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Journal articles on the topic 'Electrophysiology - Mathematical models'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 January 2023

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1

Amuzescu, Bogdan, Razvan Airini, Florin Bogdan Epureanu, Stefan A. Mann, Thomas Knott, and Beatrice Mihaela Radu. "Evolution of mathematical models of cardiomyocyte electrophysiology." Mathematical Biosciences 334 (April 2021): 108567. http://dx.doi.org/10.1016/j.mbs.2021.108567.

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2

Johnstone, Ross, Rémi Bardenet, Teun de Boer, et al. "Cell-specific mathematical models of cardiac electrophysiology." Journal of Pharmacological and Toxicological Methods 81 (September 2016): 343. http://dx.doi.org/10.1016/j.vascn.2016.02.029.

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3

Linge, S., J. Sundnes, M. Hanslien, G. T. Lines, and A. Tveito. "Numerical solution of the bidomain equations." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 367, no. 1895 (2009): 1931–50. http://dx.doi.org/10.1098/rsta.2008.0306.

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Knowledge of cardiac electrophysiology is efficiently formulated in terms of mathematical models. However, most of these models are very complex and thus defeat direct mathematical reasoning founded on classical and analytical considerations. This is particularly so for the celebrated bidomain model that was developed almost 40 years ago for the concurrent analysis of extra- and intracellular electrical activity. Numerical simulations based on this model represent an indispensable tool for studying electrophysiology. However, complex mathematical models, steep gradients in the solutions and co

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4

Lines, G. T., M. L. Buist, P. Grottum, A. J. Pullan, J. Sundnes, and A. Tveito. "Mathematical models and numerical methods for the forward problem in cardiac electrophysiology." Computing and Visualization in Science 5, no. 4 (2002): 215–39. http://dx.doi.org/10.1007/s00791-003-0101-4.

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5

Cherry, Elizabeth M., and Flavio H. Fenton. "A tale of two dogs: analyzing two models of canine ventricular electrophysiology." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (2007): H43—H55. http://dx.doi.org/10.1152/ajpheart.00955.2006.

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The extensive development of detailed mathematical models of cardiac myocyte electrophysiology in recent years has led to a proliferation of models, including many that model the same animal species and specific region of the heart and thus would be expected to have similar properties. In this paper we review and compare two recently developed mathematical models of the electrophysiology of canine ventricular myocytes. To clarify their similarities and differences, we also present studies using them in a range of preparations from single cells to two-dimensional tissue. The models are compared

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6

Jacquemet, Vincent. "Steady-state solutions in mathematical models of atrial cell electrophysiology and their stability." Mathematical Biosciences 208, no. 1 (2007): 241–69. http://dx.doi.org/10.1016/j.mbs.2006.10.007.

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7

Carlu, M., O. Chehab, L. Dalla Porta, et al. "A mean-field approach to the dynamics of networks of complex neurons, from nonlinear Integrate-and-Fire to Hodgkin–Huxley models." Journal of Neurophysiology 123, no. 3 (2020): 1042–51. http://dx.doi.org/10.1152/jn.00399.2019.

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Population models are a powerful mathematical tool to study the dynamics of neuronal networks and to simulate the brain at macroscopic scales. We present a mean-field model capable of quantitatively predicting the temporal dynamics of a network of complex spiking neuronal models, from Integrate-and-Fire to Hodgkin–Huxley, thus linking population models to neurons electrophysiology. This opens a perspective on generating biologically realistic mean-field models from electrophysiological recordings.

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Collin, Annabelle, and Sébastien Imperiale. "Mathematical analysis and 2-scale convergence of a heterogeneous microscopic bidomain model." Mathematical Models and Methods in Applied Sciences 28, no. 05 (2018): 979–1035. http://dx.doi.org/10.1142/s0218202518500264.

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The aim of this paper is to provide a complete mathematical analysis of the periodic homogenization procedure that leads to the macroscopic bidomain model in cardiac electrophysiology. We consider space-dependent and tensorial electric conductivities as well as space-dependent physiological and phenomenological nonlinear ionic models. We provide the nondimensionalization of the bidomain equations and derive uniform estimates of the solutions. The homogenization procedure is done using 2-scale convergence theory which enables us to study the behavior of the nonlinear ionic models in the homogen

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Corre, S., and A. Belmiloudi. "Coupled lattice Boltzmann simulation method for bidomain type models in cardiac electrophysiology with multiple time-delays." Mathematical Modelling of Natural Phenomena 14, no. 2 (2019): 207. http://dx.doi.org/10.1051/mmnp/2019045.

