Development And Evaluation Of An Observational System For Goalball Match Analysis

Our purpose was to develop and evaluate an observational system for goalball match analysis. We used a non-participant systematic game observation method including eight elite games, video recorded, and randomly chosen. Observational categories and performance indicators were determined for each offensive (i.e., ball control, attack preparation, and throwing) and defensive principles (i.e., defensive balance, throw reading, and blocking). The comprehensive method of development and the ideal reliability levels (kappa coefficient of 0.81-1.00) of this protocol ensure the generation of quantitative and qualitative information for players and coaches and the rigor required for scientific use. Nosso objetivo foi desenvolver e avaliar um sistema de observação para análise do jogo no goalball. Foi usado um método de observação sistemática não participante, incluindo vídeos de oito jogos de elite escolhidos aleatoriamente. Categorias de observação e indicadores de desempenho foram determinadas para cada princípio ofensivo (i.e., controle de bola, preparação do ataque e efetivação do arremesso) e defensivo (i.e., balanço defensivo, leitura da trajetória e interceptação do arremesso). O abrangente método de desenvolvimento e os níveis de confiabilidade ideais (coeficiente kappa de 0,81-1,00) desse protocolo asseguram a geração de informações quantitativas e qualitativas para jogadores e treinadores e o rigor necessário para uso científico. Nuestro objetivo fue desarrollar y evaluar un sistema de observación para el análisis del juego del . goalball. Se utilizó un método de observación sistemática no participante, que incluía vídeos de ocho juegos de élite elegidos al azar. Se determinaron las categorías de observación y los indicadores de rendimiento de cada principio ofensivo (p.ej., control del balón, preparación del ataque y lanzamiento) y defensivo (p.ej., equilibrio defensivo, lectura de la trayectoria e interceptación del lanzamiento). El método completo del desarrollo y los niveles de fiabilidad ideales (coeficiente kappa de 0,81 a 1,00) del presente protocolo aseguran la generación de información cuantitativa y cualitativa para jugadores y entrenadores, y el rigor necesario para el uso científico. © 2016

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.)