Annals of the Rheumatic Diseases最新文献

{"title":"Correspondence on 'Pulmonary arterial hypertension in adults with Still's disease: another pulmonary manifestation associated with HLA-DRB1*15' by Boucly A, et al.","authors":"Jingjing Li, Ting Ma, Wenwen Xu, Ran Wang, Jie Chen, Qiong Fu","doi":"10.1016/j.ard.2025.08.024","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.024","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111836","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":"Integrative spatial multiomics analysis reveals regulatory mechanisms of VCAM1⁺ proximal tubule cells in lupus nephritis.","authors":"Junyu Wang, Ao Zheng, Nianping Liu, Zhen Tan, Yu Shi, Tianyi Ma, Songwen Luo, Lin Zhu, Zhou Zhou, Feifei Yuan, Tiekun Li, Yuyan Gong, Jingwen Fang, Lu Liu, Xuejun Zhang, Sang-Cheol Bae, Chikashi Terao, Zhu Chen, Xiaomei Li, Guosheng Wang, Kun Qu, Chuang Guo","doi":"10.1016/j.ard.2025.08.015","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.015","url":null,"abstract":"<p><strong>Objectives: </strong>Lupus nephritis (LN) is a severe complication of systemic lupus erythematosus (SLE), characterised by kidney inflammation, tubular injury, and interstitial fibrosis. However, the spatial organisation of these heterogeneous cell populations and their regulatory mechanisms in LN remain poorly understood. The objective of this study was to investigate the regulatory mechanisms underlying region-specific kidney lesions and tubular damage in LN.</p><p><strong>Methods: </strong>We performed single-cell multiome and spatial transcriptomic analyses on kidney biopsy samples from patients with LN and controls, integrating data from the largest East Asian SLE genome-wide association studies (GWAS) (208,370 samples) to date. Validation experiments were performed using multiplex immunohistochemistry (mIHC), in vitro lentiviral-mediated transcription factor overexpression, and functional stimulation assays.</p><p><strong>Results: </strong>We identified VCAM1-expressing proximal tubule (PT_VCAM1) cells as components of an LN-specific inflammatory niche (niche 5) localised in the kidney cortex. Both in silico and in vitro experiments demonstrated that interactions between PT_VCAM1 cells and myofibroblasts, as well as immune cells in niche 5, promote their epithelial-mesenchymal transition. Trajectory analysis suggested that PT_VCAM1 cells originate from a failed-repair pathway in proximal tubule cells, regulated by transcriptional networks involving BACH2. Integrative GWAS analysis further linked SLE-associated risk single-nucleotide polymorphisms to cis-regulatory elements specific to PT_VCAM1 cells, including single-nucleotide polymorphisms within the distal enhancer of the BMP2K locus, which establishes a BACH2 motif.</p><p><strong>Conclusions: </strong>Collectively, our findings characterise PT_VCAM1 cells as injury-responsive cell states that contribute to the inflammatory and fibrotic niche in LN, linking genetic predisposition to cellular injury and disease progression.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091073","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":"Inhibition of structural damage progression with the selective interleukin-23 inhibitor guselkumab in participants with active PsA: results through week 24 of the phase 3b, randomised, double-blind, placebo-controlled APEX study.","authors":"Philip J Mease, Christopher T Ritchlin, Laura C Coates, Alexa P Kollmeier, Bei Zhou, Yusang Jiang, Karen Bensley, Koeun Im, Rattandeep Batra, Soumya D Chakravarty, Proton Rahman, Désirée van der Heijde","doi":"10.1016/j.ard.2025.08.006","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.006","url":null,"abstract":"<p><strong>Objectives: </strong>The APEX study evaluated the effects of guselkumab, a fully human, dual-acting monoclonal antibody able to bind CD64 and selectively inhibit the interleukin (IL)-23p19 subunit, on clinical and radiographic outcomes in active psoriatic arthritis (PsA).</p><p><strong>Methods: </strong>APEX (ongoing, phase 3b, double-blind, placebo-controlled) randomised (5:7:7) biologic-naïve adults with active PsA (≥3 tender, ≥3 swollen joints; C-reactive protein ≥0.3 mg/dL; ≥2 erosive joints) to subcutaneous guselkumab 100 mg every 4 weeks (Q4W); guselkumab 100 mg at week 0, week 4, then every 8 weeks (Q8W); or placebo every 4 weeks. Primary (proportion of participants achieving ≥20% improvement in American College of Rheumatology response criteria [ACR20]) and major secondary (total PsA-modified van der Heijde-Sharp [vdH-S] score least squares mean [LSM] change from baseline) endpoints at week 24 were multiplicity-controlled for comparing each guselkumab group versus placebo.