Journal of Allergy and Clinical Immunology最新文献

{"title":"Environmental risk factors and asthma primary prevention: From birth cohort studies to clinical trials","authors":"Amy A. Eapen MD, MS ,&nbsp;Soni Shankhwar PhD ,&nbsp;Erika von Mutius MD, MSc ,&nbsp;Christine C. Johnson PhD, MPH","doi":"10.1016/j.jaci.2025.07.002","DOIUrl":"10.1016/j.jaci.2025.07.002","url":null,"abstract":"<div><div>With the prevalence of pediatric asthma and allergy rising substantially since last mid-century, birth cohort studies starting in pregnancy have been pivotal in identifying prenatal and early life environmental factors that influence risk of these diseases. With these findings, researchers have been able to identify biologic mechanisms at play with the eventual goal of engineering tailored interventions to optimize immune system development and decrease the risk of allergic disorders. In this review, we describe the critical role birth cohort studies have played in starting to disentangle the environmental epidemiology and etiology of childhood-onset asthma and other allergic diseases and how these studies have guided ongoing clinical trials for asthma and allergy prevention. Lastly, we highlight important questions that remain unanswered and potential approaches to help fill these gaps in knowledge.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"156 3","pages":"Pages 535-545"},"PeriodicalIF":11.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144630475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complement factor I deficiency–associated neuroinflammatory disease among Old Order Amish","authors":"Whitney Reid MD ,&nbsp;Laura Baas BS ,&nbsp;Amy L. Stiegler PhD ,&nbsp;Titus J. Boggon PhD ,&nbsp;Portia A. Kreiger MD ,&nbsp;Kathleen E. Sullivan MD, PhD ,&nbsp;Edward M. Behrens MD ,&nbsp;Vinay V.R. Kandula MD ,&nbsp;Lambert P. van den Heuvel PhD ,&nbsp;Karlla W. Brigatti MS ,&nbsp;Vincent J. Carson MD ,&nbsp;Neil Romberg MD","doi":"10.1016/j.jaci.2025.06.021","DOIUrl":"10.1016/j.jaci.2025.06.021","url":null,"abstract":"<div><h3>Background</h3><div>Complement factor I (CFI) deficiency is an ultrarare inborn disorder of complement regulation that manifests with protean infectious, vasculitic, and neuroinflammatory symptoms.</div></div><div><h3>Objective</h3><div>We sought to functionally validate a previously unrecognized, disease-associated CFI variant (Y459S) and determine variant enrichment in the Old Order Amish population.</div></div><div><h3>Methods</h3><div>Expression and function of the CFI Y459S variant was evaluated via immunoblot, complement factor 3b degradation, and crystal structure analysis. <em>CFI</em> variant frequencies in Old Order Amish populations were determined using genomic databases hosted by the Clinic for Special Children and the Anabaptist Variant Server. Patient samples were assessed for leukocyte frequencies, cytokine concentrations, and complement component concentrations in clinical laboratories. Neuroinflammatory assessments were made by review of brain and spine magnetic resonance imaging by a blinded neuroradiologist.</div></div><div><h3>Results</h3><div>Y459S conferred a loss of function to CFI. The CFI Y459S allele is enriched more than 4500-fold among the Old Order Amish (mean allelic frequency, 0.037), with 1 in every 730 live births in this population predicted to be homozygous. A single-center cohort of 11 Amish CFI Y459S homozygous patients identified 5 patients with critical neuroinflammatory diagnoses including acute disseminated encephalomyelitis, transverse myelitis, and aseptic meningoencephalitis. Features of CFI-deficient neuroinflammation included neutrophilic cerebral spinal fluid pleocytosis, constitutive complement activation, female predominance, diverse neuroimaging findings, and (in 1 case) a clinical response to eculizumab.</div></div><div><h3>Conclusions</h3><div>CFI deficiency should be a key diagnostic consideration for patients with neuroinflammatory symptoms, neutrophilic cerebral spinal fluid pleocytosis, and complement consumption, especially if they belong to the Old Order Amish community.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"156 3","pages":"Pages 835-841"},"PeriodicalIF":11.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144547903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The nasal microbiome in early infancy is primarily shaped by the maternal nasal microbiome","authors":"Bailey E. Quinn BS ,&nbsp;José Alejandro Reyes Rodríguez BS ,&nbsp;Emmanuel Kweku Sam BS ,&nbsp;Jasmina Duliman BS ,&nbsp;Elizabeth Denn MS ,&nbsp;Sandra Lee MPH ,&nbsp;Liang Shan PhD ,&nbsp;Christiana Kuti MD ,&nbsp;Beatrice Irene Nyann MD ,&nbsp;Nicolas Rosario-Matos MD ,&nbsp;Leyao Wang PhD","doi":"10.1016/j.jaci.2025.05.004","DOIUrl":"10.1016/j.jaci.2025.05.004","url":null,"abstract":"<div><h3>Background</h3><div>The infant nasal microbiota closely mediates the risks of developing childhood respiratory diseases. However, the primary sources of these early residing bacteria remain largely unknown, preventing the development of microbiome strategies for disease prevention.