Location of the appendix at the third trimester of pregnancy: A new approach to old dilemma.

The aim of this study was to determine the location of the appendix at the third trimester of pregnancy as there are conflicting results in literature. Distances from the base of the appendix were measured intra-operatively to the anterior iliac spine (A), symphysis pubis (B) and the xyphoid process (C). The same measurements were taken from McBurney's point on the abdominal wall (A1, B1 and C1). In the allocated 21 pregnant and 18 non-pregnant women, distance A and B were 10.3 ± 0.9 cm and 18.3 ± 3.2 cm in pregnant and 6.7 ± 0.9 cm and 13.2 ± 0.9 cm in non-pregnant women (p < 0.001), respectively. Distance C was shorter in pregnant women (14.7 ± 2.5 cm vs. 23.8 ± 1.9, p < 0.001). Conversely, distance C1 was longer in pregnant women (30.3 ± 3.0 vs. 24.8 ± 5.1 cm, p = 0.004). This study provides evidence that the appendix moves cranially late in the course of the pregnancy. Therefore, McBurney's point cannot be used as a reference point to localise the appendix at the third trimester of pregnancy.

Enterostomy closure site hernias: a clinical and ultrasonographic evaluation.

BACKGROUND: Parastomal hernia with a reported incidence of up to 50% is a major problem after ostomy formation. Hernias at the closure site may be a problem after the closure of the enterostomy. In this study, in addition to physical examination, we used ultrasonography (USG) in order to find the true incidence of ostomy closure site and laparotomy incisional hernias. METHODS: We examined patients with closed enterostomy sites by both physical examination and USG for the detection of hernias. Risk factors for hernia formation, such as age, gender, body mass index (BMI), ostomy type, and surgical site infections, were determined. RESULTS: The evaluation of 31 patients with ostomies resulted in a 32% incidence of closed ostomy site hernias when patient medical history, physical examination, and ultrasonographic examination were used together. With physical examination and USG, incisional hernias at the laparotomy incision were found in 58% of cases. USG was able to detect hernias which were not clinically evident at the ostomy closure site and the laparotomy wound. BMI, age, gender, ostomy type, and surgical site infection did not have a significant effect on hernia formation. CONCLUSION: Ostomy closure site and laparotomy incisional hernias are important clinical problems with a high incidence after ostomies are closed. Closure of the enterostomy site should be regarded as a hernia repair rather than a simple fascial closure. USG is a valuable clinical tool in combination with physical examination for the detection of minor defects.

Immunologic influences of hyperthermia in a rat model of obstructive jaundice.

In this study, the effect of hyperthermia on immune response and bacterial translocation from the gut in jaundiced rats was assessed. In hyperthermic (HP; N = 8) and normothermic (NP; N = 8) preconditioning groups, rats were preconditioned by hyperthermia for 15 min at 42 degrees C or 38 degrees C, respectively. After 8 hr, the common bile duct (CBD) of each animal was ligated. In thermal (TT; N = 8) and normothermic treatment groups (NT; N = 8) the CBD of the animals was ligated, and after seven days rats were treated by hyperthermia for 15 min at 42 degrees C and 38 degrees C, respectively. The rats in the preconditioning groups (HP and NP) were killed at day 7 and rats in the treatment groups (TT and NT) were killed 8 hr after they were put in a water bath. Determination of the immunophenotypes of lymphocytes and serum levels of bilirubin was done in serum samples taken just after death. The quantity and identify of translocated bacteria were determined in tissue samples of mesenteric lymph nodes, spleen, and liver. NK cell expression as well as CD4+/CD8+ ratio were elevated in HP group when compared to NP group. CD8+ expression was found to be low in HP group when compared to NP group. CD4+, CD11b+, and B cell expressions were not found to be different between HP and NP groups. All immunologic parameters were similar when TT and NT groups were compared to each other. In the TT group, half of the rats revealed bacterial translocation, whereas in all other groups, we determined translocation in only 1/8 rats. The application of hyperthermia as preconditioning rather than applying it after the establishment of jaundice seemed to be beneficial. Hyperthermic preconditioning led an improvement in immune responses whereas the latter resulted an increase in bacterial translocation with no favorable influence on immune system. Bacterial translocation was unrelated with the immune status.

