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Effects of veliparib on microglial activation and functional outcomes following traumatic brain injury in the rat and pig.
TLDR
Results showed veliparib suppression of CCI-induced microglial activation with a delay-to-treatment interval of at least 24 hours in both rats and pigs, but with no associated functional improvement, which underscores the complexities in translating anti-inflammatory effects to clinically relevant outcomes.
Cofilin-actin rod formation in neuronal processes after brain ischemia
TLDR
Four mouse models of brain ischemia are evaluated to define the conditions that drive formation of cofilin-actin rods; early reperfusion restores ATP generating capacity, but also induces oxidative stress; and interventions that limit coFilin-Actin rod formation may help to preserve integrity of neuronal processes in permanent ischemIA.
Cofilin-actin rod formation in neuronal processes after brain ischemia
TLDR
Four mouse models of brain ischemia are evaluated to define the conditions that drive formation of cofilin-actin rods; early reperfusion restores ATP generating capacity, but also induces oxidative stress; and interventions that limit co Filin-Actin rod formation may help to preserve integrity of neuronal processes in permanent ischemIA.
Effects of Veliparib on Microglial Activation and Functional Outcomes after Traumatic Brain Injury in the Rat and Pig
The inflammation response induced by brain trauma can impair recovery. This response requires several hours to develop fully and thus provides a clinically relevant therapeutic window of opportunity.
Blast-Induced Axonal Degeneration In The Rat Cerebellum In The Absence of Head Movement
TLDR
The findings support the contentions that blast per se, independent of head movement, is sufficient to induce axonal injury, and that axons in cerebellar white matter are particularly vulnerable to direct blast‐induced injury.