Historically, cardiac arrhythmias have been interpreted as intrinsic ion channel disorders of the cardiomyocyte. However, the field is currently undergoing a fundamental paradigm shift, recognizing the brain–heart axis as the ultimate arbiter of electrical stability. Despite a wealth of preclinical evidence, the clinical translation of neuromodulatory interventions has reached a critical juncture, with many trials yielding conflicting or disappointing outcomes. This translational gap underscores a critical need to move beyond an oversimplified, efferent-centric view toward an integrated understanding of the neuro-cardiac hierarchy. This review redefines arrhythmogenesis as an emergent property of multi-level network instability, driven by 3 core mechanistic principles: spatial heterogeneity, temporal dynamics, and convergent remodeling. By synthesizing the anatomical architecture of the cardiac autonomic nervous system, integrating the often-overlooked afferent sensory limb and the intrinsic “little brain”, we illustrate how neural circuits translate systemic stressors into localized electrophysiological triggers. We examine the bidirectional neuroimmune crosstalk and neuropeptide dynamics that bridge inflammatory signaling with maladaptive remodeling. Furthermore, we explore how circadian rhythms impose temporal windows of vulnerability, transforming stable substrates into arrhythmogenic ones. Finally, we critically evaluate the therapeutic landscape, from established pharmacological blockade to the nascent frontiers of closed-loop bioelectronics and nanotechnology. By bridging molecular mechanisms with a hierarchical appraisal of clinical evidence, this review provides a roadmap for the next generation of precision neuromodulation designed to restore and sustain neuro-cardiac homeostasis.

Whole-body ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography (¹⁸F-FDG PET/CT) is central to lung cancer staging, yet report drafting remains time intensive and error sensitive, as a single mislocalized finding can alter TNM stage and treatment decisions. We cast PET/CT report drafting as TNM-accountable decision support and propose RIDE, a 2-stage dual-modality 3-dimensional framework that separates TNM-critical anchoring from narrative completion. Stage I generates TNM-oriented structured impressions from paired PET and CT volumes; stage II performs hierarchical organ-wise exemplar retrieval and prompts a large language model to synthesize complete Findings and Impression conditioned on these inspectable artifacts. We curate a multicenter whole-body FDG PET/CT cohort of 1,583 patients from 3 hospitals, all referred for suspected or confirmed lung cancer, and evaluate it on a held-out test set of 520 cases, including 276 external cases from 2 independent institutions. RIDE achieves the strongest overall drafting performance and cross-site generalization, improving a clinically grounded competency metric by +20.4 on the external set and maintaining high clinician ratings under shift (mean Likert 4.00 internal; 4.17 external) while also delivering the best TNM staging performance among evaluated baselines. These findings support workflow-decomposed, TNM-accountable PET/CT drafting as a promising decision-support approach for human verification, and prospective studies will be valuable for further characterizing its utility in real-world clinical workflows.

Bioplastics derived from hemicellulose exhibit marked potential to substitute petroleum-based plastics due to their sustainability and biodegradability. However, developing bioplastics that combine facile manufacturing processes, excellent mechanical properties, and a low carbon footprint remains challenging. Herein, we present a strategy for fabricating high-performance bioplastics (XAGP) by crosslinking xylan molecular chains via photo-induced free-radical polymerization. The XAGP exhibits high light transmittance (95%), exceptional mechanical toughness (26 MJ/m³) and mechanical strength (84 MPa), outstanding thermal stability, water-assisted processability, rapid biodegradability (10 days in nature soil), hypotoxicity in aquatic environments, and good biocompatibility (cell viability above 98%). Furthermore, cost and life cycle assessment results demonstrate that XAGP is a more sustainable alternative to commercial biodegradable plastics, offering greater cost-effectiveness and a reduced carbon dioxide emission. This work establishes a promising route for transforming pulp waste into degradable, high-performance bioplastics, providing an effective solution to both waste disposal and plastic pollution.

The understanding of type 2 inflammatory diseases is undergoing a paradigm shift from “immune imbalance” toward “immune–metabolic crosstalk”. Energy metabolism not only fuels immune responses but also fundamentally dictates the functional phenotypes of immune cells through metabolic reprogramming. By systematically integrating metabolic programming data of key immune cells across diverse tissues (skin, gut, nasal, and ocular mucosa), this review constructs a cross-disease “metabolism–signaling network” atlas. The synthesis highlights that glycolysis and mTORC1 signaling are predominantly coupled with the pro-inflammatory outputs of Th2 cells and ILC2s, whereas fatty acid oxidation (FAO) and oxidative phosphorylation (OXPHOS) sustain the homeostasis of Tregs and M2-like macrophages. Furthermore, this review characterizes how the tryptophan, glutamine, and arginine pathways fine-tune the immune tolerance boundary via the IDO–AhR–mTOR axis. We also elucidate a conserved inter-organ “hypoxia–HIF-1α–lactylation” axis, which, in conjunction with tissue-specific metabolic branches (e.g., the ceramide pathway in the skin, the SCFA circuit in the gut, and the lactate–GPR81 loop in the mucosa), collectively sculpts local microenvironments and remodeling trajectories. Ultimately, a novel diagnostic and therapeutic framework centered on metabolic phenotyping is proposed, providing prospective insights into targeting metabolic checkpoints for precision immunotherapy in type 2 inflammation.

The widespread occurrence of antimicrobial-resistance-associated contaminants in natural and engineered water systems poses a major threat to environmental and public health. Conventional contact-electro-catalysis (CEC) can generate interfacial H₂O₂ and reactive oxygen species, but its efficiency is often constrained by sluggish H₂O₂ activation and limited reactive oxygen species flux. Here, we report an additive-free contact-electro-catalysis/vacuum ultraviolet (CEC–VUV) system that uses low-cost polytetrafluoroethylene as a dielectric catalyst for rapid mitigation of antibiotics, pathogens, and antibiotic resistance genes in water. Mechanistic analyses reveal that VUV irradiation activates CEC-derived H₂O₂ and O₃ through charge–photon coupling, converting these otherwise underutilized intermediates into ^•OH. CEC continuously supplies interfacial charges and H₂O₂, while VUV promotes H₂O₂ photolysis and O₂-to-O₃ conversion. The generated O₃ is further activated at the charged polytetrafluoroethylene/water interface, establishing an interconnected H₂O₂/O₃-to-^•OH conversion network that amplifies ^•OH generation. This mechanism enables complete degradation of representative antibiotics within 10 min, complete inactivation of pathogenic bacteria within 5 min, effective antibiotic resistance gene removal in real water matrices, and stable bactericidal performance under continuous-flow operation.

With global space activities shifting from an exploration-oriented focus to large-scale development and utilization, low-cost, “airline-mode”, and high-capability space transportation capabilities have become the critical foundation for supporting the construction of space infrastructure and the flourishing of the space economy. This paper targets the “dual-hundredfold” goal, aiming for a hundredfold increase in both payload insertion mass and launch frequency compared to current levels. After analyzing the development trends and challenges of large-scale space transportation systems, key technologies—such as ultra-high-speed re-entry active thermal management, long life-cycle engines, efficient low-temperature propellant transfer control and precise sensing, aerodynamic-assisted orbital maneuvers, aerodynamic and control integration design for the payloads featuring high lift-to-drag ratios and high packing densities, and fully electric-driven pressurization and fluid transport control technologies—are discussed. Breakthroughs in these technologies are expected to revolutionize human access to space, give rise to new intercontinental travel paradigms, and reshape the global technological competition landscape and strategic balance.

Structural phase transitions driven by atomic rearrangements at the interaction interfaces of biological macromolecules, particularly proteins, are fundamental to regulating critical physiological processes, making their effective modulation key to developing targeted therapeutics. Existing induction strategies encounter substantial limitations: Chemical methods have difficulty accessing shallow binding pockets and can lead to invasive, irreversible modifications, while common visible and near-infrared modulation technologies are hindered by side effects induced by exogenous agents and restricted deep-tissue penetration. Here, using molecular dynamics simulations of the programmed cell death protein 1/programmed cell death 1 ligand 2 complex, we find terahertz light (40.2 THz) to be a reversible, nonthermal, and noninvasive physical induction modality to drive a directed structural phase transition. Energetic analyses reveal that the terahertz field markedly decreases the binding affinity by more than 3-fold and reduces the free energy barrier by nearly 3-fold. Fundamentally, our research demonstrates that this directed decoupling process originates from the coherent resonance of certain key interfacial residues. Collectively, our findings propose a universal physical strategy to modulate macromolecular interfaces, providing an essential computational framework to guide future experimental validations in noninvasive tumor immunotherapy.

Endothelial cells (ECs) sense hemodynamic forces and critically influence aortic aneurysm and dissection (AAD) development. However, the possible contribution of the mechanical sensor Piezo1 to AAD remains elusive. Single-cell mRNA sequencing identified Piezo1 as the most up-regulated mechanical sensor in ECs from AAD model mice. Immunofluorescence and immunoblotting confirmed markedly increased Piezo1 protein in human and mouse AAD samples. Disturbed flow induced by abdominal aortic constriction plus Angiotensin II up-regulated Piezo1 expression and AAD incidence, whereas Piezo1 inhibition attenuated both. Moreover, EC-specific Piezo1 deficiency was sufficient to suppress β-aminopropionitrile- and Ang II-induced AAD formation in mice. Mechanistically, we discovered the disturbed shear stress-induced opening of the endothelial barrier via Piezo1 and subsequent Ca²⁺/MLC/PYK2/SRC-mediated activation of downstream signaling. In addition, in an Ang II-induced endothelial barrier dysfunction model, Piezo1 deficiency in ECs ameliorated Ang II-induced barrier dysfunction. Further study revealed that Piezo1 activation in ECs promoted the up-regulation of CCL2 in a STAT3-dependent manner and strongly promoted the chemotactic recruitment of monocytes/macrophages to the aorta. Importantly, blocking CCR2 reduced monocyte/macrophage recruitment and subsequently attenuated Piezo1 up-regulation-aggravated AAD formation. Transcriptome analysis of human AAD samples revealed a positive correlation between Piezo1 and inflammation of the aorta. We demonstrate that Piezo1 directly links mechanical sensing under disturbed flow to a pathogenic cascade of endothelial barrier dysfunction and inflammatory cell recruitment. Consequently, interventions targeting Piezo1 or the downstream STAT3-CCL2/CCR2 signaling hold therapeutic promise for AAD.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease with limited mechanism-based therapies, and ferroptosis—an iron-dependent lipid peroxidation-driven cell death—has emerged as a critical pathogenic event. Using a machine learning model that combines molecular fingerprints and transfer learning representations to screen for ALOX15 inhibitors, we identified rosmarinic acid (RA) from natural product libraries. RA exhibited high-affinity binding to ALOX15 and maintained stable complex conformation in molecular dynamics simulations. In dextran sulfate sodium-induced colitis mice and lipopolysaccharide-treated intestinal epithelial cells (IEC-6 and mouse colonic epithelial cell), RA alleviated disease activity index, colon shortening, histological damage, and barrier protein loss (ZO-1, Occludin, and Claudin-1). Mechanistically, RA suppressed ferroptosis by restoring GPX4, SLC7A11, and FTH1; reducing ACSL4, COX-2, and lipid reactive oxygen species (ROS); and lowering intracellular Fe²⁺ and malondialdehyde. Crucially, RA disrupted the ALOX15–VDAC1 protein complex, preserved mitochondrial membrane potential, and reduced mitochondrial ROS, effects that were abrogated by ALOX15 knockdown or VDAC1 knockdown. Serum metabolomics further revealed that RA remodels lipid metabolism pathways (arachidonic acid and linoleic acid metabolism) linked to ferroptosis. Collectively, this artificial intelligence-driven discovery positions RA as a novel ferroptosis inhibitor that targets the ALOX15–VDAC1 axis, offering a promising therapeutic candidate for UC.

With the ongoing progress in coronary interventional therapy, the progression of atherosclerosis is no longer solely governed by its natural course. Postprocedural neointimal hyperplasia and plaque formation markedly increase the risk of cardiovascular events, where chronic, unresolved inflammation and the overproduction of reactive oxygen species (ROS) play a critical role in driving plaque development. Drawing inspiration from the reaction mechanisms of intracellular antioxidant defense systems, we report the de novo design of a ruthenium arene complex (RuC₆H₆) with pseudo-vacant coordination sites, which serves as efficient small-molecular antioxidant enzyme mimics for biocatalytic ROS elimination and the attenuation of vascular restenosis. Our findings reveal that the ligands in RuC₆H₆ undergo rapid hydrolysis during the reaction and chloride ligands are replaced by H₂O₂, thereby generating abundant reactive sites and conferring the complex with efficient, broad-spectrum, and stable ROS-scavenging properties. When encapsulated in liposomes (Lipid-Ru), the complex effectively reprogrammed macrophages from the M1 phenotype, diminished the secretion of inflammatory cytokines, and suppressed foam cell formation. Moreover, the Lipid-Ru administration led to a significant reduction in smooth muscle cell migration and neointimal area, ultimately alleviating vascular restenosis. This class of structurally tunable arene ruthenium complexes thus provides a promising strategy for designing biomimetic antioxidant reagents, holding considerable potential for the treatment of diverse inflammation-associated diseases.