This suggestion is explained in suggestions eight and nine.
This can be explained in terms of either saturation of the limited number of accessible active sites on the photocatalyst surface that leads to a decrease in degradation efficiency, or poisoning (deactivation) of the active sites of the catalyst.
This can be explained in two ways: either recorded patients characteristics are not the correct predictors of response, or response is not adequately defined (e.g., by FEV1, which is used in most studies).
Such effect may be explained in part by either a decrease in the rate of intestinal glucose absorption [ 23- 25] or an increase in peripheral glucose utilization [ 24, 25].
The second objective is to interpret any patterns observed and, in particular, to see if clustering can be explained in terms of either infectious agents or environmental hazards as aetiological agents.
This conundrum may be explained in part either by selective inhibition of the various isoforms of NOS or by an ancillary non-vascular function of NOS.
These findings can be explained in two ways; either by the occurrence of saturation of tubular reabsorption due to increased tubular delivery of hepcidin-25 thus exceeding reabsorption capacity or by production of hepcidin-25 locally in the kidney.
Some studies reported the presence of extremely low levels (<0.1%) of JAK2V617F in healthy people, which may be explained in two ways: either the mutation can be transient or the mutant allele burden can rise from undetectable to detectable levels throughout time and those patients are in a preclinical phase.
A decrease in the blood flow velocity measured within the middle cerebral artery may theoretically be explained in two ways: either the large and medium-size vessel (the middle cerebral artery) is dilated or there is a vasoconstriction at the level of resistance arterioles of its corresponding territory.
The lack of sister separation in PIASγ/hSgo1 doubly depleted cells could be explained in one of two ways: either, (1) PIASγ is required for cohesin removal even in the absence of the cohesin guardian, or (2) sister chromatids remain cohered at the centromeres in the absence of cohesin.
The equivalence of these protons can be explained in two different ways, either by rapid interconverting conformers of the 1,3,5-triazepane ring, which can adopt two conformations (Figure 3) on the NMR time scale, or by the virtual chemical equivalence of these protons.
