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RISS 인기검색어
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- 저자 : J. Bohlen (검색결과 2 건)
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Modelling the Thermo-Mechanical Behavior of Magnesium Alloys during Indirect Extrusion
D. Steglich,S. Erturk,J. Bohlen,D. Letzig,W. Brocks 한국소성가공학회 2010 기타자료 Vol.2010 No.6
One of the basic metal forming process for semi-finished products is extrusion. Since extrusion involves complex thermo-mechanical and multiaxial loading conditions resulting in large strains, high strain rates and an increase in temperature due to deformation, a proper yield criterion and hardening law should be used in the numerical modelling of the process. A phenomenological model based on a plastic potential has been proposed that takes strain, strain rate and temperature dependency on flow behaviour into consideration. A hybrid methodology of experiment and finite element simulation has been adopted in order to obtain necessary model parameters. The anisotropy/asymmetry in yielding was quantified by tensile and compression tests of specimens prepared from different directions. The identification of the corresponding model parameters was performed by a genetic algorithm. A fully coupled thermo-mechanical analysis has been used in extrusion simulations for calculation of the temperature field by considering heat fluxes and heat generated due to plastic deformation. The results of the approach adopted in this study appeared to be successful showing promising predictions of the experiments and thus may be extended to be applicable to other magnesium alloys or even other hcp metals.
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Neurotoxic reactive astrocytes are induced by activated microglia
Liddelow, Shane A.,Guttenplan, Kevin A.,Clarke, Laura E.,Bennett, Frederick C.,Bohlen, Christopher J.,Schirmer, Lucas,Bennett, Mariko L.,Mü,nch, Alexandra E.,Chung, Won-Suk,Peterson, Todd C.,Wilto Nature Publishing Group, a division of Macmillan P 2017 Nature Vol.541 No.7638
<P>Reactive astrocytes are strongly induced by central nervous system (CNS) injury and disease, but their role is poorly understood. Here we show that a subtype of reactive astrocytes, which we termed A1, is induced by classically activated neuroinflammatory microglia. We show that activated microglia induce A1 astrocytes by secreting Il-1 alpha, TNF and C1q, and that these cytokines together are necessary and sufficient to induce A1 astrocytes. A1 astrocytes lose the ability to promote neuronal survival, outgrowth, synaptogenesis and phagocytosis, and induce the death of neurons and oligodendrocytes. Death of axotomized CNS neurons in vivo is prevented when the formation of A1 astrocytes is blocked. Finally, we show that A1 astrocytes are abundant in various human neurodegenerative diseases including Alzheimer's, Huntington's and Parkinson's disease, amyotrophic lateral sclerosis and multiple sclerosis. Taken together these findings help to explain why CNS neurons die after axotomy, strongly suggest that A1 astrocytes contribute to the death of neurons and oligodendrocytes in neurodegenerative disorders, and provide opportunities for the development of new treatments for these diseases.</P>
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