Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The binding specificity of 16 sera from systemic lupus erythematosus (SLE) patients was studied by enzyme-linked immunosorbent assay (ELISA), using 4 native DNAs of different guanine-cytosine (G-C) content and a group of synthetic polynucleotides. All the SLE sera showed increased binding to poly(dA-dC).poly(dG-dT), compared with calf thymus DNA in the right-handed B conformation. No significant differences were noted in binding of selected SLE sera to the native DNAs that differed in G-C content or superhelicity of DNA. With poly(dG-dC).poly(dG-dC) and poly(dG-m5dC).poly(dG-m5dC), the majority of SLE sera showed a preferential binding to the salt-induced Z form, compared with the B form. In addition, an average twelve-fold increase was found in binding to Z-form brominated poly(dG-dC).poly(dG-dC) compared with B-form poly(dG-dC).poly(dG-dC), when the polymers were coated on the plates in 0.15M NaCl. The preferential binding of SLE sera to poly(dA-dC).poly(dG-dT) and to Z-DNA may be important in the formation of circulating immune complexes and subsequent vascular damage, or may provide a clue to the mechanism of production of anti-DNA antibodies in this disease.
Arthritis Rheum 1988 Mar
PMID:DNA sequence and conformation specificity of lupus autoantibodies. Preferential binding to the left-handed Z-DNA form of synthetic polynucleotides. 335

Five drugs associated with systemic lupus erythematosus were studied for their effect on the salt-induced right-handed (B) to left-handed (Z) transition of poly(dG-me5dC) X poly(dG-me5dC). Using circular dichroism spectroscopy, procainamide and hydralazine were found to reduce the midpoint of B to Z transition from 0.8M NaCl to 0.5M NaCl and to increase the rate of this transition at 1M NaCl. Isoniazid and D-penicillamine had less effect on the midpoint of transition and practically no effect on the kinetics. N-acetyl procainamide (a structurally related control for procainamide) and L-canavanine had no effect. Procainamide caused slight reduction in the helix-coil transition (melting) temperature of calf thymus DNA. At a concentration of 1:1 (DNA phosphate:drug ratio), procainamide and hydralazine also caused the aggregation of calf thymus DNA. Since altered DNA conformations, such as Z-DNA, are more immunogenic, these results suggest that the induction or stabilization of Z-DNA by these drugs might be important in the pathogenesis of at least some cases of systemic lupus erythematosus.
Arthritis Rheum 1986 May
PMID:Effects of lupus-inducing drugs on the B to Z transition of synthetic DNA. 371 55

The purpose of this study was to test whether cartilage serves as the source or repository of antigenic components active in the stimulation of inflammation in rheumatoid arthritis through an analysis of peripheral blood lymphocyte proliferation. Articular cartilage samples were obtained from patients with osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis undergoing joint replacement surgery. Each sample was homogenized and characterized biochemically with respect to the content of proteoglycan, collagen, and immunoglobulin. Proteoglycan content of rheumatoid cartilage was reduced by 71% when compared to osteoarthritic cartilage; the proteoglycan content of ankylosing spondylitis cartilage was reduced by 40% when compared to osteoarthritic cartilage. Immunoglobulins were detectable in all cartilage samples when analyzed by ELISA or end-plate titration. Lymphocyte proliferation, quantified by uptake of 3H-thymidine, was unaltered by addition of cartilage fragments, low (saline) and high salt extracts (2.0 M CaCl2), or cartilage residues. Both autologous and heterologous lymphocytes were tested against the cartilage samples with no difference in reactivity. Purified bovine articular proteoglycans and Type II collagen were also inactive. Although tetanus toxoid and phytohemagglutinin were effective stimulants of proliferation, lymphocytes from arthritis patients were suppressed relative to those of normal individuals. Analysis of arthritic articular cartilage by these techniques failed to demonstrate the presence of antigen(s) stimulating proliferation of peripheral blood lymphocytes.
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PMID:Biochemistry and antigenicity of osteoarthritic and rheumatoid cartilage. 373 34

The use of unfixed and undecalcified cryostat sections of mouse knee joints is described for the study of enzyme histochemical reactions. Non-inflamed knee joints and knee joints of mice with antigen induced arthritis have been used. Joints were embedded in gelatin and subsequently cut at low speed with a motor-driven cryostat fitted with a tungsten carbide knife at an obtuse angle (10 degrees). The sections were attached to transparent tape to keep the integrity of the tissue intact. The following histochemical reactions were carried out successfully: the tetrazolium salt reaction for dehydrogenase and reductase activity, the post-azo-coupling method for acid phosphatase and cathepsin B activity and the simultaneous azo-coupling method for esterase activity. In all cases the morphology and integrity of the sections were well kept and serial sections were obtained without any difficulty. Nonspecific staining of the tape did not occur. The localization of the final reaction product was meeting criteria for specific and precise histochemical methods with the exception of the metal salt method because of nonspecific staining of undecalcified bone. Cytophotometry of the final reaction product appeared to be reproducible and valid as demonstrated by reaction for glucose-6-phosphate dehydrogenase activity in synoviocytes from knee joints with induced arthritis. End point measurements as well as kinetic measurements of the formazan production were performed and linear relationships were found between the specific formazan formation and section thickness or incubation time, respectively. It is concluded that cryostat sections attached to transparent tape are an excellent tool for the study of the metabolism in tissues adjacent to bone matrix.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enzyme histochemical reactions in unfixed and undecalcified cryostat sections of mouse knee joints with special reference to arthritic lesions. 381 56