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In this work, we propose a mathematical model of the cardiac electrophysiology which take into account time delays in signal transmission, in order to capture the whole activities of macro- to micro-scale transport processes, and use this model to analyze the propagation of electrophysiological waves in the heart by using a developed coupling Lattice Boltzmann Method (LBM). The propagation of electrical activity in the heart is mathematically modeled by a modified bidomain system. As transmembrane potential evolves, the domain has anisotropical properties which are transposed into intracellula

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10

Lei, Chon Lok, Sanmitra Ghosh, Dominic G. Whittaker, et al. "Considering discrepancy when calibrating a mechanistic electrophysiology model." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 378, no. 2173 (2020): 20190349. http://dx.doi.org/10.1098/rsta.2019.0349.

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Uncertainty quantification (UQ) is a vital step in using mathematical models and simulations to take decisions. The field of cardiac simulation has begun to explore and adopt UQ methods to characterize uncertainty in model inputs and how that propagates through to outputs or predictions; examples of this can be seen in the papers of this issue. In this review and perspective piece, we draw attention to an important and under-addressed source of uncertainty in our predictions—that of uncertainty in the model structure or the equations themselves. The difference between imperfect models and real

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11

SACHSE, FRANK B., GUNNAR SEEMANN, MATTHIAS B. MOHR, and ARUN V. HOLDEN. "MATHEMATICAL MODELING OF CARDIAC ELECTRO-MECHANICS: FROM PROTEIN TO ORGAN." International Journal of Bifurcation and Chaos 13, no. 12 (2003): 3747–55. http://dx.doi.org/10.1142/s0218127403008910.

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Mathematical models of cardiac anatomy and physics provide information, which help to understand structure and behavior of the heart. Miscellaneous cardiac phenomena can only be adequately described by combination of models representing different aspects or levels of detail. Coupling of these models necessitates the definition of appropriate interfaces. Adequateness and efficiency of interfaces is crucial for efficient application of the combined models. In this work an integrated model is presented consisting of several models interconnected by interfaces. The integrated model allows the reco

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12

REINERTH, G. "P1567 Simulation of cardiac electrophysiology using mathematical models and computer based processing of digital image data." European Heart Journal 24, no. 5 (2003): 285. http://dx.doi.org/10.1016/s0195-668x(03)94705-1.

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13

HANCOX, JULES C., KATHRYN H. YUILL, JOHN S. MITCHESON, and MARY K. CONVERY. "PROGRESS AND GAPS IN UNDERSTANDING THE ELECTROPHYSIOLOGICAL PROPERTIES OF MORPHOLOGICALLY NORMAL CELLS FROM THE CARDIAC ATRIOVENTRICULAR NODE." International Journal of Bifurcation and Chaos 13, no. 12 (2003): 3675–91. http://dx.doi.org/10.1142/s021812740300879x.

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The atrioventricular node (AVN) is a small but critically important component of the cardiac electrical conduction system and is located at the junction between right atrium and right ventricle of the heart. It plays important roles in normal and abnormal impulse propagation. Mathematical models of the conduction properties of the AVN have been made, but detailed in silico reconstruction of AVN electrophysiology lags behind that of other cardiac regions. One important facet of detailed reconstruction of AVN electrical activity is the development of comprehensive, ionic conductance-based models

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Rudy, Yoram, and Jonathan R. Silva. "Computational biology in the study of cardiac ion channels and cell electrophysiology." Quarterly Reviews of Biophysics 39, no. 1 (2006): 57–116. http://dx.doi.org/10.1017/s0033583506004227.

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1. Prologue 582. The Hodgkin–Huxley formalism for computing the action potential 592.1 The axon action potential model 592.2 Cardiac action potential models 623. Ion-channel based formulation of the action potential 653.1 Ion-channel structure 653.2 Markov models of ion-channel kinetics 663.3 Role of selected ion channels in rate dependence of the cardiac action potential 713.4 Physiological implications of IKs subunit interaction 773.5 Mechanism of cardiac action potential rate-adaptation is species dependent 784. Simulating ion-channel mutations and their electrophysiological consequences 81

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Drovandi, C. C., N. Cusimano, S. Psaltis, et al. "Sampling methods for exploring between-subject variability in cardiac electrophysiology experiments." Journal of The Royal Society Interface 13, no. 121 (2016): 20160214. http://dx.doi.org/10.1098/rsif.2016.0214.

