19 research outputs found

    Annual mean levels of air pollutants at residential address, by year and averaged across study period, μg/m<sup>3</sup>.

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    <p>Values are mean ± SD (range);</p><p>* air pollution data were not available for two participants (one in each of Years 1 and 2 of the study) because their residential addresses were outside the Greater London area</p><p>Annual mean levels of air pollutants at residential address, by year and averaged across study period, μg/m<sup>3</sup>.</p

    Odds ratios for associations of potentially confounding variables with prevalence of lifetime (ever having had) asthma, hay fever and eczema.

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    <p>Data shown as odds ratio (OR) for unit increase in variable unless otherwise stated, with 95% confidence intervals in brackets; ORs adjusted for all variables shown in table; ETS exposure = positive urinary cotinine:creatinine ratio (CCR ≥ 30ng/mg);</p><p>* p<0.05</p><p>**p<0.01</p><p>Odds ratios for associations of potentially confounding variables with prevalence of lifetime (ever having had) asthma, hay fever and eczema.</p

    Odds ratios for associations of potentially confounding variables with prevalence of current respiratory/allergic symptoms.

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    <p>Data shown as odds ratio (OR) for unit increase in variable unless otherwise stated, with 95% confidence intervals in brackets; ORs adjusted for all variables shown in table; ETS exposure = positive urinary cotinine:creatinine ratio (CCR ≥ 30ng/mg);</p><p>* p<0.05</p><p>**p<0.01</p><p>Odds ratios for associations of potentially confounding variables with prevalence of current respiratory/allergic symptoms.</p

    Prevalence of current respiratory/allergic symptoms among all children, and by sex and ethnicity.

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    <p>Percentages are for rows, except for first column which reads vertically (e.g. 49.9% of all respondents were male; 14.1% of males have current wheeze); percentages may not add to 100.0 due to rounding</p><p>Prevalence of current respiratory/allergic symptoms among all children, and by sex and ethnicity.</p

    Exposure to air pollution as a risk factor for current and lifetime respiratory/allergic symptoms.

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    <p>Adjusted associations between air pollutants and the prevalence of current and lifetime respiratory/allergic symptoms. Odds ratios adjusted for age, sex, BMI, socio-economic deprivation (IMD score), ETS exposure and year of study, with a random effect for school. Single-pollutant models were calculated for each air pollutant. Odds ratios are for unit increase in pollutant, in μg/m<sup>3</sup>. Current symptoms defined as within the last 12 months; lifetime conditions defined as ‘having ever had’ asthma, hay fever or eczema. Vertical dotted line indicates null (OR = 1). Horizontal lines indicate 95% confidence intervals of odds ratios. * p<0.05, **p<0.01</p

    Circulating immunological correlates of time to sputum culture conversion in PTB patients of African vs.

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    <p><b>Eurasian ancestry.</b> Higher ESR and serum MMP-1 concentration associated with slower sputum culture conversion in patients of African and Eurasian ancestry alike (A–B, p≤0.0080). Higher red blood cell count and lower serum vitamin D binding protein concentration associated with slower sputum culture conversion in patients of African ancestry but faster sputum culture conversion in those of Eurasian ancestry (C–D, p≤0.0075). Lower serum concentrations of CCL11 and IL-7 associated with slower sputum culture conversion in patients of African ancestry (p≤0.0028), but did not associate with treatment response in those of Eurasian ancestry (E–F). Higher plasma concentrations of cathelicidin LL-37 and lower serum concentration of CXCL10 associated with slower sputum culture conversion in patients of Eurasian ancestry (p≤4.98×10<sup>−05</sup>), but did not associate with treatment response in those of African ancestry (G–H). Fast (solid lines) vs. slow (dashed lines) sputum clearance defined as time to sputum culture conversion <37.25 days vs. ≥37.25 days, respectively. Means ± SEM at 0, 2, 4, 6 and 8 weeks of treatment are presented. Data for all parameters except red blood cell count were normalised by log<sub>10</sub> transformation and the y-axis presented as 10∧(log value). P-values were generated using rank regression with covariates on the interaction term ‘week of sampling*speed of sputum culture conversion, with adjustment for the following covariates: age, sex, months of symptoms pre-diagnosis, duration of antimicrobial therapy pre-sampling, isoniazid sensitivity, allocation to vitamin D vs. placebo, week of sampling and subject ID. Parameters with a false discovery rate (q-value)>0.05, determined by the Benjamini Hochberg approach, were designated non-significant (ns).</p

    Serum vitamin D binding protein (DBP) concentration in patients with newly-diagnosed PTB by <b><i>DBP</i></b><b> genotype and ethnic group.</b>

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    <p>DBP concentration varied with <i>DBP</i> genotype, with patients of Gc1F/1F genotype having the lowest concentrations, and those with Gc1S/1S genotype having the highest concentrations, irrespective of ethnic group (p<0.0001 for comparison by genotype with ethnic groups pooled; p>0.05 for ethnic comparison within each genotype). Kruskal-Wallis test with Dunn's multiple comparison test. AFR, African ancestry; EUA, Eurasian ancestry.</p

    Principal component analysis (PCA) plots generated using immunological parameters which contribute to variation in baseline inflammatory profile between PTB patients of African and Eurasian ancestry.

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    <p>Each point represents one patient, and its position in the plot is determined by the combined effects of all parameters measured for that patient sample that contribute significantly to ethnic variation in inflammatory profile. The distance between sample points represents Euclidean distance. The first 3 component vectors are displayed, along with a % figure signifying the proportion of the variability in the data that each component accounts for. Points representing patients with Eurasian ancestry have been coloured according to their ethnic subgroup (Central/South Asian (blue) and European/Middle Eastern (yellow) ancestry) to demonstrate that they cluster together and that they are separated from those representing patients of African ancestry (black). One patient of mixed South Asian and European ancestry is classified as a Eurasian (green) and clusters within samples from the Eurasian subgroups. A, PCA plot of circulating immunological parameters in patients of African (n = 45), Central/South Asian (n = 55), European/Middle Eastern (n = 27) and Eurasian (n = 1) ancestry at baseline. B, PCA plot of rCFP-10-stimulated immunological parameters in patients of African (n = 13), Central/South Asian (n = 22) and European/Middle Eastern (n = 7) ancestry at baseline.</p
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