Journal of Leukocyte Biology最新文献

{"title":"Machine learning algorithm approach to complete blood count can be used as early predictor of COVID-19 outcome.","authors":"Cecília Horta Ramalho-Pinto, Lucas Haniel Araújo Ventura, Giovanna Caliman Camatta, Gabriela Silveira-Nunes, Matheus Souza Gomes, Hugo Itaru Sato, Murilo Soares Costa, Henrique Cerqueira Guimarães, Rafael Calvão Barbuto, Olindo Assis Martins-Filho, Laurence Rodrigues Amaral, Pedro Luiz Lima Bertarini, Santuza Maria Ribeiro Teixeira, Unaí Tupinambás, Andrea Teixeira-Carvalho, Ana Maria Caetano Faria","doi":"10.1093/jleuko/qiae223","DOIUrl":"10.1093/jleuko/qiae223","url":null,"abstract":"<p><p>Although the SARS-CoV-2 infection has established risk groups, identifying biomarkers for disease outcomes is still crucial to stratify patient risk and enhance clinical management. Optimal efficacy of COVID-19 antiviral medications relies on early administration within the initial 5 d of symptoms, assisting high-risk patients in avoiding hospitalization and improving survival chances. The complete blood count (CBC) can be an efficient and affordable option to find biomarkers that predict the COVID-19 prognosis due to infection-induced alterations in various blood parameters. This study aimed to associate hematological parameters with different COVID-19 clinical forms and utilizes them as disease outcome predictors. We performed a CBC in blood samples from 297 individuals with COVID-19 from Belo Horizonte, Brazil. Statistical analysis, as well as ROC Curves and machine learning Decision Tree algorithms were used to identify correlations, and their accuracy, between blood parameters and disease severity. In the initial 4 d of infection, traditional hematological COVID-19 alterations, such as lymphopenia, were not yet apparent. However, the monocyte percentage and granulocyte-to-lymphocyte ratio (GLR) proved to be reliable predictors for hospitalization, even in cases where patients exhibited mild symptoms that later progressed to hospitalization. Thus, our findings demonstrate that COVID-19 patients with monocyte percentages lower than 7.7% and a GLR higher than 8.75 are assigned to the hospitalized group with a precision of 86%. This suggests that these variables can serve as important biomarkers in predicting disease outcomes and could be used to differentiate patients at hospital admission for managing therapeutic interventions, including early antiviral administration. Moreover, they are simple parameters that can be useful in minimally equipped health care units.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142467620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multifaceted roles of neutrophils in cardiac disease.","authors":"Samantha Morrissey, Logan G Kirkland, Tasha K Phillips, Rebecca D Levit, Alex Hopke, Brian C Jensen","doi":"10.1093/jleuko/qiaf017","DOIUrl":"https://doi.org/10.1093/jleuko/qiaf017","url":null,"abstract":"<p><p>Neutrophils, the most abundant leukocytes in human blood, have long been recognized as critical first responders in the innate immune system's defense against pathogens. Some of the more notable innate anti-microbial properties of neutrophils include generation of superoxide free radicals like myeloperoxidase (MPO), production of proteases that reshape the extracellular matrix allowing for easier access to infected tissues, and release of neutrophil extracellular traps (NETs), extruded pieces of DNA that ensnare bacterial and fungi. These mechanisms developed to provide neutrophils with a vast array of specialized functions to provide the host defense against infection in an acute setting. However, emerging evidence over the past few decades has revealed a far more complex and nuanced role for these neutrophil-driven processes in various chronic conditions, particularly in cardiovascular diseases. The pathophysiology of cardiac diseases involves a complex interplay of hemodynamic, neurohumoral, and inflammatory factors. Neutrophils, as key mediators of inflammation, contribute significantly to this intricate network. Their involvement extends far beyond their classical role in pathogen clearance, encompassing diverse functions that can both exacerbate tissue damage and contribute to repair processes. Here we consider the contributions of neutrophils to myocardial infarction, heart failure, cardiac arrhythmias and non-ischemic cardiomyopathies. Understanding these complex interactions is crucial for developing novel therapeutic strategies aimed at modulating neutrophil functions in these highly morbid cardiac diseases.