Precision measurement of the B0s-B¯0s oscillation frequency with the decay B0s → D−sπ+

A key ingredient to searches for physics beyond the Standard Model in B0s mixing phenomena is the measurement of the B0s– ${{\overline{ {\mathrm {B}}}{}}^0_{\mathrm { s}}}$ oscillation frequency, which is equivalent to the mass difference Δms of the B0s mass eigenstates. Using the world's largest B0s meson sample accumulated in a dataset, corresponding to an integrated luminosity of 1.0 fb−1, collected by the LHCb experiment at the CERN LHC in 2011, a measurement of Δms is presented. A total of about 34 000 B0s → D−sπ+ signal decays are reconstructed, with an average decay time resolution of 44 fs. The oscillation frequency is measured to be Δms = 17.768 ± 0.023 (stat) ± 0.006 (syst) ps−1, which is the most precise measurement to date

Incarceration as a key variable in racial disparities of asthma prevalence

<p>Abstract</p> <p>Background</p> <p>Despite the disproportionate incarceration of minorities in the United States, little data exist investigating how being incarcerated contributes to persistent racial/ethnic disparities in chronic conditions. We hypothesized that incarceration augments disparities in chronic disease.</p> <p>Methods</p> <p>Using data from the New York City Health and Nutrition Examination Study, a community-based survey of 1999 adults, we first estimated the association between having a history of incarceration and the prevalence of asthma, diabetes, hypertension using propensity score matching methods. Propensity scores predictive of incarceration were generated using participant demographics, socioeconomic status, smoking, excessive alcohol and illicit drug use, and intimate partner violence. Among those conditions associated with incarceration, we then performed mediation analysis to explore whether incarceration mediates racial/ethnic disparities within the disease.</p> <p>Results</p> <p>Individuals with a history of incarceration were more likely to have asthma compared to those without (13% vs. 6%, p < 0.05) and not more likely to have diabetes or hypertension, after matching on propensity scores. Statistical mediation analysis revealed that increased rates of incarceration among Blacks partially contribute to the racial disparity in asthma prevalence.</p> <p>Conclusion</p> <p>Having been incarcerated may augment racial disparities in asthma among NYC residents. Eliminating health disparities should include a better understanding of the role of incarceration and criminal justice policies in contributing to these disparities.</p

Differential branching fraction and angular analysis of the decay B s0 → φμ + μ -

The determination of the differential branching fraction and the first angular analysis of the decay Bs0 → φμ + μ - are presented using data, corresponding to an integrated luminosity of 1.0 fb-1, collected by the LHCb experiment at √s=7 TeV. The differential branching fraction is determined in bins of q 2, the invariant dimuon mass squared. Integration over the full q 2 range yields a total branching fraction of B (Bs0 → φμ + μ -(7.07 -0.59+0.64± 0.71± 0.71) × 10 -7, where the first uncertainty is statistical, the second systematic, and the third originates from the branching fraction of the normalisation channel. An angular analysis is performed to determine the angular observables F L, S 3, A 6, and A 9. The observables are consistent with Standard Model expectations. [Figure not available: see fulltext.] © 2013 CERN for the benefit of the LHCb collaboration

Observation of B_{c}^{+}→J/ψD_{s}^{+} and B_{c}^{+}→J/ψD_{s}^{*+} decays

The decays B+c→J/ψD+s and B+c→J/ψD*+s are observed for the first time using a dataset, corresponding to an integrated luminosity of 3  fb−1, collected by the LHCb experiment in proton-proton collisions at center-of-mass energies of s√=7 and 8 TeV. The statistical significance for both signals is in excess of 9 standard deviations. The following ratios of branching fractions are measured to be B(B+c→J/ψD+s)B(B+c→J/ψπ+)=2.90±0.57±0.24, B(B+c→J/ψD*+s)B(B+c→J/ψD+s)=2.37±0.56±0.10, where the first uncertainties are statistical and the second systematic. The mass of the B+c meson is measured to be mB+c=6276.28±1.44(stat)±0.36(syst)  MeV/c2, using the B+c→J/ψD+s decay mode

Observation of the narrow state X(3872)-\u3e J/psi pi(+)pi(-) in (p)over-barp collisions at root s=1.96 TeV

