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Ann Thorac Surg 2004;77:1389-1390
© 2004 The Society of Thoracic Surgeons

Invited commentary

Hermann Aebert, MD

Department of Thoracic and Cardiovascular Surgery Eberhard Karls University Hoppe-Seyler-Strasse 3 D-72706 Tuebingen, Germany

e-mail: hermann.aebert@med.uni-tuebingen.de

The first 20% of the full text of this article appears below.

This article exemplifies impressively how the combination of classic physiological methods and molecular biology can result in new knowledge. Doctor Feng and colleagues observed that the decline of myocardial contractility and endothelium-dependent coronary relaxation after cardioplegic arrest is related to increased caspase-3 activation and decreased Bad phosphorylation. Why are these findings important?

The concept of apoptosis or programmed cell death has revolutionized our understanding of multicellular organism development, tissue homeostasis under normal and pathological conditions, and therapeutic interventions. If a cell is exposed to limited injury not resulting in direct necrosis, the scale beam of cell survival is inclining to apoptosis. This may be counterbalanced by anti-apoptotic factors. However, when a point of no return is reached, the . . . [Full Text of this Article]




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