Evaluation of the GrovacTM system for decontamination of retail beef trimmings to control E. coli O157:H7 and Salmonella

The Grovac™ intervention system was evaluated for its effectiveness in reducing E. coli O157:H7 and Salmonella inoculated on the surfaces of beef trimmings. Designed to be used in a batch process, the Grovac™ system involves treating beef trimmings in a mixture of citric acid and a hypotonic salt solution while tumbling under vacuum. Beef trimmings were inoculated with a five-strain cocktail of E. coli O157:H7 and Salmonella, then subjected to no treatment, water with a 1-hour drain treatment, water with an overnight drain treatment, Grovac™ with a 1-hour drain treatment, and Grovac™ with an overnight drain treatment. Data indicated that the Grovac™ system may be a viable method for retailers to use with in-house beef grinding operations to reduce E. coli O157:H7 and Salmonella risks. Reductions in these pathogen populations were 85 and 80%, respectively, after draining for 18 hours at 36°F

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.)