bioRxiv : the preprint server for biology最新文献

{"title":"<ArticleTitle xmlns:ns0=\"http://www.w3.org/1998/Math/MathML\">Alternative mutational architectures producing identical <ns0:math><ns0:mrow><ns0:mtext>M</ns0:mtext></ns0:mrow> </ns0:math> -matrices can lead to different patterns of evolutionary divergence.","authors":"Daohan Jiang, Matt Pennell","doi":"10.1101/2023.08.11.553044","DOIUrl":"10.1101/2023.08.11.553044","url":null,"abstract":"<p><p>Explaining macroevolutionary divergence in light of population genetics requires understanding the extent to which the patterns of mutational input contribute to long-term trends. In the context of quantitative traits, mutational input is typically described by the mutational variance-covariance matrix, or the <math><mrow><mtext>M</mtext></mrow> </math> -matrix, which summarizes phenotypic variances and covariances introduced by new mutations per generation. However, as a summary statistic, the <math><mrow><mtext>M</mtext></mrow> </math> -matrix does not fully capture all the relevant information from the underlying mutational architecture, and there exist infinitely many possible underlying mutational architectures that give rise to the same <math><mrow><mtext>M</mtext></mrow> </math> -matrix. Using individual-based simulations, we demonstrate mutational architectures that produce the same <math><mrow><mtext>M</mtext></mrow> </math> -matrix can lead to different levels of constraint on evolution and result in difference in within-population genetic variance, between-population divergence, and rate of adaptation. In particular, the rate of adaptation and that of neutral evolution are both reduced when a greater proportion of loci are pleiotropic. Our results reveal that aspects of mutational input not reflected by the <math><mrow><mtext>M</mtext></mrow> </math> -matrix can have a profound impact on long-term evolution, and suggest it is important to take them into account in order to connect patterns of long-term phenotypic evolution to underlying microevolutionary mechanisms.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11642737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75543993","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":"Amyloid β Induces Lipid Droplet-Mediated Microglial Dysfunction in Alzheimer's Disease.","authors":"Priya Prakash, Palak Manchanda, Evi Paouri, Kanchan Bisht, Kaushik Sharma, Jitika Rajpoot, Victoria Wendt, Ahad Hossain, Prageeth R Wijewardhane, Caitlin E Randolph, Yihao Chen, Sarah Stanko, Nadia Gasmi, Anxhela Gjojdeshi, Sophie Card, Jonathan Fine, Krupal P Jethava, Matthew G Clark, Bin Dong, Seohee Ma, Alexis Crockett, Elizabeth A Thayer, Marlo Nicolas, Ryann Davis, Dhruv Hardikar, Daniela Allende, Richard A Prayson, Chi Zhang, Dimitrios Davalos, Gaurav Chopra","doi":"10.1101/2023.06.04.543525","DOIUrl":"10.1101/2023.06.04.543525","url":null,"abstract":"<p><p>Several microglia-expressed genes have emerged as top risk variants for Alzheimer's disease (AD). Impaired microglial phagocytosis is one of the main proposed outcomes by which these AD-risk genes may contribute to neurodegeneration, but the mechanisms translating genetic association to cellular dysfunction remain unknown. Here we show that microglia form lipid droplets (LDs) upon exposure to amyloid-beta (Aβ), and that their LD load increases with proximity to amyloid plaques in brains from human patients and the AD mouse model 5xFAD. LD formation is dependent on age and disease progression and is prominent in the hippocampus in mice and humans. Despite differences in microglial LD load between brain regions and sexes in mice, LD-laden microglia exhibited a deficit in Aβ phagocytosis. Unbiased lipidomic analysis identified a decrease in free fatty acids (FFAs) and a parallel increase in triacylglycerols (TGs) as the key metabolic transition underlying LD formation. DGAT2, a key enzyme for converting FFAs to TGs, promotes microglial LD formation and is increased in 5xFAD and human AD brains. Inhibition or degradation of DGAT2 improved microglial uptake of Aβ and drastically reduced plaque load in 5xFAD mice, respectively. These findings identify a new lipid-mediated mechanism underlying microglial dysfunction that could become a novel therapeutic target for AD.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f7/ca/nihpp-2023.06.04.543525v1.PMC10274698.