Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of a 70-year-old woman with a history of gastric ulcer and several pneumonias is presented. She was found to have pulmonary emphysema, severe alpha-1-antitrypsin (alpha1AT) deficiency and raised serum mitochondrial antibodies. Surgical liver biopsy showed portal liver cirrhosis, PAS-positive, diastaseresistant globules in the hepatocytes and changes interpreted as florid duct lesion of primary biliary cirrhosis. A brother has severe alpha1AT deficiency. Two daughters had raised mitochondrial antibodies. One of the latter had a granulomatous hepatitis, a common finding in primary biliary cirrhosis. The association of alpha1AT deficiency and primary biliary cirrhosis does not seem to have been described previously.
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PMID:Alpha-1-antitrypsin deficiency, mitochondrial antibodies and possible primary biliary cirrhosis. A case report and family study. 108 Sep 23

To elucidate the role of Helicobacter pylori infection in the pathogenesis of gastric ulcer, we investigated the intracellular mucin content by measuring the periodic acid-Schiff-Alcian blue (PAS-AB)-stained substances, by means of computer, in the biopsy sample of gastric mucosa from patients with and without H. pylori infection. In the antral mucosa the intracellular PAS-AB-stained mucin content was significantly smaller in patients with infection than in patients without infection, whereas in the oxyntic gland mucosa the intracellular mucin content showed no significant change between patients with and without infection. In an animal study we investigated the effect of ammonia, which might be produced by H. pylori in the presence of urea. The ammonia, administered orally, caused a greater decrease of intracellular PAS-AB-stained mucin content in the gastric antral mucosa than in the body mucosa, in a dose-dependent manner. The results suggested that H. pylori infection had a different effect on the gastric mucosal intracellular PAS-AB-stained mucin and lowered specifically the antral intracellular PAS-AB-stained mucin content, possibly due to generation of ammonia by H. pylori.
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PMID:Different effect of Helicobacter pylori on the human gastric antral and body mucosal intracellular mucin. 170 31

Histochemically differentiated mucins have been studied in the mucosal lining of the esophagus and the stomach. Acid mucin was differentiated from neutral mucin by the alcian blue/PAS technique and sulphomucin by the high iron diamine/alcian blue technique. Neutral mucin secreted normally by the stomach mucosa was replaced by acid mucin in 17 of the 19 mucin secreting adenocarcinomas involving the lower third of the esophagus, and in 24 of the 28 mucin secreting gastric adenocarcinomas studied. The intestinal metaplasia (IM) seen in the gastric mucosa associated with adenocarcinoma, chronic gastric ulcer and chronic gastritis was classified according to the type of mucin secreted by the goblet cells. IM secreting sulphomucins was seen to be associated with gastric adenocarcinoma.
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PMID:Mucin histochemistry of the upper gastrointestinal tract. 270 46

Morphological observations were made of the behavior of biogenic amines in the gastric wall of rats with acetic acid-induced ulcer. In the normal rat stomach, abundant adrenergic fibers were seen in the adventitia of arteries and arterioles, with frequently distributed mast cells in their environs, in all gastric wall layers. Mast cells had a more frequent distribution in the antral region than in the corpus ventriculi while enterochromaffin-like cells (EC-like cells) were found with greater frequencies in the latter region of gastric wall. Adrenergic fibers were abundant around blood vessels in perilesional area of the gastric wall of rats with acetic acid ulcer. Mast cells, seen more frequently in the antral region as in the normal rats, showed degranulation in these rats. The population of PAS-positive mucous cells reached its peak in 10 days after injection of acetic acid and subsequently declined with healing of the ulcer, thus remarkably concordant with the ulcer index. Local administration of serotonin produced angiospasm in the greater omentum. The finding indicates a possible participation of arteriospasm by adrenergic nerve fibers in the pathogenesis of gastric ulcer. The results of the present study strongly suggest that biogenic amines have bearing as an aggressive factor upon the angiospasm theory of ulcerogenesis.
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PMID:A morphologic study of the behavior of biogenic amines in experimental acetic acid gastric ulcer. 716 May 98

