An electron jet pump: The Venturi effect of a Fermi liquid

A three-terminal device based on a two-dimensional electron system is investigated in the regime of non-equilibrium transport. Excited electrons scatter with the cold Fermi sea and transfer energy and momentum to other electrons. A geometry analogous to a water jet pump is used to create a jet pump for electrons. Because of its phenomenological similarity we name the observed behavior "electronic Venturi effect".Comment: Journal of Applied Physics Special Topic: Plenary and Invited Papers from the 30th International Conference on the Physics of Semiconductors, Seoul, Korea, 2010; http://link.aip.org/link/?JAP/109/10241

Relaxation of hot electrons in a degenerate two-dimensional electron system: transition to one-dimensional scattering

The energy relaxation channels of hot electrons far from thermal equilibrium in a degenerate two-dimensional electron system are investigated in transport experiments in a mesoscopic three-terminal device. We observe a transition from two dimensions at zero magnetic field to quasi--one-dimensional scattering of the hot electrons in a strong magnetic field. In the two-dimensional case electron-electron scattering is the dominant relaxation mechanism, while the emission of optical phonons becomes more and more important as the magnetic field is increased. The observation of up to 11 optical phonons emitted per hot electron allows us to determine the onset energy of LO phonons in GaAs at cryogenic temperatures with a high precision, \eph=36.0\pm0.1\,meV. Numerical calculations of electron-electron scattering and the emission of optical phonons underline our interpretation in terms of a transition to one-dimensional dynamics.Comment: 15 pages, 9 figure

Effects of Friction and Disorder on the Quasi-Static Response of Granular Solids to a Localized Force

The response to a localized force provides a sensitive test for different models of stress transmission in granular solids. The elasto-plastic models traditionally used by engineers have been challenged by theoretical and experimental results which suggest a wave-like (hyperbolic) propagation of the stress, as opposed to the elliptic equations of static elasticity. Numerical simulations of two-dimensional granular systems subject to a localized external force are employed to examine the nature of stress transmission in these systems as a function of the magnitude of the applied force, the frictional parameters and the disorder (polydispersity). The results indicate that in large systems (typically considered by engineers), the response is close to that predicted by isotropic elasticity whereas the response of small systems (or when sufficiently large forces are applied) is strongly anisotropic. In the latter case the applied force induces changes in the contact network accompanied by frictional sliding. The larger the coefficient of static friction, the more extended is the range of forces for which the response is elastic and the smaller the anisotropy. Increasing the degree of polydispersity (for the range studied, up to 25%) decreases the range of elastic response. This article is an extension of a previously published letter [1].Comment: 21 pages (PDFLaTeX), 24 figures (some of them bitmapped to save space); submitted to Phys. Rev.

Mild Electrical Stimulation with Heat Shock Ameliorates Insulin Resistance via Enhanced Insulin Signaling

Low-intensity electrical current (or mild electrical stimulation; MES) influences signal transduction and activates phosphatidylinositol-3 kinase (PI3K)/Akt pathway. Because insulin resistance is characterized by a marked reduction in insulin-stimulated PI3K-mediated activation of Akt, we asked whether MES could increase Akt phosphorylation and ameliorate insulin resistance. In addition, it was also previously reported that heat shock protein 72 (Hsp72) alleviates hyperglycemia. Thus, we applied MES in combination with heat shock (HS) to in vitro and in vivo models of insulin resistance. Here we show that 10-min treatment with MES at 5 V (0.1 ms pulse duration) together with HS at 42°C increased the phosphorylation of insulin signaling molecules such as insulin receptor substrate (IRS) and Akt in HepG2 cells maintained in high-glucose medium. MES (12 V)+mild HS treatment of high fat-fed mice also increased the phosphorylation of insulin receptor β subunit (IRβ) and Akt in mice liver. In high fat-fed mice and db/db mice, MES+HS treatment for 10 min applied twice a week for 12–15 weeks significantly decreased fasting blood glucose and insulin levels and improved insulin sensitivity. The treated mice showed significantly lower weight of visceral and subcutaneous fat, a markedly improved fatty liver and decreased size of adipocytes. Our findings indicated that the combination of MES and HS alleviated insulin resistance and improved fat metabolism in diabetes mouse models, in part, by enhancing the insulin signaling pathway

Gene regulatory network reveals oxidative stress as the underlying molecular mechanism of type 2 diabetes and hypertension

