Particle-in-cell simulation study of a lower-hybrid shock

The expansion of a magnetized high-pressure plasma into a low-pressure ambient medium is examined with particle-in-cell simulations. The magnetic field points perpendicular to the plasma's expansion direction and binary collisions between particles are absent. The expanding plasma steepens into a quasi-electrostatic shock that is sustained by the lower-hybrid (LH) wave. The ambipolar electric field points in the expansion direction and it induces together with the background magnetic field a fast E cross B drift of electrons. The drifting electrons modify the background magnetic field, resulting in its pile-up by the LH shock. The magnetic pressure gradient force accelerates the ambient ions ahead of the LH shock, reducing the relative velocity between the ambient plasma and the LH shock to about the phase speed of the shocked LH wave, transforming the LH shock into a nonlinear LH wave. The oscillations of the electrostatic potential have a larger amplitude and wavelength in the magnetized plasma than in an unmagnetized one with otherwise identical conditions. The energy loss to the drifting electrons leads to a noticeable slowdown of the LH shock compared to that in an unmagnetized plasma.

The Genetic Landscape of Renal Complications in Type 1 Diabetes

Diabetes is the leading cause of end stage renal disease. Despite evidence for a substantial heritability of diabetic kidney disease, efforts to identify genetic susceptibility variants have had limited success. We extended previous efforts in three dimensions, examining a more comprehensive set of genetic variants in larger numbers of subjects with type 1 diabetes characterized for a wider range of cross-sectional diabetic kidney disease phenotypes. In 2,843 subjects, we estimated that the heritability of diabetic kidney disease was 35% ( p=6x10-3 ). Genome-wide association analysis and replication in 12,540 individuals identified no single variants reaching stringent levels of significance and, despite excellent power, provided little independent confirmation of previously published associated variants. Whole exome sequencing in 997 subjects failed to identify any large-effect coding alleles of lower frequency influencing the risk of diabetic kidney disease. However, sets of alleles increasing body mass index ( p=2.2×10-5) and the risk of type 2 diabetes (p=6.1x10-4 ) were associated with the risk of diabetic kidney disease. We also found genome-wide genetic correlation between diabetic kidney disease and failure at smoking cessation ( p=1.1×10-4 ). Pathway analysis implicated ascorbate and aldarate metabolism ( p=9×10-6), and pentose and glucuronate interconversions ( p=3×10-6) in pathogenesis of diabetic kidney disease. These data provide further evidence for the role of genetic factors influencing diabetic kidney disease in those with type 1 diabetes and highlight some key pathways that may be responsible. Altogether these results reveal important biology behind the major cause of kidney disease.