Evidence map›Paper›PMID 27443477›Full record

ArticleAnatolian journal of cardiology2017

Endothelial nitric oxide gene polymorphisms and their association with coronary artery disease in Tunisian population.

Letaief Afef, Benothmane Leila, Charfeddine Bassem, Ernez Hajri Samia, Guider Jridi, Limem Khalifa

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In one paragraph

Article in Anatolian journal of cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 33% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Letaief AfefDepartment of Biochemistry, UR12ES07 Research Laboratory, Faculty of Medicine Ibn Jazzar; Sousse-Tunisia. letaief_a@yahoo.fr.
Benothmane LeilaDepartment of Biochemistry, UR12ES07 Research Laboratory, Faculty of Medicine Ibn Jazzar; Sousse-Tunisia.
Charfeddine BassemDepartment of Biochemistry, UR12ES07 Research Laboratory, Faculty of Medicine Ibn Jazzar; Sousse-Tunisia.
Ernez Hajri SamiaDepartment of Cardiology, Heart Failure (LR12SP09) Research Laboratory, Hospital Farhat Hached; Sousse-Tunisia.
Guider JridiDepartment of Cardiology, Heart Failure (LR12SP09) Research Laboratory, Hospital Farhat Hached; Sousse-Tunisia.
Limem KhalifaDepartment of Biochemistry, UR12ES07 Research Laboratory, Faculty of Medicine Ibn Jazzar; Sousse-Tunisia.
University of Sousse · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveBy releasing mediators, like nitric oxide (NO), vascular endothelium is considered so significant in the process of atherosclerotic . In fact, the major functions of NO consist in inhibiting the activation of platelet, relaxing the muscles (vascular and smooth ones), and modulating the growth and the migration of cells (vascular and smooth ones). Therefore, this process makes the endothelial nitric oxide synthase (NOS3) considerably important because it possesses atheroprotective activity. Polymophisms, rs1808593 (10G/T) as well as rs891512 (G24943A) within NOS3 gene, play major role in the coronary artery disease (CAD) development. The aim of the study is to evaluate the relationship between the 10G/T and G24943A polymorphisms and the CAD among Tunisian individuals.

methodsWe included, in this survey, a set of 274 patients suffering from CAD together with 162 normotensive subjects. The PCR-RFLP was applied to analyze the polymorphism of intron 23 (10G/T) gene, while the ASA-PCR was used to analyze the intronic G24943A gene polymorphism. Overall and subgroup analyses were performed. Odds ratio (OR) and 95% confidence interval (CI) were used to evaluate the association between NOS3 10G/T and G24943A polymorphisms as well as CAD risk. Statistical analysis was performed with SPSS V.10.

resultsThe genotype frequencies for G24943A polymorphism differed significantly between the CAD patients and the controls. The former had a frequency of 11.4% for the AA genotype, 34.7% for the GA genotype and 53.9% for the GG genotype. The latter had a frequency of only 2.5% for the AA genotype, 29.7% for the GA genotype and 67.7% for the GG genotype (χ2=7.62; OR=1.79; p=0.006). The CAD patient group showed a significantly-higher frequency of the A allele compared to the controls (0.28 vs. 0.16; χ2=15.20; p<0.001). The odds ratio of CAD for A vs. G allele frequency was statistically significant 1.99 (1.4-2.82) at 95% CI. The genotype distribution for the 3 investigated variants of 10G/T were not significantly different between CAD and control subjects (χ2=1.46; OR=1.72; p=0.22). Whereas, 10G/T has revealed barely allelic (χ2=4.45; OR=2.3; p=0.034) correlation with coronary artery disease Conclusion: The present study was designed so that there would be an association between the CAD and NOS3 polymorphism (G24943A). However, these results have proven that the polymorphism of 10G/T is not associated with CAD in the Tunisian population.

Indexed as

Genetic Predisposition to DiseaseCase-Control StudiesCholesterolCholesterol, HDLCholesterol, LDLCoronary Artery DiseaseFemaleHumansMaleMiddle AgedNitric Oxide Synthase Type IIIPolymorphism, GeneticTriglyceridesTunisiaCholesterolCholesterol, HDLCholesterol, LDLNitric Oxide Synthase Type IIINOS3 protein, humanTriglycerides

Identifiers

PMID27443477
PMCPMC5324859
OpenAlexW2463331039

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.