Search

In this study, the ungated AlGaN/GaN devices with special mesa structures were designed. The hypothesis of effective width expansion was tested experimentally by using ungated samples with different sizes, and an empirical expression for calculating the conduction channel effective width was given according to the experimental results. Finally, split-gate AlGaN/GaN heterostructure field-effect transistors (HFETs) with different gate lengths were prepared, and the channel electron mobility of split-gate samples was calculated by using the empirical expression and polarization Coulomb field (PCF) scattering theoretical model. The results showed that, for split-gate AlGaN/GaN HFETs, with the increase in the gate length, the total amount of additional polarization charges underneath the gate increases, resulting in the enhancement of the PCF scattering intensity. [ABSTRACT FROM AUTHOR]

Our current research aims to examine whether protocatechuic acid (PCA) can be used as a therapeutic agent for the development of cerebral aneurysm (CA) and to elucidate the mechanisms behind this. We assessed the effects of PCA at 50 and 100 mg/kg on the activation of signaling pathways for tissue necrosis factor (TNF)-α/nuclear factor (NF)-κB/nuclear factor erythroid 2 (Nrf-2) on progression and development in an elastase-induced CA model, accompanied by a high-salt diet to induce hypertension. The expression of inflammatory cytokines, chemokines, tumor necrosis factor-α, interleukins (IL)-8, IL-17, IL-6, IL-1β, and matrix metalloproteinase (MMP)-2 and MMP-9 was analyzed by ELISA, western blot, and reverse transcriptase quantative polymerase chain reaction. The expression levels of antioxidant enzymes and translocation of Nrf-2 were also determined. The group treated with PCA demonstrated a significant (P < 0.05) decrease in the aneurysmal size in rats compared to the CA-induced group. We found that PCA treatment suppressed the invasion of macrophage and activation of TNF-α/NF-κB/Nrf-2 signaling pathways. There was a significant decrease (P < 0.05) in pro-inflammatory cytokine and chemokine levels in a dose-dependent manner. We found that PCA treatment exerts protective effects by suppressing the development and progression of CA through the inhibition of inflammatory responses in macrophages via TNF-α/NF-κB/Nrf-2 signaling pathways, thus demonstrating that PCA can act as a treatment for CA.

In this study, a split-gate AlGaN/GaN heterostructure field-effect transistor with an auxiliary gate was fabricated. Through experiment and analysis, it was discovered that by applying a constant potential (usually 0 V or negative potential) to the auxiliary gate, a negative bias can be formed between the auxiliary gate and the channel. This consumes the two-dimensional electron gas in the channel, leading to significant improvements in the saturation characteristics of split-gate devices. By applying different potentials to the main gate and the auxiliary gate, a variety of device working modes can be obtained, and the threshold voltage can be altered across a large range. These advantages make split-gate devices with auxiliary gates more suitable for increasingly complex integrated circuit applications. [ABSTRACT FROM AUTHOR]

The relationship between mobility and subthreshold swing (SS) of AlGaN/GaN HFETs was investigated at 10 and 20 V drain bias using the Monte Carlo method. We find that the polarization Coulomb field (PCF) scattering dominates the mobility at both 10 and 20 V drain bias. The channel carrier mobility is reduced as the gate bias becomes more negative, which reduces SS. The influence of mobility has not been considered in the 60 mV/dec rule, and PCF scattering is crucial for SS to be lower than 60 mV/dec in AlGaN/GaN HFETs. However, when the drain bias is 10 V, the CF scattering significantly diminishes SS. When the drain bias is 20 V, the SS barely decreases. Accordingly, a lower drain–source bias is needed to appropriately reduce SS. [ABSTRACT FROM AUTHOR]

This paper demonstrates the improvement of device linearity in AlGaN/GaN heterostructure field effect transistors (HFETs) using polarization Coulomb field (PCF) scattering and investigates the relationship between device linearity and PCF scattering under 10 and 20 V drain bias. The mobility of the gate-to-source region in AlGaN/GaN HFETs is calculated using the Monte Carlo method. We find that PCF scattering decreases with an increase in gate bias (from −3 to −0.5 V) under high field conditions, leading to lower gate-to-source resistance. Under 20 V drain bias, linearity is worse than under 10 V drain bias. The transconductance drop is significant in AlGaN/GaN HFETs, which damages linearity. By adopting an appropriate drain bias, PCF scattering can alleviate transconductance drop and improve the linearity of AlGaN/GaN HFETs. [ABSTRACT FROM AUTHOR]

