<?xml version="1.0" encoding="utf-8"?><rss version="2.0"><channel><title>RSS for Postconditioning reduces infarct size and cardiac myocyte apoptosis via the opioid receptor and JAK-STAT signaling pathway</title><link>http://academic.research.microsoft.com/Rss.aspx?cata=9&amp;id=34471068</link><description>Search RSS feed for Microsoft Academic Search</description><generator>MSRA Libra RSS Burner</generator><copyright>(c)2008 Microsoft Corpration, All right reserved.</copyright><pubDate>Mon, 20 May 2013 14:35:51 GMT</pubDate><lastBuildDate>Mon, 20 May 2013 14:35:51 GMT</lastBuildDate><category /><item><title>Postconditioning reduces infarct size and cardiac myocyte apoptosis via the opioid receptor and JAK-STAT signaling pathway</title><link>http://academic.research.microsoft.com/Publication/34471068</link><pubDate>Mon, 20 May 2013 07:35:51 GMT</pubDate><guid isPermaLink="false">344710680</guid><description><![CDATA[<div><a href="http://academic.research.microsoft.com/Author/23752410">Lu You</a>, <a href="http://academic.research.microsoft.com/Author/53415045">Li Li</a>, <a href="http://academic.research.microsoft.com/Author/27530168">Qiuling Xu</a>, <a href="http://academic.research.microsoft.com/Author/26709962">Jianghua Ren</a>, <a href="http://academic.research.microsoft.com/Author/21816163">Fan Zhang</a>:
            
            <span style="margin-left:20px" /><span style="margin-left:20px"><a href="http://www.springerlink.com/content/l047t5844v6j155n">view publication</a></span></div><div>Brief intermittent episodes of ischemia and reperfusion could reduce infarct size, a phenomenon called “postconditioning” at the onset of reperfusion after a prolonged period of ischemia. To investigate whether the opioid receptors and signaling factor JAK-STAT might be responsible for the cardioprotection in ischemic postconditioning, and the possible molecular machinery of cardioprotection. Hundred and twenty healthy <a href='http://academic.research.microsoft.com/Keyword/64011/new-zealand'>New Zealand</a>  rabbits were divided into six groups. The <a href='http://academic.research.microsoft.com/Keyword/26978/myocardial-infarct'>myocardial infarct</a>  size, <a href='http://academic.research.microsoft.com/Keyword/4829/cardiac-myocyte'>cardiac myocyte</a>  apoptosis, BCL-2 and P-Stat3 <a href='http://academic.research.microsoft.com/Keyword/33125/protein-expression'>protein expression</a>  were tested in the current study. The results suggested that ischemic postconditioning might increase BCL-2 <a href='http://academic.research.microsoft.com/Keyword/33125/protein-expression'>protein expression</a>  by activating the opioid receptors and JAK-STAT signaling pathway, and also to reduce ischemia-reperfusion-induced cardiomyocyte apoptosis and to play a key role in myocardial protection. However, further research still needs to be done to unravel the underlying mechanisms.</div><div></div><div>Journal: <a href="http://academic.research.microsoft.com/Journal/7752">Molecular Biology Reports - MOL BIOL REP</a>, vol. 38, no. 1, pp. 437-443, 2011</div><div />]]></description></item></channel></rss>