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한기돈,허진혁,문승재,유호선,Han, Ki-Don,Hur, Jin-Huek,Moon, Seung-Jae,Yoo, Hoseon 한국플랜트학회 2010 플랜트 저널 Vol.6 No.1
From 2000, the world plant market, especially plant developing business related to oil and gas, has been increasing. Domestic construction companies advance to overseas plant construction market actively, and proportioning to this, an importance of utility construction is increasing. However, the project becomes large and high-tech, and many companies experience difficulty of project management due to relatively high risk of overseas construction. In this study, we built the standard process with which domestic company can evaluate the risk of overseas plant utility construction. Primary factors for risk evaluation is derived, classification system is made out, primary factor is analyzed, and counter plan is suggested. And thorough management of risk is performed by risk management organization that manages the risks, risk control methods, reports and monitors through risk sheet and risk action log from the start of project to the end.
각종 간질성폐질환에서 폐포 대식세포의 Superoxide 분비능과 식균 작용
송정섭(Jeong Sup Song),김영균(Young Kyoon Kim),김관형(Kwan Hyoung Kim),한기돈(Ki Don Han),문화식(Hwa Sik Moon),신완식(Wan Shik Shin),박성학(Sung Hak Park) 대한내과학회 1990 대한내과학회지 Vol.39 No.3
N/A Interstitial lung diseases are a heterogenous group of disorders characterized by various degrees of parenchymal alveolitis and fibrosis. Alveolar macrophages (AM) are the predominant inflammatory cell type within alveolar structures and function not only as phagocytic cells but also as secretory cells that release various secretory products involving oxygen metabolites. Alveolar macrophages from patients with interstitial lung disease are thought to participate in the injury to the alveolar wall and contribute to the development of interstitial fibrosis. To investigate the role of alveolar macrophages in interstitial lung diseases, we measured the amount of superoxide release and phagocytosis by AM after bronchoalveolar lavage (BAL) from the normal controls and cases with interstitial lung diseases. The results were summerized as follows: 1) The total number of inflammatory cells in the BAL fluids increased more in patients with interstitial lung diseases than in the controls (p<0.02). 2) The differential cell count of BAL inflammatory cells showed that lymphocytes were predominant in sarcoidosis, hypersensitivity pneumonitis, and collagen lung disease, while neutrophils were predominant in idiopathic pulmonary fibrosis and bleomycin-induced pneumonitis. 3) The superoxide release by AM in patients with interstitial lung diseases was higher than the normal controls, either spontaneously or after stimulation by phorbol myristate acetate (PMA)(p<0.05). 4) The phagocytosis of non-opsonized staphylococcus aureus by AM was elevated in the interstitial lung disease cases (p<0.02), but no difference was noted when using the opsonized staphylococcus aureus as a target. These results suggest that AM are activated in interstitial lung diseases, and increased production of oxidant by AM in interstitial lung diseases may play a critical role in tissue damage and pulmonary fibrosis. Elevation of oxygen metabolite release by AM could be a useful marker in the assessment of the activity of interstitial lung diseases.
장기간 흡연한 폐기종환자 호중구에서의 Superoxide ( O2- ) 분비
송정섭(Jeong Sup Song),김영균(Young Kyoon Kim),김관형(Kwan Hyoung Kim),한기돈(Ki Don Han),문화식(Hwa Sik Moon),박성학(Sung Hak Park) 대한내과학회 1989 대한내과학회지 Vol.36 No.4
N/A The polymorphonuclear leukocyte (PMN) may play an important role in the pathogenesis of pulmonary emphysema associated with cigarette smoking. To investigate its potential for oxidant-mediated lung injury in cigarette smokers, we studied PMN oxidative metabolism in pulmonary emphysema patients associated with long-term smoking and in nonsmoking control subjects. The results were summarized as follows: 1) The spontaneous release of O2- from the PMN in pulmonary emphysema patients (1.71±0.91 n mole) was slightly higher than in nonsmoking control subjects (1.15±0.70 n mole), (p>0.05). 2) The release of O2- from the PMN stimulated with PMA (phorbol 12-myristate 13-acetate) in pulmonary emphysema patients (73.99±11.60 n mole) was slightly lower than in nonsmoking control subjects (80.08±9.64 n mole), (p>0.05). These results suggest that long-term smoking may influence the PMN to release O2- and desensitize the PMN to a stimulating agent such as PMA in pulmonary emphysema patients.
송정섭(Jeong Sup Song),김관형(Kwan Hyoung Kim),한기돈(Ki Don Han),문화식(Hwa Sik Moon),박성학(Sung Hak Park),유태준(Tae Joon Yoo) 대한내과학회 1989 대한내과학회지 Vol.37 No.5
N/A Goodpasture`s syndrome has been used as the prototype for autoimmunity to the basement membrane. To induce autoimmune lung disease, we immunized Sprague-Dawley rats with type IU collagen, laminin or CFA (complete Freund`s adjuvant), and boosted twice biweekly. One half of the rats were exposed to 1009 09 for 48 hours or 60 hours and then sacrificed two weeks after the last immunization. The results were as follows: 1) The immunized rats of both groups showed a high antibody titer against each antigen and high lymphocyte proliferative response to concanavalin A and immunizing antigens. 2) Histopathologically; O2 exposed and immunized rats showed neutrophil and plasma rell infiltration into edematous stroma and exudate in alveoli without hemorrhage. There was no IgG depostition in lung tissue by immunofluorescence study. In conclusion, animals immunized with type IV collagen and laminin showed high antibody titer but no deposition of IgG in the alveolar basement membrane suggesting that: a) antibodies did not contact the alveolar basement membrane (ABM) b) antibodies produced are weak antibodies similar to the autologous phase of passive immunization, where the lesions produced are less severe than the heterologous and take longer to develop. Thus the 4H;md 60 hour of increased capillary permeablility may not have allowed enough contact time betwen the ABM and antibody to cause lesions. O2 injury and immune injury to ABM were additive in this rat model. Since there was no 1gCi deposition and thus no evidence for humoral injury, cell mediated immunity contributed to alveolar injury. Thus, in Goodpasture`s syndrome, cell mediated immunity as well as anitobdy and complement mediated injury may contribute to the pathologic changes seen.