pubmed-article:9119496 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9119496 | lifeskim:mentions | umls-concept:C0079488 | lld:lifeskim |
pubmed-article:9119496 | lifeskim:mentions | umls-concept:C0041942 | lld:lifeskim |
pubmed-article:9119496 | lifeskim:mentions | umls-concept:C0074722 | lld:lifeskim |
pubmed-article:9119496 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:9119496 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:9119496 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:9119496 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:9119496 | lifeskim:mentions | umls-concept:C2266864 | lld:lifeskim |
pubmed-article:9119496 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:9119496 | pubmed:dateCreated | 1997-4-24 | lld:pubmed |
pubmed-article:9119496 | pubmed:abstractText | Helicobacter pylori CPY3401 and an isogenic urease-negative mutant, HPT73, showed chemotactic responses to urea, flurofamide (a potent urease inhibitor), and sodium bicarbonate. Since urea and sodium bicarbonate are secreted through the gastric epithelial surface and hydrolysis of urea by urease on the bacterial surface is essential for colonization, the chemotactic response of H. pylori may be crucial for its colonization and persistence in the stomach. | lld:pubmed |
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pubmed-article:9119496 | pubmed:language | eng | lld:pubmed |
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pubmed-article:9119496 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:9119496 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9119496 | pubmed:month | Apr | lld:pubmed |
pubmed-article:9119496 | pubmed:issn | 0019-9567 | lld:pubmed |
pubmed-article:9119496 | pubmed:author | pubmed-author:NakazawaTT | lld:pubmed |
pubmed-article:9119496 | pubmed:author | pubmed-author:YoshiyamaHH | lld:pubmed |
pubmed-article:9119496 | pubmed:author | pubmed-author:MizoteTT | lld:pubmed |
pubmed-article:9119496 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9119496 | pubmed:volume | 65 | lld:pubmed |
pubmed-article:9119496 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9119496 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9119496 | pubmed:pagination | 1519-21 | lld:pubmed |
pubmed-article:9119496 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
pubmed-article:9119496 | pubmed:meshHeading | pubmed-meshheading:9119496-... | lld:pubmed |
pubmed-article:9119496 | pubmed:meshHeading | pubmed-meshheading:9119496-... | lld:pubmed |
pubmed-article:9119496 | pubmed:meshHeading | pubmed-meshheading:9119496-... | lld:pubmed |
pubmed-article:9119496 | pubmed:meshHeading | pubmed-meshheading:9119496-... | lld:pubmed |
pubmed-article:9119496 | pubmed:meshHeading | pubmed-meshheading:9119496-... | lld:pubmed |
pubmed-article:9119496 | pubmed:meshHeading | pubmed-meshheading:9119496-... | lld:pubmed |
pubmed-article:9119496 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9119496 | pubmed:articleTitle | Urease-independent chemotactic responses of Helicobacter pylori to urea, urease inhibitors, and sodium bicarbonate. | lld:pubmed |
pubmed-article:9119496 | pubmed:affiliation | Department of Microbiology, Yamaguchi University School of Medicine, Ube, Japan. | lld:pubmed |
pubmed-article:9119496 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9119496 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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