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  • Abstract Number: 1990 • 2018 ACR/ARHP Annual Meeting

    Luteolin Modulates Glyco-Lipo-Oxidative Protein Modifications and Inhibits Inflammatory Cytokine Release in Human Osteoarthritic Articular Chondrocytes: Comparison with Colchicine

    Berna Goker1, Zubeyir Elmazoglu2, Berivan Bitik3, Cem Nuri Aytekin4 and Cimen Karasu2, 1Internal Medicine- Rheumatology, Gazi University Medical School, Ankara, Turkey, 2Medical Pharmacology,Cellular Stress Response & Signal Transduction Research Laboratory, Gazi University Medical School, Ankara, Turkey, 3Internal Medicine-Rheumatology, Başkent University Medical School, Ankara, Turkey, 4Orthopedics & Traumatology, Yıldırım Beyazıd University, Ankara, Turkey

    Background/Purpose: The progressive destruction of osteoarthritic articular cartilage has been attributed to multifactorial cellular events, including increased oxidative modifications in proteins, abnormal inflammatory and catabolic…
  • Abstract Number: 1991 • 2018 ACR/ARHP Annual Meeting

    Measuring Balance in an Experimental Mouse Model of Osteoarthritis

    Rachel E. Miller1, Shingo Ishihara2, Zhe Wang3, Richard J. Miller4 and Anne-Marie Malfait5, 1Biochemistry, Rush University Medical Center, Chicago, IL, 2Internal Medicine, Rush University Medical Center, Chicago, IL, 3Guangzhou Institutes of Biomedicine and Health, Guangzhou, China, 4Pharmacology/Medical Humanities and Bioethics, Northwestern University, Chicago, IL, 5Biochemistry & Rheumatology, Rush University Medical Center, Chicago, IL

    Background/Purpose: Destabilization of the medial meniscus (DMM) in mice results in experimental osteoarthritis, characterized by progressive joint damage (severe damage by week 12) and associated…
  • Abstract Number: 1992 • 2018 ACR/ARHP Annual Meeting

    The Effect of 4E-BP1 on Osteoarthritis-Related Gene Expression in TGF-β1-Stimulated Chondrocytes

    Mi Hyun Lee, Ju-Ryoung Kim, Hyun Sook Hwang and Hyun Ah Kim, Hallym University Sacred Heart Hospital, Kyunggi-do, Korea, Republic of (South)

    Background/Purpose: Initiation of protein synthesis is regulated by a repressor of cap-dependent translation, eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), which prevents eukaryotic initiation factor…
  • Abstract Number: 1993 • 2018 ACR/ARHP Annual Meeting

    Evaluation of Cartilage Degeneration and Osteoarthritis Pain on Female and Male Mouse Model of Osteoarthritis

    In Young Park, Jeong-Im Hong, Hyun Sook Hwang and Hyun Ah Kim, Hallym University Sacred Heart Hospital, Kyunggi-do, Korea, Republic of (South)

    Background/Purpose: The prevalence of radiographic and symptomatic osteoarthritis (OA) is higher in women, but in animal study, male mice were more frequently used to explore…
  • Abstract Number: 1994 • 2018 ACR/ARHP Annual Meeting

    Osteoarthritis Severity Is Reduced By Intra-Articular Administration of Hydrogen Sulfide

    Elena F. Burguera1,2, Angela Vela-Anero3, Carlos Vaamonde-Garcia3, Tamara Hermida-Gómez1,2, Purificacion Filgueira-Fernandez1,2, Lucía Gato-Calvo2, Rosa Meijide-Failde4 and Francisco J Blanco5, 1CIBER-BBN, Madrid, Spain, 2Unidad de Medicina Regenerativa, Grupo de Investigación en Reumatología, Agrupación Estratégica CICA-INIBIC, Complexo Hospitalario Universitario de A Coruña (CHUAC), Sergas, Universidade de A Coruña (UDC), A Coruña, Spain, 3Department of Physiotherapy, Medicine and Biological sciences, Tissue Engineering and Regenerative Medicine group (University of A Coruña), A Coruña, Spain, 4Department of Physiotherapy, Medicine and Biological Sciences, Tissue Engineering and Regenerative Medicine group (University of A Coruña), A Coruña, Spain, 5Grupo de Investigación en Reumatología, Instituto de Investigación Biomédica de A Coruña (INIBIC), Complexo Hospitalario Universitario de A Coruña (CHUAC), Sergas. Universidade da Coruña (UDC), A Coruña, Spain

