• Journal of Korean Ophthalmic Optics Society
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• v.12 no.4
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• pp.111-117
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• 2007

The visual evoke potential(VEP) is the effective method to diagnose and treat the amblyopia or to check the infants visual ability. In order to evaluate the changes of P100 latencies and amplitudes of VEP by intensity of illumination and refractive errors, we measured latencies and amplitudes of 41 normal adults (20/20 VA) who have no ocular diseases and neurologic diseases. The results were as follows: In the scotopic condition, the latencies were N75$75.83{\pm}3.69$ msec, P100$103.48{\pm}5.34$ msec, the P100 amplitude was $14.86{\pm}2.43$ msec, and in the photopic condition, the latencies were N75$76.71{\pm}3.11$ msec, P100$107.26{\pm}5.54$ msec and the P100 amplitude was $10.35{\pm}1.75$ msec. The latencies and amplitudes of P100 in the photopic condition had higher values than those in the scotopic condition and the measures were significantly different between the scotopic and photopic condition (p<0.01). The P100 latencies were delayed both in the scotopic and photopic condition with the refractive errors and those measures were delayed more than in the photopic condition. The P100 amplitudes in the induced myopic and hyperopic conditionsreduced than in the emmetopes in both illumination conditions. The P100 latencies and amplitudes in emmetropes showed a correlation with the induced myopic conditions in the scotopic condition. Those results showed that P100 latencies and amplitudes are dependent on the illumination conditions and refractive errors. And we suggest that those results would be useful to determine and evaluate the normal range for the person considering patients' refractive errors and illumination of the test room.

• Microbiology and Biotechnology Letters
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• v.43 no.1
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• pp.45-55
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• 2015

This study was carried out to demonstrate the anti-inflammatory effect of tuna oil (TO) using LPS-induced inflammation responses and mouse models. First, nitric oxide (NO) and pro-inflammatory cytokines levels were suppressed up to 50% with increasing concentrations of TO without causing any cytotoxicity. Also, the expression of a variety of proteins, such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nuclear factor kappa B (NF-κB), was suppressed in a dosedependent manner by treatment with TO. Furthermore, TO also inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs), including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 protein kinase (p38). Moreover, in in vivo testing the formation of ear edema was reduced at the highest dose tested compared to that in the control, and a reduction of ear thickness and the number of mast cells was observed in histological analysis. In acute toxicity test, no mortalities occurred in mice administrated 5,000 mg/kg body weight of TO over a two-week observation period. Our results suggest that TO has a considerable anti-inflammatory property through the suppression of inflammatory mediator productions and that it could prove to be useful as a potential anti-inflammatory therapeutic material.

• Applied Biological Chemistry
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• v.18 no.1
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• pp.10-15
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• 1975

These studies were conducted to induce the available mutants in Takju yeasts by the irradiation of UV light. Two original strains(5-Y-5, 6-Y-6) using for irradiation of UV selected from 24 strains which were isolated from the Takju mashes And Nuruks collected from 12 local regions of Chungnam and Chungbuk provinces in Korea, and the irradiations to the yeasts with UV light were carried out at a distance 10-40cm from the sources of irradiation for 10-220 seconds. The purpose of this experiment is to report the effects of irradiating distances and times of UV light on the survival ratio of orginal yeasts, and the identification of two orginal yeasts and three mutants induced by the irradiation of UV light. The results were summarized as follows. 1) The effects of irradiating distances and times on the survival ratio on the yeasts were represented as follows. and acid productivity to the survival strains by the irradiation of UV light. The selected mutants were the strains 30-24, 40-27 which have more powerful fermentability about 10 percent than those of original strains and a strain 30-81 which have potential acid productivity. 3) The selected yeasts (5-Y-5, 6-Y-6) were identified to Saccharomyces cerevisiae by a taxonomic study of Lodder and the mutants(30-81, 40-27, 30-81) induced from above yeasts by the irradiation of UV light have almost same properties two orginal yeasts in the identical characteristics.

