빌라조경 설계사례에 관한 연구 : Case Study of Jang-chung Dong Villa

김동찬,이윤수,유재설,박익수,임동민,임상재 경희대학교 부설 디자인연구원 1998 예술· 디자인학연구 Vol.1 No.1

The goal of this study is to propose a plan for the Jang-Chung Dong Villa. This Villa is located on Jang-Chung Dong Jung-Gu, Seoul. And, this place is where high-class residential area. This Site area covers about 1925.6m². This base idea of this plan is to provide a community of dwelling houses with identity and amenity in outdoor spaces in order to create the high-class environment of outdoor spaces. Design principles are established as follow; to make spaces for flexibility in the garden related activities, to provide many chances to contact with nature, and to feel pride in the villa life.

급성전골수성백혈병에서 백혈구성분채집술에 이은 치명적인 뇌출혈 2예

오윤정,박소윤,김윤정,한동석,김현수,최진혁,남동기,임호영,김효철,주희재 아주대학교 의과학연구소 1998 아주의학 Vol.3 No.1

The aim of this study is to report 2 cases of acute promyelocytic leukemia who died from intracranial hemorrhage following leukapheresis and to provide proper preventive measures against hemorrhage following leukapheresis. From 1994 to 1997, a total of twenty-six patients with leukemia underwent leukapheresis to control hyperleukocytosis at Ajou University Hospital. Two patients with acute promyelocytic leukemia received all-trans retinoic acid but developed drug-induced hyperleukocytosis. Shortly after leukapheresis, they died from intracranial hemorrhage. The risk factors for fatal hemorrhage are thought to be coexisting disseminated intravascular coagulation(DIC), thrombocytopenia aggravated by leukapheresis, exacerbated coagulopathy related to mechanical trauma through leukapheresis and the excess use of citrate during leukapheresis. To reduce the risk of the bleeding associated with leukapheresis, it is necessary to replace platelet sufficiently before and after leukapheresis and to give calcium to correct coagulopathy induced by excess citrate which is used as anticoagulant as well as the correction of disseminated intravascular coagulation.

Debrisoquin이 Norepinephrine 및 Tyramine의 昇壓效果에 미치는 影響(1)

林東潤 조선의대 1985 The Medical Journal of Chosun University Vol.10 No.1

Taxol합성에 관한 연구. Ⅱ : 3-(2-Hydroxyethyl)-2, 2, 4-trimethyl-3-cyclohexenone SEM ether의 합성

임남수,신동수,정윤성,김정주,박두천,주우홍 昌原大學校 基礎科學硏究所 1995 基礎科學硏究所論文集 Vol.7 No.-

3-(2-Hydroxyethyl)-2,2,4-trimethyl-3-cyclohexenone SEM ether ??, an intermediate in the synthesis of taxol was provided in eight steps. The keto ketal ?? was obtained in three steps from 1,3-cyclohexanedione. Reaction of the potassium enolate of ?? with N-phenyltrifluoromethanesulfonimide provided triflate ?? in 84% yield. Thus palladium-mediated cross-coupling reaction of enol triflate ?? with vinyltributylstannane afforded diene ?? in a 89% yield. 3-(2-Hydroxyethyl)-2,2,4-trimethyl-3-Cyclohexenone SEM ether was prepared from diene ?? by sequential hydroboration [9-BBN, THF, 89%], deprotection[pTsOH ·H₂O, THF-H₂O,~100%], and silyation [SEMC], iPr₂NEt, nBu₄NI, CH₂Cl₂, 94%]

D-Amphetamine이 니코틴성 흥분작용에 의한 카테콜아민 분비작용에 미치는 영향

임건한,서유석,민선영,임지연,김용직,나광문,임동윤 朝鮮大學校 附設 醫學硏究所 2005 The Medical Journal of Chosun University Vol.30 No.1

