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cs.AI, q-bio.NC updates on arXiv.org
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Automatic Image-Level Morphological Trait Annotation for Organismal Images
arXiv:2604.01619v1 Announce Type: cross Abstract: Morphological traits are physical characteristics of biological organisms that provide vital clues on how organisms interact with their environment. Yet extracting these traits remains a slow, expert-driven process, limiting their use in large-scale ecological studies. A major bottleneck is the absence of high-quality datasets linking biological images to trait-level annotations. In this work, we demonstrate that sparse autoencoders trained on f
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Cell
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Unified modeling of 3D molecular generation via atomic interactions with PocketXMol
A versatile, atom-level generative AI model enables unified pocket-interacting tasks, from docking to de novo design, and demonstrates robust experimental validation for both small-molecule and peptide therapeutics.
Unified modeling of 3D molecular generation via atomic interactions with PocketXMol
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Microbiome and metabolite signatures for cirrhosis to HCC risk stratification: progress, controversies, and gaps
Front Cell Infect Microbiol. 2026 Mar 16;16:1793213. doi: 10.3389/fcimb.2026.1793213. eCollection 2026.ABSTRACTThe progression from cirrhosis to hepatocellular carcinoma (HCC) is a key outcome in the management of chronic liver disease. This process has a long incubation period and significant individual differences, making early warning still difficult. Clinical follow-up mainly relies on imaging examinations and alpha fetoprotein, but the ability to identify high risk precancerous states is li
Microbiome and metabolite signatures for cirrhosis to HCC risk stratification: progress, controversies, and gaps
Front Cell Infect Microbiol. 2026 Mar 16;16:1793213. doi: 10.3389/fcimb.2026.1793213. eCollection 2026.
ABSTRACT
The progression from cirrhosis to hepatocellular carcinoma (HCC) is a key outcome in the management of chronic liver disease. This process has a long incubation period and significant individual differences, making early warning still difficult. Clinical follow-up mainly relies on imaging examinations and alpha fetoprotein, but the ability to identify high risk precancerous states is limited. The imbalance of gut microbiota and its metabolites may occur earlier than the visible stage of tumors. They can affect barrier integrity, chronic inflammation, immune surveillance, and metabolic homeostasis through the gut liver axis, and participate in the formation of a pro tumor microenvironment. Therefore, such changes may provide more upstream risk stratification clues for the population with cirrhosis. This article summarizes previous research evidence and summarizes the common microbiome and metabolite characteristics of cirrhosis and high-risk populations, including a decrease in short chain fatty acid (SCFA) related symbiotic bacteria, an increase in inflammation related bacteria, bile acid spectrum shift, and other intestinal derived metabolite abnormalities. This article also outlines the key mechanisms that these features may correspond to, such as barrier damage and microbial translocation, immune suppression, etc. There are still significant uncertainties at present. The effect of SCFA is context dependent. Different etiologies, diets, medications, and complications can lead to significant confounding and affect cross cohort consistency. Subsequent research requires longitudinal cohort validation and the promotion of multi omics integration and the construction of interpretable predictive models to support clinical translation.
PMID:41918873 | PMC:PMC13033666 | DOI:10.3389/fcimb.2026.1793213
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Nature - Issue - nature.com science feeds
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DNA damage burden causes selective CUX2 neuron loss in neuroinflammation
Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10310-3DNA damage burden and inadequate repair in CUX2+ cortical layer 2/3 excitatory neurons contributes to selective vulnerability in neuroinflammatory injury.
DNA damage burden causes selective CUX2 neuron loss in neuroinflammation
Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10310-3
DNA damage burden and inadequate repair in CUX2+ cortical layer 2/3 excitatory neurons contributes to selective vulnerability in neuroinflammatory injury.-
Nature - Issue - nature.com science feeds
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Electric dipole moment drives the dynamics of the TNFR1 complex I signalosome
Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10304-1Long-range interactions mediated by protein electric dipole moments have a role in driving the assembly and disassembly of super-signalling complex I for promoting NF-κB signalling.
