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)

Gastrin- and somatostatin-immunoreactive cells in biopsies taken from the prepyloric portion of the antrum from 15 patients with duodenal ulcer, 16 patients with gastric ulcer, and a control group of 19 patients without histopathological alterations of the antral mucosa were studied using peroxidase anti-peroxidase and immunogold-silver staining methods in combination with morphometry. Numerical densities and sizes (immunoreactive areas) of the cells demonstrated were measured and compared between all three groups. Gastrin- and somatostatin-immunoreactive cells were located most frequently in the lower midzone of the gastric crypts. None of the parameters measured showed a correlation with age or sex. The group with duodenal ulcer tended to exhibit gastrin- and somatostatin-cell-hyperplasia whereas the size of both cell types remained unchanged. In comparison with the control group, the numerical density of gastrin-immunoreactive cells was significantly increased in gastric ulcer patients, whereas the numerical density of somatostatin-immunoreactive cells was decreased in this group. Immunoreactive areas of both cell types were significantly increased in patients with gastric ulcer.
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PMID:Gastrin- and somatostatin-immunoreactive cells of the antral mucosa in patients with duodenal or gastric ulcers. An immunocytochemical study. 198 75

The present study was conducted to investigate the role of the parasympathetic nervous system innervating the stomach in gastric ulcer formation, with special reference to its neuroanatomic characteristics in rats. First, the effects of electric vagal stimulation on the gastric mucosa were examined. The electric stimulation of the left or right gastric branch of the vagus nerve caused gastric mucosal lesions to develop. Interestingly, however, gastric lesions were found on the anterior wall in the rats that had received electric stimulation to the left gastric branch of the vagus nerve and on the posterior wall in the rats that had received stimulation to the right gastric branch. Next, the cells of origin projecting to the left or right gastric branch of the vagus nerve were identified by means of a horseradish peroxidase retrograde tracer method. The left and right gastric branches were found to be innervated by the left and right dorsal motor nuclei of the vagus nerve in the medulla oblongata, respectively. It has been reported that the left and right dorsal motor nuclei of the vagus nerve separately innervate the anterior or posterior gastric wall. The present results, therefore, suggest that the long-lasting excitation of neurons in the dorsal motor nucleus facilitates the site-specific formation of gastric ulcers through the left or right gastric branch of the vagus nerve.
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PMID:Site-specific formation of gastric ulcers by the electric stimulation of the left or right gastric branch of the vagus nerve in the rat. 240 89

Kainic acid injection into the dorsal motor nucleus of the vagus nerve (DMN) induced lesions in the glandular stomach of rats. A decrease in mucus production seemed to play an important role in the pathogenesis of the kainic acid-induced gastric lesions. On the other hand, by means of horseradish peroxidase tracing method, the original cells projecting to the DMN were identified in the central nucleus of the amygdala, several hypothalamic nuclei and the insular cortex. Considering that kainic acid is a long-acting neuronal excitant, it was suggested that the continual stimulation of DMN neurons facilitated gastric ulcer formation.
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PMID:Gastric lesions induced by kainic acid injection into the dorsal motor nucleus of the vagus nerve in rats. 255 87

The aims of our experiments were to clear up the possible correlations between the free radical mechanisms and the gastric cytoprotection of beta-carotene on HCl-induced gastric mucosal lesions. The beta-carotene was intragastrically given in doses of 1 and 10 mg/kg and 30 min. later 1 ml 0.6 N HCl was given to provoke the mucosal damage. After 1, 5, 15, 30 and 60 min. the animals were sacrificed. The number and severity of gastric mucosal lesions were calculated. The superoxide dismutase (SOD), glutathion peroxidase (GPX), catalase (CAT) activity and the malondialdehyde (MDA) and reduced glutathion (GSH) contents were determined from the gastric mucosa of rats. It was found that 1. beta-carotene was able to reduce the number and severity of ulcers only after 30 min.; 2. the CAT activity was decreased at 60 min. by carotene; 3. the GPX activity became dissimilar in the different groups after 15 min; 4. the changes of GSH were found to be similar ones; 5. the SOD activity was lower during the cyto-protection; 6. the MDA level remained practically unchanged. It has been concluded that 1. the free radicals are the consequences of the development of gastric ulcer and cytoprotection; 2. the scavenger character of beta-carotene is involved in its cytoprotective effect.
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PMID:The free radical mechanisms in beta-carotene induced gastric cytoprotection in HCl model. 259 22

To study how the normal gastric mucosa develops chronic gastritis, gastric ulcer or cancer, biopsies from 103 patients with non-tumor gastric diseases and operative specimens from 12 patients with stomach carcinoma were examined for epithelial antigen (EA). In the peroxidase-antiperoxidase reaction performed on paraffin-embedded and cryostat sections of the gastric mucosa, monoclonal antibodies (MAb) to antigens located on the membranes of fatty breast milk globules were employed, which had been presented by the Department of Biomedical Sciences, Tampere University (Finland). The MAb 111C12-identified antigenic determinant was found to occur in 12.8% of the nonmalignant gastric mucosa examined and 48% of the stomach carcinoma one. The detection of EA is not characteristic of the given portion of the gastric mucosa in carcinoma.
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PMID:[Detection of the epithelial membrane antigen in patients with varying status of the gastric mucosa using monoclonal antibodies]. 277 94

