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Rescuing a broken heart: A tale of two Models of Neural Crest deficiency and its impact on In Utero Heart function and Embryonic Survival via the Beta-Adrenergic pathway
Congenital heart defects occur in approximately one percent of births every year, which makes it the most frequently occurring congenital defect in patients. The aim of this project was to use two mutant neural crest (NC) mouse models to study the mechanisms underlying congenital heart failure in utero. The first mouse model was a Pax3 systemic knockout, which was lethal by mouse gestational day 14, and had appreciably reduced numbers of migratory NC cells. The second mouse model was adoi:10.7912/c2/1945 fatcat:v2fyb4s2ezdnthlmj4gd5hlxeu