흰쥐의 심장과 심근세포에서 cyclic AMP에 의한 Mg²⁺ 유리조절

강형섭,김진상,강창원,이호일,Kang, Hyung-sub,Kim, Jin-shang,Kang, Chang-won,Lee, Ho-il 대한수의학회 1999 大韓獸醫學會誌 Vol.39 No.1

Although it has been reported that hormones or chemicals, which increase in intracellular cAMP, produced $Mg^{2+}$ release from the heart, it is not well characterized whether a specific $Mg^{2+}$ exchanger is involved in cAMP-induced $Mg^{2+}$ efflux in the mammalian hearts. In this work, we studied the relationship between the increase in intracellular cAMP and ion transport system on $Mg^{2+}$ regulation in the perfused rat heart and isolated myocytes. The $Mg^{2+}$ content in the perfusate and supernatant were measured by atomic absorption spectrophotometer. The addition of membrane permeable cAMP analogue to the perfused hearts and myocytes induced a $Mg^{2+}$ efflux in the dose dependent manners. $Mg^{2+}$ efflux was stimulated by cAMP modulators (forskolin, IBMX and Ro20-1724) in the perfused hearts and myocytes. cAMP-induced $Mg^{2+}$ efflux was inhibited by $H_7$, benzamil or imipramine in the perfused hearts and myocytes, but not by EIPA. We confirmed that a significant $Mg^{2+}$ efflux was induced by an increase in intracellular cAMP in the hearts and myocytes. The cAMP-induced increase of $Mg^{2+}$ efflux in the hearts may be involved in ion transport system ($Na^+-Ca^{2+}$ and $Na^+-Mg^{2+}$ exchanger).

Development and Performance Evaluation of Hydroxyl Radical Generator using Electron Emission Type High Voltage and Low Current Discharger

강형섭,홍영표,이인호,김기범,Kang, Hyung-Sub,Hong, Young-Pyo,Lee, In-Ho,Kim, Gi-Beum The Korea Academia-Industrial cooperation Society 2017 한국산학기술학회논문지 Vol.3 No.2

본 연구는 MOSFET을 이용하여 안정적인 구형파를 구현함과 동시에 순간적인 전류의 상승을 최대한 줄여 전체 회로의 안정성 이 확보된 폐수처리용 전자방사식 OH radical generator를 개발하고자 하였다. 이와 같은 문제를 해결하고 안정성이 확보된 전자방사식 고압 저전력 방전을 이용한 폐수처리용 전자방사식 OH radical generator를 개발하고 그 성능을 평가하고자 하였다. 실험은 2016년 11월부터 2017년 3월까지 실시하였다. 그 결과 AC 체배 변환기의 입력 단에 연결되는 Power MOSFET의 drain 전류는 CR-스너버 구조의 부궤환(negative feedback) 회로를 통해 안정적이고 일정한 펄스 파형을 제공할 수 있었으며 AC 체배 변환기의 여기 전류(excitation current) 감소 및 발진 회로의 안정성을 상승시킬 수 있었다. 또한 이와 같은 회로를 갖는 전자방사식 OH radical generator에서 OH radical을 안정정적으로 발생시킬 수 있었다. 또한 살균능을 평가한 결과, E. coli, S. aureus와 S. flexneri는 60분 후 최대 99.9%이상의 살균력을 보였다. 본 연구 결과를 기반으로, MOSFET을 이용하여 안정적인 구형파를 구현함과 동시에 순간적인 전류의 상승을 최대한 줄여 전체 회로의 안정성이 확보된 살균능이 우수한 폐수처리용 전자방사식 OH radical generator를 개발하였다. In this study, we developed an electron-emission OH radical generator for waste water treatment. The stability of the circuitry was ensured by implementing stable pulse waves with a MOSFET and reducing the momentary current rise. The OH radical generator uses a high-voltage and low-current discharger. The performance of the device was evaluated experimentally, which showed that it is possible to produce a stable and uniform pulse waveform for the drain current of the power MOSFET, which is connected to the input side of an AC multiplying converter through negative feedback circuitry with CR-snubber architecture. It was also possible to reduce the excitation current of the converter and improve the stability of the oscillation circuit. In addition, the generator can generate hydroxyl radicals stably. The bactericidal activities were also evaluated, and the germicidal power for E. coli, S. aureus, and S. flexneriwas improved by 99.9% or more after 60 minutes.

