Executive cognitive functions have been postulated to include both dynamic behavioral selection and strategic goal-setting or response preparation.
Their function has been postulated to include roles in peptide-binding and presentation, but without cleavage.
Underlying mechanisms are postulated to include ischaemic hypothalamic damage and the inability of hypoxic mitochondria to generate heat.
Reasons for this have been postulated to include the fact that those with higher incomes have higher educational achievement, better living circumstances, and less risky health behaviours.
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).
Moreover, CYP4V10 transcripts were not induced, nor would this have been expected, since this sequence falls within the CYP4C/V clade containing CYP forms whose roles have been postulated to include hormone-stimulated fatty acid oxidation during starvation (cockroach, CYP4C1) [ 65] and fatty acid metabolism in the retina in vertebrates (reviewed in [ 24]).
Disruption of this balance is postulated to underlie many pathological conditions, including tumorigenesis/tissue hyperplasia (due to excess self-renewal) and tissue degeneration/aging (due to excess differentiation).
The development of hormone resistance in ER+ but endocrine-refractory metastatic disease is postulated to involve signal transduction pathways, including mammalian target of rapamycin (mTOR).
These include millions of repetitive DNA elements for which methylation is postulated to silence parasitic and transposable activity.
Furthermore, AcpM is postulated to recognize enzymes belonging to the FAS II system (Trivedi et al., 2004), including MtbHadAB, and deliver the fatty acid chain to the dehydratases.