Electric dipole moment drives the dynamics of the TNFR1 complex I signalosome
Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10304-1
Long-range interactions mediated by protein electric dipole moments have a role in driving the assembly and disassembly of super-signalling complex I for promoting NF-κB signalling.-
(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Integrated Network Toxicology and Metabolomics Elucidate Mechanisms of Carbosulfan-Induced Respiratory Toxicity in Rats
Int J Mol Sci. 2026 Feb 25;27(5):2170. doi: 10.3390/ijms27052170.ABSTRACTCarbosulfan is a widely used carbamate insecticide, yet its mechanisms of respiratory toxicity remain poorly understood. This study integrated network toxicology, untargeted metabolomics, and molecular docking to systematically investigate the potential mechanisms of carbosulfan-induced respiratory toxicity in male Sprague Dawley rats. Rats were administered a single oral dose of carbosulfan (125 or 250 mg/kg) and assessed
Integrated Network Toxicology and Metabolomics Elucidate Mechanisms of Carbosulfan-Induced Respiratory Toxicity in Rats
Int J Mol Sci. 2026 Feb 25;27(5):2170. doi: 10.3390/ijms27052170.
ABSTRACT
Carbosulfan is a widely used carbamate insecticide, yet its mechanisms of respiratory toxicity remain poorly understood. This study integrated network toxicology, untargeted metabolomics, and molecular docking to systematically investigate the potential mechanisms of carbosulfan-induced respiratory toxicity in male Sprague Dawley rats. Rats were administered a single oral dose of carbosulfan (125 or 250 mg/kg) and assessed after 12 h. Exposure resulted in significant pathological lung damage, characterized by disrupted alveolar architecture, inflammatory cell infiltration, and increased serum levels of the pro-inflammatory cytokines IL-6, IL-1β, and TNF-α. Network toxicology analysis identified 51 potential targets associated with respiratory toxicity, with core targets including SRC, EGFR, PTGS2, CXCL8, CYP3A4, and NR3C1. Enriched pathways were primarily related to neuroactive ligand-receptor interaction, VEGF signaling, and arachidonic acid metabolism. Untargeted metabolomics revealed significant metabolic perturbations in pathways central to antioxidant defense and energy homeostasis, including glutathione metabolism, the tricarboxylic acid cycle, and arginine biosynthesis. Molecular docking confirmed stable in silico binding affinities between carbosulfan and the predicted core targets. Integrative analysis suggests that carbosulfan exposure is associated with respiratory damage, potentially through interconnected mechanisms involving oxidative stress, inflammation, and disruption of cell signaling and metabolic enzyme systems. However, given the acute high-dose nature of the model and the interpretative integration of multi-omics data, these findings should be considered hypothesis-generating. This study provides a novel system-level perspective on carbosulfan-induced respiratory toxicity and highlights key pathways and targets for future validation in chronic exposure models.
PMID:41828400 | PMC:PMC12984169 | DOI:10.3390/ijms27052170
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Omics In Lung
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Integrated Network Toxicology and Metabolomics Elucidate Mechanisms of Carbosulfan-Induced Respiratory Toxicity in Rats
Int J Mol Sci. 2026 Feb 25;27(5):2170. doi: 10.3390/ijms27052170.ABSTRACTCarbosulfan is a widely used carbamate insecticide, yet its mechanisms of respiratory toxicity remain poorly understood. This study integrated network toxicology, untargeted metabolomics, and molecular docking to systematically investigate the potential mechanisms of carbosulfan-induced respiratory toxicity in male Sprague Dawley rats. Rats were administered a single oral dose of carbosulfan (125 or 250 mg/kg) and assessed
Integrated Network Toxicology and Metabolomics Elucidate Mechanisms of Carbosulfan-Induced Respiratory Toxicity in Rats
Int J Mol Sci. 2026 Feb 25;27(5):2170. doi: 10.3390/ijms27052170.
