• Journal of the Korean Chemical Society
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• v.36 no.2
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• pp.318-323
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• 1992

Following seven new nucleophilic adducts of sulfilimine compounds were prepared by the addition of 1-methyl-5-mercapto-1,2,3,4-tetrazole to vinylsulfilimine derivatives; S-Phenyl-S-2-(1-methyl-1,2,3,4-tetrazole-5-thio)-ethyl-N-p-tosylsulfilimine, S-p-tolyl-S-2-(1-methyl-1,2,3,4-tetrazole-5-thio)-ethyl-N-p-tosylsulfilimine, S-m-tolyl-S-2-(1-methyl-1,2,3,4-tetrazole-5-thio)-ethyl-N-p-tosylsulfilimine, S-p-chlorophenyl-S-2-(1-methyl-1,2,3,4-tetrazole-5-thio)-ethyl-N-p-tosylsulfilimine, S-p-bromophenyl-S-2-(1-methyl-1,2,3,4-tetrazole-5-thio)-ethyl-N-p-tosylsulfilimine, S-p-methoxyphenyl-S-2-(1-methyl-1,2,3,4-tetrazole-5-thio)-ethyl-N-p-tosylsulfilimine and S-p-nitrophenyl-S-2-(1-methyl-1,2,3,4-tetrazole-5-thio)-ethyl-N-p-tosylsulfilimine. The structures of these adducts were confirmed by elemental analyses, MP, UV, IR-and NMR-Spectra.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.3
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• pp.139-142
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• 2002

To examine intracellular signaling of human $S1P_3\;(hS1P_3),$ a sphingosine 1-phosphate (S1P) receptor in plasma membrane, $hS1P_3$ DNA was transfected into RH7777 rat hepatoma cell line, and the inhibition of forskolin-induced cAMP accumulation and activation of MAP kinases by S1P were tested. In $hS1P_3$ transformants, S1P inhibited forskolin-induced activation of adenylyl cyclase activity by about 80% and activated MAP kinases in dose-dependent and pertussis-toxin (PTX) sensitive manners. In oocytes expressing $hS1P_3$ receptor, S1P evoked $Cl^-$ conductance. These data suggested that PTX-sensitive G proteins are involved in $hS1P_3-mediated$ signaling, especially the positive action of S1P in cell proliferation. The potential advantages of rat hepatoma cells for the research of sphingosine 1-phosphate receptor are discussed.

• Journal of Life Science
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• v.21 no.2
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• pp.183-193
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• 2011

Migration and differentiation of mesenchymal stem cells are crucial for tissue regeneration in response to injury. Sphingosine-1-phosphate (S1P) is a bioactive lipid that regulates a variety of biological processes, including proliferation, survival, differentiation and motility. In the present study, we determined the role of S1P in migration and differentiation of human bone marrow-derived mesenchymal stem cells (BMSCs). S1P stimulated migration of BMSCs in a dose- and time-dependent manner, and pre-incubation of the cells with pertussis toxin completely abrogated S1P-induced migration, suggesting involvement of Gi-coupled receptors in S1P-induced cell migration. S1P elicited elevation of intracellular concentration of $Ca^{2+}$ ($[Ca^{2+}]_i$) and pretreatment with VPC23019, an antagonist of $S1P_1/S1P_3$, blocked S1P-induced migration and increase of $[Ca^{2+}]_i$. Small interfering RNA-mediated knockdown of endogenous $S1P_1$ attenuated S1P-induced migration of BMSCs. Furthermore, S1P treatment induced expression of $\alpha$-smooth muscle actin ($\alpha$-SMA), a smooth muscle marker, and pretreatment with VPC23019 abrogated S1P-induced $\alpha$-SMA expression. S1P induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), and pretreatment of cells with SB202190, an inhibitor of p38 MAPK, or adenoviral overexpression of a dominant-negative mutant of the p38 MAPK blocked S1P-induced cell migration and $\alpha$-SMA expression. Taken together, these results suggest that S1P stimulates migration and smooth muscle differentiation of BMSCs through an $S1P_1$-p38 MAPK-dependent mechanism.

