247 research outputs found

    Measurement of the branching fraction for Υ(1S)τ+τ\Upsilon (1S) \to \tau^+ \tau^-

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    We have studied the leptonic decay of the Υ(1S)\Upsilon (1S) resonance into tau pairs using the CLEO II detector. A clean sample of tau pair events is identified via events containing two charged particles where exactly one of the particles is an identified electron. We find B(Υ(1S)τ+τ)=(2.61 ± 0.12 +0.090.13)B(\Upsilon(1S) \to \tau^+ \tau^-) = (2.61~\pm~0.12~{+0.09\atop{-0.13}})%. The result is consistent with expectations from lepton universality.Comment: 9 pages, RevTeX, two Postscript figures available upon request, CLNS 94/1297, CLEO 94-20 (submitted to Physics Letters B

    Study of the B^0 Semileptonic Decay Spectrum at the Upsilon(4S) Resonance

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    We have made a first measurement of the lepton momentum spectrum in a sample of events enriched in neutral B's through a partial reconstruction of B0 --> D*- l+ nu. This spectrum, measured with 2.38 fb**-1 of data collected at the Upsilon(4S) resonance by the CLEO II detector, is compared directly to the inclusive lepton spectrum from all Upsilon(4S) events in the same data set. These two spectra are consistent with having the same shape above 1.5 GeV/c. From the two spectra and two other CLEO measurements, we obtain the B0 and B+ semileptonic branching fractions, b0 and b+, their ratio, and the production ratio f+-/f00 of B+ and B0 pairs at the Upsilon(4S). We report b+/b0=0.950 (+0.117-0.080) +- 0.091, b0 = (10.78 +- 0.60 +- 0.69)%, and b+ = (10.25 +- 0.57 +- 0.65)%. b+/b0 is equivalent to the ratio of charged to neutral B lifetimes, tau+/tau0.Comment: 14 page, postscript file also available at http://w4.lns.cornell.edu/public/CLN

    Measurement of the Decay Asymmetry Parameters in Λc+Λπ+\Lambda_c^+ \to \Lambda\pi^+ and Λc+Σ+π0\Lambda_c^+ \to \Sigma^+\pi^0

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    We have measured the weak decay asymmetry parameters (\aLC ) for two \LC\ decay modes. Our measurements are \aLC = -0.94^{+0.21+0.12}_{-0.06-0.06} for the decay mode Λc+Λπ+\Lambda_c^+ \to \Lambda\pi^+ and \aLC = -0.45\pm 0.31 \pm 0.06 for the decay mode ΛcΣ+π0\Lambda_c \to \Sigma^+\pi^0 . By combining these measurements with the previously measured decay rates, we have extracted the parity-violating and parity-conserving amplitudes. These amplitudes are used to test models of nonleptonic charmed baryon decay.Comment: 11 pages including the figures. Uses REVTEX and psfig macros. Figures as uuencoded postscript. Also available as http://w4.lns.cornell.edu/public/CLNS/1995/CLNS95-1319.p

    Observation of the Ξc+\Xi_c^+ Charmed Baryon Decays to Σ+Kπ+\Sigma^+ K^-\pi^+, Σ+Kˉ0\Sigma^+ \bar{K}^{*0}, and ΛKπ+π+\Lambda K^-\pi^+\pi^+

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    We have observed two new decay modes of the charmed baryon Ξc+\Xi_c^+ into Σ+Kπ+\Sigma^+ K^-\pi^+ and Σ+Kˉ0\Sigma^+ \bar{K}^{*0} using data collected with the CLEO II detector. We also present the first measurement of the branching fraction for the previously observed decay mode Ξc+ΛKπ+π+\Xi_c^+\to\Lambda K^-\pi^+\pi^+. The branching fractions for these three modes relative to Ξc+Ξπ+π+\Xi_c^+\to\Xi^-\pi^+\pi^+ are measured to be 1.18±0.26±0.171.18 \pm 0.26 \pm 0.17, 0.92±0.27±0.140.92 \pm 0.27 \pm 0.14, and 0.58±0.16±0.070.58 \pm 0.16 \pm 0.07, respectively.Comment: 12 page uuencoded postscript file, postscript file also available through http://w4.lns.cornell.edu/public/CLN

    Rare variant in scavenger receptor BI raises HDL cholesterol and increases risk of coronary heart disease.

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    Scavenger receptor BI (SR-BI) is the major receptor for high-density lipoprotein (HDL) cholesterol (HDL-C). In humans, high amounts of HDL-C in plasma are associated with a lower risk of coronary heart disease (CHD). Mice that have depleted Scarb1 (SR-BI knockout mice) have markedly elevated HDL-C levels but, paradoxically, increased atherosclerosis. The impact of SR-BI on HDL metabolism and CHD risk in humans remains unclear. Through targeted sequencing of coding regions of lipid-modifying genes in 328 individuals with extremely high plasma HDL-C levels, we identified a homozygote for a loss-of-function variant, in which leucine replaces proline 376 (P376L), in SCARB1, the gene encoding SR-BI. The P376L variant impairs posttranslational processing of SR-BI and abrogates selective HDL cholesterol uptake in transfected cells, in hepatocyte-like cells derived from induced pluripotent stem cells from the homozygous subject, and in mice. Large population-based studies revealed that subjects who are heterozygous carriers of the P376L variant have significantly increased levels of plasma HDL-C. P376L carriers have a profound HDL-related phenotype and an increased risk of CHD (odds ratio = 1.79, which is statistically significant)
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