Thai B. Nguyen, Ricardo Miramontes, Carlos Chillon-Marinas, Roy Maimon, Sonia Vazquez-Sanchez, Alice L. Lau, Nicolette R. McClure, Zhuoxing Wu, Keona Q. Wang, Whitney E. England, Monika Singha, Jennifer T. Stocksdale, Marie Heath, Ki-Hong Jang, Sunhee Jung, Karen Ling, Paymann Jafar-nejad, Jharrayne I. McKnight, Leanne N. Ho, Osama Al Dalahmah, Richard L. M. Faull, Joan S. Steffan, Jack C. Reidling, Cholsoon Jang, Gina Lee, Don W. Cleveland, Clotilde Lagier-Tourenne, Robert C. Spitale, Leslie M. Thompson
{"title":"Aberrant splicing in Huntington’s disease accompanies disrupted TDP-43 activity and altered m6A RNA modification","authors":"Thai B. Nguyen, Ricardo Miramontes, Carlos Chillon-Marinas, Roy Maimon, Sonia Vazquez-Sanchez, Alice L. Lau, Nicolette R. McClure, Zhuoxing Wu, Keona Q. Wang, Whitney E. England, Monika Singha, Jennifer T. Stocksdale, Marie Heath, Ki-Hong Jang, Sunhee Jung, Karen Ling, Paymann Jafar-nejad, Jharrayne I. McKnight, Leanne N. Ho, Osama Al Dalahmah, Richard L. M. Faull, Joan S. Steffan, Jack C. Reidling, Cholsoon Jang, Gina Lee, Don W. Cleveland, Clotilde Lagier-Tourenne, Robert C. Spitale, Leslie M. Thompson","doi":"10.1038/s41593-024-01850-w","DOIUrl":"10.1038/s41593-024-01850-w","url":null,"abstract":"Huntington’s disease (HD) is caused by a CAG repeat expansion in the HTT gene, leading to altered gene expression. However, the mechanisms leading to disrupted RNA processing in HD remain unclear. Here we identify TDP-43 and the N6-methyladenosine (m6A) writer protein METTL3 to be upstream regulators of exon skipping in multiple HD systems. Disrupted nuclear localization of TDP-43 and cytoplasmic accumulation of phosphorylated TDP-43 occurs in HD mouse and human brains, with TDP-43 also co-localizing with HTT nuclear aggregate-like bodies distinct from mutant HTT inclusions. The binding of TDP-43 onto RNAs encoding HD-associated differentially expressed and aberrantly spliced genes is decreased. Finally, m6A RNA modification is reduced on RNAs abnormally expressed in the striatum of HD R6/2 mouse brain, including at clustered sites adjacent to TDP-43 binding sites. Our evidence supports TDP-43 loss of function coupled with altered m6A modification as a mechanism underlying alternative splicing in HD. Nguyen et al. identify TDP-43 and METTL3 as key regulators of disrupted RNA splicing in Huntington’s disease, offering insight into how TDP-43 mislocalization and aberrant m6A RNA modification and localization relate to disease pathogenesis.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 2","pages":"280-292"},"PeriodicalIF":21.2,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41593-024-01850-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142929446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mary O’Keeffe, Sam A. Booker, Darren Walsh, Mosi Li, Chloe Henley, Laura Simões de Oliveira, Mingshan Liu, Xingran Wang, Maria Banqueri, Katherine Ridley, Kosala N. Dissanayake, Cristina Martinez-Gonzalez, Kirsty J. Craigie, Deepali Vasoya, Tom Leah, Xin He, David A. Hume, Ian Duguid, Matthew F. Nolan, Jing Qiu, David J. A. Wyllie, Owen R. Dando, Alfredo Gonzalez-Sulser, Jian Gan, Clare Pridans, Peter C. Kind, Giles E. Hardingham
{"title":"Typical development of synaptic and neuronal properties can proceed without microglia in the cortex and thalamus","authors":"Mary O’Keeffe, Sam A. Booker, Darren Walsh, Mosi Li, Chloe Henley, Laura Simões de Oliveira, Mingshan Liu, Xingran Wang, Maria Banqueri, Katherine Ridley, Kosala N. Dissanayake, Cristina Martinez-Gonzalez, Kirsty J. Craigie, Deepali Vasoya, Tom Leah, Xin He, David A. Hume, Ian Duguid, Matthew F. Nolan, Jing Qiu, David J. A. Wyllie, Owen R. Dando, Alfredo Gonzalez-Sulser, Jian Gan, Clare Pridans, Peter C. Kind, Giles E. Hardingham","doi":"10.1038/s41593-024-01833-x","DOIUrl":"10.1038/s41593-024-01833-x","url":null,"abstract":"Brain-resident macrophages, microglia, have been proposed