Odor G.,Research Institute for Natural science |
Kelling J.,Helmholtz Center Dresden |
Kelling J.,TU Chemnitz |
Gemming S.,Helmholtz Center Dresden |
Gemming S.,TU Chemnitz
Physical Review E - Statistical, Nonlinear, and Soft Matter Physics | Year: 2014
Extended dynamical simulations have been performed on a (2+1)-dimensional driven dimer lattice-gas model to estimate aging properties. The autocorrelation and the autoresponse functions are determined and the corresponding scaling exponents are tabulated. Since this model can be mapped onto the (2+1)-dimensional Kardar-Parisi-Zhang surface growth model, our results contribute to the understanding of the universality class of that basic system. © 2014 American Physical Society.
Eum D.-Y.,Research Institute for Natural science |
Byun J.-Y.,Research Institute for Natural science |
Yoon C.-H.,Research Institute for Natural science |
Seo W.-D.,NICS |
And 7 more authors.
Anti-Cancer Drugs | Year: 2011
A combined treatment with conventional chemotherapies can enhance the effectiveness of chemotherapeutic agents against cancers. Here, we have shown that the naturally occurring triterpenoids synergistically enhance the response of cervical cancer cells to taxol. Of the triterpenoid compounds, pristimerin enhanced the anticancer effect of taxol with the highest efficiency by combination. Pristimerin synergizes with taxol to inhibit clonogenic survival and tumor growth in nude mice, and to enhance cell death in cervical cancer cells. A combined treatment with taxol and pristimerin induced cervical cancer cell death by increasing intracellular reactive oxygen species levels, upregulation of death receptor death receptor 5 (DR5), activation of Bax, and dissipation of mitochondrial membrane potential. Treatment with N-acetyl-L-cysteine, a thiol-containing antioxidant completely blocked combined treatment-induced Bax translocation as well as DR5 upregulation. Moreover, inhibition of Jun N-terminal kinase/c-Jun pathway attenuated cell death by blocking DR5 upregulation and Bax activation. These results indicate that the triterpenoid, pristimerin, synergistically enhances taxol response of cervical cancer cells through DR5 expression and Bax activation. Furthermore, the reactive oxygen species-dependent activation of the Jun N-terminal kinase/c-Jun pathway is required for the DR5 upregulation and Bax activation. The molecular mechanism revealed by this study may aid in the design of future combination cancer therapies against cells with intrinsically reduced sensitivity to taxol. © 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Kang M.-J.,Yale University |
Kang M.-J.,Brown University |
Yoon C.M.,Yale University |
Yoon C.M.,Brown University |
And 9 more authors.
American Journal of Respiratory Cell and Molecular Biology | Year: 2015
Chitinase 3-like 1 (Chi3l1), which is also called YKL-40 in humans and BRP-39 inmice, is the prototypic chitinase-like protein. Recent studies have highlighted its impressive ability to regulate the nature of tissue inflammation and the magnitude of tissue injury and fibroproliferative repair. This can be appreciated in studies that highlight its induction after cigarette smoke exposure, during which it inhibits alveolar destruction and the genesis of pulmonary emphysema. IL-18 is also known to be induced and activated by cigarette smoke, and, in murine models, the IL-18 pathway has been shown to be necessary and sufficient to generate chronic obstructive pulmonary disease-like inflammation, fibrosis, and tissue destruction. However, the relationship between Chi3l1 and IL-18 has not been defined. To address this issue we characterized the expression of Chi3l1/BRP-39 in control and lung-targeted IL-18 transgenic mice. We also characterized the effects of transgenic IL-18 in mice with wild-type and null Chi3l1 loci. The former studies demonstrated that IL-18 is a potent stimulator of Chi3l1/BRP-39 and that this stimulation is mediated via IFN-g-, IL-13-, and IL-17A-dependent mechanisms. The latter studies demonstrated that, in the absence of Chi3l1/BRP-39, IL-18 induced type 2 and type 17 inflammation and fibrotic airway remodeling were significantly ameliorated, whereas type 1 inflammation, emphysematous alveolar destruction, and the expression of cytotoxic T lymphocyte perforin, granzyme, and retinoic acid early transcript 1 expression were enhanced. These studies demonstrate that IL-18 is a potent stimulator of Chi3l1 and that Chi3l1 is an important mediator of IL-18-induced inflammatory, fibrotic, alveolar remodeling, and cytotoxic responses. © Copyright 2015 by the American Thoracic Society.
Yoo H.J.,Research Institute for Natural science |
Yoon T.H.,Research Institute for Natural science
Journal of Nanoscience and Nanotechnology | Year: 2014
In this study, a simple flow cytometry protocol to evaluate nanoparticle associated biological response was proposed. Particularly, we have evaluated the effect of surface charge on the cellular nanoparticle associations and nanoparticle-induced apoptosis. Significant enhancement in side scattering intensity was observed for the HeLa cells treated with positively charged PLLZnO nanoparticles, suggesting that the PLLZnO nanoparticles may induce cell death via adsorption and endocytosis of the nanoparticles. On the other hand, the negatively charged PAAZnO nanoparticle seems to cause cell death process indirectly via the released Zn ions, with less contribution from cellular association of nanoparticles. Time- and dose-dependent studies on cellular association of ZnO nanoparticles, and ZnO associated reactive oxygen species generation were also performed for the HeLa cells exposed to the PLLZnO nanoparticle. For those cells associated with PLLZnO nanoparticle, a significant enhancement in reactive oxygen species generation was observed even at a lower concentration (10 ppm), which was not observable for the results with the whole cell population. By using this approach, we are able to distinguish biological responses (e.g., reactive oxygen species (ROS) generation) directly related to the cellular associations of NPs from those indirectly related to the cellular associations of NPs, such as the cytotoxicity caused by the NP released metal ions. Copyright © 2014 American Scientific Publishers All rights reserved.
Yoon Y.,Hanyang University |
Cho S.,Hanyang University |
Kim S.,Hanyang University |
Choi E.,Hanyang University |
And 4 more authors.
2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, EMBC 2014 | Year: 2014
We report on a microfluidic trap array that separates and captures circulating tumor cells (CTCs) from whole blood. The device is a series array of microfluidic branches that utilizes the difference in flow rates between the bypass channel and the trap channel to allow CTCs in whole blood to be separated and trapped. Once a trap has captured a cell with diameter larger than the narrow trap outlet, additional cells arriving at the branch would flow towards the bypass channel due to its lower flow resistance. Results demonstrated that it was possible to capture CTCs from the whole blood of a mouse with full-blown metastasis. With further developments, the bypass integrated microfluidic trap array could become a useful tool for the early prognosis of cancer metastasis. © 2014 IEEE.