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)

We have analyzed possible qualitative and quantitative differences in antigen expression between Helicobacter pylori strains isolated from the antrum and different locations in the duodenum of 21 duodenal ulcer (DU) patients and 20 asymptomatic subjects (AS) by enzyme-linked immunosorbent assay (ELISA) and inhibition ELISA. Almost all antral and duodenal strains grown in vitro expressed the N-acetyl-neuroaminyllactose-binding hemagglutinin, flagellins (subunits FlaA and FlaB), urease, a 26-kDa protein, and a neutrophil-activating protein. In 75% of both the DU patients and the AS, antral H. pylori strains expressed either the blood group antigen Lewis y (Le(y)) alone or together with the Le(x) antigen. However, duodenal H. pylori strains of DU patients expressed Le(y) antigen more frequently than corresponding strains of AS (P < 0.05). Presence of Le(y) on H. pylori was related to the degree of active duodenitis (P < 0.05). Duodenal H. pylori strains isolated from AS were significantly more often Lewis nontypeable than duodenal strains of DU patients (P < 0.01). Presence of H. pylori blood group antigen-binding adhesin (BabA) was significantly higher on both antral and duodenal strains isolated from DU patients than on corresponding strains isolated from AS (P < 0.05). BabA-positive duodenal H. pylori strains isolated from DU patients were associated with active duodenitis more frequently than corresponding strains isolated from AS (P < 0.01). Infection with H. pylori strains positive for Le(y) and BabA in the duodenum is associated with development of duodenal ulcer formation.
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PMID:Differences in surface-exposed antigen expression between Helicobacter pylori strains isolated from duodenal ulcer patients and from asymptomatic subjects. 1097 Mar 97

The Helicobacter pylori infection rate was determined in 124 consecutive patients with duodenal ulcers (DU), gastric ulcers (GU), duodenal erosions or gastric erosions diagnosed by endoscopy at a single institution in north-eastern peninsular Malaysia in 1996-97. Biopsies of the gastric antrum and body were subjected to the urease test, Gram staining of impression smears, culture and histopathological examination. Serology was undertaken on all patients using a locally validated commercial kit. Infection was defined as a positive result in at least one test. The infection rates were 20% (10/50), 21.2% (7/33), 16.7% (1/6) and 17.1% (6/35) in DU, GU, duodenal erosion and gastric erosion patients, respectively. The infection rate among Malays [7.0%, (6/86)] was lower than in non-Malays [47.4% (18/38)] (P < 0.001). There was a higher infection rate among males, who constituted 62.1% (77/124) of the sample. Seventy-eight patients (62.9%) were receiving non-steroidal anti-inflammatory drugs (NSAIDs) and 33 patients (26.6%) were neither receiving NSAIDs nor were infected with H. pylori. The H. pylori infection rate among peptic ulcer patients in this predominantly Malay rural population appears to be the lowest reported in the world thus far. Empirical H. pylori eradication therapy in peptic ulcer patients is clearly not indicated in this community. The possible reasons for the low prevalence of H. pylori infection are discussed.
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PMID:Further evidence for an exceptionally low prevalence of Helicobacter pylori infection among peptic ulcer patients in north-eastern peninsular Malaysia. 1128 57

Peptic ulcer accounts for about 50% of all cases of upper gastrointestinal bleeding. Acute mortality may be as high as 14%. Infection with Helicobacter plyori (Hp) and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the predominant risk factors. While the prevalence of Hp in ulcer bleeding is still debated, there is strong evidence that eradication of bacteria reduce the risk of re-bleeding significantly. The use of NSAIDs increases the frequency of ulcer bleeding about four- to sixfold on average. Additional factors such as advanced age, concomitant use of corticosteroids or anticoagulants, prior ulcer complications and co-morbid diseases may further increase the risk of bleeding. Whether or not Hp infection also represents an additive risk factor in NSAID-related bleeding remains to be clarified. The pathophysiologic action of both Hp and NSAIDs is quite complex. Hp promotes the aggressive factor acid and damages several mucosal defence mechanisms by liberating lipopolysaccharide, urease and vacuolating cytotoxin. In NSAID toxicity the cyclo-oxygenase enzymes (COX) have been studied intensively. With the advent of COX-2-selective NSAIDs, the clinical problem of NSAID-induced ulcer bleeding may be markedly reduced or abolished completely.
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PMID:Incidence and pathophysiology of peptic ulcer bleeding. 1137 51

