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To this end, we used an etiologically realistic rat model of posttraumatic epilepsy, in which the initiating fluid percussion injury closely replicates contusive closed-head injury in humans, and has been adapted to maximize epileptogenesis and focal non-convulsive seizures.
Translating these findings in vivo, we evaluated therapeutic effect of 3,4,6-O-Bu3GalNAc 3,4,6-O-Bu3GalNAc 3,4,6-O-Bu3GalNAcA when delivered via lonal inthe-aratcular sustained-release delivery using modelparticles and fofnd this method to be efficacious in posttraumatic prOAression.
To evaluate the tissue and cellular basis for these effects, we examined the impact of orally administered hCol1 in a model of posttraumatic OA (PTOA).
Z. Hu and J. Tu investigated mitochondrial function in an experimental model of posttraumatic syringomyelia.
A limitation of repetitive injury as a model of posttraumatic OA is that it disrupts endogenous repair responses.
The rabbit model of posttraumatic knee contractures simulating stable intra-articular fractures and accompanied by a period of immobilization also supports the capsular contribution to joint contractures.
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Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research past, present, and future.
Increasing predictability of animal models of posttraumatic stress disorder (PTSD) has required active collaboration between clinical and preclinical scientists.
Several experimental models of posttraumatic epilepsy are currently in use that may facilitate discovery of molecular and pathophysiological alterations underlying the process of epileptogenesis.
Despite its prevalence, killing in war is an experience that may not fit neatly into existing models of posttraumatic stress disorder (PTSD) and its treatment.
Information processing models of posttraumatic stress disorder (PTSD) suggest that PTSD is characterized by preferential allocation of attentional resources to potentially threatening stimuli.
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