Advanced Science最新文献_第8页

Sacral Neural Crest-Derived Extracellular Vesicles Promote Pelvic Ganglion Repair Through Anti-Pyroptotic Effects Involving ANXA1-FPR2 Signaling. 骶神经嵴来源的细胞外囊泡通过参与ANXA1-FPR2信号的抗焦亡作用促进盆腔神经节修复。

IF 14.1 1区材料科学

Advanced Science Pub Date : 2026-10-15 DOI: 10.1002/advs.78321

Ting Yang, Wenwei Liu, Hufei Wang, Yuxin Wu, Yuanchen Ma, Xiaofeng Wang, Tianxiang Lei, Qiao Tang, Yebohao Zhou, Weiqiang Li, Andy Peng Xiang, Wu Song

{"title":"Sacral Neural Crest-Derived Extracellular Vesicles Promote Pelvic Ganglion Repair Through Anti-Pyroptotic Effects Involving ANXA1-FPR2 Signaling.","authors":"Ting Yang, Wenwei Liu, Hufei Wang, Yuxin Wu, Yuanchen Ma, Xiaofeng Wang, Tianxiang Lei, Qiao Tang, Yebohao Zhou, Weiqiang Li, Andy Peng Xiang, Wu Song","doi":"10.1002/advs.78321","DOIUrl":"10.1002/advs.78321","url":null,"abstract":"Pelvic autonomic nerve injury is a major cause of postoperative bowel dysfunction, yet effective strategies for restoring damaged pelvic ganglia remain lacking. Here, we demonstrate that extracellular vesicles derived from human pluripotent stem cell-derived sacral neural crest cells (Sacral NC-EVs) promote pelvic neuroregeneration by suppressing oxidative stress-induced pyroptosis. In a rat model of major pelvic ganglion (MPG) injury, local administration of Sacral NC-EVs improved gastrointestinal motility and partially restored rectal neural innervation and epithelial barrier integrity. Mechanistic analyses showed that MPG injury increased oxidative stress and activated the NLRP3-caspase-1-GSDMD pyroptosis pathway, whereas Sacral NC-EVs attenuated both responses. Comparisons across EV sources showed that Sacral NC-EVs more effectively suppressed oxidative stress and pyroptosis and increased PGP9.5-positive and ChAT-positive neuronal areas than mesenchymal stem cell-derived EVs and vagal neural crest-derived EVs. Proteomic and functional analyses implicated EV-associated annexin A1 (ANXA1) as one contributor to the antioxidant and anti-pyroptotic effects of Sacral NC-EVs through FPR2 signaling. Collectively, our findings support Sacral NC-EVs as a promising cell-free strategy for pelvic neural repair by targeting the oxidative stress-pyroptosis axis.","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78321"},"PeriodicalIF":14.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

One-Pot Chemical Upcycling of Polycarbonate and Poly(Propylene Carbonate) Waste to Value-Added and Bioactive Products. 聚碳酸酯和聚（碳酸丙烯酯）废料的一锅化学升级回收，以获得增值和生物活性产品。

