• Molecules and Cells
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• v.27 no.2
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• pp.257-261
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• 2009

Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) is an important pathogen casuing aggressive periodontitis. The present study was designed to investigate the chemokines expression regulated by A. actinomycetemcomitans lipopolysaccharide (LPS). Chemokines genes expression profiling was performed in Raw 264.7 cells by analyses of microarray and reverse transcription-polymerase chain reaction (RT-PCR). Microarray results showed that the induction of monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-$1{\alpha}$ (MIP-$1{\alpha}$), MIP-$1{\beta}$, MIP-$1{\gamma}$, regulated upon activation, normal T-cell expressed and secreted (RANTES), macrophage inflammatory protein-2 (MIP-2), and interferon-${\gamma}$ inducible protein 10 (IP 10) by A. actinomycetemcomitans LPS was increased to 12.5, 1.53, 9.09, 17.3, 2.82, 16.1, and 18.1 folds at 18 h, respectively. To check these chemokines expression by A. actinomycetemcomitans LPS, we examined gene expressions by RT-PCR, and found that the expression of MIP-$1{\beta}$, MIP-$1{\gamma}$, RANTES, MIP-2, and IP 10 was increased 107.1, 93.6, 106.8, 86.5, and 162.0 folds at 18 h, respectively. These results indicate that A. actinomycetemcomitans LPS stimulates the several chemokines expressions (MIP-$1{\alpha}$, MIP-$1{\beta}$, MIP-$1{\gamma}$, RANTES, MIP-2, and IP 10) in Raw 264.7 cells.

• Biomolecules & Therapeutics
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• v.21 no.1
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• pp.42-48
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• 2013

Nystatin, a polyene antifungal antibiotic, is a cholesterol sequestering agent. The antifungal agent alters composition of the plasma membrane of eukaryotic cells, whereas its effects on cells are poorly investigated. In the current study, we investigated the question of whether nystatin was able to induce expression of macrophage inflammatory protein-1 (MIP-1). THP-1 cells rarely express MIP-$1{\alpha}$ and MIP-$1{\beta}$, however, upon exposure to nystatin, significantly elevated expression of MIP-$1{\alpha}$ and MIP-$1{\beta}$ was observed in a dose-dependent fashion at the messenger and protein levels. Cellular factors activated by nystatin as well as involved in nystatin-induced expression of MIP-1 proteins were identified in order to understand the molecular mechanisms of action of the anti-fungal agent. Treatment with nystatin resulted in enhanced phosphorylation of Akt, ERK, p38 MAPK, and JNK. Abrogation or significant attenuation of nystatin-induced expression of MIP-$1{\alpha}$ and MIP-$1{\beta}$ was observed by treatment with Akt inhibitor IV, LY294002, and SP6001250. Inhibition of ERK or p38MAPK using U0126 and SB202190 did not lead to attenuation of MIP-1 expression. In addition, inhibitors of protein kinase C, such as GF109203X and Ro-318220, also attenuated expression of MIP-1. These results indicate that nystatin is able to activate multiple cellular kinases and, among them, Akt and JNK play primary roles in nystatin-induced expression of MIP-1 proteins.

• Investigative Magnetic Resonance Imaging
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• v.13 no.2
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• pp.183-189
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• 2009

