Arthritis and Rheumatology




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سفارش




ACR Presidential Address: Rheumatologists�Folks You Can Trust

Kenneth G. Saag

doi : 10.1002/art.42475

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The Biology of Pain: Through the Rheumatology Lens

Flavia Sunzini, Andrew Schrepf, Daniel J. Clauw, Neil Basu

doi : 10.1002/art.42429

Chronic pain is a major socioeconomic burden globally. The most frequent origin of chronic pain is musculoskeletal. In inflammatory musculoskeletal diseases such as rheumatoid arthritis (RA), chronic pain is a primary determinant of deleterious quality of life. The pivotal role of peripheral inflammation in the initiation and perpetuation of nociceptive pain is well-established among patients with musculoskeletal diseases.

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The NLRP3 Conundrum

James T. Rosenbaum, Tejpal Gill, Tammy M. Martin

doi : 10.1002/art.42430

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Criteria for Hyperinflammation Developing in COVID-19: Analysis of 2 Cohorts From Different Periods of the Pandemic

Shirkhan Amikishiyev, M. Guven Gunver, Murat Bektas, Sarvan Aghamuradov, Burak Ince, Nevzat Koca, Ege Sinan Torun, Numune Aliyeva, Selma Sari, Cigdem Cetin, Banu C. Yalcin-Dulundu, Rabia Deniz, Fatih Kemik, Besim Fazil Agargun, Ubeyde Ayse Gulseren, Beliz Besisik, Onur Alkan, Ceren Bagriacik, Yavuz B. Tor, Naci Senkal, Yunus Catma, Gorkem Durak, Sevim Mese, Ali Agacfidan, Murat Kose, Mustafa Erelel, A. Atahan Cagatay, Serap Simsek-Yavuz, Sevgi Kalayoglu-Besisik, Figen Esen, Ahmet Gül

doi : 10.1002/art.42417

Hyperinflammation (HI) that develops in week 2 of COVID-19 contributes to a worse outcome. Because week 2 laboratory findings can be relatively mild, the available criteria for classification of hemophagocytic lymphohistiocytosis or macrophage activation syndrome are not helpful.

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Diversity and Clonality of T Cell Receptor Repertoire and Antigen Specificities in Small Joints of Early Rheumatoid Arthritis

Sara Turcinov, Erik af Klint, Bertrand Van Schoubroeck, Arlette Kouwenhoven, Sohel Mia, Karine Chemin, Hans Wils, Carl Van Hove, An De Bondt, Ken Keustermans, Jeroen Van Houdt, Joke Reumers, Nathan Felix, Navin L. Rao, Pieter Peeters, Frederik Stevenaert, Lars Klareskog, Murray McKinnon, Daniel Baker, Anish Suri, Vivianne Malmström

doi : 10.1002/art.42407

CD4+ T cells are implicated in rheumatoid arthritis (RA) pathology from the strong association between RA and certain HLA class II gene variants. This study was undertaken to examine the synovial T cell receptor (TCR) repertoire, T cell phenotypes, and T cell specificities in small joints of RA patients at time of diagnosis before therapeutic intervention.

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Impaired Efferocytosis by Synovial Macrophages in Patients With Knee Osteoarthritis

Luigi Del Sordo, Garth B. Blackler, Holly T. Philpott, Jared Riviere, Lakshman Gunaratnam, Bryan Heit, C. Thomas Appleton

doi : 10.1002/art.42412

Osteoarthritis (OA) exposes all joint tissues to physiologic stresses, increasing the need to clear apoptotic cells from tissues, including the synovium. We undertook this study to assess the burden of apoptotic cells in synovial tissue in patients with late-stage knee OA and to investigate whether OA impairs the macrophage-mediated clearance of apoptotic cells via efferocytosis.

