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)

Helicobacter pylori represents one of the most common and medically prominent infections worldwide. Infection with this microaerobic, gram-negative bacterium has been established as an etiologic factor in the development of peptic ulcer disease. In addition, H pylori infection has been associated firmly with the development of gastric neoplasia, including gastric adenocarcinomas and gastric mucosa-associated lymphoid tissue lymphomas. Effective antimicrobial treatment depends on sensitive and accurate diagnostic approaches. This review article discusses invasive and noninvasive strategies for diagnosis of H pylori infection. Invasive methods requiring endoscopic evaluation include bacteriologic culture and susceptibility testing, histopathologic studies, molecular diagnostics, and rapid urease testing. Noninvasive approaches include fecal antigen detection, serologic testing, and urea breath testing.
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PMID:Helicobacter pylori. Pathology and diagnostic strategies. 1264 43

The present study sought to quantitatively examine mucosal inflammatory and immune responses in dogs with gastritis and the relationship of these responses to infection with Helicobacter. Gastric biopsies from 30 dogs were evaluated for B- and T-lymphocytes, neutrophils, eosinophils, macrophages, and mast cells. Mucosal atrophy, fibrosis, cellularity, and severity of gastritis were graded qualitatively. Messenger-RNA (mRNA) for actin, interleukin-1beta (IL-1beta), IL-4, IL-8, and IL-10, transforming growth factor beta (TGF-beta), and interferon gamma (IFN-gamma) was quantified by polymerase chain reaction (PCR). The presence of Helicobacter spp. was determined by urease activity, histology, PCR, and enzyme-linked immunosorbent assay. mRNA for IL-1beta, IL-8, IL-10, TGF-beta, and IFN-gamma was detected in most dogs. IL-4 mRNA was detected in only 1 dog. Correlations were observed for IL-1beta versus IL-8 and IL-10; IL-8 versus IL-10, IFN-gamma, and TGF-beta; and IL-10 versus IFN-y. Mucosal pathology was related to cytokine mRNA expression (neutrophils to IL-8 and IFN-gamma, macrophages and lymphocytes to IFN-gamma, and fibrosis to IL-1beta). Gastritis was categorized as lymphoplasmacytic in all dogs, and its histologic severity correlated with atrophy, infiltration with lymphocytes and macrophages, and expression of IL-10 and IFN-gamma. Of the dogs examined, 76.7% were infected with Helicobacter spp. Infection was associated with increased expression of TGF-beta and fibrosis. Circulating anti-Helicobacter immunoglobulin G titers were higher in uninfected than infected dogs. We conclude that lymphoplasmacytic gastritis in dogs is characterized by concurrent activation of proinflammatory and immunomodulatory cytokines, with increased mRNA expression related to mucosal pathology. No significant associations between Helicobacter infection and proinflammatory cytokine expression, severity of gastritis, or differences in the pathogenicity of different Helicobacter spp. were found.
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PMID:Quantitative analysis of inflammatory and immune responses in dogs with gastritis and their relationship to Helicobacter spp. infection. 1571 41

"Infection Lithiasis" refers to calculi that occur with persistent urinary tract infection. Stones composed of magnesium ammonium phosphate (struvite) and carbonate apatite, called "triple phosphate" stones, are the more common type of infection lithiasis. These stones are also called "staghorn" calculi because they may grow rapidly and fill the entire collecting system. They form during urinary infection with urea-splitting micro-organism. They may originate de novo or complicate a lithiasis when pre-existing stones are colonized with urea-splitting bacteria. They represent about 2-3% of stones referred for laboratory analysis. This article reviews the epidemiology, pathogenesis, clinical features, and management of struvite stones. A singular pathologic entity recently described, called "encrusted cystitis or encrusted pyelitis", mainly caused by Corynebacterium urealyticum is also review. Infection lithiases caused by non-urease-producing bacteria may also occur and are examined in this article. Finally, the controversial role of nanobacteria in nephrolithiasis is discussed.
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PMID:[Infective lithiasis]. 1583 May 51

Helicobacter pylori (H. pylori) is the principal cause of peptic ulcer disease and important risk factor in gastric cancer. Gastric mucosal biopsy specimens taken from 110 patients were examined by polymerase chain reaction (PCR), culture and urease test. The ureA gene was detected in 52 out of 110 examined samples. The cagA gene was detected in 35 (67.3%) out of these 52 specimens (ureA+). This gene was presented in all of patients with stomach ulcer, in 75.0% of patients with duodenitis, 69.6% of patients with duodenal ulcer and 58.3% of patients with gastritis. H. pylori was detected by culture in 24 (25.3%) out of 95 samples. These results were confirmed by PCR. H. pylori was detected additionally in 20 samples only by PCR. This bacterium was detected more frequently by PCR than by culture (46.3% vs 25.3%). Results obtained by using three methods: culture, urease test and PCR were concordant in 47.0% (39 out of 83 patients). In 16 (19.3%) cases H. pylori was detected by two methods: urease test and PCR. Infection was detected only by PCR in 3 (3.6%) cases and in 25 cases (30.1%) only by urease test.
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PMID:[Comparison of diagnostic methods for Helicobacter pylori detection and identification of cagA gene in clinical specimens]. 1586 38

