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Purpose: Bladder tumors are rare in children and adolescents. For this reason, the diagnosis is sometimes delayed in pediatric patients. We aimed to describe the diagnosis, treatment, and follow-up methods of bladder urothelial neoplasms in children and adolescents., Materials and Methods: We carried out a retrospective multicenter study involving patients who were treated between 2008 and 2014. Eleven patients aged younger than 18 years were enrolled in the study. In all the patients, a bladder tumor was diagnosed using ultrasonography and was treated through transurethral resection of the bladder (TURBT)., Results: Nine of the 11 patients (82%) were admitted with gross hematuria. The average delay in diagnosis was 3 months (range, 0-16 months) until the ultrasonographic diagnosis was performed from the first episodes of macroscopic hematuria. A single exophytic tumor (1-4cm) was present in each patient. The pathology of all patients was reported as superficial urothelial neoplasm: two with papilloma, one with papillary urothelial neoplasm of low malignant potential (PUNLMP), four with low grade pTa, and four with low grade pT1. No recurrence was observed during regular cystoscopic and ultrasonographic follow-up., Conclusions: Regardless of the presence of hematuria, bladder tumors in children are usually not considered because urothelial carcinoma in this population is extremely rare, which causes a delay in diagnosis. Fortunately, the disease has a good prognosis and recurrences are infrequent. Cystoscopy may be unnecessary in the follow-up of children with bladder tumors. We believe that ultrasonography is sufficient in follow-up.

Infantile fibrosarcoma is a very rare soft tissue tumor that originates most commonly in the body and extremities. We present a neonate with an infantile fibrosarcoma that originated in the ileocecal region and was detected incidentally without symptoms. This is the first case of fibrosarcoma reported in the ileocecal region.

This study aims to investigate the acute protective effect of montelukast sodium in hepatic injury secondary to acetaminophen (APAP) intoxication. This study used 60 rats. The rats were grouped into 6 groups. The control group was administered oral distilled water 10 ml/kg, the APAP group oral APAP 1 g/kg, the montelukast sodium (MK) group oral MK 30 mg/kg, the acetaminophen+N-acetylcysteine (APAP+NAC) group oral APAP 1 g/kg, followed by a single dose of intraperitoneal NAC 1.5 g/kg three hours later, the acetaminophen+montelukast sodium (APAP+MK) group oral APAP 1 g/kg, followed by oral MK 30 mg/kg 3 h later, the acetaminophen+N-acetylcysteine+montelukast sodium (APAP+NAC+MK) group oral APAP 1 g/kg, followed by a single intraperitoneal NAC 1.5 g/kg plus oral MK 30 mg/kg 3 h later. Blood and liver tissue samples were taken 24h after drug administration. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin were studied from the blood samples. Liver tissue samples were used for histopathological examination. Compared with the control group, serum AST and ALT activities were higher in the APAP and APAP+NAC groups. APAP+NAC, APAP+MK, and APAP+NAC+MK groups had reduced serum ALT and AST activities than the group administered APAP alone. APAP+MK and APAP+NAC+MK groups had a lower serum ALP activity than the control group. Histopathologically, there was a difference between the group administered APAP alone and the APAP+MK and APAP+NAC+MK groups. MK is as protective as NAC in liver tissue in APAP intoxication in rats., (Copyright © 2015 Elsevier GmbH. All rights reserved.)

Objective: Ethyl alcohol is a substance that is widely used worldwide and known to exert toxic effects on liver. In this study, we aimed to examine the effect of L-ornithine L-aspartate (LOLA) on the toxicity of a single dose of ethyl alcohol in rats., Subjects and Method: We used 32 randomly selected male Sprague-Dawley rats weighing 200-250 g. The rats were grouped into four groups with each group containing eight rats: Group 1: the control group, Group 2: the ethyl alcohol group, Group 3: the LOLA group and Group 4: the ethyl alcohol+LOLA group. Ethyl alcohol was administered orally through a nasogastric tube at a dose of 6 g/kg after diluting with distilled water. One hour after ethyl alcohol administration, LOLA was administered to pre-specified groups orally through a nasogastric tube at a dose of 200 mg/kg after diluting with distilled water. Liver tissue and blood samples were obtained from all rats 24 hours later to study total antioxidant capacity (TAC), total oxidant status (TOS) and oxidative stress index (OSI) levels in liver samples, and aspartate aminotransferase (AST), alanine transferase (ALT), TAC, TOS and OSI levels in blood samples., Results: Serum TAC, TOS and OSI levels were higher in the groups that were administered ethyl alcohol. In addition, tissue TAC level was higher and TOS and OSI levels were lower in groups that were given ethyl alcohol. No significant changes were observed in serum and tissue TAC, TOS, OSI, ALT and AST levels in the LOLA administered groups., Conclusion: This study showed that LOLA was not biochemically effective and exerts no oxidative stress reducing activity in liver injury due to acute ethyl alcohol toxicity.

