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cs.AI, q-bio.NC updates on arXiv.org
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AdaptFuse: Training-Free Sequential Preference Learning via Externalized Bayesian Inference
arXiv:2604.03925v1 Announce Type: cross Abstract: Large language models struggle to accumulate evidence across multiple rounds of user interaction, failing to update their beliefs in a manner consistent with Bayesian inference. Existing solutions require fine-tuning on sensitive user interaction data, limiting their applicability in privacy-conscious settings. We propose AdaptFuse, a training-free framework that externalizes probabilistic computation entirely from the LLM: a symbolic module mai
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cs.AI, q-bio.NC updates on arXiv.org
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Preserving Forgery Artifacts: AI-Generated Video Detection at Native Scale
arXiv:2604.04634v1 Announce Type: cross Abstract: The rapid advancement of video generation models has enabled the creation of highly realistic synthetic media, raising significant societal concerns regarding the spread of misinformation. However, current detection methods suffer from critical limitations. They rely on preprocessing operations like fixed-resolution resizing and cropping. These operations not only discard subtle, high-frequency forgery traces but also cause spatial distortion an
Preserving Forgery Artifacts: AI-Generated Video Detection at Native Scale
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cs.AI, q-bio.NC updates on arXiv.org
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Discovering Failure Modes in Vision-Language Models using RL
arXiv:2604.04733v1 Announce Type: cross Abstract: Vision-language Models (VLMs), despite achieving strong performance on multimodal benchmarks, often misinterpret straightforward visual concepts that humans identify effortlessly, such as counting, spatial reasoning, and viewpoint understanding. Previous studies manually identified these weaknesses and found that they often stem from deficits in specific skills. However, such manual efforts are costly, unscalable, and subject to human bias, whic
Discovering Failure Modes in Vision-Language Models using RL
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cs.AI, q-bio.NC updates on arXiv.org
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ContextDrag: Precise Drag-Based Image Editing via Context-Preserving Token Injection and Position-Aligned Attention
arXiv:2512.08477v2 Announce Type: replace-cross Abstract: Drag-based image editing enables intuitive visual manipulation through point-based drag operations. Existing methods mainly rely on diffusion inversion or pixel-space warping with inpainting. However, inversion inherently introduces approximation errors that degrade texture fidelity, whereas rigid pixel-space operations discard semantic context and produce unnatural deformations. To address these issues, we introduce ContextDrag, to our
ContextDrag: Precise Drag-Based Image Editing via Context-Preserving Token Injection and Position-Aligned Attention
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cs.AI, q-bio.NC updates on arXiv.org
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GPA: Learning GUI Process Automation from Demonstrations
arXiv:2604.01676v2 Announce Type: replace-cross Abstract: GUI Process Automation (GPA) is a lightweight but general vision-based Robotic Process Automation (RPA), which enables fast and stable process replay with only a single demo. Addressing the fragility of traditional RPA and the non-deterministic risks of current vision language model-based GUI agents, GPA introduces three core benefits: (1) Robustness via Sequential Monte Carlo-based localization to handle rescaling and detection uncertai
GPA: Learning GUI Process Automation from Demonstrations
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.ABSTRACTBACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-
Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.
ABSTRACT
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.
METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-cell and spatial transcriptomics, as well as peripheral blood multi-omics data to uncover key molecular signatures in IPF. Furthermore, machine learning techniques were utilized to identify core genes, whereas functional analyses and Mendelian randomization were conducted to evaluate the causal relationships among gut microbiota, immune cells, and IPF. Additionally, experimental validation using qPCR and ELISA assays was conducted in vitro, in vivo, and in patient plasma to confirm the expression patterns of key genes.
RESULTS: Across integrated public bulk, single-cell, spatial, and blood multi-omics, CXCL13, IL33, TLR4, and IGF1 were identified as core IPF genes consistently linked to immune infiltration and fibrotic remodeling. Deconvolution, scRNA-seq, and spatial mapping localized their dysregulation to fibroblasts and immune compartments (notably B-cell, macrophage, and mast-cell axes), highlighting fibroblast-immune crosstalk in fibrotic foci. A four-gene model robustly distinguished IPF from controls across cohorts. Mendelian randomization supported a gut-immune-lung axis, indicating causal effects of specific gut taxa on IPF risk via immune phenotypes. qPCR/ELISA in TGF-β1-stimulated fibroblasts, bleomycin mouse lungs, and patient plasma corroborated upregulation of IL33, CXCL13, IGF1 and downregulation of TLR4. Drug-signature reversal nominated cucurbitacin I and temsirolimus; molecular docking was performed as a preliminary in silico, computer-simulation-based assessment of potential ligand-protein interactions between these compounds and the four core targets.
CONCLUSION: This study provides new insights into the importance of gut-immune-lung axis in IPF and identifies CXCL13, IL33, TLR4, and IGF1 as diagnostic signatures and therapeutic targets. By integrating public multi-omics resources with experimental validation, our findings offer a foundation for future diagnostic and treatment strategies aimed at modulating the gut microbiota and immune system in IPF.
PMID:41939867 | PMC:PMC13043422 | DOI:10.3389/fimmu.2026.1730289
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Omics In Lung
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Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.ABSTRACTBACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-
Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.
ABSTRACT
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.
METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-cell and spatial transcriptomics, as well as peripheral blood multi-omics data to uncover key molecular signatures in IPF. Furthermore, machine learning techniques were utilized to identify core genes, whereas functional analyses and Mendelian randomization were conducted to evaluate the causal relationships among gut microbiota, immune cells, and IPF. Additionally, experimental validation using qPCR and ELISA assays was conducted in vitro, in vivo, and in patient plasma to confirm the expression patterns of key genes.
RESULTS: Across integrated public bulk, single-cell, spatial, and blood multi-omics, CXCL13, IL33, TLR4, and IGF1 were identified as core IPF genes consistently linked to immune infiltration and fibrotic remodeling. Deconvolution, scRNA-seq, and spatial mapping localized their dysregulation to fibroblasts and immune compartments (notably B-cell, macrophage, and mast-cell axes), highlighting fibroblast-immune crosstalk in fibrotic foci. A four-gene model robustly distinguished IPF from controls across cohorts. Mendelian randomization supported a gut-immune-lung axis, indicating causal effects of specific gut taxa on IPF risk via immune phenotypes. qPCR/ELISA in TGF-β1-stimulated fibroblasts, bleomycin mouse lungs, and patient plasma corroborated upregulation of IL33, CXCL13, IGF1 and downregulation of TLR4. Drug-signature reversal nominated cucurbitacin I and temsirolimus; molecular docking was performed as a preliminary in silico, computer-simulation-based assessment of potential ligand-protein interactions between these compounds and the four core targets.
CONCLUSION: This study provides new insights into the importance of gut-immune-lung axis in IPF and identifies CXCL13, IL33, TLR4, and IGF1 as diagnostic signatures and therapeutic targets. By integrating public multi-omics resources with experimental validation, our findings offer a foundation for future diagnostic and treatment strategies aimed at modulating the gut microbiota and immune system in IPF.
PMID:41939867 | PMC:PMC13043422 | DOI:10.3389/fimmu.2026.1730289