Oh, Yoon Jung;Kim, Young Sun;Choi, Young In;Shin, Seung Soo;Park, Joo Hun;Choi, Young Hwa;Park, Kwang Joo;Park, Rae Woong;Hwang, Sung Chul
Tuberculosis and Respiratory Diseases
/
v.58
no.1
/
pp.31-42
/
2005
Background : Peroxiredoxins (Prxs) are a relatively newly recognized, novel family of peroxidases that reduce $H_2O_2$ and alkylhydroperoxide into water and alcohol, respectively. There are 6 known isoforms of Prxs present in human cells. Normally, Prxs exist in a head-to-tail homodimeric state in a reduced form. However, in the presence of excess $H_2O_2$, it can be oxidized on its catalytically active cysteine site into inactive oxidized forms. This study surveyed the types of the Prx isoforms present in the pulmonary epithelial, macrophage, endothelial, and other cell lines and observed their response to oxidative stress. Methods : This study examined the effect of exogenous, excess $H_2O_2$ on the Prxs of established cell lines originating from the pulmonary epithelium, macrophages, and other cell lines, which are known to be exposed to high oxygen partial pressures or are believed to be subject to frequent oxidative stress, using non-reducing SDS polyacrylamide electrophoresis (PAGE) and 2 dimensional electrophoresis. Result : The addition of excess $H_2O_2$ to the culture media of the various cell-lines caused the immediate inactivation of Prxs, as evidenced by their inability to form dimers by a disulfide cross linkage. This was detected as a subsequent shift to its monomeric forms on the non-reducing SDS PAGE. These findings were further confirmed by 2 dimensional electrophoresis and immunoblot analysis by a shift toward a more acidic isoelectric point (pI). However, the subsequent reappearance of the dimeric Prxs with a comparable, corresponding decrease in the monomeric bands was noted on the non-reducing SDS PAGE as early as 30 minutes after the $H_2O_2$ treatment suggesting regeneration after oxidation. The regenerated dimers can again be converted to the inactivated form by a repeated $H_2O_2$ treatment, indicating that the protein is still catalytically active. The recovery of Prxs to the original dimeric state was not inhibited by a pre-treatment with cycloheximide, nor by a pretreatment with inhibitors of protein synthesis, which suggests that the reappearance of dimers occurs via a regeneration process rather than via the de novo synthesis of the active protein. Conclusion : The cells, in general, appeared to be equipped with an established system for regenerating inactivated Prxs, and this system may function as a molecular "on-off switch" in various oxidative signal transduction processes. The same mechanisms might applicable other proteins associated with signal transduction where the active catalytic site cysteines exist.
Kim, Jong-Myung;Yu, Ji-Min;Bae, Yong-Chan;Jung, Jin-Sup
Journal of Life Science
/
v.21
no.5
/
pp.631-646
/
2011
Mesenchymal stem cells (MSC) are multipotent and can be isolated from diverse human tissues including bone marrow, fat, placenta, dental pulp, synovium, tonsil, and the thymus. They function as regulators of tissue homeostasis. Because of their various advantages such as plasticity, easy isolation and manipulation, chemotaxis to cancer, and immune regulatory function, MSCs have been considered to be a potent cell source for regenerative medicine, cancer treatment and other cell based therapy such as GVHD. However, relating to its supportive feature for surrounding cell and tissue, it has been frequently reported that MSCs accelerate tumor growth by modulating cancer microenvironment through promoting angiogenesis, secreting growth factors, and suppressing anti-tumorigenic immune reaction. Thus, clinical application of MSCs has been limited. To understand the underlying mechanism which modulates MSCs to function as tumor supportive cells, we co-cultured human adipose tissue derived mesenchymal stem cells (ASC) with cancer cell lines H460 and U87MG. Then, expression data of ASCs co-cultured with cancer cells and cultured alone were obtained via microarray. Comparative expression analysis was carried out using DAVID (Database for Annotation, Visualization and Integrated Discovery) and PANTHER (Protein ANalysis THrough Evolutionary Relationships) in divers aspects including biological process, molecular function, cellular component, protein class, disease, tissue expression, and signal pathway. We found that cancer cells alter the expression profile of MSCs to cancer associated fibroblast like cells by modulating its energy metabolism, stemness, cell structure components, and paracrine effect in a variety of levels. These findings will improve the clinical efficacy and safety of MSCs based cell therapy.
