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Öğe Delayed gastric emptying in gastroesophageal reflux disease(Springer, 2005) Demirbilek, S; Karaman, A; Gürünlüoglu, K; Akin, M; Tas, E; Aksoy, RT; Kekilli, EThe association between gastroesophageal reflux (GER) and intestinal malrotation (IM) has been well described. Delayed or impaired gastric emptying in IM is thought to be a contributing factor in the development of gastroesophageal reflux disease (GERD). The current study assessed the role of malrotation in delayed gastric emptying in children with GERD. We also evaluated the interactions between GERD, malrotation, gastric pH abnormalities, and gastric dysmotility. Sixty-seven patients between 1 and 5 years of age ( mean 3.08 +/- 1.2) and with symptoms of GER, such as emesis, reactive or recurrent lung disease, and/or growth retardation, were studied in 2001 - 2005. Upper and lower gastrointestinal contrast studies were performed for the diagnosis of malrotation. Gastric motility was evaluated with a liquid gastric emptying protocol. GER was documented by upper gastrointestinal studies, scintigraphy, and/or 24- h pH monitoring. In our series of 44 children with GERD, there was an unexpectedly high incidence of IM: 54.5% (24/44). IM has previously been known to occur in 25% of patients with GERD. GERD was found in 24 (82.7%) of 29 patients with IM. Mean nuclear gastric emptying (MNGE) was 51.6 +/- 8.04 min in patients with isolated GERD and 96.6 +/- 20.5 min in children with IM and GERD. There was a statistically significant difference in MNGE time ( p< 0.05) between children with primary GERD and in those with GERD and IM. Esophageal pH monitoring showed that mean fraction time below pH 4 was 7.06 +/- 1.1% in patients with isolated GERD and 14.7 +/- 4.1% in patients with IM and GERD. GERD is common in children between 1 and 5 years old. Using gastric emptying studies and esophageal pH monitoring, we have shown that gastric dysmotility and esophageal pH abnormalities are highly prevalent, especially in children with malrotation compared with children with isolated GERD. These findings suggest that malrotation is an important factor responsible for delayed gastric emptying in GERD. Hence, we recommend that all infants and children with GERD and delayed gastric emptying undergo careful evaluation for malrotation.Öğe Glial cell line-derived neurotrophic factor and synaptophysin expression in pelviureteral junction obstruction(Elsevier Science Inc, 2006) Demirbilek, S; Edali, MN; Gürünlüoglu, K; Türkmen, E; Tas, E; Karaman, A; Akin, MObjectives. To examine the expression of neuronal markers in congenital pelviureteral junction (PUJ) obstruction as a causative factor. The findings from some investigations have suggested that defective neuronal innervation may play an important role in the pathogenesis of PUJ obstruction. Methods. Using specific antibodies, we studied the neuronal markers of specimens from 12 cases of PUJ obstruction and 10 normal PUJs by immunohistochemistry using glial cell line-derived neurotrophic factor (GDNF), synaptophysin, S-100, and neurofilament. Results. In the PUJ obstruction specimens, staining with hematoxylin-eosin and Masson's trichrome revealed muscular hypertrophy and an increase in collagen tissue and fibrosis in the lamina propria and tunica muscularis. The most striking finding on immunohistochemistry was the marked nuclear staining of cells with synaptophysin in all layers of the PUJ obstruction specimens that was totally absent in the normal PUJ specimens. In addition, significantly less intense staining for GDNF was found in the PUJ obstruction specimens compared with the normal PUJ specimens. The underexpression of GDNF in PUJ obstruction specimens was localized in the muscular layer especially. Immunohistochemical staining for S-100 and neurofilament showed no differences in the expression level of these neuronal markers in normal and PUJ obstruction specimens. Conclusions. Because GDNF is a survival factor for central and peripheral neurons, defective expression of GDNF could play an important role in the defective neuronal innervation of PUJ obstruction. Intense nuclear expression of synaptophysin in all layers of obstructed PUJ specimens suggested that obstructed PUJs have a serious structural abnormality.