Browsing by Author "Rahman M.F.A."

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The association of fractalkine receptor (T280m) polymorphism in the pathogenesis of acute coronary syndrome in the Egyptian population
(Bentham Science Publishers B.V., 2019) Hassan D.S.; Hashad I.M.; Rahman M.F.A.; Abdel-Maksoud S.M.; Clinical Biochemistry Unit; Faculty of Pharmacy and Biotechnology; German University in Cairo; Cairo; Egypt; Biochemistry Department; Faculty of Pharmacy; October University for Modern Science and Arts; Giza; Egypt
Fractalkine (FKN) in its free and membrane bound-forms and its receptor CX3CR1are reported to have an atherosclerotic effect. The relationship of Single Nucleotide Polymorphisms (SNPs) in FKN and CX3CR1genes with the Coronary Artery Disease (CAD) risk showed conflicting results in different populations. The aim of this study was to investigate the influence of CX3CR1 threonine 280 methionine (T280M) polymorphism in the predisposition of Acute Coronary Syndrome (ACS) in Egyptians. Methods: 200 Egyptian subjects were recruited for the study. They were divided into 100 ACS patients and 100 healthy controls. Genotyping of CX3CR1 T280M was performed using a Polymerase Chain Reaction-restriction Fragment Length Polymorphism (PCR-RFLP). Serum FKN was assayed by Enzyme - Linked - Immuno- Sorbent-Assay (ELISA). Results: T and M allele frequencies for CX3CR1gene were not significantly different between ACS and Controls (p=0.76). Moreover, none of the genotypes had an atheroprotective effect. Serum analysis showed higher levels of FKN in ACS patients (p=0.041). FKN levels were not significantly different among genotypes of control and ACS groups (p=0.34) and (p=0.38) respectively. Conclusion: This study shows that CX3CR1 T280M polymorphism does not affect the incidence of ACS the Egyptian population. Moreover, none of the genotypes were associated with higher FKN levels. � 2018 Bentham Science Publishers.
Contribution of cyp27b1 and cyp24a1 genetic variations to the incidence of acute coronary syndrome and to vitamin d serum level
(Canadian Science Publishing, 2019) Fam M.S.; Hassanein S.I.; Rahman M.F.A.; Assal R.A.; Hanafi R.S.; Gad M.Z.; Clinical Biochemistry Unit; Faculty of Pharmacy and Biotechnology; German University in Cairo; Fifth Settlement; Cairo; 11432; Egypt; Biochemistry Department; Faculty of Pharmacy; October University for Modern Sciences and Arts; 6th of October; Giza 12566; Egypt; The Molecular Pathology Research Group; Department of Pharmacology and Toxicology; Faculty of Pharmacy and Biotechnology; German University in Cairo; Fifth Settlement; Cairo; 11432; Egypt; Pharmaceutical Chemistry Department; Faculty of Pharmacy and Biotechnology; German University in Cairo; Fifth Settlement; Cairo; 11432; Egypt
Cardiovascular diseases remain a major public health burden worldwide. It was reported that vitamin D protects the cardiovascular system through several mechanisms mainly by hindering atherosclerosis development. Genetic variations in vitamin D metabolic pathway were found to affect vitamin D levels. This study aimed at investigating the association between single nucleotide polymorphisms in genes involved in vitamin D metabolism, CYP27B and CYP24A1; 25-hydroxyvitamin D (25(OH)D) levels; and susceptibility to acute coronary syndrome (ACS). One hundred and eighty-five patients and 138 healthy controls were recruited. CYP24A1 rs2762939 was genotyped using fast real-time PCR, while CYP24A1 rs4809960 and CYP27B1 rs703842 were genotyped using polymerase chain reaction followed by restriction fragment length polymorphism (PCR�RFLP). 25(OH)D3 and 25(OH)D2 levels were measured using ultra-performance liquid chromatography tandem mass spectrum. Vitamin D level was significantly lower in patients than controls (p < 0.05). The GG genotype of rs2762939 was significantly associated with the risk of ACS development, but not correlated to the vitamin D level. rs4809960 and rs703842 genetic variations were not associated with ACS nor with 25(OH)D level. The genetic variant rs2762939 of CYP24A1 is remarkably associated with ACS. Meanwhile, the variants rs4809960 and rs703842 are not associated with ACS incidence. � 2019, Canadian Science Publishing. All rights reserved.
