{"title":"Impact of maternal and offspring smoking and breastfeeding on oesophageal cancer in adult offspring","authors":"Yixue Wang, Hongru Sun, Gen Li, Jingxue Xu, Siyu Wang, Shijie Zhang, Tianle Zhou, Tianshu Han, Changhao Sun, Jianqun Ma, Xiaoyuan Wang, Hang Yin","doi":"10.1038/s41467-025-56252-8","DOIUrl":"https://doi.org/10.1038/s41467-025-56252-8","url":null,"abstract":"<p>Numerous risk factors for oesophageal cancer are linked to lifestyle habits, but the role of early-life factors in its incidence and mortality is unclear. Using UK Biobank data, we explore the association among breastfeeding, maternal smoking, smoking in offspring, and oesophageal cancer risk in adult offspring via multivariable Cox regression. Here, we show that being breastfed, compared with not being breastfed, is associated with a lower risk of oesophageal cancer incidence (HR: 0.83, 95% CI: 0.70–0.98) and mortality (HR: 0.74, 95% CI: 0.61–0.89) in adult offspring. Additionally, it is associated with a reduced impact of smoking in offspring on oesophageal cancer incidence (HR: 0.79, 95% CI: 0.64-0.96) and mortality (HR: 0.73, 95% CI: 0.59-0.91). We subsequently construct a polygenic risk score for oesophageal cancer to explore the influence of genetic factors. Our findings emphasize the importance of breastfeeding, and smoking cessation to prevent oesophageal cancer.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"11 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhen Zhang, Zhenyu Xing, Xianglin Luo, Chong Cheng, Xikui Liu
{"title":"Densely populated macrocyclic dicobalt sites in ladder polymers for low-overpotential oxygen reduction catalysis","authors":"Zhen Zhang, Zhenyu Xing, Xianglin Luo, Chong Cheng, Xikui Liu","doi":"10.1038/s41467-025-56066-8","DOIUrl":"https://doi.org/10.1038/s41467-025-56066-8","url":null,"abstract":"<p>Dual-atom catalysts featuring synergetic dinuclear active sites, have the potential of breaking the linear scaling relationship of the well-established single-atom catalysts for oxygen reduction reaction; however, the design of dual-atom catalysts with rationalized local microenvironment for high activity and selectivity remains a great challenge. Here we design a bisalphen ladder polymer with well-defined densely populated binuclear cobalt sites on Ketjenblack substrates. The strong electron coupling effect between the fully-conjugated ladder structure and carbon substrates enhances the electron transfer between the cobalt center and oxygen intermediates, inducing the low-to-high spin transition for the 3<i>d</i> electron of Co(II). In situ techniques and theoretical calculations reveal the dynamic evolution of Co<sub>2</sub>N<sub>4</sub>O<sub>2</sub> active sites and reaction intermediates. In alkaline conditions, the catalyst exhibits impressive oxygen reduction reaction activity featuring an onset potential of 1.10 V and a half-wave potential of 1.00 V, insignificant decay after 30,000 cycles, pushing the overpotential boundaries of ORR electrocatalysis to a low level. This work provides a platform for designing efficient dual-atom catalysts with well-defined coordination and electronic structures in energy conversion technologies.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"137 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Griffin J. Davis, Anthony O. Omole, Yejin Jung, Wioletta Rut, Ronald Holewinski, Kiall F. Suazo, Hong-Rae Kim, Mo Yang, Thorkell Andresson, Marcin Drag, Euna Yoo
{"title":"Chemical tools to define and manipulate interferon-inducible Ubl protease USP18","authors":"Griffin J. Davis, Anthony O. Omole, Yejin Jung, Wioletta Rut, Ronald Holewinski, Kiall F. Suazo, Hong-Rae Kim, Mo Yang, Thorkell Andresson, Marcin Drag, Euna Yoo","doi":"10.1038/s41467-025-56336-5","DOIUrl":"https://doi.org/10.1038/s41467-025-56336-5","url":null,"abstract":"<p>Ubiquitin-specific protease 18 (USP18) is a multifunctional cysteine protease primarily responsible for deconjugating the interferon-inducible ubiquitin-like modifier ISG15 from protein substrates. Here, we report the design and synthesis of activity-based probes (ABPs) that incorporate unnatural amino acids into the C-terminal tail of ISG15, enabling the selective detection of USP18 activity over other ISG15 cross-reactive deubiquitinases (DUBs) such as USP5 and USP14. Combined with a ubiquitin-based DUB ABP, the USP18 ABP is employed in a chemoproteomics screening platform to identify and assess inhibitors of DUBs including USP18. We further demonstrate that USP18 ABPs can be utilized to profile differential activities of USP18 in lung cancer cell lines, providing a strategy that will help define the activity-related landscape of USP18 in different disease states and unravel important (de)ISGylation-dependent biological processes.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"33 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143020467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wesley Cardoso Generoso, Alana Helen Santana Alvarenga, Isabelle Taira Simões, Renan Yuji Miyamoto, Ricardo Rodrigues de Melo, Ederson Paulo Xavier Guilherme, Fernanda Mandelli, Clelton Aparecido Santos, Rafaela Prata, Camila Ramos dos Santos, Felippe Mariano Colombari, Mariana Abrahão Bueno Morais, Rodrigo Pimentel Fernandes, Gabriela Felix Persinoti, Mario Tyago Murakami, Leticia Maria Zanphorlin
