The EMBO JournalPub Date : 2025-04-11DOI: 10.1038/s44318-025-00422-3
Rosa Pascual,Jinming Cheng,Amelia H De Smet,Bianca D Capaldo,Minhsuang Tsai,Somayeh Kordafshari,François Vaillant,Xiaoyu Song,Göknur Giner,Michael J G Milevskiy,Felicity C Jackling,Bhupinder Pal,Toby Dite,Jumana Yousef,Laura F Dagley,Gordon K Smyth,Naiyang Fu,Geoffrey J Lindeman,Yunshun Chen,Jane E Visvader
{"title":"Fibroblast hierarchy dynamics during mammary gland morphogenesis and tumorigenesis.","authors":"Rosa Pascual,Jinming Cheng,Amelia H De Smet,Bianca D Capaldo,Minhsuang Tsai,Somayeh Kordafshari,François Vaillant,Xiaoyu Song,Göknur Giner,Michael J G Milevskiy,Felicity C Jackling,Bhupinder Pal,Toby Dite,Jumana Yousef,Laura F Dagley,Gordon K Smyth,Naiyang Fu,Geoffrey J Lindeman,Yunshun Chen,Jane E Visvader","doi":"10.1038/s44318-025-00422-3","DOIUrl":"https://doi.org/10.1038/s44318-025-00422-3","url":null,"abstract":"Fibroblasts form a major component of the stroma in normal mammary tissue and breast tumors. Here, we have applied longitudinal single-cell transcriptome profiling of >45,000 fibroblasts in the mouse mammary gland across five different developmental stages and during oncogenesis. In the normal gland, diverse stromal populations were resolved, including lobular-like fibroblasts, committed preadipocytes and adipogenesis-regulatory, as well as cycling fibroblasts in puberty and pregnancy. These specialized cell types appear to emerge from CD34high mesenchymal progenitor cells, accompanied by elevated Hedgehog signaling. During late tumorigenesis, heterogeneous cancer-associated fibroblasts (CAFs) were identified in mouse models of breast cancer, including a population of CD34- myofibroblastic CAFs (myCAFs) that were transcriptionally and phenotypically similar to senescent CAFs. Moreover, Wnt9a was demonstrated to be a regulator of senescence in CD34- myCAFs. These findings reflect a diverse and hierarchically organized stromal compartment in the normal mammary gland that provides a framework to better understand fibroblasts in normal and cancerous states.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"110 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143824782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Reconstruction of the ancient cyanobacterial proto-circadian clock system KaiABC.","authors":"Silin Li,Zengxuan Zhou,Yufeng Wan,Xudong Jia,Peiliang Wang,Yu Wang,Taisen Zuo,He Cheng,Xiaoting Fang,Shuqi Dong,Jun He,Yilin Yang,Yichen Xu,Shaoxuan Fu,Xujing Wang,Ximing Qin,Qiguang Xie,Xiaodong Xu,Yuwei Zhao,Dan Liang,Peng Zhang,Qinfen Zhang,Jinhu Guo","doi":"10.1038/s44318-025-00425-0","DOIUrl":"https://doi.org/10.1038/s44318-025-00425-0","url":null,"abstract":"Earlier in its history, the Earth used to spin faster than it does today. How ancient organisms adapted to the short day/night cycles during that time remains unclear. In this study we reconstruct and analyse the ancient circadian clock system KaiABC (anKaiABC) of cyanobacteria that existed ~0.95 billion years ago, when the daily light/dark cycle was ~18 h-long. Compared to their contemporary counterparts, anKaiABC proteins had different structures and interactions. The kinase, phosphatase, and adenosine triphosphatase (ATPase) activities of anKaiC were lower, while the anKaiA and anKaiB proteins were less effective at regulating the KaiC/anKaiC phosphorylation status. We provide evidence indicating that the anKaiABC system does not endogenously oscillate, but it can be entrained by an 18 h-long light/dark cycle. A Synechococcus strain expressing ankaiABC genes exhibits better adaptation to 9-h light/9-h dark cycles (LD9:9) that mimic the ancient 18-h day/night cycles, whereas the kaiABC-expressing strain preferentially adapts to the LD12:12 contemporary conditions. These findings suggest that, despite its lack of self-sustaining circadian oscillation, the proto-circadian system may have mediated adaptation of ancient cyanobacteria to the 18 h-long light/dark cycles present 0.95 billion years ago.