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cs.AI, q-bio.NC updates on arXiv.org
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City Editing: Hierarchical Agentic Execution for Dependency-Aware Urban Geospatial Modification
arXiv:2602.19326v3 Announce Type: replace-cross Abstract: Urban renewal requires incremental modifications to existing geospatial plans, yet manually updating complex layouts under spatial constraints is labor-intensive and error-prone. To tackle this, we propose CEAE, a hierarchical agentic framework that formulates urban renewal as machine-executable GeoJSON editing from natural-language instructions. CEAE decomposes instructions into hierarchical geometric intents, executing edits from coars
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cs.AI, q-bio.NC updates on arXiv.org
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FiberTune: Preserving Action-Fiber Visual Residuals in Vision-Language-Action Fine-Tuning
arXiv:2606.08653v2 Announce Type: replace-cross Abstract: Action-supervised fine-tuning of vision-language-action (VLA) policies fits demonstrations effectively but constrains only the directions that change predicted actions, leaving visual structure consistent across action-equivalent states free to collapse. We formalize this as residual visual collapse along local action fibers and propose FiberTune, a training-time objective that preserves teacher-structured visual residuals without adding
FiberTune: Preserving Action-Fiber Visual Residuals in Vision-Language-Action Fine-Tuning
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cs.AI, q-bio.NC updates on arXiv.org
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LightNav-0: Eliciting VLM Spatial Intelligence for Generalist Embodied Navigation
arXiv:2608.30935v2 Announce Type: replace-cross Abstract: Embodied navigation requires agents to translate heterogeneous goals and visual observations into actions across tasks, environments, and robot embodiments. Modern vision-language models (VLMs) already encode spatial priors for visual grounding, spatial reasoning, and pointing, but these capabilities are rarely elicited directly for robot control. Existing navigation systems instead rely on task- or embodiment-specific components, fragme
LightNav-0: Eliciting VLM Spatial Intelligence for Generalist Embodied Navigation
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Omics in Hepatocellular
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Integrative Multi-Omics Mendelian Randomization Analysis Identifies NIT2 as a Potential Metabolic Risk Gene in Hepatocellular Carcinoma
J Gene Med. 2026 Sep;28(9):e70111. doi: 10.1002/jgm.70111.ABSTRACTBACKGROUND: Metabolic pathways are crucial in hepatocellular carcinoma (HCC) pathogenesis, but causal metabolic genes remain unclear. This study used Summary data-based Mendelian Randomization (SMR) and colocalization to identify metabolism-related genetic loci influencing HCC risk.METHODS: Differentially expressed genes in hepatic malignancy phenotype versus normal tissues from TCGA and GTEx were analyzed. Metabolism-related cand
Integrative Multi-Omics Mendelian Randomization Analysis Identifies NIT2 as a Potential Metabolic Risk Gene in Hepatocellular Carcinoma
J Gene Med. 2026 Sep;28(9):e70111. doi: 10.1002/jgm.70111.
ABSTRACT
BACKGROUND: Metabolic pathways are crucial in hepatocellular carcinoma (HCC) pathogenesis, but causal metabolic genes remain unclear. This study used Summary data-based Mendelian Randomization (SMR) and colocalization to identify metabolism-related genetic loci influencing HCC risk.
METHODS: Differentially expressed genes in hepatic malignancy phenotype versus normal tissues from TCGA and GTEx were analyzed. Metabolism-related candidates were examined via SMR and colocalization using multi-omics data: methylation (mQTL), expression (eQTL), and protein (pQTL) quantitative trait loci.
RESULTS: Multi-omics integration identified NIT2 as a key metabolic regulator for HCC. The cg13016775 locus of NIT2 was associated with elevated HCC risk at gene (OR = 1.618, 95% CI: 1.199-2.182) and protein (OR = 4.432, 95% CI: 1.783-11.018) levels. Colocalization supported a shared causal variant (PPH4 > 0.6), linking NIT2 to hepatocarcinogenesis via metabolic regulation.
CONCLUSIONS: This study provides multi-omics evidence for NIT2 as a potential causal gene in HCC, enhancing understanding of metabolic contributions to HCC pathogenesis and highlighting integrative genomics for uncovering causal relationships.
PMID:42681890 | PMC:PMC13534973 | DOI:10.1002/jgm.70111