HIGHLIGHTS • An ultrathin and flexible carbon nanotubes/MXene/cellulose nanofibrils composite paper with gradient and sandwich structure was successfully fabricated via a facile alternating vacuum-assisted filtration process. • The composite paper exhibits excellent mechanical property and electromagnetic interference shielding performance.

Vibrio parahaemolyticus is a leading cause of foodborne infections in China and a threat to human health worldwide. The main objective of this study is to determine the prevalence and characteristic of V. parahaemolyticus isolates in fish, oyster and shrimp samples from the South China domestic consumer market. To accomplish this, we examined 504 seafood samples from 11 provinces of China. The prevalence rates were 9.38, 30.36, and 25.60%, respectively. In summer (33.33%), the prevalence of V. parahaemolyticus was more common than that detected in the winter (14.01%). In addition, we identified 98 V. parahaemolyticus strains. The antimicrobial resistance trends of our seafood isolates to 15 antimicrobial agents revealed that major isolates were resistant to ampicillin (79.59%). Furthermore, 68.38% of the isolates were identified as being multidrug resistance. The prevalence of tdh or trh genes among the isolates was 8.16 and 12.24%, respectively. ERIC-PCR and multilocus sequence typing (MLST) results enabled classification of the isolates (n = 98) into different clusters, revealing genetic variation and relatedness among the isolates. Thus, our findings demonstrate the prevalence of V. parahaemolyticus in a variety of common seafood consumed domestically in China and provides insights into the dissemination of antibiotic-resistant strains, which should improve our microbiological risk assessment knowledge associated with V. parahaemolyticus in seafoods.

Faithful inheritance of DNA methylation across cell division requires DNMT1 and its accessory factor UHRF1. However, how this axis is regulated to ensure DNA methylation homeostasis remains poorly understood. Here we show that SET8, a cell-cycle-regulated protein methyltransferase, controls protein stability of both UHRF1 and DNMT1 through methylation-mediated, ubiquitin-dependent degradation and consequently prevents excessive DNA methylation. SET8 methylates UHRF1 at lysine 385 and this modification leads to ubiquitination and degradation of UHRF1. In contrast, LSD1 stabilizes both UHRF1 and DNMT1 by demethylation. Importantly, SET8 and LSD1 oppositely regulate global DNA methylation and do so most likely through regulating the level of UHRF1 than DNMT1. Finally, we show that UHRF1 downregulation in G2/M by SET8 has a role in suppressing DNMT1-mediated methylation on post-replicated DNA. Altogether, our study reveals a novel role of SET8 in promoting DNA methylation homeostasis and identifies UHRF1 as the hub for tuning DNA methylation through dynamic protein methylation.

Insulin promotes bone formation via a well-studied canonical signaling pathway. An adapter in this pathway, insulin-receptor substrate (IRS)-1, has been implicated in the diabetic osteopathy provoked by impaired insulin signaling. To further investigate IRS-1’s role in the bone metabolism, we generated Irs-1-deficient Irs-1smla/smla mice. These null mice developed a spontaneous mutation that led to an increase in trabecular thickness (Tb.Th) in 12-mo-old, but not in 2-mo-old mice. Analyses of the bone marrow stromal cells (BMSCs) from these mice revealed their differential expression of osteogenesis-related genes and miRNAs. The expression of miR-342, predicted and then proven to target the gene encoding collagen type Iα2 (COL1A2), was reduced in BMSCs derived from Irs-1-null mice. COL1A2 expression was then shown to be age dependent in osteoblasts and BMSCs derived from Irs-1smla/smla mice. After the induction of osteogenesis in BMSCs, miR-342 expression correlated inversely with that of Col1a2. Further, Col1a2-specific small interfering RNA (siRNA) reduced alkaline phosphatase (ALP) activity and inhibited BMSC differentiation into osteocyte-like cells, both in wild-type (WT) and Irs-1smla/smla mice. Conversely, in Irs-1smla/smla osteocytes overexpressing COL1A2, ALP-positive staining was stronger than in WT osteocytes. In summary, we uncovered a temporal regulation of BMSC differentiation/bone formation, controlled via Irs-1/miR-342 mediated regulation of Col1a2 expression.—Guo, Y., Tang, C.-Y., Man, X.-F., Tang, H.-N., Tang, J., Wang, F., Zhou, C.-L., Tan, S.-W., Feng, Y.-Z., Zhou, H.-D. Insulin receptor substrate-1 time-dependently regulates bone formation by controlling collagen Iα2 expression via miR-342.

