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Auditing medical multi-agent AI reveals risks of false consensus

arXiv:2510.10185v2 Announce Type: replace-cross Abstract: Large language models are increasingly being assembled into medical multi-agent systems that emulate multidisciplinary consultation through specialist roles, peer review and consensus formation. In clinical decision support, however, apparent consensus is not enough. Clinicians also need to know whether agents checked the evidence, addressed disagreement and kept uncertainty visible. Current evaluations largely score final accuracy, leaving the safety of the collaborative process untested. Here we introduce MedAgentAudit, a clinically grounded workflow audit framework for diagnosing and quantifying collaborative failure modes in medical multi-agent systems. From 3,600 execution logs, we derive an expert-validated taxonomy of ten recurrent failures spanning task comprehension, collaborative discussion, and synthesis and decision-making. We then deploy an expert-validated automated auditor as non-interventional probes across 14,400 cases, covering six multi-agent architectures, six medical text and vision datasets, and four large language model settings per modality. Across systems, collaboration yields uneven accuracy gains and frequent process failures. Unsupported observations affect 16.63% of cases and propagate downstream. In discussion, agents repeat initial views in 98.42% of cases rather than re-examining evidence, and fail to activate specialist reasoning in 42.73%. During synthesis, final answers often substitute authority or majority count for evidence checking, showing authority bias in 28.76% (rising from 35.30% to 68.75% across rounds), self-contradiction in 18.53%, contradiction neglect in 5.48% and minority suppression in 5.11%. MedAgentAudit reframes medical AI evaluation from output scoring to process-level safety and accountability, providing a practical foundation for transparent, auditable and clinician-supervised agentic systems in medicine.
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The landscape of virtual simulation in undergraduate dental education with implications for artificial intelligence incorporation

npj Digital Medicine, Published online: 26 May 2026; doi:10.1038/s41746-026-02806-z

The landscape of virtual simulation in undergraduate dental education with implications for artificial intelligence incorporation
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SIRT3 deacetylates STEAP4 to modulate cuproptosis sensitivity via mitochondrial metabolic reprogramming in HBV-related HCC

Cell Death Differ. 2026 Mar 16. doi: 10.1038/s41418-026-01713-w. Online ahead of print.

ABSTRACT

Hepatitis B virus (HBV) infection remains a leading etiological driver of hepatocellular carcinoma (HCC). Cuproptosis is a recently defined copper-dependent form of regulated cell death that selectively eliminates mitochondria-dependent cells; whether HBV rewires this vulnerability remains unknown. Here we unveil a novel HBV X protein (HBx)-driven mechanism of cuproptosis evasion. Integrative analysis of clinical specimens, HBx-transgenic (HBx-Tg) mice, and multi-omics datasets revealed marked downregulation of STEAP4 (six-transmembrane epithelial antigen of prostate 4), a metalloreductase essential for cuproptosis sensitivity, in HBV-positive HCC. Mechanistically, HBx attenuates sirtuin 3 (SIRT3), impairing deacetylation of STEAP4 at lysine 404 and abolishing its mitochondrial targeting. Consequently, cells switch from the tricarboxylic acid (TCA) cycle respiration to glycolysis, reducing sensitivity to the copper ionophore elesclomol (ES). Restoring STEAP4 expression or pharmacological activation of SIRT3 with honokiol (HKL) re-instated mitochondrial STEAP4 localization and re-sensitized HBV-related HCC cells to cuproptosis; combination with ES produced synergistic tumor suppression in vitro and in orthotopic models. Collectively, our findings establish the SIRT3-STEAP4 axis as a novel regulator of cuproptosis resistance in HBV-related HCC. HBx-mediated repression of SIRT3 disrupts STEAP4 deacetylation and mitochondrial targeting, fostering metabolic reprogramming and evasion of copper-induced cell death. The results provide a pre-clinical rationale for copper-directed combination strategies in HBV-associated HCC.

PMID:41840161 | DOI:10.1038/s41418-026-01713-w

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