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Cardiovascular Research 2001 51(4):630-632; doi:10.1016/S0008-6363(01)00397-2
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Measuring electrophysiological changes in transgenic mouse models of cardiovascular disease

Carol A Eisenberg* and Leonard M Eisenberg

Department of Cell Biology and Anatomy, Medical University of South Carolina, 173 Ashley Ave., Suite 652, P.O. Box 250508, Charleston, SC 29425, USA

eisenbec@musc.edu

* Corresponding author. Tel.: +1-843-792-6502; fax: +1-843-792-0664

Received 20 June 2001;

KEYWORDS Heart; Electrophysiology; Connexin; Optical mapping

The first 10% of the full text of this article appears below.

See article by Eloff et al. [19] (pages 681–690) in this issue.

The ability to remove selected genes within the mouse genome has proven to be an invaluable tool in the study of vertebrate biology. Many genetically modified ‘knockout’ mice possess significant morphological abnormalities that have provided substantial insights into the function of individual genes. However, the severity of the phenotype is often the drawback to using knockout mice as disease models, since many human diseases are due to subtle genetic defects. This is especially true for genetic alterations that manifest as electrophysiological disturbances in the heart, as cardiac conduction defects, substrates for arrhythmias, and susceptibility to sudden cardiac arrest may arise without any obvious morphological abnormalities.

Cardiac function requires the organized contractility of billions of myocytes. Propagation of electrical current from cell-to-cell is mediated by gap junctions, . . . [Full Text of this Article]


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