• 생명과학회지
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• 제15권2호
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• pp.231-235
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• 2005

기질 금속단백분해효소(MMP)는 기저막이나 간질성 조직 등에 있는 세포외기질 성분을 분해하여 상처 치유, 태아의 발생, 종양세포의 침윤과 전이 등을 포함하여 조직이 재구성되는 과정에서 생리학적 및 병리학적인 과정 양쪽 모두에 매우 중요한 역할을 한다. 본 연구에서는 MMP-9 유전자의 발현을 억제하는 물질을 천연물에서 탐색하였고, 탐색된 시료 중에서 높은 역가를 가진 낙우송과의 Metasequoia glyptostroboides가 선택되었다. 여러 가지 flavonoid 성분을 가지고 있는 Metasequoia glyptostroboides를 이용하여 4개의 biflavonoid와 2개의 monoflavonoid 구조의 물질을 분리하였고, 이 flavonoid들은 sciadopitysin, isoginkgetin, bilobetin, 2, 3-dihydrohino-kiflavone, luteolin, apigenin으로 정제하여 구조를 밝히고 zymography, WST-1을 이용한 세포독성시험, northern blot 등의 실험을 통하여 각 화합물의 구조적인 특성과 함께 MMP-9 유전자 발현을 억제하는 효과가 있는 것을 확인하였다.

• Biomolecules & Therapeutics
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• 제24권1호
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• pp.25-32
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• 2016

Lichens have been known to possess multiple biological activities, including anti-proliferative and anti-inflammatory activities. Vascular cell adhesion molecule-1 (VCAM-1) may play a role in the development of atherosclerosis. Hence, VCAM-1 is a possible therapeutic target in the treatment of the inflammatory disease. However, the effect of lobaric acid on VCAM-1 has not yet been investigated and characterized. For this study, we examined the effect of lobaric acid on the inhibition of VCAM-1 in tumor necrosis factor-alpha (TNF-${\alpha}$)-stimulated mouse vascular smooth muscle cells. Western blot and ELISA showed that the increased expression of VCAM-1 by TNF-${\alpha}$ was significantly suppressed by the pre-treatment of lobaric acid ($0.1-10{\mu}g/ml$) for 2 h. Lobaric acid abrogated TNF-${\alpha}$-induced NF-${\kappa}B$ activity through preventing the degradation of $I{\kappa}B$ and phosphorylation of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK), and p38 mitogen activated protein (MAP) kinase. Lobaric acid also inhibited the expression of TNF-${\alpha}$ receptor 1 (TNF-R1). Overall, our results suggest that lobaric acid inhibited VCAM-1 expression through the inhibition of p38, ERK, JNK and NF-${\kappa}B$ signaling pathways, and downregulation of TNF-R1 expression. Therefore, it is implicated that lobaric acid may suppress inflammation by altering the physiology of the atherosclerotic lesion.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제34권1호
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• pp.28-35
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• 2008

Purpose: The nitric oxide (NO) release by inducible nitric oxide synthase (iNOS) is the key events in macrophage response to lipopolysaccharide (LPS) which is suggested to be a crucial mediator for inflammatory and innate immune responses. NO is an important mediator involved in many host defense action and may also lead to a harmful host response to bacterial infection. However, given the importance of iNOS in a variety of pathophysiological conditions, control of its expression and signaling events in response to LPS has been the subject of considerable investigation. Materials and Methods: The Raw264.7 macrophage cell line was used to observe LPS-stimulated iNOS expression. The expression of iNOS is observed by Western blot analysis and real-time RT-PCR. Protein kinase C $(PKC)-{\alpha}$ overexpressing Raw264.7 cells are established to determine the involvement of $PKC-{\alpha}$ in LPS-mediated iNOS expression. $NF-{\kappa}B$ activity is measured by $I{\kappa}B{\alpha}$ degradation and $NF-{\kappa}B$ luciferase activity assay. Results: We found that various PKC isozymes regulate LPS-induced iNOS expression at the transcriptional and translational levels. The involvement of $PKC-{\alpha}$ in LPS-mediated iNOS induction was further confirmed by increased iNOS expression in $PKC-{\alpha}$ overexpressing cells. $NF-{\kappa}B$ dependent transactivation by LPS was observed and $PKC-{\alpha}$ specific inhibitory peptide abolished this activation, indicating that $NF-{\kappa}B$ activation is dependent on $PKC-{\alpha}$. Conclusion: Our data suggests that $PKC-{\alpha}$ is involved in LPS-mediated iNOS expression and that its downstream target is $NF-{\kappa}B$. Although $PKC-{\alpha}$ is a crucial mediator in the iNOS regulation, other PKC isozymes may contribute LPS-stimulated iNOS expression. This finding is needed to be elucidated in further study.

