. The model uses a point system to assess student risk of attrition based on their participation and performance at key points during the academic year. Survey, interview, and NSSE data was used to identify points in the model that were appropriate for followup with a faculty-initiated email. This type of structured framework must be in place in order for institutions to link email correspondence with other strategies aimed at helping students and ultimately measured as part of a successful retention effort.</p>

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<author>Kjrsten Keane</author>


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<item>
<title>The Experiences of People with Psychiatric Disabilities in Disability Income and Employment Support Programs</title>
<link>http://digitalcommons.library.umaine.edu/etd/1007</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1007</guid>
<pubDate>Fri, 04 May 2012 15:18:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>This study sought to investigate the disability income and employment support program experiences of people with psychiatric disabilities (PWPD), as well as their knowledge of the Social Security Administration (SSA) work incentives. Using qualitative research methods, seventeen people were interviewed in order to learn about their experiences and knowledge. Grounded theory methods guided the study with respect to data collection, analysis, and theory development. The central category, "The Irony of Security: Program Paradoxes in the SSA and VR," describes the emergent theory that the SSA's disability income support programs, Social Security Disability Insurance (SSDI) and Supplemental Security Income (SSI), as well as the Vocational Rehabilitation (VR) program—and by extension, program staff activities—contain inherent paradoxes which hinder PWPDs ability to return to or enter employment through these means. Furthermore, the practice of empowerment, as conceptualized in social work and recovery-based initiatives, is thereby compromised in such settings.</p>

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</description>

<author>Michelle M. Alexander</author>


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<item>
<title>Moving from Middle to High School: At-Risk Student Perceptions of the Effectiveness of Transition Activities</title>
<link>http://digitalcommons.library.umaine.edu/etd/1006</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1006</guid>
<pubDate>Fri, 04 May 2012 15:18:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>An important relationship exists between early identification of at-risk students, the challenges of transitions for academic achievement and engagement with the school environment, and a high school program that provides a supportive framework to assist students with staying on track to graduation. Growing interest on the part of researchers and educators has focused on the ninth grade as a critical turning point for young adolescents, and schools have designed programs intended to effectively transition students from middle to high school. Limited research has examined the perceptions of at-risk students as they interact with these programs. The purpose of this case study was to identify at-risk student perceptions regarding the helpfulness of transition activities during their move from middle to high school. A team of school personnel in each of two Maine schools identified potential eighth-graders for participation. Qualitative data was collected and analyzed from transition documents and interviews conducted with students at two intervals: during the spring of eighth grade and again in the fall of the ninth. Findings focused on three essential components of the transition process: personal/social, procedural/organizational, and academic. While the emphasis of the formal transition activities organized by the schools was perceived as primarily academic, students highlighted the importance of the personal/social aspects, often developed through more informal avenues. Peer interactions, meaningful adult relationships, and belonging through athletics, the arts, and other extra- and co-curricular activities were cited as contributing to engagement with their ninth-grade environment. Results reflect the changing nature of student perceptions regarding the helpfulness of the transition activities, as well as offer, through the words of the participants, suggestions for improvements. The results of this study may assist administrators and educators as they design, implement, and assess transition programming in their individual settings, as well as contribute to the literature on issues related to the transition process and the critical ninth-grade year. These results will also add fourteen voices to the limited existing research on student perceptions of the transition experience, research that should continue to explore the temporal nature of this process throughout students' eighth and ninth-grade years.</p>

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<author>Pamela L. Astbury</author>


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<item>
<title>Inside the Gap: Innovative Uses of Technology and Student Teachers</title>
<link>http://digitalcommons.library.umaine.edu/etd/1005</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1005</guid>
<pubDate>Fri, 04 May 2012 15:17:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>The technological generation gap is a societal phenomenon that also reaches into school classrooms. Typically when the generation gap in technology is discussed it puts students on one side of the gap and teachers on the other, with a clear demarcation implied based on age and assumed experience. This assumption does not account for the emergence of teachers who themselves are considered digital natives, adding a potential gap between younger and more experienced teachers. This study explores the experiences of student teachers who are just entering the field and who, from a technological standpoint, have one foot on each bank of that generational chasm. It reveals their perceptions of the technological generation gap and the challenges they faced in infusing innovative uses of technology into their teaching. For this study, innovative uses of technology included, but were not limited to: blogging; creation of websites, webquests, wikis, podcasts; and the use of a myriad of technological devices such as lcd projectors in conjunction with laptops, cellphones, and mp3 players. Qualitative methods encouraged an in-depth exploration and analysis of the experiences and beliefs of nine recent interns who taught at the middle or high school level, and eight college of education professionals specializing in teacher preparation. In-depth, semi-structured interviews were conducted and the transcripts were analyzed using an inductive method of analysis. For organizational clarity, the data were first sorted by research question, and then by category within each research question. The findings present three themes associated with the implementation of innovative uses of technology by student teachers. First, the need for infusing technologically-based pedagogical practices throughout teacher preparation courses. Creating educational opportunities for pre-service teachers to learn both from university faculty and from each other would expand their knowledge, skill and confidence and knowledge in how to use and integrate technology. Second, diverse factors have an impact on the innovative uses of technology in schools. This theme revealed gaps between technologically rich schools and schools lacking technology, which has implications for relevant instruction. Third, the complexity of the technological generation gap goes far beyond a linear progression with divisions by age. It also manifests itself according to work experience, willingness to embrace new ideas, access to the technology, and acceptable behavior norms for technology use. This study presents implications for teacher preparation programs and school districts, which will need to incorporate technological advances that will prepare students for the global environment in which they will live and work as adults. It will take an infusion of creativity, a financial commitment, and a willingness among educators to embrace new technologies if we hope to advance best practices in teaching for 21st Century learners.</p>

