RESUMO
In this work, for the first time, the specific impedances of various injection solutions as well as the surface and tissue impedance after injection of these solutions were analyzed and compared regarding the radio-frequency surgical cutting process. The impedances of 0.9% NaCl, 4% gelatine, 6% hydroxyethyl starch, 10% glycerol/5% fructose, 10% glucose, 5% and 20% albumin, blood, and blood plasma as well as aqua destillata have been tested in vitro. Even if EMR and ESD are routinely used in clinical practice, there is so far no easy, fast, and safe method to remove larger lesions en bloc. We show that the impedance of the injected solution shows to be a crucial factor for safe removal, especially of larger lesions (Ø > 20 mm) and more importantly in accordance with the requirements of oncology and pathology. KEY MESSAGES: Impedance is playing a crucial factor in the radio-frequency (RF)-surgery. With a higher Impedance there will be less current necessary to reach the aimed voltage. Injection solution Aqua destillata and 10% Glucose, show significantly higher Impedances. Higher impedances lead to less surgical related complications. Minor changes in existing method to improve patent safety.
Assuntos
Impedância Elétrica , Injeções , Humanos , Soluções , AnimaisRESUMO
Apoptosis of pancreatic beta-cells is an important factor in the pathophysiology of diabetes. Previously, we have shown that the "phytoestrogen" resveratrol can induce beta-cell apoptosis dependent on the expression of sulfonylurea receptor (SUR) 1, the regulatory subunit of pancreatic ATP-sensitive K(+) channels. Here, we investigate whether 17beta-estradiol also influences beta-cell apoptosis in a SUR1-dependent manner. Therefore, islets from wild type or SUR1 knock-out mice, clonal beta-cells, or HEK293 cells expressing different SUR forms were treated with 17beta-estradiol or estrone. Different apoptotic parameters were determined and estrogen binding to SUR was analyzed. In murine islets, 17beta-estradiol treatment resulted in significant apoptotic changes, which in their nature (either apoptotic or anti-apoptotic) were dependent on the age of the animal. These effects were not observed in SUR1 knock-out mice. Furthermore, 17beta-estradiol, which specifically binds to SUR, induced enhanced apoptosis in SUR1-expressing HEK293 cells and clonal beta-cells, whereas apoptosis in recombinant cells expressing SUR2A or SUR2B (cardiac or vascular SUR-isoforms) or sham-transfected control cells was significantly lower. The apoptotic potency of 17beta-estradiol was much higher than that of resveratrol or estrone. SUR1-specific 17beta-estradiol-induced apoptosis was either abolished by the mutation M1289T in transmembrane helix 17 of SUR1 or clearly enhanced by two mutations in nucleotide binding fold 2 (R1379C, R1379L). In conclusion, 17beta-estradiol treatment modulates beta-cell apoptosis under specific involvement of SUR1 in an age-dependent manner. 17beta-Estradiol-induced apoptosis can be influenced by certain SUR1 mutations. These findings may contribute to the understanding of pathophysiological changes in beta-cell mass and could, for instance, provide interesting aspects concerning the etiology of gestational diabetes.
