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Predisposition to Myocardial Infarction Influenced by Interleukin 13 Gene Polymorphisms: A Case-Control Study
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Background: Additional inflammatory responses and subsequent damage—arising from enhance transcriptional activity or forming the more active protein due to existence of polymorphic sites in the pro-inflammatory cytokines gene loci—give rise to myocardial infarction susceptibility. Objectives: The aim of our study was to explore whether two interleukin-13 gene polymorphisms (−1512A/C and +2044G/A) could serve as underpins genetic susceptibility of myocardial infarction. Methods: The Iranian population that belong to the Parsis ethnic group was involved in the present study. A total 250 patients with definite myocardial infarction—meeting hypertension, hypercholesterolemia, hyperglycemia, and coronary artery disease requirements—were recruited from the Shiraz urban hospitals. 250 age- and sex-matched healthy individuals without a history of cardiovascular disease and heart disease related risk factors constituted the control group. PCR-restriction fragment length polymorphism technique applied to genotyping at −1512A/C and +2044G/A loci. Hardy–Weinberg equilibrium test was performed (combined cases and controls). The differences of the genotype frequencies in cases and controls were analyzed using a chi-square test. Logistic regression analysis was performed to assess the association between the genotypes and most important risk factors for myocardial infarction. All statistical analyses were performed in SPSS Version 22.0. p-values below 0.05 were hailed as statistically significant. Results: Deviation from Hardy–Weinberg equilibrium was not significant in the −1512A/C locus. Statistically significant difference between our study groups was found in genotype frequency of the −1512A/C. This variant was found in associated with myocardial infarction risk factors. The +2044G/A polymorphism was not in Hardy–Weinberg equilibrium and no significant difference observed in the distribution of +2044G/A genotype frequency among cases and controls. However, further analysis revealed that this genotype associated with an increased susceptibility to myocardial infarction risk factors. Conclusions: The presence of interleukin-13 −1512A/C and +2044G/A gene polymorphisms underpin myocardial infarction predisposition in the ethnic Parsis of the Iranian population.
Title: Predisposition to Myocardial Infarction Influenced by Interleukin 13 Gene Polymorphisms: A Case-Control Study
Description:
Background: Additional inflammatory responses and subsequent damage—arising from enhance transcriptional activity or forming the more active protein due to existence of polymorphic sites in the pro-inflammatory cytokines gene loci—give rise to myocardial infarction susceptibility.
Objectives: The aim of our study was to explore whether two interleukin-13 gene polymorphisms (−1512A/C and +2044G/A) could serve as underpins genetic susceptibility of myocardial infarction.
Methods: The Iranian population that belong to the Parsis ethnic group was involved in the present study.
A total 250 patients with definite myocardial infarction—meeting hypertension, hypercholesterolemia, hyperglycemia, and coronary artery disease requirements—were recruited from the Shiraz urban hospitals.
250 age- and sex-matched healthy individuals without a history of cardiovascular disease and heart disease related risk factors constituted the control group.
PCR-restriction fragment length polymorphism technique applied to genotyping at −1512A/C and +2044G/A loci.
Hardy–Weinberg equilibrium test was performed (combined cases and controls).
The differences of the genotype frequencies in cases and controls were analyzed using a chi-square test.
Logistic regression analysis was performed to assess the association between the genotypes and most important risk factors for myocardial infarction.
All statistical analyses were performed in SPSS Version 22.
p-values below 0.
05 were hailed as statistically significant.
Results: Deviation from Hardy–Weinberg equilibrium was not significant in the −1512A/C locus.
Statistically significant difference between our study groups was found in genotype frequency of the −1512A/C.
This variant was found in associated with myocardial infarction risk factors.
The +2044G/A polymorphism was not in Hardy–Weinberg equilibrium and no significant difference observed in the distribution of +2044G/A genotype frequency among cases and controls.
However, further analysis revealed that this genotype associated with an increased susceptibility to myocardial infarction risk factors.
Conclusions: The presence of interleukin-13 −1512A/C and +2044G/A gene polymorphisms underpin myocardial infarction predisposition in the ethnic Parsis of the Iranian population.
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