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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MSI test to distinguish between HNPCC and other predisposing syndromes -- of value in tailored surveillance.
PMID 15528791 · PMC3839337 · Disease markers · 2004 · 8 claims · 5 setups
MSI (or immunohistochemistry) testing applied to a pre-selected patient with a family history or early-onset colorectal cancer can distinguish HNPCC from unknown non-HNPCC colorectal cancer syndromes.
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Adaptation to different human populations by HIV-1 revealed by codon-based analyses.
PMID 16789820 · PMC1480537 · PLoS computational biology · 2006 · 8 claims · 8 setups
Developed two fixed effects maximum likelihood methods: one to detect selection that persists in a population (internal vs. terminal branches) and one to detect differential selection on codons between two populations.
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Size matters: just how big is BIG?: Quantifying realistic sample size requirements for human genome epidemiology.
PMID 18676414 · PMC2639365 · International journal of epidemiology · 2009 · 7 claims · 2 setups
Conventional power calculations for case-control studies disregard analytic complexity (e.g. clinical assessment errors, unmeasured aetiological determinants) and can seriously underestimate true sample size requirements
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Neurofibrillary tau pathology modulated by genetic variation of alpha-synuclein.
PMID 18661559 · PMC8957216 · Annals of neurology · 2008 · 7 claims · 5 setups
The SNCA intron 4 marker rs2572324 is associated with the extent of neurofibrillary tangle (Braak stage) pathology.
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Genome-wide prediction of functional gene-gene interactions inferred from patterns of genetic differentiation in mice and men.
PMID 18270580 · PMC2217631 · PloS one · 2008 · 8 claims · 6 setups
Pairs of unlinked SNPs showing excess genetic differentiation (LD in mouse RILs, Fst in human populations) beyond what simulations/coalescent models predict by chance represent candidate functionally interacting (epistatic) gene pairs.