Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Cascade-KDE: Robust Time-Series Restoration under Out-of-Distribution Impulse Corruptions
arXiv:2605.24055v1 Announce Type: cross Abstract: Real-world time-series data in industrial sensing, healthcare, and energy systems is often corrupted by a mixture of Gaussian noise and occasional large-magnitude impulse outliers. For tasks that depend on local shape, such as ECG morphology analysis and battery degradation monitoring, the main requirement is not only low reconstruction error but also preservation of derivative peaks and task-critical features. We propose Cascade-KDE, a training
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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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Combating Data Laundering in LLM Training
arXiv:2604.01904v1 Announce Type: cross Abstract: Data rights owners can detect unauthorized data use in large language model (LLM) training by querying with proprietary samples. Often, superior performance (e.g., higher confidence or lower loss) on a sample relative to the untrained data implies it was part of the training corpus, as LLMs tend to perform better on data they have seen during training. However, this detection becomes fragile under data laundering, a practice of transforming the
Combating Data Laundering in LLM Training
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cs.AI, q-bio.NC updates on arXiv.org
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Group Representational Position Encoding
arXiv:2512.07805v5 Announce Type: replace-cross Abstract: We present GRAPE (Group Representational Position Encoding), a unified framework for positional encoding based on group actions. GRAPE unifies two families of mechanisms: (i) multiplicative rotations (Multiplicative GRAPE) in $\operatorname{SO}(d)$ and (ii) additive logit biases (Additive GRAPE) arising from unipotent actions in the general linear group $\mathrm{GL}$. In Multiplicative GRAPE, a position $n \in \mathbb{Z}$ (or $t \in \mat
Group Representational Position Encoding
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cs.AI, q-bio.NC updates on arXiv.org
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NeuroNarrator: A Generalist EEG-to-Text Foundation Model for Clinical Interpretation via Spectro-Spatial Grounding and Temporal State-Space Reasoning
arXiv:2603.16880v2 Announce Type: replace-cross Abstract: Electroencephalography (EEG) provides a non-invasive window into neural dynamics at high temporal resolution and plays a pivotal role in clinical neuroscience research. Despite this potential, prevailing computational approaches to EEG analysis remain largely confined to task-specific classification objectives or coarse-grained pattern recognition, offering limited support for clinically meaningful interpretation. To address these limita
NeuroNarrator: A Generalist EEG-to-Text Foundation Model for Clinical Interpretation via Spectro-Spatial Grounding and Temporal State-Space Reasoning
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Omics In Lung
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Correction: Integrative multi-omics and machine learning reveals the spatial niche distribution and role of CYP27A1+TAMs in immunotherapy response in non-small cell lung cancer
Front Immunol. 2026 Mar 16;17:1822612. doi: 10.3389/fimmu.2026.1822612. eCollection 2026.ABSTRACT[This corrects the article DOI: 10.3389/fimmu.2026.1782545.].PMID:41918731 | PMC:PMC13033988 | DOI:10.3389/fimmu.2026.1822612
Correction: Integrative multi-omics and machine learning reveals the spatial niche distribution and role of CYP27A1+TAMs in immunotherapy response in non-small cell lung cancer
Front Immunol. 2026 Mar 16;17:1822612. doi: 10.3389/fimmu.2026.1822612. eCollection 2026.
ABSTRACT
[This corrects the article DOI: 10.3389/fimmu.2026.1782545.].
PMID:41918731 | PMC:PMC13033988 | DOI:10.3389/fimmu.2026.1822612
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Correction: Integrative multi-omics and machine learning reveals the spatial niche distribution and role of CYP27A1+TAMs in immunotherapy response in non-small cell lung cancer
Front Immunol. 2026 Mar 16;17:1822612. doi: 10.3389/fimmu.2026.1822612. eCollection 2026.ABSTRACT[This corrects the article DOI: 10.3389/fimmu.2026.1782545.].PMID:41918731 | PMC:PMC13033988 | DOI:10.3389/fimmu.2026.1822612
Correction: Integrative multi-omics and machine learning reveals the spatial niche distribution and role of CYP27A1+TAMs in immunotherapy response in non-small cell lung cancer
Front Immunol. 2026 Mar 16;17:1822612. doi: 10.3389/fimmu.2026.1822612. eCollection 2026.
