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Transforming growth factor ${\beta}_1$이 배양랫트 신경교세포의 성장 및 생화학적 변화에 미치는 영향
김용식,윤용하,박난향,박찬웅,Kim, Yong-Sik,Youn, Yong-Ha,Park, Nan-Hyang,Park, Chan-Woong 대한약리학회 1994 대한약리학잡지 Vol.30 No.2
Recent evidence indicates that glial cells have a wide range of funtions which are critical for maintaining a balanced homeostatic environment in the central nervous system(CNS) peripheral nervous system(PNS). Morever, astrocytes are known to participate in the tissue repair and neuroimmunologic events within the CNS through many kinds of growth factors and cytokines. We investigated the effect of $TGF\;{\beta}_1$, on the growth and biochemical changes of rat glial cells in culture. The proliferative effect was determined by $^3H-thymidine$ uptake and the double immunostain with anti-cell-specific marker and anti-Bromodeoxyuridine(BrdU) antibody. To check the effect of biochemical changes we compared the amounts of glial fibrillar acidic protein(GFAP) and the activity of glutamine synthetase(GS) in astrocyte. And the amounts of myelin basic protein and the activity of 2',3'-cyclic nucleotide phosphohydrolase(CNPase) were measured in oligodendrocyte and the amounts of peripheral myelin in Schwann cell. When $TGF\;{\beta}_1$, was treated for 2 days with cultured glial cell, $TGF\;{\beta}_1$, decreased the $^3H-thymidine$ uptake and proliferation index of double immunostain of astrocytes, which indicates the inhibition of astroglial DNA synthesis, but stimulated the growth of Schwann cell. Also, $TGF\;{\beta}_1$, decrease the GS activity and increased the amounts of GFAP in astrocyte. In the case of Schwann cells the amounts of peripheral myelin was increased when treated with $TGF\;{\beta}_1$. However, $TGF\;{\beta}_1$, didn't show any effect on the proliferation and biochemical changes in oligodendrocyte. These results suggest that $TGF\;{\beta}_1$, might have a critical action in the regulation of proliferation and biochemical changes in glial cells, especially astrocyte.
Toluene의 생물학적 분해능 향상을 위한 계면활성제의 선정
김용식,손영규,김지형,송지현,Kim Yong-Sik,Son Young-Gyu,Khim Jee-Hyeong,Song Ji-Hyeon 한국지하수토양환경학회 2005 지하수토양환경 Vol.10 No.4
Surfactants can be used to enhance the mass transfer rate of hydrophobic compounds into the biologically active liquid phase, resulting in an increase in biodegradation rate of toluene. In this study, the mass transfer rate and the biocompatibility of toluene in the presence of various surfactants were evaluated. Four anionic and non ionic surfactants were tested: sodium dodecyl sulfate (SOS), TritonX-100, Tween 80, and BYK-345 (silicone surfactant). Experimental results showed that BYK-345 at the critical micelle concentration (CMC) enhanced the solubility of toluene. However, there was no increase in the solubility of toluene by SOS and TritonX-100 at their CMCs. With the addition of each surfactant into deionized water the mass transfer rate became faster than that of the case with no surfactant. A bottle study using toluene-degrading microorganisms showed that SOS seriously