{"title":"Coordinated conformational changes in P450 decarboxylases enable hydrocarbons production from renewable feedstocks","authors":"Wesley Cardoso Generoso, Alana Helen Santana Alvarenga, Isabelle Taira Simões, Renan Yuji Miyamoto, Ricardo Rodrigues de Melo, Ederson Paulo Xavier Guilherme, Fernanda Mandelli, Clelton Aparecido Santos, Rafaela Prata, Camila Ramos dos Santos, Felippe Mariano Colombari, Mariana Abrahão Bueno Morais, Rodrigo Pimentel Fernandes, Gabriela Felix Persinoti, Mario Tyago Murakami, Leticia Maria Zanphorlin","doi":"10.1038/s41467-025-56256-4","DOIUrl":"https://doi.org/10.1038/s41467-025-56256-4","url":null,"abstract":"<p>Fatty acid peroxygenases have emerged as promising biocatalysts for hydrocarbon biosynthesis due to their ability to perform C-C scission, producing olefins - key building blocks for sustainable materials and fuels. These enzymes operate through non-canonical and complex mechanisms that yield a bifurcated chemoselectivity between hydroxylation and decarboxylation. In this study, we elucidate structural features in P450 decarboxylases that enable the catalysis of unsaturated substrates, expanding the mechanistic pathways for decarboxylation reaction. Combining X-ray crystallography, molecular dynamics simulations, and machine learning, we have identified intricate molecular rearrangements within the active site that enable the Cβ atom of the substrate to approach the heme iron, thereby promoting oleate decarboxylation. Furthermore, we demonstrate that the absence of the aromatic residue in the Phe-His-Arg triad preserves chemoselectivity for alkenes, providing a distinct perspective on the molecular determinants of decarboxylation activity. Ultimately, these findings enable the sustainable production of biohydrocarbons from industrial feedstocks.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"8 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143020468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shana M. Owens, Jeffrey M. Sifford, Gang Li, Steven J. Murdock, Eduardo Salinas, Darby Oldenburg, Debopam Ghosh, Jason S. Stumhofer, Intawat Nookaew, Mark Manzano, J. Craig Forrest
{"title":"Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment","authors":"Shana M. Owens, Jeffrey M. Sifford, Gang Li, Steven J. Murdock, Eduardo Salinas, Darby Oldenburg, Debopam Ghosh, Jason S. Stumhofer, Intawat Nookaew, Mark Manzano, J. Craig Forrest","doi":"10.1038/s41467-025-56247-5","DOIUrl":"https://doi.org/10.1038/s41467-025-56247-5","url":null,"abstract":"<p>Gammaherpesviruses are DNA tumor viruses that establish lifelong latent infections in lymphocytes. For viruses such as Epstein-Barr virus and murine gammaherpesvirus 68, this is accomplished through a viral gene-expression program that promotes cellular proliferation and differentiation, especially of germinal center B cells. Intrinsic host mechanisms that control virus-driven cellular expansion are incompletely defined. Using a small-animal model of gammaherpesvirus pathogenesis, we demonstrate in vivo that the tumor suppressor p53 is activated specifically in B cells latently infected by murine gammaherpesvirus 68. In the absence of p53, the early expansion of murine gammaherpesvirus 68 latency greatly increases, especially in germinal center B cells, a cell type whose proliferation is conversely restricted by p53. We identify the B cell-specific latency gene M2, a viral promoter of germinal center B cell differentiation, as a viral protein sufficient to elicit a p53-dependent anti-proliferative response caused by Src-family kinase activation. We further demonstrate that Epstein-Barr virus-encoded latent membrane protein 1 similarly triggers a p53 response in primary B cells. Our data highlight a model in which gammaherpesvirus latency gene-expression programs that promote B cell proliferation and differentiation to facilitate viral colonization of the host trigger aberrant cellular proliferation that is controlled by p53.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"74 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143020525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhihua Luo, Junlin Chen, Yuchu Liu, Yelin Dai, Hui Gao, Borui Zhang, Haibin Ou, Kwok-Fai So, Ji-an Wei, Li Zhang
