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Search Results for : Rheumatoid Arthritis
Merck Online Lab
Diagnosis Therapy Rehabilitation Imaging Clinical Laboratory
Chondrogenic differentiation of human subchondral progenitor cells is impaired by rheumatoid arthritis synovial fluid.
Author(s): Kr; üger, JP; Endres, M; Neumann, K; H; äupl, T; Erggelet, C; Kaps, C
Journal: J Orthop Res 2010 May 5; Vol. 28, Issue 6; Page(s) 819-27
[Medline ID - 20041492]

In microfracture, subchondral progenitors enter the cartilage defect and form cartilage repair tissue. We hypothesize that synovial fluid (SF) from rheumatoid arthritis (RA) donors affects chondrogenesis of human subchondral progenitors stimulated with transforming growth factor-beta3 (TGFB3), whereas SF from normal and osteoarthritis (OA) donors do not. Human progenitors from subchondral cortico-spongious bone (pool of n = 4) were cultured in micromasses under serum-free conditions and were stimulated with 10 ng/mL TGFB3 and with 5% SF from normal, OA, and RA donors (pool of n = 7, each). Histological staining of proteoglycan and immunostaining of type II collagen showed that progenitors stimulated with SF from RA donors show significantly reduced cartilage matrix formation compared to progenitors treated with TGFB3 or with SF from normal and OA donors (n = 3, each). Gene expression analysis of typical chondrocyte marker genes and genes encoding matrix modifying enzymes showed that SF from OA and RA donors influence the onset of TGFB3-mediated chondrogenesis (pool of 20 micromasses), but had no effect on the gene expression profile after prolonged culture in micromasses. These results suggest that SF from RA patients may impair the chondrogenic development of mesenchymal progenitors in microfracture, whereas osteoarthritic SF may has no negative effect on the cartilage matrix formation.

Autoimmune disease classification by inverse association with SNP alleles.
Author(s): Sirota, M; Schaub, MA; Batzoglou, S; Robinson, WH; Butte, AJ
Journal: PLoS Genet 2010 Mar 23; Vol. 5, Issue 12; Page(s) e1000792
[Medline ID - 20041220]

With multiple genome-wide association studies (GWAS) performed across autoimmune diseases, there is a great opportunity to study the homogeneity of genetic architectures across autoimmune disease. Previous approaches have been limited in the scope of their analysis and have failed to properly incorporate the direction of allele-specific disease associations for SNPs. In this work, we refine the notion of a genetic variation profile for a given disease to capture strength of association with multiple SNPs in an allele-specific fashion. We apply this method to compare genetic variation profiles of six autoimmune diseases: multiple sclerosis (MS), ankylosing spondylitis (AS), autoimmune thyroid disease (ATD), rheumatoid arthritis (RA), Crohn's disease (CD), and type 1 diabetes (T1D), as well as five non-autoimmune diseases. We quantify pair-wise relationships between these diseases and find two broad clusters of autoimmune disease where SNPs that make an individual susceptible to one class of autoimmune disease also protect from diseases in the other autoimmune class. We find that RA and AS form one such class, and MS and ATD another. We identify specific SNPs and genes with opposite risk profiles for these two classes. We furthermore explore individual SNPs that play an important role in defining similarities and differences between disease pairs. We present a novel, systematic, cross-platform approach to identify allele-specific relationships between disease pairs based on genetic variation as well as the individual SNPs which drive the relationships. While recognizing similarities between diseases might lead to identifying novel treatment options, detecting differences between diseases previously thought to be similar may point to key novel disease-specific genes and pathways.