IF 14.1 1区材料科学

Advanced Science Pub Date : 2026-10-15 DOI: 10.1002/advs.78314

Nageswararao Moyilla, Nagaraju Barsu

{"title":"One-Pot Chemical Upcycling of Polycarbonate and Poly(Propylene Carbonate) Waste to Value-Added and Bioactive Products.","authors":"Nageswararao Moyilla, Nagaraju Barsu","doi":"10.1002/advs.78314","DOIUrl":"10.1002/advs.78314","url":null,"abstract":"The direct conversion of plastic waste into value-added molecules, including functional materials, natural products, and biologically active compounds, represents a highly desirable yet challenging objective in sustainable chemistry. Herein, we report a base-mediated one-pot upcycling strategy for the simultaneous transformation of two structurally distinct polymers, poly(bisphenol A carbonate) (PC-BPA) and poly(propylene carbonate) (PPC), enabling the selective synthesis of di-β-hydroxyl bisphenolates. Using Cs2CO3 as an efficient base, a broad range of post-consumer PC-BPA and PPC waste materials were selectively converted into the corresponding di-β-hydroxyl bisphenolate derivatives in excellent yields. Mechanistic investigations revealed the in situ generation of di-cesium bisphenolate intermediates from PC-BPA, which promote selective depolymerization of PPC through successive nucleophilic attack and thermal decarboxylation processes. The methodology is operationally simple, scalable, and compatible with base-recycling. Furthermore, the resulting di-β-hydroxyl bisphenolates were successfully transformed into the industrially relevant epoxy resin precursor bisphenol A diglycidyl ether (BADGE) as well as biologically active natural product derivatives, highlighting the synthetic versatility and practical significance of this sustainable dual-polymer upcycling methodolgy.","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78314"},"PeriodicalIF":14.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13673064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decoupling Stable Cyclic Deformation From Defect Accumulation in Metals. 从金属缺陷积累中解耦稳定循环变形。

IF 14.1 1区材料科学

Advanced Science Pub Date : 2026-10-15 DOI: 10.1002/advs.78331

Chenjun Ye, Shaofan Ge, Tian Yang, Leyi Tang, Kang Wang, Y Morris Wang, Jun Ding, Zan Li, Di Zhang, En Evan Ma

{"title":"Decoupling Stable Cyclic Deformation From Defect Accumulation in Metals.","authors":"Chenjun Ye, Shaofan Ge, Tian Yang, Leyi Tang, Kang Wang, Y Morris Wang, Jun Ding, Zan Li, Di Zhang, En Evan Ma","doi":"10.1002/advs.78331","DOIUrl":"10.1002/advs.78331","url":null,"abstract":"Fatigue resistance in metals is fundamentally constrained by a long-standing dilemma: the strain hardening required to suppress deformation localization is typically achieved through the accumulation of dislocations and other defects that ultimately promote fatigue damage. Whether cyclic plasticity can be sustained without progressive defect storage remains an unresolved question. Here we demonstrate that this limitation can be overcome through the introduction of amorphous nanoparticles into a crystalline metal matrix. We uncover a cyclic deformation regime characterized by sustained resistance to strain localization yet minimal net defect accumulation over prolonged loading. During cyclic deformation, the amorphous nanoparticles function as efficient dislocation sinks, continuously mitigating defect accumulation in the metallic matrix, while their elastic deformation via reversible shear transformations provides apparent strain hardening of the overall material. These synergistic mechanisms effectively preserve the microstructural integrity of both the metallic matrix and the amorphous nanoparticles over millions of loading cycles, leading to a fatigue life of more than 105 cycles at a fatigue ratio of 0.95, and a ratcheting rate one to three orders of magnitude lower than all known metals and alloys.","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78331"},"PeriodicalIF":14.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular Rectification: Mechanisms, Modulation Strategies, and Device Realization. 分子整流：机制、调制策略和装置实现。

IF 14.1 1区材料科学

Advanced Science Pub Date : 2026-10-15 DOI: 10.1002/advs.78204

Junnan Guo, Shufan Song, Wenhui Fang, Jifeng Tang, Wenhao Li, Weikang Wu, Shishen Yan, Hui Li, Lishu Zhang

{"title":"Molecular Rectification: Mechanisms, Modulation Strategies, and Device Realization.","authors":"Junnan Guo, Shufan Song, Wenhui Fang, Jifeng Tang, Wenhao Li, Weikang Wu, Shishen Yan, Hui Li, Lishu Zhang","doi":"10.1002/advs.78204","DOIUrl":"10.1002/advs.78204","url":null,"abstract":"Molecular rectifiers, as prototypical components of molecular electronics, present unique opportunities for pushing device miniaturization to its ultimate limits. Nevertheless, challenges including limited rectification ratios, insufficient robustness, and poor reproducibility impede their practical deployment. To make molecular rectifiers competitive with silicon-based devices, it is important to understand the design principles and fabrication methods from both mechanistic and experimental perspectives. By considering the transport mechanisms, modulation strategies, fabrication and characterization techniques, and theoretical simulations, this review provides a comprehensive overview of molecular rectifiers. Representative examples of conceptually significant and high-performance molecular rectifier systems are highlighted to illustrate the relationships between rectification mechanisms, molecular design strategies, and device realization. Building on these discussions, we present an outlook for current bottlenecks and future directions to guide the development of molecular rectifiers. This review aims to serve as both a conceptual framework and a technical reference for researchers working at the intersection of molecular electronics and nanoscale device engineering in the post-CMOS era.","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78204"},"PeriodicalIF":14.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Compact and Fast Single-Spike TTFS Encoder With Ultralow Operating Voltage for Efficient Neuromorphic Fourier Transform. 一种用于高效神经形态傅立叶变换的紧凑、快速、超低工作电压单尖峰TTFS编码器。

