• Korean Journal of Fisheries and Aquatic Sciences
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• v.24 no.1
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• pp.21-30
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• 1991

In Summer, oxygen-deficient water masses were developed extensively in the closed eutrophic bays such as Chinhae Bay which results in mass mortality of marine organisms and severe decrease the production of the bay every year. Under the circumstances, this study was performed to investigate the oxygen depletion relating to eutrophication, and also to evaluate self-purfication capacity of Buk Bay by dissolved oxygen mass balance in 1988. The mean concentration of total inorganic nitrogen, phosphate phosphorus and chlorophyll-a were $11.06{\mu}g-at/l,\;0.80{\mu}g-at/l\;and\;1.11mg/m^3$ respectively, which were over eutrophication criteria. Oxygen-deficient water mass was formed in July with the minimum concentration of 2.08ml/l(mean) at the bottom of all stations and recovered slowly in August. The decay and reaeration coefficient calculated from dissloved oxygen sag curve were 0.222/day and 0.018ml/l/day, respectively. To maintain above 4ml/l of oxygen to prevent oxygen-deficient water mass, it is recommendable to supply as much as 0.856ml/l/day of dissolved oxygen or should be reduced the same mass loading of BOD from watershed by the construction of wastewater treatment plant.

• Fire Science and Engineering
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• v.34 no.2
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• pp.1-6
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• 2020

The energy released by various burning material has a wide range of its magnitude and transient characteristics, the measurement of the heat release rate(HRR) has been considered as one of the most challenging issue among the parameters related to fire. This study compares the measured HRR calculated by the oxygen consumption (OC) method and the carbon dioxide generation (CDG) method using a laboratory-scale fire calorimeter. The feasibility of the CDG method is examined by analyzing the relative error. The relationship between the oxygen depletion factor and CO₂ mass flow rate, which is a key parameter in HRR calculations, showed strong linearity at 6 % for the methane burner fire. The contribution of HRR by CO was less than 7% compared with the of HRR by CO₂ in the CDG calculation method. The linearity of the OC and CDG methods with respect to HRR of the referenced methane burner in a quasi-steady state was less than 1%; this indicates that the CDG method can be utilized as a complementary method in heat release rate measurement.

• Biomolecules & Therapeutics
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• v.13 no.4
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• pp.256-262
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• 2005

We examined the signaling molecules involved in the 6-hydroxydopamine (6-OHDA)-induced neuronal cell death and increase in cellular glutathione (GSH) level in SK-N-SH cells. The 6-OH-DA-induced cell death was significantly prevented by the pretreatment with N-acetylcysteine (NAC), a thiol antioxidant, and BAPTA, an intracellular $Ca^{2+}$ chelator. Although 6-OHDA induced ERK phosphorylation, the pretreatment with PD98059, an ERK inhibitor, did not block 6-OHDA-induced cell death. In addition, the 6-OHDA-induced activation of caspase-3, a key signal for apoptosis, was blocked by the pretreatment with NAC and BAPTA. While the level of reactive oxygen species (ROS) was significantly increased in the 6-OHDA-treated cells, the cellular GSH level was not altered for the first 6-hr exposure to 6-OHDA, but after then, the level was significantly increased, which was also blocked by the pretreatment with NAC and BAPTA, but not by PD98059. Depletion of GSH by pretreating the cells with DL-buthionine-(S,R)-sulfoximine (BSO), a glutathione synthesis inhibitor, rather significantly potentiated the 6-OHDA-induced death. In contrast to the pretreatment with NAC, 6-OHDA-induced cell death was not prevented by the post-treatment with NAC 30 min after 6-OHDA treatment. The results indicate that the GSH level which is increased adaptively by the 6-OHDA-induced ROS and intracellular $Ca^{2+}$ is not enough to overcome the death signal mediated through ROS-$Ca^{2+}$ -caspase pathway.

