• Tuberculosis and Respiratory Diseases
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• v.56 no.6
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• pp.670-676
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• 2004

Chemical pneumonitis is caused by the inhalation of noxious chemical substances and is a cause of occupational lung disease. Nitric acid, which is a one of the common air pollutants and a potential oxidant for refining and cleansing of metals, has a chance for occupational and environmental exposure. A 52-year-old man visited our hospital due to coughing and dyspnea after the inhalation of nitric acid fumes at his workplace. He had conditions of tachypnea (respiratory rate 26 /min) and hypoxemia ($PaO_2$ 42.6 mmHg, $SaO_2$ 80.2% in room air) in our emergency department. The chest radiographs showed diffuse interstitial infiltrates and ground glass opacity in both lungs. The patient made improvements in clinical symptoms and chest radiography after being given a supply of oxygen, antibiotics, and bronchodilator therapy without systemic glucocorticoid therapy. On his follow up visit after 4 weeks, he showed no symptoms and sequelae, and the pulmonary function test showed a normal pulmonary function.

• Tuberculosis and Respiratory Diseases
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• v.59 no.6
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• pp.690-695
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• 2005

Nitric acid is an oxidizing agent used in metal refining and cleaning, electroplating, and other industrial applications. Its accidental spillage generates oxides of nitrogen, including nitric oxide (NO) and nitrogen dioxide ($NO_2$), which cause chemical pneumonitis when inhaled. The clinical presentation of a nitric acid inhalation injury depends on the duration and intensity of exposure. In mild cases, there may be no symptoms during the first few hours after exposure, or the typical symptoms of pulmonary edema can appear within 3-24 hours. However, in cases of prolonged exposure, progressive pulmonary edema develops instantaneously and patients may not survive for more than 24 hours. We report a case of a 44-year-old male who was presented with acute respiratory distress syndrome after nitric acid inhalation. He complained of cough and dyspnea of a sudden onset after inhaling nitric acid fumes at his workplace over a four-hour period. He required endotracheal intubation and mechanical ventilation due to fulminant respiratory failure. He was managed successfully with mechanical ventilation using positive end expiratory pressure and systemic corticosteroids, and recovered fully without any deterioration in his pulmonary function.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.12 no.10
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• pp.4378-4384
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• 2011

In order to evaluate the anti-oxidative capabilities of Angelica dahurica Radix ethanol extract (ADEE), we analyzed the contents of polyphenol and flavonoid compounds and the electron donating ability from ADEE. For animal experimentation, the test agent was topically applied to the artificial tanning spots which were induced by 1,500 mJ/$cm^2$ of ultraviolet B radiation on the backs of brown guinea pigs weighing approximately 450~500g. The test agent of $30{\mu}{\ell}$ was applied (6areas per group) twice a day, five days a week, for five weeks. On completion of the experiment, the animals were sacrificed under anesthetization, and the artificial tanning spots were obtained by biopsy punch and stained with H&E to observe the histological change in the epidermis and dermis. As a result, the contents of polyphenol and flavonoid compounds in ADEE were 20.7mg/g and 19.5mg/g respectively. As the for electron-donating capability of ADEE, it was observed that ADEE displays a dose-dependent antioxidative capacity of 14.8% and 19.8% at the concentration of 500 and 1000 ${\mu}g/m{\ell}$ respectively. Tissue staining with H&E revealed that the epidermis of the control group was slightly thicker than that of the other groups. However no inflammation or any other undesirable effect on the skin tissue due to ADEE was observed. These results indicate that ADEE is of value as a natural antioxidant.

• Journal of Life Science
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• v.15 no.3 s.70
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• pp.406-414
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• 2005

