• The Journal of the Petrological Society of Korea
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• v.9 no.2
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• pp.70-83
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• 2000

The purpose of this study is to identify the petrographic and geochemical characteristics of four granitic masses and clanfy for the origin and relationship among the masses. These granitic rocks are distributed in the eastern part of Yangsan fault in the Kyongsang basin, southeastern part of Korea. Based on the mineralogy and texture, the granitic rocks are divided into three facies; granodiorite, porphyritic fine-grained granite, and equigranular granite. According to the result of modal analysis, northern part and most of the southern part of Daebon granitic rocks are plotted in granodiorite field and the rest part of the xocks are plotted in granite field. These granitic rocks belong to the sub-alkaline series, and are subdivided into calc-alkaline series. The rare earth elements normalized bv chondrite show LREE is more enriched than HREE and the lowest values in O-w m- i t e and Daebon equigranular granite. The crystallization pressures and temperatures of minimum melt compositions of granitic rocks estimated from the study area are about 0.5-1 kbar and $700~820^{\circ}C$, respectively. Referring to the petrographic characteristics, geochemical data and radiogenic age data, Oyu granite was emplaced in the Paleocene, but Daebon granodiorite, Sanseo porphyritic granite, and Hoam equigranular granite are co-magmatic differentiation products, were emplaced in the Eocene.

• Journal of Astronomy and Space Sciences
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• v.21 no.4
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• pp.283-294
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• 2004

New BV RI photometric observations of the contact binary AH Tau were performed with the 61 cm reflector and a 2K CCD camera at the Sobaeksan Optical Astronomy Observatory during seven nights from September to December, 2001. A total of 144 times of minima observed up to date, including three times of minima obtained from our observation, were analyzed. It is found that the orbital period of AH Tau has varied in a cyclic way superposed on a secular period decrease. The rate of the secular period decrease is calculated to be $1^s$ .04 per century, implying that a mass of about $3.8{\times}10^{-8}M{\odot}/yr$ from the more massive primary flows into the secondary if a conservative mass transfer is assumed. Assuming that the sinusoidal period variation is produced by a light-time effect due to an unseen third body, the resultant semi-amplitude, period, and eccentricity for the deduced light-time orbit are obtained as 35.4 years, 0.014 day and 0.52, respectively. The mass of the third-body is calculated as a tout $0.24M{\odot}$ when the third body is assumed to be coplanar with AH Tau system.

• Journal of Acupuncture Research
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• v.19 no.5
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• pp.219-233
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• 2002

면역억제활성이 알려진 Cerves korean TEMMINCK var. manchur-icus Swinhoe(Nokyong) 약침(CPH)은 다모 뿔의 녹용을 열수추출한 용액이다. 본 연구에서는 녹용 약침의 효과를 adjuvant 유발 관절염 실험용쥐를 이용하여 골체, 골강도 및 골대체율의 감소를 평가하였다. 위의 골 대사 관련 검정실험을 위하여 6주령의 암컷 실험용쥐에 20일간 약물투여를 실시하였다. 실험적인 관절염유발은 실험용쥐의 뒤쪽 다리에 Adjuvant를 주사하여 유발시킨 결과, 요부의 골 무기질함량과 밀도(BMC, BMD) 그리고 압축강도는 관절염 실험용쥐에서 감소되었다. 10일 경과 후 골형성도(BFR/BS, BFR/BV)의 조직형태학적 기준척도인 혈청 osteocalcin 수가 정상대조군과 비교해 볼 때 현저하게 감소되었다. 그러나, 몸무게로 나눈 BMC치는 관절염 유발군과 정상군 사이에 큰 차이가 보이지 않았다. 그리고 골무기질 함량은 정상군에 비해 감소하지 않았다. 20일 경과후 몸무게로 나누거나 나누지 않은 BMC치 모두, 관절염 군에서 요부 몸체의 골무기질 함량과 강도가 정상군과 비교해 볼 때 현저하게 감소되었다. 잔존 소주(小柱)의 무기질 침착 표면은 현저하게 감소하였으며 파골 세포의 수는 증가하였다. 초기부터 매일 Shinsu(B23)에 CPH 약침 투여(10, 20, $50{\mu}g/kg$)는 20일 경과후 만성적인 다리 부종을 현저하게 방지하였으며, 골 무기질함량, 골강도 및 소주골 형성등의 감소와 파골세포수 증가도 완화하였다. Adjuvant주사로 장애를 받았던 연령대비 요부 길이 증가도 유지되었다. 이러한 결과는 Adjuvant에 의한 관절염 실험용쥐의 2차적인 골관절염에서 충분히 요추 몸체뼈와 강도 감소를 나타내기 위해서는 적어도 20일이 필요하다는 것을 제시하였다. 본 결과로부터 CPH가 실험용쥐의 관절염에 대한 골체, 골강도 및 골대체율을 조절하는데 유효하게 작용하고 있음을 알 수 있었다.

