EMBO Molecular Medicine最新文献

Author Correction: CITED2 is a druggable epigenetic switch coupling neuronal maturation to regenerative decline. 作者更正：CITED2是一种可药物化的表观遗传开关，将神经元成熟与再生衰退耦合在一起。

IF 8.3 1区医学

EMBO Molecular Medicine Pub Date : 2026-05-08 DOI: 10.1038/s44321-026-00442-4

Franziska Müller, Eilidh McLachlan, Ana Catarina Costa, Jia Qu, Bishal Shrestha, Zheng Wang, Francesco De Virgiliis, Thomas Haynes Hutson, Luming Zhou, Guiping Kong, Jessica S Chadwick, Paolo La Montanara, Zhulin Yuan, Nejc Haberman, Monica M Sousa, Ilaria Palmisano, Simone Di Giovanni

引用次数: 0

Gut microbiota-modulated glutamic acid rejuvenates the quality of oocytes deteriorated by advanced reproductive age. 肠道菌群调节谷氨酸可使因高龄生殖而恶化的卵母细胞质量恢复活力。

IF 8.3 1区医学

EMBO Molecular Medicine Pub Date : 2026-05-08 DOI: 10.1038/s44321-026-00443-3

Feixue Wang, Wenjun Zeng, Zihao Zhang, Na Li, Zhaokang Cui, Jie Bai, Jiner Yan, Yu Zhang, Yilong Miao, Ling Gu, Bo Xiong

{"title":"Gut microbiota-modulated glutamic acid rejuvenates the quality of oocytes deteriorated by advanced reproductive age.","authors":"Feixue Wang, Wenjun Zeng, Zihao Zhang, Na Li, Zhaokang Cui, Jie Bai, Jiner Yan, Yu Zhang, Yilong Miao, Ling Gu, Bo Xiong","doi":"10.1038/s44321-026-00443-3","DOIUrl":"https://doi.org/10.1038/s44321-026-00443-3","url":null,"abstract":"The gut microbiota plays a vital role in maintaining the physiological function of host health and the pathogenesis of various diseases. However, its relationship with maternal age-associated decline in oocyte quality remains elusive. Here, we report that establishment of gut microbiota from young donors in aged mice by fecal microbiota transplantation (FMT) is an effective method to rejuvenate the quality of maternally aged oocytes. Specifically, young gut microbiota promoted the ovulation and maturation of aged oocytes, and inhibited occurrence of cytoplasm fragmentation and spindle/chromosome abnormalities, hence enhancing the oocyte quality and female fertility. By integrating metagenome and untargeted metabolome of intestinal digesta, as well as targeted metabolome of ovaries and micro-transcriptome of oocytes, we identified that Bacteroides_caecimuris-modulated glutamic acid levels mediated the restorative effects of young gut microbiota on the aged oocytes through strengthening the mitochondria function. In addition, we demonstrated that in vivo supplementation of glutamic acid also enhanced the quality of aged oocytes, and the improvement of oocyte quality by glutamic acid was conserved across species. Altogether, our findings highlight the importance of gut microbiota in the oocyte aging and provide potential improvement strategies for age-related decline in oocyte quality and female fertility.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Loss of mitochondrial DNA helicase in retinal macroglia drives neovascular retinopathy. 视网膜大胶质细胞线粒体DNA解旋酶缺失导致新生血管性视网膜病变。

IF 8.3 1区医学

EMBO Molecular Medicine Pub Date : 2026-05-08 DOI: 10.1038/s44321-026-00438-0

Sofiia Olander, Sinem Karaman, Fumi Suomi, Kevin Aguilar, Aleksandra Zhaivoron, Maiken Nedergaard, Lina Smeds, Jussi Tiihonen, Albert Quintana, Juan Hidalgo, Kari Alitalo, Petri Ala-Laurila, Gulayse Ince-Dunn, Anu Suomalainen