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Between-subject and within-subject variability is ubiquitous in biology and physiology, and understanding and dealing with this is one of the biggest challenges in medicine. At the same time, it is difficult to investigate this variability by experiments alone. A recent modelling and simulation approach, known as population of models (POM), allows this exploration to take place by building a mathematical model consisting of multiple parameter sets calibrated against experimental data. However, finding such sets within a high-dimensional parameter space of complex electrophysiological models is

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Nickerson, David P., and Martin L. Buist. "A physiome standards-based model publication paradigm." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 367, no. 1895 (2009): 1823–44. http://dx.doi.org/10.1098/rsta.2008.0296.

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In this era of widespread broadband Internet penetration and powerful Web browsers on most desktops, a shift in the publication paradigm for physiome-style models is envisaged. No longer will model authors simply submit an essentially textural description of the development and behaviour of their model. Rather, they will submit a complete working implementation of the model encoded and annotated according to the various standards adopted by the physiome project, accompanied by a traditional human-readable summary of the key scientific goals and outcomes of the work. While the final published,

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17

Silva, Haroldo S., Adam Kapela, and Nikolaos M. Tsoukias. "A mathematical model of plasma membrane electrophysiology and calcium dynamics in vascular endothelial cells." American Journal of Physiology-Cell Physiology 293, no. 1 (2007): C277—C293. http://dx.doi.org/10.1152/ajpcell.00542.2006.

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Vascular endothelial cells (ECs) modulate smooth muscle cell (SMC) contractility, assisting in vascular tone regulation. Cytosolic Ca2+ concentration ([Ca2+]i) and membrane potential ( Vm) play important roles in this process by controlling EC-dependent vasoactive signals and intercellular communication. The present mathematical model integrates plasmalemma electrophysiology and Ca2+ dynamics to investigate EC responses to different stimuli and the controversial relationship between [Ca2+]i and Vm. The model contains descriptions for the intracellular balance of major ionic species and the rel

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18

Aziz, Muhamad H. N., and Radostin D. Simitev. "Estimation of Parameters for an Archetypal Model of Cardiomyocyte Membrane Potentials." International Journal Bioautomation 26, no. 3 (2022): 255–72. http://dx.doi.org/10.7546/ijba.2022.26.3.000832.

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Contemporary realistic mathematical models of single-cell cardiac electrical excitation are immensely detailed. Model complexity leads to parameter uncertainty, high computational cost and barriers to mechanistic understanding. There is a need for reduced models that are conceptually and mathematically simple but physiologically accurate. To this end, we consider an archetypal model of single-cell cardiac excitation that replicates the phase-space geometry of detailed cardiac models, but at the same time has a simple piecewise-linear form and a relatively low-dimensional configuration space. I

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19

Gerach, Tobias, Steffen Schuler, Jonathan Fröhlich, et al. "Electro-Mechanical Whole-Heart Digital Twins: A Fully Coupled Multi-Physics Approach." Mathematics 9, no. 11 (2021): 1247. http://dx.doi.org/10.3390/math9111247.

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Mathematical models of the human heart are evolving to become a cornerstone of precision medicine and support clinical decision making by providing a powerful tool to understand the mechanisms underlying pathophysiological conditions. In this study, we present a detailed mathematical description of a fully coupled multi-scale model of the human heart, including electrophysiology, mechanics, and a closed-loop model of circulation. State-of-the-art models based on human physiology are used to describe membrane kinetics, excitation-contraction coupling and active tension generation in the atria a

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20

Li, Xiang, Ji-qian Zhang, and Jian-wei Shuai. "Isoprenaline: A Potential Contributor in Sick Sinus Syndrome—Insights from a Mathematical Model of the Rabbit Sinoatrial Node." Scientific World Journal 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/540496.

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The mechanism of isoprenaline exerting its effects on cardiac pacemaking and driving in sick sinus syndrome is controversial and unresolved. In this paper, mathematical models for rabbit sinoatrial node cells were modified by incorporating equations for the known dose-dependent actions of isoprenaline on various ionic channel currents, the intracellular Ca2+transient, andiNachanges induced by SCN5A gene mutations; the cell models were also incorporated into an intact SAN-atrium model of the rabbit heart that is based on both heterogeneities of the SAN electrophysiology and histological structu

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Hendrix, Maurice, Michael Clerx, Asif U. Tamuri, et al. "cellmlmanip and chaste_codegen: automatic CellML to C++ code generation with fixes for singularities and automatically generated Jacobians." Wellcome Open Research 6 (June 15, 2022): 261. http://dx.doi.org/10.12688/wellcomeopenres.17206.2.

