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Childhood asthma and the microbiome: from gut-lung axis mechanisms to precision prevention strategies

Front Immunol. 2026 Sep 2;17:1902053. doi: 10.3389/fimmu.2026.1902053. eCollection 2026.

ABSTRACT

Childhood asthma is a highly heterogeneous chronic respiratory disease, and its onset and progression are intricately linked to genetic susceptibility, environmental exposure, immune development, and the establishment of the early-life microbiome. In recent years, studies on the gut and respiratory microbiomes have suggested that the composition, metabolic functions, and interactions of microbial communities with the host immune system may be involved in the formation of asthma susceptibility, shaping of inflammatory phenotypes, and disease progression in children. The gut-lung axis, as an important pathway connecting gut microbiome, respiratory immunity, and systemic inflammatory responses, provides a new perspective for understanding the early mechanisms of childhood asthma. This article reviews the characteristics of the respiratory and gut microbiomes associated with childhood asthma, with a focus on the roles of the gut-lung axis, microbial metabolites, mucosal immune regulation, and environmental exposure. It also evaluates the research progress of probiotics, prebiotics, nutritional interventions, and novel microecological therapies. Additionally, the potential of microbial maturity, microbial metabolites, and immunophenotypes as biomarkers for risk prediction, phenotype stratification, and treatment response is analyzed. Furthermore, the role of multi-omics integration in supporting the identification of responsive populations, matching of intervention strategies, and dynamic monitoring of efficacy is discussed. Current evidence suggests that the microbiome offers promising targets for risk assessment and precision prevention of childhood asthma. However, relevant research still faces challenges such as ambiguous causality, high cohort heterogeneity, limited reproducibility of candidate biomarkers, inconsistent intervention outcomes, and insufficient evidence of long-term safety. At present, most biomarkers and multi-omics models remain in the stage of association discovery, lacking unified thresholds, cross-cohort validation, and biomarker-guided randomized controlled trials in children. Therefore, they cannot be routinely used for patient stratification or intervention selection. Future efforts should rely on standardized longitudinal birth cohorts, multi-omics integration, external validation, and high-quality clinical trials to clarify the incremental value of microbiome biomarkers over traditional clinical indicators and their clinical utility in the individualized management of childhood asthma.

PMID:42751182 | PMC:PMC13580037 | DOI:10.3389/fimmu.2026.1902053

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EvoRS: On-Policy Self-Evolution of Reward Systems for Open-Ended Reinforcement Learning

arXiv:2609.12459v1 Announce Type: new Abstract: Open-ended reinforcement learning often relies on rubric-based rewards for tasks without directly verifiable answers. Yet the policy and reward system form a dynamic feedback loop: as the policy optimizes the current reward, an initially useful reward system may become unreliable due to reward hacking or reduced response discriminability. The reward system should therefore evolve rather than remain fixed during training. Existing dynamic-rubric methods adapt evaluation criteria, but reward failures can also arise from scoring mechanisms or signal composition. We introduce EvoRS, a self-evolving RL framework that evolves the reward system from on-policy experience, representing it as an executable Reward-DAG. Specifically, an agentic designer updates this system from on-policy rollouts and reward traces to maintain train-time reliability. Across writing and roleplay, EvoRS achieves the best quality under all three judges, outperforming the policy by \(2.107\) and \(4.767\) points, respectively, while reducing reward hacking and coverage failures and preserving reward informativeness. Ablations confirm that a comprehensive fixed reward system cannot remain reliable in open-ended tasks and must evolve throughout training.
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Advancing Graph Few-Shot Learning via In-Context Learning

arXiv:2605.24410v1 Announce Type: new Abstract: Graph few-shot learning, which aims to classify nodes from novel classes with only a few labeled examples, is a widely studied problem in graph learning. However, existing methods often face two key limitations. First, the predominant graph few-shot learning paradigm relies on supervised tasks, failing to leverage the vast number of unlabeled nodes in the graph. Second, many approaches require complex task adaptation or fine-tuning during inference, limiting their efficiency and applicability. Inspired by the powerful in-context learning capabilities of large language models, we propose a novel model named VISION for adVancIng graph few-Shot learning via In-cOntext LearNing to address these challenges. Our model reframes graph few-shot learning as a fine-tuning-free sequence reasoning problem. At its core is a context-aware network that initializes nodes with role embeddings and employs a dual-context fusion module to synergistically integrate local topological structures and global task-level dependencies. This allows our model to dynamically generate class-aware representations for the query set conditioned on the support set context in a single forward pass. To effectively train our model, we introduce an unsupervised task generator that creates structure-adaptive features and constructs diverse pseudo-tasks from abundant unlabeled data. Our method unifies unsupervised meta-learning with graph in-context learning, achieving efficient inference. Extensive experiments on multiple benchmark datasets demonstrate the superiority of our model. Our public code can be found
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Deubiquitinase USP35 regulates MDM4 degradation to promote endothelial ferroptosis and renal injury progression

Cell Death Discovery, Published online: 25 May 2026; doi:10.1038/s41420-026-03128-5

Deubiquitinase USP35 regulates MDM4 degradation to promote endothelial ferroptosis and renal injury progression
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Structure of the mouse cytoplasmic lattice

Nature, Published online: 31 March 2026; doi:10.1038/s41586-026-10442-6

Structure of the mouse cytoplasmic lattice
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