Cryoglobulin evaluation: best practice?
Author(s): Sargur, R; White, P; Egner, W
Journal: Ann Clin Biochem 2010 Mar 6; Vol. 47, Issue Pt 1; Page(s) 8-16
[Medline ID - 20040794]

Cryoglobulins are serum immunoglobulins that precipitate at temperatures below 37 degrees C and re-dissolve on warming. Cryoglobulinaemia leads to variable symptoms including characteristic purpura, ischaemia of extremities, renal failure, peripheral neuropathy, abdominal pain secondary to intestinal ischaemia and arthralgias. Cryoglobulin testing is underutilized in clinical practice. It has been neglected in clinical laboratories and by clinicians due to several factors, such as the length of time it takes for serum cryoglobulin analysis to be performed in the laboratory, the perceived difficulty in getting optimal sampling conditions and a failure to appreciate that even apparently low levels of cryoglobulin can be associated with severe symptoms in some patients. The most important variable confounding standardization of cryoglobulin testing is improper sample handling. A recent report critically appraising the current practice of cryoglobulin evaluation in 137 laboratories in Europe by United Kingdom National External Quality Assurance Scheme (UKNEQAS) illustrated the wide variability in practice. Although many clinical laboratories perform cryoglobulin evaluation, there are widespread differences in the methodology used and the care with which this is ca rried out and this leads to considerable intralaboratory and interlaboratory variability. The most common sources of error are false-negative results due to loss of cryoprecipitate during transport and storage. Better standardization is needed to avoid missed diagnoses and improve the comparability of results. Laboratories should ensure that sample temperature is maintained at 37 degrees C until the serum is separated. In this article, we briefly review the classification and clinical features of cryoglobulins and suggest best practice guidelines for laboratory detection and identification of cryoglobulins.

Abrupt development of sarcoidosis with a prodromal increase in plasma osteopontin in a patient with rheumatoid arthritis during treatment with etanercept.
Author(s): Takatori, S; Kamata, Y; Murosaki, T; Iwamoto, M; Minota, S
Journal: J Rheumatol 2010 Apr 7; Vol. 37, Issue 1; Page(s) 210-1
[Medline ID - 20040649]

ABSTRACT NOT AVAILABLE

Low level (below cutoff) of anti-cyclic citrullinated peptide test results in diagnosis of rheumatoid arthritis in a high-risk population.
Author(s): Kim, DA; Kim, TY
Journal: J Rheumatol 2010 Apr 7; Vol. 37, Issue 1; Page(s) 208
[Medline ID - 19228654]

ABSTRACT NOT AVAILABLE

HLA-DRB1 alleles and rheumatoid arthritis-related pulmonary fibrosis.
Author(s): Migita, K; Nakamura, T; Koga, T; Eguchi, K
Journal: J Rheumatol 2010 Apr 7; Vol. 37, Issue 1; Page(s) 205-7
[Medline ID - 20040645]

ABSTRACT NOT AVAILABLE

Risk factors for cardiovascular disease in rheumatoid arthritis: defining treatment thresholds.
Author(s): Ravindran, V; Hughes, RA
Journal: J Rheumatol 2010 Apr 7; Vol. 37, Issue 1; Page(s) 200; author reply 201-2
[Medline ID - 19567631]

ABSTRACT NOT AVAILABLE

Images in rheumatology. Transfusion-related acute lung injury during intravenous immunoglobulin treatment.
Author(s): Voulgari, PV; Paschou, S; Svarna, E; Tsifetaki, N; Drosos, AA
Journal: J Rheumatol 2010 Apr 7; Vol. 37, Issue 1; Page(s) 190-1
[Medline ID - 20040637]

ABSTRACT NOT AVAILABLE

Can the events of early life influence the development of rheumatoid arthritis?
Author(s): Edwards, CJ
Journal: J Rheumatol 2010 Apr 7; Vol. 37, Issue 1; Page(s) 1-2
[Medline ID - 20040634]

ABSTRACT NOT AVAILABLE

Tocilizumab for rheumatoid arthritis.
Journal: Drug Ther Bull 2010 Apr 7; Vol. 48, Issue 1; Page(s) 9-12
[Medline ID - 20040568]

Tocilizumab (RoActemra-Roche) is a new biological agent available in the UK for the treatment of adults with rheumatoid arthritis.1 Unlike currently available biological agents, the drug targets the pro-inflammatory cytokine interleukin-6 (IL-6). Here, we consider the place of tocilizumab in rheumatoid arthritis and whether it offers any advantages over other biological agents.
  Page 1 of 100  




 



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