Nature Communications最新文献

{"title":"Effective extracellular payload release and immunomodulatory interactions govern the therapeutic effect of trastuzumab deruxtecan (T-DXd)","authors":"Li-Chung Tsao, John S. Wang, Xingru Ma, Sirajbir Sodhi, Joey V. Ragusa, Bushangqing Liu, Jason McBane, Tao Wang, Junping Wei, Cong-Xiao Liu, Xiao Yang, Gangjun Lei, Ivan Spasojevic, Ping Fan, Timothy N. Trotter, Michael Morse, Herbert Kim Lyerly, Zachary C. Hartman","doi":"10.1038/s41467-025-58266-8","DOIUrl":"https://doi.org/10.1038/s41467-025-58266-8","url":null,"abstract":"<p>Trastuzumab deruxtecan (T-DXd) is an antibody-drug conjugate (ADC) targeting HER2, exhibiting significant clinical efficacy in breast cancer (BC) with varying HER2 expression, including HER2-low and HER2-ultralow. However, the precise mechanism underlying its efficacy and the contribution of immune activation in these settings remain unclear. Here, we demonstrate that T-DXd efficacy in HER2-low and HER2-negative BC is independent of HER2 engagement and ADC internalization. Instead, its activity relies on extracellular proteases, such as cathepsin L (CTSL), within the tumor microenvironment. Irrespective of their HER2 status, tumor and stromal compartments of invasive BC abundantly express CTSL, which efficiently cleaves the specialized linker of T-DXd, facilitating payload release and inducing cytotoxicity against HER2-low/negative tumors. In HER2-positive BC, the antibody backbone of T-DXd engages Fcγ-receptors and drives antibody-dependent cellular phagocytosis (ADCP). Concurrently, its cytotoxic payload (DXd) induces immunogenic cell death, further activating myeloid cells via TLR4 and STING pathways to enhance tumor antigen presentation to CD8+ T cells. Notably, T-DXd cytotoxicity also upregulates tumor CD47 expression, dampening immune activation. Combining T-DXd with CD47 checkpoint blockade significantly enhances anti-tumor immune responses in a HER2-transgenic BC mouse model, while also inducing durable CD8+ T cell memory to prevent tumor recurrence after therapy cessation.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"102 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retrievable hydrogel networks with confined microalgae for efficient antibiotic degradation and enhanced stress tolerance","authors":"Minwen Jiang, Jie Zheng, Yi Tang, Hai Liu, Yawen Yao, Jianfei Zhou, Wei Lin, Yuan Ma, Jin Liu, Jiajing Zhou","doi":"10.1038/s41467-025-58415-z","DOIUrl":"https://doi.org/10.1038/s41467-025-58415-z","url":null,"abstract":"<p>Antibiotic contamination has emerged as a global challenge, increasing antibiotic resistance and threatening human health and ecosystems. Bioremediation using microorganism offers sustainable methods to degrade such pharmaceutical contaminants. However, these microorganisms exhibit reduced activity under high-stress conditions, and are difficult to recycle and potentially leak into environment as microbial pollutions. Here we report bioprinted retrievable microalgae hydrogel networks (MHNs) by confining living microalgae in double-network hydrogels, which achieves enhanced antibiotic degradation (&gt;99.3%) and recyclable ability. Particularly, coating MHN with tannic acid (MHN@TA) generates a semipermeable membrane to prevent the leakage of microalgae (&lt;0.7% for 7 days), ensuring the containment of potential microbial biohazards. The biohybrid system protects the biological activity of microalgae, enabling antibiotic degradation up to 400 mg L⁻¹. Free-standing MHN@TA fencing systems are also manufactured to demonstrate their practical applications. This study provides insights of microalgae-material interactions in bioremediation and offers design rationales for biohybrid systems.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"21 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Covalent adduct Grob fragmentation underlies LSD1 demethylase-specific inhibitor mechanism of action and resistance","authors":"Amanda L. Waterbury, Jonatan Caroli, Olivia Zhang, Paloma R. Tuttle, Chao Liu, Jiaming Li, Ji Sung Park, Samuel M. Hoenig, Marco Barone, Airi Furui, Andrea Mattevi, Brian B. Liau","doi":"10.1038/s41467-025-57477-3","DOIUrl":"https://doi.org/10.1038/s41467-025-57477-3","url":null,"abstract":"<p>Chromatin modifiers often work in concert with transcription factors (TFs) and other complex members, where they can serve both enzymatic and scaffolding functions. Due to this, active site inhibitors targeting chromatin modifiers may perturb both enzymatic and nonenzymatic functions. For instance, the antiproliferative effects of active-site inhibitors targeting lysine-specific histone demethylase 1A (LSD1) are driven by disruption of a protein-protein interaction with growth factor independence 1B (GFI1B) rather than inhibition