Linked Life Data

11785069

Source:http://linkedlifedata.com/resource/pubmed/id/11785069

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-1-10
pubmed:abstractText
Abnormal placental implantation presumed to be secondary to maternal genetic susceptibility or immune maladaptation is considered to be fundamental to the pathogenesis of preeclampsia. The reduced placental perfusion resulting in placental ischemia is hypothesized to cause the known endothelial dysfunction, which leads to the clinical manifestations of this disease. Oxidative stress is a postulated linking factor, an aberration that possibly has its genesis via cytokines released from the abnormally implanted and perfused placenta. Clearly the maternal pathophysiologic changes that subsequently produce what is recognized as preeclampsia are present long before the disease makes its clinical appearance.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0270-9295
pubmed:author
pubmed:copyrightInfo
Copyright 2002 by W.B. Saunders Company
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
54-64
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Preeclampsia: pathophysiology and practice considerations for the consulting nephrologist.
pubmed:affiliation
University of Mississippi Medical Center, Jackson, MS 39216-4505, USA.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't