Algal Extracellular Organic Matter Induced Photochemical Oxidation of Mn(II) to Solid Mn Oxide: Role of Mn(III)-EOM Complex and Its Ability to Remove 17α-Ethinylestradiol.

Photosensitizer-mediated abiotic oxidation of Mn(II) can yield soluble reactive Mn(III) and solid Mn oxides. In eutrophic water systems, the ubiquitous algal extracellular organic matter (EOM) is a potential photosensitizer and may have a substantial impact on the oxidation of Mn(II). Herein, we focused on investigating the photochemical oxidation process from Mn(II) to solid Mn oxide driven by EOM. The results of irradiation experiments demonstrated that the generation of Mn(III) intermediate was crucial for the successful photo oxidization of Mn(II) to solid Mn oxide mediated by EOM. EOM can serve as both a photosensitizer and a ligand, facilitating the formation of the Mn(III)-EOM complex. The complex exhibited excellent efficiency in removing 17α-ethinylestradiol. Furthermore, the complex underwent decomposition as a result of reactions with reactive intermediates, forming a solid Mn oxide. The presence of nitrate can enhance the photochemical oxidation process, facilitating the conversion of Mn(II) to Mn(III) and then to solid Mn oxide. This study deepens our grasp of Mn(II) geochemical processes in eutrophic water and its impact on organic micropollutant fate.

Combining the Fecal Immunochemical Test with a Logistic Regression Model for Screening Colorectal Neoplasia.

Background: The fecal immunochemical test (FIT) is a widely used strategy for colorectal cancer (CRC) screening with moderate sensitivity. To further increase the sensitivity of FIT in identifying colorectal neoplasia, in this study, we established a classifier model by combining FIT result and other demographic and clinical features. Methods: A total of 4,477 participants were examined with FIT and those who tested positive (over 100 ng/ml) were followed up by a colonoscopy examination. Demographic and clinical information of participants including four domains (basic information, clinical history, diet habits and life styles) that consist of 15 features were retrieved from questionnaire surveys. A mean decrease accuracy (MDA) score was used to select features that are mostly related to CRC. Five different algorithms including logistic regression (LR), classification and regression tree (CART), support vector machine (SVM), artificial neural network (ANN) and random forest (RF) were used to generate a classifier model, through a 10X cross validation process. Area under curve (AUC) and normalized mean squared error (NMSE) were used in the evaluation of the performance of the model. Results: The top six features that are mostly related to CRC include age, gender, history of intestinal adenoma or polyposis, smoking history, gastrointestinal discomfort symptom and fruit eating habit were selected. LR algorithm was used in the generation of the model. An AUC score of 0.92 and an NMSE score of 0.076 were obtained by the final classifier model in separating normal individuals from participants with colorectal neoplasia. Conclusion: Our results provide a new "Funnel" strategy in colorectal neoplasia screening via adding a classifier model filtering step between FIT and colonoscopy examination. This strategy minimizes the need of colonoscopy examination while increases the sensitivity of FIT-based CRC screening.

Establishment and Characterization of a CTC Cell Line from Peripheral Blood of Breast Cancer Patient.

BACKGROUND: Circulating tumor cell (CTC)-based patient-derived cells are ideal models for investigating the molecular basis of cancer. However, the rarity and heterogeneity of CTCs as well as the difficulties of primary culture limit their practical application. Establishing efficient in vitro culture methods and functionally characterizing CTCs is essential for cancer studies. To this end, we developed an experimental protocol for the isolation, expansion, and identification of breast cancer CTCs. METHODS: The CTC-3 cell line was established from peripheral blood cells of a breast cancer patient. A karyotype analysis was performed. The molecular profile was assessed by flow cytometry, quantitative real-time PCR, and western blot. The characteristics of tumors formed by CTC-3 cells were evaluated by cell growth and tumor sphere formation assays and in a mouse xenograft model. The tumors were analyzed by immunohistochemistry, immunofluorescence analysis, and hematoxylin and eosin staining. RESULTS: The CTC-3 cell line showed more aggressive growth both in vitro and in vivo than the widely used MCF-7 breast cancer cell line. CTC-3 cells were also more resistant to chemotherapeutic agents, and gene profiling indicated higher expression levels of the epithelial-to-mesenchymal transition and stemness markers as compared to MCF-7 cells. CONCLUSIONS: CTC-3 cells are a better model for investigating the malignant behavior of breast cancer than existing cell lines.

Knockdown of Thymidine Kinase 1 Suppresses Cell Proliferation, Invasion, Migration, and Epithelial-Mesenchymal Transition in Thyroid Carcinoma Cells.

Patients with advanced thyroid carcinoma have poor prognosis with low overall survival. Unfortunately, the underlying mechanisms of thyroid carcinoma progression remain unclear. The elevated expression of thymidine kinase 1 (TK1) has been implicated in the progression of thyroid carcinoma, while the role of TK1 in thyroid carcinoma progression has not been explored. The present study aimed to determine the role TK1 in the progression of thyroid cancer and to explore the underlying molecular mechanisms. In this study, it was found that serum TK1 levels were markedly increased in the patients with thyroid nodules. Further online data mining showed that TK1 expression was upregulated in thyroid carcinoma tissues, and higher expression of TK1 was correlated with shorter disease-free survival of patients with thyroid carcinoma. Silencing of TK1 suppressed cell proliferation, invasion, migration, and epithelial-mesenchymal transition, and also induced cell apoptosis in the thyroid carcinoma cell lines. Animal studies showed that TK1 knockdown inhibited in vivo tumor growth of thyroid carcinoma cells. Importantly, miR-34a-5p was found to be downregulated in the thyroid carcinoma cells. Furthermore, miR-34a-5p targeted the 3' untranslated region of TK1 and suppressed the expression of TK1 in thyroid carcinoma cell lines. In summary, first, these results demonstrated the upregulation of TK1 in thyroid nodules and thyroid carcinoma tissues; second, TK1 promoted thyroid carcinoma cell proliferation, invasion, and migration; lastly, TK1 was negatively regulated by miR-34a-5p. Our study may provide novel insights into the role of TK1 in regulating thyroid carcinoma progression.