1,187 research outputs found

    Potential Role of Nuclear Factor κB in Diabetic Cardiomyopathy

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    Diabetic cardiomyopathy entails the cardiac injury induced by diabetes independently of any vascular disease or hypertension. Some transcription factors have been proposed to control the gene program involved in the setting and development of related processes. Nuclear factor-kappa B is a pleiotropic transcription factor associated to the regulation of many heart diseases. However, the nuclear factor-kappa B role in diabetic cardiomyopathy is under investigation. In this paper, we review the nuclear factor-kappa B pathway and its role in several processes that have been linked to diabetic cardiomyopathy, such as oxidative stress, inflammation, endothelial dysfunction, fibrosis, hypertrophy and apoptosis

    Study of a Solution with COTS for the LHCb Calorimeter Upgrade

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    AbstractWe present a solution made out of Components Out of Shelf (COTS) for the analog processing of the signal of the LHCb calorimeters in the framework of the foreseen upgrade of the detector. The present proposal is based on the current functional solution, yet, to meet the stringent noise requirements, a number of modifications are proposed. Preliminary results on the prototype boards show promising results

    Integrated test environment for a part of the LHCb calorimeter - TWEPP09

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    An integrated test environment for the data acquisition electronics of the Scintillator Pad Detector (SPD) from the calorimeter of the LHCb experiment is presented. It allows to test separately every single board or to perform global system tests, while being able to emulate every part of the system and debug it. This environment is foreseen to test the production of spare electronic boards and help the maintenance of the SPD electronics along the life of the detector. The heart of the system is an Altera Stratix II FPGA while the main board can be controlled over USB, Ethernet or WiFi

    Study of η − η′ mixing from measurement of B (s)0 → J/ψη(′) decay rates

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    A study of B and B0 s meson decays into J/ψη and J/ψη0 final states is performed using a data set of proton-proton collisions at centre-of-mass energies of 7 and 8 TeV, collected by the LCHb experiment and corresponding to 3.0 fb−1 of integrated luminosity. The decay B0 → J/ψη0 is observed for the first time. The following ratios of branching fractions are measured: B(B0 → J/ψη0 ) B(B0 s → J/ψη0) = (2.28 ± 0.65 (stat) ± 0.10 (syst) ± 0.13 (fs/fd)) × 10−2 , B(B0 → J/ψη) B(B0 s → J/ψη) = (1.85 ± 0.61 (stat) ± 0.09 (syst) ± 0.11 (fs/fd)) × 10−2 , where the third uncertainty is related to the present knowledge of fs/fd, the ratio between the probabilities for a b quark to form a B0 s or a B0 meson. The branching fraction ratios are used to determine the parameters of η−η 0 meson mixing. In addition, the first evidence for the decay B0 s → ψ(2S)η 0 is reported, and the relative branching fraction is measured, B(B0 s → ψ(2S)η 0 ) B(B0 s → J/ψη0) = (38.7 ± 9.0 (stat) ± 1.3 (syst) ± 0.9(B)) × 10−2 , where the third uncertainty is due to the limited knowledge of the branching fractions of J/ψ and ψ(2S) mesons

    Sitagliptin improved glucose assimilation in detriment of fatty-acid utilization in experimental type-II diabetes: Role of GLP-1 isoforms in Glut4 receptor trafficking

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    Background: The distribution of glucose and fatty-acid transporters in the heart is crucial for energy consecution and myocardial function. In this sense, the glucagon-like peptide-1 (GLP-1) enhancer, sitagliptin, improves glucose homeostasis but it could also trigger direct cardioprotective actions, including regulation of energy substrate utilization. Methods: Type-II diabetic GK (Goto-Kakizaki), sitagliptin-treated GK (10 mg/kg/day) and wistar rats (n = 10, each) underwent echocardiographic evaluation, and positron emission tomography scanning for [ 18 F]-2-fluoro-2-deoxy-d-glucose ( 18 FDG). Hearts and plasma were isolated for biochemical approaches. Cultured cardiomyocytes were examined for receptor distribution after incretin stimulation in high fatty acid or high glucose media. Results: Untreated GK rats exhibited hyperglycemia, hyperlipidemia, insulin resistance, and plasma GLP-1 reduction. Moreover, GK myocardium decreased 18 FDG assimilation and diastolic dysfunction. However, sitagliptin improved hyperglycemia, insulin resistance, and GLP-1 levels, and additionally, enhanced 18 FDG uptake and diastolic function. Sitagliptin also stimulated the sarcolemmal translocation of the glucose transporter-4 (Glut4), in detriment of the fatty acyl translocase (FAT)/CD36. In fact, Glut4 mRNA expression and sarcolemmal translocation were also increased after GLP-1 stimulation in high-fatty acid incubated cardiomyocytes. PI3K/Akt and AMPKα were involved in this response. Intriguingly, the GLP-1 degradation metabolite, GLP-1(9-36), showed similar effects. Conclusions: Besides of its anti-hyperglycemic effect, sitagliptin-enhanced GLP-1 may ameliorate diastolic dysfunction in type-II diabetes by shifting fatty acid to glucose utilization in the cardiomyocyte, and thus, improving cardiac efficiency and reducing lipolysisThis work was supported by national grants from Ministerio de Educación y Ciencia (SAF2009-08367), Comunidad de Madrid (CCG10-UAM/BIO-5289), and PIE13/00051 and PI14/00386 (IS. Carlos III). Merck Sharp and Dohme (Darmstadt, Germany) provided sitagliptin and partial financial support to the conduct of the stud

