Because we do not have a true gold-standard set of interactions, we cannot reliably hypothesize whether the imputed interactions with large relative ranks are because of a failure of the method (i.e. evolutionarily non-parsimonious interactions) or simply false-negatives in the input data.
Although we cannot say definitively, we hypothesize that this early rehabilitation contributed to the attainment of JRP goals (Table 1) and lengths of stay that were short compared with published literature.[ 42] Based on the reported results, the JRP program was considered successful.
Similarly, we hypothesize that we cannot rule out the effects of puberty and growth during childhood and adolescence on the impressionable breast and that it is during this critical time window of susceptibility not only that breast carcinogenesis is initiated, but that tumor biology and prognosis are determined.
It is plausible that this modulation involves transport, as we have hypothesized, but we cannot exclude other possible mechanisms.
Taken together, a possible involvement of HTR4 in trypanotolerance/susceptibility in cattle might be hypothesized though we cannot exclude an implication of this serotonin receptor in more general aspects of circadian rythmicity [ 50].
Although effect by other levels of regulation such as feedback control cannot be ignored, we hypothesize that change in soluble sugar levels in 14-3-3 14-3-3 14-3-3ulted frox the regulation of carbohydrate metabolic enzymes by 14-3-3 plantsns and the loweresulted in TCA cycle.
Since the expression of genes important for cell survival are generally stable under many different stimuli and cannot fluctuate extensively, we hypothesize and show that expression variation of essential genes is lower than that of non-essential genes and decreases with toxicity degree within non-essential genes.
Although the current study cannot explain this finding, we could hypothesize that, despite their poor control, some in this group remained using basal insulin alone at study baseline because of resistance to further insulin intensification, and that this resistance limited the impact of GMC.
At this stage we cannot explain the mechanisms behind this observation, although we may hypothesize that the reduction in other granule compounds may facilitate the accumulation of β-hexosaminidase.
