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In addition to its role in erythropoiesis, erythropoietin (Epo) plays a role in tissue protection, which includes cardioprotective, nephroprotective and neuroprotective effects. The presence of Epo and its receptor (Epo-R) in pulmonary tissue also suggests a cytoprotective effect of Epo in the lung. Our project aims to document this role in a murine model under-expressing Epo. The obtained results will lead to a better understanding of the cytoprotective effects of Epo and will also give an appreciation of its beneficial effects in cases of lung injury.

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AIM: This study was designed to evaluate a new technique for a completely diverting tube ileostomy achieved through temporary occlusion of the distal ileum using a flexible rubber strip. METHODS: This prospective interventional study was conducted in one centre. Patients who underwent colorectal resections with a primary anastomosis and who were deemed as requiring a defunctioning stoma were included in the study. After completion of resection and anastomosis, the tube ileostomy was fashioned by inserting a reinforced (spiral) endotracheal tube with an inner diameter of 7.5 mm into the ileum. To provide complete faecal diversion, temporary occlusion of the distal ileum was performed using a flexible rubber strip. The primary outcome of this study was the incidence of complete diversion achieved using this method. RESULTS: Fifty consecutive patients underwent a diverted tube ileostomy using the technique described above. Defaecation before removal of the strip did not occur in any of the patients inferring that complete diversion was observed in all patients (100%). The tube was removed at postoperative week 3. After tube removal, the resulting enterocutaneous fistulas closed spontaneously in a median of 6 (2-30) days. CONCLUSION: The diverting tube ileostomy technique using an easily removable rubber strip to defunction the colorectal anastomosis is a safe and effective method that precludes the need to fashion a stoma.

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BACKGROUND: Colorectal cancers are third most common cancer in both genders. They are associated with genetic and environmental factors. Staging is important in the prognosis. Carcinoembryonic Antigen (CEA) provides preliminary information and there is a correlation between Proliferation Index (PI) and prognostic variables. Our aim is to investigate the relationship between DNA repair capacity and clinico-pathologic factors. PATIENTS AND METHODS: The blood samples taken from cancer patients were irradiated. DNA repair capacity by comet technique was calculated. The CEA values were recorded. Pathology reports were collected and PI values were calculated. s. RESULTS: Total of 30 patients; male (n: 14) and female (n: 16) with a median age of 66.37 ± 10.32 were included. Mean CEA value was 42.85 (1.46 - 422.30 µgr/ml) µgr/ml. Mean % DNA repair capacity was 44.49 ± 5.24. In the pathology; 21 (70%) were T3 tumors; 18 (60%) had lymphatic and 12 (40%) had vascular 2 invasion. Perineural invasion was present in 8 (26.7%). According to the proliferation index (PI); 16 (53.3%) were in high percentile (PI > 66%) group. CONCLUSIONS: There was a significant correlation between; perineural invasion and tumor grade (P = 0.043); lymphatic and perineural invasion (P = 0.006); lymphatic invasion and vascular invasion (P = 0.034) and the DNA repair capacity with the lymphatic invasion (P = 0.026). There was also a statistically significant (P = 0.044) relationship between PI and lymphatic invasion. As a result in colorectal cancer patients DNA repair capacity can be used as a biomarker in the staging and also in the prediction of the tumor behavior.

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OBJECTIVES: Regular screening for the BK virus (BKV) is recommended for early intervention in renal transplant patients. Identification of predictors for the development of BK viremia would improve their monitoring. We performed a retrospective study investigating whether the lymphocyte count may be a predictor of BKV development in renal transplant patients. PATIENTS AND METHODS: We retrospectively analyzed 268 renal transplant patients who were followed in our clinic from January 2011 to August 2014. The viral loads of BKV in blood detected by quantitative real-time polymerase chain reaction test were performed according to relevant guidelines. We also retrospectively monitored lymphocyte count, creatinine, immunosuppressive drug doses, and tacrolimus/cyclosporine/mTor inhibitors levels during the same time as BKV screening. Demographic and other clinical data were extracted from patients' files. The calculation of correlation coefficients and receiver operating characteristics (ROC) curve analysis were performed. RESULTS: Overall, 16 patients (5.9%) who experienced BKV-DNA positivity were included the study. Mean age of patients was 38.2 ± 12.8 years. All patients received steroid and calcineurin inhibitors (CNIs). Mycophenolate mofetil/mycophenolic acid (MMF/MPA) was administered to 14 patients. BKV-DNA was found in 64 of the 88 (72.7%) plasma samples. The lymphocyte count on the first day of positive BKV-DNA test was significantly lower than in those with negative BKV-DNA results (1700/µl vs 2400/µl, respectively; P = .009). Its AUC of the ROC curve was 0.77 (P = .012). The optimal cutoff point for lymphocyte count was 1900/µl, and sensitivity and specificity for predict BKV positivity were 75% and 78.57%, respectively. We also found that lymphocyte count negatively correlated with the first detectable BKV titers (r = -0.438; P = .015). However, there is no relation between CNI/mTOR inhibitor levels, MMF/MPA doses, lymphocyte count, and all BKV-titers. CONCLUSIONS: Decreased lymphocyte count may be a predictor for preceding BKV viremia. Clinicians should be more careful in terms of the decreased lymphocyte count in case of BKV replication in renal transplant patients.

