• Proceedings of the Materials Research Society of Korea Conference
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• 1993.11a
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• pp.141-141
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• 1993

• Proceedings of the Korean Powder Metallurgy Institute Conference
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• 2006.09a
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• pp.596-596
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• 2006

• 한국전자현미경학회:학술대회논문집
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• 1993.06a
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• pp.13-13
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• 1993

• The Korean Journal of Physiology
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• v.14 no.1
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• pp.25-30
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• 1980

It has been well known that beta-adrenoceptor is responsible for the renin release stimulatory and alpha-adrenoceptor may be inhibitory. It has been observed accidently that alpha-adrenergic agonist can inhibit renin release by just changing the medium temperature in Vitro experiment in this laboratory. A series of experiments were performed to clarify this interesting phenomena in Vitro experiment. Rat renal slices were incubated in PSS medium under gas phase at $37^{\circ}C$. The following results were observed. 1) Isoproterenol and norepinephrine resulted in renin release stimulatory in dose-dependent by the concentrations of $10^{-9}$ to $10^{-5}\;M/L$ at $37^{\circ}C$. 2) Norepinephrine resulted in renin release inhibitory in dose dependent by the concentrations of $10^{-7}$ to $10^{-5}\;M/L$, and almost no effect by isoproterenol $10^{-6}\;M/L$ at $20^{\circ}C$. 3) Phenoxybenzamine pretreatment at $37^{\circ}C$ accentuated isoproterenol stimulatory effect at $37^{\circ}C$. 4) Phenoxybenzamine pretreatment at $20^{\circ}C$ attenuated isoproterenol stimulatory effect at $37^{\circ}C$. These data suggest that the renal adrenoceptor(s) related to renin release maybe a single entity, and can be interconverted different forms in certain conditions.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.6
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• pp.425-429
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• 2009

Intracranial headaches, including migraines, are mediated by nociceptive activation of the trigeminal nucleus caudalis (TNC), but the precise mechanisms are poorly understood. We previously demonstrated that selective blockage of spinal sigma-1 receptors (Sig-1R) produces a prominent antinociceptive effect in several types of pain models. This study evaluates whether the Sig-1R antagonist (BD1047) has an antinociceptive effect on capsaicin (a potent C-fiber activator) induced headache models in rats. Intracisternal infusion of capsaicin evoked pain behavior (face grooming), which was significantly attenuated by BD1047 pretreatment. BD1047 consistently reduced capsaicin-induced Fos-like immunoreactivity (Fos-LI), a neuronal activator, in the TNC in a dose-dependent manner. Moreover, capsaicininduced phosphorylation of N-methyl-D-aspartate receptor subunit 1 was reversed by BD1047 pretreatment in the TNC. These results indicate that the Sig-1R antagonist has an inhibitory effect on nociceptive activation of the TNC in the capsaicin-induced headache animal model.

• Korean Journal of Veterinary Research
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• v.35 no.2
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• pp.255-261
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• 1995

Amitraz frequently causes the side effect of intestinal stasis or bloat in mammals. It is very similar to the side effect of xylazine or clonidine which produce the inhibition of intestinal motility through the stimulation of ${\alpha}_2$ adrenoceptor. Therefore, we examined whether amitraz causes intestinal stasis or bloat through the inhibition of intestinal motility or whether amitraz produces the inhibition of intestinal motility through the stimulation of ${\alpha}_2$ adrenopceptor. Amitraz inhibited the intestinal motility in a dose-dependent manner in isolated rabbit jejunum and isolated pig ileum. These inhibitory effects of amitraz were blocked by yohimbine but not by prazosin. The effect of intestinal contraction of carbachol or high-potassium was not affected by the pretreatment of amitraz. However, the con-traction of histamine was inhibited by the pretreatment of amitraz. It is concluded that amitraz mainly inhibits the intestinal motility through the stimulation of ${\alpha}_2$-adrenoceptor although partially antihistaminic action of amitraz can be involved.

• The Journal of Korean Medicine
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• v.24 no.2
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• pp.193-203
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• 2003

Objectives : In this study, we investigated the effect and pathway of contralateral heterotropic electroacupuncture (EA) on pain induced by fonualin in rats. Methods : Acu-points in the right forepaws, HT 7 and PC 7 were stimulated with 3~4mA, 2ms, and 10Hz after 5% formalin (50ul) s.c. injection to the left hind paw. In addition, it was investigated whether the dorsolateral funiculus (DLF), known to be related the descending inhibition, mediates analgesic effects of the contralateral heterotropic EA or whether administration of naltrexone, an opioid antagonist, blocks the effect of EA. Results : The results showed that contralateral heterotropic electroacupuncture (EA) inhibited late phase (63.311.7%) of pain induced by fonualin in the behavioral test, but sham-EA had little effect on pain behavior (85.616.8%) and no analgesic effects after transection of the dorsolateral funiculus (95.718.7%). The pretreatment of naltrexone (10mg/kg, i.p.) could not inhibit the analgesic effects of EA on formalin-induced pain behavior (70.713.1%). Also,EA suppressed formalin injection induced expression of cFos like protein (cFL) in the dorsal homo but not sham-EA. Suppressed expressions of cFL in the spinal cord were eliminated after transection of the ipsilateral dorsolateral funiculus at T10-11 leve1s. However, pretreatment of naltrexone could not prevent the suppressive expressions of cFL at the spinal cord. Conclusions : These results suggest that the analgesic effect of contralateral heterotropic electroacupuncture may be modulated through the dorsolateral funiculus constituting the descending inhibition.

