Advanced Science最新文献

{"title":"Responsive Open Microfluidic Logic for Mechanical Computing (Adv. Sci. 57/2026)","authors":"Roi Almog,&nbsp;Bat-El Pinchasik","doi":"10.1002/advs.77825","DOIUrl":"https://doi.org/10.1002/advs.77825","url":null,"abstract":"<p><b>Responsive Open Microfluidic Logic</b></p><p>This study integrates logic operations into open microfluidic systems driven by capillary flow. Using elasto-capillary coupling, geometric constraints, and responsive soft materials, the platform performs fundamental logic operations and more complex computations without external pumps. The approach enables programmable fluid handling and provides a foundation for responsive microfluidic systems, autonomous reaction control, and mechano-fluidic computing. More details can be found in the Research Article by Roi Almog and Bat-El Pinchasik (DOI: 10.1002/advs.77546).\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 57","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/advs.77825","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149177083","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}

{"title":"A Novel tRNA Half mt-5’-tiRNA-Tyr Promotes Colorectal Cancer Proliferation via Inducing HARS2 Succinylation (Adv. Sci. 57/2026)","authors":"Xinliang Gu,&nbsp;Danping Zhu,&nbsp;Xinwei Liu,&nbsp;Shangshang Hu,&nbsp;Xincheng Yang,&nbsp;Junjie Nie,&nbsp;Tao Xu,&nbsp;Yuqin Pan,&nbsp;Mu Xu,&nbsp;Huiling Sun,&nbsp;Shukui Wang","doi":"10.1002/advs.77826","DOIUrl":"https://doi.org/10.1002/advs.77826","url":null,"abstract":"<p><b>Colorectal Cancer</b></p><p>A glowing mitochondrial tRNA half awakens a blue-green mitochondrial landscape by associating with HARS2 and promoting its succinylation. Suppressed mitochondrial translation, coupled with enhanced metabolic activity, fuels malignant colorectal growth. More details can be found in the Research Article by Mu Xu, Huiling Sun, Shukui Wang, and co-workers (DOI: 10.1002/advs.77042).\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 57","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/advs.77826","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149177093","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}

{"title":"Issue Information: (Adv. Sci. 57/2026)","authors":"","doi":"10.1002/advs.77827","DOIUrl":"https://doi.org/10.1002/advs.77827","url":null,"abstract":"","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 57","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/advs.77827","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149177406","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}

{"title":"Rewiring Pyroptosis to Potentiate Cancer Immunotherapy via a Gasdermin D Agonist Bypassing Caspase-3","authors":"Dan Zhao,&nbsp;Lingling Zhang,&nbsp;Yue Wen,&nbsp;Lianghui Cheng,&nbsp;Sidan Tian,&nbsp;Fanling Meng,&nbsp;Liang Luo","doi":"10.1002/advs.76655","DOIUrl":"10.1002/advs.76655","url":null,"abstract":"<p>Pyroptosis holds great promise for evoking robust anti-tumor immunity, but many pyroptosis induction strategies rely on caspase-3 (Casp-3) activation and face challenges of the immunosuppressive nature of apoptosis and the frequent silencing of gasdermin E (GSDME), a substrate of Casp-3, in tumors. Here, we report a strategy to rewire the pyroptotic pathway by bypassing Casp-3 to directly activate gasdermin D (GSDMD). We identify a small-molecule agonist, (E)-2,3-diiodobut-2-ene-1,4-diol (DIBDO), which undergoes deiodination to release iodide ions upon activation by the tumor-abundant nucleophile glutathione, thereby catalytically generating singlet oxygen and molecular iodine. This cascade induces oxidative damage that downregulates key mediators of caspase-9 and caspase-8 pathways, thereby down-regulating Casp-3 activation. This mechanism selectively triggers GSDMD-mediated pyroptosis, provoking robust immunogenic cell death and inflammatory cytokine release to reconfigure the tumor immune microenvironment. In murine tumor models, DIBDO enhances tumor infiltration of cytotoxic T cells and synergizes with checkpoint blockade therapy to suppress both primary and distal tumors. It can also serve as an in situ or exogenous vaccine to elicit potent and durable antitumor immunity. This work presents a paradigm-shifting approach to cancer immunotherapy by decoupling pyroptosis from Casp-3 dependence, offering a promising avenue to expand the scope of immunogenic cell death-based treatments.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 57","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13393277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148560298","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}

