Sensing Mechanism and Characterization of NO2 Gas Sensors Using Gold-Black NP-Decorated Ga2O3 Nanorod Sensing Membranes.

In this work, a vapor cooling condensation system was utilized to deposit various amounts of p-type gold-black nanoparticles (NPs) onto the surface of n-type gallium oxide (Ga2O3) nanorods forming p-n heterojunction-structured sensing membranes of nitrogen dioxide (NO2) gas sensors. The role and the sensing mechanism of the various gold-black NP-decorated Ga2O3 nanorods in NO2 gas sensors were investigated. The coverage and atomic percentage of the sensing membranes were observed using high-resolution transmission electron microscopy (HRTEM) measurements and energy-dispersive spectroscopy (EDS), respectively. For the NO2 gas sensor using the sensing membrane of 60 s-deposited gold-black NP-decorated Ga2O3 nanorods under a NO2 concentration of 10 ppm, the highest responsivity of 5221.1% was obtained. This result was attributed to the spillover effect and the formation of the p-n heterojunction, which increased more ionized-oxygen adsorption sites and promoted the reaction between NO2 gas and Ga2O3 nanorods. Furthermore, the NO2 gas sensor could detect the low NO2 concentration of 100 ppb and achieved a responsivity of 56.9%. The resulting NO2 gas sensor also exhibited excellent selectivity for detecting NO2 gas, with higher responsivity at a NO2 concentration of 10 ppm compared with that of the C2H5OH and NH3 concentrations of 100 ppm.

Investigation of High-Sensitivity NO2 Gas Sensors with Ga2O3 Nanorod Sensing Membrane Grown by Hydrothermal Synthesis Method.

In this work, Ga2O3 nanorods were converted from GaOOH nanorods grown using the hydrothermal synthesis method as the sensing membranes of NO2 gas sensors. Since a sensing membrane with a high surface-to-volume ratio is a very important issue for gas sensors, the thickness of the seed layer and the concentrations of the hydrothermal precursor gallium nitrate nonahydrate (Ga(NO3)3·9H2O) and hexamethylenetetramine (HMT) were optimized to achieve a high surface-to-volume ratio in the GaOOH nanorods. The results showed that the largest surface-to-volume ratio of the GaOOH nanorods could be obtained using the 50-nm-thick SnO2 seed layer and the Ga(NO3)3·9H2O/HMT concentration of 12 mM/10 mM. In addition, the GaOOH nanorods were converted to Ga2O3 nanorods by thermal annealing in a pure N2 ambient atmosphere for 2 h at various temperatures of 300 °C, 400 °C, and 500 °C, respectively. Compared with the Ga2O3 nanorod sensing membranes annealed at 300 °C and 500 °C, the NO2 gas sensors using the 400 °C-annealed Ga2O3 nanorod sensing membrane exhibited optimal responsivity of 1184.6%, a response time of 63.6 s, and a recovery time of 135.7 s at a NO2 concentration of 10 ppm. The low NO2 concentration of 100 ppb could be detected by the Ga2O3 nanorod-structured NO2 gas sensors and the achieved responsivity was 34.2%.

ßPS-Integrin acts downstream of Innexin 2 in modulating stretched cell morphogenesis in the Drosophila ovary.

During oogenesis, a group of specialized follicle cells, known as stretched cells (StCs), flatten drastically from cuboidal to squamous shape. While morphogenesis of epithelia is critical for organogenesis, genes and signaling pathways involved in this process remain to be revealed. In addition to formation of gap junctions for intercellular exchange of small molecules, gap junction proteins form channels or act as adaptor proteins to regulate various cellular behaviors. In invertebrates, gap junction proteins are Innexins. Knockdown of Innexin 2 but not other Innexins expressed in follicle cells attenuates StC morphogenesis. Interestingly, blocking of gap junctions with an inhibitor carbenoxolone does not affect StC morphogenesis, suggesting that Innexin 2 might control StCs flattening in a gap-junction-independent manner. An excessive level of ßPS-Integrin encoded by myospheroid is detected in Innexin 2 mutant cells specifically during StC morphogenesis. Simultaneous knockdown of Innexin 2 and myospheroid partially rescues the morphogenetic defect resulted from Innexin 2 knockdown. Furthermore, reduction of ßPS-Integrin is sufficient to induce early StCs flattening. Taken together, our data suggest that ßPS-Integrin acts downstream of Innexin 2 in modulating StCs morphogenesis.

Investigation of Ga2O3-Based Deep Ultraviolet Photodetectors Using Plasma-Enhanced Atomic Layer Deposition System.

In this work, Ga2O3 films were deposited on sapphire substrates using a plasma-enhanced atomic layer deposition system with trimethylgallium precursor and oxygen (O2) plasma. To improve the quality of Ga2O3 films, they were annealed in an O2 ambient furnace system for 15 min at 700, 800, and 900 °C, respectively. The performance improvement was verified from the measurement results of X-ray diffraction, X-ray photoelectron spectroscopy, and photoluminescence spectroscopy. The optical bandgap energy of the Ga2O3 films decreased with an increase of annealing temperatures. Metal-semiconductor-metal ultraviolet C photodetectors (MSM UVC-PDs) with various Ga2O3 active layers were fabricated and studied in this work. The cut-off wavelength of the MSM UVC-PDs with the Ga2O3 active layers annealed at 800 °C was 250 nm. Compared with the performance of the MSM UVC-PDs with the as-grown Ga2O3 active layers, the MSM UVC-PDs with the 800 °C-annealed Ga2O3 active layers under a bias voltage of 5 V exhibited better performances including photoresponsivity of 22.19 A/W, UV/visible rejection ratio of 5.98 × 104, and detectivity of 8.74 × 1012 cmHz1/2W-1.

