199 research outputs found

    Softened Mechanical Properties of Graphene Induced by Electric Field

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    The understanding on the mechanical properties of graphene under the applications of physical fields is highly relevant to the reliability and lifetime of graphene-based nanodevices. In this work, we demonstrate that the application of electric field could soften the mechanical properties of graphene dramatically on the basis of the conductive AFM nanoindentation method. It has been found that the Young’s modulus and fracture strength of graphene nanosheets suspended on the holes almost stay the same initially and then exhibit a sharp drop when the normalized electric field strength increases to be 0.18 ± 0.03 V/nm. The threshold voltage of graphene nanosheets before the onset of fracture under the fixed applied load increases with the thickness. Supported graphene nanosheets can sustain larger electric field under the same applied load than the suspended ones. The excessively regional Joule heating caused by the high electric current under the applied load is responsible for the electromechanical failure of graphene. These findings can provide a beneficial guideline for the electromechanical applications of graphene-based nanodevices

    Vilsmeier-Type Reaction of Dimethylaminoalkenoyl Cyclopropanes: One-Pot Access to 2,3-Dihydrofuro [3,2-<i>c</i>]pyridin-4(5<i>H</i>)-ones

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    A domino reaction of readily available 1-carbamoyl-1-dimethylaminoalkenoylcyclopropanes in the presence of triflic anhydride (Tf<sub>2</sub>O) in <i>N,N</i>-dimethylformamide (DMF) is described, which provides a facile one-pot access to 2,3-dihydrofuro[3,2-<i>c</i>]pyridin-4(5<i>H</i>)-ones <i>via</i> tandem formylation (Vilsmeier-type reaction), intramolecular cyclization, and ring-enlargement sequences

    Aeroelastic Model Test and Field Measurement of 40-m High Lattice Tower

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    This paper was reviewed and accepted by the APCWE-IX Programme Committee for Presentation at the 9th Asia-Pacific Conference on Wind Engineering, University of Auckland, Auckland, New Zealand, held from 3-7 December 2017

    [5C + 1N] Annulations: Two Novel Routes to Substituted Dihydrofuro[3,2‑<i>c</i>]pyridines

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    Two novel routes based on [5C + 1N] annulations for the synthesis of 2,3-dihydrofuro[3,2-<i>c</i>]pyridines are described. Ammonium acetate (NH<sub>4</sub>OAc) is used as an ammonia source in both routes. The first route utilizes 1-acyl-1-[(dimethylamino)alkenoyl]cyclopropanes as a five-carbon 1,5-bielectrophilic species and combines the [5C + 1N] annulation and regioselective ring-enlargement of cyclopropyl ketone into one pot, whereas the second route utilizes 3-acyl-2-[(dimethylamino)alkenyl]-4,5-dihydrofurans as the five-carbon synthons, which involves a sequential intermolecular aza-addition, intramolecular aza-nucleophilic addition/elimination, and dehydration reaction

    A New Quasi-Steady Model for Magnus Effect of Rectangular Plate Windborne Debris

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    This paper was reviewed and accepted by the APCWE-IX Programme Committee for Presentation at the 9th Asia-Pacific Conference on Wind Engineering, University of Auckland, Auckland, New Zealand, held from 3-7 December 2017

    A numerical approach to the simulation of plate-type wind-borne debris

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    This paper was reviewed and accepted by the APCWE-IX Programme Committee for Presentation at the 9th Asia-Pacific Conference on Wind Engineering, University of Auckland, Auckland, New Zealand, held from 3-7 December 2017

    Temporal profiles of Hh response visualized by a <i>Ptc1-Kaede</i> reporter.