Aqueous ammonia in concentrations of 0.02 or 0.1% was continuously administered to rats to study its effect on the gastric mucosa histologically and cell kinetically. Furthermore, acetic acid ulcer, which is a model of chronic gastric ulcer, was experimentally induced in the stomachs of rats to assess the influence of 0.02% ammonia on the course of this ulcer. Male Donryu rats were divided into three groups given 0.02% ammonia, 0.1% ammonia or tap water. On several occasions (1, 3 and 5 days and 1, 4, 8, 12 and 24 weeks from the beginning of the experiment), the gastric mucosa in the fundic gland region and the antrum was examined histologically, and from the viewpoint of cell kinetics. The assessment in the 8th and 24th weeks employed the double labeling technique with bromodeoxyuridine and 3H-thymidine. The assessment on the other occasions used the flash labeling technique with bromodeoxyuridine. Both the 0.02% and 0.1% ammonia treatment groups showed a decrease in PAS-positive mucus and an enhanced cell cycling in the early stage of the experiment. After long periods of treatment, these groups showed a reduction in the gland height, a recovery in PAS-positive mucus and a suppression of cell cycle, suggesting direct toxicity of ammonia on the gastric mucosa. Although glandular atrophy was observed in these animals, infiltration of inflammatory cells was not observed. Thus, the relationship between ammonia and gastritis remained obscure. No ulcer developed in any group. Subsequently, we experimentally induced Ul-IV or Ul-V acetic acid ulcers in the stomachs of rats, according to the method of Okabe et al. (1971, 1972). These rats were divided into two groups given 0.02% ammonia or tap water. In the 4th and 8th weeks of the experiment, the stomachs of these rats were examined histologically and from the viewpoint of cell kinetics. The 0.02% ammonia treatment group showed a significant increase in the ulcer index (long diameter x short diameter; mm2) in the 4th and 8th weeks. This group also showed suppressed cell cycling of the regenerative epithelium and fibroblasts in the ulcer margin, suggesting direct toxicity of ammonia. Thus, healing of peptic ulcer was delayed by continuous administration of 0.02% ammonia.
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PMID:Influence of ammonia solution on gastric mucosa and acetic acid induced ulcer in rats. 751 30

Our previous works have proved that moxibustion at "ShenJue" plays a role in protecting gastric mucosa in the experimental gastric ulcer model rat. The present studies are designed to determine whether the mechanisms of moxibustion protecting gastric mucosa are mediated by mucus. The results are as follows: Either before or after the experimental gastric ulcer model had formed, moxibustion treatment would markedly increase the ratio of PAS positive staining layer to total length of gastric gland (p < 0.05), and the combined gastric mucus of stomach (P < 0.05). These results are negatively correlated to gastric ulcer area and suggest that the mechanisms of moxibustion protection on gastric mucosa are mediated by mucus in the experimental gastric ulcer model rat.
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PMID:[The relation between protective effect of moxibustion on gastric mucosa and mucus]. 792 37

Lansoprazole, one of PPIs, is a strong antacid and it cures stomach and duodenal ulcers at early stages as well as having antibiotic action towards HP. The in vitro MIC of the product is between 3.13 and 12.5 micrograms/ml and it was 12.5 micrograms/ml, which was the same as MIC of colloidal bismuth citrate, in our study. Sterilizing effect of Lansoprazole is reported to be the direct attack on HP bacteria from electron microscopic findings. Our study revealed that Lansoprazole would preserve the epithelial cells on the edge of a stomach ulcer and would protect PAS-positive substance within them. Lansoprazole is said to cure many H2-Blocker resistant ulcers and to suppress the rate of recurrence of stomach and duodenal ulcers. These effects are considered to be attributable to maintenance of mucous barrier and maintenance of cytoprotection of the gastric mucosa by Lansoprazole as well as its sterilizing action mainly on HP.
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PMID:[Activity of Lansoprazole (new proton pump inhibitor) against Helicobacter pylori and its therapeutic efficacy]. 828 44

