• Journal of the Korean Society of Food Science and Nutrition
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• v.40 no.9
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• pp.1208-1214
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• 2011

Caffeine, a psychoactive stimulant, has been implicated in the modulation of learning and memory functions due to its action as a non-selective adenosine receptors antagonist. On the contrary, some side effects of caffeine have been reported, such as an increased energy loss and metabolic rate, decrease DNA synthesis in the spleen, and increased oxidative damage to exerted on LDL particles. Therefore, the aim of this study was to develop a safe stimulant from natural plants mixture (Aralia elata, Acori graminei Rhizoma, Chrysanthemum, Dandleion, Guarana, Shepherd's purse) that can be used as a substitute for caffeine. Thirty SD rats were divided into three groups; control group, caffeine group (15.0 mg/kg, i.p.), and natural plants mixture group (NP, 1 mL/kg, p.o.). The effect of NP extract on stimulant activity was evaluated with open-field test (OFT) and plus maze test for measurement of behavioral profiles. Plasma lipid profiles, lipid peroxidation in LDL (conjugated dienes), total antioxidant capacity (TRAP) and DNA damage in white blood, liver, and brain cells were measured. In the OFT, immobility time was increased significantly by acute (once) and chronic (3 weeks) supplementation of NP and showed a similar effect to caffeine treatment. Three weeks of caffeine treatment caused plasma lipid peroxidation and DNA damage in liver cells, whereas there were no changes in the NP group. NP group showed a higher plasma HDL cholesterol concentration compared to the caffeine group. The results indicate that the natural plants mixture had a stimulant effect without inducing oxidative stress.

• The korean journal of orthodontics
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• v.27 no.4 s.63
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• pp.607-621
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• 1997

GRP was known as the modulator of Pain transmission in central nervous system and local effector to peripheral tissue causing vasodilation, increased blood flow, modulation of immune sysem, stimulation of endothelial cell proliferation, and stimulation of bone formation. Numerous study, therefore, were done to elucidate involvement of CGRP to tooth movement. To investgate the response of CGRP immunoreactive nerve cells according to cell size in trigeminal ganglion during tooth movement, immunohistochemical study was performed using rat. Experimental rats(9 weeks old, 210 gm) were divided as six groups(normal(n=6), 3 hour group(n=5), 12 hour group(n=4), 1 day group(n=5), 3 day group(n=5), 7 day group(n=5)), and were applied orthodontic force (approximately 30 gm) to upper right maxillary molar. After frozen sections of trigeminal ganglions were immunostained using rabbit antisera, the changes of CGRP immunoreactive cells in regard to cell size distribution(small cell(upto $20{\mu}m$), medium cell($20-35{\mu}m$), large cell(above $35{\mu}m$)) were observed. The results were as follows 1. The percentage of CGRP immunoreactive cells to all nerve cells in trigeminal ganglion was 33.0% in normal control group, was decreased to 24.5% in 1 day group, and was increased to 41.8% in 7 day group. 2. The percentage of small, medium, and large cells expressing CGRP immunoreactivity in normal trigeminal ganglion to all CGRP immunoreactive cells were 51.3%, 44.0%, 4.7%, respectively. 3. The percentage of small cells with CGRP immunoreactivity to all CGRP immunopositive cells was increased in 3 hour and 12 hour groups. 4. The percentage of medium cells with CGRP immunoreactivity was increaed in 3 day and 7 day groups. 5. The percentage of large cells with CGRP immunoreactivity was increaed in 7 day group. Conclusively, the small cells with CGRP immunoreactivity in trigeminal ganglion respond to orthodontic force during initial phase of tooth movement, and later the medium and large cells with CGRP immunoreactivity respond

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.835-845
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• 1998

