Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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OneLA: Scaling Linear-Attention Decoding to Large Beams in Generative Recommendation
arXiv:2609.12399v1 Announce Type: new Abstract: Generative recommendation (GR) relies on large-beam decoding to generate hundreds of candidate items, creating a new scaling challenge for recurrent linear attention. Existing linear attention serving systems either materialize a full recurrent state for every beam or repeatedly replay shared history, incurring substantial memory and traffic overhead. To address this, we present OneLA, a linear-attention decoding framework that exploits the shared
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cs.AI, q-bio.NC updates on arXiv.org
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UniPart: Towards Zero-shot Language-Grounded 3D Part Segmentation for Embodied Interaction
arXiv:2609.12898v1 Announce Type: cross Abstract: Fine-grained robotic manipulation depends on understanding parts, not only whole objects. Existing 3D foundation models tend to be either generalized but object-aware, or part-aware but limited to closed-set taxonomies, which weakens zero-shot transfer. We study text-conditioned 3D part segmentation, where a free-form phrase selects a functional part on point cloud. We introduce UniPart, a feed-forward cross-modal 3D Transformer that conditions
UniPart: Towards Zero-shot Language-Grounded 3D Part Segmentation for Embodied Interaction
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(Multiomics OR Omics) AND (Pancreatic)
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The metastatic spectrum in functional and non-functional NENs: mechanistic insights from multi-omics
Front Endocrinol (Lausanne). 2026 Aug 27;17:1782791. doi: 10.3389/fendo.2026.1782791. eCollection 2026.ABSTRACTNeuroendocrine neoplasms (NENs) are biologically heterogeneous tumors in which differentiation/grade and hormonal functionality are intersecting but non-equivalent axes. This review focuses on functional and non-functional well-differentiated neuroendocrine tumors (NETs), principally gastroenteropancreatic and pancreatic NETs, and critically evaluates how site, lineage, stage, tumor bur
The metastatic spectrum in functional and non-functional NENs: mechanistic insights from multi-omics
Front Endocrinol (Lausanne). 2026 Aug 27;17:1782791. doi: 10.3389/fendo.2026.1782791. eCollection 2026.
ABSTRACT
Neuroendocrine neoplasms (NENs) are biologically heterogeneous tumors in which differentiation/grade and hormonal functionality are intersecting but non-equivalent axes. This review focuses on functional and non-functional well-differentiated neuroendocrine tumors (NETs), principally gastroenteropancreatic and pancreatic NETs, and critically evaluates how site, lineage, stage, tumor burden, genomic and epigenetic alterations, immune-stromal remodeling, metabolic adaptation, microbiome-associated signals, and treatment pressure converge on metastasis and recurrence. Apparent outcome differences by functionality are inconsistent after clinicopathological adjustment: non-functional presentation is often enriched for delayed diagnosis and adverse features, whereas functional subtypes range from typically indolent insulinomas to clinically aggressive hormone-producing tumors. We reconcile these observations through a layered model in which lineage-defining alterations and chromatin/telomere programs establish cellular state; signaling and metabolic plasticity enable stress adaptation; and hypoxia, angiogenesis, immune cells, fibroblasts, extracellular matrix, and therapy create selective niches for dissemination and relapse. We also define computational strategies for heterogeneous multi-omics integration and a staged biomarker-validation pathway. Evidence remains dominated by pancreatic NETs, and causal support is weakest for microbiome-functionality relationships and several proposed cross-omic links. A spectrum-based framework is therefore most useful when it generates testable, site- and grade-specific hypotheses rather than treating functionality as an isolated prognostic variable.
