Intestinal epithelial cell lines capable of differentiating in monolayer culture have been difficult to obtain, prompting the use of novel approaches including immortalization with oncogenes or tumor viruses. The aim of this study was to obtain conditionally immortalized human intestinal epithelial cells (temperature-sensitive fetal human intestinal [tsFHI] cells) and study their growth and differentiation capabilities.

A nongastrin acid-stimulating peptide (NGASP) has been found in ulcerogenic pancreatic tumor syndrome without hypergastrinemia. The mechanism of gastric acid hypersecretion by NGASP was investigated in rats.

Helicobacter pylori alterations in gastric acid output and mucosal proliferation may involve the enterochromaffin-like (ECL) cell. To test whether H. pylori affects ECL cell histamine secretion and proliferation, the effect of lipopolysaccharide (LPS) on ECL cell function in vitro was investigated.

Previous studies have shown that the renin-angiotensin axis plays a pivotal role in vasoconstriction of the gastric, intestinal, and hepatic circulations during cardiogenic shock. The aim of this study was to evaluate the fundamental hemodynamic mechanism of pancreatic ischemia during cardiogenic shock induced by pericardial tamponade.

Gastric adenocarcinoma has been previously recognized as a potential complication of familial adenomatous polyposis coli (APC) and attenuated forms of APC (AAPC). This tumor has only been reported to originate from adenomatous polyps of the gastric mucosa in these clinical conditions. There have been no previous case reports of gastric adenocarcinoma arising from the more commonly found fundic gland polyps associated with AAPC or APC. We report the first definitive case of gastric adenocarcinoma arising from a hyperplastic polyp of the fundis of a patient with AAPC.

Bombesin is a neuropeptide with many biological functions and is known to stimulate bile secretion. The aim of this study was to determine the role of bombesin in bile secretion and its site of action.

The excretion of various organic anions into bile is mediated by an adenosine triphosphate-dependent conjugate export pump, which has been identified as the canalicular isoform of the multidrug resistance protein (Mrp2). Mrp2 function is impaired in various experimental models of intrahepatic and obstructive cholestasis, but the underlying molecular mechanisms are unclear. The aim of this study was to investigate these molecular mechanisms.

Small intestinal carcinomas are rare but occur with increased incidence in Crohn's disease. The aim of this study was to elucidate the genetic alterations.

Rotavirus, an important agent of gastroenteritis in children, causes diarrhea by infecting differentiated villus enterocytes in the small intestine. The aim of this study was to determine whether cytokines that can be expressed by mucosal cells have an effect on the rotavirus susceptibility of cultured human enterocytes.

Tumor necrosis factor (TNF) alpha mediates both liver injury and regeneration. Kupffer cells are thought to produce TNF because gadolinium chloride (GdCl), a drug that depletes Kupffer cells, prevents TNF-mediated injury. However, GdCl increases liver TNF and regeneration after partial hepatectomy (PH), suggesting that other cells produce TNF during regeneration. The aim of this study was to identify the source(s) of TNF after PH in normal and Kupffer cell-depleted rats.

Intraileal nutrients modulate gastrointestinal motility, but effects of maldigestion on postprandial motility are unknown. The aim of this study was to compare motor responses with ileal nutrient exposure in health and pancreatic insufficiency after a meal or intraluminal perfusion.

Because SRS identifies 90% of hepatic metastatic disease and the addition of other studies (ultrasonography, C.T. MRI, and selective mesenteric angiography) identities only 4% more, the identification of a primary lesion with SRS obviates for the most part the use of further investigations. If SRS is negative, additional studies should only be undertaken if surgery is contemplated. Because SRS may only localize 60%-70% of primary gut NETs, an additional 10%-15% may be identified by undertaking additional studies. The most sensitive test, STIR-MRI, should be undertaken next, but because it is not widely available, pancreatic protocol CT scan is almost as effective in identification of a primary lesion. If a primary gastrinoma cannot be identified by SRS or STIR-MRI, endoscopic ultrasonography should be undertaken because duodenal gastrinomas are often minute and multicentric. A similar strategy applies for insulinomas because up to 40% cannot be located by SRS and the majority are located in the pancreatic head. Thus, STIR-MRI followed by endoscopic ultrasonography is the most appropriate course. Although calcium provocation-angiography is highly effective in the identification of insulinomas, it is significantly more invasive and should be used only as a last resort. Of particular interest is the observation that in the study of gastrinomas, SRS altered clinical management in almost 50% of patients. This reflected the ability of SRS not only to identify the primary tumor location but clarify equivocal localization results generated by conventional imaging studies. It thus seems that the simplicity, superior sensitivity, high specificity, and cost-effectiveness of SRS mandate that it be the imaging modality in patients with gastrinomas. Because the cost of an SRS is $1800 and may obviate the need for multiple other topographic studies that are at least as expensive, the fiscal dictates further warrant the use of this study as the initial topographic investigation. These observations are probably applicable to all gut NETs, although the likelihood of primary identification in the instance of insulinoma patients may be somewhat less. The timely and cost-effective establishment of the type of NET, its primary site, and the detection metastatic spread will enable determination of the appropriate management strategy.