132 research outputs found

    Analysis of friction-induced vibration leading to brake squeal using a three degree-of-freedom model

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    Friction-induced vibration is a common phenomenon in nature and thus has attracted many researchers’ attention. Many of the mathematical models that have been proposed on the basis of mode coupling principle, however, cannot be utilized directly to analyse the generation of friction-induced vibration that occurs between two bodies because of a difficulty relating model parameters to definite physical meaning for real friction pairs. In this paper, a brake squeal experiment is firstly carried out by using a simple beam-on-disc laboratory apparatus. Experimental results show that brake squeal correlates with the bending mode of the beam and the nodal diameter out-ofplane mode of the disc as well as the cantilever length of the beam. Then, a specific three degree-of-freedom dynamic model is developed of the beam-on-disc system and the vibration behaviour is simulated by using the complex eigenvalue analysis method and a transient response analysis. Numerical simulation shows that the bending mode frequency of the beam a little greater than the frequency of the nodal diameter out-of-plane mode and a specific incline angle of the leading area to the normal line of the disc as well as a certain friction coefficient, are necessary conditions for the mode coupling of a frictional system. Results also show that when the frictional system is transited from a steady state to an unstable state for the variation of parameters, its kinetic and potential energy increase with time due to continuous feed-in energy from the friction force while the dynamic responses of the system change from the beating oscillation to the divergent, which leads to the friction-induced vibration and squeal noise

    Evolution of Electronic Structure as a Function of Layer Thickness in Group-VIB Transition Metal Dichalcogenides: Emergence of Localization Prototypes

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    Layered group-VIB transition metal dichalcogenides (with the formula of MX<sub>2</sub>) are known to show a transition from an indirect band gap in the thick <i>n</i>-monolayer stack (MX<sub>2</sub>)<sub><i>n</i></sub> to a direct band gap at the <i>n</i> = 1 monolayer limit, thus converting the system into an optically active material suitable for a variety of optoelectronic applications. The origin of this transition has been attributed predominantly to quantum confinement effect at reduced <i>n</i>. Our analysis of the evolution of band-edge energies and wave functions as a function of <i>n</i> using ab initio density functional calculations including the long-range dispersion interaction reveals (i) the indirect-to-direct band gap transformation is triggered not only by (kinetic-energy controlled) quantum confinement but also by (potential-energy controlled) band repulsion and localization. On its own, neither of the two effects can explain by itself the energy evolution of the band-edge states relevant to the transformation; (ii) when <i>n</i> decreased, there emerge distinct regimes with characteristic localization prototypes of band-edge states deciding the optical response of the system. They are distinguished by the real-space direct/indirect in combination with momentum-space direct/indirect nature of electron and hole states and give rise to distinct types of charge distribution of the photoexcited carriers that control excitonic behaviors; (iii) the various regimes associated with different localization prototypes are predicted to change with modification of cations and anions in the complete MX<sub>2</sub> (M = Cr, Mo, W and X = S, Se, Te) series. These results offer new insight into understanding the excitonic properties (e.g., binding energy, lifetime etc.) of multiple layered MX<sub>2</sub> and their heterostructures

    A Unified Understanding of the Thickness-Dependent Bandgap Transition in Hexagonal Two-Dimensional Semiconductors

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    Many important layered semiconductors, such as hexagonal boron nitride (hBN) and transition-metal dichalcogenides (TMDs), are derived from a hexagonal lattice. A single layer of such hexagonal semiconductors generally has a direct bandgap at the high-symmetry point K, whereas it becomes an indirect, optically inactive semiconductor as the number of layers increases to two or more. Here, taking hBN and MoS<sub>2</sub> as examples, we reveal the microscopic origin of the direct-to-indirect bandgap transition of hexagonal layered materials. Our symmetry analysis and first-principles calculations show that the bandgap transition arises from the lack of the interlayer orbital couplings for the band-edge states at K, which are inherently weak because of the crystal symmetries of hexagonal layered materials. Therefore, it is necessary to judiciously break the underlying crystal symmetries to design more optically active, multilayered semiconductors from hBN or TMDs

    A Hybrid Chalcone Combining the Trimethoxyphenyl and Isatinyl Groups Targets Multiple Oncogenic Proteins and Pathways in Hepatocellular Carcinoma Cells

