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American College of Rheumatology Guidance for COVID-19 Vaccination in Patients With Rheumatic and Musculoskeletal Diseases: Version 3
Jeffrey R. Curtis,Sindhu R. Johnson,Donald D. Anthony,Reuben J. Arasaratnam,Lindsey R. Baden,Anne R. Bass,Cassandra Calabrese,Ellen M. Gravallese,Rafael Harpaz,Andrew Kroger,Rebecca E. Sadun,Amy S. Turner,Eleanor Anderson Williams,Ted R. Mikuls
doi : 10.1002/art.41928
Volume 73, Issue 10 p. e60-e75
To provide guidance to rheumatology providers on the use of coronavirus disease 2019 (COVID-19) vaccines for patients with rheumatic and musculoskeletal diseases (RMDs).
What Did Not Work: The Drug or the Trial?
Joan T. Merrill
doi : 10.1002/art.41810
Volume 73, Issue 10 p. 1773-1775
“To Randomize, or Not to Randomize, That is the Question”
Nicolino Ruperto,Alberto Martini,Angela Pistorio,for the Paediatric Rheumatology International Trials Organisation
doi : 10.1002/art.41912
Volume 73, Issue 10 p. 1776-1779
Expert Perspective: Management of Microvascular and Catastrophic Antiphospholipid Syndrome
Doruk Erkan
doi : 10.1002/art.41891
Volume 73, Issue 10 p. 1780-1790
Discrimination of COVID-19 From Inflammation-Induced Cytokine Storm Syndromes Using Disease-Related Blood Biomarkers
Christoph Kessel,Richard Vollenberg,Katja Masjosthusmann,Claas Hinze,Helmut Wittkowski,France Debaugnies,Carole Nagant,Francis Corazza,Frédéric Vély,Gilles Kaplanski,Charlotte Girard-Guyonvarc’h,Cem Gabay,Hartmut Schmidt,Dirk Foell,Phil-Robin Tepasse
doi : 10.1002/art.41763
Volume 73, Issue 10 p. 1791-1799
Infection with the novel coronavirus SARS–CoV-2 triggers severe illness with high mortality in a subgroup of patients. Such a critical course of COVID-19 is thought to be associated with the development of cytokine storm, a condition seen in macrophage activation syndrome (MAS) and secondary hemophagocytic lymphohistiocytosis (HLH). However, specific data demonstrating a clear association of cytokine storm with severe COVID-19 are still lacking. The aim of this study was to directly address whether immune activation in COVID-19 does indeed mimic the conditions found in these classic cytokine storm syndromes.
Nonserious Infections in Patients With Rheumatoid Arthritis: Results From the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis
Katie Bechman,Kapil Halai,Mark Yates,Sam Norton,Andrew P. Cope,the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis Contributors Group,Kimme L. Hyrich,James B. Galloway
doi : 10.1002/art.41754
Volume 73, Issue 10 p. 1800-1809
To describe the frequency and predictors of nonserious infections (NSI) and compare incidence across biologic agents within the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis (BSRBR-RA).
Notch-1 and Notch-3 Mediate Hypoxia-Induced Activation of Synovial Fibroblasts in Rheumatoid Arthritis
Jianhai Chen,Wenxiang Cheng,Jian Li,Yan Wang,Jingqin Chen,Xin Shen,Ailing Su,Donghao Gan,Liqing Ke,Gang Liu,Jietao Lin,Liang Li,Xueling Bai,Peng Zhang
doi : 10.1002/art.41748
Volume 73, Issue 10 p. 1810-1819
To investigate the molecular mechanism of hypoxia-induced rheumatoid arthritis synovial fibroblast (RASF) activation via Notch-1 and Notch-3 signaling, and to evaluate its potential as a therapeutic target.
Pim Kinases as Therapeutic Targets in Early Rheumatoid Arthritis
Nicola J. Maney,Henrique Lemos,Ben Barron-Millar,Christopher Carey,Ian Herron,Amy E. Anderson,Andrew L. Mellor,John D. Isaacs,Arthur G. Pratt
doi : 10.1002/art.41744
Volume 73, Issue 10 p. 1820-1830
As well as being an established oncoprotein and therapeutic target in cancer, proviral integration site for Moloney murine leukemia virus 1 (Pim-1) is implicated in human autoimmunity. This study was undertaken to investigate Pim-1 and its family members as potential therapeutic targets in early rheumatoid arthritis (RA).