{"title":"Loss of mitochondrial DNA helicase in retinal macroglia drives neovascular retinopathy.","authors":"Sofiia Olander, Sinem Karaman, Fumi Suomi, Kevin Aguilar, Aleksandra Zhaivoron, Maiken Nedergaard, Lina Smeds, Jussi Tiihonen, Albert Quintana, Juan Hidalgo, Kari Alitalo, Petri Ala-Laurila, Gulayse Ince-Dunn, Anu Suomalainen","doi":"10.1038/s44321-026-00438-0","DOIUrl":"https://doi.org/10.1038/s44321-026-00438-0","url":null,"abstract":"Retinopathy is a common symptom in mitochondrial diseases, and a leading cause of blindness in working-age individuals, often arising as a consequence of diabetes. Here, we demonstrate that postnatal loss of the replicative helicase of mitochondrial DNA in the astrocytes and Müller glia induces neovascular retinopathy. In these retinas, the macroglia show pathological reactivation, leading to hallmark features of neovascularization with blood-retina-barrier leakage, secondary microgliosis, and complement cascade activation. Similar reactivation of astrocytes in the cerebral cortex does not compromise vascular integrity, indicating tissue-specific roles of mitochondrial metabolism in macroglia for vascular homeostasis. Three secreted angiogenic factors-Fgf2, Pgf, and Lcn2-known to contribute to diabetic retinopathy, were induced. Spike recordings of the most sensitive retinal ganglion cells revealed normal rod function and intact retinal coding. These findings highlight the critical role of glial mitochondrial metabolism in neovascular retinopathy, with important implications for therapy development for mitochondrial and common forms of vision loss.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Distinct pathophysiological mechanisms of CEP152 variants in microcephaly and brain abnormalities. CEP152变异在小头畸形和脑异常中的独特病理生理机制。

IF 8.3 1区医学

EMBO Molecular Medicine Pub Date : 2026-05-05 DOI: 10.1038/s44321-026-00427-3

Nanako Hamada, Lama AlAbdi, Tomoko Uehara, Looprasertkul Sasikarn, Takuma Nishijo, Reut Suliman-Lavie, Mais O Hashem, Majid Alfadhel, Shatha Alhefdhi, Brahim Tabarki, Malak Alghamdi, Ikuko Iwamoto, Toshiki Takenouchi, Kenjiro Kosaki, Sagiv Shifman, Seiji Mizuno, Nobuhiko Ohno, Fowzan S Alkuraya, Koh-Ichi Nagata

{"title":"Distinct pathophysiological mechanisms of CEP152 variants in microcephaly and brain abnormalities.","authors":"Nanako Hamada, Lama AlAbdi, Tomoko Uehara, Looprasertkul Sasikarn, Takuma Nishijo, Reut Suliman-Lavie, Mais O Hashem, Majid Alfadhel, Shatha Alhefdhi, Brahim Tabarki, Malak Alghamdi, Ikuko Iwamoto, Toshiki Takenouchi, Kenjiro Kosaki, Sagiv Shifman, Seiji Mizuno, Nobuhiko Ohno, Fowzan S Alkuraya, Koh-Ichi Nagata","doi":"10.1038/s44321-026-00427-3","DOIUrl":"https://doi.org/10.1038/s44321-026-00427-3","url":null,"abstract":"CEP152 is essential for centriole function and neurodevelopment, and pathogenic recessive variants in CEP152 cause primary microcephaly. We identified new compound heterozygous CEP152 variants, c.314 G > A,p.(W105*) and c.2689 A > T,p.(K897*), in a microcephalic patient and analyzed them alongside a homozygous variant c.95 A > C,p.(Q32P) associated with severe microcephaly with marked gyral simplification. In vitro assays revealed distinct effects: p.K897* prevented centrosomal localization, p.W105* led to protein degradation, and p.Q32P retained centrosomal targeting but disrupted binding to Polo-like kinase 4, a key centriole biogenesis kinase and CEP152 partner. In vivo, both Cep152W105*/K897* and Cep152Q32P/Q32P knock-in mice displayed microcephaly; notably, Cep152Q32P/Q32P mice also exhibited severe cortical defects during brain development. Cellular analyses revealed centrosome dysfunction, mitotic errors, and increased apoptosis, which were exacerbated in Cep152Q32P/Q32P brains. Morphological examination, including electron microscopy, further demonstrated structural abnormalities of the centrosomes and centrioles in Cep152Q32P/Q32P brains. Electrophysiological and gene expression analyses confirmed variant-specific neuronal impairments, which correlate with clinical severity. Collectively, these findings demonstrate that distinct CEP152 variants disrupt neurodevelopment through different mechanisms, thereby explaining the spectrum of microcephaly severity and associated phenotypes.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Costimulation loss enhances IL-2-driven Treg generation by PI3K-STAT3 inhibition in CNS autoimmunity. 在中枢神经系统自身免疫中，共刺激缺失通过抑制PI3K-STAT3增强il -2驱动的Treg生成。

