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1.
ACS Appl Mater Interfaces ; 11(51): 48086-48094, 2019 Dec 26.
Artigo em Inglês | MEDLINE | ID: mdl-31773955

RESUMO

Carbon-doped GaN (GaN:C) Schottky diodes are prepared by controlling the destruction status of the graphene interlayer (GI) on the substrate. The GI without a sputtered AlN capping layer (CL) was destroyed because of ammonia precursor etching behavior in a high-temperature epitaxy. The damaged GI, like nanographite as a solid-state carbon doping source, incorporated the epitaxial growth of the GaN layer. The secondary ion mass spectroscopy depth profile indicated that the carbon content in the GaN layer can be tuned further by optimizing the sputtering temperature of AlN CL because of the better capping ability of high crystalline quality AlN CL on GI being achieved at higher temperature. The edge-type threading dislocation density and carbon concentration of the GaN:C layer with an embedded 550 °C-grown AlN CL on a GI substrate can be significantly reduced to 2.28 × 109 cm-2 and ∼2.88 × 1018 cm-3, respectively. Thus, a Ni-based Schottky diode with an ideality factor of 1.5 and a barrier height of 0.72 eV was realized on GaN:C. The series resistance increased from 28 kΩ at 303 K to 113 kΩ at 473 K, while the positive temperature coefficient (PTC) of series resistance was ascribed to the carbon doping that induced the compensation effect and lattice scattering effect. The decrease of the donor concentration was confirmed by temperature-dependent capacitance-voltage (C-V-T) measurement. The PTC characteristic of GaN:C Schottky diodes created by dissociating the GI as a carbon doping source should allow for the future use of high-voltage Schottky diodes in parallel, especially in high-temperature environments.

2.
Micromachines (Basel) ; 9(5)2018 Apr 27.
Artigo em Inglês | MEDLINE | ID: mdl-30424138

RESUMO

In this work, a MAPbBr3 quantum dot (QD-MAPbBr3) layer was prepared by a simple and rapid method. Octylammonium bromide (OABr) gives the MAPbBr3 better exciton binding energy, good surface morphology, and stability. To form a nanocrystalline thin film on indium tin oxide (ITO) glass, the QD-MAPbBr3 film was coated by a spin-coating method in a nitrogen-filled glove box and the NiOx film was used as an adhesive layer and hole transport layer. The highest transmittance of MAPbBr3 on NiOx/ITO glass was around 75% at 700 nm. This study also reported a high transparent and perovskite bulk-free ITO/NiOx/QD-MAPbBr3/C60/Ag solar cell where the NiOx, QD-MAPbBr3, and C60 were used as a hole transport layer, active layer, and electron transport layer, respectively.

3.
J Agric Food Chem ; 62(22): 5061-71, 2014 Jun 04.
Artigo em Inglês | MEDLINE | ID: mdl-24828835

RESUMO

Glioblastoma multiforme (GBM) is one of the most lethal types of tumors and highly metastatic and invasive. The epithelial-to-mesenchymal transition (EMT) is the crucial step for cancer cells to initiate the metastasis and could be induced by many growth factors. In this study, we found that GBM8401 cells were converted to fibroblastic phenotype and the space between the cells became expanded in response to insulin-like growth factor-1 (IGF-1) treatment. Epithelial markers were downregulated and mesenchymal markers were upregulated simultaneously after IGF-1 treatment. Our results illustrate that IGF-1 was able to induce EMT in GBM8401 cells. Osthole would reverse IGF-1-induced morphological changes, upregulated the expression of epithelial markers, and downregulated the expression of mesenchymal markers. Moreover, wound-healing assay also showed that osthole could inhibit IGF-1-induced migration of GBM8401 cells. By using dual-luciferase reporter assay and real-time PCR, we demonstrated that osthole inhibited IGF-1-induced EMT at the transcriptional level. Our study found that osthole decreased the phosphorylation of Akt and GSK3ß and recovered the GSK3ß bioactivity in inhibiting EMT transcription factor Snail and Twist expression. These results showed that osthole inhibited IGF-1-induced EMT by blocking PI3K/Akt pathway. We hope that osthole can be used in anticancer therapy and be a new therapeutic medicine for GBM in the future.


Assuntos
Neoplasias Encefálicas/metabolismo , Cumarínicos/farmacologia , Medicamentos de Ervas Chinesas/farmacologia , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Glioblastoma/metabolismo , Fator de Crescimento Insulin-Like I/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Neoplasias Encefálicas/tratamento farmacológico , Neoplasias Encefálicas/genética , Linhagem Celular Tumoral , Cnidium/química , Glioblastoma/tratamento farmacológico , Glioblastoma/genética , Humanos , Fosfatidilinositol 3-Quinases/genética , Fosforilação/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-akt/genética , Transdução de Sinais/efeitos dos fármacos
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