Background: Long working hours have been associated with adverse physical and mental health outcomes; however, evidence regarding their relationship with satisfaction with work environment remains limited, particularly when long working hours are defined using a specific daily threshold. This study examined the association between working ≥10 hours per day and satisfaction with work environment among Korean wage workers, focusing on the cumulative number of such workdays per month. Methods: This cross-sectional study analyzed data from the 7th Korean Working Conditions Survey. A total of 24,269 wage workers aged ≥18 years were included after excluding self-employed workers, unpaid family workers, shift workers, and respondents with missing data. Working ≥10 hours per day was categorized as 0, 1–9, and ≥10 days per month. Satisfaction with work environment was categorized as satisfied or dissatisfied. Multiple logistic regression analyses were conducted to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for dissatisfaction with work environment according to the number of long working days, adjusting for demographic and occupational characteristics. Results: Compared with workers who did not work ≥10 hours per day, those who worked 1–9 days and ≥10 days per month showed progressively higher levels of dissatisfaction with work environment. After adjustment for demographic and occupational factors, the odds of dissatisfaction with work environment were significantly higher among workers who worked ≥10 hours per day for 1–9 days per month (OR: 1.380; 95% CI: 1.145–1.665) and ≥10 days per month (OR: 2.106; 95% CI: 1.627–2.725), demonstrating a dose–response relationship. Conclusions Among the analytic sample of Korean wage workers included in this study, working ≥10 hours per day was associated with greater dissatisfaction with work environment, with a dose–response pattern according to the number of long working days per month.

Objective: This study aimed to assess the association between exposure to gadolinium-based contrast agents (GBCAs) and the risk of parkinsonism according to the GBCA type. Materials and Methods: Individuals aged ≥40 years who underwent first-ever magnetic resonance imaging (MRI) examinations between 2011 and 2014 were identified from the Korean nationwide population-based health insurance claims database and followed up until 2022. Individuals were divided into those who underwent at least one GBCA-enhanced MRI, and those who underwent only non-enhanced MRI. GBCA-exposed individuals were further categorized into those exposed only to linear or macrocyclic GBCAs, after excluding those exposed to both types. The primary event of interest was allcause parkinsonism. Secondary events included all-cause parkinsonism requiring medication, Parkinson’s disease (PD), atypical parkinsonism, and secondary parkinsonism. Hazard ratios (HRs) were estimated using multivariable Cox proportional hazard regression models for exposure to linear and macrocyclic GBCAs, with the non-enhanced MRI group serving as a reference. The models were adjusted for age, sex, smoking status, alcohol consumption, regular exercise, body mass index, estimated glomerular filtration rate, and comorbidities. Subgroup analyses were performed according to age, sex, renal function, and history of cancer. Results: A total of 222,977 individuals were included in this study. Among them, 92,230, 48,335, and 82,412 individuals underwent non-enhanced, linear GBCA-enhanced, and macrocyclic GBCA-enhanced MRI, respectively. Exposure to linear GBCAs slightly increased the risk of all-cause parkinsonism (adjusted HR, 1.13 [97.5% confidence interval, 1.08–1.19]), while exposure to macrocyclic GBCAs did not increase the risk (adjusted HR, 1.00 [97.5% confidence interval, 0.95–1.05]).The results were similar for all-cause parkinsonism requiring medication, PD, and secondary parkinsonism, whereas no significant association was observed for atypical parkinsonism. Conclusion Exposure to linear GBCAs may slightly increase the risk of parkinsonism in adults, whereas exposure to macrocyclic GBCAs may not. Caution should be exercised when using linear GBCAs until further evidence emerges.

Purpose: To develop the 2025 update to the Korean colorectal cancer (CRC) screening guidelines by systematically evaluating recent evidence, integrating domestic data, and addressing changes since the 2015 guideline revision, thereby providing an evidence-based standard for clinicians and policymakers. Methods: A multidisciplinary committee developed the guidelines using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) methodology. The process included formulation of three key questions addressing screening efficacy, diagnostic accuracy, and optimal screening age and interval. A systematic review of international guidelines and primary literature was conducted, yielding 327 eligible studies. In addition, a utility-based analysis using a Markov model was performed to determine optimal screening ages and intervals. Results: The evidence synthesis identified high-certainty evidence supporting the use of the fecal immunochemical test (FIT) for reducing CRC mortality and moderate-certainty evidence for colonoscopy. Evidence for computed tomographic colonography (CTC) and stool DNA testing was rated as very low certainty. Based on the evidence review and cost-utility analysis, the committee conditionally recommends CRC screening for asymptomatic, average-risk adults aged 45–74 years using either colonoscopy every 10 years or FIT every 1–2 years. CTC and stool DNA testing were not recommended owing to insufficient evidence. Conclusion The 2025 Korean Guidelines for Colorectal Cancer Screening present updated, evidence-based recommendations tailored to the domestic healthcare context. By conditionally endorsing both colonoscopy and FIT for individuals aged 45–74 years, these guidelines aim to improve population-level screening effectiveness and reduce the burden of CRC in South Korea.

