• Journal of Preventive Medicine and Public Health
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• 제21권2호
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• pp.207-216
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• 1988

Premature rupture of membrane is the most frequent cause of low birth weight infant delivery which increase the maternal and fetal morbidity and perinatal mortality. A retrospective case-control study was performed on 315 mothers who delivered low birth weight infants($\leq$2.5kg) with premature rupture of membrane and as control group 546 mothers who delivered normal birth weight infants(2.9-3.7kg) without premature rupture of membrane were chosen. The results obtained from this study were as follows: 1. The proportion of low birth weight infants due to premature rupture of membrane among all low birth weight infant deliveries was 14.5%, and this is equivalent to 1.1% among all deliveries. 2. The most significant maternal risk factor of low birth weight infant deliveries with premature rupture of membrane was infections on vagina, cervix and uterus during pregnancy. Compared with control, adjusted odds ratio was 7.61(95% confidence interval(CI) 1.88-30.88, p=0.004). Other significant maternal risk factors were the history of induced abortion, spontaneous abortion, and the experience of premature delivery. The risk ratios were 1.82, 2.07, 4.42, respectively. 3. Breech presentation did increase the risk of low birth weight infant delivery with premature rupture of membrane compared with control(Adjusted Odds ratio=2.66, 95% CI 1.35-5.26, p=0.005). 4. Mothers who had not taken antenatal care were having higher risk of low birth weight infant delivery with premature rupture of membrane against control(Adjusted odds ratio=1.73, 95% CI 1.19-2.53, p=0.004). These study results show that maternal factors such as the infection of genital organs during pregnancy, the history of induced abortion and breech presentation are significantly associated with the premature rupture of membrane in the low birth weight deliveries, and that most of these risk factors are controllable ones through proper antenatal cares.

• Journal of Chest Surgery
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• 제16권2호
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• pp.199-212
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• 1983

The inhibition/influences of adenine compounds on the heart have been described repeatedly by many investigators, since the first report by Druny and Szent-Gyorgyi [1929]. These studies have shown that adenosine and adenine nucleotides have an over-all effect similar to that of acetylcholine [ACh] by slowing and weakening the heartbeat. The basic cellular and membrane events underlying the inhibitory action of adenosine on sinus rate, however, are not well understood. Furthermore, the physiological role of adenosine in regulation of the heartbeat remains still to be elucidated. Therefore, this study was undertaken in order to examine the response of rabbit SA node to adenosine and to compare the response to that of ACh. Isolated SA node preparation, whole atrial pair, or left atrlal strip was used in each experiment. Action potentials of SA node were recorded through the intracellular glass microelectrodes, which were filled with 3M KCI and had resistance of 30-50 M. All experiments were performed in a bicarbonate-buffered Tyrode solution which was aerated with 3% $CO_2-97%$ $O_2$ gas mixture and kept at $35^{\circ}C$. Spontaneous firing rate of SA node at 35C [Mean + SEM, n=16] was 154 + 3.3 beats/min. The parameters of action potentials were: maximum astolic potential [MDP], -731.7mV: overshoot [OS], 9 + 1.4mV; slope of pacemaker potential [SPP], 94 3.0mV/sec.Adenosine suppressed the firing rate of SA node in a dose dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was potentiated in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine [2mg/l] and propranolol [$5{\times}10^{-6}M$]. ACh [$10^{-6}M$] responses on action potential were similar to those of adenosine by increasing MDP and decreasing SPP. These effects of ACh disappeared by pretreatment of atropine [2mg/1]. Inhibition/effects of adenosine and ACh on sinus rate were enhanced synergistically with the simultaneous administration of adenosine and ACh. Marked decrease of overshoot potential was the most prominent feature on action potential. Dipyridamole [DPM], which is known to block the adenosine transport across cell membrane, definitely potentiated the action of adenosine . Adenosine suppressed the sinus rate and atrial contractility in the same dosage range, even in the reserpinized preparation. Above` results suggest that adenosine suppresses pacemaker activity, like ACh, by acting directly on the membrane of SA node, increasing MDP and decreasing SPP.

