Vacuum-ultraviolet based advanced oxidation and reduction processes for water treatment.

The use of vacuum-ultraviolet (VUV) photolysis in water treatment has been gaining significant interest due to its efficacy in degrading refractory organic contaminants and eliminating oxyanions. In recent years, the reactive species driving pollutant decomposition in VUV-based advanced oxidation and reduction processes (VUV-AOPs and VUV-ARPs) have been identified. This review aims to provide a concise overview of VUV photolysis and its advancements in water treatment. We begin with an introduction to VUV irradiation, followed by a summary of the primary reactive species in both VUV-AOPs and VUV-ARPs. We then explore the factors influencing VUV-photolysis in water treatment, including VUV irradiation dose, catalysts or activators, dissolved gases, water matrix components (e.g., DOM and inorganic anions), and solution pH. In VUV-AOPs, the predominant reactive species are hydroxyl radicals (˙OH), hydrogen peroxide (H2O2), and ozone (O3). Conversely, in VUV-ARPs, the main reactive species are the hydrated electron (eaq-) and hydrogen atom (˙H). It is worth noting that VUV-based advanced oxidation/reduction processes (VUV-AORPs) can transit between VUV-AOPs and VUV-ARPs based on the externally added chemicals and dissolved gases in the solution. Increase of the VUV irradiation dose and the concentration of catalysts/activators enhances the degradation of contaminants, whereas DOM and inorganic anions inhibit the reaction. The pH influences the redox potential of ˙OH, the speciation of contaminants and activators, and thus the overall performance of the VUV-AOPs. Conversely, an alkaline pH is favored in VUV-ARPs because eaq- predominates at higher pH.

Predictive model for non-malignant portal vein thrombosis associated with cirrhosis based on inflammatory biomarkers.

BACKGROUND: Portal vein thrombosis (PVT), a complication of liver cirrhosis, is a major public health concern. PVT prediction is the most effective method for PVT diagnosis and treatment. AIM: To develop and validate a nomogram and network calculator based on clinical indicators to predict PVT in patients with cirrhosis. METHODS: Patients with cirrhosis hospitalized between January 2016 and December 2021 at the First Hospital of Lanzhou University were screened and 643 patients with cirrhosis who met the eligibility criteria were retrieved. Following a 1:1 propensity score matching 572 patients with cirrhosis were screened, and relevant clinical data were collected. PVT risk factors were identified using the least absolute shrinkage and selection operator (LASSO) and multivariate logistic regression analysis. Variance inflation factors and correlation matrix plots were used to analyze multicollinearity among the variables. A nomogram was constructed to predict the probability of PVT based on independent risk factors for PVT, and its predictive performance was verified using a receiver operating characteristic curve (ROC), calibration curves, and decision curve analysis (DCA). Finally, a network calculator was constructed based on the nomograms. RESULTS: This study enrolled 286 cirrhosis patients with PVT and 286 without PVT. LASSO analysis revealed 13 variables as strongly associated with PVT occurrence. Multivariate logistic regression analysis revealed nine indicators as independent PVT risk factors, including etiology, ascites, gastroesophageal varices, platelet count, D-dimer, portal vein diameter, portal vein velocity, aspartate transaminase to neutrophil ratio index, and platelet-to-lymphocyte ratio. LASSO and correlation matrix plot results revealed no significant multicollinearity or correlation among the variables. A nomogram was constructed based on the screened independent risk factors. The nomogram had excellent predictive performance, with an area under the ROC curve of 0.821 and 0.829 in the training and testing groups, respectively. Calibration curves and DCA revealed its good clinical performance. Finally, the optimal cutoff value for the total nomogram score was 0.513. The sensitivity and specificity of the optimal cutoff values were 0.822 and 0.706, respectively. CONCLUSION: A nomogram for predicting PVT occurrence was successfully developed and validated, and a network calculator was constructed. This can enable clinicians to rapidly and easily identify high PVT risk groups.

Association and mediation analyses among multiple metal exposure, mineralocorticoid levels, and serum ion balance in residents of northwest China.