ABSTRACT
[This corrects the article DOI: 10.3389/fimmu.2026.1782545.].
PMID:41918731 | PMC:PMC13033988 | DOI:10.3389/fimmu.2026.1822612
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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AI-guided multi-omics analysis identifies NPC1-modulated susceptibility to SARS-CoV-2 infection under PM(2.5) exposure
Nat Commun. 2026 Mar 30. doi: 10.1038/s41467-026-71196-3. Online ahead of print.ABSTRACTExposure to airborne fine particulate matter (PM2.5) has been linked to increased risk of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, yet the underlying mechanisms remain unclear. Here, by leveraging a fine-tuned foundation model of single-cell transcriptomics, we uncover shared transcriptional signatures between PM2.5 exposure and SARS-CoV-2 infection. We further validate this
AI-guided multi-omics analysis identifies NPC1-modulated susceptibility to SARS-CoV-2 infection under PM(2.5) exposure
Nat Commun. 2026 Mar 30. doi: 10.1038/s41467-026-71196-3. Online ahead of print.
ABSTRACT
Exposure to airborne fine particulate matter (PM2.5) has been linked to increased risk of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, yet the underlying mechanisms remain unclear. Here, by leveraging a fine-tuned foundation model of single-cell transcriptomics, we uncover shared transcriptional signatures between PM2.5 exposure and SARS-CoV-2 infection. We further validate this association using population-level epidemiological analyses and perform genome-wide association studies (GWAS) to identify genetic variants that modulate infection risk under PM2.5 exposure. In addition, we identify NPC1 as a key modulator involved in SARS-CoV-2 infection efficiency under virus-laden PM2.5 exposure through integrative functional genomic analyses and in vitro experiments. Our findings suggest that PM2.5 facilitates viral entry through an NPC1-modulated endo-lysosomal pathway, providing a mechanistic explanation for observed pollution-related susceptibility. By integrating artificial intelligence (AI)-guided transcriptomics, epidemiology, GWAS, functional genomics, and in vitro verification, our study elucidates how environmental and genetic factors jointly influence SARS-CoV-2 susceptibility. This work highlights how AI-assisted multi-omics integration systematically decodes the health impacts of environmental exposures from molecular to population levels and informs air quality policy and infectious disease preparedness.
PMID:41912520 | DOI:10.1038/s41467-026-71196-3
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cs.AI, q-bio.NC updates on arXiv.org
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TRACE: A Multi-Agent System for Autonomous Physical Reasoning in Seismological
arXiv:2603.21152v2 Announce Type: replace-cross Abstract: Inferring the physical mechanisms that govern earthquake sequences from indirect geophysical observations remains difficult, particularly across tectonically distinct environments where similar seismic patterns can reflect different underlying processes. Current interpretations rely heavily on the expert synthesis of catalogs, spatiotemporal statistics, and candidate physical models, limiting reproducibility and the systematic transfer o
TRACE: A Multi-Agent System for Autonomous Physical Reasoning in Seismological
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cs.AI, q-bio.NC updates on arXiv.org
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SFIBA: Spatial-based Full-target Invisible Backdoor Attacks
arXiv:2504.21052v2 Announce Type: replace-cross Abstract: Multi-target backdoor attacks pose significant security threats to deep neural networks, as they can preset multiple target classes through a single backdoor injection. This allows attackers to control the model to misclassify poisoned samples with triggers into any desired target class during inference, exhibiting superior attack performance compared with conventional backdoor attacks. However, existing multi-target backdoor attacks fai
SFIBA: Spatial-based Full-target Invisible Backdoor Attacks
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Cell Death Discovery nature.com science feeds
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Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation
Cell Death Discovery, Published online: 09 March 2026; doi:10.1038/s41420-026-02950-1Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation
Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation
Cell Death Discovery, Published online: 09 March 2026; doi:10.1038/s41420-026-02950-1
Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation-
