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최현석(Choe, Hyeon-Seok),김홍상,김현진(Kim, Hyeon-Jin),임근호(Im, Geun-Ho) 대한교통학회 2006 대한교통학회 학술대회지 Vol.53 No.-
속도제한의 목적은 주어진 도로상황에 따라 차량 흐름의 안전을 위해 안전한 속도로 교통운영적 측면에서 안전한 속도를 제공하는 것이다. 그러나 속도제한은 반드시 신중히 검토되야 하며 특히 고속도로 진출입구의 속도제한은 차량의 특성을 고려해야 한다. 고속도로 진출입구에서의 속도제한은 곡선 반경에 따라 변화하는 속도를 고려해야 하며 이러한 과정에서 85 백분위 속도는 중요한 고려 요소가 된다. 본 연구보고서는 고속도로 진출입구에서의 85백분위 속도를 고려한 단계적 속도제한을 분석하였으며 고속도로 진출입구에서의 제한속도 설정 방법론에 대해 연구하였다. The purpose of the speed limit helps so that vehicle operators choose proper safety speed at diverse road situation and it is for making the vehicle flows safety. However the speed limit must be applied rather carefully. Especially, the speed limit must consider characteristic of the operating speed by the vehicle in the Highway Exits-Entrances. We also must consider the change of the operating speed according to the radius of curve in the Highway Exits-Entrances. In this way, a 85percentile speed is the important factor which influence for setting up speed limit. This report analyzed suitability about the current speed limit considering 85percentile speed in a Highway Exits-Entrances. Moreover, this report studied about methodology setting up speed limit in a Highway Exits-Entrances. This report also presented method setting up sign of speed limit.
정상 심근과 확장성 심근증 심근에서의 미토콘드리아 DNA 에 대한 분석
최현석(Hyun Seok Choi),김효수(Hyo Soo Kim),오병희(Byung Hee Oh),이명묵(Myoung Mook Lee),최성준(Seong Choon Choe),홍석근(Suk Keun Hong),손대원(Dae Won Sohn),박영배(Young Bae Park),최윤식(Yun Shik Choi),서정돈(Jung Don Seo),이영우(Youn 대한내과학회 1997 대한내과학회지 Vol.53 No.3
N/A Objective: The aim of this study is to analyze the mitochondrial DNA in failing and normal hearts. Methods: Genomic DNA was extracted from 18 failing and 4 normal hearts. The DNA was digested with each 50 units of BamH I, Pvu II, Pst I, and hybridized using DNA fragments encoding CO II (cytochrome oxidase II) and CO IU. They were detected using 'Fluorescein Gene Images' system. Results: The light microscopic feature of failing myocardium was compatible with that of primary cardiomyopathy. In southern blot analysis, there was no significant difference in mitochondrial DNA amounts between normal and failing hearts. The amount of mitochondrial DNA in hearts, whether normal or failing, was greater than that in lymphocytes. There were no abnormal bands except 16.6kb-normal band using the enzyme BamH I, Pvu II from failing and normal hearts. After digesting with Pst I, 2.1kb band was found using probe CO II and 14.5kb band using probe CO III. Conclusion : The amount of mitochondrial DNA in hearts, whether normal or failing, was greater than that in lymphocytes, which suggests that the heart is an active organ in the energy metabolism. Abnormal band was not found in southern blot analysis of the mitochondrial DNA from failing and normal hearts. The more sensitive method such as PCR is required to detect the presence of sma11 amount of mutated DNA.