Annals of the Rheumatic Diseases最新文献

{"title":"Correspondence on: 'EULAR recommendations for the treatment of systemic sclerosis: 2023 update' by Del Galdo et al.","authors":"Alper Sari, Ali Akdogan","doi":"10.1016/j.ard.2024.10.001","DOIUrl":"https://doi.org/10.1016/j.ard.2024.10.001","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143397802","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":"Efficacy of Janus kinase inhibitors in immune-mediated inflammatory diseases-a systematic literature review informing the 2024 update of an international expert consensus statement.","authors":"Victoria Konzett, Josef S Smolen, Peter Nash, Daniel Aletaha, Kevin Winthrop, Thomas Dörner, Roy Fleischmann, Yoshiya Tanaka, Jette Primdahl, Xenofon Baraliakos, Iain B McInnes, Michael Trauner, Naveed Sattar, Maarten de Wit, Jan W Schoones, Andreas Kerschbaumer","doi":"10.1016/j.ard.2025.01.023","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.023","url":null,"abstract":"<p><strong>Objective: </strong>This systematic literature review (SLR) on efficacy outcomes was performed to inform the 2024 update of the expert consensus statement on the treatment of immune-mediated inflammatory diseases (IMIDs) with Janus kinase inhibitors (JAKi).</p><p><strong>Methods: </strong>An update of the 2019 SLR was performed in MEDLINE, Embase, and the Cochrane Library. For efficacy, randomised, placebo (PLC)- or active-controlled trials on all JAKi investigated in IMIDs, as well as cohort and claims data for conditions where such studies were not available, were included.</p><p><strong>Results: </strong>In total, 10,556 records were screened, and 182 articles were included in the final analysis, investigating 21 JAKi in 51 IMIDs. Forty-three phase 2 and 59 phase 3 trials as well as 9 strategic trials and 72 pilot or cohort studies and case series were considered. JAKi demonstrated efficacy both in PLC-controlled trials as well as in head-to-head comparisons against active comparators, with 93 of 102 randomised controlled trials (RCTs) meeting their primary endpoints. Since 2019, 8 JAKi have received approval by the Federal Drug Agency and the European Medicine Agency for treatment of 11 IMIDs; of these, for 2, no approved disease-modifying antirheumatic drug (DMARD) therapy had previously been available.</p><p><strong>Conclusions: </strong>JAKi are effective for treating IMIDs, and various compounds have recently been approved. The impact of Janus kinase (JAK) selectivity for distinct JAK-STAT pathways needs further investigation, and few data are also available on sustained disease control upon tapering or withdrawal or on the optimal strategic placement of JAKi in international treatment algorithms.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143397805","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":"Characterisation of the antinociceptive effect of baricitinib in the collagen antibody-induced arthritis mouse model.","authors":"Nils Simon, Resti Rudjito, Lydia Moll, Katalin Sandor, Juan Antonio Vazquez-Mora, Zerina Kurtović, Alexandra Kuliszkiewicz, Carlos E Morado Urbina, Sven David Arvidsson, Eduardo Mendoza-Sánchez, Giovanni E López-Delgado, Qing Luo, Qiaolin Deng, Arisai Martínez Martínez, Jens Gammeltoft Gerwien, Paul Karila, Venkatesh Krishnan, Juan Miguel Jiménez-Andrade, Camilla I Svensson","doi":"10.1016/j.ard.2025.01.005","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.005","url":null,"abstract":"<p><strong>Objectives: </strong>Many rheumatoid arthritis (RA) patients continue to experience persistent pain even after successful management of joint inflammation. Clinical data indicate that RA patients treated with the JAK inhibitor baricitinib consistently achieve pain relief that cannot be entirely attributed to its anti-inflammatory effects. In this study, we investigated the antinociceptive properties of baricitinib using the collagen antibody-induced arthritis (CAIA) model in which mechanical hypersensitivity persists long after resolution of joint inflammation.</p><p><strong>Methods: </strong>The effects of baricitinib, etanercept (tumour necrosis factor inhibitor), and LP-922761 (adaptor protein-2 (AP2) associated kinase 1 (AAK1) inhibitor) on pain-like behaviour in CAIA mice were examined. Tissue samples from the late, low-grade inflammatory phase were examined for the effect of the treatments. Additionally, in vitro experiments using dorsal root ganglion (DRG) cells were conducted to assess baricitinib's influence on neuronal excitability and cell morphology.