Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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A Large-Scale Multimodal Dataset and Benchmarks for Human Activity Scene Understanding and Reasoning
arXiv:2512.07136v1 Announce Type: cross Abstract: Multimodal human action recognition (HAR) leverages complementary sensors for activity classification. Beyond recognition, recent advances in large language models (LLMs) enable detailed descriptions and causal reasoning, motivating new tasks: human action understanding (HAU) and human action reasoning (HARn). However, most LLMs, especially large vision language models (LVLMs), struggle with non-RGB modalities such as depth, IMU, and mmWave due
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Omics In Lung
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Multi-omic profiling provides insights into the heterogeneity, microenvironmental features, and biomarker landscape of small-cell lung cancer
Mol Cancer. 2025 Dec 2. doi: 10.1186/s12943-025-02514-4. Online ahead of print.ABSTRACTBACKGROUND: Greater understanding of differential therapeutic sensitivity, specifically to immunotherapy, in small-cell lung cancer (SCLC) is required.METHODS: We explored SCLC heterogeneity through integrated molecular characterization of tumor tissue samples from 159 treatment-naive patients, utilizing genetic, epigenetic, transcriptional, and proteomic profiling, immunohistochemistry staining for multiple b
Multi-omic profiling provides insights into the heterogeneity, microenvironmental features, and biomarker landscape of small-cell lung cancer
Mol Cancer. 2025 Dec 2. doi: 10.1186/s12943-025-02514-4. Online ahead of print.
ABSTRACT
BACKGROUND: Greater understanding of differential therapeutic sensitivity, specifically to immunotherapy, in small-cell lung cancer (SCLC) is required.
METHODS: We explored SCLC heterogeneity through integrated molecular characterization of tumor tissue samples from 159 treatment-naive patients, utilizing genetic, epigenetic, transcriptional, and proteomic profiling, immunohistochemistry staining for multiple biologically relevant markers including transcriptional subtype-defining proteins, and spatial immune profiling using multiplex immunofluorescence.
RESULTS: Multi-omics analysis confirmed high heterogeneity across/within neuroendocrine and non-neuroendocrine subtypes. Methylomics analysis identified four methylome clusters that may enhance subtype prediction, prognosis, and longitudinal monitoring of subtype evolution. Immunohistochemistry analysis showed high MHC-I expression in non-neuroendocrine subtypes, which have greatest potential benefit from adding immunotherapy to chemotherapy; high DLL3 expression associated with neuroendocrine subtypes and an immune-cold tumor microenvironment. Multiplex immunofluorescence demonstrated associations of MHC-I with spatial arrangement and phenotypic features of immune cells in the tumor microenvironment of high-MHC-I-expressing SCLC, providing mechanistic rationale for MHC-I as a potential biomarker of immunotherapy response.
CONCLUSIONS: This multimodal profiling analysis provides further insights into the biologic complexity of SCLC and highlights potential therapeutic vulnerabilities of distinct disease subtypes.
PMID:41331472 | DOI:10.1186/s12943-025-02514-4
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cs.AI, q-bio.NC updates on arXiv.org
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PathMind: A Retrieve-Prioritize-Reason Framework for Knowledge Graph Reasoning with Large Language Models
arXiv:2511.14256v1 Announce Type: new Abstract: Knowledge graph reasoning (KGR) is the task of inferring new knowledge by performing logical deductions on knowledge graphs. Recently, large language models (LLMs) have demonstrated remarkable performance in complex reasoning tasks. Despite promising success, current LLM-based KGR methods still face two critical limitations. First, existing methods often extract reasoning paths indiscriminately, without assessing their different importance, which
PathMind: A Retrieve-Prioritize-Reason Framework for Knowledge Graph Reasoning with Large Language Models
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cs.AI, q-bio.NC updates on arXiv.org
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Large Language Model Benchmarks in Medical Tasks
arXiv:2410.21348v3 Announce Type: replace-cross Abstract: With the increasing application of large language models (LLMs) in the medical domain, evaluating these models' performance using benchmark datasets has become crucial. This paper presents a comprehensive survey of various benchmark datasets employed in medical LLM tasks. These datasets span multiple modalities including text, image, and multimodal benchmarks, focusing on different aspects of medical knowledge such as electronic health r
Large Language Model Benchmarks in Medical Tasks
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cs.AI, q-bio.NC updates on arXiv.org
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BLM$_1$: A Boundless Large Model for Cross-Space, Cross-Task, and Cross-Embodiment Learning
arXiv:2510.24161v1 Announce Type: new Abstract: Multimodal large language models (MLLMs) have advanced vision-language reasoning and are increasingly deployed in embodied agents. However, significant limitations remain: MLLMs generalize poorly across digital-physical spaces and embodiments; vision-language-action models (VLAs) produce low-level actions yet lack robust high-level embodied reasoning; and most embodied large language models (ELLMs) are constrained to digital-space with poor genera
BLM$_1$: A Boundless Large Model for Cross-Space, Cross-Task, and Cross-Embodiment Learning
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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A statistical physics approach to integrating multi-omics data for disease-module detection
Cell Rep Methods. 2025 Sep 19:101183. doi: 10.1016/j.crmeth.2025.101183. Online ahead of print.ABSTRACTGenes associated with the same disease frequently engage in mutual biological interactions, e.g., perturbation within a specific neighborhood in the molecular interactome, often referred to as the disease module. This has propelled the advancement of network-based approaches toward elucidating the molecular bases of human diseases. Although many computational methods have been developed to inte
A statistical physics approach to integrating multi-omics data for disease-module detection
Cell Rep Methods. 2025 Sep 19:101183. doi: 10.1016/j.crmeth.2025.101183. Online ahead of print.
