Search for the Rare Decays J/Psi --> Ds- e+ nu_e, J/Psi --> D- e+ nu_e, and J/Psi --> D0bar e+ e-

We report on a search for the decays J/Psi --> Ds- e+ nu_e + c.c., J/Psi --> D- e+ nu_e + c.c., and J/Psi --> D0bar e+ e- + c.c. in a sample of 5.8 * 10^7 J/Psi events collected with the BESII detector at the BEPC. No excess of signal above background is observed, and 90% confidence level upper limits on the branching fractions are set: B(J/Psi --> Ds- e+ nu_e + c.c.)<4.8*10^-5, B(J/Psi --> D- e+ nu_e + c.c.) D0bar e+ e- + c.c.)<1.1*10^-5Comment: 10 pages, 4 figure

Study of J/psi decays to Lambda Lambdabar and Sigma0 Sigma0bar

The branching ratios and Angular distributions for J/psi decays to Lambda Lambdabar and Sigma0 Sigma0bar are measured using BESII 58 million J/psi.Comment: 11 pages, 5 figure

Genetic insights into resting heart rate and its role in cardiovascular disease

Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development

Partial wave analyses of J/psi to gamma pi^+ pi^- and gamma pi^0 pi^0

Results are presented on J/psi radiative decays to pi^+pi^- and pi^0pi^0 based on a sample of 58M J/psi events taken with the BESII detector. Partial wave analyses are carried out using the relativistic covariant tensor amplitude method in the 1.0 to 2.3 GeV/c^2 pipi mass range. There are conspicuous peaks due to the f_2(1270) and two 0^++ states in the 1.45 and 1.75 GeV/c^2 mass regions. The first 0^++ state has a mass of 1466\pm 6\pm 20 MeV/c^2, a width of 108^{+14}_{-11}\pm 25 MeV/c^2, and a branching fraction B(J/psi \to \gamma f_0(1500) \to\gamma \pi^+\pi^-) = (0.67\pm0.02\pm0.30) \times 10^{-4}. Spin 0 is strongly preferred over spin 2. The second 0^++ state peaks at 1765^{+4}_{-3}\pm 13 MeV/c^2 with a width of 145\pm8\pm69 MeV/c^2. If this 0^++ is interpreted as coming from f_0(1710), the ratio of its branching fractions to pipi and K\bar K is 0.41^{+0.11}_{-0.17}.Comment: 9 pages, 6 figure

Measurement of \chi_cJ--> K+K-K+K-

Using 14M psi(2S) events taken with the BES-II detector, chi_cJ-->K+K-K+K- decays are studied. For the four-kaon final state, the branching fractions are B(chi_c0,1,2 -->K+K-K+K-)=(3.48\pm 0.23\pm 0.47)\times 10^{-3}, (0.70\pm 0.13\pm 0.10)\times 10^{-3}, and (2.17\pm 0.20\pm 0.31)\times 10^{-3}. For the \phi K+K- final state, the branching fractions, which are measured for the first time, are B(chi_c0,1,2-->\phi K+K-)=(1.03\pm 0.22\pm 0.15)\times 10^{-3}, (0.46\pm 0.16\pm 0.06)\times 10^{-3}, and (1.67\pm 0.26\pm 0.24)\times 10^{-4}. For the \phi\phi final state, B(chi_{c0,2}-->\phi\phi)=(0.94\pm 0.21\pm 0.13)\times 10^{-3} and (1.70\pm 0.30\pm 0.25)\times 10^{-3}.Comment: 7 pages, 7 figure

Precison Measurements of the Mass, the Widths of ψ(3770)\psi(3770) Resonance and the Cross Section σ[e+e−→ψ(3770)]\sigma[e^+e^-\to \psi(3770)] at Ecm=3.7724E_{\rm cm}=3.7724 GeV

By analyzing the $R$ values measured at 68 energy points in the energy region between 3.650 and 3.872 GeV reported in our previous paper, we have precisely measured the mass, the total width, the leptonic width and the leptonic decay branching fraction of the $\psi(3770)$ to be ${M}_{\psi(3770)}=3772.4 \pm 0.4 \pm 0.3$ MeV, $\Gamma_{\psi(3770)}^{\rm tot} = 28.6 \pm 1.2 \pm 0.2$ MeV, $\Gamma_{\psi(3770)}^{ee} = 279 \pm 11 \pm 13$ eV and $B[\psi(3770)\to e^+e^-]=(0.98\pm 0.04\pm 0.04)\times 10^{-5}$, respectively, which result in the observed cross section $\sigma^{\rm obs}[e^+e^-\to \psi(3770)]=7.25\pm 0.27 \pm 0.34$ nb at $\sqrt{s}=3772.4$ MeV. We have also measured $R_{\rm uds}=2.121\pm 0.023 \pm 0.084$ for the continuum light hadron production in the region from 3.650 to 3.872 GeV.Comment: 5 pages, 2 figure

The trans-ancestral genomic architecture of glycemic traits

Glycemic traits are used to diagnose and monitor type 2 diabetes and cardiometabolic health. To date, most genetic studies of glycemic traits have focused on individuals of European ancestry. Here we aggregated genome-wide association studies comprising up to 281,416 individuals without diabetes (30% non-European ancestry) for whom fasting glucose, 2-h glucose after an oral glucose challenge, glycated hemoglobin and fasting insulin data were available. Trans-ancestry and single-ancestry meta-analyses identified 242 loci (99 novel; P < 5 x 10(-8)), 80% of which had no significant evidence of between-ancestry heterogeneity. Analyses restricted to individuals of European ancestry with equivalent sample size would have led to 24 fewer new loci. Compared with single-ancestry analyses, equivalent-sized trans-ancestry fine-mapping reduced the number of estimated variants in 99% credible sets by a median of 37.5%. Genomic-feature, gene-expression and gene-set analyses revealed distinct biological signatures for each trait, highlighting different underlying biological pathways. Our results increase our understanding of diabetes pathophysiology by using trans-ancestry studies for improved power and resolution.A trans-ancestry meta-analysis of GWAS of glycemic traits in up to 281,416 individuals identifies 99 novel loci, of which one quarter was found due to the multi-ancestry approach, which also improves fine-mapping of credible variant sets.Diabetes mellitus: pathophysiological changes and therap