18 research outputs found

    Implantable metaverse with retinal prostheses and bionic vision processing.mp4

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    Video demo of our bionic vision processing software for implantable metaverse. Developers: Ning Xi, Jiaxun Ye, Chao Ping Chen. Copyright: Smart Display Lab | Shanghai Jiao Tong University

    Sag deletion sensitizes mES cells to RA-induced apoptosis.

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    <p>mES cells with genotype of Sag<sup>+/+</sup> and Sag <sup>−/−</sup> were treated with DMSO control or 1 µM RA for indicated time periods, followed by trypan blue staining (<b>A</b>), TUNEL staining at 36 hrs (<b>B</b>, left panel), with quantification of TUNEL positive cells graphed (<b>B</b>, right panel), DNA fragmentation assay at 36 hrs (<b>C</b>), and caspase-3 activity assay at the indicated time point (<b>D</b>). *, <i>p</i><0.05.</p

    Correlation between SAG overexpression and RA resistance in AML cell lines and their sensitivity to RA and/or MLN4924.

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    <p>Proteins were extracted from 7 AML lines and subjected to immunoblotting using antibody against SAG with β-actin as the loading control (<b>A</b>). Cells were seeded in 96-well plate in triplicate and treated with various concentrations of RA (<b>B</b>, left panel), MLN4924 (<b>B</b>, right panel) or in combination at indicated concentrations of each drug for 48 hrs (<b>C</b>, HL-60 cells) and (<b>D</b>, KG-1 cells), followed by ATP-lite cell viability assay. Values were normalized to the untreated control. Shown is x ± SEM from three independent experiments with IC50 curve generated and IC50 value calculated using the Prism software.</p

    MLN4924 induces RA sensitization by inducing apoptosis.

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    <p>Cells were treated with DMSO control, RA (1.5 µM), MLN4924 (0.1 µM for HL-60, 1.0 µM for KG-1) alone or in combination for 24 hrs (HL-60) or 36 hrs (KG-1), followed by FACS analysis for apoptotic sub-G1 population. *, <i>p</i><0.05; **, <i>p</i><0.01; ***, <i>p</i><0.0001, compared to control (<b>A</b>). Cells were treated with indicated drugs at concentrations described above for 24 hrs, followed by DNA fragmentation assay (<b>B</b>) or immunoblotting using indicated antibodies (<b>C</b>).</p

    Sag deletion blocks RA-induced differentiation.

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    <p>Sag<sup>+/+</sup> and Sag<sup>−/−</sup> mES cells were seeded in 6-well plate and treated with RA at indicated concentrations for 6 days. Colonies were stained with AP (<b>A</b>) and counter-stained with hematoxylin (<b>B</b>), followed by photography. Bar size = 50 nm. Cells were seeded in geletin-coated glass coverslips and cellular stiffness was measured by AFM nanomechanical analysis at 0, 12, 18, 24 and 36 hrs post RA (1 µM) treatment. Shown is x ± SD from three independent experiments (<b>C</b>).</p

    Sag deletion sensitizes mES cells to all-trans Retinoid Acid (RA).

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    <p>Two independent pairs of mES cells with genotypes of Sag<sup>+/+</sup> and Sag<sup>−/−</sup> were seeded in 96-well plate in triplicate and treated with various concentrations of RA for 24 hrs. Cell viability was measured by ATP-lite assay. The IC50 curve was generated and IC50 value calculated by the Prism software (<b>A</b>). Cells were seeded in 6-well plate in duplicate and treated with DMSO vehicle control or RA (0.1 and 1 µM) for 6 days. The plates were stained (<b>B</b>) and the colonies with more than 50 cells were counted and plotted (<b>C</b>). Shown is x ± SEM from three independent experiments.</p

    Induction of SAG-SCF E3 ligase substrates by RA and/or MLN4924.