Down-Regulation of Dkk-1 in Platelets of Patients With Axial Spondyloarthritis
Marcin Czepiel,Ma?gorzata Stec,Mariusz Korkosz,Zofia Gu?a,Przemys?aw B?yszczuk,Jaros?aw Baran,Maciej Siedlar
doi : 10.1002/art.41739
Volume 73, Issue 10 p. 1831-1834
Axial spondyloarthritis (SpA) is a chronic autoinflammatory disease with new bone formation, which is controlled by Wnt/?-catenin signaling. Dkk-1 is an inhibitor of the Wnt pathway, and in humans, platelets represent a major source of Dkk-1. This study was undertaken to investigate whether levels of Dkk-1 in serum and platelet expression of DKK1 messenger RNA (mRNA) and Dkk-1 protein are affected in patients with axial SpA compared to healthy controls.
Efficacy, Safety, and Pharmacodynamic Effects of the Bruton’s Tyrosine Kinase Inhibitor Fenebrutinib (GDC-0853) in Systemic Lupus Erythematosus: Results of a Phase II, Randomized, Double-Blind, Placebo-Controlled Trial
David Isenberg,Richard Furie,Nicholas S. Jones,Pascal Guibord,Joshua Galanter,Chin Lee,Anna McGregor,Balazs Toth,Julie Rae,Olivia Hwang,Rupal Desai,Armend Lokku,Nandhini Ramamoorthi,Jason A. Hackney,Pedro Miranda,Viviane A. de Souza,Juan J. Jaller-Raad,Anna Maura Fernandes,Rodrigo Garcia Salinas,Leslie W. Chinn,Michael J. Townsend,Alyssa M. Morimoto,Katie Tuckwell
doi : 10.1002/art.41811
Volume 73, Issue 10 p. 1835-1846
Fenebrutinib (GDC-0853) is a noncovalent, oral, and highly selective inhibitor of Bruton’s tyrosine kinase (BTK). The efficacy, safety, and pharmacodynamics of fenebrutinib in systemic lupus erythematosus (SLE) were assessed in this phase II, multicenter, randomized, placebo-controlled study.
Predicting the Risk of Pulmonary Arterial Hypertension in Systemic Lupus Erythematosus: A Chinese Systemic Lupus Erythematosus Treatment and Research Group Cohort Study
Jingge Qu,Mengtao Li,Yanhong Wang,Xinwang Duan,Hui Luo,Cheng Zhao,Feng Zhan,Zhenbiao Wu,Hongbin Li,Min Yang,Jian Xu,Wei Wei,Lijun Wu,Yongtai Liu,Hanxiao You,Juyan Qian,Xiaoxi Yang,Can Huang,Jiuliang Zhao,Qian Wang,Xiaomei Leng,Xinping Tian,Yan Zhao,Xiaofeng Zeng
doi : 10.1002/art.41740
Volume 73, Issue 10 p. 1847-1855
Pulmonary arterial hypertension (PAH) is a life-threatening complication of systemic lupus erythematosus (SLE). However, there is no algorithm to identify those at high risk. This study was undertaken to develop a prediction model for PAH in patients with lupus that provides individualized risk estimates.
Genetic and Epigenetic Interplay Within a COLGALT2 Enhancer Associated With Osteoarthritis
Yulia S. Kehayova,Emily Watson,J. Mark Wilkinson,John Loughlin,Sarah J. Rice
doi : 10.1002/art.41738
Volume 73, Issue 10 p. 1856-1865
The osteoarthritis (OA)–associated single-nucleotide polymorphism (SNP) rs11583641 is located in COLGALT2, encoding a posttranslational modifier of collagen. In cartilage, the SNP genotype correlates with DNA methylation in a putative enhancer. This study was undertaken to characterize the mechanistic relationship between rs11583641, the putative enhancer, and COLGALT2 expression using cartilage samples from human patients and a chondrocyte cell model.