Different kinds of reactive oxygen and nitrogen species were detected in colon and breast tumors.

Several studies have shown the involvement of reactive oxygen species (ROS; O2*-, hypochlorite, hydroxyl radical, hydrogen peroxide) in carcinogenesis. With certain pathologies, nitric oxide (NO) is formed and can interact with superoxide radical (O2*-) resulting in the propagation of the highly reactive species, peroxynitrite. In order to study the molecular mechanisms underlying the ability of reactive oxygen and nitrogen species (RONS) to mediate carcinogenesis, we have measured ROS, NO, and peroxynitrite content of cancerous tissues obtained from colon and breast carcinoma cases by chemiluminescence technique. All ROS were significantly increased in cancerous colon tissues with hypochlorite making the most important contribution and suggesting the role of inflammatory cells. NO was also increased and the peroxynitrite concentration was higher in cancerous samples. For breast carcinoma cases, only O2*- was significantly increased. Hypochlorite was not detected excluding the contribution of inflammatory cells. NO concentrations were not significantly different, therefore, ROS might originate by change in the redox state of the tissue.

Scientific publications at a Turkish medical school.

The authors studied the scientific publishing trend for 1991 to 1998 at Turkey's Marmara University School of Medicine. Although publications increased both in real numbers and in ratios per faculty member, most were not original, peer-reviewed articles. Mere quantity of publications cannot accurately reflect a school's research reputation.

The effect of hyperthermic preconditioning on the immune system in rat peritonitis.

OBJECTIVE: To assess whether hyperthermic (HT) preconditioning prevents the lethal effects of peritonitis by acting on the immune system. DESIGN: Prospective, controlled, experimental study. SETTING: Laboratory and animal facility of the university. MATERIALS: Adult male Sprague-Dawley rats. INTERVENTIONS: In the HT groups animals were subjected to hyperthermia (42 degrees C, 15 min) and 8 h later peritonitis (P) (n = 14) was induced. In the normothermic (NT) groups, animals were subjected to normothermia (38 degrees C, 15 min) and 8 h later peritonitis (n = 14) was induced. Each group had a corresponding sham laparotomy group (n = 14). Six rats from each group were allowed to live 7 days for survival. In the control group (n = 4), rats were not anesthetized or heat treated. MEASUREMENTS AND RESULTS: Sixteen hours after peritonitis and laparotomy, rats were killed. Blood was taken to measure the percentage of CD(4)(+), CD(8)(+), CD(4)(+)CD(56)(+), CD(8)(+) CD(11 b)(+), NK(+), B cells and the level of tumor necrosis factor. Grading of peritonitis and the measurement of free oxygen radicals in the peritoneal fluid were undertaken. All rats in the HT + P and sham laparotomy groups survived for 7 days, while in the NT + P group two rats died in 7 days. HT decreased the severity of peritonitis and increased the free oxygen radicals in the peritoneal fluid; however, the difference did not reach statistical significance. HT prevented the decrease in CD(4)(+) and B cells and the increase in CD(11 b)(+). CONCLUSIONS: HT may have a protective role in sepsis by reducing the severity of peritonitis. A causal relation between hyperthermia and an improved immune system seems possible.

Bombesin ameliorates colonic damage in experimental colitis.

In the present study we investigated the possible therapeutic effects of bombesin on an experimentally induced colitis model in rats. Inflammation of the colon was induced by a single intracolonic administration of 30 mg of 2,4,6-trinitrobenzene sulfonic acid (TNBS) at 8 cm from the anus. Immediately after the induction of colitis, some rats were given bombesin (10 microg/kg; subcutaneously) three times a day for 14 days, while another group received vehicle treatment. On day 14, the rats were decapitated and plasma carbonyl content and tissue myeloperoxidase level, as an index of granulocyte infiltration into intestinal tissue, were determined in order to obtain an objective evaluation of colonic injury. In the colitis group, increased macroscopic damage score, elevated MPO level and high plasma carbonyl content, together with the microscopic appearance revealed severe inflammatory changes resembling IBD. Bombesin treatment attenuated the TNBS-induced colonic damage and stimulated histopathologically apparent mucosal proliferation, suggesting that bombesin may play a role in protecting gut integrity.

