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<pubDate>Thu, 21 Aug 2008 17:19:11 BST</pubDate>


	<title>CiteULike: neils distribution</title>
	<description>CiteULike: neils distribution</description>


	<link>http://www.citeulike.org/user/neils/tag/distribution</link>
	<dc:publisher>CiteULike.org</dc:publisher>
	<dc:language>en-gb</dc:language>
	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/neils/article/2884033"/>
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<item rdf:about="http://www.citeulike.org/user/neils/article/2884033">
    <title>Phylogenetic distributions of British birds of conservation concern</title>
    <link>http://www.citeulike.org/user/neils/article/2884033</link>
    <description>&lt;i&gt;Proceedings of the Royal Society B: Biological Sciences&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Recent studies suggest that species' life histories and ecology can be used to forecast future extinction risk. Threatened species often share similar traits such that if a trait predisposing a species to decline or extinction is evolutionarily conserved, then close relatives of threatened species are themselves likely to be at risk. The phylogenetic distribution of current threat has been argued to provide insight into the species that could be threatened in the future when trait data are not available. Conservation criteria are typically based on multiple indices that capture different symptoms of threat including population trends and range contraction. However, there is no reason to assume consistent phylogenetic distributions of different symptoms. I construct a molecular phylogeny of 249 species of British birds (more than 93% of the breeding and wintering species) and use this to show that the species that are threatened due to population declines are phylogenetically more closely related than expected by chance alone. However, species that are listed for other reasons, including range contraction, are distributed randomly with respect to phylogeny. I suggest that while phylogeny can be informative with respect to identifying clades that are susceptible to some measures of extinction risk, such patterns are likely to be idiosyncratic with respect to symptom and taxa.</description>
    <dc:title>Phylogenetic distributions of British birds of conservation concern</dc:title>

    <dc:creator>Gavin Thomas</dc:creator>
    <dc:identifier>doi:10.1098/rspb.2008.0549</dc:identifier>
    <dc:source>Proceedings of the Royal Society B: Biological Sciences</dc:source>
    <dc:date>2008-06-12T00:03:19-00:00</dc:date>
    <prism:publicationName>Proceedings of the Royal Society B: Biological Sciences</prism:publicationName>
    <prism:category>bird</prism:category>
    <prism:category>conservation</prism:category>
    <prism:category>distribution</prism:category>
    <prism:category>ecology</prism:category>
    <prism:category>phylogeny</prism:category>
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<item rdf:about="http://www.citeulike.org/user/neils/article/2053689">
    <title>Distribution of IRAG and cGKI-isoforms in murine tissues.</title>
    <link>http://www.citeulike.org/user/neils/article/2053689</link>
    <description>&lt;i&gt;FEBS Lett, Vol. 575, No. 1-3. (2004), pp. 19-22.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;cGMP kinase I (cGKI) signaling modulates multiple physiological processes including smooth muscle relaxation. The expression of cGKI and its substrate IRAG (Inositol 1,4,5-trisphosphate receptor associated cGMP kinase substrate) was studied. IRAG and cGKI were colocalized in the smooth muscle of aorta and colon. IRAG was present in the thalamus and in most of the myenteric plexus in the absence of cGKI. Coexpression of IRAG and cGKIbeta or cGKIalpha in COS-7 cells revealed that IRAG recruits cGKIbeta but not cGKIalpha to the endoplasmic reticulum. These results suggest that IRAG may be involved in cGKI-dependent and -independent pathways.</description>
    <dc:title>Distribution of IRAG and cGKI-isoforms in murine tissues.</dc:title>

    <dc:creator>A Geiselhöringer</dc:creator>
    <dc:creator>M Gaisa</dc:creator>
    <dc:creator>F Hofmann</dc:creator>
    <dc:creator>J Schlossmann</dc:creator>
    <dc:source>FEBS Lett, Vol. 575, No. 1-3. (2004), pp. 19-22.</dc:source>
    <dc:date>2007-12-04T01:53:36-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>FEBS Lett</prism:publicationName>
    <prism:volume>575</prism:volume>
    <prism:number>1-3</prism:number>
    <prism:startingPage>19</prism:startingPage>
    <prism:endingPage>22</prism:endingPage>
    <prism:category>145-trisphosphate</prism:category>
    <prism:category>animal</prism:category>
    <prism:category>article-pka-pkg</prism:category>
    <prism:category>c57bl</prism:category>
    <prism:category>calcium</prism:category>
    <prism:category>cell</prism:category>
    <prism:category>channel</prism:category>
    <prism:category>cos</prism:category>
    <prism:category>cyclic</prism:category>
    <prism:category>cytoplasmic</prism:category>
    <prism:category>distribution</prism:category>
    <prism:category>endoplasmic</prism:category>
    <prism:category>fusion</prism:category>
    <prism:category>gmp-dependent</prism:category>
    <prism:category>hybridization</prism:category>
    <prism:category>in</prism:category>
    <prism:category>inbred</prism:category>
    <prism:category>inositol</prism:category>
    <prism:category>isoforms</prism:category>
    <prism:category>kinase</prism:category>
    <prism:category>mice</prism:category>
    <prism:category>muscle</prism:category>
    <prism:category>nuclear</prism:category>
    <prism:category>phosphoprotein</prism:category>
    <prism:category>protein</prism:category>
    <prism:category>receptor</prism:category>
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    <prism:category>reticulum</prism:category>
    <prism:category>signal</prism:category>
    <prism:category>situ</prism:category>
    <prism:category>smooth</prism:category>
    <prism:category>tissue</prism:category>
    <prism:category>transduction</prism:category>
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