TY - JOUR
T1 - Towards in silico models of decomplexification in human endotoxemia
AU - Scheff, Jeremy D.
AU - Mavroudis, Pantelis
AU - Calvano, Steve E.
AU - Lowry, Stephen F.
AU - Androulakis, Ioannis P.
PY - 2011
Y1 - 2011
N2 - Heart rate (HR) variability (HRV) is an important variable in determining the state of a critically ill patient. This motivates the quantitative understanding of the mechanisms giving rise to changes in HRV, particularly in the context of critical illness. Human endotoxemia, a clinical model of systemic inflammation, has been modeled previously to characterize its complex dynamics. This model is extended to incorporate a semi-mechanistic model of signal transduction leading from the well-established processes at the cellular and molecular levels in the inflammatory response to systemic changes in HR and HRV as governed by the autonomic nervous system's response to inflammation. This is accomplished with an integral pulse frequency modulation model that translates the continuous, deterministic model dynamics into a series of discrete, variable heart beats. Thus, homeostatic variability and the mechanisms leading from cellular processes to systemic changes in variability under endotoxemia are assessed.
AB - Heart rate (HR) variability (HRV) is an important variable in determining the state of a critically ill patient. This motivates the quantitative understanding of the mechanisms giving rise to changes in HRV, particularly in the context of critical illness. Human endotoxemia, a clinical model of systemic inflammation, has been modeled previously to characterize its complex dynamics. This model is extended to incorporate a semi-mechanistic model of signal transduction leading from the well-established processes at the cellular and molecular levels in the inflammatory response to systemic changes in HR and HRV as governed by the autonomic nervous system's response to inflammation. This is accomplished with an integral pulse frequency modulation model that translates the continuous, deterministic model dynamics into a series of discrete, variable heart beats. Thus, homeostatic variability and the mechanisms leading from cellular processes to systemic changes in variability under endotoxemia are assessed.
KW - IPFM
KW - Inflammation
KW - Mathematical modeling
KW - Systems biology
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U2 - 10.1016/B978-0-444-54298-4.50076-3
DO - 10.1016/B978-0-444-54298-4.50076-3
M3 - Article
AN - SCOPUS:79958833311
VL - 29
SP - 1485
EP - 1489
JO - Computer Aided Chemical Engineering
JF - Computer Aided Chemical Engineering
SN - 1570-7946
ER -