iMeta最新文献

{"title":"Vitamin K2 ameliorates pregnancy- and lactation-associated osteopenia and postpartum depression.","authors":"Wanqiong Yuan, Jing Hang, Jialin Jia, Jie Huang, Xuanqi Zheng, Huan Wang, Tong Wu, Hao Liu, Junxiong Zhu, Chenggui Zhang, Jinwen He, Yundi Zhang, Hong Wang, Xin Xiong, Na He, Haofan Bai, Jiamin Yan, Huijie Leng, Weili Zhu, Yingsheng Xu, Jie Shi, Chunli Song","doi":"10.1002/imt2.70180","DOIUrl":"https://doi.org/10.1002/imt2.70180","url":null,"abstract":"<p><p>Vitamin K2 (VitK2) supplementation ameliorates comorbid pregnancy- and lactation-associated osteopenia (PLO) and postpartum depression (PPD). These improvements are accompanied by reduced relative abundance of <i>Bacteroides uniformis</i> (<i>B</i>. <i>uniformis</i>) and lower serum deoxycholic acid (DCA) levels. DCA inhibits osteoblast differentiation, promotes osteoclast differentiation, and contributes to an imbalance between hippocampal glutamatergic and GABAergic signaling. Maternal VitK2 supplementation also improves offspring cognition. These findings suggest that modulation of the gut microbiota-bile acid axis may contribute to the beneficial effects of VitK2, supporting the potential of VitK2 as a therapeutic agent for PLO and PPD.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":" ","pages":"e70180"},"PeriodicalIF":44.4,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13679786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229478","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":"<i>Lactobacillus</i> derived small RNAs protect against <i>Klebsiella pneumoniae</i> infection.","authors":"Tingting Xu, Xiuying Tao, Dan Fang, Haijie Zhang, Zhiqiang Wang, Yuan Liu","doi":"10.1002/imt2.70184","DOIUrl":"10.1002/imt2.70184","url":null,"abstract":"<p><p>Carbapenem-resistant <i>Klebsiella pneumoniae</i> (CRKP) is a major multidrug-resistant pathogen with limited treatment options. Plant-derived natural products have broad biological activities, but their protective effects against extraintestinal multidrug-resistant bacterial infections remain poorly understood. Herein, we show that selected plant-derived natural products protect mice against CRKP pulmonary infection by remodeling the gut microbiota. Fecal microbiota transplantation and microbiota-depletion experiments demonstrated that this protection was microbiota dependent, with <i>Lactobacillus</i> emerging as a key genus associated with reduced pulmonary bacterial burden. Among four isolated <i>Lactobacillus</i> species, <i>Lactobacillus murinus</i> (<i>L. murinus</i>) conferred the strongest protection against CRKP infection. Mechanistically, <i>L. murinus</i>-derived membrane vesicles (MVs) delivered the small RNA mim-miR-21a-5p to pulmonary macrophages, where it targeted <i>PDCD4</i> and activated the Nrf2/SOD2 antioxidant pathway. This signaling cascade preserved mitochondrial oxidative phosphorylation, promoted an M2-like macrophage phenotype, and ultimately restricted CRKP infection. Consistent with these findings, intestinal <i>Lactobacillus</i>, particularly <i>L. murinus</i>, was reduced in patients with CRKP infection compared with healthy controls. Collectively, our findings reveal a mechanism by which plant-derived natural products enhance host resistance to CRKP through microbiota remodeling and identify <i>L. murinus</i>-derived small RNAs and membrane vesicles as key mediator of this gut-lung protective axis.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":" ","pages":"e70184"},"PeriodicalIF":44.4,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13673929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149217364","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":"Domesticated bacterial origin genes regulate homeostasis of the insect gut microbiome and empower adaptation.","authors":"Zhenjia Zhang, Yubo Zhang, Kun Zhao, Guangyuan Cheng, Zhihao Lu, Dongju Wang, Yiqun Liu, Jianguo Wu, Liying Wang, Lisheng Zhang, Xinhai Ye, Li Yu, Wei Zhang, Yi Li","doi":"10.1002/imt2.70179","DOIUrl":"10.1002/imt2.70179","url":null,"abstract":"<p><p>Sap-sucking insects, represented by the globally distributed leafhoppers, have evolved a wide range of adaptive traits and play multiple ecological roles. However, their successful survival strategies in nature remain poorly understood. To explore the adaptive mechanisms of sap-sucking insects, we established a research system using three representative leafhopper species from the same family and found that they have acquired multiple cholesterol-dependent cytolysins (<i>CDCs</i>) derived from gram-positive bacterial genes. Furthermore, we demonstrated that these <i>CDCs</i> have been domesticated and co-evolved with leafhoppers, ultimately participating in various life activities of the host. Specifically, some <i>CDCs</i> exhibit high cytotoxicity, are specifically expressed in the egg serosa, and affect the feeding behaviors of leafhopper predators; others show non-cytotoxic activity, are