These mutations are all in highly conserved amino acids and are postulated to alter the function of brain-expressed Nav1.7.
During aging, changes in chromatin state that alter gene transcription have been postulated to result in expression of genes that are normally silenced, leading to deleterious age-related effects on cellular physiology.
Dysfunction at synapses and altered axonal transport has been postulated to be some of the earliest pathological events in Parkinson's disease (Schulz-Schaeffer, 2010; Kim-Han et al., 2011; Nakata et al., 2012).
Various perinatal factors, including birth weight, birth order, maternal age, gestational age, twin status, and parental smoking, have been postulated to affect breast cancer risk in daughters by altering the hormonal environment of the developing fetal mammary glands.
Several mechanisms such as visceral hypersensitivity and altered brain-gut interactions have been postulated to play an etiological role in dyspepsia (reviewed in [ 8, 9]).
Altered descending modulation has been postulated to contribute to migraine, leading to loss of inhibition or enhanced facilitation resulting in hyperexcitability of trigeminovascular neurons.
A variety of factors have been postulated to cause injury to glomerular cells, including circulating cytokines such as permeability altering factor, angiotensin II, macrophage infiltration and other mediators of inflammation [ 12, 13].
The potential mechanisms of PBDEs on cognitive function and hyperactivity have been postulated to include induced neuronal apoptosis, decreased neuronal migration, interrupted intracellular calcium (Ca2+) homeostasis, and altered neurotransmitter release and function (Dingemans et al. 2011).
Fibroblasts with CAF-like phenotypes have been postulated to derive from (a) resident fibroblasts, and/or (b) mesenchymal stem cells that have been progressively altered by exposure to tumor epithelial cells or their secreted factors [ 58- 60].