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</description>

<author>Maryellen Mahoney-O&apos;Neil</author>


</item>


<item>
<title>Factors Affecting Implementation Probability of State-Mandated Reform Initiatives: A Study of 6th - 8th Grade Maine Teachers</title>
<link>http://digitalcommons.library.umaine.edu/etd/1004</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1004</guid>
<pubDate>Fri, 04 May 2012 15:17:36 PDT</pubDate>
<description>
	<![CDATA[
	<p>After decades of research on school reform, initiatives to improve student learning have been largely unsuccessful at influencing practice at the classroom level. However, some schools and some teachers are successful at implementing initiatives to improve student learning. This study sought to examine factors that might affect teachers' perceived likelihood of implementation of the Maine Learning Results (MLR), Maine's standards-based learning initiative. The study explored the relationships among four teacher variables: teacher efficacy, teacher attitudes toward the MLR, teacher perceptions of organizational support, and teachers' perceived likelihood of implementing the MLR in 2003. Using a path analysis model, this study examined how the first three variables interacted to influence teachers' perceived likelihood of implementing the MLR. A survey, comprised of four separate scales with established reliability scores, was mailed to a random sample of 200 6th - gth grade, regular-education teachers. The scales were: the Ohio State Teacher Efficacy Scale, perceptions of organizational support, attitudes toward the MLR, and perceived likelihood of MLR implementation. The findings from this study established that teachers overwhelmingly agreed philosophically with high academic standards. However, they were not as supportive of state-mandated standards. Overall, teachers were confident in their teaching abilities. Their views of organizational support varied, and most expressed confidence that they would fully or mostly implement the MLR by 2003. The study found significant positive bivariate relationships among the four teacher variables ranging in strength from .20 to .43. The path analysis established that the three independent variables explained 30% of the variance in the implementation variable. It established that a causal relationship existed among these variables: positive perceptions of organizational support led to a higher teacher efficacy, more positive attitudes toward the MLR, and to an increased likelihood of teachers to perceive they would implement the MLR. The study established that teachers' perceptions of organizational support, teacher efficacy, and attitudes toward a mandated refonn can help to predict teacher perceptions of likelihood to implement a refonn. Policymakers and school administration would be well advised to keep the factors in this study in mind in the development of strategies to support mandated reform.</p>

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</description>

<author>Pamela S. Flood</author>


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<item>
<title>Preparation and Support of Professional Counselors Who Work in Rural Settings</title>
<link>http://digitalcommons.library.umaine.edu/etd/1003</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1003</guid>
<pubDate>Fri, 04 May 2012 15:17:23 PDT</pubDate>
<description>
	<![CDATA[
	<p>The professional counselor who lives and works in a rural setting enjoys the rewards of rural life, but must cope daily with the challenges of rural practice. I t i s commonly believed that the rural context uniquely affects the lives and work o f rural practitioners, yet little recognition has been paid to those effects by the counseling profession. The needs and recommendations of rural professional counselors for preparation and support need to be assessed. Models for the preparation and support of rural professional counselors need to be developed. In this qualitative study the effects of the rural setting on the practice o f 20 professional counselors who live and work in rural settings across the United States are described. The needs and recommendations for preparation and support for their work in the rural environment expressed by those counselors are examined. Implications for the practice, preparation, professional development, support, and supervision of professional counselors for work in the rural setting are discussed</p>

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</description>

<author>Deborah L. Drew</author>


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<item>
<title>Significant Adults as Protective Factors: Retrospective Views of At-Risk Youth</title>
<link>http://digitalcommons.library.umaine.edu/etd/1002</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1002</guid>
<pubDate>Fri, 04 May 2012 15:17:08 PDT</pubDate>
<description>
	<![CDATA[
	<p>Significant adults serve as protective factors in the lives of at-risk youth yet little is known regarding how they become significant to at-risk youth and what actions and behaviors identify them as protective factors. This study identifies those actions and behaviors important to at-risk youth and how those actions and behaviors define qualities and characteristics of the adults that lead to them becoming protective factors. The findings can inform the practice of organizations responsible for ensuring that qualified adults are placed with at-risk youth. The study employed a semistructured interview with 15 participants between the ages of 18 and 29 who met three criteria: They had previously been at-risk; they had at one time been in residential care; and they demonstrated evidence of successful adjustment to adulthood. Interview data were examined through constant comparative analysis to identify the important actions and behaviors attributed to adults who participants described as significant to them. Coding and sorting of the data led to the identification of qualities and characteristics that described adults as significant. In the views of these 15 participants, significant adults demonstrated a willingness to communicate with them, provided personal guidance through supportive approaches, and actively invested in youth by initiating and maintaining connections. These actions and behaviors translated into qualities and characteristics that identified the adult as significant. Participants attributed to adults three broad characteristics that made them significant to them: respectfulness and sincerity, inspiration or motivation, and nurturing. These qualities formed the basis for a dynamic relationship between the participant and the adult that often endured over time, resulting in the adult becoming a protective factor. The patterns of adult behavior and impact revealed as protective in this study can guide the recruitment, training, and performance assessment of professionals working with at-risk youth. Further, this study demonstrates the potential of in-depth qualitative research into the nature of the relationship between at-risk youth and the adults they encounter. Clearly, more examination of the dynamic of protective factors is needed.</p>

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</description>

<author>Gregg Dowty</author>


</item>


<item>
<title>Risk and Protective Factors of Secondary Traumatic Stress in Crisis Counselors</title>
<link>http://digitalcommons.library.umaine.edu/etd/1001</link>
<guid isPermaLink="true">http://digitalcommons.library.umaine.edu/etd/1001</guid>
<pubDate>Fri, 04 May 2012 15:16:51 PDT</pubDate>
<description>
	<![CDATA[
	<p>Because of the nature of their work and their consistent exposure to clients with trauma histories, crisis clinicians may experience symptoms related to secondary traumatic stress (STS). The present study examined the association between personal and work-related factors and STS symptomatology. In addition, coping strategies and self-care behaviors were examined to determine which strategies and behaviors were associated with higher levels of distress. The present study was conducted with 130 crisis clinicians whose work at community mental health crisis centers involves both crisis hotline work and response to clients in acute crisis situations. Clinicians completed packets containing a Clinician Information Form, the Brief COPE (Carver, 1997), the Impact of Event Scale (IES; Horowitz, Wilner, and Alvarez, 1979), the Professional Quality of Life Scale: Compassion Satisfaction (CS), Burnout (BO), Compassion Fatigue / Secondary Trauma (CFIST) Subscales (Stamm, 2002), and a Self-care Behavior checklist developed specifically for the present study. Exploratory correlational analyses found significant associations for the personal factors of Personal Trauma History, Gender, Percentage of Trauma Survivors in Weekly Caseload, Years as a Crisis Worker, Years in the Mental Health Field, and Supervision Hours. There were no significant associations for Age, Educational Level, or Hours with any of the dependent variables and no personal or work-related factors were significantly correlated with IES Avoidance. With regard to coping strategies and self-care behaviors, results of the exploratory correlational analyses indicated that greater utilization of each of the "maladaptive" coping strategies was significantly associated with higher reports of Avoidant symptoms, Intrusive symptoms, Burnout, and CFIST. Unexpectedly, however, none of the "adaptive" coping strategies had inverse significant relationships with any of the dependent variables. In fact, the "adaptive" coping strategy Humor correlated significantly in a positive manner with Compassion Fatigue and Burnout. As expected, reported utilization of most of the "adaptive" strategies did have a statistically significant relationship with Compassion Satisfaction. This information is important not only for research purposes, but to also provide essential information to educators and supervisors, whose responsibility it is to best prepare these crisis clinicians for the important job they do.</p>

