RESULTS: Resveratrol significantly reduced cardiac hypertrophy and remodeling in aging hearts. In addition, resveratrol significantly ameliorated aging-induced mitochondrial dysfunction (e.g., decreased oxygen respiration and increased hydrogen peroxide emission) and mitochondria-dependent apoptotic signaling (the Bax/Bcl-2 ratio, mitochondrial permeability transition pore opening sensitivity, and cleaved caspase-3 protein levels).Resveratrol also significantly attenuated aging-induced apoptosis (determined via cleaved caspase-3 staining and TUNEL-positive myonuclei) in cardiac muscles. CONCLUSION This study demonstrates that resveratrol treatment has a beneficial effect on aging-induced cardiac remodeling by ameliorating mitochondrial dysfunction and inhibiting mitochondria-mediated apoptosis in the heart.

RESULTS: Resveratrol significantly reduced cardiac hypertrophy and remodeling in aging hearts. In addition, resveratrol significantly ameliorated aging-induced mitochondrial dysfunction (e.g., decreased oxygen respiration and increased hydrogen peroxide emission) and mitochondria-dependent apoptotic signaling (the Bax/Bcl-2 ratio, mitochondrial permeability transition pore opening sensitivity, and cleaved caspase-3 protein levels).Resveratrol also significantly attenuated aging-induced apoptosis (determined via cleaved caspase-3 staining and TUNEL-positive myonuclei) in cardiac muscles. CONCLUSION This study demonstrates that resveratrol treatment has a beneficial effect on aging-induced cardiac remodeling by ameliorating mitochondrial dysfunction and inhibiting mitochondria-mediated apoptosis in the heart.

RESULTS: Resveratrol significantly reduced cardiac hypertrophy and remodeling in aging hearts. In addition, resveratrol significantly ameliorated aging-induced mitochondrial dysfunction (e.g., decreased oxygen respiration and increased hydrogen peroxide emission) and mitochondria-dependent apoptotic signaling (the Bax/Bcl-2 ratio, mitochondrial permeability transition pore opening sensitivity, and cleaved caspase-3 protein levels).Resveratrol also significantly attenuated aging-induced apoptosis (determined via cleaved caspase-3 staining and TUNEL-positive myonuclei) in cardiac muscles. CONCLUSION This study demonstrates that resveratrol treatment has a beneficial effect on aging-induced cardiac remodeling by ameliorating mitochondrial dysfunction and inhibiting mitochondria-mediated apoptosis in the heart.

RESULTS: Resveratrol significantly reduced cardiac hypertrophy and remodeling in aging hearts. In addition, resveratrol significantly ameliorated aging-induced mitochondrial dysfunction (e.g., decreased oxygen respiration and increased hydrogen peroxide emission) and mitochondria-dependent apoptotic signaling (the Bax/Bcl-2 ratio, mitochondrial permeability transition pore opening sensitivity, and cleaved caspase-3 protein levels).Resveratrol also significantly attenuated aging-induced apoptosis (determined via cleaved caspase-3 staining and TUNEL-positive myonuclei) in cardiac muscles. CONCLUSION This study demonstrates that resveratrol treatment has a beneficial effect on aging-induced cardiac remodeling by ameliorating mitochondrial dysfunction and inhibiting mitochondria-mediated apoptosis in the heart.

RESULTS: Resveratrol significantly reduced cardiac hypertrophy and remodeling in aging hearts. In addition, resveratrol significantly ameliorated aging-induced mitochondrial dysfunction (e.g., decreased oxygen respiration and increased hydrogen peroxide emission) and mitochondria-dependent apoptotic signaling (the Bax/Bcl-2 ratio, mitochondrial permeability transition pore opening sensitivity, and cleaved caspase-3 protein levels).Resveratrol also significantly attenuated aging-induced apoptosis (determined via cleaved caspase-3 staining and TUNEL-positive myonuclei) in cardiac muscles. CONCLUSION This study demonstrates that resveratrol treatment has a beneficial effect on aging-induced cardiac remodeling by ameliorating mitochondrial dysfunction and inhibiting mitochondria-mediated apoptosis in the heart.