Performance improvement of Y-doped VOx microbolometers with nanomesh antireflection layer.

In the study, the yttrium (Y)-doped vanadium oxide (VOx:Y) films used as the sensitive layers of microbolometers were deposited using a radio frequency magnetron co-sputtering system. The temperature coefficient of resistance (TCR) of the VOx:Y films was enhanced from -1.88%/°C to -2.85%/°C in comparison with that of the VOx films. To further improve the performance of microbolometers, the nanomesh antireflection layer was placed on the top surface of the microbolometers to reduce the infrared reflection. The responsivity, thermal time constant, thermal conductivity, absorptance, and detectivity of the VOx:Y microbolometers with nanomesh antireflection layer were 931.89 ± 48 kV/W, 4.48 ms, 6.19×10-8 W/K, 74.41% and 2.20×108 cmHz0.5W-1, respectively.

The Hippo pathway acts downstream of the Hedgehog signaling to regulate follicle stem cell maintenance in the Drosophila ovary.

The Hippo pathway is conserved and plays important roles in organ size control. The core components of the Hippo pathway are two kinases Hippo (Hpo), Warts (Wts), and a transcription-co-activator Yorkie (Yki). Yki activity is regulated by phosphorylation, which affects its nuclear localization and stability. To determine the role of the Hippo pathway in stem cells, we examine follicle stem cells (FSCs) in the Drosophila ovary. Yki is detected in the nucleus of FSCs. Knockdown of yki in the follicle cell lineage leads to a disruption of the follicular epithelium. Mitotic clones of FSCs mutant for hpo or wts are maintained in the niche and tend to replace the other FSCs, and FSCs mutant for yki are rapidly lost, demonstrating that the Hippo pathway is both required and sufficient for FSC maintenance. Using genetic interaction analyses, we demonstrate that the Hedgehog pathway acts upstream of the Hippo pathway in regulating FSC maintenance. The nuclear localization of Yki is enhanced when the Hedgehog signaling is activated. Furthermore, a constitutively active but not a wild-type Yki promotes FSC maintenance as activation of the Hedgehog signaling does, suggesting that the Hedgehog pathway regulates Yki through a post-translational mechanism in maintaining FSCs.

Modulation of cell morphogenesis by tousled-like kinase in the Drosophila follicle cell.

BACKGROUND: Tousled-like kinase (Tlk) is a conserved serine/threonine kinase regulating DNA replication, chromatin assembly, and DNA repair. Previous studies have suggested that Tlk is involved in cell morphogenesis in vitro. In addition, tlk genetically interact with Rho1, which encodes a key regulator of the cytoskeleton. However, whether Tlk plays a physiological role in cell morphogenesis and cytoskeleton rearrangement remains unknown. RESULTS: In tlk mutant follicle cells, area of the apical domain was reduced. The density of microtubules was increased in tlk mutant cells. The density of actin filaments was increased in the apical region and decreased in the basal region. Because area of the apical domain was reduced, we examined the levels of proteins located in the apical region by using immunofluorescence. The fluorescence intensities of two adherens junction proteins Armadillo (Arm) and DE-cadherin (DE-cad), atypical protein kinase C (aPKC), and Notch, were all increased in tlk mutant cells. The basolateral localized Discs large (Dlg) shifted apically in tlk mutant cells. CONCLUSIONS: Increase of protein densities in the apical region might be resulted from disruption of the cytoskeleton and shrinkage of the apical domain. Together, these data suggest a novel role of Tlk in maintaining cell morphology, possibly through modulating the cytoskeleton.

The Hippo pathway controls border cell migration through distinct mechanisms in outer border cells and polar cells of the Drosophila ovary.

The Hippo pathway is a key signaling cascade in controlling organ size. The core components of this pathway are two kinases, Hippo (Hpo) and Warts (Wts), and a transcriptional coactivator, Yorkie (Yki). Yes-associated protein (YAP, a Yki homolog in mammals) promotes epithelial-mesenchymal transition and cell migration in vitro. Here, we use border cells in the Drosophila ovary as a model to study Hippo pathway functions in cell migration in vivo. During oogenesis, polar cells secrete Unpaired (Upd), which activates JAK/STAT signaling of neighboring cells and specifies them into outer border cells. The outer border cells form a cluster with polar cells and undergo migration. We find that hpo and wts are required for migration of the border cell cluster. In outer border cells, overexpression of hpo disrupts polarization of the actin cytoskeleton and attenuates migration. In polar cells, knockdown of hpo and wts or overexpression of yki impairs border cell induction and disrupts migration. These manipulations in polar cells reduce JAK/STAT activity in outer border cells. Expression of upd-lacZ is increased and decreased in yki and hpo mutant polar cells, respectively. Furthermore, forced expression of upd in polar cells rescues defects of border cell induction and migration caused by wts knockdown. These results suggest that Yki negatively regulates border cell induction by inhibiting JAK/STAT signaling. Together, our data elucidate two distinct mechanisms of the Hippo pathway in controlling border cell migration: (1) in outer border cells, it regulates polarized distribution of the actin cytoskeleton; (2) in polar cells, it regulates upd expression to control border cell induction and migration.