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Until there is empirical evidence on the sensitivity to change and measurement error of these outcome measures, we cannot properly interpret results obtained from these outcome measures.
In this study, because we have no objective adherence measure with which to compare our adherence measures, we cannot identify the portion of our measurement that is error, and we cannot directly compare our findings with other studies that use related items in different populations [ 16– 16].
Without an agreed definition and adequate measures, we cannot study compassion, measure compassion or evaluate whether interventions designed to enhance compassion are effective.
In the absence of objective measures, we cannot be entirely confident that the reported levels of functional limitations in the participating countries are not influenced by different perceptions.
Therefore, with regards to behaviour measures we cannot be sure that the benefits of the interventions will be maintained over time.
Without good measures we cannot identify those that do benefit from treatments and those who do not benefit and for whom possibly other less invasive treatments may be more appropriate.
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Finally, although serum S100B measurements are a valid measure, we cannot entirely exclude alterations of blood brain barrier functioning in alcohol-addicted subjects [ 42] as the cause of these slightly higher initial S100B serum levels.
When we have the data measured, we cannot save them as a regular matrix, so we use a general set of xyz values for storing the data.
While TEM showed a continual increase in NP cluster size inside cells with increasing exposure time (Figure 5 and Additional file 1: Figure S3), indicating that agglomeration of NPs within cellular endosomes contributes to the spectral shift we measured, we cannot rule out the possibility that some NPs may remain adsorbed to the cell surface after rinsing.
Results reported here (low or normal CSF glutamate) argue against a major role for glutamate excitotoxicity, although as GABA is not routinely measured, we cannot exclude GABA deficiency as a potential seizure mechanism.
Since MMP activity in membranous fractions was not measured, we cannot exclude the possibility that differences in these activities occurred in our systems and that these differences could be regulated by S100A4.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com