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We investigated the gastric response to an ulcerogenic irritant and the change in gastric functions in an experimental rat model of obstructive jaundice, with or without biliary drainage. After biliary obstruction for 14 days, rats with ligated bile duct (BDL) were randomly divided into three groups: BDL group without biliary drainage, BDL followed by choledochoduodenostomy (CD) or a choledochovesical fistula (CVF). The gastric functions were evaluated 2 weeks after the surgery. Gastric damage, induced by orogastric administration of ethanol, was evaluated 30 min later using a lesion index and microscopic scoring was then performed on fixed stomachs. Basal gastric acid secretion was measured by the pyloric ligation method. The lesion index and maximum lesion depth did not differ in the BDL and sham groups, while they were significantly reduced in the CD group. Gastric acid output and secretory volume were reduced in the BDL group compared to the sham group, while these reductions were abolished in the CD group. Afferent denervation with capsaicin further reduced the ulcer index in the later group. Our data suggest that gastric mucosal susceptibility to injury is dependent on the normal flow of bile into the duodenal lumen, which appears to be a requirement for adaptive gastric cytoprotection.

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Although iliac artery injuries caused by pelvic fractures are uncommon, in special circumstances, such as earthquakes, traumatic arterial injury should be carefully investigated. This reports describes a case of an iliac artery pseudoaneurysm causing compressive symptoms that was successfully treated by radiologic embolization.

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OBJECTIVE AND DESIGN: The present study was designed to investigate the role of sex steroids in burn-induced remote organ injury. MATERIAL OR SUBJECTS: Male Wistar albino rats were given burn trauma (n=39), and underwent castration or sham operation at 2 h following the burn injury. TREATMENT: Rats were injected sc with either 17beta estradiol benzoate (E2, 10 mg/kg) or an androgen receptor blocker cyproterone acetate (CPA, 25 mg/kg) or vehicle, immediately after burn and at 12 h. METHODS: At 24 h of burn insult, rats were decapitated. Blood samples for RIA of testosterone, estradiol and tumor necrosis factor (TNF)-alpha and the tissue samples for myeloperoxidase activitiy (MPO) were taken. ANOVA student's t test was used for statistical analysis. RESULTS: Castration, antiandrogen and E2 treatments increased plasma estradiol levels and depressed burn-induced elevation in serum TNF-alpha levels. In the liver and lung, burn-induced increase in MPO was reduced by E2 and castration, while CPA was effective in reducing neutrophil infiltration only in the liver. CONCLUSION: We propose that treatment with estrogens or antiandrogens might be applicable in clinical situations to ameliorate systemic inflammation induced by burn.

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This study was designed to determine the effect of exogenous bombesin (10 microg/kg/day, subcutaneously, three times a day) on intestinal hypomotility and neutrophil infiltration in the early and late phases of burn injury (partial-thickness, second-degree burn of the skin). In acute (2 h after burn injury) or chronic (3 days after) burn groups, intestinal transit was delayed, which was reversed by bombesin treatment. In the acute burn group, but not in the chronic group, increased MPO activity was also reduced by bombesin treatment. The results demonstrate that bombesin ameliorates the intestinal inflammation due to burn injury, involving a neutrophil-dependent mechanism.

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The aim of this study was to investigate the effect of nitric oxide (NO) on the gastric injury induced by hemorrhagic shock. Hemorrhagic shock was created by withdrawing 3 ml blood/200 g body weight of the rats. Before the hemorrhage, N(G)-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v. bolus), D-NAME (10 mg/kg i.v. bolus), or L-arginine (100 mg/kg i.v. bolus and 10 mg/kg/min infusion) + L-NAME were administered. At the end of the 1-hour hypovolemic shock period, histological analysis, gastric ulcer index, gastric myeloperoxidase (MPO) activity, and gastric protein oxidation (PO) levels were determined. In histological analysis a destructive effect of L-NAME (NO synthase inhibitor) was demonstrated. L-NAME treatment increased gastric MPO activity, L-arginine reversed this effect and D-NAME had no effect. Tissue PO activity was found to be increased in L-NAME-treated rats; L-arginine treatment reversed this activity. It is concluded that gastric barrier function is altered after hemorrhagic shock, and L-arginine (NO precursor) can prevent mucosal injury in the stomach. This effect of NO may be on gastric blood flow and can be mediated by tissue neutrophils.

