• Toxicological Research
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• v.16 no.2
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• pp.133-139
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• 2000

This study was designed to evaluate the mechanism by which reactive nitrogen intermediates (RNI) induced the cytotoxicity of human doparminergic neuroblastoma SH-SY5Y cells. 3-Morpholino-sydnonimine (SIN-l), a donor of peroxynitrite (ONOO) and sodium nitroprusside (SNP), a donor of nitric oxide (NO) induced cell detachment and apoptotic death, as characterized by chromatin condensation, the ladder pattern fragmentation of genomic DNA and morphological nuclear changes. SIN-l also induced the activation of caspase 3-like protease in a time-dependent manner. Exogenous antioxidants, such as reduced glutathione (GSH), N-acetylcysteine (NAC), and selenium protected the cells from apoptotic death and reduced the activation of caspase 3-like protease by SIN-1. Furthermore, SIN-l directly reduced the intracellular levels of glutathione. Taken together, these data suggested that RNI including NO and peroxynitrite decrease the concentration of intracellular antioxidant such as GSH, which lead to the apoptotic death of human neuroblastoma SH-SY5Y cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.3
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• pp.863-867
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• 2004

Herba Patriniae(HP) has been known to exert anti-inflammation and -tumoral activity in Korea. However, its molecular mechanism of action is not understood. In this study, we found that HP extract induced apoptosis in androgen-dependent prostate cancer LNCaP cells as evidenced by DNA fragmentation. Our data demonstrated that HP extract-induced apoptotic cell death was accompanied by inhibition of NF- κB activation, lowering effects of intracellular prostate specific antigen(PSA) and androgen reoeptor(AR) expression in a time dependent manner. Taken together, HP extract may inhibit the proliferation of prostate cancer LNCaP cell associated with inhibition of NF- κB activation, PSA and AR expression and that of apoptosis.

• Proceedings of the KSME Conference
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• 2004.11a
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• pp.1162-1165
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• 2004

Size and crystalline phase changes of $Fe_{2}O_{3}$ nanoparticles formed in a $H_{2}/O_{2}$ flame have been investigated. At flame temperatures below $1350^{\circ}C$, the mean particle size increased monotonously with the distance from the burner edge; but in high-temperature flames above $1650^{\circ}C$, it suddenly decreased from 20 nm to ${\sim}3$ nm with the distance from the burner edge. The results of X-ray diffraction and HRTEM showed that this sudden reduction of the size of nanoparticles was accompanied by a partial phase transformation from ${\gamma}$-$Fe_{2}O_{3}$ into ${\alpha}$-$Fe_{2}O_{3}$. We suggest the structural instability due to ${\gamma}-$ to ${\alpha}-phase$ transformation as a mechanism for a rapid fragmentation of 20 nm particles into 3 nm ones.

• Proceedings of the Korean Society of Precision Engineering Conference
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• 1993.10a
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• pp.656-659
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• 1993

The failure phenomenon of Dual Basalt Fibers Reinforced Epoxy Composites(DFC) under tensile load was studied using acoustic emission(AE) technique. AE amplitude and AE energy were mainly associated with the internal microscopic failure mechanism of DFC specimen, such as fiber fracture, matrix cracking, and fiber/matrix debonding. Fiber failures in the DFC specimens were distinguishable by showing the highest AE energy amplitude. They were dependant on the fiber diameters. Matrix cracking was determined from the relatively lower AE amplitude and AE energy, whereas fiber/matrix debonding could not be successfully isolated. AE method, however, can be applicable to the fragmentation method for interfacial strength(IFSS) in DFC specimens with adjusting the threshold to isolate fiber breaks from matrix crack and debonding.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.22-40
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• 2001

Apoptosis is characterized by DNA fragmentation, chromatin condensation and plasma membrane blebbing. These apoptotic processes have been mainly associated with genetic mechanisms. Recently, these processes have been also associated with mitochondrial events that include the release of cytochrome c and Diablo/SMAC by modulation of mitochondrial membrane permeability.(omitted)

• Environmental Analysis Health and Toxicology
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• v.22 no.1 s.56
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• pp.57-64
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• 2007

