Pub Date : 2025-12-19DOI: 10.1038/s41593-025-02145-4
{"title":"Freezing forgetting in C. elegans to extend memory retention.","authors":"","doi":"10.1038/s41593-025-02145-4","DOIUrl":"https://doi.org/10.1038/s41593-025-02145-4","url":null,"abstract":"","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"12 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145786283","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}
Pub Date : 2025-12-19DOI: 10.1038/s41593-025-02139-2
Zhihua Liu,Dapeng Xie,Stephen X Zhang,Wenji Cai,Hao Zhou,Dragana Rogulja
Temperature compensation stabilizes the speed of circadian clocks. Uncompensated molecular clock cycles would accelerate severalfold with each 10 °C increase, precluding reliable timekeeping. Despite such thermal buffering, some clock-controlled behavioral cycles complete by up to two hours earlier or later depending on environmental temperatures. We show that temperature-dependent changes in the speed of behavioral cycles can be explained by changes in the speed of the clock itself. Although the speed of all clocks is insensitive to thermal energy, we found that in neurons the clock speed is regulated by temperature information. When the threshold of ~26 °C is exceeded for ~24 h, a pathway mediated by the LIM-homeodomain transcription factor Lim1 instructs the clocks in the Drosophila brain to accelerate. Clock acceleration enables earlier morning awakening. This work suggests that modestly altering the clock speed enables behavioral thermoadaptation, via regulated steps that do not compromise the reliability of circadian timekeeping.
{"title":"Behavioral adaptation to warm conditions via Lim1-mediated acceleration of neuronal clocks.","authors":"Zhihua Liu,Dapeng Xie,Stephen X Zhang,Wenji Cai,Hao Zhou,Dragana Rogulja","doi":"10.1038/s41593-025-02139-2","DOIUrl":"https://doi.org/10.1038/s41593-025-02139-2","url":null,"abstract":"Temperature compensation stabilizes the speed of circadian clocks. Uncompensated molecular clock cycles would accelerate severalfold with each 10 °C increase, precluding reliable timekeeping. Despite such thermal buffering, some clock-controlled behavioral cycles complete by up to two hours earlier or later depending on environmental temperatures. We show that temperature-dependent changes in the speed of behavioral cycles can be explained by changes in the speed of the clock itself. Although the speed of all clocks is insensitive to thermal energy, we found that in neurons the clock speed is regulated by temperature information. When the threshold of ~26 °C is exceeded for ~24 h, a pathway mediated by the LIM-homeodomain transcription factor Lim1 instructs the clocks in the Drosophila brain to accelerate. Clock acceleration enables earlier morning awakening. This work suggests that modestly altering the clock speed enables behavioral thermoadaptation, via regulated steps that do not compromise the reliability of circadian timekeeping.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"85 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145786288","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}
Pub Date : 2025-12-18DOI: 10.1038/s41593-025-02154-3
Nicole F. O. Green, Gavin J. Sutton, Javier Pérez-Burillo, Juli Wang, Samuel Bagot, Hannah G. Danon, Kieran Walsh, Akira Gokool, Samantha A. Miles, Guang Yang, Charles A. Herring, Yuheng Liang, Grant Pfundstein, Vladimir Sytnyk, Hamid Alinejad-Rokny, Ryan Lister, Joseph Rosenbluh, Johann A. Gagnon-Bartsch, Irina Voineagu
Genetic variants associated with complex traits often lie in distal enhancers. While candidate enhancers have been mapped genome wide, their functional state and gene targets in specific cell types remain unclear. Here we present AstroREG, a resource of enhancer–gene interactions in human primary astrocytes, generated by combining CRISPR inhibition (CRISPRi), single-cell RNA-seq and machine learning. By functionally testing nearly 1,000 PsychENCODE enhancers, we identified more than 150 regulatory interactions, revealing enhancers that control key astrocyte functions and genes implicated in Alzheimer’s disease. The CRISPRi screen also provided valuable ground-truth data from a primary cell type for training and benchmarking prediction models of enhancer activity. We thus developed EGrf, a random forest (RF) model trained on these data, and applied it genome wide to predict regulatory interactions with high specificity. Together, our data provide a comprehensive functional map of enhancer-mediated regulation in a key glial cell type, shedding light on brain function and disease.
