대한의사협회지 새 웹사이트 소개

The Journal of the Korean Medical Association (JKMA) established a new web site in July, 2010 available at http://jkma.org/. Here, we introduce the basic structure and concept of the new web site. The new web site provides current medical information from Korea to KMA members as well as global readers. The history of Korean medicine will also be organized in an easily accessible. Starting from this basic platform, JKMA will improve and expand other online functions in the near future. We hope every member of the Korean Medical Association enjoys browsing the content of JKMA through the new site and using the information they find in their clinical practiceope

기초의학 교육의 활성화 전략

The aim of this article is to identify roadblocks prohibiting effective education of medical students in the basic sciences and then propose strategies for designing and implementing a better curriculum in the basic sciences that remove the roadblocks thereby increasing the relevance to students' clinical experiences in medical training. Traditionally, the medical student experiences basic science education in a setting where there is little or no communication between the basic science and clinical science professors, where basic science content is given with very little clinical context, while clinical training does not enhance understanding of the scientific foundation for clinical practice. Herein, we re-address the purpose of basic science education proposing the concept of 'transfer' as a bridge to connect the basic and clinical science education. We also propose a continuing education program for staff development in the successful implementation of these proposals.ope

Changes in Myogenic Tone in Spontaneously Hypertensive Rat：Role of RhoA and Protein Kinase C

Background and Objectives: The myogenic response was originally described as a contraction of a blood vessel that occurred following an increase in intravascular distending pressure. Conversely, a reduction in intravascular pressure produces myogenic vascular relaxation. Recent attention has focused on the potential role of this myogenic mechanism in the control of tone in the resistance vasculature, and in particular on how this mechanism may contribute to the increased vascular resistance seen in hypertension. Therefore, in the present study, we investigated the role of myogenic tone in the generation and/or maintenance of hypertension. Materials and Methods: Myogenic tone was developed by stretching of the basilar arteries of WKY （Wistar Kyoto rat） and SHR （spontaneously hypertensive rats）. Contractile responses, PKC （protein kinase C） immunoblots and translocation of PKC and RhoA were measured. Results: In the presence of extracellular Ca2＋, the stretching of the resting vessel evoked a myogenic contraction in the basilar arteries of SHR and WKY. Myogenic tone was significantly greater in SHR than in WKY. However, in the absence of extracellular Ca2＋, stretching evoked a myogenic contraction in SHR, but not in WKY. The stretch-induced myogenic tone was inhibited by nifedipine. The effect of nifedipine was similar in both SHR and WKY rats. H-7, calphostin C and Y-27632, also inhibited stretch-induced myogenic tone in both SHR and WKY. The inhibitory effects of these drugs were greater in SHR than in WKY. Immunoblotting showed rho A and PKCα were translocated from the cytosol to the cell membrane with stretching in both SHR and WKY. PKCε, however, was translocated to the cell membrane with stretching in SHR, but not in WKY. Conclusion: These results suggest that stretch-induced myogenic tone is significantly greater in SHR than in WKY. Furthermore, the increase in amount and/or activity of PKCε and ROK （rhoA-associated kinase） may be a key mechanism accounting for the enhanced myogenic tone in SHR.ope

Effect of PKC-dependent change of K+ current activity on histamine-induced contraction of rabbit coronary artery

