Compute and interpret validated bedside clinical risk scores and pretest probabilities for an INDIVIDUAL patient — pick the right score for the scenario, gather inputs, run the deterministic calculator tool, and read the result against an interpretation table. Covers CHA2DS2-VASc (AF stroke risk), HAS-BLED (bleeding on anticoagulation), CURB-65 (pneumonia severity / admit decision), qSOFA (sepsis screen), Child-Pugh + MELD-Na (cirrhosis severity / transplant priority), Wells DVT and Wells PE (VTE pretest probability), ASCVD (10-year cardiovascular risk / statin decision), and eGFR CKD-EPI (kidney function / drug dosing). Use when asked things like "stroke risk for this AF patient", "should this patient be anticoagulated", "pneumonia severity — admit or not?", "sepsis screen this patient", "DVT/PE pretest probability", "10-year cardiovascular risk", "cirrhosis severity / MELD score", or "eGFR / kidney function". Pairs CHA2DS2-VASc with HAS-BLED to weigh anticoagulation. NOT for polygenic/genetic risk (use tooluniverse-polygenic-risk-score), NOT for population-level epidemiology/incidence (use tooluniverse-epidemiological-analysis), and NOT for diagnostic test sensitivity/specificity/likelihood-ratio math (use tooluniverse-diagnostic-test-evaluation).
Strategic clinical trial design feasibility assessment. Analyzes 6 dimensions (endpoint, population, comparator, effect size, duration, regulatory pathway) using precedent trials and FDA guidance. Produces enrollment projections, endpoint recommendations, and approval-pathway analysis. Use for trial-protocol design, power/sample-size estimation, comparator selection, and FDA submission strategy. Driven by precedent-based reasoning rather than first-principles math.
Interpret a missense variant via ESMC-6B Sparse Autoencoder (SAE) feature activations. For a given protein + variant, computes which interpretable SAE features (catalytic, ligand-binding, PTM, structural motif, domain, etc.) are lost or gained at the mutation site. Use when standard pathogenicity scores (AlphaMissense, ClinVar) say a variant is damaging but you need a MECHANISTIC explanation — e.g. 'why is this variant LoF?' Complements (does not replace) variant-interpretation and variant-to-mechanism skills, which focus on ACMG classification or regulatory mechanism.
Given a PDB structure, produce a per-residue annotation table: which residues sit at a binding interface (vs a partner chain), which line a ligand pocket, which are buried (core) vs solvent-exposed (surface), and optionally secondary structure. This is the structural track drawn under a DMS heatmap and the structural prior SAE feature drops are read against. Use when you need to anchor a variant-interpretation or DMS analysis to the protein's actual physical context.