of demethylase activity. Recently, next-generation precision LSD1 covalent inhibitors have been developed, which selectively block LSD1 enzyme activity by forming a compact <i>N</i>-formyl flavin adenine dinucleotide (FAD) adduct that spares the GFI1B interaction. However, the mechanism accounting for <i>N</i>-formyl-FAD formation remains unclear. Here we clarify the mechanism of these demethylase-specific inhibitors of LSD1, demonstrating that the covalent inhibitor-FAD adduct undergoes a Grob fragmentation. Using inhibitor analogs and structural biology, we identify structure-activity relationships that promote this transformation. Furthermore, we unveil an unusual drug resistance mechanism whereby distal active-site mutations can promote inhibitor-adduct Grob fragmentation even for previous generation compounds. Our study uncovers the unique Grob fragmentation underlying the mechanism of action of precision LSD1 enzyme inhibitors, offering insight into their reactivity with broader implications for drug resistance.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"34 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of tau neuronal internalization using anti-tau single domain antibodies","authors":"Clément Danis, Elian Dupré, Thomas Bouillet, Marine Denéchaud, Camille Lefebvre, Marine Nguyen, Justine Mortelecque, François-Xavier Cantrelle, Jean-Christophe Rain, Xavier Hanoulle, Morvane Colin, Luc Buée, Isabelle Landrieu","doi":"10.1038/s41467-025-58383-4","DOIUrl":"https://doi.org/10.1038/s41467-025-58383-4","url":null,"abstract":"<p>In Alzheimer’s disease, tau pathology spreads across brain regions as the disease progresses. Intracellular tau can be released and taken up by nearby neurons. We evaluated single domain anti-tau antibodies, also called VHHs, as inhibitors of tau internalization. We identified three VHH inhibitors of tau uptake: A31, H3-2, and Z70_mut1. These VHHs compete with the membrane protein LRP1, a major receptor mediating neuronal uptake of tau. A31 and Z70_mut1 bind to microtubule binding domain repeats, which are involved in the interaction with LRP1. VHH H3-2 is the only VHH from our library that reduces the internalization of both monomeric tau and tau fibrils. VHH H3-2 binds a C-terminal tau epitope with high affinity. Its three-dimensional structure in complex with a tau peptide reveals a unique binding mode as a VHH-swapped dimer. These anti-tau VHHs are interesting tools to study tau prion-like propagation in tauopathies and potentially develop novel biotherapies.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"4 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neoadjuvant Aumolertinib for unresectable stage III EGFR-mutant non-small cell lung cancer: a single-arm phase II trial","authors":"Dongliang Bian, Shuyu Ji, Yue Liu, Zhida Huang, Lei Jiang, Ming Liu, Xiao Bao, Jie Yang, Yirui Zhou, Junjie Hu, Liangdong Sun, Yingzhi Zheng, Jie Huang, Jing Liu, Xinsheng Zhu, Jing Zhang, Lele Zhang, Xiaogang Liu, Wenxin He, Dong Xie, Yuming Zhu, Chunyan Wu, Deping Zhao, Liang Duan, Gening Jiang, Peng Zhang","doi":"10.1038/s41467-025-58435-9","DOIUrl":"https://doi.org/10.1038/s41467-025-58435-9","url":null,"abstract":"<p>Aumolertinib, a third-generation epidermal growth factor receptor tyrosine kinase inhibitor (<i>EGFR</i>-TKI), is widely utilized for advanced <i>EGFR</i>-mutant non-small cell lung cancer patients (NSCLCm). This single-arm, phase II trial (NCT04685070) assessed the feasibility of neoadjuvant Aumolertinib for unresectable stage III NSCLCm. Fifty-six patients were enrolled, with 51 participants receiving neoadjuvant Aumolertinib (110 mg/day, orally) and forming the intention-to-treat population. The primary endpoint was objective response rate (ORR). Secondary endpoints included major pathological response (MPR) rate, pathological complete response (pCR) rate, complete (R0) resection rate, event-free survival (EFS), overall survival (OS), and treatment-related adverse events (TRAEs). The ORR was 70.6% (95% confidence interval: 58%-84%), meeting the pre-specified primary endpoint. Additionally, twenty-three (45.1%) participants converted into resectable disease and underwent surgery. Among them, R0 resection, MPR and pCR rates were 100%, 21.7%, and 13.0%, respectively. The median EFS and OS were not reached. While, the 1- and 2-year EFS rates were 88.2% and 58.8%, respectively. Fatigue (49.0%), alanine aminotransferase concentration elevation (39.2%), and rash (35.3%) were the most common treatment-related adverse events (TRAEs). Grade 3/4 TRAEs occurred in 5 patients (9.8%), and no grade 5 TRAE was recorded. RNA-sequencing based analysis revealed increased infiltration of CD8 + T-cells in post-treatment tumors compared to baseline, particularly in responsive and Ex19-Del mutation tumors. Collectively, neoadjuvant Aumolertinib showed promising efficacy and a surgical conversion rate with a tolerable safety profile for unresecable NSCLCm in stage III, potentially involved in the remodeling of tumor microenvironment.