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Received — 8 April 2026 ⏭

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

✇(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
By: Zhengyu Hu · Jiaqi Wang · Jialin Yu · Zheqing Hu · Jing Xue · Zhanbing Ma · Miaomiao Nian · Ruixin Qi · Tingting Zhao · Xia Cao · Hongxia Xin · Xiuyan Wang · Guilan Yang · Zhenzhen Gui · Xiaoming Liu · Juan Chen
6 April 2026 at 18:00

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

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

✇Omics In Lung
By: Zhengyu Hu · Jiaqi Wang · Jialin Yu · Zheqing Hu · Jing Xue · Zhanbing Ma · Miaomiao Nian · Ruixin Qi · Tingting Zhao · Xia Cao · Hongxia Xin · Xiuyan Wang · Guilan Yang · Zhenzhen Gui · Xiaoming Liu · Juan Chen
6 April 2026 at 18:00

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

Received — 17 March 2026 ⏭

Visual-ERM: Reward Modeling for Visual Equivalence

✇cs.AI, q-bio.NC updates on arXiv.org
By: Ziyu Liu · Shengyuan Ding · Xinyu Fang · Xuanlang Dai · Penghui Yang · Jianze Liang · Jiaqi Wang · Kai Chen · Dahua Lin · Yuhang Zang
16 March 2026 at 12:00
arXiv:2603.13224v1 Announce Type: cross Abstract: Vision-to-code tasks require models to reconstruct structured visual inputs, such as charts, tables, and SVGs, into executable or structured representations with high visual fidelity. While recent Large Vision Language Models (LVLMs) achieve strong results via supervised fine-tuning, reinforcement learning remains challenging due to misaligned reward signals. Existing rewards either rely on textual rules or coarse visual embedding similarity, both of which fail to capture fine-grained visual discrepancies and are vulnerable to reward hacking. We propose Visual Equivalence Reward Model (Visual-ERM), a multimodal generative reward model that provides fine-grained, interpretable, and task-agnostic feedback to evaluate vision-to-code quality directly in the rendered visual space. Integrated into RL, Visual-ERM improves Qwen3-VL-8B-Instruct by +8.4 on chart-to-code and yields consistent gains on table and SVG parsing (+2.7, +4.1 on average), and further strengthens test-time scaling via reflection and revision. We also introduce VisualCritic-RewardBench (VC-RewardBench), a benchmark for judging fine-grained image-to-image discrepancies on structured visual data, where Visual-ERM at 8B decisively outperforms Qwen3-VL-235B-Instruct and approaches leading closed-source models. Our results suggest that fine-grained visual reward supervision is both necessary and sufficient for vision-to-code RL, regardless of task specificity.
Received — 5 March 2026 ⏭

Learning Memory-Enhanced Improvement Heuristics for Flexible Job Shop Scheduling

✇cs.AI, q-bio.NC updates on arXiv.org
By: Jiaqi Wang · Zhiguang Cao · Peng Zhao · Rui Cao · Yubin Xiao · Yuan Jiang · You Zhou
4 March 2026 at 13:00
arXiv:2603.02846v1 Announce Type: cross Abstract: The rise of smart manufacturing under Industry 4.0 introduces mass customization and dynamic production, demanding more advanced and flexible scheduling techniques. The flexible job-shop scheduling problem (FJSP) has attracted significant attention due to its complex constraints and strong alignment with real-world production scenarios. Current deep reinforcement learning (DRL)-based approaches to FJSP predominantly employ constructive methods. While effective, they often fall short of reaching (near-)optimal solutions. In contrast, improvement-based methods iteratively explore the neighborhood of initial solutions and are more effective in approaching optimality. However, the flexible machine allocation in FJSP poses significant challenges to the application of this framework, including accurate state representation, effective policy learning, and efficient search strategies. To address these challenges, this paper proposes a Memory-enhanced Improvement Search framework with heterogeneous graph representation--MIStar. It employs a novel heterogeneous disjunctive graph that explicitly models the operation sequences on machines to accurately represent scheduling solutions. Moreover, a memoryenhanced heterogeneous graph neural network (MHGNN) is designed for feature extraction, leveraging historical trajectories to enhance the decision-making capability of the policy network. Finally, a parallel greedy search strategy is adopted to explore the solution space, enabling superior solutions with fewer iterations. Extensive experiments on synthetic data and public benchmarks demonstrate that MIStar significantly outperforms both traditional handcrafted improvement heuristics and state-of-the-art DRL-based constructive methods.
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