Experiments
Searchable full-text extractions: founding hypothesis, core claims, experimental setups, key results and statistics — pulled out of each paper as structure. Search a cell line, an assay or an entity (e.g. HUH7) and find every paper that worked with it. This corpus stands on its own: most entries carry no reproduction assessment (yet).
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Has reproduction · 33
To Explore the Key Subgroup and Their Immune Microenvironment During the Formation of Coronary Plaque With scRNA-seq.
PMID 40454289 · PMC12126265 · Cardiology research and practice · 2025 · 6 claims · 8 setups
C1 RACK1+ NK cells are a crucial subgroup for understanding coronary plaque formation, exhibiting the highest cell stemness/differentiation potential and positioned at the start of the pseudotime trajectory
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A biomarker panel for peripheral arterial disease.
PMID 18687758 · PMC3133945 · Vascular medicine (London, England) · 2008 · 7 claims · 6 setups
β2-microglobulin (β2M) and cystatin C had the highest correlation with ABI among all plasma markers tested, higher than age, smoking, or diabetes status
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Association of polymorphisms in cyclooxygenase (COX)-2 with coronary and carotid calcium in the Diabetes Heart Study.
PMID 18768181 · PMC2699582 · Atherosclerosis · 2009 · 8 claims · 6 setups
COX-2 promoter SNP rs689466 is associated with lower coronary calcified plaque (CorCP)
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Has reproduction · 56
DESE: estimating driver tissues by selective expression of genes associated with complex diseases or traits.
PMID 31694669 · PMC6836538 · Genome biology · 2019 · 8 claims · 8 setups
DESE is a unified iterative framework that estimates driver tissues of complex diseases/traits from tissue-selective expression of GWAS-associated genes, and outputs prioritized susceptibility genes as a byproduct
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Discovery and validation of new molecular targets in treating dyslipidemia: the role of human genetics.
PMID 20211435 · PMC3328807 · Trends in cardiovascular medicine · 2009 · 8 claims · 8 setups
Mendelian randomization uses genetic variants as a 'randomized trial of nature' to assess causal relationships between lipid biomarkers and CHD, overcoming confounding and reverse causality limitations of observational epidemiology.