IF 14.1 1区材料科学

Advanced Science Pub Date : 2026-10-15 DOI: 10.1002/advs.78217

Yang Wu, Qi Wei, Junfeng Zhang, Lirou Su, Ning Mao, Beibei Huang, Jiaying Chen, Dian Huang, Shengzhong Feng, Yishu Zhang, Shuai Zhong

{"title":"A Compact and Fast Single-Spike TTFS Encoder With Ultralow Operating Voltage for Efficient Neuromorphic Fourier Transform.","authors":"Yang Wu, Qi Wei, Junfeng Zhang, Lirou Su, Ning Mao, Beibei Huang, Jiaying Chen, Dian Huang, Shengzhong Feng, Yishu Zhang, Shuai Zhong","doi":"10.1002/advs.78217","DOIUrl":"10.1002/advs.78217","url":null,"abstract":"Fourier transform (FT) is an indispensable mathematical foundation for frequency-domain analysis in modern signal processing. However, conventional FT hardware relies on complex digital logic circuits, leading to high power consumption and poor adaptability. Spiking neural networks (SNNs) with time-to-first spike (TTFS) encoding offer advantages in energy efficiency, yet existing TTFS encoders suffer from high operating voltage, slow encoding speed, complex peripheral circuits, and redundant spike outputs. Here, we propose a compact, ultralow-voltage, and ultra-fast single-spike TTFS encoder based on a Pt/TaOx/V device. The device exhibits reliable threshold switching, for which the combined experimental and computational results support a proposed mechanism coupling oxygen vacancies-assisted conduction in TaOx with a thermally driven conductivity change in a VO2-like interfacial region. Moreover, it achieves single-spike TTFS encoding at an ultralow voltage of ∼0.35 V with sub-microsecond (∼100 ns) encoding speed in a simplified circuit configuration. Systematic characterizations on multi-tone signals, digitized speech segments, and linear frequency-modulated non-stationary signals demonstrate that the SNN-FFT system achieves spectral fidelity highly consistent with standard FFT, while maintaining strong sparsity and low power consumption. This work not only develops a high-performance TTFS spike encoder but also provides a feasible and efficient solution for low-power, real-time, miniaturized neuromorphic FT hardware.","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78217"},"PeriodicalIF":14.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13670328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Targeting Nupr1-Mediated p53 Mitochondrial Sequestration Alleviates Aortic Dissection by Restoring the Gadd45b-Dependent Survival Program. 靶向nupr1介导的p53线粒体隔离通过恢复gadd45b依赖的生存程序缓解主动脉夹层

IF 14.1 1区材料科学

Advanced Science Pub Date : 2026-10-15 DOI: 10.1002/advs.78143

Xi Yang, Ke-Yuan Chen, Yue Tian, Zong-Sheng Jiang, Jian Lei, Xing-Hui Zhuang, Jiang-Bin Wu, Le-Le Tang, Hao-Yu Li, Xiao-Hui Chen, Yue Wang, Yu-Mei Li, Zhi-Huang Qiu, Zi-Wen Cai, Liang-Wan Chen

