Effect of $K^+-channel$ Blockers on the $A_1-adenosine$ Receptor-Coupled Regulation of Electrically-Evoked Norepinephrine Release in the Rat Hippocampus

최봉규,김상훈,Choi, Bong-Kyu,Kim, Sang-Hoon The Korean Society of Pharmacology 1996 대한약리학잡지 Vol.32 No.3

Since it has been reported that the depolarization-induced NE release is inhibited by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus, a large body of experimental data on the post-receptor mechanism of this process has been accumulated. But, the post-receptor mechanism of presynaptic $A_1-adenosine$ receptor on the NE release has not been clearly elucidated yet. Therefore, it was attempted to clarify the participation of $K^+-channel$ in the post-receptor mechanisms of the $A_1-adenosine$ receptor-mediated control of NE release in this study. Slices from rat hippocampus were equilibrated with $^3H-norepinephrine$ and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 $VCm^{-1}$, 2 ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Adenosine, in concentrations ranging from $1{\sim}30\;{\mu}M$, decreased the NE release in a dose-dependent manner, without affecting the basal rate of release. 4AP $(1{\sim}30{\mu}M)$, a specific A-type $K^+-channel$ blocker, increased the evoked NE release in a dose-related fashion, and the basal rate of release is increased by 10 and $30{\mu}M$. TEA $(1{\sim}10{\mu}\;M)$, a nonspecific $K^+-channel$ blocker, increased the evoked NE release in a dose-dependent manner without affecting basal release. The adenosine effects were significantly inhibites by 3 ${\mu}M$ 4AP and 10 mM TEA treatment. 4AP $(30{\mu}M)-$ and TEA (10 mM)-induced increments of evoked NE release were completely abolished in $Ca^{++} free, but these were recoverd in low $Ca^{++} medium. And the effects of $K^+-channel$ blockers in low $Ca^{++} medium were inhibites and abolishes by $Mg^{++} (4 mM) adding and TTX $(0.3{\mu}M)$ adding medium, respectively. These results suggest that the decrement of the evoked NE-release by $A_1-adenosine$ receptor is mediated by 4AP and TEA sensitive $K^+-channel$.

쌀가루의 저장조건에 따른 자연균총의 생육특성

최봉규,박신영,하상도,금준석,이현유,박종대,Choi, Bong-Kyu,Park, Shin-Young,Ha, Sang-Do,Kum, Jun-Seok,Lee, Hyun-Yu,Park, Jong-Dae 한국식품영양과학회 2007 한국식품영양과학회지 Vol.36 No.7

본 연구는 쌀가루의 저장온도 및 저장기간에 따른 자연균 총 생육특성을 조사하고 안전성과 유효성을 고려한 최적의 열풍 및 마이크로파 처리 방법을 개발하여 쌀가루의 미생물학적 안전성, 저장성 및 품질유지를 최적화하고자 하였다. 마이크로파 처리(700 watt/30 sec, MT)와 열풍 처리($65^{\circ}C$/15 min, HT) 후 쌀가루의 ${\Delta}E$값은 각각 0.15와 0.27로 마이크로파 건조가 열풍 건조보다 색깔의 변화가 적은 것으로 나타났다. 건조방법에 따른 처리 직후 총균수, 효모와 곰팡이수는 MT 처리구가 2.62 log CFU/g과 0.37 log CFU/g으로 감소한 것으로 나타나, HT 처리구보다 효과적인 건조방법이었다. 저장기간에 따른 자연균총은 모든 처리구에서 유사한 성장패턴을 보였으나, MT 처리시 가장 낮은 성장률을 나타내었다. 결론적으로 저장 쌀가루의 품질특성 및 미생물학적 안전성 측면에서 마이크로파 처리는 열풍 건조 처리와 더불어 상업적 살균방법으로 검토할 필요성이 있는 것으로 평가되었다. In order to optimize microbial safety and preservation in quality retention of rice flour, commercial hot-air dry (HT, 65/15 min) and microwave dry (MT, 700 watt/30 sec) treatments were developed, and in this study, natural microflora present in rice flour exposed to different storage temperature and periods were monitored. Changes in color (E) appeared to be less on the MT rice flour than on the rice flour. Effectiveness of the MT treatment showed reduction rates for total aerobic bacteria (2.62 log CFU/g), yeasts, and molds (0.37 log CFU/g). Total aerobic bacteria showed similar growth patterns of all the treatments during storage; however, the MT treatment inhibited the growth of this organism in rice flour. In conclusion, the MT treatment was found to be a suitable drying method to substitute the HT treatment in terms of quality of rice flour and microbial safety.

