We aimed to review the current data composition of the Korean Tuberculosis and Post-Tuberculosis Cohort, which was constructed by linking the Korean Tuberculosis Surveillance System (KNTSS; established and operated by the Korean Disease Control and Prevention Agency since 2000) and the National Health Information Database (NHID; established by the National Health Insurance Service in 2012). The following data were linked: KNTSS data pertaining to patients diagnosed with tuberculosis between 2011 and 2018, NHID data of patients with a history of tuberculosis and related diseases between 2006 and 2018, and data (obtained from the Statistics Korea database) on causes of death. Data from 300 117 tuberculosis patients (177 206 men and 122 911 women) were linked. The rate of treatment success for new cases was highest in 2015 (86.7%), with a gradual decrease thereafter. The treatment success rate for previously treated cases showed an increasing trend until 2014 (79.0%) and decreased thereafter. In total, 53 906 deaths were confirmed among tuberculosis patients included in the cohort. The Korean Tuberculosis and Post-Tuberculosis Cohort can be used to analyze different measurement variables in an integrated manner depending on the data source. Therefore, these cohort data can be used in future epidemiological studies and research on policy-effect analysis, treatment outcome analysis, and health-related behaviors such as treatment discontinuation.

A hypoxic microenvironment leads to cancer progression and increases the metastatic potential of cancer cells within tumors via epithelial-mesenchymal transition (EMT) and cancer stemness acquisition. The hypoxic response pathway can occur under oxygen tensions of < 40 mmHg through hypoxia-inducible factors (HIFs), which are considered key mediators in the adaptation to hypoxia. Previous studies have shown that cellular responses to hypoxia are required for EMT and cancer stemness maintenance through HIF-1α and HIF-2α. The principal transcription factors of EMT include Twist, Snail, Slug, Sip1 (Smad interacting protein 1), and ZEB1 (zinc finger E-box-binding homeobox 1). HIFs bind to hypoxia response elements within the promoter region of these genes and also target cancer stem cell-associated genes and mediate transcriptional responses to hypoxia during stem cell differentiation. Acquisition of stemness characteristics in epithelial cells can be induced by activation of the EMT process. The mechanism of these phenotypic changes includes epigenetic alterations, such as DNA methylation, histone modification, chromatin remodeling, and microRNAs. Increased expression of EMT and pluripotent genes also play a role through demethylation of their promoters. In this review, we summarize the role of hypoxia on the acquisition of EMT and cancer stemness and the possible association with epigenetic regulation, as well as their therapeutic applications.
Anoxia* ; Chromatin Assembly and Disassembly ; DNA Methylation ; Epigenomics* ; Epithelial Cells ; Epithelial-Mesenchymal Transition* ; Fingers ; Gastropoda ; Genes, Homeobox ; Histones ; MicroRNAs ; Oxygen ; Promoter Regions, Genetic ; Response Elements ; Snails ; Stem Cells ; Transcription Factors

The detrimental effects of environmental pollutants on the health of the individual are generally accepted, although the mechanisms of these effects remain to be incompletely understood. In the present study, we examined the effects of B[a]P, 2-BP, phenol and TCDD on proinflammatory cytokine gene expression in mice spleen cells which were stimulated with anti-CD3. 10-9M TCDD increased IFN gammar and TNF alpha gene expression, but suppressed IL-1 gene expression. 10-6M phenol inhibited IL-1, IL-6 and TNF alpha gene expression, and 10-6M of 2-BP downregulated TNF alpha gene expression. However, 10-6M of B[a]P did not influence on IL-1, IL-6, IFN gammar and TNF alpha gene expression. These findings suggest that TCDD may impair the immune functions of mice by enhancing proinflammatory cytokines production, whereas phenol and 2-BP may impair the functions by inhibiting the production of these cytokines.
Animals ; Antigens, CD3/immunology ; Apoptosis/drug effects ; Benzo(a)pyrene/*toxicity ; Cells, Cultured ; Cytokines/*biosynthesis/genetics ; Environmental Pollutants/*toxicity ; Gene Expression/drug effects ; Hydrocarbons, Brominated/*toxicity ; Male ; Mice ; Mice, Inbred C3H ; Phenol/*toxicity ; RNA/chemistry/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Spleen/*drug effects/metabolism ; Tetrachlorodibenzodioxin/*toxicity