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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.

This study presents the fabrication and improved properties of an AlGaAs/InGaAs metal-oxide-semiconductor pseudomorphic high-electron-mobility transistor (MOS-PHEMT) using liquid phase deposited titanium dioxide (LPD-TiO2) as a gate dielectric. Sulfur pretreatment and postoxidation rapid thermal annealing (RTA) were consecutively employed before and after the gate dielectric was deposited to fill dangling bonds and therefore release interface trapped charges. Compared with a benchmark PHEMT, the AlGaAs/InGaAs MOS-PHEMT using LPD-TiO2 exhibited larger gate bias operation, higher breakdown voltage, suppressed subthreshold characteristics, and reduced flicker noise. As a result, the device with proposed process and using LPD-TiO2 as a gate dielectric is promising for high-speed applications that demand little noise at low frequencies.

As phagocytic cells of central nervous system, excessive activation or cell death of microglia is involved in a lot of nervous system injury and degenerative disease, such as stroke, epilepsy, Parkinson's disease, Alzheimer's disease. Accumulating evidence indicates that hypoxia upregulates HIF-1α expression leading to cell death of microglia. However, the exact mechanism of cell death induced by hypoxia in microglia is not clear. In the current study, we showed that hypoxia induced cell death and autophagy in microglia. The suppression of autophagy using either pharmacologic inhibitors (3-methyladenine, bafilomycin A1) or RNA interference in essential autophagy genes (BECN1 and ATG5) decreased the cell death induced by hypoxia in microglia cells. Moreover, the suppression of HIF-1α using either pharmacologic inhibitors (3-MA, Baf A1) or RNA interference decreased the microglia death and autophagy in vitro. Taken together, these data indicate that hypoxia contributes to autophagic cell death of microglia through HIF-1α, and provide novel therapeutic interventions for cerebral hypoxic diseases associated with microglia activation.