Search

Additional file 1: Table S1. Frequency of non-synonymous variants in CLEC18 genes among different ethnic populations from the data of 1000 Genome Project. Table S2. The 48 variants as significant cis-expression quantitative trait loci (cis-eQTL) for CLEC18 family genes (GTEx Portal). Table S3. The cis-eQTL annotation of rs75776403. Figure S1. Boxplot showing the distribution of CLEC18A transcript (mRNA) levels across rs75776403 genotypes. Table S4. The 86 quantitative traits (11 phenotype categories) included in this study (N = 68,080). Table S5. The 24 additional quantitative traits are included in this study. Table S6. Association results of rs75776403 to the quantitative traits. Table S7. The 84 binary traits (16 phenotype categories) are included in this study. Table S8. Association results of rs75776403 and binary traits. Table S9. The 19 ordered traits (4 phenotype categories) are included in this study. Table S10. Association results of rs75776403 and ordinary traits. Table S11. Phenome-wide association study for CLEC18A rs75776403 in UK Biobank (UKB) and BioBank Japan (BBJ). Table S12. Significantly enriched pathways (and/or gene sets) were identified by gene-set enrichment analysis (GSEA). Table S13. Gene-set enrichment analysis (GSEA) results of phosphoproteomics that were associated with rs75776403. Figure S2. Pairwise correlation plot showing a gene–gene correlation between genes that are involved in the cellular response to thyroid hormone stimulus (purple) and corticosteroid receptor signaling pathways (orange). CLEC18A gene is marked using a red dot. Table S14. Association between (A) rs75776403 or (B) CLEC18A mRNA level with thyroid hormone axial genes. Table S15. Gene set of cellular response to thyroid hormone stimulus and corticosteroid receptor signaling pathway in gene ontology (GO) biological process (BP) database. Table S16. Association between rs75776403 and corticosteroid receptor signaling or thyroid-stimulated pathway genes. Table S17. Association between CLEC18A and thyroid stimulated pathways or corticosteroid receptor signaling genes in adrenal gland, liver, ovary, and testis tissues from GTEx portal.

Figure S1. Linkage disequilibrium (LD) map of EDN1 gene SNPs shown (a) based on R-squared (r2) (b) based on D-prime (Dâ ). Figure S2. Linkage disequilibrium (LD) map of EDN2 gene SNPs shown (a) based on R-squared (r2) (b) based on D-prime (Dâ ). Figure S3. Linkage disequilibrium (LD) map of EDN3 gene SNPs shown (a) based on R-squared (r2) (b) based on D-prime (Dâ ). Figure S4. EDN3 gene expression across different tissues. Table S1. Baseline characteristics of study patients stratified by bacteremia events. Table S2. Analysis of association between EDN1 single-nucleotide polymorphisms (SNPs) and hospitalized infection events. Table S3. Analysis of association between EDN2 single-nucleotide polymorphisms (SNPs) and hospitalized infection events. Table S4. Analysis of association between EDN1 single-nucleotide polymorphisms (SNPs) and hospitalized bacteremia events. Table S5. Analysis of association between EDN2 single-nucleotide polymorphisms (SNPs) and hospitalized bacteremia events. (DOCX 196 kb)

The confounding factors for BAI and BDI scores. Figure S1. Correlation between BAI and BDI score in the first week (p-value

Summary of T-cell receptor (TCR) β clonotype statistics. (DOCX 14 kb)

T-cell receptor (TCR) β complementarity determining region (CDR)3 size spectratype plots of amino acid clonotypes from end-stage renal disease patients. The CDR3 length is defined as the number of amino acids between the conserved positions CDR3, i.e., cysteine (Cys)104 and phenylalanine (Phe)118. The color of the bar is annotated by the number of corresponding nucleotide read counts in the samples. (DOCX 155 kb)

Mappability to variable/diversity/joining (VDJ) regions in end-stage renal disease patients. (DOCX 13Â kb)

Overlapping read length distribution plot of end-stage renal disease patients. QC, quality control. (DOCX 260Â kb)

Summary of repertoire sequencing output and overlapping proportions in end-stage renal disease samples. (DOCX 14Â kb)

Quantification of T-cell repertoire diversity in end-stage renal disease (ESRD) patients. a The clonotype distribution plots of ESRD patients. The x-axis and y-axis are log10 scaled. The value of 1/D represents the T-cell receptor (TCR) β repertoire diversity. b Comparison of TCR repertoire diversity (log-scaled) between erythropoietin (EPO) responders and EPO resistants (p = 0.642) (DOCX 232 kb)

Schematic showing steps of T-cell receptor (TCR) β repertoire sequencing data processing. (DOCX 25 kb)

3D bar plots quantifying joint distributions of TRBV and TRBJ in end-stage renal disease (ESRD) patients. (DOCX 517Â kb)

Demographic characteristic of the study patients. Table S2. Association of EDN1_rs4714384 and cardiovascular disease in ESRD patients. Table S3. Potential function prediction of SNP in transcription factor binding site in EDN gene family. (DOCX 21Â kb)

Purpose Ultraviolet B (UVB) radiation from sunlight is a known risk factor for human corneal injury. The aim of the present study was to investigate the protective effects of green tea polyphenol epigallocatechin gallate (EGCG) on UVB radiation–induced corneal oxidative damage in male imprinting control region (ICR) mice. Methods Corneal oxidative damage was induced by exposure to UVB radiation at 560 μW/cm2. The animals received 0%, 0.1%, and 0.01% EGCG eye drops at a 5 mg/ml dose, twice daily for 8 days. Corneal surface damage was graded according to smoothness and the extent of lissamine green staining. Corneal glutathione (GSH), thiobarbituric acid-reactive substances (TBARS), and protein carbonyl levels, as well as superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), and glutathione reductase (GSH-Rd) activity in the cornea, were measured to monitor corneal injury. Results UVB radiation caused significant damage to the corneas, including apparent corneal ulceration and severe epithelial exfoliation, leading to a decrease in SOD, catalase, GSH-Px, GSH-Rd, and GSH activity in the cornea. However, the corneal TBARS and protein carbonyls increased compared with the control group. Treatment with EGCG eye drops significantly (p