Genetic and Epigenetic Fine-Tuning of TGFB1 Expression Within the Human Osteoarthritic Joint
Sarah J. Rice,Jack B. Roberts,Maria Tselepi,Abby Brumwell,Julia Falk,Charlotte Steven,John Loughlin
doi : 10.1002/art.41736
Volume 73, Issue 10 p. 1866-1877
Osteoarthritis (OA) is an age-related disease characterized by articular cartilage degeneration. It is largely heritable, and genetic screening has identified single-nucleotide polymorphisms (SNPs) marking genomic risk loci. One such locus is marked by the G>A SNP rs75621460, downstream of TGFB1. This gene encodes transforming growth factor ?1, the correct expression of which is essential for cartilage maintenance. This study investigated the regulatory activity of rs75621460 to characterize its impact on TGFB1 expression in disease-relevant patient samples (n = 319) and in Tc28a2 immortalized chondrocytes.
The Epidemiology of Psoriatic Arthritis Over Five Decades: A Population-Based Study
Paras Karmacharya,Cynthia S. Crowson,Delamo Bekele,Sara J. Achenbach,John M. Davis III,Alexis Ogdie,Alí Duarte-García,Floranne C. Ernste,Hilal Maradit-Kremers,Megha M. Tollefson,Kerry Wright
doi : 10.1002/art.41741
Volume 73, Issue 10 p. 1878-1885
To determine the incidence of psoriatic arthritis (PsA) in a US population and describe trends in incidence and mortality over 5 decades.
Somatic Mutations in UBA1 Define a Distinct Subset of Relapsing Polychondritis Patients With VEXAS
Marcela A. Ferrada,Keith A. Sikora,Yiming Luo,Kristina V. Wells,Bhavisha Patel,Emma M. Groarke,Daniela Ospina Cardona,Emily Rominger,Patrycja Hoffmann,Mimi T. Le,Zuoming Deng,Kaitlin A. Quinn,Emily Rose,Wanxia L. Tsai,Gustaf Wigerblad,Wendy Goodspeed,Anne Jones,Lorena Wilson,Oskar Schnappauf,Ryan S. Laird,Jeff Kim,Clint Allen,Arlene Sirajuddin,Marcus Chen,Massimo Gadina,Katherine R. Calvo,Mariana J. Kaplan,Robert A. Colbert,Ivona Aksentijevich,Neal S. Young,Sinisa Savic,Daniel L. Kastner,Amanda K. Ombrello,David B. Beck,Peter C. Grayson
doi : 10.1002/art.41743
Volume 73, Issue 10 p. 1886-1895
Somatic mutations in UBA1 cause a newly defined syndrome known as VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic syndrome). More than 50% of patients currently identified as having VEXAS met diagnostic criteria for relapsing polychondritis (RP), but clinical features that characterize VEXAS within a cohort of patients with RP have not been defined. We undertook this study to define the prevalence of somatic mutations in UBA1 in patients with RP and to create an algorithm to identify patients with genetically confirmed VEXAS among those with RP.
Extensive Multiple Organ Involvement in VEXAS Syndrome
Noriyuki Takahashi,Takuya Takeichi,Tetsuya Nishida,Juichi Sato,Yasuhiro Takahashi,Masahiro Yamamura,Tomoo Ogi,Masashi Akiyama
doi : 10.1002/art.41775
Volume 73, Issue 10 p. 1896-1897
Optimizing the Start Time of Biologics in Polyarticular Juvenile Idiopathic Arthritis: A Comparative Effectiveness Study of Childhood Arthritis and Rheumatology Research Alliance Consensus Treatment Plans
Yukiko Kimura,Laura E. Schanberg,George A. Tomlinson,Mary Ellen Riordan,Anne C. Dennos,Vincent Del Gaizo,Katherine L. Murphy,Pamela F. Weiss,Marc D. Natter,Brian M. Feldman,Sarah Ringold,the CARRA STOP-JIA Investigators
doi : 10.1002/art.41888
Volume 73, Issue 10 p. 1898-1909
The optimal time to start biologics in polyarticular juvenile idiopathic arthritis (JIA) remains uncertain. The Childhood Arthritis and Rheumatology Research Alliance (CARRA) developed 3 consensus treatment plans (CTPs) for untreated polyarticular JIA to compare strategies for starting biologics.
Improved Disease Course Associated With Early Initiation of Biologics in Polyarticular Juvenile Idiopathic Arthritis: Trajectory Analysis of a Childhood Arthritis and Rheumatology Research Alliance Consensus Treatment Plans Study
Mei Sing Ong,Sarah Ringold,Yukiko Kimura,Laura E. Schanberg,George A. Tomlinson,Marc D. Natter, and the CARRA Registry Investigators
doi : 10.1002/art.41892
Volume 73, Issue 10 p. 1910-1920
To investigate the effects of early introduction of biologic disease-modifying antirheumatic drugs (bDMARDs) on the disease course in untreated polyarticular juvenile idiopathic arthritis (JIA).
