1.Status of Clerkship Education and Its Evaluation in Korean Medical Schools.
Eunbae YANG ; Duk Joon SUH ; Yunseong LEE ; Sookon LEE ; Seokhwa KIM ; Eunil LEE ; Guetae CHAE ; Yeonju JO ; Ducksun AHN
Korean Journal of Medical Education 2007;19(2):111-121
PURPOSE: The aim of this study is to identify the status of clerkship education and its evaluation in Korea. METHODS: Questionnaires were sent to 943personnel in 23clinical departments of 41medical schools nationwide from April, 1 to April 10, 2004. We analyzed the 638 questionnaires that were collected from 39medical schools. RESULTS: The most frequently used methodologies for clerkship education were small group lecture(17.1%), observation of ambulatory care(15.7%), seminar(12.9%), observation and support of operation(12.4%), ward rounding(12.1%). The relative proportion of educational methodologies was varied according to the type of clinical departments. Most of the clinical clerkship activity was conducted in the university hospital. Also, the clerkship activities were educated by professors(57.8%), fellows(9.1%), residents(30.6%) and others(2.5%). The evaluation methods were written exam(21.8%), attendance(17.5%), report(14.0%), and oral exam(12.0%). In terms of evaluating items, acquirement of clinical knowledge has been mainly tested. However, students' ability to communicate, build human relationship, and clinical skills has been less frequently evaluated in most of medical schools. CONCLUSION: It is most likely that the current status of clerkship education and its evaluation in Korea is focused on the education and assessment of clinical knowledge. To improve this, the following areas need to be enriched: interaction between faculty and students, experience-based clerkship, effective feedback, time management, objectivity of evaluation, performance evaluation.
Clinical Clerkship
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Clinical Competence
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Education*
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Evaluation Studies as Topic
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Humans
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Korea
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Schools, Medical*
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Time Management
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Surveys and Questionnaires
2.Syringaresinol causes vasorelaxation by elevating nitric oxide production through the phosphorylation and dimerization of endothelial nitric oxide synthase.
Byung Hee CHUNG ; Sookon KIM ; Jong Dai KIM ; Jung Joon LEE ; Yi Yong BAEK ; Dooil JEOUNG ; Hansoo LEE ; Jongseon CHOE ; Kwon Soo HA ; Moo Ho WON ; Young Guen KWON ; Young Myeong KIM
Experimental & Molecular Medicine 2012;44(3):191-201
Nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays an important role in vascular functions, including vasorelaxation. We here investigated the pharmacological effect of the natural product syringaresinol on vascular relaxation and eNOS-mediated NO production as well as its underlying biochemical mechanism in endothelial cells. Treatment of aortic rings from wild type, but not eNOS-/- mice, with syringaresinol induced endothelium-dependent relaxation, which was abolished by addition of the NOS inhibitor NG-monomethyl-L-arginine. Treatment of human endothelial cells and mouse aortic rings with syringaresinol increased NO production, which was correlated with eNOS phosphorylation via the activation of Akt and AMP kinase (AMPK) as well as elevation of intracellular Ca2+ levels. A phospholipase C (PLC) inhibitor blocked the increases in intracellular Ca2+ levels, AMPK-dependent eNOS phosphorylation, and NO production, but not Akt activation, in syringaresinol-treated endothelial cells. Syringaresinol-induced AMPK activation was inhibited by co-treatment with PLC inhibitor, Ca2+ chelator, calmodulin antagonist, and CaMKKbeta siRNA. This compound also increased eNOS dimerization, which was inhibited by a PLC inhibitor and a Ca2+-chelator. The chemicals that inhibit eNOS phosphorylation and dimerization attenuated vasorelaxation and cGMP production. These results suggest that syringaresinol induces vasorelaxation by enhancing NO production in endothelial cells via two distinct mechanisms, phosphatidylinositol 3-kinase/Akt- and PLC/Ca2+/CaMKKbeta-dependent eNOS phosphorylation and Ca2+-dependent eNOS dimerization.
Animals
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Aorta/*drug effects/physiology
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Enzyme Activation/drug effects
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Furans/*pharmacology
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Gene Deletion
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Human Umbilical Vein Endothelial Cells/drug effects/metabolism
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Humans
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Lignans/*pharmacology
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Mice
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Mice, Inbred C57BL
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Nitric Oxide/metabolism
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Nitric Oxide Synthase Type III/genetics/*metabolism
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Phosphatidylinositol 3-Kinases/metabolism
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Phosphoinositide Phospholipase C/metabolism
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Phosphorylation/drug effects
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Protein Multimerization/*drug effects
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Proto-Oncogene Proteins c-akt/metabolism
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Vasodilation/*drug effects