Epitaxial growth and characterization of La2Zr2O 7 multilayers on biaxially textured NiW substrate by chemical solution deposition under highly reducing conditions

The paper presents the growth and characterization of highly textured La2Zr2O7 (LZO) multilayer coatings on Ni-5 at.%W (NiW) biaxially textured substrates by chemical solution deposition (CSD) under highly reducing conditions (Ar + 12%H2) in order to protect the metallic substrate from oxidation. The coating solution consists in a stoichiometric mixture of lanthanum and zirconium acetylacetonates dissolved in an excess of propionic acid. The precursor chemistry was studied by means of infrared spectroscopy, thermogravimetric-differential thermal analyses, Raman spectroscopy and X-ray diffraction carried out on the precursor powder. The as-grown multilayer LZO coating exhibits a sharp in-plane and out-of-plane texture, with the full-width-at-half-maximum of the \u3c9-scans and \u3c6-scans of about 7.2 and 8.0, respectively, close to that of the NiW substrate. The volume fraction of the c-axis oriented grains from the top layer of the coating increases with the number of layers. The LZO coating exhibits a smooth and crack-free surface, appropriate for the further epitaxial growth of a seed layer for the YBa2Cu3O7 - x (YBCO) deposition. Transmission Electron Microscopy was used to investigate the microstructure of the CSD LZO thin films deposited on flexible NiW substrates. A high density of nanovoids, with a size ranging between 10 and 30 nm, was observed in the LZO layers. YBCO films epitaxially grown by pulsed laser deposition on the CSD LZO buffer layer exhibit critical current densities, Jc, close to 1.6 MA/cm2 at 77 K and self-field and zero resistance critical temperature (Tc(R = 0)) of 90.3 K

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.)