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From Efficiency to Adaptivity: A Deeper Look at Adaptive Reasoning in Large Language Models

arXiv:2511.10788v3 Announce Type: replace Abstract: Recent advances in large language models (LLMs) have made reasoning a central benchmark for evaluating intelligence. While prior surveys focus on efficiency by examining how to shorten reasoning chains or reduce computation, this view overlooks a fundamental challenge: current LLMs apply uniform reasoning strategies regardless of task complexity, generating long traces for trivial problems while failing to extend reasoning for difficult tasks. This survey reframes reasoning through the lens of {adaptivity}: the capability to allocate reasoning effort based on input characteristics such as difficulty and uncertainty. We make three contributions. First, we formalize deductive, inductive, and abductive reasoning within the LLM context, connecting these classical cognitive paradigms with their algorithmic realizations. Second, we formalize adaptive reasoning as a control-augmented policy optimization problem balancing task performance with computational cost, distinguishing learned policies from inference-time control mechanisms. Third, we propose a systematic taxonomy organizing existing methods into training-based approaches that internalize adaptivity through reinforcement learning, supervised fine-tuning, and learned controllers, and training-free approaches that achieve adaptivity through prompt conditioning, feedback-driven halting, and modular composition. This framework clarifies how different mechanisms realize adaptive reasoning in practice and enables systematic comparison across diverse strategies. We conclude by identifying open challenges in self-evaluation, meta-reasoning, and human-aligned reasoning control.

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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