• Title/Summary/Keyword: I2C

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The Mechanism of Poly I:C-Induced Antiviral Activity in Peritoneal Macrophage

  • Pyo, Suh-Kenung
    • Archives of Pharmacal Research
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    • v.17 no.2
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    • pp.93-99
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    • 1994
  • Macrtophages play an important role in defense against virus infection by intrinsic resistance and by extrinsic resistance. Since interferon-induced enzymes which are 2'-5' oligoadenylate synthetase and p1/eIF-2 protein kinase have been shown to be involved in the inhibition of viral replication, I examined the mechanism by which poly I:C, an interferon inducer, exerts its antiviral effects in inflammatory macrophages infected with herpes simplex virus type 1 (HSV-1). The data presented here demonstrate that poly I:C-induced antiviral activity is partially due to the activation of 2'-5' pligoadenylate synthetase. The activation of 2'-5' oligoadenlate A synthetase by poly I:C is also at least mediated via the production of interferon-.betha.. Taken together, these data indicate that interferon-.betha. produced in response to poly I:C acts in an autocrine manner to activate the 2'-5' oligoadenylate synthetase and to induce resistance to HSV-1.

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The Effect of Solvents on the Formation of Complexes of Benzene with Iodine and with Iodine Monochloride (벤젠과 요오드 또는 일염화요오드 사이의 錯物에 대한 용매의 영향)

  • Choi, Sang-Up;Lee, Bu-Yong
    • Journal of the Korean Chemical Society
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    • v.9 no.4
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    • pp.161-168
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    • 1965
  • The effect of solvents on the stabilities of the $C_6H_6{\cdot}I_2$ complex and the $C_6H_6{\cdot}ICl$ complex has been investigated through ultraviolet spectrophotometric measurements. The equilibrium constants obtained at room temperature for the formation of $C_6H_6{\cdot}I_2$ complex are 0.090, 0.216 and 0.328$ lmole^{-1}$ in chloroform, cyclohexane and n-hexane, respectively. The corresponding equilibrium constants at room temperature for $C_6H_6{\cdot}ICl$ complex are 0.125, 0.676 and 0.689 $lmole^{-1}.$ These results indicate that the stabilities of the two complexes increase with decreasing dielectric constants of the solvents used, the increase in stability being more rapid in the $C_6H_6{\cdot}ICl$ complex than in the $C_6H_6{\cdot}I_2$ complex. This may support the conclusion that the dative ionic structures, $C_6H_6^+{\cdots}I_2^-$ and/or ($C_6H_6I)^+{\cdots}Cl^-,$ play important roles on the reasonance stabilization of both the $C_6H_6{\cdot}I_2$ complex and the $C_6H_6{\cdot}ICl$ complex, the roles being more important in the latter complex than in the former complex.

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A Study on I2C Communication Driver Implementation for MOST Interface (MOST 인터페이스를 위한 I2C 통신 드라이버의 구현에 관한 연구)

  • Sung, Hyun-Yong;Jang, Si-Woong
    • Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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    • 2010.05a
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    • pp.739-742
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    • 2010
  • The demand of MOST interface module is increasing with car-multimedia network system. MOST devices consist of INIC part which controls MOST network and EHC part which is used by user. The efficient data communication between EHC and INIC demands implementation of a proper device driver. This paper presents a design method for I2C communication driver which is used for transmitting control messages between nodes of MOST network. For effetive I2C communication, we design driver with NetService API. For testing the experiment, we use the MOST audio interface deivce for porting driver sources and will develop various driver on MOST device based OS.

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HE NONCOMMUTATIVE ℓ1 - ℓ2 INEQUALITY FOR HILBERT C*-MODULES AND THE EXACT CONSTANT

  • Krishna, K. Mahesh;Johnson, P. Sam
    • Nonlinear Functional Analysis and Applications
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    • v.27 no.2
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    • pp.249-259
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    • 2022
  • Let 𝓐 be a unital C*-algebra. Then it follows that $\sum\limits_{i=1}^{n}(a_ia^*_i)^{\frac{1}{2}}{\leq}\sqrt{n}\(\sum\limits_{i=1}^{n}a_ia^*_i\)^{\frac{1}{2}}$, ∀n ∈ ℕ, ∀a1, …, an ∈ 𝓐. By modifications of arguments of Botelho-Andrade, Casazza, Cheng, and Tran given in 2019, for certain n-tuple x = (a1, …, an) ∈ 𝓐n, we give a method to compute a positive element cx in the C*-algebra 𝓐 such that the equality $$\sum\limits_{i=1}^{n}(a_ia^*_i)^{\frac{1}{2}}=c_x\sqrt{n}\(\sum\limits_{i=1}^{n}a_ia^*_i\)^{\frac{1}{2}}$$ holds. We give an application for the integral of Kasparov. We also derive a formula for the exact constant for the continuous ℓ1 - ℓ2 inequality.

