Limits on New Physics from exclusive B→D(∗)ℓνˉB \to D^{(*)}\ell \bar\nu Decays

We consider the exclusive decays $B \to D^{(*)}\,\ell \bar\nu$ and study the effect of non $V-A$ structures on the observables. We extend the standard model hadronic current by additional right-handed vector as well as left- and right-handed scalar and tensor contributions and calculate the decay rates including the perturbative corrections up to order $\alpha_s$. Using the data of the exclusive semileptonic $b \to c$ decays and recent calculations of the form factors at the non-recoil point we discuss the constraints to the wrong helicity admixtures in the hadronic current.Comment: 7 page

Higher Order Power Corrections in Inclusive B Decays

We discuss order 1/m_b^4 and 1/m_b^5 corrections in inclusive semileptonic decay of a $B$ meson. We identify relevant hadronic matrix elements of dimension seven and eight and estimate them using the ground-state saturation approximation. Within this approach the effects on the integrated rate and on kinematic moments are estimated. The overall relative shift in V_{cb} turns out about +0.4% as applied to the existing fits. Similar estimates are presented for B -> X_s+\gamma decays.Comment: 30 pages, 16 figure

Proceedings of the 2nd Workshop on Flavor Symmetries and Consequences in Accelerators and Cosmology (FLASY12)

These are the proceedings of the 2nd Workshop on Flavor Symmetries and Consequences in Accelerators and Cosmology, held 30 June 2012 - 4 July 2012, Dortmund, Germany.Comment: Order 400 pages, several figures including the group picture v2: corrected author list and contributio

Highly multiplexed subcellular RNA sequencing in situ

Understanding the spatial organization of gene expression with single-nucleotide resolution requires localizing the sequences of expressed RNA transcripts within a cell in situ. Here, we describe fluorescent in situ RNA sequencing (FISSEQ), in which stably cross-linked complementary DNA (cDNA) amplicons are sequenced within a biological sample. Using 30-base reads from 8102 genes in situ, we examined RNA expression and localization in human primary fibroblasts with a simulated wound-healing assay. FISSEQ is compatible with tissue sections and whole-mount embryos and reduces the limitations of optical resolution and noisy signals on single-molecule detection. Our platform enables massively parallel detection of genetic elements, including gene transcripts and molecular barcodes, and can be used to investigate cellular phenotype, gene regulation, and environment in situ

Proceedings of the 2nd Workshop on Flavor Symmetries and Consequences in Accelerators and Cosmology (FLASY12)

These are the proceedings of the 2nd Workshop on Flavor Symmetries and Consequences in Accelerators and Cosmology, held 30 June 2012 - 4 July 2012, Dortmund, Germany

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.)