Every year, nearly 800,000 people in the United States experience a stroke, and most of these are ischemic strokes – a leading cause of death, as well as long-term disability, that present a major burden for families and health care systems. During the acute phase, ischemic stroke rapidly initiates many pathologic processes that lead to brain cell death, while during the recovery phase, endogenous neurorestorative processes that contribute to spontaneous recovery of neurologic function are believed to be activated in the post-stroke brain. This 2-phase theory largely guides the current search for therapeutic strategies to improve stroke outcome, ie, neuroprotective strategies during the acute phase, and neurorestorative strategies during the recovery phase. Our group is currently studying endogenous protective processes/pathways in both post-stroke phases. These include proteostasis-related pathways such as the unfolded protein response (UPR), SUMOylation, and O-GlcNAcylation, and modulation of neuronal activity.
Cardiac Arrest and Resuscitation
Many advances in resuscitation have led to increased numbers of cardiac arrest (CA) patients who survive the initial arrest event and are admitted to the Intensive Care Unit. Unfortunately, among this growing patient population, mortality and morbidity remain strikingly high. This is attributed to a complex set of pathophysiologic processes that include the ischemia/reperfusion-induced cascade of pathologic events in various organs and systemic immune response. Therefore, our CA research is focused not only on individual organs such as the brain, lung and intestine, but also on the systemic hormonal and immune responses.