İstanbul Üniversitesi Açık Erişim Sistemi
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Hesaplanmış globülinin (HG) antikor eksikliği için tarama testi olarak Türk yetişkin hastalarda validasyonu
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Effects of extensive mobilization and tension anastomosis in anorectal reconstruction (experimental study)
No full text© 2022, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.Purpose: Anorectoplasty and pull-through procedure can be performed with extensive mobilization or tension anastomosis, which can compromise bowel blood perfusion. We aimed to analyze the hypoxia biomarker values and histopathological findings in both conditions to correlate the occurrence of anal stenosis and defecation disorders in experimental models. Methods: We created anorectal reconstruction models with impaired vascularization of the anorectum (group I) and tension anastomosis (group II) in rats. A third group of animals underwent sham operation (group III) and another as controls (group IV). Hypoxia biomarker values were assessed in all groups. The histopathological changes on the postoperative days 3 and 35, anal stenosis and defecation disorders on day 35 were compared. Results: Hypoxia biomarker values confirmed postoperative ischemia in groups I–III compared to control. Group I and II rats had a similarly pronounced ischemia with histopathologic changes in the anorectum on the postoperative day 3 and accompanied by severe fibrosis on day 35. Compared to the sham operation, both groups showed defecation disorders with significant anal stenoses. Conclusion: Extensive rectal mobilization to about the same extent as tension anastomosis has a major impact on postoperative rectal ischemia, resulting in severe fibrotic changes in the anorectum and defecation disorders in the long term
PP081 Nitic Oxide Mediated Effects of Nebivolol in Myocardial Infarction: The Source of Nitric Oxide
No full textObjective: After MI, LV remodelling is one of the major causes of death. We previously showed the NO mediated beneficial effects of nebivolol in rat MI model, in this study we aimed to determine the source of NO. Methods: Rats were divided into four groups: sham operated (sham-control), MI-induced (MI-control), immediate nebivolol loaded (MI-neb1), orally nebivolol treated (MI-neb2). MI was induced by the ligation of the LAD. NOS related mechanisms were assessed either in acute and sub-acute period of MI by histologic, hemodynamic and biologic studies. Results: Compared to MI-control rats, physiological functions of LV (LVEDP, D!dp/dt) were prevented in nebivolol treated groups. Improvements in anatomical parameters (LEV, HW, LVW/HW) were consistent with functional improvement. Oxidative (decreased MDA, increased SOD) and nitrosative (decreased ONOO-) damage were limited also. Most dramatic change was seen in the nNOS labelling.The decrease in iNOS labelling was also prominent too. Conclusions: NOS mediated mechanisms of nebivolol can be summarized as: 1) diminishing iNOS expression together with restoration of MI induced eNOS activation both in vascular bed and myocytes at the acute period of MI, and 2) prevention of deterioration in nNOS expression in myocardial cells at the sub-acute period of MI
