Patients with a wide range of cerebrovascular disease may have difficulty in opening their mouths, resulting in failing to swallow foods and maintain their oral hygiene. K-point was introduced as an effective trigger point to stimulate the jaw opening reflex for those patients. K-point stimulation may be useful as one of methods of helping open the jaw for dental examinations, or for placing foods onto the dorsum of the tongue and swallowing them effectively. Although this method cannot always guarantee the success of the jaw opening for every patient, it may still be considered to be an effective one to apply to patients having difficulty in jaw opening and swallowing disorder.
The purpose of this study is to investigate the effects of Bee Venom Herb-Acupuncture on the jaw opening reflex evoked by tooth pulp stimulation. Rats were anesthetized with thiopental sodium given intraperitoneally in an initial dose of 80mg/kg. Maintenance doses of 5mg/kg thiopental sodium were given through a cannular in the femoral vein as required to maintain light anesthesia. To apply noxious stimuli, a pair of enameled wires were inserted into the tooth pulp of the lower incisor. The effects of conditioning stimuli were estimated as an indicator of the degree of suppression of the digastric muscle electromyogram(dEMG) in the jaw opening reflex. Bee Venom Herb- Acupuncture(0.2% solution 0.1ml/rat) was injected to Hapgok(LI4) loci. In addition, Normal Saline (0.1ml/rat) was injected to Hapgok loci so as to compare the degree of suppression elicited from Bee-Venom. By administration of Bee Venom Herb-Acupuncture, the amplitude of dEMG was maximally suppressed to $67.5{\pm}3.38%$ ipsilaterally, 73.33{\pm}8.00%$ contralaterally. Generally, the dEMG activities caused by electrical stimulation were gradually suppressed during the stimulation and maximal suppressive effect showed at 15min after its onset. However the dEMG activities by Be Venom Herb-Acupuncture were immediately suppressed after its onset and the suppressive effect continued for a long time compared to electrical stimulation. In conclusion, Bee Venom Herb-Acupuncture may have a different mechanism of analgesia from that of electro-acupuncture and contribute to the modulation of pain analgesia.
The aim of this study was to investigate the effect of herbal organic extracts on the pain response provoked by noxious stimuli on dental nerve and the peripheral nerve conduction. Cats (2-2.5Kg regardless of sex) that were chosen as experimental animals were classified into control group, Asiasari radix application group and Zingiberis rhizoma application group. They were anesthetized with ${\alpha}$-chloralose, then anterior belly of digastric muscle of both sides were exposed and wire electrodes were inserted for recording of Electromyogram (EMG). Cavities were prepared on canines until pulp of the teeth were exposed. And after the drugs solubilized for 2% and 4% concentration (W/V) in vehicle were applied, their effects were compared through the recording of EMG immediately after drug application, 30 minutes, 60 minutes, 120 minutes and 5 days after, respectively. And after both inferior alveolar nerves were exposed, 4% organic extracts of Zingiberis rhizoma and Asiasari radix were applied for 30 minutes then the change of jaw opening reflex provoked by noxious stimuli on pulpal nerves were observed immediately after washing out, at 30, 60 and 90 minutes after drug had been washed out. After saphenous nerve of both sides were exposed, one side of nerve was used for vehicle application and the other side was used for drug application for 30 minutes. Then conduction of action potential of A-${\delta}$ and C-fiders of saphenous nerves, which have changed with time, was recorded. With analysis of these records, the following results were obtained: 1. Organic extract of Zingiberis rhizoma (2% or 4% concentration) greatly suppressed EMG of digastric muscle provoked by noxious stimuli on pulpal nerve at five days after application, the suppressive: effect was greater than that of organic extract of Asiasari radix. 2. Organic extract of Asiasari radix (2% or 4% concentration) suppressed jaw opening reflex provoked by noxious stimuli on pulpal nerve, at 5 days after drug application. 3. Organic extract of Zingiberis rhizoma and Asiasari radix (immediately after 30 minutes application) suppressed neural conduction of A-${\delta}$ and C-fibers, the suppressive effect was greater on A-${\delta}$ fibers than on C-fibers. 4. Jaw opening reflex provoked by noxious stimuli on pulpal nerve in inferior alveolar nerve was greatly suppressed 30 minutes after drug application, this effect was greater by Zingiberis rhizoma than by Asiasari radix.
