Primary Blast Injury Criteria for Animal/Human TBI Models using Field Validated Shock Tubes
Technical Report,15 Aug 2016,14 Aug 2017
New Jersey Institute of Technology Newark United States
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Blast-induced Traumatic brain injury bTBI is a leading cause of morbidity in soldiers on the battlefield and training sites with long-term neurological and psychological pathologies. We evaluated the extent of lung injuries, major pathological sequelae, including oxidative stress, neuroinflammation and BBB damage, supplemented by characterization of proteome changes in hippocampus and cortex in an animal model of single primary blast TBI. Three blast overpressures, 130, 180 and 240 kPa, were used for these studies and evaluation was performed at three time points 0, 4 and 24 hours post injury. Spatiotemporal patterns of oxidative stress were examined using two isoforms NADPH oxidase 1 and 2 NOX1, NOX2, superoxide and 4-hydroxynonenal 4HNE protein adducts. Gross protein changes were evaluated via Western blot, followed by immunofluorescence signal quantification performed on entire coronal sections. One of the major findings is differential regional and cellular distribution of injury markers. Expression of NOX isoforms displayed NOX1 is increased in hippocampus and thalamus, whereas in the frontal cortex the NOX2 expression reached the highest levels. Cell-specific analysis revealed NOX1 and NOX 2 levels were significantly higher in neurons compared to astrocytes and microglia. These results demonstrate uniform pressure loading results in differential pathological response, which depends on the local tissue composition, and the response is to insult depends upon the cell type.
- Medicine and Medical Research