TENSOR PRODUCTS OF C*-ALGEBRAS WITH FIBRES GENERALIZED NONCOMMUTATIVE TORI AND CUNTZ ALGEBRAS

  • Boo, Deok-Hoon;Park, Chun-Gil
    • Journal of the Chungcheong Mathematical Society
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    • v.13 no.1
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    • pp.139-144
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    • 2000
  • The generalized noncommutative torus $T_{\rho}^d$ of rank m was defined in [2]. Assume that for the completely irrational noncommutative subtorus $A_{\rho}$ of rank m of $T_{\rho}^d$ there is no integer q > 1 such that $tr(K_0(A_{\rho}))=\frac{1}{q}{\cdot}tr(K_0(A_{\rho^{\prime}}))$ for $A_{\rho^{\prime}}$ a completely irrational noncommutative torus of rank m. All $C^*$-algebras ${\Gamma}({\eta})$ of sections of locally trivial $C^*$-algebra bundles ${\eta}$ over $M=\prod_{i=1}^{e}S^{2k_i}{\times}\prod_{i=1}^{s}S^{2n_i+1}$, $\prod_{i=1}^{s}\mathbb{PR}_{2n_i}$, or $\prod_{i=1}^{s}L_{k_i}(n_i)$ with fibres $T_{\rho}^d{\otimes}M_c(\mathbb{C})$ were constructed in [6, 7, 8]. We prove that ${\Gamma}({\eta}){\otimes}M_{p^{\infty}}$ is isomorphic to $C(M){\otimes}A_{\rho}{\otimes}M_{cd}(\mathbb{C}){\otimes}M_{p^{\infty}}$ if and only if the set of prime factors of cd is a subset of the set of prime factors of p, that $\mathcal{O}_{2u}{\otimes}{\Gamma}({\eta})$ is isomorphic to $\mathcal{O}_{2u}{\otimes}C(M){\otimes}A_{\rho}{\otimes}M_{cd}(\mathbb{C})$ if and only if cd and 2u - 1 are relatively prime, and that $\mathcal{O}_{\infty}{\otimes}{\Gamma}({\eta})$ is not isomorphic to $\mathcal{O}_{\infty}{\otimes}C(M){\otimes}A_{\rho}{\otimes}M_{cd}(\mathbb{C})$ if cd > 1 when no non-trivial matrix algebra can be ${\Gamma}({\eta})$.

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Valproic Acid Induces Transcriptional Activation of Human GD3 Synthase (hST8Sia I) in SK-N-BE(2)-C Human Neuroblastoma Cells

  • Kwon, Haw-Young;Dae, Hyun-Mi;Song, Na-Ri;Kim, Kyoung-Sook;Kim, Cheorl-Ho;Lee, Young-Choon
    • Molecules and Cells
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    • v.27 no.1
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    • pp.113-118
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    • 2009
  • In this study, we have shown the transcriptional regulation of the human GD3 synthase (hST8Sia I) induced by valproic acid (VPA) in human neuroblastoma SK-N-BE(2)-C cells. To elucidate the mechanism underlying the regulation of hST8Sia I gene expression in VPA-stimulated SK-N-BE(2)-C cells, we characterized the promoter region of the hST8Sia I gene. Functional analysis of the 5'-flanking region of the hST8Sia I gene by the transient expression method showed that the -1146 to -646 region, which contains putative binding sites for transcription factors c-Ets-1, CREB, AP-1 and NF-${\kappa}B$, functions as the VPA-inducible promoter of hST8Sia I in SK-N-BE(2)-C cells. Site-directed mutagenesis and electrophoretic mobility shift assay indicated that the NF-${\kappa}B$ binding site at -731 to -722 was crucial for the VPA-induced expression of hST8Sia I in SK-N-BE(2)-C cells. In addition, the transcriptional activity of hST8Sia I induced by VPA in SK-N-BE(2)-C cells was strongly inhibited by SP600125, which is a c-Jun N-terminal kinase (JNK) inhibitor, and $G{\ddot{O}}6976$, which is a protein kinase C (PKC) inhibitor, as determined by RT-PCR (reverse transcription-polymerase chain reaction) and luciferase assays. These results suggest that VPA markedly modulated transcriptional regulation of hST8Sia I gene expression through PKC/JNK signal pathways in SK-N-BE(2)-C cells.

The Complex Formation of Gallium Bromide with i-Butyl Bromide in Nitrobenzene) (니트로벤젠용액내에서의 브롬화갈륨과 i-브롬화부틸과의 착물형성에 관한 연구)

  • Gwon, O Cheon;NamGung, Jin Hui;Choe, Gi Jun
    • Journal of the Korean Chemical Society
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    • v.38 no.3
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    • pp.208-213
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    • 1994
  • The solubility of i-butyl bromide in nitrobenzene have been measured at 19, 25 and $40^{\circ}C$ in the presence and absence of gallium bromide. In the presence of gallium bromide, 1 : 1 complex, $i-C_4H_9Br{\cdot}GaBr_3$ is formed in the solution. The instability constant K of the complex formation was evaluated from the following equilibrium equation. $i-C_4H_9Br{\cdot}GaBr_3{\rightleftharpoons}C_4H_9Br + 1/2Ga_2Br_6.$ From these result, it seems that the stabilities of the complex formation, gallium bromide with alkyl bromide, are directly related with those of the carbonium ions of alkyl bromide.

