Models that contain the Implementer : Sung, Ruey J

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    Models   Description
1.  Cardiac action potential based on Luo-Rudy phase 1 model (Luo and Rudy 1991), (Wu 2004)
A mathematical model of the membrane action potential of the mammalian ventricular cell is introduced. The model is based, whenever possible, on recent single-cell and single-channel data and incorporates the possibility of changing extracellular potassium concentration [K]o. The fast sodium current, INa, is characterized by fast upstroke velocity (Vmax = 400 V/sec) and slow recovery from inactivation. The time-independent potassium current, IK1, includes a negative-slope phase and displays significant crossover phenomenon as [K]o is varied. The time-dependent potassium current, IK, shows only a minimal degree of crossover. A novel potassium current that activates at plateau potentials is included in the model. The simulated action potential duplicates the experimentally observed effects of changes in [K]o on action potential duration and rest potential. See papers for more and details.
2.  Kv4.3, Kv1.4 encoded K(+) channel in heart cells (Greenstein et al 2000) (XPP)
A model of canine I:(to1) (the Ca(2+)-independent transient outward current) is formulated as the combination of Kv4.3 and Kv1.4 currents and is incorporated into an existing canine ventricular myocyte model. Simulations demonstrate strong coupling between L-type Ca(2+) current and I:(Kv4.3) and predict a bimodal relationship between I:(Kv4.3) density and APD whereby perturbations in I:(Kv4.3) density may produce either prolongation or shortening of APD, depending on baseline I:(to1) current level. The model files were submitted by: Dr. Sheng-Nan Wu, Dr. Ruey J. Sung, Ya-Jean Wang and Jiun-Shian Wu e-mail: snwu@mail.ncku.edu.tw
3.  Markovian model for cardiac sodium channel (Clancy, Rudy 2002)
Complex physiological interactions determine the functional consequences of gene abnormalities and make mechanistic interpretation of phenotypes extremely difficult. A recent example is a single mutation in the C terminus of the cardiac Na(+) channel, 1795insD. The mutation causes two distinct clinical syndromes, long QT (LQT) and Brugada, leading to life-threatening cardiac arrhythmias. Coexistence of these syndromes is seemingly paradoxical; LQT is associated with enhanced Na(+) channel function, and Brugada with reduced function. Using a computational approach, we demonstrate that the 1795insD mutation exerts variable effects depending on the myocardial substrate. We develop Markov models of the wild-type and 1795insD cardiac Na(+) channels. See reference for more and details. The model files were submitted by: Dr. Jiun-Shian Wu, Dr. Sheng-Nan Wu, Dr. Ruey J. Sung, Han-Dong Chang.
4.  Markovian model for single-channel recordings of Ik_1 in ventricular cells (Matsuoka et al 2003)
The interaction between many currents in a cardiac ventricular model are examined in this paper. One of the main contributions come from a current called IK_1. An XPP version of this model was supplied by Hsieng-Jung Lai, Jiun-Shian Wu, Sheng-Nan Wu, Ruey J. Sung, Han-Dong Chang. Please see paper and model for more and details.

Re-display model names without descriptions