480 research outputs found

    On the emission reduction through the application of an electrically heated catalyst to a diesel vehicle

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    Exhaust emissions from diesel engine powered vehicles are considerably high during cold start and warm‐up, because of the poor catalyst performance due to the insufficient catalyst temperature. The controlled heat injection allowed by electrically heated catalysts can effectively reduce the catalyst light‐off time with relatively moderate fuel penalty. This paper compares the exhaust temperature and emissions of a case study diesel vehicle in cold and warm start conditions, and proposes two electrically heated catalyst control strategies, which are evaluated in terms of emission reduction and energy consumption with different target temperature settings. In addition, a new performance indicator, that is, the specific emission reduction, is used to evaluate the after‐treatment system and associated thermal management. For the worldwide harmonized light vehicle test cycle, the results without electrically heated catalyst show that from both cold and warm start conditions a large amount of operating points of the engine is located in the region of partial catalyst light off. Moreover, emissions, especially in terms of carbon monoxide and hydrocarbon, significantly decrease with the electrically heated catalyst implementation, for example, by at least 50% from cold start; however, they still tend to be rather substantial when the fuel is re‐injected after the engine cutoff phases. The exhaust temperature is lower than the target values in the sections of the driving cycle in which the electrically heated catalyst power is saturated according to the maximum level allowed by the device. The carbon dioxide penalty brought by the electrically heated catalyst ranges from 3.93% to 6.65% and from 6.49% to 9.35% for warm and cold start conditions, respectively

    Principle of Maximum Entropy Applied to Rayleigh-B\'enard Convection

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    A statistical-mechanical investigation is performed on Rayleigh-B\'enard convection of a dilute classical gas starting from the Boltzmann equation. We first present a microscopic derivation of basic hydrodynamic equations and an expression of entropy appropriate for the convection. This includes an alternative justification for the Oberbeck-Boussinesq approximation. We then calculate entropy change through the convective transition choosing mechanical quantities as independent variables. Above the critical Rayleigh number, the system is found to evolve from the heat-conducting uniform state towards the convective roll state with monotonic increase of entropy on the average. Thus, the principle of maximum entropy proposed for nonequilibrium steady states in a preceding paper is indeed obeyed in this prototype example. The principle also provides a natural explanation for the enhancement of the Nusselt number in convection.Comment: 13 pages, 4 figures; typos corrected; Eq. (66a) corrected to remove a double counting for k⊥=0k_{\perp}=0; Figs. 1-4 replace

    Causality bounds for neutron-proton scattering

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    We consider the constraints of causality and unitarity for the low-energy interactions of protons and neutrons. We derive a general theorem that non-vanishing partial-wave mixing cannot be reproduced with zero-range interactions without violating causality or unitarity. We define and calculate interaction length scales which we call the causal range and the Cauchy-Schwarz range for all spin channels up to J = 3. For some channels we find that these length scales are as large as 5 fm. We investigate the origin of these large lengths and discuss their significance for the choice of momentum cutoff scales in effective field theory and universality in many-body Fermi systems.Comment: 36 pages, 10 figures, 7 tables, version to appear in Eur. Phys. J.

    Clinical significance of altered nm23-H1, EGFR, RB and p53 expression in bilharzial bladder cancer