IF 8.3 1区医学

EMBO Molecular Medicine Pub Date : 2026-05-05 DOI: 10.1038/s44321-026-00431-7

Kyung-Ho Nam, Gil-Ran Kim, Yu-Rim Kim, Young Nam Kwon, Sung-Min Kim, Je-Min Choi

{"title":"Costimulation loss enhances IL-2-driven Treg generation by PI3K-STAT3 inhibition in CNS autoimmunity.","authors":"Kyung-Ho Nam, Gil-Ran Kim, Yu-Rim Kim, Young Nam Kwon, Sung-Min Kim, Je-Min Choi","doi":"10.1038/s44321-026-00431-7","DOIUrl":"https://doi.org/10.1038/s44321-026-00431-7","url":null,"abstract":"Costimulation blockade with CTLA-4 Ig (Abatacept) is a widely used strategy to suppress autoreactive T cells; however, its efficacy is often self-limiting due to concurrent depletion of regulatory T cells (Tregs), which depend on CD28 signaling for homeostasis. Here, we demonstrate that costimulation blockade paradoxically potentiates IL-2-driven Treg generation by selectively reprogramming intracellular cytokine signaling. We identified that IL-2 activates STAT3 only in the presence of TCR stimulation, as this pathway requires CD28-mediated PI3K-AKT signaling, which is abrogated by costimulation blockade. Consequently, CTLA-4 Ig uncouples STAT3 activation from IL-2 signaling while sparing STAT5, thereby enhancing TGF-β/Smad2/3 signaling to induce Foxp3 expression. This dual action-sustained STAT5 activation and increased Smad2/3 signaling-promoted robust Treg generation that ameliorated experimental autoimmune encephalomyelitis (EAE). Furthermore, we confirmed that this synergistic effect is conserved in human T cells from patients with multiple sclerosis (MS) upon CTLA-4 Ig and IL-2 cotreatment. Our findings suggest a strategy to expand the utility of CTLA-4 Ig therapy, providing a mechanistic rationale for combining costimulation blockade with IL-2 to restore immune tolerance in CNS autoimmunity.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HNRNPU and architectural lncRNAs as nuclear tethers of epithelial state stability. HNRNPU和结构lncrna作为上皮状态稳定性的核栓。

IF 8.3 1区医学

EMBO Molecular Medicine Pub Date : 2026-05-04 DOI: 10.1038/s44321-026-00440-6

Longlong Luo, George L Sen

{"title":"HNRNPU and architectural lncRNAs as nuclear tethers of epithelial state stability.","authors":"Longlong Luo, George L Sen","doi":"10.1038/s44321-026-00440-6","DOIUrl":"https://doi.org/10.1038/s44321-026-00440-6","url":null,"abstract":"Skin biology is commonly framed through signaling pathways that reprogram transcription in response to inflammatory and environmental cues. Here, a complementary perspective is proposed: epidermal homeostasis and disease recurrence may also depend on the physical organization of the genome within the nucleus. HNRNPU/SAF-A has emerged as an RNA-dependent architectural factor that links RNA binding to chromatin topology, while architectural long non-coding RNAs provide precedents for how RNA can scaffold nuclear compartments and influence higher-order genome organization. Building on these concepts, the Epidermal Differentiation Complex is considered as a tractable epidermal locus in which RNA-dependent nuclear tethering may help stabilize barrier gene programs. This framework further suggests that chronic inflammation could remodel chromatin architecture in ways that persist after apparent resolution, generating a \"structural scar\" that biases future responses. Although this model remains hypothetical, it is now experimentally testable. By integrating architectural RNA biology with epidermal differentiation and inflammatory memory, this Perspective provides a roadmap for investigating how nuclear structure may contribute to epithelial state stability and how it may be altered in inflammatory skin disease.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Spatially resolved ex vivo drug response profiling in SMARCB1-deficient sinonasal carcinoma. 空间分辨的smarcb1缺陷鼻窦癌体外药物反应分析。