• IMMUNE NETWORK
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• v.6 no.1
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• pp.27-32
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• 2006

Background: Chronic inflammation in the brain has known to be associated with the development of a various neurological diseases including dementia. In general, the characteristic of neuro-inflammation is the activated microglia over the brain where the pathogenesis occurs. Pro-inflammatory repertoires, interleukin-1${\beta}$ (IL-1${\beta}$) and nitric oxide (NO), are the main causes of neuro-degenerative disease, particularly in Alzheimer's disease (AD) which is caused by neuronal destruction. Those pro-inflammatory repertoires may lead the brain to chronic inflammatory status, and thus we hypothesized that chronic inflammation would be inhibited when pro-inflammatory repertoires are to be well controlled by inactivating the signal transduction associated with inflammation. Methods: In the present study, we examined whether biphenyl dimethyl dicarboxylate (DDB), an active compound from Schizandra chinensis Baillon, inhibits the NO production by a direct method using Griess reagent and by RT-PCR in the gene expression of inducible nitric oxide synthase (iNOS) and IL-1${\beta}$. Western blots were also used for the analysis of NF-${\kappa}B$ and I${\kappa}B$. Results: In the study, we found that DDB effectively inhibited IL-1${\beta}$ as well as NO production in BV-2 microglial cell, and the translocation of NF-${\kappa}B$ was comparably inhibited in the presence of DDB comparing those to the positive control, lipopolysaccharide. Conclusion: The data suggested that the DDB from Schizandra chinensis Baillon may play an effective role in inhibiting the pro-inflammatory repertoires which may cause neurodegeneration and the results imply that the compound suppresses a cue signal of the microglial activation which can induce the brain pathogenesis such as Alzheimer's disease.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.12 no.10
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• pp.4359-4368
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• 2011

Among several macroeconomic missteps blamed for the recent global financial crisis including the social problems of income distribution and the lack of proper financial remedies, two of them have received particular attention: the global BOP(Balance of Payment) imbalance and the misguided monetary policy. Such BOP imbalance was blamed for massive foreign exchange investment flows from Asia into the U.S., triggering the financial and real estate bubble in America. The latter refers to the excessively loose monetary policy of the U.S. Federal Reserve, which pushed financial institutions and households into reckless investment behavior in search of higher returns. Given the abuse of certain innovative financial techniques and new investment instruments that have been created in recent decades, both collateralized debt obligations (CDOs) and credit default swaps (CDS) enjoyed a symbiotic and toxic relationship prior to the financial crisis This paper is organized as follows: The first section analyzes the real causes of the recent financial crisis. The second details the role of CDOs and CDS. Then, to identify key determinants of the CDS spreads in an emerging capital market, the sample data of major Korean firms' CDS spreads are used to estimate the risk premium by utilizing the multiple regression analysis. The empirical test result indicates that Korean 3-year treasury bond rate(TYIELD), market to book value ratio(MV/BV), and assets size(INASSETS) are shown to demonstrate statistically significant influences on the changes of the CDS premium for sample firms.

