Purpose: Previous studies from mostly Western populations have suggested possible associations between obesity and melanoma risk. This study aimed to investigate associations between obesity status and melanoma using a nationwide cohort of Koreans. Materials and Methods: A total of 4,441,403 adults who received a national health examination in 2012 were included from the Korean National Health Insurance Service database, and followed until December 31, 2022. Obesity status was defined based on the body mass index at the baseline health examination. Cox proportional hazards analyses were performed to evaluate associations between obesity status and incident melanoma, with adjustment for confounders. Stratified analyses were performed by sex and menopausal status (in women). Results: Overall, melanoma risk increased according to obesity status (p for trend=0.024); adjusted hazard ratios (95% confidence intervals) for melanoma risk were 0.766 (0.438–1.340) in underweight; 1.292 (1.072–1.557) in overweight; 1.202 (1.002–1.442) in obesity; and 1.191 (0.798–1.778) in severe obesity compared to normal weight (reference). In stratified analyses, similar trends to those of the overall study population were observed among men and premenopausal women (p for trend=0.052 in men and 0.036 in premenopausal women). Among premenopausal women, the risk of melanoma increased linearly with obesity status. Meanwhile, among postmenopausal women, melanoma risk showed no significant difference or trend according to obesity status. Conclusion Overweight and obesity were associated with increased risk of melanoma in a population-based cohort of Koreans. Obese individuals, especially men and premenopausal women, may require more thorough prevention and screening strategies for melanoma.

Objectives: The association between statin use and depression is well studied, but the studies on the association of statin use and bipolar disorders are limited. Thus, we aimed to investigate the effects of taking statin on risk of bipolar disorder using national claims data of South Korea. Methods: A total of 5713871 subjects who did not take statin and were not diagnosed with bipolar disorder before the health examination were included. Among eligible subjects, 315537 subjects started taking statin within 1 year after taking the health examination and 5398334 subjects did not. After 9 years of follow-up, the incidence of bipolar disorder was determined for each group. Results: Compared to subjects who were not exposed to statin, subjects who were exposed to statin showed a greater incidence of bipolar disorder and an increased risk of bipolar disorder (hazard ratio [HR]: 1.66; 95% confidence interval [CI]: 1.58 to 1.75), and after adjusting for age, sex, low income, regular exercise, smoking, drinking, diabetes mellitus, hypertension, body mass index, cholesterol and depression (adjusted HR: 1.32; 95% CI: 1.24 to 1.40). Conclusions This result showed an increased risk of bipolar disorder after taking statin, but the underlying biological mechanism needs further investigations. This study has clinical implications for patients taking statins, which require early assessment and response in addition to drug treatment and lifestyle modification, considering the possibility that unhealthy lifestyle habits may appear as part of the mood symptoms of bipolar disorder.

Purpose: To evaluate how a family history of prostate cancer influences the progression of the disease in individuals with prostate cancer undergoing active surveillance. Materials and Methods: We conducted a thorough literature search in PubMed/MEDLINE, Embase, and Cochrane Library up to June 2023. This systematic review was registered in PROSPERO (CRD42023441853). The study evaluated the effects of family history of prostate cancer (intervention) on disease progression (outcome) in prostate cancer patients undergoing active surveillance (population) and compared them to those without a family history (comparators). For time to disease progression outcomes, the extracted data were synthesized using the inverse variance method on the log hazard ratios scale. Results: A total of eight studies were incorporated into this systematic review and meta-analysis. The combined hazard ratio for unadjusted disease progression was 1.06 (95% confidential interval [CI] 0.66–1.69; p=0.82). The combined hazard ratio for adjusted disease progression was 1.31 (95% CI 1.16–1.48; p<0.0001). All the enlisted studies demonstrated high quality based on the Newcastle–Ottawa scale. The certainty of evidence for univariate and multivariate analysis of disease progression was very low and low, respectively. Publication bias for all studies was not significant. Conclusions For individuals with prostate cancer opting for active surveillance, a family history of prostate cancer may serve as an independent risk factor associated with an elevated risk of disease progression. Clinicians should be counseled about the increased risk of disease progression in patients with a family history of prostate cancer undergoing active surveillance.