reduced toluene removal presumably due to the toxicity of the anionic surfactant and/or the substrate competition between the surfactant and toluene. In addition, the degradation rate of toluene was decreased in the presence of BYK-345, indicating that BYK-345 adversely affects the activity of microorganisms. However, TritonX-100 and Tween 80 did not decrease the degradation rate of toluene significantly. Rather, at the low concentration of TritonX-100 toluene degradation rate was even increased. Overall the experimental results suggest that TritonX-100 be the appropriate surfactant for enhanced biological degradation of toluene. 계면활성제는 소수성 물질(톨루엔)의 물질전달율을 증가시켜 미생물이 있는 액상으로 잘 녹아들어가게 함으로써 미생물에 의한 분해를 증가시킨다. 본 연구에서는 여러 종류의 계면활성제가 존재할 때 톨루엔의 물질전달율과 미생물에 의한 분해가 어떻게 이루어지는지에 대해 알아보았다. 사용한 계면활성제는 다음과 같다: Sodium Oodecyl Sulfate (SOS), TritonX-100, Tween 80, BYK-345 (silicone 계면활성제). 실험결과에 따르면 BYK-345는 critical micelle concentration (CMC)에서 톨루엔의 용해도를 증가시켰다. 하지만, SDS와 TritonX-100는 CMC에서 톨루엔의 용해도를 증가시키지 못했다. 증류수에 계면활성제를 첨가하면 증류수만 있는 경우보다 톨루엔의 물질전달율$(K_La)$이 증가했다. 톨루엔 분해 미생물을 이용한 회분식 실험에서 SOS는 톨루엔의 분해를 감소시켰다. 그 이유는 SDS가 미생물에 독성을 미쳤기 때문일 수도 있고, 기질로서 이용되어서 톨루엔과 경쟁관계에 놓였기 때문일 수도 있다. BYK-345를 계면활성제로 사용한 실험에서도 톨루엔의 분해가 감소했는데 이것은 BYK-345가 미생물의 활성도에 심각한 영향을 미쳤기 때문이다. 하지만, TritonX-100 와 Tween 80의 경우에는 톨루엔의 분해가 크게 감소하지 않았다. 낮은 농도의 TritonX-100의 경우에 오히려 톨루엔의 분해는 증가했다. 이와 같은 결과들을 통해 톨루엔의 생물학적 분해를 위해 가장 적절한 계면활성제는 TritonX-100임을 알 수 있었다.
MPTP와 대사물인 $MPP^+$의 도파민 신경세포에 대한 독성효과에 관한 연구
김용식,박찬웅,윤영란,윤용하,Kim, Yong-Sik,Park, Chan-Woong,Yoon, Young-Ran,Youn, Yong-Ha 대한약리학회 1995 대한약리학잡지 Vol.31 No.2
Dissociated cell cultures from rat embryonic ventral mesencephalon were used to evaluate the mechanisms of $MPP^+$ neurotoxicity. The cells were treated with MPTP or $MPP^+$ and the viability of the cells was assessed biochemically; tyrosine hydroxylase (TH) immunoreactivity, protein, intracellular ATP and lactate content and lipid peroxidation. Also the generation of the intracellular oxidants was measured after loading 2', 7‘-dichlorofluorescin diacetate to the cells. When cultures were exposed to 0.1 mM $MPP^+$, at 2 hour incubation lactate was significantly accumulated in the cells and then the intracellular ATP content and TH immunoreactivity were decreased dose- and time-dependently. But, malondialdehyde as an index for lipid peroxidation was not changed even though the generation of the intracellular oxidants was stimulated by the addition of $MPP^+$. On the other hand, 1 mM MPTP significantly reduced the TH immunoreactivity at 24 hour exposure without any change in the intracellular A TP, lactate and MDA content until 6 hour exposure. And also MPTP inhibited the generation of the intracellular oxidants from control cells and $MPP^+$ exposed cells. These results indicate that cytotoxicity of $MPP^+$ is mediated by inhibiting the mitochondrial energy metabolism rather than generating the intracellular oxidants. And MPTP would have direct action in addition to conveting to the toxic metabolite, $MPP^+$ to exert the toxicity on the dopaminergic neurons.
