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    Atorvastatin reduced soluble receptors of tnf-alpha in systemic lupus erythematosus
    (Clinical & exper rheumatology, 2016) Ferreira, G. A.; Teixeira, A. L.; Calderaro, D. C.; Sato, E. I. [UNIFESP]
    Objective The aim of this study was to evaluate the efficacy of atorvastatin to reduce the plasma levels of TNF system molecules (TNF-alpha, sTNFR1 and sTNFR2) and to assess their association with risk factors for accelerate atherosclerosis and clinical disease activity scores in SLE patients. Methods In a previous study, 64 female SLE patients received 20 mg/day of atorvastatin and 24 SLE patients (non-treated group) were followed for 8 weeks. Plasma levels of TNF-alpha, sTNFR 1 and sTNFR 2 were measured by ELISA, at baseline and at the end of the study. Results The plasma levels of sTNFR1 and sTNFR 2 showed a positive correlation with SLEDAI score. We also found a positive correlation between TNF-alpha and sTNFR 1 levels and SLICC score. Patients with current nephritis and patients with anti-dsDNA antibodies presented higher sTNFR1 and sTNFR2 levels. Patients with abdominal obesity and arterial hypertension also had higher plasma levels of soluble receptors. At the end of 8 weeks, we observed a significant decrease in sTNFR1 plasma levels in patients receiving atorvastatin [median (percentile), 876.5 (717-1284 pg/ml) vs. 748 (629.6-917.3 pg/ml), p=0.03], without difference regarding TNF-alpha and sTNFR2 plasma levels. The SLEDAI and SLICC scores were independent determinants of the plasma levels of sRTNF1. Conclusion Atorvastatin reduced soluble receptors of TNF-alpha. The plasma levels of TNF-alpha, sTNFR1 and sTNFR2 may play a role in SLE activity and atherosclerosis, and might be evaluated as targets for new therapies.
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    Marcadores genéticos e auto-imunes do diabetes melito tipo 1: da teoria para a prática
    (Sociedade Brasileira de Endocrinologia e Metabologia, 2008-03-01) Silva, Maria Elizabeth Rossi da; Mory, Denise [UNIFESP]; Davini, Elaine; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    Type 1 A diabetes mellitus (T1AD) results from the autoimmune destruction of the insulin producing pancreatic beta-cells. The largest contribution to genetic susceptibility comes from several genes located in the major histocompatibility complex on chromosome 6p21.3 (IDDM1 locus), accounting for at least 40% of the family aggregation of this disease. The highest-risk human leukocyte antigen HLA genotype for T1AD is DR3-DQA1*0501-DQB1*0201/DR4-DQA1*0301-DQB1*0302, whereas -DR15-DQA1*0102-DQB1*0602 haplotype is associated with dominant protection. Three other T1D loci associated with predisposition are the Variable Number for Tandem Repeats (VNTR) near the insulin gene (IDDM2), which accounts to 10% of genetic susceptibility, the Cytotoxic T-Lymphocyte-associated Antigen (CTLA-4)(IDDM 12) and the Protein Tyrosine Phosphatasis Nonreceptor-type 22 (PTPN22). Many other gene suspected to predispose to autoimmunity have been investigated. T1AD is frequently associated with autoimmune thyroid disease, celiac disase, Addison´s disease and many other autoimmune diseases, characterized by organ-specific autoantibodies and related to the same genetic background. Using these autoantibodies, organ specific autoimmunity may be detected before the development of clinical disease preventing significant morbidity.
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    Multi-target detection of oxidative stress biomarkers in quercetin and myricetin treated human red blood cells
    (Royal soc chemistry, 2016) Maurya, Pawan Kumar [UNIFESP]; Kumar, Prabhanshu; Nagotu, Shirisha; Chand, Subhash; Chandra, Pranjal
    Quercetin and myricetin are important dietary flavonoids with potential health benefits and interfere with reactive oxygen species metabolism. The objective of this study was multi-target spectroscopic analysis of oxidative stress biomarkers (malondialdehyde (MDA), glutathione (GSH) and sulfhydryl (-SH) groups) in quercetin and myricetin treated red blood cells (RBCs) during human aging. The study was carried out on clinically relevant blood samples obtained from 105 healthy subjects between the ages of 18-82 years. The subjects were divided into three age groups, young (18-35 years), middle (36-60 years) and old (>60 years). Oxidative stress was induced in vitro by incubating RBCs with 10(-5) M tert-butyl hydroperoxide (t-BHP). The effects of flavonoids were evaluated by detecting MDA, GSH and -SH groups by co-incubating the RBCs in the presence of flavonoid (10(-8) M to 10(-5) M final concentration) and t-BHP. The GSH/GSSG ratios were estimated to demonstrate the antioxidant power of the RBCs. The results showed elevated MDA levels (p < 0.001) after incubation with t-BHP as compared to a control. The GSH and -SH groups significantly (p < 0.001) decreased when incubated with t-BHP. In vitro administration of both flavonoids significantly attenuated the deleterious effect of oxidative stress in erythrocytes from all age groups. We showed a significant (p < 0.0001) negative correlation (r = -0.8334) between GSH/GSSG during human aging. We believe that these findings are novel and will help in the fast screening of new chemical molecules which may help against oxidative stress in RBCs, and thereby have tremendous scope in medical diagnostics and therapeutics.