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)

Both misoprostol (synthetic PGE1 analog) and De-Nol (factor releasing endogenous prostaglandins in the gastric mucosa) can be useful in the treatment of patients with gastric ulcer resistant to cimetidine according to their gastroprotective properties. 64 patients whose gastric ulcer had not healed after 6 weeks of therapy with cimetidine in daily dose of 1000 mg were treated in a comparative short-term trial to assess the relative efficacy of misoprostol (Cytotec; Searle) in daily dose of 800 micrograms (I group; n = 32) and colloidal bismuth subcitrate (De-Nol; Gist-Brocades), four times a day in dose of 5 ml diluted with 15 ml of water (II group; n = 32). Both groups of patients were comparable according to age, sex, duration of ulcer disease, smoking habits, gastric acid secretion, ulcer size and localization in the stomach. The ulcer healing was controlled endoscopically after 2 and 4 weeks of the treatment. Healing rates after 2 weeks of therapy appeared to be 47% for misoprostol and 34% for De-Nol. After 4 weeks of therapy the healing rates were 72% with misoprostol and 63% with De-Nol. No statistically significant differences in the therapeutic efficacy were observed between two groups of the patients. No correlation was found between the ulcer healing rates and size of ulcer, its localization or smoking habits. The moderate side effects (transient diarrhea) were observed in 22% of patients treated with misoprostol. These findings suggest that misoprostol is as effective as De-Nol in the treatment of gastric ulcers resistant to cimetidine.
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PMID:[Misoprostol and de-nol in the treatment of patients with cimetidine-resistant stomach ulcer]. 251 27

The antiulcer effects of OPC-12759, a novel antiulcer agent were compared with those of cetraxate in various experimental ulcer models and on gastric secretion in rats. OPC-12759 (0.3-30 mg/kg, b.i.d., p.o.) significantly accelerated the healing rate of acetic acid-induced gastric ulcer in a dose-dependent manner, while cetraxate did not. When administered orally at 0.3-30 mg/kg, b.i.d., for 7 days, pretreatment with OPC-12759 (0.3-30 mg/kg, b.i.d., p.o.) prevented the formation of acute gastric ulcers, induced by: restraint water immersion stress, aspirin, indomethacin, histamine, serotonin, platelet activating factor (PAF) and DDC. Cetraxate showed antiulcer activity against a part of the OPC-12759-positive gastric ulcer models. Given intraperitoneally at the single dosing range of 10-100 mg/kg, OPC-12759 inhibited the formation of these acute gastric ulcer models. OPC-12759 administered orally at 0.3-30 mg/kg, b.i.d., for 7 days did not inhibit basal gastric secretion in pylorus ligated rats. The results indicated that OPC-12759 possesses wide spectrum antiulcer activity as compared with cetraxate.
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PMID:Effect of OPC-12759, a novel antiulcer agent, on chronic and acute experimental gastric ulcer, and gastric secretion in rats. 254 84

It has been developed by us a simple new method for producing subacute gastric ulcer in rats, combined with a novel method for the quantitative evaluation of the healing process. Fasted rats with 120-150 g were used. The animals were anaesthesized by ether and than a polyethylene chateter was orally inserted into the stomach with a fine needle inside. After the cannule reached the gastric wall, the needle was pressed gently so as to punch the gastric wall. Drugs under study were administered orally 30 min and 24 h after the puncture. Food and water were given ad libitum from 2 h after the intervention until the end (96 h) of experiments. In order to follow the healing process of subacute ulcer, the so-called tensile strength of the ulcer was determined by inflating and expressed in mmHg. The healing rate was calculated. The antiulcer drugs: Cimetidine, Famotidin, Pirenzepine and sucralfate dose dependently and significantly increased the healing rate of ulcer. Non steroidal antiinflammatory drugs: naproxen, piroxicam, indomethacin and ibuprofen significantly delayed the healing of ulcer. ASA showed tendency to delay the healing. Strong HCl (0.5 molar) significantly delayed the healing of ulcer. N-EM given subcutaneously dose dependently delayed the healing of subacute ulcer.
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PMID:Effect of cytoprotective and antiulcer drugs on the healing process of subacute gastric ulcer in rat (a new model). 259 12

