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Brain injury from stroke, head trauma, and chronic neurologic degenerative diseases, is a major cause of morbidity and mortality. We are particularly interested in the cellular consequences of brain injury. To study this problem we work with primary cultures of neurons and astrocytes from mice and employ rodent models of stroke. Current work focuses on: 1) the role of miRNAs as a way to regulate groups of proteins important to ischemic outcome; 2) the interaction of neurons and glia during injury; 3) the role of astrocytes in global ischemia; 4)protection using heat shock proteins and cell death regulatory proteins 4) changes in mitochondrial function and signaling in injury and ways to protect mitochondria; 5) ways to improve neurogenesis after stroke; 6) the interaction of oxidative stress and inflammation in stroke; 7) computational modeling of cell death.We use gene transfer techniques to express genes and miRNAs of interest in brain cells and intact brain and analyze ways in which these can provide protection. We use fluorescent probes for pH, intracellular calcium, ROS, mitochondrial membrane potential, as well as morphologically evaluate outcome, and quantitate injury. We also use transgenic mice to analyze the effects of overexpression or loss of expression of specific genes on outcome from stroke. Mitochondria are central to energy metabolism, the regulation of inflammation, and the regulation of cell death. We study changes in mitochondria with stress. We are also interested in the interaction of oxidative stress and inflammation in stroke.