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)

Ninety patients suffering from peptic ulcer and 25 healthy subjects were examined for the content of gastrin, bombesin and somatostatin in blood and gastric juice. Among patients with duodenal ulcer, 2 groups were distinguished: group I included patients in whom peptic ulcer occurred before 30 years; the majority of the patients manifested blood hypergastrinemia, a decrease of bombesin concentration and normal somatostatin concentration; gastric juice was characterized by a lowering of somatostatin concentration and unchanged gastrin concentration; group II was made up of patients who developed peptic ulcer after 30: in the majority of the patients, gastrin concentration was reduced under basal conditions, after loading it was unchanged; in part of the patients, blood somatostatin concentration was elevated, in 16 in exacerbation and in 19 in remission; in the remainder, it was unchanged. The concentration of bombesin in blood remained unchanged. In gastric juice, gastrin concentration was increased only after histamine administration, somatostatin concentration was unchanged whatever the disease stage. In patients with gastric ulcer, gastrin concentration in blood was elevated only under basal conditions, being unchanged in gastric juice irrespective of the disease stage. Meanwhile, the concentration of bombesin was lowered both under basal conditions and after insulin administration, the concentration of somatostatin was decreased both in blood and gastric juice whatever the disease stage.
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PMID:[The content of gastrin, bombesin and somatostatin in the blood and gastric juice of patients with duodenal and gastric peptic ulcer]. 135 94

Mucosal atrophy of the gastric antrum (type B atrophic gastritis) is generally accepted as predisposing to the development of the intestinal type of gastric cancer. Since bombesin stimulates gastrin release selectively from the antral mucosa, the response can be used as a marker for antral mucosal atrophy. In this study we have investigated bombesin-stimulated plasma gastrin responses in 21 patients with the intestinal type of gastric cancer and we have compared the results with 12 patients with the diffuse type of gastric cancer, 17 patients with benign gastric ulcer, and 30 dyspeptic patients without endoscopical or histological abnormalities. Gastrin concentrations were also measured in extracts of antral biopsies. Basal plasma gastrin concentrations were not significantly different. In contrast, patients with the intestinal type of gastric cancer had a significantly lower plasma gastrin response to bombesin than did the normal subjects (P less than 0.01) and patients with the diffuse type of gastric cancer (P less than 0.05), but the result was not significantly different from that of the gastric ulcer patients. The antral gastrin content of the patients with the intestinal type of gastric cancer was significantly lower than in controls (P less than 0.005), the patients with the diffuse type of gastric cancer (P less than 0.05), and those with gastric ulcer (P less than 0.05). It is concluded that patients with the intestinal type of gastric cancer have, in contrast to those with the diffuse type of gastric cancer, an abnormally low plasma gastrin response to bombesin. This low response is due to a reduced gastrin content of the antral mucosa.
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PMID:Plasma gastrin responses to bombesin and antral gastrin concentrations in patients with the intestinal type of gastric cancer. 334 93

This study evaluated the effect of intracisternal (I.C.) administration of the brain and gastrointestinal peptides neurotensin (NT) and bombesin (BOM) on the acute development of gastric ulcers induced by cold-restraint stress (CRS) and ethanol in rats. The results of this study can be summarized as follows: In confirmation of previous observations I.C. NT (30 micrograms) and BOM (1 microgram) significantly reduced gastric ulcer incidence and severity induced by 3h of CRS. The results of the ethanol preparation indicate that although I.C. BOM (1 microgram) significantly (P less than 0.05) increased intraluminal gastric pH and mucus, it did not prevent gastric ulcer formation. NT (30 micrograms), by contrast, was totally inactive in this ethanol model. These findings support a role for brain NT and BOM in protection against psycho-behavioral, but not chemical forms of ulcer-producing stress.
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PMID:Differential effects of intracisternal neurotensin and bombesin on stress- and ethanol-induced gastric ulcers. 376 73

