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Author Correction: A base editor for the long-term restoration of auditory function in mice with recessive profound deafness
Nature Biomedical Engineering, Published online: 07 September 2026; doi:10.1038/s41551-026-01794-5
Author Correction: A base editor for the long-term restoration of auditory function in mice with recessive profound deafnessEEGBind: Detecting Source-Level Interictal Epileptiform Discharges via EEG-Centric Multimodal Binding
FrontierChallenge: Evaluating Scientific Workflow Completion
Synergistic Vision-Language Reinforcement Enables Scalable On-Demand Analysis across Diverse Clinical Tasks
Gastrointestinal motility in microgravity: a critical review of multi-level mechanisms and model-dependent effects
Front Physiol. 2026 Aug 20;17:1930628. doi: 10.3389/fphys.2026.1930628. eCollection 2026.
ABSTRACT
BACKGROUND: Gastrointestinal motility disturbances rank among the most frequently reported medical complications of spaceflight. Astronauts experience delayed gastric emptying, erratic small intestinal transit and reduced colonic propulsion. The underlying mechanisms are multifactorial. Microgravity alters intra-abdominal physical mechanics, disrupts autonomic and enteric neural circuits, shifts gastrointestinal hormone secretion profiles, inflicts oxidative stress upon effector cells, and perturbs gut microbial communities. Cross-model comparisons reveal substantial disagreement, suggesting that no single ground-based analog fully captures the pathophysiology of orbital flight.
AIM: To critically review how weightlessness affects gastric emptying, small intestinal transit and colonic motility; to critically evaluate contradictory findings across simulation platforms; and to delineate the neural, humoral, cellular and microbiological mechanisms involved.
METHODS: We searched PubMed, Web of Science and the NASA Technical Reports Server for articles published between January 1990 and June 2026 (last search 30 June 2026). Search terms included: "microgravity", "weightlessness", "spaceflight", "gastrointestinal motility", "gastric emptying", "intestinal transit", "gut microbiome", "interstitial cells of Cajal" and "oxidative stress". Studies using head-down bed rest, hindlimb unloading, clinorotation, parabolic flight and actual spaceflight were included. The review follows a critical narrative design; the full search strategy and the framework used to appraise the evidence are described in Section 1.1.
RESULTS: Altered-gravity studies suggest that gastrointestinal dysmotility may involve neurohumoral dysregulation, oxidative injury to interstitial cells of Cajal and smooth muscle, barrier dysfunction and altered enteric signaling; however, most mechanistic evidence derives from simulated models and has not been directly validated during human spaceflight. Direct human motility measurements remain sparse, and the evidence comprises a mixture of direct observations, model-dependent inferences and testable hypotheses. Cross-study agreement is poor: some head-down bed rest trials report accelerated small-bowel transit, whereas tail-suspension models and limited flight observations suggest motor suppression. These divergences may reflect model-specific confounding rather than a uniform effect of microgravity.
CONCLUSION: Current ground-based models each capture only partial aspects of orbital GI pathophysiology. Future work should combine multi-omics profiling with next-generation simulation platforms to develop evidence-based countermeasures for long-duration missions.
PMID:42694486 | PMC:PMC13539599 | DOI:10.3389/fphys.2026.1930628
DHCR24<sup>+</sup> tumor epithelial cells drive cisplatin resistance in bladder cancer by enhancing cholesterol metabolism to activate lipid raft-associated MAPK signaling
Oncogene, Published online: 29 August 2026; doi:10.1038/s41388-026-03967-7
DHCR24+ tumor epithelial cells drive cisplatin resistance in bladder cancer by enhancing cholesterol metabolism to activate lipid raft-associated MAPK signalingEvolutionary Enhanced Multi-Agent Reinforcement Learning for Cooperative Air Combat
Don't Retrain, Just Reuse: Recovering Dual-Target Molecules from Single-Target Diffusion Models
Self-supervised Hierarchical Visual Reasoning with World Model
Rethinking the Comparison Unit in Sequence-Level Reinforcement Learning: An Equal-Length Paired Training Framework from Loss Correction to Sample Construction
Pulmonary-Intestinal Axis: Shared Genetic Basis and Mediating Factors Identified Through Multi-Omics Analysis
Int J Chron Obstruct Pulmon Dis. 2026 Apr 7;21:561645. doi: 10.2147/COPD.S561645. eCollection 2026.