Background: Silica-induced lung diseases is characterized by the accumulation of inflammatory cells at early stage and fibrosis in pulmonary parenchyma and interstitium at late stage. As a consequence of inflammation, silicosis is accompanied with the expansion of interstitial collagen and the formation of fibrotic nodule. In this process, several kinds of lung cells produce cytokines which can amplify and modulate pulmonary fibrosis. The alveolar macrophage is a potent source of proflammatory cytokines and growth factor. But in the process of silicotic inflammation and fibrosis, there are many changes of the kinetics in cytokine network. And the sources of cytokines in each phase are not well known. Method: 2.5 mg of silica was instillated into the lung of C57BL/6J mice. After intratracheal instillation of silica, the lungs were removed for imunohistochemical stain at 1, 2, 7 day, 2, 4, 8, 12 week, respectively. We investigated the expression of IL-1$\beta$, IL-6, TNF-$\alpha$ and TGF-$\beta$ in lung tissue. Results: 1) The expression of IL-6 increased from 1 day after exposure to 8 weeks in vascular endothelium. Also peribronchial area were stained for IL-6 from 7 days and reached the peak level for 4 weeks. 2) The IL-1 $\beta$ was expressed weakly at the alveolar and peribronchial area through 12 weeks. 3) The TNF-$\alpha$ expressed strongly at alveolar and bronchial epithelia during early stage and maintained for 12 weeks. 4) TGF-$\beta$ was expressed strongly at bronchial epithelia and peribronchial area after 1 week and the strongest at 8 weeks. Conclusion: The results above suggests IL-6, TNF-$\alpha$ appear to be a early inflammatory response in silica induced lung fibrosis and TGF-$\beta$ play a major role in the maintenance and modulation of fibrosis in lung tissue. And the regulation of TNF-$\alpha$ production will be a key role in modultion of silica-induced fibrosis.

• Tuberculosis and Respiratory Diseases
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• v.43 no.6
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• pp.936-944
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• 1996

Background: Neutrophils or monocytes separated in vitro by the adherence to plastic surface are known to be activated by surface adherence itself and subsequent experimental data might be altered by surface adherence. Adhesion molecules and gene transcription of the inflammatory mediators are known to be associated in this process. To evaluate whether adhesion molecule and transcriptional activation of the inflammatory substances are also involved in the activation of human alveolar macrophage by the adherence procedure, we designed this experiment. Method : Bronchoalveolar lavage was performed in the person whose lung of either side was confirmed to be nonnal by chest cr and alveolar macrophage was harvested. To measure the expression of Interleukin-8(IL-8) mRNA, manganese superoxide dismutase(SOD) mRNA and CD11/CD18 mRNA in human alveolar macrophage of both adherence state and suspension state, Northern blot analysis was done at 0, 2, 4, 8 and 24hrs after the adherence to plastic surface and during suspension state. Then, phorbol myristate acetate(pMA) and N-formyl-methionyl-leucyl-phenylalanine(fMLP) were added respectively in the same experimental condition. Result : 1) Human alveolar macrophages in the adherent state induced IL-8 mRNA and SOD mRNA expression which was maximal at 8 hours after the adherence to plastic surface. But we could not observe the upregulation of CD18 mRNA by surface adherence. 2) PMA induced these mRNA expression both in the adherent cell and the nonadherem cells, but the induction of mRNA expression by fMLP occurred only in the adherent cells. Conclusion: These results suggest that adherence of huamn alveolar macropahge is an important cell-activating event that may play a critical role in the modulation of lung inflammatory respones.

• Korean Journal of Biological Psychiatry
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• v.14 no.2
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• pp.115-121
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• 2007

Objetives : Identification of target genes for ethanol in neurons is important for understanding its molecular and cellular mechanism of action and the neuropathological changes seen in alcoholics. The purpose of this study is to identify of altered gene expression after acute treatmet of ethanol in rat gliom cells. Methods : We used high density cDNA microarray chip to measure the expression patterns of multiple genes in cultured rat glioma cells. DNA microarrays allow for the simultaneous measurement of the expression of several hundreds of genes. Results : After comparing hybridized signals between control and ethanol treated groups, we found that treatment with ethanol increased the expression of 15 genes and decreased the expression of 12 genes. Upregulated genes included Orthodenticle(Drosophila) homolog 1, procollagen type II, adenosine A2a receptor, GATA bindning protein 2. Downregulated genes included diacylglycerol kinase beta, PRKC, Protein phosphatase 1, clathrin-associated protein 17, nucleoporin p58, proteasome. Conclusion : The gene changes noted were those related to the regulation of transcription, signal transduction, second messenger systems. modulation of ischemic brain injury, and neurodengeneration. Although some of the genes were previously known to be ethanol responsive, we have for the most part identified novel genes involved in the brain response to ethanol.

