156 research outputs found

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    Demonstration of the temporal matter-wave Talbot effect for trapped matter waves

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    We demonstrate the temporal Talbot effect for trapped matter waves using ultracold atoms in an optical lattice. We investigate the phase evolution of an array of essentially non-interacting matter waves and observe matter-wave collapse and revival in the form of a Talbot interference pattern. By using long expansion times, we image momentum space with sub-recoil resolution, allowing us to observe fractional Talbot fringes up to 10th order.Comment: 17 pages, 7 figure

    Kaon Production and Kaon to Pion Ratio in Au+Au Collisions at \snn=130 GeV

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    Mid-rapidity transverse mass spectra and multiplicity densities of charged and neutral kaons are reported for Au+Au collisions at \snn=130 GeV at RHIC. The spectra are exponential in transverse mass, with an inverse slope of about 280 MeV in central collisions. The multiplicity densities for these particles scale with the negative hadron pseudo-rapidity density. The charged kaon to pion ratios are K+/π=0.161±0.002(stat)±0.024(syst)K^+/\pi^- = 0.161 \pm 0.002 {\rm (stat)} \pm 0.024 {\rm (syst)} and K/π=0.146±0.002(stat)±0.022(syst)K^-/\pi^- = 0.146 \pm 0.002 {\rm (stat)} \pm 0.022 {\rm (syst)} for the most central collisions. The K+/πK^+/\pi^- ratio is lower than the same ratio observed at the SPS while the K/πK^-/\pi^- is higher than the SPS result. Both ratios are enhanced by about 50% relative to p+p and pˉ\bar{\rm p}+p collision data at similar energies.Comment: 6 pages, 3 figures, 1 tabl

    Mid-rapidity anti-proton to proton ratio from Au+Au collisions at sNN=130 \sqrt{s_{NN}} = 130 GeV

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    We report results on the ratio of mid-rapidity anti-proton to proton yields in Au+Au collisions at \rts = 130 GeV per nucleon pair as measured by the STAR experiment at RHIC. Within the rapidity and transverse momentum range of y<0.5|y|<0.5 and 0.4 <pt<<p_t< 1.0 GeV/cc, the ratio is essentially independent of either transverse momentum or rapidity, with an average of 0.65±0.01(stat.)±0.07(syst.)0.65\pm 0.01_{\rm (stat.)} \pm 0.07_{\rm (syst.)} for minimum bias collisions. Within errors, no strong centrality dependence is observed. The results indicate that at this RHIC energy, although the pp-\pb pair production becomes important at mid-rapidity, a significant excess of baryons over anti-baryons is still present.Comment: 5 pages, 3 figures, accepted by Phys. Rev. Let

    Strange anti-particle to particle ratios at mid-rapidity in sqrt(s_NN)= 130 GeV Au+Au Collisions

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    Values of the ratios in the mid-rapidity yields of anti-Lambda/Lambda = 0.71 +/- 0.01(stat.) +/- 0.04(sys.), anti-Xi+/Xi- = 0.83 +/- 0.04(stat.) +/- 0.05 (sys.), anti-Omega+/Omega- = 0.95 +/- 0.15(stat) +/- 0.05(sys.) and K+/K- 1.092 +/- 0.023(combined) were obtained in central sqrt(s_NN) = 130 GeV Au+Au collisions using the STAR detector. The ratios indicate that a fraction of the net-baryon number from the initial system is present in the excess of hyperons over anti-hyperons at mid-rapidity. The trend in the progression of the baryon ratios, with increasing strange quark content, is similar to that observed in heavy-ion collisions at lower energies. The value of these ratios may be related to the charged kaon ratio in the framework of simple quark-counting and thermal models.Comment: 6 pages, 3 figures, revtex4, now accepted by Physics Letters B. All figures improved for clarity, fig. 2 now has kaon ratio separated by technique, fig. 3 now has additional other RHIC data points. Minor clarifications in text in response to referee comments. Updated ref

    Risk profiles and one-year outcomes of patients with newly diagnosed atrial fibrillation in India: Insights from the GARFIELD-AF Registry.

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    BACKGROUND: The Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF) is an ongoing prospective noninterventional registry, which is providing important information on the baseline characteristics, treatment patterns, and 1-year outcomes in patients with newly diagnosed non-valvular atrial fibrillation (NVAF). This report describes data from Indian patients recruited in this registry. METHODS AND RESULTS: A total of 52,014 patients with newly diagnosed AF were enrolled globally; of these, 1388 patients were recruited from 26 sites within India (2012-2016). In India, the mean age was 65.8 years at diagnosis of NVAF. Hypertension was the most prevalent risk factor for AF, present in 68.5% of patients from India and in 76.3% of patients globally (P < 0.001). Diabetes and coronary artery disease (CAD) were prevalent in 36.2% and 28.1% of patients as compared with global prevalence of 22.2% and 21.6%, respectively (P < 0.001 for both). Antiplatelet therapy was the most common antithrombotic treatment in India. With increasing stroke risk, however, patients were more likely to receive oral anticoagulant therapy [mainly vitamin K antagonist (VKA)], but average international normalized ratio (INR) was lower among Indian patients [median INR value 1.6 (interquartile range {IQR}: 1.3-2.3) versus 2.3 (IQR 1.8-2.8) (P < 0.001)]. Compared with other countries, patients from India had markedly higher rates of all-cause mortality [7.68 per 100 person-years (95% confidence interval 6.32-9.35) vs 4.34 (4.16-4.53), P < 0.0001], while rates of stroke/systemic embolism and major bleeding were lower after 1 year of follow-up. CONCLUSION: Compared to previously published registries from India, the GARFIELD-AF registry describes clinical profiles and outcomes in Indian patients with AF of a different etiology. The registry data show that compared to the rest of the world, Indian AF patients are younger in age and have more diabetes and CAD. Patients with a higher stroke risk are more likely to receive anticoagulation therapy with VKA but are underdosed compared with the global average in the GARFIELD-AF. CLINICAL TRIAL REGISTRATION-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01090362

    Observation of a new boson at a mass of 125 GeV with the CMS experiment at the LHC

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    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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