932 resultados para Alfonso V, King of Aragon, 1396-1458.
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Measurements of the anisotropy parameter v(2) of identified hadrons (pions, kaons, and protons) as a function of centrality, transverse momentum p(T), and transverse kinetic energy KET at midrapidity (vertical bar eta vertical bar < 0.35) in Au + Au collisions at root s(N N) = 200 GeV are presented. Pions and protons are identified up to p(T) = 6 GeV/c, and kaons up to p(T) = 4 GeV/c, by combining information from time-of-flight and aerogel Cerenkov detectors in the PHENIX Experiment. The scaling of v(2) with the number of valence quarks (n(q)) has been studied in different centrality bins as a function of transverse momentum and transverse kinetic energy. A deviation from previously observed quark-number scaling is observed at large values of KET/n(q) in noncentral Au + Au collisions (20-60%), but this scaling remains valid in central collisions (0-10%).
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Corrections to the revision of Rhopalessa Bates, 1873 (Clarke et al. 2011), with the transfer of two species to a new genus, Rashelapso: R. durantoni (Peñaherrera-Leiva & Tavakilian, 2004) comb. nov., and R. schmidi sp. nov. (previously considered to be conspecific with Ommata (Rhopalessa) rubroscutellaris Tippmann, 1960 by the authors). Ommata (Rhopalessa) rubroscutellaris is now considered a junior synonym of Laedorcari fulvicollis (Lacordaire, 1868).
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BACKGROUND: Generation of active procoagulant cofactor factor Va (FVa) and its subsequent association with the enzyme activated factor X (FXa) to form the prothrombinase complex is a pivotal initial event in blood coagulation and has been the subject of investigative effort, speculation, and controversy. The current paradigm assumes that FV activation is initiated by limited proteolysis by traces of (meizo) thrombin. METHODS AND RESULTS: Recombinant tick salivary protein TIX-5 was produced and anticoagulant properties were studied with the use of plasma, whole blood, and purified systems. Here, we report that TIX-5 specifically inhibits FXa-mediated FV activation involving the B domain of FV and show that FXa activation of FV is pivotal for plasma and blood clotting. Accordingly, tick feeding is impaired on TIX-5 immune rabbits, displaying the in vivo importance of TIX-5. CONCLUSIONS: Our data elucidate a unique molecular mechanism by which ticks inhibit the host's coagulation system. From our data, we propose a revised blood coagulation scheme in which direct FXa-mediated FV activation occurs in the initiation phase during which thrombin-mediated FV activation is restrained by fibrinogen and inhibitors.
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Canine distemper virus (CDV) causes in dogs a severe systemic infection, with a high frequency of demyelinating encephalitis. Among the six genes transcribed by CDV, the P gene encodes the polymerase cofactor protein (P) as well as two additional nonstructural proteins, C and V; of these V was shown to act as a virulence factor. We investigated the molecular mechanisms by which the P gene products of the neurovirulent CDV A75/17 strain disrupt type I interferon (IFN-alpha/beta)-induced signaling that results in the establishment of the antiviral state. Using recombinant knockout A75/17 viruses, the V protein was identified as the main antagonist of IFN-alpha/beta-mediated signaling. Importantly, immunofluorescence analysis illustrated that the inhibition of IFN-alpha/beta-mediated signaling correlated with impaired STAT1/STAT2 nuclear import, whereas the phosphorylation state of these proteins was not affected. Coimmunoprecipitation assays identified the N-terminal region of V (VNT) responsible for STAT1 targeting, which correlated with its ability to inhibit the activity of the IFN-alpha/beta-mediated antiviral state. Conversely, while the C-terminal domain of V (VCT) could not function autonomously, when fused to VNT it optimally interacted with STAT2 and subsequently efficiently suppressed the IFN-alpha/beta-mediated signaling pathway. The latter result was further supported by a single mutation at position 110 within the VNT domain of CDV V protein, resulting in a mutant that lost STAT1 binding while retaining a partial STAT2 association. Taken together, our results identified the CDV VNT and VCT as two essential modules that complement each other to interfere with the antiviral state induced by IFN-alpha/beta-mediated signaling. Hence, our experiments reveal a novel mechanism of IFN-alpha/beta evasion among the morbilliviruses.
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[von] Mosés Bensabat Amzalak
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Gershon Katz
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Signatur des Originals: S 36/F03237
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Deficiency of dolichyl-P-Glc:Man9GlcNAc2-PP-dolichyl glucosyltransferase is the cause of an additional type of carbohydrate-deficient glycoprotein syndrome (CDGS type V). Clinically this type resembles the classical type Ia of CDGS caused by the deficiency of phosphomannomutase. As a result of the glucosyltransferase deficiency in CDGS type V nonglucosylated lipid-linked oligosaccharides accumulate. The defect is leaky and glucosylated oligosaccharides are found on nascent glycoproteins. The limited availability of glucosylated lipid-linked oligosaccharides explains the incomplete usage of N-glycosylation sites in glycoproteins. This finding is reflected in the presence of transferrin forms in serum that lack one or both of the two N-linked oligosaccharides and the reduction of mannose incorporation to about one-third of control in glycoproteins of fibroblasts.
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Given a pool of motorists, how do we estimate the total intensity of those who had a prespecified number of traffic accidents in the past year? We previously have proposed the u,v method as a solution to estimation problems of this type. In this paper, we prove that the u,v method provides asymptotically efficient estimators in an important special case.