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| pubmed-article:17307847 | lifeskim:mentions | umls-concept:C0010674 | lld:lifeskim |
| pubmed-article:17307847 | lifeskim:mentions | umls-concept:C0033809 | lld:lifeskim |
| pubmed-article:17307847 | lifeskim:mentions | umls-concept:C0042765 | lld:lifeskim |
| pubmed-article:17307847 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17307847 | lifeskim:mentions | umls-concept:C0521367 | lld:lifeskim |
| pubmed-article:17307847 | lifeskim:mentions | umls-concept:C0546816 | lld:lifeskim |
| pubmed-article:17307847 | lifeskim:mentions | umls-concept:C1155661 | lld:lifeskim |
| pubmed-article:17307847 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:17307847 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:17307847 | pubmed:dateCreated | 2007-4-18 | lld:pubmed |
| pubmed-article:17307847 | pubmed:abstractText | The inactivation of the mismatch repair (MMR) system of Pseudomonas aeruginosa modestly reduced in vitro fitness, attenuated virulence in murine models of acute systemic and respiratory infections, and decreased the initial oropharyngeal colonization potential. In contrast, the inactivation of the MMR system favored long-term persistence of oropharyngeal colonization in cystic fibrosis mice. These results may help in understanding the reasons for the low and high prevalences, respectively, of hypermutable P. aeruginosa strains in acute and chronic infections. | lld:pubmed |
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| pubmed-article:17307847 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17307847 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17307847 | pubmed:month | May | lld:pubmed |
| pubmed-article:17307847 | pubmed:issn | 0021-9193 | lld:pubmed |
| pubmed-article:17307847 | pubmed:author | pubmed-author:MoenM GMG | lld:pubmed |
| pubmed-article:17307847 | pubmed:author | pubmed-author:OliverAntonio... | lld:pubmed |
| pubmed-article:17307847 | pubmed:author | pubmed-author:BorrellNuriaN | lld:pubmed |
| pubmed-article:17307847 | pubmed:author | pubmed-author:PérezJosé LJL | lld:pubmed |
| pubmed-article:17307847 | pubmed:author | pubmed-author:MaciáMaría... | lld:pubmed |
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| pubmed-article:17307847 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17307847 | pubmed:volume | 189 | lld:pubmed |
| pubmed-article:17307847 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17307847 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17307847 | pubmed:pagination | 3665-8 | lld:pubmed |
| pubmed-article:17307847 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:17307847 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17307847 | pubmed:articleTitle | Inactivation of the mismatch repair system in Pseudomonas aeruginosa attenuates virulence but favors persistence of oropharyngeal colonization in cystic fibrosis mice. | lld:pubmed |
| pubmed-article:17307847 | pubmed:affiliation | Servicio de Microbiología, Hospital Son Dureta, C. Andrea Doria No. 55, 07014 Palma de Mallorca, Spain. | lld:pubmed |
| pubmed-article:17307847 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17307847 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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