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Results for “SYNOVIAL FLUID”

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At least 127 records · Page 7Linked to original sources
PubMed1995

[Synovial fluid on non-synovial tendon: experimental study].

The non-synovial tendon was placed in the synovial cavity of rabbit knee joint to carry out tissue culture in vivo. The surface of the cultured tendon was covered with a smooth membrane-like tissue which possessed the morphologic characteristics of the synovial membrane identified by histological and electron microscopic examinations. The tendon segments were kept free in the cavity of knee joint and adhesions were not observed. It is suggested that non-synovial tendon could transform into a synovial tendon in the environment filled with synovial fluid.

Animals↗
PubMedDate not supplied

[Time-dependent flow behavior and fibrinogen content of synovial fluid].

Normal bovine synovial fluid and synovial effusions in human non-inflammatory joint diseases do not show any decrease of viscosity for a long period of time during imposed shear loading, as is required for thixotropy. This observation is based on two different methods of measurement; the "hysteresis loop" method and the recording of the shear stress-time curve. Inflammatory synovial fluids--particularly from patients with rheumatoid arthritis and a high concentration of fibrinogen--form a visible gel after 6 to 20 hours of rest. Those gels show a hysteresis loop typical for thixotropy and a decrease of viscosity with the duration of shear loading. Due to the shearing in the rheometer precipitation occurs and fibrin clots appear. The appearance of fibrin clots induced by mechanical shear loading not known until now, can be discussed with regard to its possible participation in the symptom of morning stiffness, in the formation of rice bodies and in the destruction of joint cartilage in rheumatoid arthritis.

Animals↗
PubMed1992

Measurement of synovial fluid volume: a new dilution method adapted to fluid permeation from the synovial cavity.

A new dilution method was developed to measure the synovial fluid (SF) volume in a single knee joint of a rabbit. In this dilution method, we used 2 different kinds of dextrans, one having a mean molecular weight (M(r)) of 487,000 and labelled with fluorescein isothiocyanate (FITC) as a marker, and the other M(r) of 300,000 to give hypertonicity to the solution. By employing these high M(r) dextrans in their optimal concentrations, we were able to minimize the inevitable transsynovial shift of the fluid and marker after intraarticular injection. The original SF volume was then calculated using the fluorescence intensities of the injected and retrieved fluids. By determining the accurate volume of SF, it became possible to measure per joint the protein and hyaluronic acid contents in SF as well as the total and differential cell counts. The results obtained by this new method were reasonable and consistent, except for volume, with the reported results based on pooled samples from multiple joints. We believe that the method can contribute to the analysis of SF changes under various conditions in small laboratory animals.

Animals↗
PubMed1990

A study of the effect of rheumatoid synovial fluid on proliferation and IL-2 production by total mononuclear cells and purified CD4+ cells of synovial fluid and peripheral blood.

T cells from synovial fluid (SF) of rheumatoid arthritis (RA) patients have previously been shown to proliferate less after mitogenic stimulation and produce less interleukin 2 (IL-2) than normal T cells. To test whether SF is responsible for the reduced T-cell responses, we studied the effect of inflammatory SF on peripheral blood (PB) RA and normal mononuclear cells (MNC) and CD4+ T cells and on RA SF MNC and CD4+ cells in vitro. Most rheumatoid SF present in concentrations of 50% and 5% during in vitro stimulation increased mitogen-induced IL-2 production and proliferative response by normal PB and RA MNC and CD4+ cells. Other rheumatoid SF samples did not influence the T cell responses, while only a few samples had an inhibitory effect. The results indicate that SF contain both stimulatory and inhibitory factors and that the resultant effect on T cells may depend on the net effect of these. The results do not support the hypothesis that the apparently impaired function of SF T cells is due to contact with SF.

Arthritis, Rheumatoid↗
PubMed1977

Somatomedin activity in synovial fluid.

