During evolution, spatial correlation with hemodynamic signal only exists briefly at the maximal spread of the VSD signal.
In general, we find that during all points in the evolution of the seizure, the area of CBV signal was slightly larger than the maximal spread of each membrane potential wave (Fig. 8).
However, after 2 h, controls had reached a near maximal spread cell area of 1645.5 μm ± 231.3 while the talin1 knockdown cells were markedly smaller (465.0 μm ± 93.3, p = 0.0001), a difference that was maintained for the entire 14 h period (Fig. 2B).
GCV started to be administered 4 days after the last viral injection to facilitate maximal viral spreading and to avoid cell death induced by GCV before the virus started replicating.
This indicates that cooperativity exists between PKA- and EPAC1-regulated signalling pathways to promote maximal cell spreading following cAMP stimulation of HEK293T cells.
Therefore cooperativity must exist between EPAC and PKA signalling pathways in HUVECs that underlies the cytoskeletal reorganisation required for maximal cell spreading.
Specifically, for the given maximal time delay τ max and maximal Doppler spread ν max, the choice of T and F should satisfy [14] frac{T}{F}=frac{tau_{text{max}}}{nu_{text{max}}}.
It should be noted that while insulated from GC bias, these substitutions do nonetheless exhibit differing effects on intensity: in yeast, the maximal intensity spread between C→G (G·G mispair) and A→T (T·T mispair) is ~7%; in human, it can reach ~9%.
This suggests that EPAC1 activation alone is not sufficient to promote maximal levels of cell spreading or cortical actin bundling in HUVECs, and that there is an additional requirement for PKA.
Only difficult and time-consuming measurements, as performed for example in the G dataset, lead to an accurate assessment of the maximal lateral spread of a root system (Phillips et al. 2014).