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of CD57+γδ T cells in the immune pathogenesis of patients with sepsis.","authors":"Liman Li, Nenggang Jiang, Yongmei Jin, Chuan Yang, Yang Fu","doi":"10.1093/jleuko/qiaf015","DOIUrl":"https://doi.org/10.1093/jleuko/qiaf015","url":null,"abstract":"<p><p>The immune response goes haywire during sepsis. The aim of this study was to explore the role of CD57+γδ T cells in the immune pathogenesis of sepsis. We characterized the transcriptomic profile of peripheral γδ T cells obtained from patients with sepsis using the Smart RNA-Sequence. We also analyzed the cell count and the immune functional signatures of CD57+γδ T cells in sepsis using flow cytometry. Besides, the cytotoxicity capacity of CD57+γδ T cell subset and its responses to sepsis-related drug were validated in vitro. Here, we found that patients with sepsis exhibited a reduction in peripheral CD57+γδ T cells proportion, which was positively associated with clinical outcomes. Compared with CD57-γδ T cells, CD57+γδ T cells exhibited drastically altered immunophenotype, including decreased expression levels of costimulatory molecules, higher expression levels of pro-inflammatory factors and cytotoxic granules.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extended repertoire of CXC chemokines acting as agonists and antagonists of the human and murine atypical chemokine receptor ACKR2.","authors":"Rafael Luís, Brian F Volkman, Martyna Szpakowska, Andy Chevigné","doi":"10.1093/jleuko/qiaf013","DOIUrl":"https://doi.org/10.1093/jleuko/qiaf013","url":null,"abstract":"<p><p>Atypical chemokine receptors (ACKRs) are a subfamily of important regulators of chemokine functions. Among them, ACKR2 has long been considered as a scavenger of multiple inflammatory chemokines exclusively from the CC family. Recently, we demonstrated the ability of ACKR2 to scavenge the CXC chemokine CXCL10, previously reported to bind solely the classical receptor CXCR3. This discovery emphasized the need for systematic reassessments of chemokine-receptor pairings. In this work, we established a highly sensitive NanoBRET-based competition binding assay using a novel proprietary ACKR2 modulator (LIH222) and applied it in a comprehensive reassessment of the pairings between human and murine chemokines and their respective ACKR2 orthologues. We confirmed CXCL10 as a ligand for the human but also the mouse ACKR2. We also identified CXCL5, CXCL11 and CXCL12 as new CXC chemokines for both ACKR2 orthologues. Furthermore, we showed that CXCL2 is a ligand for the human but not the mouse ACKR2, whereas CXCL1 binds the mouse but not the human receptor. Finally, we found that N-terminally truncated CXCL5 (CXCL58-78) loses its capacity to bind ACKR2, whereas the removal of the first two residues of CXCL11 (CXCL113-73) enhances its antagonist potency, showing a tendency towards a reduction of the receptor basal interactions with β-arrestins. Altogether, this study demonstrates that ACKR2 is not exclusive to CC chemokines and although with a weaker affinity it can also bind and scavenge a subset of inflammatory and homeostatic CXC chemokines important for the regulation of the immune system.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD73 promotes the maturation of murine NK cells and their survival in the tumor microenvironment.","authors":"Brian Parra-Tello, Moira García-Gómez, Eva Rekus-Polanska, Felipe Malgue, Sebastián Charlín, Andrés Hernández-Oliveras, Javiera Reyes-Alvarez, Mario Rosemblatt, Andreas Lundqvist, Alvaro Lladser, María Rosa Bono, Daniela Sauma","doi":"10.1093/jleuko/qiaf011","DOIUrl":"https://doi.org/10.1093/jleuko/qiaf011","url":null,"abstract":"<p><p>Natural Killer (NK) cells are crucial in recognizing and eliminating tumor cells, making them pivotal in antitumor responses. Adenosine, the product of ATP hydrolysis mediated by CD39 and CD73 ectonucleotidases, has been reported to reduce the proliferation and maturation of NK cells. In this study, we investigate the expression of CD73 in NK cells and its impact on maturation, phenotype, survival, and function. Our findings reveal that while splenic NK cells express minimal levels of CD73, its expression is induced upon activation and in the tumor microenvironment upon adoptive transfer to tumor-bearing mice. Notably, within the tumor microenvironment, CD73 expression in NK cells correlates with elevated levels of PD-L1 and CD226. Accordingly, analysis of human melanoma datasets uncovers a subset of immature tumor-infiltrating NK cells expressing CD73. To further understand the role of CD73 on NK cells, we used a CD73 knockout (KO) murine model and observed that CD73-deficient NK cells display a more immature phenotype and heightened proliferative activity than wild-type (WT) NK cells. Additionally, CD73-deficient NK cells exhibit elevated levels of P2X7R and reduced CD39 expression, suggesting an increased susceptibility to ATP-induced death. Following adoptive transfer to tumor-bearing mice, CD73KO NK cells are present at a lower frequency but demonstrate similar control over tumor growth compared to WT NK cells. In conclusion, our study demonstrates the upregulation of CD73 in NK cells infiltrating tumors and underscores its role as a checkpoint regulating the functional maturation of NK cells.