to have an active role in synaptic refinement and maturation, influencing plasticity and circuit-level connectivity. Here we show that several neurodevelopmental processes previously attributed to microglia can proceed without them. Using a genetically modified mouse that lacks microglia (Csf1r∆FIRE/∆FIRE), we find that intrinsic properties, synapse number and synaptic maturation are largely normal in the hippocampal CA1 region and somatosensory cortex at stages where microglia have been implicated. Seizure susceptibility and hippocampal-prefrontal cortex coherence in awake behaving animals, processes that are disrupted in mice deficient in microglia-enriched genes, are also normal. Similarly, eye-specific segregation of inputs into the lateral geniculate nucleus proceeds normally in the absence of microglia. Single-cell and single-nucleus transcriptomic analyses of neurons and astrocytes did not uncover any substantial perturbation caused by microglial absence. Thus, the brain possesses remarkable adaptability to execute developmental synaptic refinement, maturation and connectivity in the absence of microglia. Microglia are proposed to have a role in brain development through synaptic engulfment and paracrine signaling. O’Keeffe et al. show that certain neurodevelopmental processes attributed to microglia can proceed normally even in the absence of these cells.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 2","pages":"268-279"},"PeriodicalIF":21.2,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41593-024-01833-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142929726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Miguel A. Abellanas, Maitreyee Purnapatre, Chiara Burgaletto, Michal Schwartz
{"title":"Monocyte-derived macrophages act as reinforcements when microglia fall short in Alzheimer’s disease","authors":"Miguel A. Abellanas, Maitreyee Purnapatre, Chiara Burgaletto, Michal Schwartz","doi":"10.1038/s41593-024-01847-5","DOIUrl":"https://doi.org/10.1038/s41593-024-01847-5","url":null,"abstract":"<p>The central nervous system (CNS) is endowed with its own resident innate immune cells, the microglia. They constitute approximately 10% of the total cells within the CNS parenchyma and act as ‘sentinels’, sensing and mitigating any deviation from homeostasis. Nevertheless, under severe acute or chronic neurological injury or disease, microglia are unable to contain the damage, and the reparative activity of monocyte-derived macrophages (MDMs) is required. The failure of the microglia under such conditions could be an outcome of their prolonged exposure to hostile stimuli, leading to their exhaustion or senescence. Here, we describe the conditions under which the microglia fall short, focusing mainly on the context of Alzheimer’s disease, and shed light on the functions performed by MDMs. We discuss whether and how MDMs engage in cross-talk with the microglia, why their recruitment is often inadequate, and potential ways to augment their homing to the brain in a well-controlled manner.</p>","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"78 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142929724","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}
Philip Hehlert, Thomas Effertz, Ruo-Xu Gu, Björn Nadrowski, Bart R. H. Geurten, Dirk Beutner, Bert L. de Groot, Martin C. Göpfert