Abnormalities of synovial fluid, as a lubricant and nutrient, may have relevance to the causation of certain articular diseases. The somatomedin activity in normal synovial fluid obtained from the knee joint of the ox has been studied and compared with the activity in serum from the same animal. The porcine costal cartilage bioassay of Van den Brande and Du Caju (1974) has been used with the isotopes 35S-sulphate and 3H-thymidine. The mean potency ratio of ox synovial fluid in terms of ox serum for 35S-sulphate incorporation was 0-28 (range 0-19-0-47) and for 3H-thymidine incorporation 0-35 (range 0-21-0-63). A significant correlation was found between the somatomedin activity (as measured by 35S-sulphate incorporation) and the total protein and albumin concentrations in the ox synovial fluids and the ox sera, but there was no significant relationship between the somatomedin potency ratios and the globulin concentrations. The possible relevance of these findings to injury and disease in synovial joint is discussed.

Albumins↗
PubMed1988

Detection of tumor necrosis factor alpha but not tumor necrosis factor beta in rheumatoid arthritis synovial fluid and serum.

Synovial fluids from 6 of 12 patients with rheumatoid arthritis (RA) and from 3 of 11 patients with reactive arthritis contained measurable levels of tumor necrosis factor alpha (TNF alpha). Seven of 12 sera from RA patients contained TNF alpha, while only 1 of those from reactive arthritis patients was positive. Gamma-interferon was detected in the synovial fluids and sera of only the RA patients. Tumor necrosis factor beta was not detected in any sera or synovial fluids. RA patients with detectable TNF alpha had higher erythrocyte sedimentation rates and synovial fluid leukocyte counts.

Adult↗
PubMed1988

IgE rheumatoid factors: quantification in synovial fluid and ability to induce synovial mast cell histamine release.

IgE rheumatoid factor activity was found to be significantly elevated (P less than 0.01) using an ELISA assay when paired synovial fluid and sera from 13 patients with active RA were compared to ten control samples. Synovial fluid IgE RF activity was higher than predicted by diffusion alone in 7/11 (64%) of the RA synovial fluids studied when coefficients of diffusion were determined. The specificity of IgE RF activity as measured by the ELISA was confirmed using immunoaffinity chromatography. Mast cells, obtained by enzymatic dispersion of rheumatoid synovial tissue, were sensitized with sera containing either IgE antibodies directed against ragweed or IgE with RF activity. Histamine was released upon challenge with anti-IgE antibodies (33.2% +/- 11), ragweed antigen E (34.6% +/- 11), or aggregated gamma globulin (47.6% +/- 17.9). No histamine release was observed if antigen challenge occurred in the absence of appropriate sensitization, with C3 anaphylatoxin, or after immunoadsorption of IgE from sera containing IgE RF activity.

Allergens↗
PubMed1993

Immunoaffinity purification of prostaglandin E2 and leukotriene C4 prior to radioimmunoassay: application to human synovial fluid.

When human synovial fluid as such was subjected to radioimmunoassays of prostaglandin E2 (PGE2) and leukotriene C4 (LTC4), there was no linear increase in PGE2 and LTC4 as the amount of synovial fluid was raised. For removal of substances thus disturbing the assay we developed a method of immunoaffinity purification of PGE2 and LTC4. A monoclonal antibody against PGE2 or LTC4 was coupled to BrCN-activated Sepharose 4B. When synovial fluid mixed with radiolabelled PGE2 or LTC4 was applied to the column of immobilized antibody, the ligand was adsorbed to the column and eluted with a mixture of methanol/water in a recovery of about 80%. The purified material showed a linearity between the amount of the sample and the value of radioimmunoassay. The one-step method was applied to synovial fluid from patients with rheumatoid arthritis, osteoarthritis and other joint diseases.

Animals↗
PubMed1983

Factors influencing the incorporation of fibronectin into synovial fluid cryoprotein.

