S and full research articles published in SLEEP, the official journal of the APSS. Sleep and sleep disorder scientific findings.

3-Monochloropropane-1,2-diol (3-MCPD), 2,3-epoxy-1-propanol (glycidol), and their esters are well-known food contaminants mainly formed by the heat processing of certain refined oils and coexist in various kinds of foodstuffs. However, the combined health effect and the underlying mechanism of 3-MCPD and glycidol coexposure are not well-understood. In this study, we investigated the systemic toxicity effects and the nephrotoxicity mechanisms of 3-MCPD and glycidol coexposure with in vitro and in vivo models, and next-generation sequencing (NGS) analysis. It was found that 3-MCPD and glycidol coexposure for 28 days synergistically induced toxicity in the kidney, lung, testis, and heart in C57BL/6 mice. Kidney was the most sensitive organ to coexposure, and the coexposure had a synergistic effect on inflammation and cytotoxicity through activation of the NLRP3 inflammasome, and the induction of necroptosis, and autophagic cell death in NRK-52E cells. Moreover, the NGS results revealed the genes changes associated with nephrotoxicity, inflammation and with the broad toxicity effects induced by 3-MCPD or glycidol alone or in combination, which were consistent with the results of in vitro and in vivo models. In summary, we report for the first time of the comprehensive toxicity effects and the mechanisms caused by 3-MCPD and glycidol coexposure.

The aim was to identify the risk factors for renal scarring and deteriorating renal function in children with primary vesico-ureteral reflux (VUR). Patients with primary VUR admitted to the National Cheng Kung University Hospital were retrospectively analyzed. The outcomes were renal scarring, assessed by technetium-99 m dimercaptosuccinic acid scanning, and renal function, assessed by estimated glomerular filtration rate. Univariate and multivariate models were applied to identify the corresponding independent predictors. A total of 173 patients with primary VUR were recruited. The median age of VUR diagnosis was 10.0 months (IQR: 4.0–43.0 months). After adjusting for confounding factors, it was found that older age of VUR diagnosis (≥5 years vs. <1 year, adjusted OR = 2.78, 95% CI = 1.00–7.70, p = 0.049), higher grade of VUR (high grade [IV–V] vs. none, adjusted OR = 15.17, 95% CI = 5.33–43.19, p<0.0001; low grade [I–III] vs. none, adjusted OR = 5.72, 95% CI = 2.43–13.45, p<0.0001), and higher number of UTI (≥2 vs. 0, adjusted OR = 3.21, 95% CI = 1.06–9.76, p = 0.039) were risk factors for renal scarring, whereas a younger age of VUR diagnosis (≥5 years vs. <1 year, adjusted HR = 0.16, 95% CI: 0.05–0.51, p = 0.002), renal scarring (yes vs. no, adjusted HR = 3.66, 95% CI: 1.32–10.16, p = 0.013), and APN (yes vs. no, adjusted HR = 3.10, 95% CI: 1.05–9.14, p = 0.041) were risk factors for developing chronic kidney disease stage 2 or higher. Our findings expand on the current knowledge of risk factors for renal scarring and deteriorating renal function, and this information can be used to modify the management and treatment of VUR.