</p><p><strong>Results: </strong>Baricitinib reduced CAIA-induced joint inflammation, but its antinociceptive effects were most pronounced during the late phase when etanercept was ineffective. Administering baricitinib both early and late significantly decreased CAIA-induced bone loss, synovial innervation, and baseline STAT3 phosphorylation in ankle joints and DRGs. Unlike etanercept, baricitinib effectively reduced pain-like behaviour and synovial hyperinnervation when administered exclusively in the late phase. Additionally, baricitinib modulated glial cell morphology and neuronal excitability in vitro. Notably, it inhibited AAK1 signalling in DRGs, with AAK1 kinase activity blockade providing an antinociceptive effect in the CAIA model.</p><p><strong>Conclusions: </strong>Our data suggests that baricitinib has antinociceptive effects by targeting not only immune cells but also neurons and glia cells via inhibition of 2 signalling pathways linked to chronic pain.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381636","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":"AI-driven histologic analysis of human Achilles tendinopathy provides a roadmap to unravel pathogenesis.","authors":"Guillaume Planckaert, Arne Burssens, Flore Stappers, Julie Coudenys, Sofía Demolder, Irem Kaya, Malaïka Van der Linden, Amanda Gonçalves, Kelly Lemeire, Benjamin Pavie, Edwin Van Ovost, Peter Burssens, Amber Vanhaecke, Jo Van Dorpe, Lauren Pringels, Evi Wezenbeek, Jess Snedeker, Katrien De Bock, Fiona Bonar, Jill Cook, Jan Victor, Dirk Elewaut, Eric Gracey","doi":"10.1016/j.ard.2025.01.027","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.027","url":null,"abstract":"<p><strong>Objectives: </strong>Achilles tendinopathy is a common source of pain and dysfunction, yet its pathogenesis remains poorly understood. Research on human tendons is hampered by lack of standardisation in tissue sample validation, making interpretation of results challenging. We sought to develop an automated and operator-independent approach to histologically score human tendons.</p><p><strong>Methods: </strong>We assembled a cohort of 15 tendinopathic and 10 normal control Achilles tendon samples. We stained longitudinal sections with haematoxylin and eosin and Alcian blue and developed a low temperature epitope-retrieval protocol for immunostaining of blood vessels. Histologic sections were scored by pathologists using the current gold standard Bonar score. Whole sections were then analysed with open-source software (QuPath). Histologic features were automatically quantified across the entire section and summarised in the BonAIr score. Tissue from the same patients was subsequently analysed by quantitative polymerase chain reaction and flow cytometry to validate elements of the BonAIr score.</p><p><strong>Results: </strong>We observed increased cell roundness, collagen disarrangement, ground substance, and vascularity in tendinopathy using both the Bonar and BonAIr scores. Increased cellularity was only detected by the BonAIr score. Cellular and transcriptomic analyses corroborated tendinopathic shifts in all elements of the BonAIr score and further identified elevated THY1/CD90 expression in tendinopathy. CD90⁺ cells were found to localise to areas of low collagen alignment. These results align with the concept of stromal cell dysregulation in tendinopathy.</p><p><strong>Conclusions: </strong>Automated analysis of whole tendon sections refines conventional histopathologic scoring and predicts cellular and molecular changes found in tendinopathy. The BonAIr score should be further developed for standardised assessment of tendons samples across other anatomical locations and different research centres.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373756","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 giant cell arteritis (GCA) ultrasound score (OGUS) at diagnosis and after initial treatment predicts future relapses in GCA patients: results of a multicentre prospective study.","authors":"Sara Monti, Cristina Ponte, Valentin S Schäfer, Davide Rozza, Carlo Scirè, Giulia Franchi, Alessandra Milanesi, Nikita Khmelinskii, Simon M Petzinna, Greta Carrara, Cristina Di Nicola, João Eurico Fonseca, Carlomaurizio Montecucco, Wolfgang A Schmidt, Christian Dejaco, Raashid A Luqmani","doi":"10.1016/j.ard.2025.01.018","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.018","url":null,"abstract":"<p><strong>Objectives: </strong>To test the prognostic role of ultrasonography at diagnosis of giant cell arteritis (GCA) and the change of ultrasound abnormalities during the initial weeks of follow-up for the prediction of relapse, vascular complications, or initiation of disease-modifying antirheumatic drugs (DMARDs).