</div></div><div><h3>Objective</h3><div>Our aim was to identify the primary maternal source of bacteria found in the early infant nasal microbiome.</div></div><div><h3>Methods</h3><div>We conducted a birth cohort study titled the Mother Infant Microbiome International Cohort (MIMIC) study. We recruited 95 mother-newborn dyads from 3 sites (St Louis, Mo; San Juan, Puerto Rico; and Accra, Ghana) and collected samples at 2 time points (at the infants’ birth and when they were around 2 months old). We performed analyses of 16S ribosomal RNA gene sequencing data to evaluate the maternal microbiomes (nasal, saliva, breast milk, and areola skin) as sources seeding the infant nasal microbiome.</div></div><div><h3>Results</h3><div>The infant nasal microbiome underwent a major compositional change during the first 2 months of life. The maternal nasal microbiome was identified as the primary source of bacteria in the early nasal microbiome across the 3 study regions. <em>Corynebacterium</em> was predominantly transferred from the maternal nasal microbiome. Infants were more likely to harbor a <em>Corynebacterium</em>-dominant nasal microbiome if the nasal microbiome of their mother was <em>Corynebacterium</em> dominant.</div></div><div><h3>Conclusions</h3><div>The maternal nasal microbiome is an important source of bacteria in the early nasal microbiome. A large portion of transmitted bacteria from the maternal nasal microbiome belonged to the generally beneficial bacterial genus <em>Corynebacterium</em>. The results from this study will aid in the development of early-life intervention strategies aimed at reducing the incidence of childhood respiratory diseases and asthma.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"156 3","pages":"Pages 668-678"},"PeriodicalIF":11.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144087529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tryptophan–kynurenine metabolites associate with inflammation and immunologic phenotypes in common variable immunodeficiency","authors":"Silje F. Jørgensen MD, PhD ,&nbsp;Peder R. Braadland PhD ,&nbsp;Thor Ueland PhD ,&nbsp;Mai S.A. Fraz MD, PhD ,&nbsp;Annika E. Michelsen PhD ,&nbsp;Kristian Holm Cand Scient ,&nbsp;Liv T. Osnes MD, PhD ,&nbsp;Marius Trøseid MD, PhD ,&nbsp;Per Magne Ueland MD, PhD ,&nbsp;Børre Fevang MD, PhD ,&nbsp;Pål Aukrust MD, PhD ,&nbsp;Johannes R. Hov MD, PhD","doi":"10.1016/j.jaci.2025.04.031","DOIUrl":"10.1016/j.jaci.2025.04.031","url":null,"abstract":"<div><h3>Background</h3><div>A large proportion of patients with common variable immunodeficiency (CVID) have autoimmune and inflammatory manifestations characterized by chronic T-cell– and monocyte/macrophage activation of unknown etiology. The tryptophan–kynurenine pathway has previously been linked to immune activation involving T cells and monocytes/macrophages, as well as with gut microbial dysbiosis in some inflammatory diseases.</div></div><div><h3>Objective</h3><div>We aimed to characterize the tryptophan–kynurenine pathway in CVID and its potential association with clinical/immunologic phenotype and gut microbial dysbiosis.</div></div><div><h3>Methods</h3><div>Serum concentrations of a set of tryptophan–kynurenine pathway metabolites and neopterin were measured using liquid chromatography–tandem mass spectrometry in a discovery cohort (n = 40), a validation cohort (n = 53), and healthy controls (n = 60). B-cell phenotype was analyzed in both cohorts, whereas inflammatory markers (enzyme immunoassay), lipopolysaccharide, gut microbial composition, and food frequency questionnaire were measured in the discovery cohort.</div></div><div><h3>Results</h3><div>Compared to healthy controls, CVID patients had increased metabolism of the tryptophan–kynurenine pathway as assessed by increased kynurenine/tryptophan ratio, quinolinic acid, and 3-hydroxykynurenine in both the discovery and validation cohorts. The findings were most pronounced in the subgroup with autoimmune/inflammatory complications but was to some degree also observed in CVID patients with infection only. In CVID, the metabolites in the tryptophan–kynurenine pathway associated with soluble (s) markers of monocyte (sCD14, sCD163, neopterin) and T-cell (sCD25) activation as well as B-cell phenotype (eg, naïve B cells). Individual gut microbial taxa may influence tryptophan–kynurenine pathway metabolites, but not lipopolysaccharide or diet.