Future marine zooplankton research - a perspective

During the Second Marine Zooplankton Colloquium (MZC2) 3 issues were added to those developed 11 yr ago during the First Marine Zooplankton Colloquium (MZC1). First, we focused on hot spots, i.e., locations where zooplankton occur in higher than regular abundance and/or operate at higher rates. We should be able to determine the processes leading to such aggregations and rates, and quantify their persistence. Second, information on the level of individual species, even of highly abundant ones, is limited. Concerted efforts should be undertaken with highly abundant to dominant species or genera (e.g., Oithona spp., Calanus spp., Oikopleura spp., Euphausia superba) to determine what governs their abundance and its variability. Third, zooplankton clearly influence biogeochemical cycling in the ocean, but our knowledge of the underlying processes remains fragmentary. Therefore a thorough assessment of variables that still need to be quantified is required to obtain an understanding of zooplankton contributions to biogeochemical cycling. Combining studies on the 7 issues from MZC1 with the 3 from MZC2 should eventually lead to a comprehensive understanding of (1) the mechanisms governing the abundance and existence of dominant zooplankton taxa, and (2) the control of biodiversity and biocomplexity, for example, in the tropical ocean where diversity is high. These recommendations come from an assemblage of chemical, physical and biological oceanographers with experience in major interdisciplinary studies, including modeling. These recommendations are intended to stimulate efforts within the oceanographic community to facilitate the development of predictive capabilities for major biological processes in the ocean

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.)