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</description>

<author>Catherine J. Lounsbury</author>


</item>


<item>
<title>NEWS@UTEP: Official News Feed of the University of Texas at El Paso</title>
<link>http://digitalcommons.utep.edu/utep_news/50</link>
<guid isPermaLink="true">http://digitalcommons.utep.edu/utep_news/50</guid>
<pubDate>Fri, 04 May 2012 15:15:03 PDT</pubDate>
<description>
	<![CDATA[
	<p>Weekly e-newsletter of the University of Texas at El Paso.</p>

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</description>

<author>University Communications</author>


</item>


<item>
<title>Intestinal transcriptomes of nematodes: Comparison of the parasites Ascaris suum and Haemonchus contortus with the free-living Caenorhabditis elegans</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1016</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1016</guid>
<pubDate>Fri, 04 May 2012 15:07:26 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Yong Yin et al.</author>


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<item>
<title>Leukocyte tyrosine kinase functions in pigment cell development</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1015</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1015</guid>
<pubDate>Fri, 04 May 2012 15:07:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Susana S. Lopes et al.</author>


</item>


<item>
<title>Patchin: Towards a theory and political history of Africana Agrarianism</title>
<link>http://digitalcommons.auctr.edu/dissertations/255</link>
<guid isPermaLink="true">http://digitalcommons.auctr.edu/dissertations/255</guid>
<pubDate>Fri, 04 May 2012 15:01:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>This is a theoretical dissertation that seeks to explore the implications of using an Africana agrarian development philosophy to examine the historical evolution of African-American communities and social movements in the United States. The central theme of this study is the importance of recentering the land question as a theoretical tool used to construct narratives of the cultural development of African-American rural and farming communities. Particular emphasis is placed upon using the notion of an ecological revolution to explain African-Amencan responses to the socio-economic problems that have emerged from their relationship to the American state and, the resultant paradigms that have developed, within the tradition of African-American political philosophy, to both perceive and address these issues.</p>

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</description>

<author>Kwasi Densu</author>


</item>


<item>
<title>The duals of harmonic Bergman spaces</title>
<link>http://repository.cmu.edu/math/374</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/374</guid>
<pubDate>Fri, 04 May 2012 14:58:29 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>C. V.(Charles Vernon) Coffman et al.</author>


</item>


<item>
<title>Tchebychev nets on spheres</title>
<link>http://repository.cmu.edu/math/373</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/373</guid>
<pubDate>Fri, 04 May 2012 14:58:22 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Sandra Samelson</author>


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<item>
<title>Complete isothermal Riemannian metrics on R² having compactly supported Gaussian curvature</title>
<link>http://repository.cmu.edu/math/372</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/372</guid>
<pubDate>Fri, 04 May 2012 14:58:14 PDT</pubDate>
<description>
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</description>

<author>Sandra Samelson</author>


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<item>
<title>On formulation of singularities in one-dimensional nonlinear thermoelasticity</title>
<link>http://repository.cmu.edu/math/371</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/371</guid>
<pubDate>Fri, 04 May 2012 14:58:07 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W Hrusa et al.</author>


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<item>
<title>Probabilistic analysis of the generalised assignment problem</title>
<link>http://repository.cmu.edu/math/370</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/370</guid>
<pubDate>Fri, 04 May 2012 14:58:00 PDT</pubDate>
<description>
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</description>

<author>Martin Dyer et al.</author>


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<item>
<title>Phase transitions of elastic solid materials</title>
<link>http://repository.cmu.edu/math/369</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/369</guid>
<pubDate>Fri, 04 May 2012 14:57:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Irene Fonseca</author>


</item>


<item>
<title>The displacement problem for elastic crystals</title>
<link>http://repository.cmu.edu/math/368</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/368</guid>
<pubDate>Fri, 04 May 2012 14:57:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Irene Fonseca et al.</author>


</item>


<item>
<title>Normal varieties of combinators</title>
<link>http://repository.cmu.edu/math/367</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/367</guid>
<pubDate>Fri, 04 May 2012 14:57:39 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Richard Statman</author>


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<item>
<title>Equilibrium in a simplified dynamic, stochastic economy with heterogeneous agents</title>
<link>http://repository.cmu.edu/math/366</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/366</guid>
<pubDate>Fri, 04 May 2012 14:57:32 PDT</pubDate>
<description>
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</description>

<author>Ioannis Karatzas</author>


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<item>
<title>Martingale and duality methods for utuility [i.e., utility] maximization in an incomplete market</title>
<link>http://repository.cmu.edu/math/365</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/365</guid>
<pubDate>Fri, 04 May 2012 14:57:25 PDT</pubDate>
<description>
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</description>

<author>Ioannis Karatzas</author>


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<item>
<title>Probabilistic analysis of graph algorithms</title>
<link>http://repository.cmu.edu/math/364</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/364</guid>
<pubDate>Fri, 04 May 2012 14:57:17 PDT</pubDate>
<description>
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</description>

<author>Frieze</author>


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<item>
<title>Multiphase thermomechanics with interfacial structure.</title>
<link>http://repository.cmu.edu/math/363</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/363</guid>
<pubDate>Fri, 04 May 2012 14:57:11 PDT</pubDate>
<description>
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</description>

<author>Sigurd B. Angenent et al.</author>


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<item>
<title>A random polynomial time algorithm for approximating the volume of convex bodies</title>
<link>http://repository.cmu.edu/math/362</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/362</guid>
<pubDate>Fri, 04 May 2012 14:57:03 PDT</pubDate>
<description>
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</description>

<author>Martin Dyer et al.</author>


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<item>
<title>Compositions for balanced hypergraphs</title>
<link>http://repository.cmu.edu/math/361</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/361</guid>
<pubDate>Fri, 04 May 2012 14:56:56 PDT</pubDate>
<description>
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</description>

<author>Olivia M. Carducci</author>


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<item>
<title>Conditions for mechanical self-annealing in motions of elastic-plastic oscillators</title>
<link>http://repository.cmu.edu/math/360</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/360</guid>
<pubDate>Fri, 04 May 2012 14:56:49 PDT</pubDate>
<description>
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</description>

<author>David R. Owen et al.</author>


</item>


<item>
<title>On matchings and Hamilton cycles in random graphs</title>
<link>http://repository.cmu.edu/math/359</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/359</guid>
<pubDate>Fri, 04 May 2012 14:56:42 PDT</pubDate>
<description>
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</description>

<author>Frieze</author>


</item>


<item>
<title>On the strength of mechanical and thermal damping in linear materials</title>
<link>http://repository.cmu.edu/math/358</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/358</guid>
<pubDate>Fri, 04 May 2012 14:56:34 PDT</pubDate>
<description>
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</description>

<author>Jacobo Bielak et al.</author>


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<item>
<title>Fully discrete finite element schemes for the Cahn-Hilliard equation</title>
<link>http://repository.cmu.edu/math/357</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/357</guid>
<pubDate>Fri, 04 May 2012 14:56:26 PDT</pubDate>
<description>
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</description>