{"title":"Treadmill exercise prevents stress-induced anxiety-like behaviors via enhancing the excitatory input from the primary motor cortex to the thalamocortical circuit","authors":"Zhihua Luo, Junlin Chen, Yuchu Liu, Yelin Dai, Hui Gao, Borui Zhang, Haibin Ou, Kwok-Fai So, Ji-an Wei, Li Zhang","doi":"10.1038/s41467-025-56258-2","DOIUrl":"https://doi.org/10.1038/s41467-025-56258-2","url":null,"abstract":"<p>Physical exercise effectively prevents anxiety disorders caused by environmental stress. The neural circuitry mechanism, however, remains incomplete. Here, we identified a previously unrecognized pathway originating from the primary motor cortex (M1) to medial prefrontal cortex (mPFC) via the ventromedial thalamic (VM) nuclei in male mice. Besides anatomical evidence, both ex vivo and in vivo recordings showed enhanced excitability of M1-VM inputs to the prelimbic (PrL) region of mPFC upon 14-day treadmill exercise on a chronic restraint stress (CRS) mouse model. Further functional interrogations demonstrated that the activation of this neural circuit is both necessary and sufficient to direct the anxiolytic effect of exercise training in CRS mice. Our findings provide more insights into the neural circuits connecting motor and mental regions under exercise paradigm and implicate potential targets for neuromodulation in treating anxiety disorders.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"28 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Peter C. Cook, Sheila L. Brown, Emma L. Houlder, Julio Furlong-Silva, Daniel P. Conn, Stefano A. P. Colombo, Syed Baker, Freya R. Svedberg, Gareth Howell, Margherita Bertuzzi, Louis Boon, Joanne E. Konkel, Christopher R. Thornton, Judith E. Allen, Andrew S. MacDonald
{"title":"Mgl2+ cDC2s coordinate fungal allergic airway type 2, but not type 17, inflammation in mice","authors":"Peter C. Cook, Sheila L. Brown, Emma L. Houlder, Julio Furlong-Silva, Daniel P. Conn, Stefano A. P. Colombo, Syed Baker, Freya R. Svedberg, Gareth Howell, Margherita Bertuzzi, Louis Boon, Joanne E. Konkel, Christopher R. Thornton, Judith E. Allen, Andrew S. MacDonald","doi":"10.1038/s41467-024-55663-3","DOIUrl":"https://doi.org/10.1038/s41467-024-55663-3","url":null,"abstract":"<p>Fungal spores are abundant in the environment and a major cause of asthma. Originally characterised as a type 2 inflammatory disease, allergic airway inflammation that underpins asthma can also involve type 17 inflammation, which can exacerbate disease causing failure of treatments tailored to inhibit type 2 factors. However, the mechanisms that determine the host response to fungi, which can trigger both type 2 and type 17 inflammation in allergic airway disease, remain unclear. Here we find that CD11c<sup>+</sup> DCs and CD4<sup>+</sup> T cells are essential for development of both type 2 and type 17 airway inflammation in mice repeatedly exposed to inhaled spores. Single cell RNA-sequencing with further multi-parameter cytometry shows that allergic inflammation dramatically alters the proportion of numerous DC clusters in the lung, but that only two of these (Mgl2<sup>+</sup> cDC2s and CCR7<sup>+</sup> DCs) migrate to the dLNs. Targeted removal of several DC subsets shows that Mgl2<sup>+</sup> cDC2 depletion reduces type 2, but not type 17, fungal allergic airway inflammation. These data highlight distinct DC subsets as potential therapeutic targets for the treatment of pulmonary fungal disease.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"74 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhengyan Kan, Ji Wen, Vinicius Bonato, Jennifer Webster, Wenjing Yang, Vladimir Ivanov, Kimberly Hyunjung Kim, Whijae Roh, Chaoting Liu, Xinmeng Jasmine Mu, Jennifer Lapira-Miller, Jon Oyer, Todd VanArsdale, Paul A. Rejto, Jadwiga Bienkowska