Transcriptomic Evaluation of Juvenile Localized Scleroderma Skin With Histologic and Clinical Correlation
Christina Schutt,Emily Mirizio,Claudia Salgado,Miguel Reyes-Mugica,Xinjun Wang,Wei Chen,Lorelei Grunwaldt,Kaila L. Schollaert,Kathryn S. Torok
doi : 10.1002/art.41758
Volume 73, Issue 10 p. 1921-1930
Juvenile localized scleroderma (LS) is an autoimmune disease of the skin whose pathogenesis is not well understood due to the rarity of the disease. This study was undertaken to determine the skin transcriptome in skin biopsy tissue from children with juvenile LS compared to pediatric healthy controls, with identification of significant molecular targets using RNA sequencing (RNA-Seq). In this study, differentially expressed genes (DEGs) were assessed for correlations with histopathologic and clinical features in children with juvenile LS, and were used to group the children into distinct genetic clusters based on immunophenotype.
ICBP90 Regulates MIF Expression, Glucocorticoid Sensitivity, and Apoptosis at the MIF Immune Susceptibility Locus
Jie Yao,Lin Leng,Weiling Fu,Jia Li,Christian Bronner,Richard Bucala
doi : 10.1002/art.41753
Volume 73, Issue 10 p. 1931-1942
Macrophage migration inhibitory factor (MIF) is an inflammatory and neurorendocrine mediator that counterregulates glucocorticoid immunosuppression. MIF polymorphisms, which comprise a variant promoter microsatellite (?794 CATT5–8), are linked genetically to autoimmune disease severity and to glucocorticoid resistance. While invasive stimuli increase MIF expression, MIF also is up-regulated by glucocorticoids, which serve as a physiologic regulator of inflammatory responses. This study was undertaken to define interactions between the MIF promoter, the glucocorticoid receptor (GR), and the transcription factor inverted CCAAT box binding protein 90 kd (ICBP90) (also referred to as UHRF1), which binds to the promoter in a ?794 CATT5–8 length–dependent manner, to regulate MIF transcription.
Body Fat Composition and Risk of Rheumatoid Arthritis: Mendelian Randomization Study
Sizheng S. Zhao,Cristina Maglio,David M. Hughes,James P. Cook
doi : 10.1002/art.41766
Volume 73, Issue 10 p. 1943-1944
Reply
Bowen Tang,Lars Alfredsson,Lars Klareskog,Leonid Padyukov,Huwenbo Shi,Xia Jiang
doi : 10.1002/art.41769
Volume 73, Issue 10 p. 1944-1945
Immuno-Autonomics as a Complement to Precision Medicine Guiding Treatment of Patients With Rheumatoid Arthritis: Comment on the Article by Tao et al
Andrew J. Holman
doi : 10.1002/art.41782
Volume 73, Issue 10 p. 1945-1946
Concerns Regarding P Value-Based Variable Selection of Exposure Variables and Confounding Factors: Comment on the Article by Hawker et al
Takahisa Ogawa,Yoshie Yamada,Ryo Momosaki,Junya Katayanagi,Takashi Yoshioka
doi : 10.1002/art.41771
Volume 73, Issue 10 p. 1946-1947
Reply
Gillian A. Hawker,Bheeshma Ravi,Eric Bohm,Michael J. Dunbar,C. Allyson Jones,Donald Dick,Paulose Paul,Barbara L. Conner-Spady,Tom Noseworthy,Peter Faris,James Powell,Deborah A. Marshall,On behalf of the BEST-Knee Study Team
doi : 10.1002/art.41764
Volume 73, Issue 10 p. 1947-1948
Concerns Regarding the Analysis of a Takayasu Arteritis Cohort: Comment on the Article by Goel et al
Hasan Yazici,Mert Oztas,Yusuf Yazici
doi : 10.1002/art.41784
Volume 73, Issue 10 p. 1948-1948
Reply
Ruchika Goel,Joht Singh Chandan,Rasiah Thayakaran,Nicola J. Adderley,Krishnarajah Nirantharakumar,Lorraine Harper
doi : 10.1002/art.41789
Volume 73, Issue 10 p. 1948-1950
