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Non-rolling mesh for a rolling finite-element tire model
Omid Kazemi,Adrijan P. Ribaric,Parviz E. Nikravesh,Seongho Kim 대한기계학회 2015 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.29 No.7
This paper presents a methodology for constructing a finite element based tire model suitable for ride and handling simulations of vehicles. The model is based on available high-resolution finite element models developed by tire manufacturers. Such high-resolutionmodels contain detailed structural and material characteristics of a tire that exhibit degrees-of-freedom in the order of 105 or greater. Consequently,for multibody dynamic analysis, the main objectives of the presented methodology become to reduce the number of degreesof-freedom and to preserve as much of the essential characteristics of the original model as possible. The presented tire model is formulatedwith a non-rotating reference frame that uses the rotational invariant characteristic of the tire.
Kurokawa, Manabu,Kim, Jiyeon,Geradts, Joseph,Matsuura, Kenkyo,Liu, Liu,Ran, Xu,Xia, Wenle,Ribar, Thomas J.,Henao, Ricardo,Dewhirst, Mark W.,Kim, Wun-Jae,Lucas, Joseph E.,Wang, Shaomeng,Spector, Neil L AAAS 2013 Science signaling Vol.6 No.274
<P><B>Breaking Down to Build Resistance</B></P><P>Chemotherapeutic resistance often arises because of the rewiring of signaling pathways in cancer cells. Kurokawa <I>et al.</I> found that the ubiquitin E3 ligase MDM2 triggered the breakdown of another ubiquitin E3 ligase, HUWE1. In breast cancer cells that died when exposed to the HER2 (human epidermal growth factor receptor 2) EGFR (epidermal growth factor receptor) tyrosine kinase inhibitor lapatinib, MDM2 was degraded, which enabled HUWE1 to trigger the degradation of a prosurvival protein and promote assembly and activation of a protein complex required for the execution of cell death. However, MDM2 degradation did not occur in lapatinib-resistant breast cancer cells, and thus, the abundance of HUWE1 was decreased, promoting cell survival. In a mouse xenograft model, an inhibitor of MDM2 reduced the growth of tumors generated from lapatinib-resistant breast cancer cells. Thus, MDM2 could be targeted to circumvent resistance to lapatinib in breast cancers.</P>