Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The report describes a case of a four-month-old infant, who developed acute gastric ulcer while being hospitalised because of pneumonia. One year's observation of the patient, additional tests, especially gastroscopy with histopathological evaluation of biopsy specimen, determination of gastrin level in blood serum, and therapy analysis allow to establish a diagnosis of pseudo Zollinger-Ellison syndrome.
Med Sci Monit
PMID:Bleeding from alimentary tract in pseudo Zollinger-Ellison syndrome. 1120 77

Polaprezinc, N-(3-aminopropionyl)-L-histidinatozinc, has been shown to stimulate the production of insulin-like growth factor-1 (IGF-1) in mesenchymal cells, the polypeptide playing a role in the gastric epithelial wound repair. The present study was performed to examine the effect of polaprezinc on the impaired healing of chronic gastric ulcers in adjuvant-induced arthritic rats, in relation to IGF-1. Arthritis was induced in male Dark Agouti (DA) rats by a single injection of Freund's complete adjuvant (FCA), and the gastric ulcers were induced by thermal cauterization (70 degrees C for 30 sec) 7 days after FCA injection. Omeprazole (30 mg/kg) was administered p.o. once daily, while recombinant human IGF-1 (rhIGF-1) (30 micrograms/kg, s.c.) or polaprezinc (3-10 mg/kg, p.o.) was administered twice daily, starting from 3 days after ulceration for 14 days. The healing of gastric ulcers was significantly delayed in arthritic rats as compared to normal rats on day 10 and 17 following ulceration. The expression of IGF-1 mRNA was markedly increased in the ulcerated mucosa, but this response was apparently attenuated in arthritic rats. Repeated administration of polaprezinc accelerated the healing of gastric ulcers in both normal and arthritic rats, in a dose-dependent manner, and this effect was more pronounced in arthritic rats. Likewise, treatment with omeprazole also significantly promoted the healing of gastric ulcers in both normal and arthritic rats. On the other hand, rhIGF-1 significantly promoted the gastric ulcer healing in arthritic rats without any effect on that in normal rats. These results suggest that the impaired healing of chronic gastric ulcers in arthritic rats is, at least partly, accounted for by less expression of IGF-1, and the polaprezinc improves the delayed healing of gastric ulcers in arthritic rats, probably through an increase in IGF-1 production.
Med Sci Monit
PMID:Effect of polaprezinc on impaired healing of chronic gastric ulcers in adjuvant-induced arthritic rats--role of insulin-like growth factors (IGF)-1. 1120 87

Hp and NSAID are the most common pathogens in the stomach, but their interaction on gastro-duodenal mucosa has been little studied. Hp infection in humans does not interfere with NSAID-induced gastric ulcer healing by omeprazole, therefore, there is no rationale to eradicate the germ. Hp infection induces COX-2 expression resulting in excessive biosynthesis of gastroprotective prostaglandin (PG), which should in turn counteract NSAID-induced gastropathy and contribute to healing of existing ulcers. Some investigators claim that Hp infection acts synergistically with NSAID on ulcerogenesis and propose that Hp should be eradicated, particularly at the onset of long-term NSAID therapy. Our studies in about 6500 dyspeptic patients undergoing upper endoscopy and 13C-urea breath test revealed that about 70% of these patients are Hp positive and 31% of these develop gastro-duodenal ulcers. Of these ulcers, 66% were Hp positive and NSAID negative, 3%--NSAID positive and Hp negative, 8% were both Hp positive and NSAID positive, while 23% ulcers were Hp and NSAID negative. An evidence was obtained for negative interaction between Hp infection and NSAID on risk of gastro-duodenal ulcers suggesting that Hp may attenuate the peptic ulcerogenesis. Our results support the concept 1) the interaction between Hp infection and NSAID on gastro-duodenal ulcerations is antagonistic, 2) the Hp and NSAID are independent risk factors for peptic ulcerations in humans, 3) there is no need for the Hp eradication in NSAID-treated patients, and 4) the rate of ulcer complications (hemorrhage and perforation) remains constant despite the decrease in Hp and ulcer prevalence.
Med Sci Monit 2002 Sep
PMID:Interaction of Helicobacter pylori (Hp) and nonsteroidal anti-inflammatory drugs (NSAID) on gastric mucosa and risk of ulcerations. 1221 57

In this paper we reviewed roles of SPARC in cell functions with a focus on tissue injury healing. SPARC (Secreted Protein, Acidic and Rich in Cysteine) is a matrix-associated glycoprotein that influences a variety of cellular activities in vitro and in vivo. SPARC and its related peptides bind to several proteins of the extracellular matrix (ECM), affect ECM protein expression, alter cell shape, reduce cellular adhesion, influence migration, and modulate growth factor-induced cell proliferation and angiogenesis. SPARC influences cell interactions with the extracellular milieu during embryonic development and in response to tissue injury. This paper reviews the roles of SPARC in the cellular and molecular events taking place during healing of tissue injury. We also present preliminary data on increased SPARC expression in gastritis and in granulation tissue of human gastric ulcer.
Med Sci Monit 2007 Feb
PMID:Role of SPARC--matricellular protein in pathophysiology and tissue injury healing. Implications for gastritis and gastric ulcers. 1726 93