Oxygen free radicals have been implicated in the pathogenesis of gastrointestinal mucosal injury. However, their effect on the quality of experimental gastric ulcer healing has not been investigated previously. Gastric ulcers were produced on the anterior wall of the stomach of rats by submucosal injection of 20% acetic acid. To investigate the role of oxygen radicals, rats with gastric ulcers were treated with scavengers for 6 weeks. Rats received either a daily dose of 20,000 U/kg of recombinant human Cu,Zn-SOD, a 1% solution of DMSO administered orally ad libitum, or 50 mg/kg/day of allopurinol administered orally. The quality of ulcer healing was evaluated by histologic and biochemical parameters: ulcer area, lipid peroxide levels, abnormality of regenerated mucosa, angiogenesis, and fibrosis as assessed by Azan staining, mucin content as assessed by the PAS-positive area, and polymorphonuclear leukocyte (PMN) infiltration. The treatments with SOD, DMSO, or allopurinol did not affect the ulcer area or lipid peroxide levels in the gastric mucosa, and SOD did not affect the histologic abnormality score, PMN infiltration in regenerated mucosa, the collagen fiber proliferation index, or the PAS-positive mucous score. DMSO and allopurinol significantly increased the collagen fiber proliferation index and the PAS-positive mucous score compared with controls. These results indicate that scavenging hydroxyl radicals or inhibiting xanthine oxidase enhances the quality but not the speed of gastric ulcer healing.
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PMID:Effects of oxygen radical scavengers on the quality of gastric ulcer healing in rats. 877 96

The study was performed to examine whether indomethacin administered during the initial period of acetic acid-induced gastric ulcer healing affects future ulcer recurrence. Gastric ulcers were produced in rats by subserosal injection of acetic acid. Indomethacin (1 mg/kg/day, orally) administered either alone or concomitant with ornoprostil (50 micrograms/kg/day, orally) was started on the fourth day and continued for 56 days. In rats whose ulcer healed at the 90th day after production of ulcer, endoscopy was done every 30 days to examine recurrence of ulcer. Gastric specimens were obtained 10, 30, 60, 90, and 240 days after ulcer production for histology, to quantitate the height of regenerated mucosa, thickness of fibrous tissue, degree of polymorphonuclear cell infiltration, and PAS-positive cells. Cumulative ulcer recurrence rate was significantly higher in rats initially treated with indomethacin than in controls. Increased polymorphonuclear cell infiltration was the major histologic abnormality persisting after cessation of indomethacin. Ornoprostil reversed these abnormalities caused by indomethacin. In conclusion, the administration of indomethacin during the initial period of the ulcer healing promoted persistent polymorphonuclear cell infiltration and increased ulcer recurrence rates, possibly via a prostaglandin-dependent mechanism.
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PMID:Indomethacin treatment during initial period of acetic acid-induced rat gastric ulcer healing promotes persistent polymorphonuclear cell-infiltration and increases future ulcer recurrence. Possible mediation of prostaglandins. 888 21

To investigate pathophysiological diversities in the repairing process of gastric ulcer, distribution density of basic fibroblast growth factor (bFGF)-positive fibroblasts and myofibroblasts and vascular endothelial cells, mucosal haemoglobin content, PAS-positive mucus amount and glandular index were compared in the peripheral region of an open ulcer (the unhealed group; n = 17), the central region of a red scar (the red scar group; n = 32) and the central region of the white scar (white scar group; n = 32). Density of bFGF-positive fibroblasts and myofibroblasts and vascular endothelial cells was highest in the unhealed group, followed by the red scar group, while the white scar group showed a low value close to control. Mucosal haemoglobin content was high in the red scar and unhealed groups. PAS-positive mucus amount in the unhealed and red scar groups showed lower values compared with that in the white scar group. Glandular index in the unhealed group was the lowest, followed by the red scar group, while the white scar group neared control values. Statistically significant correlations were observed between the density of bFGF-positive "fibroblasts and myofibroblasts' and density of bFGF-positive vascular endothelial cells, between the density of bFGF-positive vascular endothelial cells and mucosal haemoglobin content and between the PAS-positive mucus amount and glandular index. Discriminant analysis demonstrated that the unhealed group could be distinguished from the red and white scar groups, based on glandular index, density of bFGF-positive "fibroblasts and myofibroblasts', mucosal haemoglobin content and PAS-positive mucus amount, while the red scar group could be discriminated from the white scar group based on the density of bFGF-positive "fibroblasts and myofibroblasts', density of bFGF-positive vascular endothelial cells, glandular index, haemoglobin content and PAS-positive mucus amount. The white scar group was difficult to discriminate from control. Our present results show that the recovery of glandular formation and mucus production continues throughout the repairing process, whereas the acceleration of angiogenesis and granulation formation is observed only in unhealed ulcers and at the red scar stage.
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PMID:Study of the repairing process of gastric ulcer using multivariate analysis of bFGF-positive cells, haemodynamics, PAS-positive mucus amount and glandular index in the gastric mucosa. 891 29


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