In murine experimental setups, tolerance induced by LCs has been explained by mechanisms such as induction of Treg (Gomez de Agüero et al, 2012), immunosuppressive IL-10 release (Igyarto et al, 2009), or incomplete maturation (Azukizawa et al, 2011; Shklovskaya et al, 2011).
This feature of ΔZ variation is different from what is expected from the Chapman model of EEJ and has been explained as the effect of induction in subsurface conducting layer (Rastogi, 2004).
Other nonformal necessary truths (e.g., "nothing can be both red and green all over") are also explained as intuitive inductions: one can see a universal and necessary connection through a particular instance of it.
Transcriptional induction of SspA might be explained as a consequence of the simultaneous increase (~2.0-fold; SD5) of sigG (CAC1696) because σG regulated the synthesis of SspA in Bacillus subtilis (Jones et al. 2008).
Therefore, we postulate that induction of abnormal mitochondrial behavior is an intrinsic capacity of hDMPK A and cannot be simply explained as a result of overexpression.
Valproic acid-induced osteopathy, for example, cannot be explained by an induction of 24-hydroxylases, as valproic acid inhibits cytochrome P450 enzymes and is not a ligand of the pregnane X receptor.
The possible mechanism of the potent protection of all the tested extracts against direct mutagens such as NOPD and MMS could be explained by the induction of the oxidative defence system and/or DNA repair enzymes, which are required to protect against oxidative-like mutations.
This induction might be explained by the induction of the chemokine signaling, as identified by the KEGG software.
This would explain the induction of flagellar motility, as evidenced by the broadening of the line of cell density and the appearance of distal colonies, after 28 hours in wild type strain stab-plates.
It also gives support to the theory that suggests that LTBI is considered to be a process of constant endogenous reinfection, and explains the induction of active TB as a process that depends on the site where the reinfection occurs, for example the upper lobes, favoring bacillary growth, liquefaction of the necrotic tissues and extracellular bacillary growth, which in turn lead to cavitation[51].
