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Fatigue Damage Spectrum을 이용한 궤도차량의 진동환경 비교
김재하,최병민,우호길 한국군사과학기술학회 2000 한국군사과학기술학회지 Vol.3 No.1
This paper provides the test results of tracked vehicle at each driving condition and life cycle. Fatigue Damage Spectrum(FDS) has evaluated with the Power Spectrum Density(PSD) and the life time of equipment. Finally, provisional vibration qualification test level is evaluated.
김재하,황동기,최대근,Kim, Jai-Ha,Whang, Dong-Kee,Choe, Dae-Geun 한국군사과학기술학회 2007 한국군사과학기술학회지 Vol.10 No.4
This paper considers the mechanical properties test results of the ceramic fiber reinforced plastic using hyper temperature. These materials were developed to make antenna cover which should not only protect antenna from high temperature and high pressure but also transmit and receive radio frequency for hypersonic missile. So the bending strength tests under the room temperature and the hyper temperature for new materials were done to evaluate of their performances. Also, the conductivity, specific heat, diffusivity and density were tested.
김재하,Kim, Jae-Ha 대한약리학회 1994 대한약리학잡지 Vol.30 No.2
In rat atrium the characteristics of purinergic receptors were investigated by observing the effects of some purinergic receptor agonists and antagonists on action potential and contractile force. The statistically significant effects of $ATP(10^{-6}{\sim}10^{-3}M)$ and adenosine $(10^{-6}{\sim}10^{-3}M)$ on normal action potential characteristics were a dose-dependent shortening of action potential duration $(APD_{90})$ by both agents and hyperpolarization by $ATP(10^{-4},10^{-3}M)$. $CAP(10^{-8}{\sim}10^{-4}M)$, an $A_1$ adenosine receptor agonist, shortened $(APD_{90})$ markedly in a dose-dependent manner and these effects were almost abolished by $DPCPX\;(10^{-6}\;M), an $A_1$, adenosine receptor antagonist, but not affected by $DMPX(2{\times}10^{-6}\;M)$, an $A_2$ adenosine receptor agonist. On the other hand, CGS $21680(10^{-7}{\sim}10^{-4}M)$, an $A_2$ adenosine receptor agonist, elicited a slight shortening of $(APD_{90})$ and these effects were inhibited by DPCPX but persisted in the presence of DPMX. Adenosine $(10^{-6}{\sim}10{\-4}\;M)$ decreased the basal contraction of atrial muscle in a dose-dependent manner and these effects were not inhibited by DMPX but by DPCPX. These results suggests that purinergic receptor agonists depress the cardiac activity by a short ening of action potential duration and this effect is mostly mediated by $A_1$ adenosine receptors in rat atrium.
혈관활성 물질이 심근의 ATP-민감성 칼륨통로의활성 조절에 미치는 영향
김재하,주정민,박령화,김윤이,정한성,박형욱,정대호,이상록,윤남식,김계훈,홍영준,김주한,김원,안영근,정명호,조정관,박종춘,강정채 대한심장학회 2006 Korean Circulation Journal Vol.36 No.7
Background and Objectives:It has been known that various vasoactive agents are involved in the regulation ofcardiac function through the modification of the K+ channel activities, including the ATP-sensitive K+ channel(KATP). We examined the effects of several vasoactive agents on the cardiac KATP currents in isolated cardiac myocytes.Materials and Methods:Ventricular myocytes were isolated from the hearts of ICR mice by enzymatic digestion.The channel currents were recorded by the excised inside-out and cell-attached patch clamp configurations.Results:In the excised inside-out patches, bradykinin (BRK; 1-10 μM) and prostaglandin I2 (PGI; 10-50 μM)did not affect the channel activities, whereas the vasodilators increased the attenuated channel activities in thepresence of 100 μM ATP. BRK and PGI in parallel shifted the dose-response curves of ATP (1-1,000 μM),and this inhibited the KATP currents to the right. Endothelin (ET-1; 0.1-1 nM) and leukotriene D4 (LTD; 3-10μM) decreased the channel activities immediately after making the inside-out patches. However, the vasoconstrictorsdid not affect the attenuated channel activities by ATP. In the cell-attached patches, both BRK and PGIincreased the channel activities and these effects were markedly attenuated by glibenclamide (50 μM). ET-1 andLTD did not affect the baseline channel activities in the cell-attached patches, but they markedly attenuated thedinitrophenol-induced activities. Conclusion:It was inferred that certain vasoactive substances are involved inthe regulation of cardiac KATP channel activities, and that bradykinin and PGI2 enhance the channel activities,and ET-1 and LTD4 inhibit the channel activities. (Korean Circulation J 2006;36:516-525) 배경 및 목적: 혈관 평활근의 긴장도 조절에 관여하는 다양한 종류의 혈 관 활성 물질들이 심근에서도 K+ 통로의 활성 조절을 통한 심기능 조절에 관여함이 알려져 있다. 본 연구는 이들 심혈 관계 활성 물질이, 심근 허혈 및 재관류 시 ATP-민감성 K+(KATP) 통로가 심근세포의 허혈 손상과 부정맥 발생에 어 떤 역할을 하는지 알아보고자 하였다. 방 법: 효소(collagenase) 분리법으로 분리한 생쥐의 단일 심실근 세포로부터 excised inside-out patch(IOP) 및 cell-attached patch(CAP)를 만들고, 각각 ATP-free 실험용액과 DNP 실험용액을 관류시켜 KATP 통로의 활성을 유도하고 혈관활 성물질에 의한 통로 활성의 변동을 측정하였다. 결 과: Bradykinin(BRK, 1~10 μM)과 Prostaglandin I2(PGI, 10~50 μM)는 IOP 시행 후 나타나는 내향성의 통로 활성 에는 영향을 미치지 않았다. 그러나 세포내측에 ATP를 투 여하여 통로 활성이 약화된 상태에서는 각각 용량-의존적 으로 통로 활성을 증가시켰다. BRK와 PGI에 의한 내향성 통로 활성의 증가는 100 μM의 ATP 투여 시에 가장 현저하 였다. Endothelin(ET-1, 0.01~1 nM)과 Leukotriene D4 (LTD, 3~10 μM)는 IOP 시행 후 나타나는 내향성의 통로 활성을 각각 용량-의존적으로 감소시켰다. BRK(1~10 μM) 와 PGI(10~50 μM)는 CAP 시행 후 나타나는 내향성의 통 로 활성을 각각 용량-의존적으로 증가시켰으며 이 통로 활 성 증가 효과는 ATP-민감성 K+ 통로차단제인 glibenclamide (50 μM)에 의해서 현저히 약화되었다. ET-1(0.01~1 nM)과 LTD(3~10 μM)는 CAP 시행 후 나타나는 내향성의 통로 활 성에 영향을 미치지 않았으나, 대사억제제 dinitrophenol (50 μM)을 관류하여 유도된 통로의 활성은 용량-의존적으 로 감소시켰다. 결 론: 이상의 연구 결과로, 주요 혈관 활성 물질들은 ATP-민감 성 K+(KATP) 통로의 활성 조절에 관여하고 혈관확장제인 BRK 와 PGI는 통로 활성을 증가시키고, 혈관수축제인 ET-1과 LTD는 통로 활성을 감소시킴으로써 심근의 허혈 손상을 보 호하거나 조장하며 부정맥을 유발하는 데 관여할 것으로 추 론하였다.