Disease relevance of Stomach Ulcer

• Mice deficient in protein tyrosine phosphatase receptor type Z are resistant to gastric ulcer induction by VacA of Helicobacter pylori [1].
• Cimetidine was cost-effective in both gastric ulcer and duodenal ulcer patients in the first 2 years after healing [2].
• Progression of fundal gastritis in gastric ulcer patients [3].
• Uninvolved gastric mucosa from duodenal ulcer, gastric ulcer, and gastric cancer patients was incubated with [1-14C]glucose and [6-14C]glucose in order to assess the relative contributions of the pentose phosphate pathway and Krebs cycle to glucose metabolism [4].
• Cotreatment with the synthetic prostaglandin misoprostol was associated with a marked reduction in gastric ulcer development in patients with osteoarthritis receiving NSAIDs chronically, suggesting that prevention of prostaglandin generation in the gastric mucosa may play a pivotal role in NSAID-induced gastric ulcers [5].

Psychiatry related information on Stomach Ulcer

• These results suggest that the 2 g b.i.d. dose of sucralfate in granule form is at least as effective as the conventional dose of 1 g q.i.d. in the treatment of active gastric ulcers and could lead to better patient compliance [6].
• Electroshock convulsions, marginally but not significantly protective against such ulcers themselves, when coupled with 4-acetylpyridine administration fully prevented gastric ulcers from occurring in this murine model of experimentally induced stress [7].
• The personality assessment of 96 patients with gastric ulcer (GU) and 70 patients with duodenal ulcer (DU) was carried out using the Cattell Sixteen Personality Factor Questionnaire (16 PF) [8].
• Misoprostol treatment resulted in a significant (p < 0.05) risk reduction of gastric ulcer in the short-term (pooled RD = 13.3%; 95% confidence interval -25.7%, -0.9%) and in the long-term (RD = -8.4%; 95% confidence interval -17.7%, -1.0%) non-steroidal anti-inflammatory drug treatment [9].
• Experimental study on bromopride pharmacology in vivo. antiemetic activity, effects on intestinal transit, on bloating and on gastric ulcers; basal effects on CNS and interferences with the spontaneous motor activity [10].

High impact information on Stomach Ulcer

• Taken together, these data indicate that erroneous Ptprz signaling induces gastric ulcers [1].
• The rates of gastric-ulcer healing were significantly higher with 20 mg of omeprazole (but not 40 mg of omeprazole) than with misoprostol [11].
• Prozac or prilosec for gastric ulcer [12]?
• The cumulative incidence of gastric ulcers was 20 percent in the placebo group, 13 percent in the group of patients receiving 20 mg of famotidine twice daily (P = 0.24 for the comparison with placebo), and 8 percent in the group receiving 40 mg of famotidine twice daily (P = 0.03 for the comparison with placebo) [13].
• Cimetidine for benign gastric ulcer [14].

Chemical compound and disease context of Stomach Ulcer

• In patients with H. pylori infection and gastric ulcers unrelated to the use of nonsteroidal antiinflammatory drugs, one week of antibacterial therapy without acid suppression heals the ulcers as well as omeprazole and reduces the rate of their recurrence [15].
• These drugs also show synergism with either amoxicillin or clari- thromycin in eradicating Helicobacter pylori, an organism shown to be important in duodenal and gastric ulcer disease [16].
• METHODS: Gastric ulcers were induced in rats by acetic acid applied to the serosal surface of the stomach, and the site around the ulcer was injected with nonviral plasmid-encoding full-length complementary DNA (cDNA) of human recombinant (rh) VEGF165, rhAng1, or their combination [17].
• Repeated administration of indomethacin markedly delays spontaneous healing of experimental gastric ulcers induced in rats [18].
• Sucralfate appears useful for duodenal but not gastric ulcers [19].

