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Semahat S Demir

Publications and source records attributed to Semahat S Demir.

6 recordsLinked to original sources
PubMed2006

Interactive cell modeling web-resource, iCell, as a simulation-based teaching and learning tool to supplement electrophysiology education.

An interactive cell modeling web site, iCell (http://ssd1.bme.memphis.edu/icell/), that integrates research and education, was developed to present and to disseminate JAVA-coded models of cellular activities, and to supplement physiology education. iCell can be used to supplement the text-book material as a simulation-based teaching and learning tool. Specifically, iCell allows the students to supplement their learning experiences of the text-book cellular physiology material by running simulations in an interactive environment. The site consists of JAVA-coded models of various cardiac cells and neurons, and provides simulation data of their bioelectric transport activities at cellular level. Each JAVA-coded model allows the user to go through menu options to change model parameters, run and view simulation results. The site also has a glossary section for the scientific terms. iCell has been used as a teaching and learning tool for seven graduate courses at the Joint Biomedical Engineering Program of University of Memphis and University of Tennessee. This modeling tool was also used as a collaboration site among our physiology colleagues interested in simulations of cell membrane activities. Scientists from the fields of biosciences, engineering, life sciences and medical sciences in 17 countries have tested and utilized iCell as a simulation-based teaching, learning and collaboration environment. iCell provides us with an interactive, platform-independent, and user-friendly teaching and learning resource, and also a collaboration environment for electrophysiology to be shared over the Internet. The usage of simulations for teaching and learning will continue advancing simulation-based engineering and sciences for research and development.

Animals↗
PubMed2004

Computational modeling of cardiac ventricular action potentials in rat and mouse: review.

Little is known about the ionic mechanisms underlying the action potential heterogeneity in ventricle-associated healthy and disease conditions, even though five decades of histological, electrophysiological, pharmacological, and biochemical investigations exist. The computational modeling in murine ventricular myocytes can complement our knowledge of the experimental data and provide us with more quantitative descriptions in understanding different conditions related to normal and disease conditions. This paper initially reviews the theoretical modeling for cardiac ventricular action potentials of various species and the related experimental work. It then presents the progress of the computational modeling of cardiac ventricular cells for normal, diabetic, and spontaneously hypertensive rats. The paper also introduces recent modeling efforts for the action potential heterogeneity in mouse ventricular cells. The computational insights gained into the ionic mechanisms in rodents will continue to enhance our understanding of the heart and provide us with new knowledge for future studies to treat cardiac diseases in children and adults. Because the dissemination of computational models is very important, we continue to disseminate these models by iCell, the interactive cell modeling resource. iCell (http://ssd1.bme.memphis.edu/icell/) has been developed as a simulation-based teaching and learning tool for electrophysiology and contains JAVA applets that present models of various cardiac cells and neurons and simulation data of their bioelectric activities at cellular level.

Action Potentials↗
PubMed2003

A mathematical model of the electrophysiological alterations in rat ventricular myocytes in type-I diabetes.

Our mathematical model of the rat ventricular myocyte (Pandit et al., 2001) was utilized to explore the ionic mechanism(s) that underlie the altered electrophysiological characteristics associated with the short-term model of streptozotocin-induced, type-I diabetes. The simulations show that the observed reductions in the Ca(2+)-independent transient outward K(+) current (I(t)) and the steady-state outward K(+) current (I(ss)), along with slowed inactivation of the L-type Ca(2+) current (I(CaL)), can result in the prolongation of the action potential duration, a well-known experimental finding. In addition, the model demonstrates that the slowed reactivation kinetics of I(t) in diabetic myocytes can account for the more pronounced rate-dependent action potential duration prolongation in diabetes, and that a decrease in the electrogenic Na(+)-K(+) pump current (I(NaK)) results in a small depolarization in the resting membrane potential (V(rest)). This depolarization reduces the availability of the Na(+) channels (I(Na)), thereby resulting in a slower upstroke (dV/dt(max)) of the diabetic action potential. Additional simulations suggest that a reduction in the magnitude of I(CaL), in combination with impaired sarcoplasmic reticulum uptake can lead to a decreased sarcoplasmic reticulum Ca(2+) load. These factors contribute to characteristic abnormal [Ca(2+)](i) homeostasis (reduced peak systolic value and rate of decay) in myocytes from diabetic animals. In combination, these simulation results provide novel information and integrative insights concerning plausible ionic mechanisms for the observed changes in cardiac repolarization and excitation-contraction coupling in rat ventricular myocytes in the setting of streptozotocin-induced, type-I diabetes.