AlGaN/GaN heterostructure field-effect transistors (HFETs) with three kinds of gate lengths were fabricated, and the theory of polarization Coulomb field (PCF) scattering with the electron systems in the AlGaN/GaN HFETs was studied. There are two methods of analysis and calculation of the PCF scattering in AlGaN/GaN HFETs: one is by considering the 2-dimensional electronic gas (2DEG) of the gate-source, gate-drain, and gate regions as three independent electron systems and the other is by considering the 2DEG of the drain–source channel as a unified electron system. The calculation and analysis of the additional polarization charges underneath the gate region for the prepared AlGaN/GaN HFETs indicate that the theory of PCF scattering in AlGaN/GaN HFETs with three independent electron systems is more accurate. [ABSTRACT FROM AUTHOR]

A physics-based model for the output current–voltage (I–V) characteristics of AlGaN/GaN HFETs is developed based on AlGaAs/GaAs HFETs. It is demonstrated that Polarization Coulomb Field (PCF) scattering greatly influences channel electron mobility. With different gate biases, channel electron mobility is varied by PCF scattering. Furthermore, a more negative gate bias and a lower ratio of l g / l s d (gate length/source-drain space) of the device causes the PCF scattering to have stronger influence on channel electron mobility. This work is the first to apply PCF scattering to a physics-based model for AlGaN/GaN HFETs with I–V characteristics and the results indicate that PCF scattering is essential for a physics-based model to identify I–V characteristics of AlGaN/GaN HFETs. [ABSTRACT FROM AUTHOR]

The small-signal S parameters of the fabricated double-finger gate AlGaN/GaN high electron mobility transistors (HEMTs) were measured at various direct current quiescent operating points (DCQOPs). Under active bias conditions, small-signal equivalent circuit (SSEC) parameters such as R s and R d , and intrinsic parameters were extracted. Utilizing f T and the SSEC parameters, the effective electron velocity (νe-eff) and intrinsic electron velocity (νe-int) corresponding to each gate bias (V GS ) were obtained. Under active bias conditions, the influence mechanism of V GS on νe-eff was systematically studied, and an expression was established that correlates νe-eff, νe-int, and bias-dependent parasitic resistances. Through the analysis of the main scattering mechanisms in AlGaN/GaN HEMTs, it has been discovered that the impact of V GS on νe-eff should be comprehensively analyzed from the aspects of νe-int and parasitic resistances. On the one hand, changes in V GS influence the intensity of polar optical phonon (POP) scattering and polarization Coulomb field (PCF) scattering, which lead to changes in νe-int dependent on V GS . The trend of νe-int with changes in V GS plays a dominant role in determining the trend of νe-eff with changes in V GS . On the other hand, both POP scattering and PCF scattering affect νe-eff through their impact on parasitic resistance. Since there is a difference in the additional scattering potential corresponding to the additional polarization charges ( APC ) between the gate-source/drain regions and the region under the gate, the mutual effects of PCF scattering on the under-gate electron system and the gate-source/drain electron system should be considered when adjusting the PCF scattering intensity through device structure optimization to improve linearity. This study contributes to a new understanding of the electron transport mechanisms in AlGaN/GaN HEMTs and provides a novel theoretical basis for improving device performance.

Aberrant expression of oncogenes and/or tumor suppressors play fundamental roles in the pathogenesis of glioma. B-cell CLL/lymphoma 3 (BCL3) was previously found to be a putative proto-oncogene in human cancers and the decoy receptor DcR1 is induced in a p50/Bcl3-dependent manner and attenuates the efficacy of temozolomide in glioblastoma cells. However, its expression status, clinical significance and biological functions in glioma remain largely unknown. In the present study, the levels of BCL3 were overexpressed in glioma compared to normal brain tissues. Furthermore, high expression of BCL3 protein was confirmed by immunoblotting in glioma cells as compared with normal human astrocyte cell line. The positive expression of BCL3 was correlated with adverse prognostic features and reduced overall survival rate of glioma patients. BCL3 silencing resulted in prominent decreased proliferation, cell cycle arrest in G1 phase and increased apoptosis in U251 cells. In contrast, BCL3 overexpression in U87 cells remarkably facilitated proliferative ability and cell cycle progression and induced apoptosis. In vivo studies showed that BCL3 knockdown inhibited the tumor growth of U251 cells in a mouse xenograft model. Mechanistically, BCL3 positively regulated the abundance of STAT3, p-STAT3 and the downstream targets of STAT3 pathway including BCL2, MCL-1 and cyclin D1 in glioma cells. Furthermore, a positive correlation between BCL3 and STAT3 expression was observed in glioma specimens. Notably, we confirmed that STAT3 knockdown abolished the oncogenic roles of BCL3 in glioma. In conclusion, we suggest that BCL3 serves as an oncogene in glioma by modulating proliferation, cell cycle progression and apoptosis, and its oncogenic effects are mediated by the STAT3 signaling pathway.