Evidence map›Paper›PMID 22927777›Full record

ArticleInternational journal of medical sciences2012

Mannose binding lectin and macrophage migration inhibitory factor gene polymorphisms in Turkish children with cardiomyopathy: no association with MBL2 codon 54 A/B genotype, but an association between MIF -173 CC genotype.

Nilgun Col-Araz, Sibel Oguzkan-Balci, Osman Baspinar, Tugce Sever, Ayse Balat, Sacide Pehlivan

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Nilgun Col-ArazUniversity of Gaziantep, Faculty of Medicine, Department of Pediatrics, Gaziantep, Turkey.
Sibel Oguzkan-Balci
Osman Baspinar
Tugce Sever
Ayse Balat
Sacide Pehlivan
Gaziantep University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial inflammation is one of the commonest mechanisms in cardiomyopathy (CMP). Mannose binding lectin (MBL) is a key molecule in innate immunity, while macrophage migration inhibitory factor (MIF) is a constitutive element of the host defenses. We investigated the possible association between polymorphisms of MBL2 and MIF genes and CMP in Turkish children. Twenty-children with CMP and 30 healthy controls were analyzed for codon 54 A/B polymorphism in MBL, and -173 G/C polymorphism in MIF genes by using PCR-RFLP methods. No significant difference was found between genotypes and alleles of MBL2 gene codon 54 A/B polymorphism in patients and controls (p>0.05). However, serum uric acid levels was found higher in dilated CMP patients with AA genotype. Frequency of MIF -173 CC genotype was significantly higher in patients (p<0.05), and sodium levels were higher in patients with MIF -173 CC genotype. This study is the first to investigate the MBL and MIF gene polymorphisms in Turkish children with CMP. We conclude that CC genotype of MIF (-173) polymorphism may be a risk factor for CMP patients. However, further studies with larger samples are needed to address the exact role of this polymorphism in CMP.

Indexed as

AdolescentCardiomyopathiesChildChild, PreschoolGenetic Predisposition to DiseaseGenotypeHumansInfantMacrophage Migration-Inhibitory FactorsMannose-Binding LectinPolymorphism, GeneticTurkeyMacrophage Migration-Inhibitory FactorsMannose-Binding LectinMBL2 protein, humanCardiomyopathyChildrenMacrophage migration inhibitory factorMannose binding lectinpolymorphism.

Identifiers

PMID22927777
PMCPMC3427956
OpenAlexW2147470970

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.