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"3 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143758583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural mimicry of UM171 and neomorphic cancer mutants co-opts E3 ligase KBTBD4 for HDAC1/2 recruitment","authors":"Zhuoyao Chen, Gamma Chi, Timea Balo, Xiangrong Chen, Beatriz Ralsi Montes, Steven C. Clifford, Vincenzo D’Angiolella, Timea Szabo, Arpad Kiss, Tibor Novak, András Herner, András Kotschy, Alex N. Bullock","doi":"10.1038/s41467-025-58350-z","DOIUrl":"https://doi.org/10.1038/s41467-025-58350-z","url":null,"abstract":"<p>Neomorphic mutations and drugs can elicit unanticipated effects that require mechanistic understanding to inform clinical practice. Recurrent indel mutations in the Kelch domain of the KBTBD4 E3 ligase rewire epigenetic programs for stemness in medulloblastoma by recruiting LSD1-CoREST-HDAC1/2 complexes as neo-substrates for ubiquitination and degradation. UM171, an investigational drug for haematopoietic stem cell transplantation, was found to degrade LSD1-CoREST-HDAC1/2 complexes in a wild-type KBTBD4-dependent manner, suggesting a potential common mode of action. Here, we identify that these neomorphic interactions are mediated by the HDAC deacetylase domain. Cryo-EM studies of both wild-type and mutant KBTBD4 capture 2:1 and 2:2 KBTBD4-HDAC2 complexes, as well as a 2:1:1 KBTBD4-HDAC2-CoREST1 complex, at resolutions spanning 2.7 to 3.3 Å. The mutant and drug-induced complexes adopt similar structural assemblies requiring both Kelch domains in the KBTBD4 dimer for each HDAC2 interaction. UM171 is identified as a bona fide molecular glue binding across the ternary interface. Most strikingly, the indel mutation reshapes the same surface of KBTBD4 providing an example of a natural mimic of a molecular glue. Together, the structures provide mechanistic understanding of neomorphic KBTBD4, while structure-activity relationship (SAR) analysis of UM171 reveals analog S234984 as a more potent molecular glue for future studies.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"32 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143758584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct ventral tegmental area neuronal ensembles are indispensable for reward-driven approach and stress-driven avoidance behaviors","authors":"Ioannis Koutlas, Lefkothea Patrikiou, Stef E. van der Starre, Diaz Danko, Inge G. Wolterink-Donselaar, Mieneke C. M. Luijendijk, Roger A. H. Adan, Frank J. Meye","doi":"10.1038/s41467-025-58384-3","DOIUrl":"https://doi.org/10.1038/s41467-025-58384-3","url":null,"abstract":"<p>Assigning valence to stimuli for adaptive behavior is an essential function, involving the ventral tegmental area (VTA). VTA cell types are often defined through neurotransmitters (NT). However, valence function in VTA does not parse along NT-boundaries as, within each NT-class, certain neurons are excited by reward and others by stressors. Here we identify, in male mice, the co-activated VTA neuronal ensembles for reward and stress, and determine their role in adaptive behaviors. We show that stimuli of opposite valence (opioid vs acute social stress) recruit two distinct VTA neuronal ensembles. These two ensembles continue to be preferentially engaged by congruent valence stimuli. Stimulation of VTA stress- or reward ensembles is aversive/reinforcing, respectively. Strikingly, external valence stimuli fully require activity of these small discrete VTA ensembles for conferring approach/avoidance outcomes. Overall, our study identifies distinct VTA ensembles for positive and negative valence coding and shows their indispensability for adaptive behavior.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"33 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143758578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Flexible intelligent microwave metasurface with shape-guided adaptive programming","authors":"Fan Li, Taisong Pan, Weihan Li, Zujun Peng, Dengji Guo, Xiang Jia, Taiqi Hu, Lingxiao Wang, Wei Wang, Min Gao, Guang Yao, Le Zuo, Mei Bi, Xiaolong Weng, Wenxuan Tang, Yuan Lin","doi":"10.1038/s41467-025-58249-9","DOIUrl":"https://doi.org/10.1038/s41467-025-58249-9","url":null,"abstract":"<p>Empowering the reconfigurable metasurfaces (RM) with the capability to be mechanically deformable highlights the possibility to manipulate the electromagnetic (EM) wave across arbitrary surfaces. Such ambition is hampered by the absence of adaptivity to shape variation in current programming strategies