ctrl + v thread Sup Forums
and no cheating niggers
pic not related
Other urls found in this thread:
i.imgur.com
bored-and-imaginative.tumblr.com
shadbase.com
hentai-foundry.com
images.akamai.steamusercontent.com
i.4cdn.org
efukt.com
mobile.twitter.com
youtube.com
reddit.com
twitter.com
One-third of all congenital birth defects affect the head and face, and most craniofacial anomalies are considered to arise through defects in the development of cranial neural crest cells. Cranial neural crest cells give rise to the majority of craniofacial bones, cartilages and connective tissues. Therefore, understanding the events that control normal cranial neural crest and subsequent craniofacial development is important for elucidating the pathogenetic mechanisms of craniofacial anomalies and for the exploring potential therapeutic avenues for their prevention. Treacher Collins syndrome (TCS) is a congenital disorder characterized by severe craniofacial anomalies. An animal model of TCS, generated through mutation of Tcof1, the mouse (Mus musculus) homologue of the gene primarily mutated in association with TCS in humans, has recently revealed significant insights into the pathogenesis of TCS. Apoptotic elimination of neuroepithelial cells including neural crest cells is the primary cause of craniofacial defects in Tcof1 mutant embryos. However, our understanding of the mechanisms that induce tissue-specific apoptosis remains incomplete. In this review, we describe recent advances in our understanding of the pathogenesis TCS. Furthermore, we discuss the role of Tcof1 in normal embryonic development, the correlation between genetic and environmental factors on the severity of craniofacial abnormalities, and the prospect for prenatal prevention of craniofacial anomalies.
...
Four Questions Heading into the 2016 Season
Fran Drescher
TEENS LOVE HUGE COCKS fml
20250
¯\_(ツ)_/¯
margaretvanwyk
>A perfect mix of the Asian and White races, with wits, memes, bantz and looks to die for
...