B_s->D_s/B->D Semileptonic Form-Factor Ratios and Their Application to BR(B^0_s->\mu^+\mu^-)

We calculate form-factor ratios between the semileptonic decays \bar{B}->D^+\ell^-\bar{\nu} and \bar{B}_s->D_s^+\ell^-\bar{\nu} with lattice QCD. These ratios are a key theoretical input in a new strategy to determine the fragmentation fractions of the neutral B decays, which are needed for measurements of BR(B^0_s-> \mu^+\mu^-). We use the MILC ensembles of gauge configurations with 2+1 flavors of sea quarks at two lattice spacings of approximately 0.12 fm and 0.09 fm. We use the model-independent z-parametrization to extrapolate our simulation results at small recoil toward maximum recoil. Our results for the form-factor ratios are $f_0^{(s)}(M^2_\pi)/f_0^{(d)}(M^2_K) =1.046(44)_{stat.}(15)_{syst.}$ and $f_0^{(s)}(M^2_\pi)/f_0^{(d)}(M^2_\pi)=1.054(47)_{stat.}(17)_{syst.}$. In contrast to a QCD sum-rule calculation, no significant departure from U-spin (ds) symmetry is observed.Comment: 30 pages, 11 figures. Fig. 1 updated. Table II added. Conforms with version published in Physical Review D, except typos fixed, as in the PRD Erratum, in Table V (previously Table IV in arXiv v1). Results unchange

Vascular endothelial growth factor is an important determinant of sepsis morbidity and mortality

Sepsis, the systemic inflammatory response to infection, is a leading cause of morbidity and mortality. The mechanisms of sepsis pathophysiology remain obscure but are likely to involve a complex interplay between mediators of the inflammatory and coagulation pathways. An improved understanding of these mechanisms should provide an important foundation for developing novel therapies. In this study, we show that sepsis is associated with a time-dependent increase in circulating levels of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) in animal and human models of sepsis. Adenovirus-mediated overexpression of soluble Flt-1 (sFlt-1) in a mouse model of endotoxemia attenuated the rise in VEGF and PlGF levels and blocked the effect of endotoxemia on cardiac function, vascular permeability, and mortality. Similarly, in a cecal ligation puncture (CLP) model, adenovirus–sFlt-1 protected against cardiac dysfunction and mortality. When administered in a therapeutic regimen beginning 1 h after the onset of endotoxemia or CLP, sFlt peptide resulted in marked improvement in cardiac physiology and survival. Systemic administration of antibodies against the transmembrane receptor Flk-1 but not Flt-1 protected against sepsis mortality. Adenovirus-mediated overexpression of VEGF but not PlGF exacerbated the lipopolysaccharide-mediated toxic effects. Together, these data support a pathophysiological role for VEGF in mediating the sepsis phenotype

Study of the rare decays of B 0 s Bs0 and B 0 B0 into muon pairs from data collected during the LHC Run 1 with the ATLAS detector

A study of the decays B 0 s →μ + μ − Bs0→μ+μ− and B 0 →μ + μ − B0→μ+μ− has been performed using data corresponding to an integrated luminosity of 25 fb −1 −1 of 7 and 8 TeV proton–proton collisions collected with the ATLAS detector during the LHC Run 1. For the B 0 B0 dimuon decay, an upper limit on the branching fraction is set at B(B 0 →μ + μ − )<4.2×10 −10 B(B0→μ+μ−)<4.2×10−10 at 95 % confidence level. For B 0 s Bs0, the branching fraction B(B 0 s →μ + μ − )=(0.9 +1.1 −0.8 )×10 −9 B(Bs0→μ+μ−)=(0.9−0.8+1.1)×10−9 is measured. The results are consistent with the Standard Model expectation with a p value of 4.8 %, corresponding to 2.0 standard deviations