BackgroundFasting is the most widely prescribed and self-imposed strategy for treating excessive weight gain and obesity, and has been shown to exert a number of beneficial effects. The aim of the present study was to determine the exact role of fasting and subsequent refeeding on fat distribution in mice.MethodsC57/BL6 mice fasted for 24 to 72 h and were then subjected to refeeding for 72 h. At 24, 48 and 72 h of fasting, and 12, 24, 48 and 72 h of refeeding, the mice were sacrificed, and serum and various adipose tissues were collected. Serum biochemical parameters, adipose tissue masses and histomorphological analysis of different depots were detected. MRNA was isolated from various adipose tissues, and the expressions of thermogenesis, visceral signature and lipid metabolism-related genes were examined. The phenotypes of adipose tissues between juvenile and adult mice subjected to fasting and refeeding were also compared.ResultsFasting preferentially consumed mesenteric fat mass and decreased the cell size of mesenteric depots; however, refeeding recovered the mass and morphology of inguinal adipose tissues preferentially compared with visceral depots. Thermogenesis-related gene expression in the inguinal WAT and interscapular BAT were suppressed. Mitochondrial biogenesis was affected by fasting in a depot-specific manner. Furthermore, a short period of fasting led to an increase in visceral signature genes (Wt1, Tcf21) in subcutaneous adipose tissue, while the expression of these genes decreased sharply as the fasting time increased. Additionally, lipogenesis-related markers were enhanced to a greater extent greater in subcutaneous depots compared with those in visceral adipose tissues by refeeding. Although similar phenotypic changes in adipose tissue were observed between juvenile mice and adult mice subjected to fasting and refeeding, the alterations appeared earlier and more sensitively in juvenile mice.ConclusionsFasting preferentially consumes lipids in visceral adipose tissues, whereas refeeding recovers lipids predominantly in subcutaneous adipose tissues, which indicated the significance of plasticity of adipose organs for fat distribution when subject to food deprivation or refeeding.Electronic supplementary materialThe online version of this article (doi:10.1186/s12986-016-0159-x) contains supplementary material, which is available to authorized users.

Insulin signaling is coordinated by insulin receptor substrates (IRSs). Many insulin responses, especially for blood glucose metabolism, are mediated primarily through Irs-1 and Irs-2. Irs-1 knockout mice show growth retardation and insulin signaling defects, which can be compensated by other IRSs in vivo; however, the underlying mechanism is not clear. Here, we presented an Irs-1 truncated mutated mouse (Irs-1−/−) with growth retardation and subcutaneous adipocyte atrophy. Irs-1−/− mice exhibited mild insulin resistance, as demonstrated by the insulin tolerance test. Phosphatidylinositol 3-kinase (PI3K) activity and phosphorylated Protein Kinase B (PKB/AKT) expression were elevated in liver, skeletal muscle, and subcutaneous adipocytes in Irs-1 deficiency. In addition, the expression of IRS-2 and its phosphorylated version were clearly elevated in liver and skeletal muscle. With miRNA microarray analysis, we found miR-33 was down-regulated in bone marrow stromal cells (BMSCs) of Irs-1−/− mice, while its target gene Irs-2 was up-regulated in vitro studies. In addition, miR-33 was down-regulated in the presence of Irs-1 and which was up-regulated in fasting status. What’s more, miR-33 restored its expression in re-feeding status. Meanwhile, miR-33 levels decreased and Irs-2 levels increased in liver, skeletal muscle, and subcutaneous adipocytes of Irs-1−/− mice. In primary cultured liver cells transfected with an miR-33 inhibitor, the expression of IRS-2, PI3K, and phosphorylated-AKT (p-AKT) increased while the opposite results were observed in the presence of an miR-33 mimic. Therefore, decreased miR-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin signaling pathway in Irs-1 deficient mice.

Genetically selected chickens with better growth and early maturation show an incidental increase in abdominal fat deposition (AFD). Accumulating evidence reveals a strong association between gut microbiota and adiposity. However, studies focusing on the role of gut microbiota in chicken obesity in conventional breeds are limited. Therefore, 400 random broilers with different levels of AFD were used to investigate the gut microbial taxa related to AFD by 16S rRNA gene sequencing of 76 representative samples, and to identify the specific microbial taxa contributing to fat-related metabolism using shotgun metagenomic analyses of eight high and low AFD chickens. The results demonstrated that the richness and diversity of the gut microbiota decrease as the accumulation of chicken abdominal fat increases. The decrease of Bacteroidetes and the increase of Firmicutes were correlated with the accumulation of chicken AFD. The Bacteroidetes phylum, including the genera Bacteroides, Parabacteroides, and the species, B. salanitronis, B. fragilis, and P. distasonis, were correlated to alleviate obesity by producing secondary metabolites. Several genera of Firmicutes phylum with circulating lipoprotein lipase activity were linked to the accumulation of chicken body fat. Moreover, the genera, Olsenella and Slackia, might positively contribute to fat and energy metabolism, whereas the genus, Methanobrevibacter, was possible to enhance energy capture, and associated to accumulate chicken AFD. These findings provide insights into the roles of the gut microbiota in complex traits and contribute to the development of effective therapies for the reduction of chicken fat accumulation.

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