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Taxing Health Benefits Could Be Used To Pay For Expanded Coverage, Drive Out Unnecessary Care, Some Say
Economists say taxing health benefits not only could raise billions per year for health care reform efforts, but also could make the system run better, NPR and KHN report.

Osteoporosis-linked Fractures Have Risen Dramatically
The hospitalization rate of patients admitted for treatment of hip, pelvis and other fractures associated with osteoporosis increased by 55 percent between 1995 and 2006, according to the latest News and Numbers from the Agency for Healthcare Research and Quality.
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Vertex Initiates Phase 3 Registration Program For VX-770, An Oral CFTR Potentiator Targeting The Defective Protein Responsible For Cystic Fibrosis
Vertex Pharmaceuticals Incorporated (Nasdaq: VRTX) today announced the initiation of a Phase 3 registration program for VX-770, an investigational Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) potentiator that targets the defective CFTR protein that causes cystic fibrosis (CF). The VX-770 registration program will consist of three clinical trials, including a primary 48-week Phase 3 trial that is currently open to enrollment of patients aged 12 years and older who carry the G551D mutation on at least one allele. Two additional trials will evaluate VX-770 in patients aged 6 to 11 years with the G551D mutation on at least one allele and in patients homozygous for the F508del mutation, respectively.
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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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