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)

The distribution of Campylobacter pylori, its prevalence, and its relationship to gastritis and urease activity have been studied in 54 postmortem stomachs. Infection was confirmed by finding C. pylori in a Gram-stained smear of gastric mucus harvested from the entire stomach. Eight tissue specimens were obtained from predetermined sites from each stomach and examined for histologic gastritis and urease activity. Thirty-seven per cent of stomachs were infected, and of these 80% had widespread histologic gastritis. The detection of urease activity provided information on the distribution of the organism and had a high correlation with histologic gastritis. The organism is capable of infecting any area of the stomach. Infection is common and is more prevalent in Polynesian subjects (60%) than in Caucasians (19%).
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PMID:Distribution of Campylobacter pylori in the human stomach obtained at postmortem. 338 89

Infections with Klebsiella and Enterobacter have increased among hospitalized patients. To study such infections, relatively simple but precise methods are needed for clinical laboratories to identify the two genera accurately. Moreover, a rapid identification is essential for assisting with the therapy of the patients. For this purpose, a new 4-hr urease test was developed so that colonies could be tested directly from blood-agar plates which have been inoculated with clinical material and allowed to incubate overnight. This 4-hr test was positive with 98.5% of 202 Klebsiella species and negative with 80 Enterobacter species. As a single criterion for distinguishing between the two major genera, the new 4-hr urease test was just as accurate as a motility test (99% of the 282 isolates were accurately identified with either). The 4-hr urease test represents a simple, rapid, and reliable technique which is ideally suited for use in clinical microbiology laboratories.
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PMID:Four-hour urease test for distinguishing between Klebsiella and Enterobacter. 489 77

The virulence of urease-producing bacteria depends on the ability of urease to degrade urea into ammonia and thereby to alkalinize the urine. Infections caused by urease-producing organisms such as Proteus mirabilis are particularly difficult to manage clinically. We have shown that the layer of glycosaminoglycans at the bladder surface protects against infection by blocking the adherence of bacteria to the epithelium. To determine whether urease-producing urinary pathogens owe their virulence in part to an ability to inactivate the protective effect of the glycosaminoglycan layer, we tested the ability of ammonium chloride to alter bacterial adherence to the normal vesical mucosa. We used an in vivo adherence assay that we have described previously in rabbits. Control animals received sodium chloride adjusted to the same pH as the ammonium chloride. We found that 0.25 M ammonium chloride significantly increases bacterial adherence to normal vesical mucosa as compared to adherence in controls receiving 0.25 M sodium chloride (p less than 0.05). These data suggest that urease plays a hitherto undescribed role in bacterial virulence by altering the antiadherence activity of the glycosaminoglycan layer present at the transitional cell surface.
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PMID:Effect of ammonium on bacterial adherence to bladder transitional epithelium. 637 29

Phosphate stones are divided in two groups: I. Infection stones = triple phosphate stones (struvite and carbonate apatite). II. Calcium phosphate stones = Hydroxy apatite. Ad I. For the formation of this stone, infection with urease-producing bacteria is essential. It is important to look for factors that cause infection and for metabolic abnormalities. Three possibilities for treatment are discussed: Acidifying the urine: orally with NH4NO3 or NH4Cl; dosage is possible up to 12 g a day (metabolic acidosis!). Irrigation for instance with Renacidin ; when using a nephrostomy-tube, one can start 5 days after the operation. It is important to look for fever and flank pain. Especially useful in cases with small residual stones. Reduction of phosphate excretion in urine ( Shorr -regimen). Some aluminium combinations reduce the intestinal phosphate absorption as a result of the formation of a nonabsorbable aluminium-phosphate combination. This can be combined with a low calcium- and phosphate diet. In several publications good results are shown. Also when using a less rigid regimen, satisfactory results are seen: decrease of the phosphate excretion from 30 to 17 mmol/24 h (own investigation). Urease-inhibitors result in a lower urine-pH and a decrease of the ammonium-concentration. there are only a few publications with results, but AHA seems able to reduce the stone size in 24% of the patients. Ad II. This stone is concerning formation and treatment much like the calcium oxalate stone. In case of an alkaline urine one must look for primary hyperparathyroidism and renal tubular acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Conservative therapy of phosphate calculi]. 653 26

Certain infection stones are thought to be linked to urease-possessing bacteria such as Proteus sp. Since ureaplasma also contain urease and are predominantly located in the urogenital tract, their possible role in the formation of infection stones was studied in the rat model described by Friedlander and Braude [2]. Infection stones were produced in Sprague-Dawley and Wistar male rats after injection of ureaplasmas into the renal medulla. In Sprague-Dawley rats, six different ureaplasma strains (serotypes 3 and 5 clinical isolates) were able to produce bladder stones. Acetohydroxamic acid, a urease inhibitor, prevented the formation of the stones. There was no difference in urinary pH or the presence of leukocytes, crystals and ureaplasmas in the urine between rats which presented stones and those which did not. Ureaplasmas could be cultivated only very rarely from rat stones. Similarly, no ureaplasmas could be obtained from human stones.
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PMID:Experimental production of bladder calculi in rats by ureaplasma injection. 671 56

