The availability of complete sets of genes from many organisms makes it possible to identify genes unique to (or lost from) certain clades. This information is used to reconstruct phylogenetic trees; identify genes involved in the evolution of clade specific novelties; and for phylostratigraphy-identifying ages of genes in a given species. These investigations rely on accurately predicted orthologs. Here we use simulation to produce sets of orthologs that experience no gains or losses. We show that errors in identifying orthologs increase with higher rates of evolution. We use the predicted sets of orthologs, with errors, to reconstruct phylogenetic trees; to count gains and losses; and for phylostratigraphy. Our simulated data, containing information only from errors in orthology prediction, closely recapitulate findings from empirical data. We suggest published downstream analyses must be informed to a large extent by errors in orthology prediction that mimic expected patterns of gene evolution.Sepsis is a leading cause of death among inpatients at hospitals. However, with early detection, death rate can drop substantially. In this study, we present the top-performing algorithm for Sepsis II prediction in the DII National Data Science Challenge using the Cerner Health Facts data involving more than 100,000 adult patients. This large sample size allowed us to dissect the predictability by age-groups, race, genders, and care settings and up to 192 hr of sepsis onset. This large data collection also allowed us to conclude that the last six biometric records on average are informative to the prediction of sepsis. We identified biomarkers that are common across the treatment time and novel biomarkers that are uniquely presented for early prediction. The algorithms showed meaningful signals days ahead of sepsis onset, supporting the potential of reducing death rate by focusing on high-risk populations identified from heterogeneous data integration.Extended space travel is a goal of government space agencies and private companies. However, spaceflight poses risks to human health, and the effects on the nervous system have to be better characterized. Here, we exploited the unique experimental advantages of the nematode Caenorhabditis elegans to explore how spaceflight affects adult neurons in vivo. We found that animals that lived 5 days of adulthood on the International Space Station exhibited hyperbranching in PVD and touch receptor neurons. We also found that, in the presence of a neuronal proteotoxic stress, spaceflight promotes a remarkable accumulation of neuronal-derived waste in the surrounding tissues, suggesting an impaired transcellular degradation of debris released from neurons. Our data reveal that spaceflight can significantly affect adult neuronal morphology and clearance of neuronal trash, highlighting the need to carefully assess the risks of long-duration spaceflight on the nervous system and to develop adequate countermeasures for safe space exploration.Achieving highly active and stable oxygen reduction reaction performance at low platinum-group-metal loadings remains one of the grand challenges in the proton-exchange membrane fuel cells community. Currently, state-of-the-art electrocatalysts are high-surface-area-carbon-supported nanoalloys of platinum with different transition metals (Cu, Ni, Fe, and Co).  https://www.selleckchem.com/products/abc294640.html  Despite years of focused research, the established structure-property relationships are not able to explain and predict the electrochemical performance and behavior of the real nanoparticulate systems. In the first part of this work, we reveal the complexity of commercially available platinum-based electrocatalysts and their electrochemical behavior. In the second part, we introduce a bottom-up approach where atomically resolved properties, structural changes, and strain analysis are recorded as well as analyzed on an individual nanoparticle before and after electrochemical conditions (e.g. high current density). Our methodology offers a new level of understanding of structure-stability relationships of practically viable nanoparticulate systems.There is no efficient wastewater treatment solution for removing organic micropollutants (OMPs), which, therefore, are continuously introduced to the Earth's surface waters. This creates a severe risk to aquatic ecosystems and human health. In emerging water treatment processes based on ion-exchange membranes (IEM), transport of OMPs through membranes remains unknown. We performed a comprehensive investigation of the OMP transport through a single IEM under non-steady-state conditions. For the first time, positron annihilation lifetime spectroscopy was used to study differences in the free volume element radius between anion- and cation-exchange membranes, and between their thicknesses. The dynamic diffusion-adsorption model was used to calculate the adsorption and diffusion coefficients of OMPs. Remarkably, diffusion coefficients increased with the membrane thickness, where its surface resistance was more evident in thinner membranes. Presented results will contribute to the improved design of next-generation IEMs with higher selectivity toward multiple types of organic compounds.Arrestin-dependent activation of a G-protein-coupled receptor (GPCR) triggers endocytotic internalization of the receptor complex. We analyzed the interaction between the pattern recognition receptor (PRR) lectin-like oxidized low-density lipoprotein (oxLDL) receptor (LOX-1) and the GPCR angiotensin II type 1 receptor (AT1) to report a hitherto unidentified mechanism whereby internalization of the GPCR mediates cellular endocytosis of the PRR ligand. Using genetically modified Chinese hamster ovary cells, we found that oxLDL activates Gαi but not the Gαq pathway of AT1 in the presence of LOX-1. Endocytosis of the oxLDL-LOX-1 complex through the AT1-β-arrestin pathway was demonstrated by real-time imaging of the membrane dynamics of LOX-1 and visualization of endocytosis of oxLDL. Finally, this endocytotic pathway involving GPCR kinases (GRKs), β-arrestin, and clathrin is relevant in accumulating oxLDL in human vascular endothelial cells. Together, our findings indicate that oxLDL activates selective G proteins and β-arrestin-dependent internalization of AT1, whereby the oxLDL-LOX-1 complex undergoes endocytosis.