Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-10-19
pubmed:abstractText
Infections after ischemic stroke are known to complicate the clinical course and worsen the outcome. Neuroinflammation is one of the predominant mechanisms of secondary progression of brain injury and infection and is far from being well understood. Experimental data demonstrate that ischemic stroke patients are at a higher risk for systemic infections if they show a pronounced anti-inflammatory response after the event, which is considered an indication of a stress-mediated reduction of immune competence. Only a small number of studies describe the time course of inflammation mediators after ischemic stroke in patients with early poststroke infections. Levels of inflammation mediators after the event of stroke differ, depending on clinical severity and concomitant infectious diseases. Thus, sequential dynamics of early inflammation must be considered in the development of both mechanism-targeting anti-inflammatory and anti-infectious treatment strategies in ischemic brain damage.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1749-6632
pubmed:author
pubmed:copyrightInfo
© 2010 New York Academy of Sciences.
pubmed:issnType
Electronic
pubmed:volume
1207
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
116-22
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Linking infection and inflammation in acute ischemic stroke.
pubmed:affiliation
Department of Neurology, Medical School of Hannover, Germany. worthmann.hans@mh-hannover.de
pubmed:publicationType
Journal Article, Review