Dissipative dynamics of superfluid vortices at non-zero temperatures

We consider the evolution and dissipation of vortex rings in a condensate at non-zero temperature, in the context of the classical field approximation, based on the defocusing nonlinear Schr\"odinger equation. The temperature in such a system is fully determined by the total number density and the number density of the condensate. A vortex ring is introduced into a condensate in a state of thermal equilibrium, and interacts with non-condensed particles. These interactions lead to a gradual decrease in the vortex line density, until the vortex ring completely disappears. We show that the square of the vortex line length changes linearly with time, and obtain the corresponding universal decay law. We relate this to mutual friction coefficients in the fundamental equation of vortex motion in superfluids.Comment: 4 pages, 3 figure

Critical packing in granular shear bands

In a realistic three-dimensional setup, we simulate the slow deformation of idealized granular media composed of spheres undergoing an axisymmetric triaxial shear test. We follow the self-organization of the spontaneous strain localization process leading to a shear band and demonstrate the existence of a critical packing density inside this failure zone. The asymptotic criticality arising from the dynamic equilibrium of dilation and compaction is found to be restricted to the shear band, while the density outside of it keeps the memory of the initial packing. The critical density of the shear band depends on friction (and grain geometry) and in the limit of infinite friction it defines a specific packing state, namely the \emph{dynamic random loose packing}

Interleukin-6 Attenuates Insulin-Mediated Increases in Endothelial Cell Signaling but Augments Skeletal Muscle Insulin Action via Differential Effects on Tumor Necrosis Factor-α Expression

OBJECTIVE: The cytokine interleukin-6 (IL-6) stimulates AMP-activated protein kinase (AMPK) and insulin signaling in skeletal muscle, both of which result in the activation of endothelial nitric oxide synthase (eNOS). We hypothesized that IL-6 promotes endothelial cell signaling and capillary recruitment in vivo, contributing to increased glucose uptake. RESEARCH DESIGN AND METHODS: The effect of IL-6 with and without insulin on AMPK, insulin, and eNOS signaling in and nitric oxide (NO) release from human aortic endothelial cells (HAECs) was examined. The physiological significance of these in vitro signaling events was assessed by measuring capillary recruitment in rats during control and euglycemic-hyperinsulinemic clamps with or without IL-6 infusion. RESULTS: IL-6 blunted increases in insulin signaling, eNOS phosphorylation (Ser1177), and NO production and reduced phosphorylation of AMPK in HAEC in vitro and capillary recruitment in vivo. In contrast, IL-6 increased Akt phosphorylation (Ser473) in hindlimb skeletal muscle and enhanced whole-body glucose disappearance and glucose uptake during the clamp. The differences in endothelial cell and skeletal muscle signaling were mediated by the cell-specific, additive effects of IL-6 and insulin because this treatment markedly increased tumor necrosis factor (TNF)-alpha protein expression in HAECs without any effect on TNF-alpha in skeletal muscle. When HAECs were incubated with a TNF-alpha-neutralizing antibody, the negative effects of IL-6 on eNOS signaling were abolished. CONCLUSIONS: In the presence of insulin, IL-6 contributes to aberrant endothelial cell signaling because of increased TNF-alpha expression