Bartonella henselae is the causative agent of cat scratch disease. Although cats are the main zoonotic reservoirs of Bartonella spp., unusual cases of cat scratch disease caused by a domestic dog scratch have been recently reported. For the in vivo B. henselae infection, eight dogs were inoculated intradermally with $2{\times}10^8CFU$ of B. henselae Houston-1 suspended in 1 ml of phosphate buffered saline on day 0 and subsequent injections of the same amount given intradermally on days 21, 28, 36, 58 and 64. After in vivo canine B. henselae infection was confirmed by nested PCR, the IFN-$\gamma$ levels of the culture supernatant of PBMC stimulated with B. henselae was significantly higher in the B. henselae-PCR positive group than the B. henselae-PCR negative group. Our results showed that the canine immune responses against B. henselae were different from those of cats. Th1 activation by B. henselae stimulation was characterized in dog peripheral blood mononuclear cells, whereas Th2 activation was reported in B. henselae-infected cats.
A seven-year-old, castrated male Basset hound weighing 21.1 kg was presented for investigation of anorexia, lethargy, weight loss, melena and vomiting for 4 months. In laboratory findings, microcytic hypochromic anemia was identified, and other results were within a normal reference range. On the plain radiographs, soft tissue opacity was increased in the descending duodenal region; and on the contrast radiographs, ulcerative changes were identified in the entire segment of descending duodenum. Ultrasonographic findings included increased duodenal wall thickness and duodenal wall layering was lost. Endoscopy revealed irregular mucosal surface and luminal narrowing of the descending duodenum. There was concentrically thickened descending duodenum on the computed tomography. And the wall of the descending duodenum showed heterogenous enhancement after contrast agent injection. On histopathological findings, both chronic inflammation with mucosal proliferation and neoplastic changes with multiple small glandslike structures invading into the submucosa were identified. Based on these findings, presented case was diagnosed as an annular form duodenal adenocarcinoma. After 13 months of supportive medical treatment, the patient was expired. The purpose of this case report was to describe the duodenal adenocarcinoma in a dog.
Kim, Hyeon-Cheol;Hong, Eui-Ju;Ryu, Si-Yun;Choi, Kyoung-Seong;Yu, Do-Hyeon;Cho, Jeong-Gon;Park, Jinho;Chae, Joon-Seok;Park, Bae-Keun
Journal of Veterinary Clinics
/
v.37
no.5
/
pp.242-248
/
2020
An intestinal strigeiid trematode, Apharyngostrigea pipientis, was detected from Ardea cinerea jouyi, Egretta intermedia and Nycticorax nycticorax between July, 2006 and June, 2020 in Daejeon metropolitan city and Kangwon-do, Republic of Korea. It was observed with a light and scanning electron microscope (SEM), and molecularly analyzed with 18S rRNA genes. The infection rate of the strigeiid trematode was 25.9% (7/27). The body is cylindrical in whole mount, greatly elongated in outline and shows a strong dorsal curvature. The overall measurements are: length 4.1-4.8 mm; fore-body 1.00-1.20 mm by 0.8-0.9 mm; hind-body 3.2-3.6 mm by 0.43-0.46 mm. The body is covered by a relatively thick cuticle, devoid of spines. The oral sucker leads into a short esophagus that is devoid of a muscular pharynx. The holdfast organ is enormously developed. The vitelline follicles distributed dorsal wall of fore-body and hind-body. This strigeiid trematode especially differs from other species of genus Apharyngostrigea in morphology. Although these A. pipientis are several morphological distinctions from Apharyngostrigea cornu, the partial sequence of 18S rRNA showed the sequence homology of A. pipientis (99.9%) and A. cornu (99.8%), and this result revealed their conspecific relationship between A. cornu and A. pipientis. This is the first report of A. pipientis in the Republic of Korea.
