Xiuqin Xie, Weibin Cheng, Zhaohong Li, Rong He, Ke Yuan, Qinghua Zhang, Ruiqiang Yang, LiLi Ming, Ke Yu, Tiangang Luan, Baowei Chen
{"title":"Functional metagenomics reveals novel antibiotic resistomes in polar soils","authors":"Xiuqin Xie, Weibin Cheng, Zhaohong Li, Rong He, Ke Yuan, Qinghua Zhang, Ruiqiang Yang, LiLi Ming, Ke Yu, Tiangang Luan, Baowei Chen","doi":"10.1002/imt2.70069","DOIUrl":"https://doi.org/10.1002/imt2.70069","url":null,"abstract":"<p>Using a robust functional metagenomics approach, we demonstrated that polar environments are important reservoirs of novel antibiotic resistance genes (ARGs). DNA was initially extracted from cultured bacterial consortia in the polar soils and recombined into plasmid vectors and then transformed into <i>Escherichia coli</i> (<i>E. coli</i>) for the subsequent screening of antibiotic resistance. Consequently, we identified 671 novel polar ARGs with experimentally verified resistance against multiple clinical antibiotics (cefotaxime, folate synthesis inhibitors, and clindamycin). Bioinformatics analysis revealed that novel polar ARGs had limited mobility and dissemination potential and were seldom carried by human bacterial pathogens. Overall, this study offers a comprehensive perspective on previously overlooked novel ARGs in polar regions, advancing our understanding of environmental resistomes.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 4","pages":""},"PeriodicalIF":23.7,"publicationDate":"2025-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70069","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Probiotics restore enteric HDL3 secretion and improve prognosis in patients with end-stage renal disease","authors":"Xiaoxue Liu, Yuan Huang, Yixuan Li, Juan Chen, Xifan Wang, Xiaobin Wang, Liang Zhao, Yongting Luo, Peng An, Liwei Zhang, Chengying Zhang, Weijing Bian, Xingen Lei, Xiang Gao, Yinghua Liu, Yanling Hao, Huiyuan Guo, Xiaoxu Zhang, Pengjie Wang, Ran Wang, Hao Zhang, Bing Fang, Xiaolin Zhang, Longjiao Wang, Qinglu Qiu, Yuchan Zhang, Jingyi Qi, Songtao Yang, Yulong Yin, Fazheng Ren, Xiaoyu Wang","doi":"10.1002/imt2.70062","DOIUrl":"https://doi.org/10.1002/imt2.70062","url":null,"abstract":"<p>Randomized double-blind trials have shown that probiotic mixtures significantly increase high-density lipoprotein (HDL) levels and reduce the risk of cardiovascular disease mortality in end-stage renal disease (ESRD) patients. Meta-analysis with prospective cohort studies further confirms that elevated HDL is a protective factor for ESRD outcomes. In severe renal injury models, including 5/6 nephrectomy and apolipoprotein E-deficient (<i>ApoE<sup>−/−</sup></i>) mice, probiotics restored cardiac function, mirroring the cardioprotective effects seen in humans. Mechanistic studies indicate that probiotics enhance intestinal HDL3 production through the insulin-mediated SP1(P)-CYP27A-LXRα/β-ABCA1 pathway, thereby maintaining HDL metabolic homeostasis. This study reveals a novel link between probiotic intervention and host cholesterol metabolism, offering a previously unexplored strategy for reducing cardiovascular risk in ESRD patients.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 4","pages":""},"PeriodicalIF":23.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70062","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"PMAT2: An efficient graphical assembly toolkit for comprehensive organellar genomes","authors":"Fuchuan Han, Changwei Bi, Yicun Chen, Xiaogang Dai, Zefu Wang, Huaitong Wu, Ning Sun, Yanshu Qu, Yang Yang, Yangdong Wang, Tongming Yin","doi":"10.1002/imt2.70064","DOIUrl":"https://doi.org/10.1002/imt2.70064","url":null,"abstract":"<p>We developed PMAT2, an advanced toolkit for lineage-specific de novo assembly of plant, animal, and fungal mitochondrial genomes, as well as plant chloroplast genome. PMAT2 leverages optimized graph-based strategies tailored to organelle genome complexity, enabling complete and accurate assemblies, even with approximately 1 × highly accurate PacBio high-fidelity (HiFi) reads. By assembling 150 organellar genomes across diverse lineages, PMAT2 outperformed existing tools in assembly completeness. The source code for PMAT2 is publicly available at https://github.com/aiPGAB/PMAT2.