Yibing Jia

TL;DR: It is demonstrated that nicotine can alter fetal monkey lung development by crossing the placenta to interact directly with nicotinic receptors on non-neuronal cells in the developing lung, and that similar effects likely occur in human infants whose mothers smoke during pregnancy.

TL;DR: It is demonstrated that SCLC can synthesize, secrete, and degrade ACh and that released ACh stimulates SclC cell growth and provides a potential new target for therapeutic intervention.

TL;DR: ACh meets all the criteria for an autocrine/paracrine hormone in lung bronchial epithelium and provides a potentially important target for cholinergic drugs.

TL;DR: Cholinergic signaling is broadly up-regulated in SCC and blocking cholinergic signalling can limit basal and nicotine-stimulated growth of SCC, one approach to blocking proliferative effects of nicotine and ACh on growth of lung cancers may be through M3 mAChR antagonists, which can limit the activation of mitogen-activated protein kinase that is caused by both nicotinic and muscarinic signaling.

TL;DR: This study demonstrates that the 3' end of genes is rich in sequence polymorphisms and is suitable for the efficient discovery of gene-linked SNPs, and shows that the genomic sequences of Indian and Chinese rhesus macaque are remarkably divergent, and include numerous population-specific SNPs.