Fabrication of nanostructure via self-assembly of nanowires within the AAO template

The novel nanostructures are fabricated by the spatial chemical modification of nanowires within the anodic aluminum oxide (AAO) template. To make the nanowires better dispersion in the aqueous solution, the copper is first deposited to fill the dendrite structure at the bottom of template. During the process of self-assembly, the dithiol compound was used as the connector between the nanowires and nanoparticles by a self-assembly method. The nanostructures of the nano cigars and structure which is containing particles junction are characterized by transmission electron microscopy (TEM). These kinds of novel nanostructure will be the building blocks for nanoelectronic and nanophotonic devices

Marine extinctions revisited

In recent years, more than 130 extinctions have been estimated to have occurred in the marine realm. Here we review this body of evidence and show that this figure may actually be overestimated by as much as 50%. We argue that previous estimates have not fully taken into account critical uncertainties such as naturally variable geographical distributions, and have misinterpreted documentary evidence. However, current evidence indicates that some sharks, rays and reef-associated species, although not necessarily geographically restricted, are particularly vulnerable to anthropogenic impacts and now occur in very low numbers. Overestimating extinctions is of concern because it could reduce confidence in the credibility of the ‘extinct’ category in threatened species lists and, ultimately, be used to question the integrity of conservation and management policies. We suggest that when integrating future checklists of marine extinct species, there needs to be a more rigorous use of the terminology of extinction, and participation by specialists in each of the particular taxonomic groups involved.Pablo del Monte-Luna, Daniel Lluch-Belda, Elisa Serviere-Zaragoza, Roberto Carmona, Héctor Reyes-Bonilla, David Aurioles-Gamboa, José Luis Castro-Aguirre, Sergio A. Guzmán del Próo, Oscar Trujillo-Millán and Barry W. Broo

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.)