28 research outputs found

    Photon-Assisted CVD Growth of Graphene Using Metal Adatoms As Catalysts

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    A photon-assisted CVD growth scheme of graphene using metal adatoms as catalysts at the edge of a graphene seed on noncatalytic surfaces, such as silicon dioxide (SiO<sub>2</sub>), hexagonal boron nitride (<i>h-</i>BN), and graphene, is reported based on first-principles calculations. We systematically examine the possible graphene edge reactions with carbon precursors such as methane, ethylene, or acetylene, using Cu and Ni adatoms as catalysts. The metal atoms adsorbed at the graphene edge capture the ambient ethylene or acetylene molecules, and initiate a series of edge reactions that would be energetically unfavorable in the absence of metal adatoms catalysts. We also suggest that ultraviolet photons can be used to dissociate the stable metal–ethylene or metal–acetylene complex in order to sustain the catalytic reactions. The growth rate of the graphene seed is shown to be slightly higher when on an <i>h-</i>BN or graphene substrate. In principle, this process could also be used to heal graphene defects between flakes or improve the continuity of reduced graphene oxide films

    Jag2 expression is upregulated in hypoxia-treated rats and PASMCs.

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    (A) Visualization of Jag2 expression in the GSE85618 dataset. (B) Jag2 mRNA and protein (C) expression by qRT-PCR, immunohistochemistry, and western blotting in lung tissue of normal and hypoxia-treated rats. N = 6 rats per group. (D) Immunofluorescence double staining of α-SMA and Jag2 in lung tissues of normal and hypoxia-treated rats. Scale bar, 10 Όm. (E) Jag2 mRNA and protein expression by qRT-PCR, immunofluorescence (F), and western blotting (G) in normal and hypoxia-treated PASMCs. Each group N = 3, and three biological replicates per group for cellular experiments. Scale bar, 25 Όm. Data shown are mean ± SD; ***P < 0.001.</p

    Absence of Jag2 alleviates hypoxia-induced oxidative stress injury in rats.

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    (A)Comparison of DHE staining and quantitative analysis in rat lung tissue samples treated with Control, HPH, and HPH+Jag2i. (B) Comparison of lung SOD, MPO, and MDA activity in the different groups. (C) Representative immunoblot images and quantitative analysis of Nrf2 and HO-1 protein expression inControl, HPH, and HPH+Jag2i rats. N=6 rats per group. The values expressed are mean ± SD. *P< 0.05, **P <0.01, ***P < 0.001.</p

    Jag2 knockdown ameliorates mitochondrial dysfunction induced by hypoxia.

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    (A) JC-1 staining of the intracellular mitochondrial membrane potential of control, hypoxia, and hypoxia+Si-Jag2 groups. JC-1 aggregates produce red fluorescence; JC-1 monomer produces green fluorescence. An increase in the relative ratio of red to green fluorescence indicates mitochondrial depolarization. (B) Intracellular mitochondrial superoxide levels in the three groups were tested using the MitoSOX assay and flow cytometry. (C) Representative western blots and quantitative analysis (D) of Coxiv and Tom20 in three groups. *P<0.05, **P<0.01, ***P<0.001, each group N = 3. Three biological replicates per group for cellular experiments.</p

    Heat map and volcano plot of the GSE85618 dataset.

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    (A) A visual representation in the form of a heat map to highlight the top 40 genes that show significant differences in expression levels within the GSE85618 dataset. Each column in the heat map corresponds to a particular sample, while each row represents the expression level of a specific gene. (B) volcano plot of the GSE85618 dataset showing the fold change (x-axis) differentially expressed genes. (TIF)</p

    Inhibition of Jag2 effectively ameliorates hypoxia-induced PH in rats.

