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Biomedical subjects

J C Rhee

Publications and source records attributed to J C Rhee.

6 recordsLinked to original sources

Biliary proteins in patients with and without gallstones.

BACKGROUND: Nucleation from supersaturated bile of calcium salts of cholesterol and bilirubinate is essential in the formation of gallstone. Nucleation requires gallbladder mucin and its main component, glycoprotein, may contribute to gallstone formation by providing a nidus or matrix for precipitation of lipid components. However, biliary protein patterns of patients with gallstones have not been completely explored. METHODS: We have tried to extract, isolate and characterize the proteins in patients with gallstones and without gallstones. 21 bile samples were obtained from patients with different types of gallstones and with no stones at cholecystectomy. Biliary protein concentrations were measured by Lowry and Bensadoun methods, and individual glycoproteins from each of the patients were compared by silver staining and densimetric quantification of Sodium Dodesyl Sulfate Polyacrylamide Gel Electrophoresis. RESULTS: 1) Among 16 gallstones, 5 were cholesterol stones, 5 were calcium bilirubinate stones, and 6 were black pigment stones. 2) The mean protein concentration was highest in bile with cholesterol stones (47.6 mg/ml), 24.2 mg% in bile without gallstones, and 15.9 mg/ml in brown pigment stones. 3) Cholesterol gallstones were found to have 14.2 KD glycoproteins, whereas pigment stones were found to have 66 KD glycoproteins. CONCLUSIONS: Gallbladder proteins from both cholesterol and pigment stones play an important role in the nucleation and growth of calcium salt crystals.

Bile

The causes and management of lower GI bleeding: a study based on clinical observations at Hanyang University Hospital.

During the period of the study, lower GI bleeding patients comprised a constant 1.6% of the total admitted patients at Hanyang University Hospital annually. There were no statistically significant changes according to year. The 970 cases were classified as follows: hemorrhoid and anal fissure 65.5%, malignant neoplasm 21.1% (rectal cancer 16.9%, sigmoid colon cancer 3.3%, anal cancer 0.9%), benign neoplasm 4.2%, ulcerative colitis 3.3%, infectious colitis 2.3%, ischemic colitis 1.8%, radiation colitis 1.3%, diverticulosis 0.3%, and others 0.2%. Ulcerative colitis and rectosigmoid cancer showed increasing trends, while other disease groups showed no change in the occurrence rate. Hemorrhoid and anal fissure developed mostly in the 30s age group, benign polyp and ulcerative colitis in the 40s age group, malignant neoplasm in the 50s age group, and ischemic colitis and radiation colitis in the 60s age group. There was no sexual predominance of lower GI bleeding. About 10% of the patients admitted to the hospital needed transfusions, particularly patients with ulcerative colitis (21.9%) and radiation colitis (23.1%). 20.2% of the patients improved with supportive measures and medical treatment and 79.8% underwent surgical operation. In particular, 51.2% of the patients with benign neoplasm underwent polypectomies.

Adolescent

Mechanism of oleic acid-induced inhibition on gastric acid secretion in rats.

We investigated the existence of an enterogastrone in rats induced by duodenal administration of oleic acid. Acid secretion by the luminally perfused stomach was stimulated in anesthetized rats by intravenous infusion of 0.3 micrograms.kg-1.h-1 pentagastrin. Intraduodenal administration of 3 mmol of oleic acid produced a profound inhibition (94%) of pentagastrin-stimulated acid output in 10 rats (P less than 0.01). Of several peptides in plasma including secretin, neurotensin, somatostatin, and peptide YY, only secretin was found to increase significantly (P less than 0.001). A similar degree of inhibition of acid output (93%) was caused by porcine secretin, 5.6 pmol.kg-1.h-1, given intravenously to mimic the plasma level of secretin produced by oleic acid infusion. The inhibitory effect of oleic acid on the acid secretion was completely reversed by intravenous injection of a rabbit antisecretin serum but not by a normal rabbit serum. These observations strongly suggest that the inhibition was mediated via circulating secretin. The inhibition produced by either oleic acid or secretin was completely blocked by indomethacin. The blocking action was completely reversed by intravenous administration of 48 micrograms.kg-1.h-1 prostaglandin E2. We conclude that endogenous secretin is a major enterogastrone released by oleic acid in anesthetized rats and that the inhibitory action of secretin requires endogenous prostaglandins.

Animals

Ulcerogenic tumor syndrome of the pancreas associated with a nongastrin acid secretagogue.

Among 30 patients with islet cell neoplasms or hyperplasia who exhibited marked gastric acid hypersecretion and peptic ulceration and/or diarrhea, fasting plasma gastrin concentrations were less than 150 pg/ml in 11 patients, whereas the remaining 19 patients had hypergastrinemia. Plasma extracts from seven of these 11 patients were assayed for acid secretagogue activity in rats. All seven plasma extracts had secretagogue activity that was not found in the plasma extracts of ten patients with ordinary duodenal ulcer disease. Each of the tumor or pancreatic tissue extracts obtained from nine patients exhibited secretagogue activity in rats even though tissue gastrin content was 101.9 pmol (213.8 ng).g-1 or less. The secretagogue activity of the tumor extracts was confirmed in conscious gastric fistula dogs. The tumors' secretagogue activity, in contrast to gastrin, was destroyed by trypsin. It was eluted between porcine motilin and human gastrin I from a Sephadex G-50 (Pharmacia LKB Biotechnology, Inc., Piscataway, NJ) superfine column and was not retained by CM-cellulose, at pH 8.5. Its retention time during reverse phase HPLC on a C18 column also differed from those of G17 and G34. Thus, this secretagogue activity appeared mediated by a small, acidic peptide with a molecular size of about 2000 to 3000 daltons. The present study indicates that plasma and tumor extracts of these 11 patients contain a gastric acid secretagogue activity mediated by a nongastrin peptide. We suggest that what may be a distinct clinical entity associated with endocrine neoplasms of the pancreas should be considered in the face of excessive acid hypersecretion without fasting hypergastrinemia.

Adult