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 4","pages":""},"PeriodicalIF":23.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70064","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neoadjuvant immunotherapy driven bladder preservation for muscle invasive bladder cancer","authors":"Jiao Hu, Luzhe Yan, Jinhui Liu, Minfeng Chen, Yunbo He, Benyi Fan, Bo Peng, Long Wang, Weibin Hou, Chao Li, Bosen You, Meng Zhang, Wenze Li, Jiaxing Wang, Hongzhou Cai, Shenglin Gao, Yang Liu, Dingshan Deng, Huihuang Li, Guanghui Gong, Jiansheng Tang, Chengyong Wang, Xiaofeng Yang, Liang Wei, Guangzheng Lin, Ruizhe Wang, Xiao Guan, Shiyu Tong, Yangle Li, Wei He, Zhiyong Cai, Peihua Liu, Yu Gan, Yu Cui, Yuanqing Dai, Yi Cai, Zefu Liu, Jiatong Xiao, Zhenyu Nie, Zhenyu Ou, Jinbo Chen, Xi Guo, Xiongbing Zu","doi":"10.1002/imt2.70063","DOIUrl":"https://doi.org/10.1002/imt2.70063","url":null,"abstract":"<p>The study included 163 patients with muscle-invasive bladder cancer (MIBC) from 14 hospitals, categorized into the neoadjuvant immunotherapy-combined-modality therapy (Neoimmu-CMT), trimodal therapy (TMT), and neoadjuvant chemotherapy-combined-modality therapy (NAC-CMT) subgroups. Propensity score matching (PSM) was utilized to mitigate baseline variability. Univariate and multivariate Cox analyses were used to identify potential prognostic factors. Biomarker assessment comprised immunohistochemistry and single-cell RNA sequencing. After PSM, Neoimmu-CMT demonstrated superior efficacy over NAC-CMT and comparability to TMT. A clinical complete response to neoadjuvant treatment and lower clinical T stage were positive prognostic factors for Neoimmu-CMT. Biomarker analysis showed that the immune phenotype of the tumor microenvironment (TME) was closely associated with bladder preservation outcomes. We assessed the potential relationship between various cell types in the TME and bladder preservation outcomes using single-cell RNA sequencing. The results showed that the dynamic distribution of fibroblast and NK/T cell subclusters was associated with bladder preservation outcomes. In the future, the development of Neoimmu-CMT will substantially expand its application in bladder preservation therapies.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 4","pages":""},"PeriodicalIF":23.7,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70063","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xueqin Xie, Changchun Wu, Fuying Dao, Kejun Deng, Dan Yan, Jian Huang, Hao Lyu, Hao Lin
{"title":"scRiskCell: A single-cell framework for quantifying islet risk cells and their adaptive dynamics in type 2 diabetes","authors":"Xueqin Xie, Changchun Wu, Fuying Dao, Kejun Deng, Dan Yan, Jian Huang, Hao Lyu, Hao Lin","doi":"10.1002/imt2.70060","DOIUrl":"https://doi.org/10.1002/imt2.70060","url":null,"abstract":"<p>scRiskCell is an interpretable intelligent computational framework that leverages nearly 500,000 islet cell expression profiles from 106 donors across different continuous disease states. By calculating the intrinsic relationship between donor disease states and cell expression profiles, it assigns a pseudo-cell state index to each cell. Sorting the pseudo-indexes of cells enables the identification of risk cells truly disrupted by the disease. Importantly, scRiskCell reveals the dynamic aggregation pattern of risk cells during disease progression, providing mechanistic insights for early disease prediction and clinical dynamic monitoring of disease progression.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 4","pages":""},"PeriodicalIF":23.7,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70060","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yanhua Liu, Ling Yang, Maryam Meskini, Anjana Goel, Monique Opperman, Sagar Singh Shyamal, Ajay Manaithiya, Meng Xiao, Ruizi Ni, Yajing An, Mingming Zhang, Yuan Tian, Shuang Zhou, Zhaoyang Ye, Li Zhuang, Linsheng Li, Istuti Saraswat, Ankita Kar, Syed Luqman Ali, Shakir Ullah, Syed Yasir Ali, Shradha Kaushik, Tianmu Tian, Mingyang Jiao, Shujun Wang, Giulia Ghisleni, Alice Armanni, Sara Fumagalli, WenYu Wang, Chao Cao, Maria Carpena, Miguel A. Prieto, Antonia Bruno, Chanyuan Jin, Hanqing Hu, Yuhang Zhang, Ilse du Preez, Ashok Aspatwar, Lingxia Zhang, Wenping Gong