{"title":"CRISPRi screening in cultured human astrocytes uncovers distal enhancers controlling genes dysregulated in Alzheimer’s disease","authors":"Nicole F. O. Green, Gavin J. Sutton, Javier Pérez-Burillo, Juli Wang, Samuel Bagot, Hannah G. Danon, Kieran Walsh, Akira Gokool, Samantha A. Miles, Guang Yang, Charles A. Herring, Yuheng Liang, Grant Pfundstein, Vladimir Sytnyk, Hamid Alinejad-Rokny, Ryan Lister, Joseph Rosenbluh, Johann A. Gagnon-Bartsch, Irina Voineagu","doi":"10.1038/s41593-025-02154-3","DOIUrl":"https://doi.org/10.1038/s41593-025-02154-3","url":null,"abstract":"Genetic variants associated with complex traits often lie in distal enhancers. While candidate enhancers have been mapped genome wide, their functional state and gene targets in specific cell types remain unclear. Here we present AstroREG, a resource of enhancer–gene interactions in human primary astrocytes, generated by combining CRISPR inhibition (CRISPRi), single-cell RNA-seq and machine learning. By functionally testing nearly 1,000 PsychENCODE enhancers, we identified more than 150 regulatory interactions, revealing enhancers that control key astrocyte functions and genes implicated in Alzheimer’s disease. The CRISPRi screen also provided valuable ground-truth data from a primary cell type for training and benchmarking prediction models of enhancer activity. We thus developed EGrf, a random forest (RF) model trained on these data, and applied it genome wide to predict regulatory interactions with high specificity. Together, our data provide a comprehensive functional map of enhancer-mediated regulation in a key glial cell type, shedding light on brain function and disease.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"23 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145770707","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}
Pub Date : 2025-12-17DOI: 10.1038/s41593-025-02157-0
William A. Eimer, Alex S. Rodriguez, Michael T. DeFao, Simon Ehricke, Joseph Park, Deepak K. Vijaya Kumar, Nanda K. Navalpur Shanmugam, Sanjana Singh, Tara Sawhney, Robert D. Moir, Rudolph E. Tanzi
Tau is a microtubule-associated cytoskeletal protein, which, when hyperphosphorylated and aggregated, can result in a myriad of different tauopathies, including Alzheimer’s disease (AD). We previously showed that the principal component of senile plaques, amyloid beta (Aβ), is an antimicrobial peptide capable of binding and entrapping microbial pathogens. Here we show that tau is hyperphosphorylated in neurons in response to viral infection and can neutralize herpes simplex virus 1 (HSV-1) infectivity by directly binding to viral capsids. Our data suggest that the ‘pathogenic’ characteristics of tau hyperphosphorylation, microtubule destabilization and aggregation are part of an antiviral response, in which tau serves as a host defense protein in the innate immune system of the brain. The combined antimicrobial activities of Aβ and phosphorylated tau resulting in Aβ plaques and neurofibrillary tangles, along with neuroinflammation, suggest that AD neuropathology may have evolved as an orchestrated innate immune host defense response to microbial infection in the brain.
