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고추종자의 성숙에 따른 구조 및 저장물질의 전자현미경적 연구
김세규,김은수,김우갑,이광웅,Kim, Se-Kyu,Kim, Eun-Soo,Kim, Woo-Kap,Lee, Kwang-Woong 한국현미경학회 1995 Applied microscopy Vol.25 No.4
The ultrastructure and storage reserves of the Capsicum annuum seeds were studied in order to identify structure and to localize storage components in the endosperm using light microscopy, scanning and transmission electron microscopy. The seed coat was composed of one cell layer which contained a large number of lipid bodies, while most of the endosperm cells did not showed many lipid bodies. During seed maturation, the endosperm cells were continuously degenerated by the autophagy. Various types of plastids were also distinguished in the endosperm cells. They contained starch grains surrounded by electron-dense tiny particles, plastoglobuli, and vasicular bodies.
백서 폐동맥 내피세포에서 cytokine 및 내독소에 의한 nitric oxide 생성과 미토콘드리아 aconitase 활성도의 관계
김세규(Se Kyu Kim),장준(Joon Chang),이원영(Won Young Lee),장상호(Sang Ho Jang),박전한(Jeon Han Park),김세종(Se Jong Kim),김성규(Sung Kyu Kim),(Boaz A . Markewitz),(John R . Michael) 대한내과학회 1999 대한내과학회지 Vol.56 No.2
N/A Objective : Both constitutive and inducible forms of nitric oxide synthase exist in endothelial cells. Disorders that produce acute lung injury frequently release endotoxin and cytoknes, such as interferon(IFNγ) and tumor necrosis factor (TNFα). Endotoxin and these cytokines likely act as important mediators of cell injury. Because nitric oxide (NO) avidly reacts with iron, it may affect the activity of key enzymes, such as mitochondrial aconitase, which contain an iron-sulfur structure as a prosthetic group. Method : We studied the effect of IFNγ, TNFα and E. coli lipopolysaccharide(LPS) on NO production and mitochondrial aconitase activity in cultured rat lung microvascular endothelial cells(RLMVC). Result : Exposing RLMVC for 24 hours to IFNγ(500 U/mL), TNFα(300 U/mL) and LPS(5 ㎍/mL) significantly increases nitrite production to 20±1 μM compared to 0.07 μM in control cells(P<0.05, n=4). Cytokine treatment also reduced mitochondrial aconitase activity from 196±8 to 102±34 nmole/min/mg of cell protein(P<0.05, n=4). Treatment with the inhibitor of nitric oxide synthase N-monomethyl-L-arginine(NMMA) (0.5 mM) not only significantly blunted the cytokine- mediated increase in nitrite formation (3±0.5 μM vs 20±1 μM with cytokines, P<0.05, n=4), but also prevented the cytokine-mediated drop in aconitase activity (161± 24 vs. 196±8 nmole/min/mg of cell protein, NS). Conclusion : Exposing RLMVC to IFNγ, TNFα and E. coli LPS substantially decreases mitochondrial aconitase activity. Nitric oxide appears to mediate this effect. Our results suggest that the excessive production of NO by endothelial cells, in response to cytokines and endotoxin, may inhibit the function of the endothelial cell itself.