심장근(心臟筋) mithochondria의 $Ca^{++}$유리에 대한 $Na^+$의 영향(影響)
김용식,박찬웅,김명석,Kim, Yong-Sik,Park, Chan-Woong,Kim, Myung-Suk 대한약리학회 1981 대한약리학잡지 Vol.17 No.1
Mitochondria로 부터의 $Na^+$에 의한 $Ca^{++}$유리현상은 digitalis의 강심기전을 설명하는데 있어 세포내 $Ca^{++}$농도 증가기전을 설명할 수 있는 현상의 하나로 보여지므로 $Na^+$에 의한 $Ca^{++}$유리와 이러한 $Ca^{++}$유리가 반응액내 $Ca^{++}$ 존재 유무로 어떠한 변화를 받는지를 비교 검토하였고 steady state에서의 $Ca^{++}$ flux에 대한 $Na^+$의 효과를 관찰하였다. $Na^+$의 증가에 따라 mitochondria에 흡수된 $Ca^{++}$의 유리량과 유리율이 증가하였고, EGTA 1mM 투여로 반응액내 잔여 $Ca^{++}$을 없을 경우 $Ca^{++}$유리가 증가함을 보여, 반응액내 잔여 $Ca^{++}$이 $Na^+$에 의한 $Ca^{++}$유리를 억제하리하 믿어진다. 한편 steady state에서 unidirectionai $Ca^{++}$ influx가 $Na^+$에 의하여 감소되는 점으로 미루어, $Na^+$에 의한 $Ca^{++}$유리는 $Na^+$이 $Ca^{++}-Ca^{++}$ 교환을 직접 억제하여 $Ca^{++}$ influx를 감소시켜 나타나는 결과로 생각된다. $Na^+$에 의한 unidirectional $Ca^{++}$ influx의 억제는 $Ca^{++}-Ca^{++}$교환에 $Na^+$이 직접 작용하며, 또한 반응액내 $Ca^{++}$의 다소에 따라 $Na^+$에 의한 $Ca^{++}$ 유리정도가 변화되는 양상으로 미루어 보아 mitochondria의 $Ca^{++}$ 운반의 일부는 $Na^+$과 $Ca^{++}$이 상경적으로 작용하는 모종의 동일매개체에 의하여 이루어질 수 있으리라 생각된다. The $Na^+$-induced calcium release and the effect of sodium on the transmitochondrial calcium flux were observed in mitochondria isolated from pig ventricular myocardium by Milipore filtration technique using radioisotope $^{45}Ca$. The release of calcium from cardiac mitochondria was induced by small amount of sodium, and was promoted by increasing sodium concentration in the incubation medium. The extent of the $Na^+$-induced calcium release was much greater in the absence of extramitochondrial calcium than in the presence of calcium. At steady state of calcium binding on the mitochondrial membrane unidirectional calcium influx was inhibited by sodium and unidirectional calcium efflux was increased., From the above results, it was suggested that calcium might be released from cardiac mitochondria in exchange with sodium through the mediation of the postulated '$Na^+/Ca^{++}$ exchange' mechanism.
광주, 전남지역에서의 업종별 악성종양 발생에 관한 연구 - 1종 의료보험 자료를 중심으로 -
김용식,오원문,박형철,최진수,송인현,Kim, Yong-Sik,Oh, Won-Moon,Park, Hyung-Cheol,Choi, Jin-Su,Song, In-Hyun 대한예방의학회 1990 Journal of Preventive Medicine and Public Health Vol.23 No.2
In order to investigate the occurrence characteristics of cancer in terms of industry in Kwangju-Chonnam area, medical utilization records of industrial medical insurance corporations during the period of 1987 to 1988 were reviewed for the identification of neoplastic disease. The cases obtained from the medical records were followed up for the verification and to get additional information. Standardized incidence data were compared by occupational characteristics. Multiple logistic regression analysis was applied to analyze the difference of incidence or distribution of cancer as a whole or of some selected cancer. Total cases of cancer identified were 242 during the study period. Annual incidence rate was calculated as 123.1 per 100,000 person. The frequent types of cancer were cancers of stomach, liver, lung, colon and rectum, bladder and lymphoma in descending order. Employees of mine and other sand handling industries showed significantly higher risks for cancer of stomach and cancer as a whole. Employees of the transportation industry showed the higher risk for cancer of liver, Workers in small-sized industry (${\leqq}100$) had a higher risk for cancer than who in large-sized industry (<100). These findings suggested the effect of occupational environmental exposure to cancer development.