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FIXED POINTS AND FUZZY STABILITY OF QUADRATIC FUNCTIONAL EQUATIONS

  • Lee, Jung Rye;Shin, Dong Yun
    • Journal of the Chungcheong Mathematical Society
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    • v.24 no.2
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    • pp.273-286
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    • 2011
  • Using the fixed point method, we prove the Hyers-Ulam stability of the following quadratic functional equations $${cf\left({\displaystyle\sum_{i=1}^n\;xi}\right)+{\displaystyle\sum_{i=2}^nf}{\left(\displaystyle\sum_{i=1}^n\;x_i-(n+c-1)x_j\right)}\\ {=(n+c-1)\;\left(f(x_1)+c{\displaystyle\sum_{i=2}^n\;f(x_i)}+{\displaystyle\sum_{i in fuzzy Banach spaces.

Conformational Change of Human Annexin I by the Binding of $Ca^{2+}$, ATP and cAMP

  • Lee, Bong-Jin;An, Hee-Chul;Lee, Yeon-Hee;Han, Hee-Yong;Na, Doe-Sun
    • Journal of the Korean Magnetic Resonance Society
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    • v.2 no.2
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    • pp.141-151
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    • 1998
  • Human annexin I is a member of annexin family of calcium dependent phospholipid binding proteins, which have been implicated in various physiological roles including phospholipase A2(PLA2) inhibition, membrane fusion and calcium channel activity. In this work, the structure of N-terminally truncated human annexin I ({{{{ DELTA }}-annexin I) and its interactions with Ca2+, ATP and cAMP were studied at atomic level by using nuclear magnetic resonance (NMR) spectroscopy. The effect of Ca2+ binding on the structure of {{{{ DELTA }}-annexin I was investigated. The addition of Ca2+ to {{{{ DELTA }}-annexin I caused some changes in 13C NMR spectra. Carbonyl carbon resonances of some histidines were significantly broadened by Ca2+ binding. However, in the case of methionine, phenylalanine, and tyrosin, small changes could be observed. We found that ATP and cAMP bind {{{{ DELTA }}-annexin I, and the binding ratio of ATP to {{{{ DELTA }}-annexin I is 1. These results are well consistent with the report that cAMP and ATP interact with annexin I, and affect the calcium channels formed by annexin I. Because {{{{ DELTA }}-annexin I is a large protein with 35 kDa molecular weight, site-specific (carbonyl-13C) labeling technique was used to study the interaction sites of {{{{ DELTA }}-annexin I with Ca2+. NMR study was focused on the carbonyl carbon resonances of tyrosine, phenylalanine, methionine and histidine residues of {{{{ DELTA }}-annexin I because the number of these amino acids is small in the amino acid sequence of {{{{ DELTA }}-annexin I.

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Insulin-like Growth Factor-I Induces Plectin and MACF1 Expression in C2C12 Myotubes (C2C12 myotube에서 insulin-like growth factor-I이 plectin과 MACF1 발현에 미치는 영향)

  • Kim, Hye Jin;Hwang, Ji Sun;Kwak, Yi-Sub;Lee, Won Jun
    • Journal of Life Science
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    • v.22 no.12
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    • pp.1651-1657
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    • 2012
  • Plectin and microtubule actin cross-linking factor 1 (MACF1) are architectural proteins that contribute to the function of skeletal muscle as generators of mechanical force. However, the influence of insulin- like growth factor-I (IGF-I), a master regulator of skeletal muscle cells, on plectin and MACF1 in skeletal muscle cells has not been demonstrated. The effect of IGF-I on plectin and MACF1 gene expression was investigated by treating differentiated C2C12 murine skeletal muscle cells with 20 ng/ml of IGF-I at different time points. The IGF-I treatment increased plectin protein expression in a dose-dependent manner. The mRNA level of plectin was measured by real-time quantitative PCR to determine if plectin induction was regulated pretranslationally. IGF-I treatment resulted in a very rapid induction of plectin mRNA transcript in C2C12 myotubes. Plectin mRNA increased by 140 and 180% after 24 and 48 hours of IGF-I treatment, respectively, and returned to the control level after 72 hours of IGF-I treatment. MACF1 mRNA increased 86 and 90% after 24 and 48 hours of IGF-I treat-ment, respectively, and returned to the control level after 72 hours of IGF-I treatment. These results suggested that the plectin gene is regulated pretranslationally by IGF-I in skeletal muscle cells. In conclusion, IGF-I induces a rapid transcriptional modification of the plectin and MACF1 genes in C2C12 skeletal muscle cells and has modulating effects on a cytolinker protein as well as on contractile proteins.