As a transplant surgeon, my objectives in the clinical liver transplantation are (1) to maximize the cadaveric organ donors to meet the critical organ shortage, and (2) to optimize the functional capacity of the marginal and small-for-size liver allografts.
My bench research has been focused on the pathogenesis of brain edema in fulminant hepatic failure (FHF). FHF, or acute liver failure, is associated with massive hepatocellular necrosis and severe dysfunction of the liver in the absence of previous liver disease. In early stages, patients may recover. However, when stages III and IV of encephalopathy (comatose stages) set in, brain edema occurs. Brain edema, if uncontrolled, leads to brain herniation and death of the patients. Although the cytotoxic mechanism of brain edema in FHF has been extensively studied, evidence for a vasogenic mechanism is lacking. Moreover, effective and successful therapeutic options for brain edema are limited.
My long-term research goal has been to elucidate the vasogenic mechanisms of brain edema in FHF. Understanding the specific vasogenic mechanisms involved in causing cerebral edema in these patients is likely to yield novel approaches aimed at increasing survival.