• Tuberculosis and Respiratory Diseases
• /
• v.41 no.4
• /
• pp.319-327
• /
• 1994

Background: The pathogenetic mechanism of adult respiratory distress syndrome(ARDS) is not clearly defined yet, but it is well known that increased pulmonary capillary permeabilty is characteristic feature of ARDS. The increased alveolar-capillary permeability is usually preceded by damage of pulmonary artery endothelial cells. The released enzymes and oxygen free radicals from the activated neutrophils seem to play a predominant role in endothelial cell cytotoxicity. The activated neutrophils, however, probably are not the sole contributing factor in this type of damage because many cases of ARDS have been reported in severe neutropenia. Bacterial endotoxin perse and/or oxygen free radicals released from endothelial cells are suggested to be possible factors that contribute to the development of ARDS. The purpose of this study is to investigate the direct cytotoxicity of endotoxin and the role of oxygen free radicals released from the endothelial cells in endotoxin-induced endothelial cell cytotoxicity. Methods: First, to investigate whether endotoxin is cytotoxic to HUVE by itself, various doses of endotoxin were added to culture medium and cytotoxicity was measured. Second, to evaluate the possible role of oxygen free radical in endotoxin-induced HUVE cytotoxicity, various antioxidants were added on the endotoxin-induced HUVE cytotoxicity and cytotoxicity was measured. Third, to verify the release of oxygen free radicals from HUVE, the concentrations of hydrogen peroxide in the endotoxin-treated culture supernatant were measured. Finally, to observe the cytotoxic effect of hydrogen peroxide, HUVE cytotoxicity in the presence of various doses of hydrogen peroxide was measured. The fourth generations of subcultured HUVE from primary culture were used. The cell cytotoxicity was quantified by the chromium-51 release assay. Results: 1) Endotoxin alone showed HUVE cytotoxicity in a dose-dependent fashion. 2) Endotoxin-induced HUVE cytotoxicity was significantly attenuated by the pretreatment of catalase and DMTU. 3) Hydrogen peroxide was released from HUVE after endotoxin treatment in a dose-dependent fashion. 4) Exogenous hydrogen peroxide also showed HUVE cytotoxicity in a dose-dependent fashion. Conclusion: These results suggest that endotoxin alone can directly injure HUVE, and, oxygen-free radicals released from HUVE in response to endotoxin may also participate in the endotoxin-induced HUVE cytotoxicity.

• Journal of Korean Society of Environmental Engineers
• /
• v.30 no.3
• /
• pp.323-330
• /
• 2008

The study presents the results of 1,4-dioxane degradation using zero valent (Fe$^0$) or Fe$^{2+}$ ions with and without UV. During the reaction, the change of [Fe$^{2+}$] and [Fe$^{2+}$]/[Fe(t)], the concentration ratio of ferrous ion to total iron ion in solution was measured. Less than 10% degradation of 1,4-dioxane was observed by UV-only, Fe$^0$-only, and Fe$^{2+}$-only conditions, and also the changes of [Fe$^{2+}$] and [Fe$^{2+}$]/[Fe(t)] were minimal in each reaction. However, the oxidation of Fe$^0$ was enhanced with the irradiation of UV by approximately 25% and the improvement of 1,4-dioxane degradation was observed. Fenton reaction ($Fe^{2+}+H_2O_2$) showed higher degradation efficiency of 1,4-dioxane until 90 min, which of the degradation was stopped after that time. In the reaction of Fe$^{2+}$ and UV, the ratio of [Fe$^{2+}$]/[Fe(t)] decreased then slowly increased after a certain time indicating the reduction of Fe3+ to Fe$^{2+}$. In case of Fe$^0$ in the presence of UV, the first-order rate constant was found to be 1.84$\times$10$^{-3}$ min$^{-1}$ until 90 min, and then changed to 9.33$\times$10$^{-3}$ min$^{-1}$ when the oxidation of Fe$^{2+}$ mainly occurred. In this case [Fe$^{2+}$]/[Fe(t)] kept decreasing for the reaction. However, the addition of perchlortae (ClO$_4^-$) in the reaction of Fe$^0$ and UV induced the continuous increase of [Fe$^{2+}$]/[Fe(t)] ratio. The results mean the primary degradation factor of 1,4-dioxane is the oxidation by the radicals generated from the redox reaction between Fe$^{2+}$ and Fe$^{3+}$. Also, both UV and ClO$_4^-$ played the role inducing the reduction of Fe$^{3+}$, which is important to degrade 1,4-dioxane by enhancing the generation of radicals.