본 연구의 목적은 d-arphetamine이 흰쥐의 적출부신 관류모델에서 니코틴 수용체 흥분에 의한 카테콜아민(CA) 유리작용에 미치는 영향을 검색하여 그 작용기전을 규명하고자 하였다. D-amphetamine은 흰쥐 부신정맥내로 60분간 관류시 d-amphetamine자체는 약한 CA 분비작용을 나타내었으나, d-amphetamine (30 μM)을 비롯한 강력한 neuronal nicotine 수용체 작용제인 cytisine (50 μM) 및 epibatidine (30 μM)에 의한 CA 유리작용을 처음 4-10분 동안만 유의하게 증강시켰다. 또한, d-amphetamine (30 μM)은 60분간 부신정맥 내로 관류한 상태에서 dihydropyridine L-형 칼슘통로 개방약물인 Bay-K-8644 (10 μM)과 세포질내 칼슘저장고에서 Ca^(2+) ATPase 억제제인 cyclopiazonic acid (10 μM)의 CA 유리작용을 처음 4분간만 유의하게 증강시켰다. 그러나, 고농도의 d-amphetamine (500 μM)은 상기한 모든 분비촉진제의 CA분비작용을 오히려 억제하였다. 이와 같은 연구결과로 보면, 흰쥐 관류 부신수질에서 d-amphetamine은 낮은 농도에서는 콜린성 니코틴 수용체 흥분에 의한 카테콜아민 분비반응을 증강시키지만, 고농도에서는 오히려 억제적으로 작용함을 시사한다. 따라서, d-amphetamine은 용량에 따라서 흰쥐 적출 관류부신수질의 니코틴 수용체의 작용제 및 길항제로 이중 작용(dual action)을 나타내는 것으로 생각된다. 이러한 d-amphetamine의 작용은 흰쥐 부신수질 크롬친화세포의 dihydropyridine계 L-형 칼슘통로의 활성화 및 세포 내 칼슘저장고로부터 칼슘유리작용과 관련성이 있는 것으로 사료된다. The purpose of the present study was to examine the effect of d-amphetamine on CA release evoked by nocotinic receptor stimulation from the isolated perfused model of the rat adrenal gland, and to establish its mechanism of action. D-amphetamine(30 μM), when perfused into an adrenal vein of the rat adrenal gland for 60 min, enhanced the CA secretory responses evoked by ACh (5.32 mM), nicotine (30 μM), cytisine (50 μM, a selective neuronal nicotinic Nn-receptor agonist) and epibatidine (30 nM, a selective neuronal nicotinic Nn receptor agonist) only for the first period (4~10 min), although it alone has weak effect on CA secretion. Moreover, d-amphetamine (30 μM) in to an adrenal vein for 60 min also augmented the CA release evoked by BAY-K-8644, an activator of the dihydropyridine L-type Ca^(2+) channels, and cyclopiazonic acid, an inhibitor of cytoplasmic Ca^(2+) ATPase only for the first peroid (4 min). However, in the presence rather inhibited the CA secretory responses evoked by the above all of secretagogues. Taken together, these experimental results suggest that d-amphetamine at a low concentration enhances the CA secretion from the rat adrenal medulla evoked by stimulation of cholinergic nicotininc receptors, but at a high concentration it rather inhibits them. It semms that d-amphetamine has dual action acting as both agonist and antagonist at nicotinic receptors of the isolated perfused rat adrenal medulla, which are might be dependent on the concentration. It is also thought that these actions of d-amphetamine are probably relevant to the activation of the dihydropyridine L-type Ca^(2+) channels located on the rat adrenomedullary chromaffin cell membrane and release of Ca^(2+) from the cytoplasmic store.