Mutations in Fused in Sarcoma (FUS) have been identified in patients with amyotrophic lateral sclerosis (ALS) or Frontotemporal Dementia (FTD). Pathological FUS is mis-localized to cytosol and forms aggregates associated with stress granules (SG), while FUS is normally localized to nucleus. However, it is largely unknown how pathological FUS forms SG-aggregates and which domains are responsible for this process. In this study, we examined cellular localization and aggregation of ALS-linked FUS missense mutants (P525L, R521C, R521H, R521G), analyzed the domains responsible for cytosolic FUS aggregation in HEK293T cells, and confirmed this in cultured mouse neurons. To do this, we firstly generated missense mutants of FUS and then examined their cellular localization. We found that P525L was mostly mis-localized to cytosol and formed FUS-positive SG aggregates while R521C, R521H, or R521G was localized to both nucleus and cytosol. To further characterize the domains required for aggregate formation of cytosolic FUS, we generated different domain-deletion mutants using FUS-∆17 which has a deletion of nuclear localization signal. Interestingly, cytosolic FUS without SYGQ and RGG1 domain or cytosolic FUS without RGG2-ZnF-RGG3 domain did not form FUS-positive SG aggregates, while cytosolic FUS without RRM domain generated more aggregates compared to FUS-∆17. Taken together, these data suggest that SYGQ-RGG1 or RGG2-ZnF-RGG3 domain contributes to formation of cytosolic aggregate, while RRM domain might interfere with FUS aggregation. Therefore, our studies will provide important insight for understanding cellular pathogenesis of neurodegeneration associated with FUS aggregate as well as finding therapeutic targets for ALS or FTD.
Ji, Cheol;Cho, Kyung-Keun;Lee, Kyung Jin;Park, Sung Chan;Cho, Jung Ki;Kang, Joon Ki;Choi, Chang Rak
Journal of Korean Neurosurgical Society
/
v.30
no.3
/
pp.263-271
/
2001
Objective : Glioblastomas, the most common type of primary brain tumors, are highly invasive and cause massive tissue destruction at both the tumor invading edges and in areas that are not in direct contact with glioma cells. As a result, patients with high-grade gliomas are faced with a poor prognosis. Such grim statistics emphasize the need to better understand the mechanisms that underlie glioma invasion, as these may lead to the identification of novel targets in the therapy of high grade gliomas. Protein kinase C(PKC) is a family of serine/threonine kinases and an important signal transduction enzyme that conveys signals generated by ligand-receptor interaction at the cell surface to the nucleus. PKC appears to be critical in regulating many aspects of glioma biology. The purpose of this study was to assess accurately the role of PKC in the invasion regulation of human gliomas based on hypothesis that protein kinase C(PKC) is functional in the process of glial tumor cell invasion. Method : To test this hypothesis, U-87 malignant glioma cell line intracellular PKC levels were up and down regulated and their invasiveness was tested. Intracellular PKC level was characterized using PKC activity assays. Invasion assays including barrier migration and spheroid confrontation were used to study the relationship between PKC concentration and invasiveness. Result : The cell line which were treated by PKC inhibitor tamoxifen and hypericin exhibited decreased PKC activity and decreased invasive abilities dose dependently both in matrigel invasion assay and tumor spheroid fetal rat brain aggregates(FRBA) confrontation assay. However, the cell line that was treated by PKC activator 12-O-tetradecanylphorbol-13acetate(TPA) did not exhibit increases in either PKC activity or invasive ability. Conclusion : These studies suggest that PKC may be a useful molecular target for the chemotherapy of glioblastoma and other malignancies and that a therapeutic approach based on the ability of PKC inhibitors may be helpful in preventing invasion.
