We study the mechanisms of cell death following brain ischemia and reperfusion, focusing on the causes and consequences of reperfusion-induced inhibition of protein synthesis, or translation arrest. This translation arrest appears to be part of the post-ischemic neuronal stress response. We have evaluated classical ribosome biochemistry, intracellular stress responses and most recently began investigating mRNA regulatory mechanisms, including stress granules and HuR granules. The lab is currently funded by the National Institute of Neurological Disorders and Stroke at the NIH.
Brain ischemia and reperfusion injury: stroke, cardiac arrest and resuscitation brain damage.
Jose Rafols, Ph.D.