Newellrobinson7845

Gas storage and recovery processes in shales critically depend on nano-scale porosity and chemical composition, but information about the nanoscale pore geometry and connectivity of kerogen, insoluble organic shale matter, is largely unavailable. Using adsorption microcalorimetry, we show that once strong adsorption sites within nanoscale network are taken, gas adsorption even at very low pressure is governed by pore width rather than chemical composition. A combination of focused ion beam with scanning electron microscopy and transmission electron microscopy reveal the nanoscale structure of kerogen includes not only the ubiquitous amorphous phase but also highly graphitized sheets, fiber- and onion-like structures creating nanoscale voids accessible for gas sorption. Nanoscale structures bridge the current gap between molecular size and macropore scale in existing models for kerogen, thus allowing accurate prediction of gas sorption, storage and diffusion properties in shales.Genetic evidence indicates that haploinsufficiency of ARID1B causes intellectual disability (ID) and autism spectrum disorder (ASD), but the neural function of ARID1B is largely unknown. Using both conditional and global Arid1b knockout mouse strains, we examined the role of ARID1B in neural progenitors. We detected an overall decrease in the proliferation of cortical and ventral neural progenitors following homozygous deletion of Arid1b, as well as altered cell cycle regulation and increased cell death. Each of these phenotypes was more pronounced in ventral neural progenitors. Furthermore, we observed decreased nuclear localization of β-catenin in Arid1b-deficient neurons. Conditional homozygous deletion of Arid1b in ventral neural progenitors led to pronounced ID- and ASD-like behaviors in mice, whereas the deletion in cortical neural progenitors resulted in minor cognitive deficits. This study suggests an essential role for ARID1B in forebrain neurogenesis and clarifies its more pronounced role in inhibitory neural progenitors. Our findings also provide insights into the pathogenesis of ID and ASD.Amorphous carbon (a-C) films are characterized by extraordinary chemical inertness and unique thermophysical properties that are critical to applications requiring oxidation-resistant, low-friction, and durable overcoats. However, the increasing demands for ultrathin (a few nanometers thick) a-C films in various emerging technologies, such as computer storage devices, microelectronics, microdynamic systems, and photonics, make experimental evaluation of the structural stability and tribomechanical properties at the atomic level cumbersome and expensive. Consequently, the central objective of this study was to develop comprehensive MD models that can provide insight into the oxidation behavior and friction characteristics of ultrathin a-C films exhibiting layered through-thickness structure. MD simulations were performed for a-C films characterized by relatively low and high sp3 contents subjected to energetic oxygen atom bombardment or undergoing normal and sliding contact against each other in vacuum and oxygen atmosphere. The effect of energetic oxygen atoms on the oxidation behavior of a-C films, the dependence of contact deformation and surface attractive forces (adhesion) on surface interference, and the evolution of friction and structural changes (rehybridization) in the former a-C films during sliding are interpreted in the context of simulations performed in vacuum and oxidizing environments. The present study provides insight into the oxidation mechanism and friction behavior of ultrathin a-C films and introduces a computational framework for performing oxidation/tribo-oxidation MD simulations that can guide experimental investigations.Left ventricular remodeling following myocardial infarction (MI) is related to adverse outcome. It has been shown that an up-regulation of plasma soluble ST2 (sST2) levels are associated with lower pre-discharge left ventricular (LV) ejection fraction, adverse cardiovascular outcomes and mortality outcome after MI. The mechanisms involved in its modulation are unknown and there is not specific treatment capable of lowering plasma sST2 levels in acute-stage HF. We recently identified Yin-yang 1 (Yy1) as a transcription factor related to circulating soluble ST2 isoform (sST2) expression in infarcted myocardium. However, the underlying mechanisms involved in this process have not been thoroughly elucidated. This study aimed to evaluate the pathophysiological implication of miR-199a-5p in cardiac remodeling and the expression of the soluble ST2 isoform. Myocardial infarction (MI) was induced by permanent ligation of the left anterior coronary artery in C57BL6/J mice that randomly received antimiR199a therapy, antimiR-Ctrl or saline. A model of biomechanical stretching was also used to characterize the underlying mechanisms involved in the activation of Yy1/sST2 axis. Our results show that the significant upregulation of miR-199a-5p after myocardial infarction increases pathological cardiac hypertrophy by upregulating circulating soluble sST2 levels. AntimiR199a therapy up-regulates Sirt1 and inactivates the co-activator P300 protein, thus leading to Yy1 inhibition which decreases both expression and release of circulating sST2 by cardiomyocytes after myocardial infarction. A-769662 ic50 Pharmacological inhibition of miR-199a rescues cardiac hypertrophy and heart failure in mice, offering a potential therapeutic approach for cardiac failure.This article presents a new open source extension to the Emergency Events Database (EM-DAT) that allows researchers, for the first time, to explore and make use of subnational, geocoded data on major disasters triggered by natural hazards. The Geocoded Disasters (GDIS) dataset provides spatial geometry in the form of GIS polygons and centroid latitude and longitude coordinates for each administrative entity listed as a disaster location in the EM-DAT database. In total, GDIS contains spatial information on 39,953 locations for 9,924 unique disasters occurring worldwide between 1960 and 2018. The dataset facilitates connecting the EM-DAT database to other geographic data sources on the subnational level to enable rigorous empirical analyses of disaster determinants and impacts.