Nature Communications最新文献_第10页

Triple-effect correction for Cell Painting data with contrastive and domain-adversarial learning 基于对比和领域对抗学习的细胞绘画数据的三效校正

IF 16.6 1区综合性期刊

Nature Communications Pub Date : 2025-07-25 DOI: 10.1038/s41467-025-62193-z

Chengwei Yan, Yu Zhang, Jiuxin Feng, Heyang Hua, Zhihan Ruan, Zhen Li, Siyu Li, Chaoyang Yan, Pingjing Li, Jian Liu, Shengquan Chen

{"title":"Triple-effect correction for Cell Painting data with contrastive and domain-adversarial learning","authors":"Chengwei Yan, Yu Zhang, Jiuxin Feng, Heyang Hua, Zhihan Ruan, Zhen Li, Siyu Li, Chaoyang Yan, Pingjing Li, Jian Liu, Shengquan Chen","doi":"10.1038/s41467-025-62193-z","DOIUrl":"https://doi.org/10.1038/s41467-025-62193-z","url":null,"abstract":"Cell Painting (CP), as a high-throughput imaging technology, generates extensive cell-stained imaging data, providing unique morphological insights for biological research. However, CP data contains three types of technical effects, referred to as triple effects, including batch effects, gradient-influenced row and column effects (well-position effects). The interaction of various technical effects can obscure true biological signals and complicate the characterization of CP data, making correction essential for reliable analysis. Here, we propose cpDistiller, a triple-effect correction method specially designed for CP data, which leverages a pre-trained segmentation model coupled with a semi-supervised Gaussian mixture variational autoencoder utilizing contrastive and domain-adversarial learning. Through extensive qualitative and quantitative experiments across various CP profiles, we demonstrate that cpDistiller effectively corrects triple effects, especially well-position effects, while preserving cellular heterogeneity. Moreover, cpDistiller effectively captures system-level phenotypic responses to genetic perturbations and reliably infers gene functions and interactions both when combined with scRNA-seq data and independently. cpDistiller also demonstrates promising capability for identifying gene and compound targets, highlighting its potential utility in drug discovery and broader biological research.","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"2 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144710671","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}

引用次数: 0

Biomarkers of pediatric Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis through single-cell transcriptomics 通过单细胞转录组学研究儿童爱泼斯坦-巴尔病毒相关的噬血细胞淋巴组织细胞病的生物标志物

IF 16.6 1区综合性期刊

Nature Communications Pub Date : 2025-07-25 DOI: 10.1038/s41467-025-62090-5

Jie Shen, Yunyan He, Hong Zheng, Jianwen Xiao, Fu Li, Keke Chen, Biyun Guo, Yulei He, Lin Liu, Zhi Lin, Dan Wang, Leping Liu, Shengfeng Wang, Wen Zhou, Yingchi Zhang, Jian Wei, Yunchu Wang, Rong Hu, Daolin Tang, Dao Wang, Minghua Yang

{"title":"Biomarkers of pediatric Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis through single-cell transcriptomics","authors":"Jie Shen, Yunyan He, Hong Zheng, Jianwen Xiao, Fu Li, Keke Chen, Biyun Guo, Yulei He, Lin Liu, Zhi Lin, Dan Wang, Leping Liu, Shengfeng Wang, Wen Zhou, Yingchi Zhang, Jian Wei, Yunchu Wang, Rong Hu, Daolin Tang, Dao Wang, Minghua Yang","doi":"10.1038/s41467-025-62090-5","DOIUrl":"https://doi.org/10.1038/s41467-025-62090-5","url":null,"abstract":"Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis (EBV-HLH) is a fatal hyperinflammatory disorder distinct from self-limiting EBV-induced infectious mononucleosis (IM). However, the immunological mechanisms underlying the divergence between benign EBV infection and fulminant HLH—particularly in the absence of inherited immunodeficiency—remains unclear, and systematic comparisons of immune landscapes across EBV-associated disease spectra are lacking. In this study, by enrolling children with IM and healthy volunteers as controls, we utilize single-cell RNA sequencing to identify unique immunological characteristics of EBV-HLH. Our analysis indicates that patients with EBV-HLH exhibite widespread activation of NF-κB signaling pathway. Furthermore, excessive cytokine secretion by T and NK cells is observed, along with a shift in monocyte differentiation towards an inflammatory phenotype, and the aggregation of IDO1+ monocytes. Metabolic pathway analysis reveals that L-kynurenine, a downstream metabolite of IDO1, is specifically elevated in EBV-HLH and mediates the production of multiple pro-inflammatory cytokines. Collectively, our study maps the immune landscape in pediatric EBV-HLH at single-cell resolution, uncovering potential role of IDO1+ monocytes and L-kynurenine as biomarkers.","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"64 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144710858","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}

