Evidence map›Paper›PMID 25606383›Full record

ArticleMeta gene2014

Investigation of the monocyte diapedesis-related LFA-1 and JAM-A gene variants in Turkish coronary heart disease patients.

Bengu Tokat, Ozlem Kurt, Zehra Bugra, Oguz Ozturk, Hulya Yilmaz-Aydogan

Abstract read
In one paragraph

Article in Meta gene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

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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

6 citing papers in PubMed.

  1. Review
  2. International journal of molecular sciences · 2023
    Article
  3. Article
  4. Investigation of JAM-A (rs790056) and LFA-1 (rs8058823) gene variants in Turkish colorectal cancer patients.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2019
    Article
  5. Article
  6. 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

5 authors.

Bengu TokatDepartment of Molecular Medicine, Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey.
Ozlem KurtDepartment of Biochemistry, Faculty of Pharmacy, Istanbul University, Istanbul, Turkey.
Zehra BugraDepartment of Cardiology, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Turkey.
Oguz OzturkDepartment of Molecular Medicine, Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey.
Hulya Yilmaz-AydoganDepartment of Molecular Medicine, Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLFA-1/JAM-A interaction plays a significant role in early steps of leukocyte transendothelial migration (diapedesis) which takes part in atherosclerosis pathogenesis. In this population-based case-control study, the frequencies of JAM-A rs790056 and LFA-1 rs8058823 gene polymorphisms in patients with coronary heart disease (CHD) and healthy subjects were investigated and the correlations between the different genotypes and cardiovascular risk factors were analyzed.

methodsThe JAM-A and LFA-1 genotypes were determined in 153 patients with CHD and 124 controls by PCR-RFLP assay.

resultsIn CHD patient group, the frequency of JAM-A rs790056 TT genotype and the frequency of T allele were higher when compared with the control group (p = 0.03 and p = 0.007,respectively). In patient groups, the frequency of LFA-1 rs8058823 AA genotype was higher (p = 0.000), and the frequency of AG genotype was lower when compared with the control group (p = 0.031). In the control group, LFA-1 rs8058823 G allele carriers had higher SBP than subjects with AA genotype (p = 0.038), whereas in the CHD patient group, G allele carriers had lower DBP than subjects with AA genotype (p = 0.007). The multivariate logistic regression analysis confirmed that the JAM-A rs790056 TT genotype (OR = 2.472, p = 0.045) and LFA-1 rs8058823 AA genotype (OR = 6.751, p = 0.000) were risk factors for CHD development.

conclusionThese results suggest that the wild type genotypes and alleles of JAM-A rs790056 (TT genotype and T allele) and LFA-1 rs8058823 (AA genotype and A allele) were found to be risk factors for CHD, whereas rare genotypes and alleles were found to be higher in healthy controls thus being protective.

Indexed as

3′UTR, 3′-untranslated regionBMI, body mass indexCHD, coronary heart diseaseCI, confidence intervalCoronary heart diseaseDBP, diastolic blood pressureDiapedesisHDL-C, high density lipoprotein cholesterolHWE, Hardy-Weinberg EquilibriumJAM-AJAM-A, junctional adhesion molecule-ALDL-C, low density lipoprotein cholesterolLFA-1LFA-1, leukocyte function-associated antigen-1LVH, left ventricular hypertrophyOR, odds ratioPCR-RFLP, polymerase chain reaction–restriction fragment length polymorphismPolymorphismSBP, systolic blood pressureSNP, single nucleotide polymorphismT2DM, type 2 diabetes mellitusTC, total cholesterolTG, triglycerideVLDL-C, very low density lipoprotein cholesterol

Identifiers

PMID25606383
PMCPMC4287794

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Registered trials

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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.