732 resultados para Intergroup Contact
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Thesis (doctoral)--Université de Zurich, 1908.
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Cover title: Directory of Federal Technology Transfer.
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At head of title: Ministère des travaux publics.
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"This paper is an analysis of the data contained in a report of the ASME Research Committee on Plastic Flow of Metals entitled Rolling of metals."
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Thesis (Ph.D.)--University of Washington, 2016-06
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The author conducted 2 studies to explore the link between superiority bias in the interpersonal and intergroup domains. Australian university students evaluated the extent to which various personality traits were more or less applicable to themselves than to other Australian university students in general. They then evaluated the extent to which the same traits were more or less applicable to Australians than to people from other countries in general. As expected, the more participants evaluated themselves as superior to other university students, the more they evaluated Australians as a whole as superior to people from other countries. This link between interpersonal and intergroup superiority biases explained 22.1% of variance in Study 1 and 33.6% of variance in Study 2. The author interprets the results of the 2 studies as support for fundamental principles of social identity theory: (a) that self-concept consists of not only one's personal self but also the social groups to which one belongs and (b) that people are motivated to view both levels of self in a relatively positive fashion.
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Classic cadherins are adhesion-activated cell signaling receptors. In particular, homophilic cadherin ligation can directly activate Rho family GTPases and phosphatidylinositol 3-kinase (PI3-kinase), signaling molecules with the capacity to support the morphogenetic effects of these adhesion molecules during development and disease. However, the molecular basis for cadherin signaling has not been elucidated, nor is its precise contribution to cadherin function yet understood. One attractive hypothesis is that cadherin-activated signaling participates in stabilizing adhesive contacts ( Yap, A. S., and Kovacs, E. M. ( 2003) J. Cell Biol. 160, 11-16). We now report that minimal mutation of the cadherin cytoplasmic tail to uncouple binding of p120-ctn ablated the ability of E-cadherin to activate Rac. This was accompanied by profound defects in the capacity of cells to establish stable adhesive contacts, defects that were rescued by sustained Rac signaling. These data provide direct evidence for a role of cadherin-activated Rac signaling in contact formation and adhesive stabilization. In contrast, cadherin-activated PI3-kinase signaling was not affected by loss of p120-ctn binding. The molecular requirements for E-cadherin to activate Rac signaling thus appear distinct from those that stimulate PI3-kinase, and we postulate that p120-ctn may play a central role in the E-cadherin-Rac signaling pathway.