specifically expressed in the gut, and may regulate leafhopper growth and development by potentially maintaining the homeostasis of the leafhopper gut microbiome. This study uncovers leafhoppers as a paradigm for understanding how organisms can borrow microbial innovations to address ecological challenges and thrive as agricultural pests. It provides a comprehensive perspective to bridge the genotypes of acquired genes with the phenotypes of adaptive traits and demonstrates how homologous genes from donor organisms undergo functional differentiation in recipient hosts, enabling them to exploit new ecological niches. By decoding these mechanisms, we not only gain fundamental insights into evolutionary processes but also develop powerful strategies for sustainable pest management.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":" ","pages":"e70179"},"PeriodicalIF":44.4,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13670155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149217395","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":"Decoding ferroptosis via integrated multi-omics analyses in rice blast.","authors":"Zhibin Liang, Qing Shen, Nam Khoa Nguyen, Ruhui Long, Yuming Ma, Qiao Liu, Naweed I Naqvi, Nam-Soo Jwa, Yi-Zhen Deng","doi":"10.1002/imt2.70178","DOIUrl":"10.1002/imt2.70178","url":null,"abstract":"<p><p>The rice-<i>Magnaporthe oryzae</i> pathosystem is presented as a host-pathogen ferroptosis model. Multi-omics insights connect ferroptosis to several cellular processes, such as iron homeostasis, reactive oxygen species (ROS)/redox imbalance, and polyunsaturated fatty acid-containing phospholipid (PUFA-PL) peroxidation, under multiple regulators in rice and <i>M. oryzae</i>, respectively. Interestingly, ferroptosis drives two opposite biological outcomes: fungal infection-related development and rice immunity.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":" ","pages":"e70178"},"PeriodicalIF":44.4,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13645718/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149139700","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":"Infection mechanisms of <i>Rhizoctonia cerealis</i> in wheat.","authors":"Yan Ren, Ti Liu, Heying Zhao, Qirun Qian, Lufei Cui, Zhipeng Sun, Wenkai Yang, Peng Guo, Sisheng Wang, Lingran Zhang, Congwei Sun, Aolin Jia, Ning Zhang, Feng Chen","doi":"10.1002/imt2.70174","DOIUrl":"10.1002/imt2.70174","url":null,"abstract":"<p><p><i>Rhizoctonia cerealis</i> (<i>Rc</i>) as a major pathogen causing sharp eyespot (SE) seriously affects wheat production worldwide. We collected 1683 wheat plants exhibiting SE symptoms from 30 locations in China over 7 years. We next constructed high-quality genome maps by <i>de novo</i> sequencing of five representative <i>Rc</i> isolates and established an atlas of genomic variation by resequencing 207 isolates. We identified a key effector, RcPL3, conferring <i>Rc</i> pathogenicity. RcPL3 increased the protein accumulation of histone deacetylase TaHDA9 in wheat cytoplasm to promote <i>Rc</i> infection. TaHDA9 inhibited the E3 ubiquitin ligase TaRHC1A through deacetylation. RcPL3 indirectly inhibited the accumulation of TaRHC1A by mediating TaHDA9. TaRHC1A promoted the degradation of TaRBOH3 synthesizing reactive oxygen species (ROS) to cause wheat SE resistance. We further discovered an antagonist HY-19741 to prevent <i>Rc</i> infection. The high-quality genome maps of <i>Rc</i> and a SE RcPL3-TaHDA9-TaRHC1A-TaRBOH3 regulatory cascade will be valuable for SE prevention in wheat.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":" ","pages":"e70174"},"PeriodicalIF":44.4,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13638802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119593","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":"Gut virome orchestrates nitrogen partitioning between the host and microbiome.","authors":"Shujie Xu, Xianglin Fei, Fengqing Lin, Wenzi Wu, Jiachen Zhuang, Qiufen Mo, Xiuan Zhan, Aikun Fu","doi":"10.1002/imt2.70177","DOIUrl":"https://doi.org/10.1002/imt2.70177","url":null,"abstract":"<p><p>Dietary protein is essential for host growth and nitrogen homeostasis. How dietary protein shapes intestinal phage-bacteria interactions and influences the translation of dietary cues into host physiological outcomes remains poorly understood. We show that low-protein diet (LPD) substantially remodels the murine gut virome by altering phage-bacteria dynamics. Under LPD, nutritional stress suppresses bacterial phage release without altering the predicted proportion of lysogenic phages, leading to reduced free phage abundance and weaker bacterial lysis. Lysogenic phages carrying carbohydrate-related auxiliary metabolic genes (AMGs) may promote expansion of the bacterial host population while suppressing urease-mediated nitrogen recycling. High bacterial load coupled with low free phage availability creates a nitrogen trap that both sequesters host-accessible nitrogen and accelerates urea loss, thereby constraining host growth. Both the normal diet (ND) virome, defined by its high free phage abundance and lytic potential, and an equivalently sized LPD phage pool partially rescued nitrogen flow in mice fed a LPD. These results reveal a previously unrecognized gut \"viral shunt,\" in which balanced phage-bacteria interactions redistribute nitrogen within the gut. Together, this study highlights the ecological significance of phage-bacteria interactions in host nutritional adaptation and suggests that targeted viral manipulation may offer a potential therapeutic strategy for protein-deficiency-related disorders.