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dc.contributor.authorRodriguez-Gonzalez, Raquelen
dc.contributor.authorSobrino, Tomasen
dc.contributor.authorRodriguez-Yanez, Manuelen
dc.contributor.authorMillan, Monicaen
dc.contributor.authorBrea, Daviden
dc.contributor.authorMiranda, Elenaen
dc.contributor.authorMoldes, Octavioen
dc.contributor.authorPerez, Juanen
dc.contributor.authorLomas, Daviden
dc.contributor.authorLeira, Rogelioen
dc.contributor.authorDavalos, Antonien
dc.contributor.authorCastillo, Joseen
dc.date.accessioned2011-06-13T17:03:05Z
dc.date.available2011-06-13T17:03:05Z
dc.date.issued2011-05-11en
dc.identifier.citationJournal of Translational Medicine 2011, 9:58
dc.identifier.issn1479-5876
dc.identifier.urihttp://www.dspace.cam.ac.uk/handle/1810/237582
dc.description.abstractAbstract Background Neuroserpin has shown neuroprotective effects in animal models of cerebral ischemia and has been associated with functional outcome after ischemic stroke. Our aim was to study whether neuroserpin serum levels could be associated to biomarkers of excitotoxicity, inflammation and blood brain barrier disruption. Methods We prospectively included 129 patients with ischemic stroke (58.1% male; mean age, 72.4 ± 9.6 years) not treated with tPA within 12 hours (h) of symptoms onset (mean time, 4.7 ± 2.1 h). Poor functional outcome at 3 months was considered as a modified Rankin scale score >2. Serum levels of neuroserpin, Interleukin 6 (IL-6), Intercellular adhesion molecule-1 (ICAM-1), active Matrix metalloproteinase 9 (MMP-9), and cellular fibronectin (cFn) (determined by ELISA) and glutamate (determined by HPLC) were measured on admission, 24 and 72 h. The main variable was considered the decrease of neuroserpin levels within the first 24 h. ROC analysis was used to select the best predictive value for neuroserpin to predict poor functional outcome due to a lack of linearity. Results The decrease of neuroserpin levels within the first 24 h was negatively correlated with serum levels at 24 hours of glutamate (r = -0.642), IL-6 (r = -0.678), ICAM-1 (r = -0.345), MMP-9 (r = -0.554) and cFn (r = -0.703) (all P < 0.0001). In the multivariate analysis, serum levels of glutamate (OR, 1.04; CI95%, 1.01-1.06, p = 0.001); IL-6 (OR, 1.4; CI95%, 1.1-1.7, p = 0.001); and cFn (OR, 1.3; CI95%, 1.1-1.6, p = 0.002) were independently associated with a decrease of neuroserpin levels <70 ng/mL at 24 h after adjusting for confounding factors. Conclusions These findings suggest that neuroprotective properties of neuroserpin may be related to the inhibition of excitotoxicity, inflammation, as well as blood brain barrier disruption that occur after acute ischemic stroke.
dc.languageEnglishen
dc.language.isoen
dc.titleAssociation between neuroserpin and molecular markers of brain damage in patients with acute ischemic stroke.en
dc.typeArticle
dc.date.updated2011-06-13T17:03:05Z
dc.rights.holderRodriguez-Gonzalez et al.; licensee BioMed Central Ltd.
prism.publicationDate2011en
dcterms.dateAccepted2011-05-11en
rioxxterms.versionofrecord10.1186/1479-5876-9-58en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2011-05-11en
dc.identifier.eissn1479-5876
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idMEDICAL RESEARCH COUNCIL (G0901786)


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