Search for: All records

In this study, we compared the transient self-heating behavior of a homoepitaxial β-Ga2O3 MOSFET and a GaN-on-Si HEMT using nanoparticle-assisted Raman thermometry and thermoreflectance thermal imaging. The effectiveness of bottom-side and double-side cooling schemes using a polycrystalline diamond substrate and a diamond passivation layer were studied via transient thermal modeling. Because of the low thermal diffusivity of β-Ga2O3, the use of a β-Ga2O3 composite substrate (bottom-side cooling) must be augmented by a diamond passivation layer (top-side cooling) to effectively cool the device active region under both steady-state and transient operating conditions. Without no proper cooling applied, the steady-state device-to-package thermal resistance of a homoepitaxial β-Ga2O3 MOSFET is 2.6 times higher than that for a GaN-on-Si HEMT. Replacing the substrate with polycrystalline diamond (under a 6.5 μm-thick β-Ga2O3 layer) could reduce the steady-state temperature rise by 65% compared to that for a homoepitaxial β-Ga2O3 MOSFET. However, for high frequency power switching applications beyond the ~102 kHz range, bottom-side cooling (integration with a high thermal conductivity substrate) does not improve the transient thermal response of the device. Adding a diamond passivation over layer diamond not only suppresses the steadystate temperature rise, but also drastically reduces the transient temperature rise under high frequency operating conditions. 

We report the use of suboxide molecular-beam epitaxy ( S-MBE) to grow β-Ga 2 O 3 at a growth rate of ∼1 µm/h with control of the silicon doping concentration from 5 × 10 16 to 10 19  cm −3 . In S-MBE, pre-oxidized gallium in the form of a molecular beam that is 99.98% Ga 2 O, i.e., gallium suboxide, is supplied. Directly supplying Ga 2 O to the growth surface bypasses the rate-limiting first step of the two-step reaction mechanism involved in the growth of β-Ga 2 O 3 by conventional MBE. As a result, a growth rate of ∼1 µm/h is readily achieved at a relatively low growth temperature ( T sub ≈ 525 °C), resulting in films with high structural perfection and smooth surfaces (rms roughness of <2 nm on ∼1 µm thick films). Silicon-containing oxide sources (SiO and SiO 2 ) producing an SiO suboxide molecular beam are used to dope the β-Ga 2 O 3 layers. Temperature-dependent Hall effect measurements on a 1 µm thick film with a mobile carrier concentration of 2.7 × 10 17  cm −3 reveal a room-temperature mobility of 124 cm 2  V −1  s −1 that increases to 627 cm 2  V −1  s −1 at 76 K; the silicon dopants are found to exhibit an activation energy of 27 meV. We also demonstrate working metal–semiconductor field-effect transistors made from these silicon-doped β-Ga 2 O 3 films grown by S-MBE at growth rates of ∼1 µm/h. 

We report the use of suboxide molecular-beam epitaxy (S-MBE) to grow β-Ga2O3 at a growth rate of ∼1 μm/h with control of the silicon doping concentration from 5 × 1016 to 1019 cm−3 . In S-MBE, pre-oxidized gallium in the form of a molecular beam that is 99.98% Ga2O, i.e., gallium suboxide, is supplied. Directly supplying Ga2O to the growth surface bypasses the rate-limiting frst step of the two-step reaction mechanism involved in the growth of β-Ga2O3 by conventional MBE. As a result, a growth rate of ∼1 μm/h is readily achieved at a relatively low growth temperature (Tsub ≈ 525 ○C), resulting in flms with high structural perfection and smooth surfaces (rms roughness of <2 nm on ∼1 μm thick flms). Silicon-containing oxide sources (SiO and SiO2) producing an SiO suboxide molecular beam are used to dope the β-Ga2O3 layers. Temperature-dependent Hall effect measurements on a 1 μm thick flm with a mobile carrier concentration of 2.7 × 1017 cm−3 reveal a room-temperature mobility of 124 cm2 V−1 s −1 that increases to 627 cm2 V −1 s−1 at 76 K; the silicon dopants are found to exhibit an activation energy of 27 meV. We also demonstrate working metal–semiconductor feld-effect transistors made from these silicon-doped β-Ga2O3 flms grown by S-MBE at growth rates of ∼1 μm/h. 

In this work, β-Ga 2 O 3 fin field-effect transistors (FinFETs) with metalorganic chemical vapor deposition grown epitaxial Si-doped channel layer on (010) semi-insulating β-Ga 2 O 3 substrates are demonstrated. β-Ga 2 O 3 fin channels with smooth sidewalls are produced by the plasma-free metal-assisted chemical etching (MacEtch) method. A specific on-resistance (R on,sp ) of 6.5 mΩ·cm 2 and a 370 V breakdown voltage are achieved. In addition, these MacEtch-formed FinFETs demonstrate DC transfer characteristics with near zero (9.7 mV) hysteresis. The effect of channel orientation on threshold voltage, subthreshold swing, hysteresis, and breakdown voltages is also characterized. The FinFET with channel perpendicular to the [102] direction is found to exhibit the lowest subthreshold swing and hysteresis. 

ABSTRACT Susceptibility to breast cancer is significantly increased in individuals with germ line mutations in RECQ1 (also known as RECQL or RECQL1 ), a gene encoding a DNA helicase essential for genome maintenance. We previously reported that RECQ1 expression predicts clinical outcomes for sporadic breast cancer patients stratified by estrogen receptor (ER) status. Here, we utilized an unbiased integrative genomics approach to delineate a cross talk between RECQ1 and ERα, a known master regulatory transcription factor in breast cancer. We found that expression of ESR1 , the gene encoding ERα, is directly activated by RECQ1. More than 35% of RECQ1 binding sites were cobound by ERα genome-wide. Mechanistically, RECQ1 cooperates with FOXA1, the pioneer transcription factor for ERα, to enhance chromatin accessibility at the ESR1 regulatory regions in a helicase activity-dependent manner. In clinical ERα-positive breast cancers treated with endocrine therapy, high RECQ1 and high FOXA1 coexpressing tumors were associated with better survival. Collectively, these results identify RECQ1 as a novel cofactor for ERα and uncover a previously unknown mechanism by which RECQ1 regulates disease-driving gene expression in ER-positive breast cancer cells.