Objectives: The association between statin use and depression is well studied, but the studies on the association of statin use and bipolar disorders are limited. Thus, we aimed to investigate the effects of taking statin on risk of bipolar disorder using national claims data of South Korea. Methods: A total of 5713871 subjects who did not take statin and were not diagnosed with bipolar disorder before the health examination were included. Among eligible subjects, 315537 subjects started taking statin within 1 year after taking the health examination and 5398334 subjects did not. After 9 years of follow-up, the incidence of bipolar disorder was determined for each group. Results: Compared to subjects who were not exposed to statin, subjects who were exposed to statin showed a greater incidence of bipolar disorder and an increased risk of bipolar disorder (hazard ratio [HR]: 1.66; 95% confidence interval [CI]: 1.58 to 1.75), and after adjusting for age, sex, low income, regular exercise, smoking, drinking, diabetes mellitus, hypertension, body mass index, cholesterol and depression (adjusted HR: 1.32; 95% CI: 1.24 to 1.40). Conclusions This result showed an increased risk of bipolar disorder after taking statin, but the underlying biological mechanism needs further investigations. This study has clinical implications for patients taking statins, which require early assessment and response in addition to drug treatment and lifestyle modification, considering the possibility that unhealthy lifestyle habits may appear as part of the mood symptoms of bipolar disorder.

Objectives: The association between statin use and depression is well studied, but the studies on the association of statin use and bipolar disorders are limited. Thus, we aimed to investigate the effects of taking statin on risk of bipolar disorder using national claims data of South Korea. Methods: A total of 5713871 subjects who did not take statin and were not diagnosed with bipolar disorder before the health examination were included. Among eligible subjects, 315537 subjects started taking statin within 1 year after taking the health examination and 5398334 subjects did not. After 9 years of follow-up, the incidence of bipolar disorder was determined for each group. Results: Compared to subjects who were not exposed to statin, subjects who were exposed to statin showed a greater incidence of bipolar disorder and an increased risk of bipolar disorder (hazard ratio [HR]: 1.66; 95% confidence interval [CI]: 1.58 to 1.75), and after adjusting for age, sex, low income, regular exercise, smoking, drinking, diabetes mellitus, hypertension, body mass index, cholesterol and depression (adjusted HR: 1.32; 95% CI: 1.24 to 1.40). Conclusions This result showed an increased risk of bipolar disorder after taking statin, but the underlying biological mechanism needs further investigations. This study has clinical implications for patients taking statins, which require early assessment and response in addition to drug treatment and lifestyle modification, considering the possibility that unhealthy lifestyle habits may appear as part of the mood symptoms of bipolar disorder.

Objectives: The association between statin use and depression is well studied, but the studies on the association of statin use and bipolar disorders are limited. Thus, we aimed to investigate the effects of taking statin on risk of bipolar disorder using national claims data of South Korea. Methods: A total of 5713871 subjects who did not take statin and were not diagnosed with bipolar disorder before the health examination were included. Among eligible subjects, 315537 subjects started taking statin within 1 year after taking the health examination and 5398334 subjects did not. After 9 years of follow-up, the incidence of bipolar disorder was determined for each group. Results: Compared to subjects who were not exposed to statin, subjects who were exposed to statin showed a greater incidence of bipolar disorder and an increased risk of bipolar disorder (hazard ratio [HR]: 1.66; 95% confidence interval [CI]: 1.58 to 1.75), and after adjusting for age, sex, low income, regular exercise, smoking, drinking, diabetes mellitus, hypertension, body mass index, cholesterol and depression (adjusted HR: 1.32; 95% CI: 1.24 to 1.40). Conclusions This result showed an increased risk of bipolar disorder after taking statin, but the underlying biological mechanism needs further investigations. This study has clinical implications for patients taking statins, which require early assessment and response in addition to drug treatment and lifestyle modification, considering the possibility that unhealthy lifestyle habits may appear as part of the mood symptoms of bipolar disorder.

