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Lancet Examines Obama's Pledge To Fight HIV/AIDS
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Study Estimates Cost Added To Private Health Insurance Premiums To Cover Uncompensated Care
The average U.S. family and their employers paid an additional $1,017 in health care premiums in 2008 to pay for care of the uninsured, according to a study released on Thursday by Families USA, USA Today reports (Kim, USA Today, 5/28). According to the study, which examined federal data, the uninsured received $116 billion in health care from hospitals, physicians and other providers in 2008 and paid 37% of that amount. Government programs and charities covered an additional 26%, which left another 37%, or about $43 billion, unpaid. The study then estimated how those costs are when spread across the insured through higher premiums, the study found. According to the study, prepared by the actuarial firm Milliman, the average additional amount paid under private coverage for single individuals was about $370 per year (Werner, AP/Austin American-Statesman, 5/28). Families USA Executive Director Ron Pollack said, "This is a hidden tax on all insurance premiums, whether it is paid by business for their work or by families when they purchase their own coverage" (USA Today, 5/28).The study is available online.
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Could Hormones Explain Gender Differences In Neurological Disease?

Neurological diseases including Parkinson"s, Tourette"s, attention deficit hyperactivity disorder (ADHD), Alzheimer"s, and schizophrenia are all associated with alterations in dopamine-driven function involving the dopamine transporter (DAT). Research published recently in the open access journal BMC Neuroscience suggests that a number of estrogens acting through their receptors affect the DAT, which may explain trends in timing of women"s susceptibility to these diseases. Rebecca Alyea and Cheryl Watson from the University of Texas Medical Branch investigated how physiological estrogen levels might influence neurochemical pathways including dopamine signalling. The authors tested the rapid nongenomic effects of several physiological estrogens (estradiol, estrone, and estriol) on dopamine efflux via the DAT in a non-transfected rat neuronal cell culture model that expresses the three membrane estrogen receptors ERí±, ERöŸ, and GPR30. The authors found that estradiol-mediated dopamine efflux is DAT-specific and not dependent on extracellular Ca2+-mediated vesicular release of dopamine. Using kinase inhibitors they also showed that estradiol-mediated dopamine efflux is dependent on specific signaling kinases (protein kinase C and MEK, but not on PI3K or protein kinase A). While inhibiting dopamine efflux, estrone and estriol caused DAT to leave the plasma membrane. Previous work by Alyea and Watson indicated that the suppression of efflux occurs mainly via ERí±, and in this new study they show a physical association of ERí± and ERöŸ with DAT before and during estrogen action, and trafficking of all three estrogen receptors in and out of the plasma membrane during dopamine efflux. "The significance of estrogen-coupled regulation of the DAT by both direct and indirect (kinase-mediated) interactions between estrogen receptors and the DAT should provide insights into how neurological diseases which involve the DAT are related to developmental, gender, and life stage issues," says Watson. "Such regulation may suggest new ideas about treatment and prevention of diseases associated with extreme hormonal fluctuations such as in postpartum depression." Women experience significant estrogen level changes at various life stages such as adolescence, menopause and as a result of monthly cycles. Women are also most likely to experience the onset or exacerbations of some neurological diseases at these times. Notes: Nongenomic mechanisms of physiological estrogen-mediated dopamine efflux Rebecca A Alyea and Cheryl S Watson BMC Neuroscience (in press) Article available at journal website: http://www.biomedcentral.com/bmcneurosci/. All articles are available free of charge, according to BioMed Central"s open access policy. Charlotte Webber BioMed Central


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