• Industry Promotion Research
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• v.1 no.2
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• pp.7-11
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• 2016

$SnO_2$ films were annealed in a vacuum atmosphere conditions to research the temperature dependency of current-voltage characteristics, crystal structure and chemical properties. The $SnO_2$ film annealed in a vacuum became an amorphous structure, but the degree of amorphous structure changed in accordance with the content of oxygen vacancy, which increased at film annealed at $100^{\circ}C$ and then decreased over the sample at annealed at $150^{\circ}C$. Because the crystallinity was affected the content of oxygen vacancy. The oxygen vacancy as carriers disappeared with increasing the annealing temperatures, and the depletion layer increased. Therefore the content of exiton as optical properties increased with becoming the amorphous structure. So the intensity of PL spectra increased with increasing the annealing temperature.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.2
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• pp.121-130
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• 2019

Glutamate toxicity-mediated mitochondrial dysfunction and neuronal cell death are involved in the pathogenesis of several neurodegenerative diseases as well as acute brain ischemia/stroke. In this study, we investigated the neuroprotective mechanism of dieckol (DEK), one of the phlorotannins isolated from the marine brown alga Ecklonia cava, against glutamate toxicity. Primary cortical neurons ($100{\mu}M$, 24 h) and HT22 neurons (5 mM, 12 h) were stimulated with glutamate to induce glutamate toxic condition. The results demonstrated that DEK treatment significantly increased cell viability in a dose-dependent manner ($1-50{\mu}M$) and recovered morphological deterioration in glutamate-stimulated neurons. In addition, DEK strongly attenuated intracellular reactive oxygen species (ROS) levels, mitochondrial overload of $Ca^{2+}$ and ROS, mitochondrial membrane potential (${\Delta}{\Psi}_m$) disruption, adenine triphosphate depletion. DEK showed free radical scavenging activity in the cell-free system. Furthermore, DEK enhanced protein expression of heme oxygenase-1 (HO-1), an important anti-oxidant enzyme, via the nuclear translocation of nuclear factor-like 2 (Nrf2). Taken together, we conclude that DEK exerts neuroprotective activities against glutamate toxicity through its direct free radical scavenging property and the Nrf-2/HO-1 pathway activation.

• The Korea Journal of Herbology
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• v.28 no.6
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• pp.79-86
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• 2013

Objectives : The purpose of this study is to investigate neuroprotective effects and molecular mechanisms of luteolin against ${\beta}$-amyloid ($A{\beta}_{25-35}$)-induced oxidative cell death in BV-2 cells. Methods : The protective effects of luteolin against $A{\beta}_{25-35}$-induced cytotoxicity and apoptotic cell death were determined by MTT dye reduction assay and TUNEL staining, respectively. The apoptotic cell death was further analyzed by measuring mitochondrial transmembrane potential and expression of pro- and/or anti-apoptotic proteins. To elucidate the molecular mechanisms underlying the protective effects of luteolin, intracellular accumulation of reactive oxygen species, oxidative damages, and expression of antioxidant enzymes were examined. Results : Luteolin pretreatment effectively attenuated $A{\beta}_{25-35}$-induced apoptotic cell death indices such as DNA fragmentation, dissipation of mitochondrial transmembrane potential, increased Bax/Bcl-2 ratio, and activation of c-Jun N-terminal kinase and caspase-3 in BV-2 cells. Furthermore, $A{\beta}_{25-35}$-induced intracellular formation of reactive oxygen species and subsequent oxidative damages such as lipid peroxidation and depletion of endogenous antioxidant glutathione were suppressed by luteolin treatment. The neuroprotective effects of luteolin might be mediated by up-regulation of cellular antioxidant defense system via up-regulation of ${\gamma}$-glutamylcysteine ligase, a rate-limiting enzyme in the glutathione biosynthesis and superoxide dismutase, an enzyme involved in dismutation of superoxide anion into oxygen and hydrogen peroxide. Conclusions : These findings suggest that luteolin has a potential to protect against $A{\beta}_{25-35}$-induced neuronal cell death and damages thereby exhibiting therapeutic utilization for the prevention and/or treatment of Alzheimer's disease.