Toxic metals are vital risk factors affecting serum ion balance; however, the effect of their co-exposure on serum ions and the underlying mechanism remain unclear. We assessed the correlations of single metal and mixed metals with serum ion levels, and the mediating effects of mineralocorticoids by investigating toxic metal concentrations in the blood, as well as the levels of representative mineralocorticoids, such as deoxycorticosterone (DOC), and serum ions in 471 participants from the Dongdagou-Xinglong cohort. In the single-exposure model, sodium and chloride levels were positively correlated with arsenic, selenium, cadmium, and lead levels and negatively correlated with zinc levels, whereas potassium and iron levels and the anion gap were positively correlated with zinc levels and negatively correlated with selenium, cadmium and lead levels (all P < 0.05). Similar results were obtained in the mixed exposure models considering all metals, and the major contributions of cadmium, lead, arsenic, and selenium were highlighted. Significant dose-response relationships were detected between levels of serum DOC and toxic metals and serum ions. Mediation analysis showed that serum DOC partially mediated the relationship of metals (especially mixed metals) with serum iron and anion gap by 8.3% and 8.6%, respectively. These findings suggest that single and mixed metal exposure interferes with the homeostasis of serum mineralocorticoids, which is also related to altered serum ion levels. Furthermore, serum DOC may remarkably affect toxic metal-related serum ion disturbances, providing clues for further study of health risks associated with these toxic metals.

Identifying the predictive role and the related drugs of oxidative stress genes in the hepatocellular carcinoma.

BACKGROUND AND AIMS: Oncogenesis and tumor development have been related to oxidative stress (OS). The potential diagnostic utility of OS genes in hepatocellular carcinoma (HCC), however, remains uncertain. As a result, this work aimed to create a novel OS related-genes signature that could be used to predict the survival of HCC patients and to screen OS related-genes drugs that might be used for HCC treatment. METHODS: We used The Cancer Genome Atlas (TCGA) database and the Gene Expression Omnibus (GEO) database to acquire mRNA expression profiles and clinical data for this research and the GeneCards database to obtain OS related-genes. Following that, biological functions from Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were performed on differentially expressed OS-related genes (DEOSGs). Subsequently, the prognostic risk signature was constructed based on DEOSGs from the TCGA data that were screened by using univariate cox analysis, and the Least Absolute Shrinkage and Selection Operator (LASSO) regression, and multivariate cox analysis. At the same time, we developed a prognostic nomogram of HCC patients based on risk signature and clinical-pathological characteristics. The GEO data was used for validation. We used the receiver operating characteristic (ROC) curve, calibration curves, and Kaplan-Meier (KM) survival curves to examine the prediction value of the risk signature and nomogram. Finally, we screened the differentially expressed OS genes related drugs. RESULTS: We were able to recognize 9 OS genes linked to HCC prognosis. In addition, the KM curve revealed a statistically significant difference in overall survival (OS) between the high-risk and low-risk groups. The area under the curve (AUC) shows the independent prognostic value of the risk signature model. Meanwhile, the ROC curves and calibration curves show the strong prognostic power of the nomogram. The top three drugs with negative ratings were ZM-336372, lestaurtinib, and flunisolide, all of which inversely regulate different OS gene expressions. CONCLUSION: Our findings indicate that OS related-genes have a favorable prognostic value for HCC, which sheds new light on the relationship between oxidative stress and HCC, and suggests potential therapeutic strategies for HCC patients.

Constructing spherical-beads-on-string structure of electrospun membrane to achieve high vapor flux in membrane distillation.

Hydrophobic membranes with a reentrant-like structure have shown high hydrophobicity and high anti-wetting properties in membrane distillation (MD). Here, PVDF spherical-beads-on-string (SBS) fibers were electrospun on nonwoven fabric and used in the MD process. Such a reentrant-like structure was featured with fine fibers, a low ratio of bead length to bead diameter, and high bead frequency. It was revealed that the SBS-structured membranes exhibited an exceptional capability for vapor flux, due to the formation of a network of more interconnected macropores than that of fibers and fusiform-beads-on-string structures, ensuring unimpeded vapor diffusion. In the desalination of formulated seawater (3.5 wt.% NaCl solution), a vapor flux of 61 ± 3 kg m-2 h-1 with a salt rejection of >99.98 % was achieved at a feed temperature of 60 °C. Furthermore, this SBS structured membrane showed satisfactory seawater desalination performance with a stable flux of 40 kg m-2 h-1 over a 27 h MD process. These findings suggest a viable approach for fabricating SBS-structured membranes that significantly enhance vapor flux in MD for desalination applications. Besides, the hydrophobic membranes with SBS structure can be prepared by single-step electrospinning, and it is facile to scale-up manufacture. This strategy holds promise for advancing the development of high-performance MD membranes tailored for efficient seawater desalination processes.