引用次数: 0

Arbovirus suppression of a lectin protein-mediated broad-spectrum resistance enhances herbivorous vector performance and viral transmission 虫媒病毒抑制凝集素蛋白介导的广谱抗性增强了草食性载体的性能和病毒传播

IF 16.6 1区综合性期刊

Nature Communications Pub Date : 2025-07-25 DOI: 10.1038/s41467-025-62233-8

Zihang Yang, Wei Wu, Zhongtian Xu, Yanjun Li, Hehong Zhang, Lulu Li, Jianping Chen, Bingjian Sun, Zongtao Sun

引用次数: 0

Tumour initiated purinergic signalling promotes cardiomyocyte RBFOX1 degradation and cardiotoxicity from DNA damaging anticancer agents 肿瘤引发的嘌呤能信号传导促进心肌细胞RBFOX1降解和DNA损伤抗癌药物的心脏毒性

IF 16.6 1区综合性期刊

Nature Communications Pub Date : 2025-07-25 DOI: 10.1038/s41467-025-62172-4

Saymon Tejay, Maria Areli Lorenzana-Carrillo, Guocheng Huang, Seyed Amirhossein Tabatabaei Dakhili, Yuan -Yuan Zhao, Farah Eaton, Michelle Mendiola Pla, Dawn E. Bowles, Adam Kinnaird, D. Ian Paterson, Edith Pituskin, John R. Ussher, Evangelos D. Michelakis, Gopinath Sutendra

{"title":"Tumour initiated purinergic signalling promotes cardiomyocyte RBFOX1 degradation and cardiotoxicity from DNA damaging anticancer agents","authors":"Saymon Tejay, Maria Areli Lorenzana-Carrillo, Guocheng Huang, Seyed Amirhossein Tabatabaei Dakhili, Yuan -Yuan Zhao, Farah Eaton, Michelle Mendiola Pla, Dawn E. Bowles, Adam Kinnaird, D. Ian Paterson, Edith Pituskin, John R. Ussher, Evangelos D. Michelakis, Gopinath Sutendra","doi":"10.1038/s41467-025-62172-4","DOIUrl":"https://doi.org/10.1038/s41467-025-62172-4","url":null,"abstract":"It is well established tumour cells secrete signalling factors affecting distant normal tissues. What remains unresolved is whether these factors initiate a signalling cascade rendering terminally differentiated cardiomyocytes susceptible to apoptosis, a feature of chemotherapy-induced cardiotoxicity (CIC). Here we show in MANTICORE trial cancer patients, cumulative baseline plasma levels of the nucleoside inosine and its derivative hypoxanthine predict cardiotoxicity. We found the Zn2+ finger transcription factor ZNF281 increases synthesis and release of inosine and hypoxanthine, which bind the A2A receptor on cardiomyocytes, activating CAMKIIδ which phosphorylates the postnatal mRNA splicing factor RBFOX1, resulting in its caspase-dependent degradation. RBFOX1 loss reverts cardiomyocytes to a less mature state with open chromatin and susceptibility to DNA damage, apoptosis or CIC, when treated with DNA intercalating or alkylating anticancer agents. These findings suggest cumulative inosine and hypoxanthine levels may be a biomarker predicting patient susceptibility to DNA damaging anti-cancer agents.","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"214 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144701573","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}

