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The study explored titanium dioxide (TiO 2 ) prepared by liquid phase deposition (LPD) deposited on (NH 4 ) 2 S x -treated aluminum gallium arsenide (AlGaAs), including the surface roughness by using atomic force microscopy (AFM) measurements and electrical properties. The leakage current density of MOS capacitor is approximately 6.83 × 10 −7 A/cm 2 at zero electric field for the sample without any pretreatment. The interface trap density ( D it ) and the flat-band voltage shift (Δ V FB ) are 4.46 × 10 12 cm −2 eV −1 and 3.6 V, respectively. After the 10 min 5% (NH 4 ) 2 S x pretreatment, the leakage current density, D it , and Δ V FB can be improved to 1.04 × 10 −7 A/cm 2 at zero electric field, 2.28 × 10 12 cm −2 eV −1 , and 2 V, respectively. The paper also demonstrates the application to the AlGaAs/InGaAs metal-oxide-semiconductor pseudomorphic high-electron-mobility transistor (MOS-PHEMT) using LPD-TiO 2 after 10 min sulfide pretreatment.

Liquid phase deposition (LPD) was performed to fabricate titanium dioxide (TiO 2 ) on AlGaAs by using ammonium sulfide pretreatment. In addition, the study investigated how postoxidation rapid thermal annealing (RTA) affected the LPD-TiO 2 on (NH 4 ) 2 S x -treated AlGaAs. The deposition rate of the as-deposited LPD-TiO 2 for the 10 min 5% (NH 4 ) 2 S x -treated AlGaAs was approximately 126 nm/h. Following the 10 min 5% (NH 4 ) 2 S x pretreatment and a postoxidation RTA at 350 °C for 1 min, the root mean square value, leakage current density at 0 MV/cm, interface trap density, and flat-band voltage shift were improved to 6.20, 5.64 × 10 − 8 A/cm 2 , 6.48 × 10 11 cm − 2 eV − 1 , and 1.5 V, respectively.

Much evidence demonstrates that microglia mediated neuroinflammation is an important contributor to the inflammatory injury in intracerebral hemorrhage (ICH). Therefore, the compounds that can inhibit neuroinflammation are greatly needed. In the current study, we examined whether curcumin, present in a Chinese medicinal plant, could prevent ICH induced microglia activation and confer protection against neurotoxicity. The cytokines of microglia were measured by ELISA, p38MAPK/PKC and NF-κB were measured by Western blot and EMSA. Microglial toxicity was assessed using MTT and FACS assays. And neurological function was evaluated by animal behavioristics. We found that curcumin prevented ICH-induced inflammatory molecules through NF-κB activation via the p38MAPK/PKC pathway in vitro. In addition, curcumin protected hippocampal HT22 cells from indirect toxicity mediated by ICH-treated microglia cells. Further, curcumin also attenuated ICH-induced neurological deficit and cerebral water content in vivo. Together, our findings suggest that curcumin could suppress ICH induced inflammatory injury and represent a novel herbal sources for ICH therapeutical strategy.