• Molecules and Cells
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• v.43 no.12
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• pp.1023-1034
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• 2020

Complement fragment iC3b serves as a major opsonin for facilitating phagocytosis via its interaction with complement receptors CR3 and CR4, also known by their leukocyte integrin family names, αMβ2 and αXβ2, respectively. Although there is general agreement that iC3b binds to the αM and αX I-domains of the respective β2-integrins, much less is known regarding the regions of iC3b contributing to the αX I-domain binding. In this study, using recombinant αX I-domain, as well as recombinant fragments of iC3b as candidate binding partners, we have identified two distinct binding moieties of iC3b for the αX I-domain. They are the C3 convertase-generated N-terminal segment of the C3b α'-chain (α'NT) and the factor I cleavage-generated N-terminal segment in the CUBf region of α-chain. Additionally, we have found that the CUBf segment is a novel binding moiety of iC3b for the αM I-domain. The CUBf segment shows about a 2-fold higher binding activity than the α'NT for αX I-domain. We also have shown the involvement of crucial acidic residues on the iC3b side of the interface and basic residues on the I-domain side.

• Bulletin of the Korean Mathematical Society
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• v.47 no.3
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• pp.645-651
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• 2010

In this note we study positive solutions of the mth order rational difference equation $x_n=(a_0+\sum{{m\atop{i=1}}a_ix_{n-i}/(b_0+\sum{{m\atop{i=1}}b_ix_{n-i}$, where n = m,m+1,m+2, $\ldots$ and $x_0,\ldots,x_{m-1}$ > 0. We describe a sufficient condition on nonnegative real numbers $a_0,a_1,\ldots,a_m,b_0,b_1,\ldots,b_m$ under which every solution $x_n$ of the above equation tends to the limit $(A-b_0+\sqrt{(A-b_0)^2+4_{a_0}B}$/2B as $n{\rightarrow}{\infty}$, where $A=\sum{{m\atop{i=1}}\;a_i$ and $B=\sum{{m\atop{i=1}}\;b_i$.

• Korean Journal of Mathematics
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• v.18 no.4
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• pp.335-342
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• 2010

Let D be an integral domain with quotient field K,$\mathcal{I}(D)$ be the set of nonzero ideals of D, and $w$ be the star-operation on D defined by $I_w=\{x{\in}K{\mid}xJ{\subseteq}I$ for some $J{\in}\mathcal{I}(D)$ such that J is finitely generated and $J^{-1}=D\}$. The D is called a Pr$\ddot{u}$fer $v$-multiplication domain if $(II^{-1})_w=D$ for all nonzero finitely generated ideals I of D. In this paper, we show that D is a Pr$\ddot{u}$fer $v$-multiplication domain if and only if $(A{\cap}(B+C))_w=((A{\cap}B)+(A{\cap}C))_w$ for all $A,B,C{\in}\mathcal{I}(D)$, if and only if $(A(B{\cap}C))_w=(AB{\cap}AC)_w$ for all $A,B,C{\in}\mathcal{I}(D)$, if and only if $((A+B)(A{\cap}B))_w=(AB)_w$ for all $A,B{\in}\mathcal{I}(D)$, if and only if $((A+B):C)_w=((A:C)+(B:C))_w$ for all $A,B,C{\in}\mathcal{I}(D)$ with C finitely generated, if and only if $((a:b)+(b:a))_w=D$ for all nonzero $a,b{\in}D$, if and only if $(A:(B{\cap}C))_w=((A:B)+(A:C))_w$ for all $A,B,C{\in}\mathcal{I}(D)$ with B, C finitely generated.

• Tuberculosis and Respiratory Diseases
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• v.49 no.3
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• pp.332-342
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• 2000