• Tuberculosis and Respiratory Diseases
• /
• v.43 no.5
• /
• pp.728-735
• /
• 1996

Background : Recognition and ingestion of opsonized microorganisms by neutrophils induces the burst of oxidative metabolic activity. Products of the respiratory burst activity provide powerful oxygen dependent killing mechanism. Measurement of respiratory burst activity has been a major indicator of the functional capacity of neutrophils. We determined the respiratory burst activity of neutrophils in patients with pneumonia and observed the changes during the clinical course of pneumonia. Methods: The EDTA blood was drawn from 24 normal controls and same numbers of pneumonia patients. The respiratory burst activity(with the production of $H_2O_2$ which changes nonfluorescent DCF-DA to green fluorescent DCF) in the non-stimulated state and the stimulated state with fMLP and PMA of neutrophils was measured by flowcytometry at day 1, 3, 5, 7 and 9 of admission. Results: The respiratory burst activity of neutrophils was mildly increased by stimulation with fMLP. But there was no statistical significance between normal control and patients with pneumonia. The respiratory burst activity of neutrophils was markedly increased by stimulation with PMA in both groups. There was a significant difference in response to PMA between normal control and patients with pneumonia. The production of hydrogen peroxide from neutrophils was decreased during early course of pneumonia and it was recuperated gradually to normal level in 9 days. Conclusion : Hydrogen peroxide production from neutrophils was suppressed during early course of pneumonia and restored after treatment. It is suggested that the production of oxygen radical in response to PMA stimulation from each neutrophils is decreased rather than increased during the early course of pneumonia.

• Journal of the Korean earth science society
• /
• v.23 no.4
• /
• pp.357-368
• /
• 2002

In this study we have tried to explain the barrel-shaped morphology for young supernova remnants considering the dynamical effects of the ejecta. We consider the magnetic field amplification resulting from the Rayleigh-Taylor instability near the contact discontinuity. We can generate the synthetic radio image assuming the cosmic-ray pressure and calculate the azimuthal intensity ratio (A) to enable a quantitative comparison with observations. The postshock magnetic field are amplified by shearing, stretching, and compressing at the R-T finger boundary. The evolution of the instability strongly depends on the deceleration of the ejecta and the evolutionary stage of the remnant. the strength of the magnetic field increases in the initial phase and decreases after the reverse shock passes the constant density region of the ejecta. However, some memory of the earlier phases of amplification is retained in the interior even when the outer regions turn into a blast wave. The ratio of the averaged magnetic field strength at the equator to the one at the pole in the turbulent region can amount to 7.5 at the peak. The magnetic field amplification can make the large azimuthal intensity ratio (A=15). The magnitude of the amplification is sensitive to numerical resolution. This mens the magnetic field amplification can explain the barrel-shaped morphology of young supernova remnant without the dependence of the efficiency of the cosmic-ray acceleration on the magnetic field configuration. In order for this mechanism to be effective, the surrounding magnetic field must be well-ordered. The small number of barrel-shaped remnants may indicate that this condition rarely occurs.

• 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.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.37 no.3
• /
• pp.269-275
• /
• 2008

The avocado is a widely grown and consumed fruit that is high in nutrients and low in calories, sodium, and fats. In this study, antioxidant activities and induction of apoptosis by methanol extracts from sarcocarp, seed and peel of avocado were investigated in vitro. Contents of total polyphenols in methanol extracts from sarcocarp, seed and peel were 13.89, 137.12 and $223.45{\mu}g/mg$ respectively. Radical-scavenging activities of the methanol extracts were examined by using ${\alpha},{\alpha}$-diphenyl-${\beta}$-picrylhydrazyl (DPPH) radicals and 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) assay. The methanol extracts from the peel of avocado showed higher scavenging activities against DPPH, ABTS than those from sarcocarp and seed. Apoptosis in MDA-MB-231 cells mediated by the methanol extracts of avocado was associated with the increase of activation of caspase-3 and caspase-3 target protein, PARP. Therefore, with more researches on identification and action mechanism of active compounds, the methanol extracts from peel and seed of avocado is expected to be a natural source for the developments of functional food and medical agents to prevent human breast cancer.

