3,937 research outputs found

    An improved perturbation approach to the 2D Edwards polymer -- corrections to scaling

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    We present the results of a new perturbation calculation in polymer statistics which starts from a ground state that already correctly predicts the long chain length behaviour of the mean square end--to--end distance RN2 \langle R_N^2 \rangle\ , namely the solution to the 2~dimensional~(2D) Edwards model. The RN2\langle R_N^2 \rangle thus calculated is shown to be convergent in NN, the number of steps in the chain, in contrast to previous methods which start from the free random walk solution. This allows us to calculate a new value for the leading correction--to--scaling exponent~Δ\Delta. Writing RN2=AN2ν(1+BNΔ+CN1+...)\langle R_N^2 \rangle = AN^{2\nu}(1+BN^{-\Delta} + CN^{-1}+...), where ν=3/4\nu = 3/4 in 2D, our result shows that Δ=1/2\Delta = 1/2. This value is also supported by an analysis of 2D self--avoiding walks on the {\em continuum}.Comment: 17 Pages of Revtex. No figures. Submitted to J. Phys.

    Evaluation of web-based flexible learning

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    Arts, Education & Law Group, School of Education and Professional StudiesFull Tex

    Unsupervised Domain Adaptation for 3D Keypoint Estimation via View Consistency

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    In this paper, we introduce a novel unsupervised domain adaptation technique for the task of 3D keypoint prediction from a single depth scan or image. Our key idea is to utilize the fact that predictions from different views of the same or similar objects should be consistent with each other. Such view consistency can provide effective regularization for keypoint prediction on unlabeled instances. In addition, we introduce a geometric alignment term to regularize predictions in the target domain. The resulting loss function can be effectively optimized via alternating minimization. We demonstrate the effectiveness of our approach on real datasets and present experimental results showing that our approach is superior to state-of-the-art general-purpose domain adaptation techniques.Comment: ECCV 201

    The role of thermal and lubricant boundary layers in the transient thermal analysis of spur gears

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    An improved convection heat-transfer model has been developed for the prediction of the transient tooth surface temperature of spur gears. The dissipative quality of the lubricating fluid is shown to be limited to the capacity extent of the thermal boundary layer. This phenomenon can be of significance in the determination of the thermal limit of gears accelerating to the point where gear scoring occurs. Steady-state temperature prediction is improved considerably through the use of a variable integration time step that substantially reduces computer time. Computer-generated plots of temperature contours enable the user to animate the propagation of the thermal wave as the gears come into and out of contact, thus contributing to better understanding of this complex problem. This model has a much better capability at predicting gear-tooth temperatures than previous models

    Addressing the interplay between apoptosis and glucose metabolism in liver cirrhosis and hcc

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    Introduction: Pro-inflammatory signalling in the liver promotes the appearance of a metabolic phenotype that involves the transition from mitochondrial respiration to aerobic glycolysis. It was demonstrated that this metabolic shift occurs during the transition from healthy and early stage of liver injury (NAFLD/NASH, ALD to late stage of disease (i.e. cirrhosis), and further escalates during HCC development.1,2This metabolic signature enables dividing cells to satisfy anabolic and energetic needs for biomass production and to suppress apoptotic signalling, which is consistent with increased compensatory hepatic cell proliferation typical of cirrhotic and HCC livers. However other studies in contrast have suggested that hepatocytes are unable to sustain glycolysis during late stage of chronic liver disease.3 Method: We used unbiased gene expression analyses of microarray datasets to investigate the expression of glycolytic genes in cirrhotic and HCC livers and correlated their expression with patient outcome. Furthermore, by using a combination of in vitro and in vivo analyses we have characterised the abilities of a novel anti-apoptotic gene to regulate aerobic glycolysis in liver cirrhosis and HCC. Results: mRNA profiling showed significantly higher expression of glycolytic transcripts in cirrhotic and HCC livers compared to normal quiescent livers (P < 0.05). Up regulation of Glut1, Hk1, Hk2, G6PI, and PFKLwas seen in HCC livers compared to their adjacent non-tumour tissues (P < 0.001). Notably, expression of enzymes regulating mitochondrial activity (Pdha, Pdk) was unchanged between non-tumour tissues and late stage of HCC. Moreover, up regulation of a novel anti-apoptotic gene positively correlated with increased expression of glycolytic transcripts in a group of cirrhotic patients prospectively classified as poor prognosis based on HCC development, and promotes the aerobic glycolysis of hepatoma cells. Conclusion: In summary, our findings delineate a putative link between aerobic glycolysis and suppression of apoptosis that is an important part of the progression of cirrhosis to HCC. The identification of the mechanism regulating this link may lead to design new therapeutic strategies for human liver disease

