568 research outputs found

    Applied Plasma Research

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    Contains reports on two research projects.National Science Foundation (Grant GK-28282X1)National Science Foundation (Grant GK-33843

    Strong "quantum" chaos in the global ballooning mode spectrum of three-dimensional plasmas

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    The spectrum of ideal magnetohydrodynamic (MHD) pressure-driven (ballooning) modes in strongly nonaxisymmetric toroidal systems is difficult to analyze numerically owing to the singular nature of ideal MHD caused by lack of an inherent scale length. In this paper, ideal MHD is regularized by using a kk-space cutoff, making the ray tracing for the WKB ballooning formalism a chaotic Hamiltonian billiard problem. The minimum width of the toroidal Fourier spectrum needed for resolving toroidally localized ballooning modes with a global eigenvalue code is estimated from the Weyl formula. This phase-space-volume estimation method is applied to two stellarator cases.Comment: 4 pages typeset, including 2 figures. Paper accepted for publication in Phys. Rev. Letter

    Perpendicular momentum injection by lower hybrid wave in a tokamak

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    The injection of lower hybrid waves for current drive into a tokamak affects the profile of intrinsic rotation. In this article, the momentum deposition by the lower hybrid wave on the electrons is studied. Due to the increase in the poloidal momentum of the wave as it propagates into the tokamak, the parallel momentum of the wave increases considerably. The change of the perpendicular momentum of the wave is such that the toroidal angular momentum of the wave is conserved. If the perpendicular momentum transfer via electron Landau damping is ignored, the transfer of the toroidal angular momentum to the plasma will be larger than the injected toroidal angular momentum. A proper quasilinear treatment proves that both perpendicular and parallel momentum are transferred to the electrons. The toroidal angular momentum of the electrons is then transferred to the ions via different mechanisms for the parallel and perpendicular momentum. The perpendicular momentum is transferred to ions through an outward radial electron pinch, while the parallel momentum is transferred through collisions.Comment: 22 pages, 4 figure

    TBC1D1 Regulates Insulin- and Contraction-Induced Glucose Transport in Mouse Skeletal Muscle

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    OBJECTIVE: TBC1D1 is a member of the TBC1 Rab-GTPase family of proteins and is highly expressed in skeletal muscle. Insulin and contraction increase TBC1D1 phosphorylation on phospho-Akt substrate motifs (PASs), but the function of TBC1D1 in muscle is not known. Genetic linkage analyses show a TBC1D1 R125W missense variant confers risk for severe obesity in humans. The objective of this study was to determine whether TBC1D1 regulates glucose transport in skeletal muscle. RESEARCH DESIGN AND METHODS: In vivo gene injection and electroporation were used to overexpress wild-type and several mutant TBC1D1 proteins in mouse tibialis anterior muscles, and glucose transport was measured in vivo. RESULTS: Expression of the obesity-associated R125W mutant significantly decreased insulin-stimulated glucose transport in the absence of changes in TBC1D1 PAS phosphorylation. Simultaneous expression of an inactive Rab-GTPase (GAP) domain of TBC1D1 in the R125W mutant reversed this decrease in glucose transport caused by the R125W mutant. Surprisingly, expression of TBC1D1 mutated to Ala on four conserved Akt and/or AMP-activated protein kinase predicted phosphorylation sites (4P) had no effect on insulin-stimulated glucose transport. In contrast, expression of the TBC1D1 4P mutant decreased contraction-stimulated glucose transport, an effect prevented by concomitant disruption of TBC1D1 Rab-GAP activity. There was no effect of the R125W mutation on contraction-stimulated glucose transport. CONCLUSIONS: TBC1D1 regulates both insulin- and contraction-stimulated glucose transport, and this occurs via distinct mechanisms. The R125W mutation of TBC1D1 impairs skeletal muscle glucose transport, which could be a mechanism for the obesity associated with this mutation
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