Infection with Helicobacter pylori may be associated with a variety of gastroduodenal diseases. Although H. pylori infection is common, peptic ulcer disease and gastric cancer occur in only a small minority of infected persons. This work was intended to correlate the pathological findings with the serological response to certain H. pylori antigens. Serum samples were taken from 285 patients who underwent gastroscopy. H. pylori infection was diagnosed by histology, culture or rapid urease test (RUT). Serum IgG reactivity against H. pylori-specific antigens was studied by Western blot. There was a significant association between the diagnosis of gastric cancer and the presence of IgG antibodies against the 19.5, 33 and 136 kDa (CagA) antigens. Comparing all H. pylori-positive patients with the gastric cancer group for the presence of the 19.5, 33 and 136 kDa (CagA) antigens, the results were as follows: chi2: 17.482, p < 0.001, power P = 0.994, odds ratio (OR) for the presence of gastric cancer: 19.5 (95% confidence interval (CI): 4.11-92.56). Antibodies against CagA alone or other bands (except 33 and 19.5 kDa antigens), as well as the age of patients were not related to a diagnosis of gastric cancer. Male patients were more likely to develop duodenal ulcer. IgG antibodies against the 19.5, 33 and 136 kDa (CagA) antigens could be helpful to identify patients at enhanced risk for the development of gastric cancer.
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PMID:Serum antibody positivity for distinct Helicobacter pylori antigens in benign and malignant gastroduodenal disease. 1660 Jun 80

Infection with Helicobacter trogontum, a urease-positive helicobacter isolated from subclinically infected rats, was evaluated in B6.129P2-IL10(tm1Cgn) (interleukin-10(-/-) [IL-10(-/-)]) and C57BL/6 (B6) mice. In a first experiment, IL-10(-/-) mice naturally infected with Helicobacter rodentium had subclinical typhlocolitis but developed severe diarrhea and loss of body condition with erosive to ulcerative typhlocolitis within 1 to 3 weeks of experimental infection with H. trogontum. A second experiment demonstrated that helicobacter-free IL-10(-/-) mice dosed with H. trogontum also developed severe clinical signs and typhlocolitis within 2 to 4 weeks, whereas B6 mice colonized with H. trogontum were resistant to disease. In a third experiment, using helicobacter-free IL-10(-/-) mice, dosing with H. trogontum resulted in acute morbidity and typhlocolitis within 8 days. Acute typhlocolitis was accompanied by signs of sepsis supported by degenerative hemograms and recovery of Escherichia coli and Proteus spp. from the livers of infected mice. Quantitative PCR data revealed that H. rodentium and H. trogontum may compete for colonization of the lower bowel, as H. trogontum established higher colonization levels in the absence of H. rodentium (P < 0.003). H. trogontum-induced typhlocolitis was also associated with a significant decrease in the levels of colonization by five of eight anaerobes that comprise altered Schaedler's flora (P < 0.002). These results demonstrate for the first time that H. rodentium infection in IL-10(-/-) mice causes subclinical typhlocolitis and that infection with H. trogontum (with or without H. rodentium) induces a rapid-onset, erosive to ulcerative typhlocolitis which impacts the normal anaerobic flora of the colon and increases the risk of sepsis.
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PMID:Rapid onset of ulcerative typhlocolitis in B6.129P2-IL10tm1Cgn (IL-10-/-) mice infected with Helicobacter trogontum is associated with decreased colonization by altered Schaedler's flora. 1698 22

'Candidatus Helicobacter suis' is a spiral-shaped bacterium that colonizes the stomach of more than 60% of slaughter pigs. The role of 'Candidatus Helicobacter suis' in gastric disease of pigs is still unclear. Experimental studies in pigs are lacking because this bacterium is unculturable until now. An inoculation protocol using 'Candidatus Helicobacter suis' infected mouse stomach homogenate was used to reproduce the infection in pigs. Control animals were inoculated using negative mouse stomach homogenate. Pigs were inoculated three times with one-week intervals and euthanized 6 weeks post inoculation. Tissue samples were taken from different mucosal stomach regions to detect 'Candidatus Helicobacter suis' by PCR and urease test. Mucosal inflammation was evaluated on formalin-fixed tissue samples. Lesions in the pars oesophagea were scored macroscopically. Infection was successful in all challenged animals, with the antrum and the fundus being predominantly positive. Infection was associated with infiltration of lymphocytes and plasma cells in the antral mucosa, evolving to follicular gastritis. No apparent inflammation of the fundic stomach region was detected in the infected animals. A clear link between 'Candidatus Helicobacter suis' and pars oesophageal lesions could not be found.
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PMID:Experimental infection of pigs with 'Candidatus Helicobacter suis'. 1721 9

