• Biomedical Science Letters
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• v.18 no.4
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• pp.329-337
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• 2012

${\alpha}$-synuclein (${\alpha}$-syn) is known to be implicated in the pathogenesis of Parkinson's disease and transiently bind to biological vesicles. In this study, we examined the effect of molecular crowding on the interaction of ${\alpha}$-syn with biological vesicles by using inert polymers since the environment of proteins in cells are crowded with other macromolecules. The addition of different polymers including polyethylene glycol, dextran, and ficoll enhanced the binding of ${\alpha}$-syn to vesicles in a concentration-dependent manner and the association of ${\alpha}$-syn with vesicle was proportionally augmented by increased expression of ${\alpha}$-syn. However, molecular crowding had a neglectable effect on the vesicle binding of ${\alpha}$-syn mutants (A30P, TG6), which has been reported to show impaired vesicle binding capacity. These results suggest that transient interaction of ${\alpha}$-syn with vesicles occurs more commonly in cells than expected implying interaction with vesicles may be one of the physiological processes in which ${\alpha}$-syn is involved.

• Journal of the Korean Ceramic Society
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• v.34 no.6
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• pp.553-560
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• 1997

A fine $\alpha$-Al2O3 powder was prepared by sol-gel process for membrane application. And it was carried out by adding 1.5wt% $\alpha$-Al2O3 powders(mean size : 87 nm) as seeds to the prepared sols and by controlling the heating schedule (the heating rate and the soaking time) to prevent the microstructural change, which occured during $\theta$-to $\alpha$Al2O3 phase transformation. The seeded $\alpha$-Al2O3 particles acted as the heterogeneous nucleation sites for the $\alpha$-Al2O3 nucleation during the transformation of $\theta$- to $\alpha$-Al2O3 and resulted in increasing the driving force of phase transformation to activate the formation of $\alpha$-Al2O3 phase at 82$0^{\circ}C$. By $\alpha$-Al2O3 seeding and controlling of heating condition the phase transformation of $\theta$- to $\alpha$-Al2O3 was accomplished at low temperature and the grain growth process was depressed. Therefore, the unsupported membrane could be fabricated in $\alpha$-Al2O3 . The average diameter of pores in the fabricated membrane was 7 nm and the porosity was 47%.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.23 no.8
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• pp.1893-1898
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• 1998

We have redefined the $\alpha$ -parameter of the extended transmitters in the presence of self-phase modulation (SPM) induced chirp. The $\alpha$ -parameter is effectively lowered to about 1, when the SPM effect with the launching power of 12.5dBm (maximum launching power to avoid stimulated Brillouin scattering(SBS)) is included, compared to the $\alpha$ -parameter of the transmitter algone. The lowered $\alpha$ -parameter has improved the transmission performance significantly regardless the transmitter is operated with positive or negative chirp. The SPM-induced effective $\alpha$ -parameter can be used as a design parameter for the high speed (10 Gbps) transmission systems.

• BMB Reports
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• v.29 no.6
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• pp.530-534
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• 1996

Astrocyte are the major glial cell type in the central nervous system (CNS), and analogous to macrophage, mediates the number of immune responses such as production of cytokines including tumor necrosis factor alpha ($TNF-{\alpha}$) upon activation. $TNF-{\alpha}$ has been implicated in neuroimmunological disorders through killing oligodendrocytes and thus causing demyelination. It has been previously demonstrated that mitogen-activated T cells synthesized a 26 kDa precursor form of $TNF-{\alpha}$ which is bound to the surface of a membrane, and is later secreted as a 17 kDa mature version. In order to examine whether astrocytes would produce the transmembrane form of $TNF-{\alpha}$, astrocytes were stimulated with biological stimuli and the membrane form of $TNF-{\alpha}$ was analyzed by Western blot and FACS analysis. When astrocytes are stimulated with lipopolysaccharide (LPS), $IFN-{\gamma}/LPS$, or $IFN-{\gamma}/IL-1{\beta}$, they were able to express a membrane-anchored $TNF-{\alpha}$ of approximately 26 kDa protein which was immunoreactive to an $anti-TNF-{\alpha}$ antibody, whereas unstimulated astrocytes or astrocytes treated with $IFN-{\gamma}$ or $IL-1{\beta}$ alone was not. Our FACS data were also consistent with the immunoblot analysis. Our result suggests that the membrane form of $TNF-{\alpha}$ expressed by activated astrocytes may cause local damage to oligodendrocytes by direct cell-cell contact and contribute to demyelination observed in multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE).

