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- Rantakari, Krista, et al.
(författare)
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Early oxygen levels contribute to brain injury in extremely preterm infants
- 2021
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Ingår i: Pediatric Research. - : Springer Science and Business Media LLC. - 0031-3998 .- 1530-0447. ; 90, s. 131-139
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND Extremely low gestational age newborns (ELGANs) are at risk of neurodevelopmental impairments that may originate in early NICU care. We hypothesized that early oxygen saturations (SpO(2)), arterial pO(2) levels, and supplemental oxygen (FiO(2)) would associate with later neuroanatomic changes.METHODS SpO(2), arterial blood gases, and FiO(2) from 73 ELGANs (GA 26.4 +/- 1.2; BW 867 +/- 179 g) during the first 3 postnatal days were correlated with later white matter injury (WM, MRI, n = 69), secondary cortical somatosensory processing in magnetoencephalography (MEG-SII, n = 39), Hempel neurological examination (n = 66), and developmental quotients of Griffiths Mental Developmental Scales (GMDS, n = 58).RESULTS The ELGANs with later WM abnormalities exhibited lower SpO(2) and pO(2) levels, and higher FiO(2) need during the first 3 days than those with normal WM. They also had higher pCO(2) values. The infants with abnormal MEG-SII showed opposite findings, i.e., displayed higher SpO(2) and pO(2) levels and lower FiO(2) need, than those with better outcomes. Severe WM changes and abnormal MEG-SII were correlated with adverse neurodevelopment.CONCLUSIONS Low oxygen levels and high FiO(2) need during the NICU care associate with WM abnormalities, whereas higher oxygen levels correlate with abnormal MEG-SII. The results may indicate certain brain structures being more vulnerable to hypoxia and others to hyperoxia, thus emphasizing the role of strict saturation targets. Impact This study indicates that both abnormally low and high oxygen levels during early NICU care are harmful for later neurodevelopmental outcomes in preterm neonates. Specific brain structures seem to be vulnerable to low and others to high oxygen levels. The findings may have clinical implications as oxygen is one of the most common therapies given in NICUs. The results emphasize the role of strict saturation targets during the early postnatal period in preterm infants.
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| 2. |
- Talvi, Salli, et al.
(författare)
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Embigin deficiency leads to delayed embryonic lung development and high neonatal mortality in mice.
- 2024
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Ingår i: iScience. - 2589-0042. ; 27:2
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Tidskriftsartikel (refereegranskat)abstract
- Embigin (Gp70), a receptor for fibronectin and an ancillary protein for monocarboxylate transporters, is known to regulate stem cell niches in sebaceous gland and bone marrow. Here, we show that embigin expression is at high level during early mouse embryogenesis and that embigin is essential for lung development. Markedly increased neonatal mortality of Emb-/- mice can be explained by the compromised lung maturation: in Emb-/- mice (E17.5) the number and the size of the small airways and distal airspace are significantly smaller, there are fewer ATI and ATII cells, and the alkaline phosphatase activity in amniotic fluid is lower. Emb-/- lungs show less peripheral branching already at E12.5, and embigin is highly expressed in lung primordium. Thus, embigin function is essential at early pseudoglandular stage or even earlier. Furthermore, our RNA-seq analysis and Ki67 staining results support the idea that the development of Emb-/- lungs is rather delayed than defected.
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