Realization of tunable-performance in atomic layer deposited Hf-doped In2O3 thin film transistor via oxygen vacancy modulation.

Due to the limitation of inherent ultra-high electron concentration, the electrical properties of In2O3 resemble those of conductors rather than semiconductors prior to special treatment. In this study, the effect of various annealing treatments on the microstructure, optical properties, and oxygen vacancies of the films and transistors is systematically investigated. Our finding reveals a progressive crystallization trend in the films with increasing annealing temperature. In addition, a higher annealing temperature is also associated with the reduction in the concentration of oxygen vacancies, as well as an elevation in both optical transmittance and optical bandgap. Furthermore, with the implementation of annealing process, the devices gradually transform from no pronounced gate control to exhibit with excellent gate control and electrical performances. The atomic layer deposited Hf-doped In2O3 thin film transistor annealed at 250 °C exhibits optimal electrical properties, with a field-effect mobility of 18.65 cm2 V-1 s-1, a subthreshold swing of 0.18 V/dec, and an Ion/Ioff ratio of 2.76 × 106. The results indicate that the impact of varying annealing temperatures can be attributed to the modulation of oxygen vacancies within the films. This work serves as a complementary study for the existing post-treatment of oxide films and provides a reliable reference for utilization of the annealing process in practical applications.

Tunable-performance all-oxide structure field-effect transistor based atomic layer deposited Hf-doped In2O3 thin films.

The relocation of peripheral transistors from the front-end-of-line (FEOL) to the back-end-of-line (BEOL) in fabrication processes is of significant interest, as it allows for the introduction of novel functionality in the BEOL while providing additional die area in the FEOL. Oxide semiconductor-based transistors serve as attractive candidates for BEOL. Within these categories, In2O3 material is particularly notable; nonetheless, the excessive intrinsic carrier concentration poses a limitation on its broader applicability. Herein, the deposition of Hf-doped In2O3 (IHO) films via atomic layer deposition for the first time demonstrates an effective method for tuning the intrinsic carrier concentration, where the doping concentration plays a critical role in determine the properties of IHO films and all-oxide structure transistors with Au-free process. The all-oxide transistors with In2O3: HfO2 ratio of 10:1 exhibited optimal electrical properties, including high on-current with 249 µA, field-effect mobility of 13.4 cm2 V-1 s-1, and on/off ratio exceeding 106, and also achieved excellent stability under long time positive bias stress and negative bias stress. These findings suggest that this study not only introduces a straightforward and efficient approach to improve the properties of In2O3 material and transistors, but as well paves the way for development of all-oxide transistors and their integration into BEOL technology.

Post-annealing optimization of the heteroepitaxial La-doped SrSnO3 integrated on silicon via ALD.

Wide band gap (WBG) alkaline-earth stannate transparent oxide semiconductors (TOSs) have attracted increasing attention in recent years for their high carrier mobility and outstanding optoelectronic properties, and have been applied widely in various devices, such as flat-panel displays. Most alkaline-earth stannates are grown by molecular beam epitaxy (MBE); there are some intractable issues with the tin source including the volatility with SnO and Sn sources and the decomposition of the SnO2 source. In contrast, atomic layer deposition (ALD) serves as an ideal technique for the growth of complex stannate perovskites with precise stoichiometry control and tunable thickness at the atomic scale. Herein, we report the La-SrSnO3/BaTiO3 perovskite heterostructure heterogeneously integrated on Si (001), which uses ALD-grown La-doped SrSnO3 (LSSO) as a channel material and MBE-grown BaTiO3 (BTO) as a dielectric material. The reflective high-energy electron diffraction and X-ray diffraction results indicate the crystallinity of each epitaxial layer with a full width at half maximum (FWHM) of 0.62°. In situ X-ray photoelectron spectroscopy results confirm that there was no Sn0 state in ALD-deposited LSSO. Besides, we report a strategy for the post-treatment of LSSO/BTO perovskite heterostructures by controlling the oxygen annealing temperature and time, with a maximum oxide capacitance Cox of 0.31 µF cm-2 and a minimum low-frequency dispersion for the devices with 7 h oxygen annealing at 400 °C. The enhancement of capacitance properties is primarily attributed to a decrease of oxygen vacancies in the films and interface defects in the heterostructure interfaces during an additional ex situ excess oxygen annealing. This work expands current optimization methods for reducing defects in epitaxial LSSO/BTO perovskite heterostructures and shows that excess oxygen annealing is a powerful tool for enhancing the capacitance properties of LSSO/BTO heterostructures.

