Measurement of b hadron lifetimes in exclusive decays containing a J/psi in p-pbar collisions at sqrt(s)=1.96TeV

We report on a measurement of $b$-hadron lifetimes in the fully reconstructed decay modes B^+ -->J/Psi K+, B^0 --> J/Psi K*, B^0 --> J/Psi Ks, and Lambda_b --> J/Psi Lambda using data corresponding to an integrated luminosity of 4.3 ${\rm fb}^{-1}$, collected by the CDF II detector at the Fermilab Tevatron. The measured lifetimes are $\tau$B^+ = $1.639 \pm 0.009 ({\rm stat}) \pm 0.009 {\rm (syst) ~ ps}$, $\tau$B^0 = $1.507 \pm 0.010 ({\rm stat}) \pm 0.008 {\rm (syst) ~ ps}$ and $\tau$Lambda_b = $1.537 \pm 0.045 ({\rm stat}) \pm 0.014 {\rm (syst) ~ ps}$. The lifetime ratios are $\tau$B^+/$\tau$B^0 = $1.088 \pm 0.009 ({\rm stat})\pm 0.004 ({\rm syst})$ and $\tau$Lambda_b/$\tau$B^0 = $1.020 \pm 0.030 ({\rm stat})\pm 0.008 ({\rm syst})$. These are the most precise determinations of these quantities from a single experiment.Comment: revised version. accepted for PRL publicatio

Search for High Mass Resonances Decaying to Muon Pairs in root s=1.96 TeV p(p)over-bar Collisions

We present a search for a new narrow, spin-1, high mass resonance decaying to mu(+)mu(-) + X, using a matrix-element-based likelihood and a simultaneous measurement of the resonance mass and production rate. In data with 4.6 fb(-1) of integrated luminosity collected by the CDF detector in p (p) over bar collisions at root s = 1960 GeV, the most likely signal cross section is consistent with zero at 16% confidence level. We therefore do not observe evidence for a high mass resonance and place limits on models predicting spin-1 resonances, including M > 1071 GeV/c(2) at 95% confidence level for a Z' boson with the same couplings to fermions as the Z boson

Measurement of b Hadron Lifetimes in Exclusive Decays Containing a J/Psi in p(p)over-bar Collisions at root s=1.96 TeV

We report on a measurement of b-hadron lifetimes in the fully reconstructed decay modes B+-> J/psi K+, B-0 -> J/psi K*(892)(0), B-0 -> J/psi K-s(0), and Lambda(0)(b)-> J/psi Lambda(0) using data corresponding to an integrated luminosity of 4.3 fb(-1), collected by the CDF II detector at the Fermilab Tevatron. The measured lifetimes are tau(B+)=[1.639 +/- 0.009(stat)+/- 0.009(syst)]ps, tau(B-0)=[1.507 +/- 0.010(stat)+/- 0.008(syst)]ps, and tau(Lambda(0)(b))=[1.537 +/- 0.045(stat)+/- 0.014(syst)]ps. The lifetime ratios are tau(B+)/tau(B-0)=[1.088 +/- 0.009(stat)+/- 0.004(syst)] and tau(Lambda(0)(b))/tau(B-0)=[1.020 +/- 0.030(stat)+/- 0.008(syst)]. These are the most precise determinations of these quantities from a single experiment

Estimating The Probability Of Informed Trading: A Bayesian Approach

The collection of a large number of $B$ hadron decays to hadronic final states at the CDF II detector is possible due to the presence of a trigger that selects events based on track impact parameters. However, the nature of the selection requirements of the trigger introduces a large bias in the observed proper decay time distribution. A lifetime measurement must correct for this bias and the conventional approach has been to use a Monte Carlo simulation. The leading sources of systematic uncertainty in the conventional approach are due to differences between the data and the Monte Carlo simulation. In this paper we present an analytic method for bias correction without using simulation, thereby removing any uncertainty between data and simulation. This method is presented in the form of a measurement of the lifetime of the $B^{-}$ using the mode B -> D0 pi. The $B^-$ lifetime is measured as $\tau_{B^-}$ = 1.663 $\pm$ 0.023 $\pm$ 0.015 ps, where the first uncertainty is statistical and the second systematic. This new method results in a smaller systematic uncertainty in comparison to methods that use simulation to correct for the trigger bias

A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee

Many clinical trials have evaluated the benefit of long-term use of antiplatelet drugs in reducing the risk of clinical thrombotic events. Aspirin and ticlopidine have been shown to be effective, but both have potentially serious adverse effects. Clopidogrel, a new thienopyridine derivative similar to ticlopidine, is an inhibitor of platelet aggregation induced by adenosine diphosphate. METHODS: CAPRIE was a randomised, blinded, international trial designed to assess the relative efficacy of clopidogrel (75 mg once daily) and aspirin (325 mg once daily) in reducing the risk of a composite outcome cluster of ischaemic stroke, myocardial infarction, or vascular death; their relative safety was also assessed. The population studied comprised subgroups of patients with atherosclerotic vascular disease manifested as either recent ischaemic stroke, recent myocardial infarction, or symptomatic peripheral arterial disease. Patients were followed for 1 to 3 years. FINDINGS: 19,185 patients, with more than 6300 in each of the clinical subgroups, were recruited over 3 years, with a mean follow-up of 1.91 years. There were 1960 first events included in the outcome cluster on which an intention-to-treat analysis showed that patients treated with clopidogrel had an annual 5.32% risk of ischaemic stroke, myocardial infarction, or vascular death compared with 5.83% with aspirin. These rates reflect a statistically significant (p = 0.043) relative-risk reduction of 8.7% in favour of clopidogrel (95% Cl 0.3-16.5). Corresponding on-treatment analysis yielded a relative-risk reduction of 9.4%. There were no major differences in terms of safety. Reported adverse experiences in the clopidogrel and aspirin groups judged to be severe included rash (0.26% vs 0.10%), diarrhoea (0.23% vs 0.11%), upper gastrointestinal discomfort (0.97% vs 1.22%), intracranial haemorrhage (0.33% vs 0.47%), and gastrointestinal haemorrhage (0.52% vs 0.72%), respectively. There were ten (0.10%) patients in the clopidogrel group with significant reductions in neutrophils (< 1.2 x 10(9)/L) and 16 (0.17%) in the aspirin group. INTERPRETATION: Long-term administration of clopidogrel to patients with atherosclerotic vascular disease is more effective than aspirin in reducing the combined risk of ischaemic stroke, myocardial infarction, or vascular death. The overall safety profile of clopidogrel is at least as good as that of medium-dose aspirin