Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Who Pays for Open Review? Visible Author Reputation and Its Effect on Ratings
arXiv:2609.11983v1 Announce Type: cross Abstract: An OpenReview bug in November 2025 broke anonymity at several conferences and prompted calls for open review, which motivate us to ask what shifting from blind to open would mean for authors. Analyzing over 18,000 reviewed submissions to ICLR 2026, split into de facto open and blind groups by arXiv preprint timing, we find that ratings rise with author reputation under both mechanisms, with a steeper slope under open review that is statistically
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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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Nature - Issue - nature.com science feeds
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Ancient proteins identify various Denisovan remains from Southwest China
Nature, Published online: 09 September 2026; doi:10.1038/s41586-026-10976-9Identification and proteomic analysis of bone fragments and teeth from an excavation in Southwest China provide insight into the evolution and phenotype of Denisovans and fill a geographical gap in their documented distribution.
Ancient proteins identify various Denisovan remains from Southwest China
Nature, Published online: 09 September 2026; doi:10.1038/s41586-026-10976-9
Identification and proteomic analysis of bone fragments and teeth from an excavation in Southwest China provide insight into the evolution and phenotype of Denisovans and fill a geographical gap in their documented distribution.-
Cell
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Genomics and social practices at Mogou and other Gansu sites during prehistoric trans-Eurasian exchange
Ancient DNA from 149 individuals at 11 sites in Gansu, China, dated to around 4,700–3,000 years ago, reveals human population history during early transcontinental exchanges of agriculture and technology, as well as contemporary social practices, at the large Mogou cemetery.
Genomics and social practices at Mogou and other Gansu sites during prehistoric trans-Eurasian exchange
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Nature Cancer
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Author Correction: Low-protein diet enhances antitumor immunity in pancreatic cancer through microbiota-derived UDP-galactose
Nature Cancer, Published online: 25 August 2026; doi:10.1038/s43018-026-01241-zAuthor Correction: Low-protein diet enhances antitumor immunity in pancreatic cancer through microbiota-derived UDP-galactose
Author Correction: Low-protein diet enhances antitumor immunity in pancreatic cancer through microbiota-derived UDP-galactose
Nature Cancer, Published online: 25 August 2026; doi:10.1038/s43018-026-01241-z
Author Correction: Low-protein diet enhances antitumor immunity in pancreatic cancer through microbiota-derived UDP-galactose-
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
Cascade-KDE: Robust Time-Series Restoration under Out-of-Distribution Impulse Corruptions
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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