CellPub Date : 2025-07-22DOI: 10.1016/j.cell.2025.05.016
Hyoung-Soo Cho, Ji-Sun Yoo, Xinyang Song, Byoungsook Goh, Alos Diallo, Jesang Lee, Sumin Son, Yoon Soo Hwang, Seung Bum Park, Sungwhan F. Oh, Dennis L. Kasper
{"title":"Structure of gut microbial glycolipid modulates host inflammatory response","authors":"Hyoung-Soo Cho, Ji-Sun Yoo, Xinyang Song, Byoungsook Goh, Alos Diallo, Jesang Lee, Sumin Son, Yoon Soo Hwang, Seung Bum Park, Sungwhan F. Oh, Dennis L. Kasper","doi":"10.1016/j.cell.2025.05.016","DOIUrl":"https://doi.org/10.1016/j.cell.2025.05.016","url":null,"abstract":"Commensals are constantly shaping the host’s immunological landscape. Lipopolysaccharides found in gram-negative microbes have a terminal lipid A in their outer membrane. Here, we report that structural variations in symbiotic lipid A lead to divergent immune responses with each lipid A structure, eliciting effects distinct from those induced by classical lipid A. Certain lipid A structures can induce a sustained interferon (IFN)-β response orchestrated by Cdc42-facilitated Toll-like receptor 4 (TLR4) endocytosis and lipid droplet (LD) formation. This lipid A-directed IFN-β response is paramount for colon RORγt<sup>+</sup> regulatory T cell (Treg) induction while simultaneously suppressing colonic T<sub>H</sub>17 cells and controlling gut inflammation. Intriguingly, the quantitatively dominant penta-acylated lipid A species in Bacteroidetes fails to elicit an IFN-β response. Instead, a less abundant tetra-acylated lipid A species sustainably induces IFN-β, thereby contributing to RORγt<sup>+</sup> Treg homeostasis. Nuances in symbiont lipid A structure contribute to maintaining potent regulation of Tregs to maintain a healthy endobiotic balance.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"52 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144677398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellPub Date : 2025-07-22DOI: 10.1016/j.cell.2025.06.042
Erica Wolin, Jimmy K. Guo, Mario R. Blanco, Isabel N. Goronzy, Darvesh Gorhe, Wenzhao Dong, Andrew A. Perez, Abdurrahman Keskin, Elizabeth Valenzuela, Ahmed A. Abdou, Carl R. Urbinati, Ross Kaufhold, H. Tomas Rube, Jailson Brito Querido, Mitchell Guttman, Marko Jovanovic
{"title":"SPIDR enables multiplexed mapping of RNA-protein interactions and uncovers a mechanism for selective translational suppression upon cell stress","authors":"Erica Wolin, Jimmy K. Guo, Mario R. Blanco, Isabel N. Goronzy, Darvesh Gorhe, Wenzhao Dong, Andrew A. Perez, Abdurrahman Keskin, Elizabeth Valenzuela, Ahmed A. Abdou, Carl R. Urbinati, Ross Kaufhold, H. Tomas Rube, Jailson Brito Querido, Mitchell Guttman, Marko Jovanovic","doi":"10.1016/j.cell.2025.06.042","DOIUrl":"https://doi.org/10.1016/j.cell.2025.06.042","url":null,"abstract":"RNA-binding proteins (RBPs) regulate all stages of the mRNA life cycle, yet current methods generally map RNA targets of RBPs one protein at a time. To overcome this limitation, we developed SPIDR (split-and-pool identification of RBP targets), a highly multiplexed split-pool method that profiles the binding sites of dozens of RBPs simultaneously. SPIDR identifies precise, single-nucleotide binding sites for diverse classes of RBPs. Using SPIDR, we uncovered an interaction between LARP1 and the 18S rRNA and resolved this interaction to the mRNA entry channel of the 40S ribosome using cryoelectron microscopy (cryo-EM), providing a potential mechanistic explanation for LARP1’s role in translational suppression. We explored changes in RBP binding upon mTOR inhibition and identified that 4EBP1 preferentially associates with translationally repressed mRNAs upon mTOR inhibition. SPIDR has the potential to significantly advance our understanding of RNA biology by enabling rapid, <em>de novo</em> discovery of RNA-protein interactions at an unprecedented scale.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"4 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144677399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellPub Date : 2025-07-21DOI: 10.1016/j.cell.2025.06.035