• 한국재료학회지
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• 제5권5호
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• pp.598-605
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• 1995

Thin films of $YB_{2}Cu_{3}O_{7-d}$ were prepared on various substrated of MgO(100), $SrTiO_{3}$, and $LaAlO_{3}$ by using off-axis magentron sputtering methods and annealing in-situ. The prarameters of film fabrication processes had been optimized through a "follow the lcoal maxima" strategy to yield good quality films in therms of the critical temperature $T_{c}$ and the critical current density $J_{c}$. Optimizedproecsses employing a plane magndtron and an cylindrical magnetron yielded $T_{c}$>90K along with $J_{c}$$10^{6}$A/$\textrm{cm}^2$ at 77K and > 2${\times}$$10^{7}$A/$\textrm{cm}^2$ at 5K. The sampels, however, showed degradationinthe properties, after chemical etching for fabrication of microbridges with the line width of 2-10 mocrons. In particular, the value of $T_{c}$ for the microbridges of 2microns was as small as 80%. The degradation was strongly dependent on the line width through a formula : $T_{c}$(e)=$T_{c}$)b) [1-a exp(-1000 bL)} where $T_{c}$(e) and $T_{c}$ (b) are the values of $T_{c}$ in the absolute scale measured after and before chemical etching, respectively and L is the line width in mm. By utilizing a best fitting technique, the proper constant values of a and to b were found as exp(-1.2) and 0.22, respectively. This formula was very useful in estimatiing the upper limit of the device operationtemperature.

• 대한환경공학회지
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• 제31권10호
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• pp.865-872
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• 2009

슬러지의 감량과 최종처분 기술 개발을 위해 실험실 규모 호기성 소화공정을 279일간 운전하였다. 혐기성 소화 슬러지를 원료로 $40^{\circ}C$에서 120분간 알칼리 전처리하여 호기성 소화조에 유입시켰다. 유입 슬러지 성상과 HRT의 변화에 따라 소화효율의 변화가 있었으며 적정 HRT는 6일인 것으로 나타났다. 이때 $NH_3$-N, SCOD, TKN, TCOD, SS, VSS의 평균 제거율(소화조 유입 슬러지 기준)은 각각 97.4%, 81.7%, 68.7%, 61.4%, 50.6%, 47.0% 이었다. SS는 전처리와 호기성 소화를 통해 원료 슬러지(23,920 mg/L)의 73.9% 감량화가 가능하였다. 처리 슬러지는 약 350 mg/L의 SCOD를 포함하고 있어 액비로 활용하기에 무리가 없을 것으로 판단되었다. HRT를 5일 이상으로 유지할 경우 질산화 반응이 활성화되었으며 최대 658 mg/L의 유출 슬러지 질산성 질소 농도를 얻을 수 있었다. 암모니아성 질소 농도는 20 mg/L 내외로 크게 감소하였다.

• ETRI Journal
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• 제31권6호
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• pp.660-666
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• 2009

We investigate the effects of interfacial dielectric layers (IDLs) on the electrical properties of top-gate In-Ga-Zn-oxide (IGZO) thin film transistors (TFTs) fabricated at low temperatures below $200^{\circ}C$, using a target composition of In:Ga:Zn = 2:1:2 (atomic ratio). Using four types of TFT structures combined with such dielectric materials as $Si_3N_4$ and $Al_2O_3$, the electrical properties are analyzed. After post-annealing at $200^{\circ}C$ for 1 hour in an $O_2$ ambient, the sub-threshold swing is improved in all TFT types, which indicates a reduction of the interfacial trap sites. During negative-bias stress tests on TFTs with a $Si_3N_4$ IDL, the degradation sources are closely related to unstable bond states, such as Si-based broken bonds and hydrogen-based bonds. From constant-current stress tests of $I_d$ = 3 ${\mu}A$, an IGZO-TFT with heat-treated $Si_3N_4$ IDL shows a good stability performance, which is attributed to the compensation effect of the original charge-injection and electron-trapping behavior.

• IMMUNE NETWORK
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• 제13권6호
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• pp.283-288
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• 2013

The pro-inflammatory cytokines tumor necrosis factor-${\alpha}$ (TNF${\alpha}$) and interleukin (IL)-$1{\beta}$ are crucial mediators involved in chronic inflammatory diseases. Inflammatory signal pathways regulate inflammatory cytokine expression-mediated by p38 mitogen activated protein kinase (p38MAPK). Therefore, considerable attention has been given to p38MAPK as a target molecule for the development of a novel anti-inflammatory therapeutics. BIRB 796, one of p38MAPK inhibitor, is a candidate of therapeutic drug for chronic inflammatory diseases. In this study, we investigated the effect of BIRB 796 on inflammatory cytokine productions by lipopolysaccharide (LPS) in different immune cell types. BIRB 796 reduced LPS-mediated IL-8 production in THP-1 cells but not in Raw 264.7 cells. Further analysis of signal molecules by western blot revealed that BIRB 796 sufficiently suppressed LPS-mediated phosphorylation of p38MAPK in both cell types whereas it failed to block inhibitor of kappa B (I-${\kappa}B$) degradation in Raw 264.7 cells. Taken together, these results suggest that the anti-inflammatory function of BIRB 796 depends on cell types.

