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.

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.

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.

Purpose: Smoking is causally related to alcohol use disorder. Although polycyclic aromatic hydrocarbons (PAHs) are major neurotoxic pollutants in tobacco smoke, evidence is lacking on the role of PAHs in the relationship between smoking and alcohol use disorder. This study investigated the types of PAHs associated with smoking and whether exposure to those PAHs mediated the effect of smoking on alcohol use disorder. Materials and Methods: A total of 968 male firefighters were analyzed. Smoking history and cumulative pack-years were obtained using self-reported questionnaires. Alcohol use disorder was defined using the Alcohol Use Disorder Identification Test.PAH exposure was assessed by urinary metabolites. Regression analyses were performed between exposure (smoking), outcome (alcohol use disorder), and mediator (PAH metabolites) variables. A mediation analysis was performed to test the indirect effect of PAH metabolites on the association between smoking and alcohol use disorder. All analyses were repeated for 770 participants who were followed up after 2 years, while alcohol use disorder was redefined from follow-up data ensuring the temporal sequence of the variables. Results: Both 2-naphthol [β=0.78, 95% confidence interval (CI): 0.59–0.98] and 2-hydroxyfluorene (β=0.69, 95% CI: 0.56–0.82) were associated with smoking history. Furthermore, 2-naphthol and 2-hydroxyfluorene mediated the associations of smoking history (proportion mediated: 14.2%, 23.6% respectively) or cumulative pack-years (proportion mediated: 14.4%, 25.4% respectively) with alcohol use disorder. The results were consistent in longitudinal settings. Conclusion Exposure to PAHs mediated the association between tobacco smoking and alcohol use disorder. PAH exposure from tobacco may increase the risk of addictive disorders.

Purpose: Smoking is causally related to alcohol use disorder. Although polycyclic aromatic hydrocarbons (PAHs) are major neurotoxic pollutants in tobacco smoke, evidence is lacking on the role of PAHs in the relationship between smoking and alcohol use disorder. This study investigated the types of PAHs associated with smoking and whether exposure to those PAHs mediated the effect of smoking on alcohol use disorder. Materials and Methods: A total of 968 male firefighters were analyzed. Smoking history and cumulative pack-years were obtained using self-reported questionnaires. Alcohol use disorder was defined using the Alcohol Use Disorder Identification Test.PAH exposure was assessed by urinary metabolites. Regression analyses were performed between exposure (smoking), outcome (alcohol use disorder), and mediator (PAH metabolites) variables. A mediation analysis was performed to test the indirect effect of PAH metabolites on the association between smoking and alcohol use disorder. All analyses were repeated for 770 participants who were followed up after 2 years, while alcohol use disorder was redefined from follow-up data ensuring the temporal sequence of the variables. Results: Both 2-naphthol [β=0.78, 95% confidence interval (CI): 0.59–0.98] and 2-hydroxyfluorene (β=0.69, 95% CI: 0.56–0.82) were associated with smoking history. Furthermore, 2-naphthol and 2-hydroxyfluorene mediated the associations of smoking history (proportion mediated: 14.2%, 23.6% respectively) or cumulative pack-years (proportion mediated: 14.4%, 25.4% respectively) with alcohol use disorder. The results were consistent in longitudinal settings. Conclusion Exposure to PAHs mediated the association between tobacco smoking and alcohol use disorder. PAH exposure from tobacco may increase the risk of addictive disorders.

Purpose: Smoking is causally related to alcohol use disorder. Although polycyclic aromatic hydrocarbons (PAHs) are major neurotoxic pollutants in tobacco smoke, evidence is lacking on the role of PAHs in the relationship between smoking and alcohol use disorder. This study investigated the types of PAHs associated with smoking and whether exposure to those PAHs mediated the effect of smoking on alcohol use disorder. Materials and Methods: A total of 968 male firefighters were analyzed. Smoking history and cumulative pack-years were obtained using self-reported questionnaires. Alcohol use disorder was defined using the Alcohol Use Disorder Identification Test.PAH exposure was assessed by urinary metabolites. Regression analyses were performed between exposure (smoking), outcome (alcohol use disorder), and mediator (PAH metabolites) variables. A mediation analysis was performed to test the indirect effect of PAH metabolites on the association between smoking and alcohol use disorder. All analyses were repeated for 770 participants who were followed up after 2 years, while alcohol use disorder was redefined from follow-up data ensuring the temporal sequence of the variables. Results: Both 2-naphthol [β=0.78, 95% confidence interval (CI): 0.59–0.98] and 2-hydroxyfluorene (β=0.69, 95% CI: 0.56–0.82) were associated with smoking history. Furthermore, 2-naphthol and 2-hydroxyfluorene mediated the associations of smoking history (proportion mediated: 14.2%, 23.6% respectively) or cumulative pack-years (proportion mediated: 14.4%, 25.4% respectively) with alcohol use disorder. The results were consistent in longitudinal settings. Conclusion Exposure to PAHs mediated the association between tobacco smoking and alcohol use disorder. PAH exposure from tobacco may increase the risk of addictive disorders.