{"title":"Loss of Intestinal MSTN Promotes GLP-1 Secretion Through SGLT1 Palmitoylation.","authors":"Sheng-Zhong Han, Shuang-Yan Chang, Zhaobo Luo, Ke Sun, Biaohu Quan, Yanqiu Lv, Zhouyan Li, Xinyue Liu, Sitong Lv, Meifu Xuan, Xiaoyufan Xu, Xue Fang, Hang Chang, Rihuan Zhang, Xi-Jun Yin, Lin-Hu Quan, Jin-Dan Kang","doi":"10.1002/advs.78302","DOIUrl":"10.1002/advs.78302","url":null,"abstract":"<p><p>Intestinal glucagon-like peptide-1 (GLP-1) is secreted by intestinal L cells in a glucose-dependent manner. The localization and surface abundance of glucose-sensing proteins on the cell membrane affect the response to glucose, but the regulatory mechanism remains poorly understood. Here, we show that S-palmitoylation is required for stable plasma membrane enrichment of SGLT1 and for SGLT1-mediated GLP-1 secretion. Notably, myostatin (MSTN) was identified as a key upstream regulator of this modification. Intestinal MSTN deficiency markedly enhanced SGLT1 palmitoylation, increased its plasma membrane abundance, and thereby promoted glucose-stimulated GLP-1 secretion. Importantly, simvastatin induced intestinal MSTN upregulation and impaired glucose homeostasis, whereas MSTN deficiency largely alleviated these effects. Mechanistically, MSTN regulated the expression of the palmitoyl acyltransferase ZDHHC20, which catalyzed SGLT1 S-palmitoylation at Cys301. Blocking SGLT1 palmitoylation attenuated SGLT1 membrane enrichment and markedly suppressed the induction of GLP-1 secretion caused by MSTN deficiency. Collectively, our research results have revealed a new mechanism by which MSTN regulates intestinal endocrine function and S-palmitoylation modification promotes GLP-1 secretion, providing potential targets for regulating endogenous GLP-1 secretion in the intestine and treating metabolic diseases related to glucose imbalance.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78302"},"PeriodicalIF":14.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178128","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}

{"title":"PDHA1 Hyperactivation-Mediated Glucose Metabolism Reprogramming Fuels Neutrophil NETosis and Promotes Acute Lung Injury.","authors":"Yu-Biao Liu, Wen-Jing Zhong, Chen-Yu Zhang, Meng-Rui Chen, Nan-Shi-Yu Yang, Han-Xi Sha, Yan-Ling Qiu, Hui Chen, Jin-Tong Yang, Li-Ying Liang, Jian-Bing Xiong, Shao-Kun Liu, Cha-Xiang Guan, Jia-Xi Duan, Yong Zhou","doi":"10.1002/advs.78307","DOIUrl":"10.1002/advs.78307","url":null,"abstract":"<p><p>Neutrophil extracellular trap (NET) formation, termed NETosis, is a key driver of lung tissue injury in acute lung injury/acute respiratory distress syndrome (ALI/ARDS). However, the precise mechanisms that trigger neutrophil NETosis remain incompletely understood. Here, we observed that neutrophils from both ALI mice and ARDS patients exhibited NETosis alongside a pronounced selective metabolic shift, characterized by enhanced oxidative phosphorylation (OXPHOS) and attenuated glycolytic activity. Phosphoproteomic profiling revealed that this shift was driven by aberrant activation of pyruvate dehydrogenase E1 subunit alpha (PDHA1), resulting from its dephosphorylation at Ser293. Inhibiting PDHA1 activity, using either the inhibitor 3-fluoropyruvate (3-FP) or genetic knockdown, effectively reversed this selective metabolic reprogramming and suppressed NETosis. We further constructed neutrophil-targeted 3-FP-loaded albumin nanoparticles (3-FP-BSA NPs). These nanoparticles were specifically taken up by activated neutrophils, markedly inhibited NETosis, and alleviated lipopolysaccharide-induced ALI in mice. Mechanistically, RNA-seq revealed the enrichment of the AMPK in neutrophils during NETosis. AMPK phosphorylated PDHA1 at Ser314, which disrupted the PDHA1-pyruvate dehydrogenase kinase 1 (PDK1) interaction and inhibited PDHA1 phosphorylation at Ser293. Ultimately, PDHA1 hyperactivation-driven selective metabolic reprogramming precipitated mitochondrial stress and mtROS accumulation, thereby initiating NETosis. This study defines a targetable metabolic pathway in neutrophils and advances a specific PDHA1-nanotherapeutic strategy against ALI/ARDS.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78307"},"PeriodicalIF":14.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669207/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178147","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}