Analysis of the driving role and impact of road construction on carbon stock.

Road construction will have a large impact on the ecosystem in the road area, and carbon stock, as an important indicator to measure the scale and quantity of primary productivity of the ecosystem, will also change, but the specific pattern is not clear. It is important to study the impact of road construction on carbon stock for regional ecosystem protection and sustainable economic and social development. Based on the InVEST model, this paper quantifies the spatial and temporal changes of carbon stocks in Jinhua, Zhejiang Province, from 2002 to 2017, using remote sensing image classification data land cover types as model driving data, geodetector, trend analysis, and buffer zone analysis methods, explores the driving effect of road construction on carbon stocks, and analyzes the spatial and temporal impacts of road construction on carbon stocks within the buffer zone. Results indicate that the total carbon stock in the Jinhua area showed a decreasing trend during the 16 years, decreasing by about 8.58 × 106 t. The spatial changes in the areas with higher carbon stocks were not significant. The explanatory power of road network density on carbon stock reaches 37%, and the anisotropic effect of road construction on carbon stock is strong and had a significant driving effect on carbon storage reduction. The new highway construction will accelerate the rate of carbon stock decline in the buffer zone, and the spatial situation is generally "the farther away from the highway, the higher the carbon stock."

Chimeric RNA TNNI2-ACTA1-V1 Regulates Cell Proliferation by Regulating the Expression of NCOA3.

Chimeric RNA is a crucial target for tumor diagnosis and drug therapy, also having its unique biological role in normal tissues. TNNI2-ACTA1-V1 (TA-V1), a chimeric RNA discovered by our laboratory in porcine muscle tissue, can inhibit the proliferation of Porcine Skeletal Muscle Satellite Cells (PSCs). The regulatory mechanism of TA-V1 in PSCs remains unclear, but we speculate that NCOA3, DDR2 and RDX may be the target genes of TA-V1. In this study, we explored the effects of NCOA3, DDR2 and RDX on cell viability and cell proliferation by CCK-8 assay, EdU staining and flow cytometry. Furthermore, the regulatory pathway of proliferation in PSCs mediated by TA-V1 through NCOA3 or CyclinD1 was elucidated by co-transfection and co-immunoprecipitation (Co-IP). The results revealed that overexpression of NCOA3 significantly increased cell viability and the expression level of CyclinD1, and also promotes cell proliferation by changing cells from the G1 phase to the S phase. In addition, inhibiting the expression of NCOA3 substantially reduced cell viability and inhibited cell proliferation. Overexpression of DDR2 and RDX had no significant effect on cell viability and proliferation. Co-transfection experiments showed that NCOA3 could rescue the proliferation inhibition of PSCs caused by TA-V1. Co-IP assay indicated that TA-V1 directly interacts with NCOA3. Our study explores the hypothesis that TA-V1 directly regulates NCOA3, indirectly regulating CyclinD1, thereby regulating PSCs proliferation. We provide new putative mechanisms of porcine skeletal muscle growth and lay the foundation for the study of chimeric RNA in normal tissues.

Characterization of a Read-through Fusion Transcript, BCL2L2-PABPN1, Involved in Porcine Adipogenesis.

cis-Splicing of adjacent genes (cis-SAGe) has been involved in multiple physiological and pathological processes in humans. However, to the best of our knowledge, there is no report of cis-SAGe in adipogenic regulation. In this study, a cis-SAGe product, BCL2L2-PABPN1 (BP), was characterized in fat tissue of pigs with RT-PCR and RACE method. BP is an in-frame fusion product composed of 333 aa and all the functional domains of both parents. BP is highly conserved among species and rich in splicing variants. BP was found to promote proliferation and inhibit differentiation of primary porcine preadipocytes. A total of 3074/44 differentially expressed mRNAs (DEmRs)/known miRNAs (DEmiRs) were identified in porcine preadipocytes overexpressing BP through RNA-Seq analysis. Both DEmRs and target genes of DEmiRs were involved in various fat-related pathways with MAPK and PI3K-Akt being the top enriched. PPP2CB, EGFR, Wnt5A and EHHADH were hub genes among the fat-related pathways identified. Moreover, ssc-miR-339-3p was found to be critical for BP regulating adipogenesis through integrated analysis of mRNA and miRNA data. The results highlight the role of cis-SAGe in adipogenesis and contribute to further revealing the mechanisms underlying fat deposition, which will be conductive to human obesity control.

Study on Preparation of Superhydrophobic Copper Surface by Milling and Its Protective Performance.

