The over-arching goal of my research program has been to elucidate the mechanisms that regulate liver regeneration so as to improve the management of patients with liver diseases. In pursuit of this goal, my laboratory has accumulated extensive experience and expertise with the rodent partial hepatectomy paradigm and other experimental models of liver regeneration, and we have contributed broadly to current understanding of the mechanisms that regulate liver regeneration. Our previously published and preliminary data provide strong support for our central hypothesis that liver injuries induce changes in metabolism that initiate hepatic regeneration and, thus, that pro-regenerative therapeutic approaches targeting such metabolic alterations can be discovered. We recently reported data implicating protein acetylation as an important molecular link between the metabolic response to hepatic insufficiency and the initiation of liver regeneration, and we are also pursuing studies to examine interactions between metabolism and other mechanisms of epigenetic regulation during liver regeneration. These studies will serve as a vehicle towards new opportunities with which to improve the management of patients with acute and chronic liver disease. In a complementary area of investigation, we have sought to identify novel metabolic biomarkers of liver regeneration, and examine the utility of such markers in the management of pediatric acute liver failure (ALF) and other serious human liver disease. Such studies have informed our hypothesis that incorporation of metabolic bio-markers of liver regeneration into ALF outcomes-prediction algorithms will improve medical management of these patients, and, thus, should lead to novel opportunities with which to improve the management of human liver diseases. We recently initiated a new line of investigation, to elucidate the mechanisms that link dietary aflatoxin exposure to stunting, using a novel rat model which we developed. We are pursuing the hypothesis that toxin-induced injuries to the liver and the gut mediate such stunting.