To investigate the etiology, pathogenicity and virological properties of NYJ-1-87 strain of Aujeszky's disease virus (ADV) that was isolated from the diseased piglet in Korea, the virus at $10^{6.0}TCID_{50}/0.1ml$ was inoculated intranasally and subcutaneously into 30 to 35 days-old piglets. Results obtained through the experiments were summarized as follows. 1. Ten of the infected piglets were clinically observed for 15 days. On the 2nd day post-inoculation(pi), the signs of pyrexia, anorexia and convulsion were noted. On the 4th to 7th days pi, nervous signs of incoordination and intermittent spasm were shown in the most of piglets, and one out of 5 piglets infected intranasally was died with severe nervous signs at the 7th day pi. The signs became relieved on the 8th day pi and all of remainder were completely recovered on the 13th to 14th days pi. 2. In hematological study, prominent decrease in the number of total leukocyte and lymphocyte was shown in the ADV-infected piglets on the 6th day pi. On the 8th day pi, the cell numbers were slightly increased and returned to normal level on the 10th day pi. 3. Viral excretion of the ADV-inoculated piglets was examined by swabbing of nasal and oral cavities, and rectal feces. During the periods of the 3rd to 11th days pi, the virus was excreted intermittently from nasal and oral cavities, and rectal feces. The nasal excretions were shown the highest virus concentration of $10^{5.2}TCID_{50}/0.1ml$ at the 5th day pi. 4. Recovery of the inoculated virus from various organs of the piglets that were died or experimentally slaughtered was attempted, and the virus was isolated from the tissues of brain and tonsil by the cultured cell-inoculation method. The highest recovery rate was noted in the tonsil. By indirect immunofluorescence antibody assay using ADV-monoclonal antibody, the viral antigens were detected in tissues of spleen and liver as well as brain and tonsil on the 7th to 9th days pi. The virus was not isolated from blood and the tissues of lung and kidney throughout the experiments. 5. Titers of virus neutralizing antibody in the piglets experimentally infected with ADV became increased after the 6th to 9th days pi in both of intranasal and subcutaneous inoculation showing the highest titers of 64 to 128 on the 29th day pi. When the antibody levels were measured by radial immunodiffusion enzyme assay, the reactive diameter was enlarged to be positive after the 4th to 6th days pi in both of intranasal and subcutaneous inoculation showing the largest diameter of 13 to 14mm on the 29th day pi.
In order to know the influence of mast cells on the mammary tumor development, the growth of the mammary carcinoma, the numerical changes and the morphological findings of mast cells appeared in the tumor were microscopically observed in the rat treated with DMBA and each chemical of histamine, heparin, pyrilamine or cimetidine. The results observed were summarized as follows: The tumor induction time that represented the number of days elapsing between the 3rd DMBA administration until a first tumor became $10{\times}10mm$ in diameter was $42.5{\pm}4.7$ days, and the mean number of tumor mass per rat was $3.4{\pm}1.2$ in the DMBA-treated group. No significant difference was apparent in the tumor induction time of the histamine-treated group, heparin-treated group or pyrilamine-treated group compared with the control group, but in the cimetidine-treated group the tumor induction time was $61.8{\pm}10.6$ days (p<0.005). The mean number of tumors per rat was $2.1{\pm}0.9$ in the cimetidine-treated group in contrast to $3.4{\pm}1.3$ in the control group (p<0.005). Numerical changes of mast cells were observed according to the development of DMBA induced mammary tumors that were separated into three major classes of tumors. The numbers of mast cells in all the experimental group were inclined to increase significantly according to the mammary tumor development (p<0.005), and the histamine-treated group, heparin-treated group, or pyrilamine-treated group were nearly similar to the control group. But the mast cells in the each stage of tumor development were more numerous in the cimetidine-treated group than in the control group (p<0.005). There were not significant in the numerical changes of mast cells among the experimental groups on each stage of carcinomas separated by early stage, middle stage and late stage. In the morphological characteristics of mast cells, the degranulation was not detectable from the hyperplasia stages to the early stage of carcinoma, but its degranulation was observed at the middle stage of carcinoma. Most mast cells were nearly degranulated at the late stage of carcinoma. The histamine treated group, pyrilamine-treated group and cimetidine treated group did not differ from the control group in morphological changes of mast cells, but the degranulation was shown mild in the heparin-treated group. And the degranulation gave rise to the depletion of intercellular matrix via exocytosis all the experimental group. From above results, it is supposed that mast cells inhibit the tumor development and that the inhibition is not caused by a single-factor, but by a complex activities of mast cell mediators.
