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)

Prospective sonographic evaluation after water ingestion in 25 normal children aged 2 days to 15 years (mean 6.3 years) demonstrated that normal gastric wall thickness was less than 3 mm. Gastric walls of 5-15 mm thickness were seen in nine of about 6500 children undergoing abdominal sonographic examinations. These nine patients had a variety of unusual diseases, including varioliform gastritis, gastric ulcer, lymphoid hyperplasia, and gastric hamartoma. Previously unreported sonographic appearances were seen. The sonographic examination was instrumental in the detection of five clinically unsuspected gastric lesions and helpful in follow-up in four others.
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PMID:Sonography of the normal and abnormal stomach (excluding hypertrophic pyloric stenosis in children. 351 46

Gastric ulceration in rats is exacerbated by allowing a so-called recovery period after exposure to an ulcerogenic stressor. One hypothesis, which has support from pharmacological studies, argues that this effect is brought about by a rebound of parasympathetic activation. We tested this parasympathetic rebound hypothesis by presenting animals with a fear-inducing (sympathetic-activating) conditioned stimulus (CS) after 2 hr of water-restraint stress. Contrary to the hypothesis, presentation of such a CS increased severity of ulceration compared with those animals that did not receive the CS after restraint stress and control animals. These ulceration data favor instead a sustained activation hypothesis for ulceration, whereby presentation of the CS effectively prolonged the length of time during which animals were under stress, thus enhancing the degree of ulceration. Measurement of plasma corticosterone however indicated a negative correlation between adrenocortical activity and degree of gastric ulceration, contrary to that expected by a sustained activation hypothesis. It is suggested that this inconsistency may be because of the activating of a pituitary-endorphinogenic mediated stress analgesia.
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PMID:Quality of poststressor rest influences the ulcerative process. 358 Jan 27

The purpose of this experiment was to determine whether chronic gastric ulcers in the rat are predisposed to tumor formation when exposed to a usually noncarcinogenic dose of the carcinogen, N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG). Two groups of rats were prepared; one subjected to a standard ulcer-producing operation, the other as control. Both groups were given oral MNNG (100 mg/liter as drinking water) for 12 weeks, the carcinogen was then stopped and replaced with tap water, and the experiment terminated at 52 weeks. Results showed that a low dose of carcinogen (200 mg) did not induce tumor formation in any of the normal rats. In the presence of a chronic gastric ulcer, only intestinal metaplasia and hyperplastic glandular nodules were observed, but there were no gastric tumors. It is concluded that the presence of a chronic gastric ulcer did not increase the likelihood of gastric tumor formation in rats treated with a noncarcinogenic dose of the carcinogen MNNG.
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PMID:Chronic gastric ulcers are not predisposed to tumor formation when exposed to a low dose of carcinogen. 374 98

Effects of (-) cis-2,3-dihydro-3-(4-methylpiperazinylmethyl)-2-phenyl-1,5-benz othiazepin-4-(5H ) -one hydrochloride (BTM-1086) on various experimental gastric and duodenal ulcers were studied in rats. In the pylorus-ligated ulcer, restraint and water immersion stress ulcer, and drug-induced ulcer (indomethacin, aspirin, reserpine, serotonin, cysteamine), BTM-1086 prevented the development of ulcer at a dose of 0.1 to 1 mg/kg, p.o., but only weakly inhibited the histamine-induced gastric ulcer. The inhibitory activities of BTM-1086 were significantly higher than those of atropine sulfate. In the healing experiment with the acetic acid-induced stomach ulcer, BTM-1086 (1 mg/kg/day, p.o., X 14) showed a significant healing effect, which was higher than that of propantheline bromide. BTM-1086 at a dose of 0.2 mg/kg, i.d., remarkably inhibited the gastric secretion 6 hr after pylorus ligation. The aspirin-induced reductions of the total acid and K+ as well as the increments of the volume and Na+ in the gastric secretion were prevented dose-dependently by pretreatment with BTM-1086.
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PMID:Antiulcer effect of (-)-cis-2,3-dihydro-3-(4-methylpiperazinylmethyl) -2-phenyl-1,5-benzothiazepin-4-(5H)-one hydrochloride (BTM-1086) in experimental animals. 376 47