Yaqiao Li, Carlota Pereda Serras, Jessica Blumenfeld, Min Xie, Yanxia Hao, Elise Deng, You Young Chun, Julia Holtzman, Alice An, Seo Yeon Yoon, Xinyu Tang, Antara Rao, Sarah Woldemariam, Alice Tang, Alex Zhang, Jeffrey Simms, Iris Lo, Tomiko Oskotsky, Michael J. Keiser, Yadong Huang, Marina Sirota
{"title":"Cell-type-directed network-correcting combination therapy for Alzheimer’s disease","authors":"Yaqiao Li, Carlota Pereda Serras, Jessica Blumenfeld, Min Xie, Yanxia Hao, Elise Deng, You Young Chun, Julia Holtzman, Alice An, Seo Yeon Yoon, Xinyu Tang, Antara Rao, Sarah Woldemariam, Alice Tang, Alex Zhang, Jeffrey Simms, Iris Lo, Tomiko Oskotsky, Michael J. Keiser, Yadong Huang, Marina Sirota","doi":"10.1016/j.cell.2025.06.035","DOIUrl":"https://doi.org/10.1016/j.cell.2025.06.035","url":null,"abstract":"Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder characterized by heterogeneous molecular changes across diverse cell types, posing significant challenges for treatment development. To address this, we introduced a cell-type-specific, multi-target drug discovery strategy grounded in human data and real-world evidence. This approach integrates single-cell transcriptomics, drug perturbation databases, and clinical records. Using this framework, letrozole and irinotecan were identified as a potential combination therapy, each targeting AD-related gene expression changes in neurons and glial cells, respectively. In an AD mouse model with both Aβ and tau deposits, this combination therapy significantly improved memory performance and reduced AD-related pathologies compared with vehicle and single-drug treatments. Single-nucleus transcriptomic analysis confirmed that the therapy reversed disease-associated gene networks in a cell-type-specific manner. These results highlight the promise of cell-type-directed combination therapies in addressing multifactorial diseases like AD and lay the groundwork for precision medicine tailored to patient-specific transcriptomic and clinical profiles.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"29 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144669960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Procr+ chondroprogenitors sense mechanical stimuli to govern articular cartilage maintenance and regeneration","authors":"Qiaoling Zhu, Feng Yin, Jiachen Qin, Wanyu Shi, Yaojia Liu, Yuanyuan Zhao, Jianfang Wang, Lei Zhang, Aoyuan Fan, Dandan Cao, Qiqi Peng, Bin Zhou, Lijun Wang, Weiguo Zou, Rui Yue","doi":"10.1016/j.cell.2025.06.036","DOIUrl":"https://doi.org/10.1016/j.cell.2025.06.036","url":null,"abstract":"Protein C receptor<sup>+</sup> (Procr<sup>+</sup>) cells were identified as stem or progenitor cells in multiple adult tissues. However, whether mechanical stimuli fine-tune their activation and differentiation remain unknown. Here, we found rare Procr<sup>+</sup> cells in the superficial layer of tibial articular cartilage and meniscus, which keep replenishing chondrocytes in postnatal knee joints. Mechanical stimulation by forced running significantly increased the frequency of Procr<sup>+</sup> cells, whereas mechanical unloading by tail suspension showed opposite effects. Osteoarthritis (OA) activated Procr<sup>+</sup> cells to repair cartilage erosion, whereas genetic ablation of Procr<sup>+</sup> cells accelerated OA progression. Pharmacological or genetic inhibition of the mechanosensor Piezo1 significantly blunted cartilage regeneration by Procr<sup>+</sup> cells and exacerbated OA. In contrast, intra-articular administration of a Piezo1 agonist ameliorated OA symptoms. Purified mouse or human Procr<sup>+</sup> superficial cells robustly repair articular cartilage after expansion and <em>in vivo</em> transplantation. Together, we discovered a mechanosensitive chondroprogenitor population indispensable for articular cartilage maintenance and regeneration.