Search for W\u27 decaying to tau lepton and neutrino in proton-proton collisions at √s=8 TeV

The first search for a heavy charged vector boson in the final state with a tau lepton and a neutrino is reported, using 19.7 fb−1 of LHC data at View the MathML sources=8 TeV. A signal would appear as an excess of events with high transverse mass, where the standard model background is low. No excess is observed. Limits are set on a model in which the W′W′ decays preferentially to fermions of the third generation. These results substantially extend previous constraints on this model. Masses below 2.0 to 2.7 TeV are excluded, depending on the model parameters. In addition, the existence of a W′W′ boson with universal fermion couplings is excluded at 95% confidence level, for W′W′ masses below 2.7 TeV. For further reinterpretation a model-independent limit on potential signals for various transverse mass thresholds is also presented

Myocardial damage due to hypokalaemia and hypophosphataemia.

A case of severe hypokalaemia with stupor, skeletal muscle and heart muscle damage is reported. An initial infusion of glucose-insulin and potassium (GIK) produced a temporary clinical improvement with reduction of creatine kinase (CKMB) and elevation of serum K+. On the 4th day of treatment, neuromuscular and cardiovascular deterioration occurred accompanied by a further rise of CKMB. This deterioration was coincident with a serum phosphate of 0.26 mmol/l. The impaired left ventricular (LV) function was measured using echocardiography and detecting the ejection fraction (EF). GIK was stopped and a potassium phosphate infusion commenced. As the phosphate and potassium deficiencies were corrected, the neuromuscular and cardiac abnormalities resolved, CKMB fell to normal and LVEF rose from 40% to 72%. We suggest that additional cardiac damage due to hypophosphataemia may have occurred in this patient, who already had cardiac impairment as a result of profound hypokalaemia. Possible mechanisms are discussed