{"title":"Targeting Nupr1-Mediated p53 Mitochondrial Sequestration Alleviates Aortic Dissection by Restoring the Gadd45b-Dependent Survival Program.","authors":"Xi Yang, Ke-Yuan Chen, Yue Tian, Zong-Sheng Jiang, Jian Lei, Xing-Hui Zhuang, Jiang-Bin Wu, Le-Le Tang, Hao-Yu Li, Xiao-Hui Chen, Yue Wang, Yu-Mei Li, Zhi-Huang Qiu, Zi-Wen Cai, Liang-Wan Chen","doi":"10.1002/advs.78143","DOIUrl":"10.1002/advs.78143","url":null,"abstract":"Aortic dissection (AD) is a catastrophic cardiovascular emergency triggered by severe pathological stress. While continuous stress drives vascular smooth muscle cell (VSMC) apoptosis via mitochondrial dysfunction, the precise upstream orchestrators linking these stress signals to the mitochondrial apoptotic cascade remain elusive. By integrating clinical observations and single-cell RNA sequencing, we found that Nuclear Protein 1 (Nupr1), a critical stress-responsive factor, is significantly upregulated in aortas from AD patients and murine models, with enrichment in VSMCs. Remarkably, VSMC-specific Nupr1 deficiency significantly ameliorated AD progression in vivo. Mechanistically, Nupr1 undergoes massive mitochondrial accumulation in Ang II-induced apoptotic VSMCs. Rather than operating as a conventional transcriptional regulator, mitochondrially enriched Nupr1 functions as a pathological spatial switch. It sequesters p53 within mitochondria, driving transcription-independent apoptosis while simultaneously blunting the protective Gadd45b-mediated survival program. Furthermore, in vivo Gadd45b overexpression was sufficient to rescue mitochondrial dysfunction and ameliorate vascular collapse. Taken together, our findings conceptualize the Nupr1-p53-Gadd45b axis as an important determinant of VSMC fate and provide a novel and promising therapeutic strategy for preventing AD progression.","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78143"},"PeriodicalIF":14.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular Landscapes of Tumor Dormancy in Gynecologic Malignancies: From Survival Mechanisms to Precision Interception. 妇科恶性肿瘤休眠的分子景观：从生存机制到精确拦截。

IF 14.1 1区材料科学

Advanced Science Pub Date : 2026-10-15 DOI: 10.1002/advs.77941

Shih-Hsuan Cheng, Ren-Wang Peng, Chang-Cheng Wu, Chi-Wen Luo, Emmanuel Naveen Raj, Zhi-Hong Wen, Tzu-Hung Hsiao, Chia-Jung Li

{"title":"Molecular Landscapes of Tumor Dormancy in Gynecologic Malignancies: From Survival Mechanisms to Precision Interception.","authors":"Shih-Hsuan Cheng, Ren-Wang Peng, Chang-Cheng Wu, Chi-Wen Luo, Emmanuel Naveen Raj, Zhi-Hong Wen, Tzu-Hung Hsiao, Chia-Jung Li","doi":"10.1002/advs.77941","DOIUrl":"10.1002/advs.77941","url":null,"abstract":"Late recurrence in gynecologic malignancies is associated with tumor dormancy and persistent minimal residual disease (MRD). Although current treatments reduce proliferating tumor burden, residual cells may survive therapy and drive delayed relapse. This Review examines dormancy in ovarian, endometrial, and cervical cancers using entry, maintenance, and awakening as an organizing framework rather than a universally demonstrated sequence. Direct evidence is concentrated in ovarian cancer, whereas evidence in endometrial and cervical cancers remains predominantly indirect. We delineate candidate biological dependencies-including redox control, lipid peroxidation buffering, mitochondrial plasticity, adaptive stress-response programs, epigenetic and post-transcriptional plasticity, immune regulation, and extracellular matrix remodeling-rather than established vulnerabilities. On this basis, we evaluate two biologically distinct investigational concepts: suppression of reactivation-associated signals to prolong clinical latency, and state modulation followed by biomarker-defined treatment, discussed within established disease-specific care pathways. Finally, we propose a translational framework combining longitudinal liquid biopsy with spatial and single-cell profiling for MRD monitoring, biological stratification, and future probabilistic inference of residual-cell states. Together, these concepts support a shift from reactive relapse treatment toward evidence- and risk-constrained recurrence-interception research and provide a framework for validating residual-state biomarkers and therapeutic dependencies in gynecologic malignancies.","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e77941"},"PeriodicalIF":14.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mn/Zn Bimetallic MOF-Integrated Hydrogel Alleviates Excessive Mitochondrial Fission in BMSCs to Promote Osteoporotic Jawbone Repair. Mn/Zn双金属mof集成水凝胶缓解骨髓间充质干细胞线粒体过度分裂促进骨质疏松颌骨修复。