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Gene Expression and Autoantibody Analysis Revealing Distinct Ancestry-Specific Profiles Associated With Response to Rituximab in Refractory Systemic Lupus Erythematosus

Lucy M. Carter, Adewonuola Alase, Zoe Wigston, Antonios Psarras, Agata Burska, Emily Sutton, Md Yuzaiful Md Yusof, John A. Reynolds, The MASTERPLANS Consortium, Neil McHugh, Paul Emery, Miriam Wittmann, Ian N. Bruce, Edward M. Vital

doi : 10.1002/art.42404

Gene expression profiles are associated with the clinical heterogeneity of systemic lupus erythematosus (SLE) but are not well studied as biomarkers for therapy. We studied gene expression and response to rituximab in a multiethnic UK cohort who were refractory to standard therapy.

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Platelet LGALS3BP as a Mediator of Myeloid Inflammation in Systemic Lupus Erythematosus

Hanane El Bannoudi, MacIntosh Cornwell, Elliot Luttrell-Williams, Alexis Engel, Christina Rolling, Tessa J. Barrett, Peter Izmirly, H. Michael Belmont, Kelly Ruggles, Robert Clancy, Jill Buyon, Jeffrey S. Berger

doi : 10.1002/art.42382

Platelets are mediators of inflammation with immune effector cell properties and have been implicated in the pathogenesis of systemic lupus erythematosus (SLE).

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A Flare Risk Index Informed by Select Immune Mediators in Systemic Lupus Erythematosus

Melissa E. Munroe, Derek Blankenship, Daniele DeFreese, Mohan Purushothaman, Wade DeJager, Susan Macwana, Joel M. Guthridge, Stan Kamp, Nancy Redinger, Teresa Aberle, Eliza F. Chakravarty, Cristina Arriens, Yanfeng Li, Hu Zeng, Kathleen A. McCarthy-Fruin, Shirley-Ann Osei-Onomahm, Uma Thanarajasingam, Judith A. James, Eldon Jupe

doi : 10.1002/art.42389

Systemic lupus erythematosus (SLE) is marked by immune dysregulation linked to varied clinical disease activity. Using a unique longitudinal cohort of SLE patients, this study sought to identify optimal immune mediators informing an empirically refined flare risk index (FRI) reflecting altered immunity prior to clinical disease flare.

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Autoreactive Plasmablasts After B Cell Depletion With Rituximab and Relapses in Antineutrophil Cytoplasmic Antibody–Associated Vasculitis

Alvise Berti, Sophie Hillion, Maximilian F. Konig, Marta Casal Moura, Amber M. Hummel, Eva Carmona, Tobias Peikert, Fernando C. Fervenza, Cees G.M. Kallenberg, Carol A. Langford, Peter A. Merkel, Paul A. Monach, Philip Seo, Robert F. Spiera, Paul Brunetta, E. William St. Clair, Kristina M. Harris, John H. Stone, Guido Grandi, Jacques-Olivier Pers, Ulrich Specks, Divi Cornec

doi : 10.1002/art.42388

Autoreactive B cells are responsible for antineutrophil cytoplasmic antibody (ANCA) production in ANCA-associated vasculitis (AAV). Rituximab (RTX) depletes circulating B cells, including autoreactive B cells. We aimed to evaluate changes and associations with relapse of the circulating autoreactive B cell pool following therapeutic B cell depletion in AAV.

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Activation of a Latent Epitope Causing Differential Binding of Antineutrophil Cytoplasmic Antibodies to Proteinase 3

Marta Casal Moura, Gwen E. Thompson, Darlene R. Nelson, Lynn A. Fussner, Amber M. Hummel, Dieter E. Jenne, Daniel Emerling, Fernando C. Fervenza, Cees G. M. Kallenberg, Carol A. Langford, W. Joseph McCune, Peter A. Merkel, Paul A. Monach, Philip Seo, Robert F. Spiera, E. William St. Clair, Steven R. Ytterberg, John H. Stone, William H. Robinson, Ulrich Specks

doi : 10.1002/art.42418

Proteinase 3 (PR3) is the major antigen for antineutrophil cytoplasmic antibodies (ANCAs) in the systemic autoimmune vasculitis, granulomatosis with polyangiitis (GPA). PR3-targeting ANCAs (PR3-ANCAs) recognize different epitopes on PR3. This study was undertaken to study the effect of mutations on PR3 antigenicity.