Cadmium exacerbates liver injury by remodeling ceramide metabolism: Multiomics and laboratory evidence.

Cadmium (Cd) is a toxic heavy metal that primarily targets the liver. Cd exposure disrupts specific lipid metabolic pathways; however, the underlying mechanisms remain unclear. This study aimed to investigate the lipidomic characteristics of rat livers after Cd exposure as well as the potential mechanisms of Cd-induced liver injury. Our analysis of established Cd-exposed rat and cell models showed that Cd exposure resulted in liver lipid deposition and hepatocyte damage. Lipidomic detection, transcriptome sequencing, and experimental analyses revealed that Cd mainly affects the sphingolipid metabolic pathway and that the changes in ceramide metabolism are the most significant. In vitro experiments revealed that the inhibition of ceramide synthetase activity or activation of ceramide decomposing enzymes ameliorated the proapoptotic and pro-oxidative stress effects of Cd, thereby alleviating liver injury. In contrast, the exogenous addition of ceramide aggravated liver injury. In summary, Cd increased ceramide levels by remodeling ceramide synthesis and catabolism, thereby promoting hepatocyte apoptosis and oxidative stress and ultimately aggravating liver injury. Reducing ceramide levels can serve as a potential protective strategy to mitigate the liver toxicity of Cd. This study provides new evidence for understanding Cd-induced liver injury at the lipidomic level and insights into the health risks and toxicological mechanisms associated with Cd.

The association between trace metals in both cancerous and non-cancerous tissues with the risk of liver and gastric cancer progression in northwest China.

Liver cancer and gastric cancer have extremely high morbidity and mortality rates worldwide. It is well known that an increase or decrease in trace metals may be associated with the formation and development of a variety of diseases, including cancer. Therefore, this study aimed to evaluate the contents of aluminium (Al), arsenic (As), cadmium (Cd), cobalt (Co), chromium (Cr), copper (Cu), iron (Fe), manganese (Mn), nickel (Ni), lead (Pb), selenium (Se), and zinc (Zn) in cancerous liver and gastric tissues, compared to adjacent healthy tissues, and to investigate the relationship between trace metals and cancer progression. During surgery, multiple samples were taken from the cancerous and adjacent healthy tissues of patients with liver and gastric cancer, and trace metal levels within these samples were analysed using inductively coupled plasma mass spectrometry (ICP-MS). We found that concentrations of As, Cd, Co, Cr, Cu, Fe, Mn, Ni, Pb, Se, and Zn in tissues from patients with liver cancer were significantly lower than those in healthy controls (P < 0.05). Similarly, patients with gastric cancer also showed lower levels of Cd, Co, Cr, Mn, Ni, and Zn-but higher levels of Cu and Se-compared to the controls (P < 0.05). In addition, patients with liver and gastric cancers who had poorly differentiated tumours and positive lymph node metastases showed lower levels of trace metals (P < 0.05), although no significant changes in their concentrations were observed to correlate with sex, age, or body mass index (BMI). Logistic regression, principal component analysis (PCA), Bayesian kernel regression (BKMR), weighted quantile sum (WQS) regression, and quantile-based g computing (qgcomp) models were used to analyse the relationships between trace metal concentrations in liver and gastric cancer tissues and the progression of these cancers. We found that single or mixed trace metal levels were negatively associated with poor differentiation and lymph node metastasis in both liver and gastric cancer, and the posterior inclusion probability (PIP) of each metal showed that Cd contributed the most to poor differentiation and lymph node metastasis in both liver and gastric cancer (all PIP = 1.000). These data help to clarify the relationship between changes in trace metal levels in cancerous liver and gastric tissues and the progression of these cancers. Further research is warranted, however, to fully elucidate the mechanisms and causations underlying these findings.