ABSTRACT
Genes associated with the same disease frequently engage in mutual biological interactions, e.g., perturbation within a specific neighborhood in the molecular interactome, often referred to as the disease module. This has propelled the advancement of network-based approaches toward elucidating the molecular bases of human diseases. Although many computational methods have been developed to integrate the molecular interactome and omics profiles to extract such context-dependent disease modules, approaches that leverage multi-omics for disease-module detection are still lacking. Here, we developed a statistical physics approach based on the random-field O(n) model (RFOnM) to fill this gap. We applied the RFOnM approach to integrate gene-expression data and genome-wide association studies or mRNA data and DNA methylation for several complex diseases with the human interactome. We found that the RFOnM approach outperforms existing single omics methods in most of the complex diseases considered in this study.
PMID:40975055 | DOI:10.1016/j.crmeth.2025.101183
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Cell
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Extrachromosomal DNA replication and maintenance couple with DNA damage pathway in tumors
This study demonstrates that extrachromosomal DNA (ecDNA) replication induces DNA double-strand breaks and activates the DNA damage response (DDR). The DDR pathways, such as alt-NHEJ, are critical for ecDNA maintenance in tumor cells. Mechanistic insights into ecDNA replication and maintenance unveil a therapeutic approach for treating tumors harboring ecDNA.
Extrachromosomal DNA replication and maintenance couple with DNA damage pathway in tumors
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Omics in Hepatocellular
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Decoding per- and polyfluoroalkyl substances (PFAS) in hepatocellular carcinoma: a multi-omics and computational toxicology approach
J Transl Med. 2025 May 2;23(1):504. doi: 10.1186/s12967-025-06517-z.ABSTRACTBACKGROUND: Per- and polyfluoroalkyl substances (PFAS), particularly perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), are synthetic chemicals known for their widespread use and environmental persistence. These compounds have been increasingly linked to hepatotoxicity and the development of hepatocellular carcinoma (HCC). However, the molecular mechanisms by which PFAS contribute to HCC remain underexpl
Decoding per- and polyfluoroalkyl substances (PFAS) in hepatocellular carcinoma: a multi-omics and computational toxicology approach
J Transl Med. 2025 May 2;23(1):504. doi: 10.1186/s12967-025-06517-z.
ABSTRACT
BACKGROUND: Per- and polyfluoroalkyl substances (PFAS), particularly perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), are synthetic chemicals known for their widespread use and environmental persistence. These compounds have been increasingly linked to hepatotoxicity and the development of hepatocellular carcinoma (HCC). However, the molecular mechanisms by which PFAS contribute to HCC remain underexplored.
METHODS: This study employs a multi-omics approach that combines network toxicology, integrated machine learning, single-cell RNA sequencing, spatial transcriptomics, experimental validation, and molecular docking simulations to uncover the mechanisms through which PFAS exposure drives HCC. We analyzed publicly available transcriptomic data from several HCC cohorts and used differential gene expression analysis to identify targets associated with both PFAS exposure and HCC. We constructed a protein-protein interaction (PPI) network and a survival risk model, the PFAS-related HCC signature (PFASRHSig), based on integrated machine learning to identify prognostic biomarkers, with the goal of identifying core targets of PFAS in HCC progression and prognosis. RT-qPCR and immunohistochemical (IHC) staining were used to validate the expression levels of the targets in both tumor and normal tissues. Molecular docking simulations were conducted to assess the binding affinities between PFAS compounds and selected target proteins.
