222 research outputs found

    A Double-Blind, Randomized, Placebo-Controlled 4-Week Study on the Efficacy and Safety of the Purinergic Agents Allopurinol and Dipyridamole Adjunctive to Lithium in Acute Bipolar Mania

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    The therapeutics for Bipolar Disorders (BD) is still far from adequate and new options with improved effectiveness, safety and tolerability in a wide range of patients are necessary. Preliminary data have suggested a role for dysfunctions targeting at the purinergic system in mood disorders. This study aimed to evaluate the efficacy and tolerability of the purinergic agents allopurinol and dipyridamole combined with lithium in bipolar mania

    Observation of J/ψpJ/\psi p resonances consistent with pentaquark states in Λb0→J/ψK−p{\Lambda_b^0\to J/\psi K^-p} decays

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    Observations of exotic structures in the J/ψpJ/\psi p channel, that we refer to as pentaquark-charmonium states, in Λb0→J/ψK−p\Lambda_b^0\to J/\psi K^- p decays are presented. The data sample corresponds to an integrated luminosity of 3/fb acquired with the LHCb detector from 7 and 8 TeV pp collisions. An amplitude analysis is performed on the three-body final-state that reproduces the two-body mass and angular distributions. To obtain a satisfactory fit of the structures seen in the J/ψpJ/\psi p mass spectrum, it is necessary to include two Breit-Wigner amplitudes that each describe a resonant state. The significance of each of these resonances is more than 9 standard deviations. One has a mass of 4380±8±294380\pm 8\pm 29 MeV and a width of 205±18±86205\pm 18\pm 86 MeV, while the second is narrower, with a mass of 4449.8±1.7±2.54449.8\pm 1.7\pm 2.5 MeV and a width of 39±5±1939\pm 5\pm 19 MeV. The preferred JPJ^P assignments are of opposite parity, with one state having spin 3/2 and the other 5/2.Comment: 48 pages, 18 figures including the supplementary material, v2 after referee's comments, now 19 figure

    SARS-CoV-2 uses CD4 to infect T helper lymphocytes

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    The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.</p

    SARS-CoV-2 uses CD4 to infect T helper lymphocytes

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    The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.</p

    Measurement of the Ξ<sup>-</sup><sub>b</sub> and Ω<sup>-</sup><sub>b</sub> baryon lifetimes

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    Using a data sample of pp collisions corresponding to an integrated luminosity of 3 fb−13~ \rm fb^{-1}, the Ξb−\Xi_b^- and Ωb−\Omega_b^- baryons are reconstructed in the Ξb−→J/ψΞ−\Xi_b^- \rightarrow J/\psi \Xi^- and Ωb−→J/ψΩ−\Omega_b^- \rightarrow J/\psi \Omega^- decay modes and their lifetimes measured to be \tau (\Xi_b^-) = 1.55\, ^{+0.10}_{-0.09}~{\rm(stat)} \pm 0.03\,{\rm(syst)} ps, \tau (\Omega_b^-) = 1.54\, ^{+0.26}_{-0.21}~{\rm(stat)} \pm 0.05\,{\rm(syst)} ps. These are the most precise determinations to date. Both measurements are in good agreement with previous experimental results and with theoretical predictions

    First observation and amplitude analysis of the B−→D+K−π− decay

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    The B−→D+K−π− decay is observed in a data sample corresponding to 3.0  fb−1 of pp collision data recorded by the LHCb experiment during 2011 and 2012. Its branching fraction is measured to be B(B−→D+K−π−)=(7.31±0.19±0.22±0.39)×10−5 where the uncertainties are statistical, systematic and from the branching fraction of the normalization channel B−→D+π−π−, respectively. An amplitude analysis of the resonant structure of the B−→D+K−π− decay is used to measure the contributions from quasi-two-body B−→D∗0(2400)0K−, B−→D∗2(2460)0K−, and B−→D∗J(2760)0K− decays, as well as from nonresonant sources. The D∗J(2760)0 resonance is determined to have spin 1
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