Vlasov Simulations of Trapping and Inhomogeneity in Raman Scattering

We study stimulated Raman scattering (SRS) in laser-fusion conditions with the Eulerian Vlasov code ELVIS. Back SRS from homogeneous plasmas occurs in sub-picosecond bursts and far exceeds linear theory. Forward SRS and re-scatter of back SRS are also observed. The plasma wave frequency downshifts from the linear dispersion curve, and the electron distribution shows flattening. This is consistent with trapping and reduces the Landau damping. There is some acoustic ($\omega\propto k$) activity and possibly electron acoustic scatter. Kinetic ions do not affect SRS for early times but suppress it later on. SRS from inhomogeneous plasmas exhibits a kinetic enhancement for long density scale lengths. More scattering results when the pump propagates to higher as opposed to lower density.Comment: 4 pages, 6 figures. Submitted to "Journal of Plasmas Physics" for the conference proceedings of the 19th International Conference on Numerical Simulation of Plasma

Solving the Vlasov equation for one-dimensional models with long range interactions on a GPU

We present a GPU parallel implementation of the numeric integration of the Vlasov equation in one spatial dimension based on a second order time-split algorithm with a local modified cubic-spline interpolation. We apply our approach to three different systems with long-range interactions: the Hamiltonian Mean Field, Ring and the self-gravitating sheet models. Speedups and accuracy for each model and different grid resolutions are presented

One Dimensional Hybrid-Vlasov Simulation of a Hall Thruster

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/97103/1/AIAA2012-4313.pd

MicroRNA-27b is a regulatory hub in lipid metabolism and is altered in dyslipidemia

Cellular and plasma lipid levels are tightly controlled by complex gene regulatory mechanisms. Elevated plasma lipid content, or hyperlipidemia, is a significant risk factor for cardiovascular morbidity and mortality. MicroRNAs (miRNAs) are posttranscriptional regulators of gene expression and have emerged as important modulators of lipid homeostasis, but the extent of their role has not been systematically investigated. In this study, we performed high-throughput small RNA sequencing and detected approximately 150 miRNAs in mouse liver. We then employed an unbiased, in silico strategy to identify miRNA regulatory hubs in lipid metabolism, and miR-27b was identified as the strongest such hub in human and mouse liver. In addition, hepatic miR-27b levels were determined to be sensitive to plasma hyperlipidemia, as evidenced by its ~3-fold up-regulation in the liver of mice on a high-fat diet (42% calories from fat). Further, we showed in a human hepatocyte cell line (Huh7) that miR-27b regulates the expression (mRNA and protein) of several key lipid-metabolism genes, including Angptl3 and Gpam. Finally, we demonstrated that hepatic miR-27b and its target genes are inversely altered in a mouse model of dyslipidemia and atherosclerosis

MicroRNA-223 coordinates cholesterol homeostasis

Results from this study represent a breakthrough in our understanding of posttranscriptional control of cholesterol metabolism and how microRNAs (miRNAs) are at the heart of cholesterol regulatory circuitry and homeostasis. Although cells are adept at maintaining proper cholesterol levels, it was unknown how cells posttranscriptionally coordinate cholesterol uptake, efflux, and synthesis. MicroRNA-223 (miR-223) transcription and expression are maintained by cholesterol, and, as a feedback network, miR-223 inhibits cholesterol biosynthesis and uptake and increases cholesterol efflux. This study clearly demonstrates the extensive role that miRNAs play in coordinating metabolic adaptation to disease and general homeostasis. This work highlights a unique regulatory control point for cholesterol homeostasis and illustrates how important the study of miRNAs is to the greater understanding of dyslipidemia and cardiovascular disease

HDL-transferred microRNA-223 regulates ICAM-1 expression in endothelial cells

High-density lipoproteins (HDL) have many biological functions, including reducing endothelial activation and adhesion molecule expression. We recently reported that HDL transport and deliver functional microRNAs (miRNA). Here we show that HDL suppresses expression of intercellular adhesion molecule 1 (ICAM-1) through the transfer of miR-223 to endothelial cells. After incubation of endothelial cells with HDL, mature miR-223 levels are significantly increased in endothelial cells and decreased on HDL. However, miR-223 is not transcribed in endothelial cells and is not increased in cells treated with HDL from miR-223−/− mice. HDL inhibit ICAM-1 protein levels, but not in cells pretreated with miR-223 inhibitors. ICAM-1 is a direct target of HDL-transferred miR-223 and this is the first example of an extracellular miRNA regulating gene expression in cells where it is not transcribed. Collectively, we demonstrate that HDL’s anti-inflammatory properties are conferred, in part, through HDL-miR-223 delivery and translational repression of ICAM-1 in endothelial cells

Renormalized Dissipation in Plasmas with Finite Collisionality

SCOPUS: ar.jinfo:eu-repo/semantics/publishe