• Journal of the Institute of Electronics Engineers of Korea SD
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• v.47 no.2
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• pp.21-31
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• 2010

This paper presents a design of PLL and SSCG for reducing the EMI effect at the electronic machinery and tools for DisplayPort application. This system is composed of the essential element of PLL and Charge-Pump2 and Reference Clock Divider to implement the SSCG operation. In this paper, 270MHz/162MHz dual-mode PLL that can provide 10-phase and 1.35GHz/810MHz PLL that can reduce the jitter are designed for 2.7Gbps/162Gbps DisplayPort application. The jitter can be reduced drastically by combining 270MHz/162MHz PLL with 2-stage 5 to 1 serializer and 1.35GHz PLL with 2 to 1 serializer. This paper propose the frequency divider topology which can share the divider between modes and guarantee the 50% duty ratio. And, the output current mismatch can be reduced by using the proposed charge-pump topology. It is implemented using 0.13 um CMOS process and die areas of 270MHz/162MHz PLL and 1.35GHz/810MHz PLL are $650um\;{\times}\;500um$ and $600um\;{\times}\;500um$, respectively. The VCO tuning range of 270 MHz/162 MHz PLL is 330 MHz and the phase noise is -114 dBc/Hz at 1 MHz offset. The measured SSCG down spread amplitude is 0.5% and modulation frequency is 31kHz. The total power consumption is 48mW.

• Tuberculosis and Respiratory Diseases
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• v.40 no.2
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• pp.147-152
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• 1993

Background: There is evidence that platelet is activated in chronic obstructive pulmonary disease and activated platelet with injured endothelium contribute to the pathogenesis of pulmonary hypertension, prognostic factor of chronic obstructive pulmonary disease. So, we have investigated platelet function further in chronic obstructive pulmonary disease and effect of platelet activation on pulmonary hypertension. Method: We studied platelet aggregation ratio and alpha-granule products such as platelet factor 4(PF4) and beta-thromboglobulin (${\beta}$-TG) in control subjects and COPD without and with pulmonary hypertension subjects. Result: 1) The platelet aggregation ratio (PAR) was $0.99{\pm}0.04$ in control subjects, $0.98{\pm}0.05$ in COPD without pulmonary hypertension subjects and $0.89{\pm}0.08$ in COPD with pulmonary hypertension subjects. The platelet aggregation ratio of COPD subjects was tend to decrease than that of control subjects and the ratio of COPD with pulmonary hypertension subjects was significantly lower than that of control subjects. 2) The platelet factor 4 (PF4, IU/ml) was $4.7{\pm}1.2$ in control subjects, $18.6{\pm}4.9$ in COPD without pulmonary hypertension subjects and $57.2{\pm}12.7$ in COPD with pulmonary hypertension subjects. The level of COPD subjects was significantly higher than that of control subjects and the level of COPD with pulmonary hypertension subjects was significantly higher than that of COPD without pulmonary hypertension subjects. 3) The beta-thromboglobulin (${\beta}$-TG, IU/ml) was $34.4{\pm}5.8$ in control subjects, $80.4{\pm}18.1$ in COPD without pulmonary hypertension subjects and $93.0{\pm}14.0$ in COPD with pulmonary hypertension subjects. The level of COPD subjects was significantly higher than that of conrtrol subjects and the level of COPD with pulmonary hypertension subjects was tend to increase than that of COPD without pulmonary hypertension subjects. 4) There was no correlation between the clinical parameters and PAR, PF4 and ${\beta}$-TG but there was significant correlation among PAR, PF4 and ${\beta}$-TG. Conclusion: The platelet is activated in chronic obstructive pulmonary disease and the platelet of COPD with pulmonary hypertension is tend to be activated more than that of COPD without pulmonary hypertension. So, activated platelet may involve in the pathogenesis and maintenance of pulmonary hypertension in COPD subjects and modulation of platelet activity that might reduce pulmonary hypertension needs to be determined.

• Tuberculosis and Respiratory Diseases
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• v.52 no.2
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• pp.117-127
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• 2002

Backgroud : MUC1 mucin is a heavily glycosylated large glycoprotein and is expressed aberrantly in carcinoma. CD44 is polymorphic family of cell surface glycoproteins participating in cell-cell adhesion and modulation of the cell-matrix interaction. MUC1 mucin and CD44 expression have been implicated in a tumor invasion and metastasis in certain malignancies. In this study, the expression of MUC1 and the standard form of CD44 (CD44s) was examined in non-small cell lung cancer (NSCLC). Methods : Immunohistochemical staining using monoclonal antibodies including MUC1 glycoprotein and CD44s was performed on 80 NSCLC surgical specimens. The association between MUC1 and CD44s expression and the histological type and tumor stage was investigated. Results : Depolarized MUC1 expression in more than 10% of cancer cells was found in 12 (27.9%) out of 43 squamous cell carcinomas (SCCs) and 12 (32.4%) out of 37 adenocarcinomas (ACs). It was not associated with the tumor histological type and the TNM-stage in SCCs. Depolarized MUC1 expression correlated with the N-stage in ACs (p=0.036). CD44s was expressed in 36 (83.7%) out of 43 SCCs and 14 (37.8%) out of 37 ACs. Reduced CD44s expression correlated with the N-stage (p=0.031) and the TNM-stage (p=0.006) in SCCs. Conclusions : Depolarized MUC1 expression was related to the nodal stage in NSCLC adenocarcinoma. Reduced CD44s expression was related to nodal involvement and the TNM-stage in squamous cell carcinoma. This suggests that MUC1 and CD44s expression in NSCLC might play important roles in tumor progression and cap be used as prognostic variables.