• Journal of Life Science
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• v.10 no.6
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• pp.584-590
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• 2000

Natural products are one of the useful source of cardiovascular drugs, in particular, when they have antioxidant activity. Gagaminine, an alkaloid isolated from the roots of Cynanchum wilfordi Hemsley, has been reported to potently inhibit the aldehyde oxidase activity ({TEX}$IC_{50}${/TEX}=0.8$\mu$M) and reduce lipid peroxidation. However, the effect of gagaminine on vascular smooth muscle has not yet been investigated. In the present study, we examined whether gagaminine relaxes vascular smooth muscle by isometric tension study. In order to observe its relaxation effect on the arteries, conductivel vessel (rat thoracic aorta) and resistance vessel (pig coronary artery) were purposely used. Results indicated that gagaminine relaxed in a concentration-dependent manner $\alpha$-adrenoceptor agonist, phenylephrine (PE)-induced contraction of rat aorta. Pretreatment with gagaminine inhibited PE-induced contraction, noncompetitively. {TEX}$Ca^{2+}${/TEX}-induced contraction was significantly diminished by gagaminine. In pig coronary artery, gagaminine relaxed thromboxane receptor (U 46619)-mediated contraction in dose-dependent manner. Pretreatment with gagaminine also reduced the maximum contraction induced by KCl. These observations strongly suggest that agagminnine relaxes vascular smooth muscle, irrespective of both resistance and conductive artery. We demonstrate that gagaminine, a potent natural antioxidant, has a significant vasodilatory effect and its action mechanism van be ascribed at least in part to {TEX}$Ca^{2+}${/TEX} antagonistic action as evidenced by inhibition {TEX}$Ca^{2+}${/TEX}-induced contraction (rat aorta) and KCl-induced contraction (porcine artery). Furthermore, neither $\alpha$ -adrenoceptor nor thromboxane receptor seems responsible for the relaxation of gagaminine.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.2
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• pp.328-332
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• 2008

The purpose of this study was to identify the protective effect of Codonopis pilosula extract on cell death induced by $H_2O_2$ in SK-N-MC neuroblastoma cells. We measured the antioxidant effect by DPPH radical scavenging analysis, BSA analyssis and examined the cell viability by crystal violet and cytochrome C, Bax, Bcl-2, p53, p21 by using Western blot analysis. Codonopis pilosula extract scavenged DPPH radical in a dose-dependent manner and shown direct free radical scavenging effect, suggested that Codonopis pilosula extract have antioxidant effect in vitro. Treatment of cells with hydrogen peroxide, a reactive oxygen species, was to induce cell death and pretreatment with Codonopis pilosula extract attenuated the occurrence of $H_2O_2-induced$ cell death. To elucidate the protective mechanisms of action of Codonopis pilosula extract, Western blot analyses for Bcl-2 and Bax expression and cytochrome c release were carried out. Pretreatment with Codonopis pilosula extract induced the expression of Bcl-2 and suppressed the release of cytochrome c and Bax into the cytosol, thereby arresting $H_2O_2-induced$ apoptotic cell death. Especially p21 and p53 were decreased prior to $H_2O_2$ treatment. These results suggest that Codonopis pilosula extract is associated with the cell cycle and anti-apoptotic cell death.

• YAKHAK HOEJI
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• v.27 no.4
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• pp.271-282
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• 1983

This study is an attempt to study the influence of clonidine, which has a central sympatholytic action, on the renal function in dogs and to elucidate its mechanism of action. Clonidine ($15\mu$g/kg) injected into a cephalic vein of the dog produced a marked increase in urine flow and in amounts of $Na^{+}$ and $K^{+}$ excreted in urine, and clearances of free water and osmolar substance, the reabsorption rates of $Na^{+}$ and $K^{+}$ in renal tubules were significantly decreased. Clonidine ($50.0]mu$g/kg) administered intravenouly elicited a transient reduction in urine flow, along with inhibition of all renal functions. Intravenous clonidine-induced diuretic effect was completely blocked by pretreatment with reserpine, and was lessened by water diuresis. Clonidine ($3.0\mu$g/kg) injected tnto a carotid artery revealed a transient diuresis with a increase in clearance of free water. Clonidine injected into a renal artery showed a significant antidiuretic effect and all functions of an experimental kidney were reduced. Antidiuretic action induced by clonidine given into a renal artery markedly suppressed by pretreatment with reserpine. The above results suggest that clonidine has dual mechanisms: 1) diuretic effect due to the central sympatholytic action and inhibition of release of antidiuretic hormone, and 2) antidiutetic effect indued by indirect symptheic stimulation in the periphery.