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:3.5.1.5 (urease)
7,257 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urease is an enzyme found in plants and bacteria, but not mammals. It catalyzes the conversion of urea to carbon dioxide and ammonia. Ammonia shortens the life span of cells; and higher concentrations cause tissue necrosis and cytolysis. Twenty percent of total body urea is converted to ammonia by bacterial urease in the colon. Small injections of urease immunize animals by producing antiurease, a gamma globulin, which inactivates urease. Immunization eliminates the colonic conversion of urea to ammonia. Injection of urease produces ammonia intoxication making immunization hazardous. Although previously impossible, a non enzymatic urease antigen was synthesized by covalently bonding jack bean urease with glutaraldehyde. This antigen stimulated the production of antiurease that inactivates native urease. Helicobacter pylori, a potent urease producer, has been implicated in peptic ulcer, gastritis and other inflammatory bowel lesions. The pathogenicity of H pylori is dependent on its urease production. Immunization to urease can render H pylori non pathogenic. Cirrhotics develop encephalopathy and hyperammonemia because their livers fail to convert all the ammonia in portal venous blood to urea and collaterals develop by passing the liver. Colonic ammonia increases the turnover rate of colonic mucosa. Ammonia absorbed into the portal venous system is transported to the liver where it is reconverted to urea. Absorbed ammonia adversely influences liver function. Infections with urease producing organisms destroy the renal parenchyma and produce struvite stones. Urease immunization aids colonic healing and prevents uremic colitis. Absorbed ammonia is a noxious influence on the liver. Animals immunized to urease regenerate the liver faster and are less susceptible to hepatotoxins. Immunization to urease ameliorates cirrhosis. Proteus and other urease producers become non toxic and do not damage the renal parenchyma. Urease is responsible for the pathogenicity of infections with urease producing organisms. Immunization to urease renders urease producing organisms non pathogenic.
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PMID:Awakenings to the pathogenicity of urease and the requirement for continuous long term therapy. 799 80

Helicobacter pylori infection is found world-wide although the epidemiology of infection has not been well defined in many geographical areas. The aims of this study were to determine the prevalence of H. pylori infection and chronic gastritis and the demographic correlates of infection in a single racial group in southern India. The sample population was selected randomly from the male population register of a Tibetan refugee settlement. Demographic data and results of endoscopy with antral mucosal biopsy were evaluated in 197 subjects (median age 28, range 21-81 years). H. pylori was present in 77.2% of subjects by histology and/or urease test. Chronic gastritis and H. pylori were closely related and there was an association between the number of bacteria present and the severity of the gastritis (P < 0.04). Infection with H. pylori was inversely associated with socio-economic factors, specifically educational level (P < 0.02) and occupation (P < 0.02). Unlike other studies, the prevalence of H. pylori was not found to rise with age, being lower in those older than 40 years (P < 0.005). This difference was still apparent when adjusted for socio-economic status. The major demographic difference between younger and older subjects of low socio-economic status was the greater proportion of early life spent outside India (and in Tibet) by older subjects. Among younger subjects, residence in India for 20 years or more was associated with a greater risk of H. pylori infection (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An evaluation of factors affecting Helicobacter pylori prevalence in Tibetans exiled in India. 824 63

The incidence of gastritis with Helicobacter pylori (HP) was studied in 225 patients with active duodenal ulcer diagnosed endoscopically. The infection was diagnosed by the urease test and in some cases by histopathological examination. Infection with Helicobacter pylori was detected in 55% of the patients, a proportion much smaller than the one generally reported in the literature, a rather surprising fact for our sanitary conditions. This might mean that in our country unlike the west-European countries other pathogenetic factors could be more important than HP.
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PMID:Duodenal ulcer and infection with Helicobacter pylori. 864 86

Helicobacter pylori is an important pathogen in humans, causing chronic gastritis and playing a major role in the development of peptic ulcers and gastric cancer. The organism is highly adapted to the human stomach, largely due to its motility and ability to produce large amounts of urease. It binds specifically to the gastric mucosa via adhesion pedestals; colonization of the duodenum only occurs in the presence of gastric metaplasia. Infection with H. pylori leads to gastritis, but the majority of infected patients are asymptomatic, and it is thought that the ability of H. pylori to cause more severe disease may be related to the presence of the cagA gene. With improvements in public health and living conditions, the prevalence of H. pylori infection in developed countries is decreasing, and this is associated with a decline in the incidence of peptic ulcer and gastric cancer.
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PMID:The nature of Helicobacter pylori. 872 98

