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Results for “JOINT DISEASES”

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At least 1,477 records · Page 82Linked to original sources
PubMed2003

Estrogens reduce the expression of YKL-40 in the retina: implications for eye and joint diseases.

PURPOSE: To identify modifications in the gene expression profile of the ocular posterior segment in ovariectomized (OVX) mice with and without substitutive estradiol therapy and to select differentially expressed genes that could be relevant to the natural history of human age-related macular degeneration (AMD). METHODS: Chorioretinal tissues from two groups of 25 treated and untreated OVX mice were analyzed by using cDNA array technology. The expression level of selected genes was confirmed in triplicate by RT-PCR and related to the estrogenic status of the animals. Expression of the YKL-40 gene was further investigated in intact or diseased human retinas and in a murine model of experimental choroidal neovascularization (CNV), using laser pressure catapulting. RESULTS: Of the approximately 10,000 genes screened, only YKL-40 expression was significantly downregulated by 17-beta-estradiol. YKL-40 was expressed in intact human neural retina and in the RPE. The expression of YKL-40 was upregulated in experimental CNV and in neovascular membranes extracted from patients affected by the exudative form of AMD. CONCLUSIONS: These observations indicate that YKL-40 expression in the retina is modulated by serum levels of estradiol. This protein could be relevant to the development of AMD and is also a new mediator to take into account when evaluating the broad consequences of hormonal replacement therapy.

Adipokines↗
PubMed2004

JNK1 is not essential for TNF-mediated joint disease.

Tumour necrosis factor (TNF) signalling molecules are considered as promising therapeutic targets of antirheumatic therapy. Among them, mitogen-activated protein kinases are thought to be of central importance. Herein, we investigate the role in vivo of TNF-alpha signalling through c-Jun N-terminal kinase (JNK)1 in destructive arthritis. Human TNF transgenic (hTNFtg) mice, which develop inflammatory arthritis, were intercrossed with JNK1-deficient (JNK1-/-) mice. Animals (n = 35) of all four genotypes (wild-type, JNK1-/-, hTNFtg, JNK1-/-hTNFtg) were assessed for clinical and histological signs of arthritis. Clinical features of arthritis (swelling and decreased grip strength) developed equally in hTNFtg and JNK1-/-hTNFtg mice. Histological analyses revealed no differences in the quantity of synovial inflammation and bone erosions or in the cellular composition of the synovial infiltrate. Bone destruction and osteoclast formation were observed to a similar degree in hTNFtg and JNK1-/-hTNFtg animals. Moreover, cartilage damage, as indicated by proteoglycan loss in the articular cartilage, was comparable in the two strains. Intact phosphorylation of JNK and c-Jun as well as expression of JNK2 in the synovial tissue of JNK1-/-hTNFtg mice suggests that signalling through JNK2 may compensate for the deficiency in JNK1. Thus, JNK1 activation does not seem to be essential for TNF-mediated arthritis.

Animals↗
PubMed2003

Adalimumab - a new TNF-alpha antibody for treatment of inflammatory joint disease.

Tumour necrosis factor alpha (TNF-alpha) is a pro-inflammatory cytokine with various roles in inflammatory processes. Several TNF blockers are currently approved for use in rheumatoid arthritis (RA) as well as in other inflammatory arthropathies. The latest of these compounds is the human monoclonal antibody, adalimumab, which was obtained using phage display technology and successfully produced in a mammalian expression system. Clinical application of this compound led to significant improvement in patients suffering from RA, both as monotherapy and in combination with various disease modifying antirheumatic drugs (DMARDs), including methotrexate (MTX). Moreover, radiographic progression is significantly inhibited and quality of life improved. This article summarises the available information.

Adalimumab↗
PubMed1987

Work capacity of patients with inflammatory joint diseases. An eight-year follow-up study.

In a prospective study of recent arthritis, 103 patients had rheumatoid arthritis (RA), 63 seronegative oligoarthritis (SO), 67 reactive arthritis (REA), 20 ankylosing spondylitis (AS), and 13 psoriatic arthritis (PA). At the 8-year check-up, 36% of patients with RA were at work, compared with 69% in PA (p less than 0.002), and 85-90% in AS, SO, and REA (p less than 0.001). Correspondingly 43% of the RA patients were disabled by arthritis, compared with 23% in PA (NS), 15% in AS (p less than 0.005), none in SO, and 4% in REA (p less than 0.001). No significant differences in work capacity were noted between patients with PA, AS, SO or REA. In RA, the educational backgrounds of patients unable to work (44 patients) and able to work (37 patients) did not differ from each other or from the overall population of Finland, but a significantly (p less than 0.01) smaller number of patients with arduous work were able to continue at work. The mean age of 49 years for RA patients unable to work differed highly significantly (p less than 0.001) from the 35 years of RA patients at work. However, the weightiest cause of limited work capacity was severity of disease.

Adult↗
PubMed1988

The major leukocyte protein L1 as an indicator of inflammatory joint disease.

L1 is a major protein in granulocytes and monocytes. It is released during activation of these cells, and the plasma level of L1 is therefore thought to reflect the turnover of leukocytes. Peripheral blood from 96 patients hospitalized in a rheumatological department, was analysed for L1, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). The total patient material was divided into groups depending on diagnosis: 47 patients with rheumatoid arthritis, 27 patients with arthritis of different etiologies, 15 patients with non-inflammatory diseases and 7 patients with arteritis. Correlation analysis were made between the different laboratory parameters. A high positive correlation was found between L1 and CRP in all the groups, and with a correlation coefficient of the total patient material of 0.68 (p less than 0.001). The correlation coefficient between L1 and ESR was 0.54 (p less than 0.001) in the total patient material, and between CRP and ESR it was 0.66 (p less than 0.001). The results indicate that the L1 protein could be a new laboratory marker of inflammation in rheumatic diseases.

Antigens, Surface↗