The genetic instability of cancer cells may be related to inappropriately activated DNA repair pathways. In present study, the modulated expression of DNA-dependent protein kinase (DNA-PK), a major DNA repair protein, in human cancer metastatic cells was tested. The expressions of Ku70/80, regulatory subunit of DNA-PK, and the Ku DNA-binding activity in various highly metastatic cell lines were higher than those in each parental cell line. Also, the expression of DNA-PKcs, catalytic subunit of DNA-PK, and the kinase activity of the whole DNA-PK complex in highly metastatic cells were significantly increased as compared to those of parental cells, suggesting that the enhanced DNA repair capacity of metastatic cells could be associated with aberrant use of DNA repair, which may mediate tumor progression and metastatic potential. Increased EGFR (epidermal growth factor receptor) signaling has been associated with tumor invasion and metastasis, and the linkage between EGFR-mediated signaling and DNA-PK has been suggested. This study showed that PKI166, the new EGFR tyrosine kinase inhibitor, modulated the expressions of Ku70/80 and DNA-PKcs and also revealed the chemosensitization effect of PKI166 against metastatic cells may be in part due to inhibition of Ku70/80. These results suggest that interference in EGFR signaling by EGFR inhibitor resulted in the impairment of DNA repair activity, and thus DNA-PK could be possible molecular targets for therapy against metastatic cancer cells.

• Tuberculosis and Respiratory Diseases
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• v.39 no.6
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• pp.536-541
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• 1992

Bronchiolitis obliterans organizing pneumonia (BOOP) is a type of diffuse interstitial lung disease that primarily affects the small conducting airways and characterized by the presence of granulation tissue plugs within the lumen of small airways often extending into alveolar ducts. It is associated with a number of different causes, including a variety of infections, fume exposures, drugs, collagen diseases and idiopathic. Recently we have experienced one patient with idiopathic BOOP. The patient was a 58 year old man presented with 2 months' history of dry cough and exertional dyspnea. The phyical examination showed inspiratory crackles at both lower lung field. Chest X-ray showed bilateral multiple patchy alveolar density. Pulmonary function studies showed a moderate degree of restrictive lung disease. Open lung biopsy carried out and revealed findings characteristic of BOOP. There was a dramatic response clinically and radiologically to high dose predinisolone therapy. Chest X-ray and pulmonary function test under-taken one year later showed marked improvement. New lesion on chest PA was developed during the period of tapering of prednisolone dose, but it was soon disappeared after increasing of prednisolone dose. One year later, he is well without steroid therapy.

• Journal of Chest Surgery
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• v.32 no.7
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• pp.637-647
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• 1999

Background: Ischemia-reperfusion injury is one of the major contributing causes of early graft failure in lung transplantation. It has been suggested that triiodothyronine (T3) may ameliorate ischemia-reperfusion injury to various organs in vivo and in vitro. Predicting its beneficial effect for ischemic lung injury, we set out to demonstrate it by administering T3 into the in situ canine ischemia-reperfusion model. Material and Method: Sixteen adult mongrel dogs were randomly allocated into group A and B. T3 $(3.6\mug/kg)$ was administered before the initiation of single lung ischemia in group B, whereas the same amount of saline was administered in group A. Ischemia was induced in the left lung by clamping the left hilum for 100 minutes. After reperfusion, various hemodynamic parameters and blood gases were analyzed for 4 hours while intermittently clamping the right hilum in order to allow observation of the injured left lung function. Result: Arterial oxygen partial pressure $(PaO_2)$ decreased 30 minutes after reperfusion and recovered gradually thereafter in both groups. In group B the decrease of $PaO_2$ was less marked than in group A. The recovery of $PaO_2$ was faster in group B than in group A. The differences between the two groups were statistically significant from 30 minutes after reperfusion $(125\pm34$ mmHg and $252\pm44$ mmHg, p<0.05) until the end of the experiment $(178\pm42$mmHg and $330\pm37$ mmHg, p<0.05). The differences in the arterial carbon dioxide pressure, airway pressure and lung compliance showed no statistical significance. The malondialdehyde (MDA) level, measured from the tissue obtained 240 minutes after reperfusion, was lower in group B $(0.40\pm0.04\mu$M) than in group A $(0.53\pm0.05\mu$M, p<0.05). The ATP level of group B $(0.69\pm0.07\mu$M/g) was significantly higher than that of group A $(0.48\pm0.07\mu$M/g, p<0.05). The microscopic exami nation revealed varying degrees of injury such as perivascular neutrophil infiltration, capillary hemorrhage and interstitial congestion. There were no differences in the microscopic findings between the two groups. CONCLUSION T3 has beneficial effects on the ischemic canine lung injury including preservation of oxygenation capacity, less production of lipid peroxidation products and a higher level of tissue ATP. These results suggest that T3 is effective in pulmonary allograft preservation.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1214-1222
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• 1998