Role of endothelins in trinitrobenzene sulfonic acid-induced colitis in rats.

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.

The effects of thromboxane synthase inhibition on reperfusion injury and endothelin-1,2 levels in allograft kidney transplantation in rats.

Thromboxane A2 is a proaggregative vasoconstrictor that is synthesized and released in reperfusion injury. We aimed to investigate the effects of thromboxane synthase inhibitor, UK 38485, on endothelin-1,2 (ET) response of the renal endothelium and lipid peroxidation and protein oxidation in the early period of kidney transplantation. Four groups (n=8 in group IV and n=10 in the others) [corrected] of Sprague-Dawley rats were designed as Group I (sham nephrectomy), Group II (autotransplantation), Group III (allotransplantation) and Group IV (allotransplantation group in which the allografts were perfused with UK 38485. All subjects underwent right nephrectomy after transplantation. The grafts were flushed with 4 ml of ice-cold Ringer's lactate and in Group IV 10 microg of UK 38485 was added into the solution for each kidney. In allotransplantation groups, the kidneys were harvested from allogeneic white Wistar albino rats. The kidney grafts were allowed 120 min of reperfusion after 40 min of cold ischemic period. ET-1,2 plasma concentrations in the renal vein blood and diene conjugates (DC), hydroxyalkanals (HAA), hydroxyalkenals (HAE) and malondialdehyde (MDA) levels as the products of lipid peroxidation, protein carbonyls and protein sulfhydryls as the indicators of protein oxidation were analyzed in kidney tissue. Plasma ET-1,2 concentrations increased significantly in Group II and Group III (P<0.01) when compared to Group I but decreased in Group IV in comparison with Group III (P<0.05). DC, HAA, HAE and MDA levels increased in Groups II and III (P<0.001). Significant protein oxidation occurred only in Group III (P<0.01). Perfusion of the allografts with UK 38485 prevented lipid peroxidation and protein oxidation in Group IV. Histopathological changes were mild in the last group. We concluded that, in kidney transplantation, local administration of UK 38485 has cytopreservative effects on the allografts and this effect can be related to ET-1,2 concentrations.

Role of endothelin in obstructive jaundice.

Mediators responsible for renal changes in obstructive jaundice are not specified. This study is designed to study the role of endothelin-1 (ET-1) in obstructive jaundice in rats. Animals were randomly placed into five experimental groups. Group 1 (N = 3) was the sham-operated group. Group 2 (N = 8) after common bile duct (CBD) ligation, received bosentan, which is a nonselective endothelin receptor blocker, 50 mg/kg/day for seven days. Group 3 (N = 7) received 1 microg/kg/day captopril. Group 4 (N = 7) was given both drugs orally for seven days. Group 5 (N = 6) after CBD ligation, received Arabic gum as the vehicle. Blood was drawn from the infrahepatic vena cava for the determination of ET-1, bilirubin, creatinine, protein oxidation products, hyaluronic acid, and beta-N-acetyl-hexosaminase. Liver tissue samples were obtained to determine glutathione levels. ET-1, protein oxidation products, hyaluronic acid, bilirubin, and creatinine levels increased significantly in the control group when compared with sham. Bosentan effectively prevented ET-1 elevation but could not reverse creatinine or bilirubin elevation. Captopril with or without bosentan was cytoprotective but did not reverse increased creatinine levels. It is concluded that increased ET-1 in obstructive jaundice may be one of the contributing factors of renal damage.

Prospective multicentre trials in developing countries: willingness of surgeons to participate.