高血壓을 일으키는 아세트 알데하이드의 作用에 關한 硏究 : 副腎에서 카테콜아민의 分泌에 對하여

林東潤,文宰奎 朝鮮大學校 附設 醫學硏究所 1986 The Medical Journal of Chosun University Vol.11 No.1

Authors tried to investigate whether acetaldehyde causes release of catecliolaniiiies(CA) from Liie isolated perfused rabbit adrenal gland or not and to elucidate its mechanism or action. Acetaldehyde (300㎍) injected into adrenal vein produced the marked secretion of CA. Acetaldehyde-induced secretory effect of CA was not affected by treatment of atropine or chlorisondamine and even by atropine plus chlorisondamine. Release of CA evoked by acetaldehyde was not blocked by pretreatment with adenosine, but inhibited significantly by ouabain-treatment or calcium free Krebs solution. These results obtained suggest that acetaldehyde evokes release of CA from the isolated perfused rabbit adrenal gland by direct action, and that it may exert its hypertensive action partly through this mechanism.

Nd : YAG 레이저를 조사한 상아질 표면변화에 관한 주사전자현미경적 연구

임성삼,윤수한,박동성 大韓齒科保存學會 1997 Restorative Dentistry & Endodontics Vol.22 No.1

家兎副腎으로 부터 Adenosine에 의한 Acetylcholine의 Catecholamines 分泌의 相乘作用

林東潤,崔哲熙 朝鮮大學校 附設 醫學硏究所 1986 The Medical Journal of Chosun University Vol.11 No.1

This study is an attempt to investigate the effect of adenosine, which is known as a presynaptic modulator of neurotransmitter release from autonomic nerve ending's, on the potentiation of acetylcholine(Ach)-induced secretion of calecholamines (CA) from the isolated perfused rabbit adrenal gland. Adenosine(0.18mM), when perfused into the adrenal gIand for 30min, potentiated significantly Ach(50㎍)-induced CA secretion as compared to its corresponding value(655.6±102.5 and 353.2±59.3 ng/4min. respectively) and this potentiation lasted over 2hr. Adenosine-induced potentiation of CA secrction by Ach was antagonized by treatment with neophylline(dihyclroxypropyltheophyllinc, 0.2mM) which is an adenosine receptor blocking' agent. Adenosine also potentiated CA secretion by KCl(200㎍), a direct dePolarizinq agent, and nicotine(10㎍), but less than that evoked by Ach. Physostigmine(eaerine, 10nM), which is an anticholinesterase, weakened the effect of adenosine on Ach-induced CA seretion. and vice versa. From the above mentioned results, it is thought that adenosine-evoked potentiation of Ach-induced CA secretion is exerted via adenosine receptors on chromaffin cells and that it exhibits no specific relationship to nicotine receptors, but may produce an intracelluar effect opposite to that caused by physostigmine. And it also seems that there is a species difference in the modulation of adenosine to CA secretion from the adrenal gland.

Metoclopramide가 휜쥐의 血壓에 미치는 影響

임동윤,최동준,김규형,최철희,박재윤,문재규,김문석,황두환 中央醫學社 1988 中央醫學 Vol.53 No.9

Influences of metocopramide (MCP), which is a seletive dopaminergic antagonist, on blood pressure of the rat and its mechanism of action were investigated in the present study. MCP administered into a femoral vein of the rat caused markedly a dose-related fall in blood pressure followed by secondary transient pressor response. The depressor action evoked by MCP was not blocked by pretreatment of atropine or chlorisondamine, while the pressor action was inhibited significantly. Prazosin treatment reduced markedly both of depressor and pressor induced by MCP. MCP-evoked pressor action was not affected by clonidine, but the depressor response was attenuated significantly. Debrisoquin treatment made the inhibited response to MCP-induced pressor response, while did not affect the depressor action. Both of pressor and depressor responses evoked by MCP were not influenced by cyproheptadine. The hypertensive activity induced by nor epinephrine was weakened markedly by the infusion of MCP (1.50 mg/kg/30min.), but the pressor action evoked by dopamine not affected. These experimental data suggest that MCP produces biphasic responses (depressor and pressor) in blood pressure of the rat, and that the hypotensive activity is due to adrenergic alpha-receptors blockade, and that pressor activity is exerted through stimulation of cholinergic nicotinic receptors in autonmic ganglia.

기관내삽관에 의한 후두손상

임상철,이준규,이동훈,윤태미 全南大醫大 2004 전남의대학술지 Vol.40 No.1