Purpose: Guided bone regeneration (GBR) is the most widely used technique to regenerate and augment bones. Even though augmented bones (ABs) have been examined histologically in many studies, few studies have been conducted to examine the biological potential of these bones and the healing dynamics following their use. Moreover, whether the bone obtained from the GBR procedure possesses the same functions as the existing autogenous bone is uncertain. In particular, little attention has been paid to the regenerative ability of GBR bone. Therefore, the present study histologically evaluated the regenerative capacity of AB in the occlusive space of a rat guided bone augmentation (GBA) model. Methods: The calvaria of 30 rats were exposed, and plastic caps were placed on the right of the calvaria in 10 of the 30 rats. After a 12-week healing phase, critical-sized calvarial bone defects (diameter: 5.0 mm) were trephined into the dorsal parietal bone on the left of the calvaria. Bone particles were harvested from the AB or the cortical bone (CB) using a bone scraper and transplanted into the critical defects. Results: The newly generated bone at the defects' edge was evaluated using micro-computed tomography (micro-CT) and histological sections. In the micro-CT analysis, the radiopacity in both the augmented and the CB groups remained high throughout the observational period. In the histological analysis, the closure rate of the CB was significantly higher than in the AB group. The numbers of cells positive for runt-related transcription factor 2 (Runx2) and tartrate-resistant acid phosphatase (TRAP) in the AB group were larger than in the CB group. Conclusions: The regenerative capacity of AB in the occlusive space of the rat GBA model was confirmed. Within the limitations of this study, the regenerative ability of the AB particulate transplant was inferior to that of the CB particulate transplant.
An ultimate goal of periodontal therapy is to stop the disease process and to regenerate a functionally-oriented periodontium destroyed as a result of periodontal disease. The purpose of this study was to observe the effect of grafting granulation tissue obtained from extraction socket on the regeneration of horizontal furcation defect. Six dogs were used in this study. All mandibular first and third premolars were extracted. At 2, 3, and 5 days after extraction, tissues were obtained from extraction socket of 1 mongrel dog and examined by light microscope. Granulation tissue obtained at 5 days after extraction was chosen as the graft material. Five days later, horizontal furcation defects were created surgically at mandibular second and fourth premolars in the right and left side of the 5 beagle dogs. The entrance area of the artificially prepared "key hole" defects were about $3\;4mm^2$. By random selections, 2 exposed furcation defects were grafted with granulation tissue obtained from extraction socket as experimental group and 1 furcation defect was as control. The flaps were replaced to their original position and sutured with 4-0 chromic cat-gut. Three dogs were sacrificed 4 weeks and two dogs 8 weeks after surgery, and the prepared specimens were examined by light microscope. At 4 weeks, furcations were filled with epithelial lining and fibrous connective tissue infiltrated with chronic inflammatory cells. New bone formation was observed in all groups. Only experimental group showed new cementum formation. At 8 weeks, new cementum, functional arrangement of new PDL fiber, root resorption, and some ankylotic union of newly formed alveolar bone and root surface were observed in all groups. Experimental group showed that epithelial downgrowth was inhibited and new bone formation was more active compared to control. The success rate of the furcation defect healing was higher in experimental group than control. These results suggested that grafting of granulation tissue obtained from extraction socket which combined with reconstructive periodontal flap surgery may promote periodontal regeneration of horizontal furcation defect.
Giant cell interstitial pneumonia. a synonym for hard metal pneumoconiosis, is a unique form of pulmonary fibrosis resulting from an exposure to hard metal dust. A case of biopsy-proved giant cell interstitial pneumonia in the absence of appropriate history of exposure to hard metal dust is reported. The patient presented with clinical features of chronic interstitial lung disease or idiopathic pulmonary fibrosis. He worked in a chemical laboratory at a fertilizer plant, where he had been exposed to various chemicals such as benzene and toluene. He denied having any other hobby in his house or job at work, which may have exposed him hard metal dust. High-resolution CT scan revealed multi-lobar distribution of ground glass opacity with peripheral and basal lung predominance. The retrieved fluid of bronchoalveolar lavage contained asbestos fiber and showed neutrotphil predominance. Surgical lung biopsy was performed for a definite diagnosis. Lung specimen showed alveolar infiltration of numerous multinucleated giant cells with mild interstitial fibrosis. Upon detailed examination of the lung tissue, one asbestos body was found. An analysis for mineral contents in lung tissue was performed. Compared with the control specimen, the amount of cobalt and several hard metal components in the lung tissue of this patient was ten times higher. We speculated that the inconsistency between occupational history and the findings of pathologic and mineralogical analyses could be explained by the difference in individual immunologic reactivity to hard metal dust despite the relatively small amount of unrecognized environmental exposure(ED: It's hard to understand what this phrase is trying to say).