Biological context of Stomach Ulcer

• Moreover, in vivo functional tests during gastric ulcer healing showed that cell proliferation in the regenerative epithelia of the ulcer margin was significantly decreased by NKP608 compared with placebo; furthermore, gastric ulcer healing was significantly delayed by NKP608 both in wild-type and cyclooxygenase-2(-/-) mice [20].
• In rats in which gastric ulcers were produced with a cryoprobe, the ulcers were larger and slower to heal in those receiving indomethacin than in controls; also, immunohistochemical staining indicated significantly fewer mitotic cells in glands adjacent to the ulcer in indomethacin-treated rats (8 mitoses [SEM 3]) than in control animals (25 [5]) [21].
• CONCLUSIONS: These findings indicate that experimental gastric ulcer healing involves activation of EGF-R-ERK signal transduction pathway [22].
• These results also indicate genetic heterogeneity of gastric ulcer disease, and suggest that the pepsinogen C RFLP may be a useful subclinical marker to explain the differences in genetic aetiologies of gastric body ulcer and gastric angular or antral ulcer [23].
• These results suggest that syndecan-1 participates in cell adhesion mainly at the foveolar epithelium and plays a role in the healing of gastric ulcers by interacting with heparin-binding growth factors [24].

Anatomical context of Stomach Ulcer

• Importance of gastric acid in gastric ulcer formation in rabbits with antibody-induced prostaglandin deficiency [25].
• We investigated whether the trophic actions of prostaglandins, omeprazole, and indomethacin on gastric mucosa lead to accelerated healing of gastric ulcers in the rat [26].
• In patients with gastric ulcer lower levels of PGE were found in body mucosa with atrophic gastritis 0.83 (0.53-2.66) ng PGE/mg protein as compared with histologically normal body mucosa 2.55 (0.63-7.67), p less than 0.05 [27].
• We present endoscopic, microscopic, and histochemical studies of a patient with melanosis of the duodenum associated with a gastric ulcer and a folic acid deficiency [28].
• Comparative efficacy of cimetidine, famotidine, ranitidine, and mylanta in postoperative stress ulcers. Gastric pH control and ulcer prevention in patients undergoing coronary artery bypass graft surgery [29].

Gene context of Stomach Ulcer

• Gene therapy for gastric ulcers with single local injection of naked DNA encoding VEGF and angiopoietin-1 [17].
• The aim of this study was to investigate whether extracellular signal-regulated kinase (ERK) cascade is involved in the healing of experimental gastric ulcers [22].
• In vivo, treatment of rats with established gastric ulcers with a PAR1 antagonist each day for 1 wk resulted in a significant retardation of healing [30].
• Histological examination of several organs revealed fibrin deposition in the liver; lung; and in the stomach, associated with gastric ulcers, in 6- to 12-week-old Plg-/- mice but not in Plg+/+ or Plg+/- littermates [31].
• Activation of Raf-1 during experimental gastric ulcer healing is Ras-mediated and protein kinase C-independent [32].

Analytical, diagnostic and therapeutic context of Stomach Ulcer

• One year after treatment, recurrent gastric ulcers were detected in 1 of 22 patients (4.5 percent) in the antibacterial-treatment group and in 12 of 23 (52.2 percent) in the omeprazole group (P = 0.001) [15].
• Cimetidine, antacid, and hospitalization in the treatment of benign gastric ulcer: a multicenter double blind study [33].
• Passive immunization of unimmunized rabbits with prostaglandin E2-hyperimmune plasma led to acute gastric ulcers within 9 days, whereas passive transfer of nonimmune plasma did not produce ulcers [34].
• Gene therapy with SRF significantly accelerated experimental gastric ulcer healing and promoted re-epithelialization and muscle restoration [35].
• INTERVENTIONS: Patients who were expected to receive at least 3 months of NSAID therapy and who did not have a gastric ulcer at the time of the initial screening endoscopy were randomized to receive misoprostol, 200 micrograms four times a day, or sucralfate, 1 g four times a day [36].

References