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Stick-slip is a complex phenomenon which has been studied by researchers from many points of view. A variety of engineering factors, such as surface roughness, may contribute to this behavior. However, recent studies from basic science have shown that molecularly smooth surfaces separated by a film also exhibit stick-slip. Thus, the process may be intrinsically film-induced due to transitions between solid-like and fluid-like behavior. The authors of such studies often state that this kind of response indicates the futility of trying to describe such behavior from a continuum perspective. A purpose of this paper is to refute that point of view. Other studies, both experimental and theoretical, have indicated that continuum rheological models may be valid for films of molecular (nanometer) scale. Various rheological models which can predict stick-slip are proposed in this paper. Calculated results are similar to those of experiment.

Rheological behavior in concentrated contacts has been studied extensively. In certain conditions such as a rough concentrated contact or sliding of nominally flat surfaces, films may be of molecular (nanometer) scale. The question arises as to whether the application of any viscous fluid model is appropriate. In this study, elastohydrodynamic lubrication analysis is performed on three candidate rheological models: (1) the classical case of viscosity variation with pressure, (2) an isoviscous model which idealizes porous layers on the solid surfaces representing the molecular microstructure, and (3) an isoviscous model which includes van der Waals and solvation surface forces. The latter two models predict behavior similar to classical behavior. The study is not sufficiently sensitive to determine which model best predicts experimental results, but some credence must be given to the latter two because experimental evidence suggests that Reynolds' equation is not valid for molecularly thin films.

Ginseng has been recommended to alleviate the menopausal symptoms, which indicates that components of ginseng very likely contain estrogenic activity. We have examined the possibility that a component of Panax ginseng, ginsenoside-Rb1, acts by binding to estrogen receptor. We have investigated the estrogenic activity of ginsenoside-Rb1, in a transient transfection system using estrogen-responsive luciferase plasmids in MCF-7 cells. Ginsenoside-Rbb1 activated the transcription of the estrogen-responsive luciferase reporter gene in MCF-7 breast cancer cells at a concentration of 50 μM. Activation was inhibited by the specific estrogen receptor antagonist ICI 182,780, indicating that the estrogenic effect of ginsenoside-Rbb1 is estrogen receptor dependent. Next, we evaluated the ability of ginsenoside-Rbb1, to induce the estrogen-responsive gene c-fos by semi-quantitative RT-PCR assays and Western analyses. Ginsenoside-Rbb1 increased c-fos both at mRNA and protein levels. However, ginsenoside-Rbb1 failed to activate the glucocorticoid receptor, the retinoic acid receptor, or the androgen receptor in CV-1 cells transiently transfected with the corresponding steroid hormone receptors and hormone responsive reporter plasmids. These data support our hypothesis that ginsenoside-Rbb1 acts a weak phytoestrogen, presumably by binding and activating the estrogen receptor. [ABSTRACT FROM AUTHOR]