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cs.AI, q-bio.NC updates on arXiv.org
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CUA-Gym: Scaling Verifiable Training Environments and Tasks for Computer-Use Agents
arXiv:2605.25624v1 Announce Type: new Abstract: Reinforcement learning with verifiable rewards (RLVR) has driven breakthroughs in domains such as math, tool-use, and software engineering, yet its extension to computer-use agents (CUAs) has been bottlenecked by the scarcity of scalable training data with deterministic rewards. Constructing such data for CUAs requires consistent task instruction, executable environment, and verifiable reward. However, hand-curated benchmarks achieve high reward f
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cs.AI, q-bio.NC updates on arXiv.org
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CoSPlay: Cooperative Self-Play at Test-Time with Self-Generated Code and Unit Test
arXiv:2605.23491v2 Announce Type: replace-cross Abstract: Recently, Reinforcement Learning with Verifiable Rewards (RLVR) and Test-Time Scaling (TTS) have advanced LLM code generation through executable verification. Yet Ground-Truth Unit Tests (GT UTs) remain a bottleneck: SOTA RLVR methods require them for costly training, while existing TTS methods lose competitiveness without them. This motivates GT-free TTS, where existing methods directly use self-generated UTs to refine and select code c
CoSPlay: Cooperative Self-Play at Test-Time with Self-Generated Code and Unit Test
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(Multiomics OR Omics) AND (Pancreatic)
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High-salt diet in macrophage-associated metabolic disorders: Mechanisms and therapeutic implications
Chin Med J (Engl). 2026 May 19. doi: 10.1097/CM9.0000000000004098. Online ahead of print.ABSTRACTHigh-salt diet (HSD) has emerged as a prevalent environmental factor that exacerbates chronic inflammation and insulin resistance in obesity-associated type 2 diabetes (T2D) by modulating macrophage polarization, metabolic reprogramming, and epigenetic imprinting. Current evidence demonstrates that HSD activates p38/mitogen-activated protein kinase (MAPK), nuclear factor kappa-B (NF-κB), and NOD-like
High-salt diet in macrophage-associated metabolic disorders: Mechanisms and therapeutic implications
Chin Med J (Engl). 2026 May 19. doi: 10.1097/CM9.0000000000004098. Online ahead of print.
ABSTRACT
High-salt diet (HSD) has emerged as a prevalent environmental factor that exacerbates chronic inflammation and insulin resistance in obesity-associated type 2 diabetes (T2D) by modulating macrophage polarization, metabolic reprogramming, and epigenetic imprinting. Current evidence demonstrates that HSD activates p38/mitogen-activated protein kinase (MAPK), nuclear factor kappa-B (NF-κB), and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling pathways, by which it drives macrophage polarization toward a proinflammatory M1 phenotype while inducing a glycolysis-dominant metabolic shift, thereby establishing a persistent "metabolic memory". Moreover, HSD orchestrates metabolic memory in macrophages through coordinated epigenetic machinery, including histone modifications (Trimethylation of histone H3 at lysine 4 [H3K4me3] and Acetylation of histone H3 at lysine 27 [H3K27ac]), DNA methylation, and noncoding RNAs (e.g., long non-coding RNA MALAT1 and miR-155), leading to sustained inflammatory phenotypes. In multiple metabolic organs (e.g., adipose tissue, liver, pancreas, and gut), the HSD-macrophage axis aggravates systemic insulin resistance through shared proinflammatory signaling and other tissue-specific mechanisms. Most importantly, therapeutic strategies targeting the NLRP3 inflammasome, metabolic pathways, and epigenetic alterations offer novel approaches for managing metabolic inflammation. Future investigations are encouraged to leverage lineage tracing, single-cell sequencing, and spatial multi-omics technologies to advance the development of precision medicine for macrophage-associated metabolic disorders.
PMID:42156155 | DOI:10.1097/CM9.0000000000004098
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Oncogene - Issue - nature.com science feeds
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S100A6 promotes liver metastasis by activating FGFR3 signaling in <i>BAP1</i>-deficient uveal melanoma
Oncogene, Published online: 04 April 2026; doi:10.1038/s41388-026-03766-0S100A6 promotes liver metastasis by activating FGFR3 signaling in BAP1-deficient uveal melanoma
S100A6 promotes liver metastasis by activating FGFR3 signaling in <i>BAP1</i>-deficient uveal melanoma
Oncogene, Published online: 04 April 2026; doi:10.1038/s41388-026-03766-0
S100A6 promotes liver metastasis by activating FGFR3 signaling in BAP1-deficient uveal melanoma-
cs.AI, q-bio.NC updates on arXiv.org
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Agent Data Protocol: Unifying Datasets for Diverse, Effective Fine-tuning of LLM Agents
arXiv:2510.24702v2 Announce Type: replace-cross Abstract: Public research results on large-scale supervised finetuning of AI agents remain relatively rare, since the collection of agent training data presents unique challenges. In this work, we argue that the bottleneck is not a lack of underlying data sources, but that a large variety of data is fragmented across heterogeneous formats, tools, and interfaces. To this end, we introduce the agent data protocol (ADP), a light-weight representation
Agent Data Protocol: Unifying Datasets for Diverse, Effective Fine-tuning of LLM Agents
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cs.AI, q-bio.NC updates on arXiv.org
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ShotFinder: Imagination-Driven Open-Domain Video Shot Retrieval via Web Search
arXiv:2601.23232v3 Announce Type: replace-cross Abstract: In recent years, large language models (LLMs) have made rapid progress in information retrieval, yet existing research has mainly focused on text or static multimodal settings. Open-domain video shot retrieval, which involves richer temporal structure and more complex semantics, still lacks systematic benchmarks and analysis. To fill this gap, we introduce ShotFinder, a benchmark that formalizes editing requirements as keyframe-oriented