Leaching of heavy metals from tungsten mining tailings: A case study based on static and kinetic leaching tests.

Heavy metal (HM) leaching from tungsten mine tailings is a serious environmental risk. In this study, we assess the HM pollution level of tungsten tailings, determine the HM leaching patterns and mechanisms, and estimate the HM fluxes from a tailings reservoir. The results showed that the comprehensive pollution index (CRSi) values that decreased in order of the HM pollution levels in the tailings were cadmium (Cd) > tungsten (W) > lead (Pb) > copper (Cu) = zinc (Zn) > arsenic (As) > manganese (Mn). This result indicated that Cd, W, and Pb were priority pollutants in tailings. The Res fraction of all HMs was greater than 50%. Pb and Cd had similar species fractions with high Exc fractions, and tungsten had a considerable proportion of the Wat fraction. The general acid neutralizing capacity (GANC) test divides the leaching process of HMs into two stages, and each of stage is affected by different mechanisms. A neutral environment promoted tungsten leaching in the column leching test, while an acidic environment promoted Cd and Pb leaching. In addition, the pH effect was more obvious in the early stage. The kinetic fitting results showed that the second-order dynamic model well simulated the leaching of W, Pb, and Cd in most cases. Based on column kinetic leaching test results and tailings parameters, the annual W, Pb, and Cd fluxes were estimated to be 6.35 × 108, 1.3288 × 109, and 1.012 × 108 mg/year, respectively. The above results can guide the environmental management of tungsten tailing reservoirs, such as selecting suitable repair materials and estimating repair service times.

Genomic characterization of a newly established esophageal squamous cell carcinoma cell line from China and published esophageal squamous cell carcinoma cell lines.

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is one of the most prevalent malignancies and a major cause of cancer related death worldwide, especially in China. Cell lines are widely used disease models for basic medical research, however, well characterized ESCC cell models from China were seldom reported. Misidentifying and cross-contaminations of cell lines also hamper the way of producing solid and reproductive data. METHODS: CSEC216 was originated from a 45-year-old male ESCC patient from Chaoshan littoral, China. Specimens were minced into fragments and seeded in T-25 flask for primary culture. Immunoflourescence staining was performed for identifying the origination and proliferation activity. In vitro migration and invasion abilities was tested by transwell assay. DNA Short Tandem Repeats profiling was implemented for cell authorization. Karyotype was investigated by spectrum karyotyping. Whole genome sequencing was utilized to investigate genomic alterations. Background information and genomic mutation data of published ESCC cell lines were obtained from online databases. RESULTS: CSEC216 was an uncontaminated cell line, exhibited epithelial cell features with polygonal morphology and adherent growth as monolayer. Immuno staining demonstrated its epithelial origination and high proliferation rate. The Population Doubling time was 29.7 h. The karyotype demonstrated tumor cell patterns with aneuploidy and complex chromosomal aberrations. Mutation signatures, genes with SNA or CNA of CSEC216 and published ESCC cell lines were similar with the mutation spectrum of original ESCC tumors. CONCLUSIONS: ESCC cell line CSEC216 from high incidence region in China was established with no cross-contamination. Biological features were studied. Genomic mutation features of CSEC216 and 28 ESCC cell lines were characterized which provided thorough cytogenetic background that facilitated future usage.

Genetic Alterations in Esophageal Tissues From Squamous Dysplasia to Carcinoma.

BACKGROUND & AIMS: Esophageal squamous cell carcinoma (ESCC) is the most common subtype of esophageal cancer. Little is known about the genetic changes that occur in esophageal cells during the development of ESCC. We performed next-generation sequence analyses of esophageal nontumor, intraepithelial neoplasia (IEN), and ESCC tissues from the same patients to track genetic changes during tumor development. METHODS: We performed whole-genome, whole-exome, or targeted sequence analyses of 227 esophageal tissue samples from 70 patients with ESCC undergoing resection at Shantou University Medical College in China from 2012 through 2015 (no patients had received chemotherapy or radiation therapy); we analyzed normal tissues, tissues with simple hyperplasia, dysplastic tissues (IEN), and ESCC tissues collected from different regions of the esophagus at the same time. We also obtained 1191 nontumor esophageal biopsy specimens from the Chaoshan region (a high-risk region for ESCC) of China (a high-risk region for ESCC) and performed immunohistochemical and histologic analyses to detect inflammation. RESULTS: IEN and ESCC tissues had similar mutations and copy number alterations, at similar frequencies; these differed from mutations detected in tissues with simple hyperplasia. IEN tissues had mutations associated with apolipoprotein B messenger RNA editing enzyme, catalytic polypeptide-like-mediated mutagenesis (a DNA damage mutational signature). Genetic analyses indicated that most ESCCs were formed from early stage IEN clones. Trunk mutations (mutations shared by >10% of paired IEN and ESCC tissues) were in genes that regulate DNA repair and cell apoptosis, proliferation and adhesion. Mutations in TP53 and CDKN2A and copy number alterations in 11q (contains CCND1), 3q (contains SOX2), 2q (contains NFE2L2), and 9p (contains CDKN2A) were considered to be trunk variants; these were dominant mutations detected at high frequencies in clones of paired IEN and ESCC samples. In the esophageal biopsy samples from high-risk individuals (residing in the Chaoshan region), 68.9% had an evidence of chronic inflammation; the level of inflammation was correlated with atypical cell structures and markers of DNA damage. CONCLUSIONS: We analyzed mutations and gene copy number changes in nontumor, IEN, and ESCC samples, collected from 70 patients. IEN and ESCCs each had similar mutations and markers of genomic instability, including apolipoprotein B messenger RNA editing enzyme, catalytic polypeptide-like. Genomic changes observed in precancerous lesions might be used to identify patients at risk for ESCC.