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9706244","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":"Inhibiting NINJ1-dependent plasma membrane rupture protects against inflammasome-induced blood coagulation and inflammation.","authors":"Jian Cui, Hua Li, Dien Ye, Guoying Zhang, Yan Zhang, Ling Yang, Martha M S Sim, Jeremy P Wood, Yinan Wei, Zhenyu Li, Congqing Wu","doi":"10.1101/2023.08.30.555561","DOIUrl":"10.1101/2023.08.30.555561","url":null,"abstract":"<p><p>Systemic blood coagulation accompanies inflammation during severe infection like sepsis and COVID. We've previously established a link between pyroptosis, a vital defense mechanism against infection, and coagulopathy. During pyroptosis, the formation of gasdermin-D (GSDMD) pores on the plasma membrane leads to the release of tissue factor (TF)-positive microvesicles (MVs) that are procoagulant. Mice lacking GSDMD release fewer TF MVs. However, the specific mechanisms leading from activation of GSDMD to MV release remain unclear. Plasma membrane rupture (PMR) in pyroptosis was recently reported to be actively mediated by the transmembrane protein Ninjurin-1 (NINJ1). Here we show that NINJ1 promotes procoagulant MV release during pyroptosis. Haploinsuffciency or glycine inhibition of NINJ1 limited the release of procoagulant MVs and inflammatory cytokines and partially protected against blood coagulation and lethality triggered by bacterial flagellin. Our findings suggest a crucial role for NINJ1-dependent PMR in inflammasome-induced blood coagulation and inflammation.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/07/b7/nihpp-2023.08.30.555561v1.PMC10491273.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10315540","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":"Ventral pallidal GABAergic neurons drive consumption in male, but not female rats.","authors":"Alexandra Scott, Anika Paulson, Collin Prill, Klaiten Kermoade, Bailey Newell, Jocelyn M Richard","doi":"10.1101/2024.04.30.591876","DOIUrl":"10.1101/2024.04.30.591876","url":null,"abstract":"<p><p>Food intake is controlled by multiple converging signals: hormonal signals that provide information about energy homeostasis, but also hedonic and motivational aspects of food and food cues that can drive non-homeostatic or \"hedonic \"feeding. The ventral pallidum (VP) is a brain region implicated in the hedonic and motivational impact of food and foods cues, as well as consumption of rewards. Disinhibition of VP neurons has been shown to generate intense hyperphagia, or overconsumption. While VP gamma-Aminobutyric acidergic (GABA) neurons have been implicated in cue-elicited reward seeking and motivation, the role of these neurons in the hyperphagia resulting from VP activation remains unclear. Here, we used Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) to activate or inhibit VP GABA neurons in sated male and female rats during chow and sucrose consumption. We found that activation of VP GABA neurons increases consumption of chow and sucrose in male rats, but not female rats. We also found that, while inhibition of VP GABA neurons tended to decrease sucrose consumption, this effect was not statistically significant. Together, these findings suggest that activation of VP GABA neurons can stimulate consumption of routine or highly palatable rewards selectively in male rats.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11092650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140923957","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":"Pain persists in mice lacking both Substance P and CGRPα signaling.","authors":"Donald Iain MacDonald, Monessha Jayabalan, Jonathan Seaman, Rakshita Balaji, Alec Nickolls, Alexander Chesler","doi":"10.1101/2023.11.15.567208","DOIUrl":"10.1101/2023.11.15.567208","url":null,"abstract":"<p><p>The neuropeptides Substance P and CGRPα have long been thought important for pain sensation. Both peptides and their receptors are expressed at high levels in pain-responsive neurons from the periphery to the brain making them attractive therapeutic targets. However, drugs targeting these pathways individually did not relieve pain in clinical trials. Since Substance P and CGRPα are extensively co-expressed we hypothesized that their simultaneous inhibition would be required for effective analgesia. We therefore generated <i>Tac1</i> and <i>Calca</i> double knockout (DKO) mice and assessed their behavior using a wide range of pain-relevant assays. As expected, Substance P and CGRPα peptides were undetectable throughout the nervous system of DKO mice. To our surprise, these animals displayed largely intact responses to mechanical, thermal, chemical, and visceral pain stimuli, as well as itch. Moreover, chronic inflammatory pain and neurogenic inflammation were unaffected by loss of the two peptides. Finally, neuropathic pain evoked by nerve injury or chemotherapy treatment was also preserved in peptide-deficient mice. Thus, our results demonstrate that even in combination, Substance P and CGRPα are not required for the transmission of acute and chronic pain.