• Tuberculosis and Respiratory Diseases
• /
• v.41 no.3
• /
• pp.222-230
• /
• 1994

Background: Paraquat, a widely used herbicide, is extremely toxic, causing multiple organ failure in humans. Paraquat especially leads to irreversible progressive pulmonary fibrosis, which is related to oxygen free radicals. However, its biochemical mechanism is not clear. Natural mechanisms that prevent damage from oxygen free radicals include changes in glutathione level, G6PDH, superoxide dismutase(SOD), catalase, and glutathione peroxidase. The authors think catalase is closely related to paraquat toxicity in the lungs Method: The effects of 3-amino-1,2,4-triazole(aminotriazole), a catalase inhibitor, on mice administered with paraquat were investigated. We studied the effects of aminotriazole on the survival of mice administered with paraquat, by comparing life spans between the group to which paraquat had been administered and the group to which a combination of paraquat and aminotriazole had been administered. We measured glutathion level, glucose 6-phosphate dehydrogenase(G6PDH), superoxide dismutase(SOD), catalase, and glutathione peroxidase(GPx) in the lung tissue of 4 groups of mice: the control group, group A(aminotriazole injected), group B(paraquat administered), group C(paraquat and aminotriazole administered). Results: The mortality of mice administered with paraquat which were treated with aminotriazole was significantly increased compared with those of mice not treated with aminotriazole. Glutathione level in group B was decreased by 20%, a significant decrease compared with the control group. However, this level was not changed by the administration of aminotriazole(group C). The activity of G6PDH in all groups was not significantly changed compared with the control group. The activities of SOD, catalase, and glutathione peroxidase(GPx) in the lung tissue were significantly decreased by paraquat administration(group B); catalase showed the largest decrease. Catalase and GPX were significantly decreased by aminotriazole treatment in mice administered with paraquat but change in SOD activity was not significant(group C). Conclusion: Decrease in catalase activity by paraquat suggests that paraquat toxicity in the lungs is closely related to catalase activity. Paraquat toxicity in mice is enhanced by aminotriazole administration, and its result is related to the decrease of catalase activity rather than glutathione level in the lungs. Production of hydroxyl radicals, the most reactive oxygen metabolite, is accelerated due to increased hydrogen peroxide by catalase inhibition and the lung damage probably results from nonspecific tissue injury of hydroxyl radicals.

• Tuberculosis and Respiratory Diseases
• /
• v.44 no.3
• /
• pp.639-648
• /
• 1997

Background : Arterial hypoxemia has been noted in patients with liver cirrhosis because of bronchial vessel dilatation. Cabenes et al. reported that bronchial hyperresponsiveness to the metacholine inhalation was observed in patients of left side heart failure, he suggested that one of the mechanism was bronchial vessel dilatation. We hypothesized that patients of liver cirrhosis might have bronchial hyperresponsiveness to metacholine inhalation due to portal hypertension. We evaluate the relationship between bronchial responsiveness and severity of liver cirrhosis, severity of portal hypertension. Methods : In the 22 patients of the liver cirrhosis with clinical portal hypertension, metacholine provocation test was done and determined $PC_{20}FEV1$. We classified liver cirrhosis according to Pugh-Child classification. Esophagogastroscopies were performed for the evaluation of the relationship between bronchial hyperresponsiveness and severity of esophageal varix. Results : In the 22 cases of the liver cirrhosis with clinical portal hypertension. The causes of liver cirrhosis, alcoholic hepatitis was 9 cases, hepatitis B virus was 12 cases, hepatitis C virus was 1 case, and 151 cases (68.18%) of total 22 cases were positive in metacholine provocation test. In positive cases. There was no significant relationship between $PC_{20}FEV1$ and severity of liver cirrhosis which were classified by Pugh-Child classification or severity of esophageal varix(p<0.05). Conclusion : we observed that bronchial responsiveness to metacholine increased in the patients of liver cirrhosis and there was no significant relationship between the severity of liver cirrhosis and the severity of esophageal varix.

• Korean Journal of Agricultural and Forest Meteorology
• /
• v.19 no.4
• /
• pp.280-292
• /
• 2017

Hail is not a frequently occurring weather event, and there are even fewer reports of hail damages to forest stands. Since the 2000s, an increase in hail incidence has been documented in Europe and the United States. In Korea, severe hails occurred in Jeollanam-do province on May 31 and in Gyeongsangbuk-do province on June 1, 2017. Hail size was ranged from 0.5 to 5.0 cm in diameter in Jeollanam-do, and from 1.5 to 3.0 cm in Gyeongsangbuk-do. This study was aimed to analyze the hail damages to forests by species and topography based on damage-categorized maps created by using drones and aerial photographs, and to analyze relationships of the damages with meteorological factors. The total damaged forest area was 1,163.1ha in Jeollanam-do, and 2,942.3ha in Gyeongsangbuk-do. Among the 'severe' damaged area 326.7ha, 91% was distributed in Jeollanam-do, and concentrated in the city of Hwasun which covers 57.2% of the total 'severe' damaged area. The most heavily damaged species was Korean red pine(Pinus densiflora S. & Z.) followed by P. rigida. Most broad-leaved trees species including oaks were recovered without any dead trees found. Liliodendron tulipifera was the most severely damaged in terms of the rate of 'severe' degree individuals which are needed to be checked whether they will die or be recovered. Cause of the death of pines was considered as the combination of physical damage caused by the hail and long-lasting drought with high air temperature that occurred before and after the hail event. No pathogens and insects were found which might have affected to tree deaths. We suggested a dieback mechanism of the pine trees damaged by hail and drought.

