Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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HiRAD: A Flexible Large-Scale AGV Routing System
arXiv:2609.09752v1 Announce Type: cross Abstract: Automatic Guided Vehicles (AGVs) substantially boost warehouse throughput, but routing large-scale AGV fleets remains challenging. Classical Multi-Agent Pathfinding solvers suffer from exploding combinatorial complexity and super-quadratic runtime, while relying on idealized grid or piecewise-linear motion models that mismatch real-world kinematics. Recent Reinforcement Learning (RL) solutions improve flexibility via decentralized agent policies
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cs.AI, q-bio.NC updates on arXiv.org
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CollectionLoRA: Collecting 50 Effects in 1 LoRA via Multi-Teacher On-Policy Distillation
arXiv:2605.25378v1 Announce Type: cross Abstract: Customized image editing aims to equip pre-trained diffusion models with specific visual effects using limited paired data, typically via Low-Rank Adaptation (LoRA). As the number of desired effects grows, storing and dynamically loading numerous these effect LoRAs significantly increases deployment overhead. Furthermore, current pipelines typically cascade these effect LoRAs with acceleration modules for fast generation, which triggers severe p
CollectionLoRA: Collecting 50 Effects in 1 LoRA via Multi-Teacher On-Policy Distillation
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Omics In Lung
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Epigenome-wide Mendelian randomization with multi-omics validation identifies epigenetic drivers of idiopathic pulmonary fibrosis
Commun Biol. 2026 Apr 11. doi: 10.1038/s42003-026-10033-1. Online ahead of print.ABSTRACTIdiopathic pulmonary fibrosis (IPF) is a complex disease without clear etiology or effective therapy. While DNA methylation has been implicated in IPF pathogenesis, the tissue-specific causal effects of the epigenetic factors on IPF remain undetermined. Here, we perform epigenome-wide Mendelian randomization using blood-based methylation quantitative trait loci of 420,509 CpG sites and genome-wide associatio
Epigenome-wide Mendelian randomization with multi-omics validation identifies epigenetic drivers of idiopathic pulmonary fibrosis
Commun Biol. 2026 Apr 11. doi: 10.1038/s42003-026-10033-1. Online ahead of print.
ABSTRACT
Idiopathic pulmonary fibrosis (IPF) is a complex disease without clear etiology or effective therapy. While DNA methylation has been implicated in IPF pathogenesis, the tissue-specific causal effects of the epigenetic factors on IPF remain undetermined. Here, we perform epigenome-wide Mendelian randomization using blood-based methylation quantitative trait loci of 420,509 CpG sites and genome-wide association study for IPF to elucidate the causal effects of the CpG sites on IPF. Totally, 452 CpG sites has shown putative causal effects on IPF risk after Bonferroni correction. Among them, 13 CpG sites have shown strong colocalization evidence with genetic factors associated with IPF. Specifically, DNA methylation at CpG sites within MAN2A2 and TRIM27 shows significant differences between IPF lungs and controls, correlating with altered mRNA expressions of these genes in lung tissues. The CpG site in MAN2A2 is a binding site of ZNF384 according to transcription factor databases. RNA sequencing in the TGFβ1-induced alveolar epithelia confirms significantly reduced expression of MAN2A2 and ZNF384 comparing to the controls. Collectively, our study suggests a putative causal link between DNA methylation within MAN2A2 and IPF risk, wherein lung-specific DNA methylation in MAN2A2 may perturb the interaction between ZNF384 and MAN2A2, revealing novel roles for these genes in IPF pathogenesis.
PMID:41965819 | DOI:10.1038/s42003-026-10033-1
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Epigenome-wide Mendelian randomization with multi-omics validation identifies epigenetic drivers of idiopathic pulmonary fibrosis
Commun Biol. 2026 Apr 11. doi: 10.1038/s42003-026-10033-1. Online ahead of print.ABSTRACTIdiopathic pulmonary fibrosis (IPF) is a complex disease without clear etiology or effective therapy. While DNA methylation has been implicated in IPF pathogenesis, the tissue-specific causal effects of the epigenetic factors on IPF remain undetermined. Here, we perform epigenome-wide Mendelian randomization using blood-based methylation quantitative trait loci of 420,509 CpG sites and genome-wide associatio
Epigenome-wide Mendelian randomization with multi-omics validation identifies epigenetic drivers of idiopathic pulmonary fibrosis
Commun Biol. 2026 Apr 11. doi: 10.1038/s42003-026-10033-1. Online ahead of print.