</div></div><div><h3>Conclusion</h3><div>We found altered levels of several metabolites in the tryptophan–kynurenine pathway in two different CVID cohorts associated with systemic inflammation and B-cell phenotype.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"156 3","pages":"Pages 814-824.e11"},"PeriodicalIF":11.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toward precision medicine: Inflammatory nasal epithelial transcriptomic profiles in long COVID","authors":"Nadia Baalbaki PharmD, PhD ,&nbsp;Jelle M. Blankestijn MSc ,&nbsp;Samuel W. Kazer PhD ,&nbsp;Mahmoud I. Abdel-Aziz PhD ,&nbsp;Lizan D. Bloemsma PhD ,&nbsp;Harm Jan Bogaard MD, PhD ,&nbsp;Merel E.B. Cornelissen MSc ,&nbsp;Cornelis M. van Drunen PhD ,&nbsp;Daniëlle van Egmond BSc ,&nbsp;Esther J. Nossent MD, PhD ,&nbsp;Jaclyn M.L. Walsh BSc ,&nbsp;Jose Ordovas-Montanes PhD ,&nbsp;Korneliusz Golebski PhD ,&nbsp;Anke H. Maitland-van der Zee PhD ,&nbsp;P4O2 Consortium","doi":"10.1016/j.jaci.2025.05.023","DOIUrl":"10.1016/j.jaci.2025.05.023","url":null,"abstract":"<div><h3>Background</h3><div>Little is known about the role of the nasal epithelium in long COVID (LC).</div></div><div><h3>Objective</h3><div>We sought to assess nasal epithelial transcriptomes of patients with LC to unravel pathophysiological mechanisms for disease management.</div></div><div><h3>Methods</h3><div>Medical data and transcriptomes were obtained from participants in the Precision Medicine for More Oxygen COVID-19 cohort at 3 to 6 months (n = 40) and at 12 to 18 months (n = 15) post-COVID. Cell-type frequencies were estimated by deconvolution from a single-cell data set. Hierarchical clustering identified transcriptomic clusters and cellular clusters from which differences in gene expression, gene set enrichment, and pulmonary phenotypes were assessed. Functional validation was performed using CRISPR/Cas9 gene editing and <em>in vitro</em> assays in primary mutant nasal epithelium, and gene expression comparisons were made with healthy controls (n = 51).</div></div><div><h3>Results</h3><div>At 3 to 6 and 12 to 18 months, transcriptomes associated with inflammatory pathways (<em>P</em>_adj &lt; .05). Transcriptomic and cellular clusters were identified and were related to inflammation and ciliogenesis (<em>P</em>_adj &lt; .05). Comparison of transcriptomes of patients with and without pulmonary radiological abnormalities resulted in 613 significant differentially expressed genes (<em>P</em>_adj &lt; .05). Upregulated inflammatory genes were observed in patients with abnormalities. <em>SMURF1</em> expression was significantly increased in patients with abnormalities compared with those without abnormalities and healthy controls. <em>SMURF1</em>^−/− mutant nasal epithelial cells produced significantly lower levels (<em>P</em> &lt; .05) of proinflammatory cytokines on virus exposure compared with controls.</div></div><div><h3>Conclusions</h3><div>Nasal epithelium in LC exhibits persistent inflammatory states. <em>SMURF1</em> upregulation potentially contributes to an exacerbated inflammatory state in nasal epithelium of patients with radiological abnormalities. This study demonstrates the importance of understanding these inflammatory profiles within a clinical context and emphasizes the need for further assessment and validation of <em>SMURF1</em>’s role in LC.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"156 3","pages":"Pages 790-802"},"PeriodicalIF":11.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heterogeneity and molecular mechanisms of early-life wheeze","authors":"Conglin Liu MD, PhD ,&nbsp;Carlos A. Camargo Jr. MD, DrPH ,&nbsp;Zhaozhong Zhu ScD","doi":"10.1016/j.jaci.2025.06.027","DOIUrl":"10.1016/j.jaci.2025.06.027","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"156 3","pages":"Pages 609-611"},"PeriodicalIF":11.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144578798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiomics approach to evaluating personalized biomarkers of allergen immunotherapy","authors":"Mohamed H. Shamji PhD ,&nbsp;William T. Fulton MSc ,&nbsp;Ibrahim Animashaun MD ,&nbsp;Elizabeth Palmer PhD ,&nbsp;Katja Baerenfaller PhD ,&nbsp;Milena Sokolowska MD, PhD ,&nbsp;Domingo Barber MD, PhD ,&nbsp;Michelle Huffaker MD ,&nbsp;Carolyn Baloh MD ,&nbsp;Oliver Pfaar MD, PhD ,&nbsp;Markus Ollert MD, PhD ,&nbsp;Ludger Klimek MD, PhD ,&nbsp;Ronald L. Rabin MD ,&nbsp;Anubha Tripathi MD ,&nbsp;Alkis Togias MD ,&nbsp;Stefan Vieths PhD ,&nbsp;Wayne G. Shreffler MD, PhD ,&nbsp;Janice A. Layhadi PhD","doi":"10.1016/j.jaci.2025.06.036","DOIUrl":"10.1016/j.jaci.2025.06.036","url":null,"abstract":"<div><div>Recent advancements in genomics and “omic” technologies have ushered in a transformative era referred to as personalized or precision medicine. This