2,643 research outputs found

    Magnetic field effects on the electroluminescence of organic light emitting devices: A tool to indicate the carrier mobility

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    The magnetoelectroluminescence (MEL) of organic light emitting devices with a N, N′ -bis(l-naphthyl)- N, N′ -diphenyl- 1, l′ -biphentl- 4, 4′ -diamine:tris-(8-hydroxyquinoline) aluminum (NPB: Alq 3) mixed emission layer (EML) has been investigated. We find that MEL is maximized when the volume ratio of NPB of the mixed EML reaches 30% and the EML thickness is 40 nm. The features of MEL under various magnetic field strengths are insensitive to the change in EML thickness and mixing ratio. Meanwhile, MEL has a close relationship with the carrier mobility. We have conducted a theoretical study to further verify the relationship. Our experimental and theoretical results confirm that MEL can function as a tool to indicate the mobility. © 2010 American Institute of Physics.published_or_final_versio

    Battery management system and control strategy for hybrid and electric vehicle

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    Author name used in this publication: K. W. E. ChengAuthor name used in this publication: K. DingAuthor name used in this publication: W. TingVersion of RecordPublishe

    Stability analysis and quasinormal modes of Reissner Nordstr{\o}m Space-time via Lyapunov exponent

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    We explicitly derive the proper time (τ)(\tau) principal Lyapunov exponent (λp\lambda_{p}) and coordinate time (tt) principal Lyapunov exponent (λc\lambda_{c}) for Reissner Nordstr{\o}m (RN) black hole (BH) . We also compute their ratio. For RN space-time, it is shown that the ratio is λpλc=r0r023Mr0+2Q2\frac{\lambda_{p}}{\lambda_{c}}=\frac{r_{0}}{\sqrt{r_{0}^2-3Mr_{0}+2Q^2}} for time-like circular geodesics and for Schwarzschild BH it is λpλc=r0r03M\frac{\lambda_{p}}{\lambda_{c}}=\frac{\sqrt{r_{0}}}{\sqrt{r_{0}-3M}}. We further show that their ratio λpλc\frac{\lambda_{p}}{\lambda_{c}} may vary from orbit to orbit. For instance, Schwarzschild BH at innermost stable circular orbit(ISCO), the ratio is λpλcrISCO=6M=2\frac{\lambda_{p}}{\lambda_{c}}\mid_{r_{ISCO}=6M}=\sqrt{2} and at marginally bound circular orbit (MBCO) the ratio is calculated to be λpλcrmb=4M=2\frac{\lambda_{p}}{\lambda_{c}}\mid_{r_{mb}=4M}=2. Similarly, for extremal RN BH the ratio at ISCO is λpλcrISCO=4M=223\frac{\lambda_{p}}{\lambda_{c}}\mid_{r_{ISCO}=4M}=\frac{2\sqrt{2}}{\sqrt{3}}. We also further analyse the geodesic stability via this exponent. By evaluating the Lyapunov exponent, it is shown that in the eikonal limit , the real and imaginary parts of the quasi-normal modes of RN BH is given by the frequency and instability time scale of the unstable null circular geodesics.Comment: Accepted in Pramana, 07/09/201

    The effect of S-substitution at the O6-guanine site on the structure and dynamics of a DNA oligomer containing a G:T mismatch

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    The effect of S-substitution on the O6 guanine site of a 13-mer DNA duplex containing a G:T mismatch is studied using molecular dynamics. The structure, dynamic evolution and hydration of the S-substituted duplex are compared with those of a normal duplex, a duplex with Ssubstitution on guanine, but no mismatch and a duplex with just a G:T mismatch. The S-substituted mismatch leads to cell death rather than repair. One suggestion is that the G:T mismatch recognition protein recognises the S-substituted mismatch (GS:T) as G:T. This leads to a cycle of futile repair ending in DNA breakage and cell death. We find that some structural features of the helix are similar for the duplex with the G:T mismatch and that with the S-substituted mismatch, but differ from the normal duplex, notably the helical twist. These differences arise from the change in the hydrogen-bonding pattern of the base pair. However a marked feature of the S-substituted G:T mismatch duplex is a very large opening. This showed considerable variability. It is suggested that this enlarged opening would lend support to an alternative model of cell death in which the mismatch protein attaches to thioguanine and activates downstream damage-response pathways. Attack on the sulphur by reactive oxygen species, also leading to cell death, would also be aided by the large, variable opening