• 대한약리학회지
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• 제16권1호
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• pp.41-50
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• 1980

Chenodeoxycholic acid(CDCA) has been used as a gallstone dissolving agent since 1972. Recently, ursodeoxycholic acid(UDCA) has been reported to be effective in dissolving gallstones. Both bile acids increased bile flow. The increase in bile flow associated with an increase in cholesterol level in bile after CDCA or UDCA infusion was reported. In this study, using the smooth muscle strips of guinea pig and fowl, responses of the cholates were observed. In addition, the influence of adrenergic blocking agents on the response of the strips to cholates was investigated. Also the effects of cholates on cardiac function were examined by using isolated atria of rabbit and heart of anesthetized frog. The results are as follows: 1) All cholates, such as UDCA, CDCA, and CA produced a marked inhibitory effect on the motility in isolated duodenal strip of guinea pig and fowl, however, only UDCA showed the contraction in the isolated esophagus of fowl. These effects of cholates were blocked by propranolol. 2) In isolated guinea pig stomach strip and gall bladder, cholates exhibited a marked inhibitory effect on the motility and the effects due to UDCA and CA were blocked by phenoxybenzamine while CDCA was not affected. 3) The spontaneous and ouabain induced arrhythmia was partially abolished by cholates. However, concomitant administration of cholates with ouabain or epinephrine caused a marked prolongation in occurrence of atrial arrhythmia in comparison with ouabain or epinephrine alone in isolated rabbit atria. 4) In the heart of anesthetized frog, the epinephrine-induced arrhythmia was partially abolished by cholates. The combined treatment with cholates and ouabain or epinephrine produced a marked prolongation in occurrence of the arrhythmia in comparison with, ouabain or epinephrine alone. From the above results, it can be suggested that the effects of cholates on the smooth muscle of duodenum and esophagus are produced in response to adrenergic ${\beta}$-receptor and the effect or gall bladder and stomach is more likely due to the direct effect on the muscle. In addition, cholates exhibit a slight antiarrhythmic effect on heart, therefore, cholates can be classified as a nonselective antiarrhythmic drug, such as propranolol.

• Restorative Dentistry and Endodontics
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• 제15권1호
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• pp.1-15
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• 1990

The aim of this study was to investigate the effect of dental therapeutic agent on conduction velocity and threshold current of intradental A- and C-fibers in the cat. Inferior alveolar nerve of cat anesthetized with sodium pentobarbital was exposed and dissected until response of functional single pulp nerve until could be evoked by monopolar electrical stimulation of the crown of the lower left canine teeth. 10ms rectangular pulse was used to determine the threshold current and 1ms rectangular pulse was used to determine conduction velocity. After application of calcium chloride (1, 2, 6M), calcium hydroxide mixed with saline, potassium chloride (0.2, 0.8, 1.6M), eugenol, zinc oxide eugenol to the cavity on the labial surface, conduction velocity and threshold current of single pulp nerve unit were compared with the control. In 10 cats, 24 $A{\delta}$- and 11 C- pulp nerve units were recorded. The mean conduction velocities of $A{\delta}$- and C-fibers were 7.5m/sec (SD=5.8) and 1.2m/sec (SD=0.4), respectively. The mean threshold current was $12.3{\mu}A$ (SD=5.3) for $A{\delta}$-fibers and $24.9{\mu}A$ (SD=8.1) for C-fibers. 1, 2, 6M calcium chloride caused decrease of conduction velocity and remarkable increase of threshold current in $A{\delta}$- and C-fibers. The effect of calcium hydroxide mixed with saline was similar but smaller than calcium chloride solution. 0.2M potassium chloride had insignificant effect. In 0.8M potassium chloride, the threshold current was increased although conduction velocity was not affected. In 1.6M potassium chloride, the threshold current was increased and the conduction velocity was slowed down. Spontaneous activity was recorded frequently for first 5 min but gradually reduced both in $A{\delta}$- and C-fibers. Eugenol had irreversible effect on pulp nerve in that initially there were not certain changes in the conduction velocity and threshold current of $A{\delta}$- and C-fibers, but the responses to electrical stimulation were abruptly disappeared after sustained application and were not recovered. Contrary to eugenol, zinc oxide eugenol did not caused significant increase of the threhold current and caused time dependent decrease of the conduction velocity, and did not show any irreversible change.