• Journal of Korean Tunnelling and Underground Space Association
• /
• v.26 no.1
• /
• pp.59-78
• /
• 2024

In tunnel construction, the stability is evaluated by the settlement of adjacent structures and ground, but the shear strain of the ground is the main factor that determines the failure mechanism of the ground due to the tunnel excavation and the change of the operating load, and can be used to review the stability of the tunnel excavation and to calculate the reinforcement area. In this study, a twin tunnel excavation was simulated on a soft ground in an urban area through a laboratory model test to analyze the behavior of the twin tunnel excavation on the adjacent pile grouped foundation and adjacent ground. Both the displacement and the shear strain of ground were obtained using a close-range photogrammetry during laboratory model test. In addition, two-dimensional finite element numerical analysis was performed based on the model test. The results of a back-analysis showed that the maximum shear strain rate tends to decrease as the horizontal distance between the pillars of the twin tunnel and the vertical distance between the toe of the pile group and the crown of the tunnel were decreased. The impact of the second tunnel on the first tunnel and pile group was decreased as the horizontal distance between the pillars of the twin tunnel was increased. In addition, the vertical distance between the toe of the pile group and the crown of the tunnel had a relatively greater impact on the shear strain results than the horizontal distance of the pillars between the twin tunnels. According to the results of the close-range photogrammetry and numerical analysis, the settlement of adjacent pile group and adjacent ground was measured within the design criteria, but the shear strain of the ground was judged to be outside the range of small strain in all cases and required reinforcement.

• KDI Journal of Economic Policy
• /
• v.12 no.3
• /
• pp.71-94
• /
• 1990

This paper reviews the rationale of monetary and banking intervention by an outside authority, either the government or the central bank, and seeks to delineate clearly the optimal limits to the monetary and banking deregulation currently underway in Korea as well as on a global scale. Furthermore, this paper seeks to establish an objective and balanced view on the role of the central bank, especially in light of the current discussion on the restructuring of Korea's central bank, which has been severely contaminated by interest-group politics. The discussion begins with the recognition that the modern free banking school and the new monetary economics are becoming formidable challenges to the traditional role of the government or the central bank in the monetary and banking sector. The paper reviews six arguments that have traditionally been presented to support intervention: (1) the possibility of an over-issue of bank notes under free banking instead of central banking; (2) externalities in and the public good nature of the use of money; (3) economies of scale and natural monopoly in producing money; (4) the need for macro stabilization policy due to the instability of the real sector; (5) the external effects of bank failure due to the inherent instability of the existing banking system; and (6) protection for small banknote users and depositors. Based on an analysis of the above arguments, the paper speculates on the optimal role of the government or central bank in the monetary and banking system and the optimal degree of monetary and banking deregulation. By contrast to the arguments for free banking or laissez-faire monetary systems, which become fashionable in recent years, monopoly and intervention by the government or central bank in the outside money system can be both necessary and optimal. In this case, of course, an over-issue of fiat money may be possible due to political considerations, but this issue is beyond the scope of this paper. On the other hand, the issue of inside monies based on outside money could indeed be provided for optimally under market competition by private institutions. A competitive system in issuing inside monies would help realize, to the maxim urn extent possible, external economies generated by using a single outside money. According to this reasoning, free banking activities will prevail in the inside money system, while a government monopoly will prevail in the outside money system. This speculation, then, also implies that the monetary and banking deregulation currently underway should and most likely will be limited to the inside money system, which could be liberalized to the fullest degree. It is also implied that it will be impractical to deregulate the outside money system and to allow market competition to provide outside money, in accordance with the arguments of the free banking school and the new monetary economics. Furthermore, the role of the government or central bank in this new environment will not be significantly different from their current roles. As far as the supply of fiat money continues to be monopolized by the government, the control of the supply of base money and such related responsibilities as monetary policy (argument(4)) and the lender of the last resort (argument (5)) will naturally be assigned to the outside money supplier. However, a mechanism for controlling an over-issue of fiat money by a monopolistic supplier will definitely be called for (argument(1)). A monetary policy based on a certain policy rule could be one possibility. More importantly, the deregulation of the inside money system would further increase the systemic risk inherent in the current fractional banking system, while enhancing the efficiency of the system (argument (5)). In this context, the role of the lender of the last resort would again become an instrument of paramount importance in alleviating liquidity crises in the early stages, thereby disallowing the possibility of a widespread bank run. Similarly, prudential banking supervision would also help maintain the safety and soundness of the fully deregulated banking system. These functions would also help protect depositors from losses due to bank failures (argument (6)). Finally, these speculations suggest that government or central bank authorities have probably been too conservative on the issue of the deregulation of the financial system, beyond the caution necessary to preserve system safety. Rather, only the fullest deregulation of the inside money system seems to guarantee the maximum enjoyment of external economies in the single outside money system.