<author>Charles M. Elliott et al.</author>


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<item>
<title>Combinators hereditarily of order two</title>
<link>http://repository.cmu.edu/math/356</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/356</guid>
<pubDate>Fri, 04 May 2012 14:56:18 PDT</pubDate>
<description>
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</description>

<author>Richard Statman</author>


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<item>
<title>Combinators and the theory of partitions</title>
<link>http://repository.cmu.edu/math/355</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/355</guid>
<pubDate>Fri, 04 May 2012 14:56:11 PDT</pubDate>
<description>
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</description>

<author>Richard Statman</author>


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<item>
<title>Combinators hereditarily of order one</title>
<link>http://repository.cmu.edu/math/354</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/354</guid>
<pubDate>Fri, 04 May 2012 14:56:04 PDT</pubDate>
<description>
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</description>

<author>Richard Statman</author>


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<item>
<title>Classification of balanced sets and critical points of even functions on spheres</title>
<link>http://repository.cmu.edu/math/353</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/353</guid>
<pubDate>Fri, 04 May 2012 14:55:56 PDT</pubDate>
<description>
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</description>

<author>C. V.(Charles Vernon) Coffman</author>


</item>


<item>
<title>On the number of Hamilton cycles in a random graph</title>
<link>http://repository.cmu.edu/math/352</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/352</guid>
<pubDate>Fri, 04 May 2012 14:55:48 PDT</pubDate>
<description>
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</description>

<author>C Cooper et al.</author>


</item>


<item>
<title>Regularity of the value function for a two-dimensional singular stochastic control problem</title>
<link>http://repository.cmu.edu/math/351</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/351</guid>
<pubDate>Fri, 04 May 2012 14:55:41 PDT</pubDate>
<description>
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</description>

<author>H. Mete. Soner et al.</author>


</item>


<item>
<title>Zero investment in a high yield asset can be optimal</title>
<link>http://repository.cmu.edu/math/350</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/350</guid>
<pubDate>Fri, 04 May 2012 14:55:34 PDT</pubDate>
<description>
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</description>

<author>Gan-lin Xu</author>


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<item>
<title>A viscosity solution approach to the asymptotic analysis of queueing systems</title>
<link>http://repository.cmu.edu/math/349</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/349</guid>
<pubDate>Fri, 04 May 2012 14:55:27 PDT</pubDate>
<description>
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</description>

<author>Paul Dupuis et al.</author>


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<item>
<title>Explicit expressions for the Lyapunov exponents of certain Markov processes</title>
<link>http://repository.cmu.edu/math/348</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/348</guid>
<pubDate>Fri, 04 May 2012 14:55:20 PDT</pubDate>
<description>
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</description>

<author>A Leizarowitz</author>


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<item>
<title>Tests for injectivity in finitely generated universal Horn classes</title>
<link>http://repository.cmu.edu/math/347</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/347</guid>
<pubDate>Fri, 04 May 2012 14:55:13 PDT</pubDate>
<description>
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</description>

<author>Michael H. Albert</author>


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<item>
<title>The gradient theory of phase transitions for systems with two potential wells</title>
<link>http://repository.cmu.edu/math/346</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/346</guid>
<pubDate>Fri, 04 May 2012 14:55:06 PDT</pubDate>
<description>
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</description>

<author>Irene Fonseca et al.</author>


</item>


<item>
<title>Norm-bounded tridiagonalizing similarity transformations for matrices</title>
<link>http://repository.cmu.edu/math/345</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/345</guid>
<pubDate>Fri, 04 May 2012 14:54:59 PDT</pubDate>
<description>
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</description>

<author>William W. Hager et al.</author>


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<item>
<title>Application of average eigenvectors</title>
<link>http://repository.cmu.edu/math/344</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/344</guid>
<pubDate>Fri, 04 May 2012 14:54:52 PDT</pubDate>
<description>
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</description>

<author>Roger N. Pederson</author>


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<item>
<title>Occupancy problems and random algebras</title>
<link>http://repository.cmu.edu/math/343</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/343</guid>
<pubDate>Fri, 04 May 2012 14:54:44 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Michael H. Albert et al.</author>


</item>


<item>
<title>Elementary order varieties</title>
<link>http://repository.cmu.edu/math/342</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/342</guid>
<pubDate>Fri, 04 May 2012 14:54:38 PDT</pubDate>
<description>
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</description>

<author>Michael H. Albert</author>


</item>


<item>
<title>Multiphase thermomechanics with interfacial structure.</title>
<link>http://repository.cmu.edu/math/341</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/341</guid>
<pubDate>Fri, 04 May 2012 14:54:31 PDT</pubDate>
<description>
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</description>

<author>Morton E. Gurtin</author>


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<item>
<title>Existence and uniqueness results for semi-linear Dirichlet problems in annuli</title>
<link>http://repository.cmu.edu/math/340</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/340</guid>
<pubDate>Fri, 04 May 2012 14:54:23 PDT</pubDate>
<description>
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</description>

<author>C. V.(Charles Vernon) Coffman et al.</author>


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<item>
<title>On random minimum length spanning trees</title>
<link>http://repository.cmu.edu/math/339</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/339</guid>
<pubDate>Fri, 04 May 2012 14:54:17 PDT</pubDate>
<description>
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</description>

<author>Frieze et al.</author>


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<item>
<title>Hope and Guidance for Parents of Children with OCD: A Review of &lt;i&gt;Freeing Your Child from Obsessive-Compulsive Disorder&lt;/i&gt; [Book Review Section]</title>
<link>http://digitalcommons.unl.edu/edpsychpapers/143</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/edpsychpapers/143</guid>
<pubDate>Fri, 04 May 2012 14:54:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>A favorable review of <em>Freeing Your Child from Obsessive-Compulsive Disorder</em> by T.E. Chansky (Crown Publishers, 2004). From the review: "Closely following March and Mulle's (1998) treatment protocol, this book is guided by the philosophy that an individual with OCD must “boss back” symptoms in order to break the symptom cycle. With this approach OCD is objectified (and externalized) as a “brain bully” or enemy that can be overcome with knowledge, determination, and support. Separating the child from his/her OCD symptoms is an effective, concrete technique that children and adolescents will readily comprehend. Such a tactic reminds parents that their child is not OCD; rather, their child sometimes experiences and is challenged by symptoms of OCD. Chansky's knowledge, experience, and genuine optimism are strongly evident in this invaluable resource for parents."</p>

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</description>

<author>Richard J. Cowan et al.</author>


</item>


<item>
<title>On the independence number of random regular graphs</title>
<link>http://repository.cmu.edu/math/338</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/338</guid>
<pubDate>Fri, 04 May 2012 14:54:09 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frieze et al.</author>


</item>


<item>
<title>Interfacial energy and the Maxwell rule</title>
<link>http://repository.cmu.edu/math/337</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/337</guid>
<pubDate>Fri, 04 May 2012 14:54:01 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Irene Fonseca</author>


