Biosingularity

Archive for October 2007

A study by scientists at UCL (University College London) shows that mice lacking the insulin receptor substrate (IRS)-1 are more resistant to ageing than normal mice. The research adds to a growing body of work showing the importance of insulin signalling pathways as an ageing mechanism in mammals – and potentially humans.

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When elderly nursing home residents contract pneumonia, it is a blow to their already fragile health. Simin Nikbin Meydani, DVM, PhD of the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University and colleagues report that maintaining normal serum zinc concentration in the blood may help reduce the risk of pneumonia development in that population.

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Without sleep, the emotional centers of the brain dramatically overreact to negative experiences, reveals a new brain imaging study in the October 23rd issue of Current Biology, a publication of Cell Press. The reason for that hyperactive emotional response in sleep-deprived people stems from a shutdown of the prefrontal lobe—a region that normally keeps emotions under control.

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MIT researchers have discovered a link between a gene believed to promote long lifespan and a pathway that flushes cholesterol from the body.

The finding could help researchers create drugs that lower the risk of diseases associated with high cholesterol, including atherosclerosis (clogged arteries) and Alzheimer’s disease.

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n a series of mouse experiments, researchers at the Harvard School of Public Health (HSPH) have pinpointed a specific immune deficiency as the likely fundamental cause of ulcerative colitis, a chronic, sometimes severe inflammatory disease of the colon or large intestine that afflicts half a million Americans. Remarkably, the researchers also found that once the disease was established in mice, it could be passed from mother to offspring and even between adult animals, with potential implications for public health and prevention.

The researchers have linked ulcerative colitis in mice to a deficiency of a molecular “peacekeeper” in the immune system, allowing harmful bacteria in the large intestine to breach the bowel’s protective lining and trigger damaging inflammation.

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Although the causes of Alzheimer’s disease are not completely understood, amyloid-beta (A-beta) is widely considered a likely culprit — the “sticky” protein clumps into plaques thought to harm brain cells.

But now researchers at Washington University School of Medicine in St. Louis have uncovered evidence strengthening the case for another potential cause of Alzheimer’s. The finding also represents the first time scientists have found a connection between early- and late-onset Alzheimer’s.

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A human embryonic stem cell is reined in – prevented from giving up its unique characteristics of self-renewal and pluripotency – by the presence of a protein modification that stifles any genes that would prematurely instruct the cell to develop into heart or other specialized tissue. But, thanks to the simultaneous presence of different protein modifications, stem cells are primed and poised, ready to develop into specialized body tissue, Singapore scientists reported in last month’s issue of the journal Cell Stem Cell.

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