引用次数: 0

Identifying fibroblast-derived sFRP2 as a therapeutic target and engineering siRNA therapy for uterine scarring 鉴定成纤维细胞来源的sFRP2作为治疗靶点和工程siRNA治疗子宫瘢痕

IF 16.6 1区综合性期刊

Nature Communications Pub Date : 2025-07-25 DOI: 10.1038/s41467-025-62248-1

Juan Cheng, Siqi Zhang, Qian Gui, Zedan Pu, Zhiyu Chen, Quanfang Wei, Hongbo Qi, Jianxiang Zhang

{"title":"Identifying fibroblast-derived sFRP2 as a therapeutic target and engineering siRNA therapy for uterine scarring","authors":"Juan Cheng, Siqi Zhang, Qian Gui, Zedan Pu, Zhiyu Chen, Quanfang Wei, Hongbo Qi, Jianxiang Zhang","doi":"10.1038/s41467-025-62248-1","DOIUrl":"https://doi.org/10.1038/s41467-025-62248-1","url":null,"abstract":"Uterine scarring is a common complication following uterine injury, characterized by abnormal wound healing in the endometrial or myometrial tissue. However, the underlying mechanisms contributing to scar formation remain unclear, impeding the development of effective drugs for uterine scarring. Here, we identify that secreted frizzled-related protein 2 (sFRP2) is highly expressed in human and mouse uterine tissues with uterine scarring, particularly in uterine fibroblasts. Using female mouse models, we demonstrate that sFRP2 overexpression in the healthy uterus induces uterine scarring features and exacerbates surgery-induced fibrosis, while sFRP2 knockdown inhibits uterine scarring development and fibrotic transformation in uterine fibroblasts, highlighting the pivotal role of sFRP2 as an initiating driver in uterine scarring pathogenesis. Mechanistically, sFRP2 promotes uterine scar formation by activating the non-canonical Wnt signaling pathway and calcium influx in uterine fibroblasts. Additionally, therapeutic potential of targeting sFRP2 is demonstrated by developing siRNA against sFRP2 and engineering a lipid nanoparticle delivery system. The siRNA therapy effectively suppresses sFRP2 expression, reduces uterine scar formation, and improves pregnancy outcomes in female mice, underscoring the therapeutic potential of sFRP2 as a promising target for the prophylactic treatment of uterine scarring.","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"278 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144701575","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}

引用次数: 0

Enantioselective synthesis of chiral 2,3-cis-disubstituted piperidines and C1-substituted tetrahydroisoquinolines by asymmetric Cu-catalyzed cyclizative aminoboration 不对称铜催化环化氨基化反应对映选择性合成手性2,3-顺式二取代哌啶和c1取代四氢异喹啉

IF 16.6 1区综合性期刊

Nature Communications Pub Date : 2025-07-25 DOI: 10.1038/s41467-025-61736-8

Dazhuang Zhang, He Yang, Qinghai Zhou, Wenjun Tang

{"title":"Enantioselective synthesis of chiral 2,3-cis-disubstituted piperidines and C1-substituted tetrahydroisoquinolines by asymmetric Cu-catalyzed cyclizative aminoboration","authors":"Dazhuang Zhang, He Yang, Qinghai Zhou, Wenjun Tang","doi":"10.1038/s41467-025-61736-8","DOIUrl":"https://doi.org/10.1038/s41467-025-61736-8","url":null,"abstract":"Chiral N-heterocycles such as piperidines and tetrahydroisoquinolines are privileged structural motifs in drug discovery and pharmaceutical industry. The development of efficient and practical asymmetric synthetic methods towards pharmaceutically important chiral N-heterocycles constitutes an important subject in synthetic chemistry. Asymmetric synthesis of 2,3-cis-disubstituted piperidines bearing two consecutive chiral centers is particularly challenging in terms of both diastereoselective and enantioselective control. In this work, a regiospecific and enantioselective cyclizative aminoboration is designed to tackle this problem by employing Cu/(S, S)-Ph-BPE as the chiral catalyst, leading to a series of 2,3-cis-disubstituted piperidines as well as C1-substituted tetrahydroisoquinolines in moderate to good yields and excellent enantioselectivities. The asymmetric six-membered ring-closing aminoboration features a broad substrate scope, mild reaction conditions, and excellent functional group compatibility. DFT calculation reveals the importance of noncovalent interactions between substrate and Cu catalyst in controlling the enantioselectivity. The synthetic utility and practicality of this cyclization protocol have been exemplified by the synthesis of the key chiral intermediates of avacopan and L-733,060.","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"23 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144701814","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}

