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1.
Nanomaterials (Basel) ; 13(5)2023 Feb 27.
Artigo em Inglês | MEDLINE | ID: mdl-36903774

RESUMO

Recently, we reported that device performance degradation mechanisms, which are generated by the γ-ray irradiation in GaN-based metal-insulator-semiconductor high electron mobility transistors (MIS-HEMTs), use extremely thin gate insulators. When the γ-ray was radiated, the total ionizing dose (TID) effects were generated and the device performance deteriorated. In this work, we investigated the device property alteration and its mechanisms, which were caused by the proton irradiation in GaN-based MIS-HEMTs for the 5 nm-thick Si3N4 and HfO2 gate insulator. The device property, such as threshold voltage, drain current, and transconductance varied by the proton irradiation. When the 5 nm-thick HfO2 layer was employed for the gate insulator, the threshold voltage shift was larger than that of the 5 nm-thick Si3N4 gate insulator, despite the HfO2 gate insulator exhibiting better radiation resistance compared to the Si3N4 gate insulator. On the other hand, the drain current and transconductance degradation were less for the 5 nm-thick HfO2 gate insulator. Unlike the γ-ray irradiation, our systematic research included pulse-mode stress measurements and carrier mobility extraction and revealed that the TID and displacement damage (DD) effects were simultaneously generated by the proton irradiation in GaN-based MIS-HEMTs. The degree of the device property alteration was determined by the competition or superposition of the TID and DD effects for the threshold voltage shift and drain current and transconductance deterioration, respectively. The device property alteration was diminished due to the reduction of the linear energy transfer with increasing irradiated proton energy. We also studied the frequency performance degradation that corresponded to the irradiated proton energy in GaN-based MIS-HEMTs using an extremely thin gate insulator.

2.
Nanomaterials (Basel) ; 10(11)2020 Oct 30.
Artigo em Inglês | MEDLINE | ID: mdl-33143313

RESUMO

The device performance deterioration mechanism caused by the total ionizing dose effect after the γ-ray irradiation was investigated in GaN-based metal-insulator-semiconductor high electron mobility transistors (MIS-HEMTs) for a 5 nm-thick SiN and HfO2 gate dielectric layer. The γ-ray radiation hardness according to the gate dielectric layer was also compared between the two different GaN-based MIS-HEMTs. Although HfO2 has exhibited strong tolerance to the total ionizing dose effect in Si-based devices, there is no detail report of the γ-ray radiation effects in GaN-based MIS-HEMTs employing a HfO2 gate dielectric layer. The pulsed-mode stress measurement results and carrier mobility behavior revealed that the device properties not only have direct current (DC) characteristics, but radio frequency (RF) performance has also been mostly degraded by the deterioration of the gate dielectric quality and the trapped charges inside the gate insulator. We also figured out that the immunity to the γ-ray radiation was improved when HfO2 was employed instead of SiN as a gate dielectric layer due to its stronger endurance to the γ-ray irradiation. Our results highlight that the application of a gate insulator that shows superior immunity to the γ-ray irradiation is a crucial factor for the improvement of the total ionizing dose effect in GaN-based MIS-HEMTs.

3.
Nanomaterials (Basel) ; 10(11)2020 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-33114425

RESUMO

An enhancement-mode AlGaN/GaN metal-insulator-semiconductor high-electron- mobility-transistor was fabricated using a recess gate and CF4 plasma treatment to investigate its reliable applicability to high-power devices and circuits. The fluorinated-gate device showed hysteresis during the DC current-voltage measurement, and the polarity and magnitude of hysteresis depend on the drain voltage. The hysteresis phenomenon is due to the electron trapping at the Al2O3/AlGaN interface and charging times longer than milliseconds were obtained by pulse I-V measurement. In addition, the subthreshold slope of the fluorinated-gate device was increased after the positive gate bias stress because of the two-dimensional electron gas reduction by ionized fluorine. Our systematic observation revealed that the effect of fluorine ions should be considered for the design of AlGaN/GaN power circuits.

4.
Oncotarget ; 8(54): 92090-92105, 2017 Nov 03.
Artigo em Inglês | MEDLINE | ID: mdl-29190900

RESUMO

The epidermal growth factor receptor (EGFR) is one of the most comprehensively studied molecular targets in head and neck squamous cell carcinoma (HNSCC). However, inherent and acquired resistance are serious problems and are responsible for limited clinical efficacy and tumor recurrence. In this study, we evaluated the feasibility of immuno-positron emission tomography (PET) imaging and radioimmunotherapy (RIT) with 64Cu-/177Lu-PCTA-cetuximab in cetuximab-resistant SNU-1066 HNSCC xenografted model. The cellular uptake of 64Cu/177Lu-3,6,9,15-tetraazabicyclo[9.3.1]-pentadeca-1(15),11,13-triene-3,6,9,-triacetic acid (PCTA)-cetuximab showed good correlation with western blot and flow cytometry analysis in EGFR expression level of various HNSCC cells. 177Lu-PCTA-cetuximab selectively killed cetuximab-resistant SNU-1066 cells in vitro. 64Cu-/177Lu-PCTA-cetuximab specifically accumulated in SNU-1066 tumor and those uptakes were peaked at 48 h and 7 day, respectively in biodistribution, PET and single-photon emission computed tomography/computed tomography (SPECT/CT) imaging. RIT with single dose of 177Lu-PCTA-cetuximab exhibited significant tumor regression and markedly reduced 2-[18F]fluoro-2-deoxy-D-glucose (18F-FDG) uptake, compared to other groups. Proliferation index were dramatically decreased and apoptotic index increased in RIT group. These results suggest that a diagnostic and therapeutic convergence radiopharmaceutical, 64Cu-/177Lu-PCTA-cetuximab has the potential of target selection using immuno-PET imaging and targeted therapy by RIT in EGFR expressing cetuximab-resistant HNSCC tumors.

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