Background : The importance of pro-inflammatory cytokines, especially tumor necrosis factor $\alpha$ (INF-$\alpha$) and interleukin-1$\beta$ (IL-1$\beta$), have been extensively documented in the generation of inflammatory lung disease. Lung epithelial cells are also actively involved in initiating and maintaining inflammation by producing pro-inflammatory mediators. Understanding the mechanism of pro-inflammatory cytokine expression in lung epithelial cells is crucial to the development of new therapeutic modalities for inflammatory lung disease. Transcription of most pro-inflammatory cytokines is dependent on the activation of NF-${\kappa}B$. However, the relationship between pro-inflammatory cytokine expression and NF-${\kappa}B/I{\kappa}B$ pathway in lung epithelial cells is not clear. Methods : BEAS-2B, A549, Na-H157, NCI-H719 cells were stimulated with IL-$1{\beta}$ or TNF-$\alpha$ at various times, and then IL-8 and TNF-$\alpha$mRNA expressions were assayed by Northern blot analysis. IL-$1{\beta}$ or TNF-$\alpha$-induced NF-${\kappa}B$ activation was assessed by the nuclear translocation of p65 NF-${\kappa}B$ subunit. The degradation of $I{\kappa}B{\alpha}$ and $I{\kappa}B{\beta}$ by IL-$1{\beta}$ or TNF-$\alpha$stimulation was assayed by Western blot analysis. The phosphorylation of $I{\kappa}B{\alpha}$ was evaluated by Western blot analysis after pre-treating cells with proteasome inhibitor followed by IL-$1{\beta}$ or TNF-$\alpha$ stimulation. The basal level of IKK $\alpha$ expression was evaluated by Western blot analysis. Results: $I{\kappa}B{\alpha}$ and $I{\kappa}B{\alpha}$ was rapidly degraded after 5 minutes of incubation with IL-$1{\beta}$ or TNF-$\alpha$ in BEAS-2B, A549, and NCI-H157 cells. The activation of NF-${\kappa}B{\alpha}$ and the induction of IL-8 and TNF-$\alpha$ mRNA expression were observed by IL-$1{\beta}$ or TNF-$\alpha$ stimulation in these cells. In contrast, neither the changes in NF-${\kappa}B/I{\kappa}B$ pathway nor IL-8 and TNF-$\alpha$mRNA expression was induced by IL-$1{\beta}$ or TNF-$\alpha$ stimulation in NCI-H719 cells. IL-$1{\beta}$ and TNF-$\alpha$-induced $I{\kappa}B$ phosphorylation was observed in BEAS-2B, A549, and NCI-H157 cells, but not in NCI-H719 cells. The basal level of IKK$\alpha$ expression was not different between cell. Conclusion : NF-${\kappa}B/I{\kappa}B$ pathway plays an important role in the expression of pro-inflammatory cytokine in most lung epithelial cells. The absence of the effect on NF-${\kappa}B/I{\kappa}B$ pathway in NCI-H719 cells sæms to be due to the defect in the intracellular signal transduction pathway upstream to IKK.

• Journal of the Korean Ceramic Society
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• v.41 no.5
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• pp.401-405
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• 2004

Undoped SrB $i_2$T $a_2$O$_{9}$, donor-doped Sr$_{0.99}$B $i_2$(Ta$_{0.99}$W$_{0.01}$)$_2$O$_{9}$ and acceptor-doped SrB $i_2$(Ta$_{0.99}$Ti$_{0.01}$)$_2$O$_{8.99$ ceramics were prepared and their microstructure, ferroelectric P-E hysteresis and Curie temperature were investigated. Grain size did not influence P-E hysteresis curve in undoped SrB $i_2$T $a_2$O$_{9}$ ceramics. Donor-Doped Sr$_{0.99}$B $i_2$(Ta$_{0.99}$W$_{0.01}$)$_2$O$_{9}$ ceramics showed more saturated P-E hysteresis curve with larger remanent polarization (P$_{r}$) than undoped SrB $i_2$T $a_2$O$_{9}$ ceramics while acceptor-doped SrB $i_2$(Ta$_{0.99}$Ti$_{0.01}$)$_2$O$_{8.99}$ ceramics led to a pinched P-E hysteresis loop. Larger polarization in donor-doped Sr$_{0.99}$B $i_2$(Ta$_{0.99}$W$_{0.01}$)$_2$O$_{9}$ ceramics resulted from easier domain wall motion by Sr-vacancies.

• Journal of the Chungcheong Mathematical Society
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• v.26 no.1
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• pp.91-103
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• 2013

Let (D,B) be an admissible pair. Then recall that $B\;{\times}^L_HD^{{\rightarrow}{\pi}_D}_{{\leftarrow}i_D}\;D$ are bialgebra maps satisfying ${\pi}_D{\circ}i_D=I$. We have solved a converse in case D is a Hopf algebra. Let D be a Hopf algebra with antipode $S_D$ and be a left H-comodule algebra and a left H-module coalgebra over a field $k$. Let A be a bialgebra over $k$. Suppose $A^{{\rightarrow}{\pi}}_{{\leftarrow}i}D$ are bialgebra maps satisfying ${\pi}{\circ}i=I_D$. Set ${\Pi}=I_D*(i{\circ}s_D{\circ}{\pi}),B=\Pi(A)$ and $j:B{\rightarrow}A$ be the inclusion. Suppose that ${\Pi}$ is an algebra map. We show that (D,B) is an admissible pair and $B^{\leftarrow{\Pi}}_{\rightarrow{j}}A^{\rightarrow{\pi}}_{\leftarrow{i}}D$ is an admissible mapping system and that the generalized biproduct bialgebra $B{\times}^L_HD$ is isomorphic to A as bialgebras.

