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In other words, genetic determinism was not an absolute truth; rather, genes were as much a part of the system as they were its cause.
Reaction conditions for all genes were as follows: initial denaturation at 95°C for 10 min followed by 40 cycles of 15 s at 95°C and 1 min at 60°C.
Criteria for the selection of genes were as follows: All pair-wise comparisons for one group versus another (e.g., mock-versus-SARS-CoV or DHOV-infected cells at 12 hr) were expected to be at least 1.5-fold and at least 50% greater than the fold-change observed between any two controls (e.g., mock-infected replicate 1 versus mock-infected replicate 2 at 12 hr).
Primers for the CES genes were as follows.
Primers for the internal control genes were as before [ 19].
Primer pairs for the amplification of target genes were as follows.
Primer sequences for MSP analysis of the remaining genes were as follows: Methylation was also analysed quantitatively by pyrosequencing.
PCR primers and conditions for amplification of icaA and icaB genes were as described by Frebourg et al [ 8].
The assay numbers for the endogenous control (β-actin) and target genes were as follows: 4326315E (β-actin); Hs00275833_s1 (FZD7).
Primers specific to the chosen marker genes were as described in Raynor et al, 2002 (Table 2) [ 10].
The threshold values for positively identified genes were as follows: Z-test P-value ≤0.05, the | Z-ratio|≥1.5 and the false discovery ratio ≤0.3.
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