Evidence map›Paper›PMID 18274806›Full record

ArticleJournal of neurology2008

Apolipoprotein A5 gene C56G variant confers risk for the development of large-vessel associated ischemic stroke.

Anita Maász, Péter Kisfali, Zoltán Szolnoki, Ferenc Hadarits, Béla Melegh

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Article in Journal of neurology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
4.9field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.

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  7. Association analysis ofOncotarget · 2017
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  15. Clinical significance of apolipoprotein A5.Current opinion in lipidology · 2008
    Review
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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 at 3 institutions in 1 country.

Anita MaászUniversity of Pécs, Dept. of Medical Genetics and Child Development, Szigeti 12, 7624 Pécs, Hungary.
Péter Kisfali
Zoltán Szolnoki
Ferenc Hadarits
Béla Melegh
University of Pecs · HUBékés Megyei Központi Kórház · HUMarkusovszky Egyetemi Oktatókórház · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesIschemic stroke is a suddenly developing temporary or often permanent damage of the brain. Several candidate genes have been shown to have an impact in the pathogenesis of stroke. The aim of our study was to investigate the possible association between the C56G variant of the apolipoprotein A5 (APOA5) gene and ischemic stroke.

methodsPCR-RFLP assays were performed to detect the C56G alleles in 403 patients with classified stroke types and 171 controls.

resultsTriglyceride levels of subjects carrying 56G allele were elevated compared to the subjects with 56C allele in all stroke subgroups and in the controls. The serum total cholesterol levels did not differ between subjects with C or G alleles in each group. An accumulation of APOA5 56G allele was observed in the large-vessel associated stroke group compared to the healthy controls (10.9 vs. 5.6 %; p < 0.05), while its prevalence did not increase in any other stroke subgroups. Multivariate logistic regression analysis adjusted for differences in age, gender, BMI, serum total cholesterol levels, ischemic heart disease, hypertension, diabetes mellitus, smoking and drinking habits revealed that the APOA5 56G allele represents a susceptibility factor for large-vessel associated stroke (OR = 2.132 at 95 % CI; p < 0.05).

conclusionThe data presented here suggest that the 56G allele can confer risk exclusively for development of large-vessel associated stroke. Thereby, the 56G allele differs from the APOA5 T-1131C allelic variant, which has been previously identified as a risk factor for all subgroups of the stroke disease.

Indexed as

AllelesAdultAgedAged, 80 and overApolipoprotein A-VApolipoproteins ABrain IschemiaDNA Mutational AnalysisFemaleGene FrequencyGenetic Predisposition to DiseaseGenetic TestingGenotypeHumansHyperlipidemiasMaleAPOA5 protein, humanApolipoprotein A-VApolipoproteins ATriglycerides

Identifiers

PMID18274806
OpenAlexW2022094164

What OpenQuestion holds

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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.