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":" ","pages":"e70177"},"PeriodicalIF":44.4,"publicationDate":"2026-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13635721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119519","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":"Deciphering transcriptome complexity via long-read sequencing.","authors":"Chuwen Xu, Jia Li, Chenxi Yin, Keying Li, Tian Wang, Shiwen Gao, Yue Yu, Cheng Chang, Ye Wang, Guoqing Tong, Liang Gong, Wen Hu, Guoliang Chai, Yilai Han, Qian Qin, Suoqin Jin, Xiufen Zou, Bo Li, Tianyuan Zhang, Ana Conesa, Yunhao Wang, Dingjie Wang","doi":"10.1002/imt2.70171","DOIUrl":"https://doi.org/10.1002/imt2.70171","url":null,"abstract":"<p><p>Transcriptomics is moving beyond gene-level quantification toward isoform-resolved interrogation of alternative splicing, transcript structural variation, and repeat-derived transcription. Yet short-read sequencing remains intrinsically limited in accurately reconstructing full-length transcripts and resolving complex repetitive regions, including transposable elements. Recent advances in long-read sequencing, exemplified by Pacific Biosciences (PacBio) and Oxford Nanopore Technologies (ONT), offer a transformative opportunity to directly observe complete RNA molecules and thereby overcome these bottlenecks. However, practical adoption is hindered by demanding library construction and the need to process noisy, fast-evolving long-read data, and the field still lacks a unified resource that guides researchers through the entire experimental and analytical workflow. This review fills that gap by providing a concise, end-to-end, and implementation-oriented roadmap for long-read transcriptomics. We distill the key decisions from platform and library strategy selection to core computational processing and downstream interpretation, and we summarize emerging frontiers and best-practice recommendations. By offering a reusable framework and practical checklists, this guide empowers a broader community to exploit long reads for standardized, reproducible, isoform-level discovery at unprecedented resolution.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":" ","pages":"e70171"},"PeriodicalIF":44.4,"publicationDate":"2026-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13634186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119550","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":"Dissecting the angiogenic mechanism of pachychoroid polypoidal choroidal vasculopathy.","authors":"Xinyu Zhao, Tiantian Cheng, Wenfei Zhang, Xingwang Gu, Qing Zhao, Yaning Chen, Lihui Meng, Jiaqi Zhang, Bintao Qiu, Lili Li, Shiyu Cheng, Zicheng Wang, Chuting Wang, Yuelin Wang, Zuyi Yang, Zhengming Shi, Ye Guo, Shengzhi Liu, Youxin Chen","doi":"10.1002/imt2.70176","DOIUrl":"https://doi.org/10.1002/imt2.70176","url":null,"abstract":"<p><p>Polypoidal choroidal vasculopathy (PCV) is a distinct variant of neovascular age-related macular degeneration (AMD) and a major cause of vision loss in older adults, yet its pathogenesis remains poorly understood. Pachychoroid PCV is a subtype characterized by poor treatment response, minimal typical AMD features, and dilated choroidal vessels. Using a multicenter PCV cohort, we conducted plasma multi-omics analyses and identified enrichment of fluid shear stress and atherosclerosis (FSS-AS) signaling pathways in this subtype. The pachychoroid phenotype, together with FSS-AS enrichment, implicated altered choroidal hemodynamics in its pathogenesis. By inducing choroidal circulatory hypertension (CCH) in mice, we recapitulated, for the first time, the hallmark ocular lesions of pachychoroid PCV. Single-cell sequencing identified the cellular origin of these angiogenic lesions and implicated endothelin-1 (EDN1) as a key effector. Alleviating choroidal hypertension, reducing EDN1 expression, or pharmacologically blocking the endothelin receptor A (EDNRA, the receptor for EDN1), prevented lesion formation. In vitro, disturbed fluid shear stress upregulated EDN1 in choroidal endothelial cells and promoted pathological remodeling and angiogenesis through EDNRA. Collectively, our findings define a pathogenic cascade wherein CCH induces abnormal hemodynamics (disrupted fluid shear stress) and drives angiogenesis via the EDN1/EDNRA axis, offering mechanistic insight and identifying a potential therapeutic target for pachychoroid PCV.