Additional file 1: of Inoculation with enterococci does not affect colon inflammation in the multi-drug resistance 1a-deficient mouse model of IBD

Representation of the overall investigation of which this study forms a part. Description of data: a figure showing how this study of the impact of bacterial inoculation forms part of a larger investigation into the effects of dietary polyphenols [6, 8] on intestinal inflammation in the Mdr1a –/– mouse model of IBD. The figure shows how a common set of control mice was used for the overall investigation. (PDF 402 kb

Influence of lifestyle and genetic variants in the <i>aldo-keto reductase 1C3</i> rs12529 polymorphism in high-risk prostate cancer detection variability assessed between US and New Zealand cohorts

<div><p>Introduction</p><p>The prostate-specific antigen (PSA) based prostate cancer (PC) screening is currently being debated. The current assessment is to understand the variability of detecting high-risk PC in a NZ cohort in comparison to a US cohort with better PSA screening facilities. Aldo-keto reductase 1C3 (AKR1C3) is known for multiple functions with a potential to regulate subsequent PSA levels. Therefore, we wish to understand the influence of tobacco smoking and the AKR1C3 rs12529 gene polymorphism in this variability.</p><p>Method</p><p>NZ cohort (n = 376) consisted of 94% Caucasians while the US cohort consisted of African Americans (AA), n = 202, and European Americans (EA), n = 232. PSA level, PC grade and stage at diagnosis were collected from hospital databases for assigning high-risk PC status. Tobacco smoking status and the AKR1C3 rs12529 SNP genotype were considered as confounding variables. Variation of the cumulative % high-risk PC (outcome variable) with increasing PSA intervals (exposure factor) was compared between the cohorts using the Kolmogorov-Smirnov test. Comparisons were carried out with and without stratifications made using confounding variables.</p><p>Results</p><p>NZ cohort has been diagnosed at a significantly higher mean age (66.67± (8.08) y) compared to both AA (62.65±8.17y) and EA (64.83+8.56y); median PSA (NZ 8.90ng/ml compared to AA 6.86ng/ml and EA 5.80ng/ml); and Gleason sum (NZ (7) compared EA (6)) (p<0.05). The cumulative % high-risk PC detection shows NZ cohort with a significantly lower diagnosis rates at PSA levels between >6 - <10ng/ml compared to both US groups (p<0.05). These were further compounded significantly by smoking status and genetics.</p><p>Conclusions</p><p>High-risk PCs recorded at higher PSA levels in NZ could be due to factors including lower levels of PSA screening and subsequent specialist referrals for biopsies. These consequences could be pronounced among NZ ever smokers carrying the <i>AKR1C3</i> rs12529 G alleles making them a group that requires increased PSA screening attention.</p></div

Cumulative % high-risk PC as a fraction of all PCs by PSA groups.

<p>(NZ = New Zealanders, AA = African Americans, EA = European Americans. Points of significant differences (p<0.05) are shown according to the Kolmogorov-Smirnov test results. Full double headed arrow = maximum difference between EA and NZ. Dashed double headed arrow = maximum difference between AA and NZ).</p

Cumulative frequency of high-risk PC as a fraction of all high-risk PCs by PSA groups in study cohorts.

<p>(NZ = New Zealanders, AA = African Americans, EA = European Americans S = ever smokers NS = never smokers. Points of significant differences (p<0.05) are shown according to the Kolmogorov-Smirnov test results. Full double headed arrow = maximum difference between EA and NZ. Dashed double headed arrow = maximum difference between AA and NZ).</p

Genetic and ethnic stratification of high-risk PCs as fractions of all high-risk PCs in each PSA interval.

<p>Genetic and ethnic stratification of high-risk PCs as fractions of all high-risk PCs in each PSA interval.</p

Patient characteristics compared between the study cohorts.

<p>Patient characteristics compared between the study cohorts.</p

Cumulative frequency of high-risk PCs as a fraction of all high-risk PCs by PSA groups, genotype and tobacco smoking status.

<p>(AA = African American EA = Caucasian American NZ = New Zealanders S = ever smokers NS = never smokers. Points of significant differences (p<0.05) are shown according to the Kolmogorov-Smirnov test results. Full double headed arrow = maximum difference between EA and NZ. Dashed double headed arrow = maximum difference between AA and NZ).</p

Cumulative % high-risk PC as a fraction of all PCs by PSA groups separated by smoking status.

<p>(NZ = New Zealanders, AA = African Americans, EA = European Americans. S = ever smokers NS = never smokers. (Points of significant differences (p<0.05) are shown according to the Kolmogorov-Smirnov test results. Full double headed arrow = maximum difference between EA ever smokers and NZ ever smokers. Dashed double headed arrow = maximum difference between AA ever smokers and NZ ever smokers).</p

High-risk PC statistics against genotype, smoking status and PSA interval among study groups.

<p>High-risk PC statistics against genotype, smoking status and PSA interval among study groups.</p

Genotype and allele frequencies recorded between study cohorts.

<p>Genotype and allele frequencies recorded between study cohorts.</p