{"title":"Freestanding PZT Films for Integrated Wearable Sensing and Intelligent Acoustic Recognition.","authors":"Hailong Pan, Zhichao Xu, Rongxiao Liu, Jianmei Pei, Changhong Yang, Shifeng Huang, Michael Wübbenhorst","doi":"10.1002/advs.78091","DOIUrl":"10.1002/advs.78091","url":null,"abstract":"<p><p>Flexible, self-powered sensors are pivotal for next-generation human-machine interfaces. However, substrate-induced clamping fundamentally restricts their electromechanical performance by suppressing longitudinal deformation, thereby reducing signal sensitivity. Here, we report a high-performance freestanding PbZr_0.52Ti_0.48O₃ (PZT) thin film based on a layered Mica/Pt/LaNiO₃ heterostructure. The complete release of substrate constraints unlocks markedly enhanced properties, including a 1.4-fold increase in remanent polarization (P_r = 54 vs. 40 µC cm^- ²), a 2.2-fold enhancement in the effective converse piezoelectric coefficient (d₃₃ = 390 pm V^-1 vs. 174 pm V^-1), and an approximate 1.5-fold improvement in dielectric permittivity. Consequently, the device exhibits rapid electromechanical transduction with an ultrashort pulse duration of 500 µs, alongside high output voltage and power. Integrated onto the human body, the sensor delivers sensitive, repeatable responses to various biomechanical motions. Beyond tactile sensing, the device enables high-fidelity acoustic detection and intelligent signal analysis. By implementing harmonic evaluation and principal component analysis, the system achieves reliable discrimination among musical instruments with distinctive spectral fingerprints. Collectively, this work establishes the freestanding PZT film as a multifunctional platform integrating energy harvesting and intelligent acoustic recognition, offering new pathways for self-powered biointegrated electronics.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78091"},"PeriodicalIF":14.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13668060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178166","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}

{"title":"Hyperpolarization of [1-13C]Ketoisocaproate-d2 by Reversible Exchange with Parahydrogen Enables Profiling of Branched-Chain-Amino-Acid Metabolism in Cellulo and in Vivo","authors":"Stefan Petersen,&nbsp;Philipp R. Groß,&nbsp;Paul M. Schmidt,&nbsp;Henri de Maissin,&nbsp;Asitan Rittinger,&nbsp;Robert Willing,&nbsp;Adriana Sacristán-Martín,&nbsp;Lisa Heß,&nbsp;Jule Koch,&nbsp;Sebastian Lucas,&nbsp;Maxim Zaitsev,&nbsp;Dominik von Elverfeldt,&nbsp;Martin Grashei,&nbsp;Franz Schilling,&nbsp;Jan-Bernd Hövener,&nbsp;André F. Martins,&nbsp;Max von Delius,&nbsp;Thomas Reinheckel,&nbsp;Andreas B. Schmidt","doi":"10.1002/advs.76213","DOIUrl":"10.1002/advs.76213","url":null,"abstract":"<p>Hyperpolarized ¹³C magnetic resonance imaging (MRI) is the only method to image metabolic fluxes in real time, non-invasively, and in vivo. To date, however, most studies have used [1-¹³C]pyruvate and dynamic nuclear polarization (dDNP). Here, we establish efficient hyperpolarization (HP) of protio and partially-deuterated [1-¹³C]ketoisocaproate (KIC) using Spin-Lock-Induced-Crossing-Signal Amplification by Reversible Exchange (SLIC-SABRE), a high-throughput, uncomplex and low-cost method based on parahydrogen. We demonstrate ¹³C polarization up to ≈28% and T₁ relaxation times &gt; 200 s at 1 T in methanol-d₄. A rapid purification procedure allowed us to obtain biocompatible formulations with ≈11% ¹³C polarization at the time of injection, sufficient for in cellulo and in vivo studies. We found that branched-chain-amino-acid transaminase (BCAT) activity leads to HP [1-¹³C]leucine formation exclusively in BCAT1-high MDA-MB231 breast-cancer cells, but not in BCAT1-low MCF7 or PyB6 cells. In a proof-of-concept in vivo experiment, ¹³C magnetic resonance spectroscopy imaging of the healthy mouse brain detected [1-¹³C]leucine formation after intravenous injection of SABRE [1-¹³C]KIC-d₂. Our results demonstrate that [1-¹³C]KIC-d₂ provides a sensitive readout of BCAT1-dependent metabolism and that SLIC-SABRE can rapidly generate this probe for ¹³C MRI, extending accessible parahydrogen-based hyperpolarization to amino-acid pathways relevant to cancer biology and chemoresistance.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 57","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13336365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148300263","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}

