Phenomenology for the decay of energy-containing eddies in homogeneous MHD turbulence

We evaluate a number of simple, one‐point phenomenological models for the decay of energy‐containing eddies in magnetohydrodynamic(MHD) and hydrodynamicturbulence. The MHDmodels include effects of cross helicity and Alfvénic couplings associated with a constant mean magnetic field, based on physical effects well‐described in the literature. The analytic structure of three separate MHDmodels is discussed. The single hydrodynamic model and several MHDmodels are compared against results from spectral‐method simulations. The hydrodynamic model phenomenology has been previously verified against experiments in wind tunnels, and certain experimentally determined parameters in the model are satisfactorily reproduced by the present simulation. This agreement supports the suitability of our numerical calculations for examining MHDturbulence, where practical difficulties make it more difficult to study physical examples. When the triple‐decorrelation time and effects of spectral anisotropy are properly taken into account, particular MHDmodels give decay rates that remain correct to within a factor of 2 for several energy‐halving times. A simple model of this type is likely to be useful in a number of applications in space physics, astrophysics, and laboratory plasma physics where the approximate effects of turbulence need to be included

Current collection to long conductors with wide geometries for bare electrodynamic tether applications - A laboratory update

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/77101/1/AIAA-2002-1123-228.pd

Satellite particle collection during active states of the Tethered Satellite System (TSS)

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/76723/1/AIAA-1996-2298-205.pd

Dynamical age of solar wind turbulence in the outer heliosphere

In an evolving turbulent medium, a natural timescale can be defined in terms of the energy decay time. The time evolution may be complicated by other effects such as energy supply due to driving, and spatial inhomogeneity. In the solar wind the turbulence appears not to be simply engaging in free decay, but rather the energy level observed at a particular position in the heliosphere is affected by expansion, “mixing,” and driving by stream shear. Here we discuss a new approach for estimating the “age” of solar wind turbulence as a function of heliocentric distance, using the local turbulent decay rate as the natural clock, but taking into account expansion and driving effects. The simplified formalism presented here is appropriate to low cross helicity (non-Alfvénic) turbulence in the outer heliosphere especially at low helio-latitudes. We employ Voyager data to illustrate our method, which improves upon the familiar estimates in terms of local eddy turnover times

Role of Cross Helicity in Cascade Processes of MHD turbulence

The purpose of this work is to investigate the spectral properties of the developed isotropic (non-Alfven) MHD turbulence stationary excited by an external force, which injects the cross helicity into the flow simultaneously with the energy. It is shown that the cross helicity blocks the spectral energy transfer in MHD turbulence and results in energy accumulation in the system. This accumulation proceeds until the vortex intensification compensates the decreasing efficiency of nonlinear interactions. The formula for estimating the average turbulence energy is obtained for the set ratio between the injected helicity and energy. It is remarkable that the turbulence accumulates the injected cross helicity at its low rate injection -- the integral correlation coefficient significantly exceeds the ratio between the injected helicity and the energy. It is shown that the spectrum slope gradually increases from "5/3" to "2" with the cross helicity level.Comment: 4 page

Solar Wind Turbulence and the Role of Ion Instabilities

International audienc

Ablation of Proliferating Cells in the CNS Exacerbates Motor Neuron Disease Caused by Mutant Superoxide Dismutase

Proliferation of glia and immune cells is a common pathological feature of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Here, to investigate the role of proliferating cells in motor neuron disease, SOD1G93A transgenic mice were treated intracerebroventicularly (ICV) with the anti-mitotic drug cytosine arabinoside (Ara-C). ICV delivery of Ara-C accelerated disease progression in SOD1G93A mouse model of ALS. Ara-C treatment caused substantial decreases in the number of microglia, NG2+ progenitors, Olig2+ cells and CD3+ T cells in the lumbar spinal cord of symptomatic SOD1G93A transgenic mice. Exacerbation of disease was also associated with significant alterations in the expression inflammatory molecules IL-1β, IL-6, TGF-β and the growth factor IGF-1

