3,708 research outputs found

    Numerical investigation of cloud cavitation and cavitation noise on a hydrofoil section

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    Partial cavitating flow and cloud cavitation on a hydrofoil section are numerically investigated. A fully compressible, density based homogeneous equilibrium model is employed along with a RANS turbulence model and high-order numerical methods based on a sixthorder central compact scheme and localized artificial diffusivity scheme are used to resolve the cavitating flow and pressure waves generated by cloud cavitation. Predicted results compare well with the experimental measurements for steady/unsteady partial cavitating flows on a NACA66 hydrofoil at cavitation number, ?=1.0-1.4 and angle of attack 6 and 8 degree. Detailed experimental data from the work of Leroux et al. were provided by Prof. J.-A. Astolfi at Institut de Recherche de l Ecole Navale, France. Numerical visualizations of cloud cavity evolution and surface pressure signals show relatively good agreement with the experimental data. The re-entrant jet flow and pressure wave generated by collapse of cloud cavity are closely investigated. The mechanism associated with two different unsteady dynamics of cloud cavitation observed in previous numerical/experimental study for angle of attack 6 and 8 degree are further explored using the present computational results. The pressure pulse generated by the collapse of bubble cloud and the flow-blockage effect caused by a large cavity cloud are found to be responsible for the shifting of cloud cavitation dynamics.http://deepblue.lib.umich.edu/bitstream/2027.42/84259/1/CAV2009-final62.pd

    Stress and EEG

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    Development of software for computing forming information using a component based approach

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    ABSTRACTIn shipbuilding industry, the manufacturing technology has advanced at an unprecedented pace for the last decade. As a result, many automatic systems for cutting, welding, etc. have been developed and employed in the manufacturing process and accordingly the productivity has been increased drastically. Despite such improvement in the manufacturing technology, however, development of an automatic system for fabricating a curved hull plate remains at the beginning stage since hardware and software for the automation of the curved hull fabrication process should be developed differently depending on the dimensions of plates, forming methods and manufacturing processes of each shipyard. To deal with this problem, it is necessary to create a ā€œplug-inā€ framework, which can adopt various kinds of hardware and software to construct a full automatic fabrication system. In this paper, a framework for automatic fabrication of curved hull plates is proposed, which consists of four components and related software. In particular the software module for computing fabrication information is developed by using the ooCBD development methodology, which can interface with other hardware and software with minimum effort. Examples of the proposed framework applied to medium and large shipyards are presented

    Fully Secure Anonymous Hierarchical Identity-Based Encryption with Constant Size Ciphertexts

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    Efficient and privacy-preserving constructions for search functionality on encrypted data is important issues for data outsourcing, and data retrieval, etc. Fully secure anonymous Hierarchical ID-Based Encryption (HIBE) schemes is useful primitives that can be applicable to searchable encryptions [4], such as ID-based searchable encryption, temporary searchable encryption [1], and anonymous forward secure HIBE [9]. We propose a fully secure anonymous HIBE scheme with constant size ciphertexts

    Grape seed proanthocyanidin extract inhibits glutamate-induced cell death through inhibition of calcium signals and nitric oxide formation in cultured rat hippocampal neurons

