@article{knisley_2005, title={Comment on "Ventricular arrhythmias following exposure of failing hearts to oxidative stress in vitro"}, volume={16}, ISSN={["1540-8167"]}, DOI={10.1111/j.1540-8167.2005.40818.x}, abstractNote={The article by Brigadeau et al. in this issue of the Journal represents an important step in the search for the triggering factors that play a role in lethal tachyarrhythmias in heart failure.1 Despite the fact that heart failure carries a high risk of death or hospital readmission, the cause of death and the optimal therapy remain elusive. Death has been presumed to result most often from a lethal cardiac tachyarrhythmia, while in a percentage of patients it may result from bradyarrhythmia or pulseless activity.2,3 It should be reemphasized that the production and use of an animal model of heart failure as done by Brigadeau et al. can be an especially difficult and costly enterprise, which may increase the rarity and potential value of results obtained.4 The failure develops over time, requiring multiple examinations of live animals. Also, attempts to discover lethal arrhythmias may not reveal the desired information since an animal may die before data are obtained or may survive with no arrhythmia. Also, a single animal model may not represent all of the conditions that develop in human heart failure. Experimental reports of the effects of failure or the conditions produced in a particular model of failure have described changes in cardiac variables including ion channels, pumps or exchangers, action potentials, reactive oxygen species, and ventricular function. This has provided a wealth of information on mechanisms underlying major electrophysiological effects of failure, e.g., the classical increased action potential duration and bradycardia-induced afterdepolarizations that may trigger tachyarrhythmias. However, information on the arrhythmias themselves is essential for understanding the cause of death in failure, developments of potential therapeutic strategies, and whether proposed mechanisms apply to genesis of lethal arrhythmias. Thus, the approach of Brigadeau et al. in which data on arrhythmias were sought is highly appropriate. The article by Brigadeau et al. has specifically addressed effects of oxidative stress in a rapid pacing induced heart failure model with the addition of H2O2. This work follows their study with the rapid-paced porcine model in which no polymorphic ventricular tachyarrhythmias were found at the time of death despite delayed repolarization and uniformly decreased whole cell delayed rectifier and transient outward potassium currents.5 Also, their earlier report indicated a decrease in repolarization dispersion in the porcine model.}, number={6}, journal={JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY}, author={Knisley, SB}, year={2005}, month={Jun}, pages={637–638} }
 @article{jevremovic_gulati_hennig_diaz_cole_kleppe_cosset_simari_vile_2004, title={Use of blood outgrowth endothelial cells as virus-producing vectors for gene delivery to tumors}, volume={287}, ISSN={["1522-1539"]}, DOI={10.1152/ajpheart.00064.2004}, abstractNote={Cell-based delivery of therapeutic viruses has potential advantages over systemic viral administration, including attenuated neutralization and improved viral targeting. One of the exciting new areas of investigation is the potential ability of endothelial-lineage cells to deliver genes to the areas of neovascularization. In the present study, we compared two types of endothelial-lineage cells [outgrowth endothelial cells (OECs) and culture-modified mononuclear cells (CMMCs), also known as "endothelial progenitor cells"] for their ability to be infected with adenovirus and to home to the areas of neovascularization. Both cell types were isolated from peripheral blood of healthy human donors and expanded in culture. We demonstrate that OECs are more infectable and home better to tumors expressing VEGF on systemic administration. Furthermore, we used an adenoviral/retroviral chimeric system to convert OECs to retrovirus-producing cells. When injected systemically into tumor-bearing mice, OECs retain their ability to produce retrovirus and infect surrounding tumor cells. Our data demonstrate that OECs could be efficient carriers for viral delivery to areas of tumor neovascularization.}, number={2}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY}, author={Jevremovic, D and Gulati, R and Hennig, I and Diaz, RM and Cole, C and Kleppe, L and Cosset, FL and Simari, RD and Vile, RG}, year={2004}, month={Aug}, pages={H494–H500} }