• The Korean Journal of Physiology
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• 제18권1호
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• pp.19-35
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• 1984

Since the first report of Drury and $Szent-Gy{\ddot{o}}rgyi$ in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. These studies have shown that adenosine and adenine nucleotides have overall depressant effects, similar to those of acetylcholine. Heart beats become slow and weak. It is also well known that adenosine is a potent endogenous coronary vasodilator. Many investigations on the working mechanisms of adenosine have been focused mainly on the effects of the coronary blood flow. However, the cellular mechanisms underlying the inhibitory action of adenosine on sinus node are not well understood yet. Thus, this study was undertaken to examine the behavior of rabbit SA node under influence of adenosine. In these series of experiments three kinds of preparations were used: whole atrial pair, left atrial strip, and isolated SA node preparations. The electrical activity of SA node was recorded with conventional glass microelectrodes 30 to 50 $M{\Omega}$. The preparations were superfused with bicarbonate-buffered Tyrode solution of pH 7.35 and aerated with a gas mixture of $3%\;CO_2-97%\;O_2$ at $35^{\circ}C$. In whole atrial pair, adenosine suppressed sinoatrial rhythm in a dose-dependent manner. Effect of adenosine on atrial rate appeared at the concentration of $10^{-5}M$ and was enhanced in parallel with the increase in adenosine concentration. Inhibitory action of adenosine on pacemaker activity was more prominent in the preparation pretreated with norepinephrine, which can steepen the slope of pacemaker potential by increasing permeability of $Ca^{+2}$. Calcium ions in perfusate slowly produced a marked change in sinoatrial rhythm. Elevation of the calcium concentration from 0.3 to 8 mM increased the atrial rate from 132 to 174 beats/min, but over 10 mM $Ca^{+2}$ decreased. The inhibitory effect of adenosine on sinoatrial rhythm developed very rapidly. Atrial rate was recovered promptly from the adenosine-induced suppression by the addition of norepinephrine, but extra $Ca^{+2}$ was less suitable to restore the suppression of atrial rate. Adenosine suppressed also atrial contractility in the same dosage range that restricted pacemaker activity, even in the reserpinized preparation. In isolated SA node preparation, spontaneous firing rate of SA node at $35^{\circ}C$(mean{\pm}SEM, n=16) was $154{\pm}3.3\;beats/min. The parameters of action potentials were: maximum diastolic potential(MDP), $-73{\pm}1.7\;mV: overshoot(OS), $9{\pm}1.4\;mV: slope of pacemaker potential(SPP), $94{\pm}3.0\;mV/sec. Adenosine suppressed the firing rate of SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}M$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine and propranolol. Lowering extra $Ca^{2+}$ irom 2 mM to 0.3 mM resulted in a marked decrease of OS and SPP, but almost no change of MDP. However, increase of perfusate $Ca^{2+}$ from 2 mM to 6 or 8 mM produced a prominent decrease of MDP and a slight increase of OS and SPP. Dipyridamole(DPM), which is known to block the adenosine transport across the cell membrane, definately potentiated the action of adenosine. The results of this experiment suggest that adenosine suppressed pacemaker activity and atrial contractility simultaneously and directly, by decreasing $Ca^{2+}-permeability$ of nodal and atrial cell membranes.

• Clinical and Experimental Reproductive Medicine
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• 제15권2호
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• pp.103-117
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• 1988

Ovulation induction was done with 3 different regimens as clomid combined with HMG, HMG only, and FSH combined with HMG in 28 menstrual cycles for IVF-ET and GIFT program. The appearance of endogenous LH surge, estradiol plateau, atypical LH surge, and time from initiation to peak of LH surge in serum and urine were observed and compared in 3 groups. 1. The estradiol concentration of serum LH surge day was similar in three groups but 1st group (Clomiphene Citrate+Sequential HMG) was slightly higher at $1924.0{\pm}865.1\;pg/ml$. In regards to the existence of serum estradiol plateau, 3rd group (FSH+Sequential HMG) was highest at 60%, and 1st group and 2nd group (HMG only) were similar at 33% and 44% respectively. 2. The number of ovarian of ovarian follicle which was more than 18mm in diameter was $4.1{\pm}2.0$, $4.2{\pm}2.1$ respectibely for 2nd group and 3rd group. Although the numbers were slightly higher thean 1st group for each ovarian follicle, serum estradiol value per follicle was higher for 1st group at $583.0{\pm}261.2pg/ml$. 3. When measuring the urine LH surge according to Hi-Gonavi and according to the standard set by three different types of surge, simultameous satisfaction for 1st group, 2nd group, 3rd group was two cases, five cases, four cases respectively at 40%, and the remained cases were composed of numorous type combination which satisfied the two definition, simultaneously in this study, the LH surge starting time was determined only in the cases tow combination were satisfied simultaneously at first, but there are something to study more. In one case of the 3rd group. 4. The concentration of LH surge start in urine and serum of 2nd group was highest at306. $0{\pm}287.2IU/l$ and $34.0{\pm}9.9mIU/ml$ and 1st group was low at $116.6{\pm}66.1IU/l$ and 7.4mIU/ml. The urine and serum value of LH was highest at $1644.4{\pm}988.8IU/l$, $65.9{\pm}15.0mIU/ml$ for 2nd group, 1st group was low at urine, and 3rd group was low of serum. With pregnancy established, the LH concentration of urine was relatively high but on the contrary the LH concentration of serum was low compared to urine concentration. 5. Time from LH surge start to the maximun of urine and serum value was highest at 15. $7{\pm}9.1$ hrs and $10.8{\pm}4.9$ hrs for 1st group and 3rd group. With pregnancy established, time was shortened for urine but on the contrary serum showed an increase in time. 6. The concentration of LH which increases with time on urine was highest at 2nd group ($194.6{\pm}76.8\;IU/hour$). The lowest increase for serum was at 3rd group (2.1mIU/hour). With pregnancy established, urine showed more increase than control group ($266.5{\pm}47.4\;IU/hour$) and for serum there was similar increase ($3.4{\pm}0.8\;mIU/hour$). 7. There were two examples of non-typical surge from 1st group and 3rd group each. Among these three cases showed a reestablishment of LH surge after 10-24 hours. 8. Endogenous spontaneous Lh surge occurs once for each 2nd group and 3rd group.

