Sentence examples for postnatal defects from inspiring English sources

This includes embryotoxic/foetotoxic effects such as reduced body weight, growth and developmental retardation, organ toxicity, death, abortion, structural defects (teratogenic effects), functional effects, peri- and postnatal defects, and impaired postnatal mental or physical development up to normal pubertal development.

However, the interplay between mechanics and biology in de novo generation of bone in postnatal defects as well as healing of morcellized bone graft or massive cortical bone autografts is less well understood.

Moreover, WWOX-deficient mice die three weeks post-partum and display multiple postnatal defects, such as growth retardation and abnormalities in bone metabolism [ 52].

Furthermore, the absence of lactotriaosylceramide (Lc3cer) synthase, as shown in UDP-GlcNAc betaGal beta-1,3-N-acetylglUDP-GlcNAc betaGalase 5- (beta-1,3-N-acetylglucosaminyltransferaseed to cause preimplantation lethality [ 33] or multiple postnatal defects [ 34].

First we show that ablation of Dlk1 in the Myf5-derived myogenic cells leads to both developmental and postnatal growth/regeneration defects in myogenesis.

Recently, an adult viable model has been published that does not demonstrate hydrocephalus or significant postnatal cardiac defects.

However, as the Esrp1/Esrp2 DKO mice are not viable at birth we were unable to analyze postnatal barrier defects in DKO mice.

Yamaguchi et al. [ 51] found that the paternalKO (Tet1−/− male x wild-type female) mice had significantly fetal and postnatal growth defects.

This view is also supported by our findings of focal pre- and postnatal developmental defects, including abnormal migration with heterotopic and ectopic clusters of neurons, dysplastic changes, and subependymal nodular dysplasia detected in the brain of individuals with idiopathic and dup(15 -associated autism [ 5].

It is striking that these patients have not been described to have features reminiscent of paternal GNAS loss of function mutations, although the loss of the paternal GNAS allele (on chromosome 20) is associated with pre- and postnatal growth defect and Albright hereditary osteodystrophy [ 8].

Knockout mice lacking HB-EGF result in perinatal or postnatal lethality from defects in heart chamber and valve formation, abnormal development of lungs, and a significant defect in epidermal wound healing [36], [37] while knockout mice lacking all three major EGFR ligands (EGF, TGFA and AREG) result in mammary gland impairment and small intestine defects but are viable and fertile [38], [39].