Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Beyond Gemini-3-Pro: Revisiting LLM Routing and Aggregation at Scale
arXiv:2601.01330v1 Announce Type: new Abstract: Large Language Models (LLMs) have rapidly advanced, with Gemini-3-Pro setting a new performance milestone. In this work, we explore collective intelligence as an alternative to monolithic scaling, and demonstrate that open-source LLMs' collaboration can surpass Gemini-3-Pro. We first revisit LLM routing and aggregation at scale and identify three key bottlenecks: (1) current train-free routers are limited by a query-based paradigm focusing solely
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(Multiomics OR Omics) AND (Pancreatic)
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Single-Cell Multi-Omics in Type 2 Diabetes Mellitus: Revealing Cellular Heterogeneity and Mechanistic Insights
Int J Mol Sci. 2025 Nov 13;26(22):11005. doi: 10.3390/ijms262211005.ABSTRACTType 2 diabetes mellitus (T2DM) is a prevalent and complex metabolic disorder characterized by insulin resistance, progressive β-cell dysfunction, and severe systemic complications. Advances in single-cell multi-omics-transcriptomics, chromatin accessibility profiling, and integrative analyses-have offered unprecedented insights into the cellular heterogeneity and regulatory networks of pancreatic islets. We highlight re
Single-Cell Multi-Omics in Type 2 Diabetes Mellitus: Revealing Cellular Heterogeneity and Mechanistic Insights
Int J Mol Sci. 2025 Nov 13;26(22):11005. doi: 10.3390/ijms262211005.
ABSTRACT
Type 2 diabetes mellitus (T2DM) is a prevalent and complex metabolic disorder characterized by insulin resistance, progressive β-cell dysfunction, and severe systemic complications. Advances in single-cell multi-omics-transcriptomics, chromatin accessibility profiling, and integrative analyses-have offered unprecedented insights into the cellular heterogeneity and regulatory networks of pancreatic islets. We highlight recent discoveries in islet cell heterogeneity and β-cell pathophysiology, with a particular focus on dysfunction and dedifferentiation. We further underscore the computational frameworks that enable these discoveries, spanning data preprocessing, multi-omics integration, and machine learning-driven analyses, which collectively enable the dissection of disease-relevant cell subpopulations and the reconstruction of developmental and regulatory trajectories. We also examine how impaired signaling within islets and chronic adipose inflammation contribute to T2DM pathogenesis. Finally, we discuss key challenges in clinical translation-including limited population diversity in single-cell atlases and the interpretability of computational models-and propose future directions toward precision diagnostics and therapeutic innovation in T2DM.
PMID:41303487 | PMC:PMC12652634 | DOI:10.3390/ijms262211005
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Oncogene - Issue - nature.com science feeds
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Identification of novel germline mutations in <i>FUT7</i> and <i>EXT1</i> linked with hereditary multiple exostoses
Oncogene, Published online: 17 December 2024; doi:10.1038/s41388-024-03254-3Identification of novel germline mutations in FUT7 and EXT1 linked with hereditary multiple exostoses
Identification of novel germline mutations in <i>FUT7</i> and <i>EXT1</i> linked with hereditary multiple exostoses
Oncogene, Published online: 17 December 2024; doi:10.1038/s41388-024-03254-3
Identification of novel germline mutations in FUT7 and EXT1 linked with hereditary multiple exostoses