Introduction: Hepatic ischemia/reperfusion injury may occur after large tumor resection and liver transplantation procedures. Nitric oxide was shown to have protective effects on ischemia/reperfusion injury. Nebivolol is a compound that has been reported to improve nitric oxide release. We evaluated the effects of nebivolol in a rat liver ischemia/reperfusion model., Methods: A total of 40 rats were randomly divided into four groups (n = 10 each). Group I underwent only laparotomy, Group II was administered nebivolol and then underwent laparotomy, Group III underwent laparotomy and hepatic ischemia/reperfusion, and Group IV was administered nebivolol and then underwent laparotomy and hepatic ischemia/reperfusion. Serum AST, ALT, urea, and creatinine levels, and TAS and TOS levels of liver, lung, and kidney tissues were determined. Histopathological determination was also performed., Results: Nebivolol significantly reduced liver function tests in group IV, but it did not improve renal functions. Oxidative stress and abnormal histopathological findings were found to be reduced in liver tissue in group IV. Although the oxidative stress was increased after hepatic ischemia/reperfusion, nebivolol could not reduce the oxidative stress in kidney tissue. There were no significant differences between group III and group IV in terms of the histopathological changes in kidney tissue. There were no significant differences in lung tissue between the groups., Conclusions: The results of this study suggest that nebivolol has protective effects on liver but not on distant organs in a hepatic ischemia/reperfusion injury model. These experimental findings indicate that nebivolol may be useful in the treatment of hepatic ischemia/reperfusion injury.

Background: To investigate whether carvacrol (CAR) pretreatment reduces the severity of methotrexate (MTX)-induced hepatotoxicity in rats., Methods: A total of 24 rats were equally divided into three groups : group I, control ; group II, MTX-treated ; and group III, CAR+MTX-treated. On Day 1 group III received a one-time intraperitoneal dose of CAR (73 mg/kg), and on Day 2 both groups II and III received a single dose of intraperitoneal MTX (20 mg/kg). The rats were then sacrificed so to harvest blood and liver tissue samples to determine malondialdehyde (MDA), total antioxidant capacity (TAS), total oxidant status (TOS), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels. Histological specimens were examined via light microscopy., Results: Levels of MDA, ALT, AST and ALP in rat liver tissue samples were significantly higher in the MTX-treated group relative to the control group. However, TAS was significantly reduced in the MTX-treated group when compared to controls. Pretreating rats with CAR counteracted the effect of MTX exposure as MDA was significantly decreased and TAS was elevated in liver tissues when contrasted with the MTX-treated group. Furthermore, histological examination demonstrated significant liver injury in the MTX-treated group versus the CAR+MTX group., Conclusions: Pretreatment with CAR markedly diminished liver damage induced by MTX. Therefore, CAR administration preceding MTX treatment might be a promising therapeutic modality to prevent and/or lessen the extent of MTX-induced hepatotoxicity., (Copyright© Acta Chirurgica Belgica.)

Xanthogranulomatous cholecystitis is a rare variant of chronic cholecystitis characterized by severe proliferative fibrosis and accumulation of lipid-laden macrophages in regions of destructive inflammation. Xanthogranulomatous cholecystitis clinically and radiologically mimics early-stage gallbladder cancer, with wall thickening on computed tomography. The study included 14 xanthogranulomatous cholecystitis patients that were identified following retrospective analysis of the records of 1248 patients that underwent cholecystectomy between 2005 and 2011. Mean age of the 5 male and 9 female patients was 56.7 years. All 14 patients had gallbladder stones; 10 had a history of acute cholecystitis, 1 had cholangitis, and 2 presented with obstructive jaundice. A right-upper quadrant mass was palpable in 2 patients. All patients underwent cholecystectomy. Open surgery was planned and performed in 6 of the 14 patients, and laparoscopic cholecystectomy was planned in 8 patients, but was converted to open surgery in 1 case. In total, 1 patient developed wound infection, 1 patient had postoperative pneumonia, and 1 patient developed intraabdominal hematoma. None of the patients in the series died. Xanthogranulomatous cholecystitis is difficult to diagnose, both preoperatively and intraoperatively, and definitive diagnosis depends exclusively on pathological examination. Xanthogranulomatous cholecystitis should be a consideration in all difficult cholecystectomy cases.

