Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.3.4.6 (urease)
7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the prevalence and significance of Helicobacter pylori (H. pylori) infection, biopsies of the antral mucosa were obtained from 139 patients and 43 asymptomatic volunteers. The specimens were examined by hematoxylin-eosin staining and the ureas test. The detection rate of H. pylori by histologic examination was 91.3% in patients with duodenal ulcer, 75.0% in those with combined duodenal and gastric ulcer, 63.6% in those with gastric ulcer, 22.9% in those with gastric carcinoma, 36.4% in those with gastric adenoma, 14.3% in those with gastric hyperplastic polyp, and 51.7% in those with gastritis, and the respective percentages detected by the urease test were 91.3%, 75.0%, 54.5%, 28.6%, 27.3%, 14.3%, and 44.8%. H. pylori was also detected in 10/43 (23.3%) asymptomatic healthy volunteers by histology and the urease test. The prevalence of H. pylori was significantly higher in the patients than in the asymptomatic healthy volunteers (p < 0.05). H. pylori was detected in 62.9% of patients with endoscopic erosive gastritis and in 97.9% of those with histologically proven chronic active gastritis. The urease test was positive in 77/82 patients who were histologically positive for the organism (sensitivity: 93.9%), and it was negative in 98/100 patients who were negative by histology (specificity: 98.0%). Thus, there was over 90% agreement between the urease test and histology. Our investigations showed that H. pylori was closely related to peptic ulcers and antral gastritis, and that the urease test provides a simple, rapid and accurate diagnosis of H. pylori infection.
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PMID:Helicobacter pylori infection and gastroduodenal disease: a comparison of endoscopic findings, histology, and urease test data. 129 70

Helicobacter pylori (HP) has been shown to possibly be a pathogen of gastric carcinoma. HP has urease activity and produces ammonia in the stomach. In this study, the role of ammonia on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in rats. After 24 weeks pretreatment with MNNG (83 mg/l), 0.01% ammonia or tap water as a drinking water was administered for 24 weeks. The ammonia-treated rats showed a significantly higher incidence of gastric cancer (percent of animals with tumors and number of tumors per rat). Ammonia would thus appear to have an important role in HP-related human gastric carcinogenesis.
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PMID:Ammonia: a possible promotor in Helicobacter pylori-related gastric carcinogenesis. 151 5

The stomach provides a hostile environment to most microorganisms owing to the antibacterial effect of gastric acidity. However, over the period of mammalian evolution a highly specialized group of bacteria has evolved to inhabit the gastric mucosa. The common features of these bacteria that allow survival in the stomach and colonization of their natural ecologic niche, mucus, are a specialized form of motility, microaerophilism, and very high activity of the enzyme urease. Other important adaptations have been the acquisition of sophisticated mechanisms to evade host defences, and in certain cases tissue damage may result. The most important of these usually spiral-shaped bacteria is Helicobacter pylori. It is proposed that this bacterium is the human gastric spirillum that in most persons lives in harmony with its natural host, resulting in asymptomatic infection. However, if as yet undefined conditions are present, serious disease may result-that is, peptic ulceration. A consequence of long-term infection may be atrophic gastritis, which sets the scene for gastric carcinoma. The more the microbiology of the stomach is studied, the more species of Helicobacter are discovered, such as H. mustelae in the ferret, H. felis in cats and dogs, and 'Gastrospirillum hominis' in primates, cats, dogs, and pigs. These other helicobacters provide us with a wide spectrum of animal models of gastroduodenal disease. To understand mechanisms of pathogenesis, it is suggested that systematic study of all members of the genus will identify important colonizing factors and provide a realistic perspective on the putative virulence factors that have been proposed for H. pylori to date.
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PMID:Spiral organisms: what are they? A microbiologic introduction to Helicobacter pylori. 177 30