Association between Heavy Metals and Trace Elements in Cancerous and Non-cancerous Tissues with the Risk of Colorectal Cancer Progression in Northwest China.

Alterations in heavy metals and trace element levels may be associated with various cancers. However, the role of this interaction in colorectal cancer (CRC) progression is unclear. In recent years, Principal Component Analysis (PCA) and Bayesian Kernel Machine Regression (BKMR) models have provided new ideas for analyzing the effects of metal mixtures on CRC progression. Herein, we assessed the differences in the levels of arsenic (As), cadmium (Cd), cobalt (Co), chromium (Cr), copper (Cu), nickel (Ni), selenium (Se), and zinc (Zn) in tumors and adjacent healthy tissues, to investigate the relationship between heavy metals/trace elements and CRC progression. Surgical samples of CRC and noncancerous tissues were collected, and trace metal levels were analyzed using inductively coupled plasma mass spectrometry (ICP-MS). Logistic regression, PCA, and BKMR models were used to investigate the relationship between heavy metals and trace elements and the degree of tumor differentiation and lymph node metastasis in CRC. Cancer tissues showed lower As, Cd, Co, and Cr concentrations, and higher Se concentrations than healthy tissues (P < 0.05). In addition, CRC patients with poorly differentiated tumors and/or positive lymph node metastases had lower levels of Cd, Zn, Cu, and Se (P < 0.05). Logistic regression showed that single metal concentration was negatively correlated with CRC progression. PCA and BKMR models also showed that the metal mixture concentration was negatively correlated with CRC progression, with Cd contributing the most. Overall, changes in heavy metal and trace element levels may be related to the development of CRC; however, further mechanistic studies are required.

Enhanced Anti-Wetting Methods of Hydrophobic Membrane for Membrane Distillation.

Increasing issues of hydrophobic membrane wetting occur in the membrane distillation (MD) process, stimulating the research on enhanced anti-wetting methods for membrane materials. In recent years, surface structural construction (i.e., constructing reentrant-like structures), surface chemical modification (i.e., coating organofluorides), and their combination have significantly improved the anti-wetting properties of the hydrophobic membranes. Besides, these methods change the MD performance (i.e., increased/decreased vapor flux and increased salt rejection). This review first introduces the characterization parameters of wettability and the fundamental principles of membrane surface wetting. Then it summarizes the enhanced anti-wetting methods, the related principles, and most importantly, the anti-wetting properties of the resultant membranes. Next, the MD performance of hydrophobic membranes prepared by different enhanced anti-wetting methods is discussed in desalinating different feeds. Finally, facile and reproducible strategies are aspired for the robust MD membrane in the future.

Construction and validation of a novel nomogram to predict cancer-specific survival in patients with gastric adenocarcinoma.

Background and aims: Adenocarcinoma is one of the most common pathological types of gastric cancer. The aims of this study were to develop and validate prognostic nomograms that could predict the probability of cancer-specific survival (CSS) for gastric adenocarcinoma (GAC) patients at 1, 3, and 5 years. Methods: In total, 7747 patients with GAC diagnosed between 2010 and 2015, and 4591 patients diagnosed between 2004 and 2009 from the Surveillance, Epidemiology, and End Results (SEER) database were included in this study. The 7747 patients were used as a prognostic cohort to explore GAC-related prognostic risk factors. Moreover, the 4591 patients were used for external validation. The prognostic cohort was also divided into a training and internal validation sets for construction and internal validation of the nomogram. CSS predictors were screened using least absolute shrinkage and selection operator regression analysis. A prognostic model was built using Cox hazard regression analysis and provided as static and dynamic network-based nomograms. Results: The primary site, tumor grade, surgery of the primary site, T stage, N stage, and M stage were determined to be independent prognostic factors for CSS and were subsequently included in construction of the nomogram. CSS was accurately estimated using the nomogram at 1, 3, and 5 years. The areas under the curve (AUCs) for the training group at 1, 3, and 5 years were 0.816, 0.853, and 0.863, respectively. Following internal validation, these values were 0.817, 0.851, and 0.861. Further, the AUC of the nomogram was much greater than that of American Joint Committee on Cancer (AJCC) or SEER staging. Moreover, the anticipated and actual CSS values were in good agreement based on decision curves and time-calibrated plots. Then, patients from the two subgroups were divided into high- and low-risk groups based on this nomogram. The survival rate of high-risk patients was considerably lower than that of low-risk patients, according to Kaplan-Meier (K-M) curves (p<0.0001). Conclusions: A reliable and convenient nomogram in the form of a static nomogram or an online calculator was constructed and validated to assist physicians in quantifying the probability of CSS in GAC patients.