Purpose: The purpose of this study was to investigate the effect of carvacrol (CAR) on methotrexate (MTX)-induced renal damage in rats., Methods: Twenty-four male rats were equally divided into three groups: group I, control treatment; group II, MTX-treated; and group III, MTX+CAR-treated. A single dose of CAR (73 mg/kg) was administered intraperitoneally to group III on the first day of the experiment and a single dose of MTX (20 mg/kg) was administered intraperitoneally to groups II and III on the second day of the experiment. Blood samples and kidney tissue were obtained from each animal on day 8 for the measurement of malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI). Light microscopy was used for histopathological examination of kidney specimens., Results: MDA, TOS and OSI levels were significantly greater in the group receiving MTX alone relative to the control animals, while the TAS level was significantly reduced in the MTX group compared with the control group. The administration of CAR was associated with significantly decreased MDA, TOS, and OSI levels and increased TAS levels relative to the rats treated with MTX alone. Animals treated with CAR exhibited decreased tubular degeneration and architectural impairment relative to animals treated with MTX alone; however, the difference in histological scores did not meet the threshold of statistical significance., Conclusions: MTX treatment results in oxidative damage to the rat kidney; damage which is partially abrogated by the administration of CAR.

Aim: To evaluate the possible protective effect of pomegranate extract (PE) on rats following renal ischemia-reperfusion (I/R) injury., Materials and Methods: Twenty-four Wistar rats were divided into three groups. Sham group underwent laparotomy then waited for 45 minutes without ischemia. I/R group were subjected to left renal ischemia for 45 minutes followed by 60 minutes of reperfusion. I/R + PE group were subjected to the same renal I/R as the I/R group were also given 225 mg/kg PE peroral 30 minutes prior to the ischemia. Malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were determined on the blood samples and kidney tissues. Histopathological analyses were conducted on the kidney tissues., Results: Serum TAC levels were significantly decreased in I/R group when compared with S group (P = 0.001). Serum MDA levels were increased in I/R group; however, it was not statistically significant. In rat kidney tissues, TOS levels and OSI index were significantly increased after I/R injury, while TAC levels were decreased. In I/R + PE group, PE reversed the negative effects of I/R injury. PE pretreatment was effective in decreasing tubular necrosis score., Conclusion: PE pretreatment ameliorated the oxidative damage and histopathological changes occurring following renal I/R injury.

Purpose: To compare treatment modalities and investigate potential prognostic factors for survival in patients with malignant pleural mesothelioma (MPM)., Methods: The present study has investigated the data of 150 patients with MPM who were examined and treated in our center from 2005 to 2012., Results: The study included 87 male (58% and 63 female (42) patients. Surgical resection (pleurectomy/decortications (P/D), and extrapleural pneumonectomy (EPP)) was performed in 32 (36.7%) patients; 87 patients (58%) received chemotherapy alone and 16 (10.7%) had surgery, chemotherapy and radiotherapy (trimodal treatment). The median progression free and overall survival (PFS and OS) for all patients were 10.6 and 14.8 months, respectively. No statistically significant difference was observed between the patients who received pemetrexed/cisplatin (N=54) and gemcitabine/cisplatin (N=28) in terms of PFS and OS (p=0.145, p=0.244, respectively). Also, no statistically significant difference was registered between operated and non operated patients (PFS and OS, p=0.416, p=0.095, respectively). There was no difference in both PFS and OS rates between patients who had P/D or EPP (p=0.87, p=0.652, respectively). Log rank analysis: Eastern Cooperative Oncology Group performance status (ECOG PS) (p=0.018), histology (p<0.001), stage (p<0.001) and leukocytosis (p=0.005) were found to be significant prognostic factors of OS. At multivariate analysis, ECOG PS (p=0.016) and stage (p<0.001) were independent prognostic factors for OS., Conclusion: Median OS was approximately 1 year. ECOG PS, histological type, stage and presence of leukocytosis were prognostic factors that affected both PFS and OS. EPP or P/D surgical options did not provide difference in terms of survival. Survival rates in patients who received a combination of platinum analogues with pemetrexed or gemcitabine as front-line chemotherapy were similar.

Background: To determine the impact of caffeic acid phenethyl ester (CAPE) on abdominal adhesion formation after laparotomy., Methods: Forty female rats were allocated into four distinct groups on which laparotomy alone; laparotomy with traumatization of the uterine horns; laparotomy, traumatization of the uterine horns and intraperitoneal irrigation with saline, and laparotomy, traumatization of the uterine horns and intraperitoneal irrigation with CAPE were performed. After sacrifying the animals on the 14th postoperative day, histopathological examination and biochemical analysis were conducted to evaluate the formation of abdominal adhesions and antioxidant status., Results: In the CAPE group, total adhesion scores were significantly lower than in the control and saline groups. The CAPE group displayed less inflammation, giant cell formation, fibrosis and fibroblastic activity than the control group. On the other hand, the control group displayed higher total adhesion scores., Conclusion: The results of this study indicate that the administration of CAPE may have beneficial effects for the prevention of abdominal adhesion formation after laparotomy. Further clinical studies are mandatory to explore the actual therapeutic potential of CAPE., (Copyright © 2013 S. Karger AG, Basel.)