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This study was carried out to investigate the role of endogenous endothelins in intestinal motility following bum injury by using a nonselective endothelin-1 (ET-1) antagonist and to evaluate the ET-1-mediated reactive oxygen metabolite formation and neutrophil infiltration following burn injury. In 2 h and 3 day postburn groups, transit indices were significantly decreased as compared to corresponding sham groups. Transit index was not significantly changed by PD156252 pretreatment in the 2 h postburn group, whereas the delay in transit was abolished in the ET-antagonist treated 3 day postbum group. In the 2 h postburn group, tissue-associated myeloperoxidase (MPO) activity value was found to be increased compared to corresponding sham group, while PD156252 pretreatment partially reversed this effect. Although MPO activity levels were not significantly different between 3 day postburn and corresponding sham groups, MPO levels showed a significant increase in ET antagonist-treated group as compared to the corresponding burn group. In the early phase of the burn, there was no significant difference in protein oxidation levels among the groups. In the 3 day postburn group, protein oxidation levels in ET-antagonist-treated group showed an increase compared to its corresponding burn group. In conclusion, the results demonstrate that endogenous endothelins have an important role in the systemic response to burn injury, as observed by a delay in intestinal motility and an infiltration of neutrophils. Although the results of the animal studies are not readily applicable to burned patients, the present study may suggest that the burned patient's condition should be carefully evaluated to secure a proper and early enteral feeding.

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To determine the role of endothelins (ET) on experimental colitis, following intracolonic trinitrobenzene sulfonic acid administration, rats were given orally either bosentan (BS), a nonselective ET receptor antagonist (100 mg/kg in 5% arabic gum), or arabic gum by gavage for 2 or 14 days. Macroscopic damage scores obtained in the vehicle (1.4+/-0.4), acute (4.8+/-0.6) and chronic (3.8+/-0.3) colitis groups were significantly higher than in the control group (0). BS treatment reduced the scores in both acute (3+/- 0.5) and chronic (2.3+/-0.5) colitis groups. Myeloperoxidase (MPO) activities of colonic tissues were elevated in acute and chronic colitis groups (325.1+/-44.9 and 431.8+/-54.6 U/g wet weight) as compared with the control group (73.6+/-11 U/g wet weight). Plasma protein oxidation levels were found to be significantly increased in the chronic colitis group (1,158.1+/-63.4 nmol/ml) compared with the control, ethanol and acute colitis groups (274.3+/-23.1, 490+/-52.2 and 422.2+/-50.5 nmol/ml). BS treatment significantly reduced both the protein oxidation level (375.5+/-46.9 nmol/ml) and MPO activity (167.5+/-35.8 U/g wet weight). The results of the present study suggest the involvement of ETs in the pathogenesis of colonic injury in this animal model of colitis.

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The present study was undertaken to explore the role of nitric oxide (NO) in the pathogenesis of experimental non-steroidal anti-inflammatory drug (NSAID)-induced gastropathy. We assessed the role of NO inhibition and donation in indomethacin-induced gastric mucosal dysfunction. The stomach was perfused with vehicle (control) for 20 min, followed by indomethacin (10 mg ml-1 in 1 25 % sodium bicarbonate, pH 8 4) for 120 min. NG-nitro-L-arginine methyl ester (L-NAME, 5 and 10 mg kg-1, I.V. bolus), L-arginine, D-arginine (100 mg kg-1 I.V. bolus, 10 mg kg-1 h-1, 2 h infusion) and the NO donor glyceryl trinitrate (GTN) were given at the same time (20, 40 and 80 microg kg-1 min-1, 15 min infusion) as perfusion with indomethacin was started. Epithelial permeability was quantified by measuring blood-to-lumen clearance of 51Cr-labelled EDTA. Indomethacin caused a 20-fold increase in 51Cr-EDTA leakage compared with that of the control group. Treatment with L-NAME or L-arginine did not affect the indomethacin-induced alterations in mucosal permeability. Administration of GTN (20 microg kg-1 min-1) significantly reduced the indomethacin-induced mucosal dysfunction. By contrast, higher doses of GTN (80 microg kg-1 min-1) exacerbated epithelial dysfunction induced by indomethacin. Elevated levels of carbonyls and myeloperoxidase (MPO) observed after indomethacin administration were significantly reduced, to the control values, when GTN (20 microg kg-1 min-1) was administered along with indomethacin. These data suggest that NO from exogenous sources can exert a dual action on the integrity of the gastric mucosa challenged by indomethacin. Low doses of GTN can prevent mucosal dysfunction induced by indomethacin, while higher doses of GTN may exacerbate the increases in epithelial permeability.