Glycyrrhetinic acid (Ia) and eighteen related derivatives were examined for antiulcer activity using stress-induced gastric lesions (restraint plus water immersion at 25 degrees C) in mice and rats as screening tests. Among the compounds tested, dihemiphthalate derivatives of 18 alpha- or 18 beta-olean-12-ene-3 beta,30-diol (IV, IIId), 18 beta-olean-9(11)12-diene-3 beta,30-diol (VIc), and olean-11,13(18)-diene-3 beta,30-diol (VIIc) showed potent inhibition of gastric lesion formation at a dose of 12 or 25 mg/kg (p.o.); carbenoxolone sodium (Ib) significantly suppressed the lesion formation at a dose of 500 mg/kg (p.o.). Further evaluation of the antiulcer activity was carried out mainly for compound IIId. Compound IIId (p.o.) prevented the formation of indomethacin-induced or 0.6 N HCl-induced gastric lesions; the latter antiulcer effect was noted even in the combined treatment with indomethacin, suggesting that the effect occurs independently of endogenous prostaglandins. In contrast, compound IIId had no preventive effect against Shay rat ulcer when intragastrically (i.g.) administered; further, no antisecretory effect was seen by i.g. application in pylorus-ligated rats. Administration of compound IIId for 2 weeks accelerated the healing rate of acetic acid-induced gastric ulcer in rats. No significant change in urine excretion was observed after its consecutive administration for 3 d. These results suggest that dihemiphthalate derivatives (IIId, IV, VIc, VIIc) may produce a strong antiulcer activity, probably by strengthening some gastric mucosal defensive mechanism.
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PMID:Antiulcer activities of glycyrrhetinic acid derivatives in experimental gastric lesion models. 260

The mucosal superoxide dismutase (SOD) activities were serially examined on the acute gastric mucosal lesion (AGML) induced by water-immersion restraint stress to rats for six hours. The mucosal SOD activities gradually increased in proportion to the time up to 3 hours after the restraint stress. But it decreased 6 hours after when severe damage had been established in the mucosa. On the other hand, the mucosal SOD activities of the margins of human gastric ulcer showed to be higher on the healing stage than on the active stage. And the SOD activities of the intractable ulcer were lower than those of the curable ulcer. These results indicate that the mucosal SOD may play some important roles both on the protecting process information of AGML and on the healing process in gastric ulcer.
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PMID:[Changes in mucosal superoxide dismutase activities of gastric lesions]. 260 64

Gastric ulceration of rats stressed by restraint in 19 degrees C water for 75 min was markedly increased by allowing a 75-min postrestraint room-temperature rest period during which the rat was exposed to cues that had previously been associated with the delivery of 80 5-s uncontrollable electric shocks distributed over four sessions. This effect obtained equally without regard to whether the "danger cues" were punctate signals or constant contextual cues or whether contextual ones were interrupted by punctate safety signals. The experimental treatments used were unusual in that they equated the groups on their total conditioning history and thus allowed a more pure look at the poststress effect than heretofore. Other groups provided controls for prior shocks, rest, and their interaction as well as handling. Analyses of corticosterone after the stress or stress-rest cycle revealed only a general decline in corticosterone levels with rest undifferentiated across groups.
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PMID:Poststress effects of danger and safety signals on gastric ulceration in rats. 261 Sep 22