The purpose of this study was to investigate the analgesic effect of eugenol, capsaicin and demethoxy-NE. Young adult cats, weighing 2.0 to 3.0kg, were used. Each animal was anesthetized (${\alpha}$-chloralose 60mg per kg body weight) and divided into four groups; control, eugenol, capsaicin and demethoxy-NE group. The anterior digastric muscles were exposed and a pair of electrodes was inserted to record the electromyograms. To expose the pulp, each canine teeth was prepared with a low speed bur under cooling and used for recording anterior digastric muscular EMGs evoked by noxious stimulation of dental pulp. To observe effects on jaw opening reflex, inferior alveolar nerve of both sides were exposed for drug application and wire electrodes were inserted in anterior digstric muscle for recording the EMGs. To observe effects on action potential, saphenous nerves of both sides were exposed and three tissue pools were made from surrounding tissue. The most distal pool was used for applying stimulation, the most proximal one for recording of action potential, and the other one for drug application. One side of inferior alveolar nerve and saphenous nerve were used for eugenol, capsaicin, or demethoxy-NE application, the other side of nerve for control experiments(only vehicle application). Anterior digastric muscular EMGs evoked by noxious stimulation of dental pulp were recorded before drug application, immediate after drug application, at 60 and 120 minutes, and 5 days after drug application. Action potentials were recorded before drug application, immediate after 30 minutes drug application, at 30, 60 and 120 minutes after drug had been washed out. The results were as follows; 1. Eugenol had a continuous blocking effect on the anterior digastric muscular EMGs evoked by noxious pulp stimulation and after 5 days, showed completely blocking effect. 2. After 5 days, demethoxy-NE applied to dental pulp had a considerable blocking effect on the jaw opening retlex evoked by noxious stimulation but capsaicin had no significant effect. 3. After 5 days, eugenol group showed the strongest blocking effect among the all experimental groups on the jaw opening reflex evoked by noxious stimulation of dental pulp and capsaicin group showed the weakest blocking effect. 4. Eugenol had a completely blocking effect on the action potential conductivity of peripheral nerve. Capsaicin and demethoxy-NE had the blocking effect on the action potential conductivity of ${\alpha}$-and C-nerve fibers. 5. Capsaicin, demethoxy-NE and eugenol applied to inferior alveolar nerve surppressed the jaw opening reflex evoked by noxious stimulation of dental pulp.
This study was performed to investigate the mechanism of central analgesic effects of antidepressants. Thirty four male rats were anesthetized with pentobarbital sodium (40 mg/kg, ip). A stainless steel guide cannula and a PE tube (PE10) were implanted into the lateral ventricle and cisterna magna area. Stimulating and recording electrodes were implanted into the incisor pulp and anterior digastric muscle. Electrodes were led subcutaneously to the miniature cranial connector sealed on the top of the skull with acrylic resin. The jaw opening reflex was used in freely moving rats, and antidepressants were administered intracisternally in order to eliminate the effects of anesthetic agents on the pain assessment and evaluate the importance of the central action site of antidepressants. After 48 hours of recovery from surgery, digastric electromyogram (dEMG) of freely moving rats was recorded. Electrical shocks (200 ${\mu}sec$ duration, 0.5-2 mA intensity) were delivered at 0.5 Hz to the dental pulp every 2 minute. Intracisternal administration of $15\;{\mu}g$ imipramine suppressed dEMG elicited by noxious electrical stimulation in the tooth pulp to $76{\pm}6%$ control. Intracisternal administration of $30\;{\mu}g$ desipramine, nortriptyline, or imipramine suppressed dEMG remarkably to $48{\pm}2,\;27{\pm}8,\;or\;25{\pm}5%$ of the control, respectively. Naloxone, methysergide, and phentolamine blocked the suppression of dEMG produced by intracisternal antidepressants from $23{\pm}2\;to\;69{\pm}4%,\;from\;32{\pm}5\;to\;80{\pm}9%,\;and\;from\;24{\pm}6\;to\;77{\pm}5%$ of the control, respectively. These results indicate that antidepressants produce antinociception through central mechanisms in the orofacial area. Antinociception of intracisternal antidepressants seems to be mediated by an augmentation of descending pain inhibitory influences on nociceptive pathways.
