Research最新文献

[This corrects the article DOI: 10.34133/research.0897.].

The integration of multiband and multimode systems has substantially increased the complexity of electromagnetic interference, revealing critical limitations of existing absorbers in tuning efficiency and structural resilience. Here, we propose a nested microaerogel strategy to simultaneously improve the mechanical strength and microwave absorption (MA) performance of polyimide (PI) aerogel. By incorporating pomelo-peel-derived cellulose micronetworks and helical carbon nanocoil microaerogels to construct a gradient-nested framework, the long-standing issues of filler agglomeration and structural shrinkage in aerogels are effectively resolved. The aerogel combines low density, impact resistance, and thermal insulation with remarkable MA performance. The compressive strength reaches 1.3 MPa, which is about 20 times higher than pristine PI aerogel. Furthermore, it exhibits a minimum reflection loss of -50.16 dB, a broad effective absorption bandwidth of 7.44 GHz, and an ultrawide tunable range of 5.6 to 16.4 GHz. Benefiting from its exceptional mechanical properties and pressure-dependent tunability, the aerogel establishes a clear correlation between compression-induced capacitive response and MA performance. These features highlight its potential as a new generation of intelligent microwave absorbers with integrated sensing and adaptive regulation capabilities.

Calculations of collisions involving excited electronic states play an important role in many high-energy environments, for example, in simulating thermal energy content and heat flux in flows around hypersonic reentry vehicles, and useful data are usually not available from either experiment or theory. We apply a deep learning framework-compatibilization by deep neural network-to automatically discover and fit a compatible potential energy matrix (CPEM) for singlet oxygen atom collisions with N₂ in the ¹ A' manifold of N₂O. The procedure yields not only a fit to the CPEM and its gradient but also analytic representations of the adiabatic potential energy surfaces and their gradients across a dense 13-state manifold; these potential energy surfaces are suitable for dynamics calculations of inelastic and reactive collisions across a broad range of collision energies extending above the dissociation threshold of N₂. We propose a new asymptotically extended formulation of the curvature-driven coherent switches with decay of mixing (κCSDM) semiclassical dynamics method that resolves the conflict between differing symmetries of the interacting atom-diatom system and the completely separated final states. We use the new dynamics method with the analytic representation of potential surface gradients to compute electronically nonadiabatic cross-sections for N₂(X ) + O(¹S) collisions, primarily producing N₂(X) + O(¹D), N₂(A) + O(³P), and NO(X) + N(²D). Our methods provide new capabilities for modeling electronic energy transfer under extreme conditions, with implications across chemistry, physics, and aerospace engineering.

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.

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.

Sepsis-induced cardiac dysfunction (SICD) is a major contributor to mortality in sepsis. Kinesin family member 13B (KIF13B) has been identified as a critical protective factor for metabolic disorder and cardiovascular disease; however, the role of KIF13B in SICD remains unknown. After introducing lipopolysaccharide or cecal ligation and puncture surgery to wild-type (WT) and global Kif13b knockout (Kif13b ^-/-) mice combined with lipopolysaccharide-treated neonatal rat cardiomyocytes, we found that KIF13B expression levels were markedly down-regulated in septic hearts and cardiomyocytes. Kif13b deletion exacerbated SICD progress with reduced cardiac contractile function and resulted in increased mortality, accompanied by promoted lipid accumulation, fibrosis, and mitochondrial impairment. Mechanistically, the loss of KIF13B enhanced the lysosomal degradation of the lipid-droplet-associated protein perilipin 5 (PLIN5), thus disrupting the mitochondrial localization of PLIN5 and then impairing cardiac lipid homeostasis and proper mitochondrial function. Nevertheless, cardiac-directed AAV9-PLIN5 gene therapy sufficiently corrected cardiac dysfunction, inhibited lipid accumulation, and reduced oxidative stress in Kif13b ^-/- mice with SICD. In summary, these findings provide a new insight into the molecular mechanism underlying the pathogenesis of SICD, highlighting the KIF13B/PLIN5 axis as a potential therapeutic target for the treatment of SICD.