• Tuberculosis and Respiratory Diseases
• /
• v.40 no.2
• /
• pp.104-111
• /
• 1993

Background: Gram-negative bacterial endotoxin induced septicemia is known to be a leading cause in the development of adult respiratory distress syndrome(ARDS). The mechanism of endotoxin induced lung injury is mainly due to the activated neutrophils which injure the capillary endothelial cells by releasing oxidant radical and resulted in pulmonary edema. We studied the change of antioxidant enzyme in the case of large or small, intermittant dose of endotoxin infused rat lungs. Methods: Endotoxin was given to the rat through the peritoneal cavity in the dose of 7 mg/kg body weight in the large dose group and 1 mg/kg for 10 days in the small dose group. Bronchoalveolar lavage (BAL) was done and rats were killed at 6, 12, 24 hours after single endotoxin injection in the large dose group and 3, 7, 10 days after daily endotoxin injection for 10 days in the small dose group. The lungs were perfused with normal saline through the pulmonary artery to remove the blood and were homogenized in 5 volume of 50 mM potassium phosphate buffer containing 0.1 mM EDTA. After centrifuging at 100,000 g for 60 minute, the supernatent was removed and stored at $-70^{\circ}C$ until measuring for superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) and protein. Results: We observed the following results. 1) The lung wet/dry weight ratio and albumin concentration in the BAL fluids were increased to peak at 12 hours and neutrophil number in the BAL fluids were peak at 6 hours after endotoxin injection in the large dose group. 2) Cu, Zn SOD (IU/mg protein) was significantly decreased after 6, 12 hours after endotoxin injection in the large dose group. 3) There were no singnificant change in the level of Mn SOD, catalase, GSH-Px after endotoxin injection in both groups. Conclusion: Endotoxin in the large dose group produced the acute pulmonary edema and decreased the Cu, Zn SOD in the lung tissue after injecting endotoxin at 6 and 12 hours. These phenomenon may be due to the cell membrane damage by endotoxin. Further research would be necessary whther giving SOD by intratracheal route or method to increase the synthesis of SOD may lessen the acute lung injury by endotoxin.

• Restorative Dentistry and Endodontics
• /
• v.34 no.5
• /
• pp.406-414
• /
• 2009

The purpose of this study was to examine the effect of hydrogen peroxide at different application time and concentrations on the microtensile bond strength of resin restorations to the deep and the pulp chamber dentin. A conventional endodontic access cavity was prepared in each tooth, and then the teeth were randomly divided into 1 control group and 4 experimental groups as follows: Group 1, non treated; Group 2, with 20% Hydrogen peroxide ($H_2O_2$); Group 3, with 10% $H_2O_2$; Group 4, with 5% $H_2O_2$; Group 5, with 2.5% $H_2O_2$; the teeth of all groups except group 1 were treated for 20, 10, and 5min. The treated teeth were filled using a Superbond C&B (Sun medical Co., Shiga, Japan). Thereafter, the specimens were stored in distilled water at $37^{\circ}C$ for 24-hours and then sectioned into the deep and the chamber dentin. The microtensile bond strength values of each group were analyzed by 3-way ANOVA and Tukey post hoc test(p < 0.05). In this study, the microtensile bond strength of the deep dentin (D1) was significantly greater than that of the pulp chamber dentin (D2) in the all groups tested. The average of microtensile bond strength was decreased as the concentration and the application time of $H_2O_2$ were increased. Analysis showed significant correlation effect not only between the depth of the dentin and the concentration of $H_2O_2$ but also between the concentration of H202 and the application time(p < 0.05), while no significant difference existed among these three variables(p > 0.05). The higher $H_2O_2$ concentration, the more opened dentinal tubules under a scanning electron microscope(SEM) examination.