PMID:42724134 | PMC:PMC13559159 | DOI:10.3389/fendo.2026.1782791
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cs.AI, q-bio.NC updates on arXiv.org
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Accelerating Long-Tail Generation in Synchronous RLHF Training via Adaptive Tensor Parallelism
arXiv:2605.23945v1 Announce Type: new Abstract: Reinforcement Learning from Human Feedback (RLHF) has become a key post-training paradigm for improving model quality. However, the synchronous three-stage RLHF pipeline is often bottlenecked by the generation stage, where response-length skew causes the effective batch size to shrink rapidly during decoding, leaving GPUs underutilized while a few long responses remain unfinished. Mainstream frameworks employ a static tensor parallelism (TP) confi
Accelerating Long-Tail Generation in Synchronous RLHF Training via Adaptive Tensor Parallelism
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(Multiomics OR Omics) AND (Pancreatic)
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CR1(+) tumor-associated macrophages orchestrate an immunosuppressive niche in hepatocellular carcinoma: a genetic and multi-omics dissection
J Transl Med. 2026 May 25. doi: 10.1186/s12967-026-08301-z. Online ahead of print.ABSTRACTBACKGROUND: Hepatocellular carcinoma (HCC) remains a major global health burden and a leading cause of cancer-related mortality. Advanced disease is characterized by a profoundly immunosuppressive tumor microenvironment (TME) and limited durable responses to therapy. However, the upstream genetic determinants that drive tumor-associated macrophage (TAM) dysfunction in HCC remain poorly defined. Using an int
CR1(+) tumor-associated macrophages orchestrate an immunosuppressive niche in hepatocellular carcinoma: a genetic and multi-omics dissection
J Transl Med. 2026 May 25. doi: 10.1186/s12967-026-08301-z. Online ahead of print.
ABSTRACT
BACKGROUND: Hepatocellular carcinoma (HCC) remains a major global health burden and a leading cause of cancer-related mortality. Advanced disease is characterized by a profoundly immunosuppressive tumor microenvironment (TME) and limited durable responses to therapy. However, the upstream genetic determinants that drive tumor-associated macrophage (TAM) dysfunction in HCC remain poorly defined. Using an integrative genetic and multi-omics framework, we investigated complement receptor 1 (CR1) as a candidate regulator of this immunosuppressive niche.
METHODS: We combined Mendelian randomization (MR) and metabolite mediation analyses with bulk, single-cell, and spatial transcriptomics to define the role of CR1 in HCC. Public datasets included the TCGA-HCC cohort, a single-cell RNA-sequencing dataset comprising 53,474 high-quality cells from 21 samples, and two spatially profiled HCC sections. Clinical validation was performed in 30 paired HCC and adjacent liver tissues. Functional assays were conducted in THP-1-derived macrophages using CR1 gain- and loss-of-function approaches, phagocytosis assays, and macrophage-CD8+ T-cell co-culture experiments.
RESULTS: MR analyses implicated CR1 in HCC susceptibility at both the protein and transcript levels. pQTL analysis linked genetically predicted circulating CR1 levels to HCC risk (IVW OR = 1.403, p = 0.017), and mediation analysis identified specific metabolites as candidate intermediates. Integrative multi-omics analyses showed that CR1 was preferentially enriched in TAMs, spatially co-localized with the M2 marker CD206, and associated with reduced CD8+ T-cell infiltration, enhanced T-cell exhaustion signatures, advanced clinicopathological features, and poorer survival. In 30 paired clinical samples, CR1-high tumors exhibited increased M2-like macrophage accumulation and reduced CD8+ T-cell infiltration. Functionally, CR1 overexpression drove macrophages toward an M2-like phenotype, enhanced phagocytic activity, increased PD-L1 expression, and suppressed CD8+ T-cell proliferation as well as IFN-gamma and granzyme B production, whereas CR1 knockdown produced the opposite phenotype.
CONCLUSIONS: Our study provides the first integrated genetic, spatial, and functional evidence that CR1+ TAMs constitute a clinically relevant immunoregulatory axis in HCC. These findings extend current understanding of complement-associated immunosuppression beyond canonical complement cascade activity and support CR1 as a candidate biomarker and therapeutic target for macrophage reprogramming, with potential translational relevance for combination strategies involving immune checkpoint blockade.