Öğe Polyenylphosphatidylcholine pretreatment protects rat liver from ischemia/reperfusion injury(Elsevier Ireland Ltd, 2006) Demirbilek, S; Karaman, A; Gürünlüoglu, K; Tas, E; Akin, M; Aksoy, RT; Türkinen, EBackground: Hepatic injury induced by ischemia/reperfusion following surgery, transplantation, or circulatory shock combined with resuscitation is a major clinical problem. Polyenylphosphatidylcholine (PPC) has strong antioxidant, cytoprotective and anti-inflammatory effects. Aim: In this study, the influence of PPC pretreatment on ischemia-reperfusion (I/R) injury of the liver was examined in rats. Methods: The animals were divided into three groups: control (n = 10), I/R (n = 15) and IIR + PPC (n = 15). PPC was given 100 mg/day for 7 days before experiment. Several parameters of hepatic damage, oxidative stress, neutrophil infiltration and nuclear factor kappa beta (NF-kappa B) expression were measured as well as microscopic examination. Results: We observed that a significant reduction in AST and ALT values in the PPC treated group when compared with the ischemic group. The increases in hepatic total NO2 + NO3 and MDA, and decreases in SOD and GSH levels after reperfusion were partially, but significantly, inhibited by PPC pretreatment. I/R induced increase in hepatic myeloperoxidase content and NF-kappa B expression were also lowered by PPC pretreatment. Animals pretreated with PPC presented minimal hemorrhage and reduced signs of liver injury. Conclusion: PPC pretretament provided significant protection againts I/R injury to the liver. This treatment could be therapeutic in liver transplantation and other conditions associated with I/R injury. (c) 2005 Elsevier Ireland Ltd. All rights reserved.Öğe Protective effects of leflunomide against ischemia-reperfusion injury of the rat liver(Springer, 2006) Karaman, A; Fadillioglu, E; Turkmen, E; Tas, E; Yilmaz, ZHepatic ischemia-reperfusion (I/R) injury may be developed in some conditions, such as trauma, major hepatic resection, hemorrhagic shock or liver transplantation. I/R injury of the liver causes hepatocellular damage that may lead to hepatic failure. A considerable body of evidence indicates that reactive oxygen species (ROS) and inflammation may contribute to hepatocellular injury in liver I/R. Leflunomide is an isoxazole derivative, and a unique immunomodulatory agent. In the present study, we examined the effects of leflunomide on the neutrophil activation with oxidative stress and some antioxidant enzymes in the reperfusion following I/R in the rat liver. Thirty-two rats divided into four groups: group 1 (control); was given leflunomide 10 mg/kg, i.g.; group 2 (SHAM), animals were only laparotomized; group 3 (liver I/R), and group 4 (liver I/R + Leflunomide). In group 4, rats were pretreated with leflunomide (10 mg/kg, i.g.) two doses prior to experiment. In groups 3 and 4, occluding the hepatic pedicel for 60 min induced ischemia and reperfusion was allowed thereafter for 60 min. At the end of the reperfusion period, rats were sacrificed. superoxide dismutase, catalase, nitric oxide, xanthine oxidase, malondialdehyde, protein carbonyl and myeloperoxidase levels were determined in hepatic tissue as well as histological examination with H and E staining. Group 3 animals demonstrated severe deterioration of liver morphology and a significant liver oxidative stress. Pretreatment of animals with leflunomide markedly attenuated morphological alterations and neutrophil activation, reduced elevated oxidative stress products levels and restored the depleted hepatic antioxidant enzyme. The findings imply that ROS play a causal role in I/R-induced hepatic injury, and leflunomide exerts hepatoprotective effects probably by the anti-inflammatory effect with radical scavenging and antioxidant activities.