김용식,윤영란,박찬웅,Kim, Yong-Sik,Yoon, Young-Ran,Park, Chan-Woong The Korean Society of Pharmacology 1993 대한약리학잡지 Vol.29 No.1
허혈성 뇌손상시 칼슘길항제, 항산화제와 산소라디칼 제거제 그리고 흥분성 아미노산 수용체 길항제의 보호효과를 검토하기 위해 본 연구에서는 랫트 뇌 해마조직 절편을 산소와 포도당을 제거한 반응액에 노출시켜 실험적 허혈상태를 유도하였다. 그리고 여러 약물을 처리한 상태에서 허혈시의 뇌세포 손상정도를 생화학적 지표들(절편내 ATP와 반응액내 lactate 및 malondialdehyde (MDA)유리량)을 측정하여 검토하였다. 60분까지 허혈상태를 유발시킨 경우 시간에 따라 절편내 ATP 함량이 감소하였고 lactate 유리량이 증가하였다. 그 후 산소와 포도당이 든 반응액으로 바꿔주니 이들 생화학적 변화들이 회복되는 양상을 보였다. 그러나 본 실험조건에서 허혈상태로부터 완전히 회복되지는 않았다. 동일한 허혈조건에서 verapamil과 비타민 E는 ATP 함량 감소와 절편으로부터의 lactate 유리량의 증가에 대해 보고효과를 보였다. 그리고 verapamil과 diltiazem은 반응액내로의 MDA유리를 감소시켰다. Superoxide dismutase (SOD), glutathione과 MK-801 (NMDA 수용체 길항제)은 20분 허혈조건에서 ATP 함량을 증가시켰으나 그외 다른 조건에서 보호효과를 보이지 않았다. 허혈 후 20분간 산소와 포도당을 재공급한 경우 verapamil은 ATP 함량과 lactate 유리에 보호효과를 보였다. 한편 비타민 E는 20분 허혈 조건에서의 lactate 유리와 60분 허혈시의 MDA 유리 증가에 대해 감소효과를 보였다. 이상의 결과는 칼슘길항제와 비타민 E가 랫트 뇌절편에서의 허혈성 생화학적 손상을 방지함으로 나타난 결과로 해석되며, 칼슘갈항제의 효과가 비타민 E보다 우수함으로 미루어 칼슘길항제는 허혈성 뇌손상에 예방 및 보고효과를 보일 것으로 믿어졌다. To evaluate the protective effects of calcium antagonists, oxygen radical scavengers and excitatory amino acid (EAA) antagonist on the ischemic brain damage, we induced in vitro ischemic condition (namely, lack of oxygen and glucose) to rat hippocampal slices. And the degree of ischemic damage was determined by assaying changes in biochemical parameters such as ATP content and lactate ralease, MDA production in the presence or absence of the various drugs. During experimental ischemia for up to 60 min, ATP content was decreased and the amount of lactate release was markedly increased time-dependently. By changing the reaction medium which contained oxygen and glucose those biochemical parameters were recovered. But the recovery was not complete in this experimental condition. In the same ischemic conditions verapamil and vitamine E prevented the decrease of ATP content and the increase of lactate release from the slices. And verapamil and diltiazem decreased MDA release to the reaction medium. Superoxide dismutase (SOD) and MK-801 (as EAA receptor antagonist) protected the decrease of ATP content and reduced MDA release in 20 min ischemic condition, but glutathione affected ATP content and lactate release at the same condition. When oxygen and glucose were resupplied for 20 min after ischemic condition, verapamil showed the protective effect on the changes of ATP content and lactate release, and vitamine E decreased lactate release (at 20 min ischemia) and MDA release (at 60 min ischemia). These results showed that calcium antagonist and vitamine E protect the ischemic biochemical changes from rat hippocampal slices and calcium antagonist is more potent than vitamine E to protect the ischemical brain damege.