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Showing 2 results for Akbarian M

Akbarian M, Davachi F, Salim Zadeh A, Shahram F, Gharib Doost F, Tajy A H, Pajoohi M, Jamshidi Ar ,
Volume 60, Issue 4 (15 2002)
Abstract

Introduction: The bone mass density (BMD) may vary in different countries due to different genetic and environmental factors. This study was performed to determine the BMD of the normal population in Iran.

Methods and Materials: Subjects were selected randomly from different works and social classes in Tehran (from the lowest to the highest). For each decade and sexes, 20 normal subjects were selected (140 men and 140 women). BMD was measured with a Hologic 1000 plus machine by dual energy x-ray absorptiometry (DEXA) method for the lumber spine (L1, L2, L3, L4, L1-L4) and the femoral neck (neck, trochanter, intertrochanter, ward, total). Data were treated by polynomial approximation (3 rd degree). The obtained curves were compared with the standard Hologic curves for Caucasians.

Results: In female the peak bone mass (PBM) was 1.019 g/cm² for the lumbar spine and 0.832 for the femoral neck. In male the peak bone mass (PBM) was 0.987 g/cm² for the lumbar spine and 0.907 for the femoral neck. The BMD of both lumbar spine and femoral neck were lower than the Hologic standards. For the lumbar spine the mean difference was 6.5 percent (2 to 21 percent, CI=1) for women and 13.8 percent (2 to 36 percent, CI=1.45) for men. In femoral neck the mean difference was 5.4 percent (2 to 16 percent, CI=0.96) for women and 4.6 percent (1 to 14 percent, CI=0.96) for men.

Conclusion: The BMD of the lumbar spine and the femoral neck was lower in Iranian compared to the Hologic standards for Caucasians. This was seen in all age groups and in both sexes. It was less pronounced for the PBM in spine was lower in men than woman. The lower BMD of the spine in men was also seen in a cohort of patients with different diseases (inflammatory and non-inflammatory).


Gharibdoost F, Samadi F, Taghipoor R, Akbarian M, Shahram F, Nadji A, Jamshidi A R, Davatchi F,
Volume 65, Issue 7 (4 2007)
Abstract

Background: Heat-shock proteins are part of a strictly controlled biological system that allows organisms to respond to environmental stresses. Different proinflammatory cytokines are present in the synovial tissue of rheumatoid arthritis patients. Such tissues respond to stress and induce heat-shock proteins. In addition, synovial cells are exposed to mechanical stress caused by joint motion. The effects of mechanical stress on the metabolism of the synovial cells may be substantial, even pathogenic. Heat-shock proteins are often implicated in the pathogenesis of rheumatoid arthritis. Here, we compare the levels of heat-shock protein 70 from the synovial fluid of rheumatoid arthritis and osteoarthritis patients.

Methods: Synovial fluid samples from 34 rheumatoid arthritis patients and 34 osteoar-thritis patients were analyzed for heat-shock protein 70 by an ELISA method. Statistical analysis was performed using independent T-test and one-way ANOVA. Differences were considered statistically significant at p< 0.05.

Results: The mean value of synovial fluid heat-shock protein 70 levels in rheumatoid arthritis patients was 156.30 ±128.51 and that of osteoarthritis patients was 14.98 ±11.58. The differences were statistically significant at p<0.0001. For seven rheumatoid arthritis patients suffering from mechanical knee pain, synovial fluid analysis revealed non-inflammatory effusion. The mean value of synovial fluid heat-shock protein 70 level in inflammatory synovial fluid of rheumatoid arthritis patients was significantly higher at 191±121.73 and that of non-inflammatory synovial fluid from rheumatoid arthritis patients was 21.93 ±10.06 (p< 0.05).

Conclusion: The level of heat shock protein 70 is higher in inflammatory arthritis than in non-inflammatory arthritis. Considering that patients with rheumatoid arthritis are known to have a hypertrophic synovial-lining layer, and that heat-shock protein 70 is known to protect cells against a variety of toxic conditions as well as apoptotic death, further research is needed to determine if heat-shock protein 70 induction is a sign of significant changes in the cellular and tissue metabolism or is actively participating in the pathogenesis of rheumatoid arthritis.



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