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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-variation drift class, the target conditional is only partially identified: its identified-set diameter, the \emph{wall}, is irreducible from unlabeled data uniformly in sample size. A second, orthogonal $L^2$ projection wall quantifies what the frozen representation cannot express. Two canonical mechanism priors collapse the first wall. Under stated nuisance-rate conditions, the wall can be estimated from labeled historical windows at a $\sqrt N$ rate above the margin threshold $\gamma^\star=d_0/(2\alpha_s)$. At $\gamma=0$, the conditional lower-bound program depends on an open affinity estimate; the positive-margin lower branch also remains open. Semi-synthetic data illustrate the finite-sample mechanism with calibrated exponents. Stream-level proxies on eight industrial streams fall on the difficult side under a stated roughness bound, while the equality case $\gamma=\gamma^\star$ remains unresolved.

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 residual covariance and language-model-head Fisher sensitivity. It reuses the forwards already required by OPSD and adds neither rollouts nor inference-time modules. A matched Random control preserves the structured factor's rank and nonzero spectrum and uses per-arm gradient-RMS calibration, isolating the effect of the data-dependent orientation. Across the complete 25/50/75/100-step trajectories for Qwen3-1.7B, 4B, and 8B, Structured is never below Pure OPSD, with strict gains in 11 of the 12 model-checkpoint combinations and an exact tie at 4B step 25. Structured also exceeds matched Random in 10 of the 12 combinations. At step 75 on Qwen3-1.7B, Structured exceeds matched Random by 1.39 Macro Avg@12 points in each of two independent training reruns. A cross-fitted diagnostic also shows 4.40 times greater held-out privileged-gap capture than the matched random orientation. The results support a compact, Fisher-conditioned privileged subspace for short-budget OPSD.

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

Multi-omics approaches in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic targets and precision medicine

12 September 2026 at 18:00

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

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