ArticleInternational journal of legal medicine2015
That's not it, either-neither polymorphisms in PHOX2B nor in MIF are involved in sudden infant death syndrome (SIDS).
Article in International journal of legal medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Sudden Infant Death Syndrome (SIDS): State of the Art and Future Directions.International journal of medical sciences · 2024Review
- Non-polyalanine repeat mutation in PHOX2B is detected in autopsy cases of sudden unexpected infant death.PloS one · 2022Article
- A Common 3'UTR Variant of theFrontiers in neurology · 2021Article
- Comprehensive Analysis of Genes Associated With Sudden Infant Death Syndrome.Frontiers in pediatrics · 2021Article
- Influence of functional polymorphism in MIF promoter on sudden cardiac death in Chinese populations.Forensic sciences research · 2017Article
- A "Wear and Tear" Hypothesis to Explain Sudden Infant Death Syndrome.Frontiers in neurology · 2016Article
- Polymorphisms in genes of respiratory control and sudden infant death syndrome.International journal of legal medicine · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The occurrence of sudden infant death syndrome (SIDS) has been linked to several genetic risk factors, e.g. genes involved in the neuroadrenergic system, variations in serotonin reporter genes or mutations in long-QT syndrome genes. Additionally, polymorphisms in genes with impact in sleep disorder syndromes have been proposed to be of importance as genetic risk factors for SIDS. In this study, we investigated the polyalanine length variation of PHOX2B and the -794 CATT repeat in the MIF promoter region as well as single nucleotide polymorphisms (rs28462174, rs28727473, rs16853571, rs755622, rs12485058, rs12485068, rs4822444, rs4822445, rs4822446, rs4822447 and rs2012124) in both genes in 278 SIDS cases and 240 controls. No significant differences were found in allele distribution of neither length polymorphisms nor single nucleotide polymorphisms between SIDS cases or controls. Therefore, an importance of these variations for the occurrence of SIDS could be ruled out.
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