FOXP3 and SQSTM1/P62 correlate with prognosis and immune infiltration in hepatocellular carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common highly malignant tumours worldwide. FOXP3 and SQSTM1/P62 have been shown to be abnormally expressed in tumour cells, but their function in different tumours remains controversial. The present study was designed to evaluate the expression of FOXP3 and P62 in HCC and their prognostic value as well as their relationship with immune infiltration in HCC patients. METHODS: The Gene Expression Omnibus (GEO) database and TNMplot.com platform were used to analyse the expression of FOXP3 and P62. The Cancer Genome Atlas (TCGA) database and Kaplan-Meier plotter were used to assess the impacts of FOXP3 and P62 on clinical prognosis. In addition, TCGA database was also used to examine the correlation between the expression of FOXP3 and P62 and tumour immune infiltration using the CIBERSORT algorithm. Finally, immunohistochemistry (IHC) was used to determine expression levels of FOXP3 and P62 in 89 HCC and adjacent normal liver tissues, and their effects on clinicopathological features and prognosis were verified. RESULTS: FOXP3 expression was downregulated in HCC tissues, while P62 expression was upregulated. FOXP3 underexpression and P62 overexpression were closely related to decreased overall survival (OS) in HCC patients. Additionally, the abnormal expression of FOXP3 and P62 was closely related to the infiltration levels of 12 types of immune cells, including regulatory T cells (Tregs), M2 macrophages, M0 macrophages, and CD8 T cells. Notably, in the validation model, abnormal FOXP3 and P62 expression was significantly associated with adverse clinicopathological factors in HCC patients, including elevated α-fetoprotein (AFP) levels, poor tumour differentiation, and increased Ki67 levels. Furthermore, low FOXP3 and high P62 expression were independent risk factors for predicting OS prognosis in HCC patients. CONCLUSION: FOXP3 and P62 have been shown to be important prognostic factors in HCC patients and are associated with immune cell infiltration in HCC. These findings suggest that FOXP3 and P62 may be valuable prognostic biomarkers and potential therapeutic targets for HCC treatment.

Effects of cadmium and lead co-exposure on glucocorticoid levels in rural residents of northwest China.

Cadmium (Cd) and lead (Pb) are important environmental endocrine disruptors that are associated with adverse health problems. However, the effects of co-exposure to Cd and Pb on glucocorticoids (GCs) in the body at environmental levels are limited. A total of 468 subjects from the Dongdagou-Xinglong cohort (DDG-XL) were included in this study. We measured the serum levels of two representative endogenous GCs [cortisol (CRL) and cortisone (CRN)], and whole blood levels of Cd and Pb. Multiple linear regression models were constructed to explore the associations of single or combined Cd and Pb exposure with serum CRL and CRN levels. The interactive effects of Cd and Pb on GCs were further assessed using mediation analysis and moderation analysis. Single-heavy metal exposure analysis with adjustment for potential confounders showed that the serum CRL level decreased when the blood Cd or Pb concentration gradually increased (P trend <0.01). Additionally, subjects with high Cd or Pb exposure (Q4) had significantly reduced serum CRN levels compared to those with low Cd or Pb exposure (Q1) (P < 0.05). In Cd and Pb co-exposure analysis, significant negative dose-response relationships were observed between co-exposure to Cd and Pb and serum CRL and CRN levels. Furthermore, mediation analysis showed that Cd completely mediated the relationship between Pb and GCs, and moderation analysis suggested that Pb might weaken the negative relationship between Cd and GCs. These findings suggest that single or combined exposure to Cd and Pb interferes with the homeostasis of serum CRL and CRN levels. Furthermore, we innovatively propose that Cd and Pb may have interactive effects on GCs levels, and Pb can antagonize the negative relationship between Cd and GCs, which may provide clues for further studies on endocrine and metabolic disorders related to these heavy metals.

