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     <title>Research suggests popular diabetes drugs can cause abnormal pancreatic growth in humans</title>
   	 <description>(Medical Xpress)—Individuals who had taken a type of drug commonly used to treat Type 2 diabetes showed abnormalities in the pancreas, including cell proliferation, that may be associated with an increased risk of neuroendocrine tumors, according to a new study by researchers from UCLA and the University of Florida. Their findings were published online March 22 in the journal Diabetes.</description>
     <link>http://medicalxpress.com/news/2013-03-popular-diabetes-drugs-abnormal-pancreatic.html</link>
	 <category>Diabetes</category>
	 <pubDate>Wed, 27 Mar 2013 07:27:52 EST</pubDate>
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     <title>As Armstrong case unfolds, experts describe doping's harms</title>
   	 <description>(HealthDay)—In the wake of new allegations around Lance Armstrong's involvement in blood doping, experts are reminding the public of the devastating impact these substances can have on an athlete's health. </description>
     <link>http://medicalxpress.com/news/2012-10-armstrong-case-unfolds-experts-doping.html</link>
	 <category>Health</category>
	 <pubDate>Thu, 11 Oct 2012 19:20:01 EST</pubDate>
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     <title>The role of beta cell regeneration in type 2 diabetes</title>
   	 <description>The World Health Organization (WHO) has declared type 2 diabetes as the epidemic of the 21st century. A study is focusing on understanding the mechanisms underlying insulin resistance and the role of beta-cell regeneration.</description>
     <link>http://medicalxpress.com/news/2012-10-role-beta-cell-regeneration-diabetes.html</link>
	 <category>Diabetes</category>
	 <pubDate>Wed, 10 Oct 2012 08:16:30 EST</pubDate>
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     <title>Hormone discovered that preserves insulin production and beta cell function in diabetes</title>
   	 <description>(Medical Xpress) -- Researchers at Duke University Medical Center have found protective, anti-diabetic functions for a hormone that, like insulin, is produced by the islet cells of the pancreas. The new hormone was found to stimulate insulin secretion from rat and human islet cells and protect islet cells in the presence of toxic, cell-killing factors used in the study.</description>
     <link>http://medicalxpress.com/news/2012-07-hormone-insulin-production-beta-cell.html</link>
	 <category>Medical research</category>
	 <pubDate>Mon, 02 Jul 2012 12:00:07 EST</pubDate>
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     <title>Preventing diabetes: Researchers measure loss of human pancreas cells</title>
   	 <description>(Medical Xpress) -- A Yale University-led research team has developed a way to measure the loss of insulin-producing islet cells in the human pancreas. The death of those beta cells leads to diabetes. The finding is a crucial step in developing therapies to preserve insulin production and slow or halt the progress of diabetes. The study appears in the June issue of the Journal of Nuclear Medicine.</description>
     <link>http://medicalxpress.com/news/2012-06-diabetes-loss-human-pancreas-cells.html</link>
	 <category>Medical research</category>
	 <pubDate>Fri, 01 Jun 2012 06:44:59 EST</pubDate>
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     <title>Researchers find beta cell stress could trigger the development of type 1 diabetes</title>
   	 <description>In type 1 diabetes (T1D), pancreatic beta cells die from a misguided autoimmune attack, but how and why that happens is still unclear. Now, JDRF-funded scientists from the Indiana University School of Medicine have found that a specific type of cellular stress takes place in pancreatic beta cells before the onset of T1D, and that this stress response in the beta cell may in fact help ignite the autoimmune attack. These findings shed an entirely new light into the mystery behind how changes in the beta cell may play a role in the earliest stages of T1D, and adds a new perspective to our understanding how T1D progresses, and how to prevent and treat the disease.</description>
     <link>http://medicalxpress.com/news/2012-03-beta-cell-stress-trigger-diabetes.html</link>
	 <category>Diabetes</category>
	 <pubDate>Thu, 22 Mar 2012 16:39:04 EST</pubDate>
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