• Cross-Cultural Studies
• /
• v.52
• /
• pp.277-312
• /
• 2018

First-order cybernetics during the 1940s and 1950s aimed for control of an observed system, while second-order cybernetics during the mid-1970s aspired to address the mechanism of an observing system. The former pursues an objective, subjectless, approach to a system, whereas the latter prefers a subjective, personal approach to a system. Second-order observation must be noted since a human observer is a living system that has its unique cognition. Maturana and Varela place the autopoiesis of this biological system at the core of second-order cybernetics. They contend that an autpoietic system maintains, transforms and produces itself. Technoscientific recreation of biological autopoiesis opens up to a new step in cybernetics: what I describe as third-order cybernetics. The formation of technoscientific autopoiesis overlaps with the Fourth Industrial Revolution or what Erik Brynjolfsson and Andrew McAfee call the Second Machine Age. It leads to a radical shift from human centrism to posthumanity whereby humanity is mechanized, and machinery is biologized. In two versions of the novel Demon Seed, American novelist Dean Koontz explores the significance of technoscientific autopoiesis. The 1973 version dramatizes two kinds of observers: the technophobic human observer and the technology-friendly machine observer Proteus. As the story concludes, the former dominates the latter with the result that an anthropocentric position still works. The 1997 version, however, reveals the victory of the techno-friendly narrator Proteus over the anthropocentric narrator. Losing his narrational position, the technophobic human narrator of the story disappears. In the 1997 version, Proteus becomes the subject of desire in luring divorcee Susan. He longs to flaunt his male egomaniac. His achievement of male identity is a sign of technological autopoiesis characteristic of third-order cybernetics. To display self-producing capabilities integral to the autonomy of machinery, Koontz's novel demonstrates that Proteus manipulates Susan's egg to produce a human-machine mixture. Koontz's demon child, problematically enough, implicates the future of eugenics in an era of technological autopoiesis. Proteus creates a crossbreed of humanity and machinery to engineer a perfect body and mind. He fixes incurable or intractable diseases through genetic modifications. Proteus transfers a vast amount of digital information to his offspring's brain, which enables the demon child to achieve state-of-the-art intelligence. His technological editing of human genes and consciousness leads to digital standardization through unanimous spread of the best qualities of humanity. He gathers distinguished human genes and mental status much like collecting luxury brands. Accordingly, Proteus's child-making project ultimately moves towards technologically-controlled eugenics. Pointedly, it disturbs the classical ideal of liberal humanism celebrating a human being as the master of his or her nature.

• Journal of Life Science
• /
• v.29 no.6
• /
• pp.679-687
• /
• 2019

Litsea populifolia, a plant species of the Lauraceae family, is widely distributed in the tropical and subtropical areas of Asia. The phylogenetic relationships and botanical characteristics of L. populifolia have been reported; however, its anti-oxidative and anti-cancer activities remain unclear. In this study, we evaluated the anti-oxidative and anti-cancer effects of ethanol extracts of L. populifolia (EELP) together with the molecular mechanism of its anti-cancer activity in human lung adenocarcinoma A549 cells. EELP showed significant anti-oxidative effects with a 50% inhibitory concentration at $11.71{\mu}g/ml$, which was measured by the 2,2-diphenyl-1-picrylhydrazyl radical scavenging assay. EELP exhibited cytotoxic activity and induced cell cycle arrest at the G1 phase in A549 cells in a dose-dependent manner, whereas EELP did not have the cytotoxic effect on the normal human lung cell line IMR90. Treatment with EELP also resulted in a decreased expression of G1/S transition-related molecules-including cyclin-dependent kinase (CDK) 2, CDK6, cyclin D1, and cyclin E-both for the transcription and translation levels. EELP-induced G1 arrest was associated with the phosphorylation of checkpoint kinase 2 (CHK2), p53, cell division cycle 25 homolog A (CDC25A), and the reduction of CDC25A expression in A549 cells. Collectively, these results suggest that EELP may exert an anti-cancer effect by cell cycle arrest at the G1 phase through both p53-dependent and p53-independent (ATM/CHK2/CDC25A/CDK2) pathways in A549 cells.