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The higher rate of nsSNPs in the latter category, resulting in a higher phenotypic diversity, might be explained by uncertain gene categorization because of currently limited knowledge of gene function.
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The higher odds ratios in the additional analysis restricted to cases with anticoagulation prescriptions than those from the main analysis can be explained by a combination of the exclusion of uncertain events and differential anticoagulant prescribing by doctors.
However, it is as yet uncertain whether these findings can be explained by the concept that CTLA4 transduces 'negative' signals to activated effector T cells.
It is uncertain whether this observation can be explained by genetic differences in the populations, different environmental factors or a combination of both (gene-environment interactions) [ 36].
However, because it is uncertain whether the data may be explained by the effects of sorafenib or those of innate hepatic progressive disease, these results should be interpreted with caution.
By contrast, the lower risk of death in association with cystic kidney disease, which remained after adjustment for prognostic risk factors, is of uncertain clinical significance and plausibly could be explained by residual confounding (such as unmeasured comorbid conditions).
97, 98 Whenever MFS remains uncertain or diagnostic triggers of other diseases are observed, phenotypes should be explained by the presence of alternative syndromes, such as Loeys Dietz syndrome.
This may be explained by the extent to which strategic control is in the hands of those who have the incentives and abilities to allocate resources to uncertain and irreversible investments in innovation.
This can be explained by different scenarios.
This could be explained by human selection.
This can be explained by multiple possibilities.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com