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Received — 8 April 2026 ⏭

TreeGaussian: Tree-Guided Cascaded Contrastive Learning for Hierarchical Consistent 3D Gaussian Scene Segmentation and Understanding

✇cs.AI, q-bio.NC updates on arXiv.org
By: Jingbin You · Zehao Li · Hao Jiang · Xinzhu Ma · Shuqin Gao · Honglong Zhao · Congcong Zheng · Tianlu Mao · Feng Dai · Yucheng Zhang · Zhaoqi Wang
7 April 2026 at 12:00
arXiv:2604.03309v1 Announce Type: cross Abstract: 3D Gaussian Splatting (3DGS) has emerged as a real-time, differentiable representation for neural scene understanding. However, existing 3DGS-based methods struggle to represent hierarchical 3D semantic structures and capture whole-part relationships in complex scenes. Moreover, dense pairwise comparisons and inconsistent hierarchical labels from 2D priors hinder feature learning, resulting in suboptimal segmentation. To address these limitations, we introduce TreeGaussian, a tree-guided cascaded contrastive learning framework that explicitly models hierarchical semantic relationships and reduces redundancy in contrastive supervision. By constructing a multi-level object tree, TreeGaussian enables structured learning across object-part hierarchies. In addition, we propose a two-stage cascaded contrastive learning strategy that progressively refines feature representations from global to local, mitigating saturation and stabilizing training. A Consistent Segmentation Detection (CSD) mechanism and a graph-based denoising module are further introduced to align segmentation modes across views while suppressing unstable Gaussian points, enhancing segmentation consistency and quality. Extensive experiments, including open-vocabulary 3D object selection, 3D point cloud understanding, and ablation studies, demonstrate the effectiveness and robustness of our approach.

DIRECT: Video Mashup Creation via Hierarchical Multi-Agent Planning and Intent-Guided Editing

✇cs.AI, q-bio.NC updates on arXiv.org
By: Ke Li · Maoliang Li · Jialiang Chen · Jiayu Chen · Zihao Zheng · Shaoqi Wang · Xiang Chen
7 April 2026 at 12:00
arXiv:2604.04875v1 Announce Type: cross Abstract: Video mashup creation represents a complex video editing paradigm that recomposes existing footage to craft engaging audio-visual experiences, demanding intricate orchestration across semantic, visual, and auditory dimensions and multiple levels. However, existing automated editing frameworks often overlook the cross-level multimodal orchestration to achieve professional-grade fluidity, resulting in disjointed sequences with abrupt visual transitions and musical misalignment. To address this, we formulate video mashup creation as a Multimodal Coherency Satisfaction Problem (MMCSP) and propose the DIRECT framework. Simulating a professional production pipeline, our hierarchical multi-agent framework decomposes the challenge into three cascade levels: the Screenwriter for source-aware global structural anchoring, the Director for instantiating adaptive editing intent and guidance, and the Editor for intent-guided shot sequence editing with fine-grained optimization. We further introduce Mashup-Bench, a comprehensive benchmark with tailored metrics for visual continuity and auditory alignment. Extensive experiments demonstrate that DIRECT significantly outperforms state-of-the-art baselines in both objective metrics and human subjective evaluation. Project page and code: https://github.com/AK-DREAM/DIRECT

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

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