ABSTRACT
Contact stiffness is an important parameter for describing the contact behavior of rough surfaces. In this study, to more accurately describe the contact stiffness between grinding surfaces of steel materials, a novel microcontact stiffness model is proposed. In this model, the novel cosine curve-shaped asperity and the conventional Gauss distribution are used to develop a simulated rough surface. Based on this simulated rough surface, the analytical expression of the microcontact stiffness model is obtained using contact mechanics theory and statistical theory. Finally, an experimental study of the contact stiffness of rough surfaces was conducted on different steel materials of various levels of roughness. The comparison results reveal that the prediction results of the present model show the same trend as that of the experimental results; the contact stiffness increases with increasing contact pressure. Under the same contact pressure, the present model is closer to the experimental results than the already existing elastic-plastic contact (CEB) and finite-element microcontact stiffness (KE) models, whose hypothesis of a single asperity is hemispherical. In addition, under the same contact pressure, the contact stiffness of the same steel material decreases with increasing roughness, whereas the contact stiffness values of different steel materials under the same roughness show only small differences. The correctness and accuracy of the present model can be demonstrated by analyzing the measured asperity geometry of steel materials and experimental results.
ABSTRACT
Propofol is an intravenous anesthetic that produces its anesthetic effect, largely via the GABAA receptor in the CNS, and also reduces the N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced neutrophil respiratory burst. Because fMLP-stimulated neutrophils produce leukotriene (LT)B4, we examined the effect of propofol on LTB4 production in vivo and in vitro Cecal ligation and puncture surgery was performed in mice, with or without exposure to propofol. Propofol attenuated the production of 5-lipoxygenase (5-LOX)-related arachidonic acid (AA) derivatives in the peritoneal fluid. Also, in the in vitro experiments on fMLP-stimulated neutrophils and 5-LOX-transfected human embryonic kidney cells, propofol attenuated the production of 5-LOX-related AA derivatives. Based on these results, we hypothesized that propofol would directly affect 5-LOX function. Using meta-azi-propofol (AziPm), we photolabeled stable 5-LOX protein, which had been used to solve the X-ray crystallographic structure of 5-LOX, and examined the binding site(s) of propofol on 5-LOX. Two propofol binding pockets were identified near the active site of 5-LOX. Alanine scanning mutagenesis was performed for the residues of 5-LOX in the vicinity of propofol, and we evaluated the functional role of these pockets in LTB4 production. We demonstrated that these pockets were functionally important for 5-LOX activity. These two pockets can be used to explore a novel 5-LOX inhibitor in the future.-Okuno, T., Koutsogiannaki, S., Ohba, M., Chamberlain, M., Bu, W., Lin, F.-Y., Eckenhoff, R. G., Yokomizo T., Yuki, K. Intravenous anesthetic propofol binds to 5-lipoxygenase and attenuates leukotriene B4 production.
