Zuobiao Yuan understands the importance of conducting impactful research. But he also realizes that postdoctoral scholars cannot succeed on research alone.

Yuan, president of the University of Iowa Postdoctoral Association, intends to provide his fellow postdocs with professional development opportunities during the 2012-13 academic year. Events being planned include an alternative career seminar series, a presentation skills workshop series, and a grant writing workshop.

Established scholars in both academy and industry also will be invited to give talks regarding how to prepare for a successful career in their respective fields.

“Most postdocs only know how to do research,” says Yuan, chair of the UIPDA’s Professional Development Committee. “But research is not enough. I hope all postdocs can find the right direction to go to achieve their career goals.”

Yuan would like to see as many international postdocs as possible attend the talks and workshops.

“At the University of Iowa, 60 percent of postdocs are international, and international postdocs concentrate just on the research,” says Yuan, a postdoctoral fellow in the Department of Surgery at UI Hospitals and Clinics and native of Shanghai,China.

When Yuan isn’t involved in UIPDA activities, he is investigating the pathogenesis of acute gallstone pancreatitis. Specifically, he is examining how gallstone obstruction of the pancreatic duct may initiate acute inflammation of the pancreas. A better understanding of these processes will help improve the treatment of this potentially fatal disease.

“There is no specific treatment for pancreatitis and that is the problem,” says Yuan, who works in the lab of Associate Professor Isaac Samuel. “In the most severe form of pancreatitis, you may die in one week from multiple organ dysfunction syndrome.”

Acute gallstone pancreatitis creates this sudden inflammation of the pancreas when a gallstone blocks the pancreatic duct through which the pancreas secretes digestive juices, or enzymes, into the small intestine. Pancreatic enzymes join with bile—a liquid produced in the liver and stored in the gallbladder—to digest food.  Blockage of the pancreatic duct may cause symptoms such as abdominal pain, nausea and vomiting.

Normally, digestive enzymes secreted by the pancreas do not become active until they reach the small intestine. But when the bile-pancreatic duct is obstructed, the enzymes inside the pancreas attack, and some inflammatory mediators are released. Damage to the pancreas may then permit toxins to enter the bloodstream damaging organs outside of the abdominal cavity, such as the lungs and kidneys.

To further his research, Yuan developed a mouse model with acute pancreatitis—caused by a constricted pancreatic duct—that mimics the human disease, which can feature multiple organ dysfunction syndrome (MODS).

Using this model, Yuan and his colleagues have shown that pancreatic juice replacement within the small intestine inhibits pancreatic overproduction of the inflammatory mediator genes that play a key role in MODS. They also confirmed that pancreatic juice released from the abdomen plays an important role in exacerbating acute pancreatitis by hyperstimulating the pancreas to activate pro-inflammatory pathways in the presence of an obstructed duct.

“In our model, if we don’t treat the pancreatitis, median survival rate of the mice is three days,” Yuan says. “After treatment, the median survival rate is five days. In the future, we hope to increase the median survival rate to 15 days (the whole observation period).”

Yuan’s future work will focus on determining the mechanism of activation of the pro-inflammatory pathways in isolated pancreatic cells that produce digestive enzymes.

Samuel credits Yuan for helping make important early advances in the understanding of pancreatitis.

"As the investigation of the early stages of disease progression in humans is not possible, Dr. Yuan has helped to characterize a novel mouse model of duct ligation-induced acute pancreatitis that is associated with systemic inflammation and substantial mortality similar to that seen in severe clinical acute pancreatitis,” says Samuel, principal investigator on this project funded by the National Institutes of Health.

“With the expert help of co-workers Deborah Williard and Erik Twait in my laboratory, Dr. Yuan used this mouse model to define certain novel events in the early stages of disease pathogenesis such as the role of stress kinase activation and duodenal exclusion resulting from pancreatic duct obstruction. We consider these to be early steps in a direction to understand disease pathogenesis better, as a prerequisite to plan new therapeutic initiatives."