The initial studies of these oximes in vivo with the sarin surrogate NIMP have indicated reactivation of up to about 25% at 30 min after oxime administration and substantial attenuation of seizure behavior from some of the oximes.
Reactivation may require up to 24 hours to complete.
Fulminant toxoplasmosis in post-transplant patients may occur as a primary infection shortly after transplantation or as reactivation of latent infection, even up to 7 years after transplantation [4].
Notably, reactivation upon DTT treatment occurred up to 20 m m H2O2 and 80 min incubation time, verifying the absence of irreversible modifications and indicating very efficient protection of PTEN from constitutive inactivation by oxidative agents.
Reversible reactivation of the monomer was achieved up to 95% within 3 min from 8 M urea induced unfolded state, indicating that the catalytic site could form independent of its quaternary structure.
Studies have reported reactivation of CMV and HSV in up to 35% and 64% of critically ill patients, respectively [8] [10], [16], [17], [20].
For sarin hydrolysis, introduction of a polar side chain (H or Q) in either position alone or in combination produced similar rates of reactivation, ranging from 3.2×10−4 to 26×10−4 min−1, up to a 11-fold increase relative to wt hCE1.
Most clinically relevant in this setting is the reactivation of HBV, which can occur in up to 50%% of patients with previous hepatitis B [ 37– 40].
Several groups of functionally related genes were up-regulated up to 20 folds after reactivation, which include genes that are involved in energy generation, translation/transcription, metabolism, growth, cell division, and differentiation.