innovative approach considers the unique genetic profiles of individuals, along with a range of variability factors, to devise tailored disease treatments and prevention strategies that cater to the distinct needs of each patient. Although the terms <em>personalized medicine</em> and <em>precision medicine</em> are frequently utilized interchangeably, it is essential to delineate the subtle distinctions between them. Personalized medicine concentrates on bespoke treatments and prevention strategies that are meticulously tailored for each individual. Conversely, precision medicine utilizes advanced gene sequencing and comprehensive data analytics to formulate specific treatments and prevention strategies for defined groups of individuals based on genetic, environmental, and lifestyle factors rather than focusing exclusively on individual patients. Therefore, precision medicine constitutes an extension of traditional personalized care, improving the accuracy of diagnosis, prognosis, and therapy estimations for each patient through the application of sophisticated molecular diagnostics and advanced imaging techniques enabled by recent technological innovations. The shift from personalized to precision medicine has gained considerable traction, particularly in the wake of the 2015 US Precision Medicine Initiative, which has further stimulated advancements in this domain. This review will explore multiomics approaches that have facilitated the evaluation of personalized biomarkers associated with allergen immunotherapy, particularly in the treatment of allergic diseases. By leveraging these innovative methodologies, we aspire to cultivate more effective and individualized patient care, ultimately enhancing health outcomes for individuals with allergies.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"156 3","pages":"Pages 523-534"},"PeriodicalIF":11.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144989404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current data on biologics: Evaluating clinical remission in asthma","authors":"Ian Pavord MA, DM, FRCP, FERS, FMedSci ,&nbsp;Rohit K. Katial MD ,&nbsp;David J. Jackson FRCP, MSc, PhD ,&nbsp;Linda Rogers MD ,&nbsp;Flavia Cecilia Lega Hoyte MD ,&nbsp;Josef Smolen MD ,&nbsp;Michael E. Wechsler MD, MMSc ,&nbsp;Praveen Akuthota MD ,&nbsp;Daniel J. Jackson MD","doi":"10.1016/j.jaci.2025.05.034","DOIUrl":"10.1016/j.jaci.2025.05.034","url":null,"abstract":"<div><div>The growing interest in clinical remission in asthma is due in large measure to the observation that many patients with severe asthma demonstrate substantial and durable improvements while receiving biologic therapy. Rates of clinical asthma remission in patients treated with a biologic have ranged from 19% to 43% in retrospective real-world studies and 13% to 35% in <em>post hoc</em> analyses of randomized controlled studies of biologics. Although these studies applied different remission criteria, almost all used a 4-component remission definition consisting of exacerbations, oral corticosteroid receipt, symptom control, and lung function parameters. Available evidence suggests that patients with a type 2 inflammatory endotype with less severe disease, shorter disease duration, and fewer comorbidities are more likely to experience remission. Little is currently known about asthma clinical remission in children and adolescents treated with a biologic. Prospective studies in patients of all ages are needed to refine the definition of clinical asthma remission and identify interventions and patient characteristics associated with remission.</div><div><em>This article is part of a supplement supported by an educational grant from AstraZeneca Pharmaceuticals. The content of this article was developed independently by National Jewish Health and the article authors</em>.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"156 3","pages":"Pages S15-S19"},"PeriodicalIF":11.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145183682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic B-cell depletion: Mechanisms, clinical applications, and implications for secondary immunodeficiency","authors":"Ahmed Elmoursi MD, MPH ,&nbsp;Sara Barmettler MD, MPH","doi":"10.1016/j.jaci.2024.11.026","DOIUrl":"10.1016/j.jaci.2024.11.026","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"156 3","pages":"Pages 597-603"},"PeriodicalIF":11.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Editors’ Choice","authors":"","doi":"10.1016/j.jaci.2025.07.012","DOIUrl":"10.1016/j.jaci.2025.07.012","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"156 3","pages":"Pages 590-594"},"PeriodicalIF":11.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144989399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}