PMID- 22375134
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20211021
IS  - 1664-2295 (Electronic)
IS  - 1664-2295 (Linking)
VI  - 3
DP  - 2012
TI  - A Multiscale Approach to Blast Neurotrauma Modeling: Part II: Methodology for 
      Inducing Blast Injury to in vitro Models.
PG  - 23
LID - 10.3389/fneur.2012.00023 [doi]
LID - 23
AB  - Due to the prominent role of improvised explosive devices (IEDs) in wounding 
      patterns of U.S. war-fighters in Iraq and Afghanistan, blast injury has risen to 
      a new level of importance and is recognized to be a major cause of injuries to 
      the brain. However, an injury risk-function for microscopic, macroscopic, 
      behavioral, and neurological deficits has yet to be defined. While operational 
      blast injuries can be very complex and thus difficult to analyze, a simplified 
      blast injury model would facilitate studies correlating biological outcomes with 
      blast biomechanics to define tolerance criteria. Blast-induced traumatic brain 
      injury (bTBI) results from the translation of a shock wave in-air, such as that 
      produced by an IED, into a pressure wave within the skull-brain complex. Our 
      blast injury methodology recapitulates this phenomenon in vitro, allowing for 
      control of the injury biomechanics via a compressed-gas shock tube used in 
      conjunction with a custom-designed, fluid-filled receiver that contains the 
      living culture. The receiver converts the air shock wave into a fast-rising 
      pressure transient with minimal reflections, mimicking the intracranial pressure 
      history in blast. We have developed an organotypic hippocampal slice culture 
      model that exhibits cell death when exposed to a 530 +/- 17.7-kPa peak overpressure 
      with a 1.026 +/- 0.017-ms duration and 190 +/- 10.7 kPa-ms impulse in-air. We have 
      also injured a simplified in vitro model of the blood-brain barrier, which 
      exhibits disrupted integrity immediately following exposure to 581 +/- 10.0 kPa 
      peak overpressure with a 1.067 +/- 0.006-ms duration and 222 +/- 6.9 kPa-ms impulse 
      in-air. To better prevent and treat bTBI, both the initiating biomechanics and 
      the ensuing pathobiology must be understood in greater detail. A 
      well-characterized, in vitro model of bTBI, in conjunction with animal models, 
      will be a powerful tool for developing strategies to mitigate the risks of bTBI.
FAU - Effgen, Gwen B
AU  - Effgen GB
AD  - Department of Biomedical Engineering, Columbia University New York, NY, USA.
FAU - Hue, Christopher D
AU  - Hue CD
FAU - Vogel, Edward 3rd
AU  - Vogel E 3rd
FAU - Panzer, Matthew B
AU  - Panzer MB
FAU - Meaney, David F
AU  - Meaney DF
FAU - Bass, Cameron R
AU  - Bass CR
FAU - Morrison, Barclay 3rd
AU  - Morrison B 3rd
LA  - eng
PT  - Journal Article
DEP - 20120224
PL  - Switzerland
TA  - Front Neurol
JT  - Frontiers in neurology
JID - 101546899
PMC - PMC3285773
OTO - NOTNLM
OT  - astrocyte
OT  - blast injury
OT  - blood-brain barrier
OT  - endothelial cells
OT  - hippocampus
OT  - neuron
OT  - organotypic slice culture
OT  - shock tube
EDAT- 2012/03/01 06:00
MHDA- 2012/03/01 06:01
PMCR- 2012/02/24
CRDT- 2012/03/01 06:00
PHST- 2011/11/03 00:00 [received]
PHST- 2012/02/07 00:00 [accepted]
PHST- 2012/03/01 06:00 [entrez]
PHST- 2012/03/01 06:00 [pubmed]
PHST- 2012/03/01 06:01 [medline]
PHST- 2012/02/24 00:00 [pmc-release]
AID - 10.3389/fneur.2012.00023 [doi]
PST - epublish
SO  - Front Neurol. 2012 Feb 24;3:23. doi: 10.3389/fneur.2012.00023. eCollection 2012.