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The epistemic analysis endpoints surface the knowledge layer beneath Wu-Weism’s causal reasoning: confidence assessment, assumption identification, knowledge-gap detection, and provenance tracking for scientific evidence. Use these endpoints to build epistemic audit trails, expose uncertainty to end users, or retrieve the evidence records underpinning a session’s claims.
All endpoints on this page require authentication. Include your session token in the Authorization header.
Opens an epistemic analysis dialogue. Given a scientific question, the engine assesses the epistemic state of the available evidence: what is known, what is assumed, where the evidence is weak or missing, and how confident Wu-Weism is in its causal inferences.Responses are streamed as Server-Sent Events (SSE).
The scientific question or claim you want epistemic analysis on. Can be a hypothesis, a causal claim, or a general research question.Example: "Is there sufficient evidence that chronic cortisol elevation causally reduces hippocampal volume in adult humans?"
AI provider to use for the analysis: "anthropic", "openai", or "gemini". Defaults to the platform provider if not specified. See Authentication for BYOK key details.
Returns scientific evidence records associated with your account. These records are created when PDFs are processed through the hybrid synthesize pipeline or uploaded for epistemic analysis. Each record captures the file’s provenance, a structured summary, and the key scientific findings extracted during analysis.
Returns epistemic session data for your most recent (or active) session. Use this to retrieve the accumulated epistemic state — questions asked, assumptions surfaced, confidence trajectory, and knowledge gaps identified — across a session’s lifetime.
{ "sessionId": "s9f8e7d6-cc4d-4f1a-b802-d6e7f3a0c291", "createdAt": "2026-04-05T11:55:00Z", "questions": [ { "questionId": "q-001", "text": "Is there sufficient evidence that chronic cortisol elevation causally reduces hippocampal volume in adult humans?", "confidence": 0.74, "uncertaintyLabel": "medium", "timestamp": "2026-04-05T11:56:12Z" } ], "aggregateAssumptions": [ "Rodent models generalise to adult human hippocampal plasticity.", "Cortisol as measured in serum is a reliable proxy for tissue-level glucocorticoid exposure.", "SUTVA holds: one subject's cortisol exposure does not affect another's hippocampal volume." ], "aggregateGaps": [ "Limited longitudinal human data with causal (interventional) designs.", "Dose-response relationship between cortisol and hippocampal volume not well characterised in humans.", "Mechanistic pathway from cortisol to volume reduction (BDNF vs. neurogenesis vs. dendritic atrophy) not yet resolved." ]}