{"title":"NOMPC ion channel hinge forms a gating spring that initiates mechanosensation","authors":"Philip Hehlert, Thomas Effertz, Ruo-Xu Gu, Björn Nadrowski, Bart R. H. Geurten, Dirk Beutner, Bert L. de Groot, Martin C. Göpfert","doi":"10.1038/s41593-024-01849-3","DOIUrl":"10.1038/s41593-024-01849-3","url":null,"abstract":"The sensation of mechanical stimuli is initiated by elastic gating springs that pull open mechanosensory transduction channels. Searches for gating springs have focused on force-conveying protein tethers such as the amino-terminal ankyrin tether of the Drosophila mechanosensory transduction channel NOMPC. Here, by combining protein domain duplications with mechanical measurements, electrophysiology, molecular dynamics simulations and modeling, we identify the NOMPC gating-spring as the short linker between the ankyrin tether and the channel gate. This linker acts as a Hookean hinge that is ten times more elastic than the tether, with the linker hinge dictating channel gating and the intrinsic stiffness of the gating spring. Our study shows how mechanosensation is initiated molecularly; disentangles gating springs and tethers, and respective paradigms of channel gating; and puts forward gating springs as core ion channel constituents that enable efficient gating by diverse stimuli and in a wide variety of channels. Hehlert et al. report that the gating spring that pulls open mechanosensitive NOMPC channels is not their helical ankyrin tether, but instead an elastic hinge that suspends that tether on the channel gate.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 2","pages":"259-267"},"PeriodicalIF":21.2,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142929722","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}
Seung Ha Kim, Jaegeon Lee, Mirae Jang, Seung-Eon Roh, Soobin Kim, Ji Hwan Lee, Jewoo Seo, Jinhee Baek, Jae Yoon Hwang, In Seon Baek, Yong-Seok Lee, Eiji Shigetomi, C. Justin Lee, Schuichi Koizumi, Sun Kwang Kim, Sang Jeong Kim
{"title":"Cerebellar Bergmann glia integrate noxious information and modulate nocifensive behaviors","authors":"Seung Ha Kim, Jaegeon Lee, Mirae Jang, Seung-Eon Roh, Soobin Kim, Ji Hwan Lee, Jewoo Seo, Jinhee Baek, Jae Yoon Hwang, In Seon Baek, Yong-Seok Lee, Eiji Shigetomi, C. Justin Lee, Schuichi Koizumi, Sun Kwang Kim, Sang Jeong Kim","doi":"10.1038/s41593-024-01807-z","DOIUrl":"10.1038/s41593-024-01807-z","url":null,"abstract":"The cerebellum is activated by noxious stimuli and pathological pain but its role in noxious information processing remains unknown. Here, we show that in mice, cutaneous noxious electrical stimuli induced noradrenaline (NA) release from locus coeruleus (LC) terminals in the cerebellar cortex. Bergmann glia (BG) accumulated these LC–NA signals by increasing intracellular calcium in an integrative manner (‘flares’). BG flares were also elicited in response to an intraplantar capsaicin injection. Chemogenetic inactivation of LC terminals or BG in the cerebellar cortex or BG-specific knockdown of α1-adrenergic receptors suppressed BG flares, reduced nocifensive licking and had analgesic effects in nerve injury-induced chronic neuropathic pain. Moreover, chemogenetic activation of BG or an intraplantar capsaicin injection reduced Purkinje cell firing, which may disinhibit the output activity of the deep cerebellar nuclei. These results suggest a role for BG in computing noxious information from the LC and in modulating pain-related behaviors by regulating cerebellar output. This study shows that cerebellar Bergmann glia process noxious stimuli by integrating signals from the locus coeruleus. This mechanism modulates pain-related behaviors. These findings provide insight into cerebellar involvement in pain processing.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 2","pages":"336-345"},"PeriodicalIF":21.2,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911423","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}
{"title":"Negative self-experiences shape responses to others’ emotional states","authors":"","doi":"10.1038/s41593-024-01817-x","DOIUrl":"10.1038/s41593-024-01817-x","url":null,"abstract":"Mice react differently to others’ stress depending on their own past experience of the same (but not different) stress. Corticotropin-releasing factor (CRF) neuron activity in the medial prefrontal cortex (mPFC) specifically modulates the influence of affective past experience on emotional reactions to others, which was estrus-dependent in females and dominance-dependent in males.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 1","pages":"11-12"},"PeriodicalIF":21.2,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911421","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}
