• The Korean Journal of Food And Nutrition
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• v.25 no.1
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• pp.90-98
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• 2012

With the addition of ethanol to wax gourd extract and by acetic fermentation, 5.0% acidity vinegar was produced. After putting 10% extract(10% concentration) of Chrysanthemum zawadskii in this, and by dissolving shell, Chrysanthemum zawadskii-pearl vinegar was produced. When a 1% of ark shell, oyster shell, or ear shell was added to wax gourd vinegar, 95.6~98.4% of the shell dissolved, and when a 2% content of shell was added, 97.2~98.4% was dissolved. The acidity of vinegar which dissolved 1% shell was pH 3.0~3.17, and the acidity of vinegar which dissolved 2% shell was pH 1.11~ 1.20. The pH values of vinegar which dissolved 1%, and 2% shell contents were 4.54~4.55, and 4.86~4.95, respectively. When 1% shell was dissolved, the acidity was higher than that of commercial vinegar, with a high pH value and low level of free acid. This shows that when Chrysanthemum zawadskii 1% is added during acetic acid fermentation, the inhibition was 44.4%, and 22.2% respectively. In this regard, Chrysanthemum zawadskii should be added after the fermentation of acetic acid. The calcium content of 1% shell vinegar is 0.4%, and that of 2% vinegar is 0.78%. Non-heated native wax gourd shows an angiotensin converting enzyme inhibition rate of 21.7%, an antioxidant activity of 5.23%, and a tyrosinase inhibition rate of 5.5%. In the case of heated-extracted wax gourd, the angiotensin converting enzyme inhibition rate was 16.1%, superoxide dismutase activity was 20.5%, antioxidant activity was 23.2%, and the tyrosinase inhibition rate was 7.1%. Also, in the case of Chrysanthemum zawadskii, the angiotensin converting enzyme inhibition rate was 28.8%, the xanthine oxidase inhibition rate was 28.2%, the superoxide dismutase activity was 14.5%, the antioxidant activity was 3.2%, and the tyrosinase inhibition rate was 9.2% Data also revealed that when a 10% sample of the heated-wax gourd extract was added to A549 human lung cancer epithelial cells of, the number of cancer cells declined by 80% in 72 hours, When a 10% native extract was added, the number of cells declined by, 74% in 48 hours, and when a heated-extract of Chrysanthemum zawadskii was added, 100% of the cells died after 72 hours.

• Tuberculosis and Respiratory Diseases
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• v.54 no.4
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• pp.439-448
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• 2003

Background : Surfactant protein B(SP-B) and surfactant protein C(SP-C) are important in accelerating surface spreading of surfactant phospholipid. The glucocorticoids accelerate the morphologic differentiation of epithelial cells into type II cells and increase the rate of phosphatidylcholine synthesis. The hydrophobic surfactant protein has been shown to be upregulated by glucocorticoids in vitro, however, its regulation in vivo is not well established. Methods : The authors investigated the effects of glucocorticoid on the accumulation of mRNA encoding SP-B and SP-C protein content of the lung. Adult rats were given different doses of subcutaneous dexamethasone and sacrificed at 24 hours and 1 week. SP-B and SP-C mRNA were measured by a filter hybridization method. Results : 1) The accumulation of SP-B mRNA at 24 hours after 0.2 mg/kg dexamethasone treatment was increased by 23.7%. 2) The accumulation of SP-B mRNA at 1 week after 2 mg/kg dexamethasone treatment was significantly increased by 96.6%(P<0.001). 3) The accumulation of SP-C mRNA at 24 hours after 0.2 mg/kg dexamethasone treatment was significantly increased by 42.7%(P<0.01). 4) The accumulation of SP-C mRNA at 1 week after 2 mg/kg dexamethasone treatment was significantly increased by 60.0% (P<0.01). Conclusion : The authors concluded that dexamethasone treatment in vivo resulted in increased levels of SP-B mRNA and SP-C mRNA. These results suggested that dexamethasone stimulates the synthesis of hydrophobic proteins associated with surfactant.

• Tuberculosis and Respiratory Diseases
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• v.55 no.5
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• pp.478-487
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• 2003

Background : There have been several studies showing that the angiotensin II and angiotensin converting enzyme(ACE) contributes to the apoptosis of alveolar epithelial cells in idiopathic interstitial pneumonia and the activation of fibroblasts during the process of pulmonary fibrosis. These results suggest that the pulmonary fibrosis can be inhibited by the angiotensin II receptor antagonist(AGIIRA). This study was performed to identify the therapeutic effect of AGIIRA in idiopathic pulmonary fibrosis(IPF). Method : Thirteen patients with IPF, who were diagnosed with an open lung biopsy(6 patients) and furfilling the ATS criteria(7 patients) between March 1999 and October 2001 at the Gachon medical center, were enrolled in this study. Of these patients, eight patients were treated with a regimen including AGIIRA(AT group), and five were treated without AGIIRA(NT group). The pulmonary function tests and dyspnea(ATS scale) were measured at diagnosis and 1 year after treatment. All the data was collected to analyze the therapeutic effect of AGIIRA on the patients with IPF. Results : The AT group contained 8 patients(M:F=4:4) and the NT group contained 5 patients(M:F=3:2). There was no significant difference in the serum angiotensin II level between the two groups($202.5{\pm}58.5$ vs $163.7{\pm}47.3pg/ml$, p>0.05). The AT group showed an upward trend in TLC(+3%), FVC(+4%), FEV1(+3%) and DLco(+2%) compared to the NT group(TLC(-14%), FVC(-3%), FEV1(-4%) except for DLco(+5%)). The dyspnea score in the AT group improved significantly but not in the NT group. Conclusion : These results suggest that the angiotensin II receptor antagonist may have an effect on stabilizing IPF.