Distribution of <i>r</i>_MZ−2<i>r</i>_DZ for all traits on human twins.

<p>Data are from published papers by N.G. Martin and colleagues of the Queensland Institute of Medical Research, Brisbane (<a href="http://www.genepi.edu.au" target="_blank">www.genepi.edu.au</a>). Across a wide variety of traits the mean difference between the monozygotic twin correlation and twice the dizygotic twin correlation is close to zero, which is consistent with predominantly additive genetic variance and the absence of a large component of variance due to common environmental effects.</p

Summary of expected proportion of <i>V</i>_G that is <i>V</i>_A for different models^a.

a<p>Models defined in Methods section</p>b<p>Population size</p

Expected variance contributed by mutant genes before fixation for population size 100, specified dominance on the quantitative trait (<i>a</i> vs <i>d</i>) and selective (dis)advantage (<i>s</i> in heterozygote and homozygote)^a.

a<p>e.g., if the mutant gene is completely recessive for the trait and for fitness, <i>d</i> = −<i>a</i> and <i>s</i>(hom) = 0.</p>b<p>Equally likely to be completely dominant or recessive mutants, hence values as in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000008#pgen-1000008-t002" target="_blank">Table 2</a>.</p

Meta-analysis of MZ and DZ correlations in humans^a.

<p>These show the correlations (<i>r</i>) of phenotypes of twins, averaged over ranges of traits estimated in large data sets</p>a<p>Data from published papers by N.G. Martin and colleagues of the Queensland Institute of Medical Research, Brisbane (<a href="http://www.genepi.edu.au" target="_blank">www.genepi.edu.au</a>)</p>b<p>Opposite sex</p

Examples of expected proportion of <i>V</i>_G that is <i>V</i>_A in highly epistatic published QTL analyses assuming gene frequency distributions as in Table 2.

a<p>Values obtained from tables or by interpolation from Box 1c–e of Carlborg and Haley <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000008#pgen.1000008-Carlborg1" target="_blank">[8]</a>: key to their nomenclature: DomEp: Dominant epistasis (complex); Co-ad: Co-adaptive epistasis; D × D: dominance × dominance epistasis.</p>b<p>Uniform.</p>c<p>U-shaped with population size of 100.</p>d<p>U-shaped with population size of 1000.</p

Bias in use of E(<i>V</i>_A)/E(<i>V</i>_G) rather than E(<i>V</i>_A/<i>V</i>_G) for some models in Table 2 as a function of Numbers of Loci.

a<p>Number of loci for non-epistatic cases (complete dominance <i>a</i> = 1, <i>d</i> = 1, and overdominance <i>a</i> = 0, <i>d</i> = 1), numbers of pairs of loci for two-locus epistatic models (A × A and duplicate factor.</p>b<p>Not computed as <i>V</i>_G = 0 in some replicates.</p

Examples of expected proportion of <i>V</i>_G that is <i>V_A</i> in models of flux in linear metabolic pathways with a model flux <i>J</i>∝[Σ<i>_i</i>(1/<i>E_i</i>)]⁻¹ for a system with 10 loci in which 8 are invariant wild type and two (B, C) are mutants.

<p>Enzyme activities are <i>E_i</i> = 1 for loci 3 to 8, <i>E</i>_BB = <i>E</i>_CC = 1, values of <i>E</i>_bb and <i>E</i>_cc are listed, and heterozygotes are intermediate, e.g. <i>E</i>_Cc = ½(1+<i>E</i>_cc), assuming gene frequency distributions as in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000008#pgen-1000008-t002" target="_blank">Table 2</a>. Flux modelled as <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000008#pgen.1000008-Keightley1" target="_blank">[39]</a>.</p>a<p>Uniform</p>b<p>U-shaped with population size of 100</p>c<p>U-shaped with population size of 1000</p

Alveolar neutrophil recruitment 24 hours after LPS.

<p>Impact of carbon monoxide (CO) exposure on neutrophil (PMN) percentage (<b>A</b>) and number/ml (<b>B</b>) in lung lavage fluid of untreated animals (no LPS or CO), or mice treated with 10 ng intratracheal LPS. LPS-challenged mice were exposed to either 0 (air), 50, 100, 200, or 500 ppm CO for 24 hours both before and after LPS. *p<0.05, **p<0.01 ***p<0.001 vs LPS +0 ppm CO; n = 19 for LPS +0 ppm CO, and 8–12 for all other groups (numbers are higher in the LPS+0 ppm CO group because, as our primary control, we ran 1–2 of these animals alongside the experiments for each of the other groups).</p

Indicators of side-effects with low dose inhaled carbon monoxide.

<p><b>A</b>. Carboxyhemoglobin (COHb) level in blood of animals exposed to carbon monoxide (CO) for 24 hours both before and after lipopolysaccharide (LPS) instillation. Only COHb data from the first mouse removed from the chamber are shown to minimise the confounding effects of dropping the CO concentration upon opening the chamber. ***p<0.001 vs 0 ppm CO, n = 4–5/group. <b>B</b>. Percentage weight loss in the 24 hours following LPS instillation, in mice exposed to 0, 100, 200 or 500 ppm. ***p<0.001 vs 0 ppm CO, n = 8–12/group. <b>C</b>. CO₂ level in chamber. CO₂ levels were recorded every 30 minutes: data represent average level in the 24 hour period prior to LPS instillation (to avoid potential confounding effects of anesthetic/LPS). ***p<0.001 vs 0 ppm CO, n = 3–5 experiments, with 4 mice in the chamber each experiment.</p

Impact of CO exposure either pre- or post- LPS challenge on alveolar neutrophil recruitment.

<p>Neutrophil (PMN) % (<b>A</b>) and number/ml (<b>B</b>) in lung lavage fluid of mice exposed to 100 ppm carbon monoxide (CO) for 24 hours either before or after lipopolysaccharide (LPS) instillation. *p<0.05, **p<0.01 vs 100 ppm CO pre-LPS; n = 8/group. For comparison, data from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0011565#pone-0011565-g001" target="_blank">Figure 1</a> of the animals exposed either to 0 ppm or 100 ppm CO for 24 hours both pre- and post-LPS are shown (but not included in statistical analysis).</p