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TeraMedica Delivers Enterprise Imaging Interchange Technology Contributing To Meaningful Use Of EMRs To Healthcare Facilities With Sun Microsystems
TeraMedica Healthcare Technology announced, along with partner, Sun Microsystems, that the two companies will be offering a pre-configured solution for viewing and managing clinical images originating from different modalities and providers to bring secure, consistent image sharing to point-of-care.

Advocates Express Concern About Embryonic Stem Cell Research Guidelines As Comment Period Closes
Supporters of embryonic stem cell research have expressed concern about the impact on existing research efforts under the Obama administration"s draft guidelines outlining criteria for federal funding of stem cell research, the Washington Post reports. The public comment period for the guidelines ends Tuesday and has generated more than 20,000 comments addressing nearly every element of the proposal. The guidelines, which NIH issued in April, propose limiting federal funding for the research to stem cells derived from unused embryos created for fertility treatments and willingly donated by patients who have given written consent. Former President George W. Bush in August 2001 enacted restrictions limiting federal funding for the research to the 21 stem cell lines existing at the time. Although President Obama in March signed an executive order lifting Bush"s restrictions, some proponents of embryonic stem cell research have suggested that Obama"s plan could actually jeopardize many existing research efforts. The Obama administration is expected to issue its final version of the guidelines by July 7, the Post reports.After Bush restricted federal funding to the embryonic stem cell lines already in existence, many researchers turned to private donors and state governments for the financial support to create hundreds of new lines. Although supporters of the research initially were pleased that the Obama administration"s guidelines would allow federal funding for research on these new existing lines, some are now concerned that certain stipulations in the new guidelines could actually disqualify these research efforts from receiving federal funding. For example, NIH"s proposal requires that couples who wish to donate unused embryos for research sign a consent form indicating that they were fully informed of their alternatives. Although many fertility clinics provide information for couples about their other options, few clinics note these details in written consent forms, according to the Post. Therefore, existing stem cell lines derived from embryos donated by couples who did not sign the required consent forms could be ineligible under NIH"s draft proposal, the Post reports. In addition, many stem cell research supporters also expressed disappointment that only unused embryos created for fertility treatments would be eligible for federal funding.George Daley of the Harvard Stem Cell Institute said that the Obama administration"s guidelines "take 2009 standards and attempt to apply them retroactively, which isn"t really a standard that would allow most of the pre-existing lines to be acceptable for NIH funding." Lawrence Goldstein, director of the University of California-San Diego"s stem cell program, said, "It"s not that past practices were shoddy. But they don"t necessarily meet every letter of the new guidelines moving forward." Goldstein added that researchers would "have to throw everything out and start all over again" under the new proposed guidelines. Amy Comstock Rick, CEO of the Coalition for the Advancement of Medical Research, said that her group is "very concerned" about the funding prospects for existing research efforts, adding that if NIH officials do not modify the guidelines, "very little current research would be eligible" to receive federal funds. However, Raynard Kington, acting NIH director, said the agency is aware of the concerns and "will take them into consideration." He added that "it"s unambiguous that the intent of the president was to expand opportunities and research in this area," as long as such research is "scientifically worthy" and "ethically responsible" (Stein, Washington Post, 5/25).
News of the day
Sugar Tags On Nuclear Proteins Have An Important Developmental Function
Proteins are the executive agents that carry out all processes in a cell. Their activity is controlled and modified with the help of small chemical tags that can be dynamically added to and removed from the protein. 25 years after its first discovery, researchers at the European Molecular Biology Laboratory (EMBL) in Heidelberg have now gained insight into the role of one of these tags, a small sugar residue, that is found on many different proteins across species. In the current online issue of Science they report that the addition of this sugar tag to proteins in the nucleus of a cell is vital for normal development in fruit flies.
Cardiovascular

