Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen argyrophil cell carcinomas in 59 gastric scirrhous carcinomas were examined histologically, ultrastructurally, and immunohistochemically for polypeptide hormones, CEA, lysozyme, and HCG. In nine of these 16 tumors, polypeptides such as gastrin, somatostatin, and glucagon were demonstrated. Six of these nine tumors contained all three hormones, and three of these six tumors also had argentaffin cells. In all of these 16 tumors CEA were observed. Eight of them had CEA, lysozyme, and acid mucin synchronously. Of the above six tumors containing three peptides, three produced focal HCG. Ultrastructurally, several types of secretory granules were noted. Histologically, these 16 tumors showed poorly differentiated adenocarcinomas or signet ring cell carcinomas. Macroscopically, generalized type was 11 and localized type five. No hormonal syndrome was detected in any of the patients. It was suggested that these scirrhous argyrophil cell carcinomas of the stomach with the multifunction originate from totipotent immature cells of endodermal origin.
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PMID:Scirrhous argyrophil cell carcinoma of the stomach with multiple production of polypeptide hormones, amine, CEA, lysozyme, and HCG. 617 15

Eighteen argyrophil cell carcinomas in 101 early gastric carcinomas were explained histologically, ultrastructurally, and immunohistochemically for polypeptides, carcinoembryonic antigen (CEA), lysozyme, and human chorionic gonadotrophin (hCG). Seven of these 18 tumors had gastrin, and two of seven tumors also contained somatostatin. In all of these 18 tumors CEA were demonstrated. Seven had lysozyme and five of seven tumors also contained gastrin; hCG were present in four of the 18 tumors and two of four tumors had gastrin, CA, mucin, and lysozyme simultaneously. Argentaffin cells were found in seven of 18 tumors. Of the above seven tumors containing gastrin, three had argentaffin cells. Ultrastructurally, several types of secretory granules were noted and tumor cells resembling D1- or P cells were present in nine of the 18 tumors. Macroscopically, many of the tumors showed IIc or IIc + III type. Histologically, the 18 tumors consisted of six well differentiated adenocarcinomas and 12 poorly differentiated adenocarcinomas including signet-ring cell carcinoma. These 12 tumors frequently developed in the stomach of young females. In view of our previous investigations, it was suggested that the IIc-type argyrophil cell carcinoma histologically showing poorly differentiated adenocarcinoma may be related to scirrhous carcinoma of the stomach.
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PMID:Argyrophil cells in early gastric carcinoma: an immunohistochemical and ultrastructural study. 617 41

We studied goblet cell metaplasia and pseudopyloric gland metaplasia in 25 surgically removed, paraffin-embedded gallbladder specimens using mucin histochemistry, silver methods for endocrine cells, and the indirect immunoperoxidase method for 12 peptide hormones, secretory component, and lysozyme. Goblet cell metaplasia was closely related to the occurrence of endocrine cells that showed argentaffinity, argyrophilia, or immunoreactive gastrin, somatostatin, pancreatic polypeptide, or motilin. Mucosal areas without goblet cell metaplasia were devoid of such endocrine cells. Metaplastic pseudopyloric glands showing lysozyme immunoreactivity were positive for class III mucin with paradoxical concanavalin A staining. Specimens with florid metaplastic lesions revealed a low tendency to form Rokitansky-Aschoff sinuses whose cells never showed a metaplastic nature. We compared the pathophysiological significance of metaplastic lesions in the gallbladder with intestinal metaplasia of the stomach.
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PMID:Histochemical studies of metaplastic lesions in the human gallbladder. 654 69

A 47-year-old man was admitted with appendicitis, and appendectomy was performed. On microscopic examination of the resected specimen, the presence of goblet cell carcinoid in the tip of appendix was revealed. This tumor showed an aggressive nature with perineural and vascular invasion around the appendiceal serosa. The tumor was composed of two main cell populations: mucin-producing (goblet cell type) and silver-positive cells (endocrine differentiation). Additionally, a few cells were also positive for serotonin and lysozyme, but negative for gastrin and ACTH. These findings suggest that goblet cell carcinoid share some functional and histologic characteristics with carcinoid tumors and adenocarcinomas, although it is a distinct entity.
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PMID:Goblet cell carcinoid of the appendix. 794 43

