Sometimes healthy cells commit suicide. In the 1970s, scientists showed that a type of programmed cell death called apoptosis plays a key role in development, and the 2002 Nobel Prize in Physiology or Medicine recognized their work. As apoptotic cells degrade, they display standard characteristics, including irregular bulges in the membrane and nuclear fragmentation.
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A new study led by investigators from the University of Pittsburgh School of Medicine demonstrates that the process of necrosis, long thought to be a chaotic, irreversible pathway to cell death, may actually be triggered as part of a regulated response to stress by a powerful protein, SRP-6, that can potentially halt necrosis in its path.
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A remarkable change takes place in the brains of tiny songbirds every year, and some day the mechanism controlling that change may help researchers develop treatments for age-related degenerative diseases of the brain such as Parkinson’s and dementia.
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Researchers at the University of Pennsylvania School of Medicine have found that proteins known to promote cell death are also necessary for the maturation and proliferation of immune cells. Activation of T-cell receptors on the surface of lymphocytes by foreign antigens initiate a calcium-mediated signaling pathway that ends in cell differentiation and growth.
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Changes in the size, shape, and function of the heart (cardiac remodeling) contribute to the onset and progression of heart failure.
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The developing nervous system of vertebrates initially generates an excess of neurons.
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Recent studies show promise for significantly reducing vascular aging by inactivating TNFa, which has been linked to blood vessel dysfunction and cell death. The related report by Csiszar et al., "Vasculoprotective effects of anti-TNFa treatment in aging," appears in the January issue of The American Journal of Pathology.
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