Modifications in dietary fatty acid intake might lead to a modification in membrane phospholipid fatty acid composition. The purpose of this study was to investigate relationship between different type of oil consumption and leukocyte membrane phospholipid composition. This study was carried out in subjects utilizing butter (n = 15), margarine (n = 15), fluid oil (n = 15) and mixed types of oils (n = 15) in total 60 subjects. Leukocytes were separated from total blood by dextran sedimentation method. Membrane lipids and proteins were isolated following the cell disruption. Fatty acids of membrane phospholipids were isolated by hydrolysation with phospholipase B under ultrasonic dismembranator. Free fatty acids were identified with gas chromatography at chloroform phase. The results obtained were compared with data obtained by chromatograms of the standards. Results more prominent values of arachidic, dihomo-$\gamma$-linolenic and palmitoleic acids were found in butter-or mixed oil-user groups; eicosadienoic, eicosamonoenoic, dihomo-$\gamma$-linolenic and behenic acids in fluid oil; heptanoic, valeric, eicosadienoic and linolenic acids in margarine groups. The fatty acid composition of mixed oil was similar to butter, while other two oils were so different. From this study, it was concluded that the type of oil consumption might have an influence on phospholipid components of plasma membranes.
Asami, Yukihiro;Kim, Sun-Ok;Jang, Jun-Pil;Ko, Sung-Kyun;Kim, Bo Yeon;Osada, Hiroyuki;Jang, Jae-Hyuk;Ahn, Jong Seog
Journal of Microbiology and Biotechnology
/
v.30
no.1
/
pp.31-37
/
2020
We previously identified a new heparinase inhibitor fungal metabolite, named CRM646-A, which showed inhibition of heparinase and telomerase activities in an in vitro enzyme assay and antimetastatic activity in a cell-based assay. In this study, we elucidated the mechanism by which CRM646-A rapidly induced nucleus condensation, plasma membrane disruption and morphological changes by increasing intracellular Ca2+ levels. Furthermore, PD98059, a mitogen-activated protein kinase (MEK) inhibitor, inhibited CRM646-A-induced nucleus condensation through ERK1/2 activation in rat 3Y1 fibroblast cells. We identified CRM646-A as a Ca2+ ionophore-like agent with a distinctly different chemical structure from that of previously reported Ca2+ ionophores. These results indicate that CRM646-A has the potential to be used as a new and effective antimetastatic drug.
Proceedings of the Korean Society of Embryo Transfer Conference
/
2001.05b
/
pp.4-16
/
2001
Sperm competent for fertilization can become capacitated, bind to the zona pellucida (ZP)of an egg in a specific manner, and complete acrosomal exocytosis. Failure to carry out these functions results in infertility. Although the interactions between the ZP and the plasma membrane overlying the sperm acrosome have been considered important for sperm-egg recognition and signalling recent results have prompted a reassessment of current paradigms concerning these interactions. In this review, we're going to discuss about the roles of the acrosomal matrix, the particulate component of the acrosomal contents, in fertilization. The general hypothesis is that acrosomal exocytosis leads to the exposure of acrosomal matrix proteins that become de facto extracellula matrix(ECM) on the surface of the sperm head, and that the dynamic interactions of this newly-exposed sperm ECM with the egg ECM (the ZP) govern sperm-egg recognition and sperm penetration of the ZP. Informations from these experiments may provide new ways to address the poor ZP binding of sperm from some human infertility patients and may offer new avenues for contraception through the disruption of purposeful sperm-ZP binding.
Polyamines are essential for cell growth and differentiation; however their precise roles are unclear yet. In the present study, the cytotoxic effect of spermine (spm) on MCF-7 cells was investigated. In the MTT assay of MCF-7 cells treated with spm, cell viability was significantly decreased in a time-and dose-dependent manner. Cell viability measurement was confirmed by trypan blue staining. FACS analysis shows that sub-G1 was increased in a time-and dose-dependent manner too. When the cells were treated with spm, cells started to show morphological changes within 2 hrs. The expression of adhesion proteins (FAK and integrin ${\beta}1$), and cytoskeletal protein (actin) was checked by Western blotting analysis. Integrin ${\beta}1$ levels were slightly decreased, and FAK and actin levels were rapidly decreased with spm treatment. In confocal laser scanning microscopy, the distribution of actin did not change but the expression decreased in a dose-dependent manner with spm treatment. FAK was evenly distributed under the plasma membrane in the untreated control. However, at 10 ${\mu}M$ spm FAK seemed to move toward the cell nucleus. Integrin ${\beta}1$, which was mainly found in the focal point of the plasma membrane in the untreated control, dispersed through the entire plasma membrane in spm treatment. The present results indicate that cytotoxic effects of spm are triggered by the disruption of adhesion proteins and cytoskeletal protein.