Purpose: Collagen membranes are used extensively as bioabsorbable barriers in guided bone regeneration. However, collagen has different effects on tissue restoration depending on the type, structure, degree of cross-linking and chemical treatment. The purpose of this study was to evaluate the inflammatory reaction, bone formation, and degradation of dehydrothermal treated porcine type I atelocollagen (CollaGuide$^{(R)}$) compared to of the non-crosslinked porcine type I, III collagen (BioGide$^{(R)}$) and the glutaldehyde cross-linked bovine type I collagen (BioMend$^{(R)}$) in surgically created bone defects in rat mandible. Methods: Bone defect model was based upon 3 mm sized full-thickness transcortical bone defects in the mandibular ramus of Sprague-Dawley rats. The defects were covered bucolingually with CollaGuide$^{(R)}$, BioMend$^{(R)}$, or BioGide$^{(R)}$ (n=12). For control, the defects were not covered by any membrane. Lymphocyte, multinucleated giant cell infiltration, bone formation over the defect area and membrane absorption were evaluated at 4 weeks postimplantation. For comparison of the membrane effect over the bone augmentation, rats received a bone graft plus different covering of membrane. A $3{\times}4$ mm sized block graft was harvested from the mandibular angle and was laid and stabilized with a microscrew on the naturally existing curvature of mandibular inferior border. After 10 weeks postimplantation, same histologic analysis were done. Results: In the defect model at 4 weeks post-implantation, the amount of new bone formed in defects was similar for all types of membrane. Bio-Gide$^{(R)}$ membranes induced significantly greater inflammatory response and membrane resorption than other two membranes; characterized by lymphocytes and multinucleated giant cells. At 10 weeks postoperatively, all membranes were completely resorbed. Conclusion: Dehydrotheramal treated cross-linked collagen was safe and effective in guiding bone regeneration in alveolar ridge defects and bone augmentation in rats, similar to BioGide$^{(R)}$ and BioMend$^{(R)}$, thus, could be clinically useful.
The present study was performed to compare effects of demineralized freeze-dried bone allograft(DFDBA) with deproteinized bovine bone mineral(DBBM) on periodontal fenestration defect in rats. Twelve adult male rats weighing 500 to 540 grams were used in this study. Periodontal fenestration defects were surgically created with tapered fissure bur(${\Phi}1mm$) at the left side of buccal surface of the mandible. The defect size was from anterior border of the first molar to anterior of the ascending ramus mesiodistally and from just below the alveolar crest to apically 1.5-2mm area apicocoronally with 2mm in depth. Rats were divided into control group, test group I and II. Four defects were assigned to the test group I grafted with DBBM and other 4 defects were assigned to the test group II grafted with DFDBA. The rest of defects were the negative control group. At 10 days and 35 days after surgery, 12 rats were sacrificed through intracardiac perfusion and specimens were obtained prepared with Hematoxylin-Eosin stain for light microscopic evaluation. The results of this study were as follows : 1. In the control group, new bone, osteoid, dense connective tissue were observed in the defects at 10 days. new bone formation was not found but loose connective tissue was formed in the defect and fibrous encapsulation of graft materials was shown in two test groups at 10 days. 2. In all groups, new bone formation was shown in the defect at 35 days. And in the control group, bone formation increased at 35 days than at 10 days. 3. In the test group I and II at 35 days, graft materials were combined with new bone and joined host bone. There was very close contact between new bone, graft materials, and host bone with no gaps. 4. In the test group I and II, new bone formation was similar to that in the control group but not exeeded. In conclusion, in the test group I new bone formation was similar to that in the test group II at 35 days, but there was infiltration of inflammatory cells at 10 days. DFDBA and DBBM were considered as the biocompatible graft materials and effective in the regeneration of new bone.