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BACKGROUND/AIMS: To evaluate the involvement of ET-1 in ischemia-reperfusion (I/R) injury. METHODS: Superior artery occlusion was performed in Wistar albino rats for 30 min followed by 2-hour (early reperfusion; ER) or 24-hour (late reperfusion; LR) reperfusion periods. RESULTS: Intestinal transit was found to be reduced in the ER and LR groups (19.0 +/- 2.5%; p < 0.001 and 72.7 +/- 6.0%; p < 0.05, respectively) compared to the control group (85. 8 +/- 2.5%), while treatment with the ET receptor antagonist bosentan (BOS; 10 mg/kg i.v.) abolished this delay in LR. Myeloperoxidase activity showed a significant increase in ER (7.07 +/- 85.70 U/g; p < 0.001) compared to control (281.16 +/- 43.23 U/g), but BOS had no effect on this increase. The protein oxidation level was found to be higher in LR (5.92 +/- 0.77 nmol/mg protein; p < 0. 05) compared to the control (3.77 +/- 0.45 nmol/mg protein), and was reversed by BOS treatment. CONCLUSION: The results of the present study imply that I/R delays intestinal transit involving an endothelin-dependent mechanism.

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A case of primary omental torsion seen in a 26-year-old man is discussed. All signs and symptoms mimicked acute appendicitis. The patient underwent emergency laparotomy in which a normal appendix and serohemorrhagic fluid in the pelvis were observed. The pathological diagnosis was a primary torsioned omentum which was thus excised. This case helps to emphasize the importance of a routine exploration of the abdomen when serohemorrhagic fluid is found at the time of laparotomy in the absence of any pathological condition in the pelvis.

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Ischemia reperfusion (I/R) injury is one of the leading cause of the transplanted organ loss. In this experimental study, we investigated the effect of captopril on endothelin and eicosanoid release in I/R injury of the kidney. Rats were subjected to 60 min ischemia and 60 min of reperfusion of the left kidney in control and captopril groups. Tissue protein oxidation products, PGE2 and LTB4 levels and plasma endothelin-1 (ET-1) like activity were determined in sham operated, control and captopril groups. There were no differences in the LTB4 levels among the groups. ET-1 and PGE2 levels and protein oxidation products increased in the control group when compared with the sham. Captopril further increased both PGE2 and ET-1 concentrations and prevented protein oxidation. The increased ET-1 concentrations in the captopril treated group may imply the protective role of endothelin as the significant increase in protein oxidation products was reversed by captopril infusion. This has led us to believe that captopril might be useful in preventing I/R injury of the kidney. Also the release of endothelin from the vascular endothelium is increased by captopril and may be mediated by PGE2.

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Although postoperative pain following laparoscopic cholecystectomy (LC) is less intense than that after open surgery, postoperative morbidity nonetheless increases with LC. The aim of this study was to investigate whether local anesthetic infiltration of trocar sites during LC decreased postoperative pain and, if so, to find the optimum timing for local anesthesia (LA). Seventy patients undergoing LC were randomized into three groups. In the first (control group, n = 25) 3 ml of 0.9% NaCl was subcutaneously infiltrated around each 5-mm trocar site, 4 ml around each 10-mm site. In the second group (n = 20), the same volume of local anesthetic was administered in the same manner prior to surgery, and in the third group (n = 25) an identical dose of local anesthetic was infiltrated at the end of surgery. A visual analog scale was given to all patients, who were asked to record their pain intensity at 1, 3, 5, 7, and 12 h postoperatively. Pethidine HCl 1 mg/kg i.m. was given to those whose pain intensities were greater than 5. The mean pain intensities were 7.6, 5.9, and 5.1 in the control, preoperative, and postoperative LA groups, respectively. In the preoperative LA group, 50% of patients and in the postoperative LA group 28% of patients required analgesics compared with 76% in the control group. The main pain intensities and analgesic requirements were significantly lower in the postoperative LA group compared with other groups. We conclude that local anesthesia during LC reduces postoperative pain and that infiltration of trocar sites following surgery offers better pain relief than local anesthetic given just before the incision.