</p><p><strong>Results: </strong>Among 1020 participants (Q4W: 273; Q8W: 371; placebo: 376), significantly greater proportions of participants receiving guselkumab Q4W (66.6%) and Q8W (68.3%) versus placebo (47.0%) achieved ACR20 at week 24 (both P < 0.001). Baseline mean total vdH-S scores were 26.7 to 27.7 across groups; guselkumab Q4W- and Q8W-treated participants exhibited significantly lower rates of radiographic progression versus placebo at week 24 (total vdH-S score LSM change: 0.55 and 0.54 vs 1.35; P = 0.002 and P < 0.001, respectively). Through week 24, 38.2%, 42.5%, and 37.3% of participants receiving guselkumab Q4W, Q8W, and placebo, respectively, had ≥1 adverse event, with no new safety signals.</p><p><strong>Conclusions: </strong>Guselkumab, a fully human monoclonal antibody able to bind CD64 and simultaneously inhibit the IL-23p19 subunit, provided significantly higher rates of clinical improvement and significant inhibition of structural damage progression versus placebo, with no new safety signals, at week 24 in biologic-naïve participants with active and erosive PsA.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079424","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":"Myositis-specific autoantibodies recognising Mi2 also target the AIRE protein at a shared PHD zinc finger.","authors":"Jon Musai, Sahana Jayaraman, Katherine Pak, Iago Pinal-Fernandez, Sandra Muñoz-Braceras, Maria Casal-Dominguez, Eric Cho, Fa'alataitaua M Fitisemanu, Peter D Burbelo, Mariana J Kaplan, Blake M Warner, Adam I Schiffenbauer, Albert Selva-O'Callaghan, José César Milisenda, Lisa G Rider, H Benjamin Larman, Andrew L Mammen","doi":"10.1016/j.ard.2025.08.023","DOIUrl":"10.1016/j.ard.2025.08.023","url":null,"abstract":"<p><strong>Objectives: </strong>In patients with dermatomyositis with anti-Mi2 autoantibodies, autoantibodies can enter muscle cells, leading to the aberrant expression of genes normally repressed by the Mi2/nucleosome remodelling and deacetylation (NuRD) complex. However, the mechanism by which autoantibodies interfere with Mi2/NuRD function remains unclear. This study aimed to identify additional autoantibodies in anti-Mi2-positive patients and the epitopes recognised by these autoantibodies.</p><p><strong>Methods: </strong>Phage immunoprecipitation sequencing (PhIP-Seq) was used to screen sera from patients with anti-Mi2 autoantibody-positive myositis. Enzyme-linked immunosorbent assays (ELISAs) and luciferase immunoprecipitation system (LIPS) immunoassays were used to detect autoantibodies in sera from healthy controls, patients with myositis, and those with other autoimmune diseases.</p><p><strong>Results: </strong>PhIP-Seq identified autoantibodies recognising the autoimmune regulator (AIRE) in sera from anti-Mi2 autoantibody-positive patients. Both anti-AIRE and anti-Mi2 autoantibodies predominantly recognised a homologous region containing the plant homeodomain zinc finger type I (PHD1), which is critical for AIRE and Mi2/NuRD function. ELISA and LIPS showed that anti-Mi2 autoantibody-positive patients were positive for anti-AIRE autoantibodies, whereas AIRE reactivity was largely absent in healthy comparators, anti-Mi2 autoantibody-negative myositis, and other autoimmune diseases. Affinity-purified anti-Mi2 autoantibodies recognised both Mi2 and AIRE by ELISA, whereas anti-Mi2-depleted fractions did not recognise either protein.</p><p><strong>Conclusions: </strong>Autoantibodies targeting Mi2 recognise AIRE at a shared PHD1 epitope - a conserved motif found in numerous transcriptional regulators. These findings support a model in which anti-Mi2 autoantibodies disrupt the Mi2/NuRD complex, and potentially other PHD1-containing proteins, by interfering with chromatin binding, although further studies are needed to directly demonstrate this mechanism in vivo.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074451","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":"When habit shapes the hands.","authors":"Marc-Alexander Oestreich, Florence Aeschlimann","doi":"10.1016/j.ard.2025.08.019","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.019","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058339","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":"Antiobesity medications in rheumatology. Quo vadis?","authors":"Niki Kyriazi, Konstantinos D Vassilakis, Amalia Bakiri, Alexios Iliopoulos, George E Fragoulis","doi":"10.1016/j.ard.2025.08.013","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.013","url":null,"abstract":"<p><p>Obesity is a well-recognised comorbidity in the context of rheumatic and musculoskeletal diseases (RMDs), adversely affecting disease-related