Two groups of esophagus graft were done in canine esophagus in 34 adult mongrel dogs. For the first group segmental replacement graft was done with fresh autologous pericardium tube, and for the second, patch graft was done utilizing fresh autologous pericardium, fresh homologous pericardium,and dacron piece. All eight dogs in the first segmental replacement graft group died 2 to 5 days after operation with severe empyema caused by anastomosis disruption. Among 26 patch graft dogs 2 died during operation and 7 died 13 to 18 days after operation. For the 17 long-term patch grafted survivors esophagography and postoperative weight check were done. Postoperative stool was collected and examined for dacron patch excretion. One, two, three, and four months postoperative long-term survivors were sacrificed to obtain specimens in each group respectively and the following observations were made.I. Survival; Autologous pericardium patch group showed no mortality but in homologous pericardium and dacron patch group only two thirds were long-term survivors. II. Postoperative swallowing; There was no case which demonstrated postoperative dysphagia. About half of the cases showed postoperative weight increase and in only 3 cases weight decrease followed operation. III. Dacron patch was excreted in the stool 8 to 23 days after operation. Animals which excreted dacron patch up to 9 days after operation all died of empyema due to anastomosis disruption.IV. Postoperative esophagogram; All esophagograms in each group showed no leakage of barium, no passage disturbances and no remarkable stenotic signs.V. Morphological findings; [A] Macroscopical findings; In one month group specimens of each group dense adhesion with surrounding structures was noted and luminal surface was smooth with contraction of the patched area. In two month groups anastomosis sutures were still exposed but patched area showed lesser abnormality. In three to four months groups sutures were covered completely and patched area showed only very slight signs of contraction. [B] Microscopic findings; In one month group luminal surface of the replaced tissue [transplanted tissue] showed almost complete epithelial covering that is composed of several layers of squamous cells with no evidence of keratinization. Basement membrane was also well distinct throughout. Slight to minimal inflammatory cells comprising of large mononuclears, lymphocytes and plasma cells were observed in the subepithelial fibrous stroma consisted entirely of loose fibrous tissue containing many newly formed capillaries and fibroblastic proliferation. Scattered suture granulomas were found, few of which became acutely inflamed. In two months group repairing process progressed with lesser degree of inflammatory cell infiltration and young capillary proliferation. Fibrous tissue was more matured showing even focal collagenization.Suture granuloma persisted but with lesser reactive changes. Epithelial covering was that of a mature non-keratinizing stratified squamous epithelium. In three and four months groups the replaced area showed essentially similar histological findings. However, subepithelial stroma still consisted entirely of connective tissue without evidence of smooth muscle regeneration. In this group, inflammatory cell infiltration was minimal or negligible. Among these patch materials autologous pericardium group showed the most satisfactory repairing process.The above mentioned results may signify the feasibility of autogenous pericardium patch graft in clinical esophageal surgery.
