Using the MarsBar software (http://marsbar.sourceforge.net/), we defined 8-mm spheres surrounding each peak and averaged percent signal change within these participant-specific ROIs (the choice of a 8 mm radius was based on previous experience of the likely spatial scale of activations in such regions of interest).
The heat map shows the scale of predicted activation (shades of orange) and inhibition (shades of blue) states for each biological function across the 5 times measured in this study.
The platelets activation state ε is calculated at each time instant by solving the following differential equation: (5) d ɛ d t = k (ε max − ε ), where the constant k is inversely proportional to the time scale of platelets activation and is set to 0.005.
Importantly an investigation of this function shows that the maximum allowed period can be controlled both by the overall conductance strength of the (I_{text{h}}) current as well as the time-scale for activation of HCN channels.
The second argument is that it is administratively costly to scale the level of activation quickly up and down according to cyclical fluctuations.
In addition, we also observed consistency in the scale and range of activation scores for a given pathway across training and validation sets.
Although both non-visual arrestins became more flexible as a result of their pre-activation, the scale of such pre-activation-induced increase in structural flexibility was noticeably larger in arrestin-2 (Yun et al., 2015).
Other mechanisms such as mitochondrial membrane depolarization due to cumulative effects of Bax activation would result in a qualitatively similar signaling response, however, with a slightly modified time-scale of apoptosis activation.
We propose that the cell computes by exploiting variation in the time scales of protein activation (phosphorylation) and gene expression.
A proper scaling of the activation energy is introduced, ensuring a proper degeneration towards the stress strain rate power-law behaviour.