A Study on the Post-Receptor Mechanism of Adenosine Receptor on Norepinephrine Release in the Rat Hippocampus

최봉규,김도경,양경무,Choi, Bong-Kyu,Kim, Do-Kyung,Yang, Kyung-Moo The Korean Society of Pharmacology 1996 대한약리학잡지 Vol.32 No.1

흰쥐 해마(hippocampus)에서 norepinephrine(NE) 유리에 미치는 $A_1-adenosine$ 수용체의 post-receptor 기전에 관한 지견을 얻고자 하여 $^3H-norepinephrine$으로 평형시킨 해마 절편을 사용하여 adenosine의 $^3H-NE$ 유리에 미치는 여러가지 약물의 영향을 관찰하였다. Adenosine($1{\sim}30{\mu}M$)은 전기자극(3 Hz, 2 ms, 5 Vcm-1, 구형파)에 의한 NE 유리를 용량 의존적으로 감소시켰고, 이 효과는 선택적인 $A_1-adenosine$ 수용체 차단제인 $8-cyclopentyl-1,3-dipropylxanthine(2{\mu}M)$에 의해 차단되었다. G-단백 억제제인 N-ethylmaleimide(NEM, 10과 $30{\mu}M$)는 그 자체로써 전기자극으로 유발시킨 NE 유리를 증가시켰으며, adenosine의 NE 유리 억제효과는 NEM 전처리에 의하여 완전히 소실되었다. Protein kinase C 활성화제인 $4{\beta}-phorbol$ 12,13-dibutyrate(PDB, $1{\mu}M$)는 NE 유리 증가를 일으켰고, 이 효소 억제제인 $4{\beta}-polymyxin$ B(PMB, 0.1 mg)는 NE 유리감소를 일으켰으며, adenosine에 의한 NE 유리 감소효과는 PDB에 의해 억제되었고, PMB 전처리하에서는 감소효과가 출현하지 않았다. $Ca^{2+}$-통로 차단제인 $nifedipine(1{\mu}M$)은 adenosine의 NE 유리 억제효과에 영향을 미치지 못하고, ATP에 의존적인 $K^+-$통로 차단제인 glibenclamide역시 adenosine의 NE 유리 억제효과에 영향을 미치지 못하였다. 그러나 delayed rectifier $K^+-$통로 차단제인 tetraethylammonium(TEA, 3 mM)은 그 자체로 NE 유리를 증가 시켰으며, adenosine의 NE 유리 억제효과를 차단함을 볼 수 있었다. 8-bromo-cAMP(100과 $300{\mu}M$) 그 자체로는 NE 유리에 별다른 영향을 미치지 못하였으나 8-bromo-cAMP 전처리에 의하여 adenosine의 NE 유리 억제효과가 억제됨을 볼 수 있었다. 이상의 실험결과로 흰쥐 해마에서 $A_1-adenosine$ 수용체를 통한 adenosine의 NE 유리 감소는 G-단백에 의존적이며, 이러한 효과에 protein kinase C, TEA에 예민한 $K^+-$통로 및 adenylate cyclase계가 복합적으로 관여하고 nifedipine에 예민한 $Ca^{2+}-$통로와 glibenclamide에 예민한 $K^+-$통로는 관여하지 않는 것으로 사료된다. Since it has been reported that the depolarization-induced norepinephrine (NE) release is inhibited by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus, a large body of experimental data on the post-receptor mechanism of this process has been accumulated. But, the post-receptor mechanism of presynaptic $A_1-adenosine$ receptor on the NE release has not been clearly elucidated yet. Therefore, it was attempted to clarify the post-receptor mechanisms of the $A_1-adenosine$ receptor-mediated control of NE release in this study. Slices from rat hippocampus were equilibrated with $^3H-norepinephrine$ and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 $Vcm^{-1}$, 2 ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Adenosine, in concentrations ranging from $1{\sim}30{\mu}M$, decreased the NE release in a dose-dependent manner, without affecting the basal rate of release. The adenosine effects were significantly inhibited by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, $2{\mu}M$), a selective $A_1-receptor$ antagonist. The responses to N-ethylmaleimide (NEM, 10 & $30{\mu}M$), a SH-alkylating agent of G-protein, were characterized by increments of the evoked NE-release and the basal release, and the adenosine effects were completely abolished by NEM pretreatment. $4{\beta}-Phorbol$ 12,13-dibutyrate (PDB, $1{\mu}M$), a specific protein kinase C (PKC) activator, increased the evoked NE release, whereas polymyxin B sulfate (PMB,0.1 mg), a PKC inhibitor, decreased the release, and the adenosine effects were inhibited by these agents. Nifedipine $(1{\mu}M)$, a $Ca^{2+}-channel$ blocker of dihydropyridine analogue, did not affect the adenosine effect. Tetraethylammonium (TEA, 3 mM) increased the evoked NE release, and inhibited the adenosine effects, but glibenclamide, a ATP dependent $K^+-channel$ blocker, did not. Finally, 8-bromo cyclic AMP (100 & $300{\mu}M$), a membrane-permeable analogue of cAMP, did not alter the NE release, but adenosine effects were inhibited by pretreatment with 8br-cAMP. These results suggest that the decrement of the evoked NE-release by $A_1-adenosine$ receptor is mediated by the C-protein, which is coupled to protein kinase C, adenylate cyclase system and TEA sensitive $K^+-channel$, and that nifedipine-sensitive $Ca^{2+}-channel$ and glibenclamide-sensitive $K^+-channel$ are not involved in this process.