• 한국산업보건학회지
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• 제18권3호
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• pp.224-238
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• 2008

The aim of this study is to confirm the physicochemical property and hazard of thinner (012), which is a diluent of enamel paint used for floor coating for waterproofing and oil painting for the outer wall. The literatures of physicochemical property and hazard of thinner were surveyed and its physicochemical property were evaluated. And then, the inhalation toxicity of thinner affecting the central nervous system and reproductive organs in rats were examined by subchronic (6 h./day. 5 days/ week for 13 weeks) inhalation test. 1) According to the 13-week subchronic inhalation test, there were no significant changes in clinical test and body weight. However, a significant evidence of toxicity was observed in the hematological test and organ weight such as heart, kidney, liver and brain (p<0.01) in the 200 ppm and 1,000 ppm exposure groups in a dose response manner. In the histopathology analysis, there were no significant evidence of toxicity. Therefore, thinner was not classified as an organ targeted toxic agent. In case of Harmfulness, it could be classified as a chronic toxic agent 3($500 ppm/4hr, rat). 2) The reproductive toxicity such as extension of the period of estrous cycle, reduction of serum estradiol concentration and increase of frequency of the abnormal sperm was observed in the 1,000 ppm exposed animals. 3) The result of the physicochemical property of the test material showed that the specific gravity was 0.793, boiling point $155.8^{\circ}C$, steam pressure 2.1 kPa, ignition point $34.5^{\circ}C$, and spontaneous ignition point $280^{\circ}C$. The endothermic and exothermic values were 371.4 J/g and 159.1 J/g. respectively. The explosion limit was 214 mg/l. These data showed that thinner could be classified as an explosion agent level 1.2 and ignitive liquid agent 3 ($23-60^{\circ}C$) according to the notification No. 2008-1 of the Labor Ministry, "Classifying Standard of Chemical Materials."

• 한국산림과학회지
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• 제85권3호
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• pp.487-495
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• 1996

이 연구는 사유림의 영세성 극복과 경영활성화를 위해 국가정책사업(國家政策事業)으로 추진되고 있는 협업경영사업의 실태를 조사할 목적으로 수행되었다. 이러한 목적을 위해 협업체 관련 통계자료, 법규 및 문헌 자료들을 검토 및 분석하고, 협업체 관련 공무원과 실무자들을 대상으로 면담조사(面談調査)를 실시하였다. 또한 우편설문조사를 통해 협업체에 가입한 산주들의 협업체 운영실태에 대한 인식(認識) 현황(現況)을 조사하였다. 설문의 내용은 참여 산주들의 산림경영현황과 협업경영에 대한 일반적 태도를 중심으로 작성하였다. 조사결과 50% 이상의 응답자들이 임업경영에 대해 관심을 보이지 않고 있으며, 대다수 응답자들이 협업체의 협업경영 활동에 대해 긍정적인 인식을 지니지 못하고 있는 것으로 나타났다. 또한 기존 협업체 관련 통계자료들을 통해 전국의 협업체 수가 급속하게 증가하고 있음을 확인할 수 있었다. 그러나 협업체의 수적(數的) 증가(增加)는 개별 협업체에 대한 정부지원액의 감소를 야기(惹起)하여 오히려 경영여건을 악화시키고 있는 원인이 되고 있다. 이 외에도 기존의 협업경영 관련 법규들중 몇 가지 점들은 개별 협업체들의 발전에 부적합(不適合)한 것으로 지적되었다.

