In addition to the data indicating that ECyd restores sensitivity to CDDP, a biological mechanism explaining this sensitization has been revealed, in which MVP induction provides resistance to CDDP through the down-regulation of a drug transporter by ECyd.
Although sensitization has often been treated as a nuisance whose effects must be controlled in studies of habituation or associative learning, it remains a process worthy of study in its own right, for the behavioral changes it produces can have significant adaptive value.
Tm3+ sensitization has also been used in low phonon energy crystals.
However, in the later stage, central sensitization has no relationship with peripheral neural input [112].
On the other hand, the involvement of PAR-4 activation in TRPV1 sensitization has been poorly studied.
Recently, skin sensitization has been formulated as an adverse outcome pathway (AOP) to address the complex nature of sensitization [19].
It must be noted that, during the last three decades, sensitization has assumed a wider meaning than habituation.
However, all samples present a very low photocatalytic efficiency due to the little absorption of UV light, and dye sensitization has an effect on the photocatalytic activity.
The concept of QD sensitization has been considered to be of great promise in increasing the ηP of the organic/inorganic hybrid solar cells.
By contrast, using grand-average responses indirect evidence for sensitization has been found in chronic TTH with increased nociceptive specific reflexes and evoked potentials.
By contrast, using grand-average responses indirect evidence for sensitization has been disclosed in chronic TTH with nociceptive specific reflexes and evoked potentials.