ABNO-Functionalized Silica as an Efficient Catalyst for Enhancing Permanganate Oxidation of Emerging Contaminants.

Recent reports indicate that some soluble electron-shuttling compounds (or organic mediators) can accelerate reactions between permanganate (Mn(VII)) and contaminants of emerging concern. However, practical application is limited to homogeneous electron-shuttling compounds. This study reports on the development and application of a heterogeneous electron-shuttling catalyst for Mn(VII) reactions with bisphenol A (BPA). First, we screened a series of poly/monocyclic nitroxides, finding that 9-azabicyclo[3.3.1]nonane N-oxyl (ABNO) provides the most significant enhancement of Mn(VII)/BPA reaction kinetics, where Mn(VII) oxidizes ABNO to BPA-reactive ABNO+. Next, we immobilized ABNO onto silica (SiO2) by covalent bonding of 9-azabicyclo[3,3,1]nonan-3-one-9-oxyl (keto-ABNO) via a 3-aminopropyltriethoxysilane bridge to yield an ABNO@SiO2 heterogeneous catalyst. The performance of ABNO@SiO2 in catalyzing Mn(VII)/BPA reactions is demonstrated, with BPA reaction kinetics being highly dependent on catalyst dosage and pH conditions. The stability of ABNO@SiO2 was retained at pH 5.0 and decreased slightly at pH 7.0 over five successive Mn(VII)/BPA reaction cycles. Kinetics modeling shows that BPA reacts with immobilized ABNO+, Mn(VII), and in situ formed MnO2. Moreover, ABNO+ can form via ABNO reactions with both Mn(VII) and the in situ formed MnO2. These results indicate a promising strategy for developing practical heterogeneous catalysts for enhancing Mn(VII) reactivity and treatment applications.

The Effect of Smoking Habits on Blood Cadmium and Lead Levels in Residents Living Near a Mining and Smelting Area in Northwest China: a Cross-Sectional Study.

Few studies have focused on environmental cadmium (Cd) and lead (Pb) exposure while exploring the effect of smoking on blood Cd (BCd) and blood Pb (BPb) levels. Moreover, essential trace elements affect the absorption, accumulation, and toxicity of Cd and Pb. To investigate the effect of smoking on BCd and BPb levels under high Cd and Pb exposure and the influence of essential trace elements on the effect, 301 residents living near a mining and smelting area in Northwest China were included in our study. After collecting health information and measuring BCd, BPb, serum iron, magnesium, and total calcium levels, we analyzed the association between smoking and BCd and BPb levels and the influence of the essential trace elements on the association. The results showed that BCd and BPb levels in smokers were significantly higher than those in non-smokers. There was a dose-response association between pack-years and the odds ratios (ORs) of high BCd and BPb levels in all participants compared with non-smokers. Serum iron, magnesium, and calcium had a negative effect on the elevations of the ORs of high BCd and BPb levels. In addition, smoking-related elevations of BCd and BPb levels vary by sex, age, BMI, and age of smoking initiation. Our findings present evidence for the effect of smoking on BCd and BPb levels under high Cd and Pb exposure and may provide guidance for the prevention and control of BCd and BPb elevations in residents living in Cd- and Pb-polluted areas.

Liver cirrhosis and complications from the perspective of dysbiosis.