{"title":"Gut microbiota and tuberculosis","authors":"Yanhua Liu, Ling Yang, Maryam Meskini, Anjana Goel, Monique Opperman, Sagar Singh Shyamal, Ajay Manaithiya, Meng Xiao, Ruizi Ni, Yajing An, Mingming Zhang, Yuan Tian, Shuang Zhou, Zhaoyang Ye, Li Zhuang, Linsheng Li, Istuti Saraswat, Ankita Kar, Syed Luqman Ali, Shakir Ullah, Syed Yasir Ali, Shradha Kaushik, Tianmu Tian, Mingyang Jiao, Shujun Wang, Giulia Ghisleni, Alice Armanni, Sara Fumagalli, WenYu Wang, Chao Cao, Maria Carpena, Miguel A. Prieto, Antonia Bruno, Chanyuan Jin, Hanqing Hu, Yuhang Zhang, Ilse du Preez, Ashok Aspatwar, Lingxia Zhang, Wenping Gong","doi":"10.1002/imt2.70054","DOIUrl":"https://doi.org/10.1002/imt2.70054","url":null,"abstract":"<p>Tuberculosis (TB), caused by <i>Mycobacterium tuberculosis</i> (MTB), remains a significant global health challenge. Recent advancements in gut microbiota (GM) research have shed light on the intricate relationship between GM and TB, suggesting that GM alterations may influence host susceptibility, disease progression, and response to antituberculosis drugs. This review systematically synthesizes and analyzes the current research progress on the relationship between GM and TB, focusing on six key aspects: (1) bidirectional effects between GM dynamics and TB progression; (2) the interaction between GM and anti-TB drugs; (3) GM and TB immune response; (4) GM as a potential target for diagnosis and treatment of TB; (5) multi-omics and artificial intelligence (AI) technologies in GM-TB research; (6) current challenges and future directions in GM-TB research. We highlight the bidirectional nature of the GM–TB interaction, where MTB infection can lead to GM dysbiosis, and changes can affect the host's immune response, contributing to TB onset and progression. Advanced molecular techniques, such as next-generation sequencing and metagenomics, along with AI, play pivotal roles in elucidating these complex interactions. Future research directions include investigating the relationship between GM and TB vaccine efficacy, exploring GM's potential in TB prevention, developing microbiome-based diagnostic and prognostic tools, and examining the role of GM in TB recurrence. By addressing these areas, we aim to provide a comprehensive perspective on the latest advancements in GM and TB research and offer insights for future studies and clinical applications. Ultimately, the development of novel microbiome-based strategies may offer new tools and insights for the effective control and management of TB, a disease that continues to pose a significant threat to public health.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 4","pages":""},"PeriodicalIF":23.7,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70054","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiao Chen, Kefan Fang, Bo Li, Yingxing Li, Yuehua Ke, Weixin Ke, Tian Tian, Yifan Zhao, Linqi Wang, Jing Geng, Mark C. Leake, Fan Bai
{"title":"Macrophage-derived reactive oxygen species promote Salmonella aggresome formation contributing to bacterial antibiotic persistence","authors":"Xiao Chen, Kefan Fang, Bo Li, Yingxing Li, Yuehua Ke, Weixin Ke, Tian Tian, Yifan Zhao, Linqi Wang, Jing Geng, Mark C. Leake, Fan Bai","doi":"10.1002/imt2.70059","DOIUrl":"https://doi.org/10.1002/imt2.70059","url":null,"abstract":"<p>In this study, we reveal that macrophage-derived reactive oxygen species (ROS) can trigger the rapid formation of <i>Salmonella</i> aggresomes, which substantially contribute to the increased frequency of persisters induced by phagocytosis. <i>Salmonella</i> containing aggresomes exhibited a dormant phenotype characterized by reduced adenosine triphosphate (ATP) levels and decreased metabolic activity. Furthermore, these dormant bacteria showed upregulated expression of <i>Salmonella</i> pathogenicity island 1 (SPI-1)-encoded type III secretion system (T3SS)-related genes, followed by later expression of SPI-2 T3SS-related genes when macrophages ROS production declined. Our results demonstrate that <i>Salmonella</i> containing aggresomes can enter a dormant state to escape antibiotic attack, while crucially maintaining the ability to resuscitate when the stress environment is improved. Research on bacterial aggresomes could potentially provide therapeutic strategies to combat bacterial antibiotic persistence.