Background: The prevalence of diabetes mellitus and early-onset dementia (EOD), defined as dementia diagnosed at an age <65 years, is increasing worldwide, with significant socioeconomic implications. We investigated the association between diabetes, prediabetes, and EOD, focusing on the influence of diabetes duration on EOD risk. Methods: Using the Korean National Health Insurance Service database, we analyzed data from 1,979,509 patients aged 40–60 years who underwent health checkups in 2009. Patients were categorized into five groups: normal, impaired fasting glucose (IFG), newly diagnosed diabetes, diabetes duration <5 years, and diabetes duration ≥5 years. Cox proportional hazard models were used to estimate the adjusted hazard ratios (aHRs) for EOD after adjusting for demographic and clinical covariates. Results: During the observation period (mean 7.75 years), 8,921 patients with EOD were identified. The diabetes group demonstrated a significantly higher incidence of EOD compared to the normal group (aHR, 1.334; 95% confidence interval [CI], 1.226 to 1.451). EOD risk increased with longer diabetes duration, with the highest risk observed in patients with diabetes ≥5 years (aHR, 1.543; 95% CI, 1.368 to 1.741). No significant difference was observed between the IFG and normal groups (aHR, 0.989; 95% CI, 0.938 to 1.043). Additionally, the hypertension group exhibited a significantly higher incidence of EOD compared to the non-hypertension group (aHR, 1.364; 95% CI, 1.291 to 1.442). Conclusion Diabetes is independently associated with increased risk of EOD, and this risk increases with longer diabetes duration. This association remained significant regardless of the presence and duration of hypertension.

In patients with differentiated thyroid cancer (DTC), initial recurrence risk stratification based on clinical, histopathological, and perioperative data remains the key determinant for guiding management strategies during the first 1-2 years post-treatment. However, the adoption of ongoing risk stratification (ORS), which dynamically reassesses risk by integrating longitudinal clinical data and treatment response, enables more precise long-term prognostic assessment and facilitates highly individualized management. Building upon recent guidelines, the 2026 KTA guideline has been further refined by incorporating robust evidence from large-scale national cohorts and comprehensive systematic reviews. These updated recommendations outline contemporary concepts of ORS, risk-adapted TSH suppression targets, optimized surveillance modalities for recurrence detection, and disease-specific long-term follow-up strategies. Reflecting the paradigm shift toward de-escalated treatment, this revision integrates evolved perspectives on TSH suppression intensity, the clinical interpretation of thyroglobulin levels, and tailored follow-up intervals. These evidence-based recommendations aim to minimize unnecessary treatment and excessive surveillance in the large proportion of patients with excellent prognosis after initial therapy, while ensuring that each patient receives appropriately tailored and effective long-term management.

Background and Objectives: Cigarette smoking is a major risk factor for atherosclerosis.Nicotine, a crucial constituent of tobacco, contributes to atherosclerosis development and progression. However, evidence of the association between nicotine and neointima formation is limited. We aimed to evaluate whether nicotine enhances neointimal hyperplasia in the native epicardial coronary arteries of pigs after percutaneous coronary intervention (PCI) with drug-eluting stents (DES). Methods: After coronary angiography (CAG) and quantitative coronary angiography (QCA), we implanted 20 DES into 20 pigs allocated to 2 groups: no-nicotine (n=10) and nicotine (n=10) groups. Post-PCI CAG and QCA were performed immediately. Follow-up CAG, QCA, optical coherence tomography (OCT), and histopathological analyses were performed 2 months post-PCI. Results: Despite intergroup similarities in the baseline QCA findings, OCT analysis showed that the nicotine group had a smaller mean stent and lumen areas, a larger mean neointimal area, greater percent area stenosis, and higher peri-strut fibrin and inflammation scores than the no-nicotine group. In immunofluorescence analysis, the nicotine group displayed higher expression of CD68 and α-smooth muscle actin but lower CD31 expression than the no-nicotine group. Conclusions Nicotine inhibited re-endothelialization and promoted inflammation and NIH after PCI with DES in a porcine model.

Background: Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor erythroid- 2-related factor 2 (NRF2) pathway is a major regulator protecting cells from oxidative and metabolic stress. Studies have revealed that this pathway is involved in mediating resistance to cytotoxic chemotherapy and immunotherapy; however, its implications in oncogene-addicted tumors are largely unknown. This study aimed to elucidate whether this pathway could be a potential therapeutic target for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Methods: We measured the baseline expression of NRF2 using EGFR-mutant parental cells and acquired gefitinib resistant cells. We investigated whether NRF2 inhibition affected cell death in vitro and tumor growth in vivo using a xenograft mouse model, and compared the transcriptional changes before and after NRF2 inhibition. Results: Baseline NRF2 expression was enhanced in PC9 and PC9 with gefitinib resistance (PC9/GR) cells than in other cell lines, with a more prominent expression in PC9/ GR. The NRF2 inhibitor induced NRF2 downregulation and cell death in a dose-dependent manner. Cotreatment with an NRF2 inhibitor enhanced osimertinib-induced cell death in vitro, and potentiated tumor growth inhibition in a PC9/GR xenograft model. Finally, RNA sequencing revealed that NRF2 inhibition resulted in the altered expression of multiple genes involved in various signaling pathways. Conclusion We identified that NRF2 inhibition enhanced cell death and inhibited tumor growth in tyrosine kinase inhibitor (TKI)-resistant lung cancer with EGFR-mutation. Thus, NRF2 modulation may be a novel therapeutic strategy to overcome the resistance to EGFR-TKIs.