Terrence S. Furey

The paper identifies differential expression and splicing in IBD patients, showing distinct molecular mechanisms in CD and UC.

The paper identifies differentially expressed lncRNAs in Crohn's disease using genome-guided RNA-seq and links them to nearby protein-coding genes involved in immune response and tissue regeneration.

The paper identifies impaired fatty acid oxidation in fibroblasts from fibrostenotic Crohn's disease patients and links it to intestinal fibrosis.

The paper uses single-nucleus multiome sequencing to identify cell-type-specific regulatory mechanisms for cardiometabolic traits by integrating QTLs and GWAS signals.

WAD deconvolves bulk accessible chromatin data to estimate cell-type proportions using wavelet-based denoising and L1-minimal linear programming, achieving lower error and higher concordance than existing methods.

The paper introduces Consenrich, a method for robust signal recovery from multi-sample functional genomics data, showing improved biological insights in Alzheimer's cohort analysis.

The paper identifies novel target genes associated with IBD by analyzing eQTL in diseased colon tissue and comparing them to non-IBD eQTL.

CoVar identifies coordinated regulators driving gene expression changes by analyzing network connectivity in perturbed data, revealing key genes missed by differential expression alone.

The paper identifies miR-29 as a predictive marker for severe phenotypes in pediatric Crohn's disease through miRNA analysis and validation in mice and human patients.

The paper uses machine learning to predict clinical outcomes in pediatric Crohn's disease by analyzing gene expression from ileal and colonic tissues.

ROCCO identifies consensus open chromatin regions across multiple samples using convex optimization, improving upon existing peak calling methods.

The paper uses single-cell analysis to compare colonic epithelial cells in Crohn's disease and control patients, revealing shifts in cell composition and gene expression patterns.

The paper finds that increased colonic ACE2 expression in Crohn's disease patients is associated with a higher risk of surgery within 5 years.

The paper identifies genetic regulators of gene expression and chromatin accessibility across multiple tissues using a genetically diverse mouse population and proposes a causal model for gene regulation.

This study identifies miR-31 as a marker that stratifies Crohn’s disease patients into two subtypes with distinct clinical outcomes.