Rheumatology最新文献

{"title":"Isotype-specific autoantibody profiles associated with clinical immunological signatures in IgG4-RD.","authors":"Sheng-Yan Lin, Lin Bai, Chengqian Liao, Ling Wang, Hui Xiong, Ping Ye, Shaozhe Cai, Lingli Dong","doi":"10.1093/rheumatology/keag585","DOIUrl":"https://doi.org/10.1093/rheumatology/keag585","url":null,"abstract":"<p><strong>Objectives: </strong>IgG4-related disease (IgG4-RD) involves elevated serum IgG4 and several autoantigens, but the role of different antibody isotypes in pathogenesis remains unclear. This study systematically characterized isotype‑specific autoantibody responses against representative autoantigens and evaluated their clinical and immunological correlations.</p><p><strong>Methods: </strong>We enrolled 61 patients with IgG4‑RD, 31 with systemic lupus erythematosus (SLE), 11 with Sjögren's syndrome (SS), and 30 healthy controls (HC). Serum levels of isotype‑specific autoantibodies were measured using in‑house ELISA. Correlations with clinical and immunological parameters were evaluated using Spearman analysis with Benjamini‑Hochberg false discovery rate (FDR) correction. Tissue validation was performed via immunohistochemistry (IHC) and multiplex immunofluorescence (mIF) on submandibular gland biopsies. Longitudinal changes in autoantibody isotypes were assessed in paired pre‑ and post‑treatment sera from 12 patients.</p><p><strong>Results: </strong>IgG4‑RD exhibited broad isotype elevations extending beyond IgG4, with positivity rates of 80.33% for anti‑Annexin A11 IgG4, 59.02% for anti‑Galectin‑3 IgG4, and 100% for anti‑Prohibitin IgG4. Phenotype‑restricted patterns were observed: anti‑Galectin‑3 IgG4 was highest in Pancreato‑hepato‑biliary disease (72.73%) but lowest in Retroperitoneal fibrosis/aortitis group (16.67%), whereas anti‑Galectin‑3 IgE was more easily detected in Head‑and‑neck‑limited phenotype (26.09%). Correlation analyses identified 37 robust associations (FDR < 0.05) in IgG4‑RD, predominantly linking antigen‑specific IgG3 and IgG4 antibodies with serum immunoglobulins, CCL18, IL‑10, and IL‑6. Longitudinal paired analysis confirmed significant decrease of multiple detected autoantibodies following immunosuppressive therapy.</p><p><strong>Conclusions: </strong>Our findings demonstrate that IgG4‑RD encompasses a complex and isotopically diverse autoantibody profile that is associated with immuno-laboratory features and clinical phenotypes of IgG4-RD patients.</p>","PeriodicalId":21255,"journal":{"name":"Rheumatology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toward clinically actionable lupus biomarkers: a roadmap for research, validation, and translation.","authors":"Meredith Jackson, Maya Bader, May Y Choi, Andrea Fava, Andrea M Knight, Stanley J Naides, Harini Raghu, Robert H Terbrueggen, Victoria P Werth, Debra J Zack, Jad A Zoghbi, Teodora P Staeva, Alfred H J Kim, Peter H Schafer","doi":"10.1093/rheumatology/keag580","DOIUrl":"https://doi.org/10.1093/rheumatology/keag580","url":null,"abstract":"<p><p>Despite advances in lupus biomarker research, clinical translation has remained limited, leading to delayed diagnosis, imprecise disease monitoring, and trial-and-error treatment approaches. This roadmap, developed by the Lupus Research Alliance's Biomarker Roadmap Committee with input from patients and experts, identifies key priorities for translating research into clinical benefit. Three major clinical unmet needs are highlighted: improving diagnostic accuracy of Systemic Lupus Erythematosus (SLE) and neuropsychiatric SLE, developing sensitive longitudinal markers for disease activity (including lupus nephritis), and predicting disease progression and treatment response. We review the current state of biomarker development across these domains and highlight barriers that hinder clinical validation, assay development, and clinical adoption. We propose focused strategies to overcome these challenges, emphasizing analytically validated assays, diverse longitudinal cohorts, alignment with meaningful clinical outcomes, and consortium-based efforts. The roadmap outlines a path to transform lupus diagnosis, monitoring, and precision medicine, enabling research advances to improve patient care.</p>","PeriodicalId":21255,"journal":{"name":"Rheumatology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Outcomes of systemic sclerosis with overlapping myositis: a propensity score-matched cohort study.","authors":"Lekshmi Minikumari Rahulan, Nithin Gowda Av, Abhishek Gollarahalli Patel, Sakir Ahmed, Zafar Neyaz, Vimal Kumar Paliwal, Vikas Agarwal","doi":"10.1093/rheumatology/keag578","DOIUrl":"https://doi.org/10.1093/rheumatology/keag578","url":null,"abstract":"<p><strong>Objectives: </strong>Systemic sclerosis (SSc) carries the highest disease-specific mortality among rheumatic diseases, with cardiac involvement and interstitial lung disease (ILD) as leading causes of death. We aimed to determine whether overlapping myositis independently contributes to cardiac involvement and mortality in SSc.