Genetic Biomarkers for ALS Disease in Transgenic SOD1G93A Mice

The pathophysiological mechanisms of both familial and sporadic Amyotrophic Lateral Sclerosis (ALS) are unknown, although growing evidence suggests that skeletal muscle tissue is a primary target of ALS toxicity. Skeletal muscle biopsies were performed on transgenic SOD1G93A mice, a mouse model of ALS, to determine genetic biomarkers of disease longevity. Mice were anesthetized with isoflurane, and three biopsy samples were obtained per animal at the three main stages of the disease. Transcriptional expression levels of seventeen genes, Ankrd1, Calm1, Col19a1, Fbxo32, Gsr, Impa1, Mef2c, Mt2, Myf5, Myod1, Myog, Nnt, Nogo A, Pax7, Rrad, Sln and Snx10, were tested in each muscle biopsy sample. Total RNA was extracted using TRIzol Reagent according to the manufacturer's protocol, and variations in gene expression were assayed by real-time PCR for all of the samples. The Pearson correlation coefficient was used to determine the linear correlation between transcriptional expression levels throughout disease progression and longevity. Consistent with the results obtained from total skeletal muscle of transgenic SOD1G93A mice and 74-day-old denervated mice, five genes (Mef2c, Gsr, Col19a1, Calm1 and Snx10) could be considered potential genetic biomarkers of longevity in transgenic SOD1G93A mice. These results are important because they may lead to the exploration of previously unexamined tissues in the search for new disease biomarkers and even to the application of these findings in human studies

Delayed Recovery of Skeletal Muscle Mass following Hindlimb Immobilization in mTOR Heterozygous Mice

The present study addressed the hypothesis that reducing mTOR, as seen in mTOR heterozygous (+/−) mice, would exaggerate the changes in protein synthesis and degradation observed during hindlimb immobilization as well as impair normal muscle regrowth during the recovery period. Atrophy was produced by unilateral hindlimb immobilization and data compared to the contralateral gastrocnemius. In wild-type (WT) mice, the gradual loss of muscle mass plateaued by day 7. This response was associated with a reduction in basal protein synthesis and development of leucine resistance. Proteasome activity was consistently elevated, but atrogin-1 and MuRF1 mRNAs were only transiently increased returning to basal values by day 7. When assessed 7 days after immobilization, the decreased muscle mass and protein synthesis and increased proteasome activity did not differ between WT and mTOR+/− mice. Moreover, the muscle inflammatory cytokine response did not differ between groups. After 10 days of recovery, WT mice showed no decrement in muscle mass, and this accretion resulted from a sustained increase in protein synthesis and a normalization of proteasome activity. In contrast, mTOR+/− mice failed to fully replete muscle mass at this time, a defect caused by the lack of a compensatory increase in protein synthesis. The delayed muscle regrowth of the previously immobilized muscle in the mTOR+/− mice was associated with a decreased raptor•4EBP1 and increased raptor•Deptor binding. Slowed regrowth was also associated with a sustained inflammatory response (e.g., increased TNFα and CD45 mRNA) during the recovery period and a failure of IGF-I to increase as in WT mice. These data suggest mTOR is relatively more important in regulating the accretion of muscle mass during recovery than the loss of muscle during the atrophy phase, and that protein synthesis is more sensitive than degradation to the reduction in mTOR during muscle regrowth

Restoring Specific Lactobacilli Levels Decreases Inflammation and Muscle Atrophy Markers in an Acute Leukemia Mouse Model

The gut microbiota has recently been proposed as a novel component in the regulation of host homeostasis and immunity. We have assessed for the first time the role of the gut microbiota in a mouse model of leukemia (transplantation of BaF3 cells containing ectopic expression of Bcr-Abl), characterized at the final stage by a loss of fat mass, muscle atrophy, anorexia and inflammation. The gut microbial 16S rDNA analysis, using PCR-Denaturating Gradient Gel Electrophoresis and quantitative PCR, reveals a dysbiosis and a selective modulation of Lactobacillus spp. (decrease of L. reuteri and L. johnsonii/gasseri in favor of L. murinus/animalis) in the BaF3 mice compared to the controls. The restoration of Lactobacillus species by oral supplementation with L. reuteri 100-23 and L. gasseri 311476 reduced the expression of atrophy markers (Atrogin-1, MuRF1, LC3, Cathepsin L) in the gastrocnemius and in the tibialis, a phenomenon correlated with a decrease of inflammatory cytokines (interleukin-6, monocyte chemoattractant protein-1, interleukin-4, granulocyte colony-stimulating factor, quantified by multiplex immuno-assay). These positive effects are strain- and/or species-specific since L. acidophilus NCFM supplementation does not impact on muscle atrophy markers and systemic inflammation. Altogether, these results suggest that the gut microbiota could constitute a novel therapeutic target in the management of leukemia-associated inflammation and related disorders in the muscle