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Distinguishing the Unique Neuropathological Profile of Blast Polytrauma.

Abstract Traumatic brain injury sustained after blast exposure (blast-induced TBI) has recently been documented as a growing issue for military personnel. Incidence of injury to organs such as the lungs has decreased, though current epidemiology still causes a great public health burden. In addition, unprotected civilians sustain primary blast lung injury (PBLI) at alarming rates. Often, mild-to-moderate cases of PBLI are survivable with medical intervention, which creates a growing population of survivors of blast-induced polytrauma (BPT) with symptoms from blast-induced mild TBI (mTBI). Currently, there is a lack of preclinical models simulating BPT, which is crucial to identifying unique injury mechanisms of BPT and its management. To meet this need, our group characterized a rodent model of BPT and compared results to a blast-induced mTBI model. Open field (OF) performance trials were performed on rodents at 7 days after injury. Immunohistochemistry was performed to evaluate cellular outcome at day seven following BPT. Levels of reactive astrocytes (GFAP), apoptosis (cleaved caspase-3 expression), and vascular damage (SMI-71) were significantly elevated in BPT compared to blast-induced mTBI. Downstream markers of hypoxia (HIF-1α and VEGF) were higher only after BPT. This study highlights the need for unique therapeutics and prehospital management when handling BPT.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title oxidative medicine and cellular longevity
Publication Year Start




PMID- 28424745
OWN - NLM
STAT- In-Process
DA  - 20170420
LR  - 20170423
IS  - 1942-0994 (Electronic)
IS  - 1942-0994 (Linking)
VI  - 2017
DP  - 2017
TI  - Distinguishing the Unique Neuropathological Profile of Blast Polytrauma.
PG  - 5175249
LID - 10.1155/2017/5175249 [doi]
AB  - Traumatic brain injury sustained after blast exposure (blast-induced TBI) has
      recently been documented as a growing issue for military personnel. Incidence of 
      injury to organs such as the lungs has decreased, though current epidemiology
      still causes a great public health burden. In addition, unprotected civilians
      sustain primary blast lung injury (PBLI) at alarming rates. Often,
      mild-to-moderate cases of PBLI are survivable with medical intervention, which
      creates a growing population of survivors of blast-induced polytrauma (BPT) with 
      symptoms from blast-induced mild TBI (mTBI). Currently, there is a lack of
      preclinical models simulating BPT, which is crucial to identifying unique injury 
      mechanisms of BPT and its management. To meet this need, our group characterized 
      a rodent model of BPT and compared results to a blast-induced mTBI model. Open
      field (OF) performance trials were performed on rodents at 7 days after injury.
      Immunohistochemistry was performed to evaluate cellular outcome at day seven
      following BPT. Levels of reactive astrocytes (GFAP), apoptosis (cleaved caspase-3
      expression), and vascular damage (SMI-71) were significantly elevated in BPT
      compared to blast-induced mTBI. Downstream markers of hypoxia (HIF-1alpha and
      VEGF) were higher only after BPT. This study highlights the need for unique
      therapeutics and prehospital management when handling BPT.
FAU - Hubbard, W Brad
AU  - Hubbard WB
AUID- ORCID: 0000-0001-7018-0148
AD  - Biomedical Engineering and Mechanics, Virginia Tech, Blacksburg, VA 24061, USA.
FAU - Greenberg, Shaylen
AU  - Greenberg S
AD  - Translational Biology, Medicine, and Health, Virginia Tech, Blacksburg, VA 24061,
      USA.
FAU - Norris, Carly
AU  - Norris C
AUID- ORCID: 0000-0002-0654-0214
AD  - Biomedical Engineering and Mechanics, Virginia Tech, Blacksburg, VA 24061, USA.
FAU - Eck, Joseph
AU  - Eck J
AD  - Biomedical Engineering and Mechanics, Virginia Tech, Blacksburg, VA 24061, USA.
FAU - Lavik, Erin
AU  - Lavik E
AD  - Department of Chemical, Biochemical and Environmental Engineering, University of 
      Maryland, Baltimore County, Baltimore, MD 21250, USA.
FAU - VandeVord, Pamela
AU  - VandeVord P
AUID- ORCID: 0000-0003-3422-2704
AD  - Biomedical Engineering and Mechanics, Virginia Tech, Blacksburg, VA 24061, USA.
AD  - Research Services, Salem VAMC, Salem, VA 24153, USA.
LA  - eng
PT  - Journal Article
DEP - 20170323
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
PMC - PMC5382305
EDAT- 2017/04/21 06:00
MHDA- 2017/04/21 06:00
CRDT- 2017/04/21 06:00
PHST- 2017/01/20 [received]
PHST- 2017/02/28 [accepted]
AID - 10.1155/2017/5175249 [doi]
PST - ppublish
SO  - Oxid Med Cell Longev. 2017;2017:5175249. doi: 10.1155/2017/5175249. Epub 2017 Mar
      23.

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