References of "Louis, Edouard"
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See detailThe role of mesenchymal stem cells in the treatment of ulcerative colitis and Crohn's disease
GREGOIRE, Céline ULg; Louis, Edouard ULg; BRIQUET, Alexandra ULg et al

in The Biology and Therapeutic Applications of Mesenchymal Cells (in press)

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See detailLa maladie de Rendu-Osler: une cause rare d'encéphalopathie ammoniacale.
Dumont, R; LOLY, Jean-Philippe ULg; DELWAIDE, Jean ULg et al

in Revue Médicale de Liège (2016), 71(2), 83-89

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See detailInherited determinants of Crohn's disease and ulcerative colitis phenotypes: a genetic association study
Cleynen, Isabelle; Boucher, Gabrielle; Jostins, Luke et al

in Lancet (2016)

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See detailLe syndrome thyro-gastrique auto-immun : actualités cliniques et thérapeutiques
VALDES SOCIN, Hernan Gonzalo ULg; SID, Sélim ULg; LUTTERI, Laurence ULg et al

in Vaisseaux, Coeur, Poumons (2016), 21(4), 11-15

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See detailFamilial thyrogastric autoimmune syndrome : a study of 22 kindreds
Sid, Sélim ULg; LUTTERI, Laurence ULg; BEGUIN, Yves ULg et al

in Abstract book - 20th Annual Congress of the Belgian Society of Internal Medicine (2015, December)

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See detailComparison of serum fractionation methods by data independent label-free proteomics
Baiwir, Dominique ULg; Mazzucchelli, Gabriel ULg; Smargiasso, Nicolas ULg et al

in EuPA Open Proteomics (2015), 9

Off-line sample prefractionations applied prior to biomarker discovery proteomics are options to enable more protein identifications and detect low-abundance proteins. This work compared five commercial ... [more ▼]

Off-line sample prefractionations applied prior to biomarker discovery proteomics are options to enable more protein identifications and detect low-abundance proteins. This work compared five commercial methods efficiency to raw serum analysis using label-free proteomics. The variability of the protein quantities determined for each process was similar to the unprefractionated serum. A 49% increase in protein identifications and 12.2% of reliable quantification were obtained. A 61 times lower limit of protein quantitation was reached compared to protein concentrations observed in raw serum. The concentrations of detected proteins were confronted to estimated reference values. [less ▲]

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See detailFistula plug in fistulising ano-perineal Crohn's disease: a randomised controlled trial
Senéjoux, A.; Siproudhis, L.; Abramowitz, L. et al

in Journal of Crohn's and Colitis [=JCC] (2015)

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See detailSyndrome thyrogastrique autoimmun (STGA) : la gastrite auto-immune isolée (GAI) et celle associée à Helicobacter (Hp) ont des caractéristiques anatomocliniques différentes
VALDES SOCIN, Hernan Gonzalo ULg; MESUREUR, Thierry ULg; POLUS, Marc ULg et al

in Abstract book - Annales d'Endocrinologie - 32ème Congrès de la Société Française d'Endocrinologie (2015, October)

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See detailWhen it is not inflammatory bowel disease: differential diagnosis
Louis, Edouard ULg

in Current Opinion in Gastroenterology (2015)

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See detailOptimising the Inflammatory Bowel Disease Unit to Improve Quality Of Care: Expert Recommandations
Louis, Edouard ULg; Dotan, Iris; Ghosh, Subrata et al

in Journal of Crohn's and Colitis [=JCC] (2015)

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See detailPrioritizing likely causative genes in GWAS identified risk loci for immune-mediated inflammatory disorders using cell-type specific eQTL information.
Docampo Martínez, Elisa ULg; Fang, Ming ULg; Dmitrieva, Joelia Borisnova ULg et al

Poster (2015, May 05)

Background/Purpose: Immune-mediated inflammatory disorders (IMIDs) share many genetic risk factors. Pleiotropy may exist at different levels and most of the underlying mechanisms are still to be uncovered ... [more ▼]

Background/Purpose: Immune-mediated inflammatory disorders (IMIDs) share many genetic risk factors. Pleiotropy may exist at different levels and most of the underlying mechanisms are still to be uncovered. GWAS have identified hundreds of risk loci for IMIDs but causative genes have been identified in only a handful of cases. Recent fine-mapping efforts indicate that only a minority of risk variants are coding. This suggests that most risk variants will be regulatory hence affecting disease risk via eQTL effects. Methods: To aid in the identification of causative genes for IMIDs, we generated transcriptome information (HT12 arrays) for six blood cell types (CD4, CD8, CD19, CD14, CD15 and platelets) and intestinal biopsies at three anatomical locations (ileum, colon, rectum) for 350 healthy Caucasians. The same individuals were genotyped with SNP arrays interrogating > 700K variants, augmented by imputation from the 1KG project. To detect cis-eQTL we tested variants within 0.5 megabase windows centered on the tested probe. The nominal p-value of the best SNP within a cis-window was Sidak-corrected for the window-specific number of independent tests. The corresponding best, Sidak-corrected p-values for each probe were jointly used to estimate their respective false discovery rate.To identify likely causative genes in GWAS identified risk loci variants and also better understand pleiotropic effects, we (i) developed a method that quantifies the correlation between “disease association pattern” (DAP) and “eQTL association pattern” (EAP) and provides an empirical estimate of its significance, and (ii) evaluated the effect of fitting known risk variants as covariates in the eQTL analysis following Nica et al. (2010). We applied both approaches to celiac disease (CE) and rheumatoid arthritis (RA) and the second one to type one diabetes (T1D), multiple sclerosis (MS), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS) and psoriasis (PSO). Results: We detected > 16000 significant cis-eQTL, with a degree of sharing between cell types ranging from 38 to 90% highlighting the utility of our multi-tissue panel. GWAS variants were drivers of ciseQTL effects across the different tissues in 399 tests (23.6%), mostly in CD4 cells, and pinpointing 64 new gene-disease associations (3.7%). The number of shared loci and shared eQTL were highly correlated (rho=0.66).RA and SLE showed the highest degree of sharing. Conclusions: We identified new potential candidate genes for IMIDs and characterized pleiotropic effects through ciseQTL mapping in GWAS loci. These findings could shed a light on IMIDs pathogenesis and co-occurrence. Latest results will be presented. [less ▲]

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