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    <div><p>Small molecule inhibitors that can simultaneously inhibit multiple oncogenic proteins in essential pathways are promising therapeutic chemicals for hepatocellular carcinoma (HCC). To combine the anticancer effects of combretastatins, chalcones and isatins, we synthesized a novel hybrid molecule 3’,4’,5’-trimethoxy-5-chloro-isatinylchalcone (3MCIC). 3MCIC inhibited proliferation of cultured HepG2 cells, causing rounding-up of the cells and massive vacuole accumulation in the cytoplasm. Paxillin and focal adhesion plaques were downregulated by 3MCIC. Surprisingly, unlike the microtubule (MT)-targeting agent CA-4 that inhibits tubulin polymerization, 3MCIC stabilized tubulin polymers both in living cells and in cell lysates. 3MCIC treatment reduced cyclin B1, CDK1, p-CDK1/2, and Rb, but increased p53 and p21. Moreover, 3MCIC caused GSK3β degradation by promoting GSK3β-Ser9 phosphorylation. Nevertheless, 3MCIC inhibited the Wnt/β-catenin pathway by downregulating β-catenin, c-Myc, cyclin D1 and E2F1. 3MCIC treatment not only activated the caspase-3-dependent apoptotic pathway, but also caused massive autophagy evidenced by rapid and drastic changes of LC3 and p62. 3MCIC also promoted cleavage and maturation of the lysosomal protease cathepsin D. Using ligand-affinity chromatography (LAC), target proteins captured onto the Sephacryl S1000-C<sub>12</sub>-3MCIC resins were isolated and analyzed by mass spectrometry (MS). Some of the LAC-MS identified targets, i.e., septin-2, vimentin, pan-cytokeratin, nucleolin, EF1α1/2, EBP1 (PA2G4), cyclin B1 and GSK3β, were further detected by Western blotting. Moreover, both septin-2 and HIF-1α decreased drastically in 3MCIC-treated HepG2 cells. Our data suggest that 3MCIC is a promising anticancer lead compound with novel targeting mechanisms, and also demonstrate the efficiency of LAC-MS based target identification in anticancer drug development.</p></div

    Cell viability assay.

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    <p>Dose-response curves of five cancer cell lines and the fetal liver L02 cells treated with different concentrations of 3MCIC for 48 h. The bars are means ± SEM (n = 6 or 8).</p

    Influence of tubulin polymerization by 3MCIC.

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    <p>HepG2 cells were incubated at 37°C with 3MCIC, paclitaxel or colchicine, and assayed with α-tubulin mAb by immunofluorescence <b>(A)</b> and Western blotting <b>(B)</b> after separation of soluble (supernatant, S) and polymerized (pellet, P) tubulins. <b>(C)</b> HepG2 cell lysates were incubated at 25°C for 10 or 30 min with 3MCIC or paclitaxel respectively, and analyzed by Western blotting. In both <b>B</b> & <b>C</b>, normalized changes of the band-intensity ratios of P/S-tubulin in drug-treated groups over controls were plotted. *P<0.05, **P<0.01 and ***P<0.001 vs control (n = 3).</p

    Diminish of paxillin and focal adhesion plaques in 3MCIC-treated HepG2 cells.

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    <p><b>(A)</b> Cells were treated with 3MCIC and assayed by Western blotting. Calnexin was used as loading control. <b>(B)</b> Immunofluorescence of HepG2 cells stained with paxillin mAb (green), phalloidin (red) and Hoechst 33342, after incubation with 8 or 12 μg/ml 3MCIC for 3 h.</p

    Changes of cell-cycle control proteins in 3MCIC-treated HepG2 cells.

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    <p>Cells were treated with 8 or 12 μg/ml 3MCIC at indicated times respectively. Calnexin was used as loading control. <b>(A)</b> Western blotting of cyclins and CDKs. <b>(B)</b> Western blotting of c-Myc, E2F1, Ser567 phosphorylated p-Rb, Rb, p53 and p21.</p

    Morphological changes in 3MCIC-treated HepG2 cells.

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    <p><b>(A)</b> HepG2 cells in 6-well plates were incubated with 12 μg/ml 3MCIC for 30, 60 and 120 min, and observed under a phase-contrast inverted microscope. <b>(B)</b> Prolonged incubation of HepG2 cells with 8 and 12 μg/ml 3MCIC for 3 and 24 h, respectively.</p

    Activation of cell death pathways in 3MCIC-treated HepG2 cells.

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    <p><b>(A)</b> Western blots showing 3MCIC-induced PARP, caspase-3 and vimentin cleavages, CatD maturation, LC3 I & II upregulation, and p62 downregulation. <b>(B)</b> The TUNEL assay after 3MCIC treatment for 12 h. <b>(C)</b> Normalized relative band-intensity ratios of mature/pro-CatD in 3MCIC-treated groups over controls were plotted. <b>(D)</b> Immunofluorescence of HepG2 cells treated with 3MCIC for 3 h, and stained with p62 mAb (green), phalloillin (red) and Hoechst 33342. <b>(E)</b> The early-stage alternations of LC3 under 12 μg/ml 3MCIC treatment. Normalized relative band-intensity ratios of LC3 II/LC3 I in 3MCIC-treated groups over controls were plotted. In <b>C</b> & <b>E</b>, *P<0.05, **P<0.01 and ***P<0.001 vs control (n = 3). <b>(F)</b> LC3 immunofluorescence of HepG2 cells treated with 12 μg/ml 3MCIC at the indicated times. <b>(G)</b> A HepG2 cell was observed either by a light microscope (LM) to show the vacuoles, or by immunofluorescence (IF) with a LC3 mAb, after incubation with 12 μg/ml 3MCIC for 3 h.</p