ABSTRACT
Carbosulfan is a widely used carbamate insecticide, yet its mechanisms of respiratory toxicity remain poorly understood. This study integrated network toxicology, untargeted metabolomics, and molecular docking to systematically investigate the potential mechanisms of carbosulfan-induced respiratory toxicity in male Sprague Dawley rats. Rats were administered a single oral dose of carbosulfan (125 or 250 mg/kg) and assessed after 12 h. Exposure resulted in significant pathological lung damage, characterized by disrupted alveolar architecture, inflammatory cell infiltration, and increased serum levels of the pro-inflammatory cytokines IL-6, IL-1β, and TNF-α. Network toxicology analysis identified 51 potential targets associated with respiratory toxicity, with core targets including SRC, EGFR, PTGS2, CXCL8, CYP3A4, and NR3C1. Enriched pathways were primarily related to neuroactive ligand-receptor interaction, VEGF signaling, and arachidonic acid metabolism. Untargeted metabolomics revealed significant metabolic perturbations in pathways central to antioxidant defense and energy homeostasis, including glutathione metabolism, the tricarboxylic acid cycle, and arginine biosynthesis. Molecular docking confirmed stable in silico binding affinities between carbosulfan and the predicted core targets. Integrative analysis suggests that carbosulfan exposure is associated with respiratory damage, potentially through interconnected mechanisms involving oxidative stress, inflammation, and disruption of cell signaling and metabolic enzyme systems. However, given the acute high-dose nature of the model and the interpretative integration of multi-omics data, these findings should be considered hypothesis-generating. This study provides a novel system-level perspective on carbosulfan-induced respiratory toxicity and highlights key pathways and targets for future validation in chronic exposure models.
PMID:41828400 | PMC:PMC12984169 | DOI:10.3390/ijms27052170
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cs.AI, q-bio.NC updates on arXiv.org
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RANGER: Sparsely-Gated Mixture-of-Experts with Adaptive Retrieval Re-ranking for Pathology Report Generation
arXiv:2603.04348v1 Announce Type: cross Abstract: Pathology report generation remains a relatively under-explored downstream task, primarily due to the gigapixel scale and complex morphological heterogeneity of Whole Slide Images (WSIs). Existing pathology report generation frameworks typically employ transformer architectures, relying on a homogeneous decoder architecture and static knowledge retrieval integration. Such architectures limit generative specialization and may introduce noisy exte
RANGER: Sparsely-Gated Mixture-of-Experts with Adaptive Retrieval Re-ranking for Pathology Report Generation
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cs.AI, q-bio.NC updates on arXiv.org
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Agent Data Protocol: Unifying Datasets for Diverse, Effective Fine-tuning of LLM Agents
arXiv:2510.24702v2 Announce Type: replace-cross Abstract: Public research results on large-scale supervised finetuning of AI agents remain relatively rare, since the collection of agent training data presents unique challenges. In this work, we argue that the bottleneck is not a lack of underlying data sources, but that a large variety of data is fragmented across heterogeneous formats, tools, and interfaces. To this end, we introduce the agent data protocol (ADP), a light-weight representation
Agent Data Protocol: Unifying Datasets for Diverse, Effective Fine-tuning of LLM Agents
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cs.AI, q-bio.NC updates on arXiv.org
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REMem: Reasoning with Episodic Memory in Language Agent
arXiv:2602.13530v2 Announce Type: replace Abstract: Humans excel at remembering concrete experiences along spatiotemporal contexts and performing reasoning across those events, i.e., the capacity for episodic memory. In contrast, memory in language agents remains mainly semantic, and current agents are not yet capable of effectively recollecting and reasoning over interaction histories. We identify and formalize the core challenges of episodic recollection and reasoning from this gap, and obser
REMem: Reasoning with Episodic Memory in Language Agent
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cs.AI, q-bio.NC updates on arXiv.org
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Eureka-Audio: Triggering Audio Intelligence in Compact Language Models
arXiv:2602.13954v1 Announce Type: cross Abstract: We present Eureka-Audio, a compact yet high-performance audio language model that achieves competitive performance against models that are 4 to 18 times larger across a broad range of audio understanding benchmarks. Despite containing only 1.7B parameters, Eureka-Audio demonstrates strong performance on automatic speech recognition (ASR), audio understanding, and dense audio captioning, matching or surpassing multiple 7B to 30B audio and omni-mo