{"title":"Phosphorylated tau exhibits antimicrobial activity capable of neutralizing herpes simplex virus 1 infectivity in human neurons","authors":"William A. Eimer, Alex S. Rodriguez, Michael T. DeFao, Simon Ehricke, Joseph Park, Deepak K. Vijaya Kumar, Nanda K. Navalpur Shanmugam, Sanjana Singh, Tara Sawhney, Robert D. Moir, Rudolph E. Tanzi","doi":"10.1038/s41593-025-02157-0","DOIUrl":"https://doi.org/10.1038/s41593-025-02157-0","url":null,"abstract":"Tau is a microtubule-associated cytoskeletal protein, which, when hyperphosphorylated and aggregated, can result in a myriad of different tauopathies, including Alzheimer’s disease (AD). We previously showed that the principal component of senile plaques, amyloid beta (Aβ), is an antimicrobial peptide capable of binding and entrapping microbial pathogens. Here we show that tau is hyperphosphorylated in neurons in response to viral infection and can neutralize herpes simplex virus 1 (HSV-1) infectivity by directly binding to viral capsids. Our data suggest that the ‘pathogenic’ characteristics of tau hyperphosphorylation, microtubule destabilization and aggregation are part of an antiviral response, in which tau serves as a host defense protein in the innate immune system of the brain. The combined antimicrobial activities of Aβ and phosphorylated tau resulting in Aβ plaques and neurofibrillary tangles, along with neuroinflammation, suggest that AD neuropathology may have evolved as an orchestrated innate immune host defense response to microbial infection in the brain.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"12 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145765580","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}
Pub Date : 2025-12-16DOI: 10.1038/s41593-025-02132-9
Samira M Epp,Gabriel Castrillón,Beijia Yuan,Jessica Andrews-Hanna,Christine Preibisch,Valentin Riedl
Functional magnetic resonance imaging measures brain activity indirectly by monitoring changes in blood oxygenation levels, known as the blood-oxygenation-level-dependent (BOLD) signal, rather than directly measuring neuronal activity. This approach crucially relies on neurovascular coupling, the mechanism that links neuronal activity to changes in cerebral blood flow. However, it remains unclear whether this relationship is consistent for both positive and negative BOLD responses across the human cortex. Here we found that about 40% of voxels with significant BOLD signal changes during various tasks showed reversed oxygen metabolism, particularly in the default mode network. These 'discordant' voxels differed in baseline oxygen extraction fraction and regulated oxygen demand via oxygen extraction fraction changes, whereas 'concordant' voxels depended mainly on cerebral blood flow changes. Our findings challenge the canonical interpretation of the BOLD signal, indicating that quantitative functional magnetic resonance imaging provides a more reliable assessment of both absolute and relative changes in neuronal activity.
{"title":"BOLD signal changes can oppose oxygen metabolism across the human cortex.","authors":"Samira M Epp,Gabriel Castrillón,Beijia Yuan,Jessica Andrews-Hanna,Christine Preibisch,Valentin Riedl","doi":"10.1038/s41593-025-02132-9","DOIUrl":"https://doi.org/10.1038/s41593-025-02132-9","url":null,"abstract":"Functional magnetic resonance imaging measures brain activity indirectly by monitoring changes in blood oxygenation levels, known as the blood-oxygenation-level-dependent (BOLD) signal, rather than directly measuring neuronal activity. This approach crucially relies on neurovascular coupling, the mechanism that links neuronal activity to changes in cerebral blood flow. However, it remains unclear whether this relationship is consistent for both positive and negative BOLD responses across the human cortex. Here we found that about 40% of voxels with significant BOLD signal changes during various tasks showed reversed oxygen metabolism, particularly in the default mode network. These 'discordant' voxels differed in baseline oxygen extraction fraction and regulated oxygen demand via oxygen extraction fraction changes, whereas 'concordant' voxels depended mainly on cerebral blood flow changes. Our findings challenge the canonical interpretation of the BOLD signal, indicating that quantitative functional magnetic resonance imaging provides a more reliable assessment of both absolute and relative changes in neuronal activity.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"4 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145765284","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}
Pub Date : 2025-12-15DOI: 10.1038/s41593-025-02123-w
Judit González-Gallego, Katalin Todorov-Völgyi, Stephan A. Müller, Sophie Antesberger, Mihail Ivilinov Todorov, Rainer Malik, Rita Grimalt-Mirada, Carolina Cardoso Gonçalves, Martina Schifferer, Georg Kislinger, Isabel Weisheit, Barbara Lindner, Dennis Crusius, Joseph Kroeger, Mila Borri, Ali Erturk, Mark Nelson, Thomas Misgeld, Stefan F. Lichtenthaler, Martin Dichgans, Dominik Paquet
Blood–brain barrier (BBB) integrity is critical for brain homeostasis, with malfunctions contributing to neurovascular and neurodegenerative disorders. Mechanistic studies on BBB function have been mostly conducted in rodent and in vitro models, which recapitulate some disease features, but have limited translatability to humans and pose challenges for drug discovery. Here we report on a fully human induced pluripotent stem (iPS)-cell-derived, microfluidic three-dimensional (3D) BBB model consisting of endothelial cells (ECs), mural cells and astrocytes. Our model expresses typical fate markers, forms a barrier in vessel-like tubes and enables perfusion, including with human blood. Deletion of FOXF2 in ECs, a major risk gene for cerebral small vessel disease, induced key features of BBB dysfunction, including compromised cell junction integrity and enhanced caveolae formation. Proteomic analysis revealed dysregulated endocytosis and cell junction pathways. Disease features phenocopied those seen in mice with EC-specific Foxf2 deficiency. Moreover, lipid-nanoparticle-based treatment with Foxf2 mRNA rescued BBB deficits, demonstrating the potential for drug development.