Using milling method, a 0.1 mm flat-bottom sharp knife was used to mill the surface of Cu substrate in a CNC engraving machine to construct the microstructure of rectangular bumps, and rectangular bumps with different sizes and different distances were prepared by changing the distance between cutter tips. After deburring and stearic acid modification, a superhydrophobic Cu surface with excellent mechanical durability and stability was successfully prepared. Through friction and wear experiments, the contact angle of the superhydrophobic Cu surface decreased slightly while retaining excellent corrosion resistance.

Efficient and Facile Method of Preparing Superamphiphobic Surfaces on Cu Substrates.

Nowadays, scalable manufacturing of superamphiphobic surfaces by a simple and efficient method remains challenging. Herein, we developed a facile and efficient strategy for constructing superamphiphobic surfaces on Cu substrates, including press molding, oxidation, and fluorination modification. The prepared superamphiphobic surface not only has repellency and low viscosity to water, ethylene glycol, and 30% ethanol (surface tension: 33.53 mN·m-1) but can also achieve excellent self-cleaning properties through these liquids. Scanning electron microscopy images revealed that this superamphiphobic surface had multiple hybrid structures, including microflowers, nanoneedles, and micropillar arrays. Owing to the high chemical stability of the C-F group, the obtained surface also exhibited excellent corrosion resistance. The preparation method of superamphiphobic surfaces with all these advantages does not require complicated equipment and has great advantages in terms of low cost and high efficiency, which not only endows this method with broad application prospects but is also makes it suitable for industrial scalable production.

A Facile Method to Prepare a Superhydrophobic Magnesium Alloy Surface.

The application of superhydrophobic materials has been handicapped by complex processes and poor environmental friendliness. Magnesium alloys are widely used in daily production due to their low density and good casting properties. A facile and environmentally friendly method was proposed to prepare a superhydrophobic layer with coral-like microstructure on the surface of AZ91D magnesium alloy by high temperature heating. The prepared superhydrophobic surface has a contact angle of 159.1° and a rolling angle of 4.8°. The corrosion current of superhydrophobic surface has been reduced by about two orders of magnitude relative to the magnesium alloy substrate and its inhibition efficiency is 96.94%, which demonstrates its great corrosion resistance. In addition, the superhydrophobic surface has great thermal stability. When the temperature rises to 190 °C, the contact is still above 150°. Excellent self-cleaning and advantages in preparation efficiency, environmental protection and cost-effectiveness will boost its good application prospects.

Strain-controlled power devices as inspired by human reflex.

Bioinspired electronics are rapidly promoting advances in artificial intelligence. Emerging AI applications, e.g., autopilot and robotics, increasingly spur the development of power devices with new forms. Here, we present a strain-controlled power device that can directly modulate the output power responses to external strain at a rapid speed, as inspired by human reflex. By using the cantilever-structured AlGaN/AlN/GaN-based high electron mobility transistor, the device can control significant output power modulation (2.30-2.72 × 103 W cm-2) with weak mechanical stimuli (0-16 mN) at a gate bias of 1 V. We further demonstrate the acceleration-feedback-controlled power application, and prove that the output power can be effectively adjusted at real-time in response to acceleration changes, i.e., ▵P of 72.78-132.89 W cm-2 at an acceleration of 1-5 G at a supply voltage of 15 V. Looking forward, the device will have great significance in a wide range of AI applications, including autopilot, robotics, and human-machine interfaces.

Piezotronic Effect Modulated Flexible AlGaN/GaN High-Electron-Mobility Transistors.

Flexible electronic technology has attracted great attention due to its wide range of potential applications in the fields of healthcare, robotics, and artificial intelligence, etc. In this work, we have successfully fabricated flexible AlGaN/GaN high-electron-mobility transistors (HEMTs) arrays through a low-damage and wafer-scale substrate transfer technology from a rigid Si substrate. The flexible AlGaN/GaN HEMTs have excellent electrical performances with the Id,max achieving 290 mA/mm at Vgs = +2 V and the gm,max reaching to 40 mS/mm. The piezotronic effect provides a different freedom to optimize device performances, and flexible HEMTs can endure the larger mechanical distortions. Based on the piezotronic effect, we applied an external stress to significantly modulate the electrical performances of flexible HEMTs. The piezotronic effect modulated flexible AlGaN/GaN HEMTs exhibit great potential in human-machine interface, intelligent microinductor systems, and active sensors, etc, and introduce an opportunity to sensing or feedback external mechanical stimuli and so on.