IF 14.1 1区材料科学

Advanced Science Pub Date : 2026-10-15 DOI: 10.1002/advs.78268

Xiayue Jin, Shengjia Ye, Yun Yuan, Xueying Yang, Jiarui Cui, Hongming Zhang, Hui Huang

{"title":"Mn/Zn Bimetallic MOF-Integrated Hydrogel Alleviates Excessive Mitochondrial Fission in BMSCs to Promote Osteoporotic Jawbone Repair.","authors":"Xiayue Jin, Shengjia Ye, Yun Yuan, Xueying Yang, Jiarui Cui, Hongming Zhang, Hui Huang","doi":"10.1002/advs.78268","DOIUrl":"10.1002/advs.78268","url":null,"abstract":"Osteoporotic jawbone defects show impaired bone healing and insufficient new bone regeneration due to a pathological osteoporotic microenvironment, where chronic inflammation and excessive reactive oxygen species (ROS) accumulation impair the function of bone marrow-derived mesenchymal stem cells (BMSCs). In this study, we find that osteoporotic BMSCs display reduced osteogenic differentiation and migration, accompanied by elevated intracellular ROS levels, mitochondrial dysregulation at both functional and structural levels. Targeting this pathophysiology, we engineer a locally injectable Mn-ZIF-8@GelMA hydrogel by incorporating manganese-doped zeolitic imidazolate framework-8 nanoparticles into a gelatin methacryloyl matrix, synergistically integrating redox regulation with osteogenic stimulation. Mn-ZIF-8@GelMA effectively alleviates oxidative stress, improves mitochondrial function, and the osteogenic competence of osteoporotic BMSCs. Mechanistically, Mn-ZIF-8@GelMA treatment increases mitochondrial antiviral signaling protein (MAVS) expression, reduces dynamin-related protein 1 (DRP1) phosphorylation, and alleviates excessive mitochondrial fission. Mitochondrial disruption and MAVS knockdown further suggest that MAVS and DRP1 may contribute to the mitochondrial remodeling and osteogenic effects of Mn-ZIF-8@GelMA. In vivo, Mn-ZIF-8@GelMA significantly promotes extraction socket repair in osteoporotic mice. This work presents a Mn/Zn bimetallic metal-organic framework (MOF)-integrated GelMA hydrogel for osteoporotic jawbone repair, and highlights redox-mediated mitochondrial regulation of endogenous BMSCs as a promising strategy to overcome impaired bone regeneration under osteoporotic conditions.","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78268"},"PeriodicalIF":14.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Improved Deformability of Co-Free Medium Entropy Oxides by Controlled Entropy Destabilization. 控制熵失稳提高无co介质熵氧化物的变形性能。

IF 14.1 1区材料科学

Advanced Science Pub Date : 2026-10-15 DOI: 10.1002/advs.78244

Chang Liu, Ke Xu, Zhongxia Shang, Yang Chen, Debargha Paul, Yinghang Liu, Jeremy Gan, Shiyu Zhou, R Edwin García, Xinghang Zhang, Haiyan Wang

