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Han Zhou

Han Zhou contributes to research discovery and scholarly infrastructure.

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Published work

4 published item(s)

preprint2026arXiv

Learning Longitudinal Health Representations from EHR and Wearable Data

Foundation models trained on electronic health records show strong performance on many clinical prediction tasks but are limited by sparse and irregular documentation. Wearable devices provide dense continuous physiological signals but lack semantic grounding. Existing methods usually model these data sources separately or combine them through late fusion. We propose a multimodal foundation model that jointly represents electronic health records and wearable data as a continuous time latent process. The model uses modality specific encoders and a shared temporal backbone pretrained with self supervised and cross modal objectives. This design produces representations that are temporally coherent and clinically grounded. Across forecasting physiological and risk modeling tasks the model outperforms strong electronic health record only and wearable only baselines especially at long horizons and under missing data. These results show that joint electronic health record and wearable pretraining yields more faithful representations of longitudinal health.

preprint2026arXiv

PVRF: All-in-one Adverse Weather Removal via Prior-modulated and Velocity-constrained Rectified Flow

Adverse weather removal (AWR) in real-world images remains challenging due to heterogeneous and unseen degradations, while distortion-driven training often yields overly smooth results. We propose PVRF, a unified framework that integrates zero-shot soft weather perceptions with velocity-constrained rectified-flow refinement. PVRF introduces an AWR-specific question answering module (AWR-QA) that uses frozen vision--language models (VLMs) to estimate soft probabilities of weather types and low-level attribute scores. These perceptions condition restoration networks via attribute-modulated normalization (AMN) and weather-weighted adapters (WWA), producing an anchor estimate for refinement. We then learn a terminal-consistent residual rectified flow with perception-adaptive source perturbation and a terminal-consistent velocity parameterization to stabilize learning near the terminal regime. Extensive experiments show that PVRF improves both fidelity and perceptual quality over state-of-the-art baselines, with strong cross-dataset generalization on single and combined degradations. Code will be released at https://github.com/dongw22/PVRF.

preprint2026arXiv

STEP3-VL-10B Technical Report

We present STEP3-VL-10B, a lightweight open-source foundation model designed to redefine the trade-off between compact efficiency and frontier-level multimodal intelligence. STEP3-VL-10B is realized through two strategic shifts: first, a unified, fully unfrozen pre-training strategy on 1.2T multimodal tokens that integrates a language-aligned Perception Encoder with a Qwen3-8B decoder to establish intrinsic vision-language synergy; and second, a scaled post-training pipeline featuring over 1k iterations of reinforcement learning. Crucially, we implement Parallel Coordinated Reasoning (PaCoRe) to scale test-time compute, allocating resources to scalable perceptual reasoning that explores and synthesizes diverse visual hypotheses. Consequently, despite its compact 10B footprint, STEP3-VL-10B rivals or surpasses models 10$\times$-20$\times$ larger (e.g., GLM-4.6V-106B, Qwen3-VL-235B) and top-tier proprietary flagships like Gemini 2.5 Pro and Seed-1.5-VL. Delivering best-in-class performance, it records 92.2% on MMBench and 80.11% on MMMU, while excelling in complex reasoning with 94.43% on AIME2025 and 75.95% on MathVision. We release the full model suite to provide the community with a powerful, efficient, and reproducible baseline.

preprint2026arXiv

Unraveling the Allosteric Mechanism and Mechanical Stability of Partial and Complete Loss-of-Function Mutations in p53 DNA-Binding Domain

TP53 is the most frequently mutated tumor suppressor gene in human cancers, with mutations primarily in its DNA-binding domain (p53-DBD). Mutations in p53-DBD are categorized into hotspot mutations (resulting in complete loss-of-function) and non-hotspot mutations (inducing partial loss-of-function). However, the allosteric mechanisms underlying non-hotspot mutations remain elusive. Using p53 dimer as models, we constructed p53-WT, non-hotspot p53-E180R, and hotspot p53-R248W dimer-DNA complexes to compare the structural and functional impacts of these two mutation types. Our results reveal that both mutations weaken intramolecular interactions in p53-DBD and enhance structural flexibility. Specifically, E180R perturbs dimer interface interactions, impairing dimer stability and cooperative DNA binding; R248W disrupts interactions between the L3/L1 loops and DNA, leading to the loss of DNA-binding capacity. Steered molecular dynamics (SMD) simulations further confirm that both mutations accelerate p53 dimer dissociation, with E180R exerting the most prominent disruptive effect on the mechanical stability of the dimer interface.