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In our phase synchrony analyses, we tested the H0 hypothesis that the two series of phase values, namely ϕi and ϕj, were independent.
In our analyses, we tested the effects of feedback type on several dependent variables.
In a number of supplementary analyses we tested the robustness of the main findings.
In all analyses, we tested the previously identified potential drivers of spatial patterns and demography.
In our sensitivity analyses we tested the implications of applying higher price elasticities.
In sensitivity analyses we tested the effect of three main assumptions made in the modelling.
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As this would affect the validity of meta-analyses, we tested the hypothesis that the reported effect size decreases over time.
After the in vitro analyses, we tested whether the combination therapy could modulate the phenotypic markers of cells in the xenograft model.
Finally, in exploratory analyses, we tested whether the predicted relationships between the outcome variables and the goal variables would differ for individuals reporting high versus low levels of depressive symptoms or trait rumination.
Using the results from these analyses, we tested for the influence of blood lead on multiple outcomes using the Multiple Indicator Mult iple Causes (MIMIC) model under the umbrella of Structural Equations Modeling (SEM).
Therefore, in subsequent analyses we tested for the (rare) substitution of Leucine for isoleucine at codon 164 of dhfr, and performed a full analysis of the dhps gene at codons 436, 437, 540, 581 and 613.
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CEO of Professional Science Editing for Scientists @ prosciediting.com