• Bulletin of the Korean Chemical Society
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• v.35 no.5
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• pp.1365-1374
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• 2014

Thirteen analogs of tridecapeptide ${\alpha}$-factor (WHWLQLKPGQPMY) of Saccharomyces cerevisiae with C- or N-terminal Trp extension and isosteric replacement by Aib at position 8 and 11, Trp at position 13, D-Ala at position 9, and Orn and Glu at position 6 were synthesized and assayed for their biological activity. Receptor binding assay was carried out using our newly developed spectrophotometric method with detector peptide 14. C- or N-terminal extended analogs, ${\alpha}$-factor-$[Trp]_n$ (n =1-5) 1-5 and $[N-Trp]_1$-${\alpha}$-factor 6, were all less active than native ${\alpha}$-factor and gradual decreases in both activity and receptor affinity were observed with greater Trp extension. Trp-substituted analog at position 13, $[Trp^{13}]{\alpha}$-factor 7, exhibited about 2-fold reductions in both activity and receptor affinity. Aib-substituted analogs, $[Aib^8]{\alpha}$-factor 8 and $[Aib^{11}]{\alpha}$-factor 9, showed 5- to 10-fold reduction in activity as well as 3-fold reduction in receptor affinity compared to native ${\alpha}$-factor. $[Orn^6]{\alpha}$-factor 10 demonstrated strong potency with a 7.0-fold increase in halo activity as well as 1.8-fold increase in receptor affinity compared to native ${\alpha}$-factor. For two double substituted analogs, [$Glu^6,{\small{D}}-Ala^9$]${\alpha}$-factor 12 showed the slightly decreased potency in halo activity compared to analog 10, whereas [$Orn^6,{\small{D}}-Ala^9$]${\alpha}$-factor 11 exhibited 15-fold higher halo activity as well as nearly 3-fold higher receptor affinity compared to native ${\alpha}$-factor.

• Journal of Oral Medicine and Pain
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• v.24 no.4
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• pp.361-374
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• 1999

F. nucleatum is a gram-negative obligate anaerobe which is the principal and most frequent cause of gingival inflammation and is the predominant pathogen isolated in subsequent periodontal breakdown. It is also one of the most numerous bacteria found in subgingival plaque samples from healthy sites; its numbers are about 10-fold greater in plaque from periodontally diseased sites. The purpose of this study is to examine the effects of outer membrane(OM), outer membrane vesicle(OMV), and lipopolysaccharide(LPS) from F. nucleatum ATCC 25586 strain on the growth of human gingival fibroblasts and HOS 941 cells, and on the $TNF-{\alpha}$ production / $TNF-{\alpha}$ mRNA expression of mouse splenocytes. For the examination of cytotoxic effects, $TNF-{\alpha}$ production and $TNF-{\alpha}$ mRNA expression, the MTT assay, the ELISA and the RT-PCR were performed, respectively. All extracts of F. nucleatum tested were cytotoxic to both of human gingival fibroblasts and HOS 941 cells, and the significant difference of cytotoxic activity among the extracts was not observed. In the effects of these extracts on the $TNF-{\alpha}$ production / $TNF-{\alpha}$ mRNA expression of mouse splenocytes, all extracts of F. nucleatum tested also stimulated the $TNF-{\alpha}$ production / $TNF-{\alpha}$ mRNA expression, but the effects of the OM extracts on the $TNF-{\alpha}$ production / $TNF-{\alpha}$ mRNA expression were higher than those of the OMV and the LPS extracts. The pattern of the $TNF-{\alpha}$ mRNA expression was similar to that of the $TNF-{\alpha}$ production. These results indicate that F. nucleatum seems to contribute to the pathogenesis of periodontal diseases at least by its cytotoxicity, directly and its $TNF-{\alpha}$ production, indirectly.

• Korean Journal of Food Science and Technology
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• v.39 no.2
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• pp.217-221
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• 2007

In order to determine the effects of ginseng powder on the antioxidant enzyme activities of hepatotoxicity in $benzo({\alpha})pyrene[B({\alpha})P]-treated$ mice, the mice were divided into 5 groups. Ginseng powder was injected intraperitoneally once a day for 5 successive days, followed by the administration of $B({\alpha})P$ treatment on the fifth day. We also evaluated the relationship existing between lipid peroxidation and ginseng powder on oxidative stress. The increased activities of superoxide dismutase, catalase, and glutathione peroxidase observed following $B({\alpha})P-treatment$ were reduced as the result of ginseng powder treatment. Whereas, the glutathione content and glutathione S-transferase activity depleted by $B({\alpha})P$ were increased significantly, but the $B({\alpha})P-associated$ elevation of cytochrome P-450 activities and lipid peroxide content were reduced as the result of ginseng powder treatment. These results indicate that ginseng powder may exert a protective effect against $B({\alpha})P-induced$ hepatotoxicity in mice.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.2
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• pp.209-219
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• 1997

