Preconditioning pathways

The capacity of WRF to transform and mineralize a wide range of pollutants without a preconditioning period via co-metabolic pathways makes them interesting for the degradation of recalcitrant xenobiotics. The use of WRF and their LMEs for the removal of xenobiotics has been reviewed elsewhere [1-7]. 

The term, arrhythmogenic substrate, became a matter of interest to many researchers. The arrhythmogenic substrate means the pathologic and anatomic preconditions for the initiation of tachyarrhythmias such as myocardial fibrosis, aneurysm, the border zone between normal and ischemic or infarcted tissue, scars, diffuse myocardial injury in cardiomyopathy or the chronic alterations induced by myocarditis, and furthermore, accessory pathways or variations in the specific cardiac conduction system. These anatomic or pathologic altera-... 

Resveratrol preconditions the heart through activation of adenosine A3 receptors protecting the heart through a cAMP response element-binding (CREB)-dependent Bcl-2 pathway in addition to an Akt-Bcl-2 pathway (Das et al. 2005a, b). 

Agonist/Receptor Interactions and Signal Transduction Pathways in Ischemic Preconditioning... 

Lan, X., Wang, J., and Zhang, Y. 2005. Role of beta-adrenergic signal transduction pathway on myocardial ischemic preconditioning of rats. J. Huazhong Univ. Sci. Technol. Med. Sci. 25 709-711. 

Lange, M., Smul, T.M., Blomeyer, C.A., Redel, A., Klotz, K.N., Roewer, N., and Kehl, F. 2006. Role of the betal-adrenergic pathway in anesthetic and ischemic preconditioning against myocardial infarction in the rabbit heart in vivo. Anesthesiology 105 503-510. 

Lochner, A., Genade, S., Tromp, E., Podzuweit, T., and Moolman, J.A. 1999. Ischemic preconditioning and the beta-adrenergic signal transduction pathway. Circulation. 100 958-966. 

Protein kinase signal transduction pathways have been extensively studied and characterized in the myocardium. Ischemic preconditioning (IP) and the role of individual kinases involved is where much of the research efforts have been focused. IP is the reduction in susceptibility to myocardial infarction that follows brief periods of sublefhal ischemia (Murry et al, 1986). This reduction can manifest itself as a 4-fold reduction in infarct size, this being secondary to a delay in the onset and rate of cell necrosis during the subsequent lethal ischemia (Marber et al., 1994). 

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