Genetic variants of CYP2R1 are key regulators of serum vitamin D levels and incidence of myocardial infarction in middle-aged Egyptians
(Bentham Science Publishers B.V., 2018) Sedky N.K.; Rahman M.F.A.; Hassanein S.I.; Gad M.Z.; Clinical Biochemistry Unit; Biochemistry Department; Faculty of Pharmacy and Biotechnology; German University in Cairo; New Cairo City; 11835; Egypt; Zewail City of Science and Technology; Giza; 12566; Egypt; Biochemistry Department; Faculty of Pharmacy; October University for Modern Science and Arts (MSA); 6th of October City; Egypt
Background: Myocardial Infarction (MI) is one of the leading causes of morbidity and mortality in Egypt and worldwide. Vitamin D deficiency has long been linked to incidence of cardiovascular diseases. Several factors were reported to contribute to serum vitamin D level including exposure to sunlight. However, genetic variations in the vitamin D metabolic pathways have also been considered as strong determinants of vitamin D levels. CYP2R1 is the major 25-hydroxylase enzyme that is responsible for the 1st activation step of vitamin D. Objective: to investigate the contribution of polymorphisms in CYP2R1 gene to vitamin D deficiency and incidence of MI in Egyptians. Methods: The study included 323 subjects; 185 MI patients and 138 healthy controls. Serum 25OHD3, 25OHD2 and total 25OHD levels were measured using LC-MS/MS. SNPs rs2060793 and rs1993116 were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) which is considered one of the most commonly used techniques in genotyping. SNP rs10766197 was detected using TaqMan allele discrimination assay. Results: Serum 25OHD3, 25OHD2 and total 25OHD levels were found to be significantly lower in MI patients than controls. The three studied SNPs were associated with significantly different total 25OHD levels and their genotype distributions differed significantly between MI patients and controls where the high risk genotypes were AG/AA for rs2060793, AG/GG for rs1993116 and AG/AA for rs10766197. Additionally, the concurrent presence of high risk genotypes of the three studied SNPs rendered those individuals at extremely higher risk for MI than each individual SNP (OR 14.1, 95% CI (3.1-64.7), p-value = < 0.0001). Conclusions: Genetic variants of CYP2R1 are key determinants of serum 25OHD levels and are highly associated with MI risk. � 2018 Bentham Science Publishers.
Polymorphisms in gap junction proteins and their role in predisposition of acute myocardial infarction in Egyptians
(Bentham Science Publishers B.V., 2017) El Tahry F.A.; Hashad I.M.; Rahman M.F.A.; Gad M.Z.; Clinical Biochemistry Unit; Faculty of Pharmacy and Biotechnology; German University in Cairo; Cairo; Egypt; Biochemistry Department; Faculty of Pharmacy; October University for Modern Science and Arts; 6th of October City; Egypt
Background: Connexin (Cx) proteins are the building blocks of gap junctions. Among these, Cx37 and Cx40 are expressed on vascular system and reported to have cardioprotective role. Linking polymorphisms in genes coding for Cx and coronary artery disease (CAD) risk showed conflicting results in different populations. None has been studied before in Egyptians. Therefore, the aims of this study were to investigate the influence of Cx37 C1019T and Cx40 A71G polymorphisms on the predisposition of acute myocardial infarction (AMI) in Egyptians, to study linkage disequilibrium (LD) and combined effects of single nucleotide polymorphisms (SNPs) and to correlate the genotypes with sVCAM-1 serum levels. Methods: Total of 201 Egyptian subjects were recruited for the study. They were divided into 104 AMI patients and 97 healthy controls. Genotypes for each participant were determined using a polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). Serum sVCAM-1was measured by ELISA. Results: Allele frequencies for both Cx37 and Cx40 were not significantly different between AMI and Controls (p=0.93 and p=0.26 respectively). Moreover, studying the dominant and recessive models concluded that none of the genotypes was a risk factor. Both SNPs were not in LD (R2=0.0027). Serum analysis showed higher levels of sVCAM-1 in AMI patients (p<0.0001). sVCAM-1 levels were not significantly different among SNPs (Cx37; p=0.244 and Cx40; p=0.266). � 2017 Bentham Science Publishers.