93 research outputs found

    Evidence for νμντ\nu_\mu \to \nu_\tau appearance in the CNGS neutrino beam with the OPERA experiment

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    The OPERA experiment is designed to search for νμντ\nu_{\mu} \rightarrow \nu_{\tau} oscillations in appearance mode i.e. through the direct observation of the τ\tau lepton in ντ\nu_{\tau} charged current interactions. The experiment has taken data for five years, since 2008, with the CERN Neutrino to Gran Sasso beam. Previously, two ντ\nu_{\tau} candidates with a τ\tau decaying into hadrons were observed in a sub-sample of data of the 2008-2011 runs. Here we report the observation of a third ντ\nu_\tau candidate in the τμ\tau^-\to\mu^- decay channel coming from the analysis of a sub-sample of the 2012 run. Taking into account the estimated background, the absence of νμντ\nu_{\mu} \rightarrow \nu_{\tau} oscillations is excluded at the 3.4 σ\sigma level.Comment: 9 pages, 5 figures, 1 table

    New results on ν μ → ν τ appearance with the OPERA experiment in the CNGS beam

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    Design and Synthesis of .ALPHA.-Glucosidase Inhibitor Having DNA Cleaving Activity

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    Pharmacological activation of the ryanodine receptor in Jurkat T-lymphocytes

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    1. Recently, we provided evidence for cyclic adenosine 5′-diphosphate-ribose, cADP-ribose, as a second messenger in Jurkat T-lymphocytes upon stimulation of the T-cell receptor/CD3- complex (Guse et al., 1999). cADP-ribose mobilizes Ca(2+) from an intracellular Ca(2+) store which is sensitive to caffeine and gated by the ryanodine receptor/Ca(2+) release channel. In the present study we investigated the ability of the trypanocidal drug, suramin, to activate the ryanodine receptor of T-cells. Since suramin cannot permeate the plasma membrane, it was necessary to microinject the drug into Fura-2 loaded T-lymphocytes. 2. In a dose dependent manner suramin increased the intracellular Ca(2+) concentration. The dose-response curve is very steep and calculates for an EC(50) of 7.6±2.9 mM suramin in the injection pipette. 3. Co-injection of the selective ryanodine receptor inhibitor ruthenium red completely abolished the suramin induced Ca(2+) transient. This finding allows for the conclusion that the IP(3)-receptor sensitive Ca(2+) pool is not the primary target of the suramin induced Ca(2+) transient. 4. Furthermore, Ins(1,4,6)PS(3), an antagonist of the InsP(3)-receptor could not suppress the suramin-induced Ca(2+) signal. The suramin induced Ca(2+) transients declined very slowly; however, in the presence of Ins(1,4,6)PS(3) this decay was accelerated. In addition, suramin did not interact with the cADP-ribose binding site of the ryanodine receptor of T-cells. 5. In conclusion, suramin is found to be an agonist for the T-cell ryanodine receptor as previously found for the cardiac and skeletal muscle isoform. Therefore, suramin can be designated a universal ryanodine receptor agonist
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