A hybridoma monoclonal antibody against human pepsinogen I was used to develop an enzyme-linked immunosorbent assay for pepsinogen I in serum. In the two-step competitive procedure using antimouse immunoglobulin F(ab')2 fragment coupled to alkaline phosphatase, the measurable assay range was 8-256 micrograms/l. No cross-reactivity with rat pepsinogen 1, human pepsinogen II, gastrin I, bombesin, somatostatin and peptide YY was shown. However, there was slight cross-reactivity (0.09%) with porcine pepsinogen. The coefficients of variation within and between series were 7.6% and 13.0%. This enzyme-linked immunosorbent assay for serum pepsinogen I correlated positively with radioimmunoassay (r = 0.87, n = 92). The concentration range of serum pepsinogen I in 354 healthy controls was 15-100 micrograms/l with a lognormal distribution. Serum pepsinogen I levels were significantly higher in the subjects who developed active duodenal ulcer or active gastric ulcer, but significantly lower in those who had gastric cancer, than in control subjects.
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PMID:Enzyme-linked immunosorbent assay of serum pepsinogen I. 380 50

A case of a bombesin-producing carcinoid tumor of the lung is reported. Morphologically, the tumor was a typical argentaffinic carcinoid which contained bombesin as demonstrated by diffuse granular cytoplasmic staining using the immunoperoxidase method. Electron microscopy revealed dense-core granules measuring 100-150 nm, consistent with bombesin-containing endocrine cells. In man, bombesin-producing endocrine cells are found predominantly in the bronchopulmonary tree and scattered throughout the intestinal tract. The majority of previously reported bombesin-producing tumors have arisen, as in this case, in the lung; thus the demonstration of bombesin-like immunoreactivity in a widely metastatic tumor should direct the search for a primary lesion to the lung. Bombesin is known to have gastrin-releasing hormone activity. The presence of a gastric ulcer in the present patient raised the possibility of a bombesin-mediated Zollinger-Ellison-like syndrome, an association not previously described.
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PMID:Disseminated bombesin-producing carcinoid tumor of pulmonary origin. 388 21

To evaluate whether bombesin treatment has a facilitatory effect on the healing of chronic gastric ulcer, following the induction of ulcer by serosal application of acetic acid, rats were given bombesin (30 microg/kg/day; subcutaneously) or vehicle three times a day for 7, 14 or 21 days until they were decapitated. Neither food intake nor gastric emptying rate in either vehicle-treated or bombesin-treated groups was not statistically different from control rats. Similarly, ulcer indices and gastric myeloperoxidase (MPO) activities at the first and second weeks of injury were not different among the groups. However, in the 3-week ulcer group, bombesin treatment reduced tissue MPO level significantly back to control levels. Moreover, the analysis of the surface epithelium by scanning electron and light microscopy demonstrated a significant reduction in the severity of ulcers by bombesin treatment. Pretreatment with CCK antagonists (L-364,718 or L365,260; 25 micromol/kg/day) before bombesin treatment showed that neither of the CCK antagonists had a significant effect on the bombesin-mediated healing process, suggesting that CCK receptors are not involved in the action of bombesin. In accordance with the previous studies that show its acute gastroprotective effects, bombesin is also effective in promoting the healing process of chronic gastric ulcer in rats.
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PMID:Healing-promoting effect of bombesin treatment on chronic gastric ulcer in rats. 1204 14

Bombesin has been shown to have trophic effects on the gastrointestinal tissue. Bombesin has direct mitogenic effects besides stimulating release of gastric hormones. The aim of this study was to investigate the effect of bombesin in hemorrhagic shock-induced stress ulcers in rats, and the role of cholecystokinin (CCK) receptors in this activity. Hemorrhagic shock was created by withdrawing 3 ml blood/200 g b.w. of rats. At the end of the 1-hour hypovolemic shock period, histological analysis, gastric ulcer index, gastric myeloperoxidase activity and gastric protein oxidation levels were determined. When given before the hemorrhage, subcutaneous bombesin (10 microg/kg) reduced macroscopically gastric ulcer index (p < 0.05). Blockade of CCK-A receptors with intraperitoneal MK-329 (1 mg/kg) did not reverse bombesin-induced gastroprotection. Blockade of CCK-B receptors with intraperitoneal L-365,260 (25 mg/kg) reversed bombesin-induced gastroprotection. Blockade of the two receptors resulted in no gastroprotection at all. It is concluded that bombesin treatment attenuated hemorrhagic shock-induced stress ulcers in rats via CCK receptors.
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PMID:Role of bombesin and cholecystokinin receptors in gastric injury induced by hemorrhagic shock in the rat. 1271 34