引用次数: 0

Impact of the COVID-19 pandemic on incident diagnoses in German refugee centres 2018 to 2023 2019冠状病毒病大流行对2018年至2023年德国难民中心事件诊断的影响

IF 16.6 1区综合性期刊

Nature Communications Pub Date : 2025-07-24 DOI: 10.1038/s41467-025-61876-x

Kayvan Bozorgmehr, Stella Erdmann, Sven Rohleder, Rosa Jahn

{"title":"Impact of the COVID-19 pandemic on incident diagnoses in German refugee centres 2018 to 2023","authors":"Kayvan Bozorgmehr, Stella Erdmann, Sven Rohleder, Rosa Jahn","doi":"10.1038/s41467-025-61876-x","DOIUrl":"https://doi.org/10.1038/s41467-025-61876-x","url":null,"abstract":"The COVID-19 pandemic may have affected morbidity patterns of residents in refugee centres, but empirical evidence is scarce. We utilised linked data from a health surveillance network in refugee centres of three German federal states, employing a quasi-experimental design to examine the effects of the COVID-19 pandemic on newly diagnosed medical conditions. Doctors coded routine diagnoses on-site in healthcare facilities for refugee patients. Our analysis encompasses the timeframe from October 2018 to April 2023 and includes individual-level data for 109,175 refugees. This data resulted in 76,289 patient-months across 21 refugee centres, with a total occupancy of 144,012 person-months. Here, we employ segmented regression analyses, adjusting for time trends, socio-demographic factors, occupancy, and centre characteristics, to evaluate the COVID-19 pandemic’s impact on incident diagnosis patterns among refugees. We show how the COVID-19 pandemic altered diagnosis patterns among refugees in German centres. Notably, incidents of injuries, mental disorders, psychotherapeutic drug prescriptions, and genitourinary diseases rose, while respiratory diseases decreased, later rebounding. An increase in injury-related diagnoses suggests heightened violence experiences during flight or in centres. Mental disorder diagnoses and psychotherapeutic drug prescriptions rose, reflecting pandemic-related stressors and the pandemic’s multifaceted impact on refugee health.","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"706 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144693690","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}

引用次数: 0

Impairing the interaction between Erg11 and cytochrome P450 reductase Ncp1 enhances azoles’ antifungal activities 破坏Erg11与细胞色素P450还原酶Ncp1的相互作用可增强唑类药物的抗真菌活性

IF 16.6 1区综合性期刊

Nature Communications Pub Date : 2025-07-24 DOI: 10.1038/s41467-025-62131-z

Wanqian Li, Malcolm Whiteway, Sijin Hang, Jinhua Yu, Hui Lu, Yuanying Jiang

引用次数: 0

UCP2 inhibition eliminates pancreatic β cell autoinflammation in T2DM with islet-mitochondrial sequential targeting nanomedicines 利用胰岛-线粒体序列靶向纳米药物抑制UCP2可消除T2DM患者胰腺β细胞自身炎症

IF 16.6 1区综合性期刊

Nature Communications Pub Date : 2025-07-24 DOI: 10.1038/s41467-025-61883-y

Zerun Liu, Wensheng Chen, Jinping Zhang, Ting Huang, Ying Hong, Tianjiao Zhao, Min Liu, Qiaohui Chen, Yongqi Yang, Shuya Wang, Jue Wang, Xiaohong Ying, Yiming Li, Qiong Huang, Kelong Ai