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    <p>Abstract</p> <p>Background</p> <p>Proanthocyanidin is a polyphenolic bioflavonoid with known antioxidant activity. Some flavonoids have a modulatory effect on [Ca<sup>2+</sup>]<sub>i</sub>. Although proanthocyanidin extract from blueberries reportedly affects Ca<sup>2+ </sup>buffering capacity, there are no reports on the effects of proanthocyanidin on glutamate-induced [Ca<sup>2+</sup>]<sub>i </sub>or cell death. In the present study, the effects of grape seed proanthocyanidin extract (GSPE) on glutamate-induced excitotoxicity was investigated through calcium signals and nitric oxide (NO) in cultured rat hippocampal neurons.</p> <p>Results</p> <p>Pretreatment with GSPE (0.3-10 Ī¼g/ml) for 5 min inhibited the [Ca<sup>2+</sup>]<sub>i </sub>increase normally induced by treatment with glutamate (100 Ī¼M) for 1 min, in a concentration-dependent manner. Pretreatment with GSPE (6 Ī¼g/ml) for 5 min significantly decreased the [Ca<sup>2+</sup>]<sub>i </sub>increase normally induced by two ionotropic glutamate receptor agonists, N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). GSPE further decreased AMPA-induced response in the presence of 1 Ī¼M nimodipine. However, GSPE did not affect the 50 mM K<sup>+</sup>-induced increase in [Ca<sup>2+</sup>]<sub>i</sub>. GSPE significantly decreased the metabotropic glutamate receptor agonist (<it>RS</it>)-3,5-Dihydroxyphenylglycine-induced increase in [Ca<sup>2+</sup>]<sub>i</sub>, but it did not affect caffeine-induced response. GSPE (0.3-6 Ī¼g/ml) significantly inhibited synaptically induced [Ca<sup>2+</sup>]<sub>i </sub>spikes by 0.1 mM [Mg<sup>2+</sup>]<sub>o</sub>. In addition, pretreatment with GSPE (6 Ī¼g/ml) for 5 min inhibited 0.1 mM [Mg<sup>2+</sup>]<sub>o</sub>- and glutamate-induced formation of NO. Treatment with GSPE (6 Ī¼g/ml) significantly inhibited 0.1 mM [Mg<sup>2+</sup>]<sub>o</sub>- and oxygen glucose deprivation-induced neuronal cell death.</p> <p>Conclusions</p> <p>All these data suggest that GSPE inhibits 0.1 mM [Mg<sup>2+</sup>]<sub>o</sub>- and oxygen glucose deprivation-induced neurotoxicity through inhibition of calcium signals and NO formation in cultured rat hippocampal neurons.</p

    Proteomic and biochemical analyses reveal the activation of unfolded protein response, ERK-1/2 and ribosomal protein S6 signaling in experimental autoimmune myocarditis rat model

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    <p>Abstract</p> <p>Background</p> <p>To investigate the molecular and cellular pathogenesis underlying myocarditis, we used an experimental autoimmune myocarditis (EAM)-induced heart failure rat model that represents T cell mediated postinflammatory heart disorders.</p> <p>Results</p> <p>By performing unbiased 2-dimensional electrophoresis of protein extracts from control rat heart tissues and EAM rat heart tissues, followed by nano-HPLC-ESI-QIT-MS, 67 proteins were identified from 71 spots that exhibited significantly altered expression levels. The majority of up-regulated proteins were confidently associated with unfolded protein responses (UPR), while the majority of down-regulated proteins were involved with the generation of precursor metabolites and energy metabolism in mitochondria. Although there was no difference in AKT signaling between EAM rat heart tissues and control rat heart tissues, the amounts and activities of extracellular signal-regulated kinase (ERK)-1/2 and ribosomal protein S6 (rpS6) were significantly increased. By comparing our data with the previously reported myocardial proteome of the Coxsackie viruses of group B (CVB)-mediated myocarditis model, we found that UPR-related proteins were commonly up-regulated in two murine myocarditis models. Even though only two out of 29 down-regulated proteins in EAM rat heart tissues were also dysregulated in CVB-infected rat heart tissues, other proteins known to be involved with the generation of precursor metabolites and energy metabolism in mitochondria were also dysregulated in CVB-mediated myocarditis rat heart tissues, suggesting that impairment of mitochondrial functions may be a common underlying mechanism of the two murine myocarditis models.</p> <p>Conclusions</p> <p>UPR, ERK-1/2 and S6RP signaling were activated in both EAM- and CVB-induced myocarditis murine models. Thus, the conserved components of signaling pathways in two murine models of acute myocarditis could be targets for developing new therapeutic drugs or methods aimed at treating enigmatic myocarditis.</p
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