Role of α7-nicotinic acetylcholine receptor in nicotine-induced invasion and epithelial-to-mesenchymal transition in human non-small cell lung cancer cells.

Nicotine via nicotinic acetylcholine receptors (nAChRs) stimulates non-small cell lung cancer (NSCLC) cell invasion and epithelial to mesenchymal transition (EMT) which underpin the cancer metastasis. However, the receptor subtype-dependent effects of nAChRs on NSCLC cell invasion and EMT, and the signaling pathway underlying the effects remain not fully defined. We identified that nicotine induced NSCLC cell invasion, migration, and EMT; the effects were suppressed by pharmacological intervention using α7-nAChR selective antagonists or by genetic intervention using α7-nAChR knockdown via RNA inference.

A new motif in the N-terminal of acetylcholinesterase triggers amyloid-β aggregation and deposition.

Background And Purpose: As a molecular chaperone, acetylcholinesterase (AChE; EC 3.1.1.

[The surface states and the electron-hole pair recombination of TiO2 nanopowders].

The nanometer TiO2 was prepared by sol-gel method. The structure and composition of the nanometer TiO2 were analyzed in detail by X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), and Fourier transform infrared spectrometry (FTIR). The UV-visible spectrum and fluorescence spectrum were studied too.

[Effect of oxygen partial pressure on the band-gap of the TiO2 films prepared by DC reactive sputtering].

TiO2 films have been deposited on glass substrates using DC reactive magnetron sputtering at different oxygen partial pressures from 0.10 to 0.65 Pa.