Two groups of esophagus graft were done in canine esophagus in 34 adult mongrel dogs. For the first group segmental replacement graft was done with fresh autologous pericardium tube, and for the second, patch graft was done utilizing fresh autologous pericardium, fresh homologous pericardium,and dacron piece. All eight dogs in the first segmental replacement graft group died 2 to 5 days after operation with severe empyema caused by anastomosis disruption. Among 26 patch graft dogs 2 died during operation and 7 died 13 to 18 days after operation. For the 17 long-term patch grafted survivors esophagography and postoperative weight check were done. Postoperative stool was collected and examined for dacron patch excretion. One, two, three, and four months postoperative long-term survivors were sacrificed to obtain specimens in each group respectively and the following observations were made. I. Survival; Autologous pericardium patch group showed no mortality but in homologous pericardium and dacron patch group only two thirds were long-term survivors. II. Postoperative swallowing; There was no case which demonstrated postoperative dysphagia. About half of the cases showed postoperative weight increase and in only 3 cases weight decrease followed operation. III. Dacron patch was excreted in the stool 8 to 23 days after operation. Animals which excreted dacron patch up to 9 days after operation all died of empyema due to anastomosis disruption. IV. Postoperative esophagogram; All esophagograms in each group showed no leakage of barium, no passage disturbances and no remarkable stenotic signs. V. Morphological findings; [A] Macroscopical findings; In one month group specimens of each group dense adhesion with surrounding structures was noted and luminal surface was smooth with contraction of the patched area. In two month groups anastomosis sutures were still exposed but patched area showed lesser abnormality. In three to four months groups sutures were covered completely and patched area showed only very slight signs of contraction. [B] Microscopic findings; In one month group luminal surface of the replaced tissue [transplanted tissue] showed almost complete epithelial covering that is composed of several layers of squamous cells with no evidence of keratinization. Basement membrane was also well distinct throughout. Slight to minimal inflammatory cells comprising of large mononuclears, lymphocytes and plasma cells were observed in the subepithelial fibrous stroma consisted entirely of loose fibrous tissue containing many newly formed capillaries and fibroblastic proliferation. Scattered suture granulomas were found, few of which became acutely inflamed. In two months group repairing process progressed with lesser degree of inflammatory cell infiltration and young capillary proliferation. Fibrous tissue was more matured showing even focal collagenization. Suture granuloma persisted but with lesser reactive changes. Epithelial covering was that of a mature non-keratinizing stratified squamous epithelium. In three and four months groups the replaced area showed essentially similar histological findings. However, subepithelial stroma still consisted entirely of connective tissue without evidence of smooth muscle regeneration. In this group, inflammatory cell infiltration was minimal or negligible. Among these patch materials autologous pericardium group showed the most satisfactory repairing process. The above mentioned results may signify the feasibility of autogenous pericardium patch graft in clinical esophageal surgery.
Vasicinone, a quinazoline alkaloid from Adhatoda vasica Nees. is well known for its bronchodilator activity. However its anti-proliferative activities is yet to be elucidated. Here-in we investigated the anti-proliferative effect of vasicinone and its underlying mechanism against A549 lung carcinoma cells. The A549 cells upon treatment with various doses of vasicinone (10, 30, 50, $70{\mu}M$) for 72 h showed significant decrease in cell viability. Vasicinone treatment also showed DNA fragmentation, LDH leakage, and disruption of mitochondrial potential, and lower wound healing ability in A549 cells. The Annexin V/PI staining showed disrupted plasma membrane integrity and permeability of PI in treated cells. Moreover vasicinone treatment also lead to down regulation of Bcl-2, Fas death receptor and up regulation of PARP, BAD and cytochrome c, suggesting the anti-proliferative nature of vasicinone which mediated apoptosis through both Fas death receptors as well as Bcl-2 regulated signaling. Furthermore, our preliminary studies with vasicinone treatment also showed to lower the ROS levels in A549 cells and have potential free radical scavenging (DPPH, Hydroxyl) activity and ferric reducing power in cell free systems. Thus combining all, vasicinone may be used to develop a new therapeutic agent against oxidative stress induced lung cancer.