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-canonical NF-κB signaling in dendritic cells is required for ATP-driven indoleamine 2,3-dioxygenase 1 induction through P2Y11 receptor.","authors":"Darina Ocadlikova, Benedetta Fiordi, Sara Trabanelli, Valentina Salvestrini, Marilena Ciciarello, Dorian Forte, Emma Campazzi, Letizia Vitali, Serenella C Cipollitta, Anna Pegoraro, Camilla Jandus, Francesco Di Virgilio, Elena Adinolfi, Michele Cavo, Antonio Curti","doi":"10.1093/jleuko/qiaf010","DOIUrl":"https://doi.org/10.1093/jleuko/qiaf010","url":null,"abstract":"<p><p>Extracellular ATP released from dying cells, including tumor cells, is a key mediator of inflammation and tolerance by binding to purinergic receptors on dendritic cells, resulting in inflammasome activation (via P2X7R), dendritic cell maturation (via P2Y11R), and Indoleamine-2,3-dioxygenase 1 upregulation. However, the regulation of ATP-driven Indoleamine-2,3-dioxygenase 1 expression in human dendritic cells has been poorly investigated. In this work we aimed to investigate the ATP-driven molecular regulation of Indoleamine-2,3-dioxygenase 1 expression via purinergic receptors and to provide an in-depth characterization of ATP-driven T regulatory cells induced by Indoleamine-2,3-dioxygenase 1-expressing dendritic cells. We identified P2Y11R as being responsible for ATP-driven Indoleamine-2,3-dioxygenase 1 upregulation, and non-canonical NF-kB as a molecular pathway associated with ATP-dependent Indoleamine-2,3-dioxygenase 1 induction through P2Y11R. Then we investigated - but did not confirm - an involvement of inflammasome machinery through P2X7R in Indoleamine-2,3-dioxygenase 1 upregulation. Finally, we evaluated the role of ATP catabolism via ATP ectonucleotidases, i.e. CD39 and CD73 and its main product adenosine, in regulating the generation of Indoleamine-2,3-dioxygenase 1-driven T regulatory cells. We found that ATP-driven Indoleamine-2,3-dioxygenase 1 upregulation is associated with CD73 upregulation and adenosine production. Additionally, ATP-treated Indoleamine-2,3-dioxygenase 1-positive mature dendritic cells induce PD-1-expressing bone fide suppressive T regulatory cells via adenosine A2AR. Collectively, a more in-depth understanding of ATP-driven immune-regulatory mechanisms through Indoleamine-2,3-dioxygenase 1 regulation in human dendritic cells leading to the induction of T regulatory cells can have clinical implications for the development of Indoleamine-2,3-dioxygenase 1 inhibitors in cancer patients, especially in combination with immunotherapy such as an anti-CD73 or adenosine receptor agonist and immunogenic chemotherapy.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nexinhib20 inhibits JFC1-mediated mobilization of a subset of CD11b/CD18+ vesicles decreasing integrin avidity, but does not inhibit Rac1.","authors":"Kasra Askari, Jennifer L Johnson, Aparna Shukla, Elsa Meneses-Salas, William B Kiosses, Juan Yu, Sergio D Catz","doi":"10.1093/jleuko/qiaf012","DOIUrl":"10.1093/jleuko/qiaf012","url":null,"abstract":"<p><p>Regulated sequential exocytosis of neutrophil granules is essential in orchestrating the innate immune response, while uncontrolled secretion causes inflammation. We developed and characterized Nexinhib20, a small-molecule inhibitor that targets azurophilic granule exocytosis in neutrophils by blocking the interaction between the small GTPase Rab27a and its effector JFC1. Its therapeutic potential has been demonstrated in several pre-clinical models of inflammatory disease. Here, using neutrophils from Jfc1-KO mice, we show that JFC1 regulates the mobilization of a small subpopulation of CD11b+ granules. Nexinhib20 inhibits the mobilization of β2-integrins from a subset of CD11b+ granules to the plasma membrane in human and mouse neutrophils. The putative impact of Nexinhib20 on integrin activation is caused by decreased avidity, secondary to its effect on β2-integrin mobilization. CD11b mobilization and integrin activation were unaffected by pharmacological inhibition or activation of Rac1. Using quantitative 3-dimensional enhanced resolution microscopy, we show that neutrophil activation induces the recruitment of JFC1 to CD11b+ granules. Nexinhib20 decreased the localization of JFC1 at CD11b+ granules without affecting the association of Rac1 with CD11b. Nexinhib20 inhibits JFC1 recruitment but not endogenous Rac1 activation in living cells. Using orthogonal analyses of Rac1 activity consisting of a sensitive, time-resolved FRET, Rac1-PAK1-binding assay, and endogenous Rac1-GTP examination, we show that Nexinhib20 does not interfere with Rac1 activation. Instead, we confirmed its molecular mode of action to the inhibition of the Rab27a-JFC1 binding axis. Thus, Nexinhib20 limits β2- integrin mobilization to the cell surface, decreasing avidity, affecting active integrin availability, in a JFC1-dependent but Rac1-independent manner.