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cs.AI, q-bio.NC updates on arXiv.org
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Test-Time Deep Thinking to Explore Implicit Rules
arXiv:2605.24828v1 Announce Type: new Abstract: With the continuous advancement of Large Language Models (LLMs), intelligent agents are becoming increasingly vital. However, these agents often fail in environments governed by implicit rules--hidden constraints that cannot be observed directly and must be inferred through interaction. This causes agents to fall into repetitive trial-and-error loops, ultimately leading to task failure. To address this challenge, we propose Test-Time Exploration (
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cs.AI, q-bio.NC updates on arXiv.org
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CITYREP: A Unified Benchmark for Urban Representations Across Cities, Tasks, and Modalities
arXiv:2605.26036v1 Announce Type: new Abstract: Urban representation learning encodes complex urban environments into general-purpose embeddings for diverse downstream tasks and emerging urban foundation models. However, current evaluations are limited, typically focusing on one or two cities and tasks and relying on random splits that introduce spatial leakage, leading to inflated performance and weak support for cross-location generalization and fair comparison. To address this, we propose Ci
CITYREP: A Unified Benchmark for Urban Representations Across Cities, Tasks, and Modalities
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cs.AI, q-bio.NC updates on arXiv.org
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Claw-Anything: Benchmarking Always-On Personal Assistants with Broader Access to User's Digital World
arXiv:2605.26086v1 Announce Type: new Abstract: Large language model agents are increasingly envisioned as always-on personal assistants with access to anything relevant in the user's digital world. Yet current systems operate over only narrow slices of that world, limiting context-sensitive reasoning and effective assistance. Existing benchmarks similarly provide only partial user state and therefore fail to capture performance in such a broad, always-on setting. To address this gap, we introd
Claw-Anything: Benchmarking Always-On Personal Assistants with Broader Access to User's Digital World
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cs.AI, q-bio.NC updates on arXiv.org
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MuNet: A Mutualistic Network for Joint 3D Human Mesh Recovery and 3D Clothed Human Reconstruction from Single Images
arXiv:2605.25861v2 Announce Type: cross Abstract: 3D human mesh recovery and 3D clothed human reconstruction are inherently related, yet they have long been studied in isolation, thereby overlooking the potential gains of joint optimization. To overcome this limitation, we propose to address these two tasks within a unified framework, which allows their mutual dependencies to be effectively exploited. Building on this idea, we propose MuNet, a mutualistic network for joint 3D human mesh recover
MuNet: A Mutualistic Network for Joint 3D Human Mesh Recovery and 3D Clothed Human Reconstruction from Single Images
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cs.AI, q-bio.NC updates on arXiv.org
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Data Difficulty and the Generalization--Extrapolation Tradeoff in LLM Fine-Tuning
arXiv:2605.12906v2 Announce Type: replace-cross Abstract: Data selection during supervised fine-tuning (SFT) can critically change the behavior of large language models (LLMs). Although existing work has studied the effect of selecting data based on heuristics such as perplexity, difficulty, or length, the reported findings are often inconsistent or context-dependent. In this work, we systematically study the role of data difficulty in fine-tuning from both empirical and theoretical perspective
Data Difficulty and the Generalization--Extrapolation Tradeoff in LLM Fine-Tuning
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cs.AI, q-bio.NC updates on arXiv.org
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TimeGuard: Channel-wise Pool Training for Backdoor Defense in Time Series Forecasting
arXiv:2605.22365v2 Announce Type: replace-cross Abstract: Time Series Forecasting (TSF) is highly vulnerable to backdoor attacks, yet effective defenses remain underexplored due to challenges arising from data entanglement and shifts in task formulation. To fill this gap, we conduct a systematic evaluation of thirteen representative backdoor defenses across the TSF life cycle and analyze their failure modes. Our results reveal two fundamental issues: (1) data entanglement induces channel-level
TimeGuard: Channel-wise Pool Training for Backdoor Defense in Time Series Forecasting
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Oncogene - Issue - nature.com science feeds
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Lactic acid induces dendritic cell pyroptosis through MCT-1 to promote tumor immune evasion
Oncogene, Published online: 23 May 2026; doi:10.1038/s41388-026-03825-6Lactic acid induces dendritic cell pyroptosis through MCT-1 to promote tumor immune evasion
Lactic acid induces dendritic cell pyroptosis through MCT-1 to promote tumor immune evasion
Oncogene, Published online: 23 May 2026; doi:10.1038/s41388-026-03825-6
Lactic acid induces dendritic cell pyroptosis through MCT-1 to promote tumor immune evasion-
Omics In Lung
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FGFR1 Promotes Malignant Progression in Lung Squamous Cell Carcinoma Through Activation of Wnt/beta-Catenin Signaling
Cancer Med. 2026 Apr;15(4):e71833. doi: 10.1002/cam4.71833.ABSTRACTOBJECTIVES: This study aims to elucidate the role of FGFR1 in activating the Wnt/β-catenin signaling pathway and the underlying mechanisms by which it promotes malignant progression in lung squamous cell carcinoma (LUSC). By integrating multi-omics analysis with functional experiments, the clinical heterogeneity of FGFR1 amplification, signaling crosstalk, and their regulatory networks governing tumor phenotypes were revealed.MET
FGFR1 Promotes Malignant Progression in Lung Squamous Cell Carcinoma Through Activation of Wnt/beta-Catenin Signaling
Cancer Med. 2026 Apr;15(4):e71833. doi: 10.1002/cam4.71833.
ABSTRACT
OBJECTIVES: This study aims to elucidate the role of FGFR1 in activating the Wnt/β-catenin signaling pathway and the underlying mechanisms by which it promotes malignant progression in lung squamous cell carcinoma (LUSC). By integrating multi-omics analysis with functional experiments, the clinical heterogeneity of FGFR1 amplification, signaling crosstalk, and their regulatory networks governing tumor phenotypes were revealed.
METHODS: Using TCGA data (n = 490), we analyzed the relationship between FGFR1 copy number variation (CNV) and mRNA expression in LUSC, and validated the correlation with protein expression in a clinical cohort (n = 38). GSEA and single-gene GSEA were performed to identify signaling pathways associated with high FGFR1 expression. The interaction between FGFR1 and the Wnt/β-catenin pathway was investigated by immunohistochemistry, immunofluorescence, stable cell lines, Western blot, qPCR, and functional assays.
RESULTS: FGFR1 amplification correlated with increased mRNA and protein expression. The top 25% FGFR1 high-expression group enriched Wnt/β-catenin, PI3K-Akt, and cAMP pathways. Mechanistically, FGFR1 promoted β-catenin nuclear accumulation and enhanced β-catenin signaling through PKA-associated phosphorylation and Akt/GSK3β-related regulation of β-catenin stability, and these effects were attenuated by AKT inhibition. CTNNB1 knockdown significantly inhibited proliferation, migration, invasion, and tumor growth of LUSC cells.
CONCLUSIONS: Our findings indicate that FGFR1 activates Wnt/β-catenin signaling through coordinated regulation of β-catenin phosphorylation, stability, and subcellular localization, thereby promoting malignant progression in LUSC. These results provide a rationale for targeting the FGFR1-Wnt/β-catenin axis as a potential therapeutic strategy.
PMID:41998829 | DOI:10.1002/cam4.71833