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Per- and polyfluoroalkyl substances (PFAS) make up a diverse group of industrially derived organic chemicals that are of significant concern due to their detrimental effects on human health and ecosystems. Although other technologies are available for removing PFAS, adsorption remains a viable and effective method. Accordingly, the current study reported a novel type of graphene oxide (GO)-based adsorbent and tested their removal performance toward removing PFAS from water. Among the eight adsorbents tested, GO modified by a cationic surfactant, cetyltrimethylammonium chloride (CTAC), GO-CTAC was found to be the best, showing an almost 100% removal for all 11 PFAS tested. The adsorption kinetics were best described by the pseudo-second-order model, indicating rapid adsorption. The isotherm data were well supported by the Toth model, suggesting that PFAS adsorption onto GO-CTAC involved complex interactions. Detailed characterization using scanning electron microscopy-energy dispersive X-ray spectroscopy, Fourier transform infrared, thermogravimetric analysis, X-ray diffraction, and X-ray photoelectron spectroscopy confirmed the proposed adsorption mechanisms, including electrostatic and hydrophobic interactions. Interestingly, the performance of GO-CTAC was not influenced by the solution pH, ionic strength, or natural organic matter. Furthermore, the removal efficiency of PFAS at almost 100% in river water demonstrated that GO-CTAC could be a suitable adsorbent for capturing PFAS in real surface water.

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The gut-liver axis (GLA) plays an important role in the development of alcohol-induced liver injury. Alcohol consumption is typically associated with folic acid deficiency. However, no clear evidence has confirmed the effect of folic acid supplementation on alcohol-induced liver injury via GLA homeostasis. In this study, male C57BL/6J mice were given 56% (v/v) ethanol and 5.0 mg/kg folic acid daily by gavage for 10 weeks to investigate potential protective mechanisms of folic acid in alcohol-induced liver injury via GLA homeostasis. Histopathological and biochemical analyses showed that folic acid improved lipid deposition and inflammation in the liver caused by alcohol consumption and decreased the level of ALT, AST, TG, and LPS in serum. Folic acid inhibited the expression of the TLR4 signaling pathway and its downstream inflammatory mediators in the liver and upregulated the expression of ZO-1, claudin 1, and occludin in the intestine. But compared with the CON group, folic acid did not completely eliminate alcohol-induced intestine and liver injury. Furthermore, folic acid regulated alcohol-induced alterations in gut microbiota. In alcohol-exposed mice, the relative abundance of Bacteroidota was significantly increased, and the relative abundance of unclassified_Lachnospiraceae was significantly decreased. Folic acid supplementation significantly increased the relative abundance of Verrucomicrobia, Lachnospiraceae_NK4A136_group and Akkermansia, and decreased the relative abundance of Proteobacteria. The results of Spearman's correlation analysis showed that serum parameters and hepatic inflammatory cytokines were significantly correlated with several bacteria, mainly including Bacteroidota, Firmicutes, and unclassified_Lachnospiraceae. In conclusion, folic acid could ameliorate alcohol-induced liver injury in mice via GLA homeostasis to some extent, providing a new idea and method for prevention of alcohol-induced liver injury.

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Fructose has been reported to acutely elevate the circulating fibroblast growth factor 21 (FGF21) levels, which ultimately causes FGF21 resistance. FGF21 resistance is suggested to result in lipid metabolism disorder. Nicotinamide riboside (NR) can alleviate lipid metabolism disorder in mice. It is unknown whether NR supplementation would alleviate lipid metabolism disorder in high-fructose exposed mice via improving FGF21 resistance. In this study, C57BL/6J mice were given 20% fructose solution for free drinking with the supplementation of NR in 400 mg kg-1 day-1. The results showed that NR supplementation decreased the serum and hepatic lipid profile levels. The increase of lipid droplets in the liver and the size of adipose cells in WAT induced by a high-fructose diet were alleviated by the addition of NR. NR supplementation increased the NAD+/NADH ratio and activated the SIRT1/NF-κB pathway. The down-regulation of NF-κB is accompanied by a decrease in inflammation, which may increase the expression of the FGF21 receptor complex, namely KLB and FGFR, then restore its downstream signaling cascade, including ERK phosphorylation and EGR1 and c-FOS expression, and ultimately improve FGF21 resistance. With the FGF21 function recovery, hepatic PGC-1α expression was up-regulated, and hepatic SREBP-1c expression was down-regulated, resulting in decreased lipogenesis. Furthermore, restoration of the FGF21 signaling pathway also led to increased expression of ATGL and HSL in WAT, which promotes lipolysis. In conclusion, we found that NR supplementation could ameliorate high-fructose-induced lipid metabolism disorder by improving FGF21 resistance in the liver and WAT, which may be related to the regulation of inflammation mediated by the SIRT1/NF-κB signaling pathway.