In order to investigate the histopathological, mechanism of Rompun-induced shock, the development of mammary carcinoma, the numerical changes and the morphological findings of the mast cells appeared in the carcinoma were microscopically observed in the rat treated with DMBA and each chemical of compound 48/80 and Rompun. Also mast cell degranulation induced by Rompun was observed with electron microscope. The results observed were summarized as follows: Tumor appeared in 100% of the animals. Tumors grew more rapidly to $10{\times}10mm$ in rats depleted of mast cells ($37.7{\pm}4.2$ days) than was observed in the control group ($42.5{\pm}4.7$ days) (p<0.005). The mean number of tumors per rat was $2.8{\pm}1.3$ in the compound 48/80- treated group in contrast to $3.4{\pm}1.3$ in the control group. No significant difference was apparent in the tumor induction time of Rompun treated group compared with the compound 48/80-treated group, but the tumor measuring at least $10{\times}10mm$ appeared more quickly in the Rompun treated group than in the control group (p<0.005). The numbers of mast cells in the control group were inclined to increase significantly according to the mammary tumor development (p<0.005). In contrast, the mast cells were fewer significantly in the compound 48/80-treated group and Rompun-treated group than in the control group (p<0.005). The numbers of mast cells in the compound 48/80-treated group and Rompun-treated group were inclined to reduce significantly according to the stages of the mammary carcinoma growth in contrast to the control group respectively. The ultrastructural morphologies of mast cells at 30 minutes after Rompun injection were appeared many normal granules in the cytoplasm, but many normal and degranulated granules were scattered along the cell membrane. And at 1 hour after Rompun injection mast cell granules were disappeared nearly or rarely seen. many long cytoplasmic projections were folded back to adhere to their own surface membrane. and mast cells resulted in a reduced size of these cells. Otherwise. compound 48/80 caused extensive degranulation of mast cells by disrupting cell membrane. but mast cell degranulation by Rompun was observed exocytosis of granules through a channel. From the above results. it is concluded that the Rompun may give rise to the dealth of animals as a shock caused by mast cell degranulation.
Lee, Deok-Yong;Seo, Yeon-Soo;Kang, Sang-Gyun;Yoo, Han Sang
Korean Journal of Veterinary Research
/
v.46
no.3
/
pp.255-261
/
2006
Experimental animals have been used to biological and medical purposes and the animals must be, for these purposes, healthy and clean to microbial infection. However, the animals can be easily exposed to pathogenic microorganism via several routes. Of the routes, environmental conditions are the most important factors to keep the animals healthy and clean, especially air condition. Monitoring of air-condition has been required to keep the animal healthy and clean. However, any guideline is not available for experimental conditions with pigs. Therefore, the sampling times and points were compared in different conditions to establish an optimal protocol for monitoring of air borne bacteria. Tryptic soy agar(TSA), blood agar containing 5% defibrinated sheep blood and Sabraud dextrose agar(SDA) were used as media to capture total bacteria, pathogenic bacteria and fungi, respectively. Two methods, compulsive capture using an air-sampler and capturing fall-down bacteria were used to capture the microorganisms in the air. The points and time of capturing were different at each experiment. Air borne microorganisms were captured at three and five points in the open and closed equipments, respectively. Air was collected using an air-sampler for 1 min and 5 min and the agar plates as open status were left from 30 min to 2hr. At first, we monitored an experimental laboratory which dealt with several pathogenic bacteria and then, a protocol obtained from the investigation was applied to open or close experimental conditions with pigs. Number of bacteria was high from 10:00 to 15:00, especially on 13:30-15:30 but sharply decreased after 17:00. The tendency of the number of bacteria was similar between two methods even though the absolute number was higher with air sampler. Critical difference in the number of cells was observed at 5 min with air sampler and 2 hr with fall-down capturing method. However, 1 min with air sampler and 1 hr with fall-down capturing were the best condition to identify bacterial species collected from the air. Number of bacteria were different depending on the sampling points in closed condition but not in opened condition. Based on our results, a guide-line was suggested for screening air-borne microorganism in the experimental conditions with pigs.