• Journal of Life Science
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• v.17 no.10
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• pp.1447-1451
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• 2007

Through the screening of marine natural compounds that inhibit cancer cell proliferation, we previously reported that pectenotoxin-2 (PTX-2) isolated from marine sponges exhibits selective cytotoxicity against several cell lines in p53-deficient tumor cells compared to those with functional p53. However, the molecular mechanisms of its anti-proliferative action on malignant cell growth are not completely known. To further explore the mechanisms of its anti-cancer activity and to test whether the status of p53 in liver cancer cells correlates with their chemo-sensitivities to PTX-2, we used two well-known hepatocarcinoma cell lines, p53-deficient Hep3B and p53-wild type HepG2. We have demonstrated that PTX-2 markedly inhibits Hep3B cell growth and induces apoptosis whereas HepG2 cells are much more resistant to PTX-2 suggesting that PTX-2 seems to act by p53-independent cytotoxic mechanism. The apoptosis induced by PTX-2 in Hep3B cells was associated with the modulation of DNA fragmentation factor (DFF) family proteins, up-regulation of pro-apoptotic Bcl-2 family members such as Bax and Bcl-xS and activation of caspases (caspase-3, -8 and -9). Blockade of the caspase-3 activity by caspase-3 inhibitor, z-DEVD-fmk, prevented the PTX-2-induced growth inhibition in Hep3B cells. Moreover, treatment with PTX-2 also induced phosphorylation of AKT and extracellular-signal regulating kinase (ERK), but not c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MARK). Specific inhibitors of PI3K inhibitor (LY294002) and ERK1/2 inhibitor (PD98059) significantly blocks PTX-2-induced-anti-proliferative effects, whereas a JNK inhibitor (SP600125) and a p38 MAPK inhibitor (SB203580) have no significant effects demonstrating that the pro-apoptotic effect of PTX-2 mediated through activation of AKT and ERK signal pathway in Hep3B cells.

• Journal of the Korean Society of Food Science and Nutrition
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• v.34 no.6
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• pp.805-813
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• 2005

In our previous study, a novel herb mixture (HIM-I) of Angelim gigas radix, Cnidium officinale rhizoma, and Paeonia japonica radix was developed to protect the intestinal and immune systems and promote its recovery against radiation damage. In this study, a new herbal preparation (HemoHIM) with the high immune modulating activity was developed from HIM-I. HIM-I was fractionated into ethanol fraction (HIM-I-E) and polysaccharide fraction (HIM-I-P). And HemoHIM was prepared by adding HIM-I-P to HIM-I. The protective activities against $\gamma$ -irradiation were compared among HemoHIM, HIM-I and the fractions. HemoHIM and HIM-I significantly decreased the radiation-induced DNA damage in vitro, and scavenged hydroxyl radicals in a dose-dependent manner. HemoHIM showed similar activity to HIM-I. In vitro proliferation assay with mouse lymphocytes and bone marrow cells showed that HIM-I-P was remarkably higher than HIM-I and HIM-I-E in cell proliferating activity. HemoHIM showed higher activity than HIM-I and this might be associated with the higher polysaccharide content. The in vivo protective effects of HemoHIM and HIM-I were investigated in $\gamma$-irradiated mice. HemoHIM increased the surviving intestinal crypts to a similar extent compared with HIM-I. In contrast, HemoHIM appeared to be more effective than HIM-I in endogenous spleen colony formation assay. The recovery of white blood cells and lymphocytes in irradiated mice were significantly enhanced by the administration of HemoHIM. Also HemoHIM administration prolonged the survival of irradiated mice. These results showed that the novel herbal preparation, HemoHIM, effectively protected the self-renewal tissues and immune system, and promoted the survival of irradiated mice. Moreover, in comparison with HIM-I, HemoHIM maintained similar activity in the reduction of oxidative damage of self-renewal tissue but exhibited the higher activity in protection and proliferation of immune and hematopoietic cells. These results suggested that HemoHIM might be more effective than HIM-I in immune modulation as well as radioprotection.