{"title":"A fully iPS-cell-derived 3D model of the human blood–brain barrier for exploring neurovascular disease mechanisms and therapeutic interventions","authors":"Judit González-Gallego, Katalin Todorov-Völgyi, Stephan A. Müller, Sophie Antesberger, Mihail Ivilinov Todorov, Rainer Malik, Rita Grimalt-Mirada, Carolina Cardoso Gonçalves, Martina Schifferer, Georg Kislinger, Isabel Weisheit, Barbara Lindner, Dennis Crusius, Joseph Kroeger, Mila Borri, Ali Erturk, Mark Nelson, Thomas Misgeld, Stefan F. Lichtenthaler, Martin Dichgans, Dominik Paquet","doi":"10.1038/s41593-025-02123-w","DOIUrl":"https://doi.org/10.1038/s41593-025-02123-w","url":null,"abstract":"Blood–brain barrier (BBB) integrity is critical for brain homeostasis, with malfunctions contributing to neurovascular and neurodegenerative disorders. Mechanistic studies on BBB function have been mostly conducted in rodent and in vitro models, which recapitulate some disease features, but have limited translatability to humans and pose challenges for drug discovery. Here we report on a fully human induced pluripotent stem (iPS)-cell-derived, microfluidic three-dimensional (3D) BBB model consisting of endothelial cells (ECs), mural cells and astrocytes. Our model expresses typical fate markers, forms a barrier in vessel-like tubes and enables perfusion, including with human blood. Deletion of FOXF2 in ECs, a major risk gene for cerebral small vessel disease, induced key features of BBB dysfunction, including compromised cell junction integrity and enhanced caveolae formation. Proteomic analysis revealed dysregulated endocytosis and cell junction pathways. Disease features phenocopied those seen in mice with EC-specific Foxf2 deficiency. Moreover, lipid-nanoparticle-based treatment with Foxf2 mRNA rescued BBB deficits, demonstrating the potential for drug development.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"2 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145759746","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}
Pub Date : 2025-12-15DOI: 10.1038/s41593-025-02136-5
Katalin Todorov-Völgyi, Judit González-Gallego, Stephan A. Müller, Mihail Ivilinov Todorov, Fatma Burcu Seker, Simon Frerich, Filippo M. Cernilogar, Luise Schröger, Rainer Malik, Jiayu Cao, Gemma Llovera, Stefan Roth, Ulrike Schillinger, Martina Schifferer, Azadeh Reyahi, Dennis Crusius, Liliana D. Pedro, Mikael Simons, Peter Carlsson, Ali Ertürk, Arthur Liesz, Gunnar Schotta, Nikolaus Plesnila, Stefan F. Lichtenthaler, Dominik Paquet, Martin Dichgans
Cerebral small vessel disease (SVD) is a common chronic cerebrovascular disorder with poorly understood pathomechanisms. Genetic studies have identified FOXF2 as a major risk gene for both SVD and stroke. FOXF2 encodes a transcription factor primarily expressed in brain pericytes and endothelial cells (ECs); however, its mechanistic role in cerebrovascular disease remains unknown. Here we show that Foxf2 maintains EC function through Tie2 signaling. RNA and chromatin sequencing identified FOXF2 as a transcriptional activator of Tie2 and other endothelial lineage-specific genes. The deletion of EC-specific Foxf2 in adult mice resulted in blood–brain barrier leakage, which worsened after experimental stroke. Proteomic analyses of Foxf2-deficient mouse brain-derived and human-induced pluripotent stem cell-derived ECs that lack FOXF2 revealed a downregulation of multiple proteins involved in Tie2 signaling. Endothelial Foxf2 deficiency impaired functional hyperemia, reduced NO production and increased infarct size through disrupted Tie2 signaling, effects that were rescued by pharmacological activation of Tie2 with AKB-9778. Collectively, our results highlight the critical role of Foxf2-regulated Tie2 signaling in SVD and stroke, suggesting new avenues for therapeutic interventions.
