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Perfluorooctane sulfonate (PFOS) was widely used in industrial applications before it was listed as a persistent organic pollutant by the Conference of the Parties in the Stockholm Convention in 2009. Although the potential toxicity of PFOS has been studied, its toxic mechanisms remain largely undefined. Here, we investigated novel hub genes and pathways affected by PFOS to gain new conceptions of the toxic mechanisms of PFOS. Reduced body weight gain and abnormal ultra-structures in the liver and kidney tissues were spotted in PFOS-exposed rats, indicating successful establishment of the PFOS-exposed rat model. The transcriptomic alterations of blood samples upon PFOS exposure were analysed using RNA-Seq. GO analysis indicates that the differentially expressed gene-enriched GO terms are related to metabolism, cellular processes, and biological regulation. Kyoto encyclopaedia of gene and genomes (KEGG) and gene set enrichment analysis (GSEA) were conducted to identify six key pathways: spliceosome, B cell receptor signalling pathway, acute myeloid leukaemia, protein processing in the endoplasmic reticulum, NF-kappa B signalling pathway, and Fc gamma R-mediated phagocytosis. The top 10 hub genes were screened from a protein–protein interaction network and verified via quantitative real-time polymerase chain reaction. The overall pathway network and hub genes may provide new insights into the toxic mechanisms of PFOS exposure states. [Display omitted] • PFOS-exposed rat model successfully established. • Transcriptomic alterations of rats upon PFOS exposure analysed using RNA-seq. • Six pathways identified as potential toxic mechanisms of PFOS. • Ten hub genes screened as key genes of PFOS toxicity. • The immune system of PFOS-exposed rats significantly affected by PFOS exposure. [ABSTRACT FROM AUTHOR]

To assess the Type 2 Diabetes Mellitus (T2DM) patients in association with Chronic Microvascular Complications at Glucose Peak Time and the association among chronic microvascular complications in T2DM patients and the glucose peak period in the typical steamed bread meal test. Overall 1095 T2DM patients were classified as three groups: (1) Group G1: glucose peak time ≤ 1 h (n = 84), Group G2: 1 h < glucose peak time ≤ 2 h (n = 648) and Group G3: glucose peak time > 2 h (n = 363). The clinical characteristics, insulin characteristics and glucose peak time and chronic microvascular complications markers of patients in each group was analyzed and compared. Statistical analyses were performed using SPSS 23.0, employing chi-square tests, Kruskal-Wallis tests, one-way ANOVA, and binary logistic regression analysis, with significance set at P < 0.05. Age, length of disease, glycated hemoglobin (HbA1c), urine albumin-creatinine ratio (UACR), and the number of patients with diabetic retinopathy (DR) increased (all P < 0.05) in those with postponed glucose peak time, while insulinogenic indexes, the AUC for C-p (AUCC-p), fasting, and 120-min C-peptide (C-p) decreased (all P < 0.05). Only age was connected to patients with diabetic kidney disease (DKD) independently in binary logistic regression analysis, although delayed glucose peak time was related to the presence of patients with DR. (all P < 0.05). Delayed glucose peak time contributed to DR. Attention should be paid to condition of chronic microvascular complications in T2DM patients with a postponed peak glucose timing. • Independent correlations were found between DR and delayed glucose peak time. • 1 % reduction in HbA 1c caused by a 37 % reduction in the risk of microvascular • IGP not associated with carotid stiffness, IMT or microvascular function [ABSTRACT FROM AUTHOR]

Abstract: We developed a scaled-up procedure for vitrifying hepatocytes for hybrid liver support system applications. Hepatocyte monolayer cultured on collagen-coated polyethylene terephthalate (PET) discs constituted the basic module for a hybrid liver support system. Freshly isolated rat hepatocytes were seeded on collagen-coated PET discs with a diameter of 33mm at a density of 5×106 cells per disc, and were cultured for 24h before cryopreservation. The total duration of procedure starting from exposure to low concentrations of cryoprotectants up to cryostorage is 10min. Vitrification of the modules was achieved by using two vitrification solutions sequentially with first vitrification solution containing two cryoprotectants, ethylene glycol (EG) and sucrose, while second vitrification solution contained additionally polymer, Ficoll. Direct exposure to liquid nitrogen vapours was followed by immersion into liquid nitrogen. Recovery procedure for vitrified modules included their warming in 1 m sucrose at temperature of 38–39°C followed by subsequently washing in sucrose-based solutions of decreased concentration within 15min at room temperature. Viability, structural characteristics, and functions of cells were preserved by vitrification. Hepatocytes in the post-vitrified and warmed monolayer maintained differentiated hepatocyte characteristics both structurally and functionally. In average, protein synthesis measured as albumin production was 181.00±33.46ng/million cells and 166.10±28.11ng/million cells, for control and vitrified modules respectively. Urea production was, in average, 1.52±0.40ng/million cells and 1.36±0.31ng/million cells for a 7 day culture respectively, with no significant statistical difference between the control and vitrified modules. [Copyright &y& Elsevier]