</p><p><strong>Methods: </strong>We did a 1:1 propensity score matched retrospective cohort study of 880 SSc patients (2013 ACR/EULAR criteria) at a single centre. SSc myositis required proximal weakness and elevated muscle enzymes without alternative causes. Cardiac involvement used SCTC criteria (pericardial effusion, ventricular dysfunction, arrhythmia, conduction disease). We used standard and Firth penalised logistic regression for cardiac predictors, Cox regression for survival, and Fisher's exact test for cause specific mortality. All p values were Benjamini-Hochberg adjusted.</p><p><strong>Results: </strong>Of 880 patients, 92 (10.4%) had myositis. After matching, 92 pairs (n = 184) were analysed. Myositis independently predicted cardiac involvement (standard aOR=19.99, 95%CI 2.19-182.26, p = 0.008; Firth OR = 12.84, 95%CI 2.31-98.47, p = 0.006). Higher mRSS also predicted cardiac involvement (aOR=2.34 per 10 points, p = 0.006). Anti-Scl70 was less common in myositis (25.0% vs. 50.0%, p = 0.009). Overall mortality did not differ (13.0% vs. 9.8%, p = 0.620). In non-myositis deaths, ILD caused 33.3%; in myositis deaths, cardiac failure caused 25% and no ILD-related deaths (Fisher's p = 0.229). Cardiac involvement was significantly associated with mortality (aHR=8.09 (1.36-48.26), p = 0.022), independent of myositis.</p><p><strong>Conclusion: </strong>Overlapping myositis in SSc is associated with an increased risk of cardiac involvement and a shift in the cause-of-death profile away from ILD, without a detectable difference in overall survival over the observed median 21-month follow-up. Systematic cardiac surveillance is needed in these patients.</p>","PeriodicalId":21255,"journal":{"name":"Rheumatology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical performance of obstetric antiphospholipid syndrome classification criteria: an ambispective cohort study.","authors":"Huimin Liu, Yuzhu Zhang, Shumin Wang, Wanrong Huang, Zhengyan Hu, Jinbiao Han, Xun Zeng, Lang Qin, Rui Gao","doi":"10.1093/rheumatology/keag579","DOIUrl":"https://doi.org/10.1093/rheumatology/keag579","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the clinical performance of the 2006 Sydney and 2023 ACR/EULAR classification criteria for obstetric antiphospholipid syndrome (OAPS), compare subsequent pregnancy outcomes across classifications and develop a supplementary classification method to further identify clinically relevant non-criteria OAPS (NC-OAPS) cases missed by the Sydney-derived NC-OAPS classification.</p><p><strong>Methods: </strong>This single-center ambispective cohort included 1741 women of reproductive age enrolled from January 2020 to October 2024. Expert consensus was used to classify participants into OAPS, NC-OAPS and non-OAPS groups. The clinical performance of the 2006 Sydney criteria, 2023 ACR/EULAR criteria and Sydney-derived NC-OAPS classification were assessed. The subsequent pregnancy outcomes were followed up and compared across different groups. Moreover, a supplementary NC-OAPS classification method was developed and validated.</p><p><strong>Results: </strong>The Sydney criteria identified expert-defined OAPS with sensitivity 0.806, specificity 0.991 and AUC 0.898. The 2023 ACR/EULAR criteria showed lower sensitivity (0.267) but near-perfect specificity (0.999). Live birth rates were similar among expert-defined OAPS, NC-OAPS and non-OAPS after treatment, but OAPS had higher rates of preterm birth, fetal growth restriction and severe pre-eclampsia/eclampsia. Patients fulfilling 2023 ACR/EULAR criteria had poorer pregnancy outcomes than those identified by expert consensus or the Sydney criteria. In the validation folds, the supplementary method yielded a sensitivity of 0.732 and a specificity of 0.921.</p><p><strong>Conclusion: </strong>The 2006 Sydney criteria remain more suitable for clinical identification of OAPS, whereas the 2023 ACR/EULAR criteria may be useful for high-risk stratification. The supplementary classification method may improve recognition of NC-OAPS patients missed by existing criteria.</p>","PeriodicalId":21255,"journal":{"name":"Rheumatology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The long-term impact of juvenile idiopathic arthritis into adulthood: a systematic review.","authors":"Joseph Rawlinson-Smith, Rabia Keerio, Jenny H Humphreys, Kimme L Hyrich, Lianne Kearsley-Fleet","doi":"10.1093/rheumatology/keag583","DOIUrl":"https://doi.org/10.1093/rheumatology/keag583","url":null,"abstract":"<p><strong>Objectives: </strong>Juvenile idiopathic arthritis (JIA), a childhood-onset chronic condition, often persists into adulthood. However, most studies investigating outcomes of JIA are limited to childhood, missing the long-term impact of the condition. This systematic literature review aimed to: identify the frequency of children with JIA that (i) continue to have active disease in adulthood, (ii) have limited functional ability in adulthood, (iii) are impacted by mental health problems in adulthood, and (iv) describe the impact of JIA on quality of life in adulthood compared with non-JIA peers.