This study investigated the molecular mechanism of phenotypic switching of vascular smooth muscle cells (VSMCs), which play a crucial role in vascular remodeling using 9H-Carbazol-3-yl 4-aminobenzoate (CAB). CAB significantly attenuated platelet-derived growth factor (PDGF)-induced VSMC proliferation and migration. CAB suppressed PDGF-induced STAT3 activation by directly binding to the SH2 domain of STAT3. Downregulation of STAT3 phosphorylation by CAB attenuated CIAPIN1/JAK2/STAT3 axis through a decrease in CIAPIN1 transcription. Furthermore, abrogated CIAPIN1 decreased KLF4-mediated VSMC dedifferentiation and increased CDKN1B-induced cell cycle arrest and MMP9 suppression. CAB inhibited intimal hyperplasia in injury-induced neointima animal models by inhibition of the CIAPIN1/JAK2/STAT3 axis. However, CIAPIN1 overexpression attenuated CAB-mediated suppression of VSMC proliferation, migration, phenotypic switching, and intimal hyperplasia. Our study clarified the molecular mechanism underlying STAT3 inhibition of VSMC phenotypic switching and vascular remodeling and identified novel active CAB. These findings demonstrated that STAT3 can be a major regulator to control CIAPIN1/JAK2/STAT3 axis that may be a therapeutic target for treating vascular proliferative diseases.

Purpose: This study aimed to investigate the incidence, risk factors, and clinical course of nonalcoholic fatty liver disease (NAFLD) following pancreaticoduodenectomy, focusing on the role of adjuvant chemotherapy and other metabolic changes. Methods: A retrospective analysis was conducted on 189 patients who underwent pancreaticoduodenectomy between 2013 and 2016. NAFLD was diagnosed using computed tomography (CT) imaging, defined as a liver-tospleen attenuation ratio <0.9. Sarcopenia and sarcopenic obesity were assessed using preoperative CT scans. Logistic regression analysis was performed to identify risk factors for NAFLD development. Results: The cumulative incidence of NAFLD increased over time, with rates of 15.9% at one year, 20.4% at three years, and 35.2% at five years post-pancreaticoduodenectomy. Adjuvant chemotherapy was identified as the only significant independent predictor of NAFLD development (odds ratio, 2.74; 95% confidence interval, 1.16-6.70; P=0.023). No significant associations were found between NAFLD and pancreatic enzyme replacement therapy (PERT), sarcopenia, or sarcopenic obesity. Serial analysis of NAFLD status in long-term survivors revealed dynamic changes, with some patients experiencing spontaneous remission or recurrence. Conclusion NAFLD is a common, progressive complication following pancreaticoduodenectomy, particularly in patients receiving adjuvant chemotherapy. Although no significant associations with PERT or sarcopenia were observed, these areas warrant further investigation. Long-term monitoring and targeted management strategies are recommended to address NAFLD in this population. Future prospective studies are needed to elucidate the natural history and contributing factors of NAFLD after pancreaticoduodenectomy.

Purpose: This study aimed to investigate the incidence, risk factors, and clinical course of nonalcoholic fatty liver disease (NAFLD) following pancreaticoduodenectomy, focusing on the role of adjuvant chemotherapy and other metabolic changes. Methods: A retrospective analysis was conducted on 189 patients who underwent pancreaticoduodenectomy between 2013 and 2016. NAFLD was diagnosed using computed tomography (CT) imaging, defined as a liver-tospleen attenuation ratio <0.9. Sarcopenia and sarcopenic obesity were assessed using preoperative CT scans. Logistic regression analysis was performed to identify risk factors for NAFLD development. Results: The cumulative incidence of NAFLD increased over time, with rates of 15.9% at one year, 20.4% at three years, and 35.2% at five years post-pancreaticoduodenectomy. Adjuvant chemotherapy was identified as the only significant independent predictor of NAFLD development (odds ratio, 2.74; 95% confidence interval, 1.16-6.70; P=0.023). No significant associations were found between NAFLD and pancreatic enzyme replacement therapy (PERT), sarcopenia, or sarcopenic obesity. Serial analysis of NAFLD status in long-term survivors revealed dynamic changes, with some patients experiencing spontaneous remission or recurrence. Conclusion NAFLD is a common, progressive complication following pancreaticoduodenectomy, particularly in patients receiving adjuvant chemotherapy. Although no significant associations with PERT or sarcopenia were observed, these areas warrant further investigation. Long-term monitoring and targeted management strategies are recommended to address NAFLD in this population. Future prospective studies are needed to elucidate the natural history and contributing factors of NAFLD after pancreaticoduodenectomy.

