Les phénomènes de bose et les lois de l'électrisation de contact /

Thesis (doctoral)--Université de Zurich, 1908.

Principles of high-polymer theory and practice; fibers, plastics, rubbers, coatings, adhesives,

Includes bibliographies.

Federal Technology Transfer directory of programs, resources, contact points /

Cover title: Directory of Federal Technology Transfer.

Le granite des Pyrénées et ses phénomènes de contact ...

At head of title: Ministère des travaux publics.

The distribution of contact pressures in the rolling of metals

"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."

The Promise and the Price of Contact: Puyallup Indian Acculturation, Federal Indian Policy and the City of Tacoma, 1832-1909

Thesis (Ph.D.)--University of Washington, 2016-06

Minimal mutation of the cytoplasmic tail inhibits the ability of E-cadherin to activate Rac but not phosphatidylinositol 3-kinase - Direct evidence of a role for cadherin-activated Rac signaling in adhesion and contact formation

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.

Mobilized by Injustice: Criminal Justice Contact, Political Participation and Race

Thesis (Ph.D.)--University of Washington, 2016-06