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Träfflista för sökning "L773:1499 2752 OR L773:0315 162X srt2:(1990-1994)"

Sökning: L773:1499 2752 OR L773:0315 162X > (1990-1994)

  • Resultat 1-7 av 7
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1.
  • Elert, J, et al. (författare)
  • Muscle endurance, muscle tension and personality-traits in patients with muscle or joint pain - a pilot-study
  • 1993
  • Ingår i: Journal of Rheumatology. - 0315-162X .- 1499-2752. ; 20, s. 1550-1556
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective. To investigate the relationships between personality traits, depressive symptomatology and continuous muscle tension. Methods. These were investigated by means of a visual analog scale and the presence of continuous muscle tension during repeated isokinetic shoulder flexions in patients with muscle or joint pain and controls. Results. A significantly higher level of muscle tension between contractions was found in the patient groups in painful muscles. The patients with primary fibromyalgia and trapezius myalgia differed in degree of depressive symptomatology compared to controls. Conclusion. Inhibition of aggression correlated significantly with the tension level between contractions during the isokinetic test indicating interaction between psychological and somatic factors.
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2.
  • Maksymowych, WP, et al. (författare)
  • Polymorphism in an HLA linked proteasome gene influences phenotypic expression of disease in HLA-B27 positive individuals
  • 1994
  • Ingår i: Journal of Rheumatology. - 0315-162X .- 1499-2752. ; 21:4, s. 665-669
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To investigate the potential influence of the HLA-linked LMP (low molecular weight polypeptide) genes on disease susceptibility in HLA-B27 individuals with ankylosing spondylitis (AS).METHODS: A polymorphic CfoI restriction enzyme site in the coding region of one proteasome gene was evaluated in 125 genomic DNA samples from B27 individuals with well documented AS, 55 of whom had had acute iritis, and 42 samples from normal, ethnically matched B27 blood donors where AS was excluded.RESULTS: Analysis of individuals with B27 AS with iritis revealed significant differences in allelic distribution of this biallelic locus compared to patients with B27 AS without iritis. Furthermore, homozygosity for the disease associated allele was significantly more prevalent in patients with AS with iritis (72.7%) than in patients without iritis (38.6%) (p(uncorrected) = 0.0003) or B27 controls (45.2%) (p(uncorrected) = 0.01).CONCLUSION: Our findings support the involvement of additional HLA linked genes in the phenotypic expression of disease in B27 individuals and suggest a role for the non-B27 HLA haplotype in susceptibility to iritis.
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5.
  • Lohmander, L. S., et al. (författare)
  • Stromelysin, tissue inhibitor of metalloproteinases and proteoglycan fragments in human knee joint fluid after injury
  • 1993
  • Ingår i: Journal of Rheumatology. - 0315-162X. ; 20:8, s. 1362-1368
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective. To determine in a cross sectional study the concentrations of stromelysin, tissue inhibitor of metalloproteinases (TIMP), and proteoglycan fragments in knee synovial fluid (SF) at different times after injury to cruciate ligament or meniscus. Methods. Joint fluid samples were obtained from patients with knee injury diagnosed by arthroscopy. Concentrations of stromelysin-1 and TIMP-1 were determined by immunoassay with monoclonal and polyclonal antibodies. Cartilage proteoglycan fragments were quantified by immunoassay with polyclonal antibodies or by dye precipitation. Results. Average concentrations of stromelysin increased 40-fold in association with injury, and after about 6 months decreased to a plateau level about 10-fold increased compared to a reference group with healthy knees. TIMP and proteoglycan levels also increased in similar temporal patterns, but less markedly. Increased average SF levels of these markers were maintained for at least 17 years after injury. SF from knees with injury contained a 1.5 to 2.5 molar excess of stromelysin over TIMP, while reference joint fluids contained a 2-fold molar excess of TIMP over stromelysin. Conclusion. The persistent changes in SF markers after joint injury may be associated with the cartilage destruction and frequent development of posttraumatic osteoarthritis in this group of patients.
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  • Saxne, Tore, et al. (författare)
  • Plasminogen activators and plasminogen activator inhibitors in synovial fluid. Difference between inflammatory joint disorders and osteoarthritis
  • 1993
  • Ingår i: Journal of Rheumatology. - 0315-162X. ; 20:1, s. 91-96
  • Tidskriftsartikel (refereegranskat)abstract
    • The plasminogen activator (PA)/plasminogen activator inhibitor (PAI) system is believed to be involved in connective tissue remodelling in joint disease and both PA and PAI production has been shown in several cell types in the joint. We quantified immunoreactive PA and PAI in synovial fluid (SF) and correlated their levels to levels of cartilage derived proteoglycans, radiologically visible joint involvement and to signs of local inflammation. PAI-2 concentrations were increased, compared to normal plasma levels, in patients with rheumatoid arthritis (RA) and reactive arthritis, but not in patients with osteoarthritis (OA). Thirty percent of the patients with RA, but no patient with OA had increased concentrations of PAI-1. Increased concentrations of urokinase type PA (u-PA) were found in RA but not in OA. Tissue type PA (t-PA) concentrations were low in both disease groups. SF proteoglycan concentrations did not correlate with levels of PA or PAI. Concentrations of PAI-2 correlated significantly with SF leukocyte count and cytidine deaminase (CD) activity and u-PA concentrations correlated with CD activity. Both PAI-2 and u-PA were detected in supernatants from lysed polymorphonuclear cells. This suggests that in addition to release from synovial cells and chondrocytes these components may also be released from polymorphonuclear cells. Our results support a pathophysiological role for the fibrinolytic system in joint disease, possibly more pronounced in inflammatory disorders than in OA.
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