{"title":"Neurocognitive dynamics of human cooperation unveiled by intracranial recordings","authors":"","doi":"10.1038/s41593-024-01825-x","DOIUrl":"10.1038/s41593-024-01825-x","url":null,"abstract":"Simultaneous intracranial electroencephalographic recordings from individuals playing a dynamic cooperation game reveal unique neural profiles of high-gamma intra-brain activity and inter-brain synchronization in the temporoparietal junction and the amygdala.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 1","pages":"13-14"},"PeriodicalIF":21.2,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911422","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}
Elvisha Dhamala, Jocelyn A. Ricard, Lucina Q. Uddin, Liisa A. M. Galea, Emily G. Jacobs, Sarah W. Yip, B. T. Thomas Yeo, M. Mallar Chakravarty, Avram J. Holmes
{"title":"Considering the interconnected nature of social identities in neuroimaging research","authors":"Elvisha Dhamala, Jocelyn A. Ricard, Lucina Q. Uddin, Liisa A. M. Galea, Emily G. Jacobs, Sarah W. Yip, B. T. Thomas Yeo, M. Mallar Chakravarty, Avram J. Holmes","doi":"10.1038/s41593-024-01832-y","DOIUrl":"10.1038/s41593-024-01832-y","url":null,"abstract":"Considerable heterogeneity exists in the expression of complex human behaviors across the cognitive, personality and mental health domains. It is increasingly evident that individual variability in behavioral expression is substantially affected by sociodemographic factors that often interact with life experiences. Here, we formally address the urgent need to incorporate intersectional identities in neuroimaging studies of behavior, with a focus on research in mental health. We highlight how diverse sociodemographic factors influence the study of psychiatric conditions, focusing on how interactions between those factors might contribute to brain biology and illness expression, including prevalence, symptom burden, help seeking, treatment response and tolerance, and relapse and remission. We conclude with a discussion of the considerations and actionable items related to participant recruitment, data acquisition and data analysis to facilitate the inclusion and incorporation of diverse intersectional identities in neuroimaging. Individual variability in behavior is influenced by social identities. Here, Dhamala et al. discuss the need to incorporate social identities in neuroimaging studies of behavior and explore how to foster inclusivity in research.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 2","pages":"222-233"},"PeriodicalIF":21.2,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887937","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}
Naoto Watamura, Martha S. Foiani, Sumi Bez, Mathieu Bourdenx, Alessia Santambrogio, Claire Frodsham, Elena Camporesi, Gunnar Brinkmalm, Henrik Zetterberg, Saisha Patel, Naoko Kamano, Mika Takahashi, Javier Rueda-Carrasco, Loukia Katsouri, Stephanie Fowler, Emir Turkes, Shoko Hashimoto, Hiroki Sasaguri, Takashi Saito, AFM Saiful Islam, Seico Benner, Toshihiro Endo, Katsuji Kobayashi, Chiho Ishida, Michele Vendruscolo, Masahito Yamada, Karen E. Duff, Takaomi C. Saido