Park, Chan Seok;Lee, Sang Haak;Shim, Kon Ho;Kim, Wan Uk;Lee, Sook Young;Kim, Seok Chan;Kim, Kwan Hyoung;Moon, Hwa Sik;Song, Jeong Sup;Park, Sung Hak
Tuberculosis and Respiratory Diseases
/
v.57
no.3
/
pp.273-277
/
2004
Methotrexate is commonly used in rheumatoid arthritis as an anti-inflammatory agent, but treatment with methotrexate can lead to severe side effects, especially pulmonary complication. Interstitial pneumonitis is one of the most important pulmonary adverse effects of methotrexate and most patient present with a subacute febrile illness and peripheral eosinophilia is seen in about a half of patients. Almost all patients have abnormal chest roentgenograms and bibasilar interstitial infiltration with alveolar pulmonary consolidations is the most characteristic finding. Interstitial inflammation with mononuclear cell infiltration is a characteristic pathologic feature and findings that suggest acute hypersensitivity pneumonitis, such as bronchiolitis, granuloma formation with giant cells, and infiltration with eosinophils are often present. Methotrexate-induced pneumonitis is a potentially life threatening and unpredictable complication but it is difficult to make a definite diagnosis in the absence of high index of clinical suspicion. Early recognition and appropriate management may avoid the serious outcome. Herein we report a case of methotrexate-induced pneumonitis in a patient with rheumatoid arthritis.
We have reported that a 24 kDa protein (22U homologous; As22U) of Anisakis simplex larvae could elicit several Th2-related chemokine gene expressions in the intestinal epithelial cell line which means that As22U may play a role as an allergen. In order to determine the contribution of As22U to allergic reactions, we treated mice with 6 times intra-nasal application of recombinant As22U (rAs22U). In the group challenged with rAs22U and ovalbumin (OVA), the number of eosinophils in the bronchial alveolar lavage fluid (BALF) was significantly increased, as compared to the group receiving only OVA. In addition, mice treated with rAs22U and OVA showed significantly increased airway hyperresponsiveness. Thus, severe inflammation around the airway and immune cell recruitment was observed in mice treated with rAs22U plus OVA. The levels of IL-4, IL-5, and IL-13 cytokines in the BALF increased significantly after treatment with rAs22U and OVA. Similarly, the levels of anti-OVA specific lgE and lgG1 increased in mice treated with rAs22U and OVA, compared to those treated only with OVA. The Gro-${\alpha}$ (CXCL1) gene expression in mouse lung epithelial cells increased instantly after treatment with rAs22U, and allergy-specific chemokines eotaxin (CCL11) and thymus-and-activation-regulated-chemokine (CCL17) gene expressions significantly increased at 6 hr after treatment. In conclusion, rAs22U may induce airway allergic inflammation, as the result of enhanced Th2 and Th17 responses.
The objectives of this study were to examine the lung injury and inflammation caused by manual metal arc stainless steel(MMA-SS) welding fume inhalation and to evaluate the recovery process. Sprague-Dawley rats were exposed to MMA-SS welding fumes for 2 h per day in a whole-body exposure chamber, with a total suspended particulate(TSP) concentration of $51.4{\pm}2.8mg/m^3$(low dose) or $84.6{\pm}2.9mg/m^3$(high dose) for 30 days. The animals were sacrificed after 30 days of exposure as well as after a 30-day recovery period. To assess the inflammatory or injury responses, cellular and biochemical parameters as well as cytokines were assayed in the bronchoalveolar lavage fluid(BALF). MMA-SS welding fume exposure led to a significant elevation in the number of alveolar macrophages(AM) and polymorphonuclear cells(PMN). Additionary, the values of $\beta$-n-acetyl glucosaminidase($\beta$-NAG) and lactate dehydrogenase(LDH) in the BALF were increased in the exposed group when compared to controls. After 30 days of recovery from exposure, a significant reduction in inflammatory parameters of BALF was observed between the exposed and recovered groups. Slight, but significant elevations were noted in the number of AM and PMN in the recovered groups, and AM that had been ingested fume particles still remain in the lungs. In conclusion, these results indicated that welding fumes induced inflammatory responses and cytotoxicity in the lungs of exposed rats. Fume particles were not fully cleared from lungs even after a 30-day recovery period.