흰쥐 대동맥에서 imipramine의 혈관이완 작용기전

강형섭,이상우,백성수,조성건,김진상,Kang, Hyung-sub,Lee, Sang-woo,Baek, Sung-su,Joe, Sung-gun,Kim, Jin-shang 대한수의학회 2003 大韓獸醫學會誌 Vol.43 No.4

Although the antidepressant effects of imipramine (IMI) have been well known in several studies, the effects on cardiovascular system, particularly the vasorelaxant effects, have not known clearly. We hypothesis that IMI-induced vasorelaxation involves NO (nitrie oxide), activation of guanylate cyclase (GC) and $Ca^{2+}$ channel. The possible roles of the endothelium and $Ca^{2+}$ in IMI-induced responses were investigated using isolated rings of rat thoracic aorta and anesthesized rats. In KCl-precontracted rings. IMI produces endothelium-dependent and endothelium-independent relaxations in intact (+E) as well as endothelium-denuded (-E) rat aorta in a concentration-dependent manner. In phenylephrine (PE)-precontracted rings, the IMI-induced relaxation was significantly greater in +E rings. The IMI-induced relaxations were suppressed by nitric oxide synthase (NOS) inhibitors, N(G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME) and aminoguanidine, a non-selective GC inhibitor, methylene blue, $Na^+$ channel blockers, lidocaine and procaine, or $Ca^{2+}$ channel blockers, nifedipine and verapamil, in PE-precontracted +E rings, but not in PE-precontracted -E rings. These relaxations were also suppressed by lidocaine or procaine in -E aortic rings. However, IMI-induced relaxations were not inhibited by a PLC inhibitor 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate (NCDC), an inositol monophosphatase inhibitor, lithium, indomethacin and dexamethasone in +E and -E rings. In vivo, infusion of IMI elicited significant decrease in arterial blood pressure. After intravenous injection of saponin, NOS inhibitors. MB and nifedipine, infusion of IMI inhibited the IMI-lowered blood pressure markedly. These findings suggest that the endothelium-dependent relaxation induced by IMI is mediated by activation of NO/cGMP signaling cascade or inhibition of $Ca^{2+}$ entry through voltage-gated channel, and this mechanism may contribute to the hypotensive effects of IMI in rats.

흰쥐의 심장과 심근세포에서 dopaminergic 수용체 자극이 Mg²⁺ 조절에 미치는 영향

강형섭,김종식,김진상,Kang, Hyung-sub,Kim, Jong-shick,Kim, Jin-shang 대한수의학회 1999 大韓獸醫學會誌 Vol.39 No.3

Magnesium($Mg^{2+}$) is one of the most abundant intracellular divalent cation. Although recent studies demonstrate that adrenergic receptor stimulation evokes marked changes in $Mg^{2+}$ homeostasis, the regulation of $Mg^{2+}$ by dopaminergic receptor stimulation is not yet known. In this work, we used dopaminergic agents to identify which type(s) of receptors were involved in the mobilization of $Mg^{2+}$ by dopaminergic receptor stimulation in the perfused rat hearts, isolated myocytes and circulating blood. The $Mg^{2+}$ content was measured by atomic absorbance spectrophotometry. Dopamine(DA), apomorphine(APO) and pergolide stimulated $Mg^{2+}$ efflux in the perfused rat hearts and these effects were inhibited by haloperidol or fluphenazine, nonselective dopaminergic antagonists. SKF38393, a selective doparminergic agonist, increased $Mg^{2+}$ efflux from the perfused hearts in dose dependant manners and SKF38393-induced $Mg^{2+}$ efflux was blocked by haloperidol. However, dopaminergic agonists-induced $Mg^{2+}$ efflux was potentiated in the presence of sulpiride or eticlopride, $D_2$-selective antagonist, from the perfused hearts. This increase of $Mg^{2+}$ efflux was blocked by haloperidol or imipramine. DA or pergolide increased in circulating $Mg^{2+}$ from blood. By contrast, PPHT stimulated $Mg^{2+}$ influx(a decrease in efflux) from the perfused hearts and circulating blood. PPHT-induced $Mg^{2+}$ influx was blocked by fluphenazine in the perfused hearts. DA-stimulated $Mg^{2+}$ efflux was inhibited by dopaminergic antagoinst in the isolated myocytes. In conclusion, the flux of $Mg^{2+}$ is modulated by DA receptor activation in the rat hearts. The efflux of $Mg^{2+}$ can be increased by $D_1$-receptor stimulation and decreased by $D_2$-receptor stimulation, respectively.