Methods of synovial fluid collection and processing known to affect cryoprotein formation were examined to investigate the proposed role of fibronectin in synovial fluid cryoprecipitation. Fibronectin, a nonimmunoglobulin, noncomplement synovial fluid protein was present in all resolubilized synovial fluid cryoproteins studied. Radiolabeled fibronectin was precipitated from rheumatoid synovial fluid to a significantly greater extent (10%) than from noninflammatory (osteoarthritic) synovial fluid (2.8%), normal plasma (1.3%), or normal serum (0.5%) (p less than 0.01). Clotting of synovial fluid reduced fibronectin concentration 44% and resulted in a reduction in the amount and percent incorporation of fibronectin into cryoprotein, whereas heparinization and hyaluronidase treatment increased cryoprecipitable fibronectin. Affinity depletion of synovial fluid fibronectin resulted in loss of C1q and reduction in IgG in the cryoprotein; however, fibronectin, C1q, and IgG could not be co-eluted from affinity matrices of gelatin and protein A-Sepharose. Cryoprotein formation from pathologic synovial fluid depends in part on fibronectin and appears to involve interactions between fibronectin and fibrinogen as well as immunoglobulin complexes and complement components.

Arthritis, Rheumatoid↗
PubMed1982

Some observations and speculations on the factors influencing the concentration of phenylbutazone in synovial fluid.

Simultaneous plasma and synovial fluid samples have been obtained from patients, having reached a steady state on phenylbutazone, as a means of investigating factors influencing drug penetration into synovial fluid. Synovial fluid levels are lower than, but related to, plasma levels and are higher in rheumatoid disease (55-100% plasma levels) than in osteoarthritis (less than 50%). Patients with a more active form of the disease have higher synovial fluid drug concentrations. Results are discussed in the light of present knowledge and areas for further study are proposed.

Albumins↗
PubMed2005

RNA released from necrotic synovial fluid cells activates rheumatoid arthritis synovial fibroblasts via Toll-like receptor 3.

OBJECTIVE: To assess the expression of Toll-like receptor 3 (TLR-3) protein in synovial tissues and cultured synovial fibroblasts obtained from patients with rheumatoid arthritis (RA) and osteoarthritis (OA) and to investigate the consequences of stimulation of cultured synovial fibroblasts with TLR-3 ligands. METHODS: TLR-3 expression in synovial tissues was determined by immunohistochemistry and immunofluorescence, and expression in cultured RA synovial fibroblasts (RASFs) was determined by fluorescence-activated cell sorting and real-time polymerase chain reaction techniques. TLR-3 signaling was assessed by incubating RASFs with poly(I-C), lipopolysaccharide, palmitoyl-3-cysteine-serine-lysine-4, or necrotic synovial fluid cells from RA patients in the presence or absence of hydroxychloroquine or Benzonase. Subsequent determination of interferon-beta (IFNbeta), CXCL10, CCL5, and interleukin-6 (IL-6) protein production in the culture supernatants was performed by enzyme-linked immunosorbent assays. RESULTS: TLR-3 protein expression was found to be higher in RA synovial tissues than in OA synovial tissues. TLR-3 expression was localized predominantly in the synovial lining, with a majority of the TLR-3-expressing cells coexpressing fibroblast markers. Stimulation of cultured RASFs with the TLR-3 ligand poly(I-C) resulted in the production of high levels of IFNbeta, CXCL10, CCL5, and IL-6 protein. Similarly, coincubation of RASFs with necrotic synovial fluid cells from patients with RA resulted in up-regulation of these cytokines and chemokines in a TLR-3-dependent manner. CONCLUSION: Our findings demonstrate the expression of TLR-3 in RA synovial tissue and the activation of RASFs in vitro by the TLR-3 ligand poly(I-C) as well as by necrotic RA synovial fluid cells, and indicate that RNA released from necrotic cells might act as an endogenous TLR-3 ligand for the stimulation of proinflammatory gene expression in RASFs.

Arthritis, Rheumatoid↗
PubMedDate not supplied

[Complex-formation with hyaluronic acid as a cause of fibronectin heterogeneity in the synovial fluid].

Heterogeneity of synovial fluid fibronectin was studied by means of Laurell cross-immunoelectrophoresis in patients with rheumatoid arthritis, posttraumatic synovitis and other arthropathies. Prior to hyaluronidase treatment all the synovial fluid samples exhibited the fibronectin heterogeneity, which disappeared after the action of hyaluronidase. The data obtained suggest that complexes of fibronectin and hyaluronic acid are responsible for physico-chemical heterogeneity of fibronectin in synovial fluid.

Fibronectins↗