outcomes. Adipose tissue, through immunological mechanisms, induces a low-grade inflammatory state; as a result, there has been growing interest in evaluating the potential role of antiobesity drugs in the management of RMDs. Although they were initially approved for type 2 diabetes mellitus, obesity, and their cardiorenal associations, there is increasing evidence that glucagon-like peptide-1 receptor agonists (GLP-1 RAs) in particular may exert immunomodulatory and anti-inflammatory effects in the setting of RMDs. In this viewpoint, we discuss current data regarding the effects of GLP-1 RAs on several conditions, including osteoarthritis, systemic lupus erythematosus, rheumatoid arthritis, fibromyalgia, and osteoporosis. We also highlight ongoing studies, which appear to be promising. Furthermore, we propose that these drugs could be administered to difficult-to-manage cases or in people at an increased risk of developing RMDs (like obese psoriatic patients) or even as adjunctive therapy, considering also the cost barrier that exists in most countries. Preliminary findings are encouraging; however, as most of the available evidence is limited to a small sample size, large-scale randomised controlled trials are needed to evaluate also the long-term safety of these drugs throughout the spectrum of rheumatic disorders.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058284","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":"Lidocaine-induced tear production in primary Sjögren's disease: neurologically induced lacrimation to broaden the horizon for treatment of ocular dryness?","authors":"Dewi Rijnenberg, Eefje H M van der Heijden, Ronald L A W Bleys, Helen L Leavis, Joël A G van Roon","doi":"10.1016/j.ard.2025.08.017","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.017","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058203","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":"Association of health literacy with disease outcomes in inflammatory arthritis: a systematic review.","authors":"Mrinalini Dey, Shyam Budhathoki, Helen Elwell, Sofia Ramiro, Kaleb Michaud, Sam Norton, Maya Buch, Andrew Cope, Richard H Osborne, James Galloway, Elena Nikiphorou","doi":"10.1016/j.ard.2025.08.018","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.018","url":null,"abstract":"<p><strong>Objectives: </strong>This study aims to conduct a systematic literature review (SLR) to summarise associations between health literacy and inflammatory arthritis (IA) outcomes, to inform management.</p><p><strong>Methods: </strong>Inclusion criteria were adults with IA; studies assessing health literacy or interventions targeting health literacy; observational and qualitative studies, randomised controlled trials. Searches were performed using MeSH headings for health literacy and IA. Data were extracted on demographics, health literacy assessment and relevant outcomes, grouped into themes using vote-counting.</p><p><strong>Results: </strong>Of 3087 identified articles, 29 were included. The total number of participants across all studies was 16,402, comprising mostly females, with a mean age of 46 to 70 years. Ethnicity was reported in 13 studies; most participants were Caucasian. The most frequently reported IA was rheumatoid arthritis. Health literacy measures included: Test of Functional Health Literacy in Adults (n = 13); Single Item Literacy Screener (n = 10); Rapid Estimate of Adult Literacy in Medicine (n = 6); Health Literacy Questionnaire (n = 2). Six main associations were identified with low health literacy: higher disease activity; more disability; more mental health symptoms (including depression and anxiety); higher healthcare use; lower medication adherence; lower use of internet, telehealth and technology.</p><p><strong>Conclusions: </strong>In people with IA, low health literacy is generally associated with worse outcomes including higher disease activity, mental health symptoms and disability, higher healthcare use, lower medication adherence, and lower use of technology. This is the first SLR to synthesise associations between health literacy and outcomes in IA. Our findings should inform policy and resource allocation and improve the quality of care for patients with IA and low health literacy.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051786","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":"IL-2 signalling sustains pathogenic age-associated B cell homeostasis in lupus.","authors":"Xiaxia Han, Yang Jiang, Shuangshuang Gu, Yiwei Shen, Huihua Ding, Sheng Chen, Qiong Fu, John B Harley, Dai Dai, Nan Shen","doi":"10.1016/j.ard.2025.08.012","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.012","url":null,"abstract":"<p><strong>Objectives: </strong>Despite expanding regulatory T (Treg) cells, low-dose interleukin-2 (IL-2) therapy shows variable clinical efficacy in systemic lupus erythematosus (SLE). Here, we investigated whether previously unrecognised effects of IL-2 on age-associated B cells (ABCs) explain this therapeutic heterogeneity.