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Developmental alterations to epigenetic marks may induce long-term changes in gene expression, potentially leading to disease in later life [ 140, 141].
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Other demethylating agents are in development; these may be easier to deliver with less myelosuppression, and other schedules, for example, a 5-day schedule, may induce more marked and persistent demethylation.
In addition to direct epigenetic inheritance, epigenetic marks may be induced in the F1 generation as a result of maternal effects as discussed in the DOHaD example earlier, or via grand-parental effects where the F1 generation is female.
Acute lesions of the posterior medial orbitofrontal cortex (OFC) in humans may induce a state of reality confusion marked by confabulation, disorientation, and currently inappropriate actions.
As increasing p16INK4a levels mark aging neural stem cells (Molofsky et al, 2006), such synergistic action may induce neural stem cell aging, possibly leading to their eventual exhaustion, consistent with the self-renewal deficit in NS lacking Gli1 (see above).
Acetylation may induce active transcription, while mono, bi or tri-methylation of K27 is associated with a repressive mark on chromatin and gene expression.
It may induce nothing more than vertigo.
If they desensitise some people, they may induce empathy in others.
Too little medication may induce withdrawal symptoms like sweating, sleeplessness and abdominal discomfort.
may induce stress [2].
Caffeine may induce anxiety and insomnia.
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