Nonlinearity of the coefficient of thermal expansion in brain tissue.

The coefficient of thermal expansion (CTE) in biological tissues is an integral parameter behind the application of electromagnetic energy to biomedical technologies; however, its behavior is far from being fully characterized. In this study, we apply digital image correlation (DIC) to non-invasively measure the microscale thermal expansions of recently excised embryonic E18 rodent brain tissue slices. Although the CTE has been measured previously in soft tissues, the literature surrounding the expansion of brain tissue remains sparse.

Differential effects of FK506 on structural and functional axonal deficits after diffuse brain injury in the immature rat.

Diffuse axonal injury is a major component of traumatic brain injury in children and correlates with long-term cognitive impairment. Traumatic brain injury in adult rodents has been linked to a decrease in compound action potential (CAP) in the corpus callosum, but information on trauma-associated diffuse axonal injury in immature rodents is limited. We investigated the effects of closed head injury on CAP in the corpus callosum of 17-day-old rats.

Concussive brain trauma in the mouse results in acute cognitive deficits and sustained impairment of axonal function.

Concussive brain injury (CBI) accounts for approximately 75% of all brain-injured people in the United States each year and is particularly prevalent in contact sports. Concussion is the mildest form of diffuse traumatic brain injury (TBI) and results in transient cognitive dysfunction, the neuropathologic basis for which is traumatic axonal injury (TAI). To evaluate the structural and functional changes associated with concussion-induced cognitive deficits, adult mice were subjected to an impact on the intact skull over the midline suture that resulted in a brief apneic period and loss of the righting reflex.

Impaired axonal transport and neurofilament compaction occur in separate populations of injured axons following diffuse brain injury in the immature rat.

Diffuse brain injury is a leading cause of mortality in infants and children under 4 years of age and results in cognitive deficits in survivors. The anatomic basis for these behavioral deficits may be traumatic axonal injury (TAI), which manifests as impaired axonal transport (IAT) and neurofilament compaction (NFC), and may occur as a result of glutamate receptor activation. The extent of IAT and NFC was evaluated at 6, 24 and 72 h following non-contusive brain trauma in the 17 day-old rat to examine the causal relationship between these two pathologic entities; in addition, the effect of antagonists to the ionotropic glutamate receptors on TAI was evaluated.