Characterization of heavy metal contamination in groundwater of typical mining area in Hunan Province.

Heavy metal pollution in mining areas is a major cause of groundwater contamination, characterized by high toxicity, difficult degradability, and easy accumulation, and the source of pollution is not easily identified. Relying on the results of groundwater quality analysis tests in a typical mining area, this paper uses the SPSS 18.0 statistical analysis model to analyze the statistical characteristics of different indicator factors in the antimony mining area. The conclusions play a crucial role in implementing health and safety measures for the mining area and its surrounding residents. The statistical study results show that Mn, Se, As, and Sb are closely related to human mining activities and are polluted to varying degrees; the principal component analysis model indicates that the upstream monitoring points 26#, 22#, and 25# in the mining area groundwater are less polluted. The five monitoring points with a comprehensive principal component F > 1 are all located within the range of the metal mine cluster, indicating that the groundwater in the mining area is particularly sensitive to the impact of anthropogenic mineral extraction. This research summarizes the hydrogeological and geochemical statistical characteristics of the groundwater in the mining area, providing a reference for groundwater pollution risk diagnosis, ecological restoration, and heavy metal pollution prevention and control in this and similar mining areas.

The Chemokine CXCL7 is Correlated with LDH-A and Predicts the Prognosis of Patients with Colorectal Cancer.

OBJECTIVE: The aims of this study were to evaluate the correlation between chemokine (C-X-C) ligand 7 (CXCL7) expression and glycolysis and to explore the prognostic significance of CXCL7 in colorectal cancer (CRC). METHODS: The expression of CXCL7 and lactate dehydrogenase A (LDH-A) was measured by immunohistochemistry in tissue from 158 CRC patients. Patients were divided into high expression and low expression groups based on receiver operating characteristic curves and a cut-off value. The correlation between CXCL7 and LDH-A expression was evaluated. The overall survival (OS) times of CRC patients were explored. The risk factors related to prognosis were assessed. RESULTS: Significantly higher expression of CXCL7 and LDH-A was detected in CRC tissue than in non-CRC tissue, and was associated with N stage and tumor-node-metastasis (TNM) stage. CXCL7 expression was strongly correlated with LDH-A expression in CRC tissue. High expression of CXCL7 was validated as an independent risk factor for OS. CONCLUSION: Increased expression of CXCL7 was positively correlated with LDH-A expression and was an independent risk factor for CRC prognosis.

The p53-mediated cell cycle regulation is a potential mechanism for emodin-suppressing osteosarcoma cells.

Background: As the most common primary bone cancer, the therapy of osteosarcoma requires further study. An anthraquinone derivative, emodin, has been found to have anticancer potential. We proposed that emodin suppresses osteosarcoma by cell cycle regulation mediated by p53. Methods: This study determined the effect of emodin on viability and apoptosis of 6 osteosarcoma cell lines (p53 null cells MG63, G292, and A-673; p53 mutated cells HOS and SK-PN-DW; p53 expressing cells U2OS and 2 osteoblast cell lines), then knockdown p53 in U2OS, and observed the impacts of emodin on p53, p21, cyclin proteins, and cell cycle. Results: High dose emodin (40-160 µM) induced cell death and apoptosis of all the cell lines; medium dose emodin (20 µM) preferentially inhibited osteosarcoma cells; low dose emodin (1-10 µM) preferentially inhibited p53 expressing osteosarcoma cells. Emodin dose-dependently inhibited p53 and p21 in U2OS. Emodin at 10 µM decreased the expression of Cdk2, E2F, and Cdk1; and increased RB but had no effects on cyclin E and cyclin B. The knockdown of p53 almost eliminated all the impacts of 10 µM emodin on cell cycle proteins. Conclusions: Emodin suppresses U2OS by p53-mediated cell cycle regulation.

The role of CSTF2 in cancer: from technology to clinical application.

A protein called cleavage-stimulating factor subunit 2 (CSTF2, additionally called CSTF-64) binds RNA and is needed for the cleavage and polyadenylation of mRNA. CSTF2 is an important component subunit of the cleavage stimulating factor (CSTF), which is located on the X chromosome and encodes 557 amino acids. There is compelling evidence linking elevated CSTF2 expression to the pathological advancement of cancer and on its impact on the clinical aspects of the disease. The progression of cancers, including hepatocellular carcinoma, melanoma, prostate cancer, breast cancer, and pancreatic cancer, is correlated with the upregulation of CSTF2 expression. This review provides a fresh perspective on the investigation of the associations between CSTF2 and various malignancies and highlights current studies on the regulation of CSTF2. In particular, the mechanism of action and potential clinical applications of CSTF2 in cancer suggest that CSTF2 can serve as a new biomarker and individualized treatment target for a variety of cancer types.

Plasma levels of soluble ST2, but not IL-33, correlate with the severity of alcoholic liver disease.