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    <p>Cells were treated with indicated concentrations of MLN4924 for 24 hrs, followed by immunoblotting using cullin-1 antibody with β-actin as the loading control (<b>A</b>). Cells were treated with RA (1.5 µM), MLN4924 (0.1 µM for HL-60, 1.0 µM for KG-1) alone or in combination for 24 hrs, followed by immunoblotting using indicated antiobodies (<b>B&C</b>). mES cells were treated with RA at indicated concentrations for 24 hrs, followed by immunoblotting using NOXA antibody with β-actin as the loading control (<b>D</b>).</p

    Performance Investigation of Multilayer MoS<sub>2</sub> Thin-Film Transistors Fabricated via Mask-free Optically Induced Electrodeposition

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    Transition metal dichalcogenides, particularly MoS<sub>2</sub>, have recently received enormous interest in explorations of the physics and technology of nanodevice applications because of their excellent optical and electronic properties. Although monolayer MoS<sub>2</sub> has been extensively investigated for various possible applications, its difficulty of fabrication renders it less appealing than multilayer MoS<sub>2</sub>. Moreover, multilayer MoS<sub>2</sub>, with its inherent high electronic/photonic state densities, has higher output driving capabilities and can better satisfy the ever-increasing demand for versatile devices. Here, we present multilayer MoS<sub>2</sub> back-gate thin-film transistors (TFTs) that can achieve a relatively low subthreshold swing of 0.75 V/decade and a high mobility of 41 cm<sup>2</sup>·V<sup>–1</sup>·s<sup>–1</sup>, which exceeds the typical mobility value of state-of-the-art amorphous silicon-based TFTs by a factor of 80. Ag and Au electrode-based MoS<sub>2</sub> TFTs were fabricated by a convenient and rapid process. Then we performed a detailed analysis of the impacts of metal contacts and MoS<sub>2</sub> film thickness on electronic performance. Our findings show that smoother metal contacts exhibit better electronic characteristics and that MoS<sub>2</sub> film thickness should be controlled within a reasonable range of 30–40 nm to obtain the best mobility values, thereby providing valuable insights regarding performance enhancement for MoS<sub>2</sub> TFTs. Additionally, to overcome the limitations of the conventional fabrication method, we employed a novel approach known as optically induced electrodeposition (OIE), which allows the flexible and precise patterning of metal films and enables rapid and mask-free device fabrication, for TFT fabrication

    Integrated scanning electron microscopy (SEM), immunofluorescence (IF) and AFM imaging of intercellular adhesion structures.

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    <p><b>A:</b> Correlation of SEM imaging with AFM imaging. Identically cultured plates of confluent HaCaT cells were fixed and imaged by SEM and Multimode AFM in increasing magnifications. The lower magnification images (SEM: <b>A1, A2;</b> AFM: <b>A5, A6</b>) show the cells with clear boundaries between neighboring cells where cell-cell adhesion occurs. The higher magnification images (SEM: <b>A3,</b><b>A4;</b> AFM: <b>A7, A8</b>) show details of the adhesion junction with strand-shaped structures in parallel distribution between two cells. <b>B:</b> Correlation of IF imaging with AFM imaging. The same area on a confluent slide of HaCaT cells was captured simultaneously by IF and AFM after fixation of the cells. For IF imaging, HaCaT cells were labeled with anti-cytokeratin antibodies (red) and anti-desmoplakin antibodies (green). AFM images were captured by Bioscope AFM at increasing resolution with scan sizes of 100 µm (<b>B2</b>), 50 µm (<b>B3</b>) and 20 µm (<b>B4</b>). <b>C:</b> Correlation of IF imaging (<b>C1</b>) with AFM imaging [scan sizes of 100 µm (<b>C2</b>), 50 µm (<b>C3</b>) and 20 µm (<b>C4</b>)] after treatment with 10 µg/ml of the pathogenic anti-Dsg3 antibody Px4-3 for 24 h.</p
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