PMID:42185899 | DOI:10.1186/s12967-026-08301-z
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Omics in Hepatocellular
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CR1(+) tumor-associated macrophages orchestrate an immunosuppressive niche in hepatocellular carcinoma: a genetic and multi-omics dissection
J Transl Med. 2026 May 25. doi: 10.1186/s12967-026-08301-z. Online ahead of print.ABSTRACTBACKGROUND: Hepatocellular carcinoma (HCC) remains a major global health burden and a leading cause of cancer-related mortality. Advanced disease is characterized by a profoundly immunosuppressive tumor microenvironment (TME) and limited durable responses to therapy. However, the upstream genetic determinants that drive tumor-associated macrophage (TAM) dysfunction in HCC remain poorly defined. Using an int
CR1(+) tumor-associated macrophages orchestrate an immunosuppressive niche in hepatocellular carcinoma: a genetic and multi-omics dissection
J Transl Med. 2026 May 25. doi: 10.1186/s12967-026-08301-z. Online ahead of print.
ABSTRACT
BACKGROUND: Hepatocellular carcinoma (HCC) remains a major global health burden and a leading cause of cancer-related mortality. Advanced disease is characterized by a profoundly immunosuppressive tumor microenvironment (TME) and limited durable responses to therapy. However, the upstream genetic determinants that drive tumor-associated macrophage (TAM) dysfunction in HCC remain poorly defined. Using an integrative genetic and multi-omics framework, we investigated complement receptor 1 (CR1) as a candidate regulator of this immunosuppressive niche.
METHODS: We combined Mendelian randomization (MR) and metabolite mediation analyses with bulk, single-cell, and spatial transcriptomics to define the role of CR1 in HCC. Public datasets included the TCGA-HCC cohort, a single-cell RNA-sequencing dataset comprising 53,474 high-quality cells from 21 samples, and two spatially profiled HCC sections. Clinical validation was performed in 30 paired HCC and adjacent liver tissues. Functional assays were conducted in THP-1-derived macrophages using CR1 gain- and loss-of-function approaches, phagocytosis assays, and macrophage-CD8+ T-cell co-culture experiments.
RESULTS: MR analyses implicated CR1 in HCC susceptibility at both the protein and transcript levels. pQTL analysis linked genetically predicted circulating CR1 levels to HCC risk (IVW OR = 1.403, p = 0.017), and mediation analysis identified specific metabolites as candidate intermediates. Integrative multi-omics analyses showed that CR1 was preferentially enriched in TAMs, spatially co-localized with the M2 marker CD206, and associated with reduced CD8+ T-cell infiltration, enhanced T-cell exhaustion signatures, advanced clinicopathological features, and poorer survival. In 30 paired clinical samples, CR1-high tumors exhibited increased M2-like macrophage accumulation and reduced CD8+ T-cell infiltration. Functionally, CR1 overexpression drove macrophages toward an M2-like phenotype, enhanced phagocytic activity, increased PD-L1 expression, and suppressed CD8+ T-cell proliferation as well as IFN-gamma and granzyme B production, whereas CR1 knockdown produced the opposite phenotype.
CONCLUSIONS: Our study provides the first integrated genetic, spatial, and functional evidence that CR1+ TAMs constitute a clinically relevant immunoregulatory axis in HCC. These findings extend current understanding of complement-associated immunosuppression beyond canonical complement cascade activity and support CR1 as a candidate biomarker and therapeutic target for macrophage reprogramming, with potential translational relevance for combination strategies involving immune checkpoint blockade.
PMID:42185899 | DOI:10.1186/s12967-026-08301-z
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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CR1(+) tumor-associated macrophages orchestrate an immunosuppressive niche in hepatocellular carcinoma: a genetic and multi-omics dissection
J Transl Med. 2026 May 25. doi: 10.1186/s12967-026-08301-z. Online ahead of print.ABSTRACTBACKGROUND: Hepatocellular carcinoma (HCC) remains a major global health burden and a leading cause of cancer-related mortality. Advanced disease is characterized by a profoundly immunosuppressive tumor microenvironment (TME) and limited durable responses to therapy. However, the upstream genetic determinants that drive tumor-associated macrophage (TAM) dysfunction in HCC remain poorly defined. Using an int
CR1(+) tumor-associated macrophages orchestrate an immunosuppressive niche in hepatocellular carcinoma: a genetic and multi-omics dissection
J Transl Med. 2026 May 25. doi: 10.1186/s12967-026-08301-z. Online ahead of print.
