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RISS 인기검색어
- 검색키워드
- 저자 : 조종근(Jong Geun Cho) (검색결과 3 건)
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조성원(Sung Won Cho),심찬섭(Chan Sup Shim),황효주(Hyo Joo Whang),함승원(Seung Won Ham),조종근(Jong Geun Cho),김익수(Ik Soo Kim) 대한소화기학회 1987 대한소화기학회지 Vol.19 No.2
Mirizzi syndrome is obstruction of the common hepatic duct secondary to pressure from an impacted stone, either in the cystic duct or the neck of the gallbladder. We experienced of a 61-year-old female patient, whose clinical symptoms v:ere progressive jaun- dice, loss of appetite, pain on right upper quadrant abdomen, and fever with chill and ultrasonogram and ERCP revealed dilatation of common hepatic duct and intrahepatic duct with impacted stone on lateral wall of common hepatic duct.
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흡연이 기관지폐포세척액내의 Elastase 에 미치는 영향
박춘식(Choon Sik Park),박상흠(Sang Heum Park),조종근(Jong Geun Cho),양동호(Dong Ho Yang),어수택(Soo Tak Uh),정연태(Yun Tae Jung) 대한내과학회 1988 대한내과학회지 Vol.35 No.2
N/A Many experimental animal studies have confirmed the protease-antiprotease theory of emphysema that a destructive enzymatic activity against elastin is present within the lung in excess of antiprotease, especially α1-antitrypsin, resulting in degradation of elastin fiber and emphysema. Although cigarette smoking could lead to this imbalance by producin an excess of elastase activity, studies examining the presence of elastase in human bronchoalveolar lavage (BAL) fluid have produced variable results. To further characterize the presence and type of elastase activity in human BAL fluid, we studied 42 subjects, 20 smokers and 22 nonsmokers. We sought to discover 1) Whether BAL fluid collected from smokers and nonsmokers contained free elastolytic activity, 2) Whether BAL fluid collected from smokers contained more free elastolytic activity than that collected from nonsmokers and if this activity had primarily originated from neutrophils or macrophages. The results were as follows: 1) The percentage of recovered fluid after infusion with 100 ml of normal saline in smokers was 42.55±2.68% compared with 49.13±2.52% in nonsmokers (p<0.05). 2) The total cell count recovered from BAL fluid in smokers was 23.07±4.84×10(6) compared with 12.94±2.76×10(6) in nonsmokers (p<0.05), the macrophage count in smokers was 19.44±4.46×10(6) compared with 9.83±1.36×10(6) in nonsmokers (p<0.025), the neutrophil count in smokers was 1.82±0.37×10(6) compared with 0.42±0.10×10(6) in nonsmokers (p<0.025) and lymphocyte count in smokers was 0.97±0.20×10(6) compared with 0.85±0.16×10(6) in nonsmokers (p>0.05). 3) The percentage of macrophage recovered from BAL fluid in smokers was 89.27×1.12% compared with 88.86±0.86% in nonsmokers (p>0.05), that of neutrophils in smokers was 6.01±0.84% compared with 3.83±0.46% in nonsmokers (p<0.025) and that of lymphocytes in smoker was 4.72±0.74% compared with 7.26±0.86% in nonsmokers (p<0.05) 4) The total activity of elastase recovered from BAL fluid in smokers was 557.6±131.2 U compared with 302.0±52.1U in nonsmokers (p<0.05), the activity of neutrophil-elastase in smokers was 302.8±56.S U compared with 146.2±36.9U in nonsmokers (p<0.025) and the activity of macrophage elastase in smoker was 235.3±47.0 U compared with 148.3±30.1 U in nonsmoker (p>0.05). 5) The corrected concentration of elastase with recovered fluid volume in smokers was 12,93±2.22 U/ml compared with 6,77±1.10 U/ml in nonemokers (p<0.05), the corrected concentration of neutrophil-e1astase in smokers was 6.85±1.25U/ml compared with 3.23±0.86 U/ml in nonsmokers (p<0.05) and the corrected concentration of macrophage elastase in smokers was 5.41±1.11 U/ml compared with 3.17±0.47 U/ml in nonsmokers (p>0.05). 6) The coreected concentration of elastase with albumin in smokers was 363.10±97.69 U/ml compared with 173.70±33.93U/ml in nonsmokers (p<0.05), that of neutrophil-elastase in smokers was 204.10±65.43 U/ml compared with 90.3±24.6 U/ml in nonsmokers (p>0.05) and that of macrophage-elastase in smokers was 157.9+ 51.6 U/ml compared with 75.4±9.73 U/ml in nonsmokers (p>0.) 7) The proportion of elastase in smokers that originated from neutrophil elastase was 57.64±7.039 and 42.64+4.47A originated from macrophage elastase (p>0.05). In nonsmokers 43.79±6.79% of elastase originated from neutrophil and 52.50±7.29% from macrophages (p>0.05). 8) The neutrophil-elastase recovered from BAL fluid was correlated with the number of total recovered neutrophil count (r=0.577, p<0.005) and the macrophage-elastase was not correlated with the number of total recovered macrophage count, In conclusion, 1) Smoking increased the total count of inflammatory cells, especially neutrophils and macrophages in BAL fluid. 2) Free elastolytic activity was found in all cases of BAL fluid and smoking increased the total elastase and the fraction of neutrophil elastase in BAL fluid.
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조종근,홍대식,박희숙 순천향대학교 1988 논문집 Vol.11 No.1
The idiopathic hypereosinophilic syndrome represents a heterogenous group of disorders with the common features of prolonged eosinophilia of an undetectable cause and organ system dysfunction. The diagnostic criteria are 1) a persistant eosinophilia of 1500 eosinophils/cu mm for longer than six months or death before six months associated with signs and symtoms of hypereosinophilic disease; 2) lack of evidence for other causes of eosinophilia; 3) evidence of organ system involvement. We have experienced a case of idiopathic hypereosinophilic syndrome in a 29 years old man who complained of pain on right upper quadrant of abdomen and generalized maculopapular skin eruption. We confirmed it with biopsies of bone marrow, skin, liver and duodenum which showed diffuse eosinophilic infiltration, therefore he has been treated with prednisone and hydoxyurea with good response. And now he is treated with a small dose of prednisone.
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