Fast Shocks From Magnetic Reconnection Outflows

Magnetic reconnection is commonly perceived to drive flow and particle acceleration in flares of solar, stellar, and astrophysical disk coronae but the relative roles of different acceleration mecha- nisms in a given reconnection environment are not well understood. We show via direct numerical simulations that reconnection outflows produce weak fast shocks, when conditions for fast recon- nection are met and the outflows encounter an obstacle. The associated compression ratios lead to a Fermi acceleration particle spectrum that is significantly steeper than the strong fast shocks commonly studied, but consistent with the demands of solar flares. While this is not the only acceleration mechanism operating in a reconnection environment, it is plausibly a ubiquitous one

Current-Driven Filament Instabilities in Relativistic Plasmas. Final report

This grant has supported a study of some fundamental problems in current- and flow-driven instabilities in plasmas and their applications in inertial confinement fusion (ICF) and astrophysics. It addressed current-driven instabilities and their roles in fast ignition, and flow-driven instabilities and their applications in astrophysics

Scaling and memory in the return intervals of energy dissipation rate in three-dimensional fully developed turbulence

We study the statistical properties of return intervals $r$ between successive energy dissipation rates above a certain threshold $Q$ in three-dimensional fully developed turbulence. We find that the distribution function $P_Q(r)$ scales with the mean return interval $R_Q$ as $P_Q(r)=R_Q^{-1}f(r/R_Q)$ except for $r=1$, where the scaling function $f(x)$ has two power-law regimes. The return intervals are short-term and long-term correlated and possess multifractal nature. The Hurst index of the return intervals decays exponentially against $R_Q$, predicting that rare extreme events with $R_Q\to\infty$ are also long-term correlated with the Hurst index $H_\infty=0.639$.Comment: 5 pages, 5 figure

Therapeutic Effect of Targeting Branched-Chain Amino Acid Catabolic Flux in Pressure-Overload Induced Heart Failure.

Background Branched-chain amino acid (BCAA) catabolic defect is an emerging metabolic hallmark in failing hearts in human and animal models. The therapeutic impact of targeting BCAA catabolic flux under pathological conditions remains understudied. Methods and Results BT2 (3,6-dichlorobenzo[b]thiophene-2-carboxylic acid), a small-molecule inhibitor of branched-chain ketoacid dehydrogenase kinase, was used to enhance BCAA catabolism. After 2 weeks of transaortic constriction, mice with significant cardiac dysfunctions were treated with vehicle or BT2. Serial echocardiograms showed continuing pathological deterioration in left ventricle of the vehicle-treated mice, whereas the BT2-treated mice showed significantly preserved cardiac function and structure. Moreover, BT2 treatment improved systolic contractility and diastolic mechanics. These therapeutic benefits appeared to be independent of impacts on left ventricle hypertrophy but associated with increased gene expression involved in fatty acid utilization. The BT2 administration showed no signs of apparent toxicity. Conclusions Our data provide the first proof-of-concept evidence for the therapeutic efficacy of restoring BCAA catabolic flux in hearts with preexisting dysfunctions. The BCAA catabolic pathway represents a novel and potentially efficacious target for treatment of heart failure