Additional file 6: Figure S2. of Low levels of IgM antibodies recognizing oxidation-specific epitopes are associated with human non-alcoholic fatty liver disease

Correlation between plasma P1-IgM levels and systemic markers of liver damage, inflammation, and adipokines. Pearson R correlation between plasma IgM titers towards P1 and plasma ALT (A), AST (B), γ-GT (C), IL-1β (D), and IL-8 (E), respectively. (TIF 110 kb

Lonicera alpigena L. var. glehnii Nakai

原著和名: エゾヘウタンボク科名: スイカズラ科 = Caprifoliaceae採集地: 北海道 様似郡 様似町 幌満 (北海道 日高 様似郡 様似町 幌満)採集日: 1988/5/20採集者: 萩庭丈壽整理番号: JH031935国立科学博物館整理番号: TNS-VS-98193

Additional file 2: of Low levels of IgM antibodies recognizing oxidation-specific epitopes are associated with human non-alcoholic fatty liver disease

Data HepC cohort. (XLSX 28 kb

Overview of the screening and replication strategy for rare variants.

<p>Phase I: a) targeted re-sequencing of 122 genes was performed in a pooled design of 790 Dutch UC cases. Five hundred healthy individuals sequenced by the Genome of the Netherlands Project were used as a control cohort. After quality control, 2562 high-confidence variants were further prioritized based on allele frequency and likely pathogenicity. In total 188 SNVs were selected for replication phase 1 (Phase II), of which 171 passed the design of five Agena Biosience iPlexes. (<a href="http://agenabio.com" target="_blank">http://agenabio.com</a>) b) Phase II: genotyping of 171 variants was performed in 1021 Dutch UC cases and 1166 controls. c) Phase III: after association and gene-based analyses, genotyping of 19 variants was performed in 1026 German UC cases and 3532 healthy German controls.</p

Overview of quality control and prioritization in Phase I.

<p>a) After pooled sequencing, a total of 7969 SNVs were detected with a coverage of >360x (12 individuals* 30x coverage). b) All variants called by two alignment strategies were included and filtered using a Forward/Reverse balance between 20–80%. c) Variants previously tested in a large IBD cohort with the Immunochip (n = 527) and silent mutations (n = 335) were excluded. d) We used different strategies to select non-synonymous SNVs (coding), including splice-sites, (n = 418) (d1) and non-coding SNVs (n = 1282) (d2). d1) The coding variants were selected on the basis of allele frequency (AF): known SNVs with an AF > 0.05 were excluded. A different strategy was obtained for genes that are known to lead to spontaneous colitis when in knocked-out mice. In this group of genes we took a more liberal approach in selecting variants for further follow-up and included common variants with predicted functional consequences for follow-up genotyping. Three hundred seventy-seven SNVs remained after this step. d2) To prioritize the non-coding SNVs in regulatory regions, we selected 48 SNVs in a transcription factor binding site (TFBS), based on ENCODE data in the UCSC browser e) Further prioritization was based on damaging effect prediction by Polyphen (damaging effects between 0.8 and 1.0) and/or damaging effect predicted by Sift (n = 112). We included all nonsense variants (n = 6), the variants in splice-sites (n = 4) and variants that were significantly different in AF compared to the AF in GoNL (n = 5). We also included unknown SNVs present in more than one pool (n = 13). f) In total, 140 coding and 48 non-coding rare variants remained after filtering.</p

Predicted loss of function variants identified by pooled sequencing (Phase I), and genotyped in replication phase 1 (Phase II).

<p>Predicted loss of function variants identified by pooled sequencing (Phase I), and genotyped in replication phase 1 (Phase II).</p

Significant SNVs in Replication phase 1 (Phase II) and replication phase 2 (Phase III).

<p>Significant SNVs in Replication phase 1 (Phase II) and replication phase 2 (Phase III).</p

Additional file 1: of Multimodal treatment of perianal fistulas in Crohn’s disease: seton versus anti-TNF versus advancement plasty (PISA): study protocol for a randomized controlled trial

Dates of consent of participating centres