627 research outputs found

    Study of psi(2S) decays to X J/psi

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    Using J/psi -> mu^+ mu^- decays from a sample of approximately 4 million psi(2S) events collected with the BESI detector, the branching fractions of psi(2S) -> eta J/psi, pi^0 pi^0 J/psi, and anything J/psi normalized to that of psi(2S) -> pi^+ pi^- J/psi are measured. The results are B(psi(2S) -> eta J/psi)/B(psi(2S) -> pi^+ pi^- J/psi) = 0.098 \pm 0.005 \pm 0.010, B(psi(2S) -> pi^0 pi^0 J/psi)/B(psi(2S) -> pi^+ pi^- J/psi) = 0.570 \pm 0.009 \pm 0.026, and B(psi(2S) -> anything J/psi)/B(psi(2S) -> pi^+ pi^- J/psi) = 1.867 \pm 0.026 \pm 0.055.Comment: 13 pages, 8 figure

    First observation of psi(2S)-->K_S K_L

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    The decay psi(2S)-->K_S K_L is observed for the first time using psi(2S) data collected with the Beijing Spectrometer (BESII) at the Beijing Electron Positron Collider (BEPC); the branching ratio is determined to be B(psi(2S)-->K_S K_L) = (5.24\pm 0.47 \pm 0.48)\times 10^{-5}. Compared with J/psi-->K_S K_L, the psi(2S) branching ratio is enhanced relative to the prediction of the perturbative QCD ``12%'' rule. The result, together with the branching ratios of psi(2S) decays to other pseudoscalar meson pairs (\pi^+\pi^- and K^+K^-), is used to investigate the relative phase between the three-gluon and the one-photon annihilation amplitudes of psi(2S) decays.Comment: 5 pages, 4 figures, 2 tables, submitted to Phys. Rev. Let

    Surface electrons at plasma walls

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    In this chapter we introduce a microscopic modelling of the surplus electrons on the plasma wall which complements the classical description of the plasma sheath. First we introduce a model for the electron surface layer to study the quasistationary electron distribution and the potential at an unbiased plasma wall. Then we calculate sticking coefficients and desorption times for electron trapping in the image states. Finally we study how surplus electrons affect light scattering and how charge signatures offer the possibility of a novel charge measurement for dust grains.Comment: To appear in Complex Plasmas: Scientific Challenges and Technological Opportunities, Editors: M. Bonitz, K. Becker, J. Lopez and H. Thomse

    Resonances in J/ψϕπ+πJ/\psi \to \phi \pi ^+\pi ^- and ϕK+K\phi K^+K^-

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    A partial wave analysis is presented of J/ψϕπ+πJ/\psi \to \phi \pi ^+\pi ^- and ϕK+K\phi K^+K^- from a sample of 58M J/ψJ/\psi events in the BES II detector. The f0(980)f_0(980) is observed clearly in both sets of data, and parameters of the Flatt\' e formula are determined accurately: M=965±8M = 965 \pm 8 (stat) ±6\pm 6 (syst) MeV/c2^2, g1=165±10±15g_1 = 165 \pm 10 \pm 15 MeV/c2^2, g2/g1=4.21±0.25±0.21g_2/g_1 = 4.21 \pm 0.25 \pm 0.21. The ϕππ\phi \pi \pi data also exhibit a strong ππ\pi \pi peak centred at M=1335M = 1335 MeV/c2^2. It may be fitted with f2(1270)f_2(1270) and a dominant 0+0^+ signal made from f0(1370)f_0(1370) interfering with a smaller f0(1500)f_0(1500) component. There is evidence that the f0(1370)f_0(1370) signal is resonant, from interference with f2(1270)f_2(1270). There is also a state in ππ\pi \pi with M=179030+40M = 1790 ^{+40}_{-30} MeV/c2^2 and Γ=27030+60\Gamma = 270 ^{+60}_{-30} MeV/c2^2; spin 0 is preferred over spin 2. This state, f0(1790)f_0(1790), is distinct from f0(1710)f_0(1710). The ϕKKˉ\phi K\bar K data contain a strong peak due to f2(1525)f_2'(1525). A shoulder on its upper side may be fitted by interference between f0(1500)f_0(1500) and f0(1710)f_0(1710).Comment: 17 pages, 6 figures, 1 table. Submitted to Phys. Lett.