Nuciferine inhibits the progression of glioblastoma by suppressing the SOX2-AKT/STAT3-Slug signaling pathway.

BACKGROUND: Nuciferine (NF), extracted from the leaves of N. nucifera Gaertn, has been shown to exhibit anti-tumor and anti-viral pharmacological properties. It can also penetrate the blood brain barrier (BBB). However, the mechanism by which NF inhibits glioblastoma (GBM) progression is not well understood. We aimed to determine the anti-tumor effect of NF on GBM cell lines and clarify the potential molecular mechanism involved. METHODS: U87MG and U251 cell lines were used in vitro to assess the anti-tumor efficacy of NF. Cytotoxicity, viability, and proliferation were evaluated by MTT and colony formation assay. After Annexin V-FITC and PI staining, flow cytometry was performed to evaluate apoptosis and cell cycle changes in NF-treated GBM cells. Wound healing and Transwell assays were used to assess migration and invasion of GBM cells. Western blot analysis, immunofluorescence staining, immunohistochemistry, and bioinformatics were used to gain insights into the molecular mechanisms. Preclinical therapeutic efficacy was mainly estimated by ultrasound and MRI in xenograft nude mouse models. RESULTS: NF inhibited the proliferation, mobility, stemness, angiogenesis, and epithelial-to-mesenchymal transition (EMT) of GBM cells. Additionally, NF induced apoptosis and G2 cell cycle arrest. Slug expression was also decreased by NF via the AKT and STAT3 signaling pathways. Interestingly, we discovered that NF affected GBM cells partly by targeting SOX2, which may be upstream of the AKT and STAT3 pathways. Finally, NF led to significant tumor control in GBM xenograft models. CONCLUSIONS: NF inhibited the progression of GBM via the SOX2-AKT/STAT3-Slug signaling pathway. SOX2-targeting with NF may offer a novel therapeutic approach for GBM treatment.

Long non-coding RNA CCRR controls cardiac conduction via regulating intercellular coupling.

Long non-coding RNAs (lncRNAs) have emerged as a new class of gene expression regulators playing key roles in many biological and pathophysiological processes. Here, we identify cardiac conduction regulatory RNA (CCRR) as an antiarrhythmic lncRNA. CCRR is downregulated in a mouse model of heart failure (HF) and in patients with HF, and this downregulation slows cardiac conduction and enhances arrhythmogenicity. Moreover, CCRR silencing induces arrhythmias in healthy mice. CCRR overexpression eliminates these detrimental alterations. HF or CCRR knockdown causes destruction of intercalated discs and gap junctions to slow longitudinal cardiac conduction. CCRR overexpression improves cardiac conduction by blocking endocytic trafficking of connexin43 (Cx43) to prevent its degradation via binding to Cx43-interacting protein CIP85, whereas CCRR silence does the opposite. We identified the functional domain of CCRR, which can reproduce the functional roles and pertinent molecular events of full-length CCRR. Our study suggests CCRR replacement a potential therapeutic approach for pathological arrhythmias.

LRG1 promotes angiogenesis through upregulating the TGF­ß1 pathway in ischemic rat brain.

Stroke is a life-threatening disease that results in significant disability in the human population. Despite the advances in current stroke therapies, a host of patients do not benefit from the conventional treatments. Thus, more effective therapies are required. It has been previously reported that leucine­rich­α2­glycoprotein 1 (LRG1) is crucial during the formation of new blood vessels in retinal diseases. However, the function of LRG1 in the brain during the neovessel growth process following ischemic stroke has not been fully elucidated and the mechanism underlying its effect on angiogenesis remains unclear. The purpose of the current study was to demonstrate whether LRG1 may promote angiogenesis through the transforming growth factor (TGF)­ß1 signaling pathway in ischemic rat brain following middle cerebral artery occlusion (MCAO). In the present study, the spatial and temporal expression of LRG1, TGF­ß1, vascular endothelial growth factor (VEGF) and angiopoietin­2 (Ang­2) were detected in ischemic rat brain following MCAO using reverse transcription­quantitative polymerase chain reaction (RT­qPCR), western blot analysis and immunohistochemistry. CD34 immunohistochemistry staining was used as an indicator of microvessel density (MVD). The RT­qPCR and western blotting results revealed that the levels of LRG1 and TGF­ß1 mRNA and protein expression were significantly increased as early as 6 and 12 h after MCAO (P<0.05), respectively, peaked at 3 days and persisted at significantly higher level until 14 days, in comparison with the control group. Additionally, VEGF and Ang­2 were also increased following MCAO. Furthermore, the immunohistochemistry results suggested that the MVD was increased following MCAO. In addition, the results also revealed that the percentage of LRG1­positive cells was positively correlated with the percentage of TGF­ß1­positive cells, and the percentage of LRG1­positive and TGF­ß1­positive cells had a positively correlation with the MVD. Taken together, the present study indicated that LRG1 may promote angiogenesis through upregulating the TGF­ß1 signaling pathway in ischemic rat brain following MCAO. This may provide a potential therapeutic target for the treatment of ischemic stroke.

