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本文引用的文献

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Age-related changes in the structure of the proteoglycan subunits from human articular cartilage.人类关节软骨蛋白聚糖亚基结构的年龄相关性变化。
J Biol Chem. 1980 Jan 10;255(1):217-24.
2
Identification of core protein, an intermediate in proteoglycan biosynthesis in cultured chondrocytes from the Swarm rat chondrosarcoma.核心蛋白的鉴定,其为来自斯旺大鼠软骨肉瘤的培养软骨细胞中蛋白聚糖生物合成的一种中间体。
J Biol Chem. 1981 Aug 10;256(15):7890-7.
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Glycosaminoglycans produced by human synovial cell cultures.人滑膜细胞培养物产生的糖胺聚糖。
Coll Relat Res. 1982 Jul;2(4):313-29. doi: 10.1016/s0174-173x(82)80023-x.
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Radioimmunoassay of proteoglycans.蛋白聚糖的放射免疫测定
J Immunoassay. 1984;5(3-4):221-43. doi: 10.1080/01971528408063009.
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Evidence for an interaction between canine synovial cell proteoglycans and link proteins.
Biochim Biophys Acta. 1985 Dec 13;843(3):238-44. doi: 10.1016/0304-4165(85)90144-8.
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Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association.骨关节炎分类及报告标准的制定。膝关节骨关节炎的分类。美国风湿病协会诊断与治疗标准委员会。
Arthritis Rheum. 1986 Aug;29(8):1039-49. doi: 10.1002/art.1780290816.
7
Therapeutic effects on cartilage metabolism in arthritis as measured by release of proteoglycan structures into the synovial fluid.通过蛋白聚糖结构释放到滑液中所衡量的对关节炎软骨代谢的治疗效果。
Ann Rheum Dis. 1986 Jun;45(6):491-7. doi: 10.1136/ard.45.6.491.
8
Cartilage proteoglycans in synovial fluid and serum in patients with inflammatory joint disease. Relation to systemic treatment.炎症性关节病患者滑液和血清中的软骨蛋白聚糖。与全身治疗的关系。
Arthritis Rheum. 1987 Sep;30(9):972-9. doi: 10.1002/art.1780300903.
9
Spectrophotometric measurement of proteoglycans in osteoarthritic synovial fluid.骨关节炎滑液中蛋白聚糖的分光光度法测量
Ann Rheum Dis. 1987 May;46(5):375-9. doi: 10.1136/ard.46.5.375.
10
The role of cytokines in arthritic diseases: in vitro and in vivo measurements of cartilage degradation.细胞因子在关节炎疾病中的作用:软骨降解的体外和体内测量
Int J Tissue React. 1987;9(4):349-54.

关节炎性滑液中硫酸化糖胺聚糖和蛋白聚糖片段的测量

Measurement of sulphated glycosaminoglycans and proteoglycan fragments in arthritic synovial fluid.

作者信息

Carroll G

机构信息

Department of Rheumatic Diseases, Royal Perth (Rehabilitation) Hospital, Shenton Park, Western Australia.

出版信息

Ann Rheum Dis. 1989 Jan;48(1):17-24. doi: 10.1136/ard.48.1.17.

DOI:10.1136/ard.48.1.17
PMID:2923503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1003669/
Abstract

Immunoreactive proteoglycans (iPGs) and sulphated glycosaminoglycans (GAGs) were assayed in synovial fluid obtained from 22 patients with osteoarthritis (OA), 21 with rheumatoid arthritis (RA), 13 with gout, and five with Reiter's syndrome. A strong positive linear correlation was observed between concentrations of sulphated GAGs and iPGs in RA (r = 0.95) and gout (r = 0.94). A linear correlation was also observed in OA (r = 0.65). Patients with gout and Reiter's syndrome had significantly higher concentrations of sulphated GAGs and iPGs than patients with OA or RA. Patients with gout also had significantly higher total quantities of sulphated GAGs and iPGs in the knee joint cavity than patients with OA or RA. In all four diseases similar profiles were observed when comparisons were made between the total quantities and concentrations of sulphated GAGs and iPGs in synovial fluid. These results indicate that the observed differences in concentrations are not simply a function of dilution. The concentrations of sulphated GAGs and iPGs did not correlate closely with the type or number of inflammatory cells in the synovial fluid. Considerable variation was noted in the sulphated GAG/iPG ratios, suggesting that different mechanisms may be contributing to the release of proteoglycans in the diseases studied.

摘要

对22例骨关节炎(OA)患者、21例类风湿关节炎(RA)患者、13例痛风患者和5例赖特综合征患者的滑液进行了免疫反应性蛋白聚糖(iPGs)和硫酸化糖胺聚糖(GAGs)检测。在RA患者(r = 0.95)和痛风患者(r = 0.94)中,硫酸化GAGs和iPGs的浓度之间观察到强正线性相关性。在OA患者中也观察到线性相关性(r = 0.65)。痛风患者和赖特综合征患者的硫酸化GAGs和iPGs浓度显著高于OA或RA患者。痛风患者膝关节腔中硫酸化GAGs和iPGs的总量也显著高于OA或RA患者。在所有四种疾病中,当比较滑液中硫酸化GAGs和iPGs的总量与浓度时,观察到相似的分布情况。这些结果表明,观察到的浓度差异并非仅仅是稀释作用的结果。硫酸化GAGs和iPGs的浓度与滑液中炎症细胞的类型或数量没有密切相关性。硫酸化GAG/iPG比值存在相当大的差异,这表明在研究的疾病中,可能有不同的机制导致蛋白聚糖的释放。