</item>


<item>
<title>One dimensional infinite-horizon variational problems arising in viscoelasticity</title>
<link>http://repository.cmu.edu/math/336</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/336</guid>
<pubDate>Fri, 04 May 2012 14:53:53 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>A Leizarowitz et al.</author>


</item>


<item>
<title>On &quot;multibump&quot; bound states for certain semilinear elliptic equations</title>
<link>http://repository.cmu.edu/math/335</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/335</guid>
<pubDate>Fri, 04 May 2012 14:53:46 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Stanley Alama et al.</author>


</item>


<item>
<title>Workshop on shear bands : March 23-25, 1992 (abstracts)</title>
<link>http://repository.cmu.edu/math/334</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/334</guid>
<pubDate>Fri, 04 May 2012 14:53:39 PDT</pubDate>
<description>
	<![CDATA[
	
	]]>
</description>


</item>


<item>
<title>Singularities and uniqueness of cylindrically symmetric surfaces moving by mean curvature</title>
<link>http://repository.cmu.edu/math/333</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/333</guid>
<pubDate>Fri, 04 May 2012 14:53:32 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>H. Mete. Soner et al.</author>


</item>


<item>
<title>A Gronwall inequality for weakly Lipschitzian mappings</title>
<link>http://repository.cmu.edu/math/332</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/332</guid>
<pubDate>Fri, 04 May 2012 14:53:24 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>David R. Owen et al.</author>


</item>


<item>
<title>Shear bands as discontinuities</title>
<link>http://repository.cmu.edu/math/331</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/331</guid>
<pubDate>Fri, 04 May 2012 14:53:17 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>W. E. Olmstead et al.</author>


</item>


<item>
<title>H-measures applied to symmetric systems</title>
<link>http://repository.cmu.edu/math/330</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/330</guid>
<pubDate>Fri, 04 May 2012 14:53:10 PDT</pubDate>
<description>
	<![CDATA[
	<p>Abstract: "H-measures were recently introduced by Tartar [Thmo] as a tool that might provide much better understanding of propagating oscillations. Partial differential equations of mathematical physics can (almost always) be written in the form of a symmetric system: [n over [sigma] over k=1]A[superscript k][delta subscript k]u + Bu = f, where A[superscript k] and B are matrix functions, while u is a vector unknown function, and f a known vector function. In this work we prove a general propagation theorem for H-measures associated to symmetric systems (theorem 3). This result, combined with the localisation property ([Thmo]) is then used to obtain more precise results on the behaviour of H-measures associated to the wave equation and Maxwell's system. Particular attention is paid to the equations that change type: Tricomi's equation and variants. The H-measure is not supported in the elliptic region; it moves along the characteristics in the hyperbolic region, and bounces of [sic] the parabolic boundary, which separates the hyperbolic region from the elliptic region."</p>

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</description>

<author>N Antonic╠ü</author>


</item>


<item>
<title>Anisotropic singular perturbations : the vectorial case</title>
<link>http://repository.cmu.edu/math/329</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/329</guid>
<pubDate>Fri, 04 May 2012 14:53:03 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ana Cristina. Barroso et al.</author>


</item>


<item>
<title>Jensen&apos;s inequality in the calculus of variations</title>
<link>http://repository.cmu.edu/math/328</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/328</guid>
<pubDate>Fri, 04 May 2012 14:52:56 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Pedregal</author>


</item>


<item>
<title>Relaxation of quasiconvex functionals in B V (Ω, p) for integrands f(x,u,Δu)</title>
<link>http://repository.cmu.edu/math/327</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/327</guid>
<pubDate>Fri, 04 May 2012 14:52:49 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Irene Fonseca et al.</author>


</item>


<item>
<title>Construction of a class of integral models for heat flow in materials with memory</title>
<link>http://repository.cmu.edu/math/326</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/326</guid>
<pubDate>Fri, 04 May 2012 14:52:42 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Deborah Brandon et al.</author>


</item>


<item>
<title>On random regular graphs with non-constant degree</title>
<link>http://repository.cmu.edu/math/325</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/325</guid>
<pubDate>Fri, 04 May 2012 14:52:34 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frieze</author>


</item>


<item>
<title>Random graph orders</title>
<link>http://repository.cmu.edu/math/324</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/324</guid>
<pubDate>Fri, 04 May 2012 14:52:27 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Michael H. Albert et al.</author>


</item>


<item>
<title>Edge disjoint spanning trees in random graphs</title>
<link>http://repository.cmu.edu/math/323</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/323</guid>
<pubDate>Fri, 04 May 2012 14:52:20 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frieze et al.</author>


</item>


<item>
<title>Existence and uniqueness of multi-agent equilibrium in a stochastic, dynamic consumption investment model</title>
<link>http://repository.cmu.edu/math/322</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/322</guid>
<pubDate>Fri, 04 May 2012 14:52:13 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Ioannis Karatzas et al.</author>


</item>


<item>
<title>On the independence number of random graphs</title>
<link>http://repository.cmu.edu/math/321</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/321</guid>
<pubDate>Fri, 04 May 2012 14:52:05 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Frieze</author>


</item>


<item>
<title>Some results on the basis problem for proper combinators with pure effect</title>
<link>http://repository.cmu.edu/math/320</link>
<guid isPermaLink="true">http://repository.cmu.edu/math/320</guid>
<pubDate>Fri, 04 May 2012 14:51:58 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>

<author>Douglas E. Ensley</author>


</item>


<item>
<title>Dipole and Nondipole Angular-Distribution Effects in the Valence Photoemission of Neon</title>
<link>http://digitalcommons.library.unlv.edu/hrc_fac_articles/25</link>
<guid isPermaLink="true">http://digitalcommons.library.unlv.edu/hrc_fac_articles/25</guid>
<pubDate>Fri, 04 May 2012 14:50:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>Nondipole angular-distribution parameters <em>γ</em> and <em>δ</em> for neon 2s and 2p photoelectrons have been measured and are compared to all available theoretical data. The agreement is very good throughout the 150–1200 eV photon-energy range studied. Furthermore, the neon 2p dipole angular-distribution parameter <em>β</em> and the 2s to 2p cross-section ratio have been measured throughout the same photon-energy range. The agreement between theoretical data and experiment is excellent.</p>

