Advances in flexible sensors for intelligent perception system enhanced by artificial intelligence

Intelligent perception means that with the assistance of artificial intelligence(AI)-motivated brain,flexible sensors achieve the ability of memory,learning,judgment,and reasoning about external information like the human brain.Due to the superiority of machine learning(ML)algorithms in data processing and intelligent recognition,intelligent perception systems possess the ability to match or even surpass human perception systems.However,the built-in flexible sensors in these systems need to work on dynamic and irregular surfaces,inevitably affecting the precision and fidelity of the acquired data.In recent years,the strategy of introducing the developed functional materials and innovative structures into flexible sensors has made some progress toward the above challenges,and with the blessing of ML algorithms,accurate perception and reasoning in various scenarios have been achieved.Here,the most representative functional materials and innovative structures for constructing flexible sensors are comprehensively reviewed,the research progress of intelligent perception systems based on flexible sensors and ML algorithms is further summarized,and the intersection of the two is expected to unlock new opportunities for next-stage AI development.

BCI induces apoptosis via generation of reactive oxygen species and activation of intrinsic mitochondrial pathway in H1299 lung cancer cells

The compound(E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1 H-inden-1-one(BCI) is known as an inhibitor of dual specific phosphatase 1/6 and mitogen-activated protein kinase. However, its precise anti-lung cancer mechanism remains unknown. In this study, the effects of BCI on the viability of non-small cell lung cancer cell lines NCI-H1299, A549, and NCI-H460 were evaluated. We confirmed that BCI significantly inhibited the viability of p53(-) NCI-H1299 cells as compared to NCI-H460 and A549 cells, which express wild-type p53. Furthermore, BCI treatment increased the level of cellular reactive oxygen species and pre-treatment of cells with N-acetylcysteine markedly attenuated BCI-mediated apoptosis of NCI-H1299 cells. BCI induced cellular morphological changes, inhibited viability, and produced reactive oxygen species in NCI-H1299 cells in a dose-dependent manner. BCI induced processing of caspase-9, caspase-3, and poly ADP-ribose polymerase as well as the release of cytochrome c from the mitochondria into the cytosol. In addition, BCI downregulated Bcl-2 expression and enhanced Bax expression in a dose-dependent manner in NCI-H1299 cells. However, BCI failed to modulate the expression of the death receptor and extrinsic factor caspase-8 and Bid, a linker between the intrinsic and extrinsic apoptotic pathways in NCI-H1299 cells. Thus, BCI induces apoptosis via generation of reactive oxygen species and activation of the intrinsic pathway in NCI-H1299 cells.