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Fragestellung: Funktionseinschränkung und Instabilität im DRUG infolge einer komplexen distalen Radiusfraktur sind oft Grund für die Vorstellung beim Handchirurgen, da ursächlich eine Schädigung des TFCC vermutet wird. Während die Bedeutung dieser Struktur für die [zum vollständigen Text gelangen Sie über die oben angegebene URL]

Recent anatomical findings have suggested that facial fat distribution is complex and changes with age. Here, the authors developed a grafting technique based on the physiologic distribution and volume changes of facial fat compartments to achieve a youthful and natural-appearing face.Forty cadaveric hemifaces were used for the dissection of fat compartments and neurovascular structures in the midface area. Seventy-eight patients were treated for cheek atrophy using the authors' targeted restoration of midface fat compartment volume. The outcome was evaluated by a two-dimensional assessment, malar lipoatrophy assessment, and a satisfaction survey.The medial and lateral parts of the deep medial cheek fat compartment were separated by a septum arising from the lateral border of the levator anguli oris muscle. The angular vein traveled between the deep medial cheek fat compartment and the buccal fat pad, 12 mm from the maxilla. A total volume of 29.3 ml of fat was grafted per cheek for each patient. A 12-month follow-up revealed an average volume augmentation rate of 27.1 percent. Pleasing and elevated anterior projection of the cheek and ameliorated nasolabial groove were still obvious by 12 months after the procedure. In total, 95.2 percent of the patients were satisfied with their results.The present study provides the anatomical and clinical basis for the concept of compartmentally based fat grafting. It allows for the restoration of facial fat volume close to the physiologic state. With this procedure, a natural and youthful facial contour could be rebuilt with a high satisfaction rate.Therapeutic, IV.

[68Ga]Annexin A5 positron emission tomography (PET) reveals the externalization of phosphatidylserine as a surrogate marker for apoptosis. We tested this technique for therapy monitoring in a murine model of myocardial infarction (MI) including parathyroid hormone (PTH) treatment. MI was induced in mice, and they were assigned to the saline or the PTH group. On day 2, they received [68Ga]annexin A5 PET or histofluorescence TUNEL staining. Mice had 2-deoxy-2-[18F]fluoro-D-glucose (FDG)-PET examinations on days 6 and 30 for calculation of the left ventricular ejection fraction and infarct area. [68Ga]Annexin A5 uptake was 7.4 ± 1.3 %ID/g within the infarction for the controls and 4.5 ± 1.9 %ID/g for the PTH group (p = .013). TUNEL staining revealed significantly more apoptotic cells in the infarct area on day 2 in the controls (64 ± 9%) compared to the treatment group (52 ± 4%; p = .045). FDG-PET revealed a significant decrease in infarct size in the treatment group and an increase in the controls. Examinations of left ventricular ejection fraction on days 6 and 30 did not reveal treatment effects. [68Ga]Annexin A5 PET can detect the effects of PTH treatment as a marker of apoptosis 2 days after MI; ex vivo examination confirmed significant rescue of myocardiocytes. FDG-PET showed a small but significant reduction in infarct size but no functional improvement. ANIMAL STUDIES have suggested that parathyroid hormone (PTH) treatment after myocardial infarction (MI) shows beneficial effects on infarct size, left ventricular function, and cardiac remodeling and in general attenuates the progression of ischemic cardiomyopathy.1,2 Several mechanisms potentially mediating these effects of PTH have been proposed. First, PTH is known to induce arterial vasodilation by means of a receptor activation evoking intracellular cyclic adenosine monophosphate (cAMP) production.1,2 This pathway plausibly exerts beneficial effects on the perfusion of ischemically afflicted myocardium. Second, PTH induces the mobilization of progenitor cells from the bone marrow into the peripheral blood.3 Third, PTH increases plasma levels of cardiac stromal cell–derived factor 1 (SDF-1), a chemokine facilitating the homing of stem cells into the ischemic heart by activation of chemokine receptor type 4 (CXCR4) (SDF-1/CXCR4 axis).4 These effects lead to increased myocardial perfusion, neovascularization, and enhanced cell survival and regeneration, ultimately resulting in less apoptosis and cardiac remodeling and improved postinfarct cardiac function.1 Serial examinations by positron emission tomography (PET) enable serial in vivo molecular imaging of myocardial survival and viability in small-animal infarct models. PET with the glucose analogue 2-deoxy-2-[18F]fluoro-D-glucose (FDG-PET) gives quantitative information about the viability and the function of damaged myocardium in vivo.5 Furthermore, we recently reported that PET with [68Ga]annexin A5 serves to visualize and quantify phosphatidylserine externalization in the area at risk after myocardial ischemia6; the binding of [68Ga]annexin A5 to externalized phospholipids is considered a surrogate marker for myocardial apoptosis. Based on our earlier findings with FDG and annexin PET, we hypothesized that the myocardial viability and externalization of phosphatidylserine on day 2 after MI correlate with the long-term outcome.

Introduction: Cell-based therapies were reported to improve early kidney function in experimental models of renal ischemia-reperfusion injury. This study examines and compares the therapeutic effects of mesenchymal stem cells (MSC) and endothelial progenitor cells (EPC) as well as their regenerative[for full text, please go to the a.m. URL], 128. Kongress der Deutschen Gesellschaft für Chirurgie

Introduction: Cell therapy represents a promising therapeutic approach in kidney transplantation. This study examines the precise potentials and limits of cell therapy in renal ischemia-reperfusion injury. Materials and methods: The effects of endothelial progenitor cell therapy following a 45 min[for full text, please go to the a.m. URL], 127. Kongress der Deutschen Gesellschaft für Chirurgie