Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori infection and adenomatous polyposis coli (Apc) gene mutations have been linked to gastric cancer in humans, but possible synergistic interaction(s) between these risk factors have not been examined. Fourteen C57BL/6 wild-type and 14 Apc1638 heterozygous mice were inoculated with Helicobacter felis at 6 weeks of age and compared at various time points with a similar number of uninfected control mice of the same genotype. Both infected and uninfected Apc1638 mice had a limited incidence of atypical proliferation foci in the mucosa of the antrum and pyloric junction at 4.5 and 6 months of age, whereas polyps of the antrum and pylorus were present in all mice, regardless of infection status, at 7.5 months. In contrast, no altered gastric mucosal foci were observed in control or infected C57BL/6 mice at any time point. Interestingly, the infected Apc1638 mice had less epithelial proliferation and inflammation in the body of the stomach, lower anti-H. felis serum IgG antibody responses (although both the wild-type and Apc mutant mice had a Th1-like immune response, based on a predominantly IgG2a immunoglobulin response), and higher bacteria and urease scores than did infected wild-type C57BL/6 mice. In conclusion, the Apc1638 truncating mutation leads to gastric dysplasia and polyposis of the antrum and pyloric junction, but H. felis infection of the Apc mutant mouse does not lead to an increased rate of gastric neoplasia. In addition, our data suggest this Apc mutation may actually lead to decreased immune, inflammatory, and gastric hyperplastic responses to Helicobacter infection, suggesting the possibility of a novel role for this tumor suppressor gene in the immune and local tissue responses to gastric bacterial infection.
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PMID:Mice carrying a truncated Apc gene have diminished gastric epithelial proliferation, gastric inflammation, and humoral immunity in response to Helicobacter felis infection. 930 81

In patients with nasal polyps the colonisation of nasal polyps tissues by Helicobacter pylori was investigated using urease test (GUT plus). In this prospective clinical trials we enrolled 61 subjects who had undergone endoscopic nasal polyps surgery and 30 subjects who had undergone septoplasty (control group) were questioned and biopsy specimens of the removed polyps or the mucosal part of inferior turbinate were tested by the urease test GUT plus. In result Helicobacter pylori was not found in the nasal polyps and mucosal part of inferior turbinate tissue of any of patients including the 43 of 61 patients with nasal polyps and 7 of 30 patients with septum deviation who had symptoms of gastroesophageal reflux. In our study using the urease test GUT plus we were not able to confirm presence of Helicobacter pylori in the nasal polyps tissue. However, further epidemiologic studies using different diagnostic methods would be necessary to confirm presence of Helicobacter pylori as potential underlying pathogenetic mechanism of nasal polyposis.
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PMID:[Detection of Helicobacter pylori in nasal polyps specimens using urease test GUT plus]. 1635 53

Results of clinical and instrumental-laboratory study of 17 cases are presented. According to the rapid urease test (CLO) and histological studies, the helicobacter infection was found in 12 (70.6%) cases out of the group of 17 suffering from chronic atrophic gastritis, gastric ulcer adenomatous polyposis. Analyses of Helicobacter pylori dissemination over the gastric mucosa manifested the I (weak) degree (up to 20 microbes within field of vision) prevailing in 8 (66.7%) of 12 cases, while the II (medium) degree (up to 50 microbes within field of vision) and III (high) degree (over 50 microbes within field of vision) occurred only in 4 cases (33.3%). By comparative cytogenetic research of the peripheral blood lymphocytes we found the immunogenetic markers and characteristic features of cytogenetic disturbances in the immunocompetent cells in cases of pre-cancer Helicobacter pylori-associated diseases (chronic atrophic gastritis, gastric ulcer, adenomatous polyposis). Statistical data confirmed an increase in the percentage of cells with chromosomal aberrations, which amounted to 4.25+/-0.51 in the chronic atrophic gastritis cases, 3.5+/-0.46 in the gastric ulcer cases, 5.75+/-0.60 in the adenomatous polyposis cases for 100 analyzed metaphases. Considering the questionable role of Helicobacter pylori as a direct initiator of mutagenesis, the immune disturbances may be caused by the damage of DNA of lymphocytes resulting from the genotoxic effect of some intermediates of inflammation.
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PMID:[Chromosomal instability of peripheral blood lymphocytes in patients with precancer gastric cases]. 1698 Jul 44

The aim of this study was to identify the presence of Helicobacter pylori in nasal polyp specimens of patients with nasal polyposis. A cross-sectional study with control group was performed on fresh tissue samples from 25 patients with nasal polyps, and 25 persons with concha bollusa (control group). Patients with symptoms of gastroesophageal reflux (GERD) were not enrolled. Samples were studied by three methods: polymerase chain reaction (PCR), culture, and urease test. All the diagnostic tests were negative for H. pylori in both the case and control groups. In conclusion, there was no association between H. pylori and nasal polyposis in patients without GERD signs or symptoms in our study, and further studies are needed to assess other potential factors that may influence the development of nasal polyposis.
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PMID:Investigating Helicobacter pylori in nasal polyposis using polymerase chain reaction, urease test and culture. 2211 83

An 85-year-old woman was admitted to our hospital because of progressive hypoproteinemia and generalised oedema. Technetium-99m human albumin scintigraphy revealed protein leakage in the gastrointestinal tract. Upper gastrointestinal endoscopy revealed small whitish nodules from the gastric body up to the duodenal bulb. The urease test for Helicobacter pylori infection was positive. We diagnosed her as having protein-losing gastroenteropathy (PLGE) caused by H. pylori infection. The patient's hypoproteinemia and clinical symptoms promptly resolved after H. pylori eradication. Our results suggest that a trial of H. pylori eradication is warranted in patients with PLGE, even if endoscopy reveals neither giant rugal folds, erosion of the mucosa, nor polyposis, which are previously reported characteristic endoscopic findings of PLGE.
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PMID:Protein losing gastroenteropathy due to Helicobacter pylori infection without giant rugal folds, erosion or polyposis. 3174 54