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"25 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144669924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellPub Date : 2025-07-21DOI: 10.1016/j.cell.2025.06.038
Alexander A. Sousa, Markus Terrey, Holt A. Sakai, Christine Q. Simmons, Elena Arystarkhova, Natalia S. Morsci, Laura C. Anderson, Jun Xie, Fabian Suri-Payer, Linda C. Laux, Emmanuel Roze, Sylvie Forlani, Guangping Gao, Simon Frost, Nina Frost, Kathleen J. Sweadner, Alfred L. George, Cathleen M. Lutz, David R. Liu
{"title":"In vivo prime editing rescues alternating hemiplegia of childhood in mice","authors":"Alexander A. Sousa, Markus Terrey, Holt A. Sakai, Christine Q. Simmons, Elena Arystarkhova, Natalia S. Morsci, Laura C. Anderson, Jun Xie, Fabian Suri-Payer, Linda C. Laux, Emmanuel Roze, Sylvie Forlani, Guangping Gao, Simon Frost, Nina Frost, Kathleen J. Sweadner, Alfred L. George, Cathleen M. Lutz, David R. Liu","doi":"10.1016/j.cell.2025.06.038","DOIUrl":"https://doi.org/10.1016/j.cell.2025.06.038","url":null,"abstract":"Alternating hemiplegia of childhood (AHC) is a neurodevelopmental disorder with no disease-modifying treatment. Mutations in <em>ATP1A3</em>, encoding an Na<sup>+</sup>/K<sup>+</sup> ATPase subunit, cause 70% of AHC cases. Here, we present prime editing (PE) and base editing (BE) strategies to correct <em>ATP1A3</em> and <em>Atp1a3</em> mutations in human cells and in two AHC mouse models. We used PE and BE to correct five prevalent <em>ATP1A3</em> mutations with 43%–90% efficiency. AAV9-mediated <em>in vivo</em> PE corrects <em>Atp1a3</em> D801N and E815K in the CNS of two AHC mouse models, yielding up to 48% DNA correction and 73% mRNA correction in bulk brain cortex. <em>In vivo</em> PE rescued clinically relevant phenotypes, including restoration of ATPase activity; amelioration of paroxysmal spells, motor defects, and cognition deficits; and dramatic extension of animal lifespan. This work suggests a potential one-time PE treatment for AHC and establishes the ability of PE to rescue a neurological disease in animals.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"100 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144669925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellPub Date : 2025-07-21DOI: 10.1016/j.cell.2025.06.039
Doris Kaltenecker, Søren Fisker Schmidt, Peter Weber, Anne Loft, Pauline Morigny, Juliano Machado, Julia Geppert, Kerstin Beate Saul, Pia Benedikt, Claudia-Eveline Molocea, Rachel Scott, Kerstin Haase, Marc E. Martignoni, Ana Jimena Alfaro, Kan Kau Chow, Estefania Simoes, José Pinhata Otoch, Joanna D.C.C. Lima, Charles Swanton, Nadine Spielmann, Mauricio Berriel Diaz