6-[1S-(3S,4-Dihydro-8- hydroxy-1H-2-benzo-pyran-1-one-3-yl)- methylbutylamino]-4S,5S-dihydroxy-6-oxo-3S-ammoniohexanoate (AI-77B)-gamma-lactone-N-ethyl derivative (AI-77-C2) is a new antiinflammatory drug with antiulcer activity. In the first part of the present study the ulcerogenicity of this drug was assessed. Acidic antiinflammatory drugs--indomethacin and diclofenac--and basic antiinflammatory drugs--tiaramide and mepirizole--were used for comparison. Although AI-77-C2 was barely ulcerogenic at 7 h after dosing, some lesions developed in both stomach and intestine at 24 h. Repeated administrations over 5 days appeared to increase its ulcerogenicity and general toxicity. Marked gastric ulcers were induced by indomethacin and diclofenac, and severe intestinal ulcers were also produced at 24 h and by their repeated administration. Tiaramide did not induce marked ulcers in any case. Although the ulcerogenicity of mepirizole was weak at 7 h, severe duodenal ulcers developed at 24 h and after the repeated administration. From the results given above, it was concluded that the ulcerogenicity of AI-77-C2 was relatively low. In the next study, the antiulcer activity of AI-77-C2 was examined in several experimental ulcer models. AI-77-C2 showed a marked inhibition of all the models presently employed, i.e., the indomethacin-induced gastric ulcer, the pylorus ligation ulcer, the water immersion stress ulcer, and the acetylsalicylic acid-induced ulcer in rats. It was observed that AI-77-C2 suppressed the gastric secretion and movement. It is therefore concluded that the antiinflammatory drug AI-77-C2 has low ulcerogenicity and potent antiulcer activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ulcerogenic and antiulcerogenic effects of a new antiinflammatory drug, the gamma-lactone-N-ethyl derivative of 6-[1S-(3S,4-dihydro-8-hydroxy-1H-2-benzo- pyran-1-one-3-yl)-3-methylbutylamino]-4S,5S-dihydroxy-6-oxo-3S- ammoniohexanoate, on gastrointestinal tract in rats. 379 Jan 91

In the years 1980-1983 M. xenopi was isolated from the sputum of 37 persons, 30 of them living in the agglomeration of the regional town in the region of Northern Bohemia with 1,175,000 inhabitants. Only 7 of these 30 had manifestation of pulmonary disease. M. xenopi was found repeatedly in the sputum in 5 patients out of 7 affected and in 2 out of 23 persons who showed no signs of a disease. The prevalence was in males between the age of 52-67 years. All of them suffered from other diseases, as chronic bronchitis, TB healed after lobectomy, lung cancer, fibrotic lung lesions, diabetes mellitus, gastric ulcer healed by resection, chronic alcoholism. Investigations were made for detection of the source of infection. Bacteriological examinations of cold and warm tap water in flats of 9 persons with M. xenopi in their sputa were carried out, as well as cold and warm tap water from flats of 2 healthy persons. M. xenopi was found in tap water of 5 persons with M. xenopi in their sputum and in one of the two healthy persons. In the water of one household we found M. kansasii. We came to the conclusion, that transmission carried out in susceptible persons is most probably due to aerosol during washing and showering with water, containing these mycobacteria.
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PMID:Water-borne Mycobacterium xenopi--a possible cause of pulmonary mycobacteriosis in man. 380 13

Chronic gastric ulcers were produced by injection of 20% acetic acid (0.05 ml) into the submucosal layer of the rat stomach in order to determine the effects of the prostanoid trimoprostil on the healing and recurrence of ulcers. Local injection of acetic acid solution produced large demarcated ulcers in all animals on day 5, which rapidly decreased to reach low levels on days 40-80 and then became exacerbated on day 100. The exacerbation of the ulcer is probably recurrence. Trimoprostil was administered ad libitum in drinking water containing 0.1, 0.3 and 1.0 microgram/ml (average dose 12.4, 37 and 124 micrograms/kg/day) for a period of 14 days (day 1-15) to assess its effect on healing and for a period of 40 days (day 60-100) to assess its ability to prevent recurrence. The higher two doses of trimoprostil accelerated the spontaneous healing of the ulcers. Furthermore, trimoprostil, at both doses, prevented the observed recurrence of this type of ulcer. Trimoprostil dose-dependently (30-300 micrograms/kg, p.o.) inhibited gastric secretion in pylorus-ligated rats. Cimetidine at the antisecretory dose (1 mg/ml, 132 mg/kg/day) failed to affect the healing process of gastric ulcers, but tended to prevent the recurrence of gastric ulcers. Our present study suggests that trimoprostil is a promising antiulcer drug for the treatment of chronic gastric ulcer.
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PMID:Effects of trimoprostil on healing and recurrence of acetic acid-induced gastric ulcer in rats. 380 49