Previous studies have demonstrated that oxidative stress involving generation of reactive oxygen species (ROS) is responsible for the cytotoxic action of $TNF{\alpha}$. Protective effect of small heat shock proteins (small HSP) against diverse oxidative stress conditions has been suggeted. Although overexpression of small hsp was shown to provide an enhanced survival of $TNF{\alpha}$-sensitive cells when challenged with $TNF{\alpha}$, neither the nature of $TNF{\alpha}$-induced cytotoxicity nor the protective mechanism of small HSP has not been completely understood. In this study, we have attempted to determine whether $TNF{\alpha}$ induces oxidative DNA damage in $TNF{\alpha}$-sensitive L929 cells. We chose to measure the level of 8-hydroxy-2'-deoxyguanosine (8 ohdG), which has been increasingly recognized as one of the most sensitive markers of oxidative DNA damage. Our results clearly demonstrated that the level of 8 ohdG increased in L929 cells in a $TNF{\alpha}$ dose-dependent manner. Subsequently, we asked whether small HSP has a protective effect on $TNF{\alpha}$-induced oxidative DNA damage. To accomplish this goal, we have stably transfected L929 cells with mouse small hsp cDNA (hsp25) since these cells are devoid of endogenous small hsps. We found that $TNF{\alpha}$-induced 8 ohdG was decreased in cells overexpressing exogenous small hsp. We also found that the cell killing activity of $TNF{\alpha}$ was decreased in these cells as measured by clonogenic survival. Taken together, results from the current study show that cytotoxic mechanism of $TNF{\alpha}$ involves oxidative damage of DNA and that overexpression of the small hsp reduces this oxidative damage. We suggest that the reduction of oxidative DNA damage is one of the most important protective mechanisms of small HSP against $TNF{\alpha}$.

• Archives of Pharmacal Research
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• v.27 no.8
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• pp.850-856
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• 2004

Intraneuronal deposition containing $\alpha$-synuclein is implicated in the pathogenesis of synuclein-opathies including Parkinsons disease (PD). Although it has been demonstrated that cytoplas-mic inclusions of wild type $\alpha$-synuclein are observed in the brain of PD patients and that $\alpha$-synuclein mutations such as A30P and A53T accelerate aggregate formation, the exact mech-anism by which $\alpha$-synuclein forms insoluble aggregates is still controversial. In the present study, to understand the possible involvement of tissue transglutaminase (tTG) in aggregate formation of $\alpha$-synuclein, SH-SY5Y cell lines stably expressing wild type or mutant (A30P or A53T) $\alpha$-synuclein were created and aggregate formation of $\alpha$-synuclein was observed upon activation of tTG. The data demonstrated that $\alpha$-synuclein negligibly interacted with tTG and that activation of tTG did not result in the aggregate formation of $\alpha$-synuclein in SH-SY5Y cells overexpressing either wild type or mutant $\alpha$-synuclein. In addition, $\alpha$-synuclein was not modi-fied by activated tTG in situ. These data suggest that tTG is unlikely to be a contributing factor to the formation of aggregates of $\alpha$-synuclein in a stable cell model.

• Archives of Pharmacal Research
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• v.21 no.2
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• pp.120-127
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• 1998

Peroxisome proliferators induce hepatic peroxisome proliferation and hepatic tumors in rodents. These chemicals increase the expression of the peroxisomal $\beta$-oxidation pathway and the cytochrome P-450 4A family, which metabolizes lipids, including eicosanoids. Peroxisome proliferators transiently induce increased cell proliferation in vivo. However, peroxisome proliferators are weakly mitogenic and are not co-mitogenic with epidermal growth factor (EGF) in cultured hepatocytes. Earlier study found that the peroxisome proliferator ciprofibrate is cornitogenic with eicosanoids. In order to study possible mechanisms of the comitogenicity of peroxisome proliferator ciprofibrate and eicosanoids' we hypothesized that the co-mitogenicity may result from synergistic or additive increases of second messengers in mitogenic signal pathways. We therefore examined the effect of the peroxisome proliferator ciprofibrate, prostaglandin $F_2_{\alpha}$($PGF_2{\alpha}$) and the combination of ciprofibrate and $PGF_2{\alpha}$ with or without growth factors on the protein kinase C (PKC) activity, and inositol-1, 4, 5-triphosphate ($IP_{3-}$) and intracellular calcium ($[Ca^{2+}]_i$) concentrations in cultured rat hepatocytes. The combination of ciprofibrate and $PGF_2{\alpha}$ significantly increased particulate PKC activity. The combination of ciprofibrate and $PGF_2{\alpha}$ also significantly increased EGF, transforming growth factor-$\alpha$ ($TGF_2{\alpha}$) and hepatic growth factor (HGF)-induced particulate PKC activity. The combination of ciprofibrate and $PGF_2_\alpha$greatly increased $[Ca^{2+}]_i$. However, the increases of PKC activity and $[Ca^{2+}]_i$ by ciprofibrate and $PGF_2{\alpha}$ alone were much smaller. Neither ciprofibrate or $PGF_2{\alpha}$ alone nor the combination of ciprofibrate and $PGF_2{\alpha}$ significantly increased the formation of $IP_3$. The combination of ciprofibrate and $PGF_2{\alpha}$, however, blocked the inhibitory effect of $TGF-{\beta}$ on particulate PKC activity and formation of $IP_3$ induced by EGF. These results show that co-mitogenicity of the peroxisome proliferator ciprofibrate and eicosanoids may result from the increase in particulate PKC activity and intracellular calcium concentration but not from the formation of $IP_3$.