Effects of asynchrony on symmetry perception,Psychologische Forschung

Item does not contain fulltextThe effect of temporal image segmentation on symmetry perception was investigated by means of stimuli composed of one part surrounding another. The two parts could be presented synchronously or with a temporal offset (20-100 ms), and each part could be either symmetrical or random. The task was to discriminate completely symmetrical (S) stimuli (in Experiment 1) or completely random (R) stimuli (in Experiment 2) from partially symmetrical (PS) stimuli in which one part was symmetrical and the other random. The R stimuli showed an asynchrony effect but the S stimuli did not. Furthermore, in both experiments, the PS stimuli showed an asynchrony effect when the symmetrical part was presented last but not when the symmetrical part was presented first (independent of whether it was the surrounded part or the surrounding part). Both results suggest that symmetry is strong enough to override this kind of temporal image segmentation.8 p

Neural Mechanisms for Representing Surface and Contour Features

Contours and surfaces are basic qualities which are processed by the visual system to aid the successful behavior of autonomous beings within the environment. There is increasing evidence that the two modalities of contours and surfaces are processed in separate, but interacting visual streams or sub-systems. Neurons at early stages in the visual system show strong responses only at locations of high contrast, such as edges, but only weak responses within homogeneous regions. Thus, for the processing and representation of surfaces, the visual system has to integrate sparse local measurements into a dense, coherent representation

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.)