A Cu/Polypyrrole-Coated Stainless Steel Mesh Membrane Cathode for Highly Efficient Electrocoagulation-Coupling Anti-Fouling Membrane Filtration

Membrane filtration fouling has become a significant issue that restricts its wide application. The electrocoagulation (EC) technique combines a variety of synergistic pollutant removal technologies (including flocculation, redox, and air flotation), which can be an ideal pretreatment process for membrane filtration. In this work, a novel Cu2+-doped and polypyrrole-coated stainless steel mesh membrane (Cu/PPy–SSM) was prepared by direct current electrodeposition, and it was introduced in an electrocoagulation-membrane reactor (ECMR) to construct an EC–membrane filtration coupling system. The Cu/PPy–SSM was applied as the cathode, while an aluminum plate was used as the anode in the ECMR. The ECMR enabled an excellent humic acid (HA) removal performance and could effectively mitigate the fouling of the Cu/PPy–SSM. Its performance can be attributed to the following: (1) the Cu/PPy–SSM can repel the negatively charged pollutants under the applied electric field; (2) the cathodic hydrogen gas produced on the Cu/PPy–SSM restrains the compacting of the cake layer and delays degradation of membrane flux; and (3) the resultant porous loose structure can perform as a dynamic membrane, which can effectively promote the separation performance of the Cu/PPy–SSM. The resultant ECMR enabled an improved HA removal rate of 92.77%, and the membrane-specific flux could be stabilized at more than 86%. Response surface methodology (RSM) was used to optimize the operation parameters of the ECMR, and the predicted HA removal rate reached 93.01%. Both the experimental results and modelled predictions show that using the Cu/PPy–SSM as a cathode can lead to excellent performance of the ECMR

A New Oleanolic Acid Derivative against CCl4-Induced Hepatic Fibrosis in Rats

A novel hepatoprotective oleanolic acid derivative, 3-oxours-oleana-9(11), 12-dien-28-oic acid (Oxy-Di-OA), has been reported. In previous studies, we found that Oxy-Di-OA presented the anti-HBV (Hepatitis B Virus) activity (IC50 = 3.13 µg/mL). Remarkably, it is superior to lamivudine in the inhibition of the rebound of the viral replication rate. Furthermore, Oxy-Di-OA showed good performance of anti-HBV activity in vivo. Some studies showed that liver fibrosis may affiliate with HBV gene mutations. In addition, the anti-hepatic fibrosis activity of Oxy-Di-OA has not been studied. Therefore, we evaluated the protective effect of Oxy-Di-OA against carbon tetrachloride (CCl4)-induced liver injury in rats. Daily intraperitoneally administration of Oxy-Di-OA prevented the development of CCl4-induced liver fibrosis, which was evidenced by histological study and immunohistochemical analysis. The entire experimental protocol lasted nine weeks. Oxy-Di-OA significantly suppressed the increases of plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels (p < 0.05). Furthermore, Oxy-Di-OA could prevent expression of transforming growth factor β1 (TGF-β1). It is worth noting that the high-dose group Oxy-Di-OA is superior to bifendate in elevating hepatic function. Compared to the model group, Oxy-Di-OA in the high-dose group and low-dose group can significantly reduce the liver and spleen indices (p < 0.05). The acute toxicity test showed that LD50 and a 95% confidence interval (CIs) value of Oxy-Di-OA were 714.83 mg/kg and 639.73–798.73 mg/kg via intraperitoneal injection in mice, respectively. The LD50 value of Oxy-Di-OA exceeded 2000 mg/kg via gavage in mice. In addition, a simple and rapid high performance liquid chromatography-ultraviolet (HPLC-UV) method was developed and validated to study the pharmacokinetic characteristics of the compound. After single-dose oral administration, time to reach peak concentration of Oxy-Di-OA (Cmax = 8.18 ± 0.66 μg/mL) was 10 ± 2.19 h; the elimination half-life and area under the concentration-time curve from t = 0 to the last time of Oxy-Di-OA was 2.19 h and 90.21 μg·h/mL, respectively

CAID prediction portal: a comprehensive service for predicting intrinsic disorder and binding regions in proteins

International audienceIntrinsic disorder (ID) in proteins is well-established in structural biology, with increasing evidence for its involvement in essential biological processes. As measuring d ynamic ID beha vior e xperimentall y on a large scale remains difficult, scores of published ID predictor s ha ve tried to fill this gap. Unfortunatel y, their heterogeneity makes it difficult to compare perf ormance, conf ounding biologists wanting to make an informed choice. To address this issue, the Critical Assessment of protein Intrinsic Disorder (CAID) benchmarks predictors for ID and binding regions as a community blind-test in a standardized computing environment. Here we present the CAID Prediction Portal, a web server executing all CAID methods on user-defined sequences. The server generates standardized output and facilitates comparison between methods, producing a consensus prediction highlighting high-confidence ID regions. The website contains extensive documentation explaining the meaning of different CAID statistics and providing a brief description of all methods. Predictor output is visualized in an interactive feature viewer and made available for download in a single table, with the option to recover previous sessions via a priv ate dashboar d. The CAID Prediction Portal is a valuable resource for researchers interested in studying ID in proteins. The server is available at the URL: https://caid.idpcentral.org