• The Journal of Internal Korean Medicine
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• v.31 no.2
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• pp.254-263
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• 2010

Objectives : The neuroprotective effects of bee venom (BV) have been demonstrated in many studies, but bee venom has many side effects. So we used sweet bee venom (SBV), which has high molecular elements removed to reduce the side effects. I examined the neuroprotective effect of sweet bee venom in 1-methyl-4-phenylpyridine ($MPP^+$)-induced human neuroblastoma SH-SY5Y cells. Methods : To observe the possible toxicity of SBV itself, SH-SY5Y cells were treated with SBV in various concentrations for 3 h and $MPP^+$ in concentrations (1 and 5mM) for 24h. To investigate the protective effect of SBV against $MPP^+$ toxicity, SH-SY5Y cells were pretreated with vehicle or nontoxic concentrations of SBV for 3h and the cells were not washed, followed by incubation with respective concentrations of SBV and 1 mM $MPP^+$ for 24h. To investigate the protective effect of SBV against $MPP^+$ toxicity, SH-SY5Y cells were pretreated with vehicle or nontoxic concentrations of SBV for 3h and the cells were not washed, followed by incubation with respective of SBV(0.5%), 1 mM $MPP^+$, 5uM AKT inhibitor(LY984002) and 10uM ERK inhibitor(PD98059) for 24 h. The protective effect was measured by cell viability assay. To investigate the degree of apoptosis, caspase-3 enzyme activity was measured in control, $MPP^+$, SBV+$MPP^+$. Results : SBV (0.5%) pretreatment protected the SH-SY5Y cells against $MPP^+$-induced apoptotic cell death. The cell viability was higher in the SH-SY5Y cells that were pretreated with vehicle or nontoxic concentrations of SBV than those not pretreated. The caspase-3 activity was lower in the pretreated groups than these not pretreated. ERK and AKT enzymes have a role in the neuroprotective effects of the sweet bee venom. Conclusions : The results demonstrate that SBV has a protective effect on dopaminergic neurons against $MPP^+$ toxicity. This data suggest that SBV could be a potential therapeutic tool for neurodegenerative diseases such as Parkinson's disease(PD).

• Journal of Life Science
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• v.25 no.6
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• pp.656-662
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• 2015

Natural products and natural product structures play a general and highly significant role in drug discovery and development process because it has various merits and potentials for new drug source that have extensive clinical experience, development time contraction, excellent stability and safety. In several neurological disorders, neuronal death and excessive activation of microglia (neuro-inflammation) are observed. A number of drug discovery-related neuronal cell death and neuro-inflammation was studied from natural products, respectively. However, until now, it has not been possible to study dual-protection molecules recorded in the Natural Product library. In the present study, using the natural product-derived library of the Institute for Korea Traditional Medical Industry, we investigated dual-protective molecules against glutamate (a classical excitatory neurotransmitter)-induced oxidative stress mediated neuronal cell death and LPS-induced excessive activated microglial cells (immune cells of the brain). Chrysophanol, extracted from Rheum palmatum, had dual-protective effects against both glutamate-induced neuronal cell death and LPS-induced NO production, triggering proinflammatory cytokines and microglia activation and resulting in neuroinflammation. Flow-cytometry analysis revealed that chrysophanol had a scavenger effect, scavenging glutamate- and LPS-induced reactive oxygen species (ROS) produced by neuronal and microglial cells, respectively. Based on the present study, chrysophanol may have an important protective role against neuronal cell death and neuroinflammation in the brain. The results may be helpful for studying drug development candidates for treating central nervous system disorders.

• Journal of Life Science
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• v.30 no.11
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• pp.939-946
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• 2020

Stroke is one of the leading causes of neurological disability worldwide and stroke patients exhibit a range of motor, cognitive, and psychiatric impairments. GPR88 is an orphan G protein-coupled receptor (GPCR) that is highly expressed in striatal medium spiny neurons; its deletion results in poor motor coordination and motor learning. There are currently no studies on the involvement of GPR88 in stroke or in post-stroke brain function recovery. In this study, we found a decrease in GPR88 protein and mRNA expression levels in an ischemic mouse model using Western blot and real-time PCR, respectively. In addition, we observed that, among the three types of cells derived from the brain (brain microvascular endothelial cells, BV2 microglial cells, and HT22 hippocampal neuronal cells), the expression of GPR88 was highest in HT22 neuronal cells, and that GPR88 expression was downregulated in HT22 cells under oxygen-glucose deprivation (OGD) conditions. Moreover, pretreatment with RTI- 13951-33 (10 mg/kg), a brain-penetrant GPR88 agonist, ameliorated brain injury following ischemia, as evidenced by improvements in infarct volume, vestibular-motor function, and neurological score. Collectively, our results suggest that GPR88 could be a potential drug target for the treatment of central nervous system (CNS) diseases, including ischemic stroke.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.219-228
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• 2015