Helicobacter pylori is a microaerophilic, Gram-negative, spiral rod, the role of which in different gastric diseases has been investigated worldwide since the beginning of the 1980s. H. pylori has been shown to be the causative agent in active chronic gastritis, and it is regularly found in patients endoscopied for duodenal ulcer. The bacterium is also frequently isolated from persons with gastric ulcer, gastric carcinoma and non-ulcer dyspepsia. Apart from cultivation of the bacterium, other diagnostic procedures include various staining methods and urease tests of gastric biopsy samples. The application of non-invasive diagnostic methods, serology and urea breath tests, is rapidly increasing. H. pylori is susceptible to several antimicrobials in vitro, but eradication of the bacterium from the gastric mucosa is not always achieved. The best results until now have been obtained with the combined use of bismuth salts and two antibiotics. In active chronic gastritis and duodenal ulcer patients, eradication of the bacteria has resulted in healing of the disease with permanent decrease of circulating antibodies and negative urease tests. H. pylori has been found worldwide and the infection shows an age-dependent increase. Man, apparently, is the reservoir of the bacterium, but the exact mechanisms of interhuman transmission are still not defined.
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PMID:Helicobacter pylori and associated gastroduodenal diseases. Review article. 185 43

Biopsy specimens of human gastric mucosa of patients with gastric complaints and subjected to endoscopic examination were cultured microaerobically, and Campylobacter pyloridis was detected in 46 out of 80 cases (57.5%). The organism was found in 13 out of 22 patients with gastritis, 11 out of 16 with gastric ulcer scar, 7 out of 16 with gastric ulcer, 3 out of 9 with gastric polyp, 4 out of 5 with gastric carcinoma, 2 out of 2 with esophagus carcinoma, and 6 out of 9 with other gastric diseases. The isolates were identified as C. pyloridis, demonstrating its characteristic features such as positive for oxidase and catalase, negative for reduction of nitrite and nitrate, positive for urease, no growth at 25 C, growth at 37 C, not tolerant to 1% glycine, and resistant to nalidixic acid. Positive alkaline phosphatase activity was considered as an additional feature characteristic for the strains of C. pyloridis. The major cellular fatty acids were tetradecanoic acid and 19-carbon-cyclopropane acid. This pattern is unique among Campylobacter species. The survival of the organism for a longer period than 60 min at pH 2.5 indicates its significant resistance to acidic environment.
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PMID:Isolation of Campylobacter pyloridis from human gastric mucosa and characterization of the isolates. 343 27

Historical review of the pathological investigation on stomach cancer in Japan shows that the central problem had been whether or not gastric cancer developed from chronic peptic ulcer. This theory of ulcer cancer sequence was developed from chronic peptic ulcer. This theory of ulcer cancer sequence was supported by many researchers after the war in the period of 1946-64. Subsequently, systematic studies made at the Cancer Institute revealed that carcinoma arises from the gastric mucosa independently of chronic ulcer. The pathological interest then shifted toward investigation of the histogenesis and biological characteristics of gastric carcinoma. It is concluded that gastric carcinoma can be classified into two types; undifferentiated carcinoma (UCA or gastric type) and differentiated one (DCA or intestinal type). The former arises from the ordinary mucosa and cancer phenotype of this carcinoma resembles to that of the ordinary mucosa, and the latter arises from the metaplastic epithelium of intestinal type showing a cancer phenotype resembling to that of the intestinal metaplastic epithelium. These two carcinomas are also different in biological behaviors, such as growth pattern, invasiveness, metastasis, and prognosis. The frequency of UCA is almost the same in both sexes. DCA, however, occurs more often in male than in female. The time trend data indicates that in both sexes the number of DCA decreased, but that of UCA is steady, so that the ratio of DCA to UCA decreased since 1965. These results combined with the concept of the basic and variable cancer leads to a conclusion that UCA is a basic cancer and DCA is a variable cancer of the stomach.
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PMID:Pathological studies of human gastric cancer. 676 3

