ArticleMolecular biology reports2011
Contribution of SELP and PSGL-1 genotypes and haplotypes to the presence of coronary heart disease in Tunisians.
Article in Molecular biology reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 4 of them syntheses that pooled 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.
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.
Who cites it
6 citing papers in PubMed, 4 syntheses or guidelines pooled it, 15 citations in OpenAlex.
- Influence of two common polymorphisms in the EPHX1 gene on warfarin maintenance dosage: a meta-analysis.BioMed research international · 2015Pooled it
- Correlations of SELE and SELP genetic polymorphisms with myocardial infarction risk: a meta-analysis and meta-regression.Molecular biology reports · 2014Pooled it
- SELP genetic polymorphisms may contribute to the pathogenesis of coronary heart disease and myocardial infarction: a meta-analysis.Molecular biology reports · 2014Pooled it
- Heterogeneous effect of two selectin gene polymorphisms on coronary artery disease risk: a meta-analysis.PloS one · 2014Pooled it
- Review
- Plasma P-selectin level is associated with severity of coronary heart disease in Chinese Han population.The Journal of international medical research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
P-selectin (SELP) and its counter-receptor, P-selectin glycoprotein ligand-1 (PSGL-1), play key role in the transient attachment of leukocytes to endothelial cells predisposing to coronary heart disease (CHD). In the current report, 293 angiographically proven CHD patients and 327 age, gender, and race-matched controls were included. Our aim was to evaluate the contribution to CHD of the following SNPs: C-2123G, G-1969A and T715P in SELP, Met62Ile and the VNTR variants in PSGL-1 gene in a North African population from Tunisia. While there were no significant differences in the distribution of SELP or PSGL-1 alleles or genotypes between patients and controls, a trend for a significant association of the C-2123G genotypes distribution with incident CHD was observed (P=0.06). Assuming an additive model of transmission, the risk was 74% higher among subjects carrying the GG genotypes in comparison to those carrying the CC genotype (OR=1.74 [1.01-2.98], P=0.04) and 80% higher in the recessive model (OR=1.80 [1.08-3.01], P=0.02). Haplotype analysis did not identify any specific SELP or PSGL-1 haplotypes to be associated with CHD. The present study demonstrated no evidence of association between individual SELP or PSGL-1 SNPs or haplotypes with incident CHD. However, this study replicates absence of association of the mostly studied SNP, T715P, previously reported in individuals with African origin.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.