An innovative nipple reconstruction technique for minimizing postoperative scars: The teardrop flap

최봉규,김일국 대한미용성형외과학회 2020 Archives of Aesthetic Plastic Surgery Vol.26 No.2

Nipple reconstruction methods include various techniques, such as the local flap technique, free nipple grafting, and filler injection. The local flap technique can provide less donor site morbidity than a free nipple graft, but leaves an additional scar near the nipple. We present a novel method for reconstruction of the nipple using a flap located on one side of the nipple. The flap has a teardrop shape consisting of a circle and two wings folded to one side. The two wings form a pillar and cap, and the de-epithelialized tip of one wing fills the internal dead space of the new nipple. We applied this nipple reconstruction technique in the case of a 61-year-old patient who had a vertical scar due to inverted-T reduction mammoplasty. The patient had lost her nipple in previous breastconserving surgery. The immediate postoperative nipple projection was 10 mm. At the 7-month follow-up visit, the nipple projection was 7.5 mm. The teardrop flap is an innovative technique that leaves no additional scar by using the scar already present on one side of the nipple.

Interaction of Forskolin with the Effect of $N^6-Cyclopentyladenosine$ on $[^3H]-Acetylcholine$ Release in Rat Hippocampus

최봉규,박희만,강연욱,국영종,Choi, Bong-Kyu,Park, Hie-Man,Kang, Yeon-Wook,Kook, Young-Johng The Korean Society of Pharmacology 1992 대한약리학잡지 Vol.28 No.2

As it has been reported that the depolarization-induced acetylcholine (ACh) release is modulated by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus and various lines of evidence indicate the involvement of adenylate cyclase system in $A_1-adenosine$ post-receptor mechanism in hippocampus, it was attempted to delineate the role of adenylate cyclase system in the $A_1-receptor-mediated$ control of ACh release in this study. Slices from rat hippocampus were incubated with $[^3H]-choline$ and the release of the labelled products was evoked by electrical stimulation $(3\;Hz,\;5\;Vcm^{-1},\;2\;ms,\;rectangular\;pulses)$, and the influence of various agents on the evoked tritium-outflow was investigated. $N^6-cyclopentyladenosine$ (CPA), a specific $A_1-adenosine$ receptor agonist, in concentrations ranging from 0.1 to $10\;{\mu}M$, decreased the $[^3H]-ACh$ release in a dose-dependent manner without the changes of basal rate of release. 8-cyclopentyl-1,3-dipropylxanthine $(DPCPX,\;1{\sim}10\;{\mu}M)$, a selective $A_1-receptor$ antagonist, increased the $[^3H]-ACh$ release in a dose-related fashion with slight increase of basal tritium-release. And the CPA effects were significantly inhibited by DPCPX $(2\;{\mu}M)$ pretreatment and the dose-response curve produced by CPA was shifted to the right. The responses to N-ethylmaleimide $(NEM,\;10\;&\;30\;{\mu}M)$, a SH-alkylating agent of G-protein, were characterized by increments of the evoked ACh-release and the basal release, and the CPA effect were completely abolished by NEM pretreatment. Forskolin, a specific adenylate cyclase activator, in concentrations ranging from 0.3 to $10\;{\mu}M$, increased the evoked ACh-release in a dose-dependent manner and the CPA effects were inhibited by forskolin. These results indicate that the $A_1-adenosine$ heteroreceptor plays an important role in ACh-release via nucleotide-binding protein Gi in the rat hippocampus and that the adenylate cyclase system might be participated in this process.