Kim, Kyuseok;Lee, Jeong Hun;Suh, Gil Joon;Youn, Yeo Kyu;Kang, Young Joon;Kim, Min A;Cho, Sang-Gi;Shin, Hyo-Keun
Journal of Trauma and Injury
/
v.19
no.1
/
pp.14-20
/
2006
Purpose: Although hypothermia has been used in many clinical situations, such as post cardiopulmonary resuscitation, stroke, traumatic brain injury, septic shock, and hemorrhagic shock, the mechanism by which it works has not been clearly elucidated. We aimed to evaluate the effect of hypothermia on the plasma nitric oxide (NO) concentration, lung iNOS expression, and histologic changes in intestinal ischemia-reperfusion (IR). Method: Male Sprague-Dawley rats were randomly divided into the hypothermia group (HT, n=8, $27{\sim}30^{\circ}C$) and the normothermia group (NT, n=8, $36{\sim}37^{\circ}C$). They underwent 30 min of intestinal ischemia by clamping the superior mesenteric artery, which was followed by 1.5 h of reperfusion. They were then sacrificed. The acute lung injury (ALI) score, the plasma NO concentration, and lung iNOS gene expression were measured. Results: Compared with the HT group, the NT group showed severe infiltrations of inflammatrory cells, alveolar hemorrhages, and interstitial hypertrophies in lung tissues. There were significant differences in the ALI scores between the NT and the HT groups ($8.7{\pm}1.5/HPF$ in NT vs $5.8{\pm}1.2/HPF$ in HT, p=0.008). Although the plasma NO concentration was slightly lower in the HT group, there was no significant difference between the two groups ($0.80{\pm}0.24{\mu}mol/L$ in NT vs $0.75{\pm}0.30{\mu}mol/L$ in HT, p=0.917). Lung iNOS gene expression was stronger in the NT group than in the HT group. The band density of the expression of iNOS in lung tissues was significantly increased in the NT group compared to the HT group ($5.54{\pm}2.75$ in NT vs$0.08{\pm}0.52$ in HT, p=0.002). Conclusions: This study showed that hypothermia in intestinal IR reduces inflammatory responses, ALI scores, and iNOS gene expression in lung tissues. There was no significant effect of hypothermia on the plasma NO concentration.
The purpose of this study was to investigate the effect of antioxidants (vitamin E, selenium, and coenzyme $Q_{10}$) on the bleomycin-induced pulmonary lesions in male rats. Sprague-Dawley male rats were divided into 4 treatment groups ($T_1$, $T_2$, $T_3$, $T_4$) and 4 control groups ($C_1$, $C_1$, $C_3$, $C_4$). The treatment groups of rats weie given a single intratracheal dose of bleomycin (1.5 units/rat) and control groups of rats were given a single intratracheal dose of normal saline (0.15ml/rat). The rats in the $T_1$ group and $C_1$, group were dosed with normal saline (0.5ml/kg/day), the rats in the $T_2$ group and $C_2$ group were dosed with vitamin E (50mg/kg/day), the rats in the $T_3$ group and $C_3$ group were dosed with sodium selenite (3mg/kg/day) and the rats in the $T_4$ gronp and $C_4$ group were dosed with coenzyme $Q_{10}$ (2.5mg/kg/day) intraperitoneally for 7 days or 14 days, respectively. Animals were killed at 7th and 14th day after dosing with bleomycin or saline. The results obtained were as follows: 1. Lung wet weight of treatment groups of rats was increased significantly while body weight gain of them was decreased significantly in comparison with that of control groups of rats (p<0.01). 2. The ratio(%) of lung wet weight to final body weight of treatment groups of rats was increased significantly in comparison with that of control groups of rats (p<0.01). 3. The main histopathological findings of lungs observed in rats at 7th day after dosing with bleomycin were proliferation of the type II alveolar epithelial cells and fibroblasts, increased invading of macrophages into lesions, round cell infiltration and perivascular edema. 4. Lung fibrous tissues were markedly increased in rats observed at 14th day after dosing with bleomycin. 5. Pumonary lesions observed in rats dosed with bleomycin and antioxidants(vitamin E, selenium, coenzyme $Q_{10}$) were not significantly different from those of rats given bleomycin alone.
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.