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Articles by Phil S. Tsao in JoVE
JoVE Clinical and Translational Medicine
Human Interne borstslagader (IMA) Transplantatie en stenting: een humaan model aan de ontwikkeling van in-stent restenose Studie
1University Heart Center Hamburg, TSI-Lab, Germany, 2Cardiovascular Research Center, University of Hamburg, 3Department of Medicine, Cardiology Division, Pulmonary Hypertension Program, University of Alberta, 4Department of Medicine, Stanford University School of Medicine, 5Department of Biomedical Sciences, Institute of Physiology, Pathophysiology, and Biophysics, University of Veterinary Medicine, Vienna, 6Translumina GmbH, Hechingen, 7Department of Cardiothoracic Surgery, Stanford University School of Medicine
Deze video toont een model om de ontwikkeling van intima hyperplasie studeren na stent met behulp van een menselijk vat (IMA) in een immunodeficiënte rat model.
Other articles by Phil S. Tsao on PubMed
Dimethylarginine Dimethylaminohydrolase Overexpression Suppresses Graft Coronary Artery Disease
Graft coronary artery disease (GCAD) is the leading cause of death after the first year of heart transplantation. The reduced bioavailability of endothelium-derived nitric oxide (NO) may play a role in endothelial vasodilator dysfunction and the structural changes that are characteristic of GCAD. A potential contributor to endothelial pathobiology is asymmetric dimethylarginine (ADMA), an endogenous NO synthase inhibitor. We hypothesized that lowering ADMA concentrations by dimethylarginine dimethylaminohydrolase (DDAH) overexpression in the recipient might suppress GCAD and long-term immune responses in murine cardiac allografts.
