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To further test this conclusion, the team performed computer simulations designed to distinguish between natural selection and "genetic drift," a change in the frequency of genetic variants due just to chance.
Although many documents discuss excess returns caused by medium-term momentum and long-term reversal in the US market, we empirically test this conclusion using the method of Jegadeesh and Titman (1993).
Depletion of CD8 cells during CCL3 depletion is required to test this conclusion.
We discuss what experiments would be required to test this conclusion more generally.
To test this conclusion further we employed several methods that are known to inhibit clathrin-mediated endocytosis.
To further test this conclusion, we then extended our analysis to adult wing development, for which the role of EGFR regulatory cascade is well established [41].
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We tested this conclusion employing LM-PCR protocols designed to avoid bias.
We tested this conclusion by growing 1.65 × 10 Fhit-deficient and UVC-surviving Fhit-deficient cells in 6-thioguanine and counting surviving colonies, as an assay for frequency of HPRT mutations.
For instance, although the majority of studies have reported that the rs3775290 variant T allele was associated with an increased cancer risk (odds ratio [OR] > 1), four studies testing this conclusion did not reach statistical significance (P > 0.05) [ 5– 8] and only one additional study produced significant results (P < 0.05) [ 9].
As a further test of this conclusion, the paclitaxel analog 4 was designed as a compound which has all the chemical functionality necessary for activity, but which cannot adopt the T-Taxol conformation.
The chi-square test confirmed this conclusion by showing that the two types of promoters differed in windows centered at −94 to −65, and pinpoint the difference to be centered within basonuclin binding site B (Fig. 6C).
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