Park, Sun Young;Lee, Sung Hoon;Kim, Eun Joo;Choi, So Woong;Kim, Ji Young;Cho, Seong A;Cho, Jun Cheol;Lee, Hae Kwang
Journal of the Society of Cosmetic Scientists of Korea
/
v.40
no.2
/
pp.195-201
/
2014
Body fluid has been studied for diverse fields like Ringer's solutions, artificial joint fluids, cell growth culture media because it plays a crucial role in controlling body temperature and acts as a solvent for diverse metabolite processes in the body and delivery media of mineral, energy source, hormone, signal and drug from and to cell via blood or lymphatic vessel by osmotic pressure or active uptake. Stratum corneum containing extracellular lipids and NMF (natural moisturizing factor) absorbs atmospheric water residing outside of cells and utilize it to hydrate inside of their own. This process is related to skin barrier function. In this study, we conducted the cell viability test with Cell Bio Fluid $Sync^{TM}$, which mimicks body fluids including amino acids, peptides, and monosaccharides to strengthen skin barrier, and the clinical skin improvement test with cosmetics containing Cell Bio Fluid $Sync^{TM}$. In the cell viability test, HaCaT cell was treated with PBS for 3 hours, followed by the treatment of a cell culture medium (DMEM) and isotonic solution (PBS) and Cell Bio Fluid $Sync^{TM}$ for 3 hours each. Then, MTT assay and image analysis were conducted. In the clinical skin improvement test, twenty-one healthy women participated. Participants applied cosmetics containing Cell Bio Fluid $Sync^{TM}$ on their face for a week and evaluated the skin hydration, skin roughness, brightness and evenness. All measurements were conducted after they washed off their face and took a rest under the constant temperature ($22{\pm}2^{\circ}C$) and constant humidity conditions ($50{\pm}5%$) for 20 minutes. All the data were analyzed by SPSS (version 21) software program. Results showed that Cell Bio Fluid $Sync^{TM}$ improved both the cell viability and in vivo skin conditions such as skin hydration, roughness, brightness and evenness.
Park, Jong-In;Shin, Eun-Hyuk;Han, Young-Yih;Park, Hee-Chul;Lee, Jai-Ki;Choi, Doo-Ho
Progress in Medical Physics
/
v.23
no.1
/
pp.8-14
/
2012
In order to develop a Patient respiratory management system includinga biofeedback function for4-dimentional radiation therapy, this study investigated anoptimal tracking algorithmfor moving target using IR (Infra-red) camera as well as commercial camera. A tracking system was developed by LabVIEW 2010. Motion phantom images were acquired using a camera (IR or commercial). After image process were conducted to convert acquired image to binary image by applying a threshold values, several edge enhance methods such as Sobel, Prewitt, Differentiation, Sigma, Gradient, Roberts, were applied. The targetpattern was defined in the images, and acquired image from a moving targetwas tracked by matching pre-defined tracking pattern. During the matching of imagee, thecoordinateof tracking point was recorded. In order to assess the performance of tracking algorithm, the value of score which represents theaccuracy of pattern matching was defined. To compare the algorithm objectively, we repeat experiments 3 times for 5 minuts for each algorithm. Average valueand standard deviations (SD) of score were automatically calculatedsaved as ASCII format. Score of threshold only was 706, and standard deviation was 84. The value of average and SD for other algorithms which combined edge detection method and thresholdwere 794, 64 in Sobel, 770, 101 in Differentiation, 754, 85 in Gradient, 763, 75 in Prewitt, 777, 93 in Roberts, and 822, 62 in Sigma, respectively. According to score analysis, the most efficient tracking algorithm is the Sigma method. Therefore, 4-dimentional radiation threapy is expected tobemore efficient if threshold and Sigma edge detection method are used together in target tracking.
