Alumni professorships combine unrestricted gifts from medical alumni and former house staff with gifts from friends of the School of Medicine.

"The Washington University Medical Center Alumni Association launched these professorships in 1978 to help attract and retain renowned physicians and scientists," said William A. Peck, M.D., executive vice chancellor for medical affairs and dean of the School of Medicine. "Nerbonne and Ornitz already have made significant contributions to the field of molecular biology, and we are delighted to honor them with these positions."

Nerbonne's research focuses on defining the molecular mechanisms that control electrical activity in the heart and the changes that occur in heart disease. Most of her work centers on one class of molecules -- voltage-gated potassium (K+) selective ion channels. These channels mediate K+ movement across the membranes of individual cardiac muscle cells, thereby maintaining the normal rhythm of the heart. Indeed, in some congenital and acquired cardiac arrhythmias, mutations in the genes that encode K+ channel proteins produce rhythmic disturbances that can cause sudden death.

"We would like to understand how these channels function in the normal heart," Nerbonne said, "and we would like to know how to control their activity so that we might stop or prevent cardiac arrhythmias."

Nerbonne combines biochemistry, molecular genetics and electrophysiology to investigate the expression and function of these channels. Her team provided the first definitive proof that cardiac cells express multiple types of voltage-gated K+ channels with distinct properties and functional roles. The team discovered that variations in the expression levels of these channels in different regions of the heart are critical for maintaining normal cardiac electrical activity and have demonstrated that manipulating the expression of the genes encoding these channels can have profound physiological consequences.

Nerbonne's team also has pioneered efforts aimed at defining the molecular structures of voltage-gated cardiac K+ channels and has shown that distinct genes encode each of the various K+ channels identified thus far.

She and her colleagues also have shown that there are marked changes in the expression and the properties of voltage-gated K+ channels in patients with chronic heart rhythm abnormalities, as well as in a variety of other myocardial disease states.

"These findings," Nerbonne said, "suggest that there are common pathways in a variety of cardiac diseases that lead to altered K+ channel expression and functioning. We would now like to define the underlying molecular mechanisms involved in mediating these changes and to identify means to reverse these changes to prevent rhythm disturbances and restore normal cardiac function."

In addition to her extensive research on the heart, Nerbonne also has pioneered investigations into the molecular basis of K+ channels in the central and peripheral nervous systems.

Nerbonne has received several honors and awards for her work, including an Established Investigator Award from the American Heart Association. She also is a Founding Fellow in Basic Cardiovascular Sciences of the American Heart Association.

While Nerbonne studies electrical communication between cells in the heart and the nervous system, Ornitz's work examines a form of chemical communication between developing cells throughout the body. He is known for his research on fibroblast growth factors (FGFs) -- a family of proteins that regulate cell development -- and FGF receptors -- proteins on the surface of cells onto which FGFs bind.

Early in his career, Ornitz identified a molecule that could trigger FGFs to communicate with cells. He also began examining and cataloguing the differences between the 22 known FGFs, a project more than half complete at present.

In exploring the unique roles of each FGF, Ornitz has identified several critical developmental functions. For example, a mutation in FGF receptor 3 appears to cause the most common form of human dwarfism, achondroplasia. This was the first growth factor mutation found to decrease growth. The receptor also seems to be involved in inner ear development.

Ornitz's team also discovered that FGF9 is linked to lung development and gender differentiation. Two other growth factors, FGF17 and FGF14, appear to be involved in the development of the central nervous system. Surprisingly, mice that lack FGF14 are anatomically normal but have severe behavioral problems, particularly in the coordination and use of muscles. His most recent work identified FGF18 as a regulator of embryonic bone growth.

"I plan to continue this research into the role of FGFs in development," Ornitz said. "This research is critical for understanding the cause of a wide array of developmental disorders, including those that affect the central nervous system, the lungs, the skeleton and the cardiovascular system."