We evaluated the performance of a new latex agglutination test, Pyloriset Dry (Orion Diagnostica, Espoo, Finland), in the simultaneous detection of immunoglobulin G (IgG), IgA, and IgM antibodies to Helicobacter pylori and compared it with that of the Pyloristat test (BioWhittaker, Fontenay-sous-Bois, France), an enzyme-linked immunosorbent assay detecting IgG to H. pylori, for 96 untreated dyspeptic patients who had undergone gastroduodenal endoscopy. Infection was diagnosed in 56 cases by positive culture and/or positive Giemsa stain and rapid urease test (antral biopsies) and was associated with chronic gastritis in 52 patients. Forty noninfected patients did not have chronic gastritis. The sensitivity of Pyloriset Dry was 91.1%. The sensitivity of Pyloristat was 91.1 or 82.1%, depending on whether equivocal results were considered positive or negative, respectively. Both tests had a specificity of 87.5%. Their performances were not statistically different. Thus, Pyloriset Dry is an alternative to serological tests for adults, particularly when a small number of serum samples has to be tested.
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PMID:Evaluation of Pyloriset Dry, a new rapid agglutination test for Helicobacter pylori antibody detection. 878 87

In cirrhosis, Helicobacter pylori infection may be implicated, together with portal hypertension, bile reflux and alcohol abuse, in damage to gastric mucosa. Aim of this study was to define the influence of non-alcoholic liver disease on the incidence of Helicobacter pylori infection and on the diagnostic accuracy of specific serology. Enrolled in the study were 232 individuals, 105 also had cirrhosis. Infection by Helicobacter pylori, diagnosed by a positive concordance of quick urease test and histology, was detected in 97 (48 with cirrhosis) out of 184 patients. Severe gastritis was more frequent in patients with Helicobacter pylori infection than in patients without. Cirrhosis did not significantly affect the prevalence of Helicobacter pylori infection or the histological features of gastritis. Specific anti-Helicobacter pylori IgG and IgA assay (Bio-Rad GAP test) was used for serological diagnosis. Anti-Helicobacter pylori IgG showed a high sensitivity (85% in cirrhotics, 89% in non-cirrhotics) and low specificity being more evident in cirrhotics (38% vs 56% non-cirrhotics). Serum specific IgA showed low sensitivity (approximately 25% in both groups) and specificity of 79% in cirrhotics vs 84% in non-cirrhotics. In conclusion, non-alcoholic cirrhosis does not affect the incidence of Helicobacter pylori infection and the histological features of chronic gastritis but does decrease diagnostic efficiency of serological tests for Helicobacter pylori.
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PMID:Cirrhosis negatively affects the efficiency of serologic diagnosis of Helicobacter pylori infection. 889 48

Infection with Helicobacter pylori causes chronic active gastritis and has been associated with gastric and duodenal ulcer disease. In biopsy samples of 110 patients with clinical symptoms of active gastritis, H. pylori was detected by means of the polymerase chain reaction (PCR), using species-specific primers defining a 858 bp DNA fragment of H. pylori urease beta-subunit. Sensitivity and specificity of the PCR was compared with culture, histology and Warthin-Starry stain (WSs), detection of H. pylori urease antibodies in serum and urease testing with the Campylobacter-like organism (CLO) test. PCR yielded specific amplification products in 53 cases, whereas culture of the organisms was positive in a subset of 50 cases. Only direct detection in histological sections of biopsy specimens had a higher sensitivity, with 65 positive samples. In contrast, the CLO test was negative in eleven culture-positive and PCR-positive cases. Significant urease antibody titres were found in 39 patients with histologically confirmed diagnosis. These results placed the sensitivity of PCR between tat of the Warthin-Starry stain (WSs) and that of culture. Therefore, PCR can be proposed as a useful rapid and time-saving technique for the detection of H.pylori in gastritis. For epidemiological purposes, fingerprinting with arbitrarily chosen primers by AP-PCR was evaluated. Strain-specific patterns with up to 13 fragments were achieved with 10-nucleotide or longer primers (21-nt) with a G + C content > or = 55%. Thirty-five of 40 strains investigated by this method were distinguishable with a single primer. These results suggest a high level of DNA sequence diversity within this species with the possibility of confirming the clonality in consecutive isolates from a single individual. Alternatively, an increased in-vivo mutation rate could be responsible for DNA divergence, resulting in specific strains for each individual patient.
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PMID:Molecular biology in diagnosis and epidemiology of Helicobacter pylori: PCR for the detection and AP-PCR for characterization of patient isolates. 908 10