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"39 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143822451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Temporal refinement of Dach1 expression contributes to the development of somatosensory neurons.","authors":"Tünde Szemes,Alba Sabaté San José,Abdulkader Azouz,Maren Sitte,Gabriela Salinas,Younes Achouri,Sadia Kricha,Laurence Ris,Kristy Red-Horse,Eric J Bellefroid,Simon Desiderio","doi":"10.1038/s44318-025-00427-y","DOIUrl":"https://doi.org/10.1038/s44318-025-00427-y","url":null,"abstract":"During somatosensory neurogenesis, neurons are born in an unspecialized transcriptional state. Several transcription factors in these cells follow a broad-to-restricted expression trajectory as development proceeds, giving rise to neuron subtypes with different identities. The relevance of this temporal refinement of transcription factor expression remains unclear as the functions of transcription factors with broad-to-restricted expression patterns have been mostly studied in those neuron subtypes in which they remain active. Here we show that Dach1 encodes a bona fide transcription factor with a broad-to-restricted expression pattern retained and required in tactile somatosensory neurons. In developing nociceptors, Prdm12 contributes to Dach1 silencing. Using genetic approaches to prevent its temporal restriction during mouse somatosensory development, we reveal that Dach1 expression refinement is a prerequisite for the acquisition of an appropriate transcriptional profile in those somatosensory neuron subtypes in which it becomes ultimately silenced. These findings highlight the essential role played by Dach1 during somatosensory neuron development and demonstrate that the temporal pattern of broad-to-restricted expression followed by several transcription factors is physiologically important for the development of somatosensory neurons.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"217 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ductal or Ngn3+ cells do not contribute to adult pancreatic islet beta-cell neogenesis in homeostasis.","authors":"Xiuzhen Huang,Huan Zhao,Hui Chen,Zixin Liu,Kuo Liu,Zan Lv,Xiuxiu Liu,Ximeng Han,Maoying Han,Jie Lu,Qiao Zhou,Bin Zhou","doi":"10.1038/s44318-025-00434-z","DOIUrl":"https://doi.org/10.1038/s44318-025-00434-z","url":null,"abstract":"The adult pancreatic ducts have long been proposed to contain rare progenitors, some of which expressing Ngn3, that generate new beta cells in endocrine-islet homeostasis. Due to their postulated rarity and the lack of definitive markers, the existence or absence of ductal endocrine progenitors remains unsettled despite many studies. Genetic lineage tracing of ductal cells or Ngn3+ cells with currently available CreER drivers has been complicated by off-target labeling of pre-existing beta cells. Here, using dual-recombinase-mediated intersectional genetic strategy and newly-derived Ngn3-2A-CreER and Hnf1b-2A-CreER knock-in drivers, we succeeded in specifically labeling Ngn3-positive cells and Hnf1b-positive ductal cells without marking pre-existing beta cells. These data revealed no evidence of de novo generation of insulin-producing beta cells from ductal cells or endogenous Ngn3-positive cells in the adult pancreas during homeostasis.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"SLC25A1 and ACLY maintain cytosolic acetyl-CoA and regulate ferroptosis susceptibility via FSP1 acetylation.","authors":"Wei Li,Jing Han,Bin Huang,Tengteng Xu,Yihong Wan,Dan Luo,Weiyao Kong,Ying Yu,Lei Zhang,Yong Nian,Bo Chu,Chengqian Yin","doi":"10.1038/s44318-025-00369-5","DOIUrl":"https://doi.org/10.1038/s44318-025-00369-5","url":null,"abstract":"Ferroptosis, an iron-dependent form of programmed cell death characterized by excessive lipid hydroperoxides accumulation, emerges as a promising target in cancer therapy. Among the solute carrier (SLC) superfamily, the cystine/glutamate transporter system antiporter components SLC3A2 and SLC7A11 are known to regulate ferroptosis by facilitating cystine import for ferroptosis inhibition. However, the contribution of additional SLC superfamily members to ferroptosis remains poorly understood. Here, we use a targeted CRISPR-Cas9 screen of the SLC superfamily to identify SLC25A1 as a critical ferroptosis regulator in human cancer cells. SLC25A1 drives citrate export from the mitochondria to the cytosol, where it fuels acetyl-CoA synthesis by ATP citrate lyase (ACLY). This acetyl-CoA supply sustains FSP1 acetylation and prevents its degradation by the proteasome via K29-linked ubiquitin chains. K168 is the primary site of FSP1 acetylation and deacetylation by KAT2B and HDAC3, respectively. Pharmacological inhibition of SLC25A1 and ACLY significantly enhances cancer cell susceptibility to ferroptosis both in vitro and in vivo. Targeting the SLC25A1-ACLY axis is therefore a potential therapeutic strategy for ferroptosis-targeted cancer intervention.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"47 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143062080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The EMBO JournalPub Date : 2025-01-28DOI: 10.1038/s44318-024-00359-z