The NLRP3 inflammasome is a pivotal component of the innate immune system, responding to infections and cellular damage. Its dysregulation has been implicated in numerous inflammatory diseases, although the mechanisms controlling its activation remain incompletely elucidated. Recent studies have highlighted the importance of posttranslational modifications, such as ubiquitination and SUMOylation, in regulating inflammasome activation. In this study, we demonstrate that SENP6, a SUMO-specific protease, negatively regulates NLRP3 inflammasome activation by promoting K48-linked polyubiquitination of NLRP3. SENP6-deficient macrophages exhibit enhanced NLRP3 activation and increased secretion of interleukin-1β (IL-1β) and IL-18, resulting in amplified inflammatory responses. Mechanistically, SENP6 interacts with NLRP3 and promotes its degradation through the autophagy-lysosomal pathway via K48-linked polyubiquitination. We further identified that SENP6 deSUMOylated NLRP3 at specific lysine residues (K23, K204, and K689), which was essential for maintaining NLRP3 stability. Additionally, SENP6 recruits the E3 ubiquitin ligase MARCHF7 to promote NLRP3 ubiquitination and subsequent degradation. In vivo, SENP6 deficiency exacerbates NLRP3 activation and lung inflammation in lipopolysaccharide-induced endotoxic shock-associated lung injury, and enhances inflammatory responses in alum-induced peritonitis. Our findings reveal a novel mechanism whereby SENP6 modulates NLRP3 inflammasome activation via SUMOylation, ubiquitination, and degradation, providing new insights into potential therapeutic strategies for inflammasome-related pathologies.

Autophagy is integral to the rapid proliferation of esophageal squamous cell carcinoma (ESCC), and its regulation presents a promising avenue for therapeutic intervention. Recent studies have elucidated the interplay between autophagy and glucose metabolism, while there is a paucity of anticancer drugs that concurrently target these 2 biological processes. In this study, we identified a natural compound, p-hydroxylcinnamaldehyde (CMSP), originally isolated from Cochinchina momordica seed (CMS) by our research team, which exhibits substantial anticancer activity against ESCC in both in vitro and in vivo models. The study demonstrates that CMSP induces apoptosis in ESCC cell lines and patient-derived organoid (PDO) models by disrupting autophagic flux. Mechanistically, CMSP specifically binds to the glycolytic enzyme LDHA in the cytoplasm, hindering its phosphorylation by blocking its membrane translocation and thereby disrupting its interaction with FGFR1. This inhibition results in decreased lactate production from glycolysis, reduced lysosomal acidity, and suppression of the AMPK/mTOR pathway, ultimately resulting in the blockade of autophagy and the induction of apoptosis. Furthermore, in vivo studies underscore the potential clinical application of CMSP in ESCC by disrupting autophagy. In summary, we propose a novel therapeutic strategy for the precision treatment of ESCC by simultaneously targeting glycolysis-mediated autophagy.

Meniscal injuries are common in the knee joint. Minor meniscal injuries usually respond well to conservative treatment, while severe cases often require complete meniscal replacement. Meniscal injuries cause inflammatory responses that importantly hinder meniscal tissue regeneration. Despite ongoing advances in research, considerable breakthroughs in meniscal regeneration remain out of reach. This study introduces programmable macrophage mimics (PMMs), which enable sequential regulation from anti-inflammatory responses to meniscal fibrocartilage regeneration. PMMs were prepared by encapsulating the transforming growth factor-β3 and insulin-like growth factor-1 growth factors within mesoporous silica nanoparticles modified with branched polyethyleneimine via disulfide bonding. This design allows the initial adsorption of proinflammatory cytokines followed by the controlled release of growth factors that promote adipose-derived stem cell (ADSC) differentiation into fibrochondrocytes. The PMMs were integrated into meniscus-specific acellular matrix hydrogels (mGC), which provided suitable mechanical properties critical for effective regeneration. In rabbit osteoarthritis models, ADSC-loaded PMMs@mGC hydrogels showed marked fibrocartilage regeneration. Additionally, the team developed an advanced biofabrication approach that combines a 3-dimensionally printed polycaprolactone framework designed for total meniscus replacement. This research suggests that PMMs act as a bifunctional "core-shell" nano-delivery system, offering a promising therapeutic strategy for managing inflammatory meniscal conditions.

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.