The histological change of the biliary mucosa in clonorchiasis is characterized as adenomatous hyperplasia, and cross-sectioned mucosa looks like intestinal mucosa. In addition to the glandular hyperplasia, the metaplasia of mucin secreting cells is also known. The present study investigated the presence of intestinal secretion from the biliary mucosal cells of rabbits and rats with Clonorchis sinensis infection. The rabbit was infected with 300 and the rat was infected with 100 metacercariae of C. sinensis. A part of the animals were followed up after praziquantel treatment. The rabbit livers were prepared for histochemistry to observe any endocrine secretion and the bile duct mucosa of the mice was processed for the activity of brush border membrane (BBM)-bound enzymes of the small intestine. Immunohistochemistry with the polyclonal antibodies and biotin-streptavidin-peroxidase staining kit showed no positive cells for gastrin and secretin, but a few cells were positive for serotonin. The proliferated biliary mucosa of the mice revealed no activity of disaccharidases and aminopeptidase. Only alkaline phosphatase activity was found both in the control and the infected. The hyperplastic biliary mucosal cells showed no gastrointestinal secretory functions. The serotonin secreting cells may be one of the inflammatory cells.
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PMID:Secretions of the biliary mucosa in experimental clonorchiasis. 851 95

Malignant transformation in bile duct hamartomas has been previously reported in very rare instances. Here, we describe a unique case of a neuroendocrine tumor of the liver arising within an area of unusually large hamartoma with predominant bile duct component, hitherto unreported and distinct from the conventional von Meyenburg complex. The tumor was apparently secreting gastrin and chromogranin, with associated gastrinoma syndrome over several years. The histologic picture was reminiscent of a moderately differentiated adenocarcinoid, with positive mucin staining in a signet ring pattern. Tumor cells showed positive staining for neuron-specific enolase, chromogranin A, gastrin, and serotonin. Staining for pancreatic hormone peptides was negative. Resection of the tumor was apparently curative, with complete resolution of the patient's symptoms.
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PMID:Adenocarcinoid of the liver arising within an area of hamartoma with predominant bile duct component. 887 46

The presence of the extracellular calcium-sensing receptor on human antral gastrin cells was investigated. Reverse transcription PCR using mRNA isolated from gastrin cell- enriched cell cultures identified a product with a sequence identical to part of the human parathyroid-secreting cell calcium-sensing receptor. Immunocytochemistry with an antibody to the extracellular region of the receptor immunostained all gastrin cells (but not mucin or somatostatin cells), and detected appropriate-sized bands in Western blots of whole cell lysates. Increasing extracellular calcium levels from 0.5 to 9 mM stimulated gastrin release in a concentration-dependent manner, with maximal release obtained at 7.2 mM. A known agonist of the calcium receptor, spermine also stimulated gastrin release. Microfluorimetry of identified gastrin cells demonstrated that increasing extracellular calcium resulted in an initial rapid rise in intracellular calcium followed by a plateau level that returned to basal levels immediately after removal of the elevated calcium. The traces were consistent with activation of a receptor-mediated mechanism rather than a concentration-dependent influx of calcium. In conclusion, these data indicate that G cells express the calcium-sensing receptor, and that activation of the receptor may explain the acid rebound phenomenon associated with calcium-containing antacid preparations.
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PMID:Expression of the calcium-sensing receptor on human antral gastrin cells in culture. 915 73

In order to establish the measurement of gastric mucin secreted from cultured mucous cells, rat gastric mucin was purified from secreted mucus with Sepharose CL-4B column chromatography. Gastric mucin was measured by dot blot analysis using an enzyme-linked lectin (soybean agglutinin) assay in a good concentration-dependent manner. Surface epithelial cells were dispersed by limited digestion of a rat everted stomach and collected by density gradient centrifugation with Percoll. These cells were inoculated onto gelled collagen dishes, then cultured in a medium supplemented with 10% fetal calf serum under a 5% CO2 atmosphere in air. Changing the medium after a 2-d culture, the cells were cultured for another 3 d. During the culture, the numbers of cells each day were almost equal, but mucin contents in the cells increased, and then dropped at day 5 after inoculation. At that time, the edge of the cell layer peeled off and the cells adhered to each other. Using 2-d cultured cells, the effects of some secretagogues on mucin secretion were investigated. Carbachol, secretin, CCK-8 and prostaglandin E2 (PGE2) strongly stimulated mucin secretion, and gastrin I weakly did. However, histamine offered no stimulation.
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PMID:Gastric mucin secretion from cultured rat epithelial cells. 917 25

