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.

Background: Tacrolimus is a key immunosuppressant after liver transplantation.Although guideline-recommended trough levels are 4–10 ng/mL, concerns about nephrotoxicity, metabolic complications, and malignancies have led to interest in minimizing tacrolimus use. However, the effects of lower tacrolimus levels on graft rejection and hepatocellular carcinoma (HCC) recurrence remain unclear. Methods: We conducted a single-center, retrospective study of adult patients (≥19 years) who underwent living donor liver transplantation between January 2000 and December 2021. Patients were divided into low tacrolimus (FK) (<6 ng/mL) and high FK (≥6 ng/mL) groups based on tacrolimus levels measured 1–2 years post-transplantation. We analyzed overall survival, biopsy-proven rejection-free survival, and HCC recurrence-free survival in relevant subgroups. Cox proportional hazards regression identified predictors of mortality, rejection, and HCC recurrence. Results: Among 1,117 recipients, 941 were in the low FK group and 176 in the high FK group. Landmark analysis showed significantly better 10-year overall survival in the low FK group (82.8% vs. 68.8%, p=0.016), while rejection-free survival did not differ significantly beyond 2 years (p=0.098), despite early separation favoring the low FK group (p<0.001). Higher tacrolimus levels independently predicted increased mortality (hazard ratio [HR]=1.98, 95% confidence interval [CI] 1.35–2.89; p<0.001) and rejection (HR=2.20, 95% CI 1.48–3.27; p<0.001). Among 614 HCC patients, landmark analysis revealed no significant difference in recurrence-free survival (77.7% vs. 81.2%, p=0.288) or overall survival (77.3% vs. 65.8%, p=0.215), and FK levels were not independently associated with either outcome. Conclusion Maintaining tacrolimus levels below 6 ng/mL was associated with better survival and rejection outcomes without increasing HCC recurrence, suggesting dose minimization may be feasible in selected patients.

In liver transplantation, the primary concern is to ensure an adequate future liver remnant (FLR) volume for the donor, while selecting a graft of sufficient size for the recipient. The living donor–resection and partial liver segment 2−3 transplantation with delayed total hepatectomy (LD−RAPID) procedure offers a potential solution to expand the donor pool for living donor liver transplantation (LDLT).We report the first case involving a cirrhotic patient with autoimmune hepatitis and hepatocellular carcinoma, who underwent left lobe LDLT using the LD−RAPID procedure. The living liver donor (LLD) underwent a laparoscopic left hepatectomy, including middle hepatic vein. The resection on the recipient side was an extended left hepatectomy, including the middle hepatic vein orifice and caudate lobe. At postoperative day 7, a computed tomography scan showed hypertrophy of the left graft from 320 g to 465 mL (i.e., a 45.3% increase in graft volume body weight ratio from 0.60% to 0.77%). After a 7-day interval, the diseased right lobe was removed in the second stage surgery. The LD−RAPID procedure using left lobe graft allows for the use of a small liver graft or small FLR volume in LLD in LDLT, which expands the donor pool to minimize the risk to LLD by enabling the donation of a smaller liver portion.

Purpose: : This study aimed to assess the effectiveness of an advanced practice nurse (APN)-driven ventilator weaning protocol for patients undergoing cardiac surgeries. Methods: : A retrospective analysis was conducted on 226 patients admitted to the intensive care unit (ICU) of a tertiary hospital between January and June 2020, following a cardiac surgery. Patients were divided into an APN protocol-applied group (experimental group, n=152) and a control group managed based on doctors' judgment (n=74). Ventilator weaning criteria and clinical outcomes, including duration of ventilation, length of ICU stay, and rate of reintubation, were compared between the two groups. Results: : Patients in the control group were older and had a higher incidence of massive bleeding from chest tube drainage (＞100 cc/hr) at baseline. The average duration of ventilation was significantly shorter in the experimental group compared to the control group (7.44 vs. 21.61 hours, p ＜.001). Furthermore, the mean length of ICU stay was shorter in the experimental group compared to the control group (47.96 vs. 77.97 hours, p ＜.001). There was no difference in the rate of reintubation between the two groups. Conclusion : These findings suggest that an APN-driven ventilator weaning protocol can improve clinical outcomes without significant complications. These results support the adoption of APN-driven mechanical ventilator weaning protocols in clinical practice.

Purpose: To determine the efficacy of immediate pars plana vitrectomy as the primary treatment for acute endophthalmitis in patients with a visual acuity (VA) of hand motion (HM) or better. Methods: A total of 149 patients who were referred to a single center for acute endophthalmitis after cataract surgery over the 13-year study period were retrospectively analyzed. Only patients presenting with a VA of at least HM were included. Patients were initially treated with either primary vitrectomy or intravitreal antibiotic injection alone, and their visual outcomes and reintervention rates after initial treatment were compared. Results: There was no significant difference in the proportion of good (final VA ≥20 / 40) and poor (VA ≤ counting finger) visual outcomes between the groups. However, subgroup analysis of patients with a VA of HM (92 eyes) showed that the incidence of reintervention (14 of 72 eyes [19.4%] vs. 9 of 20 eyes [45.0%]) and poor visual outcomes (10 of 72 eyes [13.9%] vs. 8 of 20 eyes [40.0%]) were lower after prompt vitrectomy than after intravitreal antibiotic injection alone (p = 0.019 and p = 0.022, respectively). For those with a VA of at least counting finger, no significant difference was observed between the groups. Conclusions For patients with endophthalmitis presenting with a VA of HM, performing a prompt vitrectomy reduced the incidence of reintervention and poor visual outcomes than the administration of intravitreal antibiotics alone. Our results suggest that primary vitrectomy for patients with endophthalmitis presenting with a VA of HM could be more beneficial than intravitreal antibiotic injection alone.

Purpose: The effects of aerobic exercise training on soleus muscle morphology, mitochondria-mediated apoptotic signaling, and atrophy/hypertrophy signaling in ovariectomized rat skeletal muscle were investigated. Methods: Female Sprague-Dawley rats were divided into control (CON), ovariectomy (OVX), and ovariectomy plus exercise (OVX+EX) groups. After ovarian excision, exercise training was performed using a rat treadmill at 20 m/min, 50 min/day, 5 days/week for 12 weeks. Protein levels of mitochondria-mediated apoptotic signaling and atrophy/hypertrophy signaling in the skeletal muscle (soleus) were examined through western immunoblot analysis. Results: The number of myocytes and myocyte cross-sectional area (CSA) were increased and the extramyocyte space was decreased in the OVX group compared to those in the CON group. However, aerobic exercise training significantly increased myocyte CSA and decreased extramyocyte space in the OVX+EX group compared to those in the OVX group. The protein levels of proapoptotic signaling and muscle atrophy signaling were significantly increased, whereas the protein levels of muscle hypertrophy signaling were significantly decreased in the OVX group compared to that in the CON group. Aerobic exercise training significantly decreased the protein levels of proapoptotic signaling and increased the protein level of antiapoptotic protein in the OVX+EX group compared to that in the OVX group. Aerobic exercise training significantly increased the protein levels of hypertrophy signaling and decreased protein levels of atrophy signaling in the OVX+EX group compared to those in the OVX group. Conclusions Treadmill exercise improved estrogen deficiency-induced impairment in skeletal muscle remodeling, mitochondria-mediated apoptotic signaling, and atrophy/hypertrophy signaling in skeletal muscle.