Albert Henry
MD 🇮🇩 | MSc 🇬🇧 | PhD 🇬🇧
Research officer - Garvan Institute of Medical Research 🇦🇺
Honorary research fellow - University College London 🇬🇧
Interested in genetics, phenotypes, and anything in-between
- Reposted by Albert Henry[Not loaded yet]
- Reposted by Albert HenryNSW CVRN Rising Stars Seminar – 11 Sept Join us at VCCRI to hear from Dr Albert Henry @alberthenry.bsky.social (Garvan Institute), a rising leader in data science, cardiovascular genetics and systems biology. 📅 Wed 11 Sept | 📍VCCRI Register now: shorturl.at/r7eWD
- 1. 🚨New preprint: tinyurl.com/tenk10k-causal. We explored causal effects of gene expression in immune cell types on complex traits and diseases by combining single-cell expression quantitative trait loci (sc-eQTL) mapping in 5M+ cells from 1,925 donors in TenK10K study and GWAS. 🧵
- 2. Our study presents a catalogue of cell type-specific causal effects of gene expression on 53 diseases (8,672 genes), and 31 biomarker traits (16,085 genes) across 28 peripheral immune cell types identified using Mendelian randomisation (MR) with sc-eQTL genetic instruments.
- 3. We identified 190,449 gene-trait associations, including 34% not found by gene-level analysis of GWAS data, and 61% not found by MR using whole blood eQTL. Associations found only by sc-eQTL MR are often restricted to fewer cell types, implicating cell type specificity.
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View full threadBig thanks to co-first author Anne Senabouth, supervisor Joseph Powell, co-authors Rika Tyebally @blakebowen.bsky.social @lawrencehuang.bsky.social Jayden Fan @petercallen.bsky.social @anglixue.bsky.social @htanudisastro.bsky.social @annasecuomo.bsky.social @dgmacarthur.bsky.social, and many others!
- 🚨 Our latest GWAS of heart failure subtypes is now out in Nature Genetics! rdcu.be/eb9O0 A massive global collaboration from HERMES Consortium involving >40 studies with >150,000 heart failure cases. 🧵 highlighting key findings 1/
- Heart failure (HF) is a complex disease associated with many etiologies and risk factors. Here, we study how genetic variation influence risk of different HF subtypes and integrate these results with other genomic information to uncover disease etiology 2/
- First, we collected data from 49 GWAS comprising >150k HF cases and performed meta-analyses on 4 subsets of HF phenotypes: 1. Overall HF (HF-all) 2. non-ischaemic HF (ni-HF) 3. ni-HF with reduced (<50%) ejection fraction (ni-HFrEF) 4. ni-HF with preserved (≥50%) ejection fraction (ni-HFpEF) 3/
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View full threadLastly, it goes without saying that it takes a village to publish this study. I'd like to take this opportunity to thank my previous PhD and postdoc advisor at UCL, Dr. Tom Lumbers who led this project, friends and collaborators within the HERMES Consortium, and all the study participants. END/
- ICYMI: We delve into the molecular etiology of dilated cardiomyopathy, combining genomics, cellular transcriptomics, and clinical phenotype in population biobanks & clinical cohorts. Read the full paper below 👇
- Genome-wide association analyses in Nature Genetics provide insights into the molecular etiology of dilated cardiomyopathy, which may inform the design of genetic testing strategies and may facilitate the development of targeted therapeutics. go.nature.com/4fIkNmh 🧪