for RM. Herein, we present a flexible intelligent surface platform (FISP) as a solution to achieve flexible RM with highly stable performance under dynamic deformation. The geometry acquisition module in FISP enables real-time awareness of RM’s deformation with the conformal sensor array. By merging the actual shape of flexible RM into the input of the adaptive algorithm driven by the artificial neural network, the deformed flexible RM in FISP can be autonomously encoded by the bias voltage supply module to ensure robust performance under various deformation conditions. The versatility of FISP in manipulating EM waves is demonstrated by its applications in electromagnetic illusion, carpet cloaking, and data transmission, illustrating the prospects for seamlessly integrating flexible electronics and RM in the development of future EM metasurfaces.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"1 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A deep learning framework for instrument-to-instrument translation of solar observation data","authors":"R. Jarolim, A. M. Veronig, W. Pötzi, T. Podladchikova","doi":"10.1038/s41467-025-58391-4","DOIUrl":"https://doi.org/10.1038/s41467-025-58391-4","url":null,"abstract":"<p>The constant improvement of astronomical instrumentation provides the foundation for scientific discoveries. In general, these improvements have only implications forward in time, while previous observations do not benefit from this trend, and the joint use of data sets from different instruments is typically limited by differences in calibration and quality. We provide a deep learning framework for Instrument-To-Instrument translation of solar observation data, enabling homogenized data series of multi-instrument data sets. This is achieved by unpaired domain translations with Generative Adversarial Networks, which eliminate the need for spatial or temporal overlap to relate instruments. We demonstrate that the available data sets can directly profit from instrumental improvements, by applying our method to four different applications of ground- and space-based solar observations. We obtain a homogenized data series of 24 years of space-based observations of the solar EUV corona and line-of-sight magnetic field, solar full-disk observations with increased spatial resolution, real-time mitigation of atmospheric degradations in ground-based observations, and unsigned magnetic field estimates from the solar far-side based on EUV imagery. The direct comparison to simultaneous high-quality observations shows that our method produces images that are perceptually similar, and enables more homogeneous multi-instrument data sets without the requirement of spatial or temporal alignment.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"66 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cross-ancestry genome-wide association study identifies implications of SORL1 in cerebral beta-amyloid deposition","authors":"Jun Pyo Kim, Sang-Hyuk Jung, Beomjin Jang, Minyoung Cho, Minku Song, Jaeyoung Kim, Beomsu Kim, Hyunwoo Lee, Daeun Shin, Eun Hye Lee, Hyemin Jang, Bo-Hyun Kim, Hongki Ham, Dokyoon Kim, Towfique Raj, Carlos Cruchaga, Hee Jin Kim, Duk L. Na, Sang Won Seo, Hong-Hee Won","doi":"10.1038/s41467-025-57751-4","DOIUrl":"https://doi.org/10.1038/s41467-025-57751-4","url":null,"abstract":"<p>GWAS of Alzheimer’s disease have been predominantly based on European ancestry cohorts with clinically diagnosed patients. Increasing the ancestral diversity of GWAS and focusing on imaging brain biomarkers for Alzheimer’s disease may lead to the identification of new genetic loci. Here, we perform a GWAS on cerebral β-amyloid deposition measured by PET imaging in 3,885 East Asians and a cross-ancestry GWAS meta-analysis with data from 11,816 European participants. Our GWAS analysis replicates known loci (<i>APOE4</i>, <i>CR1</i>, and <i>FERMT2</i>) and identifies a novel locus near <i>SORL1</i> that is significantly associated with β-amyloid deposition. Single-nucleus expression analysis shows that <i>SORL1</i> is differentially expressed according to β-amyloid positivity in microglia. Our joint association analysis using the <i>SORL1</i> lead variant (rs76490923) and the <i>APOE4</i> allele demonstrates that the risk of β-amyloid deposition is reduced by up to 43.5% in <i>APOE4</i> non-carriers and up to 55.6% in <i>APOE4</i> carriers, according to the allelic dosage of the rs76490923 T allele. Our findings suggest that <i>SORL1</i> may play an important role in the pathogenesis of Alzheimer’s disease, particularly in relation to β-amyloid deposition.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"107 4 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143758582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}