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규칙적인 수영훈련이 마우스 비장세포의 ROS생성과 림프구 증식에 미치는 영향
곽이섭,박전한,김세종,장윤수,이봉기,Kwak, Yi-Sub,Park, Jeon-Han,Kim, Se-Jong,Jang, Yun-Soo,Lee, Bong-Ki 대한면역학회 2002 Immune Network Vol.2 No.2
Background: Aerobic training can be defined as any physical exercise that increases the heart rate and enhances the body's intake of oxygen long enough to benefit the condition of body. Running, cycling, and swimming are examples of aerobic activities. This type of exercise optimises immune functions. Recently several experimental findings suggested that the regular swimming training increase immune response, but there have been very few reports which compare warm water exercise with cold water exercise in spleen lymphocytes. Methods: This study was designed to examine the effects of regular swimming training on Index, the number of lymphocytes, proliferative activity and production of reactive oxygen species (ROS) by splenocytes in BALB/c mice. Thirty six mice (6 week old) were performed 10 weeks of regular swimming training and they were divided into 6 groups according to the regular swimming training (CRG: control resting group, CEG: control exercise group, WRG: warm water trained resting group, WEG: warm water trained exercise group, CORG: cold water trained resting group, COEG: cold water exercise group). Analytical items were weight change, spleen index, the number of lymphocytes, proliferative activity and production of ROS. All data were expressed as mean and standard deviation by using SPSS package program (ver. 10.0). Results: The swimming training significantly decreased body weight, and increased spleen index, the number of lymphocytes and proliferative activity in the presence or absence of Con A and LPS added conditions. For the WRG and CORG, the quantity of ROS from splenocytes was higher than CRG, whereas, ROS by spleen lymphocytes was lower following 90 min acute exercise stress. Conclusion: These results suggested that the swimming training not only increases the number of lymphocytes but also increases proliferative activity by splenocytes in vitro.
기본의학 교육과정 개선 방안 - 연세의대 광혜교육과정을 중심으로 -
류숙희,안덕선,이원택,박전한,정현수,박무석,양은배,Ryue, Sook-Hee,Ahn, Duk Sun,Lee, Won Taek,Park, Jeon Han,Jung, Hyun Su,Park, Mu Seuk,Yang, Eun Bae 연세대학교 의과대학 2009 의학교육논단 Vol.11 No.2
Medical Students' competencies depend on the medical school curriculum. Basic medical education, in particular, is an important starting point for further medical competency development. We aimed to identify the most important areas of reform in the basic medical education curriculum of Yonsei Medical School. To accomplish this, we sought case studies of different medical schools and discussion points for quality improvement methods. A qualitative comparison method saturated through the systematic discussions on the emerging thematic approaches to determine the current directions in medical school curriculum reform. The discussions, which involved 7 experts, spanned 8 months and were based on a literature review, with focus on the 7 selected case studies. From the discussions, we concluded that in order to improve basic medical education curriculum, the following measures need to be carried out. First, an outcome-based curriculum is to be designed. The expected outcome is to be deliberately and succinctly defined and should be expressed as teaching and learning objectives. Second, the core subjects and elective subjects are to be classified on the basis of the aim, content, and passage level of the subjects. Hence, the core curriculum must be treated as a standard part of medical knowledge, and the elective curriculum must be richer and more in-depth. Third, universities should institutionalize regular evaluation of their departments. Appropriate and just evaluations should be made, and feedback given to the school's administrative department. Fourth, the departmental and administrative management of the basic medical education curriculum should be harmonized with each other. Finally, teaching and learning resources are to be increased and diversified and made available to professors and students for basic medical education.
유철호(Chul Ho Yoo),이승헌(Seung Hun Lee),박전한(Jeon Han Park),전수일(Soo Il Chun) 대한피부과학회 1989 대한피부과학회지 Vol.27 No.2
Tsutsugamushi disease, an infectious disease by Rickettsia(R.) tsntsugamushi, is characterized by eschar, fever and rash. Eschar caused by chigger bite, is pre sent on 47 94% of patients with documented R. tsutsugamushi. We recently noticed one case of R. tsutsugamushi infection. Patient had fever, heaclache, lymphadenopathy, erythematous maculopapules and eschar. The R. tsu tsugamushi was isolated from serum of the patient. Histopathologic findings of eschar show epidermal ulceration overlying a zone of coagulative necrosis of upper dermis and necrotizing vasculitis. E]ectron microscopic findings of endothelial cells of capillary show rickettsia with cell division.