Mouse 갑상선에서 α₁-adrenoceptor 자극에 의한 thyroxine 유리 억제기전

강형섭,김송규,강창원,김진상,이호일,Kang, Hyung-sub,Kim, Song-kyu,Kang, Chang-won,Kim, Jin-sang,Lee, Ho-il 대한수의학회 1998 大韓獸醫學會誌 Vol.38 No.4

Thyroid function is mainly regulated through cAMP and phophatidylinositol, and it is well known that TSH-stimulated thyroxine ($T_4$) release is inhibited by catecholamine from mouse thyroids via the ${\alpha}_1$-adrenoceptor stimulation. Previous study has established that the inhibition of $T_4$ release by ${\alpha}_1$-adrenoceptor stimulation results in activated protein kinase C (PKC). The purpose of this study was to determine if ion transport systems are involved in the inhibition of $T_4$ release elicited by ${\alpha}_1$-adrenergic agonist in mouse thyroids. TSH-, IBMX- and cAMP analogue-stimulated $T_4$ release were significantly inhibited by methoxamine, R59022 (diacylglycerol kinase inhibitor), and MDL (adenylate cyclase inhibitor). TSH-stimulated $T_4$ release could be inhibited by Bay K 8644 and cyclopiazoic acid, but not by verapamil and tetrodotoxin. The addition of nifedipine ($Ca^{2+}$ channel blocker), tetrodotoxin and lidocaine ($Na^+$ channel blockers), but not amiloride (EIPA) and ryanodine, completely blocked the inhibitory effects of methoxamine on $T_4$ release. TSH-stimulated $T_4$ release was also inhibited by benzamil ($Na^+-Ca^{2+}$ exchange inhibitor). TSH-, IBMX- and cAMP-stimulated $T_4$ release were inhibited by methoxamine or R59022, these effects were reversed by nifedipine. but not by verapamil. Furthermore, nifedipine reversed the inhibitory effects of benzamil and R59022 on TSH-stimulated $T_4$ release. These data suggest that the observed ${\alpha}_1$-adrenoceptor-mediated inhibition of $T_4$ release in mouse thyroids is the result of an increase in intracellular $Na^+$ or $Ca^{2+}$ effected via activation of fast $Na^+$ or nifedipine-sensitive $Ca^{2+}$ channels, and that $Na^+-Ca^{2+}$ exchange may play an important role in reducing thyroid hormone by increasing intracellular $Ca^{2+}$.

기니픽 심장과 심근 세포에서 ${\alpha}_1-Adrenergic$ 자극에 의한 $Mg^{2+}$ 유리조절

강형섭,장성은,김진상,Kang, Hyung-Sub,Chang, Sung-Eun,Kim, Jin-Sang 대한약리학회 1997 The Korean Journal of Physiology & Pharmacology Vol.1 No.6

$Mg^{2+}$ is the fourth most abundant cation in cellular organisms. Although the biological chemistry and the physiological roles of the magnesium ion were well known, the regulation of intracellular $Mg^{2+}$ in mammalian cells is not fully understood. More recently, however, the mechanism of $Mg^{2+}$ mobilization by hormonal stimulation has been investigated in hearts and in myocytes. In this work we have investigated the regulation mechanism responsible for the $Mg^{2+}$ mobilization induced by ${\alpha}1-adrenoceptor$ stimulation in perfused guinea pig hearts or isolated myocytes. The $Mg^{2+}$ content of the perfusate or the supernatant was measured by atomic absorbance spectrophotometry. The elimination of $Mg^{2+}$ in the medium increased the force of contraction of right ventricular papillary muscles. Phenylephrine also enhanced the force of contraction in the presence of $Mg^{2+}$-free medium. ${\alpha}1-Agonists$ such as phenylephrine were found to induce $Mg^{2+}$ efflux in both perfused hearts or myocytes. This was blocked by prazosin, a ${\alpha}1-adrenoceptor$ antagonist. $Mg^{2+}$ efflux by phenylephrine was amplified by $Na^+$ channel blockers, an increase in extracellular $Ca^{2+}$ or a decrease in extracellular $Na^+$. By contrast, the $Mg^{2+}$ influx was induced by verapamil, nifedipine, ryanodine, lidocaine or tetrodotoxin in perfused hearts, but not in myocytes. $W_7$, a $Ca^{2+}/calmodulin$ antagonist, completely blocked the pheylephrine-, A23187-, veratridine-, $Ca^{2+}-induced$ $Mg^{2+}$ efflux in perfused hearts or isolated myocytes. In addition, $Mg^{2+}$ efflux was induced by $W_7$ in myocytes but not in perfused heart. In conclusion, An increase in $Mg^{2+}$ efflux by ${\alpha}1-adrenoceptor$ stimulation in hearts can be through $IP_3$ and $Ca^{2+}-calmodulin$ dependent mechanism.

