توجه: محتویات این صفحه به صورت خودکار پردازش شده و مقاله‌های نویسندگانی با تشابه اسمی، همگی در بخش یکسان نمایش داده می‌شوند.
۱Uremia Effect on White Blood Cell Count in Patients with Renal Failure
اطلاعات انتشار: International Journal of Medical Laboratory، دوم،شماره۱، ۲۰۱۵، سال
تعداد صفحات: ۴
Introduction: It is believed that uremia causes destruction of white blood cells (WBC) and thus causes leukopenia. Therefore this study had an attempt to assess the effect of uremia on WBC count. Materials and Methods: This case control study was conducted on 120 uremic patients and 100 samples as control group. All samples were examined for determination of urea and creatinine in their serum and complete blood counts were determined. Results and Conclusion: In healthy individuals, the mean value of urea was 14.5±1.9 mg\dL and the mean value of creatinine was 0.9±0.2 mg\dL (male) and 0.66±3.2 mg\dL (female). In the patient group, the mean value of urea was 83±2.4 mg\dL. The mean value of creatinin in male and female were 2.4±1.3 mg\dL and 2.1±1.7 mg\dL respectively. The mean of WBC count in case and control groups were 6.08± 2.24 and 6.17± 2.43x109\L respectively (p=0.71). Our results indicate that uremia cannot change leukocyte count.

۲Association of miR–132 and miR–185 Genes Methylation and their Expression Profile with Risk of Congenital Factor XIII Deficiency
اطلاعات انتشار: Journal of Cell and Molecular Research، هفتم،شماره۱، ۲۰۱۵، سال
تعداد صفحات: ۷
Congenital factor XIII deficiency is a very rare bleeding disorder, but because of the high rate of consanguineous marriages, it is common in Sistan and Baluchestan Province of Iran. The discovery of promoter hypermethylation of numerous miRNAs in human diseases has demonstrated an epigenetic mechanism for aberrant miRNA expression. The present study has analyzed methylation and expression status of miR–185 and miR–132 genes in patients with inherited factor XIII deficiency in a sample of South–Eastern Iranian population. Promoter methylation of miR–185 and miR–132 was investigated by Methylation Specific Polymerase Chain Reaction (MS PCR) in blood samples of 75 factor XIII deficient individuals and 74 healthy controls. Expression level of these genes was also assessed in 15 blood samples of patients and 15 healthy controls using real–time quantitative reverse transcription PCR. Analysis of miR–132 and miR–185 promoter hypermethylation did not show any significant difference between cases and controls. Relative gene expression analysis in cases (n=15) with congenital factor XIII deficiency and healthy controls (n=15) revealed no statistically significant relationship for miR–132 (p = 0.126) and miR–185 (p = 0.165) genes. Our findings indicated that promoter methylation as well as gene expression of miR–132 and miR–185 had no significant effect on etiology of factor XIII deficiency.
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