The gut-liver axis refers to the intimate relationship and rigorous interaction between the gut and the liver. The intestinal barrier's integrity is critical for maintaining liver homeostasis. The liver operates as a second firewall in this interaction, limiting the movement of potentially dangerous compounds from the gut and, as a result, contributing in barrier management. An increasing amount of evidence shows that increased intestinal permeability and subsequent bacterial translocation play a role in liver damage development. The major pathogenic causes in cirrhotic individuals include poor intestinal permeability, nutrition, and intestinal flora dysbiosis. Portal hypertension promotes intestinal permeability and bacterial translocation in advanced liver disease, increasing liver damage. Bacterial dysbiosis is closely related to the development of cirrhosis and its related complications. This article describes the potential mechanisms of dysbiosis in liver cirrhosis and related complications, such as spontaneous bacterial peritonitis, hepatorenal syndrome, portal vein thrombosis, hepatic encephalopathy, and hepatocellular carcinoma, using dysbiosis of the intestinal flora as an entry point.

[MicroRNA Methylation in the Diagnosis and Treatment of Hepatocellular Carcinoma].

MicroRNAs,a group of short non-coding RNAs that regulate gene expression at post-transcriptional level,play a role in a variety of cell activities.Methylation is an essential topic in the study of transcriptional regulation at the genomic level.It is associated with diverse diseases such as tumor and aging by regulating gene expression and silencing.Studies have demonstrated that the abnormal methylation of miRNA can regulate the expression of miRNA and affect the expression and function of the target genes,which is a key signal for the occurrence and development of hepatocellular carcinoma.This research achievement provides a new idea for deciphering the molecular mechanism of the pathogenesis of hepatocellular carcinoma and exploring the therapeutic targets.

Abatement of Organic Contaminants by Mn(VII)/TEMPOs: Effects of TEMPOs Structure, Organic Contaminant Speciation, and Active Oxidizing Species.

In this study, a representative redox mediator, 2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPO), and its para-substituted derivatives (TEMPOs: 4-hydroxyl-TEMPO, 4-acetylamino-TEMPO, and 4-amino-TEMPO) significantly accelerated the abatement of trace organic contaminants (TrOCs, i.e., bisphenol-A (BPA), phenol, amines, and phenylbutazone) by Mn(VII) over a wide pH range of 4.0-9.0. The addition of substituents at para to the > N-O• moiety significantly influenced the degradation kinetics of TrOCs by changing the reduction potentials of TEMPOs and the corresponding oxoammonium cations (TEMPOs+); a linear relationship was observed between the substituents' para Hammett sigma constants and the reduction potentials of TEMPOs and TEMPOs+. Pseudo-first-order reaction rate constants (kobs, min-1) of TrOC degradation by Mn(VII)/TEMPOs were also affected by the pKa of the TrOCs. Generally, the highest kobs values for individual TrOCs were observed at pH near the pKa even for TEMPOs+ with relatively pH-invariant reduction potentials. Overall, TrOC abatement kinetics were related to a combination of reactive species (Mn(VII), in situ formed MnO2, and TEMPOs+). For BPA, the relative contributions (R) of reactive species ranked as R(TEMPOs+) > R(Mn(VII)) > R(in situ formed MnO2) at pH 4.0-8.0, whereas R(Mn(VII)) > R(TEMPOs+) at pH 9.0 mainly owing to a change in BPA speciation as the pH approached the pKa1 value for BPA. The results of this study are useful for the development of heterogeneous TEMPO-based redox mediators and future applications of TEMPO-mediated oxidation systems for accelerated abatement of TrOCs in water.

Association among Helicobacter pylori Infection, Tooth Loss, and Heavy Medal Exposure in a Chinese Rural Population.

Previous research suggests that heavy metals may be associated with increased susceptibility to Helicobacter pylori infection. This study investigated the effect of heavy metal exposure (Pb and Cd) on tooth loss and H. pylori infection in a Chinese rural population, who live near a mining and smelting area. Blood samples were collected from the study participants to estimate the lead (Pb) and cadmium (Cd) exposure levels. H. pylori infection was analyzed using the 14C-urea breath test, and the number of missing teeth (MT), filled teeth (FT), and missing or filled teeth (MFT) were counted by conducting a physical examination. Regression analysis was used to assess the difference between H. pylori-positive and -negative individuals in the MT, FT, and MFT groups, adjusting for confounders. The H. pylori infection prevalence was higher in individuals in the high Cd or high Pb groups than that in the low Cd or low Pb groups (p < 0.05). In addition, greater numbers of FT and MFT were observed in individuals in the high Pb group than those in the low Pb group (p < 0.05). We further found 8.7% (95% CI, 2.8−23.8%, p = 0.017) of the effect of the high BPb level on H. pylori infection risk could be statistically explained by FT using amediation analyses in adjusted models, and 6.8% (95% CI, 1.6−24.8%, p = 0.066) by MFT. Furthermore, FT and MFT were significantly associated with increased risk for H. pylori infection (odds ratio (OR) = 4.938, 95% confidence interval (CI): 1.125−21.671; OR = 3.602, 95% CI: 1.218−10.648, respectively). Pb and Cd exposure may be associated with tooth loss and increased susceptibility to H. pylori infection, and tooth loss may be an independent risk factor for H. pylori infection.