IF 8.3 1区医学

EMBO Molecular Medicine Pub Date : 2026-05-02 DOI: 10.1038/s44321-026-00437-1

Philipp Jurmeister, Susanne Flach, Linda Bergmayr, Konstanze Schleich, Edgar Chimal Calderon, Liliana H Mochmann, Yauheniya Zhdanovich, Doreen Klingler, Ada Pusztai, Anna Kübler, Christoph Walz, Christoph Benedikt Westphalen, Alexander Beck, Maximilian Leitheiser, Gerben E Breimer, Johannes A Rijken, Lot Devriese, Philipp Baumeister, Alena Skálová, Simon Schallenberg, Frederick Klauschen, Andreas Mock

{"title":"Spatially resolved ex vivo drug response profiling in SMARCB1-deficient sinonasal carcinoma.","authors":"Philipp Jurmeister, Susanne Flach, Linda Bergmayr, Konstanze Schleich, Edgar Chimal Calderon, Liliana H Mochmann, Yauheniya Zhdanovich, Doreen Klingler, Ada Pusztai, Anna Kübler, Christoph Walz, Christoph Benedikt Westphalen, Alexander Beck, Maximilian Leitheiser, Gerben E Breimer, Johannes A Rijken, Lot Devriese, Philipp Baumeister, Alena Skálová, Simon Schallenberg, Frederick Klauschen, Andreas Mock","doi":"10.1038/s44321-026-00437-1","DOIUrl":"https://doi.org/10.1038/s44321-026-00437-1","url":null,"abstract":"SMARCB1-deficient sinonasal carcinoma (SDSC) is a rare, highly aggressive malignancy with limited therapeutic options and no established preclinical models. Here, single-nucleus RNA sequencing (snRNAseq), spatial transcriptomics, and ex vivo patient-derived tissue slice culture (TSC) were combined to resolve intratumoral heterogeneity, niche organization, and treatment vulnerabilities in an index SDSC. snRNAseq identified three malignant subpopulations, including two specialized states marked by ALDH1A1 and NTN4. Spatial profiling mapped these states to distinct niches. The ALDH1A1+ compartment localized to a basal-associated niche with intermingled p63-positive basal cells adjacent to stroma, showed reduced proliferative activity, and displayed stem-like transcriptional features. Ex vivo drug testing revealed a striking response: the mTOR inhibitor Sapanisertib induced extensive tumor necrosis and was associated with near-complete depletion of ALDH1A1+ and NTN4+ states, accompanied by strong stress/apoptosis signatures and reduced endothelial cells. In an additional retrospective cohort of 12 SDSC, ALDH1A1 was present in all cases with heterogeneous spatial patterns and higher levels in recurrences. Mesothelin was expressed in the index case and a subset of tumors, supporting mesothelin-directed therapeutic strategies.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interstitial and recruited macrophages prevent tuberculosis relapse by limiting immune evasion. 间质和募集的巨噬细胞通过限制免疫逃避来预防结核病复发。

IF 11.1 1区医学

EMBO Molecular Medicine Pub Date : 2026-04-29 DOI: 10.1038/s44321-026-00432-6

Valerie Vinette,Anthony Castro,Heather Kim,Carolina Trujillo,Min Xie,Martin Gengenbacher,Thomas R Ioerger,Sabine Ehrt