Action Potentials↗
PubMed2003

Computational model of the ventricular action potential in adult spontaneously hypertensive rats.

INTRODUCTION: Cardiac hypertrophy has substantial clinical significance because many hypertrophic cells have markedly prolonged repolarization behavior, which may lead to increased risk for cardiac arrhythmias. Spontaneously hypertensive rat (SHR) is one model of hypertension that is studied extensively and is considered to be the best laboratory model of human hypertension. We extended our previously published model of the rat ventricular myocyte to simulate the effects of hypertrophy in SHR. METHODS AND RESULTS: In SHR it has been shown that the membrane capacitance is increased, the density of transient outward K+ current is decreased, the sarcoplasmic reticulum Ca2+ ATPase activity is reduced, and the cell volumes are increased compared to those of the normal rat. We introduced these changes into our previous model of the rat ventricular myocyte and simulated the ventricular action potential of SHR. Our results demonstrated increased action potential duration (APD) and increased peak systolic value of the intracellular calcium transient in SHR. Simulations with reduced extracellular K+ concentration ([K+]o) have shown that there is increased APD shortening in SHR compared to that of the normal rat. CONCLUSIONS: Our computational model qualitatively simulated the electrophysiologic changes observed in SHR and provided the plausible mechanistic linkage between the prolonged APD and increased inotropy. Our model results also demonstrated the electrophysiologic changes observed with reduced [K+]o in SHR, a finding that is clinically significant in hypertensive patients with left ventricular hypertrophy undergoing diuretic treatment.

Action Potentials↗
PubMed2002

Mathematical model of the rapidly activating delayed rectifier potassium current I(Kr) in rabbit sinoatrial node.

INTRODUCTION: A rapidly activating delayed rectifier potassium current (I(Kr)) is known to have an important role in determining the properties of spontaneous pacing in enzymatically isolated rabbit sinoatrial node (SAN) cells. The functional characteristics of I(Kr) are conferred by its dependence on time, voltage, and external potassium. The aim of this study was to develop a rigorous mathematical representation for I(Kr) based on experimental findings and to investigate the role of I(Kr) in the automaticity and intercellular communication of SAN cells. METHODS AND RESULTS: A Markov model was developed using available experimental data for I(Kr) in rabbit SAN. The dependence of I(Kr) on external potassium, [K+]o, was incorporated using data from both in vitro preparations and results from heterologous expression experiments for this ether-a-go-go related gene product. Our simulation results show the following. (1) I(Kr) is the dominant repolarizing current in rabbit SAN cells. (2) Deactivation of I(Kr) contributes to the net current change during the early diastolic depolarization phase. (3) Inward rectification of I(Kr) results in a decrease in membrane resistance during repolarization relative to plateau. (4) The complex [K+]o dependence of I(Kr) confers [K+]o insensitivity on isolated cells, which may account for the sensitivity of pacing rate to elevated [K+]o at the tissue level. CONCLUSION: Model results show that I(Kr) mediates diastolic depolarization by the kinetics of its decay and by lowering resistance during late repolarization. In elevated [K+]o, increased chord conductance is balanced by the changes in kinetics and voltage dependence of I(Kr) so that the pacing rate of single cells may be more [K+]o insensitive than expected. In addition, elevated [K+]o increases I(Kr) magnitude during repolarization but lowers resistance, so current flow through gap junctions is less able to hyperpolarize pacing cells.

Action Potentials↗