ArticleInternational journal of legal medicine2013
Association between polymorphisms in the P2RY1 and SSTR2 genes and sudden infant death syndrome.
Article in International journal of legal medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Sudden infant death syndrome revisited: serotonin transporter gene, polymorphisms and promoter methylation.Pediatric research · 2022Article
- Gene variants associated with obstructive sleep apnea (OSA) in relation to sudden infant death syndrome (SIDS).International journal of legal medicine · 2021Article
- Evidence for an association of interferon gene variants with sudden infant death syndrome.International journal of legal medicine · 2019Article
- Sudden infant death syndrome: exposure to cigarette smoke leads to hypomethylation upstream of the growth factor independent 1 (GFI1) gene promoter.Forensic science, medicine, and pathology · 2016Article
- Candidate gene variants of the immune system and sudden infant death syndrome.International journal of legal medicine · 2016Article
- That's not it, either-neither polymorphisms in PHOX2B nor in MIF are involved in sudden infant death syndrome (SIDS).International journal of legal medicine · 2015Article
- Polymorphisms in genes of respiratory control and sudden infant death syndrome.International journal of legal medicine · 2015Article
- Purine and purinergic receptors.Brain and neuroscience advancesReview
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
introductionSudden infant death syndrome (SIDS) is a multifactorial syndrome and we believe that an inefficient respiratory response to certain homeostatic stressors, such as hypoxia and hypercapnia, is a key factor in the etiology of SIDS. Hence, we genotyped two single nucleotide polymorphisms (SNPs) in genes of importance for respiratory control: P2RY1 (adenosine diphosphate/adenosine triphosphate receptor) and SSTR2 (somatostatin receptor).
methodsTwo SNPs, Rs1466113 (C > G dimorphism in SSTR2) and rs701265 (A > G dimorphism in P2RY1), were typed in 175 SIDS cases and 195 controls and 275 SIDS cases and 338 controls, respectively. Genotyping was performed using TaqMan technology.
resultsThe determined genotype frequencies were SSTR2: CC (14.4 %), CG (49.7 %), GG (35.9 %) in controls and CC (17.1 %), CG (49.1 %), and GG (33.8 %) in SIDS; P2RY1: AA (70.6 %), AG (28.7 %), GG (0.7 %) in SIDS and AA (68.3 %), AG (27.9 %), and GG (3.8 %) in the control group. For rs701265 in P2RY1, homozygous G carriers were significantly more frequent in the control group (p = 0.02).
conclusionWe think that allele G provides a protective effect in events of ventilatory stress. Moreover, the significant lack of P2Y1 G allele homozygotes in the SIDS group shows that respiratory response plays an important role in the etiology of SIDS. Thus, we believe it is worthwhile to further investigate functional polymorphisms within genes that are involved in respiratory control in the future.
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