• Tuberculosis and Respiratory Diseases
• /
• v.48 no.2
• /
• pp.166-179
• /
• 2000

Background: The main reason for the failure of anti-cancer chemotherapy is the build up of resistance by cancer cells to apoptosis. The activation of NF-${\kappa}B$ in many cancer cell lines is reported to be underlying mechanism behind the build up of resistance of cancer cells to apoptosis. However, this relationship varied depending on the cells used in the experiments. In this study, the role of NF-${\kappa}B$ activation in the TNF-$\alpha$-induced apoptosis in lung cancer cell line was evaluated. Methods: NCI-H157 cells were used in all experiments. Cells were exposed to a high dose of TNF-$\alpha$(20 ng/ml) for 24 or 48 hours with or without blocking NF-${\kappa}B$ activation. TNF-$\alpha$-induced activation of NF-${\kappa}B$ was inhibited either by overexpression of $I{\kappa}B{\alpha}$-super repressor($I{\kappa}B{\alpha}$-SR) or by pre-treatment with proteasome inhibitor. Cell viability and apoptosis were evaluated with MTT assay and Western blot analysis for PARP fragment, respectively. Results: Cell viability of NCI-H157 cells was not affected by TNF-$\alpha$ treatment alone; however, combined treatment with TNF-$\alpha$ and cycloheximide reduced cell viability significantly, indicating that resistance to TNF-$\alpha$ is mediated by the new proteins synthesized after TNF-$\alpha$ stimulation. To evaluate the role of NF-${\kappa}B$ in the transcription of anti-apoptotic proteins. delete NF-${\kappa}B$ activation was inhibited before TNF-$\alpha$ stimulation. as described above. $AD5I{\kappa}B{\alpha}$-SR-transduction inhibited TNF-$\alpha$-induced nuclear translocation of p65. TNF-$\alpha$-induced cell death and apoptosis increased after inhibition of TNF-$\alpha$-induced activation of NF-${\kappa}$ by methods. Conclusion: These results suggest that TNF-$\alpha$-induced activation of NF-${\kappa}B$ may be closely related to the acquisition of the resistance to TNF-$\alpha$-induced apoptosis in lung cancer cells. Therefore. blocking of NF-${\kappa}B$ pathway can be a useful therapeutic modality in the treatment of lung cancer.

• Childhood Kidney Diseases
• /
• v.5 no.2
• /
• pp.78-86
• /
• 2001

Purpose: Rapidly progressive glomerulonephritis (RPGN) is characterized by the rapid increase in serum creatitnin and crescents formation involving more than $50\%$ of glomeruli. 10 patients who had been treated for RPGN were studied retrospectively for thier underlying diseases and clinical features Method: Cilinical review was performed on 10 children who were diagnosed with RPGN by clinical features and renal biopsy and followed up at department of pediatrics during tile last 10 years, from May 1990 to May 2000. Result: There were 6 males and 4 females between the ages of 2.1 and 14.3 years (mean $10.9{\pm}3.8$). 3 had Henoch-$Sch{\ddot{o}}nlein$ purpura nephritis; 2, idiopathic rapidly progressive glomerulonephritis; 2, lupus nephritis; 1, hemolytic uremic syndrome; 1, membranous glomerulonephritis and 1, microscopic polyangiitis. The most common chief complaints were gross hematuria and oliguria. Initial clinical features included proteinuria, edema, hypertension, nausea and arthralgia. Mean serum BUN was $74.2{\pm}39.1\;mg/dL$ mean serum creatinin, $3.2{\pm}1.8\;mg/dL$ and mean creatinin clearance, $26.5{\pm}13.2\;mL/min/1.73m^2$. Antineutrophil cytoplasmic antibody was positive only in microscopic polyangiitis. ANA and Anti-DNA antibody were positive in two lupus nephritis patients. Serum complements were decreased in 4 patients. All patients except Hemolytic uremic syndrome received steroid pulse therapy and immunosupressive agents. 3 patients were performed acute peritoneal dialysis and 2 patients were given plasmapheresis. At the last follow up, 1 patient was dead, 4 patients had elevated serum creatinin, 2 of these 4 patients were on chronic ambulatory peritoneal dialysis and 6 patients had normal renal function. Conclusion: Rapidly progressive glomerulonephritis is a medical emergency that requires very rapid diagnosis, classification, and therapy. Appropriate therapy selected on the basis of underlying disease mechanism can substantially improve renal survival. (J. Korean Soc Pediatr Nephrol 2001 ; 5 : 78-86)