New insight into birth defect synpolydactyly
Johnson & Johnson has announced it has extended its previously announced cash tender offer, through its wholly-owned subsidiary, Binder Merger Sub, Inc., for all outstanding shares of common stock of Omrix Biopharmaceuticals, Inc. until 12:00 midnight (Eastern time), on Dec. 26, 2008, unless further extended. The tender offer was originally scheduled to expire at 12:00
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Birth defects characterized by malformation of the limbs are relatively common.
New insight into one form of the birth defect synpolydactyly, where individuals have 1 or more digit (finger or toe) duplicated and 2 or more digits fused together, has now been provided by Stefan Mundlos and colleagues, at Universit?medizin Berlin, Germany, who studied a mouse model of the condition.
One form of synpolydactyly is caused by mutations in the HOXD13 gene. To understand how these mutations cause disease the authors analyzed mice carrying one of these mutations, Spdh/Spdh mice. Surprisingly, the protein generated by the mutated gene was found to have lost a function of the normal Hoxd13 protein and to have gained a new function. Specifically, the mutant protein was unable to facilitate normal levels of production of the soluble factor RA, and intrauterine treatment with RA restored normal digit formation in Spdh/Spdh mice. As RA was shown to normally suppress the generation of cells that produce and maintain cartilage, the loss-of-function mutated Hoxd13 therefore indirectly promotes the formation of cartilage. Importantly, further analysis indicated the mutated protein also directly induced the generation of cells that produce and maintain cartilage, whereas normal Hoxd13 did not. Thus, mutated Hoxd13 causes syndpolydactyly by inducing the generation of cells that produce and maintain cartilage, both directly and indirectly.
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A worldwide group of scientists has created an infectious prion disease in a mouse model, in a step that may help unravel the mystery of this progressive disease that affects the nervous system in humans and animals. The research team, including Christina J. Sigurdson, D.V.M., Ph.D., assistant professor of pathology at the University of California,
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A possible new therapeutic target for pancreatic cancer, the most lethal form of human cancer, has been identified in the proteins whose DNA recipe comes from gene, “Seven-In-Absentia,” according to researchers at the American Society for Cell Biology (ASCB) 48th Annual Meeting, Dec. 13-17, 2008 in San Francisco. In their studies with the fruit fly,
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Researchers have unraveled crucial details of how aging causes broken bones to heal slowly, or not at all, according to study results published today in the Journal of Bone and Mineral Research. The research team also successfully conducted preclinical tests on a potential new class of treatments designed to “rescue” healing capability lost to aging.
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