• 대한전자공학회논문지SP
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• 제46권6호
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• pp.78-87
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• 2009

본 논문은 IP 기반 비디오 서비스의 화질 측정을 위하여 새로운 비참조 기반의 블록 열화 측정 알고리즘을 제안한다. 제안하는 방법은 IP 기반 비디오 서비스의 화질 측정을 위하여, 네트워크에 의한 블록 열화와 영상 압축에 의한 블록 열화를 구분한다. 또한 비참조 기반으로 블록 열화를 검출하기 위하여, 주변 블록과의 차와 비디오 수신 단말기의 오류 수정 알고리즘의 패턴을 이용하고, 열화된 블록의 세기와 분포를 이용하여 화질 저하 원인을 측정한다. 제안한 방법의 정확도를 확인하기 위하여, SSCQE 방법을 이용한 MOS 실험 결과와 제안한 방법을 이용하여 화질 측정한 결과를 비교하였다. 기존 알고리즘에 비하여 블록 열화 측정의 정확도가 1.3배의 성능 향상된 것을 확인할 수 있었다.

• 수산경영론집
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• 제30권2호
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• pp.55-77
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• 1999

As the population grows, the importance of the fishery industry continues to rise. It is therefore vital to support and promote sustainable fishery industry. However, the fishery production has been declining, mainly due to overdevelopment and depletion in fishery resources and stricter limits on development limits caused by growing concerns over the marine environment and ecology. Recently, international activities related to marine environmental and its ecosystems conservation, have been vigorously pursued. The United Nations Convention on The Law of The Sea has stipulated the protection and conservation of the marine environment, and the implementation of fishery resources development, made in harmony with the environment and fishery resources and based upon scientific findings and principles has become important. Accordingly, fishery industry must pay thorough attention to marine ecological and environmental problems and its international fisheries regime. Fisheries development can affect fishery resources, their environment and ecosystems. Adverse ecological effects resulting from fishery resources development practices in general include overdevelopment and incidental development of non target species, physical degradation of seabed habitants and degraduation of water quality. It has now become more important than ever to build up fishery resources development while achieving the conservation of biodiversity and the marine environment, as well as the restoration of destroyed ecosystems. To maintain fishery industry, it is necessary to develop bioeconomic fishery production system and industry policies for the ESSD(environmentally sound and sustainable development) given that maintenance of a favourable marine environment will ensure the fishery resources productivity. These bioeconomic system and policies are necessary to ensure the sustainability and viability of the fishery industry under ESSD fisheries concepts.

• Journal of Ginseng Research
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• 제44권1호
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• pp.67-78
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• 2020

Background: Gintonin (GT), a novel ginseng-derived exogenous ligand of lysophosphatidic acid (LPA) receptors, has been shown to induce cell proliferation and migration in the hippocampus, regulate calcium-dependent ion channels in the astrocytes, and reduce β-amyloid plaque in the brain. However, whether GT influences autophagy in cortical astrocytes is not yet investigated. Methods: We examined the effect of GT on autophagy in primary cortical astrocytes using immunoblot and immunocytochemistry assays. Suppression of specific proteins was performed via siRNA. LC3 puncta was determined using confocal microscopy. Results: GT strongly upregulated autophagy marker LC3 by a concentration- as well as time-dependent manner via G protein-coupled LPA receptors. GT-induced autophagy was further confirmed by the formation of LC3 puncta. Interestingly, on pretreatment with an mammalian target of rapamycin (mTOR) inhibitor, rapamycin, GT further enhanced LC3-II and LC3 puncta expression. However, GT-induced autophagy was significantly attenuated by inhibition of autophagy by 3-methyladenine and knockdown Beclin-1, Atg5, and Atg7 gene expression. Importantly, when pretreated with a lysosomotropic agent, E-64d/peps A or bafilomycin A1, GT significantly increased the levels of LC3-II along with the formation of LC3 puncta. In addition, GT treatment enhanced autophagic flux, which led to an increase in lysosome-associated membrane protein 1 and degradation of ubiquitinated p62/SQSTM1. Conclusion: GT induces autophagy via mTOR-mediated pathway and elevates autophagic flux. This study demonstrates that GT can be used as an autophagy-inducing agent in cortical astrocytes.