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    <p>(A) Schematic drawing of the <i>Ptc1-Kaede</i> BAC reporter. A cassette containing Kaede and Kanamycin resistant gene was recombined to replace the first exon of <i>ptc1</i>. (B) <i>Ptc1-Kaede</i> fish showed <i>kaede</i> expression in a pattern similar to the expression of <i>ptc1</i> in wild type embryos at 19-som stage. (C) Inhibition of Hh signaling using cyclopamine blocked <i>Ptc1-Kaede</i> expression, while overexpression of dnPKA mRNA induced ectopic expression of the transgene. Fluorescent signal in cyclopamine-treated fish is due to auto-fluorescence of the yolk (asterisk). (D) Schematic drawings of PHRESH analysis. Photoconversion of the <i>Ptc1-Kaede</i> reporter can be used to determine the timing of Hh response (see text for details). (E) <i>Ptc1-Kaede</i> fish were photoconverted at 25 hpf, and imaged at 36 hpf. Single optical sections of a lateral view, dorsal view, and cross-section are shown. Arrows indicate <i>Ptc1-Kaede<sup>red</sup></i> cells in the lateral floor domain. Note that dorsally located KA′ cells also only express <i>Ptc1-Kaede<sup>red</sup></i> (arrowheads). (F) <i>Ptc1-Kaede</i> fish were photoconverted at 24 hpf, and stained with the GABA antibody (blue) at 35 hpf. Arrows indicate GABA-positive KA″ cells. (G) <i>Gata2-GFP</i> fish were co-labeled with <i>ptc1</i> (green), and the GFP antibody (red). Images shown are the dorsal view of an 18 hpf embryo (top) and the lateral view of a 24 hpf embryo (bottom). KA″ cells are indicated by arrows. Scale bars: 200 µm in B–C and 20 µm in E–G.</p

    Lineage analysis of the LFP domain.

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    <p>(A) Schematic drawings of scatter labeling and time-lapse imaging. <i>Gata2-GFP</i> fish were injected with <i>H2B-mCherry</i> mRNA (red) into a single blastomere at 16- to 32-cell stage. Scatter labeled embryos with nuclear mCherry expression (red) were imaged in the dorsal view starting at 3-somite stage (11 hpf) for about 11 hours. At the end of the time-lapse, an image with both the green and red channels was acquired to identify <i>Gata2-GFP</i>-expressing KA″ cells (green). (B) Observed division patterns in the LFP domain. Of a total of 25 cell divisions tracked, 16 were LFP/LFP divisions, 6 were KA″/LFP divisions, and 3 were KA″/KA″ divisions. KA″ cells (green) were identified base on the expression of <i>Gata2-GFP</i> reporter. (C) <i>Gata2-GFP</i> fish (green) was scatter labeled by <i>H2B-mCherry</i> (red) and imaged from 11 hpf for about 11 hours. Two examples are shown. Top panel: merged images with both the red channel and the bright field of a single optical slice at the start of the movie at 11 hpf. The underlying notochord (brackets) is visible but out of focus. Middle and bottom panels: the merged image with both green and red channels and the green channel alone of a confocal projection at the end of the movie around 22 hpf. KA″ cells (arrows) can be distinguished from LFP cells (arrowheads) based on the expression of <i>Gata2-GFP</i> (green) at 22 hpf. Medial floor plate cells are indicated by white dots. Lineage related cells confirmed by cell tracking are indicated (also see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002762#pgen.1002762.s001" target="_blank">Figure S1</a> and <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002762#pgen.1002762.s004" target="_blank">Video S1</a>). For example, cell 1 generates a KA″ cell (cell 1a) and an LFP cell (cell 1b). Of the 7 examples shown here, cells 1 and 6 undergo KA″/LFP divisions, cell 7 undergoes KA″/KA″ division, and cells 2–5 divide symmetrically giving rise to two LFP cells (LFP/LFP divisions). Note that cells 4 and 6 are more dorsally located and therefore not in focus in images at 11 hpf (top panels). Scale bars: 20 µm.</p

    Interaction between Notch and Hh signaling in KA″ specification.