Purpose : To evaluate the usefulness of three-dimensional (3D) maximal intensity projection (MIP) reconstruction method in breast MRI. Materials and Methods : Total 54 breasts of consecutive 27 patients were examined by breast MRI. Breast MRI was performed using GE Signa Excite Twin speed (GE medical system, Wisconsin, USA) 1.5T. We obtained routine breast MR images including axial T2WI, T1WI, sagittal T1FS, dynamic contrast-enhanced T1FS, and subtraction images. 3D MIP reconstruction images were obtained as follows; subtraction images were obtained using TIPS and early stage of contrast-enhanced TIPS images. And then 3D MIP images were obtained using the subtraction images through advantage workstation (GE Medical system). We detected and analyzed the lesions in the 3D MIP and routine MRI images according to ACR $BIRADS^{(R)}$ MRI lexicon. And then we compared the findings of 3D MIP and those of routine breast MR images and evaluated whether 3D MIP had additional information comparing to routine MR images. Results : 3D MIP images detect the 43 of 56 masses found on routine MR images (76.8%). In non-mass like enhancement, 3D MIP detected 17 of 20 lesions (85 %). And there were one hundred sixty nine foci at 3D MIP images and one hundred nine foci at routine MR images. 3D MIP images detected 14 of 23 category 3 lesions (60.9%), 11 of 16 category 4 lesions (68.87%), 28 of 28 Category 5 lesions (100%). In analyzing the enhancing lesions at 3D MIP images, assessment categories of the lesions were correlated as the results at routine MR images (p-value < 0.0001). 3D MIP detected additional two daughter nodules that were descriped foci at routine MR images and additional one nodule that was not detected at routine MR images. Conclusion : 3D MIP image has some limitations but is useful as additional image of routine breast MR Images.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.37C no.12
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• pp.1303-1309
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• 2012

In this paper, we propose a handover scheme for seamless mobile multicast service in next generation access networks. For this, we drew optimum handover scheme when applying MIP(mobile IP), FMIP(Fast MIP), HMIP(Heterogeneous MIP), PMIP(Proxy MIP) to XG-PON1. And, we analyze handover scheme for seamless mobile multicast service in XG-PON1. The prosed handover scheme remove tunnel convergence and reduces handover delay, packet delivery cost.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.18 no.2
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• pp.286-297
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• 1996

The proliferation of bone marrow stem cell compartment is thought to be under both positive and negative controls by cytokines and colony stimulation factors. Macrophage inflammatory $protein-1{\alpha}(MIP-1{\alpha})$ has been assessed for its potential to protect hematopoietic stem cells from cytotoxic effects of a cycle-specific antineoplastic agents. We have tested the ability of $MIP-1{\alpha}$ to suppress the proliferation of stem cell line Du.528.101 in variety of active status by using $[^{3}H]-thymidine$ incorporation test. The results were as follows. 1. The effect of $MIP-1{\alpha}$ on steady-state Du.528.101 cell represented the cell growth suppression at the concentration of 10, 50, 100nM of $MIP-1{\alpha}$(P<0.001). 2. $MIP-1{\alpha}$ stimulated the proliferation of Du.528.101 cells previously treated with IL-1 at the concentration of 5, 50nM of $MIP-1{\alpha}$(P<0.01). 3. The suppression effect of MIP-1 on Du.528.101 cells at the concentration of 5, 50nM was shown when cells were treated with $MIP-1{\alpha}$ before activation with $IL-1{\beta}(P<0.01)$. 4. The growth rate of synchronized cells were slower than that of non-synchronized ones, and $MIP-1{\alpha}$ represented the similar suppression effect on both synchronized and non-synchronized cells.

• The Korea Journal of Herbology
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• v.28 no.5
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• pp.113-119
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• 2013

