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Background: Previous studies investigated the relation of prenatal exposure to bisphenol A (BPA) and birth outcomes, but these results were inconsistent. The aim of this study was to investigate the relation of prenatal exposure to BPA and birth outcomes, provide comprehensive results based on current studies. Methods: The PubMed, Cochrane databases, and Web of Science databases were searched systematically by two researchers respectively from their inceptions to Oct. 2018, using the following keywords “bisphenol A, birth weight, birth length, head circumference, gestational age, birth outcomes”. We extracted β coefficient and 95% confidence interval (CI) or β coefficient and standard deviation (SD) from included study. The subgroup analysis was performed to evaluate the potential heterogeneity between studies. We conducted sensitivity analysis by excluding the each individual study to assess the results whether were stable. Finally, the publication bias was performed by accumulative forest plot. Results: Seven studies with 3004 participants met the inclusion criteria. BPA had significant positively association with birth weight (β = 21.92, 95%CI: 1.50–42.35, P = .04). No significant associations were found between BPA and birth length, head circumference and gestational age (All of P > .05). Conclusion: This meta-analysis demonstrated that the BPA was positively associated with birth weight. Therefore, further studies are needed to investigate the critical sensitive period of influencing fetal development and to investigate the difference on gender.

Alcoholic liver disease (ALD) is the most common complication of alcohol abuse, while we lack safe and effective treatment for ALD. This study aimed to explore the effects of nicotinamide riboside (NR) on lipid metabolism and gut microflora‐bile acid axis in alcohol‐exposed mice. NR significantly improved liver histopathological damage and abnormal liver function. NR as a provider of nicotinamide adenine dinucleotide (NAD+) increased the NAD+/NADH ratio. Meanwhile, NR inhibited the activation of the protein phosphatase 1 signaling pathway, decreased the liver triglyceride and total bile acid levels, and reduced lipid accumulation. According to the results of gut microflora species analysis, NR intervention changed the microbial community structure at the phylum, family and genus levels, and the species abundances returned to a level similar to these of the normal control group. Besides, the results of high‐performance liquid chromatograph‐mass spectrometry showed that NR intervention resulted in fecal bile acid levels tending to be normal with decreased chenodeoxycholic acid level and increased deoxycholic acid and hyocholic acid levels. Spearman's correlation analysis showed a correlation between gut microflora and bile acids. Therefore, NR supplementation has the potential to prevent ALD, and its mechanism may be related to regulating lipid metabolism disorders and the gut microflora‐bile acid axis.

BackgroundPhenylacetylglutamine (PAGln)—a newly discovered microbial metabolite produced by phenylalanine metabolism—is reportedly associated with cardiovascular events via adrenergic receptors. Nonetheless, its association with cardiovascular outcomes in heart failure (HF) patients remains unknown.ObjectivesThis study aimed to prospectively investigate the prognostic value of PAGln for HF.MethodsPlasma PAGln levels were quantified by liquid chromatography‐tandem mass spectrometry. We first assessed the association between plasma PAGln levels and the incidence of adverse cardiovascular events in 3152 HF patients (including HF with preserved and reduced ejection fraction) over a median follow‐up period of 2 years. The primary endpoint was the composite of cardiovascular death or heart transplantation. We then assessed the prognostic role of PAGln in addition to the classic biomarker N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP). The correlation between PAGln levels and β‐blocker use was also investigated.ResultsIn total, 520 cardiovascular deaths or heart transplantations occurred in the HF cohort. Elevated PAGln levels were independently associated with a higher risk of the primary endpoint in a dose‐response manner, regardless of HF subtype. Concurrent assessment of PAGln and NT‐proBNP levels enhanced risk stratification among HF patients. PAGln further showed prognostic value at low NT‐proBNP levels. Additionally, the interaction effects between PAGln and β‐blocker use were not significant.ConclusionsPlasma PAGln levels are an independent predictor of an increased risk of adverse cardiovascular events in HF. Our work could provide joint and complementary prognostic value to NT‐proBNP levels in HF patients.

Background: Alcoholic liver disease is caused as a result of chronic alcohol consumption. In this study, we used an alcoholic liver injury mouse model to investigate the effect of fucoidan on ethanol-induced liver injury and steatosis and the underlying mechanisms. Methods: All mice were randomly divided into four groups: 1) control group, 2) model group, 3) diammonium glycyrrhizinate treatment group (200 mg/kg body weight), and 4) fucoidan treatment group (300 mg/kg body weight). Administration of ethanol for 8 weeks induced liver injury and steatosis in mice. Results: Fucoidan treatment decreased serum alanine aminotransferase activity, serum total cholesterol levels, and hepatic triglyceride levels, and improved the morphology of hepatic cells. Fucoidan treatment upregulated the expression of AMPKα1, SIRT1, and PGC-1α and inhibited the expression of ChREBP and HNF-1α. The levels of hepatic IL-6 and IL-18 were significantly decreased in the fucoidan group. Further, the levels of cytochrome P450-2E1 (CYP2E1), glucose-regulated protein (GRP) 78, and 3-nitrotyrosine (3-NT) in hepatic tissues were reduced in the fucoidan group as compared to the model group. Fucoidan significantly reversed the reduction of ileac Farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) levels induced by alcohol- feeding and reduced CYP7A1 (cholesterol 7α-hydroxylase) expression and total bile acid levels in the liver tissue. In addition, fucoidan regulated the structure of gut flora, with increased abundance of Prevotella and decreased abundance of Paraprevotella and Romboutsia as detected by 16S rDNA high-throughput sequencing. Conclusion: Fucoidan inhibited alcohol-induced steatosis and disorders of bile acid metabolism in mice through the AMPKα1/SIRT1 pathway and the gut microbiota–bile acid–liver axis and protected against alcohol- induced liver injury in vivo.

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Medical students' perceptions of the medical school learning environment (MSLE) have an important impact on their professional development, and physical and mental health. Few studies reported potential factors that influenced medical students' perceptions of MSLE. Thus, the main goal of this study was to identify influencing factors for medical students' perception levels of MSLE. The perception levels of MSLE were assessed by the Johns Hopkins Learning Environment Scale. The univariate and multivariate logistic regression analyses were performed to identify significant predictors for the perceptions of MSLE. The nomograms were established to predict medical students' perception levels of MSLE. In the multivariate logistic regression model, gender, university category, grade, mother education level, learning environment of schools, interests in medicine, and Kolb learning experience were significantly associated with medical students' perceptions of MSLE. Correspondently, the nomograms were built based on significant variables identified by the univariate logistic regression analysis. The validation of the nomograms showed that the model had promising predictive accuracy, discrimination, and accordance (area under the curve (AUC) = 0.751). This study identified influencing factors of medical students' perceptions of MSLE. It is essential to implement corresponding interventions to improve medical students' perceptions.