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dc.date.accessioned2020-02-03T20:08:31Z
dc.date.available2020-02-03T20:08:31Z
dc.date.created2019-02-20T09:57:50Z
dc.date.issued2018
dc.identifier.citationBjørnvall, Christina Dybdrodt Opdal, Siri Hauge Rognum, Torleiv Ole Ferrante, Linda . Polymorphisms in the myeloid differentiation primary response 88 pathway do not explain low expression levels in sudden infant death syndrome. Acta Paediatrica. 2018, 1-5
dc.identifier.urihttp://hdl.handle.net/10852/72662
dc.description.abstractAim The aim of this study was to investigate if a range of known rare and common genetic variants in the Toll‐like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88) pathway were present or overrepresented in sudden infant death syndrome (SIDS) compared to controls. Methods Genetic variations in the genes encoding TLR4, MyD88 and Interleukin‐1 receptor‐associated kinase 4 were analysed. The subjects investigated included 158 SIDS cases with a median age of 15.25 weeks (2–47 weeks), 80 cases of infectious death with a median age of 24.9 weeks (0–285 weeks) and 199 adult controls with a median age of 50 years (11–86 years). The cases were collected in the years 1988–2017, and the autopsies were performed at the Department of Forensic Sciences at Oslo University Hospital, Oslo, Norway. Results The results showed that none of the genetic variants selected from the MyD88 pathway were associated with neither SIDS nor infectious death. Most of the rare genetic variants were homozygote for the common allele in all groups, while the rest revealed allelic variation. Conclusion The genetic variations investigated in this study did not appear to be involved in the pathogenesis of SIDS.
dc.languageEN
dc.titlePolymorphisms in the myeloid differentiation primary response 88 pathway do not explain low expression levels in sudden infant death syndrome
dc.typeJournal article
dc.creator.authorBjørnvall, Christina Dybdrodt
dc.creator.authorOpdal, Siri Hauge
dc.creator.authorRognum, Torleiv Ole
dc.creator.authorFerrante, Linda
cristin.unitcode185,53,18,18
cristin.unitnameAvdeling for rettsmedisinske fag
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.fulltextpostprint
cristin.qualitycode1
dc.identifier.cristin1679011
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Acta Paediatrica&rft.volume=&rft.spage=1&rft.date=2018
dc.identifier.jtitleActa Paediatrica
dc.identifier.volume108
dc.identifier.issue7
dc.identifier.startpage1262
dc.identifier.endpage1266
dc.identifier.doihttps://doi.org/10.1111/apa.14696
dc.identifier.urnURN:NBN:no-75812
dc.type.documentTidsskriftartikkel
dc.type.peerreviewedPeer reviewed
dc.source.issn0803-5253
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/72662/1/Bj%25C3%25B8rnvall_Polymorphisms%2Bin%2Bthe%2Bmyeloid%2Bdifferentiation%2Bprimary%2Bresponse%2B88%2Bpathway_Cristin-post%2B1679011.pdf
dc.type.versionAcceptedVersion


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