Starmer, Frank C

Research Interests:

Though trained formally as an electrical engineer, Eugene Stead talked me into starting my career in the Cardiology Division of the Department of Medicine at Duke. My first research project was to explore the nature of electically induced ventricular fibrillation which introduced me to reentrant cardiac arrhythmias. Though VF is complex, this work ignited my curioisity about the underlying nature of cellular communication - whether electrical via gap junctions or chemical via ligand-receptor interactions. Along the way, I found myself developing the computational infrastructure for the Cardiology Databank, starting the Computer Science Department and eventually finding my way to the laboratory.

With my long term collaborator, Augustus Grant, we explored single cardiac ion channels, drug interactions with cardiac ion channels and found ourselves returning to my initial interests in reentrant cardiac arrhythmias, in this case, induced by drug-channel interactions. Our first serious computational model was characterizing use-dependent ion channel blockade using basic chemical processes. With models of cardiac cells we identified both numerically and with in vitro experiments, the determinants of the cardiac vulnerable period. In our hands, computational biology provided us a unique look at underlying modeled processes in contrast to laboratory investigations where much was hidden.

Work with Valentin Krinsky in his autowave laboratory in Pushchino Russia introduced me to the concept of generic properties of excitable media. Since then I have focused on identifying minimally complex models of biological processes, primarly as a tool for exporing how added complexity modulates the underlying generic behavior. For me, identifying the minmally complex physical basis of generic biological processes (e.g. excitation, propagation, ligand-receptor binding and transporters) via computational and experimental models is simply great fun.

Selected Publications:

Starmer, CF. The role of intrinsic and induced vulnerability in electrically induced cardiac arrhythmias. J. Cardiovas. Electrophysiol. 2006 17:1369-70.

Starmer CF, Colatsky TJ, Grant AO. What happens when cardiac Na channels lose their function? 1--numerical studies of the vulnerable period in tissue expressing mutant channels. Cardiovasc Res. 2003 Jan;57(1):82-91

Ivashikina, N.V., Sokolov, O.A. and Starmer, C.F. Modeling nitrate absorption in maize seedlings. Agrochemistry 2001 7:10-17 (in Russian)

Starobin JM, Starmer CF. Boundary-layer analysis of waves propagating in an excitable medium: Medium conditions for wave-front-obstacle separation. Phys. Rev. E.P 1996 Jul;54(1):430-437

Starmer CF, Romashko DN, Reddy RS, Zilberter YI, Starobin J, Grant AO, Krinsky VI. Proarrhythmic response to potassium channel blockade. Numerical studies of polymorphic tachyarrhythmias. Circulation. 1995 Aug 1;92(3):595-605

Starmer CF, Lastra AA, Nesterenko VV, Grant AO. Proarrhythmic response to sodium channel blockade. Theoretical model and numerical experiments. Circulation. 1991 Sep;84(3):1364-77.

Starmer CF. Characterizing activity-dependent processes with a piecewise exponential model. Biometrics. 1988 Jun;44(2):549-59.

Starmer CF, Grant AO. Phasic ion channel blockade. A kinetic model and parameter estimation procedure. Mol Pharmacol. 1985 Oct;28(4):348-56.

Sperling O, Wyngaarden JB, Starmer CF. The kinetics of intramolecular distribution of 15N in uric acid after administration of (15N) glycine. A reappraisal of the significance of preferential labeling of N-(3+9) of uric acid in primary gout. J Clin Invest. Oct;52(10):2468-85.

Grizzle JE, Starmer CF, Koch GG. Analysis of categorical data by linear models. Biometrics. 1969 Sep;25(3):489-504.