Ultrasonography was performed for 15 patients with gastric ulcers, after tap water ingestion using 5-MHz and/or 7.5-MHz transducers. Sonographic signs of gastric ulcer were classified as gastric wall edema associated with ulcer crater (six cases) and gastric wall edema only (nine cases). The latter nine included two cases of perforation of gastric ulcers that were depicted as gastric wall edema associated with fluid collection. Ultrasonography proved useful for detecting benign ulcerations and can be used to supplement follow-up examinations, but it cannot replace endoscopy and contrast radiography.
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PMID:Ultrasonography of benign gastric ulcers. Characteristic features and sequential follow-ups. 267 74

110 patients with benign gastric ulcer and concomitant joint diseases (rheumatoid arthritis, osteoarthrosis) were treated in a comparative short-term clinical trial to assess the relative efficacy of calcitonin (daily 100 MRC of salmon calcitonin intramuscularly), cimetidine (daily 1000 mg orally) and colloidal bismuth subcitrate (De-Nol-four times a day in doses of 5 ml diluted with 15 ml of water). Groups of patients were comparable according to age, sex, duration of ulcer disease, smoking habits, gastric acid secretion and mean ulcer size. The ulcer healing was controlled endoscopically after 2 and 4 weeks of the treatment. There was no significant difference in the ulcer healing rate between three groups neither after 2 weeks (calcitonin-36.7% of healed ulcers, cimetidine-37.5% and De-Nol-35.0% nor after 4 weeks respectively (76.7%, 72.5% and 77.5%). In the calcitonin group a gradual joint pain relief was observed in 84% of patients who complained arthralgia. The moderate side effects (headache, nausea, flush) were observed only in the patients treated with calcitonin (8 subjects). We suggest that calcitonin may be considered as a valid anti-ulcer drug in the peptic ulcer patients with concomitant rheumatological diseases especially with osteoporosis.
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PMID:Calcitonin versus cimetidine or De-Nol in gastric ulcer treatment. An endoscopically controlled trial. 307 78

Gastric stasis and duodenogastric reflux have each been implicated in the pathogenesis of various upper gastrointestinal disorders. However, the relationship between intragastric bile and gastric emptying has not been explored. In each of nine healthy volunteers (seven men and two women, ages 22-47 years), gastric emptying of 300 ml 10% dextrose labeled with [99mTc]DTPA was measured twice using gamma camera imaging. During one study, 20 min after ingestion of the test meal, 525 mg of freeze-dried, sterilized human T-tube bile dissolved in 20 ml water was introduced into the stomach via a previously sited fine-bore nasogastric tube. Intragastric bile salt concentrations were calculated to be within the range 1.7-2.9 mM. In control studies, 20 ml of water alone was similarly introduced. Emptying at 20 min was comparable for both groups of studies (38 +/- 3% vs 39 +/- 4%; mean values +/- SEM). For each individual study, emptying from 20 to 60 min was well represented by a single exponential function (r = 0.81-0.99). Half-emptying times for curves fitted over this period were similar in the two groups (bile: T1/2 = 18.8 +/- 2.6 min; control T1/2 = 18.8 +/- 1.9 min). These results indicate that intragastric bile, in concentrations similar to those found in patients with gastric ulcer, has no effect on gastric emptying of dextrose in normal subjects.
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PMID:Intragastric bile does not perturb gastric emptying of liquids in humans. 334 20

A metallothionein isoform metallothionein-II was isolated from the livers of zinc acetate-treated rats. Metallothionein-II, which showed a single band on polyacrylamide gel electrophoresis, was subjected to two kinds of anti-ulcer screening systems. It was shown that intravenously administered metallothionein-II suppressed the formation of rat water-immersion stress- and HCl-ethanol-induced gastric ulcer significantly. The effect may partly be derived from the zinc contained in the metallothionein-II. However, the effect of metallothionein-II was much stronger than that of an equivalent mole of zinc. Apparently, metallothionein-II had an anti-ulcerogenic activity not based on the effect of intrinsic zinc.
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PMID:Suppression of gastric ulcer induced by stress and HCL-ethanol by intravenously administered metallothionein-II. 334 6


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