• Tuberculosis and Respiratory Diseases
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• v.54 no.4
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• pp.449-458
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• 2003

Background : Cyclosporin A(CsA) and tacrolimus(FK506) have been widely used as immunosuppressants. The effects of CsA, or FK506, on the $I{\kappa}B/NF-{\kappa}B$ pathway have been shown to vary according to the cell type. However, their effects on the $I{\kappa}B/NF-{\kappa}B$ pathway have not been reported in bronchial epithelial cells. In this study, the effects of CsA and FK506 on the $I{\kappa}B/NF-{\kappa}B$ pathway in bronchial epithelial cells, monocytes, lymphocytes and alveolar macrophages were evaluated. The relationship between their effects on the $I{\kappa}B/NF-{\kappa}B$ pathway and $I{\kappa}B$ kinase(IKK) activity was also investigated. Methods : BEAS-2B and A549 cells, pulmonary alveolar macrophages, peripheral blood monocytes and lymphocytes were used. The cells were pre-treated with CsA, or FK506, for various time periods, followed by stimulation with TNF-${\alpha}$, LPS or IL-$1{\beta}$. The $I{\kappa}B{\alpha}$ expressions were assayed by Western blot analyses. The IKK activity was evaluated by an in vitro immune complex kinase assay, using GST-$I{\kappa}B{\alpha}$ as the substrate. Results : Neither CsA nor FK506 affected the level of $I{\kappa}B{\alpha}$ expression in any of the cell types used in this study. CsA pre-treatment inhibited the TNF ${\alpha}$-induced $I{\kappa}B{\alpha}$ degradation in bronchial epithelial cells. In contrast, the TNF ${\alpha}$-induced $I{\kappa}B{\alpha}$ degradation was not affected by FK506 pre-treatment. However, FK506 suppressed the cytokine-induced $I{\kappa}B{\alpha}$ degradation in the pulmonary alveolar macrophages, peripheral blood monocytes and lymphocytes. The inhibitory effect of CsA, or FK506, on $I{\kappa}B{\alpha}$ degradation was not related to IKK. Conclusions : CsA and FK506 suppressed the $I{\kappa}B{\alpha}$ degradation in bronchial epithelial cells, monocytes, lymphocytes and alveolar macrophages, so this may not be mediated through IKK.

• Bulletin of the Korean Mathematical Society
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• v.34 no.1
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• pp.81-91
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• 1997

Let X be a finite set of elements that we shall call points. Let I be a set called an indexing set. A mapping $B : I \longrightarrow P(X)$ is called a family of blocks on X. For each $i \in I, B(i)$ is also written as $B_i$. We always assume $$\mid$B_i$\mid$ \geq 2$ for each $i \in I$.

• Journal of Digital Convergence
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• v.11 no.7
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• pp.201-207
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• 2013

The chirp signaling has been mainly used in radar systems due to its good correlation characteristics, and nowadays it is applied to real time locating system(RTLS). The RTLS with chirp signaling was chosen as a standard such as ISO/IEC 24730-5 and IEEE 802.15.4a. In this paper, the performance of a real time locating system with chirp signaling was evaluated and simulated with relative distance error rates. We considered three cases of S/I = -30[dB], -20[dB], and -10[dB] with Rician factor K=10 and K=20. The performance was enhanced with K factor improvement by 25%, 27% and 50% for respective three cases of S/I. As results, in case of S/I < -20[dB], the minimum signal power is required for performance improvement even though the line of sight component is helpful. And also, in case of S/I ${\geq}$ -20[dB], as the line of sight component is stronger the better performance is obtained.

• Honam Mathematical Journal
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• v.36 no.4
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• pp.913-919
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• 2014

We investigate the relationships between the space X and the hyperspaces concerning admissibility and connectedness im kleinen. The following results are obtained: Let X be a Hausdorff continuum, and let A, $B{\in}C(X)$ with $A{\subset}B$. (1) If X is c.i.k. at A, then X is c.i.k. at B if and only if B is admissible. (2) If A is admissible and C(X) is c.i.k. at A, then for each open set U containing A there is a continuum K and a neighborhood V of A such that $V{\subset}IntK{\subset}K{\subset}U$. (3) If for each open subset U of X containing A, there is a continuum B in C(X) such that $A{\subset}B{\subset}U$ and X is c.i.k. at B, then X is c.i.k. at A. (4) If X is not c.i.k. at a point x of X, then there is an open set U containing x and there is a sequence $\{S_i\}^{\infty}_{i=1}$ of components of $\bar{U}$ such that $S_i{\longrightarrow}S$ where S is a nondegenerate continuum containing the point x and $S_i{\cap}S={\emptyset}$ for each i = 1, 2, ${\cdots}$.