Chen Chen, Mohsen Nayebi Kerdabadi, Dongjie Wang +2cs.LG cs.AI
Longitudinal prediction from electronic health records (EHRs) is limited by the sparsity and irregularity in patient trajectories, and knowledge augmentation with external knowledge graphs (KGs) offers a promising way to alleviate these issues. However, most existing methods perform fixed, context-agnostic topology augmentation by adding the same KG nodes and edges regardless of a patient's evolving state. We propose ReTA, a Reinforcement learning-based dynamic Topology Augmentation framework that casts KG import as a per-visit, budget-aware policy. ReTA first constructs an offline refined pool of KG-grounded templates, then learns a policy to select one augment action per visit from three options: Soft Import, which enriches node features without modifying graph topology, Hard Import, which grafts a compact KG subgraph onto the visit graph to create message-passing shortcuts, and Skip, which leaves the visit unaugmented when the base encoder is already confident. To stabilize learning, ReTA employs a decoupled encoder that processes semantic and structural signals in separate channels and fuses them via adaptive gating. Experiments on MIMIC-III and MIMIC-IV across diagnosis prediction, mortality, and readmission show that ReTA consistently outperforms strong baselines while remaining efficient, transfers across datasets and knowledge graphs, and yields interpretable augmentation patterns. The robust gains under sparse supervision highlight the advantage of ReTA's dynamic decision to import knowledge, boosting accuracy while curbing costs.
Hao Ding, Daniel Semchin, Paul M. Thompson +1cs.CV cs.LG
Predicting how a subcortical structure's shape will evolve from a few prior scans could support prognosis and clinical-trial enrichment. Existing longitudinal mesh predictors either extrapolate shape trajectories via high-dimensional embeddings or regress vertex deformations directly. We instead predict the surface's intrinsic geometry in continuous time: a single per-structure graph network predicts the future per-vertex first fundamental form (metric tensor) for an arbitrary causal multiple-visit history and an arbitrary prediction horizon, conditioned on a Fourier encoding of the lead time. The predicted metric is decoded into a surface by a differentiable As-Rigid-As-Possible solver, and the model is trained end-to-end on the rigid-aligned vertex error. Training through the reconstruction keeps the decoded prediction a valid surface and consistently improves it. On 14 subcortical structures from the ADNI dataset, the proposed mesh evolution model (MT-GNN) predicts best among the evaluated methods at every horizon ($-2.29\%$ mean vertex error vs. the temporal mean, $p{=}6.1{\times}10^{-5}$, beating it on 14/14 structures), ahead of geodesic shape regression (DCM, $-0.19\%$) and a mesh transformer (TransforMesh, $-0.45\%$; $p{=}1.2{\times}10^{-4}$), with the lead widening as the horizon grows.
Longitudinal prediction of Alzheimer's disease biomarkers increasingly informs clinical decisions, and a forecast is only useful if it also reports how much to trust it. Conformal prediction supplies this by wrapping any forecaster in a prediction band with a finite-sample coverage guarantee under exchangeability. However, standard population-level conformal prediction guarantees only marginal coverage and may mask substantial under-coverage within clinically important subgroups. We introduce a general mechanism-driven framework for auditing and repairing such subgroup under-coverage. Across two cohorts (ADNI, OASIS-3), two base forecasters, and nine attributes spanning genetic risk, demographics, and clinical severity, we find that population-level bands under-cover high-risk subgroups in 57 of 68 audited combinations, despite achieving nominal marginal coverage. We trace these failures to two mechanisms: (A) \emph{rarity}, where a group-conditional band calibrated on only $n$ patients covers at most $k/(n+1)$; and (B) \emph{tail-heaviness}, where a population-wide band is too narrow for a heavy-tailed subgroup and additional data cannot close the gap. Under-coverage falls disproportionately on patients with high genetic risk and disease severity (6.1 pp mean deficit, 95\% CI [3.3, 8.9]), while demographic groups remain at the target level on average (0.0 pp, CI [$-1.9$, 1.7]). We pair each mechanism with a corresponding conformal correction: cross-conformal pooling for rarity, per-subgroup calibration for tail-heaviness, and a coverage-safe marginal floor when both arise. Together, these corrections restore target coverage for nearly every high-risk subgroup across both cohorts and forecasters.
Predicting future structural MRI of a brain is challenging because longitudinal changes are often subtle and confined to specific anatomical regions, while most subject-specific brain structure remains stable over time. An effective model should therefore preserve global brain structural consistency while remaining sensitive to fine-grained disease progression. Existing latent-space-based methods improve computational efficiency, but suffer from information loss during their compression-reconstruction procedure. In contrast, direct voxel-space methods avoid latent reconstruction but commonly use a unified prediction pathway to model brain structure and progression-related changes. Subtle local changes may therefore be overshadowed by the dominant stable brain structure. To address these challenges, we propose ProgFormer, a hierarchical voxel-space Diffusion Transformer for longitudinal brain MRI prediction. ProgFormer uses a coarse pathway to perform the primary volumetric prediction from 3D patch tokens. This pathway models overall brain structure and longitudinal context. The fine pathway then uses the coarse representations as spatio-temporal grounding for voxel-level refinement within individual patches. The two pathways jointly estimate a velocity field directly in voxel space through conditional flow matching, enabling end-to-end prediction without a separately learned image autoencoder. The predicted future scan is then generated from Gaussian noise by integrating the estimated velocity field over a sequence of Euler steps. Extensive experimental results on three widely used benchmarks, ADNI, AIBL, and OASIS, under both pairwise and trajectory settings demonstrate favourable performance compared against several state-of-the-art methods.
Resistance to first-line osimertinib in EGFR-mutant non-small-cell lung cancer (NSCLC) is the canonical example of predictable clonal evolution under therapeutic pressure, yet no public benchmark exists for training or evaluating computational models on the corresponding longitudinal patient trajectories. We introduce OncoTraj, a public benchmark of 813 EGFR-mutant NSCLC patients receiving first-line osimertinib, harmonized from three real-world clinical-genomic sources: MSK-CHORD (672 patients), AACR Project GENIE BPC NSCLC (34 patients), and the FLAURA molecular-resistance supplement (107 patients). OncoTraj defines three locked tasks: (A) binary classification of progression by a fixed 12-month landmark, (B) regression of time-to-first-progression in days, and (C) six-class classification of the dominant resistance mechanism. We release the harmonized dataset, patient-level train/validation/test splits with an audited no-leakage guarantee, an open-source evaluation harness, and six reference baselines spanning a majority-class predictor, logistic regression, random forest, XGBoost, an LSTM, and a multi-task transformer. With v1's single-timepoint snapshot features, no task clears chance on clean within-source evaluation: the uniformity of this ceiling across every model class localizes the limit to the input modality (single-snapshot tissue NGS rather than serial ctDNA), not the algorithm. The benchmark does recover a reproducible literature-consistent association: TP53 co-mutation raises the 12-month progression rate from 29% to 59% cohort-wide. OncoTraj establishes a reproducible, leakage-audited baseline and converts the modality limit into concrete design requirements for a serial-ctDNA-enriched v2.