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Beyond Static Vision: Scene Dynamic Field Unlocks Intuitive Physics Understanding in Multi-modal Large Language Models

arXiv:2604.03302v1 Announce Type: cross Abstract: While Multimodal Large Language Models (MLLMs) have demonstrated impressive capabilities in image and video understanding, their ability to comprehend the physical world has become an increasingly important research focus. Despite their improvements, current MLLMs struggle significantly with high-level physics reasoning. In this work, we investigate the first step of physical reasoning, i.e., intuitive physics understanding, revealing substantial limitations in understanding the dynamics of continuum objects. To isolate and evaluate this specific capability, we introduce two fundamental benchmark tasks: Next Frame Selection (NFS) and Temporal Coherence Verification (TCV). Our experiments demonstrate that even state-of-the-art MLLMs perform poorly on these foundational tasks. To address this limitation, we propose Scene Dynamic Field (SDF), a concise approach that leverages physics simulators within a multi-task fine-tuning framework. SDF substantially improves performance, achieving up to 20.7% gains on fluid tasks while showing strong generalization to unseen physical domains. This work not only highlights a critical gap in current MLLMs but also presents a promising cost-efficient approach for developing more physically grounded MLLMs. Our code and data are available at https://github.com/andylinx/Scene-Dynamic-Field.
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DP-OPD: Differentially Private On-Policy Distillation for Language Models

arXiv:2604.04461v1 Announce Type: cross Abstract: Large language models (LLMs) are increasingly adapted to proprietary and domain-specific corpora that contain sensitive information, creating a tension between formal privacy guarantees and efficient deployment through model compression. Differential privacy (DP), typically enforced via DP-SGD, provides record-level protection but often incurs substantial utility loss in autoregressive generation, where optimization noise can amplify exposure bias and compounding errors along long rollouts. Existing approaches to private distillation either apply DP-SGD to both teacher and student, worsening computation and the privacy--utility tradeoff, or rely on DP synthetic text generation from a DP-trained teacher, avoiding DP on the student at the cost of DP-optimizing a large teacher and introducing an offline generation pipeline. We propose \textbf{Differentially Private On-Policy Distillation (DP-OPD)}, a synthesis-free framework that enforces privacy solely through DP-SGD on the student while leveraging a frozen teacher to provide dense token-level targets on \emph{student-generated} trajectories. DP-OPD instantiates this idea via \emph{private generalized knowledge distillation} on continuation tokens. Under a strict privacy budget ($\varepsilon=2.0$), DP-OPD improves perplexity over DP fine-tuning and off-policy DP distillation, and outperforms synthesis-based DP distillation (Yelp: 44.15$\rightarrow$41.68; BigPatent: 32.43$\rightarrow$30.63), while substantially simplifying the training pipeline. In particular, \textbf{DP-OPD collapses private compression into a single DP student-training loop} by eliminating DP teacher training and offline synthetic text generation. Code will be released upon publication at https://github.com/khademfatemeh/dp_opd.
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Parallel Universes, Parallel Languages: A Comprehensive Study on LLM-based Multilingual Counterfactual Example Generation

arXiv:2601.00263v2 Announce Type: replace-cross Abstract: Counterfactuals refer to minimally edited inputs that cause a model's prediction to change, serving as a promising approach to explaining the model's behavior. Large language models (LLMs) excel at generating English counterfactuals and demonstrate multilingual proficiency. However, their effectiveness in generating multilingual counterfactuals remains unclear. To this end, we conduct a comprehensive study on multilingual counterfactuals. We first conduct automatic evaluations on both directly generated counterfactuals in the target languages and those derived via English translation across six languages. Although translation-based counterfactuals offer higher validity than their directly generated counterparts, they demand substantially more modifications and still fall short of matching the quality of the original English counterfactuals. Second, we find the patterns of edits applied to high-resource European-language counterfactuals to be remarkably similar, suggesting that cross-lingual perturbations follow common strategic principles. Third, we identify and categorize four main types of errors that consistently appear in the generated counterfactuals across languages. Finally, we reveal that multilingual counterfactual data augmentation (CDA) yields larger model performance improvements than cross-lingual CDA, especially for lower-resource languages. Yet, the imperfections of the generated counterfactuals limit gains in model performance and robustness.
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Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition

Front Immunol. 2026 Mar 20;17:1787094. doi: 10.3389/fimmu.2026.1787094. eCollection 2026.

