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  • Acute pyrophosphate arthropathy  (1)
  • Growth factors  (1)
  • Histogenesis  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Leukaemia inhibitory factor stimulates proteoglycan resorption in porcine articular cartilage (1993)
    Springer
    Rheumatology international 13 (1993), S. 5-8 
    Details
    ISSN: 1437-160X
    Keywords: Arthritis ; Cytokines ; Chondrocytes ; Growth factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Leukaemia inhibitory factor (LIF) is a secretory glycoprotein produced by tumour, mesenchymal and haemopoietic cells. LIF has been found to have pleiotropic actions that include the capacity to regulate cell differentiation, promote acute-phase protein synthesis and stimulate calcium release in bone explants. In view of its similarity to other cytokines that affect cartilage metabolism, the effects of LIF on proteoglycan resorption were examined in pig cartilage explants. Endotoxinfree recombinant mouse LIF was found to produce a dose-dependent increase in sulphated glycosaminoglycan (S-GAG) release (ED50=123 U/ml, approx. 25–50 pM). Statistically significant stimulation was observed with doses of 100 U/ml or greater. When pig cartilage was stimulated with maximum concentrations of LIF and either interleukin 1α (IL-1α), interleukin 1β (IL-1β) or tumour necrosis factor α (TNFα), in each case a significantly greater release of S-GAGs was observed than with the respective cytokines alone (P〈0.05). Comparison of the areas under the curves showed that the action of LIF was additive, and not synergistic with other catabolic cytokines. Dose-response studies showed that transforming growth factor β (TGFβ) produced a partial inhibition of LIF-stimulated release of S-GAGs (ED50=4.5 U/ml). Statistically significant inhibition was observed with doses of 2U/ml or greater. These results showed that LIF stimulated proteoglycan resorption in vitro and that this effect was modulated by other cytokines. Whether LIF contributes to the progressive destruction of cartilage in septic or chronic inflammatory arthritis remains to be determined.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00290327
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Comparison of keratan sulphate concentrations and the size distribution of proteoglycans in the synovial fluid of patients with osteoarthritis and pyrophosphate arthropathy (1991)
    Springer
    Rheumatology international 11 (1991), S. 63-68 
    Details
    ISSN: 1437-160X
    Keywords: Keratan sulphate ; Proteoglycans ; Osteoarthritis ; Chronic pyrophosphate arthropathy ; Acute pyrophosphate arthropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to evaluate the effect of calcium pyrophosphate dihydrate (CPPD) deposition on articular cartilage catabolism, the proteoglycans released into normal synovial fluid were compared with those in synovial fluid obtained from patients with osteoarthritis (OA), chronic pyrophosphate arthropathy (CPA) and acute pyrophosphate arthropathy (APA). Keratan sulphate (KS) was measured by the modified 1,9-dimethylmethylene blue (DMB) assay in synovial fluids treated with chondroitin ABC lyase. This enzyme was found to eliminate all of the sulphated glycosaminoglycans in synovial fluid except KS. In OA, CPA and APA the concentrations of KS were found to be significantly higher than in normal synovial fluid (NSF) (P〈0.01). Similar KS concentrations were observed in CPA and APA. In CPA they were significantly higher than in OA (P〈0.02). The size distribution of proteoglycan fragments varied between different patients with the same disease, but only minor differences were observed in patients with OA and CPA who were matched for age, sex and disease severity. Furthermore, the size distribution of proteoglycan fragments in the acute and chronic phases of pyrophosphate arthritis was similar. Thus although in pyrophosphate arthritis the rate at which proteoglycans are released from the cartilage may be greater than in OA or normal joints, the fundamental processes governing the release of these macromolecules may be the same.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00291147
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Localized fibrous tumour of serosal surfaces (1986)
    Springer
    Virchows Archiv 409 (1986), S. 349-363 
    Details
    ISSN: 1432-2307
    Keywords: Mesothelioma ; Serous membrane ; Localized tumour ; Histogenesis ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is uncertain whether localized lesions of serosal membranes have a kinship to mesotheliomas or are truly fibromatous in nature. Ultrastructural and immunohistochemical investigations were carried out on 12 localized benign and malignant pleural and peritoneal tumours from 10 patients. Electron microscopic findings, including the consistent and non-fibroblastic cellular organization of localized neoplasms, the presence of some form of intercellular junctions in 7 of 10 cases, basal lamina deposition in 3 cases, and polarized microvilli in one case indicated a form of mesothelial differentiation. Using monoclonal and polyclonal antibodies, positive immunostaining of tumour cells for cytokeratin peptides was detected in one case, while antibody to vimentin stained four cases. Light microscopic, ultrastructural and immunohistochemical features of one benign localized serosal tumour, with a unique blend of epithelial and spindle cells, provided further evidence for a histogenic link between localized serosal tumours and diffuse epithelial mesotheliomas. On the basis of the current findings and reports in the literature, it would appear that the majority of localized tumours of serosal membranes are a subset of mesothelioma, while a minority are fibromas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00708252
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    Paper (German National Licenses)
    Fulltext
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