Although several mechanisms have been postulated for alcoholic cardiomyopathy, including oxidative damage, accumulation of triglycerides, altered fatty acid extraction, decreased myofilament Ca2+ sensitivity, and impaired protein synthesis, neither the mechanism nor the ultimate toxin has been unveiled.
The etiopathogenesis of hydranencephaly is heterogeneous, and so several theories have been postulated for its occurrence.
Several mechanisms have been postulated for the causal role of UA in the progression of renal disease.
Several mechanisms have been postulated for alcoholic cardiomyopathy including oxidative damage, accumulation of triglycerides, altered fatty acid extraction, decreased myofilament Ca2+ sensitivity, and impaired protein synthesis.
Several hypotheses have been postulated for causing overflow metabolism of acetate, mainly involving imbalance between glucose uptake and TCA cycle or energy and biomass generation throughput [ 44, 47].
Several mechanisms have been postulated for this relationship including the neurotoxic effects of chronic hypercortisolaemia, reduced levels of neurotrophic factors [ 39], alterations in glial-neuronal networks, vascular disease and inflammatory processes [ 40].
Several functions have been postulated for SODs in chloroplasts like protection to oxidative stress (by controlling superoxide and hydrogen peroxide in the water water cycle and control of free redox-active metals), photoprotection, regulation of electron transport and signaling.
Several mechanisms have been postulated for oleocanthal protective effect against AD such as inhibition of Aβ and tau aggregation supported by in vitro results and enhancement of stereotaxically microinjected Aβ clearance across the BBB of wild-type mice.
Several regulatory mechanisms have been postulated for this type of asRNA.
Several biological mechanisms have been postulated for susceptible populations to heat-related mortality, particularly the elderly [ 7].