Components of dental resin-based restorative materials are reported to leach from the filling materials even after polymerization. Hydroquinone (HQ) is one of the major monomers used in the dental resin and is known as a carcinogen. Thus, carcinogenic risk of HQ leaching from the dental resin becomes a public health concern. The present study attempted to examine the carcinogenic potentials of HQ on the human epithelial cell, which is the target cell origin of the most of oral cancers. Cytotoxicity of HQ was observed above 50${\mu}M$ as measured by LDH assay, indicating a relatively low toxicity of this substance in human epithelial cells. The parameters of neoplastic cellular transformation such as cell saturation density, soft agar colony formation and cell aggregation were analyzed to examine the carcinogenic potential of HQ. The study showed that 2-week exposure of HQ showed the tendency of increase in the saturation density and the significant enhancement of soft agar colony formation at the highest dose, 50 ${\mu}M$ only. It is suggested that HQ has a weak potential of carcinogenicity. When cells were treated with HQ and TPA, a well-known tumor promoter, the parameters of neoplastic cellular transformation was significantly increased. This result indicates that the potential risk of carcinogenicity from HQ is largely dependent upon the presence of promoter. Exposure of 50 ${\mu}M$ HQ increased the time-dependent apoptosis as measured by the ELISA kit. This concentration coincides with a dose of neoplastic transformation, indicating a possible link between apoptosis and HQ-induced cellular transformation. Hydroquinone generated Reactive Oxygen Species (ROS) which was evidenced by the treatment of antioxidants such as trolox and N-acetyl cysteine and the GSH depleting agent, BSO. Antioxidants blocked the generation of ROS and the GSH depleting agent, BSO dramatically increased the ROS production. Since HQ is known to increase ROS production thru activation of transcriptional factor such as c-Myb and Pim-1, it is speculated that ROS generation by HQ plays a role in the activation of oncogene, which may lead to neoplastic transformation. In addition, ROS is involved in the alteration of signal transduction, which regulates the apoptosis in many cellular systems. Thus, ROS-mediated apoptosis may be involved in the HQ-induced carcinogenic processes. Protein kinase C (PKC) is known to play pivotal roles in neoplastic transformation of cells and its high expression is often found in a variety of types of tumors including oral cancer. PKC translocation of PKC-${\alpha}$ was observed following HQ exposure. Altered signaling system may also play a role in the transformation process. Taken together, HQ leached from the dental resin does not pose a significant threat as a cancer causing agent, but its carcinogenic potential can be significantly elevated in the presence of promoter. The mechanism of HQ-induced carcinogenesis involved ROS generation, apoptosis and altered signaling pathway. The present study will provide a valuable data to estimate the potential risk of HQ as a carcinogen and understand mechanism of HQ-induced carcinogenesis in human epithelial cells.
Sa, Doo-Hwan;Choi, Hee-Cheol;Kim, Young-Lok;Lee, Seung-Hoon
Journal of the Institute of Electronics Engineers of Korea SD
/
v.43
no.11
s.353
/
pp.58-68
/
2006
This work proposes a 10b 250MS/s $1.8mm^2$ 85mW 0.13um CMOS A/D Converter (ADC) for high-performance integrated systems such as next-generation DTV and WLAN simultaneously requiring low voltage, low power, and small area at high speed. The proposed 3-stage pipeline ADC minimizes chip area and power dissipation at the target resolution and sampling rate. The input SHA maintains 10b resolution with either gate-bootstrapped sampling switches or nominal CMOS sampling switches. The SHA and two MDACs based on a conventional 2-stage amplifier employ optimized trans-conductance ratios of two amplifier stages to achieve the required DC gain, bandwidth, and phase margin. The proposed signal insensitive 3-D fully symmetric capacitor layout reduces the device mismatch of two MDACs. The low-noise on-chip current and voltage references can choose optional off-chip voltage references. The prototype ADC is implemented in a 0.13um 1P8M CMOS process. The measured DNL and INL are within 0.24LSB and 0.35LSB while the ADC shows a maximum SNDR of 54dB and 48dB and a maximum SFDR of 67dB and 61dB at 200MS/s and 250MS/s, respectively. The ADC with an active die area of $1.8mm^2$ consumes 85mW at 250MS/s at a 1.2V supply.