<p>Abstract</p> <p>Background</p> <p>The prevalence of diabetes is increasing worldwide. It has been long known that increased rates of inflammatory diseases, such as obesity (OBS), hypertension (HT) and cardiovascular diseases (CVD) are highly associated with type 2 diabetes (T2D). T2D and/or OBS can develop independently, due to genetic, behavioral or lifestyle-related variables but both lead to oxidative stress generation. The underlying mechanisms by which theses complications arise and manifest together remain poorly understood. Protein-protein interactions regulate nearly every living process. Availability of high-throughput genomic data has enabled unprecedented views of gene and protein co-expression, co-regulations and interactions in cellular systems.</p> <p>Methods</p> <p>The present work, applied a systems biology approach to develop gene interaction network models, comprised of high throughput genomic and PPI data for T2D. The genes differentially regulated through T2D were 'mined' and their 'wirings' were studied to get a more complete understanding of the overall gene network topology and their role in disease progression.</p> <p>Results</p> <p>By analyzing the genes related to T2D, HT and OBS, a highly regulated gene-disease integrated network model has been developed that provides useful functional linkages among groups of genes and thus addressing how different inflammatory diseases are connected and propagated at genetic level. Based on the investigations around the 'hubs' that provided more meaningful insights about the cross-talk within gene-disease networks in terms of disease phenotype association with oxidative stress and inflammation, a hypothetical co-regulation disease mechanism model been proposed. The results from this study revealed that the oxidative stress mediated regulation cascade is the common mechanistic link among the pathogenesis of T2D, HT and other inflammatory diseases such as OBS.</p> <p>Conclusion</p> <p>The findings provide a novel comprehensive approach for understanding the pathogenesis of various co-associated chronic inflammatory diseases by combining the power of pathway analysis with gene regulatory network evaluation.</p

Analytical expressions for stopping-power ratios relevant for accurate dosimetry in particle therapy

In particle therapy, knowledge of the stopping-power ratios (STPRs) of the ion beam for air and water is necessary for accurate ionization chamber dosimetry. Earlier work has investigated the STPRs for pristine carbon ion beams, but here we expand the calculations to a range of ions (1 <= z <= 18) as well as spread out Bragg peaks (SOBPs) and provide a theoretical in-depth study with a special focus on the parameter regime relevant for particle therapy. The Monte Carlo transport code SHIELD-HIT is used to calculate complete particle-fluence spectra which are required for determining STPRs according to the recommendations of the International Atomic Energy Agency (IAEA). We confirm that the STPR depends primarily on the current energy of the ions rather than on their charge z or absolute position in the medium. However, STPRs for different sets of stopping-power data for water and air recommended by the International Commission on Radiation Units & Measurements (ICRU) are compared, including also the recently revised data for water, yielding deviations up to 2% in the plateau region. In comparison, the influence of the secondary particle spectra on the STPR is about two orders of magnitude smaller in the whole region up till the practical range. The gained insights enable us to propose an analytic approximation for the STPR for both pristine and SOBPs as a function of penetration depth, which parametrically depend only on the initial energy and the residual range of the ion, respectively.Comment: 21 pages, 5 figures, fixed bug with figures in v

Reversal of stress fibre formation by Nitric Oxide mediated RhoA inhibition leads to reduction in the height of preformed thrombi

Evidence has emerged to suggest that thrombi are dynamic structures with distinct areas of differing platelet activation and inhibition. We hypothesised that Nitric oxide (NO), a platelet inhibitor, can modulate the actin cytoskeleton reversing platelet spreading, and therefore reduce the capability of thrombi to withstand a high shear environment. Our data demonstrates that GSNO, DEANONOate, and a PKG-activating cGMP analogue reversed stress fibre formation and increased actin nodule formation in adherent platelets. This effect is sGC dependent and independent of ADP and thromboxanes. Stress fibre formation is a RhoA dependent process and NO induced RhoA inhibition, however, it did not phosphorylate RhoA at ser188 in spread platelets. Interestingly NO and PGI2 synergise to reverse stress fibre formation at physiologically relevant concentrations. Analysis of high shear conditions indicated that platelets activated on fibrinogen, induced stress fibre formation, which was reversed by GSNO treatment. Furthermore, preformed thrombi on collagen post perfused with GSNO had a 30% reduction in thrombus height in comparison to the control. This study demonstrates that NO can reverse key platelet functions after their initial activation and identifies a novel mechanism for controlling excessive thrombosis