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Biomedical subjects

Wiley Souba

Publications and source records attributed to Wiley Souba.

3 recordsLinked to original sources

Developing the young academic surgeon.

In the past, the process of developing the young academic surgeon was arguably less strategic, one that was often not deliberately managed and monitored, leading in some cases to academic drift and disillusionment. Once upon a time it was assumed that greatness was genetic and that the next triple threat would emerge when a pre-programmed set of genes was turned on. Today, as the complexities and vicissitudes of our work increase, it is practically impossible for even the most gifted young person to be successful without careful attention to career development. Faculty development must be deliberate and strategic--every junior faculty member is unique and will require a customized career development plan that is well thought out, linked to measurable goals, monitored routinely and buttressed by effective mentoring. This approach will require time and commitment--precious commodities that are in short supply as the demands on our time are only escalating. By recruiting the right people (those who fit with the organization's values and goals) and providing the right environment, we can optimize the growth and satisfaction of our young faculty and, in so doing, create departments that are leaders in carrying out our missions of research, education and patient care. We cannot afford to have our young people fail--it is simply too costly, both from a financial and a human perspective.

Academic Medical Centers↗

Developing the young academic surgeon.

In the past, the process of developing the young academic surgeon was arguably less strategic, one that was often not deliberately managed and monitored, leading in some cases to academic drift and disillusionment. Once upon a time it was assumed that greatness was genetic and that the next triple threat would emerge when a pre-programmed set of genes was turned on. Today, as the complexities and vicissitudes of our work increase, it is practically impossible for even the most gifted young person to be successful without careful attention to career development. Faculty development must be deliberate and strategic--every junior faculty member is unique and will require a customized career development plan that is well thought out, linked to measurable goals, monitored routinely and buttressed by effective mentoring. This approach will require time and commitment--precious commodities that are in short supply as the demands on our time are only escalating. By recruiting the right people (those who fit with the organization's values and goals) and providing the right environment, we can optimize the growth and satisfaction of our young faculty and, in so doing, create departments that are leaders in carrying out our missions of research, education and patient care. We cannot afford to have our young people fail--it is simply too costly, both from a financial and a human perspective.

Academic Medical Centers↗

Arginine transport in catabolic disease states.

Arginine appears to be a semiessential amino acid in humans during critical illness. Catabolic disease states such as sepsis, injury, and cancer cause an increase in arginine utilization, which exceeds body production, leading to arginine depletion. This is aggravated by the reduced nutrient intake that is associated with critical illness. Arginine depletion may have negative consequences on tissue function under these circumstances. Nutritional regimens containing arginine have been shown to improve nitrogen balance and lymphocyte function, and stimulate arginine transport in the liver. We have studied the effects of stress mediators on arginine transport in vascular endothelium, liver, and gut epithelium. In vascular endothelium, endotoxin stimulates arginine uptake, an effect that is mediated by the cytokine tumor necrosis factor-alpha (TNF-alpha) and by the cyclo-oxygenase pathway. This TNF-alpha stimulation involves the activation of intracellular protein kinase C (PKC). A significant increase in hepatic arginine transport activity also occurs following burn injury and in rats with progressive malignant disease. Surgical removal of the growing tumor results in a normalization of the accelerated hepatic arginine transport within days. Chronic metabolic acidosis and sepsis individually augment intestinal arginine transport in rats and Caco-2 cell culture. PKC and mitogen-activated protein kinases are involved in mediating the sepsis/acidosis stimulation of arginine transport. Understanding the regulation of plasma membrane arginine transport will enhance our knowledge of nutrition and metabolism in seriously ill patients and may lead to the design of improved nutritional support formulas.

Animals↗