This study was performed to examine the mean arterial pressure and nociceptive jaw opening reflex after microinjection of glutamate into the amygdala in freely moving rats, and to investigate the mechanisms of antinociceptive action of amygdala. Animals were anesthetized with pentobarbital sodium (40 mg/kg, ip). A stainless steel guide cannula (26 gauge) was implanted in the amygdala and lateral ventricle. Stimulating and recording electrodes were implanted into each of the incisor pulp and anterior digastric muscle. Electrodes were led subcutaneously to the miniature cranial connector sealed on the top of the skull with acrylic resin. After 48 hours of recovery from surgery, mean arterial pressure and digastric electromyogram (dEMG) were monitored in freely moving rats. Electrical shocks (200 ${\mu}sec$ duration, $0.5{\sim}2$ mA intensity) were delivered at 0.5 Hz to the dental pulp every 2 minutes. After injection of 0.35 M glutamate into the amygdala, mean arterial pressure was increased by $8{\pm}2$ mmHg and dEMG was suppressed to $71{\pm}5%$ of the control. Injection of 0.7 M glutamate elevated mean arterial pressure by $25{\pm}5$ mmHg and suppressed dEMG to $20{\pm}7%$ of the control. The suppression of dEMG were maintained for 30 minutes. Naloxone, an opioid receptor antagonist, inhibited the suppression of dEMG elicited by amygdaloid injection of glutamate from $28{\pm}4\;to\;68{\pm}5%$ of the control. Methysergide, a serotonin receptor antagonist, also inhibited the suppression of dEMG from $33{\pm}5\;to\;79{\pm}4%$ of the control. However, phentolamine, an ${\alpha}-adrenergic$ receptor antagonist, did not affect the suppression of dEMG. These results suggest that the amygdala can modulate both cardiovascular and nociceptive responses and that the antinociception of amygdala seems to be attributed to an augmentation of descending inhibitory influences on nociceptive pathways via serotonergic and opioid pathways.
Journal of the korean academy of Pediatric Dentistry
/
v.23
no.3
/
pp.717-728
/
1996
The effects of electro-acupuncture on the pain threshold and the amplitude of dEMG(di-gastric EMG) evoked by the noxious electric stimulation on teeth and gingiva in dogs were studied. Experiments were carried out with 10 dogs weighing 5-8kg. Each animal was anestheticed with Entobar given intraperitoneally in an initial dose of 30mg/kg. Maintenance dose of 5mg/kg/hr was given through a cannula, in the femoral vein, as required to keep up light anesthesia. Bipolar stimulating wire electrodes, 0.1mm in diameter, insulated except for tips, were inserted into the upper canine and palatal gingiva. Rectangular aluminium plate electrodes (15$\times$5mm) were placed on acupuncture points, called Yin-Hsiang, located at both sides of the upper jaw. Rectangular biphasic current pulses of 2Hz, with a $250{\mu}sec$ duration, were delivered for 15 minutes. The dEMG activities were recorded from the anterior belly of the digastric muscle(one of the jaw opening muscles) using bipolar wire electrodes. The magnitude of the jaw opening reflex at different intensties of electro-acupuncture(1volt 4volt and 10volt) was estimated by averaging the 30 superimposed dEMGs recorded on an oscilloscope and audiomonitor. Data were analysed statistically with ANOV A and paired t-test. The obtained results were as follows: 1. Pain thresholds were increased 7.7 %, 15.4 %, 17.3 % in the teeth and 11.1 %, 19.0 %, 25.4 % in the gingiva as the intensities of electro-acupuncture increased incrementally. 2. Amplitudes of dEMG were decreaed 8.3%, 22.4%, 27.4% in the teeth and 9.8%, 36.5%, 42.2 % in the gingiva as the intensities of electro-acupuncture increased incrementally. 3. Inhibition of pain responses by the electroacupuncture was more effective in the gingiva than in the teeth.