Background and Objectives : Histamine, released from mast cells in atheromatous plaque, has been known to cause cardiac ischemia or sudden cardiac death in atherosclerosis patient. Previous reports have suggested that histamine induced coronary vasoconstriction was due to increase in IP(3) and DAG, which induce release of Ca2+ from SR and increase the Ca2+ sensitivity of contractile element via activation of PKC. Recently, it was reported that application of histamine cause depolarization of intestinal smooth muscle, which may contribute to histamine-induced contraction via augmenting Ca2+ influx through activation of Ca2+ channels. However, the underyling mechanism of histamine-induced depolarization and its contribution to the magnitude of coronary vasoconstriction are still uncertain. Method : To elucidate the underlying mechanism of Ca2+ influx change during histamine-induced vasoconstriction, we examined the effect of Ca2+ channel antagonist and PKC blocker on histamine-induced contractions, and then measured the effect of PKC antagonist on whole cell K+ current using patch clamping method in rabbit coronary smooth muscle cells. Results : Application of histamine induced phasic and tonic constraction of coronary rings via activation of H(1) receptors. Pretreatment of Ca2+ channel antagonist (nifedipine, 1 µM) or PKC blockers (10 nM staurosporine and 10 µM Gö6976) markedly inhibited histamine-induced tonic contraction, which suggest that the magnitude of tonic contraction depend on the Ca2+ influx. Application of 4-AP, a blocker of voltage-dependent K+ channels, increased resting tone of coronary rings, and combined treatment of nifedipine blocked this 4-AP induced increase of resting tone. Application of active analoge of DAG (1,2-DiC8) significantly inhibited the activity of voltage-dependent K+ current in single smooth muscle cell, meanwhile the inactive analogue of DAG (1,3-DiC8) has no apparent effect on the activity of voltage-dependent K+ current. Furthermore, pretreatment of calphostin C (1 µM), a blocker of PKC, diminished the 1,2-DiC8-induced inhibition of K+ current. Conclusion : PKC dependent inhibition of voltage-dependent K+ current may be responsible for the maintaining of histamine-induced tonic contraction in rabbit coronary artery.ope

Dr. Myung-Sun Kim(1897-1982): An Eternal Teacher of Yonsei Univeristy

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The Effectiveness of an Instructor’s Intervention Using Questioning Strategy in Physiology Class

This study was done to analyze students’ learning and its lasting effect by teaching strategy involving questioning. This study was performed with 68 students who were enrolled in a physiology class of the Yonsei University College of Medicine in Seoul, Korea, in 2003. The students were randomly divided into 2 groups. One group was taught in a way where students asked questions and the instructor answered the questions. For the other group of students, the instructor asked questions, and the students answered the questions. We performed a pre-test before the study begins and post-tests immediately, 3 weeks, and 6 weeks after the study. The results were analyzed by using analysis of covariance and repeated measures analysis of variance. A higher learning effect was observed in a group where questions were asked by students compared with the other group. The post-test results showed no significant difference in the lasting effect of learning according to the teaching strategy. Students’ learning significantly improved when students asked questions and the instructor answered the questions compared with the strategy of the instructor asking questions and students answering to the questions.ope

Comparison of contractile mechanisms of sphingosylphosphorylcholine and sphingosine-1-phosphate in rabbit coronary artery

AIMS: Although stimulation with sphingosylphosphorylcholine (SPC) or sphingosine-1-phosphate (S1P) generally leads to similar vascular responses, the contractile patterns and their underlying signalling mechanisms are often distinct. We investigated the different reliance upon Ca2+-dependent and Ca2+-sensitizing mechanisms of constriction in response to SPC or S1P in coronary arteries. METHODS AND RESULTS: Contractile responses, changes in [Ca2+]i, and phosphorylation of myosin light chain phosphatase-targeting subunit (MYPT1) were measured. SPC induced a concentration-dependent sustained contraction. S1P evoked a rapid rise in force (initial transient), which was followed by a secondary sustained force. In the absence of extracellular Ca2+, the concentration dependency of constriction to SPC was shifted to the right, but with no change in maximum force, whereas S1P-induced contraction was significantly blunted. Cyclopiazonic acid (CPA) significantly decreased the initial transient force induced by S1P. In isolated single cells, S1P markedly increased [Ca2+]i, whereas only a modest elevation was noted with SPC. The S1P-induced elevation of [Ca2+]i was abolished by pre-treatment with CPA and was significantly reduced in the absence of extracellular Ca2+. In beta-escin-permeabilized strips, SPC augmented pCa 6.3-induced force; this was significantly inhibited by fasudil hydrochloride. S1P induced little or no augmentation of pCa 6.3-induced force. In intact arteries, SPC-induced contraction was completely inhibited by fasudil hydrochloride. Fasudil hydrochloride had no effect on the initial transient force induced by S1P but significantly inhibited the secondary sustained force. SPC induced a several-fold increase in Thr696 and Thr853 phosphorylation of MYPT1, but S1P did not affect phosphorylation of MYPT1. CONCLUSION: Our results suggest that constriction of coronary arteries in response to the bioactive lipid S1P or SPC occurs by distinct signalling pathways. Activation of the RhoA/RhoA-associated kinase pathway and subsequent phosphorylation of MYPT1 play a key role in SPC-induced coronary contraction, whereas elevation of [Ca2+]i is crucial for S1P-induced coronary constriction.ope