{"title":"In vivo hyperphosphorylation of tau is associated with synaptic loss and behavioral abnormalities in the absence of tau seeds","authors":"Naoto Watamura, Martha S. Foiani, Sumi Bez, Mathieu Bourdenx, Alessia Santambrogio, Claire Frodsham, Elena Camporesi, Gunnar Brinkmalm, Henrik Zetterberg, Saisha Patel, Naoko Kamano, Mika Takahashi, Javier Rueda-Carrasco, Loukia Katsouri, Stephanie Fowler, Emir Turkes, Shoko Hashimoto, Hiroki Sasaguri, Takashi Saito, AFM Saiful Islam, Seico Benner, Toshihiro Endo, Katsuji Kobayashi, Chiho Ishida, Michele Vendruscolo, Masahito Yamada, Karen E. Duff, Takaomi C. Saido","doi":"10.1038/s41593-024-01829-7","DOIUrl":"10.1038/s41593-024-01829-7","url":null,"abstract":"Tau pathology is a hallmark of several neurodegenerative diseases, including frontotemporal dementia and Alzheimer’s disease. However, the sequence of events and the form of tau that confers toxicity are still unclear, due in large part to the lack of physiological models of tauopathy initiation and progression in which to test hypotheses. We have developed a series of targeted mice expressing frontotemporal-dementia-causing mutations in the humanized MAPT gene to investigate the earliest stages of tauopathy. MAPTInt10+3G>A and MAPTS305N;Int10+3G>A lines show abundant hyperphosphorylated tau in the hippocampus and entorhinal cortex, but they do not develop seed-competent fibrillar structures. Accumulation of hyperphosphorylated tau was accompanied by neurite degeneration, loss of viable synapses and indicators of behavioral abnormalities. Our results demonstrate that neuronal toxicity can occur in the absence of fibrillar, higher-order structures and that tau hyperphosphorylation is probably involved in the earliest etiological events in tauopathies showing isoform ratio imbalance. Mice expressing humanized mutant tau exhibit synaptic loss and behavioral abnormalities in the absence of abnormal tau conformers, suggesting that hyperphosphorylated tau can be pathological, at least in tauopathies caused by tau isoform imbalance.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 2","pages":"293-307"},"PeriodicalIF":21.2,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41593-024-01829-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142879932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cagney E. Coomer, Daria Naumova, Mustafa Talay, Bence Zolyomi, Nathaniel J. Snell, Altar Sorkaç, Jean Michel Chanchu, Ji Cheng, Ivana Roman, Jennifer Li, Drew Robson, David L. McLean, Gilad Barnea, Marnie E. Halpern
{"title":"Transsynaptic labeling and transcriptional control of zebrafish neural circuits","authors":"Cagney E. Coomer, Daria Naumova, Mustafa Talay, Bence Zolyomi, Nathaniel J. Snell, Altar Sorkaç, Jean Michel Chanchu, Ji Cheng, Ivana Roman, Jennifer Li, Drew Robson, David L. McLean, Gilad Barnea, Marnie E. Halpern","doi":"10.1038/s41593-024-01815-z","DOIUrl":"10.1038/s41593-024-01815-z","url":null,"abstract":"Deciphering the connectome, the ensemble of synaptic connections that underlie brain function, is a central goal of neuroscience research. Here we report the in vivo mapping of connections between presynaptic and postsynaptic partners in zebrafish, by adapting the trans-Tango genetic approach that was first developed for anterograde transsynaptic tracing in Drosophila. Neural connections were visualized between synaptic partners in larval retina, brain and spinal cord and followed over development. The specificity of labeling was corroborated by functional experiments in which optogenetic activation of presynaptic spinal cord interneurons elicited responses in known motor neuronal postsynaptic targets, as measured by trans-Tango-dependent expression of a genetically encoded calcium indicator or by electrophysiology. Transsynaptic signaling through trans-Tango reveals synaptic connections in the zebrafish nervous system, providing a valuable in vivo tool to monitor and interrogate neural circuits over time. The trans-Tango genetic strategy, which mediates signaling across synapses, was adapted to identify neural connections in a vertebrate nervous system, with synaptic partners confirmed in the retina and spinal cord of larval zebrafish.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 1","pages":"189-200"},"PeriodicalIF":21.2,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142849011","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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