Abstract

The objective of our research program is to conduct an integrated multidisciplinary inquiry into the mechanisms and treatment of ischemic brain injury. Our investigations, grounded in experimental animal models of cerebral ischemia, have as their ultimate goal the identification of those factors responsible for ischemic injury which may be amenable to therapeutic or prophylactic intervention. The Program Project consists of six investigative proposal together with Core facilities supporting the research program in the areas of brain metabolite analysis, animal physiology, radioisotopic tracer strategies, morphology, computer science/image-processing, and animal behavior. The Cores contribute substantively to the implementation of each Project and unify the Projects by common methodological approaches. Program areas include: (1) treatable mechanisms of brain injury in foal cerebral ischemia; (2) mechanisms of functional recovery following cerebral infarction; (3) an analysis of glutamatergic mediation of ischemic vulnerability; (4) the effect of mild selective cerebral hypothermia in protecting against ischemic brain injury; (5) studies of early indices of cellular damage in the hippocampal slice preparation; and (6) an analysis of local cortical electrophysiological and ion-transport alterations in acute focal cerebral ischemia and their relationship to ultimate tissue injury.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Program Projects (P01)
Project #
2P01NS005820-25
Application #
3099241
Study Section
Neurological Disorders Program Project Review A Committee (NSPA)
Project Start
1976-08-01
Project End
1995-07-31
Budget Start
1990-08-01
Budget End
1991-07-31
Support Year
25
Fiscal Year
1990
Total Cost
Indirect Cost

  Institution

Name
University of Miami School of Medicine
Department
Type
Schools of Medicine
DUNS #
City
Miami
State
FL
Country
United States
Zip Code
33146

  Publications

Dave, Kunjan R; Della-Morte, David; Saul, Isabel et al. (2013) Ventricular fibrillation-induced cardiac arrest in the rat as a model of global cerebral ischemia. Transl Stroke Res 4:571-8
Della-Morte, D; Raval, A P; Dave, K R et al. (2011) Post-ischemic activation of protein kinase C ? protects the hippocampus from cerebral ischemic injury via alterations in cerebral blood flow. Neurosci Lett 487:158-62
Dave, Kunjan R; Anthony Defazio, Richard; Raval, Ami P et al. (2009) Protein kinase C epsilon activation delays neuronal depolarization during cardiac arrest in the euthermic arctic ground squirrel. J Neurochem 110:1170-9
DeFazio, R Anthony; Raval, Ami P; Lin, Hung W et al. (2009) GABA synapses mediate neuroprotection after ischemic and epsilonPKC preconditioning in rat hippocampal slice cultures. J Cereb Blood Flow Metab 29:375-84
Della-Morte, D; Dave, K R; DeFazio, R A et al. (2009) Resveratrol pretreatment protects rat brain from cerebral ischemic damage via a sirtuin 1-uncoupling protein 2 pathway. Neuroscience 159:993-1002
Park, Hee-Pyoung; Nimmagadda, Anitha; DeFazio, Richard A et al. (2008) Albumin therapy augments the effect of thrombolysis on local vascular dynamics in a rat model of arteriolar thrombosis: a two-photon laser-scanning microscopy study. Stroke 39:1556-62
Dave, Kunjan R; DeFazio, R Anthony; Raval, Ami P et al. (2008) Ischemic preconditioning targets the respiration of synaptic mitochondria via protein kinase C epsilon. J Neurosci 28:4172-82
Kim, Eun J; Raval, Ami P; Perez-Pinzon, Miguel A (2008) Preconditioning mediated by sublethal oxygen-glucose deprivation-induced cyclooxygenase-2 expression via the signal transducers and activators of transcription 3 phosphorylation. J Cereb Blood Flow Metab 28:1329-40
Nimmagadda, Anitha; Park, Hee-Pyoung; Prado, Ricardo et al. (2008) Albumin therapy improves local vascular dynamics in a rat model of primary microvascular thrombosis: a two-photon laser-scanning microscopy study. Stroke 39:198-204
Kim, E; Raval, A P; Defazio, R A et al. (2007) Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro. Neuroscience 145:931-41

Showing the most recent 10 out of 15 publications