Alcoholic liver disease (ALD) is a complication that is a burden on global health and economy. Interleukin-33 (IL-33) is a newly identified member of the IL-1 cytokine family and is released as an "alarmin" during inflammation. Soluble suppression of tumourigenicity 2 (sST2), an IL-33 decoy receptor, has been reported as a new biomarker for the severity of systemic and highly inflammatory diseases. Here, we found the levels of plasma sST2, increased with the disease severity from mild to severe ALD. Importantly, the plasma sST2 levels in ALD patients not only correlated with scores for prognostic models (Maddrey's discriminant function, model for end-stage liver disease and Child-Pugh scores) and indexes for liver function (total bilirubin, international normalized ratio, albumin, and cholinesterase) but also correlated with neutrophil-associated factors as well as some proinflammatory cytokines. In vitro, lipopolysaccharide-activated monocytes down-regulated transmembrane ST2 receptor but up-regulated sST2 mRNA and protein expression and produced higher levels of tumour necrosis factor-α (TNF-α). By contrast, monocytes pretreated with recombinant sST2 showed decreased TNF-α production. In addition, although plasma IL-33 levels were comparable between healthy controls and ALD patients, we found the IL-33 expression in liver tissues from ALD patients was down-regulated at both RNA and protein levels. Immunohistochemical staining further showed that the decreased of IL-33-positive cells were mainly located in liver lobule area. These results suggested that sST2, but not IL-33, is closely related to the severity of ALD. Consequently, sST2 could be used as a potential biomarker for predicting the prognosis of ALD.

Association Between Aldehyde Dehydrogenase 2 Glu504Lys Polymorphism and Alcoholic Liver Disease.

BACKGROUND: Only a subset of patients with excessive alcohol use develop alcoholic liver disease (ALD), though the exact mechanism is not completely understood. Once ingested, alcohol is metabolized by 2 key oxidative enzymes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). There are 2 major ALDH isoforms, cytosolic and mitochondrial, encoded by the aldehyde ALDH1 and ALDH2 genes, respectively. The ALDH2 gene was hypothesized to alter genetic susceptibility to alcohol dependence and alcohol-induced liver diseases. The aim of this study is to determine the association between aldehyde dehydrogenase 2 (rs671) glu504lys polymorphism and ALD. METHODS: ALDH2 genotyping was performed in 535 healthy controls and 281 patients with ALD. RESULTS: The prevalence of the common form of the single nucleotide polymorphism rs671, 504glu (glu/glu) was significantly higher in patients with ALD (95.4%) compared to that of controls (73.7%, P < 0.0001). Among controls, 23.7% had the heterozygous (glu/lys) genotype compared to 4.6% in those with ALD (odds ratio [OR] = 0.16, 95% CI: 0.09-0.28). The allele frequency for 504lys allele in patients with ALD was 2.3%, compared to 14.5% in healthy controls (OR = 0.13, 95% CI: 0.07-0.24). CONCLUSIONS: Patients with ALDH2 504lys variant were less associated with ALD compared to those with ALDH2 504glu using both genotypic and allelic analyses.

Primary biliary cirrhosis-associated hepatocellular carcinoma in Chinese patients: incidence and risk factors.

AIM: To investigate the incidence, characteristics, and risk factors for hepatocellular carcinoma (HCC) in Chinese patients with primary biliary cirrhosis (PBC). METHODS: We reviewed the data of 52 PBC-associated HCC patients treated at Beijing 302 Hospital from January 2002 to December 2013 and analyzed its incidence and characteristics between the two genders. The risk factors for PBC-associated HCC were analyzed via a case-control study comprising 20 PBC patients with HCC and 77 matched controls without HCC. The matched factors included gender, age, follow-up period and Child-Pugh scores. Conditional logistic regression was used to evaluate the odds ratios of potential risk factors for HCC development. A P < 0.05 was considered statistically significant. RESULTS: The incidence of HCC in Chinese PBC patients was 4.13% (52/1255) and was significantly higher in the males (9.52%) than in the females (3.31%). Among the 52 PBC patients with HCC, 55.76% (29/52) were diagnosed with HCC and PBC simultaneously, and 5.76% (3/52) were diagnosed with HCC before PBC. The males with PBC-associated HCC were more likely than the females to have undergone blood transfusion (18.75% vs 8.33%, P = 0.043), consumed alcohol (31.25% vs 8.33%, P = 0.010), smoked (31.25% vs 8.33%, P = 0.010), had a family history of malignancy (25% vs 5.56%, P = 0.012), and had serious liver inflammation, as indicated by the elevated levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and γ-glutamyl transpeptidase (P < 0.05). Conditional logistic regression analysis revealed that body mass index (BMI) ≥ 25 [adjusted odds ratio (AOR) = 1.116, 95%CI: 1.002-1.244, P = 0.045] and history of alcohol intake (AOR = 10.294, 95%CI: 1.108-95.680, P = 0.040) were significantly associated with increased odds of HCC development in PBC patients. CONCLUSION: HCC is not rare in Chinese PBC patients. Risk factors for PBC-associated HCC include BMI ≥ 25 and a history of alcohol intake. In addition to regular monitoring, PBC patients may benefit from abstinence from alcohol and body weight control.