Efficient reductive and oxidative decomposition of haloacetic acids by the vacuum-ultraviolet/sulfite system.

Haloacetic acids (HAAs), as a representative category of halogenated disinfection byproducts, are widely detected in disinfected water. In this work, the vacuum ultraviolet (VUV)/sulfite process under N2 saturated conditions was proposed to eliminate a series of HAAs (i.e., monochloroacetic acid (MCAA), difluoroacetic acid (DFAA), trifluoroacetic acid (TFAA), dichloroacetic acid (DCAA), etc.). The in situ generated hydrated electron (eaq-) demonstrated to be the main species to fulfill the initial degradation and dechlorination of MCAA, while hydroxyl radicals (˙OH) were in charge of the mineralization of MCAA. This means that the VUV/sulfite system is a combination of advanced reduction and oxidation processes (ARPs and AOPs). A significant enhancement of MCAA removal was observed with increasing pH values from 6.0 to 10.0, and surprisingly, kobs correlated well with the proportion of SO32- as the pH changed. This can be explained by the production of eaq- from VUV irradiation of SO32- rather than HSO3- and also due to eaq- being more stable under alkaline conditions. Increasing the sulfite dosage also elevated the degradation of MCAA. However, the addition of certain anions (i.e., chloride (Cl-), bicarbonate (HCO3-), and nitrate (NO3-)) and dissolved organic matter (DOM) inhibited the removal of MCAA to varying degrees. The VUV/sulfite system was effective toward various types of halogenated disinfection byproducts, supporting its broad applicability. Nevertheless, even in real waters, the VUV/sulfite system was also promising for the simultaneous abatement of HAAs and other oxyanions.

Screening and validation of biomarkers for cadmium-induced liver injury based on targeted bile acid metabolomics.

Although cadmium (Cd) is a toxic heavy metal that reportedly causes liver injury, few studies have investigated biomarkers of Cd-induced liver injury. The purpose of this study is to investigate the role of bile acid (BA) in Cd-induced liver injury and determine reliable and sensitive biochemical parameters for the diagnosis of Cd-induced liver injury. In this study, 48 Sprague-Dawley rats were randomly divided into six groups and administered either normal saline or 2.5, 5, 10, 20, and 40 mg/kg/d cadmium chloride for 12 weeks. A total of 403 subjects living in either a control area (n = 135) or Cd polluted area (n = 268) of Dongdagou-Xinglong (DDGXL) cohort were included, a population with long-term low Cd exposure. The BA profiles in rats' liver, serum, caecal contents, faeces, and subjects' serum were detected using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Changes in rats' and subjects' liver injury indices, rats' liver pathological degeneration, and rats' liver and subjects' blood Cd levels were also measured. Cadmium exposure caused cholestasis and an increase in toxic BAs, leading to liver injury in rats. Among them, glycoursodeoxycholic acid (GUDCA), glycolithocholic acid (GLCA), taurolithocholic acid (TLCA), and taurodeoxycholate acid (TDCA) are expected to be potential biomarkers for the early detect of Cd-induced liver injury. Serum BAs can be used to assess Cd-induced liver injury as a simple, feasible, and suitable method in rats. Serum GUDCA, GLCA, TDCA, and TLCA were verified to be of value to evaluate Cd-induced liver injury and Cd exposure in humans. These findings provided evidence for screening and validation of additional biomarkers for Cd-induced liver injury based on targeted BA metabolomics.