    Background/Purpose: Hydrogen sulphide (H2S) is recognized as a therapeutic target in osteoarthritis (OA). Exogenous supplementation with synthetic salts in in vitro models of OA has…
  • Abstract Number: 1995 • 2018 ACR/ARHP Annual Meeting

    Heparan Sulfates from Human Osteoarthritic Cartilage Display Increased Sulfation Pattern, Decrease the Protein Binding Capacity to FGF-2 and Increase the Binding to VEGF and Induce Changes of Human Mesenchymal Stem Cell Behavior

    Sarah Shamdani1, Florent Eymard2,3, sandrine Chantepie3, Camille Flageollet1, Nadia Henni-Chebra1, Yoan Jouan1, Eric Hay4, Martine Cohen-Solal5,6,7,8, Dulce Papy-Garcia3, Xavier Chevalier9,10 and Patricia Albanese1, 1Val de Marne, Cell Growth, Tissue Repair and Regeneration Laboratory (CRRET), UPEC EA 4397/ERL CNRS 9215, F-94000, Créteil, France, Créteil, France, 2Department of Rheumatology, APHP Henri Mondor Hospital, Creteil, France, 3Val de Marne, Cell Growth, Tissue Repair and Regeneration Laboratory (CRRET), UPEC EA 4397/ERL CNRS 9215, F-94000, Créteil, France, Creteil, France, 4Rheumatology Department, Lariboisiere Hospital, Inserm UMR-1132, BIOSCAR, Paris, France, 5Paris Diderot University, Paris, France, 6Rhumatologie A, INSERM U606 Hôpital Lariboisière, Centre Viggo Petersen, Paris, France, 7Department of rheumatology and of bone and joint imaging, hospital Lariboisiere, Paris, France, Hôpital Lariboisière, Paris, France, 8INSERM UMR1132, Paris Diderot University, Paris, France, 994, Cell Growth, Tissue Repair and Regeneration Laboratory (CRRET), UPEC EA 4397/ERL CNRS 9215, F-94000, Créteil, France, Creteil, France, 10Rheumatology, Hopital Henri Mondor, APHP, Creteil, France

    Background/Purpose: The major Glycosaminoglycan (GAGs) component of the cartilage ECM are Chondroitin Sulfates (CS) and Keratan sulfates (KS). Heparan Sulfates (HS) are also present in…
  • Abstract Number: 1996 • 2018 ACR/ARHP Annual Meeting

    Adenosine A2A Receptor (A2AR) Stimulation Enhances Mitochondrial Metabolism and Mitigates Reactive Oxygen Species-Mediated Mitochondrial Injury

    Cristina Castro1, Carmen Corciulo2, Maria de la Encarnacion Solesio Torregrosa3, Evgeny Pavlov4 and Bruce N. Cronstein5, 1Medicine, NYU School of Medicine, New York, NY, 2Department of Medicine, Division of Rheumatology, New York University School of Medicine, New York, NY, 3NYU College of Dentistry, New York City, NY, 4Assistant Professor, Basic Science and Craniofacial Biology, NYU College of Dentistry, New York City, NY, 5Rheumatology, New York University School of Medicine, Division of Rheumatology, New York, NY

    Background/Purpose: Osteoarthritis (OA) is the most common form of arthritis, affecting nearly 10% of the US population. With age and injury, chondrocytes have diminished mitochondrial…
  • Abstract Number: 1997 • 2018 ACR/ARHP Annual Meeting