Struvite (magnesium ammonium phosphate) uroliths are found more frequently in the urinary tracts, of dogs than are other types of uroliths. Infection of the urinary tract with urease-producing bacteria, especially staphylococci, plays an important role in urolith formation. An inherited predisposition to urinary tract infection may be associated with the high rat of occurrence of struvite uroliths in some dogs. Diagnosis of struvite urolithiasis should encompass analysis of the mineral composition of calculi and identification of concomitant urinary tract infection. Since urinary tract infections occur as sequelae to abnormalities in local or systemic host-defense mechanisms, appropriate effort should be directed toward detection of these abnormalities. Therapy of struvite urolithiasis should encompass relief of obstruction to outflow when necessary, elimination of existing calculi, eradication or control of urinary tract infection, and prevention of recurrence. Although surgical removal remains as the preferred method to eliminate struvite uroliths from dogs, nonsurgical methods of urolith dissolution should be considered. Recurrence of struvite uroliths may be prevented by various combinations of antimicrobial therapy, administration of urease inhibitors, acidification of urine, and induction of diuresis.
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PMID:Canine struvite urolithiasis: problems and their dissolution. 728 47

Helicobacter pylori infection is characterized by an inflammatory response in the gastric epithelium, the intensity of which appears to be type-strain specific. Infections caused by Type 1 H. pylori organisms, i.e., those expressing VacA (the cytotoxin) and CagA (the cytotoxin-associated protein), are associated with a strong polymorph mucosal infiltration in vivo, and with increased secretion of interleukin-8 by epithelial cells. The inflammatory potential of Type II strains (non-cytotoxic, VacA- and CagA-negative) is probably less pronounced. The small urease subunit, porins, and other substances produced by H. pylori show neutrophil chemotactic activities in vitro. These bacterial components promote the adhesion of polymorphs to endothelial cells and stimulate polymorphs to generate oxygen reactive metabolites. This can severely damage the gastroduodenal mucosa.
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PMID:Progress in defining the inflammatory cascade. 760 Jan 33

Eight ferrets specific-pathogen-free for Helicobacter mustelae were given, per dose, approximately 3.0 x 10(7) CFU of either the wild-type parent strain of H. mustelae (NCTC 12032) (two ferrets) the isogenic urease-negative mutant strain of H. mustelae (10::Tn3Km) (four ferrets), or sterile culture broth (two ferrets). Infection status was monitored by endoscopic gastric biopsy for urease activity, histopathology, and culture and by serology at 3, 6, 10, and 21 weeks. All ferrets were necropsied at 25 weeks. Both negative control ferrets remained uninfected, both ferrets receiving the H. mustelae wild-type parent strain became infected after two doses of the organism, and all four ferrets given two doses of the isogenic urease-negative mutant strain of H. mustelae remained uninfected throughout the 6-month study. Histopathology correlated with infection status. H. mustelae-infected ferrets exhibited diffuse mononuclear inflammation in the subglandular region and the lamina propria of the gastric mucosa, while uninfected ferrets showed no or minimal inflammation. These results suggest that urease activity is essential for colonization of the ferret stomach by H. mustelae.
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PMID:Inability of an isogenic urease-negative mutant stain of Helicobacter mustelae to colonize the ferret stomach. 764 14

In patients with systemic sclerosis peristaltic abnormalities may delay gastric emptying, giving rise to bacterial overgrowth, including possibly Helicobacter pylori (HP). Infection with Helicobacter is an important risk factor for esophageal and gastric diseases, including esophagitis, gastritis and gastric cancer. The purpose of this prospective study was to assess gastric HP infection in patients with systemic sclerosis. In 12 patients with systemic sclerosis the newly introduced breath test with 13C-labelled urea was used for indirect detection of gastric urease activity due to HP infection. Five out of 12 patients gave Helicobacter-positive results (42%); 7 patients were negative for Helicobacter colonization (58%). Thus, the risk for gastric diseases caused by HP infection is enhanced in patients with systemic sclerosis compared with white healthy, asymptomatic persons examined in other studies. Helicobacter-positive patients were treated with 2 x 20 mg omeprazole and 4 x 500 mg amoxicillin over 14 days. Afterwards the 13C-urea breath test was repeated and showed negative results for Helicobacter in all systemic sclerosis patients treated. Dual therapy with omeprazole and amoxicillin therapy effectively eradicated HP. The 13C-urea breath test did not cause any side-effects and is therefore considered to be a non-invasive, non-toxic and safe method for the diagnosis and therapeutic control of Helicobacter-status.
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PMID:Helicobacter pylori in patients with systemic sclerosis: detection with the 13C-urea breath test and eradication. 781 72

Infection with the bacterium Helicobacter pylori is associated with both the development of gastritis and an attenuation in the hydrophobic properties of the stomach. In order to better understand the effect of ammonium, one of the major products of H. pylori urease on these properties, a series of in vivo and in vitro experiments was performed. In the in vivo studies rats were intragastrically administered NH4Cl alone and in combination with the mucolytic agent, Muco-Mist, in various dosing strategies and concentrations. It was determined that the intragastric administration of four consecutive doses of a NH4Cl/Muco-Mist mixture (20 mmol/L/5%) was capable of converting the stomach from a hydrophobic to hydrophilic state as determined by contact angle analysis. Further, the treated rats became more susceptible to the injurious effect of luminal acid as determined by measuring the haemoglobin concentration of a collected gastric perfusate. In the in vitro studies it was determined that exposure of the hydrophobic surface of a synthetic mucus gel layer to increasing concentrations of NH4Cl (0-20 mmol/L) resulted in a rapid transition to a hydrophilic state and an associated increase in the flux of H+ across its surface. Helicobacter pylori may induce an attenuation in both mucosal hydrophobicity and barrier properties by producing high concentrations of NH4+ in the mucus gel layer. The molecular mechanism of this action may be related to the chemical similarities of NH4+ and choline-based phospholipids which contribute to the stomach's hydrophobic surface.
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PMID:Effect of ammonium ion on the hydrophobic and barrier properties of the gastric mucus gel layer: implications on the role of ammonium in H. pylori-induced gastritis. 788 Oct 13


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