Yan Huang,Hua Lu,Yao Liu,Jiabei Wang,Qingan Xia,Xiangmin Shi,Yan Jin,Xiaolin Liang,Wei Wang,Xiaopeng Ma,Yangyi Wang,Meng Gong,Canjun Li,Chunlei Cang,Qinghua Cui,Ceshi Chen,Tao Shen,Lianxin Liu,Xiangting Wang
{"title":"Micropeptide hSPAR regulates glutamine levels and suppresses mammary tumor growth via a TRIM21-P27KIP1-mTOR axis.","authors":"Yan Huang,Hua Lu,Yao Liu,Jiabei Wang,Qingan Xia,Xiangmin Shi,Yan Jin,Xiaolin Liang,Wei Wang,Xiaopeng Ma,Yangyi Wang,Meng Gong,Canjun Li,Chunlei Cang,Qinghua Cui,Ceshi Chen,Tao Shen,Lianxin Liu,Xiangting Wang","doi":"10.1038/s44318-024-00359-z","DOIUrl":"https://doi.org/10.1038/s44318-024-00359-z","url":null,"abstract":"mTOR plays a pivotal role in cancer growth control upon amino acid response. Recently, CDK inhibitor P27KIP1 has been reported as a noncanonical inhibitor of mTOR signaling in MEFs, via unclear mechanisms. Here, we find that P27KIP1 degradation via E3 ligase TRIM21 is inhibited by human micropeptide hSPAR through its C-terminus (hSPAR-C), causing P27KIP1's cytoplasmic accumulation in breast cancer cells. Furthermore, hSPAR/hSPAR-C also serves as an inhibitor of glutamine transporter SLC38A2 expression and thereby decreases the cellular glutamine levels specifically in cancer cells. The resultant glutamine deprivation sequentially triggers translocation of cytoplasmic P27KIP1 to lysosomes, where P27KIP1 disrupts the Ragulator complex and suppresses mTORC1 assembly. Administration of hSPAR or hSPAR-C significantly impedes breast cancer cell proliferation and tumor growth in xenograft models. These findings define hSPAR as an intrinsic control factor for cellular glutamine levels and as a novel tumor suppressor inhibiting mTORC1 assembly.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"30 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143056734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The EMBO JournalPub Date : 2025-01-28DOI: 10.1038/s44318-025-00368-6
Yongxiang Zhao,Pietro Vidossich,Biff Forbush,Junfeng Ma,Jesse Rinehart,Marco De Vivo,Erhu Cao
{"title":"Structural basis for human NKCC1 inhibition by loop diuretic drugs.","authors":"Yongxiang Zhao,Pietro Vidossich,Biff Forbush,Junfeng Ma,Jesse Rinehart,Marco De Vivo,Erhu Cao","doi":"10.1038/s44318-025-00368-6","DOIUrl":"https://doi.org/10.1038/s44318-025-00368-6","url":null,"abstract":"Na+-K+-Cl- cotransporters functions as an anion importers, regulating trans-epithelial chloride secretion, cell volume, and renal salt reabsorption. Loop diuretics, including furosemide, bumetanide, and torsemide, antagonize both NKCC1 and NKCC2, and are first-line medicines for the treatment of edema and hypertension. NKCC1 activation by the molecular crowding sensing WNK kinases is critical if cells are to combat shrinkage during hypertonic stress; however, how phosphorylation accelerates NKCC1 ion transport remains unclear. Here, we present co-structures of phospho-activated NKCC1 bound with furosemide, bumetanide, or torsemide showing that furosemide and bumetanide utilize a carboxyl group to coordinate and co-occlude a K+, whereas torsemide encroaches and expels the K+ from the site. We also found that an amino-terminal segment of NKCC1, once phosphorylated, interacts with the carboxyl-terminal domain, and together, they engage with intracellular ion exit and appear to be poised to facilitate rapid ion translocation. Together, these findings enhance our understanding of NKCC-mediated epithelial ion transport and the molecular mechanisms of its inhibition by loop diuretics.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143056732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"SLC13A2 promotes hepatocyte metabolic remodeling and liver regeneration by enhancing de novo cholesterol biosynthesis.","authors":"Li Shi,Hao Chen,Yuxin Zhang,Donghao An,Mengyao Qin,Wanting Yu,Bin Wen,Dandan He,Haiping Hao,Jing Xiong","doi":"10.1038/s44318-025-00362-y","DOIUrl":"https://doi.org/10.1038/s44318-025-00362-y","url":null,"abstract":"Metabolic requirements of dividing hepatocytes are prerequisite for liver regeneration after injury. In contrast to transcriptional dynamics during liver repair, its metabolic dependencies remain poorly defined. Here, we screened metabolic genes differentially regulated during liver regeneration, and report that SLC13A2, a transporter for TCA cycle intermediates, is decreased in rapid response to partial hepatectomy in mice and recovered along restoration of liver mass and function. Liver-specific overexpression or depletion of SLC13A2 promoted or attenuated liver regeneration, respectively. SLC13A2 