B/Nb and d11B systematics in the Phlegrean Volcanic District (PVD)

Boron concentration and isotopic compositions were determined in representative products from the Phlegrean Volcanic District (PVD), which includes Campi Flegrei (CF), and the islands of Procida and Ischia. The most primitive products (from Procida and Ischia islands) are moderately enriched in B (4.6-12 ppm), whereas more evolved products of CF and Ischia Island are more enriched (21-118 ppm). The content of B is positively correlated with Nb, Zr, Th, La and, generally, with all incompatible elements. N11B values are generally lower and more uniform in samples from CF (-6.8 to -10.6%) compared with those from Procida (-3.6 to -8.5%) and Ischia (-2.8 to -8.4%) islands. Overall, B-enrichments relative to fluid-immobile elements of PVD are only slightly higher than those observed in mid-ocean ridge basalts and there is no significant correlation between d11B and B/immobile element ratios. For CF samples including the Campanian Ignimbrite (CI) and most post-CI products, d11B is negatively correlated with 87Sr/86Sr, with extreme compositions represented by evolved products of the CI (higher d11B, lower 87Sr/86Sr) and less evolved shoshonite (lower d11B, higher 87Sr/86Sr). In contrast, samples from Procida, Ischia, and pre-CI products and one young shoshonite from CF define a distinct correlation with primitive trachybasalt as the high d11B, low 87Sr/86Sr end-member, and young shoshonites as the low d11B, high 87Sr/86Sr endmember. The overall interpretation of the geochemical and isotopic data suggests three conclusions: (1) Geochemical and isotopic variations of post-CI products from CF can be explained by mixing/mingling between at least two distinct magmas, i.e. the CI and the young shoshonite (Minopoli 1). (2) The isotopic trend described by Procida trachybasalts, Ischia samples, pre-CI samples from CF and Pigna St. Nicola shoshonite is a mantle trend suggesting the involvement in their genesis of a distinct component depleted in B, with low d11B and high 87Sr/86Sr. A similar component has been invoked to explain the differences between Stromboli potassic lavas and more typical calcalkaline rocks of the Aeolian Islands. This component is consistent with ‘sediments or melts thereof’ introduced into the mantle by subduction, but depleted in B due to metamorphic reactions accompanying subduction. (3) The displacement from the mantle trend of CI and Minopoli 1 shoshonite magmas is probably due to crustal contamination processes

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.)