</p><p><strong>Methods: </strong>Prospective, multicentre study of patients with new onset GCA undergoing serial ultrasound assessment at fixed time points. The Outcome Measures in Rheumatology (OMERACT) GCA ultrasonography score (OGUS) was used to quantify vessel wall abnormalities. Relapse was defined as recurrence of GCA-related symptoms or rise of inflammatory markers requiring treatment. A multivariable Poisson model with robust variance estimator was applied, including age, sex, large vessel GCA, glucocorticoid cumulative dose, and baseline OGUS as covariates.</p><p><strong>Results: </strong>Ninety-seven patients were assessed in 849 visits. Thirty-five (36.1%) patients experienced a total of 66 relapses, with median time to relapse of 210 days (IQR, 94.5-323.5). Higher OGUS at diagnosis was associated with an increased risk of relapse within 12 months (incidence rate ratio [IRR] for each 1 point increase in OGUS: 1.85; 95% CI, 1.05-3.32). At multivariable analysis, OGUS normalisation (score <1) over the first 3 weeks was negatively associated with subsequent relapses (IRR, 0.44; 95% CI, 0.22-0.88) and predicted time to first relapse. OGUS reduction over the first 12 weeks was inversely associated with initiation of DMARDs. Ischaemic/aortic complications were rare.</p><p><strong>Conclusions: </strong>Ultrasonography has a prognostic role in GCA and can inform risk stratification. Higher OGUS at diagnosis is associated with relapse, while a higher degree and rapidity of improvement in the first weeks are linked with lower relapse rate.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370130","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":"Somatic gain-of-function mutation in TLR7 causes early-onset systemic lupus erythematosus.","authors":"Yi Zeng, Panfeng Tao, Jun Wang, Ting Li, Yue Du, Xiuli Wang, Wei Wang, Siming Peng, Wei Wang, Mingsheng Ma, Hongmei Song, Xiaomin Yu, Qing Zhou","doi":"10.1016/j.ard.2025.01.011","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.011","url":null,"abstract":"<p><strong>Objectives: </strong>We identified a case of early-onset systemic lupus erythematosus (SLE) characterised by acute immune thrombocytopenia, recurrent fever, pneumonia, myocardial damage, thyroid dysfunction, lymphadenopathy, hepatosplenomegaly, and intracranial calcification. Our objective was to investigate the genetic and molecular mechanisms underlying the disease.</p><p><strong>Methods: </strong>Whole exome sequencing and targeted sequencing were performed and a somatic mutation in TLR7 was identified. RNA sequencing, quantitative polymerase chain reaction (qPCR), intracellular cytokine staining, and phospho-flow cytometry were performed to characterise inflammatory signatures. In addition, nuclear factor κB dual-luciferase reporter assays, qPCR, and RNA pull-down assays were performed to assess the functional impact of the TLR7 mutation on immune signalling.</p><p><strong>Results: </strong>We identified a novel somatic TLR7 mutation (p.Phe506Ser) that is likely to arise during early embryonic development. This mutation led to transcriptional upregulation of proinflammatory cytokines and interferon-stimulated genes, such as TNF and IFI27, with significant increases in intracellular cytokine expression, including TNF, following stimulation with the ligand single-stranded RNA (ssRNA) and the agonist R848 in the patient's peripheral blood mononuclear cells (PBMCs). In addition, functional analysis in HEK293T cells demonstrated that the mutant TLR7 exhibited increased binding affinity for ssRNA and enhanced responsiveness to agonists, resulting in hyperactivation of TLR7-mediated signalling.</p><p><strong>Conclusions: </strong>We report the first case of early-onset SLE caused by a somatic TLR7 gain-of-function mutation. Our findings demonstrate that the TLR7 F506S mutation drives excessive proinflammatory signalling in the patient's PBMCs, contributing to disease pathogenesis.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370312","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":"Impact of clinical subtype and sex on first-line biologic therapy discontinuation in axial spondyloarthritis.","authors":"Patricia Remalante-Rayco, Emmanuel S Baja, Zeynep Baskurt, Tina Chim, Carlo Irwin A Panelo, Evelyn Osio-Salido, Robert D Inman, Leonila F Dans, Nigil Haroon","doi":"10.1016/j.ard.2025.01.007","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.007","url":null,"abstract":"<p><strong>Objectives: </strong>To estimate the main and interaction effects of axial spondyloarthritis (axSpA) subtype and sex on first biologic disease-modifying antirheumatic drug (bDMARD) discontinuation.