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For propensity score matching, for example, we can use the matched samples and regress the outcome of interest on the treatment variable to estimate the causal effect.
For example, sample 76629543 was clustered further away from the other matched samples and bottom right corner.
The percentage methylation was unchanged in two matched samples and was reduced in two samples compared to matched normal mucosa.
We used the Student's T test for matched samples and the Khi-2 test for the analysis of qualitative variables.
Our criteria for differential regulation were: (1) two-fold difference in expression with matched samples, and (2) non-overlapping 95% confidence intervals.
Normal and tumour DNA are hybridized to different arrays, therefore avoiding the need for matched samples and allowing for a pool of normal samples to be used as a control.
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(2) All the variables are one-year lagged and the definition of variables are presented in Appendix A. We re-estimate model (1) using the matched sample and the results are reported in Table 5.
However, we used a matched sample and report robust effect sizes.
Research using a larger matched sample and follow-up with patients receiving both the CA and the RAI-HC could be used to further explore the issues discussed in this paper.
First, we examined whether the observed results might be different for the nonelderly patients (aged <65 years) with a 1 4 matched sample, and the results are shown in supplementary Table A2 (available in an online appendix).
They were able to match stimuli which contained novel elements, also in random orientations, and to match sample and choice stimuli that contained different elements.
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