The pathogenesis and pathophysiology of Acanthamoeba infections remain incompletely understood. Phospholipases are known to cleave phospholipids, suggesting their possible involvement in the host cell plasma membrane disruption leading to host cell penetration and lysis. The aims of the present study were to determine phospholipase activities in Acanthamoeba and to determine their roles in the pathogenesis of Acanthamoeba. Using an encephalitis isolate (T1 genotype), a keratitis isolate (T4 genotype), and an environmental isolate (T7 genotype), we demonstrated that Acanthamoeba exhibited phospholipase $A_2$ (PLA$_2$). and phospholipase D (PLD) activities in a spectrophotometry-based assay. Interestingly, the encephalitis isolates of Acanthamoeba exhibited higher phospholipase activities as compared with the keratitis isolates, but the environmental isolates exhibited the highest phospholipase activities. Moreover, Acanthamoeba isolates exhibited higher PLD activities compared with the PLA$_2$. Acanthamoeba exhibited optimal phospholipase activities at $37^{\circ}C$ and at neutral pH indicating their physiological relevance. The functional role of phospholipases was determined by in vitro assays using human brain microvascular endothelial cells (HBMEC), which constitute the blood-brain barrier. We observed that a PLD-specific inhibitor, i.e., compound 48/80, partially inhibited Acanthamoeba encephalitis isolate cytotoxicity of the host cells, while PLA$_2$-specific inhibitor, i.e., cytidine 5'-diphosphocholine, had no effect on parasite-mediated HBMEC cytotoxicity. Overall, the T7 exhibited higher phospholipase activities as compared to the T4. In contract, the T7 exhibited minimal binding to, or cytotoxicity of, HBMEC.
Cholinergic innervation of the hippocampus is known to be correlated with learning and memory. The cholinergic agonist carbachol (CCh) modulate synaptic plasticity and produced long-term synaptic depression (LTD) in the hippocampus. However, the exact mechanisms by which the cholinergic system modifies synaptic functions in the hippocampus have yet to be determined. This study introduces an acetylcholine receptor-mediated LTD that requires internalization of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors on the postsynaptic surface and their intracellular mechanism in the hippocampus. In the present study, we showed that the application of the cholinergic agonist CCh reduced the surface expression of GluA2 on synapses and that this reduction was prevented by the M1 muscarinic acetylcholine receptor antagonist pirenzepine in primary hippocampal neurons. The interaction between GluA2 and the glutamate receptor-interacting protein 1 (GRIP1) was disrupted in a hippocampal slice from a rat upon CCh simulation. Under the same conditions, the binding of GluA2 to adaptin-α, a protein involved in clathrin-mediated endocytosis, was enhanced. The current data suggest that the activation of LTD, mediated by the acetylcholine receptor, requires the internalization of the GluA2 subunits of AMPA receptors and that this may be controlled by the disruption of GRIP1 in the PDZ ligand domain of GluA2. Therefore, we can hypothesize that one mechanism underlying the LTD mediated by the M1 mAChR is the internalization of the GluA2 AMPAR subunits from the plasma membrane in the hippocampal cholinergic system.
Lee, Junguee;Oh, Dong Hyun;Park, Ki Cheol;Choi, Ji Eun;Kwon, Jong Beom;Lee, Jongho;Park, Kuhn;Sul, Hae Joung
Molecules and Cells
/
v.41
no.3
/
pp.224-233
/
2018
Primary cilia are solitary, non-motile, axonemal microtubule-based antenna-like organelles that project from the plasma membrane of most mammalian cells and are implicated in transducing hedgehog signals during development. It was recently proposed that aberrant SHH signaling may be implicated in the progression of idiopathic pulmonary fibrosis (IPF). However, the distribution and role of primary cilia in IPF remains unclear. Here, we clearly observed the primary cilia in alveolar epithelial cells, fibroblasts, and endothelial cells of human normal lung tissue. Then, we investigated the distribution of primary cilia in human IPF tissue samples using immunofluorescence. Tissues from six IPF cases showed an increase in the number of primary cilia in alveolar cells and fibroblasts. In addition, we observed an increase in ciliogenesis related genes such as IFT20 and IFT88 in IPF. Since major components of the SHH signaling pathway are known to be localized in primary cilia, we quantified the mRNA expression of the SHH signaling components using qRT-PCR in both IPF and control lung. mRNA levels of SHH, the coreceptor SMO, and the transcription factors GLI1 and GLI2 were upregulated in IPF compared with control. Furthermore, the nuclear localization of GLI1 was observed mainly in alveolar epithelia and fibroblasts. In addition, we showed that defective KIF3A-mediated ciliary loss in human type II alveolar epithelial cell lines leads to disruption of SHH signaling. These results indicate that a significant increase in the number of primary cilia in IPF contributes to the upregulation of SHH signals.
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.