OBJECTIVE: To assess the feasibility of conducting a multicentre study among surgeons in Turkey. DESIGN: Prospective open multicentre study. SETTING: Teaching hospitals in Turkey. SUBJECTS: Surgeons working in 23 university and 15 state hospitals. INTERVENTIONS: Surgeons willing to participate were asked to look for the presence of Meckel's diverticulum in all patients undergoing laparotomy. MAIN OUTCOME MEASURES: To find out the number of surgeons willing to participate in the study and once they agreed to see how they fulfilled the requirements. RESULTS: 14 agreed to participate (12 from universities and 2 from state hospitals) and completed the study. A total of 2781 patient records were collected. University hospitals were more willing to participate than state hospitals (52% compared with 13%) but state hospitals contributed 20% of the patients. The number of patients contributed in the first and second halves of the study did not differ, reflecting no diminution of the enthusiasm. CONCLUSION: This study, with no financial support, showed that it is possible to conduct multicentre studies among surgeons in developing countries such as Turkey. Increased awareness of the importance of publication may have helped to obtain this result.

Nitric oxide and endothelin relationship in intestinal ischemia/reperfusion injury.

Gastrointestinal mucosal blood flow is dependent on a balanced release of vasoactive substances from endothelium. Nitric oxide (NO) may increase the flow by vasodilatation and/or antiaggregation whereas endothelin (ET) may decrease it by vasoconstriction and aggregation. NO and ET may have counterbalancing effects on each other in tissue damage. In order to test this hypothesis, in this study on rats, L-arginine to increase NO levels and N(G)-nitro-L-arginine methyl esther (L-NAME) to decrease NO levels have been used in an intestinal ischemia/ reperfusion (I/R) injury model and portal vein ET response was evaluated. Lipid peroxidation product measurements and chemiluminescence (CL) studies were also carried out in ileal tissue samples. Intestinal I/R injury caused an increase in portal venous ET levels with levels of 9.4+/-0.5 fmol/ml in sham operation and 14.8+/-1.6 fmol/ml in I/R group. ET level of L-NAME-sh group was lower than that of sham-operated group and also ET level of L-NAME-I/R group was lower than that of I/R group. This yielded the conclusion that inhibition of NO synthesis decreases portal venous ET levels in this model. Increased NO production by L-arginine caused increased ET levels in sham operated groups but this effect was not observed in I/R injury state. This study also showed that inhibition of NO synthesis has a protective role by reducing the reperfusion damage in this model. It is likely that NO and ET have a feedback effect on each other both under physiologic conditions and I/R injury.

Captopril prevents the oxidative damage to proteins after renal ischemia reperfusion injury: role of endothelin-1.

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.

Primary torsion of the omentum mimicking acute appendicitis: report of a case.

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.

The effect and timing of local anesthesia in laparoscopic cholecystectomy.

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.

Preoperative albendazole treatment for liver hydatid disease decreases the viability of the cyst.

OBJECTIVE: Although in experimental models the efficacy of albendazole has been demonstrated, more clinical data are required. In this study, the effect of preoperative albendazole treatment was investigated in patients with liver hydatid cysts. DESIGN: This is a prospective non-randomized study. METHODS: In this study, the viability was assessed by the gross appearance of the cyst and intracystic pressure (ICP). The study consisted of 70 patients with 89 liver hydatid cysts in two groups. The patients in the first group (n = 29) received 10 mg/kg albendazole orally for 3 weeks before surgery. Thirty-five cysts were evaluated in this group. The second group (n = 41) with 54 liver hydatid cysts received no preoperative treatment. RESULTS: In the first group receiving preoperative albendazole, 20 cysts were viable and 15 non-viable. The median ICP was 21 (range 8-56) cm H2O in viable and 0 (range 0-8) cm H2O in non-viable cysts. In the second group, 43 cysts were viable and 11 non-viable. The median ICP was 35 (range 8-75) cm H2O in viable and 0 (range 0-2) cm H2O in non-viable cysts. The ICP values of viable cysts in the first group receiving preoperative albendazole were significantly lower (P < 0.05). The number of non-viable cysts was also significantly higher in the group treated with preoperative albendazole (P < 0.05). CONCLUSION: Albendazole in this study has proved to be effective in decreasing the viability of liver hydatid cysts when given for 3 weeks preoperatively.

Gastric functions in portal hypertension. Role of endothelin.

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.