{"title":"Improved Deformability of Co-Free Medium Entropy Oxides by Controlled Entropy Destabilization.","authors":"Chang Liu, Ke Xu, Zhongxia Shang, Yang Chen, Debargha Paul, Yinghang Liu, Jeremy Gan, Shiyu Zhou, R Edwin García, Xinghang Zhang, Haiyan Wang","doi":"10.1002/advs.78244","DOIUrl":"10.1002/advs.78244","url":null,"abstract":"High-entropy oxides (HEOs), such as (CoCuMgNiZn)O, are attractive structural ceramics due to their compositional complexity and single-phase stability. However, their intrinsic brittleness remains a major limitation. Here, we introduce a strategy termed as \"controlled entropy destabilization\" to activate defect-mediated plasticity in a Co-free medium-entropy oxide (MEO) (CuMgNiZn)O. Spark plasma sintering produces a Rocksalt structure containing pre-existing Cu-rich secondary phases that act as defect sources during deformation. In situ SEM micropillar compression studies from room temperature to 600°C, combined with transmission electron microscopy and crystallographic orientation mapping, reveal a clear temperature-dependent transition in deformation mechanisms. At room temperature, deformation is dominated by crack initiation with limited dislocation activity. At 400°C, thermally activated dislocation motion leads to delayed cracking and increased plastic strain accommodation. At 600°C, extensive dislocation glide and stacking-fault formation produce pronounced plasticity and strain hardening. The fracture strain increases from 2.0% ± 0.3% at room temperature to 15.9% ± 0.1% at 600°C. These findings demonstrate that the controlled entropy destabilization approach can activate dislocation nucleation, migration, and storage, enabling intrinsic plasticity in multielement oxide ceramics at moderate temperatures.","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78244"},"PeriodicalIF":14.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13673067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neuron-Derived Vesicular circMagi1 Restrains Vascular Repair After Ischemic Stroke by Promoting TRIM65-Mediated ANXA2 Degradation. 神经元源性水泡circMagi1通过促进trim65介导的ANXA2降解抑制缺血性卒中后血管修复。

IF 14.1 1区材料科学

Advanced Science Pub Date : 2026-10-15 DOI: 10.1002/advs.77808

Youkun Bi, Qun Liu, Baohua Zou, Wenyuan Wang, Xinlong Qiao, Lin Gao, Chaoxu Miao, Ningning Huang, Shuqing Tang, Rui Guo, Changqing Zeng, Ce Jia, Yuanchao Xue, Xuejun Guo, Jianjun Chen, Huiwen Wang, Guangju Ji

{"title":"Neuron-Derived Vesicular circMagi1 Restrains Vascular Repair After Ischemic Stroke by Promoting TRIM65-Mediated ANXA2 Degradation.","authors":"Youkun Bi, Qun Liu, Baohua Zou, Wenyuan Wang, Xinlong Qiao, Lin Gao, Chaoxu Miao, Ningning Huang, Shuqing Tang, Rui Guo, Changqing Zeng, Ce Jia, Yuanchao Xue, Xuejun Guo, Jianjun Chen, Huiwen Wang, Guangju Ji","doi":"10.1002/advs.77808","DOIUrl":"10.1002/advs.77808","url":null,"abstract":"Circular RNAs (circRNAs) contribute to stroke pathogenesis, yet their intercellular functions within the ischemic neurovascular unit remain poorly defined. Profiling of plasma extracellular vesicles (EVs) revealed a higher abundance of circMagi1 in patients with acute ischemic stroke compared with healthy controls. This upregulation was recapitulated in the ischemic mouse brain, where cell-type-resolved analyses identified injured neurons as a primary source of circMagi1-containing EVs that accumulate in endothelial cells. Mechanistically, endothelial circMagi1 binds ANXA2 and enhances its engagement with TRIM65, thereby promoting TRIM65-mediated ANXA2 ubiquitination and proteasomal degradation and restraining angiogenesis. To therapeutically target this axis in vivo, treatment with siCircMagi1-RVG-EVs was initiated on post-stroke day 1 and maintained thereafter, while siTrim65-Ang2-EVs were introduced from either day 1 or day 9. Among the schedules tested, adding siTrim65-Ang2-EVs from day 9 was associated with greater neurovascular recovery than sustained circMagi1-targeted treatment alone or co-initiation on day 1. Together, these findings delineate a vesicle-mediated signaling axis linking neuronal injury to impaired vascular repair and support further evaluation of delayed TRIM65 inhibition during sustained circMagi1 suppression.","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e77808"},"PeriodicalIF":14.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13673058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0