{"title":"Real-world clinical multi-omics analyses reveal bifurcation of ER-independent and ER-dependent drug resistance to CDK4/6 inhibitors","authors":"Zhengyan Kan, Ji Wen, Vinicius Bonato, Jennifer Webster, Wenjing Yang, Vladimir Ivanov, Kimberly Hyunjung Kim, Whijae Roh, Chaoting Liu, Xinmeng Jasmine Mu, Jennifer Lapira-Miller, Jon Oyer, Todd VanArsdale, Paul A. Rejto, Jadwiga Bienkowska","doi":"10.1038/s41467-025-55914-x","DOIUrl":"https://doi.org/10.1038/s41467-025-55914-x","url":null,"abstract":"<p>To better understand drug resistance mechanisms to CDK4/6 inhibitors and inform precision medicine, we analyze real-world multi-omics data from 400 HR+/HER2- metastatic breast cancer patients treated with CDK4/6 inhibitors plus endocrine therapies, including 200 pre-treatment and 227 post-progression samples. The prevalences of <i>ESR1</i> and <i>RB1</i> alterations significantly increase in post-progression samples. Integrative clustering analysis identifies three subgroups harboring different resistance mechanisms: ER driven, ER co-driven and ER independent. The ER independent subgroup, growing from 5% pre-treatment to 21% post-progression, is characterized by down-regulated estrogen signaling and enrichment of resistance markers including <i>TP53</i> mutations, <i>CCNE1</i> over-expression and Her2/Basal subtypes. Trajectory inference analyses identify a pseudotime variable strongly correlated with ER independence and disease progression; and revealed bifurcated evolutionary trajectories for ER-independent vs. ER-dependent drug resistance mechanisms. Machine learning models predict therapeutic dependency on <i>ESR1</i> and <i>CDK4</i> among ER-dependent tumors and <i>CDK2</i> dependency among ER-independent tumors, confirmed by experimental validation.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"38 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ankur Garg, Kin Fan On, Yang Xiao, Elad Elkayam, Paolo Cifani, Yael David, Leemor Joshua-Tor
{"title":"The molecular basis of Human FN3K mediated phosphorylation of glycated substrates","authors":"Ankur Garg, Kin Fan On, Yang Xiao, Elad Elkayam, Paolo Cifani, Yael David, Leemor Joshua-Tor","doi":"10.1038/s41467-025-56207-z","DOIUrl":"https://doi.org/10.1038/s41467-025-56207-z","url":null,"abstract":"<p>Glycation, a non-enzymatic post-translational modification occurring on proteins, can be actively reversed via site-specific phosphorylation of the fructose-lysine moiety by FN3K kinase, to impact the cellular function of the target protein. A regulatory axis between FN3K and glycated protein targets has been associated with conditions like diabetes and cancer. However, the molecular basis of this relationship has not been explored so far. Here, we determined a series of crystal structures of HsFN3K in the apo-state, and in complex with different nucleotide analogs together with a sugar substrate mimic to reveal the features important for its kinase activity and substrate recognition. Additionally, the dynamics in sugar substrate binding during the kinase catalytic cycle provide important mechanistic insights into HsFN3K function. Our structural work provides the molecular basis for rational small molecule design targeting FN3K.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"20 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Decui Tang, Shuoyao He, Yani Yang, Yuqi Zeng, Mengyi Xiong, Ding Ding, Weijun Wei, Yifan Lyu, Xiao-Bing Zhang, Weihong Tan
{"title":"Microenvironment-confined kinetic elucidation and implementation of a DNA nano-phage with a shielded internal computing layer","authors":"Decui Tang, Shuoyao He, Yani Yang, Yuqi Zeng, Mengyi Xiong, Ding Ding, Weijun Wei, Yifan Lyu, Xiao-Bing Zhang, Weihong Tan","doi":"10.1038/s41467-025-56219-9","DOIUrl":"https://doi.org/10.1038/s41467-025-56219-9","url":null,"abstract":"<p>Multiple receptor analysis-based DNA molecular computation has been developed to mitigate the off-target effect caused by nonspecific expression of cell membrane receptors. However, it is quite difficult to involve nanobodies into molecular computation with programmed recognition order because of the “always-on” response mode and the inconvenient molecular programming. Here we propose a spatial segregation-based molecular computing strategy with a shielded internal computing layer termed DNA nano-phage (DNP) to program nanobody into DNA molecular computation and build a series of kinetic models to elucidate the mechanism of microenvironment-confinement. We explain the contradiction between fast molecular diffusion and effective DNA computation using a “diffusion trap” theory and comprehensively overcome the kinetic bottleneck of DNP by determining the rate-limiting step. We predict and verify that identifying trace amount of target cells in complex cell mixtures is an intrinsic merit of microenvironment-confined DNA computation. Finally, we show that DNP can efficiently work in complex human blood samples by shielding the interference of erythrocytes and enhance phagocytosis of macrophages toward target cells by blocking CD47-SIRPα pathway.</p>","PeriodicalId":19066,"journal":{"name":"Nature Communications","volume":"33 1","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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