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Garlic oil (GO) is a kind of natural extract extracted from garlic, which has strong antioxidant activity. This study elucidates the protective mechanism of GO against alcohol-induced high triglyceride levels. Sixty male Sprague Dawley rats were assigned to five groups, including a control group (CON), a model group (MOD) treated with alcohol 56% v/v at 8 ml kg-1 day-1 for 2 weeks then 10 ml kg-1 day-1 for 8 weeks, a low-dose GO group (GO-L) given GO at 20 mg kg-1 day-1, a high-dose GO group (GO-H) given GO at 40 mg kg-1 day-1, and a positive group (POS) given diammonium glycyrrhizinate at 200 mg kg-1 day-1. The results showed that GO could significantly reduce the serum and liver triglyceride levels caused by alcohol exposure (p < .05). The GO-H group significantly reduced MDA level, increased SOD and GSH-Px levels in serum, liver, and colon (p < .05), significantly increased the levels of Sirt1 and PGC-1α proteins and reduced FoxO1 protein level in liver (p < .05), and significantly increased the levels of ZO-1 and Claudin1 proteins in the colon compared to the MOD group (p < .05). The 16S rRNA sequencing showed that the intestinal flora of the GO-H group was significantly changed compared with the MOD group. In summary, GO has the potential to improve high triglyceride levels in serum and liver induced by alcohol exposure, which may be related to the inhibition of oxidative stress regulation of Sirt1 and its downstream proteins, and to the restoration of the intestinal barrier and intestinal flora.

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Folic acid, as a key source of methyl donor in DNA methylation, has been proved to play a beneficial role in inflammation modulation, which is usually impaired in alcoholic liver disease (ALD). However, the role of folic acid in alcoholic liver inflammation and injury remain elusive. In this study, we sought to uncover the potential protective mechanism by which folic acid ameliorates alcoholic liver injury. 100 male C57BL/6J mice were randomly divided into 5 groups: normal saline group, folic acid control group (5 mg per kg BW), ethanol model group (56% v/v, 10 mL per kg BW), folic acid + ethanol group, and 5-Aza + ethanol group (0.1 mL per 20 g BW). Liquor (10 mL per kg BW) was orally administered 1 h after the folic acid treatment for 10 consecutive weeks. The results showed that folic acid-inhibited ethanol-induced serum TG, TC, and LDL elevation attenuated hepatic fat accumulation and maintained ALT at a normal level. 10 weeks of ethanol administration simultaneously upregulated the hepatic proportion of Th17 and Treg cells to different extents and broke the homeostasis of liver immunization. Folic acid limited ethanol-induced inflammatory injury by increasing the frequency of hepatic Treg cells. Importantly, this effect may be caused by decreased DNMT3a, which in turn downregulates the methylated levels of CPG2 and CPG3 in the Foxp3 promoter region, changing the abundance of Foxp3 expression and improving the Th17/Treg imbalance. In summary, our findings demonstrated that folic acid supplementation may relieve ethanol-induced Th17/Treg disbalance through altering Foxp3 promoter methylation patterns, suggesting that folic acid may be a feasible preventive strategy for ALD.

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The classification of six types of white blood cells (WBCs) is considered essential for leukemia diagnosis, while the classification is labor-intensive and strict with the clinical experience. To relieve the complicated process with an efficient and automatic method, we propose the Attention-aware Residual Network based Manifold Learning model (ARML) to classify WBCs. The proposed ARML model leverages the adaptive attention-aware residual learning to exploit the category-relevant image-level features and strengthen the first-order feature representation ability. To learn more discriminatory information than the first-order ones, the second-order features are characterized. Afterwards, ARML encodes both the first- and second-order features with Gaussian embedding into the Riemannian manifold to learn the underlying non-linear structure of the features for classification. ARML can be trained in an end-to-end fashion, and the learnable parameters are iteratively optimized. 10800 WBCs images (1800 images for each type) is collected, 9000 images and five-fold cross-validation are used for training and validation of the model, while additional 1800 images for testing. The results show that ARML achieving average classification accuracy of 0.953 outperforms other state-of-the-art methods with fewer trainable parameters. In the ablation study, ARML achieves improved accuracy against its three variants: without manifold learning (AR), without attention-aware learning (RML), and AR without attention-aware learning. The t-SNE results illustrate that ARML has learned more distinguishable features than the comparison methods, which benefits the WBCs classification. ARML provides a clinically feasible WBCs classification solution for leukemia diagnose with an efficient manner.

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The deposition of CaCO3 scale in circulating cooling water on metal surface is a major concern in industry. This paper focuses on the feasibility of electrochemical methods to study the scale inhibition performance of 1-hydroxyethylidene-1,1-diphosphonic acid (HEDP) and 2-phosphonobutane-1,2,4-tricarboxylic acid (PBTCA), Polyacrylic Acid (PAA), including linear sweep voltammetry, chronoamperometry, and electrochemical impedance spectroscopy (EIS). In addition, the coverage, morphology and structure of deposited CaCO3 crystal on titanium alloy surface in the absence and presence of inhibitors were investigated by X-ray diffraction (XRD) and scanning electron microscopy (SEM). A new method for calculating the efficiency of scale inhibitors was proposed so that it can be calculated by using the change in residual current density (ir). In order to prove the feasibility and accuracy of such method, the efficiencies of inhibitors were evaluated using ir and charge transfer resistance (Rct), respectively. In addition, molecular dynamics (MD) simulations were performed to evaluate the interaction between the scale inhibitor molecule and the CaCO3 crystal. The experimental results show that both the residual current density obtained by chronoamperometry and the charge transfer resistance obtained by electrochemical impedance spectroscopy can be used to evaluate the efficiency of scale inhibitors, and there is high consistency from the calculation results. It is also confirmed by X-ray diffraction and scanning electron microscopy studies that the presence of inhibitor reduces the surface coverage of CaCO3 at metal electrode and that the crystal structure of CaCO3 is transformed from the original aragonite into the most unstable vaterite. The best inhibition efficiency of PBTCA for CaCO3 deposit is confirmed by the results of MD simulations.