[Protective effects of recombinant human erythropoietin on oligodendrocyte after cerebral infarction].

OBJECTIVE: To study biological effect of recombinant human erythropoietin (RhEPO) on the expression of oligodendrocyte in the neuron glia antigen 2(NG2), Nogo receptor-interacting protein 1(LINGO-1), myelin basic protein (MBP) and myelin associated glycoprotein (MAG), and to explore the protective mechanism of RhEPO for oligodendrocyte after cerebral infarction. METHODS: Experimental rats were randomly divided into the treatment group (RhEPO at a dose of 3 000 U/kg) or saline control group. Both groups received intraperitoneal injection of RhEPO after cerebral ischemia in 30 min, 3 h, 6 h, 12 h and 24 h, which was administered daily for 7 days. The modified neurological severity score (mNSS) and histology were analyzed, and immunohistochemistry was used to detect the protein expression of NG2, MAG, MBP and LINGO-1. RESULTS: The overall mNSS of RhEPO treatment group significantly decreased compared with the saline control group on the seventh day after cerebral infarction (P<0.05). Such treatment effect was more obvious in the treatment group at 30 min and 3 h (P<0.01). Compared with the saline control group, the numbers of NG2 positive cells increased in RhEPO treatment group. In contrast, the expression of LINGO-1 protein significantly decreased (P<0.05), with a dramatic decrease observed at 30 min and 3 h (P<0.01). However, the expression of MBP protein decreased more significantly in saline control group, while the level of the MAG protein expression increased. The differences were statistically significant (P<0.05), especially at 30 min (P<0.01). CONCLUSIONS: After cerebral ischemia, RhEPO promotes the proliferation of NG2 positive cells, and inhibits the expression of LINGO-1 and MAG proteins. RhEPO improves the proliferation and differentiation of oligodendrocyte precursor cells, which in turn protects neuronal function, particularly at the early phase of ischemia.

Reciprocal activation between ATPase inhibitory factor 1 and NF-κB drives hepatocellular carcinoma angiogenesis and metastasis.

UNLABELLED: Hepatocellular carcinoma (HCC) is a highly vascularized tumor with frequent extrahepatic metastasis. Active angiogenesis and metastasis are responsible for rapid recurrence and poor survival of HCC. However, the mechanisms that contribute to tumor metastasis remain unclear. Here we evaluate the effects of ATPase inhibitory factor 1 (IF1), an inhibitor of the mitochondrial H(+)-adenosine triphosphate (ATP) synthase, on HCC angiogenesis and metastasis. We found that increased expression of IF1 in human HCC predicts poor survival and disease recurrence after surgery. Patients with HCC who have large tumors, with vascular invasion and metastasis, expressed high levels of IF1. Invasive tumors overexpressing IF1 were featured by active epithelial-mesenchymal transition (EMT) and increased angiogenesis, whereas silencing IF1 expression attenuated EMT and invasion of HCC cells. Mechanistically, IF1 promoted Snai1 and vascular endothelial growth factor (VEGF) expression by way of activating nuclear factor kappa B (NF-κB) signaling, which depended on the binding of tumor necrosis factor (TNF) receptor-associated factor 1 (TRAF1) to NF-κB-inducing kinase (NIK) and the disruption of NIK association with the TRAF2-cIAP2 complex. Suppression of the NF-κB pathway interfered with IF1-mediated EMT and invasion. Chromatin immunoprecipitation assay showed that NF-κB can bind to the Snai1 promoter and trigger its transcription. IF1 was directly transcribed by NF-κB, thus forming a positive feedback signaling loop. There was a significant correlation between IF1 expression and pp65 levels in a cohort of HCC biopsies, and the combination of these two parameters was a more powerful predictor of poor prognosis. CONCLUSION: IF1 promotes HCC angiogenesis and metastasis by up-regulation of Snai1 and VEGF transcription, thereby providing new insight into HCC progression and IF1 function. (Hepatology 2014;60:1659-1673).