    Observation of the B0 →ρ0ρ0 decay from an amplitude analysis of B0 → (π+π-) (π+π-) decays

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    Proton-proton collision data recorded in 2011 and 2012 by the LHCb experiment, corresponding to an integrated luminosity of 3.0 fb−1 , are analysed to search for the charmless B0 → ρ 0ρ 0 decay. More than 600 B0 → (π +π −)(π +π −) signal decays are selected and used to perform an amplitude analysis, under the assumption of no CP violation in the decay, from which the B0 → ρ 0ρ 0 decay is observed for the first time with 7.1 standard deviations significance. The fraction of B0 → ρ 0ρ 0 decays yielding a longitudinally polarised final state is measured to be fL = 0.745+0.048 −0.058(stat) ± 0.034(syst). The B0 → ρ 0ρ 0 branching fraction, using the B0 → φK∗ (892)0 decay as reference, is also reported as B(B0 → ρ 0ρ 0 ) = (0.94 ± 0.17(stat) ± 0.09(syst) ± 0.06(BF)) × 10−6

    Searches for Λ0b and Ξ0b decays to K0Spπ− and K0SpK− final states with first observation of the Λ0b→K0Spπ− decay

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    A search for previously unobserved decays of beauty baryons to the final states K0 S pπ− and K0 S pK− is reported. The analysis is based on a data sample corresponding to an integrated luminosity of 1.0 fb−1 of pp collisions. The Λ 0 b → K0pπ− decay is observed with a significance of 8.6 σ, with branching fraction B(Λ 0 b → K0 pπ−) = (1.26 ± 0.19 ± 0.09 ± 0.34 ± 0.05) × 10−5 , where the uncertainties are statistical, systematic, from the ratio of fragmentation fractions fΛ0 b /fd, and from the branching fraction of the B0→ K0π +π − normalisation channel, respectively. A first measurement is made of the CP asymmetry, giving ACP (Λ 0 b → K0 pπ−) = 0.22 ± 0.13 (stat) ± 0.03 (syst). No significant signals are seen for Λ 0 b → K0 S pK− decays, Ξ0 b decays to both the K0 S pπ− and K0 S pK− final states, and the Λ 0 b → D− s (→ K0 SK−)p decay, and upper limits on their branching fractions are reported

    The Front End Electronics of the Scintillator Pad Detector of LHCb Calorimeter

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    In this paper the Front End electronics of the Scintillator Pad Detector (SPD) is outlined. The SPD is a sub-system of the Calorimeter of the LHCb experiment designed to discriminate between charged and neutral particles for the first level trigger. The system design is presented, describing its different functionalities implemented through three different cards and several ASICs. These functionalities are signal processing and digitization, data transmission, interface with control and timing systems of the experiment, low voltage power supply distribution and monitoring. Special emphasis is placed on installation and commissioning subjects such as cabling, grounding, shielding and power distribution

    Observation of Z production in proton-lead collisions at LHCb

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    The first observation of Z boson production in proton-lead collisions at a centreof-mass energy per proton-nucleon pair of √ sNN = 5 TeV is presented. The data sample corresponds to an integrated luminosity of 1.6 nb−1 collected with the LHCb detector. The Z candidates are reconstructed from pairs of oppositely charged muons with pseudorapidities between 2.0 and 4.5 and transverse momenta above 20 GeV/c. The invariant dimuon mass is restricted to the range 60 − 120 GeV/c2 . The Z production cross-section is measured to be σZ→µ+µ− (fwd) = 13.5 +5.4 −4.0 (stat.) ± 1.2(syst.) nb in the direction of the proton beam and σZ→µ+µ− (bwd) = 10.7 +8.4 −5.1 (stat.) ± 1.0(syst.) nb in the direction of the lead beam, where the first uncertainty is statistical and the second systematic
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