The liberation period in Korea was when creative imagination and various debates existed about plans for political, economic, and social systems. Among them was the debate over the national health security underlying the social safety net. Although the US influenced the Korean health security after liberation, major political groups on the Korean peninsula also expressed various opinions. However, previous studies have shown little interest in national health security, which operates the public health and medical care systems. To overcome these limitations, this study focuses on the ideas on national health security presented by major political groups, analyzing the reply proposal of “Jŏnpyŏng” and the health care proposal of the US military government, which has not been reviewed before.
The opinions of major political groups including the right-wing Im-hyŏp and left-wing Min-chŏn diverged on national health security issue regarding insurance coverage, measures to secure financial resources, items of insurance benefits, and measures to stabilize the supply and demand of medical personnel. The claims of the US military government can be understood by “Labor Problems and Policies in Korea (Korean Subcommittee),” “Korean Labor Report (Stewart Meacham),” and “Proposed Political Platform Provisional Korean Democratic Government (Sub-commission #2).”
The major political groups and the US military government agreed on the need for social protection against death, old age, disability, disease, injury, and unemployment. All of them claimed national health security, in which the roles of the private sector and the government were mixed, should be gradually introduced. The major political groups, in particular, proposed to (1) set workers as beneficiaries of insurance, (2) share financial resources jointly among the state, employers, and workers, and (3) promote the expansion of the number of doctors and medical institutions and prefer cooperative operations of the hospitals established in small administrative units.
This paper argues that the ideas on national health security during the liberation period did not completely deviate from the global trend immediately after World War II when countries tried to expand the number of people covered by national health security and strengthen its coverage. Although these ideas were not fully reflected in the Constitution of 1948, it is significant in that the Constitution codified for the first time the state’s responsibility for those who have no ability for living due to their health conditions.

Purpose: Following the withdrawal of propacetamol in Europe owing to safety issues, the regulatory authority of South Korea requested a post-marketing surveillance study to investigate its safety profile. Materials and Methods: We conducted nested case-control and case-time-control (CTC) analyses of cases and controls identified for outcomes of interest, including anaphylaxis, thrombosis, and Stevens–Johnson syndrome (SJS), using the claims database of South Korea, 2010–2019. Risk-set sampling was used to match each case with up to 10 controls for age, sex, cohort entry date, and follow-up duration. Exposure to anaphylaxis, thrombosis, and SJS was assessed within 7, 90, and 30 days of the index date, respectively. We calculated odds ratios (OR) with 95% confidence intervals (CIs) using conditional logistic regression to assess the risk of outcomes associated with propacetamol. Results: We identified cases of anaphylaxis (n=61), thrombosis (n=95), and SJS (n=1) and matched them to controls (173, 268, and 4, respectively). In the nested case-control analysis, the ORs for anaphylaxis and SJS were inestimable given the small number of propacetamol users during the risk period; meanwhile, the OR for thrombosis was 1.60 (95% CI 0.71–3.62). In the CTC design, the effect estimate was only estimated for thrombosis (OR 0.56, 95% CI 0.09–3.47). Conclusion In both nested case-control and CTC analyses, propacetamol was not associated with an increased risk of anaphylaxis, thrombosis, or SJS. The findings from this study, which used routinely collected clinical data, provide reassuring real-world evidence regarding the safety of propacetamol in a nationwide population to support regulatory decision-making.

STATs (signal transducers and activators of transcription) are proteins with dual functions: signal transducers in the cytoplasm and transcriptional activators in the nucleus. STAT proteins act as transcription factors activated by phosphorylation on its tyrosine residues upon stimulation by various cytokines. The phosphorylated STAT molecules then form homo- or heterodimers through SH2-mediated interaction and translocate into the nucleus to activate the transcription of various target genes. STAT5 recognizes the interferon-gamma activated site TTCNNNGAA (GAS sequence) in the promoter region of the beta-casein gene. Except for prolactin-dependent beta-casein production in mammary gland cells, the biological consequences of STAT5a activation in various systems are not clear. Here we showed that STAT5a was phosphorylated 10 min after desferrioxamine (DFO) treatment, and reached a maximum induction at 4 h in mammary epithelial cells (HC11) and transfected COS-7 cells. Under hypoxic conditions (2% O2), a maximal phosphorylation of STAT5a was observed within 6 h. EMSA (electrophoretic mobility shift assay) showed that DFO or hypoxia enhanced the binding activities of STAT5a DNA to beta-casein gene promoter in mammary epithelial cells (HC11) and transfected COS-7 cells. These results showed that DFO or hypoxia induces tyrosine phosphorylation of STAT5a and also increases the binding activity of STAT5a DNA in mammary epithelial cells. Our data suggest that the STAT5 may act as a mediator in hypoxia-mediated gene expression.
Animals ; Anoxia/*genetics/*metabolism ; Caseins/genetics ; Cell Line ; DNA/genetics/metabolism ; DNA-Binding Proteins/*metabolism ; Deferoxamine/pharmacology ; Epithelial Cells/drug effects/*metabolism ; Gene Expression Regulation ; Mammary Glands, Animal/cytology/*metabolism ; Mice ; Phosphorylation/drug effects ; Phosphotyrosine/metabolism ; Promoter Regions (Genetics)/genetics ; Protein Binding ; Response Elements/*genetics ; Support, Non-U.S. Gov't ; Trans-Activators/*metabolism

Hypoxia, a common consequence of solid tumor growth in breast cancer or other cancers, serves to propagate a cascade of molecular pathways which include angiogenesis, glycolysis, and various cellcycle control proteins. As we have shown previously, hypoxia activates STAT5 (signal transducer and activator of transcription 5) and increases its binding activity to the GAS element in mammary epithelial cells. In this study we attempted to elucidate the mechanism by which cyclin D1 is regulated by the STAT5 protein under hypoxic conditions. Our data demonstrate that hypoxia (2% O2) or desferrioxamine (DFO) induces tyrosine and serine phosphorylation of STAT5 in human breast cancer cells (MCF-7) and mammary epithelial cells (HC11). Imunoprecipitation and subsequent Western analysis showed that Jak2 leads to the tyrosine phosphorylation and activation of STAT5a or STAT5b under hypoxic conditions. Using a transfected COS-7 cell model system, we demonstrate that the activity of a cyclin D1 promoter-luciferase construct increased under hypoxic conditions or DFO treatment. The activity of the STAT5b/cyclin D1 promoter increased significantly by 12 h of hypoxia, whereas the activity of the STAT5a/cyclin D1 promoter was unaffected under hypoxic conditions. These increases in promoter activity are predominantly mediated by the Jak2/ STAT5b signaling pathway. We have shown by EMSA that hypoxia induces STAT5 to bind to the cyclin D1 promoter (GAS-1) in MCF-7 and HC11 cells. These data suggest that STAT5b may mediate the transcriptional activation of cyclin D1 after hypoxic stimulation.
Anaerobiosis/genetics ; Animals ; Breast Neoplasms/*genetics/metabolism ; COS Cells ; Cell Hypoxia/genetics ; Cercopithecus aethiops ; Cyclin D1/*genetics ; Deferoxamine/pharmacology ; Female ; *Gene Expression Regulation, Neoplastic ; Humans ; Phosphorylation/drug effects ; Promoter Regions (Genetics) ; Protein-Tyrosine Kinase/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Research Support, Non-U.S. Gov't ; Serine/metabolism ; Tumor Cells, Cultured ; Tyrosine/metabolism