Electromagnetic gyrokinetic turbulence in finite-beta helical plasmas

A saturation mechanism for microturbulence in a regime of weak zonal flow generation isinvestigated by means of electromagnetic gyrokinetic simulations. The study identifies a newsaturation process of the kinetic ballooning mode (KBM) turbulence originating from the spatial structure of the KBM instabilities in a finite-beta Large Helical Device (LHD) plasma.Specifically, the most unstable KBM in LHD has an inclined mode structure with respect to the mid-plane of a torus, i.e., it has a finite radial wave-number in flux tube coordinates, in contrast to KBMs in tokamaks as well as ion-temperature gradient modes in tokamaks and helical systems. The simulations reveal that the growth of KBMs in LHD is saturated by nonlinear interactions of oppositely inclined convection cells through mutual shearing as well as by the zonal flow. The saturation mechanism is quantitatively investigated by analysis of the nonlinear entropy transfer that shows not only the mutual shearing but also a self-interaction with an elongated mode structure along the magnetic field line

Antigen and Thapsigargin Promote Influx of Ca2+ in Rat Basophilic RBL-2H3 Cells by Ostensibly Similar Mechanisms That Allow Filling of Inositol 1,4,5-Trisphosphate-Sensitive and Mitochondrial Ca2+ Stores

In single, Fura 2-loaded RBL-2H3 cells, antigen and thapsigargin depleted the same intracellular pool of Ca2+ in the absence of external Ca2+; provision of external Ca2+ induced immediate increases in levels of free Ca2+ ([Ca2+](i)). These increases were dependent on the presence of external Ca2+ and, presumably, on influx of Ca2+ across the cell membrane. Both stimulants enhanced intracellular accumulation of 45Ca2+ through ostensibly similar mechanisms because accumulation was blocked to similar extents by various multivalent cations or by depolarization with K+. Because thapsigargin blocked reuptake of Ca2+ into inositol 1,4,5-trisphosphate sensitive stores, uptake occurred independently of the refilling of these stores. Uptake was dependent instead on sequestration of 45Ca2+ in a pool of high capacity that was insensitive to thapsigargin, caffeine, GTP and inositol 1,4,5-trisphosphate but sensitive to ionomycin and mitochondrial inhibitors. The existence of an inositol 1,4,5-trisphosphate-insensitive pool was also apparent in permeabilized cells; at 0.1 μM [Ca2+](i), uptake of 45Ca2+ was largely confined (\u3e 80%) to the inositol 1,4,5-trisphosphate-sensitive pool, but at 2 μM [Ca2+](i) uptake was largely (\u3e 60%) into the inositol 1,4,5-trisphosphate-insensitive pool. Provision of mitochondrial inhibitors along with thapsigargin to block uptake into both pools, did not impair the thapsigargin-induced increase in [Ca2+](i) or influx of Ca2+, as indicated by changes in Fura 2 fluorescence, but did block the intracellular accumulation of 45Ca2+. The studies illustrate the utility of simultaneous measurements of [Ca2+](i) and 45Ca2+ uptake for a full accounting of Ca2+ homoeostasis as exemplified by the ability to distinguish between influx and mitochondrial uptake of Ca2+

Had the planet mars not existed: Kepler's equant model and its physical consequences

We examine the equant model for the motion of planets, which has been the starting point of Kepler's investigations before he modified it because of Mars observations. We show that, up to first order in eccentricity, this model implies for each orbit a velocity which satisfies Kepler's second law and Hamilton's hodograph, and a centripetal acceleration with an inverse square dependence on the distance to the sun. If this dependence is assumed to be universal, Kepler's third law follows immediately. This elementary execice in kinematics for undergraduates emphasizes the proximity of the equant model coming from Ancient Greece with our present knowledge. It adds to its historical interest a didactical relevance concerning, in particular, the discussion of the Aristotelian or Newtonian conception of motion