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This article describes the composition of Wnt signaling pathway and the process of neurogenesis after cerebral ischemia, and emphatically introduces the recent studies on the mechanisms of this pathway for post-stroke neurogenesis and the therapeutic possibility of activating the pathway to improve neurogenesis after stroke.Since the effect of electro-dewatering (EDW) on sludge water holding capacity was unknown, tests were conducted in this study to investigate the water holding capacity of EDW sludge and the potential mechanism related to the sludge physicochemical characteristics, EPS properties and sludge structure. Sludge was dewatered to the average moisture content (AMC) of 80%, 70% and 60% with different applied voltages at 20, 30 and 40V in EDW, respectively. Then the dewatered sludge near the anode and cathode were rewatered. The variation of sludge water holding capacity in EDW process was evaluated in terms of filterability and saturated moisture content (SMC), and the filterability was assessed by the specific resistance to filtration (SRF) of rewatered sludge. The results indicated that SRF of rewatered sludge near the cathode increased greatly. The proteins/polysaccharides (PN/PS) of loosely bound extracellular polymeric substances (LB-EPS) was significantly positively correlated with SRF (r = 0.891, p less then 0.01). Moreover, the exposure of hydrophobic sites or groups in PN near the cathode improved the surface hydrophobicity of sludge, which reduced the filterability. In addition, higher voltage could destroy the sludge structure near the anode at the later stage of EDW process, leading to the decrease of SRF and SMC. These results expanded the knowledge about changes in sludge properties and water holding capacity during EDW process.MoS2 nanosheet-decorated TiO2 nanocomposites were prepared via facile liquid-phase exfoliation of natural molybdenite combined with in situ hydrolysis route. These materials were used as a photocathode for the first time in microbial fuel cell (MFC) to reduce hexavalent chromium (Cr (VI)). Results showed the maximum power density of 1 wt% MoS2/TiO2-based MFC was 3.7 and 1.9 times higher than that of blank graphite and TiO2-based MFC, respectively. This MFC achieved 99.57% removal of Cr (VI) with a concentration of 20 mg L-1 within 8 h under visible light illumination at pH 2 and high degradation rate of 2.49 g m-3 h-1. The introduction of MoS2 nanosheets as a cocatalyst can expand the absorption of visible light, thereby leading to increased electronic participation in Cr (VI) reduction. Moreover, the appropriate amounts of MoS2 nanosheets also contribute to electrons migration and additional active site. The enhanced power output and Cr (VI) reduction efficiency of MFC can be attributed to the synergistic coupling between bioanode and MoS2/TiO2 photocathode. On the basis of its facile and scalable synthetic strategy as well as its stable and outstanding photoelectrocatalytic performance for MFC, this MoS2/TiO2 nanocomposite showed potential in the efficient treatment of wastewater.Previous studies have evaluated the relationship between prenatal air pollution exposure and low birth weight, but the results are inconsistent. The purpose of this meta-analysis is to quantitatively analyze the relationship between maternal air pollutant exposure and low birth weight (LBW). PubMed and Web of Science databases were searched to obtain the studies on the relationship between the prenatal exposure of air pollutants and LBW that published as of June 2020. The pooled effects of air pollutant exposure and LBW were calculated using random-effect model (for studies with significant heterogeneity) or fixed-effect model (for studies without significant heterogeneity). Totally, 54 studies were included in this meta-analysis. The pooled effect of PM2.5, PM10, NO2, CO, SO2, and O3 exposure on LBW were 1.081 (95% CI 1.043, 1.120), 1.053 (95% CI 1.030, 1.076), 1.030 (95% CI 1.008, 1.053), 1.007 (95% CI 1.001, 1.014), 1.125 (95% CI 1.017, 1.244), and 1.045 (95% CI 1.005, 1.086), respectively. NO2 (per 10 ppb increase) and CO (per 100 ppb increase) exposure in the first trimester were positively correlated with LBW, of which the pooled effect was 1.022 (95% CI 1.009, 1. 035) and 1.008 (95% CI 1.004, 1.012), respectively. PM2.5 (per 10 μg/m3 increase) exposure in the third trimester significantly affected the LBW, of which the pooled effect was 1.053 (95% CI 1.010, 1.097). In addition, PM10 (per 10 μg/m3 increase) exposure in the second trimester also significantly affected the LBW, with the pooled effect of 1.011 (95% CI 1.005, 1.017). Prenatal exposure of the major air pollutants during the entire pregnancy could increase the risk of LBW, while the susceptible window of the pollutants varied.In utero exposure to bisphenol A (BPA) in early stages of development has been reported to exert adverse health effects on offspring later in life. Epigenetic alterations, particularly DNA methylation, may be one plausible biological mechanism involved. We examined the association between maternal BPA exposure and DNA methylation in cord blood. We randomly selected 96 paired samples of maternal urine and infant cord blood collected from the Shanghai-Minhang Birth Cohort. BPA levels in maternal urine were measured using high-performance liquid chromatography (HPLC). Three cord blood samples with maternal BPA levels >2.0 μg/g Cr and three samples with undetected BPA were randomly selected for genome-wide methylation analysis using methylated DNA binding domain sequencing (MBD-Seq). The genes with hypermethylated promoter regions were chosen for validation using quantitative methylation-specific polymerase chain reaction (Q-MSP). Based on MBD-seq results, we observed that maternal BPA exposure was primarily associated with hypermethylation of genes involved in signal transduction in the nervous system. Raphin1 in vivo Using Q-MSP, we further validated the association between maternal BPA exposure and promoter hypermethylation of three genes in multiple linear regression models a log unit increase in BPA was associated with 12.63% (95%CI 7.99, 17.26), 11.17%, (95%CI 3.31, 19.02), and 16.57% (95% CI 10.59, 22.56) increase in promoter of CAPS2, TNFRSF25, and HKR1 methylation, respectively. Our findings provide evidence that in utero exposure to BPA could alter the offspring's epigenome by altering DNA methylation pattern.

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