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Hundreds of different mathematical models have been proposed for describing electrophysiology of various cell types. These models are quite complex (nonlinear systems of typically tens of ODEs and sometimes hundreds of parameters) and software packages such as the Cancer, Heart and Soft Tissue Environment (Chaste) C++ library have been designed to run simulations with these models in isolation or coupled to form a tissue simulation. The complexity of many of these models makes sharing and translating them to new simulation environments difficult. CellML is an XML format that offers a widely-ad

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22

Fink, Martin, Wayne R. Giles, and Denis Noble. "Contributions of inwardly rectifying K + currents to repolarization assessed using mathematical models of human ventricular myocytes." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 364, no. 1842 (2006): 1207–22. http://dx.doi.org/10.1098/rsta.2006.1765.

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Repolarization of the action potential (AP) in cardiac muscle is a major determinant of refractoriness and excitability, and can also strongly modulate excitation–contraction coupling. In clinical cardiac electrophysiology, the Q-T interval, and hence action potential duration, is both an essential marker of normal function and an indicator of risk for arrhythmic events. It is now well known that the termination of the plateau phase of the AP and the repolarization waveform involve a complex interaction of transmembrane ionic currents. These include a slowly inactivating Na + current, inactiva

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Hendrix, Maurice, Michael Clerx, Asif U. Tamuri, et al. "chaste codegen: automatic CellML to C++ code generation with fixes for singularities and automatically generated Jacobians." Wellcome Open Research 6 (October 12, 2021): 261. http://dx.doi.org/10.12688/wellcomeopenres.17206.1.

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Hundreds of different mathematical models have been proposed for describing electrophysiology of various cell types. These models are quite complex (nonlinear systems of typically tens of ODEs and sometimes hundreds of parameters) and software packages such as the Cancer, Heart and Soft Tissue Environment (Chaste) C++ library have been designed to run simulations with these models in isolation or coupled to form a tissue simulation. The complexity of many of these models makes sharing and translating them to new simulation environments difficult. CellML is an XML format that offers a solution

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Edwards, Andrew G., and William E. Louch. "Species-Dependent Mechanisms of Cardiac Arrhythmia: A Cellular Focus." Clinical Medicine Insights: Cardiology 11 (January 1, 2017): 117954681668606. http://dx.doi.org/10.1177/1179546816686061.

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Although ventricular arrhythmia remains a leading cause of morbidity and mortality, available antiarrhythmic drugs have limited efficacy. Disappointing progress in the development of novel, clinically relevant antiarrhythmic agents may partly be attributed to discrepancies between humans and animal models used in preclinical testing. However, such differences are at present difficult to predict, requiring improved understanding of arrhythmia mechanisms across species. To this end, we presently review interspecies similarities and differences in fundamental cardiomyocyte electrophysiology and c

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Romero, Lucía, Esther Pueyo, Martin Fink, and Blanca Rodríguez. "Impact of ionic current variability on human ventricular cellular electrophysiology." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 4 (2009): H1436—H1445. http://dx.doi.org/10.1152/ajpheart.00263.2009.

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Abnormalities in repolarization and its rate dependence are known to be related to increased proarrhythmic risk. A number of repolarization-related electrophysiological properties are commonly used as preclinical biomarkers of arrhythmic risk. However, the variability and complexity of repolarization mechanisms make the use of cellular biomarkers to predict arrhythmic risk preclinically challenging. Our goal is to investigate the role of ionic current properties and their variability in modulating cellular biomarkers of arrhythmic risk to improve risk stratification and identification in human

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Kügler, Philipp. "Modelling and Simulation for Preclinical Cardiac Safety Assessment of Drugs with Human iPSC-Derived Cardiomyocytes." Jahresbericht der Deutschen Mathematiker-Vereinigung 122, no. 4 (2020): 209–57. http://dx.doi.org/10.1365/s13291-020-00218-w.