    How citation boosts promote scientific paradigm shifts and Nobel Prizes

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    Nobel Prizes are commonly seen to be among the most prestigious achievements of our times. Based on mining several million citations, we quantitatively analyze the processes driving paradigm shifts in science. We find that groundbreaking discoveries of Nobel Prize Laureates and other famous scientists are not only acknowledged by many citations of their landmark papers. Surprisingly, they also boost the citation rates of their previous publications. Given that innovations must outcompete the rich-gets-richer effect for scientific citations, it turns out that they can make their way only through citation cascades. A quantitative analysis reveals how and why they happen. Science appears to behave like a self-organized critical system, in which citation cascades of all sizes occur, from continuous scientific progress all the way up to scientific revolutions, which change the way we see our world. Measuring the "boosting effect" of landmark papers, our analysis reveals how new ideas and new players can make their way and finally triumph in a world dominated by established paradigms. The underlying "boost factor" is also useful to discover scientific breakthroughs and talents much earlier than through classical citation analysis, which by now has become a widespread method to measure scientific excellence, influencing scientific careers and the distribution of research funds. Our findings reveal patterns of collective social behavior, which are also interesting from an attention economics perspective. Understanding the origin of scientific authority may therefore ultimately help to explain, how social influence comes about and why the value of goods depends so strongly on the attention they attract.Comment: 6 pages, 6 figure

    Fluid-structure interaction simulation of prosthetic aortic valves : comparison between immersed boundary and arbitrary Lagrangian-Eulerian techniques for the mesh representation

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    In recent years the role of FSI (fluid-structure interaction) simulations in the analysis of the fluid-mechanics of heart valves is becoming more and more important, being able to capture the interaction between the blood and both the surrounding biological tissues and the valve itself. When setting up an FSI simulation, several choices have to be made to select the most suitable approach for the case of interest: in particular, to simulate flexible leaflet cardiac valves, the type of discretization of the fluid domain is crucial, which can be described with an ALE (Arbitrary Lagrangian-Eulerian) or an Eulerian formulation. The majority of the reported 3D heart valve FSI simulations are performed with the Eulerian formulation, allowing for large deformations of the domains without compromising the quality of the fluid grid. Nevertheless, it is known that the ALE-FSI approach guarantees more accurate results at the interface between the solid and the fluid. The goal of this paper is to describe the same aortic valve model in the two cases, comparing the performances of an ALE-based FSI solution and an Eulerian-based FSI approach. After a first simplified 2D case, the aortic geometry was considered in a full 3D set-up. The model was kept as similar as possible in the two settings, to better compare the simulations' outcomes. Although for the 2D case the differences were unsubstantial, in our experience the performance of a full 3D ALE-FSI simulation was significantly limited by the technical problems and requirements inherent to the ALE formulation, mainly related to the mesh motion and deformation of the fluid domain. As a secondary outcome of this work, it is important to point out that the choice of the solver also influenced the reliability of the final results

    Mendelian randomization study of B-type natriuretic peptide and type 2 diabetes: evidence of causal association from population studies

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    <p>Background: Genetic and epidemiological evidence suggests an inverse association between B-type natriuretic peptide (BNP) levels in blood and risk of type 2 diabetes (T2D), but the prospective association of BNP with T2D is uncertain, and it is unclear whether the association is confounded.</p> <p>Methods and Findings: We analysed the association between levels of the N-terminal fragment of pro-BNP (NT-pro-BNP) in blood and risk of incident T2D in a prospective case-cohort study and genotyped the variant rs198389 within the BNP locus in three T2D case-control studies. We combined our results with existing data in a meta-analysis of 11 case-control studies. Using a Mendelian randomization approach, we compared the observed association between rs198389 and T2D to that expected from the NT-pro-BNP level to T2D association and the NT-pro-BNP difference per C allele of rs198389. In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. The association between rs198389 and T2D observed in case-control studies (odds ratio = 0.94 per C allele, 95% CI 0.91-0.97) was similar to that expected (0.96, 0.93-0.98) based on the pooled estimate for the log-NT-pro-BNP level to T2D association derived from a meta-analysis of our study and published data (hazard ratio = 0.82 per SD, 0.74-0.90) and the difference in NT-pro-BNP levels (0.22 SD, 0.15-0.29) per C allele of rs198389. No significant associations were observed between the rs198389 genotype and potential confounders.</p> <p>Conclusions: Our results provide evidence for a potential causal role of the BNP system in the aetiology of T2D. Further studies are needed to investigate the mechanisms underlying this association and possibilities for preventive interventions.</p&gt
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