    Adenosine A2A Receptors Maintain Chondrocyte and Cartilage Homeostasis By Maintaining Expression of Anti-Inflammatory Regulators (Nur-77) and Suppressing Expression of Pro-Inflammatory Mediators

    Carmen Corciulo1, Cristina Castro2, Samson Jacob3, David Fenyo3 and Bruce N. Cronstein4, 1Department of Medicine, Division of Rheumatology, New York University School of Medicine, New York, NY, 2Medicine, NYU School of Medicine, New York, NY, 3Institute for Systems Genetics, NYU School of Medicine, New York, NY, 4Rheumatology, New York University School of Medicine, Division of Rheumatology, New York, NY

    Background/Purpose: We have recently reported that adenosine A2A receptor (A2AR) knockout mice develop spontaneous osteoarthritis (OA) and intra-articular injection of adenosine prevents OA progression in…
  • Abstract Number: 1998 • 2018 ACR/ARHP Annual Meeting

    Autophagy-Related Molecules Detected in Blood and Cartilage Are Biomarkers of Joint Damage in OA

    Beatriz Carames1, Irene Lorenzo Gomez1, Jose Antonio Pinto Tasende2, Natividad Oreiro Villar2 and Francisco J Blanco1, 1Cartilage Biology Group, Rheumatology Division, INIBIC-CHUAC, A Coruña, A Coruña, Spain, 2Clinical Rheumatology Division, Complejo Hospitalario Universitario A Coruña (CHUAC), A Coruña, A Coruña, Spain

    Background/Purpose: In osteoarthritis (OA), defects in cellular homeostasis, and in particular in autophagy, are evident and precede joint damage. We have shown that there is…
  • Abstract Number: 1999 • 2018 ACR/ARHP Annual Meeting

    Aberrant Expression of the GluN2B N-Methyl D-Aspartate Receptor Subunit in Osteoarthritic Chondrocytes Causes Disease-Associated Changes in Chondrocyte Phenotype through Altered Expression of Core Components of the Chondrocyte Circadian Clock

    Maggie Kalev-Zylinska1, James Hearn1, Jing Rong1, Mark Zhu2, Jacob Munro3, Jillian Cornish4, Nicola Dalbeth1 and Raewyn Poulsen2, 1University of Auckland, Auckland, New Zealand, 2Medicine, University of Auckland, Auckland, New Zealand, 3Orthopaedics, Auckland City Hospital, Auckland, New Zealand, 4Department of Medicine, University of Auckland, Auckland, New Zealand

    Background/Purpose: Circadian clocks are key regulators of cell behaviour. Disruption to cell clocks is implicated in a range of diseases. Expression of two core clock…
  • Abstract Number: 2000 • 2018 ACR/ARHP Annual Meeting

    Interleukin-1β, Oxidative Stress and Basic Calcium Phosphate Crystals Induce Osteoarthritis-like Changes in Chondrocyte Phenotype By Altering the Expression of PERIOD2, a Core Component of the Chondrocyte Circadian Clock

    Jing Rong1, Mark Zhu2, Jacob Munro3, Geraldine M. McCarthy4, Jillian Cornish5, Nicola Dalbeth1 and Raewyn Poulsen2, 1University of Auckland, Auckland, New Zealand, 2Medicine, University of Auckland, Auckland, New Zealand, 3Orthopaedics, Auckland City Hospital, Auckland, New Zealand, 4Mater Misericordiae University Hospital, Dublin, Ireland, 5Department of Medicine, University of Auckland, Auckland, New Zealand

    Background/Purpose: Almost all cells contain a circadian clock. Cell clocks are key regulators of cell activity and cell differentiation. In osteoarthritis (OA), chondrocytes inappropriately undergo…
  • Abstract Number: 2001 • 2018 ACR/ARHP Annual Meeting