cs.AI, q-bio.NC updates on arXiv.org
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Can Multimodal LLMs See Science Instruction? Benchmarking Pedagogical Reasoning in K-12 Classroom Videos
arXiv:2602.18466v1 Announce Type: cross Abstract: K-12 science classrooms are rich sites of inquiry where students coordinate phenomena, evidence, and explanatory models through discourse; yet, the multimodal complexity of these interactions has made automated analysis elusive. Existing benchmarks for classroom discourse focus primarily on mathematics and rely solely on transcripts, overlooking the visual artifacts and model-based reasoning emphasized by the Next Generation Science Standards (N
Can Multimodal LLMs See Science Instruction? Benchmarking Pedagogical Reasoning in K-12 Classroom Videos
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cs.AI, q-bio.NC updates on arXiv.org
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Foundation and Large-Scale AI Models in Neuroscience: A Comprehensive Review
arXiv:2510.16658v2 Announce Type: replace Abstract: The development of large-scale artificial intelligence (AI) models is influencing neuroscience research by enabling end-to-end learning from raw brain signals and neural data. In this paper, we review applications of large-scale AI models across five major neuroscience domains: neuroimaging and data processing, brain-computer interfaces and neural decoding, clinical decision support and translational frameworks, and disease-specific applicatio
Foundation and Large-Scale AI Models in Neuroscience: A Comprehensive Review
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cs.AI, q-bio.NC updates on arXiv.org
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SelfAI: A self-directed framework for long-horizon scientific discovery
arXiv:2512.00403v2 Announce Type: replace-cross Abstract: Scientific discovery increasingly entails long-horizon exploration of complex hypothesis spaces, yet most existing approaches emphasize final performance while offering limited insight into how scientific exploration unfolds over time, particularly balancing efficiency-diversity trade-offs and supporting reproducible, human-in-the-loop discovery workflows. We introduce SelfAI, a self-directed, multi-agent-enabled discovery system that au
SelfAI: A self-directed framework for long-horizon scientific discovery
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cs.AI, q-bio.NC updates on arXiv.org
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Group Representational Position Encoding
arXiv:2512.07805v4 Announce Type: replace-cross Abstract: We present GRAPE (Group Representational Position Encoding), a unified framework for positional encoding based on group actions. GRAPE unifies two families of mechanisms: (i) multiplicative rotations (Multiplicative GRAPE) in $\operatorname{SO}(d)$ and (ii) additive logit biases (Additive GRAPE) arising from unipotent actions in the general linear group $\mathrm{GL}$. In Multiplicative GRAPE, a position $n \in \mathbb{Z}$ (or $t \in \mat
Group Representational Position Encoding
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cs.AI, q-bio.NC updates on arXiv.org
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One Token Is Enough: Improving Diffusion Language Models with a Sink Token
arXiv:2601.19657v4 Announce Type: replace-cross Abstract: Diffusion Language Models (DLMs) have emerged as a compelling alternative to autoregressive approaches, enabling parallel text generation with competitive performance. Despite these advantages, there is a critical instability in DLMs: the moving sink phenomenon. Our analysis indicates that sink tokens exhibit low-norm representations in the Transformer's value space, and that the moving sink phenomenon serves as a protective mechanism in
One Token Is Enough: Improving Diffusion Language Models with a Sink Token
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cs.AI, q-bio.NC updates on arXiv.org
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Step 3.5 Flash: Open Frontier-Level Intelligence with 11B Active Parameters
arXiv:2602.10604v2 Announce Type: replace-cross Abstract: We introduce Step 3.5 Flash, a sparse Mixture-of-Experts (MoE) model that bridges frontier-level agentic intelligence and computational efficiency. We focus on what matters most when building agents: sharp reasoning and fast, reliable execution. Step 3.5 Flash pairs a 196B-parameter foundation with 11B active parameters for efficient inference. It is optimized with interleaved 3:1 sliding-window/full attention and Multi-Token Prediction