Notes

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Objectives Sapovirus is increasingly recognized as an important cause of acute gastroenteritis (AGE) worldwide, however studies of prevalence, genetic diversity and strain-specific clinical implications have been scarce. Methods To fill this knowledge gap, we used reverse transcription real-time PCR and sequencing of the partial major capsid protein VP1 gene to analyze stool specimens and rectal swabs obtained from 3347 children with AGE and 1355 asymptomatic controls (all less then 18 years old) collected between December 2014 and August 2018 in Alberta, Canada. γGCS inhibitor Results Sapovirus was identified in 9.5% (317/3347) of the children with AGE and 2.9% of controls. GI.1 (36%) was the predominant genotype identified, followed by GI.2 (18%), GII.5 (8%) and GII.3 (6%). Rare genotypes GII.1, GII.2, GV.1, GII.4, GIV.1, GI.3 and GI.7 were also seen. Sapovirus was detected year-round, peaking during the winter months of November to January. The exception was the 2016-2017 season when GI.2 overtook GI.1 as the predominant strain with a high detection rate persisting into April. We did not observe significant difference in the severity of gastroenteritis by genogroup or genotype. Repeated infection by sapovirus of different genogroups occurred in three controls who developed AGE later. Conclusions Our data suggests that sapovirus is a common cause of AGE in children with high genetic diversity.Determinants of protective immunity against SARS-CoV-2 infection require the development of well-standardized, reproducible antibody assays. This need has led to the emergence of a variety of neutralization assays. Head-to-head evaluation of different SARS-CoV-2 neutralization platforms could facilitate comparisons across studies and laboratories. Five neutralization assays were compared using forty plasma samples from convalescent individuals with mild-to-moderate COVID-19 four cell-based systems using either live recombinant SARS-CoV-2 or pseudotyped viral particles created with lentivirus (LV) or vesicular stomatitis virus (VSV) packaging and one surrogate ELISA-based test that measures inhibition of the spike protein receptor binding domain (RBD) binding its receptor, human angiotensin converting enzyme 2 (hACE2). Vero, Vero E6, HEK293T expressing hACE2, and TZM-bl cells expressing hACE2 and transmembrane serine protease 2 were tested. All cell-based assays showed 50% neutralizing dilution (ND50) geometric mean titers (GMTs) that were highly correlated (Pearson r = 0.81-0.89) and ranged within 3.4-fold. The live-virus assay and LV-pseudovirus assays with HEK293T/hACE2 cells showed very similar mean titers 141 and 178, respectively. ND50 titers positively correlated with plasma IgG targeting SARS-CoV-2 spike and RBD (r = 0.63-0.89), but moderately correlated with nucleoprotein IgG (r = 0.46-0.73). ND80 GMTs mirrored ND50 data and showed similar correlation between assays and with IgG concentrations. The VSV-pseudovirus assay and LV-pseudovirus assay with HEK293T/hACE2 cells in low and high-throughput versions were calibrated against the WHO SARS-CoV-2 IgG standard. High concordance between the outcomes of cell-based assays with live and pseudotyped virions enables valid cross-study comparison using these platforms. 249.The use of human tissue stem cell-derived organoids has advanced our knowledge of human physiologic and pathophysiological processes that are unable to be studied using other model systems. Increases in the understanding of human epithelial tissues including intestine, stomach, liver, pancreas, lung, and brain have been achieved using organoids. However, it is not yet clear whether these cultures recapitulate in vivo organ-to-organ signaling or communication. In this work, we demonstrate that mature stem cell-derived intestinal and liver organoid cultures each express functional molecules that modulate bile acid uptake and recycling. These organoid cultures can be physically coupled in a Transwell® system and display increased secretion of FGF19 (intestine) and downregulation of CYP7A (liver) in response to apical exposure of the intestine to bile acids. This work establishes that organoid cultures can be used to study and therapeutically modulate interorgan interactions and advance the development of personalized approaches to medical care.Extracellular vesicles (EVs) contain biological molecules and are secreted by cells into the extracellular milieu. The endothelial sodium channel (EnNaC) plays an important role in modulating endothelial cell stiffness. We hypothesized EVs secreted from human aortic endothelial cells (hAoEC) positively regulate EnNaC in an autocrine dependent manner. A comprehensive lipidomic analysis using targeted mass spectrometry was performed on multiple preparations of EVs isolated from the conditioned media of hAoEC or complete growth media of these cells. Cultured hAoEC challenged with EVs isolated from the conditioned media of these cells resulted in an increase in EnNaC activity when compared to the same concentration of media derived EVs or vehicle alone. EVs isolated from the conditioned media of hAoEC but not human fibroblast cells were enriched in MARCKS Like Protein 1 (MLP1). The pharmacological inhibition of the negative regulator of MLP1, protein kinase C, in cultured hAoEC resulted in an increase in EV size and release compared to vehicle or pharmacological inhibition of protein kinase D. The MLP1 enriched EVs increased the density of actin filaments in cultured hAoEC compared to EVs isolated from human fibroblast cells lacking MLP1. We quantified 141 lipids from glycerolipids, glycerophospholipids, and sphingolipids in conditioned media EVs that represented twice the number found in control media EVs. The concentrations of sphingomyelin, lysophosphatidylcholine and phosphatidylethanolamine were higher in conditioned media EVs. These results provide the first evidence for EnNaC regulation in hAoEC by EVs and provide insight into a possible mechanism involving MLP1, unsaturated lipids, and bioactive lipids.The peroxisome proliferator activated receptors (PPARs) are a group of transcription factors belonging to the nuclear receptor superfamily. Since most target genes of either PPARs are implicated in lipid and glucose metabolism, regulation by PPARs could be used as a screening tool to identify novel genes involved in lipid or glucose metabolism. Here, we identify Adtrp, a serine hydrolase enzyme that was reported to catalyze the hydrolysis of fatty acid esters of hydroxy fatty acids (FAHFAs), as a novel PPAR-regulated gene. Adtrp was significantly upregulated by PPARα activation in mouse primary hepatocytes, liver slices, and whole liver. In addition, Adtrp was upregulated by PPARγ activation in 3L3-L1 adipocytes and in white adipose tissue. ChIP-SEQ identified a strong PPAR binding site in the immediate upstream promoter of the Adtrp gene. Adenoviral-mediated hepatic overexpression of Adtrp in diet-induced obese mice caused a modest increase in plasma non-esterified fatty acids but did not influence diet-induced obesity, liver triglyceride levels, liver lipidomic profiles, liver transcriptomic profiles, and plasma cholesterol, triglycerides, glycerol, and glucose levels.
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