Gastric infection with Helicobacter pylori activates a mucosal inflammatory response by mononuclear cells and neutrophils that includes expression of cytokines interleukin-1 beta (IL-1 beta), IL-6, tumor necrosis factor alpha, and IL-8. In this study, we analyzed the IL-8 response of human gastric cancer cell lines (Kato III, AGS, and MKN28) to H. pylori infection in vitro. IL-8 mRNA expression was detected by reverse transcription-PCR amplification of RNA extracted from epithelial cells after incubation with different H. pylori wild-type and mutant strains, and IL-8 secretion was measured by an enzyme-linked immunosorbent assay. Exposure to viable H. pylori induced IL-8 mRNA and protein synthesis in all three gastric cell lines but not in nongastric epithelial cell lines. Heat-killed H. pylori and a crude cytotoxin preparation did not induce significant IL-8 secretion. IL-8 mRNA peaked between 2 and 4 h postinfection, and IL-8 protein production was maximal 24 h postinfection. Exposure of gastric carcinoma cells to other gastrointestinal bacteria, such as Pseudomonas aeruginosa, Campylobacter jejuni, and Escherichia coli, but not Campylobacter fetus, induced IL-8 synthesis. Wild-type strains that expressed the vacuolating cytotoxin (Tox+) and a cytotoxin-associated gene (cagA) product (CagA+) induced significantly more IL-8 than did CagA- Tox- strains. However, there was no decrease in IL-8 induction by isogenic mutants of CagA-, Tox-, or Cag- Tox- strains or by a mutant lacking the urease subunits. These results indicate that exposure to H. pylori and other gram-negative organisms that do not colonize the gastric mucosa induces IL-8 production by gastric carcinoma cells in vitro. Although the CagA+ Tox+ phenotype of H. pylori is associated with enhanced IL-8 production by gastric cell lines, other bacterial constituents are clearly essential.
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PMID:Interleukin-8 response of gastric epithelial cell lines to Helicobacter pylori stimulation in vitro. 772 72

The pathogenesis of gastric carcinoma developing after infection with Helicobacter pylori now seems to be clear. The release of urease, alcohol dehydrogenase, enzymes and cytotoxin on the one hand, and chemotactic factors, PAF and heat-shock proteins on the other trigger chronic inflammation and epithelial metaplasia and dysplasia in the stomach. Under the influence of additional carcinogens, the epithelial changes progress to severe dysplasia and finally carcinoma. As a result of chronic inflammation, MALT lymphomas can also be induced. These can be made to regress by eradicating Hp. The possibility of being able to prevent up to 80% of the carcinomas of the stomach by eradicating Hp holds out good prospects, over the long-term, for the prevention of these tumors. Accurate identification of the patient groups carrying a high risk is now necessary.
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PMID:[MALT lymphoma, stomach carcinoma--role of Helicobacter pylori. Are chances for prevention on the horizon?]. 784 83

