My long term goals are solve basic science and clinically translational problems using integrative muscle physiology methods - e.g. from the molecule to in vivo. I am currently focused on researching the mechanisms that control cardiac relaxation and filling in order to improve our ability to diagnose diastolic diseases and determine how mechanisms can be modulated to improve cardiac performance. (Link to all of my Pubmed indexed articles)
I've come to the Campbell Muscle Lab to 1) bring my experience in integrative physiology and diastolic function to seek sarcomere level therapies for heart failures and 2) learn from and leverage the Campbell Muscle Lab expertise in crossbridge kinetics and modeling.
With these interests and experience, I am currently pursing transmural measurements of calcium and sarcomere lengths in unloaded cardiomyocytes. I also have a new line of research that upends the current dogma that afterload "controls" diastolic relaxation. These new experiments in loaded myocytes, trabeculae, and in vivo show that myocardial relengthening is essential in the control of relaxation.
My graduate Studies focused on physical and kinematic characterization of diastolic function. My major findings showed how many diastolic parameters from transmitral Doppler echocardiography (DT, Emax, etc) are heart rate independent and this is predicted by a damped-harmonic oscillator model of the ventricle. Furthermore, the isovolumic relaxation phase is better characterized by a damped-harmonic oscillator model, rather than the monoexponential (tau) and logistic function models of isovolumic relaxation. This work utilized clinical echocardiographic and pressure-volume data to confirm predictions made by the physical models. Pubmed my work with Sandor J Kovacs, PhD MD at Washington University in St Louis
I have postdoctoral experience in integrative physiology, translating the cellular and molecular function of the giant protein Titin to in vivo function. My major contributions describe how titin based viscosity and stiffness translate from sarcomeric function to reveal themselves in vivo. This work primarily utilized biological models of altered passive tension and titin isoform expression to study integrative physiology. Pubmed my work with Henk L Granzier, PhD at The University of Arizona
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