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        압력손실을 줄이기 위한 준비작동식 유수검지장치 본체 구조 개선

        홍승태 ( Seung Tae Hon ),정재한 ( Jae Han Jeong ),남준석 ( Jun Seok Nam ),권영규 ( Young Kyu Kwon ),한철수 ( Chul Su Han ),유승준 ( Seung Joon Yo ) 한국화학공학회 2015 Korean Chemical Engineering Research(HWAHAK KONGHA Vol.53 No.1

        다이어프램 방식 준비작동식 유수검지장치의 압력손실을 줄이기 위하여 본체 구조를 개선하였다. 개정된 유수제어밸브의 압력손실시험 기술기준을 통과하기 위해서는 압력손실이 20.7 kPa을 초과하여서는 안된다. 압력손실시험은 한국소방산업기술원 유수제어밸브 기술기준에 따라서 실시하였다. 준비작동식 유수검지장치는 습식 유수검지장치에 비해 압력손실이 크게 발생하였는데, 그 원인을 유체의 유동현상과 관련하여 분석하였다. 준비작동식 유수검지장치의 본체 내부 구조는 유로의 단면 크기와 방향 변화로 인해 압력손실 요인이 많았다. 이러한 압력손실 요소를 제거하기 위해 습식 유수검지장치와 비슷한 클래퍼 타입으로 구조를 변경하였다. 구조 변경 후 압력손실 값은 호칭 80A인 경우80.9 kPa에서 14.4 kPa로 감소하였으며, 호칭 100A인 경우 171.0 kPa에서 14.2 kPa로 감소하여 기술기준에 적합한 압력손실 값을 얻을 수 있었다. The body structure of diaphragm type preaction valve was improved in order to reduce the pressure drop. The pressure drop must be kept within 20.7 kPa to pass the revised (2012. 2. 9) standard for alarm valve and preaction valve. The pressure drop test was carried out by KFI (Korea Fire Institute) standard. The pressure drop of a preaction valve was higher than that of an alarm valve. Causes for increasing the pressure drop were investigated with the fluid flow in the valve. The preaction valve had more pressure drop factors (changes in velocity and direction) compared with the alarm valve. Inner structure of the preaction valve was changed to the clapper type to remove the pressure drop factors. In 80A and 100A size of preaction valves, the pressure drop was reduced from 80.9 and 171.0 kPa to 14.4 and 14.2 kPa respectively, after the change of the structure.

      • Cyclophosphamide가 家兎의 肝細胞에 미치는 影響에 관한 電子顯微鏡的 硏究

        한철수,이방헌,이정균 한양대학교 의과대학 1984 한양의대 학술지 Vol.4 No.1

        Cyclophosphamide (Cytoxan, Endoxan), synthesized by Arnod, Bourseaux and Brock, is an anticancer agent with antitumor effects against a wide variety of human neoplasms, including Hodgkin's disease, lymphosarcoma, Burkitt's lymphoma and acute lymphoblastic leukemia. More recently, its immunosuppressive properties have been exploited successfully in the treatment of nonneoplastic diseases such as rheumatoid arthritis and lupus erythematosus. The cytotoxic and other effects of cyclophosphamide as alkylating agent are directly related to the alkylation of components of DNA, and the breakdown of cyclophosphamide into biologically active alkylating compounds takes place principally in the liver. Thus the author observed the ulltrastructural changes of cytoplasmic oganelles in the hepatic parenchymal cells in order to investigate the effect of cyclophosphamide on the normal rabbits. Healthy normal rabbits, weighing 1500 gram each, were divided into the control and cyclophosphamide treatment group. Cyclophosphamide in distilled water was given intravenoously through ear vein in a dose of 40 mg per kg of body weight for nine days. Control animals were injected intravenously with isotonic saline solution. The animals were killed on the 9th day of cyclophosphamide treatment. Liver specimen of 1㎣ size were prefixed in the 2% glutaraldehyde-2.5% paraformaldehyde phosphate solution (pH 7.2) and postfixed in the 1% osmic acid. The ultrathin sections (600-800 A。), double-stsined with uranyl acetate and lead citrate, were observed with JEM 100 B electron microscope. The results which were observed in the hepatic parenchymal cells from the cyclophosphamide-treated rabbits were as follows; 1) The dilatation of the cisternae of rough endoplasmic reticulum associated with detachment of membrane bound-ribosomes and marked deplection of polysome in cytoplasm were observed. 2) There was proliferation of smooth endoplasmic reticulum in hepatocytes of midzonal area of the lobules associated with depletion of glycogen particles. 3) A few lysosomes and pronounced formation of autophagic vacuoles as well as multivesicular body were also noted. Through the experiment, there were no alterations in the morphology of the nuclei or nucleoli. Conequently, it is suggested that cyclophosphamide would induce the degenrative changes of cytoplasmic organelles of the hepatic parenchymal cells on prolonged treatment in rabbits.

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