Research in Dr. Sandra Hewett's lab focuses on elucidating the molecular and biochemical mechanisms by which post-ischemic inflammation contributes to the progression of acute neuronal injury with a focus on astrocyte-neuron interactions. Studies have determined that the brain damage associated with acute injury ―most commonly caused by cerebral ischemia, head trauma or seizure ― is mediated by over-stimulation of excitatory amino acid (EAA) receptors as well as inflammatory factors. While inflammatory cells from the periphery contribute to neuronal damage there is evidence that inflammatory genes expressed in parenchymal cells of the CNS also play a deleterious role. Molecules of interest in her lab include inducible forms of nitric oxide (NO) synthase and cyclooxygenase (COX), L-12/15 lipoxygenase (12/15 LO) and IL-1ß. The role of astrocyte system xc- (cystine/glutamate transporter) in injury and protection is also being explored. Both in vitro and in vivo models of injury are employed taking a “molecules to mouse” and “mouse to molecules” approach to the essential questions posed.