Brief hypoxia conditions monocytes to protect reperfused cardiocytes against cell death via the CD11b receptor

10.1016/S1053-2498(02)01161-0Journal of Heart and Lung Transplantation229979-985JHLT

Fusion Energy-Production from a Deuterium-Tritium Plasma in the Jet Tokamak

The paper describes a series of experiments in the Joint European Torus (JET), culminating in the first tokamak discharges in deuterium-tritium fuelled mixtures. The experiments were undertaken within limits imposed by restrictions on vessel activation and tritium usage. The objectives were: (i) to produce more than one megawatt of fusion power in a controlled way; (ii) to validate transport codes and provide a basis for accurately predicting the performance of deuterium-tritium plasma from measurements made in deuterium plasmas; (iii) to determine tritium retention in the torus systems and to establish the effectiveness of discharge cleaning techniques for tritium removal; (iv) to demonstrate the technology related to tritium usage; and (v) to establish safe procedures for handling tritium in compliance with the regulatory requirements. A single-null X-point magnetic configuration, diverted onto the upper carbon target, with reversed toroidal magnetic field was chosen. Deuterium plasmas were heated by high power, long duration deuterium neutral beams from fourteen sources and fuelled also by up to two neutral beam sources injecting tritium. The results from three of these high performance hot ion H-mode discharges are described: a high performance pure deuterium discharge; a deuterium-tritium discharge with a 1% mixture of tritium fed to one neutral beam source; and a deuterium-tritium discharge with 100% tritium fed to two neutral beam sources. The TRANSP code was used to check the internal consistency of the measured data and to determine the origin of the measured neutron fluxes. In the best deuterium-tritium discharge, the tritium concentration was about 11% at the time of peak performance, when the total neutron emission rate was 6.0 x 10(17) neutrons/s. The integrated total neutron yield over the high power phase, which lasted about 2 s, was 7.2 x 10(17) neutrons, with an accuracy of +/- 7%. The actual fusion amplification factor, Q(DT), was about 0.15. With an optimum tritium concentration, this pulse would have produced a fusion power of almost-equal-to 5 MW and a nominal Q(DT) almost-equal-to 0.46. The same extrapolation for the pure deuterium discharge would have given almost-equal-to 11 MW and a nominal Q(DT) = 1.14, so that the total fusion power (neutrons and alpha-particles) would have exceeded the total losses in the equivalent deuterium-tritium discharge in these transient conditions. Techniques for introducing, tracking, monitoring and recovering tritium were demonstrated to be highly effective: essentially all of the tritium introduced into the neutral beam system and, so far, about two thirds of that introduced into the torus have been recovered

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)