7,709 research outputs found

    A Memristor Model with Piecewise Window Function

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    In this paper, we present a memristor model with piecewise window function, which is continuously differentiable and consists of three nonlinear pieces. By introducing two parameters, the shape of this window function can be flexibly adjusted to model different types of memristors. Using this model, one can easily obtain an expression of memristance depending on charge, from which the numerical value of memristance can be readily calculated for any given charge, and eliminate the error occurring in the simulation of some existing window function models

    Modeling the Flux-Charge Relation of Memristor with Neural Network of Smooth Hinge Functions

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    The memristor was proposed to characterize the flux-charge relation. We propose the generalized flux-charge relation model of memristor with neural network of smooth hinge functions. There is effective identification algorithm for the neural network of smooth hinge functions. The representation capability of this model is theoretically guaranteed. Any functional flux-charge relation of a memristor can be approximated by the model. We also give application examples to show that the given model can approximate the flux-charge relation of existing piecewise linear memristor model, window function memristor model, and a physical memristor device

    Modeling the AgInSbTe Memristor

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    The AgInSbTe memristor shows gradual resistance tuning characteristics, which makes it a potential candidate to emulate biological plastic synapses. The working mechanism of the device is complex, and both intrinsic charge-trapping mechanism and extrinsic electrochemical metallization effect are confirmed in the AgInSbTe memristor. Mathematical model of the AgInSbTe memristor has not been given before. We propose the flux-voltage controlled memristor model. With piecewise linear approximation technique, we deliver the flux-voltage controlled memristor model of the AgInSbTe memristor based on the experiment data. Our model fits the data well. The flux-voltage controlled memristor model and the piecewise linear approximation method are also suitable for modeling other kinds of memristor devices based on experiment data

    In an Attempt to Introduce Long-range Interactions into Small-world Networks

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    Distinguishing the long-range bonds with the regular ones, the critical temperature of the spin-lattice Guassian model built on two typical Small-world Networks (SWNs) is studied. The results show much difference from the classical case, and thus may induce some more accurate discussion on the critical properties of the spin-lattice systems combined with the SWNs.Comment: 4 pages, 3 figures, 18 referenc

    Data-Driven Dynamic Modeling of Coupled Thermal and Electric Outputs of Microturbines

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    Microturbines (MTs) are among the most successfully commercialized distributed energy resources, especially when they are used for combined heat and power generation. However, the interrelated thermal and electrical system dynamic behaviors have not been fully investigated. This is technically challenging due to the complex thermo-fluid-mechanical energy conversion processes, which introduce multiple time-scale dynamics and strong nonlinearity into the analysis. To tackle this problem, this paper proposes a simplified model which can predict the coupled thermal and electric output dynamics of MTs. Considering the time-scale difference of various dynamic processes occurring within MTs, the electromechanical subsystem is treated as a fast quasi-linear process, while the thermo-mechanical subsystem is treated as a slow process with high nonlinearity. A three-stage subspace identification method is utilized to capture the dominant dynamics and predict the electric power output. For the thermo-mechanical process, a radial basis function model trained by the particle swarm optimization method is employed to handle the strong nonlinear characteristics. Experimental tests on a Capstone C30 MT show that the proposed modeling method can well capture the system dynamics, and produce a good prediction of the coupled thermal and electric outputs in various operating modes

    Rapamycin inhibits ALDH activity, resistance to oxidative stress, and metastatic potential in murine osteosarcoma cells

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    Osteosarcoma (OS) is the most common primary malignancy of bone. Mortality is determined by the presence of metastatic disease, but little is known regarding the biochemical events that drive metastases. Two murine OS cell lines, K7M2 and K12, are related but differ significantly in their metastatic potentials: K7M2 is highly metastatic whereas K12 displays much less metastatic potential. Using this experimental system, the mammalian target of rapamycin (mTOR) pathway has been implicated in OS metastasis. We also discovered that aldehyde dehydrogenase (ALDH, a stem cell marker) activity is higher in K7M2 cells than K12 cells. Rapamycin treatment reduces the expression and enzymatic activity of ALDH in K7M2 cells. ALDH inhibition renders these cells more susceptible to apoptotic death when exposed to oxidative stress. Furthermore, rapamycin treatment reduces bone morphogenetic protein-2 (BMP2) and vascular endothelial growth factor (VEGF) gene expression and inhibits K7M2 proliferation, migration, and invasion in vitro. Inhibition of ALDH with disulfiram correlated with decreased mTOR expression and activity. In conclusion, we provide evidence for interaction between mTOR activity, ALDH activity, and metastatic potential in murine OS cells. Our work suggests that mTOR and ALDH are therapeutic targets for the treatment and prevention of OS metastasis. © 2013 Xiaodong Mu et al