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</description>

<author>Oliver Hemmers et al.</author>


</item>


<item>
<title>Ultrafast resonance-enhanced multiphoton ionization in the azabenzenes: Pyridine, pyridazine, pyrimidine, and pyrazine</title>
<link>http://digitalcommons.unl.edu/physicsuiterwaal/17</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsuiterwaal/17</guid>
<pubDate>Fri, 04 May 2012 14:44:45 PDT</pubDate>
<description>
	<![CDATA[
	<p>We report on the ultrafast photoionization of pyridine, pyridazine, pyrimidine, and pyrazine. These four molecules represent a systematic series of perturbations into the structure of a benzene ring which explores the substitution of a C–H entity with a nitrogen atom, creating a heterocyclic structure. Data are recorded under intense-field, single-molecule conditions. The pulses (50 fs, 800 nm) are focused into the molecular vapor, and ion mass spectra are recorded for intensities of ∼10<sup>13</sup> W/cm<sup>2</sup> to ∼10<sup>15</sup> W/cm<sup>2</sup>. We measure ion yields in the absence of the focal volume effect without the need for deconvolution of the data. For all targets, stable singly- and doubly-charged parent ions (C<sub>6-n</sub>H<sub>6-n</sub>N<sub>n</sub> <sup>+(+)</sup>) are observed with features suggesting resonance-enhanced ionization. From the intensity dependence of the ion yield, we infer that excitation occurs both through 1ππ* transitions (remnants of the benzene structure) and through <sup>1</sup>nπ<sup>*</sup> transitions, the latter being a result of Rydberg-like excitations of the lone pair electrons of the nitrogen atoms. Stability against intensefield fragmentation is also discussed.</p>

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</description>

<author>Timothy D. Scarborough et al.</author>


</item>


<item>
<title>Dissociative electron attachment and vibrational excitation of CF3Cl: Effect of two vibrational modes revisited</title>
<link>http://digitalcommons.unl.edu/physicsfabrikant/7</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsfabrikant/7</guid>
<pubDate>Fri, 04 May 2012 14:40:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>We present a study of dissociative electron attachment and vibrational excitation processes in electron collisions with the CF<sub>3</sub>Cl molecule. The calculations are based on the two-dimensional nuclear dynamics including the C-Cl symmetric stretch coordinate and the CF<sub>3</sub> symmetric deformation (umbrella) coordinate. The complex potential energy surfaces are calculated using the ab initio R-matrix method. The results for dissociative attachment and vibrational excitation of the umbrella mode agree quite well with experiment whereas the cross section for excitation of the C-Cl symmetric stretch vibrations is about a factor-of-three too low in comparison with experimental data.</p>

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</description>

<author>Michal Tarana et al.</author>


</item>


<item>
<title>Migratory dermal dendritic cells act as rapid sensors of protozoan parasites</title>
<link>http://digitalcommons.wustl.edu/open_access_pubs/1014</link>
<guid isPermaLink="true">http://digitalcommons.wustl.edu/open_access_pubs/1014</guid>
<pubDate>Fri, 04 May 2012 14:38:55 PDT</pubDate>
<description>
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</description>

<author>Lai Guan Ng et al.</author>


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<item>
<title>The sweep rate dependence of the electrical control of magnetic coercivity</title>
<link>http://digitalcommons.unl.edu/physicsducharme/84</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsducharme/84</guid>
<pubDate>Fri, 04 May 2012 14:36:24 PDT</pubDate>
<description>
	<![CDATA[
	<p>The sweep rate dependence of the coercive field in magnetic thin films is well-known. Here we present an experimental investigation of the dependence of electric field control of magnetization on the magnetic field sweep rate. Our sample is a ferroelectric/ferromagnetic heterostructure, with a soft polymer ferroelectric in contact with a transition metal ferromagnet, Co. Previous work on these heterostructures revealed a large change in coercive field and anisotropy when the ferroelectric polarization was switched from up to down. The present work shows that faster sweep rates increase the changes in coercive field that arise from switching the ferroelectric polarization. Our data indicate that the field sweep rate is an important parameter in the investigation of magnetoelectric coupling.</p>

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</description>

<author>Abhijit Mardana et al.</author>


</item>


<item>
<title>Orientational imaging in polar polymers by piezoresponse force microscopy</title>
<link>http://digitalcommons.unl.edu/physicsducharme/83</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsducharme/83</guid>
<pubDate>Fri, 04 May 2012 14:34:40 PDT</pubDate>
<description>
	<![CDATA[
	<p>We report orientational imaging of the polarization distribution in nanostructured ferroelectric copolymer of polyvinylidene fluoride-trifluoroethylene (PVDF-TrFE) and collagen fibrils using vertical and lateral modes of piezoresponse force microscopy (PFM). In PVDF-TrFE, detection of azimuthal variations in the lateral PFM signal is attributed to the alignment of the molecular chains along different directions. Local switching in PVDF-TrFE is shown to proceed via 120 degrees or 180 degrees rotation of dipoles around the molecular chain, depending upon the strength of the applied electric field. Analysis of the vertical and lateral PFM signals in collagen reveals polar anisotropy of the electromechanical properties along the axes of the fibrils. The surface plots of the piezoelectric response are constructed for both materials based on their piezoelectric tensors and are shown to be consistent with the observed vertical and lateral PFM maps.</p>

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</description>

<author>Pankaj Sharma et al.</author>


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<item>
<title>Effect of gadolinium doping on the electronic band structure of europium oxide</title>
<link>http://digitalcommons.unl.edu/physicsdowben/248</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsdowben/248</guid>
<pubDate>Fri, 04 May 2012 14:30:13 PDT</pubDate>
<description>
	<![CDATA[
	<p>High quality films of EuO and Eu<sub>0.96</sub>Gd<sub>0.04</sub>O were grown on p-type Si(100) via pulsed laser deposition. X-raydiffraction results show that the addition of Gd changes the growth texture from [001] to [111]. Angular-resolved photoemission spectroscopy reveals electron pockets around the X points in Gd-doped EuO, indicating that the band gap in EuO is indirect. Combined photoemission and inverse photoemission measurements showan apparent transition from n-type to p-type behavior, which is likely due to band bending near the polar (111) surface.</p>

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</description>

<author>Juan Colon Santana et al.</author>


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<item>
<title>Relational Aggression: Not Just a Female Issue</title>
<link>http://digitalcommons.unl.edu/edpsychpapers/142</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/edpsychpapers/142</guid>
<pubDate>Fri, 04 May 2012 14:23:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>In recent decades, relational aggression has been type-cast as a female form of aggression and the literature has focused on the “gender dichotomy” in our understanding of aggressive behaviors. Girls have been characterized as more relational aggressive (e.g., threatening to withdraw from a relationship and manipulating relationships to damage others) than boys; and boys have been characterized as more physically aggressive than girls. However, other researchers have found no or weak gender differences in relational aggression. Our understanding of gender differences in aggressive behavior and how this affects the developmental progression of bullying and relational aggression among school-aged youth is murky, at best.</p>