• Journal of the Korean Magnetics Society
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• v.25 no.6
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• pp.175-179
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• 2015

The half-metallicity and magnetism of the (001) surfaces of $(AlP)_1/(CrP)_1$ superlattice were investigated by means of FLAPW (Full-potential Liniarized Augmented Plane Wave) method. We considered four types of (001) surface termination, i.e., Al(S)-, Cr(S)-, P(S)Al(S-1)- and P(S)Cr(S-1)-term systems. We found that only Cr(S)-term system maintains the half-metallicity at the surface as only this system has the calculated magnetic moment of integer number of bohr magnetons. The magnetic moment of Cr(S) atom in the system was $3.02{\mu}_B$ which was increased from the bulk value by the effects of band narrowing and increased spin-splitting at the surface. The electronic density of states of the P(S) atom in the P(S)Al(S-1)-term showed very sharp surface states due to the broken $p_z$ bonds at the surface. We found there is still a strong p-d hybridization between the P(S) and Cr(S-1) layers in the P(S)Cr(S-1)-term which causes a considerable increase of magnetic moment of P(S) atom.

• Biomolecules & Therapeutics
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• v.27 no.4
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• pp.373-380
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• 2019

Sphingosine kinase 1 and its product, sphingosine 1-phosphate (S1P), as well as their receptors, have been implicated in inflammatory responses. The functions of receptors $S1P_1$ and $S1P_2$ on cell motility have been investigated. However, the function of $S1P_3$ has been poorly investigated. In this study, the roles of $S1P_3$ on inflammatory response were investigated in primary peritoneal macrophages. $S1P_3$ receptor was induced along with sphingosine kinase 1 by stimulation of lipopolysaccharide (LPS). LPS treatment induced inflammatory genes, such iNOS, COX-2, $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$. TY52156, an antagonist of $S1P_3$ suppressed the induction of inflammatory genes in a concentration dependent manner. Suppression of iNOS and COX-2 induction was further confirmed by western blotting and NO measurement. Suppression of $IL-1{\beta}$ induction was also confirmed by western blotting and ELISA. Caspase 1, which is responsible for $IL-1{\beta}$ production, was similarly induced by LPS and suppressed by TY52156. Therefore, we have shown $S1P_3$ induction in the inflammatory conditions and its pro-inflammatory roles. Targeting $S1P_3$ might be a strategy for regulating inflammatory diseases.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.33 no.9C
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• pp.669-675
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• 2008

For an odd prime p, n=4k and $d=((p^2k+1)/2)^2$, there are $(p^{2k}+1)/2$ distinct decimated sequences, s(dt+1), $0{\leq}l<(p^{2k}+1)/2$, of a p-ary m-sequence, s(t) of period $p^n-1$. In this paper, it is shown that the cross-correlation function between s(t) and s(dt+l) takes the values in $\{-1,-1{\pm}\sqrt{p^n},-1+2\sqrt{p^n}\}$ and their, cross-correlation distribution is also derived.

• Honam Mathematical Journal
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• v.1 no.1
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• pp.1-9
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• 1979

Positive Local Coordmate($(x^1,x^2,{\cdots}x^n)$)을 갖는 Oriented Manifold M을 생각한다. M이 Compact Carrier를 갖는 경우, M위의 n차(次) Differential Form ${\phi}^{(n)}$의 적분(積分)을 $${\int}{\phi}^{(n)}=\sum_{\alpha}{\int}_{-{\infty}}^{\infty}{\cdots}{\int}_{-{\infty}}^{\infty}f_{\alpha}{\phi}^{(n)}dx^1{\cdots}dx^n$$로 정의(定義)하며 (정의(定義) 7), M위의 p 차(次)의 Differential form $\beta^{(p)}$와 Differential simplex $S^{(p)}=(S^{(p)},\;{\pi},\;{\varepsilon})$에 대하여 $S^{(p)}$위의 $\beta^{(p)}$의 적분(積分)을 $${\int}_{^{(p)}S}{\beta}^{(p)}={\int}_{S^{(p)}}{\varepsilon}{\pi}^*{\beta}^{(p)}={\int}_{E^p}f{\cdot}{\varepsilon}{\cdot}{\pi}^*{\beta}^{(p)}$$로 정의(定義)한다 (정의(定義) 9). 단(但) $\bar{S}^{(p)}$는 $S^{(p)}=(p_0{\cdot}p_1{\cdots}p_p)$에 의(依)하여 Spanning 되는 $E^p$의 Subspace이고 f는 $\bar{S}^{(p)}$의 특성함수(特性函數)이다. 이때 (n-1)차(次)의 Differential Form ${\beta}^{(n-1)}$이 Compart인 Carrier를 가지면 ${\int}d{\beta}^{(n-1)}=0$이 됨을 고찰(考察)하며(정리(定理 8), (p-1)차(次) Differential Form ${\beta}^{(p-1)$과 p차(次) Differential Chain $C^{(p)}$에 관(關)하여 $${\int}_{C^{(p)}}d{\beta}^{(p-1)}={\int}_{{\partial}C^{(p)}}{\beta}^{(p-1)}$$이 성립(成立)함을 구명(究明)하려 한다(정리(定理) 10).