ABSTRACT
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a systemic condition with comorbidities beyond the lung (eg, cardiovascular and metabolic disorders), and gastrointestinal (GI) disorders are also common. The shared genetic basis of COPD-GI comorbidity and its mediating factors remain unclear. We hypothesized that COPD and GI diseases share pleiotropic genetic architecture implicating lipid-metabolic pathways, with smoking mediating part of the association.
METHODS: We analyzed publicly available European-ancestry GWAS summary statistics for COPD (Global Biobank Meta-analysis Initiative), 15 GI diseases (FinnGen), and smoking phenotypes (UK Biobank). Genetic correlation was estimated using linkage disequilibrium score regression (LDSC) and high-definition likelihood (HDL). Multi-trait analysis of GWAS (MTAG) boosted COPD discovery by leveraging genetically correlated GI traits. We integrated locus-to-gene mapping with multi-tissue expression quantitative trait loci (eQTL) and plasma protein quantitative trait loci (pQTL) evidence to prioritize shared loci, genes, and proteins. Bidirectional two-sample Mendelian randomization (MR) tested causal directions, and two-step mediation MR evaluated smoking.
RESULTS: COPD showed significant genetic correlation with nine GI diseases. We identified six comorbidity-associated loci (three with CADD > 12.37) and 13 unique candidate pleiotropic genes; APOE was supported by proteomic evidence. Enrichment analyses highlighted lipid-metabolism pathways. MR suggested COPD increases risk of gastroesophageal reflux disease (GERD), irritable bowel syndrome (IBS), acute appendicitis, and gastric ulcer, while diverticular disease showed reverse causality toward COPD. Smoking partially mediated the COPD effect on GERD, acute appendicitis, and gastric ulcer.
CONCLUSION: COPD and multiple GI disorders share a distributed pleiotropic genetic basis within the broader systemic comorbidity spectrum of COPD. Multi-omics evidence supports a genomic pulmonary-intestinal axis in which lipid metabolism and smoking-related mechanisms contribute to COPD and GI comorbidity, providing targets for risk stratification and potential intervention.
PMID:41978582 | PMC:PMC13070119 | DOI:10.2147/COPD.S561645
Large Language Model–Based Analysis of Statin Therapy Discussions and Sentiment on Social Media: Cross-Sectional Observational Study
Development and multi-center evaluation of domain-adapted speech recognition for human-AI teaming in real-world gastrointestinal endoscopy
Efficient Reasoning with Balanced Thinking
UniMark: Artificial Intelligence Generated Content Identification Toolkit
Predicting Neuromodulation Outcome for Parkinson's Disease with Generative Virtual Brain Model
LatentPilot: Scene-Aware Vision-and-Language Navigation by Dreaming Ahead with Latent Visual Reasoning
Expressive Power of Implicit Models: Rich Equilibria and Test-Time Scaling
Gut-Brain Axis Dysregulation in Inflammatory Bowel Disease: Implications for Coagulation Abnormalities and Extraintestinal Manifestations
Int J Gen Med. 2026 Mar 24;19:590621. doi: 10.2147/IJGM.S590621. eCollection 2026.
ABSTRACT
Inflammatory bowel disease (IBD) involves chronic intestinal inflammation driven by gut-brain axis imbalance, fostering complications through an "inflammation-neuro-coagulation" triad. Current staging systems inadequately capture the dynamics of this multidimensional network. Therefore, integrated multi-omics analyses-including metagenomics, metabolomics, and single-cell transcriptomics-are essential to construct dynamic models that monitor coagulation, microbiome, and metabolism for precise assessment of disease activity and thrombotic or bleeding risks. Interventions targeting gut-brain axis nodes, such as eliminating tissue factor-positive (TF⁺) T cells or modulating vagal activity, show potential to disrupt the inflammation-coagulation cycle, although rigorous randomized trials are still needed. Artificial intelligence (AI)-assisted systems that integrate real-time biomarker monitoring with multi-omics predictions represent a novel paradigm for managing IBD-related coagulation dysfunction. Key challenges include elucidating gut-brain-liver axis regulation of coagulation and characterizing platelet functional heterogeneity. Future efforts must prioritize ethically compliant multi-omics platforms and racially stratified risk models to advance personalized coagulation management in IBD.
PMID:41913906 | PMC:PMC13033200 | DOI:10.2147/IJGM.S590621