Endothelial activation of caspase-9 promotes neurovascular injury in retinal vein occlusion.

Central nervous system ischemic injury features neuronal dysfunction, inflammation and breakdown of vascular integrity. Here we show that activation of endothelial caspase-9 after hypoxia-ischemia is a critical event in subsequent dysfunction of the blood-retina barrier, using a panel of interrelated ophthalmic in vivo imaging measures in a mouse model of retinal vein occlusion (RVO). Rapid nonapoptotic activation of caspase-9 and its downstream effector caspase-7 in endothelial cells promotes capillary ischemia and retinal neurodegeneration.

Direct Observation of Low Strain, High Rate Deformation of Cultured Brain Tissue During Primary Blast.

The Veterans Health Administration determined that over 250,000 U.S. service members were diagnosed with a traumatic brain injury (TBI) between 2008 and 2018, of which a great proportion were due to blast exposure.

Phosphodiesterase-4 inhibition restored hippocampal long term potentiation after primary blast.

Due to recent military conflicts and terrorist attacks, blast-induced traumatic brain injury (bTBI) presents a health concern for military and civilian personnel alike. Although secondary blast (penetrating injury) and tertiary blast (inertia-driven brain deformation) are known to be injurious, the effects of primary blast caused by the supersonic shock wave interacting with the skull and brain remain debated. Our group previously reported that in vitro primary blast exposure reduced long-term potentiation (LTP), the electrophysiological correlate of learning and memory, in rat organotypic hippocampal slice cultures (OHSCs) and that primary blast affects key proteins governing LTP.