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Our threshold models detected modest geographical variation in exercise participation.
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Although these limitations may have diminished our ability to detect modest associations with postnatal exposure to PCBs, the use of a pharmacokinetic model enabled us to retrospectively investigate early PCB exposures in a cohort with no measured levels in infancy.
Perhaps the dilution in relatively large cells was too effective to detect modest contributions of tracer through preferential flow paths.
Assuming a recessive mode of inheritance, the association was not significant in either population study but our power to detect modest effects was limited.
Forth, our relatively small sample size may not sufficiently powerful to detect modest association.
5 However, the study was underpowered to detect modest effects.
Thus, we were not well-powered to detect modest risks.
Second, the sample size was too small to detect modest changes in glycemic control.
The discrepancy between these results may reflect the issue of heterogeneity to detect modest effect sizes.
Subject numbers could limit statistical power to detect modest differences in glycemia reflected by CGM.
However, the number of subjects affected was too small to reliably detect modest reductions in immunogenicity.
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