IRR for CRC for tertiles of intake of dietary factors for the studied polymorphisms.

<p>^a Analysis adjusted for smoking status, alcohol intake, HRT status (women only), BMI, use of NSAID, intake of red and processed meat, and dietary fibre.</p><p>^b P-value for interaction between polymorphisms and dietary factors for the adjusted estimates</p><p>Women: Tertiles of red and processed meat (<74.7773 g, 74.7773 g < and < 102.086 g, >102.086 g), fish (<27.2196 g, 27.2196 g < and < 43.6676 g, > 43.6676 g), dietary fibre (<16.9701 g, 16.9701 g < and < 22.0983 g, > 22.0983 g), cereals (<135.539 g, 135.539 g < and < 190.481 g, > 190.481 g), fruit (<141.858 g, 141.858 g < and < 266.488 g, > 266.488 g), vegetables (<121.870 g, 121.870 g < and < 213.721 g, > 213.721 g), laktose (<7.54871 g, 7.54871 g < and < 17.1355 g, > 17.1355 g), dairy products (<218.144 g, 218.144 g < and < 454.235 g, > 454.235 g), alcohol (<4.31931 g, 4.31931 g < and < 12.9957 g, > 12.9957 g).</p><p>Men: Tertiles of red and processed meat (<116.935 g, 116.935 g < and < 159.387 g, >159.387 g), fish (<33.3477 g, 33.3477 g < and < 52.7767 g, > 52.7767 g), dietary fibre (<17.5748 g, 17.5748 g < and < 22.4931 g, > 22.4931 g), cereals (<166.378 g, 166.378 g < and < 233.859 g, > 233.859 g), fruit (<90.9913 g, 90.9913 g < and < 193.509 g, > 193.509 g), vegetables (<105.532 g, 105.532 g < and < 186.459 g, > 186.459 g), laktose (<7.93777 g, 7.93777 g < and < 17.2082 g, > 17.2082 g), dairy products (<217.360 g, 217.360 g < and < 461.449 g, > 461.449 g), alcohol (<14.4960 g, 14.4960 g < and < 37.1134 g, > 37.1134 g).</p><p>IRR for CRC for tertiles of intake of dietary factors for the studied polymorphisms.</p

Linkage disequilibrium-maps for A) <i>NLRP3</i>, B) <i>TLR5</i>, and C) <i>TLR10/1</i>.

<p>Numbers in squares represent r². Darker red indicates stronger linkage disequilibrium. Maps were made using Haploview software version 4.2 and CEPH/CEU HapMap dataset (Phase II+III merged, release 28/ August10). HapMap data were downloaded by respective genes (<i>TLR5</i> and <i>NLRP3</i>) and for <i>TLR10/1</i> data spanning both genes. To simplify LD-maps, SNPs were selected in the following way: NLRP3: minor allele frequency (MAF) >0.1, Hardy-Weinberg equilibrium (HW) p-value >0.01, genotype>50%, force include: rs10754558, force exclude #4–29; TLR5: MAF >0.1, HW p-value >0.01, genotype>50%, force include rs5744176, force exclude # 17–25; TLR10/1: MAF >0.1, HW p-value >0.01, genotype>50%, force include rs11096957, force exclude #4–58, 98–111.</p

Baseline clinical characteristics and treatment response of the study population.

<p>SD: standard deviation; DMARD: disease modifying anti-rheumatic drugs; VAS: visual analogue scale; ΔVAS: baseline VAS minus follow-up VAS; TJC: tender joint count; SJC: swollen joint count; HAQ: health assessment questionnaire; CRP: C-reactive protein; DAS28: disease activity score (28-joints); EULAR: European League Against Rheumatism; ACR50: American College of Rheumatology, 50% improvement; RelDAS28: relative change in DAS28;</p><p>^#: Two-sided t-test p-value of difference in means/proportions between seropositive and seronegative patients; Seropositive: Positive for IgM-RF</p><p>Baseline clinical characteristics and treatment response of the study population.</p

Odds ratio for association between polymorphisms in <i>IL18</i>, <i>NLRP3</i>, <i>TLR1</i> and <i>TLR5</i> and EULAR good/moderate vs. none and good vs. moderate/non-response, respectively.

<p>For <i>TLR5</i> rs5744174, patients were also stratified on diagnosis based on IgM-RF (seropositive-/seronegative RA). Log scale, 95% confidence interval.</p

<i>NFKB1</i> mRNA levels in morphologicallynon-affected and affected tissues normalised to the <i>β-actin</i> mRNA level.

<p>NS = not significant.</p>a<p>P-value for the comparison to the expression levels in tissue from healthy individuals using Kruskal Wallis and Dunńs Multiple Comparison test.</p>b<p>P-value for the comparison of the expression levels in normal and affected tissue from the same individual using Paired Student’s t-test.</p

Characteristics of study participants.

1<p>There were significantly more males in the group with mild dysplasia and colorectal cancer compared to the group of healthy individuals (p<0.001, Chi squared test).</p>2<p>The age is significant higher among patients with CRC compared to the three other groups (Kruskal-Wallis and Dunn's Multiple Comparison test, p<0.001).</p>3<p>Normal endoscopy.</p

Polymorphisms’ effect on anti−/pro-inflammatory signal and chance of good anti-TNF response (EULAR good/moderate or ACR50).

<p>EULAR (*): European League Against Rheumatism ACR50 (#): American College of Rheumatology response criterion (50% improvement).</p

Genotypes of associated polymorphisms and adjusted odds ratios for associations between gene variants and EULAR anti-TNF treatment response.

<p>Logistic regression, adjusted (Adj.) for sex, age, HAQ, CRP, DMARD at baseline, IgM RF status (seropositive/seronegative). CI: confidence interval, Freq.: Frequency, OR: odds ratio, EULAR: European League Against Rheumatism, P-value: *<0.05, **<0.01.</p

<i>ABCB1</i> mRNA levels in morphologically normal and affected tissues normalised to the <i>β-actin</i> mRNA level.

<p><i>*P-</i>value <0.05, **<i>P-</i>value <0.01, ***<i>P-</i>value <0.001.</p

Odds ratio (OR) for association between <i>NLRP3</i> (rs4612666) variant allele and EULAR good/moderate response (log scale, 95% confidence interval).

<p>Patients stratified on diagnose (seropositive-/seronegative RA) or smoking status. Smoking as independent predictor of EULAR good/moderate response: OR = 1.018, p = 0.941.</p