Information transfer through disordered media by diffuse waves

We consider the information content h of a scalar multiple-scattered, diffuse wave field $\psi(\vec{r})$ and the information capacity C of a communication channel that employs diffuse waves to transfer the information through a disordered medium. Both h and C are shown to be directly related to the mesoscopic correlations between the values of $\psi(\vec{r})$ at different positions $\vec{r}$ in space, arising due to the coherent nature of the wave. For the particular case of a communication channel between two identical linear arrays of $n \gg 1$ equally-spaced transmitters/receivers (receiver spacing a), we show that the average capacity $\propto n$ and obtain explicit analytic expressions for $/n$ in the limit of $n \to \infty$ and $k \ell \to \infty$, where $k= 2\pi/ \lambda$, $\lambda$ is the wavelength, and $\ell$ is the mean free path. Modification of the above results in the case of finite but large n and $k \ell$ is discussed as well.Comment: REVTeX 4, 12 pages, 7 figure

Superconducting gap in the presence of bilayer splitting in underdoped Bi(Pb)2212

The clearly resolved bilayer splitting in ARPES spectra of the underdoped Pb-Bi2212 compound rises the question of how the bonding and antibonding sheets of the Fermi surface are gapped in the superconducting state. Here we compare the superconducting gaps for both split components and show that within the experimental uncertainties they are identical. By tuning the relative intensity of the bonding and antibonding bands using different excitation conditions we determine the precise {\bf k}-dependence of the leading edge gap. Significant deviations from the simple cos($k_{x}$)-cos($k_{y}$) gap function for the studied doping level are detected.Comment: 5 pages, 4 figures (revtex4

The management of diabetic ketoacidosis in children

The object of this review is to provide the definitions, frequency, risk factors, pathophysiology, diagnostic considerations, and management recommendations for diabetic ketoacidosis (DKA) in children and adolescents, and to convey current knowledge of the causes of permanent disability or mortality from complications of DKA or its management, particularly the most common complication, cerebral edema (CE). DKA frequency at the time of diagnosis of pediatric diabetes is 10%–70%, varying with the availability of healthcare and the incidence of type 1 diabetes (T1D) in the community. Recurrent DKA rates are also dependent on medical services and socioeconomic circumstances. Management should be in centers with experience and where vital signs, neurologic status, and biochemistry can be monitored with sufficient frequency to prevent complications or, in the case of CE, to intervene rapidly with mannitol or hypertonic saline infusion. Fluid infusion should precede insulin administration (0.1 U/kg/h) by 1–2 hours; an initial bolus of 10–20 mL/kg 0.9% saline is followed by 0.45% saline calculated to supply maintenance and replace 5%–10% dehydration. Potassium (K) must be replaced early and sufficiently. Bicarbonate administration is contraindicated. The prevention of DKA at onset of diabetes requires an informed community and high index of suspicion; prevention of recurrent DKA, which is almost always due to insulin omission, necessitates a committed team effort

Optimization and Evaluation of Antiparasitic Benzamidobenzoic Acids as Inhibitors of Kinetoplastid Hexokinase 1

Kinetoplastid-based infections are neglected diseases that represent a significant human health issue. Chemotherapeutic options are limited due to toxicity, parasite susceptibility, and poor patient compliance. In response, we studied a molecular-target-directed approach involving intervention of hexokinase activity—a pivotal enzyme in parasite metabolism. A benzamidobenzoic acid hit with modest biochemical inhibition of Trypanosoma brucei hexokinase 1 (TbHK1, IC50=9.1 μm), low mammalian cytotoxicity (IMR90 cells, EC50>25 μm), and no appreciable activity on whole bloodstream-form (BSF) parasites was optimized to afford a probe with improved TbHK1 potency and, significantly, efficacy against whole BSF parasites (TbHK1, IC50=0.28 μm; BSF, ED50=1.9 μm). Compounds in this series also inhibited the hexokinase enzyme from Leishmania major (LmHK1), albeit with less potency than toward TbHK1, suggesting that inhibition of the glycolytic pathway may be a promising opportunity to target multiple disease-causing trypanosomatid protozoa

Libxc: a library of exchange and correlation functionals for density functional theory

The central quantity of density functional theory is the so-called exchange-correlation functional. This quantity encompasses all non-trivial many-body effects of the ground-state and has to be approximated in any practical application of the theory. For the past 50 years, hundreds of such approximations have appeared, with many successfully persisting in the electronic structure community and literature. Here, we present a library that contains routines to evaluate many of these functionals (around 180) and their derivatives.Comment: 15 page

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease