Exigent demands for multifunctional composites integrating proficient thermal management and electromagnetic shielding functionalities arise directly from the accelerating sophistication and power intensification of modern electronic systems. Drawing inspiration from the efficient grasping tentacles of sea anemones, this study pioneers a bioinspired strategy for thermal and electromagnetic management in high-power electronics: architecting bioinspired carbon nanotubes (CNTs) interfaces on copper foam. Notably, the sea anemone tentacle-like CNTs architected on copper foam not only anchor abundant poly(styrene-ethylene-propylene-styrene)/n-docosane to enhance the composites’ latent heat capacity and leakage resistance but also interconnect with expanded graphite to establish multi-path thermal conduction networks while creating electromagnetic wave-reflecting heterogeneous interfaces. By leveraging CNTs as structural bridges, this design integrates the copper foam, expanded graphite, and polymer matrix into a continuous composite (CuFCE-2), achieving superb thermal conductivity (4.71 W/m·K). Consequently, CuFCE-2 excels in thermal management, suppressing chip temperatures by 60.6 °C (transient shock) and 15.7 °C (steady state). Critically, synergistic coordination across these bioinspired heterogeneous interfaces achieves prominent electromagnetic interference shielding, averaging 111.1 dB in the X-band (8.2 to 12.4 GHz). Collectively, the straightforward preparation method and exceptional properties of CuFCE-2 endow it with substantial application potential in electronics and communications, aerospace and defense, as well as new energy and energy storage systems.

Abdominal aortic aneurysm (AAA) is a life-threatening aortic disease without effective pharmacological therapies. Mounting evidences suggested that RNA-binding proteins (RBPs) exert pivotal roles in various diseases including AAA. The public human AAA microarray dataset and the RBP database were used to screen the involved RBPs during AAA formation. The integrated analysis identified zinc finger protein 36 (ZFP36) as a potential mediator of AAA. Underexpression of ZFP36 was observed in aortic vascular smooth muscle cells (VSMCs) within aneurysms from patients and angiotensin II (AngII)-induced mice. Zfp36 deficiency in VSMCs augmented extracellular matrix (ECM) degeneration, VSMC phenotypic switch, and apoptosis, which promoted AAA formation in the AngII-infused model. In contrast, VSMC-specific overexpressing Zfp36 inhibited AAA formation. Mechanically, guanylate binding protein 2 (GBP2), a GTPase related to interferon-γ signaling, was identified as a direct target gene of ZFP36 by analyzing the bulk sequencing data. We confirmed that ZFP36 regulates VSMC phenotypic switch via manipulating Yes-associated protein1/TEA domain transcription factor 1 (YAP1/TEAD1) signaling in a GBP2-dependent manner. Additionally, we further verified that dexamethasone (Dex) could promote glucocorticoid receptor nuclear translocation and Zfp36 transcription. In vivo Dex administration prevented AAA formation in a ZFP36-dependent manner. These findings revealed the regulatory role of ZFP36/GBP2/YAP1/TEAD1 signaling in VSMC phenotypic switch and AAA formation, and provided a novel strategy (Dex) for AAA treatment.

The topological Hall effect (THE), a transport signature emerging from chiral spin textures induced by structural symmetry breaking and the Dzyaloshinskii–Moriya interaction (DMI), represents a rich frontier in condensed matter physics with promising applications in spintronic devices. To enhance the DMI and thereby induce THE in SrRuO₃ (SRO), we introduce a structural-symmetry-breaking strategy that disrupts the Ru–O termination at the rigid substrate interface. This disruption triggers a transition from a rigid epitaxial interface to a freestanding membrane with unsaturated surface bonds, resulting in asymmetric surface terminations (Sr–O on top and Ru–O at the bottom). Unlike its rigid counterpart, which shows no detectable THE, the freestanding SRO exhibits a pronounced THE signal, persisting up to 100 K while preserving high crystallinity and electronic coherence. The ability to generate robust THE in transferable oxide membranes has direct implications for next-generation spintronics, offering compelling prospects for creating low-power magnetic memory and logic devices based on chiral spin textures.

Zincology, the rigorous cross-disciplinary study of zinc metabolism and its multifaceted biological and applied roles in health and disease, delivers a transformative framework for resolving long-standing uncertainties in biomedical research. As a central regulator of cellular function and a versatile element in applied fields, zinc dyshomeostasis underpins diverse high-burden pathologies, including renal, metabolic, cardiovascular, and neurodegenerative disorders, yet its mechanisms remain fragmented across disciplines. This Perspective marks the first formal definition of Zincology as a distinct cross-disciplinary discipline, clarifying zinc’s context-dependent dual role: systemic deficiency exacerbates biological injury through compromised antioxidant defense and inflammation, while local excess drives pathogenesis—exemplified by the Zn–protein kinase B (AKT)–forkhead box protein O1 (FOXO1)–glucose-6-phosphatase catalytic subunit (G6PC) axis in kidney disease. We synthesize Zincology’s core principles to integrate systemic and local zinc metabolism, dissect its pathogenic role in the aforementioned disorders, and outline cross-disciplinary research directions with implications extending beyond biomedicine. Leveraging Zincology’s multidisciplinary rigor, we establish zinc homeostasis as a unifying framework for deciphering disease mechanisms, with kidney disease serving as a paradigmatic model to validate its core tenets, bridging fragmented basic, clinical, industrial, and environmental research to address global critical unmet medical and societal needs. Notably, Zincology extends beyond biomedicine to encompass engineering, ecology, and other frontier fields, representing a comprehensive cross-disciplinary system that links basic science with diverse applied domains.

Biological stress responses operate across multiple scales, yet the coordination mechanisms remain poorly characterized. Here, we present comprehensive systems-level characterization of coordinated plant and endophytic microbiome responses during xenobiotic stress, integrating ultrastructural analysis, proteomics, and microbiome profiling in rice seedlings exposed to ciprofloxacin. We discovered a sophisticated multi-level defense system with chloroplasts as a key hub within a highly integrated cross-organellar network, comprising 36% of all differentially expressed proteins. The system operates through 3 integrated mechanisms: (a) differential cellular accumulation patterns showing 14-fold tissue-specific differences, (b) reactive-oxygen-species-associated metabolic processes with reduced toxicity of transformation products, and (c) restructuring of endophytic bacterial communities toward stress-resistant genera. This work indicates that biological systems deploy hierarchical, integrated responses spanning from organellar to ecosystem levels. The chloroplast-centered response represents a comprehensive characterization of multicompartmental responses with implications across multiple biological fields. Our findings illustrate how multidisciplinary systems approaches can uncover emergent properties of multiscale biological responses invisible to single-scale analyses, providing a framework for investigating multiscale responses across diverse biological systems.

Intracranial hemorrhage (ICH) represents a subtype of stroke characterized by increased mortality and disability rates. Early evacuation of the hematoma is essential for the effective management of ICH. Currently, minimally invasive surgery (MIS) has emerged as a promising alternative to traditional craniotomy by offering advantages, such as reduced operating time, minimal surgical trauma, and accelerated recovery. Nonetheless, postoperative rebleeding remains an important complication that adversely affects the functional outcomes and survival rates of the affected patients. Thus, acquiring a thorough understanding of postoperative rebleeding following MIS for ICH is crucial for enhancing neurological functional outcomes. This review aimed to synthesize current evidence regarding the definition of postoperative rebleeding following MIS for ICH, elucidate the mechanisms contributing to this phenomenon, and identify the associated risk factors, including both surgical and patient-related factors. In addition, the review discusses contemporary strategies for the prevention and management of postoperative rebleeding. Furthermore, it explores prospective advances in dynamic risk prediction and early detection of postoperative rebleeding using artificial intelligence and real-time biosensors. This review offers a reference for clinical practice and guides future studies aimed at reducing the risk of postoperative rebleeding after MIS for ICH, thereby enhancing the outcomes of patients.

Apoptosis and autophagy are fundamental pathophysiological programs governing cell fate decisions under stress, particularly during anticancer therapy. However, the interplay between apoptosis and autophagy in cancer chemoresistance remains incompletely understood. Here, we identify the apoptosis-related protein in the transforming growth factor-β signaling pathway (ARTS) as a key molecular transferring apoptotic signal to autophagic machinery to promote cell survival and chemoresistance. ARTS was highly expressed in chemoresistant breast cancer tissues and was associated with poor patient prognosis. ARTS conferred resistance to doxorubicin and docetaxel by inducing protective autophagy in vitro and in vivo cancer models. Mechanistically, upon proapoptotic signaling triggered by chemotherapeutic agents, ARTS translocated from the mitochondrial intermembrane space into the cytosol, where it induced autophagy through triggering seven in absentia homolog 1-mediated degradation of Livin and subsequent engagement of the mouse double minute 2 homolog (MDM2)–p53 axis, thereby promoting cancer cell survival. Pharmacologic inhibition of caspases or autophagic flux attenuated ARTS-mediated chemoresistance. Overall, this study delineates an apoptosis-dependent ARTS–Livin–MDM2–p53 pathway that drives autophagy and confers chemoresistance in breast cancer.

Majorana zero modes (MZMs) localized in vortex cores of topological superconductors are widely regarded promising building blocks for fault-tolerant quantum computation. However, their unambiguous detection is hindered by the extremely small energy spacing separating them from conventional Caroli-de Gennes-Matricon states. Using a microscopic Bogoliubov-de Gennes approach, we demonstrate that nonmagnetic impurities, rather than suppressing, can substantially enhance the energy gap between MZMs and other vortex core excitations. The robustness of MZMs against local perturbations ensures that while conventional states are shifted by impurity-induced potentials, the MZMs remain intact. This results in a pronounced zero-bias peak in the local density of states. Our results dispute the widespread assumption that large \mathrm{\Delta }/E_F values—where \mathrm{\Delta } is the superconducting gap and E_F is the Fermi energy—are required to detect MZMs, and instead indicate that purposefully engineered pinning centers in conventional s-wave superconductors offer a practical and experimentally accessible alternative.

Copper complexes hold a promise for electroluminescent applications, owing to their dual emissive feature based on the moderate spin-orbital coupling effect of Cu⁺ ion for controllable singlet–triplet conversion. However, efficient red dual emission from copper complexes remains an important challenge, because emission wavelengths and thermally activated delayed fluorescence (TADF)/phosphorescence (PH) ratios are simultaneously correlated to electronic effects. Herein, fluorine atoms with suitable electron-withdrawing inductive effect were introduced into a typical tridentate phosphine ligand coordinated CuI skeleton, namely, TTPPCuI, to reduce the lowest unoccupied molecular orbital (LUMO) energy levels, giving rise to narrowed energy gaps between the highest occupied molecular orbital and LUMO, corresponding to emission wavelengths red shifted from 574 to 603 nm. Fluorine atoms simultaneously enhance metal-ligand charge transfer, therefore adjusting positive and reverse intersystem crossing for dual emission balance, leading to TADF/PH ratios changing from 56/44 over 75/25 to 83/17. The devices based on these fluorinated CuI complexes realized efficient red electroluminescence with the maximum wavelength and external quantum efficiency beyond 600 nm and 20%, respectively. These results demonstrate that, based on electronic effects from functional groups, ligand engineering is a feasible way for comprehensively manipulating excited-state characteristics of dual-emissive copper complexes.

Global public databases now contain extensive information about disease, environment, and society, but much of these data have been used only for descriptive summaries rather than for exploring deeper causes of health differences between countries. This commentary discusses how combining data from multiple international sources can reveal new patterns that support fairer and more effective health policies. Using 2 recent examples, we show how this approach can be used to answer important public-health questions, fill gaps in existing databases, and translate scientific evidence into preventive policy. Future ecological studies should continue to connect health data with environmental and social indicators to better understand and reduce global health inequalities.