Pregnant rats were given caffeine (0.0%, 0.017%, 0.034% or 0.05%) in their drinking water throughout gestation. Offspring were cross-fostered to non-caffeine-treated mothers at birth. A dose-related increase in offspring mortality was observed at 24 hr and at 10 days post partum. Prenatal caffeine exposure did not significantly influence open-field ambulation or defecation when tested at 48, 68, or 196 days of age. A significant dose-related increase in restraint-stress gastric ulcer susceptibility was detected at 200 days of age. Offspring from rats treated with 0.05% caffeine during pregnancy, developed significantly more frequent and significantly more severe gastric lesions than did offspring from control rats or from rats prenatally exposed to 0.017% and 0.034% caffeine. Prenatal caffeine exposure may: (1) predispose organisms to increased gastric disease susceptibility as adults and (2) interfere with neonatal feeding ability and thereby produce infant mortality.
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PMID:Effects of prenatal caffeine administration on offspring mortality, open-field behavior and adult gastric ulcer susceptibility. 400 Mar 67

The effects of 5-acetylspiro[benzofuran-2(3H),1'-cyclopropan]-3-one (AG 629), a newly synthesized compound, on various experimentally induced ulcers were investigated. Oral or intraduodenal administration of AG 629 in a dose range of 25-100 mg/kg inhibited water-immersion stress ulcer, exertion ulcer, Shay ulcer, indometacin- and acetylsalicylic acid (ASA)-induced gastric ulcer, and indomethacin-induced small intestinal ulcer in rats, histamine-induced gastric ulcer in guinea pigs, and ASA-induced gastric ulcer in dogs, though it was not effective against cysteamine-induced duodenal ulcer in rats. AG 629 in doses of 6.3-25 mg/kg p.o. twice a day significantly promoted the healing of acetic acid- or thermal-cortisone-induced gastric ulcers and acetic acid-induced duodenal ulcers in rats. AG 629 (25-100 mg/kg i.d.) inhibited the secretion of gastric acid and pepsin in pylorus-ligated rats and the acid secretion stimulated by distension of the rat stomach with air, whereas this compound did not affect acid secretion stimulated by histamine, pentagastrin, carbachol or 2-deoxy-D-glucose. This study shows that AG 629 has both prophylactic and curative effects on various ulcers. The anti-ulcer effect of this agent seems to be mediated primarily by increasing mucosal resistance and secondarily by an antisecretory activity.
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PMID:Effects of 5-acetylspiro[benzofuran-2(3H),1'-cyclopropan]-3-one, a new anti-ulcer agent, on experimental acute and chronic ulcers. 407 15

Fasting serum gastrin has been measured by radioimmunoassay in 72 patients with duodenal ulcer and compared with that in normals, patients with gastric ulcer, and with the Zollinger-Ellison syndrome. The mean (+/- SEM) gastrin levels were 15.7 +/- 1.5 pg/ml in the duodenal ulcer group, 32.1 +/- 4.3 pg/ml in normals, 118 +/- 18.1 pg/ml in gastric ulcer, and between 450 and 2,000 pg/ml in the Zollinger-Ellison syndrome. There were no difficulties in distinguishing simple ulcer from the Zollinger-Ellison syndrome as the presence of hyperchlorhydria in combination with hypergastrinaemia led to a confident diagnosis of the latter disease.The effect of protein, glucose, and cream feeding with and without atropine was also assessed in a group of these patients with duodenal ulcer. As in normals, there was no stimulation of gastrin release by either atropine alone, distilled water, glucose, or cream. However, protein alone produced a greater rise in serum gastrin levels compared with that in normals and prior atropinization augmented this response greatly in duodenal ulcer. This indicates an increased amount of releasable gastrin in the latter disease, the release of which, under basal conditions, is suppressed by the high acidity in the antrum.
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PMID:Serum gastrin in duodenal ulcer. I. Basal levels and effect of food and atropine. 513 20


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