@article {Simula.SC.448,
	title = {Electrotonic Coupling Between Human Atrial Myocytes and Fibroblasts Alters Excitability and Repolarization},
	journal = {Biophysical Journal},
	volume = {97},
	number = {8},
	year = {2009},
	month = {October},
	pages = {2179-2190},
	abstract = {Atrial fibrosis has been implicated in the development and maintenance of atrial arrhythmias, and is characterized by expansion of the extracellular matrix and an increased number of fibroblasts (Fbs). Electrotonic coupling between atrial myocytes and Fbs may contribute to the formation of an arrhythmogenic substrate. However, the role of these cell-cell interactions in the function of both normal and diseased atria remains poorly understood. The goal of this study was to gain mechanistic insight into the role of electrotonic Fb-myocyte coupling on myocyte excitability and repolarization. To represent the system, a human atrial myocyte (hAM) coupled to a variable number of Fbs, we employed a new ionic model of the hAM, and a variety of membrane representations for atrial Fbs. Simulations elucidated the effects of altering the intercellular coupling conductance, electrophysiological Fb properties, and stimulation rate on the myocyte action potential. The results demonstrate that the myocyte resting potential and action potential waveform are modulated strongly by the properties and number of coupled Fbs, the degree of coupling, and the pacing frequency. Our model provides mechanistic insight into the consequences of heterologous cell coupling on hAM electrophysiology, and can be extended to evaluate these implications at both tissue and organ levels.},
	author = {Maleckar, Molly and Joseph L. {Greenstein} and Wayne R. {Giles} and Natalia A. {Trayanova}}
}
@article {Simula.SC.450,
	title = {K+ Current Changes Account for the Rate Dependence of the Action Potential in the Human Atrial Myocyte},
	journal = {American Journal of Physiology - Heart and Circulatory Physiology},
	volume = {297},
	number = {4},
	year = {2009},
	note = {Should be listed in 2010 Annual Report},
	month = {October},
	pages = {1398-1410},
	abstract = {Ongoing investigation of the electrophysiology and pathophysiology of the human atria requires an accurate representation of the membrane dynamics of the human atrial myocyte. However, existing models of the human atrial myocyte action potential do not accurately reproduce experimental observations with respect to the kinetics of key repolarizing currents or rate dependence of the action potential and fail to properly enforce charge conservation, an essential characteristic in any model of the cardiac membrane. In addition, recent advances in experimental methods have resulted in new data regarding the kinetics of repolarizing currents in the human atria. The goal of this study was to develop a new model of the human atrial action potential, based on the Nygren et al. model of the human atrial myocyte and newly available experimental data, that ensures an accurate representation of repolarization processes and reproduction of action potential rate dependence and enforces charge conservation. Specifically, the transient outward K(+) current (I(t)) and ultrarapid rectifier K(+) current (I(Kur)) were newly formulated. The inwardly recitifying K(+) current (I(K1)) was also reanalyzed and implemented appropriately. Simulations of the human atrial myocyte action potential with this new model demonstrated that early repolarization is dependent on the relative conductances of I(t) and I(Kur), whereas densities of both I(Kur) and I(K1) underlie later repolarization. In addition, this model reproduces experimental measurements of rate dependence of I(t), I(Kur), and action potential duration. This new model constitutes an improved representation of excitability and repolarization reserve in the human atrial myocyte and, therefore, provides a useful computational tool for future studies involving the human atrium in both health and disease.},
	author = {Maleckar, Molly and Joseph L. {Greenstein} and Wayne R. {Giles} and Natalia A. {Trayanova}}
}
@misc {Simula.SC.540,
	title = {Coupling of Human Atrial Myocytes and Myofibroblasts Can Lead to Conduction Disturbances},
	howpublished = {HRS Scientific Sessions 2008},
	year = {2008},
	month = {May},
	author = {Maleckar, Molly and Joseph L. {Greenstein} and Wayne R. {Giles} and Natalia A. {Trayanova}}
}
@article {Simula.SC.452,
	title = {Mathematical Simulations of Ligand-Gated and Specific Cell-Type Effects in the Human Atrium},
	journal = {Progress in Biophysics and Molecular Biology},
	volume = {98},
	number = {2-3},
	year = {2008},
	pages = {161-70},
	author = {Maleckar, Molly and Joseph L. {Greenstein} and Natalia A. {Trayanova} and Wayne R. {Giles}}
}
