Sentence examples for maximum activation at from inspiring English sources

Time-dependent stimulation of MG-63 cells with LPA resulted in a rapid and transient phosphorylation of p42/44 MAPK, reaching a maximum activation at approx. 5 min after stimulation (Fig. 2B).

Using an anti phospho-CREB anti phospho-CREBognizes phosphorylantibodyine 133, we observed a very rapid (5 min), BPA-induced acthattion of Crecognizes-1 cells, with maximum activation at 30 min. This activation was phosphorylatedbecauserine completely abolished CREB phosphorylation (data not shown).

Three min after the addition of TEA, we observed non-inactivated outward K+ currents activated at −30 mV with a maximum activation state at +40 mV for a conductance of 50 nS.

Without TEA, we detected non-inactivated outward currents, which activated at −40 mV and reached a maximum activation state at +80 mV for a conductance of 90 nS.

We also detected slow activated outward currents with maximum activation states at +20 mV for a conductance of 48 nS and an inactivating component that turned on at 80 mV, as demonstrated by the tail current at the steady state (Figure 4c, e).

In all cases the voxel of maximum activation is at Brodmann area 31, Cingulate Gyrus, Limbic Lobe.

Model output and display: the output of the model is the position of the cleaning module with the maximum activation level at iteration i(ma i ).

The methylene blue adsorption capacity achieves a maximum value of 71.4 mg/g when the activated carbon is prepared either at minimum activation time and maximum activation temperature or at maximum activation time and minimum activation temperature conditions.

Maximum activation was achieved at (X, Y, Z) = (-3, 52, 1), corresponding to Broadmann area 10, anterior cingulate, limbic lobe.

In a time-course assay (0 24 h) with a 10  μ M CDDP treatment, we observed maximum activation of P70S6K/Akt/Erk phosphorylation at 12 h in the SOKV-3 cells and at 6 h in the CAOV-3 cells.

As described in Fig. 6, for construct β2-K-62-25, mutation E122 W appeared to reduce the amplitude of the agonist-induced signal (from 63.5% to 51% at maximum activation) and to increase dissociation constant (from 149 nM to 247 nM) but these effects did not reach statistical significance (p = 0.12 for amplitudes; p = 0.24 for affinities).