One hundred fourteen patients with definite or classic rheumatoid arthritis were followed prospectively between January 1976 and April 1981 to monitor their toxicity pattern to D-penicillamine. The influence of previous sodium aurothiomalate therapy on the toxicity pattern of D-penicillamine is described. There was no significant difference in overall outcome of the patients treated with D-penicillamine with respect to adverse effects, whether they had previous gold toxicity, previous gold therapy but no toxicity, or no previous gold therapy. The time from gold toxicity to the start of D-penicillamine therapy was greater in those who did not develop D-penicillamine toxicity compared with those who did. This difference just reached statistical significance. Total gold salt received had no effect on eventual outcome of D-penicillamine treatment, and the toxicity pattern of D-penicillamine in those patients who had previous gold therapy was similar to those patients who had never received gold therapy.
Arthritis Rheum 1982 Aug
PMID:Prior gold therapy does not influence the adverse effects of D-penicillamine in rheumatoid arthritis. 621 61

In inflammatory rheumatism treated by gold therapy synoviocytes A are stuffed with gold salt deposits leading to a therapeutic thesaurismosis. These deposits are localized in lysosomes, then called aurosomes. However they may be rarely near collagen fibers or free, particularly in ankylosing spondylitis synovitis. Their structural morphological aspect is the same in several human rheumatic diseases and in rabbit experimental arthritis whatever the gold salt used. In such deposits, microprobe analysis shows gold and sulphur. This latter is probably given by the cell. Therapeutic effect of gold salts may imply the effect of the thiol moiety and the gold metal one.
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PMID:[Ultrastructural and microanalytic study of gold depots in the synovial membrane of man and animals during treatment with sodium aurothiopropanol sulfonate]. 645 70

Incorporation of radioactive precursors into macromolecules was studied with human normal and osteoarthritic articular cartilage organ culture. Analysis of the salt extracted matrix components separated by cesium chloride buoyant density gradient centrifugation showed an increase in the specific activities of all gradient fractions prepared from the osteoarthritic cartilage. Further analysis of these fractions showed the osteoarthritic cartilage contained 5 times as much sulfate incorporated into proteoglycans, and an even greater amount of 3H-glucosamine incorporated into material sedimenting to the middle of the gradient. Greater than half of this radioactive middle fraction appears to be hyaluronate, as judged by the position it elutes from a DEAE column and its susceptibility to hyaluronidase digestion. This study supports earlier findings showing increased rates of macromolecular synthesis in osteoarthritis, and in addition, an even greater synthetic rate for hyaluronic acid is demonstrated.
Arthritis Rheum 1984 Jan
PMID:Biochemical and metabolic abnormalities in normal and osteoarthritic human articular cartilage. 669 59

The ability of gold sodium thiomalate to inhibit production of the second complement component (C2) by monocytes stimulated by a lymphokine (monocyte complement stimulator is demonstrated. This gold salt inhibits C2 production irreversibly if monocytes are incubated with it before or during lymphokine stimulation. Thiomalic acid is not inhibitory. Monocytes already stimulated by lymphokine are resistant to inhibition of C2 production by gold sodium thiomalate. Gold salts do not reduce monocyte viability, phagocytic ability (latex heads) accessory cell function (as measured by the ability to present antigen to autologous lymphocytes), or capacity to act as stimulating cells in mixed leukocyte culture. Gold sodium thiomalate's inhibition of monocyte responsiveness to lymphokine may be significant in explaining the therapeutic benefit of gold salts in rheumatoid arthritis.
Arthritis Rheum 1982 Mar
PMID:Gold inhibition of the production of the second complement component by lymphokine-stimulated human monocytes. 680 42

In rats with adjuvant-induced arthritis, the effect of (+)-catechin (CA) and 0-(beta-hydroxyethyl) rutosides (HR) on the crosslinking of collagen was studied. Compared with controls the arthritic group showed an increase in the reversibility of neutral salt-soluble collagen gel, solubility of acid-insoluble collagen to denaturing agents and the ratio of alpha/beta subunits of neutral salt-soluble collagen. These results suggest an impaired maturation of collagen in arthritic animals. Administration of CA or HR to the arthritic animals caused a decrease in the reversibility of collagen gel and in the solubility of acid-insoluble collagen to denaturing agents and to pronase. In addition, the electrophoretic patterns of neutral salt-soluble collagen on SDS polyacrylamide gels also showed a decrease in the alpha/beta ratio. All these results may collectively indicate that both flavonoids promote the crosslinking of collagen in arthritic animals.
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PMID:Bioflavonoid-mediated stabilization of collagen in adjuvant-induced arthritis. 683 39

Fisher rats from a inbred colony, when fed on a salt-free high-protein diet, developed only a mild arthritis after adjuvant injection. Their spleen cells failed to respond in vitro to concanavalin A (a T-cell mitogen), although they possessed a B-cell function of plaque formation to sheep red blood cells. When a full salt supplement was included in the diet, or magnesium or copper or zinc was included in the drinking water, adjuvant-induced arthritis was severe and the response to the T-cell mitogen was restored. The above results suggest that these trace elements may stabilize or activate certain cell populations needed for some immune responses in rats.
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PMID:Effect of diet on adjuvant-induced disease and mitogenic responses of Fisher rats. 686 67


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