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This study investigated the effects of portal hypertension on gastric motor and secretory functions and the role of endothelin in rats. Control; sham-operated; endothelin-A receptor blocker, BQ 485 (1 microgram/kg)-treated; portal hypertensive; and portal hypertension +, endothelin-A receptor blocker-treated rats were subjected to tests of gastric secretory, motor, and mucosal function studies as well as gastric wall polymorphonuclear infiltration. Portal hypertension was induced by partial portal vein ligation. Portal hypertension suppressed gastric acid and total fluid secretion and delayed gastric emptying. An increase in mucosal permeability and no alteration in gastric wall myeloperoxidase activity were observed. The effects of portal hypertension on gastric secretory, motor, and mucosal functions were reversed by treatment with endothelin-A receptor blocker, BQ-485. It is concluded that portal hypertension suppresses the gastric motor and secretory functions and endothelin plays an important role in the pathophysiology of gastric alterations associated with portal hypertension.

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We studied the effects of the specific endothelin (ETA) receptor antagonist, BQ-123, on reperfusion injury in a rat model of kidney transplantation. First, Sprague-Dawley rats were divided into three groups: a sham nephrectomy (SNEPH), an autotransplantation (AUTO-Tx), and an allotransplantation (ALLO-Tx) group. In a fourth group, ALLO-Tx + BQ, allografts were flushed with 20 micrograms BQ-123 containing cold Ringer's lactate before transplantation. For the allograft groups, kidneys from white Wistar albino rats were transplanted into allogeneic Sprague Dawley recipients. Grafts were allowed 120 min of reperfusion after 40 min of cold ischemia. ET-1,2 plasma concentrations in the renal venous blood, and kidney tissue prostaglandin (PG) E2 and leukotriene (LT) B4 levels were studied. Diene conjugates (DC), hydroxyalkanals (HAA), hydroxyalkenals (HAE) and malondialdehyde (MDA) levels, as the products of lipid peroxidation, and protein carbonyls (PC) and protein sulphydryls (PS), as the parameters of protein oxidation, were also analyzed in the kidney tissue. Plasma ET concentrations increased significantly in the AUTO-Tx and ALLO-Tx groups (P < 0.05 and P < 0.01, respectively) but this increase was reversed in the ALLO-Tx + BQ group. None of the lipid peroxidation products except DCs (P < 0.05) increased in the AUTO-Tx group, whereas they all increased in the ALLO-Tx group (P < 0.01). Protein oxidation parameters also changed significantly (P < 0.01) in the ALLO-Tx group but did not in the AUTO-Tx group (P < 0.05). The differences in PGE2 and LTB4 levels were not significant. Histopathologic examination revealed prominent glomerular and tubular injury in the AUTO-Tx and ALLO-Tx groups but less in the ALLO-Tx + BQ group. In the last group, all parameters of lipid peroxidation (P < 0.001 for all) and PCs decreased, and PSs were preserved (P < 0.001 for both) when compared with the AUTO-Tx and ALLO-Tx groups. We conclude that BQ-123, in addition to inhibiting the binding of ET-1,2 to the ETA receptor, may also inhibit the release and/or synthesis of ET-1,2 and prevent reperfusion injury in kidney transplantation.

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The reactive oxygen metabolites (ROMs) and the vascular endothelial factors such as endothelins (ETs) and thromboxane A2 (TxA2) were found to be mediators of the reperfusion component of ischemia-reperfusion (I/R) injury. Captopril (CPT), a sulfydryl (-SH) group containing angiotensin-converting enzyme inhibitor, has been shown to reverse I/R injury by its ROM scavenging effect. In this experimental study, the effects of CPT and BM 13.177 (a TxA2 receptor antagonist) were assessed on liver I/R injury in rats. Four groups of Wistar albino rats were either sham-operated, control, CPT or BM 13.177-treated. The middle and left lateral hepatic arteries and portal veins were occluded in each group but the sham and the corresponding agents were given to the animals prior to I/R injury. After I/R injury, blood was drawn from the suprahepatic inferior vena cava for ET-1-like activity assay and liver tissue samples were obtained for the determination of prostaglandin E2 (PGE2), leukotriene C4 (LTC4) and histopathologic examination. PGE2 and ET-1 levels were increased significantly in the control group compared with the sham-operated group. In the CPT group, LTC4, PGE2 and ET-1 levels were significantly increased compared with the control group, while only ET-1 levels were not different from those of the control group in the BM 13.177-treated group. It is concluded that ET-1 release increases in response to I/R injury in rat liver and CPT further increases this release. It also appears that CPT has a stimulatory effect on arachidonic acid metabolism in addition to its free radical scavenging effect.

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