</p><p><strong>Methods: </strong>The literature was searched for published reports of observational studies that measured outcomes in adults aged 18 years or over with an existing diagnosis of JIA. Outcomes of interest included disease activity, functional ability, mental health, and quality of life.</p><p><strong>Results: </strong>Forty-four studies were included. When limited to studies that identified participants during childhood, 33-66% of adults with JIA had active disease, and 28-58% had limited functional ability. Mental health diagnoses were found in up to 19% of adults with JIA, and physical health-related quality of life measures were consistently lower in adults with JIA compared with non-JIA comparators.</p><p><strong>Conclusion: </strong>Despite being a childhood-onset condition, a substantial proportion of adults with JIA experience active disease, limited functional ability, and mental health problems beyond 18 years old, as well as report poorer physical health-related quality of life. This is valuable information to support future research into the impact of JIA in adulthood, and how best to support individuals throughout the life-course of their condition.</p>","PeriodicalId":21255,"journal":{"name":"Rheumatology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular risk associated with first-line Janus kinase inhibitors versus TNF inhibitors in patients with RA: a nationwide cohort study.","authors":"Oh Chan Kwon, Hye Sun Lee, So Young Jeon, Min-Chan Park","doi":"10.1093/rheumatology/keag582","DOIUrl":"https://doi.org/10.1093/rheumatology/keag582","url":null,"abstract":"<p><strong>Objective: </strong>To compare the risk of major adverse cardiovascular events (MACE) between tumor necrosis factor inhibitors (TNFi) and Janus kinase inhibitors (JAKi) when initiated as first-line advanced therapy in patients with rheumatoid arthritis (RA).</p><p><strong>Methods: </strong>Using the Korean nationwide claims database, we identified patients newly diagnosed with RA between 2010 and 2015. Patients who initiated TNFi or JAKi as first-line advanced therapy were selected for analysis. Patients were followed from initiation of TNFi or JAKi through June 2024. The primary outcome was incident MACE, defined as myocardial infarction, ischemic stroke, or coronary revascularization. Multivariable Cox proportional hazards models were applied in the total cohort. We additionally performed propensity score (PS)-matched analyses to address confounding by indication. Prespecified subgroup analyses were conducted according to baseline cardiovascular risk factors.</p><p><strong>Results: </strong>The study included 6,174 patients (TNFi = 5,152; JAKi = 1,022). The incidence rates of MACE were 4.1 and 3.6 per 1,000 person-years in the TNFi and JAKi groups, respectively. MACE risk did not differ significantly between JAKi and TNFi in the total study cohort (adjusted hazard ratio [HR] 0.636, 95% confidence interval [CI] 0.283 to 1.429) or in the PS-matched population (adjusted HR 0.715, 95% CI 0.187 to 2.739). Results were consistent across all prespecified subgroups, including patients with baseline cardiovascular risk factors.</p><p><strong>Conclusion: </strong>First-line use of JAKi was not associated with an increased risk of MACE compared with TNFi. These findings provide real-world evidence supporting the cardiovascular safety of JAKi as first-line advanced therapy in patients with RA.</p>","PeriodicalId":21255,"journal":{"name":"Rheumatology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD40-CD40L interactions in systemic autoimmune diseases.","authors":"Motomu Hashimoto, Masao Katsushima, Fabienne Mackay, Chaim Putterman","doi":"10.1093/rheumatology/keag565","DOIUrl":"https://doi.org/10.1093/rheumatology/keag565","url":null,"abstract":"<p><p>Systemic autoimmune diseases arise from a heterogeneous interplay of genetic, epigenetic, and environmental factors that culminates in loss of tolerance, chronic inflammation, and tissue injury. Among the pathways linking susceptibility to effector disease, CD40-CD40L is a central regulator of antigen presentation, T-B cell collaboration, and germinal centre responses, while also contributing to extrafollicular autoantibody production. In this review, we first introduce the disease-specific rationale for targeting CD40-CD40L interactions, with a particular focus on systemic lupus erythematosus, Sjögren's disease, and rheumatoid arthritis. We then summarize the multifaceted roles of CD40-CD40L signalling across adaptive immunity, innate immune priming, tissue inflammation, and platelet-driven thrombo-inflammation. Finally, we review the therapeutic translation of this pathway, highlighting insights from early trials of anti-CD40/CD40L antibodies and recent advances in Fc-silent antibody engineering that preserve target binding while minimizing platelet activation. Together, these data support CD40-CD40L blockade as a renewed and promising mechanism-based strategy in systemic autoimmune rheumatic diseases.