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cs.AI, q-bio.NC updates on arXiv.org
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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 substantia
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cs.AI, q-bio.NC updates on arXiv.org
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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 bi
DP-OPD: Differentially Private On-Policy Distillation for Language Models
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cs.AI, q-bio.NC updates on arXiv.org
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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
Parallel Universes, Parallel Languages: A Comprehensive Study on LLM-based Multilingual Counterfactual Example Generation
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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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.ABSTRACTPulmonary 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 a
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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Omics In Lung
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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.ABSTRACTPulmonary 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 a
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