Fast responders have blinders on: ERP correlated of response inhibition in competition

Contains fulltext : 73184.pdf (publisher's version ) (Closed access)Recent studies have demonstrated that individuals acting in a social context form shared representations, resulting in incorporating another person's action plan into their own. The present study investigated the extent to which shared representations are formed in a competitive task. Specifically, it was tested whether in competition the process of response inhibition is affected by explicit knowledge of another's task. Event-related potential (ERP) correlates of response inhibition were measured while pairs of participants competed with each other on a speeded go/no-go task. Participants were instructed to always try to respond faster than their direct competitor. No-go stimuli requiring an inhibitory response of the other person as well (compatible action) or no-go stimuli to which the other person should respond (incompatible action) were directly compared. Behavioral performance measures and response inhibition, as reflected in the no-go P3, were decreased on incompatible actions compared to compatible ones. Interestingly, both the behavioral and the ERP effects were caused by the slow responding and thus unsuccessful competitors. These findings indicate that shared representations are formed in competitive tasks, but differently for successful and unsuccessful competitors. Only the slow responders are impeded by incompatible actions. The present study therefore demonstrates that the formation of shared representations is not a fully automatic process. People can differ in the extent to which they incorporate the other's action plan into their own and this may be closely related to successful performance in competitive action

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.)