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Abstract As a potentially life threatening side effect, pharmaceutical compounds may trigger cardiac arrhythmias by impeding the heart’s electrical and mechanical function. For this reason, any new compound needs to be tested since 2005 for its proarrhythmic risk both during the preclinical and the clinical phase of the drug development process. While intensive monitoring of cardiac activity during clinical tests with human volunteers constitutes a major cost factor, preclinical in vitro tests with non cardiac cells and in vivo tests with animals are currently under serious debate because of t

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Pan, Michael, Peter J. Gawthrop, Kenneth Tran, Joseph Cursons, and Edmund J. Crampin. "Bond graph modelling of the cardiac action potential: implications for drift and non-unique steady states." Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences 474, no. 2214 (2018): 20180106. http://dx.doi.org/10.1098/rspa.2018.0106.

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Mathematical models of cardiac action potentials have become increasingly important in the study of heart disease and pharmacology, but concerns linger over their robustness during long periods of simulation, in particular due to issues such as model drift and non-unique steady states. Previous studies have linked these to violation of conservation laws, but only explored those issues with respect to charge conservation in specific models. Here, we propose a general and systematic method of identifying conservation laws hidden in models of cardiac electrophysiology by using bond graphs, and de

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Rasmusson, R. L., J. W. Clark, W. R. Giles, E. F. Shibata, and D. L. Campbell. "A mathematical model of a bullfrog cardiac pacemaker cell." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 2 (1990): H352—H369. http://dx.doi.org/10.1152/ajpheart.1990.259.2.h352.

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Previous models of cardiac cellular electrophysiology have been based largely on voltage-clamp measurements obtained from multicellular preparations and often combined data from different regions of the heart and a variety of species. We have developed a model of cardiac pacemaking based on a comprehensive set of voltage-clamp measurements obtained from single cells isolated from one specific tissue type, the bullfrog sinus venosus (SV). Consequently, sarcolemmal current densities and kinetics are not influenced by secondary phenomena associated with multicellular preparations, allowing us to

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O'Hara, Thomas, and Yoram Rudy. "Quantitative comparison of cardiac ventricular myocyte electrophysiology and response to drugs in human and nonhuman species." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 5 (2012): H1023—H1030. http://dx.doi.org/10.1152/ajpheart.00785.2011.

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Explanations for arrhythmia mechanisms at the cellular level are usually based on experiments in nonhuman myocytes. However, subtle electrophysiological differences between species may lead to different rhythmic or arrhythmic cellular behaviors and drug response given the nonlinear and highly interactive cellular system. Using detailed and quantitatively accurate mathematical models for human, dog, and guinea pig ventricular action potentials (APs), we simulated and compared cell electrophysiology mechanisms and response to drugs. Under basal conditions (absence of β-adrenergic stimulation), N

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UGARTE, JUAN P., CATALINA TOBÓN, ANTÓNIO M. LOPES, and J. A. TENREIRO MACHADO. "A COMPLEX ORDER MODEL OF ATRIAL ELECTRICAL PROPAGATION FROM FRACTAL POROUS CELL MEMBRANE." Fractals 28, no. 06 (2020): 2050106. http://dx.doi.org/10.1142/s0218348x20501066.

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Cardiac tissue is characterized by structural and cellular heterogeneities that play an important role in the cardiac conduction system. Under persistent atrial fibrillation (persAF), electrical and structural remodeling occur simultaneously. The classical mathematical models of cardiac electrophysiological showed remarkable progress during recent years. Among those models, it is of relevance the standard diffusion mathematical equation, that considers the myocardium as a continuum. However, the modeling of structural properties and their influence on electrical propagation still reveal severa

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Heijman, Jordi, Henry Sutanto, Harry J. G. M. Crijns, Stanley Nattel, and Natalia A. Trayanova. "Computational models of atrial fibrillation: achievements, challenges, and perspectives for improving clinical care." Cardiovascular Research 117, no. 7 (2021): 1682–99. http://dx.doi.org/10.1093/cvr/cvab138.

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Abstract Despite significant advances in its detection, understanding and management, atrial fibrillation (AF) remains a highly prevalent cardiac arrhythmia with a major impact on morbidity and mortality of millions of patients. AF results from complex, dynamic interactions between risk factors and comorbidities that induce diverse atrial remodelling processes. Atrial remodelling increases AF vulnerability and persistence, while promoting disease progression. The variability in presentation and wide range of mechanisms involved in initiation, maintenance and progression of AF, as well as its a

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32

Doste, Ruben, та Alfonso Bueno-Orovio. "Multiscale Modelling of β-Adrenergic Stimulation in Cardiac Electromechanical Function". Mathematics 9, № 15 (2021): 1785. http://dx.doi.org/10.3390/math9151785.

