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Jo, M.J.,Paek, A.R.,Choi, J.S.,Ok, C.Y.,Jeong, K.C.,Lim, J.H.,Kim, S.H.,You, H.J. North-Holland ; Elsevier Science Ltd 2015 european journal of pharmacology Vol.769 No.-
<P>The proto-oncogene c-Myc has been implicated in a variety of cellular processes, such as proliferation, differentiation and apoptosis. Several c-Myc targets have been studied; however, selective regulation of c-Myc is not easy in cancer cells. Herein, we attempt to identify chemical compounds that induce cell death in c-Myc-overexpressing cells (STF-cMyc and STF-Control) by conducting MTS assays on approximately 4000 chemical compounds. One compound, C604, induced cell death in STF-cMyc cells but not STF-Control cells. Apoptotic proteins, including caspase-3 and poly(ADP-ribose) polymerase (PAPP), were cleaved in C604-treated STF-cMyc cells. In addition, 5W620, HCT116 and NCI-H23 cells, which exhibit higher basal levels of c-Myc, underwent apoptotic cell death in response to C604, suggesting a role for C604 as an inducer of apoptosis in cancer cells with c-Myc amplification. C604 induced cell cycle arrest at the G2/M phase in cells, which was not affected by apoptotic inhibitors. Interestingly, C604 induced accumulation of c-Myc and Cdc25A proteins. In summary, a chemical compound was identified that may induce cell death in cancer cells with c-Myc amplification specifically through an apoptotic pathway. (C) 2015 Elsevier B.V. All rights reserved.</P>
THE NEW TYPE BROAD BEAM ION SOURCES AND APPLICATIONS
You, D.W.,Feng, Y.C.,Wang, Y.,Kuang, Y.Z. The Korean Vacuum Society 1995 Applied Science and Convergence Technology Vol.4 No.s2
The broad beam ion sources of hot filament plasma type have widely used for modifications of materials and thin films, and the new type intensive current broad beam metal ion source including reactive gaseous ion beams is needed for preparing the hard coating films such as DLC, $\beta-C_3N_4$ Carbides, Nitrides, Borides etc. Now a electorn beam evaporation(EBE) broad beam metal ion source has been developed for this purpose in our lab. CN film has been formed by the EBE ion source. Study of the CN film shows that it has high hardness(HK=5800kgf/$\textrm {mm}^2$)and good adhesion. This method can widely changes the ratio of C/N atom's concentrations from 0.14 to 0.6 and has high coating rate. The low energy pocket ion source which was specially designed for surface texturing of medical silicon rubber was also developed. It has high efficiency and large uniform working zone. Both nature texturing and mesh masked texturing of silicon rubbers were performed. The biocompatibility was tested by culture of monocytes, and the results showed improved biocompatibility for the treated silicon rubbers. In addition, the TiB2 film synthesized by IBED is being studied recently in our lab. In this paper, the results which include the hardness, thickness of the films and the AES, XRD analysis as well as the tests of the oxidation of high temperature and erosion will be presented.
