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Discrete-Time Sliding Mode Controller for Linear Time-Varying Systems with Disturbances
Park, Kang-Bak Institute of Control 2000 Transaction on control, automation and systems eng Vol.2 No.4
In this paper, a discrete-time sliding mode controller for linear time-varying systems with disturbances is proposed. The proposed method guarantees the systems state is globally uniformly ultimately bounded(G.U.U.B) under the existence of time-varying disturbances.
박현,윤갑희,가강현,박원철 한국임학회 2000 한국산림과학회지 Vol.89 No.5
Syzygites megalocarpus occurred on the fruit bodies of Tricholoma matsutake, Leccinum rugosiceps, Pulveroboletus ravenelii, Russula emetica, and Amanita pseudoporphyria in the field. We could select Malt Extract Agar, Mueller Hinton Medium and Potato Dextrose Agar as optimal media among eight media. Syzygites megalocarpus showed an optimal temperature around 23℃ with optimal pH 6.0. Growth of S. megalocarpus on PDA was inhibited by 36.5% at 5% NaCl compared with without NaCl and did not grow at more than 8% NaCl in 2 days after inoculation. However, it grew 1.1 ㎝ in 10% NaCl in 5 days after inoculation. Growth of Tricholoma matsutake on PDA was inhibited by increasing contration of NaCl and did not nearly grow at 2.5% NaCl in 60 days after inoculation. Because S. megalocarpus grew at high concentration of NaCl, we concluded that NaCl should not use for controlling S. megalocarpus on the fruit body of T. matsutake.
Kang, Jeong-Woo,Park, Yun Sun,Lee, Dong Hun,Kim, Jung-hee,Kim, Man Sub,Bak, Yesol,Hong, Jintae,Yoon, Do-Young American Society for Biochemistry and Molecular Bi 2012 The Journal of biological chemistry Vol.287 No.42
<P>IL-32α is known as a proinflammatory cytokine. However, several evidences implying its action in cells have been recently reported. In this study, we present for the first time that IL-32α plays an intracellular mediatory role in IL-6 production using constitutive expression systems for IL-32α in THP-1 cells. We show that phorbol 12-myristate 13-acetate (PMA)-induced increase in IL-6 production by IL-32α-expressing cells was higher than that by empty vector-expressing cells and that this increase occurred in a time- and dose-dependent manner. Treatment with MAPK inhibitors did not diminish this effect of IL-32α, and NF-κB signaling activity was similar in the two cell lines. Because the augmenting effect of IL-32α was dependent on the PKC activator PMA, we tested various PKC inhibitors. The pan-PKC inhibitor Gö6850 and the PKCϵ inhibitor Ro-31-8220 abrogated the augmenting effect of IL-32α on IL-6 production, whereas the classical PKC inhibitor Gö6976 and the PKCδ inhibitor rottlerin did not. In addition, IL-32α was co-immunoprecipitated with PMA-activated PKCϵ, and this interaction was totally inhibited by the PKCϵ inhibitor Ro-31-8220. PMA-induced enhancement of STAT3 phosphorylation was observed only in IL-32α-expressing cells, and this enhancement was inhibited by Ro-31-8220, but not by Gö6976. We demonstrate that IL-32α mediated STAT3 phosphorylation by forming a trimeric complex with PKCϵ and enhanced STAT3 localization onto the IL-6 promoter and thereby increased IL-6 expression. Thus, our data indicate that the intracellular interaction of IL-32α with PKCϵ and STAT3 promotes STAT3 binding to the IL-6 promoter by enforcing STAT3 phosphorylation, which results in increased production of IL-6.</P>