    Measurement of the Branching Fraction of J/psi --> pi+ pi- pi0

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    Using 58 million J/psi and 14 million psi' decays obtained by the BESII experiment, the branching fraction of J/psi --> pi+ pi- pi0 is determined. The result is (2.10+/-0.12)X10^{-2}, which is significantly higher than previous measurements.Comment: 9 pages, 8 figures, RevTex

    Search for K_S K_L in psi'' decays

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    K_S K_L from psi'' decays is searched for using the psi'' data collected by BESII at BEPC, the upper limit of the branching fraction is determined to be B(psi''--> K_S K_L) < 2.1\times 10^{-4} at 90% C. L. The measurement is compared with the prediction of the S- and D-wave mixing model of the charmonia, based on the measurements of the branching fractions of J/psi-->K_S K_L and psi'-->K_S K_L.Comment: 5 pages, 1 figur

    First Measurements of eta_c Decaying into K^+K^-2(pi^+pi^-) and 3(pi^+pi^-)

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    The decays of eta_c to K^+K^-2(pi^+pi^-) and 3(pi^+pi^-) are observed for the first time using a sample of 5.8X10^7 J/\psi events collected by the BESII detector. The product branching fractions are determined to be B(J/\psi-->gamma eta_c)*B(eta_c-->K^+K^-pi^+pi^-pi^+pi^-)=(1.21+-0.32+- 0.23)X10^{-4},B(J/ψ>gammaetac)B(etac>K0Kˉ0pi+pi)=(1.29+0.43+0.32)X104,B(J/\psi-->gamma eta_c)*B(eta_c-->K^{*0}\bar{K}^{*0}pi^+pi^-)= (1.29+-0.43+-0.32)X10^{-4}, and (J/\psi-->gamma eta_c)* B(eta_c-->pi^+pi^-pi^+pi^-pi^+pi^-)= (2.59+-0.32+-0.48)X10^{-4}. The upper limit for eta_c-->phi pi^+pi^-pi^+pi^- is also obtained as B(J/\psi-->gamma eta_c)*B(eta_c--> phi pi^+pi^-pi^+pi^-)< 6.03 X10^{-5} at the 90% confidence level.Comment: 11 pages, 4 figure

    Ischemic-Preconditioning Induced Serum Exosomal miR-133a-3p Improved Post-Myocardial Infarction Repair via Targeting LTBP1 and PPP2CA

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    Na Yang,1,2,&ast; Yong-Bo Hou,2,3,&ast; Tian-Hao Cui,2 Jun-Ma Yu,2 Shu-Fang He,4,5 Hai-Juan Zhu1 1Department of Anesthesiology, Maternal and Child Medical Center of Anhui Medical University, Hefei, Anhui, People’s Republic of China; 2Department of Anesthesiology, The Third Affiliated Hospital of Anhui Medical University (The First People’s Hospital of Hefei), Hefei, Anhui, People’s Republic of China; 3Department of Anesthesiology, Wannan Medical College, Wuhu, Anhui, People’s Republic of China; 4Department of Anesthesiology and Perioperative Medicine, The Second Affiliated Hospital of Anhui Medical University, Hefei, People’s Republic of China; 5Key Laboratory of Anesthesiology and Perioperative Medicine of Anhui Higher Education Institutes, Anhui Medical University, Hefei, Anhui, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Shu-Fang He; Hai-Juan Zhu, Email [email protected]; [email protected]: Ischemic preconditioning-induced serum exosomes (IPC-exo) protected rat heart against myocardial ischemia/reperfusion injury. However, whether IPC-exo regulate replacement fibrosis after myocardial infarction (MI) and the underlying mechanisms remain unclear. MicroRNAs (miRs) are important cargos of exosomes and play an essential role in cardioprotection. We aim to investigate whether IPC-exo regulate post-MI replacement fibrosis by transferring cardioprotective miRs and its action mechanism.Methods: Exosomes obtained from serum of adult rats in control (Con-exo) and IPC groups were identified and analyzed, subsequently intracardially injected into MI rats following ligation. Their miRs profiles were identified using high-throughput miR sequencing to identify target miRs for bioinformatics analysis. Luciferase reporter assays confirmed target genes of selected miRs. IPC-exo transfected with selected miRs antagomir or NC were intracardially administered to MI rats post-ligation. Cardiac function and degree of replacement fibrosis were detected 4 weeks post-MI.Results: IPC-exo exerted cardioprotective effects against excessive replacement fibrosis. MiR sequencing and RT-qPCR identified miR-133a-3p as most significantly different between IPC-exo and Con-exo. MiR-133a-3p directly targeted latent transforming growth factor beta binding protein 1 (LTBP1) and protein phosphatase 2, catalytic subunit, alpha isozyme (PPP2CA). KEGG analysis showed that transforming growth factor-β (TGF-β) was one of the most enriched signaling pathways with miR-133a-3p. Comparing to injection of IPC-exo transfected with miR-133a-3p antagomir NC, injecting IPC-exo transfected with miR-133a-3p antagomir abolished protective effects of IPC-exo on declining excessive replacement fibrosis and cardiac function enhancement, while increasing the messenger RNA and protein expression of LTBP1, PPP2CA, and TGF-β 1in MI rats.Conclusion: IPC-exo inhibit excessive replacement fibrosis and improve cardiac function post-MI by transferring miR-133a-3p, the mechanism is associated with directly targeting LTBP1 and PPP2CA, and indirectly regulating TGF-β pathway in rats. Our finding provides potential therapeutic effect of IPC-induced exosomal miR-133a-3p for cardiac repair. Keywords: ischemic preconditioning, myocardial infarction, Exosomes, MicroRNAs, cardiac function, myocardial fibrosi
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