김현정 ( Hyon Jeong Kim ),신의철 ( Eui Cheol Shin ),유남진 ( Nam Jin Yoo ),박전한 ( Jeon Han Park ),김성재 ( Sung Jae Kim ),강응식 ( Eung Shick Kang ),장준섭 ( Jun Seop Jahng ) 대한류마티스학회 2001 대한류마티스학회지 Vol.8 No.2
목적: 골관절염(osteoarthritis)은 관절연골의 점차적인 소실과 이에 따른 활액막과 연골하골의 이차적인 변화를 특징으로 하는 질환으로서 특히 노년층에서 높은 유병율을 보이는데 원인 및 병인에 대해서는 아직 뚜렷하게 규명된 바가 없다. 한편, 세포사멸(apoptosis)은 세포괴사(cell necrosis)와는 상대되는 개념의 세포 사망으로서 염증반응이 없이 진행되는 것이 특징이고 자가면역질환, 종양, 퇴행성 뇌질환 등의 기전연구에서 그 역할이 규명되고 있다. 최근 몇몇 연구에 의하면, 골관절염의 연골세포가 정상관절의 연골세포에 비해 높은 비율의 세포사멸을 보이며, 또한 Fas에 대한 항체를 처치한 경우에도 부분적으로 세포사멸을 일으킨다고 하였다. 본 연구는 골관절염의 연골세포에서 일어나는 세포사멸의 양상을 정상관절의 연골세포와 비교하고, 세포사멸과 관련한 수용체/리간드의 발현을 조사하여 골관절염의 병인에 있어서 세포사멸의 조절기전을 알아보았다. 방법: 골관절염으로 인공슬관절 치환술을 시행받은 환자의 관절연골과 외상에 의해 슬상절단술을 시행 받은 환자의 절단지에서 채취한 관절연골을 재료로, TUNEL assay를 통해 세포사멸의 정도와 위치를 비교하였고 관절연골 조직에서 RNA를 분리하여 역전사중합효소연쇄반응을통해 세포사멸의 조절에 참여하는 Fas 관련분자 및 bcl-2family, TRAIL 및 그 수용체와 인터루킨-18 (IL-18)의 mRNA 발현정도를 조사하였으며 면역조직화학염색을 통하여 FasL 단백의 발현을 알아보았다. 결과: 형광 dUTP를 이용한 TUNEL assay에서 골관절염이 없는 정상 대조군 관절연골 4례 모두에서는 세포사멸을 보이는 세포를 찾아볼 수 없었으나 골관절염의 관절연골 7례의 표본 중 6례에서 전형적인 세포사멸 세포들을 관찰할 수 있었다. 역전사중합효소연쇄반응에서는 caspase-3, caspase-8, Fas 및 FasL의 mRNA 발현정도가 골관절염의 연골에서 정상 대조군 연골에 비해 증가하였으며, 특히 FasL는 일부 골관절염에서 현저히 증가된 양상을 보였다. FasL의 유도체로 알려진 IL-18은 FasL가 증가된 환자에서 함께 강한 발현을 보였다. 면역조직화학염색에서는 정상 대조군 연골에서보다 골관절염의 연골에서 FasL 단백이 현저히 강하게 발현됨을 관찰하였다. 결론: 본 연구는 골관절염 환자의 관절연골에서 의미있게 증가한 세포사멸과 FasL의 발현을 관찰하였으며, 이는 Fas/FasL 경로를 통한 세포사멸이 골관절염에서 일어나는 관절연골의 퇴화에 기여할 것을 시사한다. 또한 FasL의 유도체 중 하나인 IL-18의 발현도 관찰되었다. 이상의 결과는 차후 골관절염 치료에 있어서 새로운 접근을 제시하는 데 일조할 것으로 기대된다.
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
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.