ABSTRACT
Idiopathic pulmonary fibrosis (IPF) is a complex disease without clear etiology or effective therapy. While DNA methylation has been implicated in IPF pathogenesis, the tissue-specific causal effects of the epigenetic factors on IPF remain undetermined. Here, we perform epigenome-wide Mendelian randomization using blood-based methylation quantitative trait loci of 420,509 CpG sites and genome-wide association study for IPF to elucidate the causal effects of the CpG sites on IPF. Totally, 452 CpG sites has shown putative causal effects on IPF risk after Bonferroni correction. Among them, 13 CpG sites have shown strong colocalization evidence with genetic factors associated with IPF. Specifically, DNA methylation at CpG sites within MAN2A2 and TRIM27 shows significant differences between IPF lungs and controls, correlating with altered mRNA expressions of these genes in lung tissues. The CpG site in MAN2A2 is a binding site of ZNF384 according to transcription factor databases. RNA sequencing in the TGFβ1-induced alveolar epithelia confirms significantly reduced expression of MAN2A2 and ZNF384 comparing to the controls. Collectively, our study suggests a putative causal link between DNA methylation within MAN2A2 and IPF risk, wherein lung-specific DNA methylation in MAN2A2 may perturb the interaction between ZNF384 and MAN2A2, revealing novel roles for these genes in IPF pathogenesis.
PMID:41965819 | DOI:10.1038/s42003-026-10033-1
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cs.AI, q-bio.NC updates on arXiv.org
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RAE-AR: Taming Autoregressive Models with Representation Autoencoders
arXiv:2604.01545v1 Announce Type: new Abstract: The latent space of generative modeling is long dominated by the VAE encoder. The latents from the pretrained representation encoders (e.g., DINO, SigLIP, MAE) are previously considered inappropriate for generative modeling. Recently, RAE method lights the hope and reveals that the representation autoencoder can also achieve competitive performance as the VAE encoder. However, the integration of representation autoencoder into continuous autoregre
RAE-AR: Taming Autoregressive Models with Representation Autoencoders
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cs.AI, q-bio.NC updates on arXiv.org
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AeroTherm-GPT: A Verification-Centered LLM Framework for Thermal Protection System Engineering Workflows
arXiv:2604.01738v1 Announce Type: new Abstract: Integrating Large Language Models (LLMs) into hypersonic thermal protection system (TPS) design is bottlenecked by cascading constraint violations when generating executable simulation artifacts. General-purpose LLMs, treating generation as single-pass text completion, fail to satisfy the sequential, multi-gate constraints inherent in safety-critical engineering workflows. To address this, we propose AeroTherm-GPT, the first TPS-specialized LLM Ag
AeroTherm-GPT: A Verification-Centered LLM Framework for Thermal Protection System Engineering Workflows
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cs.AI, q-bio.NC updates on arXiv.org
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The Latent Space: Foundation, Evolution, Mechanism, Ability, and Outlook
arXiv:2604.02029v1 Announce Type: new Abstract: Latent space is rapidly emerging as a native substrate for language-based models. While modern systems are still commonly understood through explicit token-level generation, an increasing body of work shows that many critical internal processes are more naturally carried out in continuous latent space than in human-readable verbal traces. This shift is driven by the structural limitations of explicit-space computation, including linguistic redunda
The Latent Space: Foundation, Evolution, Mechanism, Ability, and Outlook
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cs.AI, q-bio.NC updates on arXiv.org
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MedLA: A Logic-Driven Multi-Agent Framework for Complex Medical Reasoning with Large Language Models
arXiv:2509.23725v3 Announce Type: replace Abstract: Answering complex medical questions requires not only domain expertise and patient-specific information, but also structured and multi-perspective reasoning. Existing multi-agent approaches often rely on fixed roles or shallow interaction prompts, limiting their ability to detect and resolve fine-grained logical inconsistencies. To address this, we propose \textsc{MedLA}, a logic-driven multi-agent framework built on large language models. Eac