Christopher Baker

Christopher Baker, Stephen Hinton, Akashdeep Nijjar et al.

The speed and accuracy of an artificial teammate fundamentally alter the failure states of Human-AI integration. While high-speed AI interventions risk inducing reflexive blind compliance, delayed interventions can induce ambiguous cognitive conflict. This study investigates how the fundamental characteristics of an in-task AI assistant, Fast/Less-Accurate (FLA-AI) versus Slow/Accurate (SA-AI) impact the synergy of Collaborative Brain-Computer Interface (cBCI) teams in a Virtual Reality drone task. Seventeen operators completed continuous search tasks under high cognitive workload while their spatial covariance was mapped using a 2D Adaptive Riemannian Oracle. The results mathematically demonstrate that AI timing dictates the mechanism of team failure. Fast AI induced instant, blind compliance; human accuracy under deception collapsed to 50.2%, and pure behavioural teams (N=8) failed to scale beyond 74.1%. In contrast, Slow AI induced delayed cognitive conflict; humans hesitated (61.1% accuracy), but N=8 behavioural teams eventually recovered to 100.0%. Crucially, the Riemannian Oracle mathematically adapted to these states: it heavily restricted temporal windows (< 0.8s) to intercept fast reflexive compliance, while widening windows (> 1.2s) to capture delayed cognitive conflict. Integrating these isolated veridical signals via Hybrid Fusion successfully rescued the Fast AI team (+7.6% at N=8) and significantly accelerated the recovery of smaller Slow AI teams (+6.9% at N=4). These findings prove that cBCI synergy is heavily contingent on the temporal dynamics of trust, providing a critical framework for designing dynamically gated Human-AI systems.

Christopher Baker, Karen Rafferty, Hui Wang

Precision oncology is currently limited by the small-N, large-P paradox, where high-dimensional genomic data is abundant, but high-quality drug response samples are often sparse. While deep learning models achieve high predictive accuracy, they remain black boxes that fail to provide the causal mechanisms required for clinical decision-making. We present a Neuro-Symbolic Agentic Framework that bridges this gap by integrating a quantitative machine learning World Model with an LLM-based agentic reasoning layer. Our system utilises a forensic data pipeline built on the Sanger GDSC dataset (N=83), achieving a robust predictive correlation (r=0.504) and a significant performance gain through the explicit modelling of clinical context, specifically Microsatellite Instability (MSI) status. We introduce the concept of Inverse Reasoning, where the agentic layer performs in silico CRISPR perturbations to predict how specific genomic edits, such as APC or TP53 repair, alter drug sensitivity. By distinguishing between therapeutic opportunity and contextual resistance, and validating these findings against human clinical data (p=0.023), our framework provides a transparent, biologically grounded path towards explainable AI in cancer research.