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</description>

<author>Susan M. Swearer Napolitano</author>


</item>


<item>
<title>Electron and hole traps in Ag-doped lithium tetraborate (Li2B4O7) crystals</title>
<link>http://digitalcommons.unl.edu/physicsdowben/247</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsdowben/247</guid>
<pubDate>Fri, 04 May 2012 14:23:17 PDT</pubDate>
<description>
	<![CDATA[
	<p>Electron paramagnetic resonance (EPR), electron-nuclear double resonance (ENDOR), and thermoluminescence (TL) are used to characterize the primary electron and hole trapping centers in a lithium tetraborate (Li<sub>2</sub>B<sub>4</sub>O<sub>7</sub>) crystal doped with Ag<sup>+</sup>. Three defects, two holelike and one electronlike, are observed after exposure at room temperature to 60 kV x-rays. The as-grown crystal contains both interstitial Ag<sup>+</sup> ions and Ag<sup>+</sup> ions substituting for Liþ ions. During the irradiation, substitutional Ag<sup>+</sup> ions (4d<sup>10</sup>) trap holes and two distinct Ag<sup>2+</sup> centers (4d<sup>9</sup>) are formed. These Ag<sup>2+</sup> EPR spectra consist of doublets (i.e., the individual <sup>107</sup>Ag and <sup>109</sup>Ag hyperfine lines are not resolved). One of these hole centers is an isolated unperturbed Ag2þ ion and the other is a Ag<sup>2+</sup> ion with a nearby perturbing defect. EPR and ENDOR angular-dependence data provide the g matrix and the <sup>107</sup>Ag and <sup>109</sup>Ag hyperfine matrices for the more intense isolated hole center. In contrast, the electronlike EPR spectrum produced during the irradiation exhibits large nearly isotropic hyperfine interactions with <sup>107</sup>Ag and <sup>109</sup>Ag nuclei and a neighboring I¼3/2 nucleus (either <sup>7</sup>Li or <sup>11</sup>B). This spectrum is assigned to a trapped electron shared between an interstitial Ag ion and the substitutional I¼3/2 ion. Upon warming, the radiation-induced trapped electrons and holes seen with EPR recombine between 100 and 200 degrees C, in agreement with a single strong TL peak observed near 160 degrees C.</p>

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</description>

<author>A. T. Brant et al.</author>


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<item>
<title>An Examination of the Deteriorative Mechanisms and Enabling Factors at the Wanamaker Memorial Tower in Philadelphia</title>
<link>http://repository.upenn.edu/hp_theses/157</link>
<guid isPermaLink="true">http://repository.upenn.edu/hp_theses/157</guid>
<pubDate>Fri, 04 May 2012 14:16:27 PDT</pubDate>
<description>
	<![CDATA[
	<p>The Wanamaker Tower is in a precarious physical state; as will be demonstrated in this thesis; exterior problems with source moisture control have let to the start of failure of the decorative marble cladding of the interior spaces. The physical conservation problem is compounded by the absence of a constituency or advocacy for stewardship of the tower due to family disinterest and the dissolution of the parish congregation. This thesis will examine the condition of the Tower and the mechanisms of deterioration leading to those conditions. This thesis will also present a conservation plan aimed at addressing the treatment of the conditions as well as the future stewardship needs of the Wanamaker Memorial Tower.</p>

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</description>

<author>Katherine Verone</author>


</item>


<item>
<title>Student in library stacks</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/16</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/16</guid>
<pubDate>Fri, 04 May 2012 14:15:56 PDT</pubDate>
<description>
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</description>


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<item>
<title>Saint Joseph&apos;s Hall</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/15</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/15</guid>
<pubDate>Fri, 04 May 2012 14:15:54 PDT</pubDate>
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</description>


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<item>
<title>O&apos;Connor Windows</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/14</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/14</guid>
<pubDate>Fri, 04 May 2012 14:15:52 PDT</pubDate>
<description>
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</description>


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<item>
<title>Nobili Hall</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/13</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/13</guid>
<pubDate>Fri, 04 May 2012 14:15:49 PDT</pubDate>
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</description>


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<item>
<title>NCIP</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/12</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/12</guid>
<pubDate>Fri, 04 May 2012 14:15:47 PDT</pubDate>
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</description>


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<item>
<title>Main campus sign</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/11</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/11</guid>
<pubDate>Fri, 04 May 2012 14:15:45 PDT</pubDate>
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</description>


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<item>
<title>LARAW instructor with student</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/10</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/10</guid>
<pubDate>Fri, 04 May 2012 14:15:42 PDT</pubDate>
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</description>


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<item>
<title>Jesuit emblem</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/9</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/9</guid>
<pubDate>Fri, 04 May 2012 14:15:39 PDT</pubDate>
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</description>


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<item>
<title>Ignatius statue</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/8</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/8</guid>
<pubDate>Fri, 04 May 2012 14:15:37 PDT</pubDate>
<description>
	<![CDATA[
	
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</description>


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<item>
<title>Ignatius statue in bw</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/7</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/7</guid>
<pubDate>Fri, 04 May 2012 14:15:34 PDT</pubDate>
<description>
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</description>


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<item>
<title>Graduating students</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/6</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/6</guid>
<pubDate>Fri, 04 May 2012 14:15:32 PDT</pubDate>
<description>
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</description>


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<item>
<title>Front of law school</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/5</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/5</guid>
<pubDate>Fri, 04 May 2012 14:15:29 PDT</pubDate>
<description>
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</description>


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<item>
<title>Dean with students in moot court room</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/4</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/4</guid>
<pubDate>Fri, 04 May 2012 14:15:27 PDT</pubDate>
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</description>


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<item>
<title>Dean in front of library</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/3</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/3</guid>
<pubDate>Fri, 04 May 2012 14:15:24 PDT</pubDate>
<description>
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</description>


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<item>
<title>Bannan Hall</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/2</link>
<guid isPermaLink="true">http://digitalcommons.law.scu.edu/campusphotos/2</guid>
<pubDate>Fri, 04 May 2012 14:15:21 PDT</pubDate>
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<title>Adobe Wall Lodge</title>
<link>http://digitalcommons.law.scu.edu/campusphotos/1</link>
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<pubDate>Fri, 04 May 2012 14:15:18 PDT</pubDate>
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<title>Berry phase from a randomly fluctuating magnetic field</title>
<link>http://digitalcommons.unl.edu/physicsskomski/69</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsskomski/69</guid>
<pubDate>Fri, 04 May 2012 14:13:39 PDT</pubDate>
<description>
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	<p>The quantum-mechanical Berry phase due to a randomly fluctuating magnetic field is calculated by exploiting an analogous random-walk problem in polymer physics. The phase depends on the time correlations of the magnetic field, despite the adiabatic nature of the Berry phase. A probability distribution for the phase is obtained, and how this phase could affect the magnetotransport in granular magnetic nanostructures is briefly discussed.</p>