Abnormal aggregation of α-synuclein is a key element in the pathogenesis of several neurodegenerative diseases, including Parkinson’s disease (PD), dementia with Lewy bodies, and multiple system atrophy. α-synuclein aggregation spreads through various brain regions during the course of disease progression, a propagation that is thought to be mediated by the secretion and subsequent uptake of extracellular α-synuclein aggregates between neuronal cells. Thus, aggregated forms of this protein have emerged as promising targets for disease-modifying therapy for PD and related diseases. Here, we generated and characterized conformation-specific antibodies that preferentially recognize aggregated forms of α-synuclein. These antibodies promoted phagocytosis of extracellular α-synuclein aggregates by microglial cells and interfered with cell-to-cell propagation of α-synuclein. In an α-synuclein transgenic model, passive immunization with aggregate-specific antibodies significantly ameliorated pathological phenotypes, reducing α-synuclein aggregation, gliosis, inflammation, and neuronal loss. These results suggest that conformation-specific antibodies targeting α-synuclein aggregates are promising therapeutic agents for PD and related synucleinopathies.

Purpose: Natural medicinal plant extracts have recently attracted attention as health beneficial foods and potential therapeutic agents for prevention of various diseases. This study was undertaken to measure the anti-inflammatory effect of the ethanol-water fraction obtained from the above-ground portion of Spiraea prunifolia var. simpliciflora, a wild-growing plant in Korea. The final fraction used in this study was the H 2 O-EtOH (40:60) fraction (SP60), which had the highest antioxidant activity, as determined in previous studies. Methods: The amounts of nitric oxide (NO), tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β production were measured in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells exposed to SP60. Western blot was performed to measure the expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and the activation of nuclear factor (NF)-κB. Results: SP60 exerted no cytotoxicity up to concentrations of 125 μg/mL. The levels of inflammatory cytokines, such as NO, TNF-α, IL-6, and IL-1β, were significantly decreased in LPS-stimulated RAW264.7 cells exposed to SP60. In addition, the expression levels of iNOS, COX-2, and phosphorylated p65 showed a concentration-dependent decrease subsequent to SP60 treatment. These results indicate that SP60 inhibits the LPS-induced production of inflammatory cytokines, iNOS, and COX-2, by inhibiting the activation of NF-κB, which is responsible for the expression of inflammatory mediators. Conclusion The results presented in this study indicate that the H 2 O-EtOH (40:60) fraction (SP60) extracted from the above-ground portion of Spiraea prunifolia var. simpliciflora has

Purpose: This study assessed the relationship between newly developed normal-tension glaucoma (NTG) and androgen deprivation therapy (ADT) in patients with prostate cancer. Materials and Methods: A retrospective population-based cohort study was performed. During the period between 2008 and 2017, a total of 218203 prostate cancer patients were identified in a nationwide claims database in the Republic of Korea. The final analysis included 170874 patients (42909 in the ADT group, 127965 in the control group) after applying the inclusion and exclusion criteria. The incidences of NTG according to ADT duration were compared with controls. Exact matching was conducted to adjust comorbidities between cohorts. Cox proportional hazard regression models were performed after controlling for latent confounding factors, and adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the incidence of NTG according to ADT were obtained. Results: In the matched cohort, the ADT group was associated with a significantly reduced risk of NTG in multivariable analysis compared to the control group. The risk of NTG decreased in patients who underwent ADT for less than 2 years (HR=0.824; 95% CI, 0.682–0.995; p=0.0440) and in those using ADT over 2 years (HR=0.796; 95% CI, 0.678–0.934; p=0.0051), compared to the controls. Conclusion Medical castrations for patients with prostate cancer results in a lower incidence of newly diagnosed NTG compared to no ADT. These findings suggest that testosterone may be involved in the pathogenesis of NTG.