Maria L. Cepero

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Traumatic brain injury (TBI) pathology includes contusions, cavitation, cell death, all of which can be exacerbated by inflammation. We hypothesized that an anti-inflammatory drug, rolipram, may reduce pathology after TBI, since in several CNS injury models rolipram reduces inflammation and improves cell survival and functional recovery. Adult male C57BL/6(More)
Incubation of normal mouse peritoneal cells consisting of over 90% phagocytizing macrophages with delta 9-tetrahydrocannabinol (THC) resulted in a inhibition of phagocytic function. The THC in a dose-related manner suppressed the percentage of macrophages per culture which ingested yeast and the average number of yeast particles ingested by the(More)
Traumatic brain injury (TBI), ranging from mild concussion to severe penetrating wounds, can involve brain regions that contain damaged or lost synapses in the absence of neuronal death. These affected regions significantly contribute to sensory, motor and/or cognitive deficits. Thus, studying the mechanisms responsible for synaptic instability and(More)
BACKGROUND Traumatic brain injury (TBI) continues to be a major source of death and disability worldwide, and one of the earliest and most profound deficits comes from vascular damage and breakdown of the blood-brain barrier (BBB). Cerebral vascular endothelial cells (cvECs) and endothelial progenitor cells (EPCs) have been shown to play essential roles in(More)
Astrocytes have been recently identified as important components of the tripartite synaptic complex. There is growing evidence that astrocytes regulate synaptic functions, in part, through the release of gliotransmitters. In a recent study, we have demonstrated that ephrinB3 could stimulate astrocytic release of D-serine through activation of EphB3 and(More)
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