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"APOE aggregation in microglia, seeds b-amyloidosis in Alzheimer's disease.","authors":"Miguel A Jiménez-Acosta, Cristina A Luckie-Duque, Marco A Meraz-Ríos","doi":"10.1093/jleuko/qiaf007","DOIUrl":"https://doi.org/10.1093/jleuko/qiaf007","url":null,"abstract":"","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Flow cytometric measurement of CFTR-mediated chloride transport in human neutrophils.","authors":"Alejandra Montanez-Barragan, Frank H Robledo-Avila, Raul Rascon, Karen S McCoy, Benjamin T Kopp, Santiago Partida-Sanchez","doi":"10.1093/jleuko/qiaf006","DOIUrl":"10.1093/jleuko/qiaf006","url":null,"abstract":"<p><p>Immune cells express a variety of ion channels and transporters in the plasma membrane and intracellular organelles, responsible of the transference of charged ions across hydrophobic lipid membrane barriers. The correct regulation of ion transport ensures proper immune cell function, activation, proliferation, and cell death. Cystic fibrosis (CF) is a genetic disease in which the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) chloride channel gene is defective, consequently, the CFTR protein is dysfunctional, and the chloride efflux in CF cells is markedly impaired. Cystic fibrosis is characterized by chronic inflammation in the airways, mainly triggered by neutrophilic infiltration and recurring bacterial infections, causing the decline of lung function and eventually respiratory failure. Novel modulator-based therapies have improved lung function in people with Cystic Fibrosis (pwCF) by increasing expression and function of CFTR in the plasma membrane of lung cells, however, the effects of these drugs in the lung recruited inflammatory cells, specifically neutrophils, remains unknown. Given the complex biology of neutrophils and their short lifespan, we aimed to develop a fluorometric method to evaluate CFTR-mediated chloride transport in human neutrophils by using flow cytometry and the intracellular chloride-binding MQAE dye. Our results show that CFTR-mediated chloride transport in human neutrophils or human neutrophil-like cell lines can be consistently evaluated in vitro by this methodology. Additionally, this assay measured increased chloride efflux in neutrophils collected from pwCF under modulator therapy, as compared to healthy donors, indicating this method can evaluate restoration of CFTR-mediated chloride transport in CF neutrophils.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell RNA Sequencing Revealed the Immunophenotypic Features of Macrophages in Cardiac Transplants and Uncovered Lgals9 Promoted Their Polarization towards The M2b Subtype.","authors":"Yuexing Zhu, Xinguo Zheng, Chao Chen, Ye Xu, Yuxi Fan, Zhouqi Tang, Yingqi Zeng, Chen Feng, Hedong Zhang, Xiaojun Chen, Zhongquan Qi, Tengfang Li, Longkai Peng, Minjie Lin, Weili Chen, Fenghua Peng, Xin Jiang, Helong Dai","doi":"10.1093/jleuko/qiaf009","DOIUrl":"https://doi.org/10.1093/jleuko/qiaf009","url":null,"abstract":"<p><p>Macrophages play a crucial role in the immune response during allograft rejection in organ transplantation. Therefore, our study aimed to explore the genomic features of macrophages in mouse heart transplants and use single-cell RNA sequencing to investigate Galectin-9 (Gal-9, Lgals9), a lectin that can mediate the activation and differentiation of immune cells through ligand-receptor interactions, and the effects of its regulation in transplantation. We discovered a new subset of macrophages called \"Myoz2+ macrophages\", which specifically expressed genes related to myocardial contraction. We identified a distinct differentiation trajectory and process for the Saa3+ macrophage population, representing anti-inflammatory functionality. Also, we observed a significant downregulation of Lgals9 expression in the macrophages after mouse heart transplantation. Then, we validated our findings using RT-qPCR and Western blotting and also investigated the impact of Lgals9 on macrophage function through flow cytometry and ELISA. Furthermore, in vitro, we found that rLgals9 (Recombinant Mouse Galectin-9 Protein) treated macrophages polarized towards the M2b phenotype at appropriate concentrations.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}