• Biomolecules & Therapeutics
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• v.11 no.2
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• pp.112-118
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• 2003

1-Methylated $\beta$-carbolines (harmaline and harmalol) and antioxidants (N-acetylcysteine and ascorbate) reduced the loss of cell viability in differentiated PC 12 cells treated with 5 mM glutamate. $\beta$-Carbolines prevented the glutamate-induced decrease in mitochondrial membrane potential, cytochrome c release and caspase-3 activation in PC 12 cells. $\beta$-Carbolines reduced the formation of reactive oxygen species and depletion of glutathione due to glutamate in PC12 cells. $\beta$-Carbolines revealed a scavenging action on hydrogen peroxide and reduced the iron and EDTA-mediated degradation of 2-deoxy-D-ribose. The results suggest that I-methylated $\beta$-carbolines attenuate the cytotoxic effect of glutamate on PC12 cells by reducing the alteration of mitochondrial membrane permeability that seems to be mediated by oxidative stress.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.4
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• pp.207-212
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• 2006

Mitochondrial permeability transition has been shown to be involved in neuronal cell death. Mitochondrial monoamine oxidase (MAO)-B is considered to play a part in the progress of nigrostriatal cell death. The present study examined the effect of MAO inhibitors against the toxicity of 1-methyl-4-phenylpyridinium $(MPP^+)$ in relation to the mitochondrial permeability transition. Chlorgyline (a selective inhibitor of MAO-A), deprenyl (a selective inhibitor of MAO-B) and tranylcypromine (nonselective inhibitor of MAO) all prevented cell viability loss, cytochrome c release, caspase-3 activation, formation of reactive oxygen species and depletion of GSH in differentiated PC12 cells treated with $500\;{\mu}M$$MPP^+$. The MAO inhibitors at $10\;{\mu}M$ revealed a maximal inhibitory effect and beyond this concentration the inhibitory effect declined. On the basis of concentration, the inhibitory potency was tranylcypromine, deprenyl and chlorgyline order. The results suggest that chlorgyline, deprenyl and tranylcypromine attenuate the toxicity of $MPP^+$ against PC12 cells by suppressing the mitochondrial permeability transition that seems to be mediated by oxidative stress.

• Journal of the Korean Institute of Electrical and Electronic Material Engineers
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• v.20 no.3
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• pp.268-272
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• 2007

A fully integrable InP/InGaAs HPT with an ITO emitter contact was first fabricated by employing a $SiO_2$ passivation layer. The electrical and the optical characteristics of the HPT with a passivation layer were measured and compared with those of the HPT without a passivation layer. The only noticeable difference was the increased emitter series resistance of the HPT with a passivation layer. AES analysis was performed to explain the reason of the increased emitter series resistance. Results show that PECVD $SiO_2$ deposition and annealing processes cause the diffusion of oxygen to the interface and the depletion of tin at the interface, which may be responsible for the increase of the series resistance.

• Journal of the Korean institute of surface engineering
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• v.29 no.6
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• pp.607-614
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• 1996

Yttrium(Y) coating was incorporated by ion-plating method either directly on the TiAl substrate or after pack aluminizing on TiAl to improve the oxidation resistance of TiAl alloy. After Y-coating, heat treatment at low oxygen partial pressure was carried out. Performance of various coating was evaluated by isothermal and cyclic oxidation tests. A simple Y-coating without pack aluminizing can give a detrimental effect on the. oxidation resistance of TiAl alloy, because it enhances formation of $TiO_2$. On the other hand, a composite coating of aluminide-yttrium has shown excellent oxidation resistance. A continuous protective $Al_2O_3$ scale is formed on the aluminized TiAl, and Y-coating improves $Al_2O_3$ scale adherence and substantially prevents depletion of Al in the aluminide-coating layer.