RESULTS: Functional enrichment studies revealed that PFAS targets were associated with metabolic signaling pathways, which are actively involved in lipid, glucose, drug metabolism, etc. Through integrated machine learning and PPI network analysis, we identified six genes, APOA1, ESR1, IGF1, PPARGC1A, SERPINE1, and PON1, that serve as core targets of PFAS in both HCC progression and prognosis. These targets were further validated via bulk RNA-seq, single-cell RNA-seq, and spatial transcriptomics, which revealed differential expression patterns across various cell types in the HCC tumor microenvironment. The results of RT-qPCR and IHC staining were consistent with the in silico findings. Molecular docking simulations revealed strong binding affinities between PFAS compounds and these core targets, supporting their potential roles in PFAS-induced hepatocarcinogenesis.
CONCLUSIONS: Our study highlights key molecular targets and pathways involved in PFAS-induced liver carcinogenesis and proposes a robust survival risk model (PFASRHSig) for HCC. These findings provide new insights into PFAS toxicity mechanisms and offer potential therapeutic targets for mitigating the health risks associated with PFAS exposure. Collectively, our findings help in advancing clinical applications by providing insights into disease mechanisms and potential therapeutic interventions.
PMID:40317014 | PMC:PMC12049027 | DOI:10.1186/s12967-025-06517-z
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Omics In Lung
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Molecular mechanisms and therapeutic targets of acute exacerbations of chronic obstructive pulmonary disease with Pseudomonas aeruginosa infection
Respir Res. 2025 Mar 26;26(1):115. doi: 10.1186/s12931-025-03185-x.ABSTRACTBACKGROUND: Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of global mortality, with acute exacerbations of COPD (AECOPD) significantly increasing the disease's morbidity and mortality. Among the pathogens implicated in AECOPD, Pseudomonas aeruginosa (P. aeruginosa) is increasingly recognized as a major co-infecting bacterium. Despite its clinical importance, the molecular mechanisms and therapeutic targe
Molecular mechanisms and therapeutic targets of acute exacerbations of chronic obstructive pulmonary disease with Pseudomonas aeruginosa infection
Respir Res. 2025 Mar 26;26(1):115. doi: 10.1186/s12931-025-03185-x.
ABSTRACT
BACKGROUND: Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of global mortality, with acute exacerbations of COPD (AECOPD) significantly increasing the disease's morbidity and mortality. Among the pathogens implicated in AECOPD, Pseudomonas aeruginosa (P. aeruginosa) is increasingly recognized as a major co-infecting bacterium. Despite its clinical importance, the molecular mechanisms and therapeutic targets underlying AECOPD with P. aeruginosa infection remain inadequately understood.
METHODS: We employed a multi-omics approach, integrating proteomic analyses of bronchoalveolar lavage fluid (BALF) and plasma with transcriptomic analysis of peripheral blood. A discovery cohort of 40 AECOPD with P. aeruginosa infection patients and 20 healthy controls was analyzed, followed by validation in an independent cohort of 20 patients and 10 controls. Differentially expressed proteins (DEPs) and genes (DEGs) were identified and subjected to protein-protein interaction (PPI) network analysis, weighted gene co-expression network analysis (WGCNA), and immune infiltration analysis. Molecular docking simulations were conducted to explore potential therapeutic agents.
RESULTS: Our integrative analysis identified key biomarkers, which played critical roles in oxidative stress and neutrophil extracellular trap (NET) formation, both of which were pivotal in the pathogenesis of AECOPD with P. aeruginosa infection. The combined analysis of BALF, plasma, and peripheral blood underscored the interplay between local lung changes and systemic immune responses. Functional enrichment analyses highlighted significant pathways related to bacterial defense, inflammation, and immune activation. Validation in an independent cohort confirmed the diagnostic value of three key proteins (AZU1, MPO, and RETN), with high area under the curve (AUC) values in ROC analyses. Molecular docking indicated strong binding affinities of these proteins with Pioglitazone and Rosiglitazone, suggesting potential therapeutic utility.
CONCLUSIONS: This study provides a comprehensive understanding of the molecular mechanisms underlying AECOPD with P. aeruginosa infection, highlighting the pivotal roles of oxidative stress and NET formation in disease progression. The identified biomarkers offer promising diagnostic and therapeutic targets. Our findings pave the way for novel strategies to improve outcomes for AECOPD patients with P. aeruginosa infection. While the study design limits our ability to establish causality, these results provide important insights that warrant further investigation, particularly through longitudinal studies, to confirm the specific contributions of P. aeruginosa in exacerbations.
CLINICAL TRIAL NUMBER: Not applicable.
PMID:40140846 | PMC:PMC11948814 | DOI:10.1186/s12931-025-03185-x
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Cell
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Multiscale drug screening for cardiac fibrosis identifies MD2 as a therapeutic target
A multiscale drug discovery platform integrating human induced pluripotent stem cells, 3D-engineered heart tissues, and animal models identifies artesunate as a safe and potent antifibrotic compound.