The Principal component analysis (PCA) is a well-known data analysis method that is useful in linear feature extraction and data compression. The PCA is a linear transformation that applies an orthogonal rotation to the original data, so as to maximize the retained variance. PCA is a classical technique for obtaining an optimal overall mapping of linearly dependent patterns of correlation between variables (e.g. neurons). PCA provides, in the mean-squared error sense, an optimal linear mapping of the signals which are spread across a group of variables. These signals are concentrated into the first few components, while the noise, i.e. variance which is uncorrelated across variables, is sequestered in the remaining components. PCA has been used extensively to resolve temporal patterns in neurophysiological recordings. Because the retinal signal is stochastic process, PCA can be used to identify the retinal spikes. With excised rabbit eye, retina was isolated. A piece of retina was attached with the ganglion cell side to the surface of the microelectrode array (MEA). The MEA consisted of glass plate with 60 substrate integrated and insulated golden connection lanes terminating in an 8${\times}$8 array (spacing 200 $\mu$m, electrode diameter 30 $\mu$m) in the center of the plate. The MEA 60 system was used for the recording of retinal ganglion cell activity. The action potentials of each channel were sorted by offline analysis tool. Spikes were detected with a threshold criterion and sorted according to their principal component composition. The first (PC1) and second principal component values (PC2) were calculated using all the waveforms of the each channel and all n time points in the waveform, where several clusters could be separated clearly in two dimension. We verified that PCA-based waveform detection was effective as an initial approach for spike sorting method.
The analysis of wide-angle seismic reflection and refraction data plays an important role in lithospheric-scale crustal structure study. However, it is extremely difficult to develop an appropriate velocity structure model directly from the observed data, and we have to improve the structure model step by step, because the crustal structure analysis is an intrinsically non-linear problem. There are several subjective processes in wide-angle crustal structure modelling, such as phase identification and trial-and-error forward modelling. Because these subjective processes in wide-angle data analysis reduce the uniqueness and credibility of the resultant models, it is important to reduce subjectivity in the analysis procedure. From this point of view, we describe two software tools, PASTEUP and MODELING, to be used for developing crustal structure models. PASTEUP is an interactive application that facilitates the plotting of record sections, analysis of wide-angle seismic data, and picking of phases. PASTEUP is equipped with various filters and analysis functions to enhance signal-to-noise ratio and to help phase identification. MODELING is an interactive application for editing velocity models, and ray-tracing. Synthetic traveltimes computed by the MODELING application can be directly compared with the observed waveforms in the PASTEUP application. This reduces subjectivity in crustal structure modelling because traveltime picking, which is one of the most subjective process in the crustal structure analysis, is not required. MODELING can convert an editable layered structure model into two-way traveltimes which can be compared with time-sections of Multi Channel Seismic (MCS) reflection data. Direct comparison between the structure model of wide-angle data with the reflection data will give the model more credibility. In addition, both PASTEUP and MODELING are efficient tools for handling a large dataset. These software tools help us develop more plausible lithospheric-scale structure models using wide-angle seismic data.
본 웹사이트에 게시된 이메일 주소가 전자우편 수집 프로그램이나
그 밖의 기술적 장치를 이용하여 무단으로 수집되는 것을 거부하며,
이를 위반시 정보통신망법에 의해 형사 처벌됨을 유념하시기 바랍니다.
[게시일 2004년 10월 1일]
이용약관
제 1 장 총칙
제 1 조 (목적)
이 이용약관은 KoreaScience 홈페이지(이하 “당 사이트”)에서 제공하는 인터넷 서비스(이하 '서비스')의 가입조건 및 이용에 관한 제반 사항과 기타 필요한 사항을 구체적으로 규정함을 목적으로 합니다.
제 2 조 (용어의 정의)
① "이용자"라 함은 당 사이트에 접속하여 이 약관에 따라 당 사이트가 제공하는 서비스를 받는 회원 및 비회원을
말합니다.
② "회원"이라 함은 서비스를 이용하기 위하여 당 사이트에 개인정보를 제공하여 아이디(ID)와 비밀번호를 부여
받은 자를 말합니다.
③ "회원 아이디(ID)"라 함은 회원의 식별 및 서비스 이용을 위하여 자신이 선정한 문자 및 숫자의 조합을
말합니다.
④ "비밀번호(패스워드)"라 함은 회원이 자신의 비밀보호를 위하여 선정한 문자 및 숫자의 조합을 말합니다.