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10705526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138810265","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":"Mesoscale functional architecture in medial posterior parietal cortex.","authors":"Riichiro Hira, Leah B Townsend, Ikuko T Smith, Che-Hang Yu, Jeffrey N Stirman, Yiyi Yu, Spencer LaVere Smith","doi":"10.1101/2023.08.27.555017","DOIUrl":"10.1101/2023.08.27.555017","url":null,"abstract":"<p><p>The posterior parietal cortex (<b>PPC</b>) in mice has various functions including multisensory integration^1-3, vision-guided behaviors^4-6, working memory^7-13, and posture control^14,15. However, an integrated understanding of these functions and their cortical localizations in and around the PPC and higher visual areas (<b>HVAs</b>), has not been completely elucidated. Here we simultaneously imaged the activity of thousands of neurons within a 3 × 3 mm² field-of-view, including eight cortical areas around the PPC, during behavior with a two-photon mesoscope¹⁶. Mice performed both a vision-guided task and a choice history-dependent task, and the imaging results revealed distinct, localized, behavior-related functions of two medial PPC areas. Neurons in the anteromedial (<b>AM</b>) HVA responded to both vision and choice information, and thus AM is a locus of association between these channels. By contrast, the anterior (<b>A</b>) HVA stores choice history with sequential dynamics and represents posture. Mesoscale correlation analysis on the intertrial variability of neuronal activity demonstrated that neurons in area A shared fluctuations with the primary somatosensory area, while neurons in AM exhibited diverse, area-dependent interactions. Pairwise interarea interactions among neurons were precisely predicted by the anatomical input correlations, with the exception of some global interactions. Thus, the medial PPC has two distinct modules, areas A and AM, which each have distinctive modes of cortical communication. These medial PPC modules can serve separate higher-order functions: area A for transmission of information including posture, movement, and working memory; and area AM for multisensory and cognitive integration with locally processed signals.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11642780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89084812","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":"Disrupted endosomal trafficking of the Vangl-Celsr polarity complex underlies congenital anomalies in trachea-esophageal morphogenesis.","authors":"Nicole A Edwards, Scott A Rankin, Adhish Kashyap, Alissa Warren, Zachary N Agricola, Alan P Kenny, Matthew J Kofron, Yufeng Shen, Wendy K Chung, Aaron M Zorn","doi":"10.1101/2023.10.11.561909","DOIUrl":"10.1101/2023.10.11.561909","url":null,"abstract":"<p><p>Disruptions in foregut morphogenesis can result in life-threatening conditions where the trachea and esophagus fail to separate properly, such as esophageal atresia (EA) and tracheoesophageal fistulas (TEF). The developmental basis of these congenital anomalies is poorly understood, but recent genome sequencing reveals that <i>de novo</i> variants in intracellular trafficking genes are enriched in EA/TEF patients. Here, we confirm that mutation of orthologous genes in <i>Xenopus</i> disrupts trachea-esophageal separation similar to EA/TEF patients. We show that the Rab11a recycling endosome pathway is required to localize Vangl-Celsr polarity complexes at the luminal cell surface where opposite sides of the foregut tube fuse. Partial loss of endosome trafficking or Vangl-Celsr complexes disrupts epithelial polarity and mutant cells accumulate at the fusion point, fail to downregulate Cadherin, and do not separate into distinct trachea and esophagus. These data provide insights into the mechanisms of congenital anomalies and general paradigms of tissue fusion during organogenesis.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10592723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49694469","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":"diplo-locus: A lightweight toolkit for inference and simulation of time-series genetic data under general diploid selection.","authors":"Xiaoheng Cheng, Matthias Steinrücken","doi":"10.1101/2023.10.12.562101","DOIUrl":"10.1101/2023.10.12.562101","url":null,"abstract":"<p><p>Whole-genome time-series allele frequency data are becoming more prevalent as ancient DNA (aDNA) sequences and data from evolve-and-resequence (E&R) experiments are generated at a rapid pace. Such data presents unprecedented opportunities to elucidate the dynamics of genetic variation under selection. However, despite many methods to infer parameters of selection models from allele frequency trajectories available in the literature, few provide user-friendly implementations for large-scale empirical applications. Here, we present diplo-locus, an open-source Python package that provides functionality to simulate and perform inference from time-series data under the Wright-Fisher diffusion with general diploid selection. The package includes Python modules as well as command-line tools and is available at: https://github.com/steinrue/diplo_locus.