We report the observation of a narrow state decaying into J/psipi(+)pi(-) and produced in 220 pb(-1) of (p) over barp collisions at roots=1.96 TeV in the CDF II experiment. We observe 730+/-90 decays. The mass is measured to be 3871.3+/-0.7(stat)+/-0.4(syst) MeV/c(2), with an observed width consistent with the detector resolution. This is in agreement with the recent observation by the Belle Collaboration of the X(3872) meson

Measurement of the cross-section for Z → e+e- production in pp collisions at s√=7 TeV

A measurement of the cross-section for pp → Z → e+e− is presented using data at s√=7 TeV corresponding to an integrated luminosity of 0.94 fb−1. The process is measured within the kinematic acceptance p T > 20 GeV/c and 2 120 GeV/c 2. The cross-section is determined to be $\sigma \left( {\mathrm{pp}\to \mathrm{Z}\to {{\mathrm{e}}^{+}}{{\mathrm{e}}^{-}}} \right)=76.0\pm 0.8\pm 2.0\pm 2.6\;\mathrm{pb}$ where the first uncertainty is statistical, the second is systematic and the third is the uncertainty in the luminosity. The measurement is performed as a function of Z rapidity and as a function of an angular variable which is closely related to the Z transverse momentum. The results are compared with previous LHCb measurements and with theoretical predictions from QCD

Effect of alirocumab on mortality after acute coronary syndromes. An analysis of the ODYSSEY OUTCOMES randomized clinical trial

Background: Previous trials of PCSK9 (proprotein convertase subtilisin-kexin type 9) inhibitors demonstrated reductions in major adverse cardiovascular events, but not death. We assessed the effects of alirocumab on death after index acute coronary syndrome. Methods: ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) was a double-blind, randomized comparison of alirocumab or placebo in 18 924 patients who had an ACS 1 to 12 months previously and elevated atherogenic lipoproteins despite intensive statin therapy. Alirocumab dose was blindly titrated to target achieved low-density lipoprotein cholesterol (LDL-C) between 25 and 50 mg/dL. We examined the effects of treatment on all-cause death and its components, cardiovascular and noncardiovascular death, with log-rank testing. Joint semiparametric models tested associations between nonfatal cardiovascular events and cardiovascular or noncardiovascular death. Results: Median follow-up was 2.8 years. Death occurred in 334 (3.5%) and 392 (4.1%) patients, respectively, in the alirocumab and placebo groups (hazard ratio [HR], 0.85; 95% CI, 0.73 to 0.98; P=0.03, nominal P value). This resulted from nonsignificantly fewer cardiovascular (240 [2.5%] vs 271 [2.9%]; HR, 0.88; 95% CI, 0.74 to 1.05; P=0.15) and noncardiovascular (94 [1.0%] vs 121 [1.3%]; HR, 0.77; 95% CI, 0.59 to 1.01; P=0.06) deaths with alirocumab. In a prespecified analysis of 8242 patients eligible for ≥3 years follow-up, alirocumab reduced death (HR, 0.78; 95% CI, 0.65 to 0.94; P=0.01). Patients with nonfatal cardiovascular events were at increased risk for cardiovascular and noncardiovascular deaths (P<0.0001 for the associations). Alirocumab reduced total nonfatal cardiovascular events (P<0.001) and thereby may have attenuated the number of cardiovascular and noncardiovascular deaths. A post hoc analysis found that, compared to patients with lower LDL-C, patients with baseline LDL-C ≥100 mg/dL (2.59 mmol/L) had a greater absolute risk of death and a larger mortality benefit from alirocumab (HR, 0.71; 95% CI, 0.56 to 0.90; Pinteraction=0.007). In the alirocumab group, all-cause death declined wit h achieved LDL-C at 4 months of treatment, to a level of approximately 30 mg/dL (adjusted P=0.017 for linear trend). Conclusions: Alirocumab added to intensive statin therapy has the potential to reduce death after acute coronary syndrome, particularly if treatment is maintained for ≥3 years, if baseline LDL-C is ≥100 mg/dL, or if achieved LDL-C is low. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01663402