    Adenosine A2A Receptor Stimulation Regulates Autophagy in Chondrocytes

    Benjamin Friedman1, Carmen Corciulo2, Cristina Castro3 and Bruce N. Cronstein1, 1Rheumatology, New York University School of Medicine, New York, NY, 2Department of Medicine, Division of Rheumatology, New York University School of Medicine, New York, NY, 3Medicine, NYU School of Medicine, New York, NY

    Background/Purpose: Osteoarthritis (OA) is a debilitating condition characterized by chondrocyte dysfunction and loss of cartilage. Autophagy, a homeostatic process that occurs in times of cellular…
  • Abstract Number: 2002 • 2018 ACR/ARHP Annual Meeting

    Dynamic Compression of Articular Cartilage Explants Increases Formation and Decreases Degradation of Type II Collagen

    Amalie Engstrøm1,2, Anne C. Bay-Jensen2, Morten A. Karsdal2 and Christian S. Thudium2, 1Department of Biomedical Science, University of Copenhagen, København, Denmark, 2Nordic Bioscience, Herlev, Denmark

    Background/Purpose: Mechanical loading is recognized as a major factor in initiation and progression of osteoarthritis (OA). Conversely loading is believed to play an essential role…
  • Abstract Number: 2003 • 2018 ACR/ARHP Annual Meeting

    Chondrocyte Size in Articular Cartilage As a Marker of Osteoarthritis Severity

    Paula Gratal1, Aranzazu Mediero2, Iván Prieto-Potin1, Ana Lamuedra1, Gabriel Herrero-Beaumont1 and Raquel Largo1, 1Bone and Joint Research Unit, IIS-Fundación Jiménez Díaz UAM, Madrid, Spain, 2Joint and Bone Research Unit, IIS-Fundación Jiménez Díaz UAM, Madrid, Spain

    Background/Purpose: Terminal differentiating growth plate chondrocytes are mainly characterized by an increase of their cell size and by the expression of hypertrophic markers such as…
  • Abstract Number: 2004 • 2018 ACR/ARHP Annual Meeting

    Effective Inhibition of Metalloproteases By a Viscosupplement Based on a Hyaluronic Acid Amide (HYADD®4)

    Cynthia Secchieri1, Devis Galesso1, Cristian Guarise1, Mauro Pavan1, Stefano Moro2 and Veronica Salmaso2, 1Fidia Farmaceutici, Abano Terme, Italy, 2Pharmaceutical and Pharmacological Sciences, University of Padova, Padova, Italy

    Background/Purpose: Osteoarthritis (OA) is a disease which results in the degeneration of articular cartilage. The progression of OA involves inflammation in the early stage of…
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All abstracts accepted to ACR Convergence are under media embargo once the ACR has notified presenters of their abstract’s acceptance. They may be presented at other meetings or published as manuscripts after this time but should not be discussed in non-scholarly venues or outlets. The following embargo policies are strictly enforced by the ACR.

Accepted abstracts are made available to the public online in advance of the meeting and are published in a special online supplement of our scientific journal, Arthritis & Rheumatology. Information contained in those abstracts may not be released until the abstracts appear online. In an exception to the media embargo, academic institutions, private organizations, and companies with products whose value may be influenced by information contained in an abstract may issue a press release to coincide with the availability of an ACR abstract on the ACR website. However, the ACR continues to require that information that goes beyond that contained in the abstract (e.g., discussion of the abstract done as part of editorial news coverage) is under media embargo until 10:00 AM CT on October 25. Journalists with access to embargoed information cannot release articles or editorial news coverage before this time. Editorial news coverage is considered original articles/videos developed by employed journalists to report facts, commentary, and subject matter expert quotes in a narrative form using a variety of sources (e.g., research, announcements, press releases, events, etc.).

Violation of this policy may result in the abstract being withdrawn from the meeting and other measures deemed appropriate. Authors are responsible for notifying colleagues, institutions, communications firms, and all other stakeholders related to the development or promotion of the abstract about this policy. If you have questions about the ACR abstract embargo policy, please contact ACR abstracts staff at [email protected].

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