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)

Helicobacter pylori (Hp) is associated with gastritis and peptic ulcers. It may also induce gastric atrophy (GA) and intestinal metaplasia (IM), and these changes may be the precursors of gastric carcinoma. The aim of this study was to determine if GA or IM is associated with Hp infection in elderly patients. Consecutive patients admitted for gastroscopy were recruited. Multiple biopsies were taken for histology and rapid urease (CLO) tests along with IgG enzyme-linked immunosorbent assay antibodies and (13)C-urea breath tests. Statistical analysis was by chi(2) tests. 114 patients were recruited, the average age was 78.9 + or - 5.4 years. Histology was available on 105 patients, 80 (76.2%) had gastritis, and 61/80 (76.25%) had evidence of definite current Hp infection. Seven patients had reflux gastritis, and these were excluded from the analysis described below. 20 patients had GA and 24 IM. The relationship between Hp and GA or IM was investigated by dividing patients into four groups: Group 1 patients (n = 57) were taken to be definitely currently infected (GA 7 patients, IM 11, both 1). Group 2 patients (n = 18) had old infection (GA 2, IM 4, both 3). Group 3 patients (n = 16) have never been infected previously (GA 1, IM 1, both 3). Group 4 patients (n = 4) had a poor immunological response to Hp (GA 1, IM 1, both 0). There were no significant differences in the numbers of patients with GA or IM in any group as compared with any other, with the exception of less patients with histological evidence of combined GA and IM among patients with definite current infection as compared with those with either previous infection (p = 0.04) or 'never' infection (p = 0.03). We conclude that the mucosal changes of GA or IM are not consistently associated with Hp infection in the elderly.
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PMID:Lack of association between helicobacter pylori and gastric atrophy or intestinal metaplasia in elderly patients. 913 79

Helicobacter pylori is recognized as an important cause of chronic antral gastritis and peptic ulceration. Moreover, H. pylori associated inflammatory process has been linked with gastric carcinoma. Many putative virulence factors of H. pylori have been suggested, including motility, urease and cytotoxins production and bacterial adhesins. An accessory function of CagA antigen and bacterial heat-shock proteins in the pathogenesis of H. pylori infections have been also considered. H. pylori-induced immunological response is discussed as regards local and general antibody production, the interaction of the bacteria with the phagocytes and still controversial involvement of T cells. Data on the importance of cytokines and inflammatory mediators in the disruption of the gastric mucosal barriers as well as the evidence to support a role for H. pylori as a risk factor for gastric carcinoma are also presented.
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PMID:[Immunologic reactions in infections caused by Helicobacter pylori]. 923 61

Helicobacter pylori is a gram-negative bacterium which causes chronic gastritis and plays important roles in peptic ulcer disease, gastric carcinoma, and gastric lymphoma. H. pylori has been found in the stomachs of humans in all parts of the world. In developing countries, 70 to 90% of the population carries H. pylori. In developed countries, the prevalence of infection is lower. There appears to be no substantial reservoir of H. pylori aside from the human stomach. Transmission can occur by iatrogenic, fecal-oral, and oral-oral routes. H. pylori is able to colonize and persist in a unique biological niche within the gastric lumen. All fresh isolates of H. pylori express significant urease activity, which appears essential to the survival and pathogenesis of the bacterium. A variety of tests to diagnose H. pylori infection are now available. Histological examination of gastric tissue, culture, rapid urease testing, DNA probes, and PCR analysis, when used to test gastric tissue, all require endoscopy. In contrast, breath tests, serology, gastric juice PCR, and urinary excretion of [15N]ammonia are noninvasive tests that do not require endoscopy. In this review, we highlight advances in the detection of the presence of the organism and methods of differentiating among types of H. pylori, and we provide a background for appropriate chemotherapy of the infection.
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PMID:Helicobacter pylori. 933 70

