angial matrix expansion and type IV collagen accumulation in Effect of simvastatin on proliferative nephritis and cell-cycle glomeruli. Although it might simply reflect the reduction in protein expression.mesangial cells, glomerular PDGF-B chain expression was re-Background. Mesangial cell proliferation is important in duced. There was no significant difference in plasma lipids subsequent mesangial matrix expansion in glomerular injury. levels at day 2 and day 4. In vehicle-treated GN rats, the Therefore, the regulation of mesangial cell proliferation may number of CDK2ϩ/OX-7ϩ cells (CDK2-expressed mesangial be critical in the treatment of glomerulonephritis. Inhibition of cells) in glomeruli increased significantly from day 4 to day 7.
3-hydro-3-methylglutaryl coenzyme A (HMG-CoA) reductaseAlthough simvastatin suppressed mesangial cell proliferation, inhibits the production of mevalonate and has been shown to the increase in the number of glomerular CDK2ϩ/OX-7ϩ cells suppress proliferation in many cell types, including mesangial was also attenuated by simvastatin treatment. There was no cells in vitro. It is expected that HMG-CoA reductase inhibitor difference in the number of p27Kip1ϩ/OX-7ϩ cells (p27Kip1may suppress mesangial cell proliferation and subsequent proexpressed mesangial cells) in the glomerulus between vehiclegression of glomerulonephritis. Recently, the tight relationship treated and simvastatin-treated GN rats. between cell-cycle regulatory protein expression and mesangial Conclusion. Simvastatin suppressed mesangial cell proliferacell proliferation in experimental glomerulonephritis was demtion and subsequent matrix expansion, and macrophage infilonstrated. The aim of the present study is to examine the effect tration into glomeruli in anti-Thy 1.1 GN rats. The antiproliferof simvastatin, one of the HMG-CoA reductase inhibitors, on ative effect of simvastatin in this model was also associated the glomerular cell proliferation and on the expression of with the reduction of CDK2 expression in mesangial cells. CDK2 or p27Kip1 in mesangial cells in experimental glomerulonephritis in vivo.Methods. The effect of simvastatin on a rat mesangial proliferative glomerulonephritis induced by antithymocyte antibody Mesangial cell proliferation and accumulation of mes-(anti-Thy 1.1 GN) was studied. Administration of simvastatin angial extracellular matrix protein are central histologic or vehicle (for control GN) were started from two days before feature in most of progressive glomerular diseases. These disease induction, and was continued to the day of nephrecprocess may precede the development of glomeruloscletomy. Nephrectomy was done at days 0, 2, 4, 7, 12 and 20 after disease induction. Immunohistochemistry for proliferating cells, rosis that is characterized by an increased amount of macrophages, ␣-smooth muscle actin, type IV collagen and extracellular matrix and represents a progressive obliter-PDGF-B chain was performed, respectively, in addition to ative process. Recent experimental studies demonstr...
Rheumatoid factor and anti-cyclic citrullinated peptides were found in a high proportion of patients with palindromic rheumatism. The clinical features of the disease in our study were different in rheumatoid factor and anti-cyclic citrullinated peptide positive and negative patients.
Bcl-2 may account in part for the maintenance of hypercellularity in human glomerular diseases through preventing cell death and by counteracting bax which may be expressed to regulate excessive proliferation. This process is associated with the effect of PDGF B-chain expression. Bax expression may be important in the cell loss leading to glomerulosclerosis and TGF-beta1 participates in this process by increasing bax expression. Thus, the balance of bcl-2/bax expression may be critical in the course of human glomerular diseases.
Aim:To determine the frequency of anti-cyclic citrullinated peptide antibody (anti-CCP) in a group of patients with rheumatoid arthritis and another group with other rheumatic diseases.
Patients and methods:Anti-CCP1 and rheumatoid factor (RF) titres were determined in 320 serum samples; 136 from RA patients, 184 from control patients (165 patients with rheumatic diseases other than RA, and 21 patients with lymphoproliferative diseases).
Results:The sensitivity of Anti-CCP was 62.5% (95% CI: 53-70%) for the diagnosis of RA with a specificity of 89.1% (95% CI: 83-93%). The sensitivity of RF was 85.3% (95% CI: 79-91%). The specificity was 64.7% (95% CI: 57-71%).
Conclusions:Anti-CCP1 has not very high specificity for RA regarding other rheumatic disease. However it is still very helpful for the diagnosis of RA.
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