Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Beyond the Aggregation Dilemma: Prior-Retaining Decoupled Learning for Multimodal Graphs
arXiv:2605.24684v1 Announce Type: cross Abstract: Multimodal Attributed Graph Learning (MAGL) integrates intrinsic node attributes with structural topology via graph aggregation. However, as pretrained encoders evolve into Large Foundation Models (LFMs), the landscape of MAGL fundamentally shifts: under high-confidence LFM priors, mandatory aggregation introduces topological noise that overwhelms discriminative signals, triggering a counter-intuitive performance inversion where sophisticated MA
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cs.AI, q-bio.NC updates on arXiv.org
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Profiling-Driven Adaptive Distributed Transformer Inference on Embedded Edge Deployment
arXiv:2605.25682v1 Announce Type: cross Abstract: Distributing Transformer inference across embedded edge devices can alleviate individual memory and compute constraints, yet practical benefits on real hardware remain unclear: prior work relies largely on simulations that overlook hardware-specific communication overheads. We present a hardware prototype study on NVIDIA Jetson Orin Nano devices connected over WiFi. Our key finding is that the dominant bottleneck is not just network bandwidth bu
Profiling-Driven Adaptive Distributed Transformer Inference on Embedded Edge Deployment
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cs.AI, q-bio.NC updates on arXiv.org
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AgentArk: Distilling Multi-Agent Intelligence into a Single LLM Agent
arXiv:2602.03955v3 Announce Type: replace Abstract: While large language model (LLM) multi-agent systems achieve superior reasoning performance through iterative debate, practical deployment is limited by their high computational cost and error propagation. This paper proposes AgentArk, a novel framework to distill multi-agent dynamics into the weights of a single model, effectively transforming explicit test-time interactions into implicit model capabilities. This equips a single agent with th
AgentArk: Distilling Multi-Agent Intelligence into a Single LLM Agent
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cs.AI, q-bio.NC updates on arXiv.org
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Safety in Embodied AI: A Survey of Risks, Attacks, and Defenses
arXiv:2605.02900v2 Announce Type: replace-cross Abstract: Embodied Artificial Intelligence (Embodied AI) integrates perception, cognition, planning, and interaction into agents that operate in open-world, safety-critical environments. As these systems gain autonomy and enter domains such as transportation, healthcare, and industrial or assistive robotics, ensuring their safety becomes both technically challenging and socially indispensable. Unlike digital AI systems, embodied agents must act un
Safety in Embodied AI: A Survey of Risks, Attacks, and Defenses
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Omics in Hepatocellular
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PRXL2B facilitates the progression of hepatocellular carcinoma and the therapeutic efficacy of oncolytic adenovirus H101 through the PI3K/AKT/PD-L1 axis
Biosci Trends. 2026 May 21. doi: 10.5582/bst.2026.01000. Online ahead of print.ABSTRACTOncolytic adenovirus H101 has shown antitumor activity in hepatocellular carcinoma (HCC), but the molecular determinants of treatment response remain unclear. In this study, a Hepa1-6 subcutaneous tumor model was established in C57BL/6 mice and treated with intratumoral H101, followed by integrated transcriptomic and proteomic analyses to identify candidate genes associated with H101 response. PRXL2B was selec
PRXL2B facilitates the progression of hepatocellular carcinoma and the therapeutic efficacy of oncolytic adenovirus H101 through the PI3K/AKT/PD-L1 axis
Biosci Trends. 2026 May 21. doi: 10.5582/bst.2026.01000. Online ahead of print.
ABSTRACT
Oncolytic adenovirus H101 has shown antitumor activity in hepatocellular carcinoma (HCC), but the molecular determinants of treatment response remain unclear. In this study, a Hepa1-6 subcutaneous tumor model was established in C57BL/6 mice and treated with intratumoral H101, followed by integrated transcriptomic and proteomic analyses to identify candidate genes associated with H101 response. PRXL2B was selected for further investigation using public multi-omics datasets, tissue microarray-based immunohistochemistry, in vitro functional assays, mechanistic analyses, and in vivo validation experiments. Integrated multi-omics analyses identified PRXL2B as a candidate gene downregulated after H101 treatment. Public datasets and tissue-based validation further showed that PRXL2B was upregulated in HCC tissues. In MHCC97H and HCCLM3 cells, PRXL2B knockdown inhibited proliferation, migration, and invasion, promoted apoptosis and cell-cycle arrest, and enhanced the antitumor effect of H101. Mechanistically, PRXL2B silencing reduced AKT phosphorylation and PD-L1 expression. In vivo, PRXL2B knockdown suppressed tumor growth, and the combination of PRXL2B knockdown and H101 produced the strongest antitumor effect. These findings indicate that PRXL2B promotes malignant phenotypes in HCC and may modulate H101 efficacy through the PI3K/AKT/PD-L1 axis. Targeting PRXL2B may therefore represent a potential strategy to enhance the therapeutic efficacy of oncolytic virus therapy in HCC.
PMID:42161529 | DOI:10.5582/bst.2026.01000