ABSTRACT
BACKGROUND: Hepatocellular carcinoma (HCC) remains a major global health burden and a leading cause of cancer-related mortality. Advanced disease is characterized by a profoundly immunosuppressive tumor microenvironment (TME) and limited durable responses to therapy. However, the upstream genetic determinants that drive tumor-associated macrophage (TAM) dysfunction in HCC remain poorly defined. Using an integrative genetic and multi-omics framework, we investigated complement receptor 1 (CR1) as a candidate regulator of this immunosuppressive niche.
METHODS: We combined Mendelian randomization (MR) and metabolite mediation analyses with bulk, single-cell, and spatial transcriptomics to define the role of CR1 in HCC. Public datasets included the TCGA-HCC cohort, a single-cell RNA-sequencing dataset comprising 53,474 high-quality cells from 21 samples, and two spatially profiled HCC sections. Clinical validation was performed in 30 paired HCC and adjacent liver tissues. Functional assays were conducted in THP-1-derived macrophages using CR1 gain- and loss-of-function approaches, phagocytosis assays, and macrophage-CD8+ T-cell co-culture experiments.
RESULTS: MR analyses implicated CR1 in HCC susceptibility at both the protein and transcript levels. pQTL analysis linked genetically predicted circulating CR1 levels to HCC risk (IVW OR = 1.403, p = 0.017), and mediation analysis identified specific metabolites as candidate intermediates. Integrative multi-omics analyses showed that CR1 was preferentially enriched in TAMs, spatially co-localized with the M2 marker CD206, and associated with reduced CD8+ T-cell infiltration, enhanced T-cell exhaustion signatures, advanced clinicopathological features, and poorer survival. In 30 paired clinical samples, CR1-high tumors exhibited increased M2-like macrophage accumulation and reduced CD8+ T-cell infiltration. Functionally, CR1 overexpression drove macrophages toward an M2-like phenotype, enhanced phagocytic activity, increased PD-L1 expression, and suppressed CD8+ T-cell proliferation as well as IFN-gamma and granzyme B production, whereas CR1 knockdown produced the opposite phenotype.
CONCLUSIONS: Our study provides the first integrated genetic, spatial, and functional evidence that CR1+ TAMs constitute a clinically relevant immunoregulatory axis in HCC. These findings extend current understanding of complement-associated immunosuppression beyond canonical complement cascade activity and support CR1 as a candidate biomarker and therapeutic target for macrophage reprogramming, with potential translational relevance for combination strategies involving immune checkpoint blockade.
PMID:42185899 | DOI:10.1186/s12967-026-08301-z
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cs.AI, q-bio.NC updates on arXiv.org
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TABQAWORLD: Optimizing Multimodal Reasoning for Multi-Turn Table Question Answering
arXiv:2604.03393v1 Announce Type: new Abstract: Multimodal reasoning has emerged as a powerful framework for enhancing reasoning capabilities of reasoning models. While multi-turn table reasoning methods have improved reasoning accuracy through tool use and reward modeling, they rely on fixed text serialization for table state readouts. This introduces representation errors in table encoding that significantly accumulate over multiple turns. Such accumulation is alleviated by tabular grounding
TABQAWORLD: Optimizing Multimodal Reasoning for Multi-Turn Table Question Answering
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cs.AI, q-bio.NC updates on arXiv.org
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Four Generations of Quantum Biomedical Sensors
arXiv:2603.29944v2 Announce Type: replace-cross Abstract: Quantum sensing technologies offer transformative potential for ultra-sensitive biomedical sensing, yet their clinical translation remains constrained by classical noise limits and a reliance on macroscopic ensembles. We propose a unifying generational framework to organize the evolving landscape of quantum biosensors based on their utilization of quantum resources. First-generation devices utilize discrete energy levels for signal trans
Four Generations of Quantum Biomedical Sensors
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Cell
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Pyruvate is a natural suppressor of interferon signaling by inducing STAT1 protein pyruvylation
Yibo et al. identify protein pyruvylation as a post-translational modification that can modulate immune signaling and host antiviral response.