Fast 웹서비스를 위한 Fast XML 인코딩 시스템 구현

최봉규,조태범,정회경,Choi, Bong-Kyu,Cho, Tae-Beom,Jung, Hoe-Kyung 한국정보통신학회 2007 한국정보통신학회논문지 Vol.11 No.4

웹서비스는 서로 다른 플랫폼간의 통합을 가능하게 하였으나, 네트워크 환경이나 임베디드 시스템과 같이 상대적으로 느린 통신 매체에 자주 접속하거나 모바일과 같이 자원이 한정적인 소형 기기에서 사용 할 경우 전체 응용프로그램의 성능을 저하시키는 문제가 발생하고 있다. 이에 ITU-T(International Telecommunication Union - Telecommunication)와 ISO(International Organization for Standardization)/ IEC(International Electrotechnical Commission) 에서 공동으로 바이너리 XML 인코딩 표준을 제안하게 되었으며, 현재 진행 중인 바이너리 XML 인코딩 표준으로는 Fast Infoset과 Fast Schema가 있다. 본 논문에서는 웹서비스의 성능 향상을 위해 현재 표준화가 진행 중인 Fast Infoset 알고리즘과 Fast Schema 알고리즘을 도입하여 Fast XML 인코딩 시스템을 구현하였다. 또한, 구현된 Fast XML 인코더를 통하여 개발자나 사용자들이 Fast 웹서비스 시스템을 구축하는데 있어 참고 할 수 있는 테스트 베드를 제공한다. Web services came true a services integration, but the XML document decreases the efficiency or the whole application program with connects frequently in relatively slow communication media like network environment embedded system or use the resource limited small-sized instrument like mobile. Thereupon, ITU-T and ISO/IEC suggested encoding standard of binary XML. In this paper, implementation, of Fast XML encoding system through introduction Fast Infoset algorithm and Fast Schema algorithm for web services increase performance. And, offered of test bed that build of Fast Web Services system through Fast XML Encoder.

Influence of Adenosine and Magnesium on Acetylcholine Release in the Rat Hippocampus

최봉규,윤영복,Choi, Bong-Kyu,Yoon, Young-Bok The Korean Society of Pharmacology 1993 대한약리학잡지 Vol.29 No.2

As it has been reported that the depolarization-induced ACh release is modulated by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus and various lines of evidence indicate the adenosine effect is magnesium dependent, the present study was undertaken to delineate the role of endogenus adenosine as a modulator of hippocampal acetylcholine release in this study. Slices from the rat hippocampus were equilibrated with $[^3H]-choline$ and the release of the labelled product, $[^3H]-ACh$, was evoked by electrical stimulation(3Hz, $5\;V\;cm^{-1},$ 2ms, rectangular pulses), and the influence of various agents on the evoked tritium outflow was investigated. Adenosine, in concentrations ranging from $0.3\;to\;100\;{\mu}M$, decreased the $[^3H]-ACh$ release in a dose-dependent manner without changing the basal rate of release. $DPCPX(1{\sim}10{\mu}M)$, a selective $A_1-receptor$ antagonist, increased the $[^3H]-ACh$ release in a dose-related fashion with slight increase of basal tritium release. And the effects of adenosine were significantly inhibited by $DPCPX(2{\mu}M)$ treatment. CPCA, a specific $A_2-agonist$, in concentration ranging from $0.3\;to\;30\;{\mu}M$ decreased evoked tritium outflow with increase of basal rate of tritium release, and these effects were also abolished by $DPCPX(2{\mu}M)$ pretreatment. But, $CGS(0.1{\sim}10{\mu}M)$, a recently introduced potent $A_2-agonist$, did not alter the evoked tritium outflow. When the magnesium concentration of the medium was reduced to 0 mM, there was no change in evoked ACh release by adenosine. In contrast, increasing the magnesium concentration to 4 mM, the inhibitory effects of adenosine were significantly potentiated. These results indicate that $A_1-adenosine$ heteroreceptor is involved in ACh-release in the rat hippocampus and the inhibitory effects of adenosine mediated by $A_1-receptor$ is magnesium-dependent.