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Low Concentrations of C5a Complement Receptor Antibodies Are Linked to Disease Activity and Relapse in Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Sebastian Klapa, Antje Müller, Andreas Koch, Anja Kerstein-Stähle, Wataru Kähler, Harald Heidecke, Susanne Schinke, Markus Huber-Lang, Martin Nitschke, Silke Pitann, Solveig Augustin, Christian M. Karsten, Gabriela Riemekasten, Peter Lamprecht

doi : 10.1002/art.42410

To examine concentrations of circulating antibodies targeting C3a and C5a complement receptors in antineutrophil cytoplasmic autoantibody (ANCA)–associated vasculitis (AAV) and analyze their association with disease activity.

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Identification of a Distinct Monocyte-Driven Signature in Systemic Sclerosis Using Biophysical Phenotyping of Circulating Immune Cells

Alexandru-Emil Matei, Markéta Kubánková, Liyan Xu, Andrea-Hermina Györfi, Evgenia Boxberger, Despina Soteriou, Maria Papava, Julia Prater, Xuezhi Hong, Christina Bergmann, Martin Kräter, Georg Schett, Jochen Guck, Jörg H. W. Distler

doi : 10.1002/art.42394

Pathologically activated circulating immune cells, including monocytes, play major roles in systemic sclerosis (SSc). Their functional characterization can provide crucial information with direct clinical relevance. However, tools for the evaluation of pathologic immune cell activation and, in general, of clinical outcomes in SSc are scarce.

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Cell-Mediated Cytotoxicity in Lyme Arthritis

David Ordóñez, Robert B. Lochhead, Klemen Strle, Annalisa Pianta, Sheila Arvikar, Ildiko Van Rhijn, Anat Stemmer-Rachamimov, Allen C. Steere

doi : 10.1002/art.42408

Obliterative microvascular lesions are found in the synovial tissue of ~50% of patients with post-antibiotic Lyme arthritis (LA) and correlate with autoantibodies to certain vascular antigens. In this study, we identified lymphocytes with cytotoxic potential that may also mediate this feature of synovial pathology.

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Amplification of Inflammation by Lubricin Deficiency Implicated in Incident, Erosive Gout Independent of Hyperuricemia

Khaled Elsaid, Tony R. Merriman, Leigh-Ana Rossitto, Ru Liu-Bryan, Jacob Karsh, Amanda Phipps-Green, Gregory D. Jay, Sandy Elsayed, Marwa Qadri, Marin Miner, Murray Cadzow, Talia J. Dambruoso, Tannin A. Schmidt, Nicola Dalbeth, Ashika Chhana, Jennifer Höglund, Majid Ghassemian, Anaamika Campeau, Nancy Maltez, Niclas G. Karlsson, David J. Gonzalez, Robert Terkeltaub

doi : 10.1002/art.42413

In gout, hyperuricemia promotes urate crystal deposition, which stimulates the NLRP3 inflammasome and interleukin-1β (IL-1β)–mediated arthritis. Incident gout without background hyperuricemia is rarely reported.

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Altered Risk of Incident Gout According to Changes in Metabolic Syndrome Status: A Nationwide, Population-Based Cohort Study of 1.29 Million Young Men

Yeonghee Eun, Kyungdo Han, Seung Woo Lee, Kyunga Kim, Seonyoung Kang, Seulkee Lee, Hoon-Suk Cha, Eun-Mi Koh, Hyungjin Kim, Jaejoon Lee

doi : 10.1002/art.42381

Few data are available on whether changes in metabolic syndrome affect incident gout. This study was undertaken to assess associations between metabolic syndrome status and incident gout, as well as changes in the clinical characteristics of metabolic syndrome and incident gout, in a cohort of young men.

