Christopher S. Thom

This study shows Tpm1 promotes platelet adhesion and clot contraction independently of its role in embryonic hematopoiesis, linking it to thrombotic disease risk.

The paper defines murine bone marrow mesenchymal and stromal cell progenitor identities and temporal emergence using a single cell atlas from fetal life to 18 months.

The paper identifies Adipoq+ stromal cells in bone marrow as a source of IGF-1 that promotes endocortical bone formation in mature female mice without affecting trabecular bone or hematopoiesis.

This study identifies platelet traits as key risk factors for stroke using Mendelian Randomization and subclustering, revealing mechanisms involving platelet reactivity and endothelial cell adhesion.

The paper uses in vitro hematopoiesis systems to analyze gene expression and chromatin organization during HPC formation, identifying genetic impacts on blood traits and disease.

This study identifies signaling pathways supporting nascent HSC release during EHT using single-cell RNA sequencing from human embryonic cells.

This study uses Mendelian randomization to show that genetic predisposition to smoke tobacco indirectly reduces red blood cell count by increasing alcohol intake.

This study uses Mendelian randomization to assess the causal effect of height on cardiovascular diseases, finding that established risk factors largely explain the association, with minimal residual effect.

This study uses single-cell RNA-sequencing to analyze the individual and combined effects of Trisomy 21 and GATA1s on hematopoietic progenitor cells, revealing their impact on lineage skew and proliferation.

The paper develops TSABL predictors to identify causal variants in GWAS loci by leveraging trait-specific regulatory features and genomic annotations.

This study uses Mendelian randomization to show that obesity and truncal adiposity have opposing genetic effects on blood traits, with BMI reducing hemoglobin and hematocrit while truncal adiposity increases them.

This study shows smoking increases type 2 diabetes risk through BMI, but not coronary artery disease risk, using Mendelian randomization.

The paper identifies shared genetic signals across hematopoietic traits and disease phenotypes using colocalization analysis, revealing novel associations and potential therapeutic targets.

This study identifies TPM1 as a causal gene for hematopoietic traits using genome-wide association data and CRISPR/Cas9 knockout in iPSCs, showing enhanced in vitro hematopoiesis.