</p><p><strong>Methods: </strong>Integrated transcriptomic analysis was used to identify the prevalent signalling pathways associated with lupus pathogenic ABCs. The effects of IL-2 on ABCs were examined. TLR7-driven lupus-prone mice were administered to assess the efficacy of IL-2 therapy. IL-2 responsiveness of ABC was further evaluated in patients with SLE through bioinformatic analysis.</p><p><strong>Results: </strong>Transcriptomic and single-cell analyses revealed elevated IL-2 signalling in ABCs, with a more pronounced IL-2 signature in patients with SLE than in healthy controls. IL2RB, a subunit of the IL-2 receptor, was significantly enriched in ABCs and showed increased chromatin accessibility at its promoter. IL-2 promoted ABC survival and differentiation in a stage-dependent manner. Prior IL-2 administration to recipient mice promoted the persistence of adoptively transferred ABCs. In lupus-prone mice, IL-2 administration increased both ABC and Treg populations without ameliorating disease manifestations with ABC's promotion being more dependent on the disease condition. Additionally, ABCs showed elevated expression of IL-2 receptor correlating with ABC frequency in our cohorts, and activation of IL-2 signalling was further observed in B cells and ABCs from patients with SLE.</p><p><strong>Conclusions: </strong>This study identified ABCs as a novel target of IL-2, expanding the understanding of IL-2's role in SLE beyond the traditional Treg-centric view and offering insights into the variable therapeutic efficacy of IL-2 in this context.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051862","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 analysis uncovers subtype-specific mechanisms and biomarkers in idiopathic inflammatory myopathies.","authors":"Yizhi Xiao, Shasha Xie, Yanjuan Liu, Yu Jiang, Hongdong Li, Huali Zhang, Xiaoxia Zuo, Hui Luo, Honglin Zhu","doi":"10.1016/j.ard.2025.08.011","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.011","url":null,"abstract":"<p><strong>Objectives: </strong>Idiopathic inflammatory myopathies (IIM) are autoimmune disorders with distinct subtype features, but their molecular mechanisms remain unclear. This study integrated multiomics data to identify subtype-specific molecular signatures and evaluate their prognostic significance in a Han Chinese IIM cohort.</p><p><strong>Methods: </strong>RNA sequencing, proteomics, and metabolomics were generated on muscle tissues from 203 patients with IIM (including 44 in a validation cohort) and 18 controls. Differential expression was analysed for exons, intron retentions (IRs), proteins, and metabolites, integrated via multiomics factor analysis (MOFA). Pathway enrichment, single-sample Gene Set Enrichment Analysis (ssGSEA), correlation with clinical features, receiver operating characteristic curve, and survival analyses were conducted.</p><p><strong>Results: </strong>MOFA distinguished dermatomyositis (DM), immune-mediated necrotising myopathy (IMNM), and antisynthetase syndrome (ASyS) from controls, identifying 798, 748, and 297 subtype-specific features and pathways, respectively, which were further validated in an independent cohort. In DM, upregulated interferon (IFN) and cytokine pathways were prominent, with 11 IFN-related genes altered at exon, IR, and protein levels, alongside changes in related metabolites. IFNs and cytokine scores correlated with skin manifestations, perifascicular atrophy/necrosis, inflammation, and relapse risk. IMNM showed changes in myosin, actin, and troponin genes, with enrichment of cytoskeleton and extracellular matrix (ECM) pathways that were positively linked to muscle necrosis, regeneration, and inflammation. Protein-level of ECM-related pathways predicted a favourable prognosis. ASyS displayed distinct metabolic signatures (nucleosides, ketones, phosphatidylserine) and endothelial dysfunction, with key metabolism-regulated genes (FABP3, AKR1C2, AKR1C3) showing multiomics alterations associated with necrosis, inflammation, and prognosis.</p><p><strong>Conclusions: </strong>This multiomics analysis elucidates distinct molecular mechanisms in IIM subtypes, identifying potential biomarkers for personalised prognosis and therapy.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039007","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}