Helical Magnetorotational Instability in Magnetized Taylor-Couette Flow

Hollerbach and Rudiger have reported a new type of magnetorotational instability (MRI) in magnetized Taylor-Couette flow in the presence of combined axial and azimuthal magnetic fields. The salient advantage of this "helical'' MRI (HMRI) is that marginal instability occurs at arbitrarily low magnetic Reynolds and Lundquist numbers, suggesting that HMRI might be easier to realize than standard MRI (axial field only). We confirm their results, calculate HMRI growth rates, and show that in the resistive limit, HMRI is a weakly destabilized inertial oscillation propagating in a unique direction along the axis. But we report other features of HMRI that make it less attractive for experiments and for resistive astrophysical disks. Growth rates are small and require large axial currents. More fundamentally, instability of highly resistive flow is peculiar to infinitely long or periodic cylinders: finite cylinders with insulating endcaps are shown to be stable in this limit. Also, keplerian rotation profiles are stable in the resistive limit regardless of axial boundary conditions. Nevertheless, the addition of toroidal field lowers thresholds for instability even in finite cylinders.Comment: 16 pages, 2 figures, 1 table, submitted to PR

A HIDDEN FIGURE, A BEAUTIFUL MIND IN THE THEORY OF MATHEMATICAL GAMES

Alain A. Lewis, an African-American researcher, was a 1983 Ford Foundation Postdoctoral Fellow at Cornell University. He obtained a B.A. in Philosophy, Economics, and Statistics from George Washington University in 1969, and a Ph.D. in Applied Mathematics from Harvard University in 1979. The title of his dissertation: “A Nonstandard Theory of Games.” His advisor was Kenneth Arrow. It was during his first year at Cornell, where his sponsor was Prof. Anil Nerode, that he enjoyed his Ford award. The result, which is an important application of game theory, is described by Philip Mirowski in the book Machine Dreams as: “…now considered in some circles as an underground classic in the theory of computational economics.

Partial differential equations in fluid dynamics

This book concerns partial differential equations applied to fluids problems in science and engineering

Mitochondrial oxidative stress contributes to diastolic dysfunction through impaired mitochondrial dynamics

Diastolic dysfunction (DD) underlies heart failure with preserved ejection fraction (HFpEF), a clinical syndrome associated with aging that is becoming more prevalent. Despite extensive clinical studies, no effective treatment exists for HFpEF. Recent findings suggest that oxidative stress contributes to the pathophysiology of DD, but molecular mechanisms underpinning redox-sensitive cardiac remodeling in DD remain obscure. Using transgenic mice with mitochondria-targeted NOX4 overexpression (Nox4TG618) as a model, we demonstrate that NOX4-dependent mitochondrial oxidative stress induces DD in mice as measured by increased E/E′, isovolumic relaxation time, Tau Glantz and reduced dP/dtmin while EF is preserved. In Nox4TG618 mice, fragmentation of cardiomyocyte mitochondria, increased DRP1 phosphorylation, decreased expression of MFN2, and a higher percentage of apoptotic cells in the myocardium are associated with lower ATP-driven and maximal mitochondrial oxygen consumption rates, a decrease in respiratory reserve, and a decrease in citrate synthase and Complex I activities. Transgenic mice have an increased concentration of TGFβ and osteopontin in LV lysates, as well as MCP-1 in plasma, which correlates with a higher percentage of LV myocardial periostin- and ACTA2-positive cells compared with wild-type mice. Accordingly, the levels of ECM as measured by Picrosirius Red staining as well as interstitial deposition of collagen I are elevated in the myocardium of Nox4TG618 mice. The LV tissue of Nox4TG618 mice also exhibited increased ICaL current, calpain 2 expression, and altered/disrupted Z-disc structure. As it pertains to human pathology, similar changes were found in samples of LV from patients with DD. Finally, treatment with GKT137831, a specific NOX1 and NOX4 inhibitor, or overexpression of mCAT attenuated myocardial fibrosis and prevented DD in the Nox4TG618 mice. Together, our results indicate that mitochondrial oxidative stress contributes to DD by causing mitochondrial dysfunction, impaired mitochondrial dynamics, increased synthesis of pro-inflammatory and pro-fibrotic cytokines, activation of fibroblasts, and the accumulation of extracellular matrix, which leads to interstitial fibrosis and passive stiffness of the myocardium. Further, mitochondrial oxidative stress increases cardiomyocyte Ca2+ influx, which worsens CM relaxation and raises the LV filling pressure in conjunction with structural proteolytic damage.http://deepblue.lib.umich.edu/bitstream/2027.42/175138/2/Mitochondrial oxidative stress contributes to diastolic dysfunction through impaired mitochondrial dynamics.pdfPublished versionDescription of Mitochondrial oxidative stress contributes to diastolic dysfunction through impaired mitochondrial dynamics.pdf : Published versio