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Review Provides New Insights Into The Causes Of Anorexia
New imaging technology provides insight into abnormalities in the brain circuitry of patients with anorexia nervosa (commonly known as anorexia) that may contribute to the puzzling symptoms found in people with the eating disorder. In a review paper published on line in Nature Reviews Neuroscience, Walter Kaye, MD, professor of psychiatry and director of the Eating Disorders Program at the University of California, San Diego, and colleagues describe dysfunction in certain neural circuits of the brain which may help explain why people develop anorexia in the first place, and behaviors such as the relentless pursuit of dieting and weight loss.
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Editorial, Opinion Piece Discuss Issues Related To Routine HIV Testing
A recent directive to streamline the HIV testing consent process in Massachusetts as well as consent forms "no longer hav[ing] to accompany test specimens to the lab," are bringing "the state closer to a CDC recommendation that clinicians provide HIV screening on an opt-out basis," according to a Boston Globe editorial. "The opt-out provision is at the heart" of legislation sponsored by state Sen. Patricia Jehlen (D) that would end the state"s requirement of written consent for HIV testing "and instead have healthcare providers inform patients verbally that the test is planned but that they can decline it," the editorial states, adding, "The Jehlen bill would help destigmatize HIV testing itself" (7/6).
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OptumHealth Provides Free Counseling Help Line For People In Missouri And Oklahoma Affected By Tornadoes
OptumHealth Inc. announced that it is providing a free help line to people in Missouri and Oklahoma who are trying to cope with the emotional consequences of the recent tornadoes that hit the region. Staffed by experienced master"s-level behavioral health specialists, the free help line offers assistance to callers seeking help in dealing with stress, anxiety and the grieving process. Callers may also receive referrals to a database of community res to help them with specific concerns, such as financial and legal issues.
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Heart Muscle Protein Can Replace Its Missing Skeletal Muscle Counterpart To Give Mice With Myopathy A Long And Active Life

A heart muscle protein can replace its missing skeletal muscle counterpart to give mice with myopathy a long and active life, show Nowak et al. The findings were published online on May 25, 2009 (http://www.jcb.org) and will appear in the June 1, 2009 print issue of the Journal of Cell Biology. The contraction machinery protein, actin, exists in different forms in the adult heart and skeletal muscles. The heart form, ACTC, is also the dominant form in skeletal muscle of the fetus. But during development, the skeletal form, ACTA1, increases in production and by birth has taken over. It is not clear why the switch occurs, or why it doesn"t occur in the heart, but it happens in every higher vertebrate and, for that reason, has been considered vitally important. Mutations to the ACTA1 gene cause a rare but serious myopathy. Most patients die within the first year of life and some are born almost completely paralyzed. Mice lacking ACTA1 die nine days after birth. Nowak et al. wondered if ACTC could compensate for a lack of ACTA1. The two proteins differ only slightly but, like the developmental switch in production, this difference is conserved across species. Many researchers therefore assumed such compensation would never work. But it did. Nowak and colleagues crossed Acta1 mutant mice with transgenic mice that express human ACTC at high levels in skeletal muscle cells. The resulting mice didn"t die at nine days. In fact, almost all of them (93.5%) survived more than three months, and some more than two years. The mice"s locomotor performance was comparable with wild-type, as was their overall muscle strength (though individual muscle fibers were slightly weaker), and their endurance was actually higher - they ran faster and for longer. This begs the question, Why do we even have ACTA1? Besides pondering that, Nowak and colleagues are also working out how to boost endogenous ACTC as a possible therapy for ACTA1-lacking patients. Nowak, K.J., et al. 2009. J. Cell Biol. doi:10.1083/jcb.200812132 Rita Sullivan Rockefeller University Press


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