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    (A) Fluorescence microscopy images of lung tissue four weeks after intratracheal AAV.1Jag2 instillation, where green fluorescence represents the expression and localization of AAV1 in lung tissue. DAPI stains the nuclei blue. Scale bar=10ÎŒm. (B) Representative immunoblot images and quantitative analysis of Jag2 protein expression in the control and AAV1.Jag2 groups. (C) Waveform diagram and quantitative analysis of RVSP (mmHg) in the indicated groups. (D) Representativemicroscopic images of distal pulmonary vascular stained with H&E, immunostained for α-SMA, and Masson trichrome in control, HPH, and HPH+Jag2i rats. Scale bar=10ÎŒm. (E) Fulton index RV/(LV+S) in the three groups. (F) The relative medial thickness expressed as a ratio of (total vascular area ‐ lumen area) to total vascular area (media/CSA). N=6 rats per group. Data shown are mean ± SD; **P < 0.01, ***P < 0.001.</p

    The Unusual Mechanism of Partial Fermi Level Pinning at Metal–MoS<sub>2</sub> Interfaces

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    Density functional theory calculations are performed to unravel the nature of the contact between metal electrodes and monolayer MoS<sub>2</sub>. Schottky barriers are shown to be present for a variety of metals with the work functions spanning over 4.2–6.1 eV. Except for the p-type Schottky contact with platinum, the Fermi levels in all of the studied metal–MoS<sub>2</sub> complexes are situated above the midgap of MoS<sub>2</sub>. The mechanism of the Fermi level pinning at metal–MoS<sub>2</sub> contact is shown to be unique for metal–2D-semiconductor interfaces, remarkably different from the well-known Bardeen pinning effect, metal-induced gap states, and defect/disorder induced gap states, which are applicable to traditional metal–semiconductor junctions. At metal–MoS<sub>2</sub> interfaces, the Fermi level is partially pinned as a result of two interface behaviors: first by a metal work function modification by interface dipole formation due to the charge redistribution, and second by the production of gap states mainly of Mo d-orbitals character by the weakened intralayer S–Mo bonding due to the interface metal–S interaction. This finding would provide guidance to develop approaches to form Ohmic contact to MoS<sub>2</sub>

    Primers for real-time PCR (rat).

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    Notch pathway has played a significant role in the pathophysiology of pulmonary hypertension (PH). However, the role of Jagged 2 (Jag2), one ligand of Notch, remains to be elucidated.Therefore, determining the contribution of Jag2 to PH and its impact on pulmonary artery smooth muscle cells (PASMCs) was the aim of this investigation. Adeno-associated virus-mediated Jag2 inhibition was used to explore the role of Jag2 in peripheral pulmonary vascular remodeling assessed in a rat model of chronic hypoxia (10% O2, 4 weeks) induced pulmonary hypertension. In vitro, the effect of Jag2 silencing on hypoxia (1% O2, 24h) induced rat PASMCs was determined. Group differences were assessed using a 2-sided unpaired Student’s t-test for two groups and one-way ANOVA for multiple groups. Jag2 upregulation was first confirmed in rats with sustained hypoxia-induced PH using publicly available gene expression data, experimental PH rat models and hypoxia induced rat PASMCs. Jag2 deficiency decreased oxidative stress injury, peripheral pulmonary vascular remodeling (0.276±0.020 vs. 0.451±0.033 ÎŒm, PPJag2 knockdown decreased proliferation (1.227±0.051 vs. 1.45±0.07, P = 0.012), increased apoptosis (16.733%±0.724% vs. 6.56%±0.668%, P</div

    Immunoblot images of α-SMA, PCNA and Sirt1.

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    (A) Representative immunoblot images and quantitative analysis of α-SMA and PCNA protein expression in Control, HPH, and HPH+ Jag2i rats. N=6 rats per group. (B) Representative western blots and quantitative analysis of Sirt1 protein expression in Control and Si-Sirt1 groups. (C) Representative western blots and quantitative analysis of Sirt1 protein expression in Control, Hypoxia and Hy+Si-Jag2 groups. *P (TIF)</p

    Jag2 deficiency prevents proliferation and promotes apoptosis in hypoxia-treated PASMCs.

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    (A) PASMCs were transfected with Si-NC or Si-Jag2 and analyzed by qRT-PCR and western blotting (B). (C) PASMC viability in control, hypoxia, and hypoxia+Si-Jag2 groups was detected by the CCK8 assay. (D) EdU analysis of PASMCs in the indicated groups. (E) Flow cytometry and quantitative analysis of apoptosis in the three groups. (F) Representative western blots and quantitative analysis of Bax/Bcl2 in the three groups. *P<0.05, **P<0.01, ***P<0.001, each group N = 3. Three biological replicates per group for cellular experiments.</p
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