Sentence examples for activation c from inspiring English sources

a Magnetic twisting cytometry; b mechano-sensitive ion-channel activation; c targeted ion-channel activation; and d receptor clustering [26].

Maximal oxidative phosphorylation plotted as a function of HO-1 expression (A) and of AMPK activation (B), and HO-1 expression plotted as a function of AMPK activation (C).

The specificity of Shp2 inhibition by DCA has been tested and confirmed by a number of experiments in this study: a) inhibition of purified Shp2 was examined against a list of other PTPs; b) DCA was shown to suppress growth factor-stimulated Erk activation; c) DCA was found to have no effect on Shp2−/− cells.

Complement activation (C) usually precedes hemodynamic disturbances in serious infections.

Figure 8 illustrates the simulated first ECG-lead (A), the action potential traces at a basal ventricular location (B) as well as activation (C) and repolarization (D) maps for control, IC50 and twice IC50 doses of a sodium blocker.

Increased tissue renewal (B, B′ ) and SREBP activation (C, C′, quantified in D, p < 0.001, Mann Whitney test) are apparent following a 3-day dietary supplementation with JH analogue (JHa).

Apoptotic cells are potent complement activators; and proposed mechanisms include IgM-mediated classical pathway activation, C-reactive protein (CRP -mediated CRP -mediatedhway aclassical, and IgM-mediated lectin pathway activation.

While based on the literature we do believe that our activation (c-FOS) data in IO and caudal RPa are related to BAT activity, we cannot rule out the possibility that at least part of the responses observed might be related to other functions, such as motor control, as previously described (Welsh and Llinás, 1997; Apps, 1999).

Maximakinin is an agonist of the human and rabbit B2R with a 8 12 fold lesser potency, but a prolonged duration of action relative to BK (ERK MAP kinase activation, c-Fos induction in HEK 293 cells).

Additionally, AEA has proved to be effective in preventing both NTG-induced activation (c-Fos) of neurons in the nucleus trigeminalis caudalis (NTC) and NTG-induced hyperalgesia at the formalin test [23].

In considering how PLC activity may relate to migraine and its comorbidities, many of these distinct conditions share a multifaceted pathophysiology, with alterations in molecules as diverse as serotonin, adrenaline, estrogen, cannabinoids, and glutamate, and include the activation of several GPCRs, protein kinase mediated signaling, and early gene activation (c-fos) [36, 37].