{"title":"UCP2 inhibition eliminates pancreatic β cell autoinflammation in T2DM with islet-mitochondrial sequential targeting nanomedicines","authors":"Zerun Liu, Wensheng Chen, Jinping Zhang, Ting Huang, Ying Hong, Tianjiao Zhao, Min Liu, Qiaohui Chen, Yongqi Yang, Shuya Wang, Jue Wang, Xiaohong Ying, Yiming Li, Qiong Huang, Kelong Ai","doi":"10.1038/s41467-025-61883-y","DOIUrl":"https://doi.org/10.1038/s41467-025-61883-y","url":null,"abstract":"Pancreatic β-cell dysfunction and mass loss are core pathologies of type 2 diabetes mellitus (T2DM), which are closely related to intense autoinflammation. However, the molecular mechanisms regulating β-cell autoinflammation remain unclear. Here, we show that STING is significantly elevated in T2DM β cells. We also clarify the key role of uncoupling protein 2 (UCP2), and reveal that interleukin-1β (IL-1β) drives β cells to produce autoinflammation through the UCP2/mtDNA/STING axis in T2DM. To inhibit UCP2 activity in vivo, we design a tailored nanomedicine, Mito-G, with sequential targeting from islets to β-cell mitochondria. Mito-G is a negatively charged ultra-small nanomedicine synthesized by polymerization of genipin (a potent UCP2 inhibitor) and glycine. It can specifically reach β cells and have a natural mitochondrial targeting. In this work, Mito-G effectively eliminates β-cell auto-inflammation by specifically inhibiting β-cell UCP2 activity in vivo, providing a paradigm for targeting autoinflammation of β cells to treat T2DM.","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"182 1","pages":"6840"},"PeriodicalIF":16.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144701625","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}

引用次数: 0

PEAK1 maintains tight junctions in intestinal epithelial cells and resists colitis by inhibiting autophagy-mediated ZO-1 degradation PEAK1维持肠上皮细胞的紧密连接，并通过抑制自噬介导的ZO-1降解来抵抗结肠炎

IF 16.6 1区综合性期刊

Nature Communications Pub Date : 2025-07-24 DOI: 10.1038/s41467-025-62107-z

Zaikuan Zhang, Yajun Xie, Qiying Yi, Jianing Liu, Lin Yang, Runzhi Wang, Jing Cai, Xinyi Li, Xiaosong Feng, Shixiang Yao, Zheng Pan, Magdalena Paolino, Qin Zhou

{"title":"PEAK1 maintains tight junctions in intestinal epithelial cells and resists colitis by inhibiting autophagy-mediated ZO-1 degradation","authors":"Zaikuan Zhang, Yajun Xie, Qiying Yi, Jianing Liu, Lin Yang, Runzhi Wang, Jing Cai, Xinyi Li, Xiaosong Feng, Shixiang Yao, Zheng Pan, Magdalena Paolino, Qin Zhou","doi":"10.1038/s41467-025-62107-z","DOIUrl":"https://doi.org/10.1038/s41467-025-62107-z","url":null,"abstract":"Tight junctions are crucial for maintaining intestinal barrier homeostasis, but how organisms modulate these junctions remain unclear. Here, we show a role for PEAK1 at cell-cell contact sites, where it interacts with ZO-1 via a conserved region spanning amino acids 714-731. This interaction masks the LC3-interacting region on ZO-1, preventing autophagy-mediated ZO-1 degradation and preserving the integrity of tight junctions in intestinal epithelial cells. Src-mediated phosphorylation of PEAK1 at Y724 promotes the binding between PEAK1 and ZO-1 to stabilize ZO-1 in intestinal epithelial cells. Additionally, PEAK1 binds to CSK to positively regulate Src activity. Loss of PEAK1 in intestinal epithelial cells leads to decreased Src activity and lower ZO-1 protein levels, resulting in disrupted tight junctions, both in vitro and in vivo. In mice, Peak1 deficiency increases intestinal epithelium permeability and exacerbates inflammation in experimentally induced colitis models. Our findings reveal PEAK1’s critical role in maintaining tight junction integrity and resistance to intestinal inflammation, extending its known function from promoting tumor cell proliferation and migration to essential physiological processes. These insights refine our understanding of the mechanisms regulating tight junctions and offer potential therapeutic targets for enhancing epithelial barrier function and treating related diseases.","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"18 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144693687","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}

引用次数: 0