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β-adrenergic receptor stimulation (β-ARS) is a physiological mechanism that regulates cardiovascular function under stress conditions or physical exercise. Triggered during the so-called “fight-or-flight” response, the activation of the β-adrenergic receptors located on the cardiomyocyte membrane initiates a phosphorylation cascade of multiple ion channel targets that regulate both cellular excitability and recovery and of different proteins involved in intracellular calcium handling. As a result, β-ARS impacts both the electrophysiological and the mechanical response of the cardiomyocyte. β-A

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Li, L., S. A. Niederer, W. Idigo, et al. "A mathematical model of the murine ventricular myocyte: a data-driven biophysically based approach applied to mice overexpressing the canine NCX isoform." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 4 (2010): H1045—H1063. http://dx.doi.org/10.1152/ajpheart.00219.2010.

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Mathematical modeling of Ca2+ dynamics in the heart has the potential to provide an integrated understanding of Ca2+-handling mechanisms. However, many previous published models used heterogeneous experimental data sources from a variety of animals and temperatures to characterize model parameters and motivate model equations. This methodology limits the direct comparison of these models with any particular experimental data set. To directly address this issue, in this study, we present a biophysically based model of Ca2+ dynamics directly fitted to experimental data collected in left ventricu

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Parikh, Jaimit, Adam Kapela та Nikolaos M. Tsoukias. "Can endothelial hemoglobin-α regulate nitric oxide vasodilatory signaling?" American Journal of Physiology-Heart and Circulatory Physiology 312, № 4 (2017): H854—H866. http://dx.doi.org/10.1152/ajpheart.00315.2016.

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We used mathematical modeling to investigate nitric oxide (NO)-dependent vasodilatory signaling in the arteriolar wall. Detailed continuum cellular models of calcium (Ca2+) dynamics and membrane electrophysiology in smooth muscle and endothelial cells (EC) were coupled with models of NO signaling and biotransport in an arteriole. We used this theoretical approach to examine the role of endothelial hemoglobin-α (Hbα) as a modulator of NO-mediated myoendothelial feedback, as previously suggested in Straub et al. ( Nature 491: 473–477, 2012). The model considers enriched expression of inositol 1,

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González-González, Gabriela, Víctor M. Velasco-Herrera, and Alicia Ortega-Aguilar. "Use of Covariance Analysis in Electroencephalogram Reveals Abnormalities in Parkinson’s Disease." Applied Sciences 11, no. 20 (2021): 9633. http://dx.doi.org/10.3390/app11209633.

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Covariance analysis from wavelet data in electroencephalographic records (EEG) was, for the first time, applied in this study to unravel information contained in the standard EEG, which was previously not taken into consideration due to the mathematical models used. The methodology discussed here could be applied to any neurological condition, including the important early stages of neurodegenerative diseases. In this study, we analyzed EEG from control (CL) participants and participants with diagnosed Parkinson’s disease (PD), who were age-matched women in an eyes-closed resting state, to tes

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Guthrie, Sarah. "Anne Elizabeth Warner. 25 August 1940—16 May 2012." Biographical Memoirs of Fellows of the Royal Society 70 (March 10, 2021): 441–62. http://dx.doi.org/10.1098/rsbm.2020.0046.

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Anne Warner applied physiological techniques to developmental biology, elucidating the mechanisms of cell interaction and communication that pattern the early embryo. Through her determination and passion for science, she contributed crucial discoveries in the fields of muscle physiology, cellular differentiation and gap junction communication. She spent the majority of her career at University College London, which became her intellectual home and where she acquired a Royal Society Foulerton Research Professorship, becoming a highly respected and influential figure. In her work on gap junctio

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Quintanilla, Jorge G., Shlomo Shpun, José Jalife, and David Filgueiras-Rama. "Novel approaches to mechanism-based atrial fibrillation ablation." Cardiovascular Research 117, no. 7 (2021): 1662–81. http://dx.doi.org/10.1093/cvr/cvab108.

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Abstract Modern cardiac electrophysiology has reported significant advances in the understanding of mechanisms underlying complex wave propagation patterns during atrial fibrillation (AF), although disagreements remain. One school of thought adheres to the long-held postulate that AF is the result of randomly propagating wavelets that wonder throughout the atria. Another school supports the notion that AF is deterministic in that it depends on a small number of high-frequency rotors generating three-dimensional scroll waves that propagate throughout the atria. The spiralling waves are thought

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Almassy, Janos, Jong Hak Won, Ted B. Begenisich, and David I. Yule. "Apical Ca2+-activated potassium channels in mouse parotid acinar cells." Journal of General Physiology 139, no. 2 (2012): 121–33. http://dx.doi.org/10.1085/jgp.201110718.