Objectives : The purpose of this study was to investigate the effects of Angelicae Gigantis Radix Water Extract(AG) on the production of proinflammatory mediators in RAW 264.7 cells stimulated with lipopolysaccharide(LPS). Method : RAW 264.7 cells were cotreated with AG(50 and 100 ug/mL) and lipopolysaccharide(LPS; 1 ug/mL) for 24 hours. After 24 hour treatment, using Bead-based multiplex cytokine assay, concentrations of various cytokines such as interleukin(IL)-6, IL-$1{\beta}$, IL-10, tumor necrosis factor-alpha(TNF-${\alpha}$), granulocyte colony-stimulating factor(G-CSF), granulocyte macrophage colony-stimulating factor(GM-CSF), interferon inducible protein-10(IP-10), leukemia inhibitory factor(LIF), lipopolysaccharide-induced chemokine(LIX), monocyte chemoattractant protein-1(MCP-1), macrophage colony-stimulating factor(M-CSF), macrophage inflammatory protein(MIP)-$1{\alpha}$, MIP-$1{\beta}$, MIP-2, Regulated on Activation, Normal T cell Expressed and Secreted(RANTES) and vascular endothelial growth factor(VEGF) were measured. Result : AG significantly inhibited LPS-induced production of TNF-${\alpha}$, MIP-$1{\alpha}$, G-CSF, RANTES, IL-10, and M-CSF from LPS-stimulated RAW 264.7 cells at the concentrations of 50 and 100 ug/mL. AG significantly inhibited LPS-induced production of MIP-$1{\beta}$, MIP-2, GM-CSF, and IL-6 from LPS-stimulated RAW 264.7 cells at the concentrations of 50 ug/mL. AG significantly inhibited LPS-induced production of VEGF from LPS-stimulated RAW 264.7 cells at the concentrations of 100 ug/mL. But AG did not show any significant effect on the production of MCP-1, LIF, LIX, IP-10 and IL-$1{\beta}$ from LPS-induced RAW 264.7 cells. Conclusion : These results suggest that AG has anti-inflammatory effect related with its inhibition of proinflammatory mediators such as TNF-${\alpha}$, MIP-$1{\alpha}$, G-CSF, RANTES, IL-10, MIP-$1{\beta}$, MIP-2, GM-CSF, IL-6, VEGF and M-CSF in LPS-induced macrophages.

• Journal of Life Science
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• v.16 no.5
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• pp.840-849
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• 2006

Severe brain injuries induced by toxin pose one of the most important problems on our health care because of their high morbidity and mortality, are implicated to leucocyte infiltration more premature or immature brain than mature brain. Chemokines are the induction meditators for infiltration of inflammatory cells to the inflammation sites. In order to study the mechanism of leucocyte infiltration, the expression of several chemokines, MCP-1, $MIP-1{\alpha}$ and MIP-2 was studied in lipopolysaccharide(LPS)-stimulated neonatal and adult brain. One week old Sprague-Dawley rats or adult male rats weighing 300-350 g were used for the experiment. After anesthetization, $1\;{\mu}l$ LPS (0.5 mg/ml) subsequently was injected in the right caudate nucleus of the brain with stereotaxic frame. Animals were sacrificed at 6 hours, 24 hours, and 72 hours after injection. The present study was carried out using RT-PCR for the mRNA and immunohistochemistry for the expression of the proteins. In the neonatal rat brain, prominent interstitial edema with significant accumulation of leukocytes was detected at 24 and 72 hours after LPS injection. A semiquantitative analysis of RT-PCR revealed that the MCP-1, $MIP-1{\alpha}$, and MIP-2 mRNA expression peaked at 24 hours in neonatal and adult rat brain. Neonatal rats showed about 2.6, 1.4, and 1.2 times more expression of the MCP-1, $MIP-1{\alpha}$, and MIP-2 than that of the adult rats in the brain tissue. Immunohistochemical analysis also showed that MCP-1 immunoreactivity was paralleled with the RT-PCR results. MCP-1 protein was significantly detected at 24 and 72 hours in the brain parenchyma. $MIP-1{\alpha}$protein was highly expressed at 24 hours. The results of leukocyte infiltration in H&E stain was parallelled with that of the immunohistochemistry. Chemokine proteins were markedly detected at 24 hours after injection of LPS and neutrophil influx into intraparenchymal was prominent at 24 hours. These results suggest that the leukocyte infiltration in the intracranial infection may be controlled by mechanisms influenced by chemokine producing cells in the central nervous system such as microglia, astrocyte and endothelial cell.

• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.3
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• pp.330-336
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• 2014

This study aimed at examining the anti-inflammatory effects of Scutellariae Radix & Lonicerae Caulis water extract(SC). RAW 264.7 mouse macrophage cells were treated with $25{\sim}200{\mu}g/m{\ell}$ SC for 24 hours. Cell viability was then measured using MTT assays. The nitric oxide(NO) production and the creation of several cytokines in LPS-stimulated RAW 264.7 cells were investigated. SC inhibited significantly increasing the production of NO in LPS-induced RAW 264.7 cell at the density of 25, 50 and $200{\mu}g/m{\ell}$. SC inhibited significantly the TNF-${\alpha}$ of the RAW 264.7 cell induced by LPS at the density of $50{\mu}g/m{\ell}$. SC inhibited significantly the MIP-$1{\alpha}$ of the RAW 264.7 cell induced by LPS at the density of 25, 50 and $100{\mu}g/m{\ell}$. SC inhibited significantly the MIP-$1{\beta}$, MIP-2 at the density of 50, $100{\mu}g/m{\ell}$ in the RAW 264.7 cell increased by LPS, respectively. SC did not affect the production levels of VEGF in RAW 264.7 cell. As a result, SC significantly inhibited the inductions of MIP-$1{\alpha}$, MIP-$1{\beta}$, MIP-2 and NO in LPS-induced RAW 264.7 cell without causing the toxicity. These results signify that SC has anti-inflammatory effects on controlling the over inflammatory reaction on the RAW 264.7 cell.

• Journal of Periodontal and Implant Science
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• v.23 no.1
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• pp.48-55
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• 1993

Macrophage inflammatory $protein-1{\alpha}(MIP-1{\alpha})$ from activated T cell or macrophage, which is small inducible cytokine of unkown biological function, has been shown to display inflammation chemokinetic activities, as well as myelosuppressive effect on more immature progenitor cells. In this paper we show the $MIP-1{\alpha}$ mRNA expression and the presence of $MIP-1{\alpha}$ binding sites from murine macrophage cell line RAW 264.7, and primary cells of mouse bone marrow and spleen. $MIP-1{\alpha}$ mRNA was induced from LPS-stimulated RAW 264.7, but not inhibited by cyclosporin A treatment, and also was expressed from mouse splenocyted and bone marrow cell which were not increased by ferritin or lactoferrin treatment. The results of receptor binding assay showed that radiolabeled RAW 264.7 cell with kd value of 0.91 nM, and binding sites per cell of 378. bone marrow cell and splenocyte also appeared to have $MIP-1{\alpha}$ binding sites 33 and 11 per cell, respectiviely.

• The Korean Journal of Mycology
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• v.46 no.2
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• pp.161-176
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• 2018

Fungal ${\beta}$-glucan, known to have immunostimulatory and antitumor activities, can be recognized by host immune cells as one of the pathogen-associated molecular patterns (PAMPs). Although there are several reports on the diverse immunostimulatory activities of ${\beta}$-glucan, little is known about the intracellular signal transduction of ${\beta}$-glucan. Stimulation of RAW264.7 macrophage cells with ${\beta}$-glucan from Ganoderma lucidum induced the expressions of dectin-1, toll-like receptor 2 (TLR2), TLR4, and TLR6 at the transcription stage. Treatment with ${\beta}$-glucan also induced inflammatory mediators such as macrophage inflammatory proteins (MIP)-$1{\alpha}$, MIP-$1{\beta}$, MIP-$1{\gamma}$, interleukin (IL)-$1{\beta}$, and tumor necrosis factor (TNF)-${\alpha}$. Treatment of the cells with polymyxin B, an inhibitor of lipopolysaccharides (LPS), blocked the induction of inflammatory mediators in LPS- or ${\beta}$-glucan-stimulated systems. Pretreatment of the cells in our cell culture system with LY294002, a phosphoinositide 3-kinase (PI3K) inhibitor, or U0126, a mitogen-activated protein kinase/extracellular-signal-regulated kinase (MAPK/ERK) kinase (MEK)1/MEK2 inhibitor, led to a reduction in the induction of inflammatory mediators in a concentration-dependent manner. These results show that stimulation of the macrophage cells by ${\beta}$-glucan induced the expressions of both dectin-1 and TLRs. We also found that the PI3K/Akt and MEK pathways were involved in the induction of inflammatory mediators in macrophage cells during intracellular signal transduction of ${\beta}$-glucan.