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In this study, a novel AlGaN/GaN heterostructure field-effect transistor based on open-gate technology was fabricated. Sample transistors of different structures and sizes were constructed. Through measurements, it was found that by changing the width of the opening, the threshold voltage of the device could be easily modulated across a larger range. The open-gate device had two working modes with different transconductance. When the gate-source voltage VGS ≤ − 4.5 V, only the open region was conductive, and a new working mechanism modulated the channel current. Corresponding theoretical analysis and calculations showed that its saturation mechanism was related to a virtual gate formed by electron injection onto the surface. Also, the gate-source voltage modulated the open channel current by changing the channel electron mobility through polarization Coulomb field scattering. When used as class-A voltage amplifiers, open-gate devices can achieve effective voltage amplification with very low power consumption. [ABSTRACT FROM AUTHOR]

E-mode P-GaN/AlGaN/GaN heterostructure field-effect transistors (HFETs) of various sizes were fabricated, and their parasitic source resistance (RS) was measured. The measurement results showed that RS varied greatly with changing gate bias, and the degree of RS change also differed with the gate bias of different-sized device samples. Through theoretical analysis, it is found that polarization Coulomb field (PCF) scattering caused by the device process and gate bias can affect electron mobility ( μ GS ) in the gate-source region, which causes the variations in μ GS for different-sized devices and same-sized devices under different gate biases. When μ GS changes with the device size and gate bias, the RS will change accordingly. Our study is the first to discover the gate bias dependency of RS for E-mode P-GaN/AlGaN/GaN HFETs due to PCF scattering, which provides a new idea for further in-depth studies on the RS of E-mode P-GaN/AlGaN/GaN HFETs and device performance optimization. [ABSTRACT FROM AUTHOR]

FGF2 is a neurotrophic factor that can act as a key regulatory molecule of neuroprotection, neurogenesis, and angiogenesis in various injuries. To explore the genetic background of the FGF2 gene on DPN development, this study analyzed the correlation between SNPs in the 3'UTR of the FGF2 gene and their interaction with environmental factors in DPN patients of Han Chinese nationality. Sanger sequencing was used to analyze the FGF2 genotypes at the rs1048201, rs3804158, rs41348645, rs6854081, rs3747676, rs7683093, rs1476215, and rs1476217 loci in 150 DPN patients, 150 NDPN patients, and 150 healthy control patients. Plasma FGF2 levels were measured in all subjects by using ELISAs. Subjects carrying the T allele at the rs1048201 locus in the FGF2 gene had a significantly lower risk of developing DPN compared with subjects carrying the C allele (OR = 0.43, 95% CI = 0.33–0.56, p < 0.01). Subjects with the G genotype at the rs6854081 locus had an exceptionally higher risk of developing DPN than subjects with the T allele (OR = 1.66, 95% CI = 1.39–1.89, p < 0.01). Individuals harboring the G allele at the rs7683093 locus had a markedly higher risk of DPN than patients with the C allele (OR = 1.63, 95% CI = 1.36–1.87, p < 0.01). Finally, individuals having the A genotype at the rs1476215 locus had a significantly higher risk of DPN than individuals carrying the T allele (OR = 1.82, 95% CI = 1.53–2.02, p < 0.01). There was an interaction between age and alcohol consumption and the SNP rs7683093. SNPs at rs1048201, rs6854081, rs7683093, and rs1476215 in the FGF2 3'UTR were strongly associated with plasma levels of FGF2 (p < 0.05). SNPs at the rs1048201, rs6854081, rs7683093, and rs1476215 loci in the FGF2 gene were significantly associated with the risk of DPN. A possible mechanism is that these SNPs affect the expression level of FGF2 by interrupting the binding of microRNAs to target sites in the 3'UTR. [ABSTRACT FROM AUTHOR]

NCAPG2 (non-SMC condensin II complex subunit G2), as an important factor in cell mitosis, has been the focus in the study of different cancers. However, the role of NCAPG2 in the malignancy of glioblastoma cells remains unknown. The findings from the present study demonstrated that NCAPG2 was significantly increased in human glioblastoma tissues and was associated with poor clinical outcome. Moreover, NCAPG2 could promote proliferation, migration, and invasion and regulate cell cycle in glioblastoma cells. Investigation of the molecular mechanism indicated that NCAPG2 regulated HBO1 phosphorylation and H4 histone acetylase activation, modulated the activation of Wnt/β-catenin pathway, and the binding of MCM protein to chromatin to exert its role. Furthermore, knockdown of HBO1 was found to reverse the effect of NCAPG2 overexpression on cell proliferation, migration, invasion, and cell cycle. In addition, knockdown of NCAPG2 attenuated glioblastoma tumorigenesis in vivo. Taken together, the findings demonstrated that NCAPG2 facilitates the malignancy of glioblastoma cells and xenograft tumor growth via HBO1 activation by phosphorylation. These results improve our understanding of the mechanism underlying glioblastoma progression and may contribute to the identification of novel biomarkers and therapeutic targets for glioblastoma. [ABSTRACT FROM AUTHOR]