</p>","PeriodicalId":21255,"journal":{"name":"Rheumatology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149196304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The trajectory of gout: mapping pathogenic cell states from flares to tophus.","authors":"Shuwei Li, Xiaofeng Zhou, Zhechen Liu, Nicola Dalbeth, Hanlin Xu, Yinghui Hua","doi":"10.1093/rheumatology/keag581","DOIUrl":"https://doi.org/10.1093/rheumatology/keag581","url":null,"abstract":"<p><p>The clinical course of gout is typically divided into four stages: asymptomatic hyperuricemia, gout flares, intercritical gout and tophaceous gout. However, the cellular and molecular mechanisms driving transitions between these stages remain unclear. Current clinical practice lacks stage-specific precision therapeutic strategies. In recent years, the development of single-cell sequencing technologies has provided tools to reveal dynamic cell state transitions during gout progression. This review synthesizes existing single-cell evidence to systematically delineate the immune and stromal cell landscapes across the stages of gout, and explores their roles in inflammation initiation, spontaneous resolution, and tissue remodeling, with the aim to provide a theoretical framework for stage-adapted therapies.</p>","PeriodicalId":21255,"journal":{"name":"Rheumatology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical characteristics and severity classification in Mixed Connective Tissue Disease: a nationwide retrospective study.","authors":"Satoshi Kubo, Yurie Kanda, Hideto Kameda, Masataka Kuwana, Hidehiko Narazaki, Takao Fujii, Keishi Fujio, Yoshinao Muro, Konomi Akamatsu, Koichiro Ohmura, Takehisa Ogura, Yuichiro Shirai, Yujiro Tanabe, Ran Nakashima, Yumi Tsuchida, Shingo Nakayamada, Hisanori Hasegawa, Shintaro Hirata, Shusaku Fukaya, Takashi Kato, Hidekata Yasuoka, Yuta Yamashita, Michihito Kono, Tatsuya Atsumi, Yoshiya Tanaka","doi":"10.1093/rheumatology/keag577","DOIUrl":"https://doi.org/10.1093/rheumatology/keag577","url":null,"abstract":"<p><strong>Objectives: </strong>To characterize clinical manifestations, major organ involvement, real-world treatment patterns, and factors associated with severity classification in Japanese patients with mixed connective tissue disease (MCTD), aiming to clarify its heterogeneous clinical spectrum.</p><p><strong>Methods: </strong>This nationwide retrospective multicenter study analyzed clinical data from 249 patients who strictly fulfilled the 2019 Japanese Ministry of Health, Labour and Welfare diagnostic criteria for MCTD, derived from an initial real-world registry of 311 clinically diagnosed patients. Clinical features, autoantibodies, and therapeutic regimens were summarized and compared between patients with severe versus non-severe disease.</p><p><strong>Results: </strong>The cohort was 93.1% female (median onset age 40.6 years). Common findings, specifically Raynaud's phenomenon and/or swelling of the fingers or dorsum of the hands, were present in 100%. Phenotypically, an overlap of systemic lupus erythematosus (SLE)-like and systemic sclerosis (SSc)-like features was most frequent (56.0%), while 32.0% had manifestations across all three phenotypic domains (SLE-, SSc-, and IIM-like). Major organ involvement occurred in 32.9% of patients, including pulmonary arterial hypertension in 12.8%. Approximately 28.7% of evaluable patients were classified as severe. Off-scale-high anti-U1-RNP antibody status was not associated with severity classification (p = 0.492) or with broad phenotypic categories. Glucocorticoids and immunosuppressive agents were used in 66.7% and 56.5% of the patients, respectively.</p><p><strong>Conclusions: </strong>Mixed connective tissue disease exhibits marked clinical heterogeneity. Severity classification was not associated with off-scale-high anti-U1-RNP antibody status or broad phenotypic categories. These findings support rigorous cardiopulmonary screening and management tailored to the dominant clinical phenotype.</p>","PeriodicalId":21255,"journal":{"name":"Rheumatology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149196339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond disease labels: towards a stratified spectrum model for giant cell arteritis and polymyalgia rheumatica.","authors":"Mohammed Hassan Abu-Zaid","doi":"10.1093/rheumatology/keag554","DOIUrl":"https://doi.org/10.1093/rheumatology/keag554","url":null,"abstract":"","PeriodicalId":21255,"journal":{"name":"Rheumatology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149196352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}