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Ahn, Hak Jun,Koketsu, Mamoru,Yang, Eun Mi,Kim, Yong Man,Ishihara, Hideharu,Yang, Hyun Ok Wiley Subscription Services, Inc., A Wiley Company 2006 Journal of cellular biochemistry Vol.99 No.3
<P>We examined the ability of the synthetic selenium compound, 2-(4-methylphenyl)-1,3-selenazol-4-one (hereafter designated 3a), to induce apoptosis in a human ovarian cancer cell line (SKOV3) and a human leukemia cell line (HL-60). Flow cytometry showed that 3a treatment induced apoptosis in both cell lines to degrees comparable to that of the positive control, paclitaxel. Apoptosis was measured by PS externalization, DNA fragmentation and decreased mitochondrial membrane potential (MMP). However, analysis of the mechanism of action revealed differences between the responses of the two cell lines. Treatment with 3a arrested the cell cycle and induced caspase-3 activation in HL-60 cells, but not in SKOV3 cells. In contrast, 3a treatment induced apoptosis through translocation of AIF, a novel pro-apoptotic protein, in SKOV3 cells, but not in HL-60 cells. Collectively, our data demonstrated that 3a induced apoptosis in both cell lines, but via different action mechanisms. J. Cell. Biochem. 99: 807–815, 2006. © 2006 Wiley-Liss, Inc.</P>
Ahn, Hak Jun,Hwang, Soon Young,Nguyen, Ngoc Hoan,Lee, Ik Jae,Lee, Eun Jeong,Seong, Jinsil,Lee, Jong-Soo Korean Society for Molecular and Cellular Biology 2019 Molecules and cells Vol.42 No.7
Tumor cells can vary epigenetically during ionizing irradiation (IR) treatment. These epigenetic variegations can influence IR response and shape tumor aggressiveness. However, epigenetic disturbance of histones after IR, implicating in IR responsiveness, has been elusive. Here, we investigate whether altered histone modification after IR can influence radiation responsiveness. The oncogenic CXCL12 mRNA and protein were more highly expressed in residual cancer cells from a hepatoma heterotopic murine tumor microenvironment and coculture of human hepatoma Huh7 and normal IMR90 cells after radiation. H3K4 methylation was also enriched and H3K9 methylation was decreased at its promoter region. Accordingly, invasiveness and the subpopulation of aggressive $CD133^+/CD24^-$ cells increased after IR. Histone demethylase inhibitor IOX1 attenuated CXCL12 expression and the malignant subpopulation, suggesting that responses to IR can be partially mediated via histone modifications. Taken together, radiation-induced histone alterations at the CXCL12 promoter in hepatoma cells are linked to CXCL12 upregulation and increased aggressiveness in the tumor microenvironment.
Ahn, Sung Hoon,Kim, Dong Jun,Chi, Won Seok,Kim, Jong Hak WILEY‐VCH Verlag 2013 ADVANCED MATERIALS Vol.25 No.35
<P>Jong Hak Kim and co‐workers report on page 4893 a unique, effective design structure for a photoanode, consisting of an SnO<SUB>2</SUB> nanotube‐TiO<SUB>2</SUB> nanosheet core‐shell (SNT@TNS), interdispersed in an organized mesoporous TiO<SUB>2</SUB> film. The high efficiency results from the effects of combining the well‐organized structure of the TiO<SUB>2</SUB> film and the excellent electron transport, as well as the good light scattering of SNT@TNS. </P>
안병운,최용수,박성준,윤종학 한국공작기계학회 2003 한국공작기계학회 추계학술대회논문집 Vol.2003 No.-
In micro hole punching process the burr occurs inevitably, but the burr must be minimized in order to improve the quality and accuracy of the product. In this study, magnetic field assisted polishing technique is applied to remove the burr which exists in nozzles for ink jet printer head and proved to be a feasible for deburring by experiment. The deburring characteristics of sheet metals was investigated changing with polishing time. After the deburring, the burr size has remarkably reduced and roundness of the hole also has improved.
Ahn, G-One,Seita, Jun,Hong, Beom-Ju,Kim, Young-Eun,Bok, Seoyeon,Lee, Chan-Ju,Kim, Kwang Soon,Lee, Jerry C.,Leeper, Nicholas J.,Cooke, John P.,Kim, Hak Jae,Kim, Il Han,Weissman, Irving L.,Brown, J. Mar National Academy of Sciences 2014 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.111 No.7
<P>Emerging evidence indicates that myeloid cells are essential for promoting new blood vessel formation by secreting various angiogenic factors. Given that hypoxia-inducible factor (HIF) is a critical regulator for angiogenesis, we questioned whether HIF in myeloid cells also plays a role in promoting angiogenesis. To address this question, we generated a unique strain of myeloid-specific knockout mice targeting HIF pathways using human S100A8 as a myeloid-specific promoter. We observed that mutant mice where HIF-1 is transcriptionally activated in myeloid cells (by deletion of the von Hippel–Lindau gene) resulted in erythema, enhanced neovascularization in matrigel plugs, and increased production of vascular endothelial growth factor (VEGF) in the bone marrow, all of which were completely abrogated by either genetic or pharmacological inactivation of HIF-1. We further found that monocytes were the major effector producing VEGF and S100A8 proteins driving neovascularization in matrigel. Moreover, by using a mouse model of hindlimb ischemia we observed significantly improved blood flow in mice intramuscularly injected with HIF-1–activated monocytes. This study therefore demonstrates that HIF-1 activation in myeloid cells promotes angiogenesis through VEGF and S100A8 and that this may become an attractive therapeutic strategy to treat diseases with vascular defects.</P>