Facile synthesis ofß-Ga2O3based high-performance electronic devices via direct oxidation of solution-processed transition metal dichalcogenides.

Gallium oxide (Ga2O3) is a promising wide bandgap semiconductor that is viewed as a contender for the next generation of high-power electronics due to its high theoretical breakdown electric field and large Baliga's figure of merit. Here, we report a facile route of synthesizingß-Ga2O3via direct oxidation conversion using solution-processed two-dimensional (2D) GaS semiconducting nanomaterial. Higher order of crystallinity in x-ray diffraction patterns and full surface coverage formation in scanning electron microscopy images after annealing were achieved. A direct and wide bandgap of 5 eV was calculated, and the synthesizedß-Ga2O3was fabricated as thin film transistors (TFT). Theß-Ga2O3TFT fabricated exhibits remarkable electron mobility (1.28 cm2Vs-1) and a good current ratio (Ion/Ioff) of 2.06 × 105. To further boost the electrical performance and solve the structural imperfections resulting from the exfoliation process of the 2D nanoflakes, we also introduced and doped graphene inß-Ga2O3TFT devices, increasing the electrical device mobility by ∼8-fold and thereby promoting percolation pathways for the charge transport. We found that electron mobility and conductivity increase directly with the graphene doping concentration. From these results, it can be proved that theß-Ga2O3networks have excellent carrier transport properties. The facile and convenient synthesis method successfully developed in this paper makes an outstanding contribution to applying 2D oxide materials in different and emerging optoelectronic applications.

Leptocarpin Suppresses Proliferation, Migration, and Invasion of Human Osteosarcoma by Targeting Type-1 Insulin-Like Growth Factor Receptor (IGF-1R).

BACKGROUND Leptocarpin (LTC) has drawn much attention for suppressing tumor growth or reducing inflammation. However, the effect of LTC on osteosarcoma has rarely been reported. Our object was to determine whether LTC suppresses MG63 cell proliferation, migration, and invasion, and whether type-1 insulin-like growth factor receptor (IGF-1R) is one of the targets in LTC suppressing osteosarcoma. MATERIAL AND METHODS Cytotoxicity of LTC was performed by use of a cell-counting kit-8 (CCK-8). RNA interference (RNAi) or pEABE-bleo IGF-1R plasmid were used for silencing or overexpressing IGF-1R, Western blot (WB) analysis was used for IGF-1R expression, CCK-8 for proliferation, and transwell assay for migration and invasion. RESULTS LTC (23.533 µM) treatment for 48 h was taken as the 50% inhibiting concentration (IC50), which significantly (P<0.05) suppressed MG63 cells proliferation, migration, and invasion. LTC (IC50) obviously inhibited IGF-1R expression in MG63 cells, with similar effect to small interfering RNA (siRNA), while pEABE-bleo IGF-1R transfection overexpressed IGF-1R. siRNA silencing IGF-1R suppressed MG63 cells proliferation, migration, and invasion, while pEABE-bleo IGF-1R transfection was significantly (P<0.05) promoted. With or without siRNA or pEABE-bleo IGF-1R transfection, LTC (IC50) suppressed MG63 cells proliferation, migration, and invasion. The effect of LTC (IC50) combined with siRNA on suppressing MG63 cells proliferation, migration, and invasion was more obvious, while the effect of LTC (IC50) combined with pEABE-bleo IGF-1R transfection was less significant (P<0.05). CONCLUSIONS LTC suppressed osteosarcoma proliferation, migration, and invasion by inhibiting IGF-1R expression. IGF-1R is one of the targets in LTC suppressing osteosarcoma.

[Effects of intravenous and inhalational anesthetics on short-latency somatosensory evoked potentials].

OBJECTIVE: To choose suitable general anesthetics dosages when short-latency somatosensory evoked potentials (SLSEP) is monitored during operation. METHODS: 150 ASA I-II neurosurgical patients undergoing elective operations were randomly divided into intravenous anesthesia group of 90 patients and inhalation anesthesia group of 60 patients. The intravenous anesthesia group was further divided into 9 subgroups of 10 patients treated with different anesthetics of different dosages: propofol (1.5 mg/kg, 2 mg/kg, and 3 mg/kg), midazolam (0.2 mg/kg, 0.3 mg/kg, and 0.4 mg/kg), and etomidate (0.15 mg/kg, 0.3 mg/kg, and 0.4 mg/kg). The intravenous anesthetics were given and upper limb SLSEP was monitored continuously. The inhalation anesthesia group was further divided into enflurane, isoflurane and desflurane subgroups of 20 patients each. The inhalational anesthetics were given at the concentrations corresponding to the end-expiratory concentrations of 0 to 0.3, 0.5, 0.75, 1.0 and 1.5 MAC. The changes of N(14), N(20) and central conduction time (CCT) were recorded. In addition to SLSEP, EKG, NIBP, SpO(2), P(ET) CO(2) were monitored as well as end-tidal anesthetic concentration. During the experiment SpO(2) was maintained > 95% and P(ET) CO(2) was maintained at the range of 35 - 45 mmHg by mask oxygen or assisted ventilation. RESULTS: The intravenous anesthetic propofol significantly decreased N(20) amplitude and produced less effect on the latency of N(14), N(20) and CCT. Midazolam significantly decreased the N(20) amplitude and prolonged the latency of N(20) and CCT. Etomidate significantly increased the N(20) amplitude, and the change did not recover when the patients had opened their eyes 10 minutes after medication. All three inhalational anesthetics significantly decreased the N(20) amplitude and prolonged the N(20) latency and CCT. N(20) amplitude disappeared in some patients treated with enflurane when the end-expiratory concentration was 1.0 MAC, while disappeared in some patients treated with isoflurane and desflurane when the end-expiratory concentration was 1.5 MAC for these 2 drugs. CONCLUSION: When using SLSEP monitoring, the most suitable general anesthetic is etomidate during the induction stage and isoflurane and desflurane during the maintenance stage with the end-expiratory concentration below 1.0 MAC.