scholarly journals The Etiology and Evolution of Fetal Brain Injury

10.5772/38441 ◽  
2012 ◽  
Author(s):  
Andrew Macnab
Keyword(s):  
Brain Injury ◽  
Fetal Brain

scholarly journals The Absence of TLR4 Prevents Fetal Brain Injury in the Setting of Intrauterine Inflammation

2018 ◽  
Vol 26 (8) ◽  
pp. 1082-1093 ◽  
Author(s):  
Natalia M. Tulina ◽  
Amy G. Brown ◽  
Guillermo O. Barila ◽  
Michal A. Elovitz
Keyword(s):  
Brain Injury ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Quantitative Polymerase Chain Reaction ◽  
Fetal Brain ◽  
Notch Signaling Pathway ◽  
Mouse Strains ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway

Background: Exposure to intrauterine inflammation during pregnancy is linked to brain injury and neurobehavioral disorders in affected children. Innate immunity, specifically Toll-like receptor (TLR) signaling pathways are present throughout the reproductive tract as well as in the placenta, fetal membranes, and fetus. The TLR pathways are mechanistically involved in host responses to foreign pathogens and may lead to brain injury associated with prenatal inflammation. Objective: We aimed to determine whether the activation of the TLR4 signaling pathway, in the mother and fetus, is critical to fetal brain injury in the setting of intrauterine inflammation. Methods: A mini-laparotomy was performed on time pregnant C57B6 mice and 2 knockout mouse strains lacking the function of the Tlr4 and Myd88 genes on embryonic day 15. Intrauterine injections of Escherichia coli lipopolysaccharide or saline were administered as described previously. Dams were killed 6 hours postsurgery, and placental, amniotic fluid, and fetal brain tissue were collected. To assess brain injury, quantitative polymerase chain reaction (qPCR) analysis was performed on multiple components of the NOTCH signaling pathway, including Hes genes. Interleukin (IL) IL6, IL1β, and CCL5 expression was assessed using qPCR and enzyme-linked immunosorbent assay. Results: Using an established mouse model of intrauterine inflammation, we demonstrate that the abrogation of TLR4 signaling eliminates the cytokine response in mother and fetus and prevents brain injury associated with increased expression of transcriptional effectors of the NOTCH signaling pathway, Hes1 and Hes5. Conclusions: These data show that the activation of the TLR4 signaling pathway is necessary for the development of fetal brain injury in response to intrauterine inflammation.

scholarly journals 898: Placental fetal side thickness correlates with fetal brain injury

2020 ◽  
Vol 222 (1) ◽  
pp. S559
Author(s):  
Anna Chudnovets ◽  
Jun Lei ◽  
Quan Na ◽  
Jie Dong ◽  
Irina Burd
Keyword(s):  
Brain Injury ◽  
Fetal Brain

Neonatal platelet counts and the timing of fetal brain injury

1997 ◽  
Vol 176 (1) ◽  
pp. S61
Author(s):  
Lisa M. Korst ◽  
Jeffrey P. Phelan ◽  
Young Mi Wang
Keyword(s):  
Brain Injury ◽  
Fetal Brain ◽  
Platelet Counts

Occiput posterior presentations are increased in fetal brain injury

2003 ◽  
Vol 189 (6) ◽  
pp. S211
Author(s):  
Cortney Kirkendall ◽  
Jeffrey Phelan
Keyword(s):  
Brain Injury ◽  
Fetal Brain

Neonatal Platelet Counts in Fetal Brain Injury

1999 ◽  
Vol 16 (02) ◽  
pp. 79-83 ◽  
Author(s):  
Lisa Korst ◽  
Jeffrey Phelan ◽  
Young Mi Wang ◽  
Myoung Ahn
Keyword(s):  
Brain Injury ◽  
Fetal Brain ◽  
Platelet Counts

Fetal brain injury

2004 ◽  
Vol 31 (2) ◽  
pp. 123-137 ◽  
Author(s):  
H. Brunel ◽  
N. Girard ◽  
S. Confort-Gouny ◽  
A. Viola ◽  
K. Chaumoitre ◽  
...  
Keyword(s):  
Brain Injury ◽  
Fetal Brain
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