Efforts to expand Medicaid while controlling spending must be informed by a deeper understanding of the extent to which the high medical costs associated with severe obesity (having a body mass index of [Formula: see text] or higher) determine spending at the state level. Our analysis of population-representative data indicates that in 2013, severe obesity cost the nation approximately $69 billion, which accounted for 60 percent of total obesity-related costs. Approximately 11 percent of the cost of severe obesity was paid for by Medicaid, 30 percent by Medicare and other federal health programs, 27 percent by private health plans, and 30 percent out of pocket. Overall, severe obesity cost state Medicaid programs almost $8 billion a year, ranging from $5 million in Wyoming to $1.3 billion in California. These costs are likely to increase following Medicaid expansion and enhanced coverage of weight loss therapies in the form of nutrition consultation, drug therapy, and bariatric surgery. Ensuring and expanding Medicaid-eligible populations' access to cost-effective treatment for severe obesity should be part of each state's strategy to mitigate rising obesity-related health care costs.

Objectives:To determine the current immune status of high-risk populations of New South Wales and Victoria to the arboviral pathogens, Murray Valley encephalitis (MVE) and Kunjin (KUN) viruses, which are associated with Australian encephalitis (AE), and Ross River (RR) and Kokobera (KOK) viruses which are associated with polyarthritis. Further, to estimate seroconversion rates to these viruses in high-risk populations over the 10-year period 1981-1991. Design and study population: Blood was taken from 2873 permanent residents, children and adults from previously identified high-risk areas in western NSW and northern Victoria. Samples were tested by the haemagglutination-inhibition (HI) test for antibodies to the four viruses. All sera were also tested for MVE and KUN antibodies by the more specific neutralisation test (NT). Ninety-five of the subjects had been seronegative when sampled 10 years previously.Results: Age standardised prevalence rates for f1avivirus HI antibodies (MVE, KUN, KOK) ranged from 66% (Bourke) to 15% (Forbes), and were similar to those observed 10 years previously. However, specific NT antibodies to MVE and KUN were uncommon in all districts except Bourke, indicating a very high level of susceptibility to Australian encephalitis, should a fresh epidemic occur. Whereas KUN virus seems enzootic in NSW and Victoria, MVE did not appear to have been present since the last outbreak in 1974, even in Bourke. Flavivirus antibody rates (as detected by the broadly reactive HI test) greatly exceeded those specifically attributable to MVE and KUN (NT test) or KOK, leading to the speculation that unidentified flaviviruses are responsible for most human infections. Ross River virus antibody prevalence rates exceeded those of flaviviruses in all districts, ranging from 72% (Bourke) to 25% (Cohuna), and were uniformly higher than those observed in 1981. Ten-year seroconversion rates in seronegative panels were 8.5% for flaviviruses and 24.2% for RR virus, and are broadly consistent with the cross-sectional study. Conclusions: Although f1avivirus and

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The suprachiasmatic nucleus (SCN) contains a circadian clock that generates endogenous rhythmicity and entrains that rhythmicity with the day-night cycle. The neurochemical events that transduce photic input within the SCN and mediate entrainment by resetting the molecular clock have yet to be defined. Because GABA is contained in nearly all SCN neurons we tested the hypothesis that GABA serves as this signal in studies employing Syrian hamsters (Mesocricetus auratus). Activation of GABAA receptors was found to be necessary and sufficient for light to induce phase delays of the clock. Remarkably, the sustained activation of GABAA receptors for more than three consecutive hours was necessary to phase delay the clock. The duration of GABAA receptor activation required to induce phase delays would not have been predicted by either the prevalent theory of circadian entrainment or by expectations regarding the duration of ionotropic receptor activation necessary to produce functional responses. Taken together, these data identify a novel neurochemical mechanism essential for phase delaying the “master” circadian clock within the SCN as well as identifying an unprecedented action of an amino acid neurotransmitter involving the sustained activation of ionotropic receptors.

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