Public Defence: Johanna Marie Lundesgaard Eidahl
MSc Johanna Marie Lundesgaard Eidahl at Institute of Clinical Medicine will be defending the thesis “Postmortem evaluation of brain edema - Possible significance for the study of sudden unexplained death in infants and small children - A physical, radiological, immunohistochemical and genetic approach” for the degree of PhD (Philosophiae Doctor).
Photo: Ine Eriksen, UiO
Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Trial Lecture – time and place
See Trial Lecture.
- First opponent: Principal Associate Robin Haynes, Harvard Medichal School
- Second opponent: Senior Consultant Marianne Arnestad, Oslo University Hospital
- Third member and chair of the evaluation committee: Senior researcher Guttorm Haraldsen, University of Oslo
Chair of the Defence
Professor Emeritus Ola Didrik Saugstad, Faculty of Medicine, University of Oslo
Group Leader Siri Hauge Opdal, Oslo University Hospital
Brain edema is considered a possible element of the pathogenesis in sudden infant death syndrome (SIDS). The edema could be the result of a dysregulated brain water homeostasis, including genetic variation in the aquaporin 4 (AQP4) gene. In this project, a new method for evaluation of postmortem brain edema in adults has been developed, and further applied in children and infants. In infants, there are a striking relationship between age and both brain water content and brain-weight-to-head-circumference ratio; brain water content being highest at birth and then falling, and brain-weight-to-head-circumference being low at birth, but increasing with age. Morphological studies of AQP4 expression in the hippocampus shows that the expression is highest around birth, and then declines with increasing age. Furthermore, the AQP4 expression was lower in infants with the AQP4 rs2075575 CT/TT genotypes compared to infants with the CC genotype. This indicates that AQP4 expression in the hippocampus may be influenced by both age and genotype, and strengthens the hypothesis that rs2075575 CT/TT represents a genetic risk factor for a subset of SIDS.
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