AlGaN-channel high-electron-mobility transistor (HEMT) with high Al composition of 0.51 has been developed. The epitaxial layers were grown on a free-standing AlN substrate to improve crystalline quality. The fabricated device exhibited a maximum drain current (Idsmax) of 25.2 mA/mm with a maximum transconductance (gmmax) of 4.7 mS/mm. The characteristic features of the device were a high source-to-drain breakdown voltage of 1800 V and a high applicable gate-to-source voltage of 4 V in the forward direction. Temperature dependence of DC characteristics demonstrated that the drain current degradation at elevated temperatures for the AlGaN-channel HEMT was appreciably small as compared with the conventional AlGaN/GaN HEMT. This is the first report showing successful DC operation of AlGaN-channel HEMT with high Al composition of over 0.5.
This paper describes high-temperature electron transport properties of AIGaN-channel HEMT fabricated on a free-standing A1N substrate, estimated at temperatures between 25 and 300°C. The AIGaNchannel HEMT exhibited significantly reduced temperature dependence in DC and RF device characteristics, as compared to those for the conventional A1GaN/GaN HEMT, resulting in larger values in both saturated drain current and current gain cutoff frequency at 300°C. Delay time analyses suggested that the temperature dependence of the AIGaN-channel HEMT was primarily dominated by the effective electron velocity in the A1GaN channel. These results indicate that an A1GaN-channel HEMT fabricated on an AIN substrate is promising for high-performance device applications at high temperatures. key words: AlGaN channel, high temperature, HEMT was still larger for the conventional A1GaN/GaN HEMT than that for the A1GaN-channel device, and no data have been reported on the high-temperature RF performance for the AlGaN-channel HEMT. In this paper, DC and RF performance of A1GaNchannel HEMTs fabricated on an A1N substrate is presented. The maximum drain current and the current gain cutoff frequency measured at temperatures from RT to 300°C are compared between devices with an AIGaN channel and a GaN channel. The mechanism responsible for the superior performance for the developed A1GaN-channel HEMT at high temperatures is discussed.
In this paper, we report on AlGaN/GaN metal–insulator–semiconductor high-electron-mobility transistors (MIS-HEMTs) fabricated using ZrO2/Al2O3 as a gate dielectric stack. Gate leakage characteristics as well as dynamic on-resistance due to current collapse have been studied for a ZrO2 (2 nm)/Al2O3 (2 nm)/AlGaN/GaN MIS-HEMT and compared with those for MIS-HEMTs with a single gate insulator of Al2O3 (4 nm) and ZrO2 (4 nm). It was found that an Al2O3 gate insulator was effective in reducing the forward gate leakage and in suppressing the current collapse, whereas the use of the ZrO2 dielectric resulted in a suppressed reverse gate leakage current. The composite ZrO2/Al2O3 MIS-HEMT exhibited superior thermal stability in both gate leakage and dynamic on-resistance up to 200 °C.
Cortical dysplasia, complex, with other brain malformations 3 (CDCBM3) is a rare autosomal dominant syndrome caused by Kinesin family Member 2A (KIF2A) gene mutation. Patients with CDCBM3 exhibit posterior dominant agyria/pachygyria with severe motor dysfunction. Here, we report an 8‐year‐old boy with CDCBM3 showing a typical, but relatively mild, clinical presentation of CDCBM3 features. Whole‐exome sequencing identified a heterozygous mutation of NM_001098511.2:c.1298C>A [p.(Ser433Tyr)]. To our knowledge, the mutation has never been reported previously. The variant was located distal to the nucleotide binding domain (NBD), in which previously‐reported variants in CDCBM3 patients have been located. The computational structural analysis showed the p.433 forms the pocket with NBD. Variants in KIF2A have been reported in the NBD for CDCBM3, in the kinesin motor 3 domain, but not in the NBD in epilepsy, and outside of the kinesin motor domain in autism spectrum syndrome, respectively. Our patient has a variant, that is not in the NBD but at the pocket with the NBD, resulting in a clinical features of CDCBM3 with mild symptoms. The clinical findings of patients with KIF2A variants appear restricted to the central nervous system and facial anomalies. We can call this spectrum “KIF2A syndrome” with variable severity.
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