However, based on the relationship between sirtuins and oxidative stress14 and the evidence from the above-described in vitro data13, it can be hypothesized that either pharmacological or genetic activation of SIRT1 could prevent fat-induced decrease in β-cell function in vivo.
It can be hypothesized that, either the electrostatic interactions of the highly cationic C-ter domain with the negatively charged N-ter domain and extracellular loops of CXCR4 [40], or the steric hindrance promoted by the bulky basic residues in the γ-wt C-ter domain, impair the specific interaction with CXCR4 and therefore reduce the agonist potency of γ-wt.
Data on clinical status was not considered in these studies and it can be hypothesized that either the oldest residents were less ill or that physicians were more cautious when prescribing to very old patients.
In contrast, expression of most chloroplast antioxidant enzymes is induced up to a certain stress level, but decreased in response to severe oxidative stress conditions, such as application of high concentrations of H2O2 [ 4, 9, 19] [Heiber et al., unpublished data], it is hypothesized that either a plus-minus regulator or interacting antagonistic signalling pathways control gene expression.
It has been hypothesized that upregulation of either KGF or KGFR expression may contribute to venous invasion, possibly through induction of VEGF-A expression, thus causing a higher risk of metastasis [39].
It has been hypothesized that CMV either directly infects the vessels of the heart and replicates at low levels, or is delivered to the vessel wall by infected circulating monocytes arriving at sites of cardiovascular injury or inflammation [24].
It has been hypothesized that the magnetochromes can either donate electrons to Fe(III) and participate in magnetite [mixture of Fe(III) and Fe(II)] formation or accept electrons from magnetite to maintain a redox balance, or they can act as redox buffers to maintain a proper ratio of maghemeite (all ferric irons) and magnetite.
It has been hypothesized that oxidative stress either via increasing reactive oxygen species or by depleting the antioxidants may modulate the genesis of early glycated proteins in vivo (10, 11).