• Journal of Korean Neurosurgical Society
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• 제63권1호
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• pp.56-68
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• 2020

Objective : To analyze the incidence and treatment trends of hemorrhagic stroke (HS), according to HS subtypes, using nationwide data in Korea from January 2008 to December 2016. Methods : We used data from the national health-claim database provided by the National Health Insurance Service for 2008-2016 using the International Classification of Diseases. The crude incidence and age-standardized incidence of each disease associated with HS, which included intracranial aneurysm (IA), hypertensive intracerebral hemorrhage (ICH), and arteriovenous malformation (AVM), were calculated and additional analysis was conducted according to age and sex. Changes in trends in treatment methods and number of treatments were analyzed for each cerebrovascular disease using the Korean Classification of Diseases procedure codes. Results : In 2016, the total number of newly diagnosed adult patients with HS was 24169, showing a decrease by 7.0% since 2008; the age-standardized incidence of HS was 46.2 per 100000 person-years. The age-standardized incidence of unruptured IA (UIA) in adults was 71.4 per 100000 person-years-increased by 2.6-fold since 2008-while that of ruptured IA (RIA) was 12.6 per 100000 person-years, which had decreased at a rate of 20.3% since 2008. The number of coil embolization (CE) for UIA increased by 3.4-fold over 9 years and exceeded that of clipping since 2008. With respect to RIA, CE increased by 2.0-fold over 9 years and exceeded that of clipping from 2014. As for spontaneous ICH in adults, the age-standardized incidence was 31.3 per 100000 person-years in 2016-decreased by 34.7% since 2008-and 14.6% of patients diagnosed with ICH were treated in 2016, which was not significantly different from the proportion of patients treated since 2008. The age-standardized incidence of unruptured AVM (UAVM) was 2.0 per 100000 person-year in 2016, while that of ruptured AVM (RAVM) was 2.4 per 100000 person-years in 2016, showing a decreasing rate of 17.2% from 2008. The total number of treated patients with AVM declined since 2014. Conclusion : In Korea, age-related cerebral vascular diseases, such as RIA, ICH, and RAVM, demonstrated a declining trend in age-standardized incidence; meanwhile, UIA and UAVM demonstrated an increased trend in both crude incidence and age-standardized incidence for 9 years. The increase in the elderly population, management of hypertension, and development of diagnostic and endovascular techniques appear to have influenced this trend.

• The Korean Journal of Physiology and Pharmacology
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• 제14권2호
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• pp.83-89
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• 2010

In this study, we studied whether hydrogen sulfide ($H_2S$) has an effect on the pacemaker activity of interstitial cells of Cajal (ICC), in the small intestine of mice. The actions of $H_2S$ on pacemaker activity were investigated using whole-cell patch-clamp technique, intracellular $Ca^{2+}$ analysis at $30^{\circ}C$ and RT-PCR in cultured mouse intestinal ICC. Exogenously applied sodium hydrogen sulfide (NaHS), a donor of hydrogen sulfide, caused a slight tonic inward current on pacemaker activity in ICC at low concentrations (50 and $100{\mu}m$), but at high concentration ($500{\mu}m$ and 1 mM) it seemed to cause light tonic inward currents and then inhibited pacemaker amplitude and pacemaker frequency, and also an increase in the resting currents in the outward direction. Glibenclamide or other potassium channel blockers (TEA, $BaCl_2$, apamin or 4-aminopydirine) did not have an effect on NaHS-induced action in ICC. The exogenous application of carbonilcyanide p-triflouromethoxyphenylhydrazone (FCCP) and thapsigargin also inhibited the pacemaker activity of ICC as NaHS. Also, we found NaHS inhibited the spontaneous intracellular $Ca^{2+}$ ($[Ca^{2+}]_i$) oscillations in cultured ICC. In doing an RT-PCR experiment, we found that ICC enriched population lacked mRNA for both CSE and CBS, but was prominently detected in unsorted muscle. In conclusion, $H_2S$ inhibited the pacemaker activity of ICC by modulating intracellular $Ca^{2+}$. These results can serve as evidence of the physiological action of $H_2S$ as acting on the ICC in gastrointestinal (GI) motility.