제 3 조 (이용약관의 효력 및 변경)
① 이 약관은 당 사이트에 게시하거나 기타의 방법으로 회원에게 공지함으로써 효력이 발생합니다.
② 당 사이트는 이 약관을 개정할 경우에 적용일자 및 개정사유를 명시하여 현행 약관과 함께 당 사이트의
초기화면에 그 적용일자 7일 이전부터 적용일자 전일까지 공지합니다. 다만, 회원에게 불리하게 약관내용을
변경하는 경우에는 최소한 30일 이상의 사전 유예기간을 두고 공지합니다. 이 경우 당 사이트는 개정 전
내용과 개정 후 내용을 명확하게 비교하여 이용자가 알기 쉽도록 표시합니다.
제 4 조(약관 외 준칙)
① 이 약관은 당 사이트가 제공하는 서비스에 관한 이용안내와 함께 적용됩니다.
② 이 약관에 명시되지 아니한 사항은 관계법령의 규정이 적용됩니다.
제 2 장 이용계약의 체결
제 5 조 (이용계약의 성립 등)
① 이용계약은 이용고객이 당 사이트가 정한 약관에 「동의합니다」를 선택하고, 당 사이트가 정한
온라인신청양식을 작성하여 서비스 이용을 신청한 후, 당 사이트가 이를 승낙함으로써 성립합니다.
② 제1항의 승낙은 당 사이트가 제공하는 과학기술정보검색, 맞춤정보, 서지정보 등 다른 서비스의 이용승낙을
포함합니다.
제 6 조 (회원가입)
서비스를 이용하고자 하는 고객은 당 사이트에서 정한 회원가입양식에 개인정보를 기재하여 가입을 하여야 합니다.
제 7 조 (개인정보의 보호 및 사용)
당 사이트는 관계법령이 정하는 바에 따라 회원 등록정보를 포함한 회원의 개인정보를 보호하기 위해 노력합니다. 회원 개인정보의 보호 및 사용에 대해서는 관련법령 및 당 사이트의 개인정보 보호정책이 적용됩니다.
제 8 조 (이용 신청의 승낙과 제한)
① 당 사이트는 제6조의 규정에 의한 이용신청고객에 대하여 서비스 이용을 승낙합니다.
② 당 사이트는 아래사항에 해당하는 경우에 대해서 승낙하지 아니 합니다.
- 이용계약 신청서의 내용을 허위로 기재한 경우
- 기타 규정한 제반사항을 위반하며 신청하는 경우
제 9 조 (회원 ID 부여 및 변경 등)
① 당 사이트는 이용고객에 대하여 약관에 정하는 바에 따라 자신이 선정한 회원 ID를 부여합니다.
② 회원 ID는 원칙적으로 변경이 불가하며 부득이한 사유로 인하여 변경 하고자 하는 경우에는 해당 ID를
해지하고 재가입해야 합니다.
③ 기타 회원 개인정보 관리 및 변경 등에 관한 사항은 서비스별 안내에 정하는 바에 의합니다.
제 3 장 계약 당사자의 의무
제 10 조 (KISTI의 의무)
① 당 사이트는 이용고객이 희망한 서비스 제공 개시일에 특별한 사정이 없는 한 서비스를 이용할 수 있도록
하여야 합니다.
② 당 사이트는 개인정보 보호를 위해 보안시스템을 구축하며 개인정보 보호정책을 공시하고 준수합니다.
③ 당 사이트는 회원으로부터 제기되는 의견이나 불만이 정당하다고 객관적으로 인정될 경우에는 적절한 절차를
거쳐 즉시 처리하여야 합니다. 다만, 즉시 처리가 곤란한 경우는 회원에게 그 사유와 처리일정을 통보하여야
합니다.
제 11 조 (회원의 의무)
① 이용자는 회원가입 신청 또는 회원정보 변경 시 실명으로 모든 사항을 사실에 근거하여 작성하여야 하며,
허위 또는 타인의 정보를 등록할 경우 일체의 권리를 주장할 수 없습니다.
