| pubmed-article:20569812 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20569812 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:20569812 | lifeskim:mentions | umls-concept:C0008495 | lld:lifeskim |
| pubmed-article:20569812 | lifeskim:mentions | umls-concept:C0456103 | lld:lifeskim |
| pubmed-article:20569812 | lifeskim:mentions | umls-concept:C0011900 | lld:lifeskim |
| pubmed-article:20569812 | lifeskim:mentions | umls-concept:C1833334 | lld:lifeskim |
| pubmed-article:20569812 | lifeskim:mentions | umls-concept:C0872252 | lld:lifeskim |
| pubmed-article:20569812 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:20569812 | pubmed:dateCreated | 2010-6-23 | lld:pubmed |
| pubmed-article:20569812 | pubmed:abstractText | Intrauterine infection is a unique pathologic process that raises the risk for early-onset neonatal sepsis (EONS). By acting synergistically with prematurity, EONS increases the risk for adverse neonatal outcomes, including intraventricular hemorrhage and cerebral palsy. Although several pathways for the pathogenesis of fetal damage have been proposed, the basic molecular mechanisms that modulate these events remain incompletely understood. Discovery of clinically and biologically relevant biomarkers able to reveal key pathogenic pathways and predict pregnancies at risk for antenatal fetal damage is a priority. Proteomics provides a unique opportunity to fill this gap. | lld:pubmed |
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| pubmed-article:20569812 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20569812 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