Infection with Helicobacter pylori strains containing the cag Pathogenicity Island (cag PAI) is strongly correlated with the development of severe gastric disease, including gastric and duodenal ulceration, mucosa-associated lymphoid tissue lymphoma, and gastric carcinoma. Although in vitro studies have demonstrated that the expression of genes within the cag PAI leads to the activation of a strong host inflammatory response, the functions of most cag gene products and how they work in concert to promote an immunological response are unknown. We developed a transcriptional reporter that utilizes urease activity and in which nine putative regulatory sequences from the cag PAI were fused to the H. pylori ureB gene. These fusions were introduced in single copies onto the H. pylori chromosome without disruption of the cag PAI. Our analysis indicated that while each regulatory region confers a reproducible amount of promoter activity under laboratory conditions, they differ widely in levels of expression. Transcription initiating upstream of cag15 and upstream of cag21 is induced when the respective fusion strains are cocultured with an epithelial cell monolayer. Results of mouse colonization experiments with an H. pylori strain carrying the cag15-ureB fusion suggested that this putative regulatory region appears to be induced in vivo, demonstrating the importance of the urease reporter as a significant development toward identifying in vivo-induced gene expression in H. pylori.
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PMID:Differential gene expression from two transcriptional units in the cag pathogenicity island of Helicobacter pylori. 1140 55

Over the past decade, several Helicobacter species have been isolated from rodents. With the advent of PCR for the diagnosis of infectious agents, it has become clear that several previously uncharacterized Helicobacter species also colonize rodents. In this report, we describe a novel urease-negative helicobacter, Helicobacter typhlonius sp. nov., which was isolated from colonies of laboratory mice independently by two laboratories. Infection of immunodeficient mice by this bacterium resulted in typhlocolitis similar to that observed with other helicobacter infections. H. typhlonius is genetically most closely related to H. hepaticus. Like H. hepaticus, it is a spiral bacterium with bipolar sheathed flagella. However, this novel species contains a large intervening sequence in its 16S rRNA gene and is biochemically distinct from H. hepaticus. Notably, H. typhlonius does not produce urease or H(2)S nor does it hydrolize indoxyl-acetate. Compared to other Helicobacter species that commonly colonize rodents, H. typhlonius was found to be less prevalent than H. hepaticus and H. rodentium but as prevalent as H. bilis. H. typhlonius joins a growing list of helicobacters that colonize mice and are capable of inducing enteric disease in various strains of immunodeficient mice.
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PMID:Helicobacter typhlonius sp. nov., a Novel Murine Urease-Negative Helicobacter Species. 1168 8

Infection with Helicobacter pylori is chronic despite a vigorous cellular and humoral immune response and causes severe pathology in some patients. In this study, phage display was used as a new approach in order to investigate the role of the host's humoral immune response in the pathogenesis of H. pylori gastritis. Human monoclonal single-chain Fv (scFv) antibody fragments against H. pylori cell lysate and the H. pylori urease were isolated from an immune phage display library, constructed from peripheral blood lymphocytes of an H. pylori-infected patient. After affinity selection, 23% of the clones tested showed binding activity against a lysate of the H. pylori Sydney strain in enzyme-linked immunosorbent assay (ELISA) and 9% bound the H. pylori urease. Further characterization by PCR-fingerprint analysis and sequencing revealed that two closely related H. pylori binders and one antiurease scFv could be isolated. The selected scFvs were highly specific as analyzed by ELISA and immunoblots using various bacterial lysates and recombinant proteins. Analysis of the humoral immune response following H. pylori infection using human monoclonal antibodies might contribute to a better understanding of the pathogenesis of the disease. Moreover, using immune phage display libraries, it might be possible for relevant epitopes of H. pylori antigens to be determined, which might be of use for vaccine development.
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PMID:Generation and characterization of human monoclonal scFv antibodies against Helicobacter pylori antigens. 1211 24

