No abstract

Surface cleaning using cavitation bubble dynamics is investigated numerically through modeling of bubble dynamics, dirt particle motion, and fluid material interaction. Three fluid dynamics models; a potential flow model, a viscous model, and a compressible model, are used to describe the flow field generated by the bubble all showing the strong effects bubble explosive growth and collapse have on a dirt particle and on a layer of material to remove. Bubble deformation and reentrant jet formation are seen to be responsible for generating concentrated pressures, shear, and lift forces on the dirt particle and high impulsive loads on a layer of material to remove. Bubble explosive growth is also an important mechanism for removal of dirt particles, since strong suction forces in addition to shear are generated around the explosively growing bubble and can exert strong forces lifting the particles from the surface to clean and sucking them toward the bubble. To model material failure and removal, a finite element structure code is used and enables simulation of full fluid-structure interaction and investigation of the effects of various parameters. High impulsive pressures are generated during bubble collapse due to the impact of the bubble reentrant jet on the material surface and the subsequent collapse of the resulting toroidal bubble. Pits and material removal develop on the material surface when the impulsive pressure is large enough to result in high equivalent stresses exceeding the material yield stress or its ultimate strain. Cleaning depends on parameters such as the relative size between the bubble at its maximum volume and the particle size, the bubble standoff distance from the particle and from the material wall, and the excitation pressure field driving the bubble dynamics. These effects are discussed in this contribution.

Material pitting from cavitation bubble collapse is investigated numerically including two-way fluid–structure interaction (FSI). A hybrid numerical approach which links an incompressible boundary element method (BEM) solver and a compressible finite difference flow solver is applied to capture non-spherical bubble dynamics efficiently and accurately. The flow codes solve the fluid dynamics while intimately coupling the solution with a finite element structure code to enable simulation of the full FSI. During bubble collapse high impulsive pressures result from the impact of the bubble re-entrant jet on the material surface and from the collapse of the remaining bubble ring. A pit forms on the material surface when the impulsive pressure is large enough to result in high equivalent stresses exceeding the material yield stress. The results depend on bubble dynamics parameters such as the size of the bubble at its maximum volume, the bubble standoff distance from the material wall, and the pressure driving the bubble collapse. The effects of these parameters on the re-entrant jet, the following bubble ring collapse pressure, and the generated material pit characteristics are investigated.

We have previously demonstrated that costunolide, a biologically active compound that was isolated from the stem bark of Magnolia sieboldii, induced apoptosis in human cancer cells. In the present study, we investigated the underlying mechanisms and suggest that costunolide induces apoptosis in human promonocytic leukemia U937 cells by depleting the intracellular thiols. Costunolide treatment rapidly depleted the intracellular reduced glutathione (GSH) and protein thiols, and this preceded the occurrence of apoptosis. Pretreatment with sulfhydryl compounds such as GSH, N-acetyl-L-cysteine, dithiothreitol and 2-mercaptoethanol almost completely blocked the costunolide-induced apoptosis, highlighting the significance of the intracellular thiol level in the process. Furthermore, overexpression of Bcl-2 also significantly attenuated the effects of costunolide. The apoptosis-inducing activity of costunolide is likely to depend on the exomethylene moiety because derivatives in which this group was reduced, such as dihydrocostunolide and saussurea lactone, did not deplete the cellular thiols and showed no apoptotic activity. Taken together, the present study demonstrates that the costunolide-induced apoptosis depends on intracellular thiols contents, which are modulated by Bcl-2.

We investigated the in vitro effects of acteoside on the proliferation, cell cycle regulation and differentiation of HL-60 human promyelocytic leukemia cells. Acteoside inhibited the proliferation of HL-60 cells in a concentration- and time-dependent manner with an IC50, approximately 30 microM. DNA flow cytometric analysis indicated that acteoside blocked cell cycle progression at the G1 phase in HL-60 human promyelocytic leukemia cells. Among the G1 phase cell cycle-related proteins, the levels of cyclin-dependent protein kinase (CDK)2, CDK6, cyclin D1, cyclin D2, cyclin D3 and cyclin E were reduced by acteoside, whereas the steady-state level of CDK4 was unaffected. The protein and mRNA levels of CDK inhibitors (cyclin-dependent kinase inhibitors), such as p21(CIP1/WAF1) and p27(KIP1), were gradually increased after acteoside treatment in a time-dependent manner. In addition, acteoside markedly enhanced the binding of p21(CIP1/WAF1) and p27(KIP1) to CDK4 and CDK6, resulting in the reduction of CDK2, CDK4 and CDK6 activities. Moreover, the hypophosphorylated form of retinoblastoma increased, leading to the enhanced binding of protein retinoblastoma (pRb) and E2F1. Our results further suggest that acteoside is a potent inducer of differentiation of HL-60 cells based on biochemical activities and the expression level of CD14 cell surface antigen. In conclusion, the onset of acteoside-induced G1 arrest of HL-60 cells prior to the differentiation appears to be tightly linked to up-regulation of the p21(CIP1/WAF1) and p27(KIP1) levels and decreases in the CDK2, CDK4 and CDK6 activities. These findings, for the first time, reveal the mechanism underlying the anti-proliferative effect of acteoside on human promyelocytic HL-60 cells.