Browsing by Author "Frazier III, Eric"
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Item Impact of Calcium Store Overload and Electrical Dynamics on Cardiac Myocytes(2015) Alexander, Amanda M.; DeNardo, Erin K.; Frazier III, Eric; McCauley, Michael; Rojina, Nicholas; Coulibaly, Zana; Peercy, Bradford E.; Izu, Leighton T.The heart's main function of pumping blood to the body is a complicated process separated into two major steps. Initially, the heart is relaxed and blood flows freely into the ventricles and atria from the veins, then the atria contracts and pumps more blood to the ventricles. The atria relaxes and the inlet valves between these and the ventricles close, producing the initial thump of the heartbeat, as pressure builds while the ventricles contract. This pressure also forces the outlet valves open, allowing blood to ow into the arteries and aorta. As the ventricles relax, the outlet valves then close, producing the second thump of the heartbeat. Once the atria and ventricles are relaxed, the inlet valves reopen, allowing the compartments to ll with blood again as the process repeats. If the heart's contractile abilities are impaired in any way, the rest of the body cannot perform properly. Despite advances in cardiology research, cardiac arrhythmia remains an influential cause of morbidity and mortality in the United States. Recent advances involve the application of devices, such as pacemakers or de brillators, and the outlook of antiarrhythmic drug therapy up to this point is grim, so it is necessary to understand how some pathological conditions within cardiac myocytes can lead to dysfunction of these cells. Calcium mishandling can play a major role in disruption of overall cardiac function by preventing the ability of the heart muscles to relax between heartbeats and thus impair their pumping blood to the bodyItem Spontaneous Calcium Release in Cardiac Myocytes: Store Overload and Electrical Dynamics(Illinois State University, 2015) Alexander, Amanda M.; DeNardo, Erin K.; Frazier III, Eric; McCauley, Michael; Rojina, Nicholas; Coulibaly, Zana; Peercy, Bradford E.; Izu, Leighton T.Heart disease is the leading cause of mortality in the United States. One cause of heart arrhythmia is calcium (Ca²⁺) mishandling in cardiac muscle cells. We adapt Izu's et al. mathematical reaction-diffusion model of calcium in cardiac muscle cells, or cardiomyocytes, [14], implemented by Gobbert [12], and analyzed in Coulibaly et al. [8] to include calcium being released from the sarcoplasmic reticulum (SR), the effects of buffers in the SR, particularly calsequestrin, and the effects of Ca²⁺ influx due to voltage across the cell membrane. Based on simulations of the model implemented in parallel using MPI, our findings aligned with known biological models and principles, giving us a thorough understanding of several factors that influence Ca²⁺ dynamics in cardiac myocytes. Speci cally, dynamic calcium store will cap previous calcium blow-up seen in the model. Calcium channels located in spatial opposition of calcium release units produce more predictable intracellular calcium propagation. And we used multi-parametric calcium dynamics tables, which act as a multidimensional bifurcation diagram, to visualize parameter boundaries between different biophysical dynamics.