Nanomaterials have been used to create unique devices at the nanoscale level. However, the toxicities of nanomaterials have not been fully tested and the risk of nanomaterials has been raised as an emerging issue in these days. In this study, the cytotoxicity of silver nanoparticles was tested using cultured mouse leydig cells. As results, silver nanoparticles showed cytotoxicity with the generation of reactive oxygen species (ROS). With the increased level of ROS, intracellular glutathione level was decreased. DNA fragmentation and caspase-3 activation suggested the apoptotic mechanism of cell death in leydig cells treated with silver nanoparticles.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.318.3-319
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• 2002

Peroxynitrite(ONOO-), formed from the reaction of superoxide(O2-) and nitric oxide(NO), is a potent oxidant that contributes to oxidation of various cellular constituents including lipids. amino acids, sulphydryls and nucleotides. It can cause cellular injury such as DNA fragmentation and apoptotic cell death. Also. the toxicity of ONOO- has been reported to be involved in inflammatory and nurodegenerative diseases such as Alzheimer's disease, Parkinson's disease. and atherosclerosis. (omitted)

• Toxicological Research
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• v.18 no.3
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• pp.275-283
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• 2002

Fungal metabolite, gliotoxin is an epipolythiodioxopiperazin (ETP) class and has various roles including immunomodulatory and apoptotic effects. This study was designed to evaluate the mechanism by which gliotoxin exerts the apoptosis on human promyelocytic leukemic HL-60 cells. Herein, we demonstrated that the gliotoxin decreased the cell viability in a time-dependent manner Gliotoxin-induced cell death was confirmed us apoptosis characterized by chromatin condensation and ladder-pattern fragmentation of genomic DNA. Gliotoxin increased the catalytic activities of caspase-3 and caspase-9. Activation of caspase-3 was further confirmed by degradation of procaspase-3 and poly(ADP-ribose) polymerase (PARP) by gliotoxin in HL-60 cells. Furthermore, gliotoxin induced the changes of mitochondrial transmembrane potential (MTP). Antioxidants, including GSH and NAC, markedly inhibited apoptosis with conistent suppression of enzymatic activity of caspase-3, caspase-9, and MTP loss in gliotoxin-treated cells. Taken together, we suggest that gliotoxin function as an oxidant and ploys proapoptotic roles in HL-60 cells via activation of intrinsic caspase cascades as well as mitochondrial dysfunction.

• Archives of Pharmacal Research
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• v.29 no.12
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• pp.1140-1146
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• 2006

Ceramide analogs are potential chemotherapeutic agents. We report that a ceramide analog induces apoptosis in human prostate cancer cells. The ceramide analog induced cell death through an apoptotic mechanism, which was demonstrated by DNA fragmentation, the cleavage of poly ADP ribose polymerase (PARP), and a loss of membrane asymmetry. Treating the cells with ceramide analog resulted in the release of various proapoptotic mitochondrial proteins including cytochrome c and Smac/DIBLO into the cytosol, and a decrease in the mitochondrial membrane potential. In addition, the ceramide analog decreased the phospho-Akt and phospho-Bad levels. The expression of the antiapoptotic Bcl-2 decreased slightly with increasing Bax to Bcl-2 ratio. These results suggest that the ceramide analog induces apoptosis by regulating multiple signaling pathways that involve the mitochondrial pathway.

• Journal of the Korean Society of Tobacco Science
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• v.7 no.2
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• pp.169-178
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• 1985

In the previous paper, the kinetics of cellulose were described. In this study, the ability of some additives to act as a flame promoter for cellulose was investigated using dynamic thermogravimetry and differential scanning calorimetry. The treated cellulose was thermally decomposed through the two model as previously noted with the untreated cellulose. The first step was associated with the flaming combustion of volatile material released in the fraunentation process and the second was caused by the glowing combustion of carbonaceous residue. The first group of the additives, which could be divided into two groups by the pyrolytic mechanism of cellulose, appeared to catalyze the fragmentation, maximizing the degradation to produce tarry products, with gaseous flammable substrate. The heat evolved in flaming combustion mode was increased significantly by the treatment of the cellulose retained 1-5% of the first group additives.