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Distinguishing the Unique Neuropathological Profile of Blast Polytrauma

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Images show similar number of microglia. IBA-1 expression, marking microglia, in the amygdala was not significantly different between groups.
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fig4: Images show similar number of microglia. IBA-1 expression, marking microglia, in the amygdala was not significantly different between groups.

Mentions: IBA-1, which is involved in phagocytosis and actin reorganization in microglia, is constitutively expressed in microglia. Though not specific to activated microglia, IBA-1 is usually used to assess morphology (ramified or ameboid), which gives information about microglial modulation in disease states. Although there is no significant difference between the BPT group and sham, there is slight elevation in IBA-1 expression in the BPT group compared to sham (Figure 4).


Distinguishing the Unique Neuropathological Profile of Blast Polytrauma
Images show similar number of microglia. IBA-1 expression, marking microglia, in the amygdala was not significantly different between groups.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5382305&req=5

fig4: Images show similar number of microglia. IBA-1 expression, marking microglia, in the amygdala was not significantly different between groups.
Mentions: IBA-1, which is involved in phagocytosis and actin reorganization in microglia, is constitutively expressed in microglia. Though not specific to activated microglia, IBA-1 is usually used to assess morphology (ramified or ameboid), which gives information about microglial modulation in disease states. Although there is no significant difference between the BPT group and sham, there is slight elevation in IBA-1 expression in the BPT group compared to sham (Figure 4).

View Article: PubMed Central - PubMed

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.

No MeSH data available.