Status of Clerkship Education and Its Evaluation in Korean Medical Schools

Purpose: The aim of this study is to identify the status of clerkship education and its evaluation in Korea. Methods: Questionnaires were sent to 943 personnel in 23 clinical departments of 41 medical schools nationwide from April, 1 to April 10, 2004. We analyzed the 638 questionnaires that were collected from 39 medical 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.ope

Role of protein kinase C- or RhoA-induced Ca2+-sensitization in stretch-induced myogenic tone

Objective: It has been suggested that Ca2+ sensitization mechanisms might contribute to myogenic tone. However, specific mechanisms have yet to be fully identified. Therefore, we investigated the role of protein kinase C (PKC)- or RhoA-induced Ca2+ sensitization in myogenic tone of the rabbit basilar vessel. Methods: Myogenic tone was developed by stretch of rabbit basilar artery. Fura-2 Ca2+ signals, contractile responses, PKC immunoblots, translocation of PKC and RhoA, and phosphorylation of myosin light chains were measured. Results: Stretch of the resting vessel evoked a myogenic contraction and an increase in the intracellular Ca2+ concentration ([Ca2+]i) only in the presence of extracellular Ca2+. Stretch evoked greater contraction than high K+ at a given [Ca2+]i. The stretch-induced increase in [Ca2+]i and contractile force were inhibited by treatment of the tissue with nifedipine, a blocker of voltage-dependent Ca2+ channel, but not with gadolinium, a blocker of stretch-activated cation channels. The PKC inhibitors, H-7 and calphostin C, and a RhoA-activated protein kinase (ROK) inhibitor, Y-27632, inhibited the stretch-induced myogenic tone without changing [Ca2+]i. Immunoblotting using isoform-specific antibodies showed the presence of PKCα and PKCε in the rabbit basilar artery. PKCα, but not PKCε, and RhoA were translocated from the cytosol to the cell membrane by stretch. Phosphorylation of the myosin light chains was increased by stretch and the increased phosphorylation was blocked by treatment of the tissue with H-7 and Y-27632, respectively. Conclusions: Our results are consistent with important roles for PKC and RhoA in the generation of myogenic tone. Furthermore, enhanced phosphorylation of the myosin light chains by activation of PKCα and/or RhoA may be key mechanisms for the Ca2+ sensitization associated myogenic tone in basilar vessels.ope

Electrophysiologic mechanism underlying action potential prolongation by sevoflurane in rat ventricular myocytes

BACKGROUND: Despite prolongation of the QTc interval in humans during sevoflurane anesthesia, little is known about the mechanisms that underlie these actions. In rat ventricular myocytes, the effect of sevoflurane on action potential duration and underlying electrophysiologic mechanisms were investigated. METHODS: The action potential was measured by using a current clamp technique. The transient outward K current was recorded during depolarizing steps from -80 mV, followed by brief depolarization to -40 mV and then depolarization up to +60 mV. The voltage dependence of steady state inactivation was determined by using a standard double-pulse protocol. The sustained outward current was obtained by addition of 5 mm 4-aminopyridine. The inward rectifier K current was recorded from a holding potential of -40 mV before their membrane potential was changed from -130 to 0 mV. Sevoflurane actions on L-type Ca current were also obtained. RESULTS: Sevoflurane prolonged action potential duration, whereas the amplitude and resting membrane potential remained unchanged. The peak transient outward K current at +60 mV was reduced by 18 +/- 2% (P < 0.05) and 24 +/- 2% (P < 0.05) by 0.35 and 0.7 mm sevoflurane, respectively. Sevoflurane had no effect on the sustained outward current. Whereas 0.7 mm sevoflurane did not shift the steady state inactivation curve, it accelerated the current inactivation (P < 0.05). The inward rectifier K current at -130 mV was little altered by 0.7 mm sevoflurane. L-type Ca current was reduced by 28 +/- 3% (P < 0.05) and 33 +/- 1% (P < 0.05) by 0.35 and 0.7 mm sevoflurane, respectively. CONCLUSIONS: Action potential prolongation by clinically relevant concentrations of sevoflurane is due to the suppression of transient outward K current in rat ventricular myocytes.ope