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Observation of the Cosmic Near-Infrared Background with the CIBER rocket
MinGyu Kim,T. Matsumoto,Hyung Mok Lee,T. Arai,J. Battle,J. Bock,S. Brown,A. Cooray,V. Hristov,B. Keating,P. Korngut,Dae-Hee Lee,L. R. Levenson,K. Lykke,P. Mason,S. Matsuura,U. W. Nam,T. Renbarger,A. S 한국천문학회 2012 天文學會報 Vol.37 No.1
Controls on KSTAR Superconducting Poloidal Field (PF) Magnets
Hahn, Sang-Hee,Kim, K.H.,Choi, J.H.,Ahn, H.S.,Lee, D.K.,Park, K.R.,Eidietis, N.W.,Leuer, J.A.,Walker, M.L.,Yang, H.L.,Kim, W.C.,Oh, Y.K. The Korean Society of Superconductivity and Cryoge 2008 한국초전도저온공학회논문지 Vol.10 No.4
As a part of the plasma control system (PCS) for the first plasma campaign of KSTAR, seven sets of fast feedback control loop for the superconducting poloidal field magnet power supply (PF MPS) have been implemented. A special real-time digital communication interface has been developed for the simultaneous exchanges of the current/voltage data from the 7 sets of 12-thyristor power supplies in a 200 microsecond control cycle. Preliminary power supply tests have been performed before actual cooldown of the device. A $29mH/50m{\Omega}$ solenoid dummy has been fabricated for a series of single power supply tests. Connectivity and response speed of the plasma control system have been verified. By changing hardware cabling, this load was also used to estimate mutual inductance coupling effects of two geometrically adjacent solenoid coils on each power supply. After the cooldown was complete, each pair of the up/down symmetric PF coils has been serially connected and tested as part of the device commissioning process. Bipolar operation and longer pulse attempts have been investigated. The responses of the coils and power supplies corresponding to the plasma magnetic controls in plasma discharges are also analyzed for the future upgrades.
Ahn, Hee-Yul,K.R. Hadizadeh Kharrazi,Yun, Y-P,Park, J-B,Choi, W,H. Vetter,A. Sachinidis 이화여자대학교 세포신호전달연구센터 2000 고사리 세포신호전달 심포지움 Vol. No.2
Vascular smooth muscle cells(VSMCs) proliferation may participate in the pathophysiology of cardiovascular diseases. Platelet-derived growth factor-BB(PDGF-BB) is a potent mitogenic factor for VSMCs. Epigallocatechin gallate(EGCG) is the main compound of green tea and is believed to be the active component in tea for the prevention against several diseases. We investigated the effect of EGCG on the PDGF-BB-induced proliferation of VSMCs. VSMCs were preincubated in serum-free medium for 24 h(quiescent VSMCs) before EGCG was added to the medium. Following 24 h incubation with EGCG per se, VSMCs were trypsinized and cell counts were determined using CASY-1 system based on the coulter counter principle(Scharfe). Treatment of the cells with 0μM, 20μM, 50μM and 100μM EGCG resulted in a decrease of cell counts from 1.49×10^(6) ± 1.2×10^(5)(0μM) to 9.7×10^(5) ± 1.1×10⁴, 5.3×10^(5) ± 6.3×10⁴, 3.8×10^(5) ± 2.5×10⁴ counts/ml(mean±SD, n=3), respectively. Stimulation of quiescent cells with 50 ng/ml PDGF-BB for 24 h resulted in a 35% increase in cell counts. In the presence of 50μM EGCG, the effect of PDGF-BB on cell counts was abrogated. Activation of the 42 and 44 kDa mitogen-activated protein kinase(MAP) kinases(p44^(mapk)/p42^(mapk)) was deteced by chemiluminescence western blotting method using primary antibodies which recognizes the Tyr204-phosphorylated active isoforms. Stimulation of quiescent VSMCs with 50 ng/ml PDGF-BB caused at 5 min an 8-fold increase of the the p44^(mapk)/p42^(mapk) phosphorylation above control levels. Pretreatment of cells for 24 h with 50㎍/ml EGCG resulted in 70% inhibition of the p44^(mapk)/p42^(mapk) phosphorylation. Stimulation of the cells with PDGF-BB caused a maximal increase in [Ca^(2+)]_(i) from 40±10(basal value) to 145±15nM(mean±SD, n=4) at 25 sec(determined by the fura-2 method). Preincubation of VSMCs for 24 h with EGCG resulted in a complete inhibition of the PDGF-BB-induced increase in [Ca^(2+)]_(i). These results demonstrate that EGCG may exert its anti-proliferative effects via inhibition of the PDGF-BB-induced intracellular signaling events like stimulation of the p44^(mapk)/p42^(mapk) and elevation of [Ca^(2+)]_(i).
