• 대한소아치과학회지
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• 제31권1호
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• pp.19-25
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• 2004

치과적 장애인이란 치과진료 시 치과의사에게 자발적인 협조가 힘든 사람을 의미한다. 본 연구는 서울대학 치과병원 장애인진료실에서 치료받은 치과적 장애인 환자들의 임상진료 실태를 마취과적으로 분석하고 향후 장애인 치과치료에 대한 지침을 마련하고자 하였다. 1999년 1월부터 2002년 10월까지 서울대학교 치과병원 장애인진료실에 내원한 장애인 환자들을 대상으로 조사한 결과, 총 89명의 환자들에게 93건의 치과진료가 시행되었다. 환자의 대다수는 정신지체였고 전신마취 하 보존치료를 받았다. 주로 마취유도제는 thiopental, 근이완제는 vecuronium을 이용하였으며 산소, 아산화질소, enflurane을 함께 흡입시켜 마취를 유지하였다. 총 마취지속시간과 회복실 체류시간은 각각 $164.4{\pm}57.2$ 분과 $106.2{\pm}50.5$ 분이었고 회복 과정에서 심각한 합병증은 관찰되지 않았다. 본 연구는 외래환자마취에 기반한 서울대학교 치과병원 장애인진료실의 치료방침에 따라 특별한 문제없이 성공적인 마취가 가능하였음을 보여 주었다. 또한 증가하는 장애인 치과치료에 대한 수요를 충족시키기 위해서 적절한 시설과 인력을 갖춘 보다 맡은 외래환자마취 센터의 필요성도 제시한다고 할 수 있다.

• International Journal of Oral Biology
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• 제32권2호
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• pp.51-57
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• 2007

Cyclosporin A (CsA) plays an important role in clinical medicine and basic biology as an immunosuppressant and a mitochondrial permeability blocker, respectively. It was reported that CsA has a protective role by preventing apoptosis and promoting the proliferation in severed neurons. However, the molecular mechanisms for CsA-induced neuronal cell proliferation are unclear. In this study, we examined the mechanisms underlying the CsA-induced proliferation of PC12 cells. CsA increased the viability of PC12 cells in a dose(over $0.1{\sim}10\;{\mu}M$)-and time-dependent manner. The level of ROS generation was decreased in the CsA-treated PC12 cells. Expression of Bcl-2, an antiapoptotic molecule that inhibits the release of cytochrome c from the mitochondria into the cytosol, was upregulated, whereas Bax, a proapototic molecule, was not changed in the CsA-treated PC12 cells. CsA downregulated the mRNA expression of VDAC 1 and VDAC 3, but VDAC 2 was not changed in the CsA-treated PC12 cells. The level of cytosolic cytochrome c released from the mitochondria and the caspase-3 activity were attenuated in the CsA-treated PC12 cells. These results suggest that the mitochondria-mediated apoptotic signal and Bcl-2 family may play an important role in CsA-induced proliferation in PC12 cells.

• Animal cells and systems
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• 제2권4호
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• pp.483-488
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• 1998

We previously found that a potent gonadotropin-releasing hormone (GnRH) agonist, buserelin, decreases GnRH promoter activity together with GnRH mRNA level, providing evidence for an autoregulatory mechanism operating at the level of GnRH gene transcription in immortalized GT1-1 neuronal cells. To examine whether agonist-induced decrease in GnRH mRNA level requires the continuous presence of buserelin, we performed a pulse-chase experiment of buserelin treatment. Short-term exposure (15 min) of GT1-1 neuronal cells to buserelin ($10{\mu}M$) was able to decrease GnRH mRNA levels when determined 24 h later. When GT1-1 cells were treated with buserelin ( $10{\mu}M$) for 30 min and then incubated for 1, 3, 6, 12, 24, and 48 h after buserelin removal, a significant decrease in GnRH mRNA levels was observed after the 12 h incubation period. These data indicate that inhibitory signaling upon buserelin treatment may occur rapidly, but requires a long time (at least 12 h) to significantly decrease the GnRH mRNA level. To examine the possible involvement of de novo synthesis and/or mRNA stability in buserelin-induced decrease in GnRH gene expression, actinomycin D ($5{\mu}m/ml$), a potent RNA synthesis blocker, was co-treated with buserelin. Actinomycin D alone failed to alter basal GnRH mRNA Revel, but blocked the buserelin-induced decrease in GnRH mRNA level at 12 h of post-treatment. These data suggest that buserelin may exert its inhibitory action by altering the stability of GnRH mRNA. Moreover, a polvsomal RNA separation by sucrose gradient centrifugation demonstrated that buserelin decreased the translational efficiency of the transcribed GnRH mRNA. Taken together, these results clearly indicate that GnRH agonist buserelin acts as an inhibitory signal at multiple levels such as transcription mRNA stability, and translation.

