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dc.contributor.authorSvetlov, S.I.
dc.contributor.authorPrima, V.
dc.contributor.authorGlushakova, O.
dc.contributor.authorSvetlov, A.
dc.contributor.authorKirk, D.R.
dc.contributor.authorGutierrez, H.
dc.contributor.authorSerebruany, V.L.
dc.contributor.authorCurley, K.C.
dc.contributor.authorWang, K.K.W.
dc.contributor.authorHayes, R.L.
dc.date.accessioned2017-11-03T18:17:41Z
dc.date.available2017-11-03T18:17:41Z
dc.date.issued2012
dc.identifier.citationSvetlov, S.I., Prima, V., Glushakova, O., Svetlov, A., Kirk, D.R., Gutierrez, H., Serebruany, V.L., Curley, K.C., Wang, K.K.W., Hayes, R.L. Neuro-glial and systemic mechanisms of pathological responses in rat models of primary blast overpressure compared to "composite" blast (2012) Frontiers in Neurology, FEB, art. no. Article 15, . Cited 48 times.en_US
dc.identifier.urihttp://hdl.handle.net/11141/2176
dc.descriptionBiomarkers, Blast, Brain injury, Neuro-glia damage, Rat models, Systemic responsesen_US
dc.description.abstractA number of experimental models of blast brain injury have been implemented in rodents and larger animals. However, the variety of blast sources and the complexity of blast wave biophysics have made data on injury mechanisms and biomarkers difficult to analyze and compare. Recently, we showed the importance of rat position toward blast generated by an external shock tube. In this study, we further characterized blast producing moderate traumatic brain injury and defined "composite" blast and primary blast exposure set-ups. Schlieren optics visualized interaction between the head and a shock wave generated by external shock tube, revealing strong head acceleration upon positioning the rat on-axis with the shock tube (composite blast), but negligible skull movement upon peak overpressure exposure off-axis (primary blast). Brain injury signatures of a primary blast hitting the frontal head were assessed and compared to damage produced by composite blast. Low to negligible levels of neurodegeneration were found following primary blast compared to composite blast by silver staining. However, persistent gliosis in hippocampus and accumulation of GFAP/CNPase in circulation was detected after both primary and composite blast. Also, markers of vascular/endothelial inflammation integrin alpha/beta, soluble intercellular adhesion molecule-1, and L-selectin along with neurotrophic factor nerve growth factor-beta were increased in serum within 6 h post-blasts and persisted for 7 days thereafter. In contrast, systemic IL-1, IL-10, fractalkine, neuroendocrine peptide Orexin A, andVEGF receptor Neuropilin-2 (NRP-2) were raised predominantly after primary blast exposure. In conclusion, biomarkers of major pathological pathways were elevated at all blast set-ups. The most significant and persistent changes in neuro-glial markers were found after composite blast, while primary blast instigated prominent systemic cytokine/chemokine, Orexin A, and Neuropilin-2 release, particularly when primary blast impacted rats with unprotected body. © 2012 Svetlov, Prima, Glushakova, Svetlov, Kirk, Gutierrez, Serebruany, Curley, Wang and Hayes.en_US
dc.language.isoen_USen_US
dc.rightsCopyright: © 2012 Svetlov, Prima, Glushakova, Svetlov, Kirk, Gutierrez, Serebruany, Curley, Wang and Hayes.en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0/en_US
dc.titleNeuro-glial and systemic mechanisms of pathological responses in rat models of primary blast overpressure compared to "composite" blasten_US
dc.typeArticleen_US
dc.identifier.doi10.3389/fneur.2012.00015


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Copyright: © 2012 Svetlov, Prima, Glushakova, Svetlov, Kirk, Gutierrez, Serebruany, Curley, Wang and Hayes.
Except where otherwise noted, this item's license is described as Copyright: © 2012 Svetlov, Prima, Glushakova, Svetlov, Kirk, Gutierrez, Serebruany, Curley, Wang and Hayes.