{"title":"Functional liver genomics identifies hepatokines promoting wasting in cancer cachexia","authors":"Doris Kaltenecker, Søren Fisker Schmidt, Peter Weber, Anne Loft, Pauline Morigny, Juliano Machado, Julia Geppert, Kerstin Beate Saul, Pia Benedikt, Claudia-Eveline Molocea, Rachel Scott, Kerstin Haase, Marc E. Martignoni, Ana Jimena Alfaro, Kan Kau Chow, Estefania Simoes, José Pinhata Otoch, Joanna D.C.C. Lima, Charles Swanton, Nadine Spielmann, Mauricio Berriel Diaz","doi":"10.1016/j.cell.2025.06.039","DOIUrl":"https://doi.org/10.1016/j.cell.2025.06.039","url":null,"abstract":"In cancer cachexia, the presence of a tumor triggers systemic metabolic disruption that leads to involuntary body weight loss and accelerated mortality in affected patients. Here, we conducted transcriptomic and epigenomic profiling of the liver in various weight-stable cancer and cancer cachexia models. An integrative multilevel analysis approach identified a distinct gene expression signature that included hepatocyte-secreted factors and the circadian clock component REV-ERBα as key modulator of hepatic transcriptional reprogramming in cancer cachexia. Notably, hepatocyte-specific genetic reconstitution of REV-ERBα in cachexia ameliorated peripheral tissue wasting. This improvement was associated with decreased levels of specific cachexia-controlled hepatocyte-secreted factors. These hepatokines promoted catabolism in multiple cell types and were elevated in cachectic cancer patients. Our findings reveal a mechanism by which the liver contributes to peripheral tissue wasting in cancer cachexia, offering perspectives for future therapeutic interventions.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"112 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144669928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellPub Date : 2025-07-21DOI: 10.1016/j.cell.2025.06.037
Daniela C. Soto, José M. Uribe-Salazar, Gulhan Kaya, Ricardo Valdarrago, Aarthi Sekar, Nicholas K. Haghani, Keiko Hino, Gabriana La, Natasha Ann F. Mariano, Cole Ingamells, Aidan Baraban, Zoeb Jamal, Tychele N. Turner, Eric D. Green, Sergi Simó, Gerald Quon, Aida M. Andrés, Megan Y. Dennis
{"title":"Human-specific gene expansions contribute to brain evolution","authors":"Daniela C. Soto, José M. Uribe-Salazar, Gulhan Kaya, Ricardo Valdarrago, Aarthi Sekar, Nicholas K. Haghani, Keiko Hino, Gabriana La, Natasha Ann F. Mariano, Cole Ingamells, Aidan Baraban, Zoeb Jamal, Tychele N. Turner, Eric D. Green, Sergi Simó, Gerald Quon, Aida M. Andrés, Megan Y. Dennis","doi":"10.1016/j.cell.2025.06.037","DOIUrl":"https://doi.org/10.1016/j.cell.2025.06.037","url":null,"abstract":"Duplicated genes expanded in the human lineage likely contributed to brain evolution, yet challenges exist in their discovery due to sequence-assembly errors. We used a complete telomere-to-telomere genome sequence to identify 213 human-specific gene families. From these, 362 paralogs were found in all modern human genomes tested and brain transcriptomes, making them top candidates contributing to human-universal brain features. Choosing a subset of paralogs, long-read DNA sequencing of hundreds of modern humans revealed previously hidden signatures of selection, including for T cell marker <em>CD8B</em>. To understand roles in brain development, we generated zebrafish CRISPR “knockout” models of nine orthologs and introduced mRNA-encoding paralogs, effectively “humanizing” larvae. Our findings implicate two genes in possibly contributing to hallmark features of the human brain: <em>GPR89B</em> in dosage-mediated brain expansion and <em>FRMPD2B</em> in altered synapse signaling. Our holistic approach provides insights and a comprehensive resource for studying gene expansion drivers of human brain evolution.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"31 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144669929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellPub Date : 2025-07-17DOI: 10.1016/j.cell.2025.06.033
Zhongyang Wu, Scott D. Pope, Nasiha S. Ahmed, Diana L. Leung, Yu Hong, Stephanie Hajjar, Cathleen Krabak, Zhe Zhong, Krishnan Raghunathan, Qiuyu Yue, Diya M. Anand, Elizabeth B. Kopp, Daniel Okin, Weiyi Ma, Ivan Zanoni, Jonathan C. Kagan, Jay R. Thiagarajah, Diana C. Hargreaves, Ruslan Medzhitov, Xu Zhou