Central analgesic effect of capsaicin was assessed by the tail flick reflex (TFR) test, using male Sprague-Dawley rats under anesthesia with pentobarbital sodium (induction with 40 mg/kg and maintenance with $4{\sim}8\;mg/kg/hr$). Level of norepinephrine in the spinal cord was also measured. Capsaicin, $35{\sim}150\;{\mu}g$, was injected intrathecally, and the TFR latency was measured before, 10, 30, and 60 minutes after the drug administration. TFR latency was increased 100% or more immediately by intrathecal capsaicin, from 2.9 seconds to the maximum of 7.0 seconds at 10 minute after the drug; P<0.01. The increase in TFR latency was maintained during the course of experiment of 2 hours. Concomitant reduction of NE content in the spinal cord was observed; from 16 ng/mg protein to 7 ng/mg protein. On the other hand, subcutaneous injection of capsaicin of 50 mg/kg did not change the TFR latency although the NE content reduced similarly to the case of intrathecal injection. Pretreatment of the animal with 0.5 mg/kg of MK-801 reversed the increase of TFR latency and NE reduction induced by intrathecal capsaicin. These results suggest that capsaicin causes analgesia at the spinal cord level by activating the excitatory amino acid-NE-dorsal horn interneurons axis of the descending inhibitory pain modulation pathway.
Background: Elevated testicular temperature disrupts spermatogenesis and causes infertility. In the present study, the protective effect of enzymatically biotransformed Panax ginseng Meyer by pectinase (GINST) against chronic intermittent heat stress-induced testicular damage in rats was investigated. Methods: Male Sprague-Dawley rats (4 wk old, 60-70 g) were divided into four groups: normal control (NC), heat-stress control (HC), heat-stress plus GINST-100 mg/kg (HG100), and heat-stress plus GINST-200 mg/kg (HG200) treatment groups. Each dose of GINST (100 mg/kg and 200 mg/kg) was mixed separately with a regular pellet diet and was administered orally for 24 wk. For inducing heat stress, rats in the NC group were maintained at $25^{\circ}C$, whereas rats in the HC, HG100, and HG200 groups were exposed to $32{\pm}1^{\circ}C$ for 2 h daily for 6 mo. At week 25, the testes and serum from each animal were analyzed for various parameters. Results: Significant (p < 0.01) changes in the sperm kinematic values and blood chemistry panels were observed in the HC group. Furthermore, spermatogenesis-related molecules, sex hormone receptors, and selected antioxidant enzyme expression levels were also altered in the HC group compared to those in the NC group. GINST (HS100 and HS200) administration significantly (p < 0.05) restored these changes when compared with the HC group. For most of the parameters tested, the HG200 group exhibited potent effects compared with those exhibited by the HG100 group. Conclusion: GINST may be categorized as an important medicinal herb and a potential therapeutic for the treatment of male subfertility or infertility caused by hyperthermia.
Kim, Se-Jin;Lee, Jong Ho;Yang, Chang Yeol;Kang, Taek-Jun;Cho, Myoung Rae;Hong, Ki-Jeong
Korean journal of applied entomology
/
v.54
no.4
/
pp.393-400
/
2015
An insect parasitic mite was found on a larva from Japanese apricot seed. The mite was identified as Pyemotes moseri Yu et Liang (Acarina: Pyemotidae) new to Korea. The host larva was identified as Eurytoma maslovskii using mitochondrial DNA sequencing analysis. We conducted preliminary study on its reproduction and parasitization capacity in laboratory condition. A mated female mite reared on Eurytoma maslovskii larva. We counted and sexed newborn progenies and then eliminated them during periodical observations. To test parasitization capacity, a PCR tube containing mass reared P. moseri and Japanese apricot seeds (assumed bear larva of E. maslovskii) placed in a stainless bath filled with potting soil. One month later, we surveyed the seeds whether the E. maslovskii larva parasitized by mite or not. We repeated this experiment three times with five replications each. Average life span (days from parasitization to the end of reproduction) of gravid females was 24.4 days (n=8). A gravid female reproduced 104.0 female progenies (n=8). Although there were more than seven Japanese apricot seeds per bath containing larva or pupa, we found parasitization only in two seeds.
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.