DocumentCode :
2340515
Title :
Apoptosis as a mediator of delayed tissue damage in progressive stroke: a computational study
Author :
Revett, Kenneth ; Kola, Jay
Author_Institution :
Sch. of Comput. Sci., Westminster Univ., London
fYear :
0
fDate :
0-0 0
Abstract :
This paper presents a computational model of ischemic stroke that focuses on the role of apoptosis as a mediator of delayed tissue. There is strong evidence that apoptosis (programmed cell death) occurs subsequent to ischemia, but its role as a mediator of delayed cell death has not been examined quantitatively. In this computational study, evidence is presented suggesting that apoptosis can cause tissue damage in a delayed fashion, with a temporal profile similar to that reported in cases of progressive stroke. The results from this study indicate that tissue damage is bi-phasic. In the acute phase (1-3 hours post-ictus), damage in the ischemic focus occurs as a result of severe metabolic insufficiency (necrosis). After a substantial time delay, a second form of cell death becomes apparent - mediated by apoptosis. The combination of necrosis and apoptosis accounts for the final infarct volume occurring in this model of ischemic stroke
Keywords :
biological tissues; cellular biophysics; medical computing; apoptosis; delayed tissue damage; infarct volume; ischemic stroke; metabolic insufficiency; necrosis; programmed cell death; progressive stroke; Animals; Blood; Calcium; Chemicals; Computational modeling; Delay effects; Ischemic pain; Neurofeedback; Neurotransmitters; Tissue damage;
fLanguage :
English
Publisher :
ieee
Conference_Titel :
Computational Intelligence Methods and Applications, 2005 ICSC Congress on
Conference_Location :
Istanbul
Print_ISBN :
1-4244-0020-1
Type :
conf
DOI :
10.1109/CIMA.2005.1662334
Filename :
1662334
Link To Document :
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