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Alexander Fulton

Publications and source records attributed to Alexander Fulton.

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Systematic Reconstruction of Disease Networks from Longitudinal Blood Data for Causal Discovery and Intervention Analysis

We explore the hyperparameters and introduce a methodological framework to convert disease patterns from time series data of blood test results into correlation graphs for causal hypothesis exploration. The networks represent hypotheses that can then be validated or rejected both for causal discovery and causal analysis (under intervention). We synthetically recreated a repository of 105 typical disease longitudinal patterns extracted from medical guidance and research literature of common blood markers to build a systematic pipeline to translate multidimensional clinical data into intervenable disease networks for causal discovery and causal analysis. This study demonstrates that knowledge graphical models reconstructed from longitudinal data can transform routine medical data into clinically interpretable structures. By integrating multiple thresholding strategies and causal graph design, the framework has the purpose to move beyond statistical correlation toward clinically and testable inference networks. These results highlight a practical pathway for more transparent, explainable, and scalable tools in clinical decision support for AI training, precision healthcare and predictive medicine, offering interpretable, clinically actionable outputs that support safer use of AI in differential diagnosis.

q-bio.OT

Multi-omic Enriched Blood-Derived Digital Signatures Reveal Mechanistic and Confounding Disease Clusters for Differential Diagnosis

Understanding disease relationships through blood biomarkers offers a pathway toward data-driven taxonomy and precision medicine. In this study, we constructed a digital blood twin, a computational model derived from 103 disease signatures comprising longitudinal hematological and biochemical analytes. Profiles were standardized into a unified disease-analyte matrix, and pairwise Pearson correlations were computed to assess similarity across conditions. Hierarchical clustering revealed consistent grouping of hematopoietic disorders, while metabolic, endocrine, and respiratory diseases were more heterogeneous, reflecting weaker internal cohesion. To evaluate cluster structure, the tree was partitioned at a stringent distance threshold, yielding 16 groups. Enrichment analysis of the largest and most heterogeneous cluster demonstrated convergence on cytokine-signaling pathways, indicating shared inflammatory mechanisms that transcend conventional clinical boundaries. PCA and UMAP corroborated the correlation-based results, consistently separating hematological diseases as a distinct cluster. Random Forest feature selection identified neutrophils, mean corpuscular volume, red blood cell count, and platelet count as the most discriminative analytes, reinforcing the role of hematopoietic markers as key drivers of disease stratification. Collectively, these findings show that blood-derived digital signatures can recover clinically meaningful disease clusters while uncovering mechanistic overlaps across categories. This network physiology framework highlights the potential of integrating routine laboratory data with computational methods to refine disease ontology, map comorbidities, and advance precision diagnostics.

q-bio.OT