increased cleavage of SREBP2, and expression of cholesterol metabolism genes, including LDLR and HMGCR. Mechanistically, SLC13A2 promotes import of citrate into hepatocytes, serving as building block for ACLY-dependent acetyl-CoA formation and de novo synthesis of cholesterol. In line, the pre-administration of the HMGCR inhibitor lovastatin abolished SLC13A2-mediated liver regeneration. Similarly, ACLY inhibition suppressed SLC13A2-promoted cholesterol synthesis for hepatocellular proliferation and liver regeneration in vivo. In sum, this study demonstrates that citrate transported by SLC13A2 acts as an intermediate metabolite to restore the metabolic homeostasis during liver regeneration, suggesting SLC13A2 as a potential drug target after liver damage.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142989727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The EMBO JournalPub Date : 2025-01-15DOI: 10.1038/s44318-024-00343-7
Kazumi Shimaoka,Kei Hori,Satoshi Miyashita,Yukiko U Inoue,Nao K N Tabe,Asami Sakamoto,Ikuko Hasegawa,Kayo Nishitani,Kunihiko Yamashiro,Saki F Egusa,Shoji Tatsumoto,Yasuhiro Go,Manabu Abe,Kenji Sakimura,Takayoshi Inoue,Takuya Imamura,Mikio Hoshino
{"title":"The microcephaly-associated transcriptional regulator AUTS2 cooperates with Polycomb complex PRC2 to produce upper-layer neurons in mice.","authors":"Kazumi Shimaoka,Kei Hori,Satoshi Miyashita,Yukiko U Inoue,Nao K N Tabe,Asami Sakamoto,Ikuko Hasegawa,Kayo Nishitani,Kunihiko Yamashiro,Saki F Egusa,Shoji Tatsumoto,Yasuhiro Go,Manabu Abe,Kenji Sakimura,Takayoshi Inoue,Takuya Imamura,Mikio Hoshino","doi":"10.1038/s44318-024-00343-7","DOIUrl":"https://doi.org/10.1038/s44318-024-00343-7","url":null,"abstract":"AUTS2 syndrome is characterized by intellectual disability and microcephaly, and is often associated with autism spectrum disorder, but the underlying mechanisms, particularly concerning microcephaly, remain incompletely understood. Here, we analyze mice mutated for the transcriptional regulator AUTS2, which recapitulate microcephaly. Their brains exhibit reduced division of intermediate progenitor cells (IPCs), leading to fewer neurons and decreased thickness in the upper-layer cortex. Increased expression of the AUTS2 transcriptional target Robo1 in the mutant animals suppresses IPC division, and transcriptomic and chromatin profiling shows that AUTS2 primarily represses transcription of genes like Robo1 in IPCs. Regions around the transcriptional start sites of AUTS2 target genes are enriched for the repressive histone modification H3K27me3, which is reduced in Auts2 mutants. Furthermore, we find that AUTS2 interacts with Polycomb complex PRC2, with which it cooperates to promote IPC division. These findings shed light on the microcephaly phenotype observed in the AUTS2 syndrome.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"119 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142989344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Recruitment of autophagy initiator TAX1BP1 advances aggrephagy from cargo collection to sequestration.","authors":"Bernd Bauer,Jonas Idinger,Martina Schuschnig,Luca Ferrari,Sascha Martens","doi":"10.1038/s44318-024-00280-5","DOIUrl":"https://doi.org/10.1038/s44318-024-00280-5","url":null,"abstract":"Autophagy mediates the degradation of harmful material within lysosomes. In aggrephagy, the pathway mediating the degradation of aggregated, ubiquitinated proteins, this cargo material is collected in larger condensates prior to its sequestration by autophagosomes. In this process, the autophagic cargo receptors SQSTM1/p62 and NBR1 drive cargo condensation, while TAX1BP1, which binds to NBR1, recruits the autophagy machinery to facilitate autophagosome biogenesis at the condensates. The mechanistic basis for the TAX1BP1-mediated switch from cargo collection to its sequestration is unclear. Here we show that TAX1BP1 is not a constitutive component of the condensates. Its recruitment correlates with the induction of autophagosome biogenesis. TAX1BP1 is sufficient to recruit the TBK1 kinase via the SINTBAD adapter. We define the NBR1-TAX1BP1-binding site, which is adjacent to the GABARAP/LC3 interaction site, and demonstrate that the recruitment of TAX1BP1 to cargo mimetics can be enhanced by an increased ubiquitin load. Our study suggests that autophagosome biogenesis is initiated once sufficient cargo is collected in the condensates.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142490374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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