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</description>

<author>Ralph Skomski</author>


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<title>Imaging and Control of Surface Magnetization Domains
in a Magnetoelectric Antiferromagnet</title>
<link>http://digitalcommons.unl.edu/physicsbinek/77</link>
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<pubDate>Fri, 04 May 2012 14:10:53 PDT</pubDate>
<description>
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	<p>We report the direct observation of surface magnetization domains of the magnetoelectric Cr<sub>2</sub>O<sub>3</sub> using photoemission electron microscopy with magnetic circular dichroism contrast and magnetic force microscopy. The domain pattern is strongly affected by the applied electric field conditions. Zero-field cooling results in an equal representation of the two domain types, while electric-field cooling selects one dominant domain type. These observations confirm the existence of surface magnetization, required by symmetry in magnetoelectric antiferromagnets.</p>

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</description>

<author>Ning Wu et al.</author>


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<title>Magnetometry and transport data complement polarized neutron reflectometry in magnetic depth profiling</title>
<link>http://digitalcommons.unl.edu/physicsbinek/76</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/physicsbinek/76</guid>
<pubDate>Fri, 04 May 2012 14:05:54 PDT</pubDate>
<description>
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	<p>Exchange coupled magnetic hard layer/soft layer thin films show a variety of complex magnetization reversal mechanisms depending on the hierarchy of interaction strengths within and between the films. Magnetization reversal can include uniform rotation, soft layer biasing, as well as exchange spring behavior. We investigate the magnetization reversal of a CoPt/Permalloy/Ta/Permalloy heterostructure. Here, Stoner-Wohlfarth-type uniform magnetization rotation of the virtually free Permalloy layer and exchange spring behavior of the strongly pinned Permalloy layer are found in the same sample. We investigate the complex magnetization reversal by polarized neutron reflectometry, magnetometry, and magneto-transport. The synergy of combining these experimental methods together with theoretical modeling is key to obtain the complete quantitative depth resolved information of the magnetization reversal processes for a multilayer of mesoscopic thickness.</p>

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</description>

<author>Yi Wang et al.</author>


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<item>
<title>BC Law Magazine Fall/Winter 2011</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/39</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/39</guid>
<pubDate>Fri, 04 May 2012 14:05:24 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>Dance Exchange: An Internship Report</title>
<link>http://scholarworks.uno.edu/aa_rpts/136</link>
<guid isPermaLink="true">http://scholarworks.uno.edu/aa_rpts/136</guid>
<pubDate>Fri, 04 May 2012 14:05:22 PDT</pubDate>
<description>
	<![CDATA[
	<p>As an administrative intern at Dance Exchange in Takoma Park, MD I had the opportunity to study this organization in a transitional phase following the departure of its founder Liz Lerman.  I worked with Dance Exchange from September 6th, 2012 to December 16th, 2012. During that time I updated their media and donor lists, social media outlets, maintained the social media outlets, and assisted in the planning and execution of their HOME events, among other tasks. This paper will serve as an organizational analysis of Dance Exchange.  Following this analysis, I will offer suggestions on how Dance Exchange might proceed so as to best benefit the organization and help them continue to be a presence in the field of modern dance.</p>

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</description>

<author>Colleen Robinson</author>


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<item>
<title>BC Law Magazine Spring/Summer 2011</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/38</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/38</guid>
<pubDate>Fri, 04 May 2012 14:05:21 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Fall/Winter 2010</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/37</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/37</guid>
<pubDate>Fri, 04 May 2012 14:05:17 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Spring/Summer 2010</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/36</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/36</guid>
<pubDate>Fri, 04 May 2012 14:05:15 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Fall/Winter 2009</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/35</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/35</guid>
<pubDate>Fri, 04 May 2012 14:05:11 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Spring/Summer 2009</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/34</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/34</guid>
<pubDate>Fri, 04 May 2012 14:05:08 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Fall/Winter 2008</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/33</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/33</guid>
<pubDate>Fri, 04 May 2012 14:05:04 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Spring/Summer 2008</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/32</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/32</guid>
<pubDate>Fri, 04 May 2012 14:05:00 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Fall/Winter 2007</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/31</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/31</guid>
<pubDate>Fri, 04 May 2012 14:04:57 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Spring/Summer 2007</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/30</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/30</guid>
<pubDate>Fri, 04 May 2012 14:04:54 PDT</pubDate>
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</description>

<author>Boston College  Law School</author>


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<item>
<title>BC Law Magazine Fall/Winter 2006</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/29</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/29</guid>
<pubDate>Fri, 04 May 2012 14:04:52 PDT</pubDate>
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<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Spring/Summer 2006</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/28</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/28</guid>
<pubDate>Fri, 04 May 2012 14:04:47 PDT</pubDate>
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<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Fall/Winter 2005</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/27</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/27</guid>
<pubDate>Fri, 04 May 2012 14:04:45 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Spring/Summer 2005</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/26</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/26</guid>
<pubDate>Fri, 04 May 2012 14:04:42 PDT</pubDate>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Fall/Winter 2004</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/25</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/25</guid>
<pubDate>Fri, 04 May 2012 14:04:39 PDT</pubDate>
<description>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Spring/Summer 2004</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/24</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/24</guid>
<pubDate>Fri, 04 May 2012 14:04:37 PDT</pubDate>
<description>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Fall/Winter 2003</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/23</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/23</guid>
<pubDate>Fri, 04 May 2012 14:04:33 PDT</pubDate>
<description>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Spring/Summer 2003</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/22</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/22</guid>
<pubDate>Fri, 04 May 2012 14:04:30 PDT</pubDate>
<description>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Fall/Winter 2002</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/21</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/21</guid>
<pubDate>Fri, 04 May 2012 14:04:27 PDT</pubDate>
<description>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Spring/Summer 2002</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/20</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/20</guid>
<pubDate>Fri, 04 May 2012 14:04:24 PDT</pubDate>
<description>
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</description>

<author>Boston College Law School</author>


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<item>
<title>BC Law Magazine Fall 2001</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/19</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/19</guid>
<pubDate>Fri, 04 May 2012 14:04:21 PDT</pubDate>
<description>
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</description>

<author>Boston College Law School</author>


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<item>
<title>Boston College Law School Magazine Spring 2001</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/18</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/18</guid>
<pubDate>Fri, 04 May 2012 14:04:18 PDT</pubDate>
<description>
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</description>

<author>Boston College Law School</author>


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<item>
<title>Boston College Law School Magazine Spring 1996</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/17</link>
<guid isPermaLink="true">http://lawdigitalcommons.bc.edu/bclsm/17</guid>
<pubDate>Fri, 04 May 2012 14:04:15 PDT</pubDate>
<description>
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</description>

<author>Boston College Law School</author>


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<item>
<title>Boston College Law School Magazine Fall 2000</title>
<link>http://lawdigitalcommons.bc.edu/bclsm/16</link>
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<pubDate>Fri, 04 May 2012 14:04:13 PDT</pubDate>
<description>
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</description>

<author>Boston College Law School</author>


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<title>Boston College Law School Magazine Spri