• 약학회지
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• 제34권4호
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• pp.224-237
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• 1990

A single uniform population of specific, saturable, high affinity binding site of $[^3H]QNB$ guinuclidinyl benzilate(QNB) was identified in the rat cerebral microsomes. The Kd value(37.2 pM) for $[^3H]QNB$ calculated from the kinetically derived rate constants was in agreement with the Kd value(48.9 pM) determined by analysis of saturation isotherms at various receptor concentrations. Dimenhydrinate(DMH), histamine $H_1-blocker$, increased Kd value for $[^3H]QNB$ QNB without affecting the binding site concentrations and this effect resulted from the ability of DMH to slow $[^3H]QNB-receptor$ association. Pirenzepine inhibition curve of $[^3H]QNB$ binding was shallow(nH = 0.52) indicating the presence of two receptor subtypes with high ($M_1-site$) and low($M_2-site$) affinity for pirenzepine. Analysis of these inhibition curves yielded that 68% of the total receptor populations were of the $M_1-subtype$ and the remaining 32% of the $M_2-subtype$. Ki values for the $M_1-$ and $M_2-subtypes$ were 2.42 nM and 629.3 nM, respectively. Ki values for $H_1-blockers$ that inhibited $[^3H]QNB$ binding varied with a wide range ($0.02-2.5\;{\mu}M$). The Pseudo-Hill coefficients for inhibition of $[^3H]QNB$ binding by most of $H_1-blockers$ examined except for oxomemazine inhibition of $[^3H]QNB$ binding were close to one. The inhibition curve for oxomemazine in competition with $[^3H]QNB$ was shallow(nH = 0.74) indicating the presence of two receptor populations with different affinities for this drug. The proportion of high and low affinity was 33:67. The Ki values for oxomemazine were $0.045{\pm}0.016\;{\mu}M$ for high affinity and $1.145{\pm}0.232\;{\mu}M$ for low affinity sites. These data indicate that muscarinic receptor blocking potency of $H_1-blockers$ varies widely between different drugs and that most of $H_1-blockers$ examined are nonselective antagonist for the muscarinic receptor subtypes, whereas oxomemazine might be capable of distinguishing between subclasses of muscarinic receptor.

• 한국임상수의학회지
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• 제32권1호
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• pp.9-15
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• 2015

본 연구는 10 kg 미만의 소형견에서 흉강경을 이용한 우측 중폐엽 절제술을 적용할 때, 적합한 포트 접근법의 설정을 위하여 실시되었다. 평균 체중 $8.67{\pm}0.49kg$의 비글견 10마리에서 전신 마취를 실시한 후 기관 내시경 유도하에 우측 주기관지를 폐쇄하여 편측성 분리폐 환기를 실시하였다. 포트는8-6-10 늑간과 8-6-5 늑간을 통한 두 가지 접근법으로 위치시켰고, 흉강경 우중폐엽 절제술에는 복강경용 자가 절단 스테플러와 검체 회수 주머니가 사용되었다. 각 접근법은 1) 시각화, 2) triangulation; 흉강내 기구간 충돌, 3) 스테플러의 폐문부 접근 및 적용의 용이성, 4) 검체 회수 주머니 사용의 장해 여부, 5) 술자의 편의도의 5가지 항목을 점수화하여 평가하였다. 모든 개체에서 편측성 분리 폐 환기에 의해 양호한 작업 공간이 확보되었고, 성공적인 흉강경 우중폐엽 절제술이 완료되었다. 어느 경우에서도 포트 위치를 수정할 필요는 없었으며, 의인성 합병증 역시 발생하지 않았다. 두가지 접근법 모두 높은 점수를 얻어, 이들은 10 kg미만의 개에서 편측성 분리폐 환기하에 자가 절단 스테플러를 이용한 흉강경 우중폐엽 절제술을 실시함에 적합한 것으로 확인되었다.