Purpose: In high-risk non-muscle-invasive bladder cancer (NMIBC), intravesical Bacillus Calmette-Guérin (BCG) is the standard adjuvant therapy post-transurethral resection of bladder tumor (TURBT). Intravesical gemcitabine, used as an alternative or second-line therapy amid BCG shortages, lacks outcome studies in the Korean population. Materials and Methods: Patients who received weekly intravesical gemcitabine for 6 weeks after TURBT from 2019 to 2022 were retrospectively investigated. Based on the American Urological Association risk classification, patients with high- or very high-risk NMIBC who refused cystectomy were included. Maintenance treatment was performed depending on their risk. Recurrence was defined as histologic confirmation on subsequent cystoscopic biopsies or TURBT. Disease free survival (DFS) was evaluated by the Kaplan–Meier method. Results: The study included 60 patients, comprising 45 high-risk (group 1) patients with a median age of 76 years and 15 very high-risk (group 2) patients with a median age of 68 years. Among them, 28 patients had previously received intravesical BCG.Over a median follow-up of 22 months, recurrence occurred in 31 patients in group 1 and 11 in group 2. The DFS rates of the highrisk group and the very high-risk group were 57.8% versus 40% at 1 year, 20.7% versus 21.3% at 2 years and 20.7% versus 21.3% at 3 years, respectively (p=0.831). Tis stage (p=0.042) and prostatic urethra invasion (p=0.028) were significant predictors of DFS.Cancer-specific mortality rates were 2.2% in group 1 and 6.7% in group 2 (p=0.441). Conclusions Similar DFS outcome between high-risk and very high-risk patients were observed based on short-term results in Korea. This finding is crucial for clinical practice; however, studies analyzing more patients and long-term outcomes are needed.

Purpose: This study aimed to investigate the incidence, risk factors, and clinical course of nonalcoholic fatty liver disease (NAFLD) following pancreaticoduodenectomy, focusing on the role of adjuvant chemotherapy and other metabolic changes. Methods: A retrospective analysis was conducted on 189 patients who underwent pancreaticoduodenectomy between 2013 and 2016. NAFLD was diagnosed using computed tomography (CT) imaging, defined as a liver-tospleen attenuation ratio <0.9. Sarcopenia and sarcopenic obesity were assessed using preoperative CT scans. Logistic regression analysis was performed to identify risk factors for NAFLD development. Results: The cumulative incidence of NAFLD increased over time, with rates of 15.9% at one year, 20.4% at three years, and 35.2% at five years post-pancreaticoduodenectomy. Adjuvant chemotherapy was identified as the only significant independent predictor of NAFLD development (odds ratio, 2.74; 95% confidence interval, 1.16-6.70; P=0.023). No significant associations were found between NAFLD and pancreatic enzyme replacement therapy (PERT), sarcopenia, or sarcopenic obesity. Serial analysis of NAFLD status in long-term survivors revealed dynamic changes, with some patients experiencing spontaneous remission or recurrence. Conclusion NAFLD is a common, progressive complication following pancreaticoduodenectomy, particularly in patients receiving adjuvant chemotherapy. Although no significant associations with PERT or sarcopenia were observed, these areas warrant further investigation. Long-term monitoring and targeted management strategies are recommended to address NAFLD in this population. Future prospective studies are needed to elucidate the natural history and contributing factors of NAFLD after pancreaticoduodenectomy.