Sentence examples for component of the terminal from inspiring English sources

As shown in Fig. 1, the q-axis component of the terminal voltage (tilde{U}_{text{PCC}}) is the input of the PLL.

For the control strategy of the UPFC shunt converter, the q-axis component of the terminal voltage for shunt transformer (dot{U}_{1}) is forced to zero, i.e., the d-axis and q-axis components of (dot{U}_{1}) are: left{ begin{array}{ll} U_{1d} = U_{1} hfill U_{1q} = 0 hfill end{array} right.

Similarly, for the control strategy of the UPFC series converter, the q-axis component of the terminal voltage for series transformer (dot{U}_{2}) is forced to zero, i.e., the d-axis and q-axis components of (dot{U}_{2}) are: left{ begin{array}{l} U_{2d} = U_{2} hfill U_{2q} = 0 hfill end{array} right.

Colocalization is only observed as a result of close proximity between synaptophysin-immunoreactive vesicles and M6a as a component of the terminal membrane.

Caspase 3 activation is considered to be a key cellular component of the terminal and irreversible phase of apoptotic death caused by DNA damaging agents.

Together with vitronectin, clusterin is a component of the terminal complement complex and mediates the folding of extracellular proteins as a chaperone [26].

Filaggrin proteins are crucial components of the terminal differentiation of the epidermis by aggregating keratin filaments.

Remarkably, these proteins are all components of the terminal web in C. elegans intestine [ 17].

Similarly, in KCl- and NaCl-exposed cells, the corresponding components of the terminal electron transport chain exhibited signs of reduced activity after 6 h of incubation.

As to the other components of the terminal web, while the loss of a single protein, other than IFC-2, does not induce major defects on intestine organization [ 30], a pronounced defective phenotype is observed after simultaneous down-regulation of two or three IF proteins [ 31] - a fact that has been interpreted in light of the redundancy of IF proteins in nematodes.

Marked susceptibility to meningococcal disease is seen in individuals with rare complement defects (especially loss of components of the terminal pathway, which is necessary for bacteriolysis and not opsonphagocytosis), those receiving C5 inhibitors (i.e. eculizumab), and inherited defects of the AP (i.e. properdin and factor D deficiencies).