{"title":"Regulation of inflammatory responses by pH-dependent transcriptional condensates","authors":"Zhongyang Wu, Scott D. Pope, Nasiha S. Ahmed, Diana L. Leung, Yu Hong, Stephanie Hajjar, Cathleen Krabak, Zhe Zhong, Krishnan Raghunathan, Qiuyu Yue, Diya M. Anand, Elizabeth B. Kopp, Daniel Okin, Weiyi Ma, Ivan Zanoni, Jonathan C. Kagan, Jay R. Thiagarajah, Diana C. Hargreaves, Ruslan Medzhitov, Xu Zhou","doi":"10.1016/j.cell.2025.06.033","DOIUrl":"https://doi.org/10.1016/j.cell.2025.06.033","url":null,"abstract":"Inflammation is an essential defense response but operates at the cost of normal tissue functions. Whether and how the negative impact of inflammation is monitored remains largely unknown. Acidification of the tissue microenvironment is associated with inflammation. Here, we investigated whether macrophages sense tissue acidification to adjust inflammatory responses. We found that acidic pH restructured the inflammatory response of macrophages in a gene-specific manner. We identified mammalian BRD4 as an intracellular pH sensor. Acidic pH disrupts transcription condensates containing BRD4 and MED1 via histidine-enriched intrinsically disordered regions. Crucially, a decrease in macrophage intracellular pH is necessary and sufficient to regulate transcriptional condensates <em>in vitro</em> and <em>in vivo</em>, acting as negative feedback to regulate the inflammatory response. Collectively, these findings uncovered a pH-dependent switch in transcriptional condensates that enables environment-dependent control of inflammation, with a broader implication for calibrating the magnitude and quality of inflammation by the inflammatory cost.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"24 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144645287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CellPub Date : 2025-07-17DOI: 10.1016/j.cell.2025.06.032
Yunhui Ge, Tongyi Dou, Thu Uyen Nguyen, Gaya P. Yadav, Theodore G. Wensel, Jiansen Jiang, Pengxiang Huang
{"title":"Structural insights into brain thyroid hormone transport via MCT8 and OATP1C1","authors":"Yunhui Ge, Tongyi Dou, Thu Uyen Nguyen, Gaya P. Yadav, Theodore G. Wensel, Jiansen Jiang, Pengxiang Huang","doi":"10.1016/j.cell.2025.06.032","DOIUrl":"https://doi.org/10.1016/j.cell.2025.06.032","url":null,"abstract":"Adequate delivery of thyroid hormones to the brain is crucial for normal neurological development. MCT8 and OATP1C1, two solute carrier (SLC) transporters, mediate the passage of thyroid hormones across the blood-brain barrier and into the central nervous system. Mutations in MCT8 result in Allan-Herndon-Dudley syndrome (AHDS), an X-linked birth defect characterized by neurodevelopmental impairments and peripheral hyperthyroidism, whereas OATP1C1 deficiency is linked to brain hypometabolism and progressive neurodegeneration. Here, we report cryoelectron microscopy (cryo-EM) structures of MCT8 and OATP1C1 bound with the active thyroid hormone triiodothyronine (T3) and the prohormone thyroxine (T4) at 2.9 and 2.3 Å resolutions, respectively. Combined with functional studies, we elucidate their distinct thyroid hormone recognition and transport mechanisms and explain disease mutations. Although extracellular allosteric sites are not a common feature of SLC transporters, we identify one in OATP1C1. Collectively, these findings illuminate key aspects of thyroid hormone transport, a fundamental process in development and disease.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"13 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144645288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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