17 research outputs found

    Combined Interventional Radiological and Endoscopical Approach for the Treatment of a Postoperative Biliary Stricture and Fistula

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    A 43-year old woman was admitted 11 days after open cholecystectomy with a iatrogenic bile duct injury. On admission the patient showed an uncontrolled biliary fistula through an external drain placed at an emergency laparotomy for biliary peritonitis with fever and jaundice. PTC showed a biliary stricture type II (Bismuth). A percutaneous drainage was performed to decompress the biliary system. Three weeks later, percutaneous balloon dilatation of the stricture was performed. However, bile leakage persisted. In a combined transhepatic/ endoscopic procedure, the percutaneous biliary drainage was replaced by a nasobiliary tube. One week later, no stricture was found and the biliary leak was sealed. The patient could be discharged without symptoms or signs of cholestasis. The multidisciplinary management of post-operative biliary fistula is presented, comparing the role of interventional radiology, endoscopy and surgery

    Significance of proliferative activity and DNA ploidy in pancreatic cancer and chronic pancreatitis

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    Summary: Background: Precise preoperative assessment of diagnosis and prognosis in patients with pancreatic tumors would facilitate improvement of treatment strategies. In this context, we evaluated the significance of the proliferative index and of static DNA cytophotometry in the diagnosis and prognosis of pancreatic tumors. Methods: Consecutive surgical specimens from 26 patients with ductal pancreatic cancers and eight patients with chronic pancreatitis were investigated by: 1. Staging; 2. Conventional histological and cytological grading; 3. MIB-1 (Ki-67 labeling) proliferating index; and 4. Static DNA cytophotometry. Results: All patients with chronic pancreatitis had a normal MIB-1 labeling index and a euploid DNA content. In contrast, patients with pancreatic cancers rarely had a normal labeling index (1 of 26 patients) or a euploid DNA content (6 of 26 patients). Staging significantly correlated with survival time. However, it did not correlate with cytological criteria. Cytological criteria, such as conventional grading, MIB-1 proliferating index, and DNA ploidy, were not significantly correlated with survival time. Conventional grading was significantly correlated (p<0.02) with proliferating index, but not with DNA ploidy. Conclusion: Proliferating index and DNA ploidy are relevant cytological markers that can help to discriminate between chronic pancreatitis and pancreatic cancer. The prognostic significance of these markers in pancreatic cancer patients, however, seems to be less relevant than tumor stage and of limited relevance for the individual cancer patien

    Significance of proliferative activity and DNA ploidy in pancreatic cancer and chronic pancreatitis

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    http://helguera.library.vanderbilt.edu The J. León Helguera Collection of Colombiana provides access to unique primary sources on 19th-century Colombian history and culture. The result of a half-century of collecting on three continents, the collection is one of the largest and most wide-ranging in the United States. Materials are grouped into three separate types: broadsides, 1825-1972; pamphlets (including novenas), 1785-1969; and programas, 1819-1914. (RSS

    Role of the different isoforms of cyclooxygenase and nitric oxide synthase during gastric ulcer healing in cyclooxygenase-1 and -2 knockout mice

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    Traditional NSAIDs, selective cyclooxygenase (COX)-2 inhibitors, and inhibitors of nitric oxide synthase (NOS) impair the healing of preexisting gastric ulcers. However, the role of COX-1 (with or without impairment of COX-2) and the interaction between COX and NOS isoforms during healing are less clear. Thus we investigated healing and regulation of COX and NOS isoforms during ulcer healing in COX-1 and COX-2 deficiency and inhibition mouse models. In this study, female wild-type COX-1(-/-) and COX-2(-/-) mice with gastric ulcers induced by cryoprobe were treated intragastrically with vehicle, selective COX-1 (SC-560), COX-2 (celecoxib, rofecoxib, and valdedoxib), and unselective COX (piroxicam) inhibitors. Ulcer healing parameters, mRNA expression, and activity of COX and NOS were quantified. Gene disruption or inhibition of COX-1 did not impair ulcer healing. In contrast, COX-2 gene disruption and COX-2 inhibitors moderately impaired wound healing. More severe healing impairment was found in dual (SC-560 + rofecoxib) and unselective (piroxicam) COX inhibition and combined COX impairment (in COX-1(-/-) mice with COX-2 inhibition and COX-2(-/-) mice with COX-1 inhibition). In the ulcerated repair tissue, COX-2 mRNA in COX-1(-/-) mice, COX-1 mRNA in COX-2(-/-) mice, and, remarkably, NOS-2 and NOS-3 mRNA in COX-impaired mice were more upregulated than in wild-type mice. This study demonstrates that COX-2 is a key mediator in gastric wound healing. In contrast, COX-1 has no significant role in healing when COX-2 is unimpaired but becomes important when COX-2 is impaired. As counterregulatory mechanisms, mRNA of COX and NOS isoforms were increased during healing in COX-impaired mice
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