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Ca2+ activation of Cl and K channels is a key event underlying stimulated fluid secretion from parotid salivary glands. Cl channels are exclusively present on the apical plasma membrane (PM), whereas the localization of K channels has not been established. Mathematical models have suggested that localization of some K channels to the apical PM is optimum for fluid secretion. A combination of whole cell electrophysiology and temporally resolved digital imaging with local manipulation of intracellular [Ca2+] was used to investigate if Ca2+-activated K channels are present in the apical PM of par

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Nickerson, D. P., A. Corrias, and M. L. Buist. "Reference descriptions of cellular electrophysiology models." Bioinformatics 24, no. 8 (2008): 1112–14. http://dx.doi.org/10.1093/bioinformatics/btn080.

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Groenendaal, Willemijn, Francis A. Ortega, Armen R. Kherlopian, Andrew C. Zygmunt, Trine Krogh-Madsen, and David J. Christini. "Cell-Specific Cardiac Electrophysiology Models." PLOS Computational Biology 11, no. 4 (2015): e1004242. http://dx.doi.org/10.1371/journal.pcbi.1004242.

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Izhikevich, Eugene M. "Hybrid spiking models." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 368, no. 1930 (2010): 5061–70. http://dx.doi.org/10.1098/rsta.2010.0130.

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I review a class of hybrid models of neurons that combine continuous spike-generation mechanisms and a discontinuous ‘after-spike’ reset of state variables. Unlike Hodgkin–Huxley-type conductance-based models, the hybrid spiking models have a few parameters derived from the bifurcation theory; instead of matching neuronal electrophysiology, they match neuronal dynamics. I present a method of after-spike resetting suitable for hardware implementation of such models, and a hybrid numerical method for simulations of large-scale biological spiking networks.

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Öğmen, H. "On the Mechanisms Underlying Directional Selectivity." Neural Computation 3, no. 3 (1991): 333–49. http://dx.doi.org/10.1162/neco.1991.3.3.333.

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Recent efforts in the understanding of motion detection and directional selectivity include electrophysiological studies using single photoreceptor stimulations and a combination of electrophysiology and neuropharmacology. Results of the former have been interpreted in favor of facilitator motion detection models while results of the latter have been interpreted in favor of inhibitory models. In this paper, this conflicting data interpretation problem is addressed by mathematically modeling some effects of neuropharmacological substances and by applying this formalism to a neural network model

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Clayton, Richard H., Yasser Aboelkassem, Chris D. Cantwell, et al. "An audit of uncertainty in multi-scale cardiac electrophysiology models." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 378, no. 2173 (2020): 20190335. http://dx.doi.org/10.1098/rsta.2019.0335.

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Models of electrical activation and recovery in cardiac cells and tissue have become valuable research tools, and are beginning to be used in safety-critical applications including guidance for clinical procedures and for drug safety assessment. As a consequence, there is an urgent need for a more detailed and quantitative understanding of the ways that uncertainty and variability influence model predictions. In this paper, we review the sources of uncertainty in these models at different spatial scales, discuss how uncertainties are communicated across scales, and begin to assess their relati

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Roberts, Byron N., Pei-Chi Yang, Steven B. Behrens, Jonathan D. Moreno, and Colleen E. Clancy. "Computational approaches to understand cardiac electrophysiology and arrhythmias." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 7 (2012): H766—H783. http://dx.doi.org/10.1152/ajpheart.01081.2011.

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Cardiac rhythms arise from electrical activity generated by precisely timed opening and closing of ion channels in individual cardiac myocytes. These impulses spread throughout the cardiac muscle to manifest as electrical waves in the whole heart. Regularity of electrical waves is critically important since they signal the heart muscle to contract, driving the primary function of the heart to act as a pump and deliver blood to the brain and vital organs. When electrical activity goes awry during a cardiac arrhythmia, the pump does not function, the brain does not receive oxygenated blood, and

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Pongui Ngoma, D. V., V. D. Mabonzo, L. J. P. Gomat, G. Nguimbi, and B. B. Bamvi Madzou. "PARAMETER IDENTIFICATION PROBLEM TO FIND THE CARDIAC POTENTIAL WAVE FORM IN IONIC MODELS." Advances in Mathematics: Scientific Journal 11, no. 11 (2022): 991–1017. http://dx.doi.org/10.37418/amsj.11.11.2.