Infection with Helicobacter pylori has been shown to be at the origin of various gastric pathologies. However, it has not yet been established whether the etiology of such diseases, particularly of gastric cancer, is related to the production of free radicals or to mutagenesis. The aim of this study was to determine whether a six-month infection with Helicobacter pylori increased the amount of lipid peroxidation, nitric oxide, and DNA damage in Mongolian gerbils (Meriones unguiculatus). H. pylori was characterized genotypically and administered orally to the animals. Four tests were applied to identify the presence of bacteria at one, two, four, and six months after the inoculation, namely, isolation and identification in culture, the urease test, the ELISA assay, and immunohistochemical staining of gastric biopsies. The infection was considered to be successful when three of the above-mentioned tests were positive. The infection occurred in 30% of the animals in the first month after the H. pylori inoculation and in 60-70% of the animals in the later stages. Levels of malondialdehyde, nitric oxide, and DNA damage (using the "comet" assay) were determined in the gastric tissue of the animals at one, two, four, and six months. We found statistically significant increases in malondialdehyde and nitric oxide levels from the second month on. The comet assay in animals infected with H. pylori showed a significant increase in the mean tail length throughout the observation period. We conclude that our results support the assumption that oxidative damage and DNA breakage produced by the infection with H. pylori are some of the initial alterations occurring in the development of gastric diseases.
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PMID:Genotoxic and oxidative damage induced by Helicobacter pylori in Meriones unguiculatus. 1772 29

Urinary tract infections and urosepsis are complications which can precede or follow a kidney stone treatment. Often the stones themselves are the source of infection, whether they are infection stones or not. Systemic infections are difficult to foresee, and neither a pre-operative negative urine culture nor an antibiotic prophylaxis avoid infectious complications for certain. The primary predictive risk factors of urosepsis are: patient conditions, urinary tract infection or a history of recurrent infections, characteristics of the stone, and anatomy of the urinary tract. Infection stones are still a matter of debate, concerning both the aetiology of the disease and its treatment. Positive cultures are not only found with struvite stones, but also with apatite and calcium oxalate stones. Currently, a long-term antibiotic therapy is advised in patients affected by infection stones. Antibiotic therapy should prevent not only septic complications but also recurrence or re-growth of stones after treatment. Different antibiotic modalities are recommended, sometimes together with urease inhibitors. Mid-stream urine culture is the easiest available pre-treatment parameter notwithstanding its poor predictive value. In case of suspected or proven urinary infection, an appropriate antibiotic therapy should always be administered prior to surgical procedure. There is, however, controversy regarding the antibiotic use, its role, expediency, and duration of prophylaxis in relation to the various surgical procedures, and the way infectious complications are considered and classified. When antibiotic prophylaxis is considered, its duration should be clearly established prior to surgery; duration may vary depending on the type of surgery or the type of antibiotic. Furthermore, prophylaxis should be administered only for a limited amount of time. In infection stones, in immuno-compromised patients or in patients with anatomical anomalies or diabetes, the risk of post-treatment infection and sepsis is higher Hence there is agreement on the need for prophylaxis and antibiotic therapy The most recent literature has shown excellent results with fluoroquinolones both in prophylaxis and therapy, concerning post-operative infection control after percutaneous as well as ureteroscopic removal of stones. No agreement has yet been reached on antibiotic prophylaxis modalities prior to percutaneous or ureteroscopic removal and its usefulness for SWL.
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PMID:Infections and urolithiasis: current clinical evidence in prophylaxis and antibiotic therapy. 1853 18

Corynebacterium urealyticum, formerly known as coryneform CDC group D2, was first recognized to be involved in human infections 30 years ago. It is a slow-growing, lipophilic, asaccharolytic and usually multidrug-resistant organism with potent urease activity. Its cell wall peptidoglycan, menaquinone, mycolic and cellular fatty acid composition is consistent with that of the genus Corynebacterium. DNA-DNA hybridization studies and 16S rDNA sequencing analysis have been used to determine the degree of relatedness of C. urealyticum to other corynebacterial species. The genome of the type strain consists of a circular chromosome with a size of 2 369 219 bp and a mean G + C content of 64.2%, and analysis of its genome explains the bacterium's lifestyle. C. urealyticum is a common skin colonizer of hospitalized elderly individuals who are receiving broad-spectrum antibiotics. It is an opportunistic pathogen causing mainly acute cystitis, pyelonephritis, encrusted cystitis, and encrusted pyelitis. More infrequently, it causes other infections, but mainly in patients with urological diseases. Infections are more common in males than in females, and treatment requires administration of antibiotics active against the organism in vitro, mainly glycopeptides, as well as surgical intervention, the latter mostly in cases of chronic infection. Mortality directly associated with infection by this organism is not frequent, but encrusted pyelitis in kidney-recipient patients may cause graft loss. The outcome of infection by this organism is reasonably good if the microbiological diagnosis is made and patients are treated appropriately.
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PMID:Microbiological and clinical features of Corynebacterium urealyticum: urinary tract stones and genomics as the Rosetta Stone. 1855 35


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