{"title":"The stroke risk gene Foxf2 maintains brain endothelial cell function via Tie2 signaling","authors":"Katalin Todorov-Völgyi, Judit González-Gallego, Stephan A. Müller, Mihail Ivilinov Todorov, Fatma Burcu Seker, Simon Frerich, Filippo M. Cernilogar, Luise Schröger, Rainer Malik, Jiayu Cao, Gemma Llovera, Stefan Roth, Ulrike Schillinger, Martina Schifferer, Azadeh Reyahi, Dennis Crusius, Liliana D. Pedro, Mikael Simons, Peter Carlsson, Ali Ertürk, Arthur Liesz, Gunnar Schotta, Nikolaus Plesnila, Stefan F. Lichtenthaler, Dominik Paquet, Martin Dichgans","doi":"10.1038/s41593-025-02136-5","DOIUrl":"https://doi.org/10.1038/s41593-025-02136-5","url":null,"abstract":"Cerebral small vessel disease (SVD) is a common chronic cerebrovascular disorder with poorly understood pathomechanisms. Genetic studies have identified FOXF2 as a major risk gene for both SVD and stroke. FOXF2 encodes a transcription factor primarily expressed in brain pericytes and endothelial cells (ECs); however, its mechanistic role in cerebrovascular disease remains unknown. Here we show that Foxf2 maintains EC function through Tie2 signaling. RNA and chromatin sequencing identified FOXF2 as a transcriptional activator of Tie2 and other endothelial lineage-specific genes. The deletion of EC-specific Foxf2 in adult mice resulted in blood–brain barrier leakage, which worsened after experimental stroke. Proteomic analyses of Foxf2-deficient mouse brain-derived and human-induced pluripotent stem cell-derived ECs that lack FOXF2 revealed a downregulation of multiple proteins involved in Tie2 signaling. Endothelial Foxf2 deficiency impaired functional hyperemia, reduced NO production and increased infarct size through disrupted Tie2 signaling, effects that were rescued by pharmacological activation of Tie2 with AKB-9778. Collectively, our results highlight the critical role of Foxf2-regulated Tie2 signaling in SVD and stroke, suggesting new avenues for therapeutic interventions.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"16 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145759779","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}
Pub Date : 2025-12-12DOI: 10.1038/s41593-025-02168-x
Alex James Major,Ahmed Abdaltawab,Jessica M Phillips,Tian Wang,Eric Kenji Lee,Maxwell J Lichtenfeld,Chandramouli Chandrasekaran,Yuri B Saalmann,Alexander Maier,Robert Desimone,Earl K Miller,André M Bastos,Diego Mendoza-Halliday
{"title":"A. J. Major et al. reply.","authors":"Alex James Major,Ahmed Abdaltawab,Jessica M Phillips,Tian Wang,Eric Kenji Lee,Maxwell J Lichtenfeld,Chandramouli Chandrasekaran,Yuri B Saalmann,Alexander Maier,Robert Desimone,Earl K Miller,André M Bastos,Diego Mendoza-Halliday","doi":"10.1038/s41593-025-02168-x","DOIUrl":"https://doi.org/10.1038/s41593-025-02168-x","url":null,"abstract":"","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"100 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145732584","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}
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