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10614779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71415601","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":"Enabling Electric Field Model of Microscopically Realistic Brain.","authors":"Zhen Qi, Gregory M Noetscher, Alton Miles, Konstantin Weise, Thomas R Knösche, Cameron R Cadman, Alina R Potashinsky, Kelu Liu, William A Wartman, Guillermo Nunez Ponasso, Marom Bikson, Hanbing Lu, Zhi-De Deng, Aapo R Nummenmaa, Sergey N Makaroff","doi":"10.1101/2024.04.04.588004","DOIUrl":"10.1101/2024.04.04.588004","url":null,"abstract":"<p><p>Modeling brain stimulation at the microscopic scale may reveal new paradigms for various stimulation modalities. We present the largest map to date of extracellular electric field distributions within a layer L2/L3 mouse primary visual cortex brain sample. This was enabled by the automated analysis of serial section electron microscopy images with improved handling of image defects, covering a volume of 250 × 140 × 90 μm ³ . The map was obtained by applying a uniform brain stimulation electric field at three different polarizations and accurately computing microscopic field perturbations using the boundary element fast multipole method. We used the map to identify the effect of microscopic field perturbations on the activation thresholds of individual neurons. Previous relevant studies modeled a macroscopically homogeneous cortical volume. Our result shows that the microscopic field perturbations - an 'electric field spatial noise' with a mean value of zero - only modestly influence the macroscopically predicted stimulation field strengths necessary for neuronal activation. The thresholds do not change by more than 10% on average. Under the stated limitations and assumptions of our method, this result justifies the conventional theory of \"invisible\" neurons embedded in a macroscopic brain model for transcranial magnetic and transcranial electrical stimulation. However, our result is solely sample-specific and largely neglects the effect of the microcapillary network. Furthermore, we only considered the uniform impressed field and a single- pulse stimulation time course.</p><p><strong>Significance statement: </strong>This study is arguably the first attempt to model brain stimulation at the microscopic scale, enabled by automated analysis of modern scanning electron microscopy images of the brain. It concentrates on modeling microscopic perturbations of the extracellular electric field caused by the physical cell structure and is applicable to any type of brain stimulation.</p><p><strong>Data availability statement: </strong>Post-processed cell CAD models (383, stl format), microcapillary CAD models (34, stl format), post-processed neuron morphologies (267, swc format), extracellular electric field and potential distributions at different polarizations (267x3, MATLAB format), *.ses projects files for biophysical modeling with Neuron software (267x2, Neuron format), and computed neuron activating thresholds at different conditions (267x8, Excel tables, without the sample polarization correction from Section 2.8) are made available online through <b>BossDB</b> , a volumetric open-source database for 3D and 4D neuroscience data.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11030228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140862863","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>bamSliceR</i>: a Bioconductor package for rapid, cross-cohort variant and allelic bias analysis.","authors":"Yizhou Peter Huang, Lauren Harmon, Eve Deering-Gardner, Xiaotu Ma, Josiah Harsh, Zhaoyu Xue, Hong Wen, Marcel Ramos, Sean Davis, Timothy J Triche","doi":"10.1101/2023.09.15.558026","DOIUrl":"10.1101/2023.09.15.558026","url":null,"abstract":"<p><p>The NCI Genomic Data Commons (GDC) provides controlled access to sequencing data from thousands of subjects, enabling large-scale study of impactful genetic alterations such as simple and complex germline and structural variants. However, efficient analysis requires significant computational resources and expertise, especially when recalling variants from raw sequence reads. We thus developed <b><i>bamSliceR</i></b> , an R/Bioconductor package that builds upon the <b><i>GenomicDataCommons</i></b> package to extract aligned sequence reads from cross-GDC meta-cohorts, followed by targeted analysis of variants and effects (including transcript-aware variant annotation from transcriptome-aligned GDC RNA data). Here we demonstrate population-scale genomic & transcriptomic analyses with minimal compute burden via <b><i>bamSliceR</i></b> , identifying recurrent, clinically relevant sequence and structural variants in the TARGET AML and BEAT-AML cohorts. We then validate results in the (non-GDC) Leucegene cohort, demonstrating how the <b><i>bamSliceR</i></b> pipeline can be seamlessly applied to replicate findings in non-GDC cohorts. These variants directly yield clinically impactful and biologically testable hypotheses for mechanistic investigation. <b><i>bamSliceR</i></b> has been submitted to the Bioconductor project, where it is presently under review, and is available on GitHub at https://github.com/trichelab/bamSliceR.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10516001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41158809","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}