Purpose: Smoking is causally related to alcohol use disorder. Although polycyclic aromatic hydrocarbons (PAHs) are major neurotoxic pollutants in tobacco smoke, evidence is lacking on the role of PAHs in the relationship between smoking and alcohol use disorder. This study investigated the types of PAHs associated with smoking and whether exposure to those PAHs mediated the effect of smoking on alcohol use disorder. Materials and Methods: A total of 968 male firefighters were analyzed. Smoking history and cumulative pack-years were obtained using self-reported questionnaires. Alcohol use disorder was defined using the Alcohol Use Disorder Identification Test.PAH exposure was assessed by urinary metabolites. Regression analyses were performed between exposure (smoking), outcome (alcohol use disorder), and mediator (PAH metabolites) variables. A mediation analysis was performed to test the indirect effect of PAH metabolites on the association between smoking and alcohol use disorder. All analyses were repeated for 770 participants who were followed up after 2 years, while alcohol use disorder was redefined from follow-up data ensuring the temporal sequence of the variables. Results: Both 2-naphthol [β=0.78, 95% confidence interval (CI): 0.59–0.98] and 2-hydroxyfluorene (β=0.69, 95% CI: 0.56–0.82) were associated with smoking history. Furthermore, 2-naphthol and 2-hydroxyfluorene mediated the associations of smoking history (proportion mediated: 14.2%, 23.6% respectively) or cumulative pack-years (proportion mediated: 14.4%, 25.4% respectively) with alcohol use disorder. The results were consistent in longitudinal settings. Conclusion Exposure to PAHs mediated the association between tobacco smoking and alcohol use disorder. PAH exposure from tobacco may increase the risk of addictive disorders.

Purpose: Smoking is causally related to alcohol use disorder. Although polycyclic aromatic hydrocarbons (PAHs) are major neurotoxic pollutants in tobacco smoke, evidence is lacking on the role of PAHs in the relationship between smoking and alcohol use disorder. This study investigated the types of PAHs associated with smoking and whether exposure to those PAHs mediated the effect of smoking on alcohol use disorder. Materials and Methods: A total of 968 male firefighters were analyzed. Smoking history and cumulative pack-years were obtained using self-reported questionnaires. Alcohol use disorder was defined using the Alcohol Use Disorder Identification Test.PAH exposure was assessed by urinary metabolites. Regression analyses were performed between exposure (smoking), outcome (alcohol use disorder), and mediator (PAH metabolites) variables. A mediation analysis was performed to test the indirect effect of PAH metabolites on the association between smoking and alcohol use disorder. All analyses were repeated for 770 participants who were followed up after 2 years, while alcohol use disorder was redefined from follow-up data ensuring the temporal sequence of the variables. Results: Both 2-naphthol [β=0.78, 95% confidence interval (CI): 0.59–0.98] and 2-hydroxyfluorene (β=0.69, 95% CI: 0.56–0.82) were associated with smoking history. Furthermore, 2-naphthol and 2-hydroxyfluorene mediated the associations of smoking history (proportion mediated: 14.2%, 23.6% respectively) or cumulative pack-years (proportion mediated: 14.4%, 25.4% respectively) with alcohol use disorder. The results were consistent in longitudinal settings. Conclusion Exposure to PAHs mediated the association between tobacco smoking and alcohol use disorder. PAH exposure from tobacco may increase the risk of addictive disorders.

Background/Aims: The prevalence and incidence of ulcerative colitis (UC) in Korea is increasing. Each patient has a different disease course and treatment response. Recently, with the development of biologic agents, histological remission has become a treatment goal. In this study, we aimed to identify the predictors of histological remission after first-line biologic agent treatment in patients with biologic agent-naïve UC. Methods: We retrospectively analyzed the medical records of 92 patients who had been diagnosed with UC and treated with first-line biologic agent treatment at our center, between 2015 and 2022. The clinical characteristics, laboratory test results, and endoscopic and biopsy findings were analyzed. Histological remission was defined as the absence of cryptitis, crypt abscesses, and inflammatory cells on histology. Univariate and multivariate logistic regression analyses were performed to identify the predictors of histological remission after first-line treatment. Results: Of the total 92 patients, 25 (27.2%) achieved histological remission. Each cohort had a varied body mass index (BMI) distribution, with a statistically significant overweight ratio, as defined by the Asian-Pacific BMI category of 23–25 kg/m2, of 48.0% in the histological remission cohort (P= 0.026). A causal correlation between the overweight category and histological remission was confirmed (odds ratio, 3.883; 95% confidence interval, 1.141–13.212; P= 0.030). Conclusions We confirmed that the overweight category was a predictor of histological remission after first-line treatment with a biological agent. However, as BMI does not account for skeletal muscle mass, future studies are required to confirm the correlation between skeletal muscle mass and histological remission.

Safe and effective sedation depends on various factors, such as the choice of sedatives, sedation techniques used, experience of the sedation provider, degree of sedation-related education and training, equipment and healthcare worker availability, the patient’s underlying diseases, and the procedure being performed. The purpose of these evidence-based multidisciplinary clinical practice guidelines is to ensure the safety and efficacy of sedation, thereby contributing to patient safety and ultimately improving public health. These clinical practice guidelines comprise 15 key questions covering various topics related to the following: the sedation providers; medications and equipment available; appropriate patient selection; anesthesiologist referrals for high-risk patients; pre-sedation fasting; comparison of representative drugs used in adult and pediatric patients; respiratory system, cardiovascular system, and sedation depth monitoring during sedation; management of respiratory complications during pediatric sedation; and discharge criteria. The recommendations in these clinical practice guidelines were systematically developed to assist providers and patients in sedation-related decision making for diagnostic and therapeutic examinations or procedures. Depending on the characteristics of primary, secondary, and tertiary care institutions as well as the clinical needs and limitations, sedation providers at each medical institution may choose to apply the recommendations as they are, modify them appropriately, or reject them completely.