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Bile from the liver and enzymes from the pancreas are both transported via the common bile duct to the small intestine, where they are integral in the digestion of foods, particularly fats. In experimental or therapeutic situations where the secretions from either one of these organs is diverted to a more distal region of the intestine, intestinal and pancreatic growth result. The pancreatic growth is thought to be stimulated by excessive release of the pancreatic hormone cholecystokinin. The increased growth of the pancreas and may presage future adverse occurrences such as pancreatitis (inflammation of the pancreas) and malignant pancreatic tumors. To determine the effects of a pharmacological antagonist of cholecystokinin (CCK) on pancreatic growth, a study was carried out with male rats that were subjected to either pancreaticobiliary diversion (PBD; accomplished by transplanting a section of the lower intestine to the area between the stomach and initial small intestine) or a sham operation. Half of the animals in each group were given a potent CCK antagonist (CR-1409). PBD resulted in a 91 and 137 percent increase in blood levels of CCK at 7 and 14 days, respectively, after the operation. The weight of the pancreas was significantly increased by PBD, and there were numerous biochemical and functional indices of cell proliferation (such as increased RNA content, incorporation of radioactive bromodeoxyuridine, and cell birth rate). Administration of CR-1409 completely abolished the increase in pancreatic weight and cell birth rate, while having no effect on blood levels of CCK. Hence, the effect of CR-1409 is likely due to its ability to block the CCK receptor. (Consumer Summary produced by Reliance Medical Information, Inc.)

Presents a comparison of the cholecystokinin-releasing effect of saturated and unsaturated fat in man. Research methods.

Presents preliminary communication studying meal-stimulated gastrin release, pentagastrin-stimulated gastric acid secretion, and the presence or absence of antral CP (Campylobacter pylori) in patients with duodenal ulcers. Experimental methods.

Background: Portable electronic devices are increasingly being used for clinical assessment of individuals with cognitive deficits. Prior to implementation of tablet-based assessments, comparison with other standard measures is needed., Objective: The study purpose was to compare an iPad administered cognitive assessment known as the Standardized Touchscreen Assessment of Cognition (STAC) to the Cognitive Linguistic Quick Test (CLQT) and the Cognitive Assessment of Minnesota (CAM)., Methods: Eighty-eight neurotypical participants completed the STAC, CAM, and CLQT in a randomized order. The researchers compared the participants' responses across similar subtests. Performance across iPad comfort levels was also explored., Results: Findings revealed moderate correlations in some areas of assessment: generative naming and immediate visual memory. The correlations varied across age groups within each area of assessment with no consistent pattern. Additionally, people with comfort using an iPad performed significantly better on three areas of STAC assessment (generative naming category and first letter, and auditory working memory) compared to people who reported no iPad comfort., Conclusions: Initial testing of the STAC in a neurotypical population identified moderate correlations with standard measures in some subtests; however, additional testing of the STAC is needed to determine the clinical utility and validity of assessing populations with cognitive impairments.

We have developed and validated a new radioimmunoassay for cholecystokinin. In order to establish that the antiserum binds large and small forms of CCK to an equal extent, we used the microbial enzyme clostripain, which cleaves large forms of CCK yielding CCK 8. Cleavage by clostripain of synthetic and purified forms of CCK, and CCK extracted at from human jejunum and CCK in human plasma was found not to affect immunoactivity, indicating that the antiserum reacts similarly with all forms of CCK. There is controversy over whether intraduodenal trypsin inhibits release of CCK in man. We used our radioimmunoassay to investigate whether chymotrypsin, rather than trypsin, could be the major mediator of negative feedback control of CCK release. Six normal subjects received an intraduodenal infusion of L-phenylalanine and L-tryptophan on two occasions, with the addition of either 1 g/l bovine chymotrypsin or 1 g/l albumin. Plasma CCK concentrations rose in response to the amino acid infusion, but were not affected by the addition of chymotrypsin, indicating that this enzyme is not a mediator of CCK feedback regulation in man.

The possibility that Campylobacter pylori (CP) in the gastric antrum stimulates gastrin release in duodenal ulcer (DU) disease was examined in 31 patients. The 25 patients with antral colonisation with CP had higher basal and meal-stimulated plasma gastrin concentrations, and higher peak acid output (PAO), than did the 6 without CP in the autumn.