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    <p>(A) Embryos treated with DMSO alone, compound E, cyclopamine, or both compound E and cyclopamine from 14 hpf to 25 hpf, were stained for the expression of <i>tal2</i>. (B) Quantification of total number of KA″ cells in experiments shown in A. Note that the fewer data points in compound E treatment is due to the fact that most compound E-treated embryos had many <i>tal2</i>-positive cells in close clusters which prevents reliable scoring. The two data points thus underestimate the total number of KA″ cells in E-treated embryos. Cyc: cyclopamine. (C) <i>hsp-Gal4; UAS-NICD</i> embryos and non-transgenic sibling controls were left uninjected or injected with Shh mRNA, heat-shocked at 11.5 hpf, and stained at 24 hpf for the expression of <i>tal2</i>. Brackets in A and C indicate the dorsal-ventral extent of the LFP domain. Scale bars: 50 µm. (D) <i>hsp-Gli1</i> embryos and non-transgenic controls were injected with compound E at 15 hpf, and heat-shocked at 16 hpf, and stained at 22 hpf for the expression of <i>nkx2.9</i>. Arrows denote the two rows of LFP domains in dorsal views. (E) Model of KA″ specification. At the early stage (t<sub>0</sub>), LFP progenitors have high level of Notch signaling activity and thereby maintain the progenitor state and Hh responsiveness (Notch<sup>ON</sup> Hh<sup>ON</sup>). Active Hh signaling in progenitor cells is required for specifying the KA″ identity in subsequent cell divisions. LFP progenitors can undergo three different types of divisions: symmetric LFP/LFP divisions, asymmetric KA″/LFP divisions (shown here), and symmetric KA″/KA″ divisions. Divisions of LFP progenitors at t<sub>1</sub> generate daughter cells with similar competence to either acquire the KA″ fate or maintain the LFP progenitor fate. Cell-cell interactions or stochastic fluctuations in Notch signaling result in cells with different levels of Notch signaling (t<sub>2</sub>). Cells that maintain high levels of Notch signaling will remain as LFP progenitors and continue to respond Shh (Notch<sup>ON</sup> Hh<sup>ON</sup>). In contrast, cells that have attenuated Notch signaling will lose Hh response and differentiate into KA″ interneurons (Notch<sup>OFF</sup> Hh<sup>OFF</sup>). Since sustained Notch or Hh signaling disrupt the differentiation of KA″ cells, formation of KA″ cells initially depends on the activation and then the attenuation of Notch and Hh signaling.</p

    Prolonged Hh response interferes with KA″ specification.

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    <p>(A) Quantification of KA″ specification in embryos overexpressing GFP-Gli1. <i>hsp-GFP-Gli1</i> embryos and their non-transgenic sibling controls were heat-shocked at indicated stages, and stained at 25 hpf for the expression of <i>tal2</i>. (B) <i>hsp-GFP-Gli1</i> and control embryos were heat-shocked at 14 hpf, and stained at 24 hpf for the expression of <i>tal2</i> and <i>nkx2.9</i>. Induction of GFP-Gli1 results in a reduction of <i>tal2</i>-positive KA″ cells (arrows) and expansion of <i>nkx2.9</i>-expressing LFPs. (C) <i>Ptc1-Kaede</i> control embryos, and <i>Ptc1-Kaede; hsp-GFP-Gli1</i> embryos were heat-shocked at 14 hpf, photoconverted at 24 hpf, and stained with the GABA antibody (blue) at 36 hpf. Induced expression of GFP-Gli1 results in a reduction of KA″ cells (arrows). Note that at 36 hpf, GFP-Gli1 expression has minimal contribution to the green fluorescence. (D) <i>Ptc1-Kaede</i> control embryos, and <i>Ptc1-Kaede</i> embryos injected with Shh mRNA, Ptc1 and Ptc2 morpholinos, or dnPKA mRNA were photoconverted at 24 hpf, and stained with the GABA antibody (blue) at 36 hpf. Arrows indicated GABA-positive cells in the LFP domain. Note that Shh and dnPKA overexpression induced many ectopic GABAergic neurons (arrowheads) throughout the dorsal-ventral axis of the spinal cord, and most of them appeared to lose Hh response by 24 hpf as indicated by the expression of <i>Ptc1-Kaede<sup>red</sup></i>. Scale bars: 20 µm.</p
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