A 78-year-old man with primary gastric plasmacytoma showing massive rod-shaped intracytoplasmic inclusions is presented. The patient was initially diagnosed as having a benign gastric ulcer and underwent partial gastrectomy. Around the ulcer of the resected stomach specimen, diffuse proliferation of plasma cells with massive rod-shaped intracytoplasmic inclusions was noticed by light microscopy. Immunohistochemically, these cells were found to contain IgM-kappa-type immunoglobulin upon peroxidase-antiperoxidase (PAP) staining. Electron microscopy showed that the intracytoplasmic inclusions were localized in the rough endoplasmic reticulum and had a lattice structure with a periodicity of about 120 A.
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PMID:Gastric plasmacytoma with rod-shaped intracytoplasmic inclusions. Report of a case studied by light and electron microscopy and immunohistochemistry. 285 Dec 59

Healing gastric ulcers were examined immunohistochemically for the presence of myofibroblasts containing actin microfilaments. Twenty five surgical specimens of the gastric ulcer corresponding to the initial healing stage and the proliferative healing stage, and 30 surgical specimens of the acetic acid-induced ulcers in rats at 3, 8 (initial healing stage), and 15 (proliferative healing stage) days after ulcer induction were fixed and cut into 4-micron sections, which were then treated with anti-actin serum, peroxidase-antiperoxidase and incubated for the localization of actin. Controls were prepared using non-immune serum or preabsorbed immune serum. Actin-positive fibroblasts were seen at the edge and the floor of the ulcer in the initial healing stage, but not in the edge of the ulcer in the proliferative healing stage. Such cells may be responsible for the contraction of the ulcer caliver observed clinically in the initial healing stage of the gastric ulcer.
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PMID:Immunohistochemical localization of the actin in the healing stage of gastric ulcers. 344 12

The gamma-glutamyl-transferase activity, the total glutathione content, the GSH-peroxidase activity, and the GSH S-transferase activity using an aryl substrate were estimated in the S9 fraction of gastric biopsy specimens taken from patients with normal stomach morphology (n = 24), acute gastritis (n = 15), chronic-atrophic gastritis (n = 10), gastric ulcer (n = 9), and carcinoma of the stomach (n = 12). The total glutathione content of normal gastric mucosal specimens was significantly higher than that of human liver biopsy specimens, whereas the GSH-peroxidase and the GSH S-aryltransferase activities were much lower than those found in the liver. Specimens of gastric ulcer had significantly lower enzyme activities of GSH-peroxidase and GSH-aryltransferase, whereas gastric cancer tissue had significantly lower concentrations of total glutathione. The intraindividual comparison of tumorous and non-tumorous tissue showed a consistent decrease of total glutathione as well as of GSH-aryltransferase activity in carcinomatous tissue.
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PMID:Glutathione and GSH-dependent enzymes in the human gastric mucosa. 670 2

The healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin were investigated with reference to the enzyme activity of both prolylhydroxylase and collagenase as related to histological findings. The rats were observed by endoscopy on the 3rd day after the subserosal injection of acetic acid; rats with ulcers were divided into three groups: non-treated, and cimetidine- and calcitonin-treated. The latter two groups were treated for 7 days. Prolylhydroxylase activity in active ulcers in the non-treated group was slightly higher on the 3rd day and significantly higher on the 10th day than the activity in control rats that had received subserosal injections of physiological saline solution on the respective days. In non-treated rats, the healed ulcer on the 10th day showed lower prolylhydroxylase activity than that in the active ulcer on the same day. Cimetidine did not affect prolylhydroxylase activity, but, with calcitonin, there was higher prolylhydroxylase activity in the healed than in the active ulcer, although the difference was not significant. Interstitial collagenase showed the highest activity on the 3rd day and decreased on the 10th day in non-treated rats. Collagenase activity was higher in the cimetidine-treated group, than that in the non-treated group, and numerous peroxidase-positive granulocytes were seen in the mucosa and submucosa. Calcitonin did not affect collagenase activity. The participation of both enzymes is indispensable in the healing process and the effects of anti-ulcer agents on these enzymes must be considered.
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PMID:Wound healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin, with special reference to prolylhydroxylase and collagenase enzyme activity. 764 95

Gastric and duodenal biopsies from 90 patients with various acid peptic disorders-reflux esophagitis (n = 24), gastric ulcer (n = 13), duodenal ulcer (n = 47) and nonulcer dyspepsia (n = 6)-were examined. Seven patients with minimal dyspeptic symptoms and an endoscopically and histologically normal stomach and duodenum served as controls. Immunoperoxidase staining for gastrin-producing G cells, somatostatin-producing D cells and serotonin-producing EC cells was carried out on fundic, antral and duodenal biopsies, and was quantified using a Zeiss MOP Videoplan using the peroxidase-antiperoxidase technique of Sternberger. In the gastric antrum, a G:D:EC cell ratio of approximately 1.6:1:1-was observed. In the duodenum the corresponding ratio was 1:1:2.4. No significant differences were observed within any of the major diagnostic categories. Patient age, sex, duration of symptoms, smoking habits, alcohol consumption and nonsteroidal anti-inflammatory drug use had no effect on endocrine cell densities. Reduced G cell density in the descending duodenum was observed in the presence of mild duodenitis in four patients. In four patients with evidence of antral intestinal metaplastic changes, a significant increase in duodenal G cell densities was found. These results suggest that a change in the number of G, D or EC cells does not play a primary role in the pathophysiology of acid peptic disorders in the majority of patients.
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PMID:Immunocytochemical and morphometric studies of gastrin-, somatostatin- and serotonin-producing cells in the stomach and duodenum of patients with acid peptic disorders. 919 76


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