Recently many reports have shown a strong association between Helicobacter pylori infection in the stomach and recurrent peptic ulcer. Moreover, prospective cohort serological studies showed that H. pylori infected individuals have significantly increased rate of gastric cancer in the USA. H. pylori is a gram-negative spiral organism which has urease activity and produces ammonia and CO2 from urea, and nestles in the gastric pits and overlaying mucus gel layer. Many diagnostic methods of H. pylori infection are available; ie bacterial culture, 13C-urea breath test, histology, serum IgG antibody against H. pylori. We developed a new method, ie tissue IgA antibody against H. pylori and detection of H. pylori DNA in the gastric juice by PCR method. Triple therapies with metronidazole, bismuth compounds, and amoxicillin or tetracyclin are difficult to use in Japan because of their sever side effects. Thus, new methods with proton pump inhibitor (PPI) and amoxicillin have been introduced. We treated 14 patients of whom were H. pylori positive-active peptic ulcer with 30 mg/day of lansoprazole, a new PPI, plus 1,500 mg/day of amoxicillin for 2 weeks and 8 (57%) patients were eradicated. Gastric carcinogenesis are multi-steps and multifactorials process. Hypothetical sequence of intestinal type of gastric cancer is that superficial gastritis-->atrophic gastritis-->intestinal metaplasia-->dysplasia-->gastric cancer and H. pylori infection may play a role in the early stage of the sequence. We examined mucosal IgA antibody against H. pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in 25 resected specimens after gastrectomy for gastric cancer. Positivity rates of tissue H. pylori IgA antibody were lower in the mucosa of intestinal metaplasia than in non-metaplastic gastric mucosa and were negative in carcinoma. Causal relationship between H. pylori infection and gastric cancer is not proven and factors other than H. pylori infection are also important in the gastric carcinogenesis. Finally we introduce 2 reports: (1) NIH Consensus Conference: Helicobacter pylori in peptic ulcer disease (JAMA. 1994; 272: 65-69). The consensus panel concluded that 1. ulcer patients with H. pylori infection require treatment with antimicrobial agents in addition to antisecretory drugs whether on first presentation with the illness or on recurrence; 2. the value of treating nonulcerative dyspepsia patients with H. pylori infection remains to be determined; and 3. the interesting relationship between H. pylori infection and gastric cancer requires further exploration. (2) World Health Organization: Working Group Meeting (Reported in World Congress of Gastroenterology, Los Angeles, 1994). H. pylori plays a causal role in the chain of events leading to cancer of the stomach. Group I: definite carcinogen.
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PMID:[Helicobacter pylori in peptic ulcer and gastric cancer]. 785 88

Helicobacter pylori is a microaerophilic bacterium initially found in the gastric antrum of patients with peptic ulcer disease. As a result, H. pylori is now believed to have a pathophysiologic role in gastritis as well as in peptic ulcer disease. Several recent studies showed that it may be associated with duodenal ulcer relapse and that eradication therapy using antibiotics may significantly decrease the ulcer recurrence rate in duodenal ulcer patients. Moreover, epidemiological studies suggest that it may increase the relative risk of carcinoma in the stomach and preliminary studies seem to indicate that some low-grade lymphoma in the stomach may regress after H. pylori eradication. Although the mechanisms by which H. pylori induces mucosal injury and/or neoplasm is not clearly understood, several modifications in gastric functions have been reported. The most specific way of detecting H. pylori in tissue is a combination of culture and histologic staining of mucosal biopsy specimens obtained by endoscopy. Rapid urease test, cytology and PCR procedures performed on biopsies may give rapid, sensitive and specific results. Breath test using 13C- or 14C-radiolabelled urea and serology tests are of particular importance when H. pylori diagnosis is needed via no invasive procedures. Helicobacter pylori is supposed to interact with G and D cells. Gastrin and somatostatin are synthetized and released from antral G and gastric D cells respectively. The gastric D cells are in close contact with either G and parietal cells. Gastrin stimulates gastric acid secretion and epithelial gastric cell proliferation (parietal and EC-L cells) while somatostatin inhibits these effects. Chronic gastritis is associated with fundic duodenal ulcer disease. In this situation, basal gastrin and meal- or bombesin-stimulated gastrin in the serum (especially gastrin G17) have been found to be higher in H. pylori positive than in negative patients. Moreover, gastrin decreases up to normal levels after eradication of H. pylori. The long term effect of a such hypergastrinemia is not so far established. The mechanism underlaying hormonal modification is poorly understood. Since no G/D cell ratio modification could be found after H. pylori eradication while the amount of somatostatin increases, one would suggest functional alteration of either G or D cells in the H. pylori-related chronic gastritis. The role of inflammatory mediators on the gastrin release and the processing of progastrin induced by the bacterium need further investigations.
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PMID:[Helicobacter pylori, a rediscovered bacterium. Implication in gastroduodenal diseases]. 789 50


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