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BASIC REVIEW

The New Genetics and Chronic Obstructive Pulmonary Disease

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Pages 257-264 | Published online: 02 Jul 2009

Figures & data

Figure 1 A simplified diagram showing key inflammatory pathways and cells implicated in the pathogenesis of COPD (reproduced with permission from Resp. Research – Wood et al., 2006).

Figure 1 A simplified diagram showing key inflammatory pathways and cells implicated in the pathogenesis of COPD (reproduced with permission from Resp. Research – Wood et al., 2006).

Figure 2 LD and Tag SNPS. In (a), all 10 SNPs are in complete LD; genotyping one SNP will, therefore, provide information about all 10. In (b), the unshaded SNPs are in complete LD with each other as are the shaded SNPs. In this case, genotyping one shaded and one unshaded will provide information about all 10 sites.

Figure 2 LD and Tag SNPS. In (a), all 10 SNPs are in complete LD; genotyping one SNP will, therefore, provide information about all 10. In (b), the unshaded SNPs are in complete LD with each other as are the shaded SNPs. In this case, genotyping one shaded and one unshaded will provide information about all 10 sites.

Figure 3 The effects of sample size on power as a function of allele frequency in a recessive and dominant model of inheritance. The bold line shows that for a dominant model, a sample size of 2,000 has 90% power to detect an association for a minor allele frequency of 5%, but only about 40% power in a recessive model with a minor allele frequency of 15% (power figures obtained using CaTS software and graph drawn from data.

Figure 3 The effects of sample size on power as a function of allele frequency in a recessive and dominant model of inheritance. The bold line shows that for a dominant model, a sample size of 2,000 has 90% power to detect an association for a minor allele frequency of 5%, but only about 40% power in a recessive model with a minor allele frequency of 15% (power figures obtained using CaTS software and graph drawn from data.

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