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cs.AI, q-bio.NC updates on arXiv.org
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The Anatomy and Boundary of Adaptation under Temporal Tabular Shift
arXiv:2609.12136v1 Announce Type: cross Abstract: Prequential adaptation of frozen tabular foundation models under temporal drift, with each label revealed only after prediction, helps some deployments and harms others, yet current practice does not predict which. We study the sources and limits of these gains. A diagnostic anatomy attributes gains to four recurring mechanisms under a streaming protocol that removes three optimistic biases and quantifies a fourth. Within an agnostic total-varia
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cs.AI, q-bio.NC updates on arXiv.org
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SCOPE-OPSD: Fisher-Conditioned Privileged Subspaces for On-Policy Self-Distillation
arXiv:2609.12579v1 Announce Type: cross Abstract: On-policy self-distillation (OPSD) scores student-generated prefixes with a solution-conditioned self-teacher, yet transfers supervision only through next-token probabilities. We ask whether the aligned final-layer discrepancy offers a useful second channel, and how to test that channel without confusing its geometry with auxiliary strength. SCOPE-OPSD projects the privileged teacher-student residual onto a frozen rank-64 factor estimated from r
SCOPE-OPSD: Fisher-Conditioned Privileged Subspaces for On-Policy Self-Distillation
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Cell Death Discovery nature.com science feeds
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Hepatic Usp2 orchestrates de novo lipogenesis through G3bp2 stabilization and β-catenin activation
Cell Death Discovery, Published online: 14 September 2026; doi:10.1038/s41420-026-03333-2Hepatic Usp2 orchestrates de novo lipogenesis through G3bp2 stabilization and β-catenin activation
Hepatic Usp2 orchestrates de novo lipogenesis through G3bp2 stabilization and β-catenin activation
Cell Death Discovery, Published online: 14 September 2026; doi:10.1038/s41420-026-03333-2
Hepatic Usp2 orchestrates de novo lipogenesis through G3bp2 stabilization and β-catenin activation-
Omics In Lung
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Multi-omics approaches in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic targets and precision medicine
Front Pharmacol. 2026 Aug 28;17:1899849. doi: 10.3389/fphar.2026.1899849. eCollection 2026.ABSTRACTIdiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with limited therapeutic options and marked molecular heterogeneity. Despite available antifibrotic therapies, disease progression remains poorly predictable, highlighting the need for improved mechanistic understanding and therapeutic targeting. This review summarizes recent advances in multi-omics research to elucidate
Multi-omics approaches in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic targets and precision medicine
Front Pharmacol. 2026 Aug 28;17:1899849. doi: 10.3389/fphar.2026.1899849. eCollection 2026.
ABSTRACT
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with limited therapeutic options and marked molecular heterogeneity. Despite available antifibrotic therapies, disease progression remains poorly predictable, highlighting the need for improved mechanistic understanding and therapeutic targeting. This review summarizes recent advances in multi-omics research to elucidate the molecular mechanisms underlying IPF and to identify potential biomarkers and pharmacological targets. Multi-omics studies, including genomics, epigenomics, transcriptomics, proteomics, metabolomics, microbiome profiling, and single-cell sequencing, have revealed key pathogenic mechanisms in IPF. Genetic susceptibility factors such as MUC5B promoter variants and telomere-related genes contribute to disease risk. Epigenetic regulation, including DNA methylation, histone modifications, and non-coding RNAs, plays a central role in fibrotic remodeling. Transcriptomic and proteomic analyses have identified dysregulated signaling pathways, including TGF-β, mTOR, cellular senescence, and extracellular matrix remodeling. Metabolomic alterations indicate disrupted lipid and amino acid metabolism. Importantly, integration of multi-omics datasets enables the identification of molecular endotypes, candidate biomarkers, and potential therapeutic targets. However, challenges including data integration, tissue heterogeneity, limited cohort size, and the need for functional validation remain important barriers to clinical translation. Continued development of multi-omics approaches may facilitate more accurate disease classification and support the development of personalized therapeutic strategies for IPF.
PMID:42729333 | PMC:PMC13561894 | DOI:10.3389/fphar.2026.1899849