Behaviour and Population Dynamics of Entomopathogenic Nematodes Following Application

Entomopathogenic nematodes (EPN) of the genera Steinernema and Heterorhabditis are widely used in inundative biological pest control programmes. It has long been recognised that increased understanding of the ecology of EPN is important for better predictions of field performance and environmental risk (Ehlers & Hokkanen, 1996; Gaugler, Lewis, & Stuart, 1997). Increasingly, EPN are also finding a place as model organisms for fundamental studies in behavioural ecology and evolutionary biology (Campos-Herrera, Barbercheck, Hoy, & Stock, 2012). In this chapter, I consider the fate of EPN used in biocontrol, focussing largely on inundative application to soil. The aim is to provide an overview of the transformation of a biotechnological product to an ecological entity, rather than a review of this rather broad topic. There are already several extensive reviews relevant to the subject, including EPN behaviour and their fate in soil (e.g. Griffin, 2012; Kaya, 2002; Lewis, Campbell, Griffin, Kaya, & Peters, 2006; Stuart, Barbercheck, Grewal, Taylor, & Hoy, 2006; see also Chap. 4). It should be noted that, while the concept of this chapter is to follow the fate of commercially produced EPN when applied to soil, many of the laboratory studies cited have used nematodes produced in insects rather than taken from commercial formulations

Thrombin-receptor antagonist vorapaxar in acute coronary syndromes

BACKGROUND Vorapaxar is a new oral protease-activated–receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platelet activation. METHODS In this multinational, double-blind, randomized trial, we compared vorapaxar with placebo in 12,944 patients who had acute coronary syndromes without ST-segment elevation. The primary end point was a composite of death from cardiovascular causes, myocardial infarction, stroke, recurrent ischemia with rehospitalization, or urgent coronary revascularization. RESULTS Follow-up in the trial was terminated early after a safety review. After a median follow-up of 502 days (interquartile range, 349 to 667), the primary end point occurred in 1031 of 6473 patients receiving vorapaxar versus 1102 of 6471 patients receiving placebo (Kaplan–Meier 2-year rate, 18.5% vs. 19.9%; hazard ratio, 0.92; 95% confidence interval [CI], 0.85 to 1.01; P = 0.07). A composite of death from cardiovascular causes, myocardial infarction, or stroke occurred in 822 patients in the vorapaxar group versus 910 in the placebo group (14.7% and 16.4%, respectively; hazard ratio, 0.89; 95% CI, 0.81 to 0.98; P = 0.02). Rates of moderate and severe bleeding were 7.2% in the vorapaxar group and 5.2% in the placebo group (hazard ratio, 1.35; 95% CI, 1.16 to 1.58; P<0.001). Intracranial hemorrhage rates were 1.1% and 0.2%, respectively (hazard ratio, 3.39; 95% CI, 1.78 to 6.45; P<0.001). Rates of nonhemorrhagic adverse events were similar in the two groups. CONCLUSIONS In patients with acute coronary syndromes, the addition of vorapaxar to standard therapy did not significantly reduce the primary composite end point but significantly increased the risk of major bleeding, including intracranial hemorrhage