The relationship between infection stone and Corynebacterium species was investigated in vitro and in vivo. Urease activity of urease-splitting Corynebacterium species was evaluated by 2 methods; an increase in pH of human urine after inoculation of Corynebacterium species and direct measurement of urease activity of 10(7) CFU organisms from amounts of ammonia by indophenol method. Formation of infection bladder stone was induced in male Wistar rats by implanting a zinc disc and inoculating 10(6) CFU organisms surgically into the bladder. Urine was alkalinized by the inoculation of Corynebacterium renale, C. pilosum and group D2 Corynebacterium. C. renale and C. pilosum had strong urease activity, and group D2 Corynebacterium had moderate activity. C. pseudodiphtheriticum did not produce the elevation of urinary pH and had little urease activity. Infection stones were formed in 100% of rats by inoculation of C. renale and C. pilosum and 88% of rats by group D2. Urinary pH was elevated in all inoculated rats. In conclusion, C. renale, C. pilosum and group D2 Corynebacterium may play a role in formation of infection stones.
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PMID:[An experimental study of infection stone formation by Corynebacterium species]. 908 46

Infection with Helicobacter pylori (H. pylori) is now recognized as a major factor in the pathogenesis of gastric disease, and the successful therapy regimens require a combination of H2 blockers with gastroprotective and antimicrobial agents. Ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene) amino]-4-thiazolyl] methyl]thio]ethyl]amino]methylene]-4-bromo-benzenesulfonamide, CAS 100981-43-9, FI-3542) is the only drug combining acid-suppressant activity with remarkable gastroprotective and anti-H. pylori properties. The drug not only displays a potent anti-H. pylori activity alone, but also exerts a strong potentiating effect on the efficacy of antimicrobial agents commonly used for H. pylori eradication, and the successful ulcer therapy with ebrotidine induces a significant (4-fold) increase in the H. pylori aggregation titer of gastric mucin. Moreover, the drug exhibits a strong inhibitory effect on H. pylori urease activity, the extent of which exceeds that of ranitidine, omeprazole and lansoprazole. Ebrotidine has also been demonstrated to exert a potent inhibitory action on the enzymatic activities directed towards mucus perimeter of gastric mucosal defense, causing a marked inhibition of H. pylori protease, lipase and phospholipase A2 activities. Another important property of ebrotidine is its ability to efficiently counteract the disruptive effects of H. pylori lipopolysaccharide on the integrity of gastric epithelium. This includes countering the interference by the lipopolysaccharide in mucosal integrin receptor interaction with proteins of extracellular matrix and the reversal of H. pylori disruptive effect on the binding of mucin to its gastric epithelial receptor. Furthermore, most recent data indicate that ebrotidine has the ability to reverse the impairment caused by H. pylori in feedback inhibition of gastrin release by somatostatin. This activity of ebrotidine apparently stems from the drug's ability to counter the untoward effect of H. pylori on the binding of somatostatin to its specific receptor on the gastric mucosal G-cells. The unique combination of acid suppressant, gastroprotective and anti-H. pylori activities makes ebrotidine a drug of choice in the treatment of gastric disease caused by H. pylori.
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PMID:Anti-Helicobacter pylori activities of ebrotidine. A review of biochemical and animal experimental studies and data. 920 47

Many putative virulence determinants of Helicobacter pylori are believed to trigger and worsen the gastroduodenal mucosa damage observed in infected patients. H. pylori urease reacts with the gastric urea and generates ammonia; ammonia combines with water and yields ammonium hydroxide, which is cytotoxic. Ammonia may also inhibit cell proliferation and cause indirect mucosal injury by stimulating neutrophils. Phospholipases may damage the gastric mucosa by degrading phospholipids and generating precursors of ulcerogenic components. Other enzymes, such as protease, neuraminidase, fucosidase, and alcohol dehydrogenase, can contribute to damage of the gastric epithelium by destroying the integrity of mucus or by inducing lipid peroxidation. Infection by vacuolating cytotoxic (VacA+) H. pylori strains is considered to constitute increased risk for development of peptic ulcer and gastric cancer. Exploration of the vacA gene structure has shown the existence of strongly toxigenic strains, and has confirmed at the molecular level the increased ulcerogenic potential of VacA+ H. pylori strains. A pathogenicity island called cag has been recently described in Type 1 H. pylori strains (VacA+/CagA+).cag contains the cagA gene (whose expression is associated with toxigenicity) and many genes, some of which are highly homologous to virulence genes of other virulent bacteria, that account for the enhanced pathogenic potential of CagA+ organisms.
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PMID:Helicobacter pylori factors involved in the development of gastroduodenal mucosal damage and ulceration. 947 42


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