More than 90% of the laboratory results for haemoglob in level, leucocyte count, and neutrophil count were available at each visit, with no difference between the randomization arms. Using the complete data method, the sample size remained large enough to demonstrate small statistical differences, even if the clinical signi?cance appears small. For the lymphocyte counts, however, only 33% of the laboratory results were available at 32 and 35 wk of gestation and at delivery. It is possible that the absence of signi?cant difference in lymphocyte evolution between the two groups could be explained by a lack of power. In comparing the ability of these constructs to promote luciferase gene expression during C2C12 differentiation to that of the wildtype construct, it is readily apparent that both can barely support transcription above the minTATA construct and that there is absolutely no induction when differentiation is triggered. It thus appears that the exonic sequence is necessary but not sufficient to enhance transcription. The PRI hypothesis predicts this outcome as both regions contain binding sites conserved in order and in spacing. One curious feature of this study is that, although there is strong differential reporter gene activity, MYOD binding does not appear to change between growing myoblasts and differentiating myotubes. The difference in activation but lack of change in MYOD ChIP could be explained by the strong recruitment of MYOG and the E-protein HEB upon the onset of differentiation. Perhaps MYOD positions the DNA and facilitates transcription by interacting with the canonical TFIID complex in myoblasts, but, having effected the necessary chromosomal arrangement, is swapped for a myogenin/HEB complex upon differentiation, which Schizandrin-B promotes even stronger transcriptional output. Two separate E-boxes in the ADAMTS5 exonic enhancer are required for robust transcriptional activation upon myogenic differentiation. This property is shared by the muscle-specific Diniconazole creatine kinase enhancer in which a pair of E-boxes has been shown to be required for cooperative binding to MYOD and subsequent transcriptional activation. It has been speculated that multiple site recognition is important for decoding the concentration of MYOD and stably engaging transcription machinery.