Local and average fields inside surface-disordered waveguides: Resonances in the one-dimensional Anderson localization regime

We investigate the one-dimensional propagation of waves in the Anderson localization regime, for a single-mode, surface disordered waveguide. We make use of both an analytical formulation and rigorous numerical simulation calculations. The occurrence of anomalously large transmission coefficients for given realizations and/or frequencies is studied, revealing huge field intensity concentration inside the disordered waveguide. The analytically predicted s-like dependence of the average intensity, being in good agreement with the numerical results for moderately long systems, fails to explain the intensity distribution observed deep in the localized regime. The average contribution to the field intensity from the resonances that are above a threshold transmission coefficient $T_{c}$ is a broad distribution with a large maximum at/near mid-waveguide, depending universally (for given $T_{c}$) on the ratio of the length of the disorder segment to the localization length, $L/\xi$. The same universality is observed in the spatial distribution of the intensity inside typical (non-resonant with respect to the transmission coefficient) realizations, presenting a s-like shape similar to that of the total average intensity for $T_{c}$ close to 1, which decays faster the lower is $T_{c}$. Evidence is given of the self-averaging nature of the random quantity $\log[I(x)]/x\simeq -1/\xi$. Higher-order moments of the intensity are also shown.Comment: 9 pages, 9 figure

Harnessing hypoxic adaptation to prevent, treat, and repair stroke

The brain demands oxygen and glucose to fulfill its roles as the master regulator of body functions as diverse as bladder control and creative thinking. Chemical and electrical transmission in the nervous system is rapidly disrupted in stroke as a result of hypoxia and hypoglycemia. Despite being highly evolved in its architecture, the human brain appears to utilize phylogenetically conserved homeostatic strategies to combat hypoxia and ischemia. Specifically, several converging lines of inquiry have demonstrated that the transcription factor hypoxia-inducible factor-1 (HIF1-1) mediates the activation of a large cassette of genes involved in adaptation to hypoxia in surviving neurons after stroke. Accordingly, pharmacological or molecular approaches that engage hypoxic adaptation at the point of one of its sensors (e.g., inhibition of HIF prolyl 4 hydroxylases) leads to profound sparing of brain tissue and enhanced recovery of function. In this review, we discuss the potential mechanisms that could subserve protective and restorative effects of augmenting hypoxic adaptation in the brain. The strategy appears to involve HIF-dependent and HIF-independent pathways and more than 70 genes and proteins activated transcriptionally and post-transcriptionally that can act at cellular, local, and system levels to compensate for oxygen insufficiency. The breadth and depth of this homeostatic program offers a hopeful alternative to the current pessimism towards stroke therapeutics

Random-Matrix Theory of Quantum Transport

This is a comprehensive review of the random-matrix approach to the theory of phase-coherent conduction in mesocopic systems. The theory is applied to a variety of physical phenomena in quantum dots and disordered wires, including universal conductance fluctuations, weak localization, Coulomb blockade, sub-Poissonian shot noise, reflectionless tunneling into a superconductor, and giant conductance oscillations in a Josephson junction.Comment: 85 pages including 52 figures, to be published in Rev.Mod.Phy

Токсическое поражение миокарда, спровоцированное острым отравлением газообразным хлором, у пациента с коронарным атеросклерозом

Acute chlorine gas poisoning leads to activation of the sympathetic nervous system and, as a consequence, dysfunction of the cardiovascular system (CVS). We report a clinical case of toxic myocardial injury with gaseous  chlorine. In a man with coronary artery disease and polypathy, toxic  myocardial injury mimicked acute coronary syndrome (ACS) and was accompanied by a large area of left ventricular microvascular dysfunction, which did not coincide with the areas of blood supply of altered coronary arteries; the dynamics of electrocardiographic changes resembled  myocardial stunning in Takotsubo syndrome (TS). The effect of chlorine on CVS, features of clinical and instrumental diagnostics and differentiation of primary / secondary CT and ACS are discussed. Острое отравление газообразным хлором приводит к активации симпатической нервной системы и, как следствие, дисфункции сердечно-сосудистой системы (ССС).  Представлен клинический случай токсического поражения миокарда — газообразным хлором. У мужчины с ишемической болезнью сердца и полипатией токсическое поражение миокарда имитировало острый коронарный  синдром (ОКС) и сопровождалось большой площадью  микрососудистой дисфункции левого желудочка, не совпадающей с зонами кровоснабжения измененных  коронарных артерий; динамика электрокардиографических  изменений напоминала оглушение миокарда при синдроме такоцубо (СТ). Обсуждаются воздействие хлора на ССС,  особенности клинико-инструментальной диагностики и дифференциации первичного/вторичного СТ и ОКС.

L-Ascorbic Acid: A True Substrate for HIF Prolyl Hydroxylase?

L-Ascorbate (L-Asc), but not D-isoascorbate (D-Asc) and N-acetylcysteine (NAC) suppress HIF1 ODD-luc reporter activation induced by various inhibitors of HIF prolyl hydroxylase (PHD). The efficiency of suppression by L-Asc was sensitive to the nature of HIF PHD inhibitor chosen for reporter activation. In particular, the inhibitors developed to compete with alpha-ketoglutarate (alphaKG), were less sensitive to suppression by the physiological range of L-Asc (40-100muM) than those having a strong iron chelation motif. Challenging those HIF activators in the reporter system with D-Asc demonstrated that the D-isomer, despite exhibiting the same reducing potency with respect to ferric iron, had almost no effect compared to L-Asc. Similarly, no effect on reporter activation was observed with cell-permeable reducing agent NAC up to 1mM. Docking of L-Asc and D-Asc acid into the HIF PHD2 crystal structure showed interference of Tyr310 with respect to D-Asc. This suggests that L-Asc is not merely a reducing agent preventing enzyme inactivation. Rather, the overall results identify L-Asc as a co-substrate of HIF PHD that may compete for the binding site of alphaKG in the enzyme active center. This conclusion is in agreement with the results obtained recently in cell-based systems for TET enzymes and jumonji histone demethylases, where L-Asc has been proposed to act as a co-substrate and not as a reducing agent preventing enzyme inactivation