흰쥐 대동맥에서 cyclic nucleotide phosphodiesterase 억제제들의 혈관 이완 특성

강형섭,최철호,김진상,Kang, Hyung-sub,Choi, Cheol-ho,Kim, Jin-shang 대한수의학회 2003 大韓獸醫學會誌 Vol.43 No.4

Vascular smooth muscle relaxation is modulated by an increase in cGMP subsequent to nitric oxide (NO) production by endothelial cells. The effects of cAMP and cGMP phosphodiesterase (PDE) inhibitors were investigated in phenylephrine-precontracted rat aorta rings by using the specific inhibitors of PDE I, III, IV and V as relaxing agents (calmodulin-activated PDE inhibitors, IBMX and $W_7$, type I; cAMP-specific PDE inhibitors, milrinone, type IV; Ro 20-1724, type III and cGMP-specific PDE inhibitor, zaprinast, type V). All the PDE inhibitors produced a concentration-dependent relaxation in the ring with intact endothelium (+E). Except for milrinone, all the PDE inhibitors-induced relaxations were inhibited by removal of extracellular $Ca^{2+}$, $N^G$-nitro-L-arginine, $N^G$-nitro-L-arginine methyl ester, methylene blue (MS) or nifedipine. The specific PDE I and PDE IV inhibitors both produced endothelium-independent relaxations which were inhibited by MS in -E rings. However, zaprinast had no effect in -E rings. Except for milrinone, sodium nitroprusside (a NO donor)-induced relaxation was significantly augmented by all PDE inhibitors in +E rings. The results suggest that I) the vasorelaxant properties of IBMX, $W_7$, Ro 20-1724 and zaprinast are dependent on endothelium or on interaction with $Ca^{2+}$ regulation, 2) each PDE is differently distributed in vascular tissues (endothelial and smooth muscle cells), 3) the vasodilations of PDE inhibitors are due to the increase of cAMP and cGMP formation through inhibition of cAMP- and cGMP-PDE and 4) the vasodilation action of milrinone does not involve in endothelial-cyclic nucleotide system.

기니픽 심장에서 histamine H₂-수용체 자극에 의한 Mg²⁺ 유리에 대한 phosphodiesterase 억제제의 효과

강형섭,김진상,Kang, Hyung-sub,Kim, Jin-shang 대한수의학회 2000 大韓獸醫學會誌 Vol.40 No.3

Several recent studies demonstrate that receptor-mediated cAMP (adenosine 3',5'-monophosphate) production evokes marked change in magnesium ($Mg^{2+}$) homeostasis. The effects of dimaprit or/and phosphodiesterase (PDE) inhibitors on the $Mg^{2+}$ release from perfused guinea pig heart and collagenase-dispersed myocytes was studied to clarify an association of $H_2-histaminergic$ receptor-mediated $Mg^{2+}$ regulation with intracellular cAMP-degradation system. $Mg^{2+}$ efflux was stimulated in perfused hearts and myocytes by IBMX (3-isobutyl-1-methylxanthine), a calmodulin-sensitive PDE inhibitor, but not by RO 20-1724(4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone) or papaverine, cAMP-specific PDE inhibitors. $Mg^{2+}$ efflux was also be induced by dimaprit, a H-2-agonist. $Mg^{2+}$ effluxes induced by dimaprit were augmented by the presence of the PDE inhibitors. The augmentation of dimaprit-induced $Mg^{2+}$ effluxes by the PDE inhibitors were inhibited by ranitidine, a $H_2-antagonist$, and imipramine, a $Na^{+}-Mg^{2+}$ exchange inhibitor, in perfused hearts and myocytes and were also inhibited by amiloride in perfused hearts. These results suggest that the $H_2$-stimulated $Mg^{2+}$ effluxes from guinea pig heart can be regulated by the cytosolic nonspecific-dependent PDE systems and that it is induced by the $Na^{+}-Mg^{2+}$ exchanger stimulation.