Infection with Helicobacter pylori (H. pylori) is now recognized as a major factor in the pathogenesis of gastric disease, and the successful therapy regimens require a combination of H2 blockers with gastroprotective and antimicrobial agents. Ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene) amino]-4-thiazolyl] methyl]thio]ethyl]amino]methylene]-4-bromo-benzenesulfonamide, CAS 100981-43-9, FI-3542) is the only drug combining acid-suppressant activity with remarkable gastroprotective and anti-H. pylori properties. The drug not only displays a potent anti-H. pylori activity alone, but also exerts a strong potentiating effect on the efficacy of antimicrobial agents commonly used for H. pylori eradication, and the successful ulcer therapy with ebrotidine induces a significant (4-fold) increase in the H. pylori aggregation titer of gastric mucin. Moreover, the drug exhibits a strong inhibitory effect on H. pylori urease activity, the extent of which exceeds that of ranitidine, omeprazole and lansoprazole. Ebrotidine has also been demonstrated to exert a potent inhibitory action on the enzymatic activities directed towards mucus perimeter of gastric mucosal defense, causing a marked inhibition of H. pylori protease, lipase and phospholipase A2 activities. Another important property of ebrotidine is its ability to efficiently counteract the disruptive effects of H. pylori lipopolysaccharide on the integrity of gastric epithelium. This includes countering the interference by the lipopolysaccharide in mucosal integrin receptor interaction with proteins of extracellular matrix and the reversal of H. pylori disruptive effect on the binding of mucin to its gastric epithelial receptor. Furthermore, most recent data indicate that ebrotidine has the ability to reverse the impairment caused by H. pylori in feedback inhibition of gastrin release by somatostatin. This activity of ebrotidine apparently stems from the drug's ability to counter the untoward effect of H. pylori on the binding of somatostatin to its specific receptor on the gastric mucosal G-cells. The unique combination of acid suppressant, gastroprotective and anti-H. pylori activities makes ebrotidine a drug of choice in the treatment of gastric disease caused by H. pylori.
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PMID:Anti-Helicobacter pylori activities of ebrotidine. A review of biochemical and animal experimental studies and data. 920 47

Although clusters of pancreatic acinar cells (CPACs) have been reported in gastric mucosa of adults, they have not been described in children. We reviewed 283 pediatric gastric (239 antral and 44 corpus) mucosal biopsies during a 2-year period and detected CPACs in 10 antral biopsy samples. These biopsy samples were stained immunohistochemically for pancreatic exocrine markers (trypsin, chymotrypsin, alpha-amylase, and lipase) and a panel of regulatory substances (insulin, glucagon, somatostatin, pancreatic polypeptide, gastrin, and serotonin). Double immunostaining for colocalization of chromogranins and trypsin as well as mucin and trypsin also were performed on all cases. CPACs were seen in antral mucosa in a background of either normal or minimally inflamed mucosa, without any atrophy or metaplasia, and were positive for all pancreatic exocrine markers. Stray chromogranin-positive cells in the CPACs were also immunopositive for somatostatin, gastrin, or serotonin. All CPACs showed a few hybrid (amphicrine) cells that coexpressed both chromogranin and trypsin. In one case, ultrastructural examination showed such cells to contain both zymogen and neurosecretory granules. Although the presence of CPACs exclusively in the antrum is most likely the result of a sampling bias, the presence of hybrid cells with an amphicrine phenotype suggests that CPACs probably result from an aberration of stem cell differentiation.
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PMID:Pancreatic acinar cell clusters in pediatric gastric mucosa. 942 22


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