مقاله G-protein coupled-receptor 65 5´UTR gene polymorphism in the pathogenesis of systemic lupus erythematosus

توجه : به همراه فایل word این محصول فایل پاورپوینت (PowerPoint) و اسلاید های آن به صورت هدیه ارائه خواهد شد

 مقاله G-protein coupled-receptor 65 5´UTR gene polymorphism in the pathogenesis of systemic lupus erythematosus دارای ۸ صفحه می باشد و دارای تنظیمات در microsoft word می باشد و آماده پرینت یا چاپ است

فایل ورد مقاله G-protein coupled-receptor 65 5´UTR gene polymorphism in the pathogenesis of systemic lupus erythematosus  کاملا فرمت بندی و تنظیم شده در استاندارد دانشگاه  و مراکز دولتی می باشد.

توجه : در صورت  مشاهده  بهم ریختگی احتمالی در متون زیر ،دلیل ان کپی کردن این مطالب از داخل فایل ورد می باشد و در فایل اصلی مقاله G-protein coupled-receptor 65 5´UTR gene polymorphism in the pathogenesis of systemic lupus erythematosus،به هیچ وجه بهم ریختگی وجود ندارد

بخشی از متن مقاله G-protein coupled-receptor 65 5´UTR gene polymorphism in the pathogenesis of systemic lupus erythematosus :

سال انتشار : ۲۰۱۷

تعداد صفحات :۸

Systemic lupus erythematosus (SLE) is a complex autoimmune disease with unknown etiology. G-protein-coupled receptor 65 (GPR65) candidates as an SLE-locus for functioning in T cell receptor-mediated self-reactive T cell death in the thymus. This is also involved in anti-inflammatory actions and apoptosis as remarkable features of autoimmune diseases. This study investigated the relationship between the rs10139328 polymorphism at the 5´UTR of a GPR65 gene and SLE. This case-control study consisted of 102 SLE patients (98 females, 4 males) and 118 age- and gender-matched healthy controls (113 females, 5 males). Genotyping of the rs10139328 polymorphism was determined using an amplification refractory mutation system-polymerase chain reaction (ARMS-PCR). Data was analyzed using SPSS software. The Pearson chi-square was the test of choice for assessing the association between the rs10139328 polymorphism and SLE. The probable influences of sunlight and family history on SLE were evaluated by performing logistic regression. Except for one heterozygote subject among the control group, the study population was homozygote for the selected polymorphism. No statistical difference was seen in genotype distribution between the cases and the controls (P> 0.05). Statistical analysis revealed that sun exposure directly increased SLE susceptibility (P < 0.001). Having a family history of SLE increased the risk of disease occurrence by more than two times (OR = 2.38, 95% CI: 1.28 – 4.41, P= 0.006). The results of the current study do not support the importance of the studied polymorphism in a GPR65 gene in the pathogenesis of SLE among southwestern Iranian patients.