</p><p><strong>Methods: </strong>This retrospective cohort study included nonradiographic axSpA (nr-axSpA) and radiographic axSpA (r-axSpA) patients initiating tumour necrosis factor or interleukin-17 inhibitors. Modified Poisson regressions were used to estimate risk ratios (RRs) for the association of subtype and sex with discontinuation, adjusting for baseline covariates. Interaction was assessed using the relative excess risk due to interaction (RERI) and ratio of RRs. In addition, bDMARD survival rates were analysed using Kaplan-Meier curves.</p><p><strong>Results: </strong>Among 469 patients, 64% discontinued their first bDMARD. Nr-axSpA (RR, 1.80; 95% CI, 1.26-2.59) and female sex (RR, 1.49; 95% CI, 1.081-2.045) were significantly associated with discontinuation. Positive interaction trends between subtype and sex were observed on additive (RERI 0.49, 95% CI, -0.78 to 1.75) and multiplicative (RR ratio, 1.05; 95% CI, 0.55-2.03) scales, though not statistically significant. Nr-axSpA females had twice the discontinuation risk of r-axSpA males (hazard ratio, 2.30; 95% CI, 1.68-3.15, P < .001). bDMARD survival over 20 years was significantly lower in nr-axSpA and female patients.</p><p><strong>Conclusions: </strong>Nr-axSpA and female patients face a significantly higher risk of bDMARD discontinuation and shorter bDMARD survival. Although the combined effect of subtype and sex trended higher, it was not statistically significant. These findings underscore the need to address potential treatment challenges in female nr-axSpA patients.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370208","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":"Risk of developing psoriatic arthritis in patients with psoriasis initiating treatment with different classes of biologics.","authors":"Paolo Gisondi, Francesco Bellinato, Carlotta Galeone, Federica Turati, Luca Idolazzi, Alen Zabotti, Dennis McGonagle, Giampiero Girolomoni","doi":"10.1016/j.ard.2025.01.006","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.006","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the risk of psoriatic arthritis (PsA) in plaque psoriasis (PsO) patients receiving different classes of biologics.</p><p><strong>Methods: </strong>A retrospective observational study involving consecutive bionaïve PsO patients starting biologic treatment was performed. We compared the occurrence of PsA by the class of the biologic (tumour necrosis factor [TNF], interleukin [IL]-17, or IL-23 inhibitors) using inverse probability of treatment weighting (IPTW) in the setting of multiple treatments to balance pretreatment covariates across cohorts and thus adjust for potential confounders. An IPTW Cox regression model was used to estimate hazard ratios (HRs) of PsA for IL-17 and IL-23 inhibitors versus TNF inhibitors.</p><p><strong>Results: </strong>In total, 622 patients, 430 (62.4%) males, mean ± SD age 46.9 ± 12.9 years, were included. They have been treated with TNF (n = 317, 50.9%), IL-17 (n = 164, 26.4%) or IL-23 inhibitors (n = 141, 22.7%) and followed for 2510 person-years (a mean of 4.1 ± 2.1 years per person). TNF, IL-17, and IL-23 inhibitor cohorts had a total of 1569, 486, and 455 person-years of follow-up. A total of 60 (10%) out of 622 patients on biologic therapy developed incident PsA during the observation period: 45 (14.2%) in the TNF, 9 (5.5%) in the IL-17, and 6 (4.3%) in the IL-23 inhibitor cohorts. After IPTW, the 3 treatment cohorts were well-balanced, and the HRs of PsA were 0.63 (95% CI, 0.38-1.05) for IL-17 and 0.57 (95% CI, 0.34-0.96) for IL-23 compared with the TNF treatment group.</p><p><strong>Conclusions: </strong>The risk of developing PsA appeared slightly different in patients receiving diverse classes of biologics.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370265","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":"Biologic classification and clinical classification of axSpA: related but not (yet) synonymous.","authors":"Zoya Qaiyum, Robert D Inman","doi":"10.1016/j.ard.2024.12.003","DOIUrl":"https://doi.org/10.1016/j.ard.2024.12.003","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370263","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":"Correspondence on 'Unveiling inflammatory and prehypertrophic cell populations as key contributors to knee cartilage degeneration in osteoarthritis using multi-omics data integration' by Fan et al.","authors":"Kohei Nishitani, Yu Kobori, Hiroyuki Yoshitomi, Akinori Murakami, Koichi Murata, Takayuki Fujii, Yugo 侑吾 Morita, Takashi Sono, Shuichi Matsuda","doi":"10.1016/j.ard.2024.11.001","DOIUrl":"https://doi.org/10.1016/j.ard.2024.11.001","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143363343","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}