My current focus involves the application of mathematical and engineering techniques to the analysis of physiologic processes. Of particular interest is the development of quantitative models that describe the behavior of neural and sensory systems and their associated pathology.

The cochlea is the organ responsible for transduction of acoustic to biologic signals. The cochlea is divided into three isolated compartments: an endolymphatic compartment containing a high concentration of potassium, and two surrounding perilymphatic compartments with relatively low potassium concentration. Experimental evidence shows that proper function of the cochlea depends on the circulation of potassium ions between cochlear compartments and the establishment of precise potassium gradients. Mutations in genes encoding potassium channel proteins and gap junctions can lead to genetic, non-syndromic forms of hearing loss. To date, no comprehensive model of cochlear potassium transport exists. I have chosen to make computational modeling of potassium transport in the cochlea the topic of my dissertation. Establishing a computational model for potassium cycling in the cochlea will elucidate mechanisms of deafness, and will aid in the development of various approaches for treating hearing loss. The model will also enable us to explore unknown deficits by allowing simulation of other channel deficiencies, which will streamline future research efforts in this field by suggesting specific gene targets to investigate.

This research will involve a combination of compartmental modeling of ion transport and analysis of the differential equations governing cochlear electrophysiology. The bulk of our initial parameters for the model will come from the wealth of published experimental data obtained from voltage-clamped cells. Given the coupled, non-linear differential relationships that describe channel behavior in a given cell, an accurate model of the cochlear potassium cycle will be computationally intensive.