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":" ","pages":"e70176"},"PeriodicalIF":44.4,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119597","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":"Different gut microbiome dysbioses impact the evolutionary fate of hypervirulent <i>Klebsiella pneumoniae</i>.","authors":"Carey Lim, Jialing Zheng, Guoxiang Cheam, Melvin Yong, Hanrong Chen, Andrew Ting, Yahua Chen, Qingqing Wang, Niranjan Nagarajan, Yunn-Hwen Gan","doi":"10.1002/imt2.70175","DOIUrl":"10.1002/imt2.70175","url":null,"abstract":"<p><p>The intestinal microbiota acts as a barrier against pathogen colonization, yet how specific ecological perturbations shape the evolutionary fate of invading pathogens remains unclear. Here, we show that the mode of gut perturbation and type of dysbiosis determine whether hypervirulent <i>Klebsiella pneumoniae</i> (hv<i>Kp</i>) persist or clear from the intestines. Transient ampicillin exposure creates a permissive, low-diversity intestinal niche dominated by facultative anaerobes, which supports long-term, high-density hv<i>Kp</i> colonization. The dysbiotic state creates an altered redox environment to favor these oxygen-using bacteria and is associated with the rapid emergence of hypomucoid variants. This occurs via contractions in the poly-T tract in the promoter of the <i>rmpA</i> regulator that controls capsule hypermucoviscosity, as well as mutations in the poly-G tract within the coding sequence. This evolutionary trajectory reflects a virulence-persistence trade-off in high-nutrient, low-competition environment. Conversely, osmotic perturbation via laxative treatment elicits only a transient window of colonization-susceptibility that is rapidly closed by the recovery of a <i>Bacteroides</i>-enriched community that is consistent with their ability to actively suppress pathogen colonization via short-chain fatty acids (SCFAs). Furthermore, SCFAs such as butyrate are more effective in inhibiting hypomucoid <i>rmpA</i> variants relative to wild-type bacteria, providing a possible explanation for how an osmotically perturbed gut microbiome constrains the expansion of these mutants. These findings provide insights into how transient antibiotic exposure could potentially drive long-term intestinal pathobiont colonization while laxative-induced osmotic perturbations do not rewire the energy and metabolic landscape of the gut microbiome, enabling rapid recovery and colonization resistance despite an initial plunge in diversity. Our work reveals that the specific mode of perturbation affects the trajectory for pathogen adaptation, and highlights the potential role of commensal competition in constraining pathogen evolution.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":" ","pages":"e70175"},"PeriodicalIF":44.4,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13601767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149042363","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":"Gut <i>Enterococcus faecium</i> derived leucic acid mediates the antiobesity effect of dietary fiber.","authors":"Baifei Hu, Qianru Gao, Junmin Hui, Mengqiong Wang, Haiyan Gao, Kai Li, Junping Zheng, Zhe Dai, Songlin Liu, Hongtao Liu","doi":"10.1002/imt2.70173","DOIUrl":"10.1002/imt2.70173","url":null,"abstract":"<p><p>Obesity is a globally prevalent metabolic disorder closely associated with gut microbiota dysbiosis. However, the precise roles of gut microbiota and microbial metabolism in this disease remain unclear. Through fecal metagenomic data mining and clinical cohort validation, we identified a gut bacterial strain with anti-obesity potential, <i>Enterococcus faecium</i> (<i>E. faecium</i>). It inhibited adipocyte enlargement, dyslipidemia, and hepatic steatosis in obese mice by metabolizing leucine to produce leucic acid (LEA). Colonization with <i>E. faecium</i> or exogenous LEA supplementation improved obesity-associated metabolic phenotypes. Mechanistically, <i>E. faecium</i> metabolized leucine into LEA via putative branched-chain amino acids metabolic enzymes. The bacterium-derived LEA regulated mitochondrial oxidative phosphorylation and thus alleviated obesity. Furthermore, using a high-content screening system and an in vitro fermentation model, we found that the dietary fiber glucomannan exerted anti-obesity effects by promoting the growth of <i>E. faecium</i>. This study reveals the critical role of microbial metabolism and LEA production in ameliorating the onset and progression of obesity, providing a theoretical basis for dietary fiber intervention strategies targeting the gut microbiota.</p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":" ","pages":"e70173"},"PeriodicalIF":44.4,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149018749","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}