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How does understanding of p75 TrkA interaction mechanisms affect pain treatment; i.e., can we predict appropriate drug doses independent of understanding the underlying p75 TrkA interaction mechanism, or is dosing dependent on the mechanism?
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This risk is dose dependent.
Further, this self-suppression is dose dependent.
Against MAP there is dose dependent inhibition by the immunosuppressants.
Doxorubicin cardiotoxicity is dose dependent.
The action of methylnaltrexone is dose dependent.
Muscle paralysis is dose dependent and reversible.
Their severity is dose dependent [ 10].
This hemolytic effect is dose dependent.
The effect is dose dependent, long lasting and statistically significant.
Tat-induced inhibition of substrate oxidation is dose dependent.
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