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New approach counters diabetes in mice trials
Key Excerpts from Article on Website of San Francisco Chronicle (San Francisco's leading newspaper)


San Francisco Chronicle (San Francisco's leading newspaper), December 11, 2008
Posted: January 2nd, 2009
http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2008/12/11/...

When he was just 7 years old, Sacramento native Nate DeFelice was told he had Type 1 diabetes. So when he joined a diabetes research project at Ben-Gurion University [in Israel] two years ago, he hoped it would be a meaningful experience. As it turns out, the project could change his life and those of millions of other diabetics. DeFelice, 27, never dreamed that he would help discover a potential cure for his disease, see the beginning of a Federal Drug Administration-approved clinical trial in the United States, and co-author a scientific paper along with seven other researchers published in October by the National Academy of Sciences. Type 1 diabetes, usually diagnosed in childhood, is caused by a failure of the insulin-producing cells in the pancreas called "islets." They require daily injections of insulin, which helps break down glucose in the blood. When Ben-Gurion University biochemistry Professor Dr. Eli Lewis asked for volunteers to participate in new research on diabetes, DeFelice jumped at the chance. Lewis, DeFelice and the other researchers have focused their investigations on islet transplantation. The Israeli team then opted for a new approach, ... focusing ... on inflammation caused by the transplant itself. Lewis grafted healthy islets into diabetic mice and treated them with an anti-inflammatory drug called alpha-1-antitrypsin, or AAT. Within months, they discovered three encouraging results: AAT enabled the newly grafted islets to survive indefinitely, successfully secreting insulin. The researchers stopped administering AAT and the islets continued to function. The mice's immune systems remained intact and were able to reject additional grafts while the original transplant continued to function.

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