Background: Rosacea is a chronic inflammatory skin disorder characterized by erythema, papules, ocular symptoms, and heightened sensitivity. Patients with neurogenic symptoms such as burning or stinging remain particularly difficult to manage. Current guidelines often underrepresent energy-based devices (EBDs), pigmentary sequelae, psychosocial burden, and ocular comorbidities. Objective: To examine Korean dermatologists’ expert perspectives on rosacea management, focusing on skin sensitivity, neurogenic symptoms, pigmentary changes, psychosocial impact, ocular involvement, and EBD use. Methods: A web-based, 29-item survey was administered to 25 board-certified Korean dermatologists (May–June 2025). Quantitative and qualitative responses were analyzed. Results: Erythematotelangiectatic and papulopustular phenotypes with sensitivity skin predominated. EBDs (pulsed dye laser, intense pulsed light) were frequently used but limited by cost and sensitivity issues. Neurogenic symptoms were recognized but rarely treated with neuromodulators. Post-inflammatory hyperpigmentation was infrequent, yet monitoring was inconsistent.Psychosocial and ocular aspects were acknowledged but seldomly systematically addressed.Respondents expressed interest in emerging adjunctive treatments such as cold plasma, skin boosters, and holistic care approaches. Conclusion Korean dermatologists adopt individualized strategies for rosacea, yet practice gaps remain regarding neurogenic symptoms, pigmentary complications, and psychosocial and ocular comorbidities. Findings support the need for updated multidisciplinary, phenotype-driven guidelines aligned with real-world practice.

Delirium is a common acute neuropsychiatric syndrome, and its early detection may improve clinical outcomes. This narrative review synthesized findings from 11 original studies and two systematic reviews that employed wearable sensors (actigraphy) to predict or detect delirium. In surgical, intensive care unit, and geriatric populations, delirium has consistently been associated with disrupted rest–activity rhythms, including lower daytime activity, increased nighttime activity, and fragmented sleep–wake cycles. Characteristic motor patterns also differed based on the motor subtype (hyperactive vs. hypoactive). Several studies have demonstrated that continuous wrist accelerometry can objectively detect the onset of delirium and classify motor subtypes. Notably, one machine learning model showed improved prediction accuracy, increasing from approximately 62% to 74% when motion features were included. Overall, continuous motion monitoring appears feasible and may serve as a promising non-invasive tool for early delirium detection and risk stratification. However, the findings remain heterogeneous, and motion-based algorithms alone show only moderate sensitivity. Further validation in larger and more diverse cohorts, as well as integration with clinical risk factors, is required before clinical implementation.

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 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 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.

Objective: The association of lipid parameters with cardiovascular disease (CVD) and the impact of kidney function on this association have not been thoroughly evaluated in patients with type 2 diabetes mellitus (T2DM). Methods: Using the Korean National Health Insurance Service Cohort database, we identified 2,343,882 subjects with T2DM in 2015–2016. Baseline lipid levels and kidney function were evaluated and followed up until December 2020. Subjects were classified into three groups according to their estimated glomerular filtration rate (eGFR): ≥60, 30–59, or <30 mL/min/ 1.73 m2 . We analyzed the diabetes group with eGFR ≥60 and low-density lipoprotein cholesterol (LDL-C) <70 mg/dL as a reference group. Results: The risk of CVD began to increase at LDL-C ≥100 mg/dL in the eGFR ≥60 mL/min/m2group. The risk of CVD in the eGFR 30–59 mL/min/m2 group was increased by 43%, even in the LDL-C <70 mg/dL, and the risk increased progressively with LDL-C category. Among subjects with eGFR 30–59 mL/min/m2 , LDL-C 70–99, 100–129, 130–159, and ≥160 mg/ dL were significantly associated with the risk of CVD, with hazard ratio (95% confidence interval) of 1.48 (1.43–1.53), 1.54 (1.49–1.60), 1.55 (1.48–1.63), and 1.88 (1.77–2.00), respectively. In the eGFR <30 mL/min/m2 group, a 3.3-fold increased risk of CVD was seen, even at LDL-C <70 mg/dL. Conclusion The cutoff levels of LDL-C that increase CVD risk in patients with T2DM depend on kidney function, which influences the relationship between LDL-C and CVD risk in patients with T2DM.

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: and Purpose The National Brain Biobank of Korea (NBBK) is a brain bank consortium supported by the Korea Disease Control and Prevention Agency and the Korea National Institute of Health, and was launched in 2015 to support research into neurodegenerative disease dementia (NDD). This study aimed to introduce the NBBK and describes clinicopathological correlations based on analyses of data collected from the NBBK. Methods: Four hospital-based brain banks have been established in South Korea: Samsung Medical Center Brain Bank (SMCBB), Seoul National University Hospital Brain Bank (SNUHBB), Pusan National University Hospital Brain Bank (PNUHBB), and Myongji Hospital Brain Bank (MJHBB). Clinical and pathological data were collected from these brain banks using standardized protocols. The prevalence rates of clinical and pathological diagnoses were analyzed in order to characterize the clinicopathological correlations. Results: Between August 2016 and December 2023, 185 brain specimens were collected and pathologically evaluated (SNUHBB: 117; PNUHBB: 27; SMCBB: 34; MJHBB: 7). The age at consent was 70.8±12.6 years, and the age at autopsy was 71.7±12.4 years. The four-most-common clinical diagnoses were Alzheimer’s disease (AD) dementia (20.0%), idiopathic Parkinson’s disease (15.1%), unspecified dementia (11.9%), and cognitively unimpaired (CU) (11.4%).Most cases of unspecified dementia had a pathological diagnosis of central nervous system (CNS) vasculopathy (31.8%) or AD (31.8%). Remarkably, only 14.2% of CU cases had normal pathological findings. The three-most-common pathological diagnoses were AD (26.5%), CNS vasculopathy (14.1%), and Lewy body disease (13.5%). Conclusions These clinical and neuropathological findings provide a deeper understanding of the mechanisms underlying NDD in South Korea.

Gastric cancer is one of the most common cancers in both Korea and worldwide. Since 2004, the Korean Practice Guidelines for Gastric Cancer have been regularly updated, with the 4th edition published in 2022. The 4th edition was the result of a collaborative work by an interdisciplinary team, including experts in gastric surgery, gastroenterology, endoscopy, medical oncology, abdominal radiology, pathology, nuclear medicine, radiation oncology, and guideline development methodology. The current guideline is the 5th version, an updated version of the 4th edition. In this guideline, 6 key questions (KQs) were updated or proposed after a collaborative review by the working group, and 7 statements were developed, or revised, or discussed based on a systematic review using the MEDLINE, Embase, Cochrane Library, and KoreaMed database. Over the past 2 years, there have been significant changes in systemic treatment, leading to major updates and revisions focused on this area.Additionally, minor modifications have been made in other sections, incorporating recent research findings. The level of evidence and grading of recommendations were categorized according to the Grading of Recommendations, Assessment, Development and Evaluation system. Key factors for recommendation included the level of evidence, benefit, harm, and clinical applicability. The working group reviewed and discussed the recommendations to reach a consensus. The structure of this guideline remains similar to the 2022 version.Earlier sections cover general considerations, such as screening, diagnosis, and staging of endoscopy, pathology, radiology, and nuclear medicine. In the latter sections, statements are provided for each KQ based on clinical evidence, with flowcharts supporting these statements through meta-analysis and references. This multidisciplinary, evidence-based gastric cancer guideline aims to support clinicians in providing optimal care for gastric cancer patients.