引用次数: 0

Regulatory challenges of personalized medicine in the real world: are the right patients being treated with CD19-targeting CAR T-cells? 现实世界中个性化医疗的监管挑战：是否有合适的患者接受靶向cd19的CAR -t细胞治疗？

IF 11.1 1区医学

EMBO Molecular Medicine Pub Date : 2026-04-27 DOI: 10.1038/s44321-026-00436-2

Attila Sebe,Rafael Hernani,Jan Müller-Berghaus

{"title":"Regulatory challenges of personalized medicine in the real world: are the right patients being treated with CD19-targeting CAR T-cells?","authors":"Attila Sebe,Rafael Hernani,Jan Müller-Berghaus","doi":"10.1038/s44321-026-00436-2","DOIUrl":"https://doi.org/10.1038/s44321-026-00436-2","url":null,"abstract":"Despite the clinical success of CD19-directed CAR T-cell therapies, less than 50% of patients achieve long-term remission. Emerging evidence indicates that loss or reduced expression of CD19-due to mutations, deletions, alternative splicing-is a significant, underrecognized mechanism of treatment failure. Notably, CD19-negative subpopulations can be detected even prior to therapy, and patients with low CD19 expression consistently show poorer outcomes. Although current clinical guidelines do not mandate routine CD19 testing before treatment, this situation reflects both scientific and technical challenges. Importantly, patients with partial/ low CD19 expression may still benefit from therapy, complicating the definition of \"target positivity.\" From a regulatory perspective, targeted therapies should ideally be used only when target expression is confirmed. This principle is difficult to implement, considering the scarcity of data and the difficulties of current diagnostic tools, risking both undertreatment and overtreatment. EU regulators have addressed the issue by introducing harmonized warnings in product information, but more is needed. We highlight this regulatory-clinical gap and advocate for improved diagnostic standards, better data integration, and dialogue among clinicians, developers, and regulators.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":"57 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147753281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Disease-stage-specific immunometabolic remodeling in pediatric obstructive sleep apnea: a single-cell transcriptomic atlas of adenoid tissue. 儿童阻塞性睡眠呼吸暂停的疾病阶段特异性免疫代谢重塑：腺样组织的单细胞转录组图谱

IF 11.1 1区医学

EMBO Molecular Medicine Pub Date : 2026-04-27 DOI: 10.1038/s44321-026-00419-3

Qin Yang,Yunfei Cui,Xiao Huang,Junlin Liu,Xiaopeng Ma,George Fu Gao,Hongguang Pan,Shijie Qin

{"title":"Disease-stage-specific immunometabolic remodeling in pediatric obstructive sleep apnea: a single-cell transcriptomic atlas of adenoid tissue.","authors":"Qin Yang,Yunfei Cui,Xiao Huang,Junlin Liu,Xiaopeng Ma,George Fu Gao,Hongguang Pan,Shijie Qin","doi":"10.1038/s44321-026-00419-3","DOIUrl":"https://doi.org/10.1038/s44321-026-00419-3","url":null,"abstract":"Hypertrophied adenoids in children can impair breathing and lead to obstructive sleep apnea (OSA), often accompanied by abnormal growth and weakened stamina and immunity. However, the cause of the pathological transformation in these originally immune-enhancing lymphoid tissues remains unclear. Our study provides the first single cell transcriptomic and immune repertoire atlas of adenoids from normal snoring to mild, moderate, and severe OSA, and identified markedly asynchronous functional modules, transcriptional regulatory networks and intercellular communications during the progression of OSA. Children with severe OSA exhibited exhibit active Hippo, Notch, and Wnt signaling, alongside significant downregulation of energy synthesis. Analysis revealed compromised T-cell and B-cell immunity, as well as reduced antigen processing by innate immune cells, coupled with diminished cell-cell communication in severe OSA group. T-cell receptor and B-cell receptor sequencing results also support more infection imprints and abnormal germinal centers and antibody class switching. Mechanistically, HIF1A-mediated hypoxic signaling likely drives the downregulation of key immune components (including HLA and interferon molecules), positioning it as a promising therapeutic target for OSA.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":"32 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147753280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0