187 research outputs found

    Gell-Mann--Okubo Mass Formula for an SU(4) Meson Hexadecuplet

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    Using a linear mass spectrum of an SU(4)SU(4) meson hexadecuplet, we derive the Gell-Mann--Okubo mass formula for the charmed mesons, in good agreement with experiment. Possible generalization of this method to a higher symmetry group is briefly discussed.Comment: 11 pages, LaTe

    Towards resolution of the scalar meson nonet enigma

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    By the application of a linear mass spectrum to a composite system of both the pseudoscalar and scalar meson nonets, we find three mass relations for the masses of the scalar states which suggest the qqˉq\bar{q} assignment for the scalar meson nonet: a0(1320),a_0(1320), K0(1430),K_0^\ast (1430), f0(1500),f_0(1500), f0(980).f_0'(980).Comment: 16 pages, LaTe

    Relativistic mass distribution in event-anti-event system and ``realistic'' equation of state for hot hadronic matter

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    We find the equation of state p,ρT6,p,\rho \propto T^6, which gives the value of the sound velocity c2=0.20,c^2=0.20, in agreement with the ``realistic'' equation of state for hot hadronic matter suggested by Shuryak, in the framework of a covariant relativistic statistical mechanics of an event--anti-event system with small chemical and mass potentials. The relativistic mass distribution for such a system is obtained and shown to be a good candidate for fitting hadronic resonances, in agreement with the phenomenological models of Hagedorn, Shuryak, {\it et al.} This distribution provides a correction to the value of specific heat 3/2, of the order of 5.5\%, at low temperatures.Comment: 19 pages, report TAUP-2161-9

    Mass Spectrum of a Meson Nonet is Linear

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    It is argued that the mass spectrum of a meson nonet is linear, consistent with the standard Gell-Mann--Okubo mass formula and leading to an extra Gell-Mann--Okubo mass relation for the masses of the isoscalar states. This relation is shown to hold with an accuracy of up to \sim 3\% for all well-established nonets. It also suggests a new qqˉq\bar{q} assignment for the scalar meson nonet.Comment: 11 pages, LaTeX, 4 postscript figures following the main tex

    Varespladib and cardiovascular events in patients with an acute coronary syndrome: the VISTA-16 randomized clinical trial

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    IMPORTANCE: Secretory phospholipase A2(sPLA2) generates bioactive phospholipid products implicated in atherosclerosis. The sPLA2inhibitor varespladib has favorable effects on lipid and inflammatory markers; however, its effect on cardiovascular outcomes is unknown. OBJECTIVE: To determine the effects of sPLA2inhibition with varespladib on cardiovascular outcomes. DESIGN, SETTING, AND PARTICIPANTS: A double-blind, randomized, multicenter trial at 362 academic and community hospitals in Europe, Australia, New Zealand, India, and North America of 5145 patients randomized within 96 hours of presentation of an acute coronary syndrome (ACS) to either varespladib (n = 2572) or placebo (n = 2573) with enrollment between June 1, 2010, and March 7, 2012 (study termination on March 9, 2012). INTERVENTIONS: Participants were randomized to receive varespladib (500 mg) or placebo daily for 16 weeks, in addition to atorvastatin and other established therapies. MAIN OUTCOMES AND MEASURES: The primary efficacy measurewas a composite of cardiovascular mortality, nonfatal myocardial infarction (MI), nonfatal stroke, or unstable angina with evidence of ischemia requiring hospitalization at 16 weeks. Six-month survival status was also evaluated. RESULTS: At a prespecified interim analysis, including 212 primary end point events, the independent data and safety monitoring board recommended termination of the trial for futility and possible harm. The primary end point occurred in 136 patients (6.1%) treated with varespladib compared with 109 patients (5.1%) treated with placebo (hazard ratio [HR], 1.25; 95%CI, 0.97-1.61; log-rank P = .08). Varespladib was associated with a greater risk of MI (78 [3.4%] vs 47 [2.2%]; HR, 1.66; 95%CI, 1.16-2.39; log-rank P = .005). The composite secondary end point of cardiovascular mortality, MI, and stroke was observed in 107 patients (4.6%) in the varespladib group and 79 patients (3.8%) in the placebo group (HR, 1.36; 95% CI, 1.02-1.82; P = .04). CONCLUSIONS AND RELEVANCE: In patients with recent ACS, varespladib did not reduce the risk of recurrent cardiovascular events and significantly increased the risk of MI. The sPLA2inhibition with varespladib may be harmful and is not a useful strategy to reduce adverse cardiovascular outcomes after ACS. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01130246. Copyright 2014 American Medical Association. All rights reserved

    Catechol-O-Methyltransferase Val158Met Polymorphism Associates with Individual Differences in Sleep Physiologic Responses to Chronic Sleep Loss

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    Val158Met polymorphism was a novel marker in healthy adults of differential vulnerability to chronic partial sleep deprivation (PSD), a condition distinct from total sleep loss and one experienced by millions on a daily and persistent basis. allelic frequencies were higher in whites than African Americans.-related treatment responses and risk factors for symptom exacerbation

    The tuberculosis necrotizing toxin kills macrophages by hydrolyzing NAD.

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    Mycobacterium tuberculosis (Mtb) induces necrosis of infected cells to evade immune responses. Recently, we found that Mtb uses the protein CpnT to kill human macrophages by secreting its C-terminal domain, named tuberculosis necrotizing toxin (TNT), which induces necrosis by an unknown mechanism. Here we show that TNT gains access to the cytosol of Mtb-infected macrophages, where it hydrolyzes the essential coenzyme NAD(+). Expression or injection of a noncatalytic TNT mutant showed no cytotoxicity in macrophages or in zebrafish zygotes, respectively, thus demonstrating that the NAD(+) glycohydrolase activity is required for TNT-induced cell death. To prevent self-poisoning, Mtb produces an immunity factor for TNT (IFT) that binds TNT and inhibits its activity. The crystal structure of the TNT-IFT complex revealed a new NAD(+) glycohydrolase fold of TNT, the founding member of a toxin family widespread in pathogenic microorganisms
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