ABSTRACT

Pulmonary fibrosis (PF) significantly increases the risk of lung cancer (LC), but the mechanisms underlying this transition remain unclear. This overview positions macrophage heterogeneity as a central node within the PF-LC continuum. First, we describe important subpopulations of profibrotic and pro-tumor macrophages, including SPP1+, MERTK+, TREM2+, and MARCO+ cells, using high-resolution spatial and single-cell omics technologies. Next, we analyze the fundamental mechanisms that determine their function: the fibrotic microenvironment (e.g., extracellular matrix stiffness, hypoxia) induces profound metabolic reprogramming (e.g., Warburg effect, lipid peroxidation) and stabilizes epigenetic memory (e.g., DNA methylation, histone modifications), locking them into a pathogenic state. This reprogramming occurs through two main pathways: (1) metabolic reprogramming, characterized by aerobic glycolytic conversion and dysregulated lipid metabolism, which stimulates both pathogenic functions and suppression of T cell activity; (2) Epigenetic modifications, including stabilized alterations in DNA methylation, histone modifications, and superactivator patterns, which maintain cells in a tumor-promoting phenotype. As central nodes of communication, these macrophages interact pathologically with fibroblasts and epithelial cells through secreted factors and extracellular vesicles, forming self-reinforcing feedback loops that promote disease progression. We are studying the crucial role of new technologies, particularly multi-omic spatial models and high-precision organoids, in fostering mechanistic discoveries. These discoveries pave the way for new macrophage-focused therapeutic strategies, including the precise stratification of patients using biomarkers from liquid biopsies (such as soluble SPP1 and MARCO) and the development of targeted drug delivery systems for the selective modulation of macrophage function, thus establishing a new paradigm for therapeutic interventions in pulmonary fibrosis with concomitant lung cancer.

PMID:41939908 | PMC:PMC13046558 | DOI:10.3389/fimmu.2026.1787094

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Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition

Front Immunol. 2026 Mar 20;17:1787094. doi: 10.3389/fimmu.2026.1787094. eCollection 2026.

ABSTRACT

Pulmonary fibrosis (PF) significantly increases the risk of lung cancer (LC), but the mechanisms underlying this transition remain unclear. This overview positions macrophage heterogeneity as a central node within the PF-LC continuum. First, we describe important subpopulations of profibrotic and pro-tumor macrophages, including SPP1+, MERTK+, TREM2+, and MARCO+ cells, using high-resolution spatial and single-cell omics technologies. Next, we analyze the fundamental mechanisms that determine their function: the fibrotic microenvironment (e.g., extracellular matrix stiffness, hypoxia) induces profound metabolic reprogramming (e.g., Warburg effect, lipid peroxidation) and stabilizes epigenetic memory (e.g., DNA methylation, histone modifications), locking them into a pathogenic state. This reprogramming occurs through two main pathways: (1) metabolic reprogramming, characterized by aerobic glycolytic conversion and dysregulated lipid metabolism, which stimulates both pathogenic functions and suppression of T cell activity; (2) Epigenetic modifications, including stabilized alterations in DNA methylation, histone modifications, and superactivator patterns, which maintain cells in a tumor-promoting phenotype. As central nodes of communication, these macrophages interact pathologically with fibroblasts and epithelial cells through secreted factors and extracellular vesicles, forming self-reinforcing feedback loops that promote disease progression. We are studying the crucial role of new technologies, particularly multi-omic spatial models and high-precision organoids, in fostering mechanistic discoveries. These discoveries pave the way for new macrophage-focused therapeutic strategies, including the precise stratification of patients using biomarkers from liquid biopsies (such as soluble SPP1 and MARCO) and the development of targeted drug delivery systems for the selective modulation of macrophage function, thus establishing a new paradigm for therapeutic interventions in pulmonary fibrosis with concomitant lung cancer.

PMID:41939908 | PMC:PMC13046558 | DOI:10.3389/fimmu.2026.1787094

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