Background : The intrapleural hypofibrinolysis is caused by mainly excessive concentration of pleural plasminogen activator inhibitor-1 antigen(PAI-1 Ag), which binds tissue type plasminogen activator. In pleural inflammation induced by sclerosing agents for pleurodesis, levels of pleural PAI-1 antigen increase in relation to decreasing D-dimer levels. It has been known that the pleural mesothelial cells have the capability of secreting PAI-1 Ag in response to inflammation in vivo. Therefore, we estimated whether pleural inflammation changes the balance between fibrinolytic and coagulative properties in exudative pleural effusions. Method : The thirty cases was included in our study. We determined the pleural levels of glucose, lactic dehydrogenase(LDH), pH and the counts of white blood cell(WBC), polymorpho leukocyte(PMN), lymphocyte as the parameters of pleural inflammation and cellular components of pleural fluid. The plasma level of fibrinogen in fluid and the neutrophil count in blood were determined. The levels of D-dimer, PAI-1 Ag and thrombinantithrombin III complex(TAT) were determined by ELISA(Behring, Marburg, Germany). Result : The causes of pleural effusion were as following : tuberculous in 14 cases, malignant in 10 cases and parapneumonic in 6 cases. The levels of pleural D-dimer, PAI-1 Ag and TAT was significantly higher than that of plasma(p<0..001). The severity of pleural inflammation did not correlated with pleural D-dimer, PAI-1 Ag, TAT and their plasma levels. But the level of pleural TAT correlated with pleural WBC and lymphocyte count. Conclusion : We found that the severity of pleural inflammations did not correlated with pleural D-dimer, PAI-1 Ag, TAT and the possibility of local production of PAI-1 antigen is present.

• Tuberculosis and Respiratory Diseases
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• v.47 no.4
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• pp.517-524
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• 1999

Background : Airway inflammation and hyperresponsiveness are recognized as major characteristics of bronchial asthma. Airway inflammation has usually been assessed by invasive methods, e.g. BAL or bronchial biopsy, but recent studies proposed induced sputum as another reliable and non-invasive tool to investigate airway inflammation in asthmatic patients. Thus, the relationship between airway inflammation assessed by induced sputum and airway hyperresponsiveness was investigated in asthmatic patient. Method : Airway responsiveness was determined by the concentration that caused a 20% decrease in $FEV_1$($PC_{20}$) after inhaling incremental concentrations of methacholine. The numbers of inflammatory cells and the concentration of eosinophilic cationic protein(ECP) were assessed in induced sputum obtained by inhalation of hypertonic saline(3%). Result: We analyzed sputum induced in 15 stable asthmatic patients. The differential cell count(%) of macrophages, neutrophils, eosinophils and lymphocytes in induced sputum were $39.1{\pm}27.0%$, $29.6{\pm}21.0%$, $28.8{\pm}18.8%$, $1.3{\pm}3.1%$ respectively. The mean value of baseline FEV1(predicted) and ECP were $76.3{\pm}30.3%$ and $1,101{\pm}833{\mu}g/L$ respectively. The geometric mean value of $PC_{20}$ was 0.56 mg/mL. The relationships between the sputum eosinophil and ECP in induced sputum, and between sputum eosinophil and degree of airway responsiveness($PC_{20}$) were found to be significantly correlated (r=0.81, p<0.05 and r=-0.78, p<0.05, respectively). Sputum neutrophils and $PC_{20}$ were not correlated to each other (r=0.11, p=0.69) and a significant negative correlation was found between ECP and baseline $FEV_1$(predicted)(r=-0.62, p<0.05). Conclusion : The results of this study suggest that an induced sputum via a inhalation of hypertonic saline is useful to determine a patient's status of airway inflammation, and airway inflammation is one of the major causal factors in the development of bronchial hyperresponsiveness in asthmatic patients.