Baek, Min K,Kim, Mi H,Jang, Hee J,Park, Jung S,Chung, Ik J,Shin, Boo A,Ahn, Bong W,Jung, Young D National Hellenic Research Foundation 2008 Oncology reports Vol.20 No.6
<P>Overexpression of epidermal growth factor (EGF) and urokinase plasminogen activator receptor (uPAR) have been observed in human gastric cancers. However, the interaction between EGF and uPAR in gastric cancer has not been well elucidated. In this study, we investigated the effect of EGF on uPAR expression and the underlying signal pathways in human gastric cancer AGS cells. EGF induced uPAR mRNA expression in a time- and concentration-dependent manner. EGF also induced uPAR promoter activity. In addition, EGF induced the activation of extracellular signal regulated kinase-1/2 (ERK-1/2) and P38 mitogen-activated protein kinase (MAPK) but not the activation of c-Jun amino terminal kinase. A specific inhibitor of MEK-1 (an upstream effector of ERK-1/2) and a dominant negative MEK-1 were able to suppress the EGF-induced uPAR promoter activity. Site-directed mutagenesis and electrophoretic mobility shift assays demonstrated that the binding sites of transcription factors, activator protein-1 (AP-1) and nuclear factor (NF)-kappaB, are involved in the EGF-induced uPAR transcription. Suppression of the EGF-induced uPAR promoter activity by the AP-1 decoy oligonuclotide, as well as expression vectors encoding mutated-type NF-kappaB-inducting kinase and I-kappaB, confirmed that the activation of AP-1 and NF-kappaB are essential for the EGF-induced uPAR upregulation. The AGS cells pretreated with EGF showed a remarkably enhanced invasiveness and this effect was partially abrogated by uPAR neutralizing antibodies and by the inhibitors of ERK-1/2, AP-1, and NF-kappaB. The above results suggest that EGF induces uPAR expression via ERK-1/2, AP-1, and NF-kappaB signaling pathways and, in turn, stimulates cell invasiveness in human gastric cancer AGS cells.</P>
Zhu, Ping,Baek, Sung Hee,Bourk, Eliot M.,Ohgi, Kenneth A.,Garcia-Bassets, Ivan,Sanjo, Hideki,Akira, Shizuo,Kotol, Paul F.,Glass, Christopher K.,Rosenfeld, Michael G.,Rose, David W. Elsevier 2006 Cell Vol.124 No.3
<P><B>Summary</B></P><P>Defining the precise molecular strategies that coordinate patterns of transcriptional responses to specific signals is central for understanding normal development and homeostasis as well as the pathogenesis of hormone-dependent cancers. Here we report specific prostate cancer cell/macrophage interactions that mediate a switch in function of selective androgen receptor antagonists/modulators (SARMs) from repression to activation in vivo. This is based on an evolutionarily conserved receptor N-terminal L/HX<SUB>7</SUB>LL motif, selectively present in sex steroid receptors, that causes recruitment of TAB2 as a component of an N-CoR corepressor complex. TAB2 acts as a sensor for inflammatory signals by serving as a molecular beacon for recruitment of MEKK1, which in turn mediates dismissal of the N-CoR/HDAC complex and permits derepression of androgen and estrogen receptor target genes. Surprisingly, this conserved sensor strategy may have arisen to mediate reversal of sex steroid-dependent repression of a limited cohort of target genes in response to inflammatory signals, linking inflammatory and nuclear receptor ligand responses to essential reproductive functions.</P>