22,228 research outputs found

    Tunable heat pump by modulating the coupling to the leads

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    We follow the nonequilibrium Green's function formalism to study time-dependent thermal transport in a linear chain system consisting of two semi-infinite leads connected together by a coupling that is harmonically modulated in time. The modulation is driven by an external agent that can absorb and emit energy. We determine the energy current flowing out of the leads exactly by solving numerically the Dyson equation for the contour-ordered Green's function. The amplitude of the modulated coupling is of the same order as the interparticle coupling within each lead. When the leads have the same temperature, our numerical results show that modulating the coupling between the leads may direct energy to either flow into the leads simultaneously or flow out of the leads simultaneously, depending on the values of the driving frequency and temperature. A special combination of values of the driving frequency and temperature exists wherein no net energy flows into or out of the leads, even for long times. When one of the leads is warmer than the other, net energy flows out of the warmer lead. For the cooler lead, however, the direction of the energy current flow depends on the values of the driving frequency and temperature. In addition, we find transient effects to become more pronounced for higher values of the driving frequency.Comment: 10 pages; version 2 accepted for publication in PR

    Cyclin B1/Cdk1 phosphorylation of mitochondrial p53 induces anti-apoptotic response.

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    The pro-apoptotic function of p53 has been well defined in preventing genomic instability and cell transformation. However, the intriguing fact that p53 contributes to a pro-survival advantage of tumor cells under DNA damage conditions raises a critical question in radiation therapy for the 50% human cancers with intact p53 function. Herein, we reveal an anti-apoptotic role of mitochondrial p53 regulated by the cell cycle complex cyclin B1/Cdk1 in irradiated human colon cancer HCT116 cells with p53(+/+) status. Steady-state levels of p53 and cyclin B1/Cdk1 were identified in the mitochondria of many human and mouse cells, and their mitochondrial influx was significantly enhanced by radiation. The mitochondrial kinase activity of cyclin B1/Cdk1 was found to specifically phosphorylate p53 at Ser-315 residue, leading to enhanced mitochondrial ATP production and reduced mitochondrial apoptosis. The improved mitochondrial function can be blocked by transfection of mutant p53 Ser-315-Ala, or by siRNA knockdown of cyclin B1 and Cdk1 genes. Enforced translocation of cyclin B1 and Cdk1 into mitochondria with a mitochondrial-targeting-peptide increased levels of Ser-315 phosphorylation on mitochondrial p53, improved ATP production and decreased apoptosis by sequestering p53 from binding to Bcl-2 and Bcl-xL. Furthermore, reconstitution of wild-type p53 in p53-deficient HCT116 p53(-/-) cells resulted in an increased mitochondrial ATP production and suppression of apoptosis. Such phenomena were absent in the p53-deficient HCT116 p53(-/-) cells reconstituted with the mutant p53. These results demonstrate a unique anti-apoptotic function of mitochondrial p53 regulated by cyclin B1/Cdk1-mediated Ser-315 phosphorylation in p53-wild-type tumor cells, which may provide insights for improving the efficacy of anti-cancer therapy, especially for tumors that retain p53

    A sharp estimate for cover times on binary trees

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    We compute the second order correction for the cover time of the binary tree of depth nn by (continuous-time) random walk, and show that with probability approaching 1 as nn increases, \sqrt{\tau_{\mathrm{cov}}}=\sqrt{|E|}[\sqrt{2\log 2}\cdot n - {\log n}/{\sqrt{2\log 2}} + O((\log\logn)^8], thus showing that the second order correction differs from the corresponding one for the maximum of the Gaussian free field on the tree.Comment: 14 pages, no figur
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