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Final models were determined using a change in estimate approach, where variables were retained if significant (p < 0.05) or confounders (defined as a 10%% change in adjusted odds ratio).
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The best fitting polynomial transformation that captured this change was determined using a modification of a SAS macro from Sauerbrei [ 24].
Genes expressed differentially between H and FS were determined using a log2 fold change of ≥3·0.
Differentially regulated metabolites were determined using a threshold of fold change greater than 1.5 between butanol-treated samples and controls.
In our study the elements that constituted the HKC-intervention were determined using a theoretically based behavioural change system.
The extent of biofilm formation was determined using a microarray scanner from changes in fluorescence intensities due to FUN 1 metabolic processing.
Changes in the target mRNA content relative to β-actin mRNA were determined using a comparative CT method to calculate changes in CT, and ultimately fold and percent change.
The variance of change was determined using a correlation factor of 0.5.
Motivation to quit was also determined using a questionnaire based on 'Stage of Change' [ 11].
Gene expression levels, expressed as "relative fold change", were determined using a method comparable to the 2-ΔΔCt method described by Pfaffl [ 16], where the point of peak cycling acceleration was extrapolated to represent maximum fold change.
Enthalpy changes were determined using a Setaram C80D microcalorimeter equipped with high pressure cells.
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