Recent advances in molecular biology and channel biophysics hold the promise of providing quantitative mechanisms for normal and abnormal cardiac electrical activity. However, the information from the new molecular technology has not been integrated into mathematical models of normal and abnormal electrical activity in the heart. This talk will examine the emerging problem of how to utilize data at the molecular and biophysical levels concerning the properties of K⁺ channels, how their time dependent characteristics are modified by drug binding and how such information can be integrated into cellular models with predictive value to be used for rational drug design.

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