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dc.contributor.authorKlings, Elizabeth S.en_US
dc.contributor.authorFarber, Harrison W.en_US
dc.date.accessioned2012-01-12T17:19:49Z
dc.date.available2012-01-12T17:19:49Z
dc.date.copyright2001
dc.date.issued2001-7-13
dc.identifier.citationKlings, Elizabeth S, Harrison W Farber. "Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease" Respiratory Research 2(5): 280-285. (2001)
dc.identifier.issn1465-993X
dc.identifier.urihttp://hdl.handle.net/2144/3394
dc.description.abstractAcute chest syndrome (ACS) of sickle cell disease (SCD) is characterized pathologically by vaso-occlusive processes that result from abnormal interactions between sickle red blood cells (RBCs), white blood cells (WBCs) and/or platelets, and the vascular endothelium. One potential mechanism of vascular damage in ACS is by generation of oxygen-related molecules, such as superoxide (O2-), hydrogen peroxide (H2O2), peroxynitrite (ONOO-), and the hydroxyl (•OH) radical. The present review summarizes the evidence for alterations in oxidant stress during ACS of SCD, and the potential contributions of RBCs, WBCs and the vascular endothelium to this process.en_US
dc.description.sponsorshipAmerican Lung Association (RT-030-N); American Heart Association (0150155N)en_US
dc.language.isoenen_US
dc.publisherBioMed Centralen_US
dc.rightsCopyright 2001 BioMed Central Ltden_US
dc.subjectAcute chest syndrome (ACS)en_US
dc.subjectEndotheliumen_US
dc.subjectHemoglobinen_US
dc.subjectNitric oxide (NO)en_US
dc.subjectOxidant stressen_US
dc.titleRole of Free Radicals in the Pathogenesis of Acute Chest Syndrome in Sickle Cell Diseaseen_US
dc.typearticleen_US
dc.identifier.doi10.1186/rr70
dc.identifier.pubmedid11686897
dc.identifier.pmcid59517


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