Moving-boundary problems solved by adaptive radial basis functions

The objective of this paper is to present an alternative approach to the conventional level set methods for solving two-dimensional moving-boundary problems known as the passive transport. Moving boundaries are associated with time-dependent problems and the position of the boundaries need to be determined as a function of time and space. The level set method has become an attractive design tool for tracking, modeling and simulating the motion of free boundaries in fluid mechanics, combustion, computer animation and image processing. Recent research on the numerical method has focused on the idea of using a meshless methodology for the numerical solution of partial differential equations. In the present approach, the moving interface is captured by the level set method at all time with the zero contour of a smooth function known as the level set function. A new approach is used to solve a convective transport equation for advancing the level set function in time. This new approach is based on the asymmetric meshless collocation method and the adaptive greedy algorithm for trial subspaces selection. Numerical simulations are performed to verify the accuracy and stability of the new numerical scheme which is then applied to simulate a bubble that is moving, stretching and circulating in an ambient flow to demonstrate the performance of the new meshless approach. (C) 2010 Elsevier Ltd. All rights reserved

Macroscopical Entangled Coherent State Generator in V configuration atom system

In this paper, we propose a scheme to produce pure and macroscopical entangled coherent state. When a three-level ''V'' configuration atom interacts with a doubly reasonant cavity, under the strong classical driven condition, entangled coherent state can be generated from vacuum fields. An analytical solution for this system under the presence of cavity losses is also given

The role of c-Myc in phagocytosis of mycobacteria in human macrophages

Poster Presentation (Doctor’s Session)This journal issue contain proceedings of the CongressMycobacterium tuberculosis is an intracellular pathogen and the causative agent of the disease tuberculosis. Macrophages are the major immunocytes to initiate host immunity against mycobacteria. Among the multiple strategies employ by macrophages to defence against mycobacteria, phagocytosis is the first step. Throughphagocytosis, macrophages could not only clear the pathogens from infection sites, but also present antigens derived from the engulfed bacteria to lymphoid cells. c-Myc is a transcription factor that regulates a variety of target genes. It can form a complex with Max and bind to the enhancer box sequences of the promoter to mediate the transcription. Recently, our group revealed that c-Myc has a potential role in regulating the antimicrobial responses in macrophages. Here, we further revealed that c-Myc may play a positive role in phagocytosis and contribute to host defense to mycobacteria. Pretreatment of c-Myc inhibitor, 10058-F4, could significantly reduce the amount of mycobacteria internalised by macrophages. The acidification of phagolysosome in mycobacteria infected macrophages was also inhibited by 10058-F4. Further investigation showed that macrophages phagocytose mycobacteria in a PI3K/Akt independent pathway. And the action of c-Myc inhibitor does not affect the expression levels of Rho family GTPases. However, we found that 10058-F4 could significantly inhibit phorsphorylation of ERK1/2 kinase, which has been indicated to play a role in FcR mediated phagocytosis in macrophage. In conclusion, c-Myc may play a role in phagocytosis of mycobacteria through regulating phorsphorylation of ERK1/2.published_or_final_versio

The role of oncogene in mycobacteria-induced antophagy in human macrophages

Poster PresentationMacrophages are the major immunocytes to initiate both innate and adaptive immune responses against Mycobacterium tuberculosis (Mtb), a causative agent of tuberculosis. Upon mycoabcteria infection, macrophages could eliminate the intracellular bacteria through different cell death pathways, including apoptosis and autophagy. c-Myc is a transcription factor that regulates a variety of target genes and control different cellular functions such as proliferation and immune resposnse. Recently, our group revealed that c-Myc has a potential role in regulating the antimicrobial responses in macrophages. Here we use BCG, a live attenuated strain of Mycobacterium bovis, which is similar to Mtb in antigenic composition, as a model to study the role of c-Myc in regulating mycobacteria-induced autophagy. We first investigated the role of c-Myc in BCG-induced LC3BII levels. Knocking down c-Myc by siRNA could decrease BCG-induced LC3BII levels. We found that BCG-induced autophagy is dependent on JNK and p38 and independent on PI3K or ERK pathways. And knocking down of c-Myc could significantly inhibit phosphorylation of p38. In conclusion, c-Myc may play a positive role in mycobacteria-induced autophagy in human macrophages.published_or_final_versio