Increased epithelial cell proliferation is associated with an increased risk of gastric carcinoma. Helicobacter pylori infection is an established risk factor for gastric cancer and the organism has recently been classified as a group I carcinogen by an IARC working group. In this study, we describe differences in gastric epithelial cell proliferation between a H. pylori eradicated group (n = 21) and a not eradicated group (n = 8) after anti-H. pylori eradication therapy to show that increased cell proliferation is associated with H. pylori infection. H. pylori infection was determined by rapid urease test and immunohistochemical method with anti-H. pylori polyclonal antibody. Gastric epithelial cell proliferation was assessed using immunohistochemical method using Ki-67 monoclonal antibody. Ki-67 positive cells in H. pylori associated chronic active gastritis were observed in the glandular neck and the upper portion of foveolar epithelium. Patients who cleared their H. pylori infections showed a significant decrease of Ki-67 labeling index after therapy (0.73 +/- 0.10 vs. 0.48 +/- 0.08, p < 0.01). By contrast, Ki-67 labeling index before and after treatment in patients who remained positive for H. pylori showed no significant difference (0.78 +/- 0.08 vs 0.74 +/- 0.10, p > 0.05). These results indicate that H. pylori infection increases the proliferation of gastric foveolar epithelium, which is reduced by the eradication therapy. We suggest that anti-H. pylori eradication therapy can prevent mucosal cell proliferation to be closely associated with gastric carcinogenesis.
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PMID:Decreased gastric proliferation of foveolar epithelial cells after the eradication of Helicobacter pylori. 936

Helicobacter pylori has been implicated in the etiology of peptic ulcer disease, chronic gastritis, gastric carcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Although significant progress has been made in treating this infection with combinations of either antimicrobial agents or antimicrobial agents plus proton pump inhibitors, these antimicrobial-based treatments continue to be suboptimal. Over the past few years it has become increasingly recognized that direct mucosal immunization can induce protection from infection at mucosal surfaces. Therefore, prevention of H. pylori infection by oral immunization is an alternative approach for the control of H. pylori disease. Using the Helicobacter felis mouse model or H. pylori mouse model, both prophylactic and therapeutic oral immunizations have been shown to be effective against H. pylori. In addition, several H. pylori proteins have been identified as potential candidate vaccines, and a phase 1 clinical trial has been completed that demonstrates the safety and tolerability of urease as a vaccine antigen. Such antigens in combination with a safe mucosal adjuvant could be used in the form of an oral vaccine administered during childhood before exposure to H. pylori to prevent infection. In addition, therapeutic immunization alone or as an adjunct to antimicrobial therapy may be capable of achieving a cure rate approaching 100%.
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PMID:What is the role for vaccination in Helicobacter pylori? 939 76

The role of Helicobacter pylori in gastric carcinogenesis is a subject of an increasing interest. In this report we describe a prospective study on the resected stomachs to establish the prevalence of H. pylori in different types of gastric carcinoma. The material consisted of 62 consecutive patients operated on stomach adenocarcinomas Fifty six percent of the patients were intestinal type, 34%--diffuse type and 10%--mixed type. The presence of H. pylori was studied in specimens from surgically removed stomachs. The conformation of the bacterial infection was done by means of rapid urease test, microbiological culture, Warthin-Starry and immunohistochemical staining. The overall prevalence of H. pylori infection was 69% (43/62). There was a statistically significant difference in the infection rates between the types of carcinoma--75% in the intestinal type and 62% in the diffuse type. The most sensitive was immunohistochemical staining. The bacterial colonies were cumulated far from the tumor tissue. In cardiac cancer the most intense of infection was an antrum and lower part of gastric body. In opposite; in antrum and pylorus cancer the scope of colonisation increased in fundus and subcardiac region with statistical signification. We could not detect H. pylori in the tumor tissue itself as in the normal mucosa of the stomach. In gastric antrum the most intense colonisation was detected on mucosal atrophy, but in the upper part of the stomach--on the mucosal metaplasia.
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PMID:Topography of Helicobacter pylori infection in gastric cancer patients. 944 64

