Browsing by Author "M. Shaban, Gamal"

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    C242T polymorphism of NADPH oxidase p22phox gene reduces the risk of coronary artery disease in a random sample of Egyptian population
    (Springer Netherlands, 2014) M. Hashad, Ingy; F. Abdel Rahman, Mohamed; M. Abdel-Maksoud, Sahar; S. Amr, Khalda; K. Effat, Laila; M. Shaban, Gamal; Z. Gad, Mohamed
    The p22phox protein subunit is essential for NADPH oxidase activity. The prevalence of C242T variants of p22phox gene was studied in 101 healthy Egyptian controls and 104 acute myocardial infarction (AMI) Egyptian patients. Contribution of oxidative stress, represented by serum oxidized-LDL (ox-LDL), in development of AMI was also examined and correlated with C242T gene variants. Genotyping and ox-LDL were assessed by PCR–RFLP and ELISA. Results showed that wild type CC genotype is prevalent in 27 % of controls; CT and TT are in 72 and 1 %. In patients, the distribution was 40.2, 59.8 and 0 % for CC, CT and TT; respectively, showing a significant difference (p = 0.0259). Serum ox-LDL levels were higher in patients than controls (p ≤ 0.0001). Subjects having CT genotype had lower levels of ox-LDL than CC genotype (p ≤ 0.005). C242T polymorphism of p22phox gene of NADPH oxidase is a novel genetic marker associated with reduced susceptibility to AMI.
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    Nitric Oxide Regulating Proteins as Biochemical and Genetic Markers of Coronary Artery Disease
    (Springer Netherlands, 2016) Z. Gad, Mohamed; M. Abdel-Maksoud, Sahar; I. Hassanein, Sally; M. Hashad, Ingy; F. Abdel Rahman, Mohamed; A. Abu el Maaty, Mohamed; M. Shaban, Gamal; Abou-Aisha, Khaled
    Cardiovascular disease (CVD) remains the leading cause of death worldwide. Despite huge efforts and great advances in studying the genetic component of CVD, there is still a great need for exploring the genetic and environmental factors contributing to the development of this disease. Among these factors evolve modulation of nitric oxide (NO) homeostasis and oxidative stress as central players according to recent reports. A wide range of biochemical disturbances, including reduced bioavailability of NO and oxidative stress, has been shown to be associated with endothelial dysfunction (ED). Many studies described the contribution of ED in the predisposition of CVD, particularly coronary artery disease (CAD). Recent evidence indicates that ED may be genetically determined. This chapter points out to the key players that influence vascular NO levels and their role in the protection against and/or predisposition to CAD