Abstract

        Background and Objective: Normal hemoglobin (Hb) is formed of a heme group and a protein group known as globin. Globin is made of four polypeptide chains and in hemoglobinopathies, the structure of one of these four polypeptide chain becomes abnormal. Cellulose acetate method is a common way to differentiate haemoglobinopathies. Inability to identify the components of Hb low concentrations and incapability to isolate all Hb types are among the disadvantages of this method. The aim of this study was to report the prevalence of hemoglobinopathies in the North of Iran by capillary electrophoresis method.

      Methods: All patients with suspected hemoglobinopathies, referred by physicians for electrophoresis, have been studied in a private center in the city of Gorgan, Iran. The level of HbA2, HbA, HbF and other Hb was recorded.

       Results: Overall, 725 blood samples were analyzed using the capillary method. HbE was reported in 2 patients, HbH was observed in 2 patients and Hb Barts was reported in 3 patients. Using the capillary method, among patients with the SDG area, only 4 of 38 (10.52%) had HbS and the majority of them (89.48%) had HbD.

      Conclusion: HbD is the most common hemoglobinopathy in the North of Iran.

        Keywords: Hemoglobinopathy; hemoglobin D; Capillary Electrophoresis; Iran

ABSTRACT

          Background and Objective: Genetic variations in the gene encoding endothelial nitric oxide synthase (eNOS) enzyme affect the susceptibility to cardiovascular disease. Identification of the way these changes affect eNOS structure and function in laboratory conditions is difficult and time-consuming. Thus, it seems essential to perform bioinformatics studies prior to laboratory studies to find  the variants that are more important. This study aimed to predict the damaging effect of changes in the coding region of eNOS using homology- and structure-based algorithms (SIFT and PolyPhen).

           Methods: First, the single nucleotide polymorphisms in the coding region (cSNPs) of the human eNOS gene were extracted from dbSNP. Resulting amino acid changes were reported as primary data required for the study. Then, position and type of amino acid changes along with the complete amino acid sequence were separately entered into the SIFT and PolyPhen tools for analysis.

         Results: Of 144 single nucleotide changes, 38 changes by the SIFT, 47 changes by the PolyPhen and 18 amino acid substitutions by both tools were predicted as damaging.

          Conclusion: It is predicted that 18 amino acid changes may have damaging phenotypic effects on the structure of the eNOS enzyme that may affect its performance by potentially affecting the enzyme’s various functional regions. Therefore, computational prediction of potentially damaging nsSNPs and prioritizing amino acid changes may be useful for investigating protein performance using targeted re-sequencing and gene mutagenesis experiments.

Background and Objective: The cell division cycle 25 (CDC25)is a familyof highly conserved dual-specificity phosphatases that activate cyclin-dependent kinase complexes. These complexes are the main cell cycle regulators. Mammalian cells ,exposure to DNA damaging radiations such as ionizing radiation and ultraviolet light, prevent cell cycle progression by activation of checkpoint pathways and lead to cell death.

      Methods: In this study, mice were exposed to different doses of ionizing radiation. Their total cellular protein was extracted from the bone marrow. After determining and matching the protein concentrations, CDC25A phosphatase levels were measured by western blotting.

        Results: The results showed that exposure to different doses of ionizing radiation in vivo significantly increased the expression of CDC25A compared to control group (P <0.05).

        Conclusion: Exposure to ionizing radiation increases the expression of CDC25A phosphatase, which increases the possibility of tumorigenesis in that area by increasing bone marrow cell proliferation.

        Keywords: Cell Cycle, CDC25A, Ionizing Radiation, Cyclin-Dependent Kinase.