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cs.AI, q-bio.NC updates on arXiv.org
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Cheers: Decoupling Patch Details from Semantic Representations Enables Unified Multimodal Comprehension and Generation
arXiv:2603.12793v1 Announce Type: cross Abstract: A recent cutting-edge topic in multimodal modeling is to unify visual comprehension and generation within a single model. However, the two tasks demand mismatched decoding regimes and visual representations, making it non-trivial to jointly optimize within a shared feature space. In this work, we present Cheers, a unified multimodal model that decouples patch-level details from semantic representations, thereby stabilizing semantics for multimod
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(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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NExT-Guard: Training-Free Streaming Safeguard without Token-Level Labels
arXiv:2603.02219v1 Announce Type: cross Abstract: Large language models are increasingly deployed in streaming scenarios, rendering conventional post-hoc safeguards ineffective as they fail to interdict unsafe content in real-time. While streaming safeguards based on token-level supervised training could address this, they necessitate expensive annotations and suffer from severe overfitting. In this work, we challenge the paradigm that streaming safety must rely on token-level supervised traini
NExT-Guard: Training-Free Streaming Safeguard without Token-Level Labels
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cs.AI, q-bio.NC updates on arXiv.org
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MultiDiffSense: Diffusion-Based Multi-Modal Visuo-Tactile Image Generation Conditioned on Object Shape and Contact Pose
arXiv:2602.19348v1 Announce Type: cross Abstract: Acquiring aligned visuo-tactile datasets is slow and costly, requiring specialised hardware and large-scale data collection. Synthetic generation is promising, but prior methods are typically single-modality, limiting cross-modal learning. We present MultiDiffSense, a unified diffusion model that synthesises images for multiple vision-based tactile sensors (ViTac, TacTip, ViTacTip) within a single architecture. Our approach uses dual conditionin
MultiDiffSense: Diffusion-Based Multi-Modal Visuo-Tactile Image Generation Conditioned on Object Shape and Contact Pose
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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