만성폐쇄성폐질환에서 우심실 기능 부전에 따른 혈액응고 및 섬유소용해계 변화
김영 ( Young Kim ),장윤수 ( Yoon Soo Chang ),김형중 ( Hyung Jung Kim ),김세규 ( Se Kyu Kim ),장준 ( Joon Chang ),안철민 ( Chul Min Ahn ),김성규 ( Sung Kyu Kim ),곽진영 ( Jin Young Kwak ),최진화 ( Jin Hwa Choi ) 대한결핵 및 호흡기학회 2006 Tuberculosis and Respiratory Diseases Vol.60 No.6
배경: COPD 환자에서 흡연은 폐혈관에 직접 작용하여 혈관 수축, 확장 및 혈관세포 증식을 조절하는 매개물질을 분비하여 혈관의 부적절한 개형 및 생리 현상을 초래하여 폐성고혈압을 유발한다. COPD 환자에서는 종종 급성 및 만성 폐혈전증이 일어나고 혈장내 응고전구물질 및 섬유소용해계의 표지자들이 증가되어 있다. 그러나 COPD 환자에서 혈액 응고계 및 섬유소용해계가 우심실 기능 장애에 어떤 기여를 하는지는 잘 알려져 있지 않다. 본 연구에서는 진행된 COPD 환자에서 multidetector CT scan (MDCT)을 이용하여 측정한 우심실 기능에 따른 혈액내 응고계 및 섬유소용해 계의 변화를 알아보고자 하였다. 방법: GOLD 지침에 따라 COPD로 진단한 26명에서 심장 MDCT scan을 이용하여 우심실 박출계수를 구하였다. 혈액내 thrombin antithrombin (TAT) 및 plasminogen activator inhibitor (PAI)-1은 enzyme linked immunoassay 방법으로 측정하였다. 결과: COPD 환자의 혈중 TAT는 10.5±19.8㎍/L으로 정상인의 혈중 TAT 3.4±2.5㎍/L보다 의미 있게 증가되었으나 (p<0.01) COPD 환자의 혈중 PAI-1는 29.6±20.7ng/㎖으로 정상인의 혈중 PAI-1 25.9±17.9ng/㎖와 비교하여 의미 있는 변화가 없었다. COPD 환자에서 혈중 TAT는 MDCT scan으로 측정한 우심실 박출계수와 의미 있는 역 상관관계를 보였으나 (r=-0.645, p<0.01) 혈중 PAI-1은 우심실 박출계수와 상관관계를 보이지 않았다 (r=0.022, p=0.92). 결론: COPD 환자에서 혈중내 응고계는 활성화되어 있으며 혈중 TAT는 우심실 기능 장애의 의미있는 표지자로 사료된다. Background: Pulmonary hypertension in COPD patients is the result of a direct effect of tobacco smoke on the intrapulmonary vessels with the abnormal production of the mediators that control vasoconstriction, vasodilatation, and vascular cell proliferation, which ultimately lead to aberrant vascular remodeling and physiology. COPD patients are prone to the development of an acute and chronic thromboembolism with an elevation of the plasma procoagulant and fibrinolytic markers However, the roles of the coagulation and fibrinolysis system on the right ventricular dysfunction in COPD patients are not well defined. We examined the alteration of the coagulation and fibrinolysis system in COPD patients according to the right ventricular function measured using cardiac multidetector computed tomography (MDCT). Methods: The right ventricular ejection fraction (RVEF) was measured using cardiac MDCT in 26 patients who were diagnosed with COPD according to the definition of the GOLD guideline. The plasma level of thrombin antithrombin (TAT) and plasminogen activator inhibitor (PAI)-1 were measured using an enzyme linked immunoassay. Results: The plasma TAT was markedly elevated in COPD patients (10.5±19.8㎍/L) compared with those of the control (3.4±2.5㎍/L) (p<0.01). However, the plasma PAI-1 in COPD patients (29.6±20.7ng/㎖) was similar to that in the controls. The plasma TAT showed a significant inverse relationship with the RVEF measured by the cardiac MDCT in COPD patients (r=-0.645, p<0.01). However, the plasma PAI-1 did not show a relationship with the RVEF (r=0.022, p=0.92). Conclusion: These results suggest that the coagulation system in COPD patients is markedly activated, and that the plasma level of TAT might be a marker of a right ventricular dysfunction in COPD patients. (Tuberc Respir Dis 2006; 60: 625-630)
비소세포성 폐암 세포주에서 Farnesyl Transferase Inhibitor SCH66336과 인슐린양 성장 인자 결합 단백-3의 병용처리에 의한 세포고사 상승 작용
김영 ( Young Kim ),김세규 ( Se Kyu Kim ),김형중 ( Hyung Jung Kim ),장준 ( Joon Chang ),안철민 ( Chul Min Ahn ),김성규 ( Sung Kyu Kim ),장윤수 ( Yoon Soo Chang ) 대한결핵 및 호흡기학회 2005 Tuberculosis and Respiratory Diseases Vol.58 No.2
연구배경 : 인슐린 양 성장 인자 결합 단백질-3 (IGF binding protein-3, IGFBP-3)는 생체내와 실험관내에서 인슐린 양 성장인자 매개 신호전달 체계를 억제하여 비소세포성 폐암 세포의 증식을 조절하는 것으로 알려져 있다. 이에 본 연구에서는 비소세포성 폐암의 치료에 있어 IGFBP-3를 이용한 치료전략의 개발을 위하여 IGFBP-3(Ad5CMV-BP3)와 FTI SCH66336의 병용치료 상승작용을 분석하였다. 방법 : 비소세포성 Background : Insulin-like growth factor binding protein (IGFBP)-3 regulates non-small cell lung cancer(NSCLC) cell proliferation in vitro and in vivo by inhibiting IGF-mediated signaling pathways. To have better strategies for the treatment of lung cancer