• Journal of the Korean Society of Food Science and Nutrition
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• v.34 no.7
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• pp.973-979
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• 2005

To investigate the effect of Pinus densiflora on biochemical parameters in type I diabetic rats, we evaluated the changes of body weight, fasting blood glucose level, oral glucose tolerance test (OGTT) and biochemical parameters after the intraperitoneal injection of distilled solution of Pinus densiflora in streptozotocin (STZ)­induced rats. Thirty-seven male Sprague Dawley rats $(180\pm10g)$ were divided into four groups; diabetic mellitus (DM) group received STZ (50 mg/kg BW, i.v.); low level of pine extract (LP) group received Pinus densiflora (5 mg/kg BW, i.p.), high level of pine extract (HP) group received Pinus densiflora (10 mg/kg BW, i.p.) after the single injection of STZ (50 mg/kg BW, i.v.), respectively. Normal control (NC) group received saline. The change of fasting blood glucose level and OGTT were measured using glucocard II, and the change of biochemical parameter were measured by Automatic Chemistry Analyzer (Hitach-747, Japan). Mean body weight change of DM group was retarded greatly by STZ-exposure. While, body weights of LP and HP groups were progressively increased with some fluctuation, although the increase rates were slower than that of NC group. Fasting blood glucose levels of LP and HP groups were reduced by Pinus densiflora injection, although the fasting blood glucose levels were higher than that of NC group. The results of OGTT was significantly improved in both of LP and HP group compared to DM group. Increases of blood glucose, alanine aminotransferase (ALT), alkaline phosphatase (ALP) and blood urea nitrogen (BUN) levels by STZ-exposure were attenuated by the Pinus densiflora treatment (p<0.05). From the results, it was suggested that Pinus densiflora has a tendency to decrease STZ-induced toxicity in terms of monitoring fasting blood glucose, OGTT and some biochemical parameters of rat.

• Tuberculosis and Respiratory Diseases
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• v.50 no.4
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• pp.426-436
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• 2001

Background : Chronic obstructive pulmonary disease(COPD) is one of the major contributors to morbidity and mortality among the adult population. Cigarette smoking(CS) is undoubtedly the single most important factor in the pathogenesis of COPD. However, its mechanism is unclear. The current hypothesis regarding the pathogenesis of COPD postulates that an imbalance between proteases and antiproteases leads to the destructive changes in the lung parenchyma. This study had two aims. First, to evaluate the effect of CS exposure on histologic changes of the lung parenchyme, and second, to evaluate the effect of CS exposure on the expression of the gelatinolytic enzymes in BAL fluid cells in guinea pigs. Methods : Two groups of five guinea pigs were exposed to the whole smoke of 20 commercial cigarettes per day, 5 hours/day, 5 days/week, for 6weeks, and 12 weeks, respectively, using a smoking apparatus. Five age-matched guinea pigs exposed to room air were used as controls. Five or more sections were microscopically extamined(${\times}400$) and the number of cellular infiltration of the alveolar wall was measured in order to evaluate the effect of CS exposure on the histologic changes of lung parenchyme. The statistical significance was analyzed by a linear regression method. To evaluate the expression of the gelatinolytic enzymes in intraalveolar cells, BAL fluid was obtained and the intraalveolar cells were separated by centrifugation (500 g for 10 min at $4^{\circ}C$). Two sets of culture plates were loaded with $1{\times}10^6$ intraalveolar cells. One plate, contained O.1mM EDTA, a inhibitor of matrix metalloproteases(MMPs), and the other plate had no EDTA. Both plates were incubated for 48 hours at $37^{\circ}C$. After incubation, gelatinolytic protease expression in the supernatants was analyzed by gelatin zymography. Results : At the end of CS exposure, the level of blood carboxy Hb had increased significantly(4.1g/dl in control group, 24g/dl immediately after CS exposure, 18g/dl 30 min after CS exposure, 15g/dl 1 hour after CS exposure). Alveolar inflammatory cells were identified in the CS exposed guinea pigs. The number of alveolar cellular cells observed in a microscopic field ($400{\times}$) was $121.4{\pm}7.2$, $158.0{\pm}20.2$, $196.8{\pm}32.8$, in the control, the 6 weeks, and the 12 weeks group, respectively. The increased extent of inflammatory cellular infiltration of the lung parenchema showed a statistically significant linear relationship with the duration of CS exposure(p=0.001, $r^2=0.675$). Several types of gelatinolytic enzymes in the intraalveolar cells of CS exposed guinea pigs were expressed, of which some were inhibited by EDT A. However, the gelatinolytic enzymes were not expressed in the control groups. Conclusion : CS exposure increases inflammatory cellular infiltration of the alveolar wall and the expression of gelatinolytic proteases in guinea pigs. EDTA inhibits some of the gelatinolytic proteases. These findings suggest a possibility that CS exposure may increase MMP expression in the lungs of guinea pigs.