Baseline Dopamine Levels And Our Motivation To Eat Influenced By Fat Hormone

As we all know from experience, people eat not only because they are hungry, but also because the food just simply tastes too good to pass up. Now, a new study in the August 6th Cell Metabolism, a Cell Press publication, helps to explain how leptin, a hormone produced by fat tissue, influences that motivation to eat. The researchers describe for the first time a new bunch of leptin-responsive (LepRb) neurons in the brain"s lateral hypothalamic area (LHA). Those LHA neurons feed directly into the mesolimbic dopamine system seated in the ventral tegmental area (VTA) of the brain, which controls the rewarding properties we assign to things. "Dopaminergic neurons in the VTA and their downstream targets represent the site of action for drugs of abuse, and also control motivation for food, sex or a fancy car," explained Martin Myers, Jr., of the University of Michigan, Ann Arbor. Put simply, "they control our wanting of stuff." The study therefore adds to growing evidence that leptin doesn"t turn the appetite on and off just by controlling satiety - for instance, whether we feel hungry or full. "Most who have studied leptin in the brain have focused on an important circuit in the ARC," and the leptin-responsive neurons there, Myers said. ARC stands for arcuate nucleus and is an area in the brain"s hypothalamus that controls energy balance by controlling satiety. "It has been assumed that leptin action in the ARC - if not the be all and end all - was responsible for the vast majority of leptin"s effect on appetite." But in fact, neurons bearing leptin receptors exist in many other parts of the brain too. Earlier studies revealed the role of leptin action on the VTA and its influence on dopamine. The new findings show that leptin also has direct effects on the LHA, which in turn exerts greater influence on the dopamine system of the VTA. The new study shows that leptin injected in the LHAs of rats causes the animals to eat less and lose weight. Leptin action in the LHA also raises dopamine content in the brains of otherwise leptin-deficient animals. While in general higher dopamine release tends to be associated with wanting things - food or something else - Myers said he suspects the higher dopamine at baseline may in fact dampen the response to food temptations, making them easier to resist. "Some people may over-eat rewarding food because of a perceived "reward deficit,"" Myers suggested. "When leptin is turned up, it might fix that deficit and make us feel better about a lot of things." It"s not yet clear how the leptin-responsive neurons in the LHA and VTA work together to control dopamine and with it our motivations, according to the researchers. "The unique roles played by these subpopulations of LHA LepRb neurons, as well as those played by VTA LepRb neurons, remain unclear, but could include the requirement for leptin to differentially regulate specific populations of midbrain dopamine neurons and/or to distinctly modulate the incentive for feeding relative to other behaviors. Going forward, it will be important to determine how these various populations of mesolimbic dopamine system-interacting LepRb neurons differ in terms of their wiring and the control of different aspects of mesolimbic dopamine signaling." The new findings do highlight the LHA neurons as a major link between leptin"s anorectic action and the mesolimbic dopamine system, they conclude. "These findings reveal important mechanisms that underlie the regulation of the mesolimbic dopamine system by a crucial signal of energy stores. In the future, it will be crucial to address the potential dysregulation of these neurons in states of obesity." The researchers include Gina M. Leinninger, University of Michigan, Ann Arbor, MI; Young-Hwan Jo, Albert Einstein College of Medicine, Bronx, NY; Rebecca L. Leshan, University of Michigan, Ann Arbor, MI; Gwendolyn W. Louis, University of Michigan, Ann Arbor, MI; Hongyan Yang, University of Michigan, Ann Arbor, MI; Jason G. Barrera, University of Cincinnati, Cincinnati, OH; Hilary Wilson, University of Cincinnati, Cincinnati, OH; Darren M. Opland, University of Michigan, Ann Arbor, MI; Miro A. Faouzi, University of Michigan, Ann Arbor, MI; Yusong Gong, University of Michigan, Ann Arbor, MI; Justin C. Jones, University of Michigan, Ann Arbor, MI; Christopher J. Rhodes, University of Chicago, Chicago, IL; Streamson Chua, Jr., Albert Einstein College of Medicine, Bronx, NY; Sabrina Diano, Yale University, New Haven, CT; Tamas L. Horvath, Yale University, New Haven, CT; Randy J. Seeley, University of Michigan, Ann Arbor, MI; Jill B. Becker, University of Michigan, Ann Arbor, MI; Heike Munzberg, University of Michigan, Ann Arbor, MI; and Martin G. Myers Jr., University of Michigan, Ann Arbor, MI. Cathleen Genova Cell Press


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