A Study on the Post-Receptor Mechanism of Adenosine Receptor on Acetylcholine Release in the Rat Hippocampus

최봉규,오재희,Choi, Bong-Kyu,Oh, Jae-Hee The Korean Society of Pharmacology 1994 대한약리학잡지 Vol.30 No.3

Since it was been reported that the depolarization-induced ACh release is inhibited by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus, a large body of experimental data on the post-receptor mechanism of this process has been accumulated. But, the post-receptor mechanism of presynaptic $A_1-adenosine$ receptor on the ACh release has not been clearly elucidated yet. Therefore, it was attempted to clarify the post-receptor mechanisms of the $A_1-adenosine$ receptor-mediated control of ACh release in this study. Slices from rat hippocampus were equilibrated with $^3H-choline$ and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 $VCm^{-1}$, 2ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Adenosine, in concentrations ranging from $0.3{\sim}300\;{\mu}M$, decreased the ACh release in a dose-dependent manner, without affecting the basal rate of release. The adenosine effects were significantly inhibited by $DPCPX\;(2\;{\mu}M)$, a selective $A_1-receptor$ antagonist. The responses to N-ethylmaleimide $(10&30{\mu}M)$, a SH-alkylating agent of G-protein, were characterized by increments of the evoked ACh-release and the basal release, and the adenosine effects were completely abolished by NEM pretreatment. PDB $(1{\sim}10\;{\mu}M)$, a specific protein kinase C (PKC) activator, increased, whereas PMB $(0.03{\sim}1\;mg)$, a PKC inhibitor, decreased the evoked ACh-release, and the adenosine effects were not affected by these agents. Nifedipine $(1\;{\mu}M)$, a $Ca^{2+}\;-channel$ blocker of dihydropyridine analogue, significantly inhibited the adenosine effect, but glibenclamide, a $K^+-channel$ blocker, did not. Finally, 8-bromo cyclic AMP $(100\;&\;300{\mu}M)$, a membrane-permeable analogue of cAMP, did not alter the ACh release, but adenosine effects were inhibited by pretreatment with large dose of 8-br-cAMP $(300\;{\mu}M)$. These results indicate that the decrement of the evoked ACh-release by $A_1-adenosine$ receptor is mediated by the G-protein, and nifedipine-sensitive $Ca^{2+}-channel$ and adenylate cyclase system are coupled partly to this effect, and that protein kinase C and glibenclamide-sensitive $K{^+}-channel$ are not involved in this process.

흰쥐 해마에서 Acetylcholine 유리에 미치는 Adenosine 수용체의 역할

최봉규,김도경,Choi, Bong-Kyu,Kim, Do-Kyung 대한약리학회 1994 대한약리학잡지 Vol.30 No.2

As it has been reported that the depolarization induced acetylcholine(ACh) release is modulated by activation of presynaptic $A_1-adenosine$ heteroreceptor and various lines of evidence indicate the $A_2-receptor$ is present In hippocampus, this study was undertaken to delineate the role of adenosine receptors on hippocampal ACh release. Slices from the rat hippocampus were equilibrated with $[^3H]-choline$ and the release of the labelled product, $[^3H]-ACh$, which evoked by electrical stimulation(3 Hz, $5\;Vcm^{-1}$, 2 ms, rectangular pulses) was measured, and the influence of various agents on the evoked tritium outflow was Investigated. Adenosine$(0.3{\sim}100\;{\mu}M)$ and CPA$(0.1{\sim}30\;{\mu}M)$ decreased the $[^3H]-ACh$ release in a dose-dependent manner without changing the basal rate of release. DPCPX$(1{\sim}10\;{\mu}M)$, a selective $A_1-receptor$, antagonist, increased the $[^3H]-ACh$ release in a dose related fashion with slight increase of basal tritium release. And the effects of adenosine and CPA were significantly inhibited by $DPCPX(2\;{\mu}M)$ treatment. CPCA, a specific $A_2-agonist$, in concentration ranging from 0.3 to 30 ${\mu}M$, decreased the evoked tritium outflow, and these effects were also abolished by $DPCPX(2\;{\mu}M)$ treatment. But the CPCA effects were not affected by $DMPX(2\;{\mu}M)$, a specific Aa-antagonist, treatment. However, CGS 21680c, a recently introduced potent $A_2-agonist$, in concentration ranging from 0.1 to $10{\mu}M$, did not alter the evoked tritium outflow. These results indicate that the decrement of the evoked ACh release by adenosine is mediated by $A_1-heteroreceptor$, but $A_2-adenosine$ receptor is not involved in ACh release in the rat hippocampus.

가상계와 물질계의 경계가 사라지는 시대에 토마스 머튼에게서 찾는 목회 페러다임

최봉규 한국실천신학회 2018 한국실천신학회 정기학술세미나 Vol.2018 No.05