The major thrust of work in my laboratory is to gain a more comprehensive understanding of the adaptation process in response to massive small bowel resection. As a surgeon/scientist, I have directed a productive research program focused in this area for the past 20 years. This has been possible through a unique, collaborative team comprised of myself, a PhD molecular biologist, and a PhD cell biologist. In addition, this laboratory has been the training ground for over 40 graduate and post-graduate fellows – the majority of whom have progressed to academic positions throughout the country. Our laboratory has pioneered a murine model for small bowel resection and has made many seminal contributions toward understanding the pathogenesis of adaptation. We have used this unique surgical model to establish a critical role for epidermal growth factor receptor signaling as a major regulator of the magnitude of adaptation responses. We have also identified specific genes that are fundamental for the induction of enterocyte proliferation (p21) as well as a key gene necessary for enterocyte apoptosis (Bax). Employing indirect calorimetry and nuclear magnetic resonance, we have extended our studies to include an understanding of metabolic responses and body compositional changes in association with massive intestinal loss. Since moving from the University of Cincinnati in 2007, I have been able to embrace the outstanding research environment of the Washington University School of Medicine. This move has enabled the development of multiple key collaborations which have significantly enhanced our research program.
Appendicitis,inguinal hernia, necrotizing enterocolitis, omphalocele, umbilical hernia, biliary atresea, Hirschsprung’s disease, imperforate anus, intussusception, malrotation/volvulus, cystic hygroma, duodenal atresia, gastroschisis, hiatal hernia (pediatric), pyloric stenosis, and esophageal atresia.