축하드립니다. Prog Biophys Mol Biol. 2006 Jan-Apr;90(1-3):186-206. Impact factor of this journal 2003: 5.346 Journal Citation Reports® 2003, published by Thomson Scientific Progress in Biophysics & Molecular Biology covers the ground between the physical and biological sciences. It indicates to the physicist the great variety of unsolved problems awaiting attention in the biological sciences. The biologist and biochemist will find that this journal presents new and stimulating ideas on structural and functional problems of the living organism. This journal will be of particular interest to biophysicists, biologists, biochemists and molecular biologists. Role of stretch-activated channels on the stretch-induced changes of rat atrial myocytes. Youm JB, Han J, Kim N, Zhang YH, Kim E, Joo H, Hun Leem C, Joon Kim S, A Cha K, Earm YE. Mitochondrial Signaling Laboratory, Department of Physiology and Biophysics, College of Medicine, Cardiovascular and Metabolic Disease Center, Biohealth Products Research Center, Inje University, Busan 614-735, Republic of Korea. The role of stretch-activated channels (SACs) on the stretch-induced changes of rat atrial myocytes was studied using a computer model that incorporated various ion channels and transporters including SACs. A relationship between the extent of the stretch and the activation of SACs was formulated in the model based on experimental findings to reproduce changes in electrical activity and Ca(2+) transients by stretch. Action potentials (APs) were significantly changed by the activation of SACs in the model simulation. The duration of the APs decreased at the initial fast phase and increased at the late slow phase of repolarisation. The resting membrane potential was depolarised from -82 to -70mV. The Ca(2+) transients were also affected. A prolonged activation of SACs in the model gradually increased the amplitude of the Ca(2+) transients. The removal of Ca((2+)) permeability through SACs, however, had little effect on the stretch-induced changes in electrical activity and Ca(2+) transients in the control condition. In contrast, the removal of the Na(+) permeability nearly abolished these stretch-induced changes. Plotting the peaks of the Ca((2+)) transients during the activation of the SACs along a time axis revealed that they follow the time course of the Na(i)(+) concentration. The Ca((2+)) transients were not changed when the Na(i)(+) concentration was fixed to a control value (5.4mM). These results predicted by the model suggest that the influx of Na(+) rather than Ca(2+) through SACs is more crucial to the generation of stretch-induced changes in the electrical activity and associated Ca(2+) transients of rat atrial myocytes.