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Most hydrochromic materials only exhibit either absorption or fluorescence changes, which greatly restrict their applications. Herein, we reported a new hydrochromic dye capable of a absorption/fluorescence dual-mode change via transforming rhodamine B from its structure of lactone to pyrroline. Taking advantage of its excellent physico-chemical properties, this hydrochromic dye has been applied in water-jet printing, which has fast coloration speed, good reversibility, high resolution, and absorption/fluorescence two-mode display. Based on its fluorescence property, its application in information encryption has been illustrated. This dual-mode hydrochromic dye shows great potential in multifunctional integrated devices.

In a seminal work, Gozar et al. reported on the high-temperature interface superconductivity in bilayers of insulating La2CuO4 and metallic La2−xSrxCuO4 (x=0.45). An interesting question to address is how general and robust this interface superconductivity is. In the past, the cuprate bilayers were grown in a unique atomic-layer molecular beam epitaxy system, with a Sr doping range of x≤0.47, and the atomically flat interface was thought to be indispensable. Here, we have fabricated bilayers of La2CuO4 and La2−xSrxCuO4 by pulsed laser deposition. We have tried to extend the nominal doping range of Sr from the previous maximum of 0.47 to the present 1.70 (the nominal Sr content in the targets). X-ray diffraction result indicates that our La2−xSrxCuO4 films with x≤0.60 have very high crystalline quality; but the film crystalline structure degrades gradually with further increasing x, and finally the structure is fully lost when x reaches 1.40 and higher. Although the film quality scatters dramatically, our experiments show that there exists superconductivity for bilayers in nearly the entire over-doped Sr range, except for a non-superconducting region at x∼0.80. These observations demonstrate that the interface superconductivity in copper oxides is very general and robust.

Water solubility and adjustable fluorescence properties have been successfully implemented in the hydrochromic amino rhodamine via copolymerization. Four copolymers have been synthesized and clearly characterized by UV-Vis spectroscopy, proving greater detail than the commonly used NMR and IR technologies. The four copolymers have good solubility in pure water and in many common organic solvents, while preserving the hydrochromism of the dye monomer. Based on aggregation and dispersion of the copolymers as adjusted by solvent media and temperature, reversible fluorescence properties were successfully realized. Furthermore, their luminescence in solid state was observed. These studies are of great significance for expanding the application of hydrochromic dyes in biological fields and promoting green industrialization.

Colorectal cancer (CRC) is one of the most common malignancies worldwide with substantial mortality and morbidity. Alisertib (ALS) is a selective Aurora kinase A (AURKA) inhibitor with unclear effect and molecular interactome on CRC. This study aimed to evaluate the molecular interactome and anticancer effect of ALS and explore the underlying mechanisms in HT29 and Caco-2 cells. ALS markedly arrested cells in G2/M phase in both cell lines, accompanied by remarkable alterations in the expression level of key cell cycle regulators. ALS induced apoptosis in HT29 and Caco-2 cells through mitochondrial and death receptor pathways. ALS also induced autophagy in HT29 and Caco-2 cells, with the suppression of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), but activation of 5′ AMP-activated protein kinase (AMPK) signaling pathways. There was a differential modulating effect of ALS on p38 MAPK signaling pathway in both cell lines. Moreover, induction or inhibition of autophagy modulated basal and ALS-induced apoptosis in both cell lines. ALS potently suppressed epithelial to mesenchymal transition (EMT) in HT29 and Caco-2 cells. Collectively, it suggests that induction of cell cycle arrest, promotion of apoptosis and autophagy, and suppression of EMT involving mitochondrial, death receptor, PI3K/Akt/mTOR, p38 MAPK, and AMPK signaling pathways contribute to the cancer cell killing effect of ALS on CRC cells.