Consequences of catch-and-release angling on the physiology, behaviour and survival of wild steelhead Oncorhynchus mykiss in the Bulkley River, British Columbia

Steelhead, the anadromous form of rainbow trout (Oncorhynchus mykiss), is one of the most coveted recreationally targeted salmonids worldwide, and catch-and-release (C&R) is commonly used as a conservation strategy to protect wild stocks. Nevertheless, little research has examined how wild steelhead respond to capture and handling. During a summer-run recreational fishery on the Bulkley River in British Columbia, we used non-lethal blood sampling and radio telemetry to assess the physiological stress response, post-release behaviour, and survival of wild steelhead exposed to either 0 s, 10 s, or 30 s of air exposure, over a range of water temperatures, fight times, and landing methods. Steelhead that were air exposed following landing had greater reflex impairment and moved further downstream immediately following release than fish kept in the water, though there was no observed difference in movement two weeks after cap

Environmental drivers of habitat use by a marine fish on a heterogeneous and dynamic reef flat

Intertidal and subtidal zones consist of heterogeneous habitats and dynamic environmental conditions, providing diverse options for fish to take advantage of marine resources. We explored how various environmental factors affected habitat use of an ecologically and economically important tropical marine fish, bonefish (Albula vulpes), on a fringing reef flat in Culebra, Puerto Rico, using a fine-scale acoustic telemetry positioning system. Machine learning algorithms and Bayesian inference via integrated nested Laplace approximation indicated diel period was the most important predictor of bonefish habitat use; bonefish occupied seagrass and mixed bottom (seagrass, macroalgae, sand) habitats most often at night, a deep-water soft sediment lagoon during the day,

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.)