② 당 사이트가 관계법령 및 개인정보 보호정책에 의거하여 그 책임을 지는 경우를 제외하고 회원에게 부여된
ID의 비밀번호 관리소홀, 부정사용에 의하여 발생하는 모든 결과에 대한 책임은 회원에게 있습니다.
③ 회원은 당 사이트 및 제 3자의 지적 재산권을 침해해서는 안 됩니다.
제 4 장 서비스의 이용
제 12 조 (서비스 이용 시간)
① 서비스 이용은 당 사이트의 업무상 또는 기술상 특별한 지장이 없는 한 연중무휴, 1일 24시간 운영을
원칙으로 합니다. 단, 당 사이트는 시스템 정기점검, 증설 및 교체를 위해 당 사이트가 정한 날이나 시간에
서비스를 일시 중단할 수 있으며, 예정되어 있는 작업으로 인한 서비스 일시중단은 당 사이트 홈페이지를
통해 사전에 공지합니다.
② 당 사이트는 서비스를 특정범위로 분할하여 각 범위별로 이용가능시간을 별도로 지정할 수 있습니다. 다만
이 경우 그 내용을 공지합니다.
제 13 조 (홈페이지 저작권)
① NDSL에서 제공하는 모든 저작물의 저작권은 원저작자에게 있으며, KISTI는 복제/배포/전송권을 확보하고
있습니다.
② NDSL에서 제공하는 콘텐츠를 상업적 및 기타 영리목적으로 복제/배포/전송할 경우 사전에 KISTI의 허락을
받아야 합니다.
③ NDSL에서 제공하는 콘텐츠를 보도, 비평, 교육, 연구 등을 위하여 정당한 범위 안에서 공정한 관행에
합치되게 인용할 수 있습니다.
④ NDSL에서 제공하는 콘텐츠를 무단 복제, 전송, 배포 기타 저작권법에 위반되는 방법으로 이용할 경우
저작권법 제136조에 따라 5년 이하의 징역 또는 5천만 원 이하의 벌금에 처해질 수 있습니다.
제 14 조 (유료서비스)
① 당 사이트 및 협력기관이 정한 유료서비스(원문복사 등)는 별도로 정해진 바에 따르며, 변경사항은 시행 전에
당 사이트 홈페이지를 통하여 회원에게 공지합니다.
② 유료서비스를 이용하려는 회원은 정해진 요금체계에 따라 요금을 납부해야 합니다.
제 5 장 계약 해지 및 이용 제한
제 15 조 (계약 해지)
회원이 이용계약을 해지하고자 하는 때에는 [가입해지] 메뉴를 이용해 직접 해지해야 합니다.
제 16 조 (서비스 이용제한)
① 당 사이트는 회원이 서비스 이용내용에 있어서 본 약관 제 11조 내용을 위반하거나, 다음 각 호에 해당하는
경우 서비스 이용을 제한할 수 있습니다.
- 2년 이상 서비스를 이용한 적이 없는 경우
- 기타 정상적인 서비스 운영에 방해가 될 경우
② 상기 이용제한 규정에 따라 서비스를 이용하는 회원에게 서비스 이용에 대하여 별도 공지 없이 서비스 이용의
일시정지, 이용계약 해지 할 수 있습니다.
제 17 조 (전자우편주소 수집 금지)
회원은 전자우편주소 추출기 등을 이용하여 전자우편주소를 수집 또는 제3자에게 제공할 수 없습니다.
제 6 장 손해배상 및 기타사항
제 18 조 (손해배상)
당 사이트는 무료로 제공되는 서비스와 관련하여 회원에게 어떠한 손해가 발생하더라도 당 사이트가 고의 또는 과실로 인한 손해발생을 제외하고는 이에 대하여 책임을 부담하지 아니합니다.
제 19 조 (관할 법원)
서비스 이용으로 발생한 분쟁에 대해 소송이 제기되는 경우 민사 소송법상의 관할 법원에 제기합니다.
[부 칙]
1. (시행일) 이 약관은 2016년 9월 5일부터 적용되며, 종전 약관은 본 약관으로 대체되며, 개정된 약관의 적용일 이전 가입자도 개정된 약관의 적용을 받습니다.