Pure titanium dioxide TiO2 photocatalytic substrates exhibit antibacterial activity only when they are irradiated with ultraviolet light, which comprises high-energy wavelengths that damage all life. Impurity doping of TiO2-related materials enables visible light to stimulate photocatalytic activity, which enhances opportunities for TiO2 to be used as a disinfectant in living environments. Boron-doped TiO2 displays visible-light-responsive bactericidal properties. However, because boron-derived compounds also exert notable antibacterial effects, most reports did not clearly demonstrate the extent to which the bactericidal property of boron-doped TiO2 is contributed by visible-light-stimulated photocatalysis. In addition, TiO2 thin films have considerable potential for applications in equipment that requires sterilization; however, the antibacterial properties of boron-doped TiO2 thin films have been examined by only a few studies. We found that boron-doped TiO2 thin films displayed visible-light-driven antibacterial properties. Moreover, because boron compounds may have intrinsic antibacterial properties, using control groups maintained in the dark, we clearly demonstrated that visible light stimulated the photocatalysis of boron-doped TiO2 thin films but not the residue boron compounds display antibacterial property. The bactericidal effects induced by visible light are equally potent for the elimination of the model organism Escherichia coli and human pathogens, such as Acinetobacter baumannii, Staphylococcus aureus, and Streptococcus pyogenes. The antibacterial applications of boron-doped TiO2 thin films are described, and relevant perspectives discussed.

An adaptive ferroelectric field-effect transistor (FET) with a floating gate has been developed using a thin film of lead titanate ( PbTiO3) deposited on a n/p+ substrate by rf sputtering. This device utilizes the charge storage on the floating gate to control the n layer conductivity of a n/p+ Si substrate and performs a memory function, in which the drain conductance changes in proportion to the charge storage density on the floating gate. The device is a bulk channel field transistor structure and different from the conventional surface channel-type floating gate memory device. Thus, it possesses higher mobility and fast access time (<160 ns). The FET has low write/erase voltages (≤10 V) and its write/erase cycles are more than 106.

An infrared optical field effect transistor has been developed using a thin film of lead titanate (PbTiO3) deposited on a n/p+ Si substrate by rf sputtering, in which the drain conductance changes in proportion to the infrared light power. A fast response with a rise time of 2.3 μs has been obtained that is about 150% faster than the other types of thermal infrared optical field effect transistor. The developed infrared sensor is a bulk channel field effect transistor structure, that possesses higher mobility. Thus, faster speed can be obtained. In addition, the sensor has been prepared on a Si substrate, which offers the potential to develop Si-based infrared optical-electric integrated circuits.

Hepatocellular carcinoma is one of the most common primary malignant tumors of the digestive system. Compound 5-chloro-N′-(2,4-dimethoxybenzylidene)-1H-indole-2-carbohydrazide (IHZ-1/ZJQ-24) is a novel indole hydrazide derivative. In a recent study, we demonstrated that IHZ-1 inhibits tumor growth and induces cell apoptosis through inhibiting the kinase activity of mTORC1 without activation of AKT, which is associated with JNK/IRS-1 activation. However, the impact and mechanisms of JNK activation by IHZ-1 in hepatocellular carcinoma remains entirely unknown. Here, we find that IHZ-1 increases the generation of intracellular ROS and enhances autophagy. The phosphorylation of JNK induced by IHZ-1 was reversed by the decreased ROS level. Moreover, inhibition of ROS/JNK or autophagy equally attenuated apoptotic effect induced by IHZ-1. Our findings suggest that the activation of JNK by IHZ-1 treatment is dependent on the generation of ROS that mediates apoptosis and autophagy in hepatocellular carcinoma.

Accumulating evidence indicates that the increased burden of senescent cells (SCs) in aged organisms plays an important role in many age-associated diseases. The pharmacological elimination of SCs with “senolytics” has been emerging as a new therapy for age-related diseases and extending the healthy lifespan. In the present study, we identified that cycloastragenol (CAG), a secondary metabolite isolated from Astragalus membrananceus, delays age-related symptoms in mice through its senolytic activity against SCs. By screening a series of compounds, we found that CAG selectively kills SCs by inducing SCs apoptosis and that this process is associated with the inhibition of Bcl-2 antiapoptotic family proteins and the PI3K/AKT/mTOR pathway. In addition, CAG treatment also suppressed the development of the senescence-associated secretory phenotype (SASP) in SCs, thereby inhibiting cell migration mediated by the SASP. Furthermore, the administration of CAG for 2 weeks to mice with irradiation-induced aging alleviated the burden of SCs and improved the animals’ age-related physical dysfunction. Overall, our studies demonstrate that CAG is a novel senolytic agent with in vivo activity that has the potential to be used in the treatment of age-related diseases.