Infectious agents have long been suspected of playing a role in the initiation of Crohn's disease. The objective of this study was to search for likely microbial agents in diseased tissues using immunocytochemical techniques.

A case of multiple focal nodular hyperplasia of the liver occurring in a 22-year-old woman with musculoskeletal hemihypertrophy and anomalous vascular supply to the liver is described. The patient had Klippel-Trénaunay-Weber syndrome and abdominal pain and tender massive hepatomegaly. Visceral angiography showed marked dilatation of the celiac axis and both the main trunk and peripheral branches of the hepatic artery. Large abdominal veins drained from the dome of the liver into the hepatic veins. The vascular anomalies were evident on contrast-enhanced computed tomography and magnetic resonance imaging. Multiple focal nodular hyperplasia was confirmed by laparoscopic liver biopsy. The findings in this patient support the concept that multiple focal nodular hyperplasia characteristically occurs in a syndromic form and is induced by an irregular arterial supply in the liver, with localized hyperfusion that leads to nodular areas of hepatocyte hyperproliferation.

Although potentially noxious compounds are used routinely to disinfect endoscopes, reports of their inadvertent introduction to the gastrointestinal tract, usually attributed to the retention of disinfectant within endoscope channels, are rare. This case report describes the clinical features of glutaraldehyde-induced colitis and the pathology of the mucosal injury in four patients, in at least one of whom the disinfectant was not retained in the endoscope itself. Within 3 months, three patients experienced severe acute proctocolitis < 6 hours after a sigmoidoscopy showing no abnormalities, performed in a small endoscopy unit. Investigation of the unit's protocols suggested that the most likely cause was retention of 2% glutaraldehyde disinfectant in the endoscope channels, and changes were made to prevent this. When a fourth case occurred 5 months later, the source of the glutaraldehyde was found to be the tubing connecting water bottles to the endoscopes, which was disinfected rigorously but flushed inconsistently between cases. Glutaraldehyde-induced colitis seems similar to ischemic colitis in biopsy specimens and cannot be diagnosed by histological analysis alone. Acute colitis occurring within 24 hours of a colonoscopy showing no abnormalities should be considered iatrogenic and should lead to an investigation of procedures in use for cleaning and disinfecting endoscopic equipment.

Free radicals are important mediators of reperfusion injury; however, the mechanism(s) of oxyradical production after liver reimplantation are not well understood. A model of cold storage and reperfusion using low-level chemiluminescence to directly measure oxyradical production during reperfusion was developed.

It has been reported that hepatic iron concentration (HIC) may influence response to therapy in chronic viral hepatitis. The aim of this study was to determine the relationship between HIC and response to interferon alfa therapy in patients with chronic hepatitis C.

We sought to determine in a double-blinded, placebo-controlled study if the nonsteroidal anti-inflammatory drug sulindac causes regression of sporadic colonic polyps. The impetus for this study is the profound regressive effect of sulindac on polyps in familial adenomatous polyposis.

In the intestine, the cystic fibrosis transmembrane conductance regulator (CFTR) has been localized to the apical pole of crypt epithelial cells. Recent data indicate that some villus cells may also express CFTR, although the identity of these cells has not been established. The aim of the current study was to characterize the distribution, morphology, and surface marker expression of CFTR-expressing villus cells.

Nitric oxide has many physiological functions and may play an important role in modulating tissue injury. However, the mechanism of NO action in ischemia/reperfusion injury is completely unknown. This report investigates the role of NO in hepatic reperfusion injury.

The frequency of colorectal adenomas, the precursor lesions for most cases of colorectal carcinoma, has been generally measured as prevalence rates of adenomas at autopsy or colonoscopy. The aim of this study was to estimate the incidence rate of adenomas and compare it with the adenoma recurrence rate.

Chronic colitis is associated with an increased risk of colorectal neoplasia, creating a need for early diagnosis in this population. Little is yet known of the genetic changes of early lesions. Cases of colitis-associated neoplasia were analyzed for APC and K-ras mutations with special emphasis given to the spectrum of noninvasive lesions.

The inability to precisely measure the area of Barrett's metaplasia has impaired the study of its natural history and response to therapy. This study used a novel computer program that creates two-dimensional maps of the esophagus allowing for calculation of the area of Barrett's metaplasia.

The central subnucleus of the nucleus of the solitary tract has been implicated in central reflex control of esophageal peristalsis. This study determined the presence of nitric oxide synthase in the brain stem circuit controlling esophageal peristalsis by combining transsynaptic retrograde tract tracing with pseudorabies virus and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH) histochemistry.

Monocyte-chemoattractant protein 1 (MCP-1) activates macrophages and increases the migration of monocytes into tissue during inflammation. It was hypothesized that MCP-1 expression is involved in intestinal inflammation.

The case of a 50-year-old man with abdominal pain and abnormal liver test results is described. Endoscopic retrograde cholangiopancreatography with manometric studies showed biliary dilatation, poor ductal drainage, and sphincter of Oddi dysfunction. Clinical and radiographic clues suggested the possibility of an ampullary lesion; a small ampullary adenoma was detected after endoscopic sphincterotomy, and ampullary carcinoma was found in the operative specimen. Malignancy can cause sphincter dysfunction not only in the esophagus (as pseudoachalasia) but in the ampulla of Vater as well.

The cellular oncogene c-yes and its viral homologue v-yes (the transforming gene of Yamaguchi 73 and Esh avian sarcoma viruses) encode 62-kilodalton, cytoplasmic, membrane-associated, protein-tyrosine kinases. For the related Src kinase, a close correlation exists between elevated kinase activity and cell transformation. Previously, we observed elevated Yes activity in many human colon carcinomas. Colonic neoplasia provides an opportunity to study tumor progression because most carcinomas arise from adenomas, which in turn arise from normal epithelia. The malignant potential of adenomas varies with size, histology, and degree of dysplasia. Large adenomas (> or = 2 cm) with villous architecture and severe dysplasia are most likely to develop carcinoma.

Secretin has been shown to mediate feedback control of pancreatic secretion of fluid and bicarbonate in rats, guinea pigs, and dogs. However, little is known about secretin in the feedback regulation in humans. We investigated the roles of secretin, cholecystokinin, neurotensin, and pancreatic polypeptide on feedback regulation of pancreatic secretion in 10 human volunteers.

The molecular pathogenesis of esophageal cancers is not completely understood. Frequent allelic losses occur on chromosome 5q, suggesting the presence of a tumor-suppressor gene that is important in esophageal tumorigenesis. Because the APC gene is located on chromosome 5q, we sought to determine its involvement as a candidate tumor-suppressor gene in esophageal carcinogenesis.

Secretin is an inhibitory hormone of gastric acid secretion. However, its inhibitory mechanism has not been well understood. Possible roles of both somatostatin and prostaglandins were investigated.