Objectives: It has been well known that electroacupuncture(EA) has an analgesic effect and there is a pain control system in the central nervous system(CNS). The pain control system is composed of three major nuclei, which are periaqueductal gray(PAG), raphe nuclei, and the pain inhibitory complex located in the spinal cord. It has been suggested that the analgesic effect of EA might be the result of activation of the pain control system in the CNS. However, there may be a possibility that other nuclei are also involved in this pain modulation. Thus, we investigated whether the posterior intralaminar thalamic nuclei (PTIN) are involved in the pain modulation. Methods: To measure the level of pain, the jaw opening reflex (JOR) was used as a pain index. The magnitude of JOR is estimated by averaging the area of 10 successive responses. JOR was evoked by tooth-pulp stimulation with bipolar electrode carrying stimulus with the following parameters: intensity ranging from 420uA to 680ulA, 0.3ms duration of square pulse, and 0.5 Hz. Hapkog($LI_4$) and Taechung ($LR_3$) were the chosen acupoints. The Hapkog point was stimulated ipsilaterally at 5V, 3 Hz, for 15min in total, and the Taechung was stimulated at 2-3 V, 3 Hz, and for a total of 15 or 30 minutes. Different intensities of stimulation were given the PITN; one was given at $300{\mu}A$ and the other was at 500uA. The position stimulated in these nuclei by Paxinos Atlas was AP; from bregma $-4.0{\sim}-4.3mm,\;L; 0.5{\sim}1.8mm,\;D;\;4.8{\sim}6.3mm$. Results: The Hapkog point had a significant analgesic effect (P<0.05). However, the Taechung point had no effect. Both types of stimulation in the PITN did not reveal any analgesic effects. Conclusions: From these results, it was suggested that the posterior intralaminar thalamic nuclei are not involved in the modulation of pain.
The purpose of this study is to prove the analgesic effects of apitoxin and its mechanism via jaw-opening reflex(JOR) and measuring expression of mRNA in Phospholipase and Tryptophan hydroxylase(TPH) using RT-PCR. The experiments were carried out on Sprague-Dawley rats(300-400g) and mastocytoma(P-185 HTR) for JOR and RT-PCR, respectively. Rats anesthetized with thiopental sodium (80mg/kg) were used in the Tooth Pulp stimulation induced JOR. The amplitude of a digastric electromyogram (dEMG) was recorded during the stimulation at an intensity of 1.5 times the threshold for JOR. Apitoxin used in this experiment was diluted with normal saline by 1:1000. Apitoxin was injected intravenously into the test group while normal saline to the control group. However, it was injected directly into the cell of mastocytoma. We referred to base sequence registered in Genbank in designing primers for RT-PCR. The results were as follows; (1)Compared with control group, analgesic effect started to show right after Sprague-Dawely rats were treated with apitoxin($71.50{\pm}8.08$) and lasted for 50 minutes. (2)As a result of the experiment of RT-PCR, we witnessed significant changes in the degree of expression of phospholipase or rate-limiting enzyme of biosynthesis of prostaglandins with $10{\mu}g/ml$ apitoxin.($31.74{\pm}18.98%$, P<0.05) (3)As a result of the experiment of RT-PCR, we witnessed significant changes in the degree of expression of TPH or rate-limiting enzyme in biosynthesis of serotonin with $10{\mu}g/ml$ apitoxin.($131.37{\pm}16.87%$, P<0.05). These results suggest that $10{\mu}g/ml$ apitoxin have the most analgesic effects. This study showed that apitoxin has analgesic effects and held good for 50 minutes. The injection of apitoxin has brought out changes in the degree of expression of phospholipase and TPH. These results strongly suggest that analgesic mechanism by apitoxin is closely related to prostaglandins and serotonin.
It is well known that stress induces analgesia. This study was designed to demonstrate the stress-induced analgesia by employing hemorrhage and restraint and to investigate its mechanism and sex difference. The degree of pain was assessed by measuring the magnitude of jaw opening reflex produced by a noxious electrical stimulation in the dental pulp and by measuring the latency to withdraw the tail from a heat ray. Restraint showed an antinociceptive response. A significant increase in pain threshold on bleeding was shown and the increase was larger in male group than in female group. The tail flick latency (TFL) on bleeding after AVP antagonist injection into the ventricle was decreased and the decrease was greater in male rats than in female rats. Castration resulted in a significant reduction of TFL. This effect was reversed by treatment with sex hormones. TFL was decreased during hemorrhage in castrated rats. This response was opposite to that in non-castrated rats. TFL was further decreased during hemorrhage after infusion of AVP antagonist, and there was a significant sex difference. These results suggest that both restraint and hemorrhage produce an antinociception and that, in hemorrhage-induced analgesia, AVP and sex hormones may play an important role and male rats show a greater analgesic response.
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.