• Journal of Yeungnam Medical Science
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• 제8권2호
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• pp.95-105
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• 1991

흰쥐 적출소장의 수축성에 미치는 GABA의 영향을 관찰하여 다음과 같은 결과를 얻었다. 1. GABA는 소장을 이완시켰으며 그 이완 작용은 십이지장, 공장 그리고 회장의 순이었다. GABA A수용체 효현제인 muscimol 역시 소장을 이완시켰으며, 그 효능의 강도는 십이지장, 공장 그리고 회장의 순이었다. 그러나 GABA B수용체 효현제인 baclofen은 소장의 운동성에 유의한 영향을 미치지 못하였다. 2. 상경적 GABA A수용체 길항제인 bicuculline과 비 상경적 GABA A수용체 길항제인 picrotoxin은 십이지장에 대한 GABA와 muscimol의 이완 작용을 현저히 억제시켰다. 그리고 bicuculline의 억제 작용이 picrotoxin 보다 강하였다. 3. Sodium channel blocker인 tetrodotoxin은 GABA의 이완 작용을 봉쇄하였다. 4. 신경절 봉쇄적인 hexamethonium은 십이지장에 대한 GABA의 이완작용을 길항하지 못하였다. 이상의 실험 결과로 볼 때 흰쥐 소장의 자발 수축운동에 대한 GABA의 이완작용은 소장이 부위에 따라 다르게 나타나며, 그 작용은 postganglionic presynaptic neuron에 존재하는 GABA A 수용체에 작용함으로써 나타나는 것으로 사료된다.

• 폴리머
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• 제28권2호
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• pp.143-148
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• 2004

옥타메틸싸이클로테트라실록산과 1,3,5-트리메틸싸이클로트리실록산 및 1,3,5,7-테트라비닐-1,3,5,7-테트라메틸싸이클로테트라실록산을 테트라메틸암모늄 실록산올레이트 촉매 하에서 1,1,3,3-테트라메틸디실록산과 평형중합으로 이들을 공중합시켜 $\alpha$,$\omega$-하이드로겐 폴리(메틸-디메틸-메틸비닐)실록산 전구체를 제조하였다. 제조된 $\alpha$,$\omega$-하이드로겐 폴리(메틸-디메틸-메틸비닐)실록산 전구체에 디메틸아크릴아마이드를 백금촉매 작용 하에서 반응시켜 아크릴아마이드 변성 $\alpha$,$\omega$-하이드로겐 폴리(메틸-디메틸-메틸비닐)실록산 전구체 (APMDMS)를 제조하였으며 여기에 금속산화물인 NiO, FeO를 배위결합시켜 금속산화물이 2차 결합으로 부가된 APMDMS-MO를 제조하였다. 제조된 화합물의 구조를 FT-IR과 $^1$H-NMR로 분석하여 확인하였다. $\alpha$,$\omega$-비닐 폴리디메틸실록산과 APMDMS-MO를 백금촉매 존재 하에서 컴파운딩시켜 금속산화물 함유 액상 실리콘 고무 복합체를 제조하였으며 이 화합물을 이용하여 제조된 쉬이트의 열 전도도는 0.29 W/mW로 액상 실리콘 고무 복합체의 0.215 W/mK 보다 우수하였고 체적 저항은 1.64${\times}$$10^{5}$$\Omega$ㆍcm로 낮은 값을 나타내었다. 또한 디메틸아크릴아마이드 변성 액상 실리콘 고무 복합체의 기계적 및 열적특성은 UTM과 TGA로 측정하였다.다.

• The Korean Journal of Physiology
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• 제26권1호
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• pp.55-68
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• 1992

The effects of changes in extracellular $Na^+\;and\;Ca^+$ concentration on the membrane potential and contractility were studied in the antral circular muscle of guinea pig stomach in order to elucidate the existence and the nature of $Na^+/Ca^{2+}$ exchange mechanism. All experiments were performed in tris buffered Tyrode solution which was aerated with 100% $O_2$ and kept at $35^{\circ}C.$ The treatment of $10^{-5}$ ouabain was performed to induce intracellular $Na^+$ loading prior to the start of experiment. The results were as follows: 1. $Na^+$-free Tyrode or high $Ca^{2+}$-Tyrode solution hyperpolarized the membrane potential and induced contracture. The time course of contracture was similar to that of change in membrane potential. 2. The degree of hyperpolarization and the amplitude of contracture decreased in accordance with the increase of extracellular $Na^+$ concentration. 3. $Na^+$-free contracture was developed even after blocking the influence of intrinsic nerves by the pretreatment with atropine, guanethidine and TTX. 4. $Ca^{2+}$-channel blockers(D-600 or $Mn^{2+}$) and the blocker of intracellular $Ca^{2+}$ release from sarcoplasmic reticulum(ryanodine) did not suppress the development of $Na^+$-free contracture. And also, dinitrophenol had no effect on $Na^+$-free contracture. 5. Dose-response relationship between extracellular $Na^+$ concentrations and the magnitude of contractures showed a sigmoid pattern. The slope of straight line from Hill plot was 2.7. 6. In parallel with the increase of extracellular $Ca^{2+}$ concentration, the amplitude of contracture increased dose dependently and was maximum at 8 mM $Ca^{2+}$-Tyrode solution. 7. The relationship between extracellular $Ca^{2+}$ concentrations and the magnitude of contractures showed hyperbolic pattern. The slope of straight line from Hill plot was 1.1. From the above results, it is suggested that $Na^+/Ca^{2+}$ exchange mechanism exists in the antral circular muscle of guinea pig stomach and this mechanism affects the membrane potential electrogenically.