국부이진패턴 히스토그램을 이용한 측면 차량 검출

강형섭(Kang Hyung-Sub),조동찬(Cho Dong-Chan),고경우(Ko Kyung-Woo),김회율(Kim Whoi-Yul) 한국방송·미디어공학회 2010 한국방송공학회 학술발표대회 논문집 Vol.2010 No.7

본 논문에서는 주행 중인 차량에서 전방을 향해 장착된 카메라를 통해 입력된 영상에서 측면에 부분적으로 나타나는 차량을 검출하는 방법을 제안한다. 기존 연구에서는 모션 벡터를 이용하여 주변 배경과 관측되는 차량 사이의 모션 벡터 차이를 이용하여 측면 차량을 검출하고 있다. 그러나 모션 벡터를 이용할 경우 정지된 차량이나 전방에서 다가오는 차량의 경우 검출하기 어려운 점이 있다. 이러한 문제를 해결하기 위해 본 논문에서는 모션 벡터를 사용하지 않고 차량 측면 모습에서 특징 정보를 추출하여 SVM 분류기를 통해 측면 차량을 검출하는 방법을 제안한다. 차량 측면 모습의 특징을 뽑기 위해 영상의 밝기 변화에 강인한 국부 이진 패턴을 사용하였고 ROI영역 내에서 차량이 나타나는 위치에 상관없이 차량의 측면 모습을 찾아내기 위해 국부 이진 패턴의 히스토그램을 이용하였다. 실험결과에서는 제안하는 방법이 정지된 차량을 포함하여 88.5%의 정확도로 측면 차량을 검출하는 것을 확인하였다.

기니픽 심장과 심근 세포에서 α<SUB>1</SUB>-Adrenergic 자극에 의한 Mg<SUP>2⁢</SUP> 유리조절

강형섭(Hyung Sub Kang),장성은(Sung Eun Chang),김진상(Jin Sang Kim) 대한생리학회-대한약리학회 1997 The Korean Journal of Physiology & Pharmacology Vol.1 No.6

<P> Mg<SUP>2⁢</SUP> is the fourth most abundant cation in cellular organisms. Although the biological chemistry and the physiological roles of the magnesium ion were well known, the regulation of intracellular Mg<SUP>2⁢</SUP> in mammalian cells is not fully understood. More recently, however, the mechanism of Mg<SUP>2⁢</SUP> mobilization by hormonal stimulation has been investigated in hearts and in myocytes. In this work we have investigated the regulation mechanism responsible for the Mg<SUP>2⁢</SUP> mobilization induced by α<SUB>1</SUB>-adrenoceptor stimulation in perfused guinea pig hearts or isolated myocytes. The Mg<SUP>2⁢</SUP> content of the perfusate or the supernatant was measured by atomic absorbance spectrophotometry. <P> The elimination of Mg<SUP>2⁢</SUP> in the medium increased the force of contraction of right ventricular papillary muscles. Phenylephrine also enhanced the force of contraction in the presence of Mg<SUP>2⁢</SUP>-free medium. α<SUB>1</SUB>-Agonists such as phenylephrine were found to induce Mg<SUP>2⁢</SUP> efflux in both perfused hearts or myocytes. This was blocked by prazosin, a α<SUB>1</SUB>-adrenoceptor antagonist. Mg<SUP>2⁢</SUP> efflux by phenylephrine was amplified by Na<SUP>⁢</SUP> channel blockers, an increase in extracellular Ca<SUP>2⁢</SUP> or a decrease in extracellular Na<SUP>⁢</SUP>. By contrast, the Mg<SUP>2⁢</SUP> influx was induced by verapamil, nifedipine, ryanodine, lidocaine or tetrodotoxin in perfused hearts, but not in myocytes. W<SUB>7</SUB>, a Ca<SUP>2⁢</SUP>/calmodulin antagonist, completely blocked the pheylephrine-, A23187-, veratridine-, Ca<SUP>2⁢</SUP>-induced Mg<SUP>2⁢</SUP> efflux in perfused hearts or isolated myocytes. In addition, Mg<SUP>2⁢</SUP> efflux was induced by W<SUB>7</SUB> in myocytes but not in perfused heart. <P> In conclusion, An increase in Mg<SUP>2⁢</SUP> efflux by α<SUB>1</SUB>-adrenoceptor stimulation in hearts can be through IP<SUB>3</SUB> and Ca<SUP>2⁢</SUP>-calmodulin dependent mechanism.