Infection by Helicobacter pylori is recognized as a risk factor for gastric cancer and peptic ulcer disease. Venezuela has regions with different gastric cancer risks; the Andean region has the highest gastric cancer mortality in the country. We performed a cross-sectional study on 357 patients who underwent endoscopy attending 2 private (n = 76) and one public hospital in Caracas, Venezuela (n = 215), and one public hospital in the Andes (n = 66) to determine H. pylori infection (by a rapid biopsy urease test and histology). The proportion of infected patients in Caracas was significantly higher in public hospitals (72%) than in private hospitals (46%; P = 0.00001), and there was no significant variation the Andes and Caracas (P = 0.7001). When analyzing the data from the public hospital in Caracas, we found that the frequency of infected patients was significantly higher during the rain (96%) than during the dry months (70%, P = 0.00000001). Differences in prevalence of infection in symptomatic patients was not related to the risk of gastric cancer but to socioeconomic differences. Rain-dependent factors that may be exacerbating the clinical activity of nonulcer dyspepsia in people infected with H. pylori deserve further study.
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PMID:Short report: socioeconomic and seasonal variations of Helicobacter pylori infection in patients in Venezuela. 1213 67

Infection stones (ammonium magnesium phosphate) and catheter encrustations have a common cause-urease producing microorganisms. With their rapid growth and frequent recurrences, infection stones are among the most troublesome of urinary system stones. For many patients with a long-term indwelling catheter, encrustations can be a severe problem. Urine composition is important, because, urine calcium enhances the crystallization process and urine citrate inhibits it. The role of non-urease producing microorganisms in stone forming processes is not well understood. Stones can now be successfully treated with a low morbidity index by percutaneous stone surgery or extracorporeal shock wave lithotripsy (ESWL) and recurrence of stone formation is then avoided by prolonged antibiotic treatment and oral citrate. Catheter encrustations and damage caused by ammonia released during urease activity can, however, be a serious problem in patients with indwelling catheters and our remedies are unsatisfactory.
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PMID:Uropathogens and urinary tract concretion formation and catheter encrustations. 1213 38

Infection stones make up approximately 15% of urinary stone diseases and are thus an important group. These stones are composed of struvite and/or carbonate apatite. The basic precondition for the formation of infection stones is a urease positive urinary tract infection. Urease is necessary to split urea to ammonia and CO(2). As a result, ammonia ions can form and at the same time alkaline urine develops, both being preconditions for the formation of struvite and carbonate apatite crystals. When these crystals deposit themselves infection stones form. If these infections are not treated and the stones are not removed, the kidney will be damaged. For stone removal modern methods are available, e.g. ESWL and/or instrumental urinary stone removal. Here especially less invasive methods are preferable. Any treatment must be adjusted to the patient individually. Patients should be examined frequently for recurrent urinary tract infections and stone recurrences and, newly arising infections must be resolutely treated. Good therapy and prophylaxis are possible with present-day treatment modalities.
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PMID:Urinary infection stones. 1213 39

Infection stones make up approximately 15% of urinary stone diseases and are thus an important group. These stones are composed of struvite and/or carbonate apatite. The basic precondition for the formation of infection stones is a urease-positive urinary tract infection. Urease is necessary to split urea into ammonia and CO(2). As a result, ammonia ions can form and at the same time alkaline urine develops, both being preconditions for the formation of struvite and carbonate apatite crystals. When these crystals are deposited infection stones form. Pathogenetically, various risk factors play a role: urinary obstruction, neurogenic bladder, dRTA, and MSK. If these infections are not treated and the stones are not removed, the kidney will be damaged. Modern methods are available for stone removal, e.g., ESWL and/or instrumental urinary stone removal. Here, especially less invasive methods are preferable. Any treatment must be adjusted to the patient individually. Patients should be examined frequently for recurrent urinary tract infections and stone recurrences, and new infections must be resolutely treated. Good therapy and prophylaxis are possible with present-day treatment modalities.
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PMID:[Infection-induced urinary stones]. 1257 84


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