    Optical and electrical properties of efficiency enhanced polymer solar cells with Au nanoparticles in a PEDOT-PSS layer

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    We unveil new device physics and provide details of device mechanisms by investigating polymer solar cells (PSCs) incorporating Au nanoparticles (NPs) into the hole collection poly(3,4-ethylenedioxythiophene) poly(styrenesulfonate) (PEDOT:PSS) layer. Theoretical and experimental results show that the very strong near field around Au NPs due to Localized Surface Plasmonic Resonance (LSPR) mainly distributes laterally along the PEDOT:PSS layer rather than vertically into the adjacent active layer, leading to minimal enhancement of light absorption in the active layer. This finding can be extended to a typical class of solar cells incorporating metallic NPs in spacing layers adjacent to the active layer. With optical effects proven to be minor contributors to device performance improvements, we investigate the electrical properties of the PSCs and obtain insights into the detailed device mechanisms. Improvements in power conversion efficiency (PCE) of solar cells are found to originate from the enlarged active layer/PEDOT:PSS interfacial area and improved PEDOT:PSS conductivity. At high NP concentrations, reduced exciton quenching at donor/acceptor junctions is found to cause PCE deterioration. Our findings indicate that it is highly important to investigate both optical and electrical effects for understanding and optimizing PSC performances. © 2011 The Royal Society of Chemistry.postprin

    Insulating charge density wave for a half-filled SU(N) Hubbard model with an attractive on-site interaction in one dimension

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    We study a one-dimensional SU(N) Hubbard model with an attractive on-site interaction and N>2N>2 at half-filling on the bipartite lattice using density-matrix renormalization-group method and a perturbation theory. We find that the ground state of the SU(N) Hubbard model is a charge density wave state with two-fold degeneracy. All the excitations are found to be gapful, resulting in an insulating ground state, on contrary to that in the SU(2) case. Moreover, the charge gap is equal to the Cooperon gap, which behaves as 2Nt2/(N1)U-2Nt^2/(N-1)U in the strong coupling regime. However, the spin gap Δs\Delta_{s} and the quasiparticle gap Δ1\Delta_{1} as well open exponentially in the weak coupling region, while in the strong coupling region, they linearly depend on UU such that ΔsU(N1)\Delta_{s}\sim -U(N-1) and Δ1U(N1)/2\Delta_{1}\sim -U(N-1)/2.Comment: 7 pages, 7 figure

    Inhibition of mapk signalling promotes cell cycle arrest and sensitises intrahepatic cholangiocarcinoma cells to chemotherapy

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    Introduction: Intrahepatic cholangiocarcinoma (ICC) is the second most common primary hepatic malignancy, accounting for approximately 15% of cases of primary liver cancer. Although new treatments have increased survival for many other cancers, including the more common primary hepatocellular carcinoma, treatment strategies and survival for patients with ICC have seen little improvement. Our previous studies suggest that the mitogen-activated protein kinase (MAPK) signalling plays a central role in the regulation of cell proliferation in human ICC. However the molecular mechanisms are poorly understood. In this study, we aim to explore whether inhibition of the MAPK pathway and its downstream effectors enhances the sensitisation of ICC cells to the chemotherapeutic agent cisplatinum. Method: We used a combinatorial approach of immunohistochemical and gene expression analyses to investigate the expression of MAPK-related genes in ICC tumours. Furthermore, by using in-vitroand in-vivoanalyses we have characterised the function of a novel MAPK downstream effector in ICC cells. Results: The expression of MAPK signalling was determined by immunohistochemical staining in tumour samples from a cohort of 14 ICC patients. High expression of phospho-activated MAPK was observed in 71.4% (10/14) of ICC cases as compared with surrounding nontumour tissue. Likewise, expression of JDP, a downstream effector of the MAPK signalling, was scored as high intensity in 64.3% (9/14). Strikingly, elevated expression of JDP transcripts was also observed in two independent cohorts of human ICC (n = 149 and n = 109 per group, respectively) compared to surrounding normal liver tissue. Consistent with the in-vivo analyses of human samples, immunoblotting analyses showed constitutive activation of MAPK and expression of JDP in ICC-derived cells (i.e. SG231, CCLP-1 and HuCCT1). Using loss-of-function analyses, we demonstrates that knockdown of JDP in ICC-derived cells resulted in cell cycle arrest and reduced expression of cell cycle regulators (i.e. cyclins), and had minimal effect on apoptosis. Chemical inhibition of JDP significantly sensitises ICC-derived cells to cisplatinum (P < 0.001). Conclusion: These results demonstrate that enhanced activation of MAPK signalling is important for ICC cell proliferation and suggest that targeting its downstream effectors is a potential therapeutic strategy for ICC
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