Gut-Specific Delivery of T-Helper 17 Cells Reduces Obesity and Insulin Resistance in Mice
Hong, C.P.,Park, A.,Yang, B.G.,Yun, C.H.,Kwak, M.J.,Lee, G.W.,Kim, J.H.,Jang, M.S.,Lee, E.J.,Jeun, E.J.,You, G.,Kim, K.S.,Choi, Y.,Park, J.H.,Hwang, D.,Im, S.H.,Kim, J.F.,Kim, Y.K.,Seoh, J.Y.,Surh, C. Elsevier North Holland [etc.] 2017 Gastroenterology Vol.152 No.8
<P>BACKGROUND & AIMS: Obesity and metabolic syndrome have been associated with alterations to the intestinal microbiota. However, few studies examined the effects of obesity on the intestinal immune system. We investigated changes in subsets of intestinal CD4(+) T-helper (T-H) cells with obesity and the effects of gut-tropic T(H)17 cells in mice on a high-fat diet (HFD). METHODS: We isolated immune cells from small intestine and adipose tissue of C57BL/6 mice fed a normal chow diet or a HFD for 10 weeks and analyzed the cells by flow cytometry. Mice fed a vitamin A-deficient HFD were compared with mice fed a vitamin A-sufficient HFD. Obese RAG1-deficient mice were given injections of only regulatory T cells or a combination of regulatory T cells and T(H)17 cells (wild type or deficient in integrin beta 7 subunit or interleukin 17 [IL17]). Mice were examined for weight gain, fat mass, fatty liver, glucose tolerance, and insulin resistance. Fecal samples were collected before and after T cell transfer and analyzed for microbiota composition by metagenomic DNA sequencing and quantitative polymerase chain reaction. RESULTS: Mice placed on a HFD became obese, which affected the distribution of small intestinal CD4(+) T-H cells. Intestinal tissues from obese mice had significant reductions in the proportion of T(H)17 cells but increased proportion of T(H)1 cells, compared with intestinal tissues from nonobese mice. Depletion of vitamin A in obese mice further reduced the proportion of T(H)17 cells in small intestine; this reduction correlated with more weight gain and worsening of glucose intolerance and insulin resistance. Adoptive transfer of in vitro-differentiated gut-tropic T(H)17 cells to obese mice reduced these metabolic defects, which required the integrin beta 7 subunit and IL17. Delivery of T(H)17 cells to intestines of mice led to expansion of commensal microbes associated with leanness. CONCLUSIONS: In mice, intestinal T(H)17 cells contribute to development of a microbiota that maintains metabolic homeostasis, via IL17. Gut-homing T(H)17 cells might be used to reduce metabolic disorders in obese individuals.</P>
Park, M.K.,You, H.J.,Lee, H.J.,Kang, J.H.,Oh, S.H.,Kim, S.Y.,Lee, C.H. Pergamon Press 2013 European journal of cancer Vol.49 No.7
Epithelial-mesenchymal-transition (EMT) is a key event for tumour cells to initiate metastasis leading to switching of E-cadherin to N-cadherin. Transglutaminase-2 (Tgase-2) expression is increased in TGF-β1-induced EMT in A549 lung cancer cells or other lung cancer cells. The role and underlying mechanism of Tgase-2 in N-cadherin switching of TGF-β1-induced EMT are not known. The involvement and mechanisms of Tgase-2 were investigated in A549 cells using chemical inhibitors, gene silencing and over-expression. TGF-β1-induced EMT was suppressed by cystamine or gene silencing of Tgase-2. Suppression of Tgase-2 or the c-Jun-N-terminal kinase (JNK) inhibitor, SP600125, significantly reduced and over-expression of Tgase-2 increased the expression of N-cadherin. The relationship between Tgase-2 and JNK in the TGF-β1-induced EMT of A549 cells was examined using Tgase-2 over-expressed A549 cells (A549<SUB>TG2</SUB>) and Tgase-2 silenced A549 cells (A549<SUB>shTG2</SUB>). JNK activation was significantly increased in A549<SUB>TG2</SUB> cells and decreased in A549<SUB>shTG2</SUB> cells. In contrast, PP2A expression was decreased in A549<SUB>TG2</SUB> and A549 cells and increased in A549<SUB>shTG2</SUB> cells. The involvement of Tgase-2 in N-cadherin expression was also confirmed in an in vivo lung cancer orthotopic model by injection of A549<SUB>WT</SUB> and A549<SUB>shTG2</SUB> cells into SCID mice. Tgase-2 expressing A549<SUB>WT</SUB> cells-injected mice group showed increased expressions of N-cadherin and JNK activation, but decreased expression of PP2A in lung cancer tissue comparing with the A549<SUB>shTG2</SUB> cells-injected group. These results suggested that Tgase-2 induces N-cadherin expression of TGF-β1-induced EMT via JNK activation by PP2A down-regulation, and Tgase-2/PP2A/JNK might be a novel axis that affects N-cadherin switching in the EMT of A549 lung cancer cells.