Background. Mitochondria play a critical role in ischemia-reperfusion injury of the heart. The purpose of the present study was to analyze the intracellular region-specific functional state of mitochondria after cold ischemia-reperfusion in a rat heart transplant model.Methods. Imaging of the mitochondrial functional state in situ in nonfixed myocardial fibers was performed by confocal microscopy of mitochondrial flavoprotein autofluorescence as redox state indicator; fluorescence of Rhod-2, a specific probe for mitochondrial calcium; and of tetramethylrhodamine ethyl ester fluorescence to monitor the mitochondrial membrane potential.Results. This imaging demonstrated that, in contrast to control fibers, 10-hr heart cold storage, heterotopic cardiac transplantation, and 24-hr reperfusion result in a highly heterogeneous mitochondrial functional state (mitochondrial calcium content, redox state, and inner membrane potential), thus suggesting local permeability transitions and heterogeneous mitochondrial damage.Conclusions. Imaging of in situ mitochondria allows topologic assessment of mitochondrial defects and heterogeneity, consequently providing new insights into the mechanisms of cardiac ischemia-reperfusion injury.
Background and aims: Surgical resection is currently the cornerstone of liver tumor treatment in children. In adults radiofrequency ablation (RFA) is an established minimally invasive treatment option for small focal liver tumors. Multiprobe stereotactic RFA (SRFA) with intraoperative image fusion to confirm ablation margins allows treatment for large lesions. We describe our experience with SRFA in children with liver masses. Methods: SRFA was performed in 10 patients with a median age of 14 years (range 0.5-17.0 years) suffering from liver adenoma (n ¼ 3), hepatocellular carcinoma (n ¼ 1), hepatoblastoma (n ¼ 2), myofibroblastic tumor (n ¼ 1), hepatic metastases of extrahepatic tumors (n ¼ 2) and infiltrative hepatic cysts associated with alveolar echinococcosis (n ¼ 1). Overall, 15 lesions with a mean lesion size of 2.6 cm (range 0.7-9.5 cm) were treated in 11 sessions. Results: The technical success rate was 100%, as was the survival rate. No transient adverse effects higher than grade II (Clavien and Dindo) were encountered after interventions. The median hospital stay was 5 d (range 2-33 d). In two patients who subsequently underwent transplant hepatectomy complete ablation was histologically confirmed. Follow-up imaging studies (median 55 months, range 18-129 months) revealed no local or distant recurrence of disease in any patient. Conclusions: SRFA is an effective minimal-invasive treatment option in pediatric patients with liver tumors of different etiologies.
Peptic ulcer in the excluded segment of a gastric bypass has been reported in the literature in only 17 cases. We report a 54-year-old woman with a perforated duodenal ulcer, who had undergone laparoscopic Roux-en-Y gastric bypass surgery for morbid obesity 15 months previously. She was successfully treated by a laparoscopic repair of the perforated duodenal ulcer.
Summary Chronic rejection (CR) remains an unsolved hurdle for long‐term heart transplant survival. The effect of cold ischemia (CI) on progression of CR and the mechanisms resulting in functional deficit were investigated by studying gene expression, mitochondrial function, and enzymatic activity. Allogeneic (Lew→F344) and syngeneic (Lew→Lew) heart transplantations were performed with or without 10 h of CI. After evaluation of myocardial contraction, hearts were excised at 2, 10, 40, and 60 days for investigation of vasculopathy, gene expression, enzymatic activities, and mitochondrial respiration. Gene expression studies identified a gene cluster coding for subunits of the mitochondrial electron transport chain regulated in response to CI and CR. Myocardial performance, mitochondrial function, and mitochondrial marker enzyme activities declined in all allografts with time after transplantation. These declines were more rapid and severe in CI allografts (CR‐CI) and correlated well with progression of vasculopathy and fibrosis. Mitochondria related gene expression and mitochondrial function are substantially compromised with the progression of CR and show that CI impacts on progression, gene profile, and mitochondrial function of CR. Monitoring mitochondrial function and enzyme activity might allow for earlier detection of CR and cardiac allograft dysfunction.
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