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    <p>Abstract</p> <p>Background</p> <p>Clinical characterization of bladder carcinomas is still inadequate using the standard clinico-pathological prognostic markers. We assessed the correlation between <it>nm23-H1</it>, <it>Rb, EGFR </it>and <it>p53 </it>in relation to the clinical outcome of patients with muscle invasive bilharzial bladder cancer (MI-BBC).</p> <p>Methods</p> <p><it>nm23-H1</it>, <it>Rb, EGFR and p53 </it>expression was assessed in 59 MI-BBC patients using immunohistochemistry and reverse transcription (RT-PCR) and was correlated to the standard clinico-pathological prognostic factors, patient's outcome and the overall survival (OS) rate.</p> <p>Results</p> <p>Overexpression of <it>EGFR </it>and <it>p53 </it>proteins was detected in 66.1% and 35.6%; respectively. Loss of <it>nm23-H1</it>and <it>Rb </it>proteins was detected in 42.4% and 57.6%; respectively. Increased <it>EGFR and </it>loss of <it>nm23-H1 </it>RNA were detected in 61.5% and 36.5%; respectively. There was a statistically significant correlation between <it>p53 </it>and <it>EGFR </it>overexpression (<it>p </it>< 0.0001), <it>nm23 </it>loss (protein and RNA), lymph node status (<it>p </it>< 0.0001); between the incidence of local recurrence and <it>EGFR </it>RNA overexpression (p= 0.003) as well as between the incidence of metastasis and altered <it>Rb </it>expression (<it>p </it>= 0.026), <it>p53 </it>overexpression (<it>p </it>< 0.0001) and mutation (<it>p </it>= 0.04). Advanced disease stage correlated significantly with increased <it>EGFR </it>(protein and RNA) (<it>p </it>= 0.003 & 0.01), reduced <it>nm23-H1 </it>RNA (<it>p </it>= 0.02), altered <it>Rb </it>(<it>p </it>= 0.023), and <it>p53 </it>overexpression (<it>p </it>= 0.004). OS rates correlated significantly, in univariate analysis, with <it>p53 </it>overexpression (<it>p </it>= 0.011), increased <it>EGFR </it>(protein and RNA, <it>p </it>= 0.034&0.031), <it>nm23-H1 RNA </it>loss (<it>p </it>= 0.021) and aberrations of ≥ 2 genes. However, multivariate analysis showed that only high <it>EGFR </it>overexpression, metastatic recurrence, high tumor grade and the combination of ≥ 2 affected markers were independent prognostic factors.</p> <p>Conclusion</p> <p><it>nm23-H1, EGFR </it>and <it>p53 </it>could be used as prognostic biomarkers in MI-BBC patients. In addition to the standard pathological prognostic factors, a combination of these markers (≥ 2) has synergistic effects in stratifying patients into variable risk groups. The higher is the number of altered biomarkers, the higher will be the risk of disease progression and death.</p

    Nucleon-Nucleon Interaction: A Typical/Concise Review

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    Nearly a recent century of work is divided to Nucleon-Nucleon (NN) interaction issue. We review some overall perspectives of NN interaction with a brief discussion about deuteron, general structure and symmetries of NN Lagrangian as well as equations of motion and solutions. Meanwhile, the main NN interaction models, as frameworks to build NN potentials, are reviewed concisely. We try to include and study almost all well-known potentials in a similar way, discuss more on various commonly used plain forms for two-nucleon interaction with an emphasis on the phenomenological and meson-exchange potentials as well as the constituent-quark potentials and new ones based on chiral effective field theory and working in coordinate-space mostly. The potentials are constructed in a way that fit NN scattering data, phase shifts, and are also compared in this way usually. An extra goal of this study is to start comparing various potentials forms in a unified manner. So, we also comment on the advantages and disadvantages of the models and potentials partly with reference to some relevant works and probable future studies.Comment: 85 pages, 5 figures, than the previous v3 edition, minor changes, and typos fixe

    Ras mutation cooperates with β-catenin activation to drive bladder tumourigenesis

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    Mutations in the Ras family of proteins (predominantly in H-Ras) occur in approximately 40% of urothelial cell carcinoma (UCC). However, relatively little is known about subsequent mutations/pathway alterations that allow tumour progression. Indeed, expressing mutant H-Ras within the mouse bladder does not lead to tumour formation, unless this is expressed at high levels. The Wnt signalling pathway is deregulated in approximately 25% of UCC, so we examined if this correlated with the activation of MAPK signalling in human UCC and found a significant correlation. To test the functional significance of this association we examined the impact of combining Ras mutation (H-RasQ61L or K-RasG12D) with an activating β-catenin mutation within the mouse bladder using Cre-LoxP technology. Although alone, neither Ras mutation nor β-catenin activation led to UCC (within 12 months), mice carrying both mutations rapidly developed UCC. Mechanistically this was associated with reduced levels of p21 with dependence on the MAPK signalling pathway. Moreover, tumours from these mice were sensitive to MEK inhibition. Importantly, in human UCC there was a negative correlation between levels of p-ERK and p21 suggesting that p21 accumulation may block tumour progression following Ras mutation. Taken together these data definitively show Ras pathway activation strongly cooperates with Wnt signalling to drive UCC in vivo
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