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In this paper, we have defined an optimization problem allowing to directly find the shape of the cardiac wave of some ionic models. This allowed us to compare some of these ionic models via a parameter identification problem instead of comparing them directly by plotting the graphs for given values of the parameters. Compared to the empirical methods used to adjust one or two parameters at a time encountered in electrophysiology, we believe that our parameter identification approach is reliable and able to simultaneously identify four to eleven parameters of an ionic model. Using this approac

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Crampin, Edmund J., Nicolas P. Smith, A. Elise Langham, Richard H. Clayton, and Clive H. Orchard. "Acidosis in models of cardiac ventricular myocytes." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 364, no. 1842 (2006): 1171–86. http://dx.doi.org/10.1098/rsta.2006.1763.

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The effects of acidosis on cardiac electrophysiology and excitation–contraction coupling have been studied extensively. Acidosis decreases the strength of contraction and leads to altered calcium transients as a net result of complex interactions between protons and a variety of intracellular processes. The relative contributions of each of the changes under acidosis are difficult to establish experimentally, however, and significant uncertainties remain about the key mechanisms of impaired cardiac function. In this paper, we review the experimental findings concerning the effects of acidosis

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CHAPELLE, DOMINIQUE, ANNABELLE COLLIN, and JEAN-FRÉDÉRIC GERBEAU. "A SURFACE-BASED ELECTROPHYSIOLOGY MODEL RELYING ON ASYMPTOTIC ANALYSIS AND MOTIVATED BY CARDIAC ATRIA MODELING." Mathematical Models and Methods in Applied Sciences 23, no. 14 (2013): 2749–76. http://dx.doi.org/10.1142/s0218202513500450.

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Computational electrophysiology is a very active field with tremendous potential in medical applications, albeit it leads to highly intensive simulations. We here propose a surface-based electrophysiology formulation, motivated by the modeling of thin structures such as cardiac atria, which greatly reduces the size of the computational models. Moreover, our model is specifically devised to retain the key features associated with the anisotropy in the diffusion effects induced by the fiber architecture, with rapid variations across the thickness that cannot be adequately represented by naive av

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Collin, Annabelle, Sébastien Imperiale, Philippe Moireau, Jean-Frédéric Gerbeau, and Dominique Chapelle. "Apprehending the effects of mechanical deformations in cardiac electrophysiology: A homogenization approach." Mathematical Models and Methods in Applied Sciences 29, no. 13 (2019): 2377–417. http://dx.doi.org/10.1142/s0218202519500490.

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We follow a formal homogenization approach to investigate the effects of mechanical deformations in electrophysiology models relying on a bidomain description of ionic motion at the microscopic level. To that purpose, we extend these microscopic equations to take into account the mechanical deformations, and proceed by recasting the problem in the framework of classical two-scale homogenization in periodic media, and identifying the equations satisfied by the first coefficients in the formal expansions. The homogenized equations reveal some interesting effects related to the microstructure — a

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Bordas, Rafel, Bruno Carpentieri, Giorgio Fotia, et al. "Simulation of cardiac electrophysiology on next-generation high-performance computers." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 367, no. 1895 (2009): 1951–69. http://dx.doi.org/10.1098/rsta.2008.0298.

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Models of cardiac electrophysiology consist of a system of partial differential equations (PDEs) coupled with a system of ordinary differential equations representing cell membrane dynamics. Current software to solve such models does not provide the required computational speed for practical applications. One reason for this is that little use is made of recent developments in adaptive numerical algorithms for solving systems of PDEs. Studies have suggested that a speedup of up to two orders of magnitude is possible by using adaptive methods. The challenge lies in the efficient implementation

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Niederer, Steven A., Eric Kerfoot, Alan P. Benson, et al. "Verification of cardiac tissue electrophysiology simulators using an N -version benchmark." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 369, no. 1954 (2011): 4331–51. http://dx.doi.org/10.1098/rsta.2011.0139.

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Ongoing developments in cardiac modelling have resulted, in particular, in the development of advanced and increasingly complex computational frameworks for simulating cardiac tissue electrophysiology. The goal of these simulations is often to represent the detailed physiology and pathologies of the heart using codes that exploit the computational potential of high-performance computing architectures. These developments have rapidly progressed the simulation capacity of cardiac virtual physiological human style models; however, they have also made it increasingly challenging to verify that a g

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