357 research outputs found

    Interaction Between Hot Carrier Aging and PBTI Degradation in nMOSFETs: Characterization, Modelling and Lifetime Prediction

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    Modelling of the interaction between Hot Carrier Aging (HCA) and Positive Bias Temperature Instability (PBTI) has been considered as one of the main challenges in nanoscale CMOS circuit design. Previous works were mainly based on separate HCA and PBTI instead of Interacted HCA-PBTI Degradation (IHPD). The key advance of this work is to develop a methodology that enables accurate modelling of IHPD through understanding the charging/discharging and generation kinetics of different types of defects during the interaction between HCA and PBTI. It is found that degradation during alternating HCA and PBTI stress cannot be modelled by independent HCI/PBTI. Different stress sequence, i.e. HCA-PBTI-HCA and PBTI-HCA-PBTI, lead to completely different degradation kinetics. Based on the Cyclic Anti-neutralization Model (CAM), for the first time, IHPD has been accurately modelled for both short and long channel devices. Complex degradation mechanisms and kinetics can be well explained by our model. Our results show that device lifetime can be underestimated by one decade without considering interaction

    Rab1A Is an mTORC1 Activator and a Colorectal Oncogene

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    SummaryAmino acid (AA) is a potent mitogen that controls growth and metabolism. Here we describe the identification of Rab1 as a conserved regulator of AA signaling to mTORC1. AA stimulates Rab1A GTP binding and interaction with mTORC1 and Rheb-mTORC1 interaction in the Golgi. Rab1A overexpression promotes mTORC1 signaling and oncogenic growth in an AA- and mTORC1-dependent manner. Conversely, Rab1A knockdown selectively attenuates oncogenic growth of Rab1-overexpressing cancer cells. Moreover, Rab1A is overexpressed in colorectal cancer (CRC), which is correlated with elevated mTORC1 signaling, tumor invasion, progression, and poor prognosis. Our results demonstrate that Rab1 is an mTORC1 activator and an oncogene and that hyperactive AA signaling through Rab1A overexpression drives oncogenesis and renders cancer cells prone to mTORC1-targeted therapy

    Frictional drag between non-equilibrium charged gases

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    The frictional drag force between separated but coupled two-dimensional electron gases of different temperatures is studied using the non-equilibrium Green function method based on the separation of center-of-mass and relative dynamics of electrons. As the mechanisms of producing the frictional force we include the direct Coulomb interaction, the interaction mediated via virtual and real TA and LA phonons, optic phonons, plasmons, and TA and LA phonon-electron collective modes. We found that, when the distance between the two electron gases is large, and at intermediate temperature where plasmons and collective modes play the most important role in the frictional drag, the possibility of having a temperature difference between two subsystems modifies greatly the transresistivity.Comment: 8figure

    Characterization of starch synthetic genes and starch granule during seeds development between synthetic hexaploid wheat and its parents

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    To study the development of starch granules in polyploid wheats, we investigated the expression of starch synthetic genes between the synthetic hexaploid wheat SHW-L1, its parents T. turgidum AS2255 and diploid Ae. tauschii AS60. The synthetic hexaploid wheat SHW-L1 showed significantly higher starch content and grain weight than its parents. Scanning electron microscopy (SEM) showed that SHW-L1 rapidly developed starch granules than AS2255 and AS60. The amount of B-type granule in AS60 was less than that in SHW-L1 and AS2255. RT-qPCR result showed that the starch synthetic genes AGPLSU1, AGPLSU2, AGPSSU1, AGPSSU2, GBSSI, SSIII, PHO1 and PHO2 expressed at earlier stages with larger quantity in SHW-L1 than in its parents during wheat grain development. The expression of the above mentioned genes in AS60 was slower than in SHW-L1 and AS2255. The expression pattern of starch synthase genes was also associated with the grain weight and starch content in all three genotypes. The results suggested that the synthetic hexaploid wheat inherited the pattern of starch granule development and starch synthase gene expression from tetraploid parent. The results suggest that tetraploid wheat could plays more important role for starch quality improvement in hexaploid wheat

    Partial Wave Analysis of J/ψγ(K+Kπ+π)J/\psi \to \gamma (K^+K^-\pi^+\pi^-)

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    BES data on J/ψγ(K+Kπ+π)J/\psi \to \gamma (K^+K^-\pi^+\pi^-) are presented. The KKˉK^*\bar K^* contribution peaks strongly near threshold. It is fitted with a broad 0+0^{-+} resonance with mass M=1800±100M = 1800 \pm 100 MeV, width Γ=500±200\Gamma = 500 \pm 200 MeV. A broad 2++2^{++} resonance peaking at 2020 MeV is also required with width 500\sim 500 MeV. There is further evidence for a 2+2^{-+} component peaking at 2.55 GeV. The non-KKˉK^*\bar K^* contribution is close to phase space; it peaks at 2.6 GeV and is very different from KKˉK^{*}\bar{K^{*}}.Comment: 15 pages, 6 figures, 1 table, Submitted to PL

    2-Aminophenoxazine-3-one and 2-amino-4,4α-dihydro-4α,7-dimethyl-3H-phenoxazine-3-one cause cellular apoptosis by reducing higher intracellular pH in cancer cells

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    We examined intracellular pH (pHi) of ten cancer cell lines derived from different organs and two normal cell lines including human embryonic lung fibroblast cells (HEL) and human umbilical vein endothelial cells (HUVEC) in vitro, and found that pHi of most of these cancer cells was evidently higher (pH 7.5 to 7.7) than that of normal cells (7.32 and 7.44 for HEL and HUVEC, respectively) and that of primary leukemic cells and erythrocytes hitherto reported (≤7.2). Higher pHi in these cancer cells could be related to the Warburg effect in cancer cells with enhanced glycolytic metabolism. Since reversal of the Warburg effect may perturb intracellular homeostasis in cancer cells, we looked for compounds that cause extensive reduction of pHi, a major regulator of the glycolytic pathway and its associated metabolic pathway. We found that phenoxazine compounds, 2-aminophenoxazine-3-one (Phx-3) and 2-amino-4,4α-dihydro-4α,7-dimethyl-3H-phenoxazine-3-one (Phx-1) caused a rapid and drastic dose-dependent decrease of pHi in ten different cancer cells within 30 min, though the extent of the decrease of pHi was significantly larger for Phx-3 (ΔpHi = 0.6 pH units or more for 100 µM Phx-3) than for Phx-1 (ΔpHi = 0.1 pH units or more for 100 µM Phx-1). This rapid and drastic decrease of pHi in a variety of cancer cells caused by Phx-3 and Phx-1 possibly perturbed their intracellular homeostasis, and extensively affected the subsequent cell death, because these phenoxazines exerted dose-dependent proapoptotic and cytotoxic effects on these cells during 72 h incubation, confirming a causal relationship between ΔpHi and cytotoxic effects due to Phx-3 and Phx-1. Phx-3 and Phx-1 also reduced pHi of normal cells including HEL and HUVEC, although they exerted less proapoptotic and cytotoxic effects on these cells than on cancer cells. Drugs such as Phx-3 and Phx-1 that reduce pHi and thereby induce cellular apoptosis might serve as benevolent anticancer drugs
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