The peptic ulcer of gastric tube using for esophageal reconstruction is rare. We report herein five cases of peptic ulcer of gastric tube used for esophageal reconstruction after esophagectomy for esophageal carcinoma. The reconstructive route, in all cases, was posterior mediastinum. In one case, 10 days after esophagectomy, he had high grade fever and pneumonia of right lower lobe of lung. Endoscopic examination revealed a deep ulcerative lesion on anterior wall of gastric tube and fistula formation on membranous part of trachea. The partial resection of gastric tube was performed for closing to tracheo-gastro fistula. In other four cases, the location of ulcer was middle or lower third of gastric tube. One had multiple peptic ulcer and other had single. Two cases of four underwent post irradiation therapy. One case of then, the Helicobacter infection detected using by rapid urease test and histological examination. We analyzed of Helicobacter pylori infection and serum gastrin level of gastric tube in outpatients who have used gastric tube for esophageal reconstruction after radical esophagectomy. Helicobacter pylori infection was positive at 56% (9/16) of all patients. The serum gastrin level of patients who was positive of Helicobacter pylori infection is not significantly higher than that of patients who was negative. We consider that post operative irradiation therapy and Helicobacter infection might play in development of peptic ulcer of gastric tube.
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PMID:[Five cases of peptic ulcer of gastric tube after radical esophagectomy for esophageal carcinoma and analysis of Helicobacter pylori infection at gastric tube]. 945 13

Helicobacter pylori is a Gram-negative bacterial pathogen associated with gastritis, peptic ulceration, and gastric carcinoma. The bacteria express a strong urease activity which is known to be essential for colonization of gnotobiotic pigs and nude mice. UreA and UreB, two structural subunits of the active enzyme, were expressed in the attenuated Salmonella typhimurium live vaccine SL3261 strain. Evaluation of protection against H. pylori was performed in Balb/c mice by oral immunization with a single dose of the vaccine strain. Five weeks after immunization, mice were challenged orally three times with a mouse-adapted H. pylori wild type strain and, six weeks later, mice were sacrificed to determine H. pylori infection by detection of urease activity from the antral region of the mouse stomachs. In several independent experiments, we observed 100% infection with H. pylori in the non-immunized mice and no infection (100% protection) in the mice immunized with S. typhimurium expressing recombinant UreA and UreB. Specific humoral and mucosal antibody responses against UreA and UreB were observed in mice immunized as indicated by western blots and ELISA assays. These data shows that oral immunization of mice with urease subunits delivered by an attenuated Salmonella strain induced a specific immune response and protected mice against H. pylori colonization. Single oral dose immunization with UreA and UreB delivered by a live Salmonella vaccine vector appears to be an attractive candidate for human vaccination against H. pylori infection. In addition, this model will aid to elucidate the effective protection mechanisms against H. pylori in the gastric mucosa.
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PMID:Protection of mice against gastric colonization by Helicobacter pylori by single oral dose immunization with attenuated Salmonella typhimurium producing urease subunits A and B. 949

The neoplasms and gastric mucosa colonization with Helicobacter pylori was studied in 40 stomachs resected for expansive (n = 20) and infiltrative (n = 20) carcinoma using Giemsa staining histological sections, histochemical reactions to oxyreductase, and urease test. In expansive carcinoma of the stomach, H. pylori was identifiable both in the tumour and surrounding gastric mucosa in 70 per cent of cases; infiltrative carcinoma appeared to be associated with gastric mucosa H. pylori in 80 per cent, whereas tumour H. pylori were recordable in 30 per cent of cases, which fact is dependent upon the histological structure of carcinoma. The role H. pylori plays in cancerogenesis is discussed.
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PMID:[Helicobacter pylori and stomach cancer]. 978 7

A prospective study was conducted in 26 patients with benign oral ulcers and oral carcinoma and 26 age and sex matched controls to determine the prevalence of Helicobacter pylori in oral mucosal biopsies. Oral mucosal biopsies were subjected to rapid urease test, campylobacter like organism (CLO) test, histopathological examination and bacteriological culture for demonstration of H pylori. Urease test was positive for H pylori in 3 (11.4%) out of 26 cases and CLO test in 2 (14%) out of 14 cases. On histology, H pylori was identified in 4 (15.38%) out of 26 cases. The spiral organism was universally absent in culture of both patients and controls. These pilot data negate the casual association of H pylori in oral mucosal lesions.
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PMID:Absence of Helicobacter pylori in oral mucosal lesions. 983 66


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