Pyruvate is a natural suppressor of interferon signaling by inducing STAT1 protein pyruvylation
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cs.AI, q-bio.NC updates on arXiv.org
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Four Generations of Quantum Biomedical Sensors
arXiv:2603.29944v1 Announce Type: cross Abstract: Quantum sensing technologies offer transformative potential for ultra-sensitive biomedical sensing, yet their clinical translation remains constrained by classical noise limits and a reliance on macroscopic ensembles. We propose a unifying generational framework to organize the evolving landscape of quantum biosensors based on their utilization of quantum resources. First-generation devices utilize discrete energy levels for signal transduction
Four Generations of Quantum Biomedical Sensors
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cs.AI, q-bio.NC updates on arXiv.org
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AVA-Bench: Atomic Visual Ability Benchmark for Vision Foundation Models
arXiv:2506.09082v4 Announce Type: replace-cross Abstract: The rise of vision foundation models (VFMs) calls for systematic evaluation. A common approach pairs VFMs with large language models (LLMs) as general-purpose heads, followed by evaluation on broad Visual Question Answering (VQA) benchmarks. However, this protocol has two key blind spots: (i) the instruction tuning data may not align with VQA test distributions, meaning a wrong prediction can stem from such data mismatch rather than a VF
AVA-Bench: Atomic Visual Ability Benchmark for Vision Foundation Models
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cs.AI, q-bio.NC updates on arXiv.org
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ToolTree: Efficient LLM Agent Tool Planning via Dual-Feedback Monte Carlo Tree Search and Bidirectional Pruning
arXiv:2603.12740v1 Announce Type: new Abstract: Large Language Model (LLM) agents are increasingly applied to complex, multi-step tasks that require interaction with diverse external tools across various domains. However, current LLM agent tool planning methods typically rely on greedy, reactive tool selection strategies that lack foresight and fail to account for inter-tool dependencies. In this paper, we present ToolTree, a novel Monte Carlo tree search-inspired planning paradigm for tool pla
ToolTree: Efficient LLM Agent Tool Planning via Dual-Feedback Monte Carlo Tree Search and Bidirectional Pruning
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cs.AI, q-bio.NC updates on arXiv.org
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Asynchronous Verified Semantic Caching for Tiered LLM Architectures
arXiv:2602.13165v2 Announce Type: replace-cross Abstract: Large language models (LLMs) now sit in the critical path of search, assistance, and agentic workflows, making semantic caching essential for reducing inference cost and latency. Production deployments typically use a tiered static-dynamic design: a static cache of curated, offline vetted responses mined from logs, backed by a dynamic cache populated online. In practice, both tiers are commonly governed by a single embedding similarity t
Asynchronous Verified Semantic Caching for Tiered LLM Architectures
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cs.AI, q-bio.NC updates on arXiv.org
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The Choice of Divergence: A Neglected Key to Mitigating Diversity Collapse in Reinforcement Learning with Verifiable Reward
arXiv:2509.07430v4 Announce Type: replace-cross Abstract: A central paradox in fine-tuning Large Language Models (LLMs) with Reinforcement Learning with Verifiable Reward (RLVR) is the frequent degradation of multi-attempt performance (Pass@k) despite improvements in single-attempt accuracy (Pass@1). This is often accompanied by catastrophic forgetting, where models lose previously acquired skills. While various methods have been proposed, the choice and function of the divergence term have bee
The Choice of Divergence: A Neglected Key to Mitigating Diversity Collapse in Reinforcement Learning with Verifiable Reward
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cs.AI, q-bio.NC updates on arXiv.org
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CausalFlip: A Benchmark for LLM Causal Judgment Beyond Semantic Matching
arXiv:2602.20094v1 Announce Type: new Abstract: As large language models (LLMs) witness increasing deployment in complex, high-stakes decision-making scenarios, it becomes imperative to ground their reasoning in causality rather than spurious correlations. However, strong performance on traditional reasoning benchmarks does not guarantee true causal reasoning ability of LLMs, as high accuracy may still arise from memorizing semantic patterns instead of analyzing the underlying true causal struc