30 research outputs found

    Universality of Frequency and Field Scaling of the Conductivity Measured by Ac-Susceptibility of a Ybco-Film

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    Utilizing a novel and exact inversion scheme, we determine the complex linear conductivity σ(ω)\sigma (\omega ) from the linear magnetic ac-susceptibility which has been measured from 3\,mHz to 50\,MHz in fields between 0.4\,T and 4\,T applied parallel to the c-axis of a 250\,nm thin disk. The frequency derivative of the phase σ/σ\sigma ''/\sigma ' and the dynamical scaling of σ(ω)\sigma (\omega) above and below Tg(B)T_g(B) provide clear evidence for a continuous phase transition at TgT_g to a generic superconducting state. Based on the vortex-glass scaling model, the resulting critical exponents ν\nu and zz are close to those frequently obtained on films by other means and associated with an 'isotropic' vortex glass. The field effect on σ(ω)\sigma(\omega) can be related to the increase of the glass coherence length, ξgB\xi_g\sim B.Comment: 8 pages (5 figures upon request), revtex 3.0, APK.94.01.0

    System Size and Energy Dependence of Jet-Induced Hadron Pair Correlation Shapes in Cu+Cu and Au+Au Collisions at sqrt(s_NN) = 200 and 62.4 GeV

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    We present azimuthal angle correlations of intermediate transverse momentum (1-4 GeV/c) hadrons from {dijets} in Cu+Cu and Au+Au collisions at sqrt(s_NN) = 62.4 and 200 GeV. The away-side dijet induced azimuthal correlation is broadened, non-Gaussian, and peaked away from \Delta\phi=\pi in central and semi-central collisions in all the systems. The broadening and peak location are found to depend upon the number of participants in the collision, but not on the collision energy or beam nuclei. These results are consistent with sound or shock wave models, but pose challenges to Cherenkov gluon radiation models.Comment: 464 authors from 60 institutions, 6 pages, 3 figures, 2 tables. Submitted to Physical Review Letters. Plain text data tables for the points plotted in figures for this and previous PHENIX publications are (or will be) publicly available at http://www.phenix.bnl.gov/papers.htm

    Improved Measurement of Double Helicity Asymmetry in Inclusive Midrapidity pi^0 Production for Polarized p+p Collisions at sqrt(s)=200 GeV

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    We present an improved measurement of the double helicity asymmetry for pi^0 production in polarized proton-proton scattering at sqrt(s) = 200 GeV employing the PHENIX detector at the Relativistic Heavy Ion Collider (RHIC). The improvements to our previous measurement come from two main factors: Inclusion of a new data set from the 2004 RHIC run with higher beam polarizations than the earlier run and a recalibration of the beam polarization measurements, which resulted in reduced uncertainties and increased beam polarizations. The results are compared to a Next to Leading Order (NLO) perturbative Quantum Chromodynamics (pQCD) calculation with a range of polarized gluon distributions.Comment: 389 authors, 4 pages, 2 tables, 1 figure. Submitted to Phys. Rev. D, Rapid Communications. Plain text data tables for the points plotted in figures for this and previous PHENIX publications are (or will be) publicly available at http://www.phenix.bnl.gov/papers.htm

    J/psi Production and Nuclear Effects for d+Au and p+p Collisions at sqrt(s_NN) = 200 GeV

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    J/psi production in d+Au and p+p collisions at sqrt(s_NN) = 200 GeV has been measured by the PHENIX experiment at rapidities -2.2 < y < +2.4. The cross sections and nuclear dependence of J/\psi production versus rapidity, transverse momentum, and centrality are obtained and compared to lower energy p+A results and to theoretical models. The observed nuclear dependence in d+Au collisions is found to be modest, suggesting that the absorption in the final state is weak and the shadowing of the gluon distributions is small and consistent with Dokshitzer-Gribov-Lipatov-Altarelli-Parisi-based parameterizations that fit deep-inelastic scattering and Drell-Yan data at lower energies.Comment: 331 authors, 6 pages text, 3 figures. Published in PRL. Version 2 has minor changes required during the review and production process. Of significant note are that (a) the original Figs. 3 and 4 are combined into a single Fig. 3 and (b) the value of (p_T)**2 at x_F=0 changed from 3.17+/-0.33 to 3.03+/-0.40. Plain text data tables for the points plotted in figures for this and previous PHENIX publications are publicly available at http://www.phenix.bnl.gov/papers.htm

    Distribution and Evolution of von Willebrand/Integrin A Domains: Widely Dispersed Domains with Roles in Cell Adhesion and Elsewhere

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    The von Willebrand A (VWA) domain is a well-studied domain involved in cell adhesion, in extracellular matrix proteins, and in integrin receptors. A number of human diseases arise from mutations in VWA domains. We have analyzed the phylogenetic distribution of this domain and the relationships among ∼500 proteins containing this domain. Although the majority of VWA-containing proteins are extracellular, the most ancient ones, present in all eukaryotes, are all intracellular proteins involved in functions such as transcription, DNA repair, ribosomal and membrane transport, and the proteasome. A common feature seems to be involvement in multiprotein complexes. Subsequent evolution involved deployment of VWA domains by Metazoa in extracellular proteins involved in cell adhesion such as integrin β subunits (all Metazoa). Nematodes and chordates separately expanded their complements of extracellular matrix proteins containing VWA domains, whereas plants expanded their intracellular complement. Chordates developed VWA-containing integrin α subunits, collagens, and other extracellular matrix proteins (e.g., matrilins, cochlin/vitrin, and von Willebrand factor). Consideration of the known properties of VWA domains in integrins and extracellular matrix proteins allows insights into their involvement in protein–protein interactions and the roles of bound divalent cations and conformational changes. These allow inferences about similar functions in novel situations such as protease regulators (e.g., complement factors and trypsin inhibitors) and intracellular proteins (e.g., helicases, chelatases, and copines)
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