• The Korean Journal of Physiology and Pharmacology
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• 제20권1호
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• pp.25-33
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• 2016

Ion channels in carcinoma and their roles in cell proliferation are drawing attention. Intracellular $Ca^{2+}$ ($[Ca^{2+}]_i$)-dependent signaling affects the fate of cancer cells. Here we investigate the role of $Ca^{2+}$-activated $K^+$ channel (SK4) in head and neck squamous cell carcinoma cells (HNSCCs) of dif-ferent cell lines; SNU-1076, OSC-19 and HN5. Treatment with $1{\mu}M$ ionomycin induced cell death in all the three cell lines. Whole-cell patch clamp study suggested common expressions of $Ca^{2+}$-activated $Cl^-$ channels (Ano-1) and $Ca^{2+}$-activated nonselective cation channels (CAN). 1-EBIO, an activator of SK4, induced outward $K^+$ current (ISK4) in SNU-1076 and OSC-19. In HN5, ISK4 was not observed or negligible. The 1-EBIO-induced current was abolished by TRAM-34, a selective SK4 blocker. Interestingly, the ionomycin-induced cell death was effectively prevented by 1-EBIO in SNU-1076 and OSC-19, and the rescue effect was annihilated by combined TRAM-34. Con-sistent with the lower level of ISK4, the rescue by 1-EBIO was least effective in HN5. The results newly demonstrate the role of SK4 in the fate of HNSCCs under the $Ca^{2+}$ overloaded condition. Pharmacological modulation of SK4 might provide an intriguing novel tool for the anti-cancer strategy in HNSCC.

• The Korean Journal of Physiology and Pharmacology
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• 제20권1호
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• pp.9-14
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• 2016

Adenosine 3',5'-cyclic monophosphate (cAMP) participates in the regulation of numerous cellular functions, including the $Na^+-K^+$-ATPase (sodium pump). Ouabain, used in the treatment of several heart diseases, is known to increase cAMP levels but its effects on the atrium are not understood. The aim of the present study was to examine the effect of ouabain on the regulation of atrial cAMP production and its roles in atrial endothelin-1 (ET-1) secretion in isolated perfused beating rabbit atria. Our results showed that ouabain ($3.0{\mu}mol/L$) significantly increased atrial dynamics and cAMP levels during recovery period. The ouabain-increased atrial dynamics was blocked by KB-R7943 ($3.0{\mu}mol/L$), an inhibitor for reverse mode of $Na^+-Ca^{2+}$ exchangers (NCX), but did not by L-type $Ca^{2+}$ channel blocker nifedipine ($1.0{\mu}mol/L$) or protein kinase A (PKA) selective inhibitor H-89 ($3.0{\mu}mol/L$). Ouabain also enhanced atrial intracellular cAMP production in response to forskolin and theophyline ($100.0{\mu}mol/L$), an inhibitor of phosphodiesterase, potentiated the ouabain-induced increase in cAMP. Ouabain and 8-Bromo-cAMP ($0.5{\mu}mol/L$) markedly increased atrial ET-1 secretion, which was blocked by H-89 and by PD98059 ($30{\mu}mol/L$), an inhibitor of extracellular-signal-regulated kinase (ERK) without changing ouabain-induced atrial dynamics. Our results demonstrated that ouabain increases atrial cAMP levels and promotes atrial ET-1 secretion via the mitogen-activated protein kinase (MAPK)/ERK signaling pathway. These findings may explain the development of cardiac hypertrophy in response to digitalis-like compounds.