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)

Serum alkaline phosphatase (AP) electrophoretic phenotype and the level of its activity inhibited by l-phenylalanine 5 mM (the stereospecific inhibitor of the intestinal AP isoenzyme) were investigated in 312 subjects (132 healthy controls, 89 patients with duodenal ulcer, 31 with gastric ulcer and 60 family members of the duodenal ulcer patients) in correlation with the ABO blood group system and secretory status. In the control subjects, those with A(II) blood group showed a predominance of the p degrees electrophoretic phenotype while phenotypes p+ and p++ were more frequent in the controls with O(I) and B(III) blood groups and in the secretory ones. In the patients with duodenal ulcer and their family members the frequency of phenotypes p+ and p+ was significantly higher than in the controls. The same distribution of frequencies was observed for the level of AP activity inhibited by l-phenylalanine. The results obtained are discussed in the light of a possible genetic linkage.
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PMID:Study of serum intestinal alkaline phosphatase isoenzyme in correlation with the ABO blood group system and secretory status in ulcer patients. 59 22

In duodenal ulcer alkaline phosphatase activity was the highest in mucosa of pyloric region of curvature ventriculi minor and it decreased distinctly in the tissues removed from pylorus. In cases of gastric ulcer, the enzymatic activity was high throughout the curvatura ventriculi minor reaching the maximal value at the ulcerous zone. Alkaline phosphatase from gastric mucosa resembled the enzyme from intestine in its inhibition patterns with 1-phenylalanine and in inactivation properties at 56 degrees within 15 min; but, as distinct from the latter, the enzyme was more stable at 65 degrees within 5 min, maintaining 50% of the initial activity.
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PMID:[Distribution and properties of the alkaline phosphatase in the human gastric mucosa in peptic ulcer]. 66 46

The mechanism of the inhibitory action of rebamipide, a new mucosal protective drug, was studied using rats with diethyldithiocarbamate-induced gastric antral ulcers. Rebamipide reduced ulcer formation and inhibited the elevation in lipid peroxide concentration in the gastric mucosa. Rebamipide inhibited both luminol- and lucigenin-dependent chemiluminescence of neutrophils activated by formyl-methionyl-leucyl-phenylalanine. Rebamipide did not alter the reduction of cytochrome c induced by the xanthine-xanthine oxidase system or the NADPH-dependent microsomal lipid peroxidation in the liver. These findings suggest that rebamipide prevents diethyldithiocarbamate-induced gastric ulcer formation by inhibiting neutrophil activation.
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PMID:Antiulcer mechanism of action of rebamipide, a novel antiulcer compound, on diethyldithiocarbamate-induced antral gastric ulcers in rats. 131 72

The amino acids in human gastric juice were measured in the hospital control (n = 9), gastric ulcer (n = 10), duodenal ulcer (n = 12), gastroduodenal ulcer (n = 9), and gastric cancer patients (n = 16) by high performance liquid chromatography, and the total of 15 kinds of amino acids was correlated with value determined by Ninhydrin method. The patients with gastric cancer had elevated levels of all amino acids, especially alanine, leucine, valine and threonine. In all but the gastric cancer disease groups, the aromatic amino acids, phenylalanine and tyrosine as well as leucine were at high levels in 15 amino acids. The different patterns of amino acids in these four groups tended to correlate with the variabilities of protein loss from the gastric wall.
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PMID:Amino acid patterns in human gastric juice in health and gastric disease. 406 60

Rebamipide is the first anti-gastric ulcer and antigastritis drug that not only increases endogenous prostaglandin in gastric mucosa but also scavenges oxygen-derived free radicals and inhibits their production. In the present paper, we have reviewed the antioxidative and antiinflammatory properties of rebamipide mainly demonstrated by in vitro studies. The study, using the electron paramagnetic resonance (EPR) spin trapping technique, showed that superoxide production was inhibited by rebamipide when isolated human neutrophils were stimulated with opsonized zymosan or Helicobacter pylori water extract in a dose-dependent manner. Chemiluminescence generated from neutrophils activated by H. pylori or formyl-methionyl-leucyl-phenylalanine was also decreased by the treatment with rebamipide. Rebamipide, at concentrations of 10(-5) and 10(-6) M, reduced the adherence of neutrophils to endothelial cells as well as the CD18 expression on neutrophils induced by H. pylori water extract. The EPR study also demonstrated the direct hydroxyl radical scavenging activity of rebamipide, and a kinetic study showed that the second-order rate constant for the reaction between rebamipide and hydroxyl radical was 2.24 x 10(10) M(-1)/s(-1). The inhibitory effect of rebamipide on lipid peroxidation induced by a free radical initiator was also demonstrated by the in vitro system using rat gastric mucosal homogenates. These data indicate that rebamipide offers a potential for protection against reactive oxygen- and activated neutrophil-associated gastric mucosal injury by scavenging hydroxyl radical and inhibiting neutrophil activation or lipid peroxidation.
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PMID:In vitro studies indicating antioxidative properties of rebamipide. 975 24

Micro-Raman spectroscopy was employed to identify gastritis tissues and gastric ulcer tissues. The primary spectral differences between the two types of samples include, for gastric ulcer tissues, (1) the intensity of the peak at 781 cm(-1) ascribed to cytosine decreases, while the peaks ascribed to adenine and thymine respectively at 793 and 823 cm(-1) become stronger; (2) the bands of amide I and amide III at 1654 and 1320-1270 cm(-1) respectively, characteristic of alpha-helix structural protein, lose their intensities, and the tryptophan band at 1332 cm(-1) and phenylalanine band at 1003 cm(-1) reduced significantly, while the tryptophan marker at 1554 cm(-1) up shiftes to 1556 cm(-1) with increasing intensity; (3) a blue shift of 1073 cm(-1) line, the characteristic Raman band of lipid, and a reduction in the ratio of 1303 cm(-1) assigned to in-phase CH2 twisting motion to 1268 cm(-1) from =CH in-plane deformation were observed; (4) statistic analysis shows that the ratio of Raman intensities at bands 1449 cm(-1) originating from CH2 group to 1660 cm(-1) from amide I provides a promising standard to distinguish the two tissues.
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PMID:[Micro-Raman spectra for gastritis and gastric ulcer tissues]. 1830 90