RESUMO
The LHC searches for light compressed top squarks have resulted in considerable bounds in the case where the top squark decays to a neutralino and a charm quark. However, in the case where the top squark decays to a neutralino, a bottom quark, and two fermions via an off-shell W boson, there is currently a significant unconstrained region in the top-squark-neutralino mass plane, still allowing for top squark masses in the range 90-140 GeV. In this Letter we propose a new monojetlike search for light top squarks, optimized for the four-body decay mode, in which at least one b-tagged jet is required. We show that, by using the existing 8 TeV LHC data set, such a search would cover the entire unconstrained region. Moreover, in the process of validating our tools against an ATLAS monojet search, we show that the existing limit can be extended to exclude also top squark masses below 100 GeV.
RESUMO
The relationships among growth hormone (GH), leptin, and resting energy expenditure (REE) are not understood. It has been reported that in malnourished hemodialysis patients, GH increases muscle protein synthesis, a process that requires energy. The present study evaluated the arterial levels and the forearm exchange of leptin, as well as the REE of the same patients during their participation in the same study, in four sequential 6-wk periods: I, baseline; II, GH treatment; III, washout; and IV, GH + intradialytic parenteral nutrition. During periods II and IV, patients received GH (5 mg three times per week). REE rose by 5% in period II, declined during period III, and rose by 7% during period IV. Basal leptin levels were low (2.0 +/- 0.19 ng/L). Insulin and leptin levels, as well as leptin release from the forearm, were unchanged during periods I through III but rose (+ 36%; P: < 0.05) during period IV. Changes in arterial leptin were directly related to changes in forearm leptin release (P: < 0.002), indicating a role of leptin production by peripheral tissues on leptinemia. Changes in leptin release were directly related to insulin (P: < 0.001) and, less consistently, to insulin-like growth factor-binding protein-1 levels (P: < 0.02). Similarly, variations in leptin levels were directly related to insulin (P: < 0.01). Variations in REE were not related to variations in leptin or insulin levels but to changes in muscle protein synthesis (P: < 0.025). The data show that in malnourished hemodialysis patients, treatment with GH is not invariably associated with an increase in leptin production. An increase in leptin release by peripheral tissues and leptin levels occurs only in the setting of hyperinsulinemia. The increase in REE that is induced by treatment with GH is not dependent on changes in leptin but is largely accounted for by the energy cost of the stimulation of muscle protein synthesis.