{"title":"SOX5 Orchestrates Malignant Evolution via Promoter-Centric Chromatin Remodeling in MYC-Driven B-Cell Lymphoma","authors":"Yiyou Mao,&nbsp;Zhenyuan Jia,&nbsp;Xiao-Qin Mu,&nbsp;Ruilin Wang,&nbsp;Jianli Ma,&nbsp;Qingyuan Zhang,&nbsp;Yuwei Deng","doi":"10.1002/advs.76656","DOIUrl":"10.1002/advs.76656","url":null,"abstract":"<p>Early events that bias germinal-center B cells toward malignant evolution remain incompletely defined. Here, we uncover Sex-determining Region Y Box 5 (<i>SOX5</i>) as an early-stage epigenetic modifier in myelocytomatosis oncogene (<i>MYC</i>)-driven B-cell lymphoma. Single-cell transcriptomics of lymph nodes from CRISPR/Cas9-engineered <i>Myc^Cd19-Cre</i> B-cell lymphoma chimeric mice resolve a Ki67–high proliferative compartment at an early stage with enriched <i>SOX5</i> transcripts. CRISPRa, CRISPR knockout, and multi-omic profiling reveal a <i>SOX5</i>-centered chromatin program defined by de novo promoter-proximal occupancy coupled to contraction of promoter accessibility. Mechanistically, <i>SOX5</i> binding at the Proteolytic Signal-Containing Nuclear Protein (<i>PCNP</i>) promoter represses its transcription, thereby reducing apoptosis and alleviating G2/M arrest. Consequently, B-cell–targeted adeno-associated virus 6 (AAV6)-sh<i>SOX5</i> reduces Ki67-positive <i>PAX5</i>-positive malignant B cells and partially restores follicular architecture. Together, <i>SOX5</i>-mediated, promoter-centric repression of <i>PCNP</i> and other effectors installs and maintains an early-stage proliferative state in <i>MYC</i>-driven B-cell lymphoma, which nominates <i>SOX5</i>-directed intervention as a candidate therapeutic strategy for further investigation.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 57","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13379260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467833","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}

{"title":"Targeting Cannabinoid 1 Receptor in Macrophages Alleviates Psoriatic Skin Inflammation Through the AUF1-NLRP3 Axis.","authors":"Hongseo Choi, Sukyoung Han, Jinho Kim, Ji Hye Han, Eunsu Kim, Yeonjeong Heo, Minju Lee, Jooyoung Lee, Heerim You, Soyoun Lee, Su-Hee Han, Ilrok Yoon, Sung Anjeon, Hyerim Kang, Seungyeon Ryu, Hyun-Ji Park, Eunha Kim, Chul Hwan Bang, Ji Hyun Lee, Josephine M Egan, Jung-Woong Kim, Eun Kyung Lee, Wook Kim","doi":"10.1002/advs.78313","DOIUrl":"10.1002/advs.78313","url":null,"abstract":"<p><p>Psoriasis is a chronic inflammatory skin disease associated with systemic metabolic dysregulation; however, the molecular pathways linking metabolic signaling to skin inflammation remain poorly understood. Here, we identify cannabinoid 1 receptor (CB1R) in macrophages as a key immunometabolic regulator of psoriatic inflammation and a potential therapeutic target. CB1R expression was increased in macrophages infiltrating psoriatic lesional skin in both humans and mice, and both pharmacological inhibition and genetic deletion of CB1R markedly attenuated psoriasis-like pathology in mouse models by reducing epidermal hyperplasia, inflammation, and barrier dysfunction in a macrophage-dependent manner. Mechanistically, CB1R signaling in macrophages suppressed expression of the RNA-binding protein AUF1, leading to stabilization of Nlrp3 mRNA and enhanced NLRP3 inflammasome activation. AUF1 directly bound an AU-rich region within the Nlrp3 3' untranslated region and promoted mRNA destabilization, thereby limiting inflammasome activation and IL-1β production. Restoration of AUF1 expression, either by CB1R inhibition or overexpression, reduced NLRP3 levels and alleviated psoriasis-like pathology, whereas Nlrp3 deficiency abrogated these effects. Collectively, these findings define a CB1R-AUF1-NLRP3 signaling axis that links metabolic signaling to inflammasome-driven skin inflammation in macrophages. Targeting macrophage CB1R may therefore represent a promising therapeutic strategy for psoriasis and other immunometabolic inflammatory diseases.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78313"},"PeriodicalIF":14.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178039","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}