    Rapamycin inhibits ALDH activity, resistance to oxidative stress, and metastatic potential in murine osteosarcoma cells

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    Osteosarcoma (OS) is the most common primary malignancy of bone. Mortality is determined by the presence of metastatic disease, but little is known regarding the biochemical events that drive metastases. Two murine OS cell lines, K7M2 and K12, are related but differ significantly in their metastatic potentials: K7M2 is highly metastatic whereas K12 displays much less metastatic potential. Using this experimental system, the mammalian target of rapamycin (mTOR) pathway has been implicated in OS metastasis. We also discovered that aldehyde dehydrogenase (ALDH, a stem cell marker) activity is higher in K7M2 cells than K12 cells. Rapamycin treatment reduces the expression and enzymatic activity of ALDH in K7M2 cells. ALDH inhibition renders these cells more susceptible to apoptotic death when exposed to oxidative stress. Furthermore, rapamycin treatment reduces bone morphogenetic protein-2 (BMP2) and vascular endothelial growth factor (VEGF) gene expression and inhibits K7M2 proliferation, migration, and invasion in vitro. Inhibition of ALDH with disulfiram correlated with decreased mTOR expression and activity. In conclusion, we provide evidence for interaction between mTOR activity, ALDH activity, and metastatic potential in murine OS cells. Our work suggests that mTOR and ALDH are therapeutic targets for the treatment and prevention of OS metastasis. © 2013 Xiaodong Mu et al

    Notch signaling is associated with ALDH activity and an aggressive metastatic phenotype in murine osteosarcoma cells

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    Osteosarcoma (OS) is the most common primary malignancy of bone, and pulmonary metastatic disease accounts for nearly all mortality. However, little is known about the biochemical signaling alterations that drive the progression of metastatic disease. Two murine OS cell populations, K7M2 and K12, are clonally related but differ significantly in their metastatic phenotypes and therefore represent excellent tools for studying metastatic OS molecular biology. K7M2 cells are highly metastatic, whereas K12 cells display limited metastatic potential. Here we report that the expression of Notch genes (Notch1, 2, 4) are up-regulated, including downstream targets Hes1 and Stat3, in the highly metastatic K7M2 cells compared to the less metastatic K12 cells, indicating that the Notch signaling pathway is more active in K7M2 cells. We have previously described that K7M2 cells exhibit higher levels of aldehyde dehydrogenase (ALDH) activity. Here we report that K7M2 cell ALDH activity is reduced with Notch inhibition, suggesting that ALDH activity may be regulated in part by the Notch pathway. Notch signaling is also associated with increased resistance to oxidative stress, migration, invasion, and VEGF expression in vitro. However, Notch inhibition did not significantly alter K7M2 cell proliferation. In conclusion, we provide evidence that Notch signaling is associated with ALDH activity and increased metastatic behavior in OS cells. Both Notch and ALDH are putative molecular targets for the treatment and prevention of OS metastasis. © 2013 Mu, Isaac, Greco, Huard and Weiss

    Rapamycin inhibits ALDH activity, resistance to oxidative stress, and metastatic potential in murine osteosarcoma cells

    Get PDF
    Osteosarcoma (OS) is the most common primary malignancy of bone. Mortality is determined by the presence of metastatic disease, but little is known regarding the biochemical events that drive metastases. Two murine OS cell lines, K7M2 and K12, are related but differ significantly in their metastatic potentials: K7M2 is highly metastatic whereas K12 displays much less metastatic potential. Using this experimental system, the mammalian target of rapamycin (mTOR) pathway has been implicated in OS metastasis. We also discovered that aldehyde dehydrogenase (ALDH, a stem cell marker) activity is higher in K7M2 cells than K12 cells. Rapamycin treatment reduces the expression and enzymatic activity of ALDH in K7M2 cells. ALDH inhibition renders these cells more susceptible to apoptotic death when exposed to oxidative stress. Furthermore, rapamycin treatment reduces bone morphogenetic protein-2 (BMP2) and vascular endothelial growth factor (VEGF) gene expression and inhibits K7M2 proliferation, migration, and invasion in vitro. Inhibition of ALDH with disulfiram correlated with decreased mTOR expression and activity. In conclusion, we provide evidence for interaction between mTOR activity, ALDH activity, and metastatic potential in murine OS cells. Our work suggests that mTOR and ALDH are therapeutic targets for the treatment and prevention of OS metastasis. © 2013 Xiaodong Mu et al
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