• Journal of the Korean Chemical Society
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• v.25 no.6
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• pp.390-393
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• 1981

Eight new compounds were prepared by the addition reaction of thioglycolic acid to ${\beta}$-nitrostyrene and its derivatives. s-[2-Nitro-1-phenylethyl]-thioglycolic acid; s-[2-nitro-1-(p-methyl)phenylethyl]-thioglycolic acid; s-[2-nitro-1-(p-methoxy)phenylethyl]-thioglycolic acid; s-[2-nitro-1-(p-chloro)phenylethyl]-thioglycolic acid; s-[2-nitro-1-(p-bromo)phenylethyl]-thioglycolic acid; s-[2-nitro-1-(p-nitro)phenylethyl]-thioglycolic acid; s-[2-nitro-1-(3-methoxy-4-ethoxy)phenylethyl]-thioglycolic acid; s-[2-nitro-1-(3,4,5-trimethoxy)phenylethyl]-thioglycolic acid; The structure of these compound were identified by elemental analysis, UV, IR and NMR spectral data.

• Korean Journal of Agricultural Science
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• v.22 no.1
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• pp.103-109
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• 1995

The model foods were prepared by simulating mositure, protein and starch, and they were heated for 30 mins, at $80^{\circ}C$ and then cooled at $25^{\circ}C$ in water bath. Their rheological properties were investigated by the use of Brookfield wide-gap rotational viscometer at $30{\sim}60^{\circ}C$, and the rotation speed ranged from 0.6 to 6 rpm and solid content ranged from 8% to 11%, the results obtained were as follows. 1. All the model foods ($P_1S_3$, $P_2S_2$, $P_1S_1$, $P_2S_1$, $P_3S_1$, $P_4S_0$) exhibited pseudoplastic behaviors with yeild stress and were thixotropic foods which showed time - dependent structural decays, but the starch food of 8 ~ 11 % solid content did not show the flow behavior. 2. The correlation between the rheological parameters and the protein content of model foods in various moisture content did not appeared a constant relationship. 3. The change of shear stress against shear rate in high starch foods was larger than that in high protein foods and the structure at initial shear time was decayed with a quatic equation according to the Tiu's Model and structural decay was in parallel with the increase of shear rate. 4. The temperature dependency of the apparent viscosity of $P_1S_2$, and $P_2S_1$ was fully expressed by Arrhenius equation and activation energies of their food were 2.35 and $1.34Kcal/g{\cdot}mol$, respectively.

• Biomolecules & Therapeutics
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• v.27 no.6
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• pp.522-529
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• 2019

M1/M2 polarization of immune cells including microglia has been well characterized. It mediates detrimental or beneficial roles in neuroinflammatory disorders including cerebral ischemia. We have previously found that sphingosine 1-phospate receptor subtype 1 ($S1P_1$) in post-ischemic brain following transient middle cerebral artery occlusion (tMCAO) can trigger microglial activation, leading to brain damage. Although the link between $S1P_1$ and microglial activation as a pathogenesis in cerebral ischemia had been clearly demonstrated, whether the pathogenic role of $S1P_1$ is associated with its regulation of M1/M2 polarization remains unclear. Thus, this study aimed to determine whether $S1P_1$ was associated with regulation of M1/M2 polarization in post-ischemic brain. Suppressing $S1P_1$ activity with its functional antagonist, AUY954 (5 mg/kg, p.o.), attenuated mRNA upregulation of M1 polarization markers in post-ischemic brain at 1 day and 3 days after tMCAO challenge. Similarly, suppressing $S1P_1$ activity with AUY954 administration inhibited M1-polarizatioin-relevant $NF-{\kappa}B$ activation in post-ischemic brain. Particularly, $NF-{\kappa}B$ activation was observed in activated microglia of post-ischemic brain and markedly attenuated by AUY954, indicating that M1 polarization through $S1P_1$ in post-ischemic brain mainly occurred in activated microglia. Suppressing $S1P_1$ activity with AUY954 also increased mRNA expression levels of M2 polarization markers in post-ischemic brain, further indicating that $S1P_1$ could also influence M2 polarization in post-ischemic brain. Finally, suppressing $S1P_1$ activity decreased phosphorylation of M1-relevant ERK1/2, p38, and JNK MAPKs, but increased phosphorylation of M2-relevant Akt, all of which were downstream pathways following $S1P_1$ activation. Overall, these results revealed $S1P_1$-regulated M1/M2 polarization toward brain damage as a pathogenesis of cerebral ischemia.