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Dr Mehrnoosh Shanaki, Dr Hassan Ehteram, Ms Hajar Nasiri, Dr Mehdi Azad, Dr Fatemeh Kouhkan, Dr Reza Pakzad , Dr Naser Mobarra,
Volume 6, Issue 4 (11-2016)
Abstract

Abstract
Background:

Thalassemias are the most common inherited blood disorders caused by some mutations which can reduce the synthesis of globin chains. Iron overload and its organ deposition are responsible for functional abnormalities and tissue injury in patients who affected by β-thalassemia major. The aim of this case-control study was evaluation of hematological parameters, oxidative stress and some serum liver and kidney risk factors which play crucial role for early prediction and prevention of patients to end-stage tissue failure and mortality.
Materials and Methods:

the present study consisted of Fifty young adult subjects with β-thalassemia major (β- TM) (aged<18 years) and same number age and sex- matched healthy subjects as control group. Hematological and biochemical laboratory parameters included Urea, Creatinine, Uric Acid, Aspartate Aminotransferase (AST), Alanine transaminase (ALT), Alkaline phosphatase (ALP) (pars azmoon kit), oxidative stress biomarker PAB, giving a redox index (chemically), and serum high-sensitivity C-reactive protein (hs-CRP) were evaluated.
Results:

Urea, Creatinine and Uric Acid were significantly decreased in patients group (P<0.001); in spite of, serum ferritin, liver biomarkers AST, ALT, ALP and risk factor biomarker PAB were statistically increased in patients versus control group(P<0.001), whereas hs-CRP(P>0.05) was not significantly difference in study groups. Exception hs-CRP and PAB (P>0.05), liver risk factors had a positive correlation with ferritin and serum Urea, Creatinine and Uric Acid tests had negative meaningful with hematological parameters (P<0.001). Likewise, PAB with AST showed a positive correlation (P<0.001) and irreversibly with urea and creatinine (P<0.001). We did not find a slight correlation between hs-CRP in the company to hematological and biochemical laboratory finding (P>0.05).

Conclusion:

Higher level of risk factors PAB values and key liver enzyme profiles are able to involve in the prognostic pathological consequences in patients with β-thalassemia major. Even so, they contribute toward the gradual development of tissue injuries.


Dr Mehdi Azad, Dr Farshad Forooghi, Dr Hassan Ehteram, Mr Mousa Vatanmakan, Mrs Hajar Nasiri, Dr Naser Mobarra,
Volume 7, Issue 2 (3-2017)
Abstract

Background: Stem Cell differentiation is a process composed of vast variety of factors which are controlled by a network of certain mechanisms. This study aims to determine the possible role of DNA methylation, a potent regulator of VHL, ECAD and RUNX3 genes during Erythroid differentiation driven by miR-451.

Materials and Methods: To determine the methylation status of promoters and the expression levels of VHL, ECAD and RUNX3 genes, Methylation Specific PCR (MSP) and real-time PCR were used, respectively, on both Cord Blood CD34+ Hematopoietic Stem Cells and differentiated cells. To measure the expression levels of mir-451, mirna qpcr technique was used.

Results: Our findings demonstrated a similar methylation pattern for the target genes before and after differentiation by miR-451. However, the expression levels were significantly increased after differentiation. Gene expression and surface marker analysis results further confirmed the potential of miR-451 for driving erythroid differentiation from hematopoietic stem cells.

Discussion: Our findings ruled out DNA methylation effect on the regulation of VHL, ECAD, and RUNX3 genes during miR-451 mediated erythroid differentiation. However, having CpG islands in their promoters, these three genes are candidates to be controlled by methylation which may not able to be detected by MSP method.

Conclusion: Taken together in this study we have shown a successful erythroid differentiation mediated by miR-451 which is at least in part, independent of DNA methylation. Further understanding of the underlying mechanisms driven by eryhtroid differentiation may lead to therapeutic measures to alter disorders of hematopoietic stem cell differentiation.



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