175 research outputs found

    Role of the IRS-1 and/or -2 in the pathogenesis of insulin resistance in Dahl salt-sensitive (S) rats

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    Insulin resistance is a common finding in hypertensive humans and animal models. The Dahl salt-sensitive (S) rat is an ideal model of genetically predetermined insulin resistance and salt-sensitive hypertension. Along the insulin signaling pathway, the insulin receptor substrates 1 and 2 (IRS-1 and -2) are important mediators of insulin signaling. IRS-1 and/or IRS-2 genetic variant(s) and/or enhanced serine phosphorylation correlate with insulin resistance. The present commentary was designed to highlight the significance of IRS-1 and/or -2 in the pathogenesis of insulin resistance. An emphasis will be given to the putative role of IRS-1 and/or -2 genetic variant(s) and serine phosphorylation in precipitating insulin resistance

    Light cone QCD sum rules study of the semileptonic heavy ΞQ\Xi_{Q} and ΞQ\Xi'_{Q} transitions to Ξ\Xi and Σ\Sigma baryons

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    The semileptonic decays of heavy spin--1/2, Ξb(c)\Xi_{b(c)} and Ξb(c)\Xi'_{b(c)} baryons to the light spin-- 1/2, Ξ\Xi and Σ\Sigma baryons are investigated in the framework of the light cone QCD sum rules. In particular, using the most general form of the interpolating currents for the heavy baryons as well as the distribution amplitudes of the Ξ\Xi and Σ\Sigma baryons, we calculate all form factors entering the matrix elements of the corresponding effective Hamiltonians in full QCD. Having calculated the responsible form factors, we evaluate the decay rates and branching fractions of the related transitions.Comment: 30 Pages, 5 Figures and 18 Table

    Study of J/Psi decays into eta Kstar Kstar-bar

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    We report the first observation of \mPJpsi \to \mPeta\mPKst\mAPKst decay in a \mPJpsi sample of 58 million events collected with the BESII detector. The branching fraction is determined to be (1.15±0.13±0.22)×103(1.15 \pm 0.13 \pm 0.22)\times 10^{-3}. The selected signal event sample is further used to search for the \mPY resonance through \mPJpsi \to \mPeta \mPY, \mPY\to\mPKst\mAPKst. No evidence of a signal is seen. An upper limit of \mathrm{Br}(\mPJpsi \to \mPeta \mPY)\cdot\mathrm{Br}(\mPY\to\mPKst\mAPKst) < 2.52\times 10^{-4} is set at the 90% confidence level.Comment: 11 pages, 4 figure

    Search for the Xb and other hidden-beauty states in the π+π−ϒ(1S) channel at ATLAS

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    This Letter presents a search for a hidden-beauty counterpart of the X(3872) in the mass ranges of 10.05–10.31 GeV and 10.40–11.00 GeV, in the channel Xb→π+π−ϒ(1S)(→μ+μ−), using 16.2 fb−1 of pp   collision data collected by the ATLAS detector at the LHC. No evidence for new narrow states is found, and upper limits are set on the product of the Xb cross section and branching fraction, relative to those of the ϒ(2S), at the 95% confidence level using the CLS approach. These limits range from 0.8% to 4.0%, depending on mass. For masses above 10.1 GeV, the expected upper limits from this analysis are the most restrictive to date. Searches for production of the ϒ(13DJ), , and states also reveal no significant signals

    Polyimides membranes for pervaporation and biofuels separation

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    10.1016/j.progpolymsci.2009.06.001Progress in Polymer Science (Oxford)34111135-1160PRPS

    Downregulation of TIM-3 mRNA expression in peripheral blood mononuclear cells from patients with systemic lupus erythematosus

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    The T-cell immunoglobulin and mucin domain (TIM) family is associated with autoimmune diseases, but its expression level in the immune cells of systemic lupus erythematosus (SLE) patients is not known. The aim of this study was to investigate whether the expression of TIM-3 mRNA is associated with pathogenesis of SLE. Quantitative real-time reverse transcription-polymerase chain reaction analysis (qRT-PCR) was used to determine TIM-1, TIM-3, and TIM-4 mRNA expression in peripheral blood mononuclear cells (PBMCs) from 132 patients with SLE and 62 healthy controls. The PBMC surface protein expression of TIMs in PBMCs from 20 SLE patients and 15 healthy controls was assayed by flow cytometry. Only TIM-3 mRNA expression decreased significantly in SLE patients compared with healthy controls (P0.05). SLE patients with lupus nephritis (LN) had a significantly lower expression of TIM-3 mRNA than those without LN (P=0.001). There was no significant difference in the expression of TIM-3 mRNA within different classes of LN (P>0.05). Correlation of TIM-3 mRNA expression with serum IgA was highly significant (r=0.425, P=0.004), but was weakly correlated with total serum protein (rs=0.283, P=0.049) and serum albumin (rs=0.297, P=0.047). TIM-3 mRNA expression was weakly correlated with the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI; rs=-0.272, P=0.032). Our results suggest that below-normal expression of TIM-3 mRNA in PBMC may be involved in the pathogenesis of SLE
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