Excessive microglial activation and subsequent neuroinflammation lead to synaptic loss and dysfunction as well as neuronal cell death, which are involved in the pathogenesis and progression of several neurodegenerative diseases. Thus, the regulation of microglial activation has been evaluated as effective therapeutic strategies. Although dieckol (DEK), one of the phlorotannins isolated from marine brown alga Ecklonia cava, has been previously reported to inhibit microglial activation, the molecular mechanism is still unclear. Therefore, we investigated here molecular mechanism of DEK via extracellular signal-regulated kinase (ERK), Akt and nicotinamide adenine dinuclelotide phosphate (NADPH) oxidase-mediated pathways. In addition, the neuroprotective mechanism of DEK was investigated in microglia-mediated neurotoxicity models such as neuron-microglia co-culture and microglial conditioned media system. Our results demonstrated that treatment of anti-oxidant DEK potently suppressed phosphorylation of ERK in lipopolysaccharide (LPS, $1{\mu}g/ml$)-stimulated BV-2 microglia. In addition, DEK markedly attenuated Akt phosphorylation and increased expression of $gp91^{phox}$, which is the catalytic component of NADPH oxidase complex responsible for microglial reactive oxygen species (ROS) generation. Finally, DEK significantly attenuated neuronal cell death that is induced by treatment of microglial conditioned media containing neurotoxic secretary molecules. These neuroprotective effects of DEK were also confirmed in a neuron-microglia co-culture system using enhanced green fluorescent protein (EGFP)-transfected B35 neuroblastoma cell line. Taken together, these results suggest that DEK suppresses excessive microglial activation and microglia-mediated neuronal cell death via downregulation of ERK, Akt and NADPH oxidase-mediated pathways.

• Journal of Food Hygiene and Safety
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• v.23 no.3
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• pp.248-256
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• 2008

To investigate the epidemiological characteristics of 68 Listeria monocytogenes isolates, including 11 reference strains and 57 isolates from imported US beef, domestic meats(beef, pork, chicken meat), raw milk, and milk plants. L. monocytogenes was to evaluate the production of virulence proteins, such as hemolysin(LLO) and lecithinase(LCP), the adsorption of Congo red(CRA), and to detect virulence genes using the polymerase chain reaction(PCR). In the study of virulence protein production, 68(100%), 62(91.2%), and 54(79.4%) of the 68 L. monocytogenes strains were positive for LLO production, the LCP test, and the CRA test, respectively, while strains of other species, such as L. innocua, L. gray, L. murrayi, and L. welshimeri, were not. There were no significant differences between L. monocytogenes serotypes and the ability to produce LLO or LCP. L. monocytogenesstrains had very high hemolytic titers(2 to 16 fold), while the other Listeria species, other than L. ivanovii and L. seeligeri, did not. The hemolysin activities of L. monocytogenes, L. ivanovii, and L. seeligeri usually exceeded 1.0 HU/mg, while those of other Listeria spp. were less than 0.04 HU/mg. In the PCR assay, all of the L. monocytogenes strains contained the hlyA, plcA, plcB, inlA, and inlB virulence genes and produced a product of the expected size. In the PCR of the actA gene, the expected 385-bp product was seen in 39(57.4%) L. monocytogenesstrains, while an unexpected 268-bp product was seen in 29(42.6%) strains. Most L. monocytogenes strains isolated from Hanwoo beef produced the 385-bp actA gene product, while strains of imported US beef usually produced the 268-bp actA gene product. By contrast, no virulence gene products were amplified in the other Listeria spp.