http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
FEASIBILITY STUDY OF AN INNOVATIVE URBAN ELECTRIC-HYBRID MICROCAR
Alessandro Ferraris,Federico Micca,Alessandro Messana,Andrea Giancarlo Airale,Massimiliana Carello 한국자동차공학회 2019 International journal of automotive technology Vol.20 No.2
This paper presents the feasibility study of a new platform for electric-hybrid quadricycles, developed by addressing important concepts like passive safety and comfort, which often represent a shortcoming in this vehicle category. Starting from packaging of energy storage system and macroscopic subsystems as the main technological constraint, the study has been entirely developed in a virtual environment, with finite element verifications on preliminary models, and a subsequent cooperation phase between computer aided design and finite element analysis softwares, with a guideline for the main tests being that each could feasibly be carried out on a complete vehicle model in order to validate the original assumptions. The resulting design, with a body curb mass of less than 100 kg, was capable of integrating optimal static stiffness characteristics and crash performance, together with improved vehicle dynamics thanks to an innovative suspension archetype.
Scatena, Roberto,Messana, Irene,Martorana, Giuseppe Ettore,Gozzo, Maria Luisa,Lippa, Silvio,Maccaglia, Alessandro,Bottoni, Patrizia,Vincenzoni, Federica,Nocca, Giuseppina,Castagnola, Massimo,Giardina, Korean Society for Biochemistry and Molecular Biol 2004 Journal of biochemistry and molecular biology Vol.37 No.4
Experimental hyperoxia represents a suitable in vitro model to study some pathogenic mechanisms related to oxidative stress. Moreover, it allows the investigation of the molecular pathophysiology underlying oxygen therapy and toxicity. In this study, a modified experimental set up was adopted to accomplish a model of moderate hyperoxia (50% $O_2$, 96 h culture) to induce oxidative stress in the human leukemia cell line, U-937. Spectrophotometric measurements of mitochondrial respiratory enzyme activities, NMR spectroscopy of culture media, determination of antioxidant enzyme activities, and cell proliferation and differentiation assays were performed. The data showed that moderate hyperoxia in this myeloid cell line causes: i) intriguing alterations in the mitochondrial activities at the levels of succinate dehydrogenase and succinate-cytochrome c reductase; ii) induction of metabolic compensatory adaptations, with significant shift to glycolysis; iii) induction of different antioxidant enzyme activities; iv) significant cell growth inhibition and v) no significant apoptosis. This work will permit better characterization the mitochondrial damage induced by hyperoxia. In particular, the data showed a large increase in the succinate cytochrome c reductase activity, which could be a fundamental pathogenic mechanism at the basis of oxygen toxicity.
( Roberto Scatena ),( Irene Messana ),( Giuseppe Ettore Martorana ),( Maria Luisa Gozzo ),( Silvio Lippa ),( Alessandro Maccaglia ),( Patrizia Bottoni ),( Federica Vincenzoni ),( Giuseppina Nocca ),( 생화학분자생물학회 2004 BMB Reports Vol.37 No.4
Experimental hyperoxia represents a suitable in vitro model to study some pathogenic mechanisms related to oxidative stress. Moreover, it allows the investigation of the molecular pathophysiology underlying oxygen therapy and toxicity. In this study, a modified experimental set up was adopted to accomplish a model of moderate hyperoxia (50% 0₂, 96 h culture) to induce oxidative stress in the human leukemia cell line, U-937. Spectrophotometric measurements of mitochondria) respiratory enzyme activities, NMR spectroscopy of culture media, determination of antioxidant enzyme activities, and cell proliferation and differentiation assays were performed. The data showed that moderate hyperoxia in this myeloid cell line causes: i) intriguing alterations in the mitochondria) activities at the levels of succinate dehydrogenase and succinate-cytochrome c reductase; ⅱ) induction of metabolic compensatory adaptations, with significant shift to glycolysis; ⅲ) induction of different antioxidant enzyme activities; ⅳ) significant cell growth inhibition and ⅴ) no significant apoptosis. This work will permit better characterization the mitochondrial damage induced by hyperoxia. In particular, the data showed a large increase in the succinate cytochrome c reductase activity, which could be a fundamental pathogenic mechanism at the basis of oxygen toxicity.