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Association of Gout Polygenic Risk Score With Age at Disease Onset and Tophaceous Disease in European and Polynesian Men With Gout

Nicholas A. Sumpter, Riku Takei, Murray Cadzow, Ruth K. G. Topless, Amanda J. Phipps-Green, Rinki Murphy, Janak de Zoysa, Huti Watson, Muhammad Qasim, Alexa S. Lupi, Abhishek Abhishek, Mariano Andrés, Tania O. Crișan, Michael Doherty, Lennart Jacobsson, Matthijs Janssen, Tim L. Jansen, Leo A. B. Joosten, Meliha Kapetanovic, Frédéric Lioté, Hirotaka Matsuo, Geraldine M. McCarthy, Fernando Perez-Ruiz, Philip Riches, Pascal Richette, Edward Roddy, Blanka Stiburkova, Alexander So, Anne-Kathrin Tausche, Rosa J. Torres, Till Uhlig, Tanya J. Major, Lisa K. Stamp, Nicola Dalbeth, Hyon K. Choi, Ana I. Vazquez, Megan P. Leask, Richard J. Reynolds, Tony R. Merriman

doi : 10.1002/art.42393

To determine whether a gout polygenic risk score (PRS) is associated with age at gout onset and tophaceous disease in European, East Polynesian, and West Polynesian men and women with gout.

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Aberrant Naive CD4–Positive T Cell Differentiation in Systemic Juvenile Idiopathic Arthritis Committed to B Cell Help

Julia Kuehn, Susanne Schleifenbaum, Michaela Hendling, Sandra Siebenhandl, Julie Krainer, Sabrina Fuehner, Antje Hellige, Carolin Park, Claas Hinze, Helmut Wittkowski, Dirk Holzinger, Lorenz Thurner, Andreas Weinhäusel, Dirk Foell, Christoph Kessel

doi : 10.1002/art.42409

Systemic juvenile idiopathic arthritis (JIA) features characteristics of autoinflammation and autoimmunity, culminating in chronic arthritis. In this study, we hypothesized that aberrant or incomplete polarization of T helper cells contributes to disease pathology.

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NLRP3 Attenuates Intraocular Inflammation by Inhibiting AIM2-Mediated Pyroptosis Through the Phosphorylated Salt-Inducible Kinase 1/Sterol Regulatory Element Binding Transcription Factor 1 Pathway

Jiayu Meng, Na Li, Xianyang Liu, Shengjun Qiao, Qian Zhou, Jun Tan, Ting Zhang, Zhifang Dong, Xiaopeng Qi, Aize Kijlstra, Liming Mao, Peizeng Yang, Shengping Hou

doi : 10.1002/art.42420

The NLRP3 inflammasome has been shown to be involved in the development of uveitis, but the exact mechanism remains elusive. This study was undertaken to explore the role of NLRP3 in the development of uveitis.

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Early Increase of Circulating Transitional B Cells and Autoantibodies to Joint-Related Proteins in Patients With Metastatic Melanoma Developing Checkpoint Inhibitor–Induced Inflammatory Arthritis

Mariele Gatto, Sara Bjursten, Charlotte A. Jonsson, Monica Leu Agelii, Caroline Jonell, Sarah McGrath, Erik Lönnblom, Outi Sareila, Rikard Holmdahl, Anna Rudin, Max Levin, Inger Gjertsson

doi : 10.1002/art.42406

To investigate potential associations between B cell–related immunologic changes and development of inflammatory arthritis (IA) after treatment with immune checkpoint inhibitors (ICIs).

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Positron emission tomography/magnetic resonance imaging of the sacroiliac joints and spine to monitor effects of anti–tumor necrosis factor therapy in axial spondyloarthritis: comment on the article by Bruckmann et al

Jerney de Jongh, Gerben J. C. Zwezerijnen, Maqsood Yaqub, Conny J. van der Laken

doi : 10.1002/art.42400

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Reply

Xenofon Baraliakos, Christoph Rischpler, Nils-Martin Bruckmann

doi : 10.1002/art.42399

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