Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2009-11-9
pubmed:abstractText
Hyperoxia-induced acute lung injury has been used for many years as a model of oxidative stress mimicking clinical acute lung injury and the acute respiratory distress syndrome. Excess quantities of reactive oxygen species (ROS) are responsible for oxidative stress-induced lung injury. ROS are produced by mitochondrial chain transport, but also by NADPH oxidase (NOX) family members. Although NOX1 and NOX2 are expressed in the lungs, their precise function has not been determined until now.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1535-4970
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
180
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
972-81
pubmed:dateRevised
2010-11-22
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
NADPH oxidase-1 plays a crucial role in hyperoxia-induced acute lung injury in mice.
pubmed:affiliation
Department of Pediatrics and Department of Pathology and Immunology, Centre Médical Universitaire, 1, rue Michel Servet, 1211 Geneva 4, Switzerland. Stephanie.Carnesecchi@unige.ch
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural