5,140 research outputs found

    Multiplicity dependence of σψ(2S)/σJ/ψ\sigma_{\psi(2S)}/\sigma_{J/\psi} in pppp collisions at s=13\sqrt{s}=13 TeV

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    International audienceThe ratio of production cross-sections of ψ(2S)\psi(2S) over J/ψJ/\psi mesons as a function of charged-particle multiplicity in proton-proton collisions at a centre-of-mass energy s=13\sqrt{s}=13 TeV is measured with a data sample collected by the LHCb detector, corresponding to an integrated luminosity of 658 pb1^{-1}. The ratio is measured for both prompt and non-prompt ψ(2S)\psi(2S) and J/ψJ/\psi mesons. When there is an overlap between the rapidity ranges over which multiplicity and charmonia production are measured, a multiplicity-dependent modification of the ratio is observed for prompt mesons. No significant multiplicity dependence is found when the ranges do not overlap. For non-prompt production, the ψ(2S)toJ/ψ\psi(2S)-to-J/\psi production ratio is roughly independent of multiplicity irrespective of the rapidity range over which the multiplicity is measured. The results are compared to predictions of the co-mover model and agree well except in the low multiplicity region. The ratio of production cross-sections of ψ(2S)\psi(2S) over J/ψJ/\psi mesons are cross-checked with other measurements in di-lepton channels and found to be compatible

    CEPC Technical Design Report -- Accelerator

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    International audienceThe Circular Electron Positron Collider (CEPC) is a large scientific project initiated and hosted by China, fostered through extensive collaboration with international partners. The complex comprises four accelerators: a 30 GeV Linac, a 1.1 GeV Damping Ring, a Booster capable of achieving energies up to 180 GeV, and a Collider operating at varying energy modes (Z, W, H, and ttbar). The Linac and Damping Ring are situated on the surface, while the Booster and Collider are housed in a 100 km circumference underground tunnel, strategically accommodating future expansion with provisions for a Super Proton Proton Collider (SPPC). The CEPC primarily serves as a Higgs factory. In its baseline design with synchrotron radiation (SR) power of 30 MW per beam, it can achieve a luminosity of 5e34 /cm^2/s^1, resulting in an integrated luminosity of 13 /ab for two interaction points over a decade, producing 2.6 million Higgs bosons. Increasing the SR power to 50 MW per beam expands the CEPC's capability to generate 4.3 million Higgs bosons, facilitating precise measurements of Higgs coupling at sub-percent levels, exceeding the precision expected from the HL-LHC by an order of magnitude. This Technical Design Report (TDR) follows the Preliminary Conceptual Design Report (Pre-CDR, 2015) and the Conceptual Design Report (CDR, 2018), comprehensively detailing the machine's layout and performance, physical design and analysis, technical systems design, R&D and prototyping efforts, and associated civil engineering aspects. Additionally, it includes a cost estimate and a preliminary construction timeline, establishing a framework for forthcoming engineering design phase and site selection procedures. Construction is anticipated to begin around 2027-2028, pending government approval, with an estimated duration of 8 years. The commencement of experiments could potentially initiate in the mid-2030s

    The mechanisms of ferroptosis and its role in atherosclerosis

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    Ferroptosis is a newly identified form of non-apoptotic programmed cell death, characterized by the iron-dependent accumulation of lethal lipid reactive oxygen species (ROS) and peroxidation of membrane polyunsaturated fatty acid phospholipids (PUFA-PLs). Ferroptosis is unique among other cell death modalities in many aspects. It is initiated by excessive oxidative damage due to iron overload and lipid peroxidation and compromised antioxidant defense systems, including the system Xc-/ glutathione (GSH)/glutathione peroxidase 4 (GPX4) pathway and the GPX4-independent pathways. In the past ten years, ferroptosis was reported to play a critical role in the pathogenesis of various cardiovascular diseases, e.g., atherosclerosis (AS), arrhythmia, heart failure, diabetic cardiomyopathy, and myocardial ischemia-reperfusion injury. Studies have identified dysfunctional iron metabolism and abnormal expression profiles of ferroptosis-related factors, including iron, GSH, GPX4, ferroportin (FPN), and SLC7A11 (xCT), as critical indicators for atherogenesis. Moreover, ferroptosis in plaque cells, i.e., vascular endothelial cell (VEC), macrophage, and vascular smooth muscle cell (VSMC), positively correlate with atherosclerotic plaque development. Many macromolecules, drugs, Chinese herbs, and food extracts can inhibit the atherogenic process by suppressing the ferroptosis of plaque cells. In contrast, some ferroptosis inducers have significant pro-atherogenic effects. However, the mechanisms through which ferroptosis affects the progression of AS still need to be well-known. This review summarizes the molecular mechanisms of ferroptosis and their emerging role in AS, aimed at providing novel, promising druggable targets for anti-AS therapy

    Search for Bc+π+μ+μB_c^+\to\pi^+\mu^+\mu^- decays and measurement of the branching fraction ratio B(Bc+ψ(2S)π+)/B(Bc+J/ψπ+){\cal B}(B_c^+\to\psi(2S)\pi^+)/{\cal B}(B_c^+\to J/\psi \pi^+)