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 4","pages":""},"PeriodicalIF":23.7,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Correction to “Gut–X axis”","authors":"","doi":"10.1002/imt2.70057","DOIUrl":"https://doi.org/10.1002/imt2.70057","url":null,"abstract":"<p>Lin, Xu, Zuxiang Yu, Yang Liu, Changzhou Li, Hui Hu, Jia-Chun Hu, Mian Liu, et al. 2025. “Gut–X axis.” <i>iMeta</i> 4: e270. https://onlinelibrary.wiley.com/doi/abs/10.1002/imt2.270</p><p>1. In Figure 7 of the “Gut–Heart Axis” section, the word “myocarditis” was incorrect; this should be “myocardial injury.” The paragraph “myocardial injury” includes diseases or pathological injuries that fall under the category of myocardial injury and cannot be equated with the category of cardiomyopathy. This is a misuse of the noun here. Furthermore, in Figure 7 of the “Gut–Heart Axis” section, the word “PAGly” should be deleted. Because the paragraph “myocardial injury” didn't describe “PAGly.” The revised Figure 7 and figure legend are as follows.</p><p>2. In the “Gut–Heart Axis” section, the word “PAGIn” was incorrect, it should be “PAGln.”</p><p>3. The corresponding author's name “Leming, Zheng” is misspelled, it should be “Lemin, Zheng.”</p><p>We apologize for these errors.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 4","pages":""},"PeriodicalIF":23.7,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Multi-omics insights into surface charge effects to decode the interplay of nanoplastics and bacterial antibiotic resistance","authors":"Houyu Li, Yinuo Ding, Yan Xu, Wei Liu","doi":"10.1002/imt2.70056","DOIUrl":"https://doi.org/10.1002/imt2.70056","url":null,"abstract":"<p>Multi-omics approaches revealed how nanoplastics with different surface charges influence antibiotic resistance in <i>Escherichia coli</i> K12. Positively charged nanoplastics enhanced antibiotic resistance by upregulating genes and proteins linked to oxidative stress tolerance and efflux pumps, and promoted antibiotic resistance genes transfer via conjugation and transformation. In contrast, negatively charged nanoplastics disrupted biofilm formation and metabolism, potentially reducing antibiotic resistance. These findings highlight the critical role of nanoplastics' surface properties in shaping microbial resistance dynamics and highlight emerging risks posed by nanoplastics to public health through accelerated antibiotic resistance propagation.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 4","pages":""},"PeriodicalIF":23.7,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70056","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"METTL5-mediated 18S rRNA m6A modification enhances ribosome assembly and ABA response in Arabidopsis","authors":"Ping Li, Yu Zhang, Songyao Zhang, Jinqi Ma, Sheng Fan, Lisha Shen","doi":"10.1002/imt2.70055","DOIUrl":"https://doi.org/10.1002/imt2.70055","url":null,"abstract":"<p>METTL5 catalyzes the <i>N</i><sup>6</sup>-methyladenosine (m<sup>6</sup>A) methylation at A<sub>1771</sub> in 18S rRNA, a modification essential for its association with the ribosomal protein RPL24A, facilitating the assembly of 80S ribosome. This facilitates the translation of mRNAs encoding the detoxifying glutathione S-transferase (GST) enzymes, thereby maintaining normal reactive oxygen species (ROS) levels and ensuring proper abscisic acid (ABA) responses. In <i>mettl5</i> mutants, the absence of m<sup>6</sup>A<sub>1771</sub> compromises RPL24A incorporation and ribosome assembly, impairing the translation of GSTs. This results in ROS excessive accumulation and hypersensitivity to ABA.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 4","pages":""},"PeriodicalIF":23.7,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}