• Korean Journal of Ecology and Environment
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• v.41 no.spc
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• pp.77-85
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• 2008

Grazing rates (GR) and pseudofaeces production (PFP) of native snail, Chinese mystery snail (Cipangopaludina chinensis malleata Reeve) on natural colonial morphs of Microcystis aeruginosa was measured. C. chinensis was collected from the upstream of the Geum River (Boryeong, Korea), where they co-habituated with Unio douglasiae and Lanceolaria acrorhyncha. The experiments were performed to evaluate the GR and PFP at different conditions such as; incubation time (1, 3, 5, 7, 9 and 11 hr), body size (3 to 6.1 cm, n=28), snail density (0.5, 1, 1.5 and 2.0 ind. $L^{-1}$) and prey concentration (168.3, 336.7, 505.0 and $673.0{\mu}g\;Chl-{\alpha}L^{-1}$). All experiments were triplicated, and conducted in transparent acrylic vessel (3L in volume). Regarding feeding time, a highest GR (0.538L $gAFDW^{-1}h^{-1}$) and PFP $(7.18mgAFDW^{-1})$ appeared at 1hr and 7hr after snail stocking, respectively. Interestingly, the snail, smaller than 4.5cm in body size, showed a wide range of GR ($-4.173{\sim}1.087L\;gAFDW^{-1}h^{-1}$) for the initial period (1 and 4hrs of stocking), compared to those greater than 4.5cm, which showed a stable FR, higher than 0.5L $gAFDW^{-1}h^{-1}$. Upon density effect, the density of 1.5 ind. $L^{-1}$ induced the most effective inhibition on Microcystis biomass with highest PFP. On the prey concentration, highest GR (0.897L $gAFDW^{-1}h^{-1}$) and PFP (3.67 mg $gAFDW^{-1}h^{-1}$) were induced at the level of $168.3{\mu}g\;Chl-{\alpha}L^{-1}$ and $673{\mu}g\;Chl-{\alpha}L^{-1}$, respectively. GR and PFP of this freshwater snail on the cyanobacterial bloom (M. aeruginosa) varied with the feeding conditions, and they were comparatively high for a short period of time less than 7hrs regardless of the stocking condition. Our results suggest that this freshwater snail has a potential to control cyanobacterial bloom when provided with suitable condition.

• Korean Journal of Environmental Biology
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• v.20 no.1
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• pp.73-77
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• 2002

The effect of salicylic acid (SA) on C $d^{2+}$ - induced physiological toxicity in Commelina communis was investigated. 3- weeks old Commelina communis was transferred to and grown in Hoagland solution in the presence or absence of 100 $\mu$M C $d^{2+}$ and SA for 3 weeks. In the treatment of C $d^{2+}$ + SA, the length of stem was increased to 0.7 cm for 3 weeks (C $d^{2+}$, 2.1cm; control, 7.2 cm). C $d^{2+}$ + SA reduced total chlorophyll content up to 86%, and changed chlorophyll a/b ratio below 1.6. C $d^{2+}$ + SA also reduced about 40-78% of water potential, but C $d^{2+}$ increased 16-39% from 1 week to 3 weeks. C $d^{2+}$ + SA also inhibited 27% of Fv/Fm, but in case of C $d^{2+}$, Fv/Fm was not changed. The treatment of C $d^{2+}$ + SA showed about 37-58% inhibition of photosynthetic activity when measured at various light intensity (500-1000 $\mu$mol $m^{-2}$ $s^{-1}$ ). In the case of C $d^{2+}$ treatment, photosynthetic activity was inhibited to 12-15%. Similar effect was found in terms of stomatal conductance. Therefore, it could be concluded that the treatment of C $d^{2+}$ + SA into plant decrease or block various physiological activities and lend to die by double effects of both chemicals.cts of both chemicals..

• Journal of Life Science
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• v.16 no.6
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• pp.904-910
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• 2006

Dendritic cells (DCs) are the only antigen presenting cells (APCs) capable of initiating immune responses, which is crucial for priming the specific cytotoxic T lymphocyte (CTL) response and tumor immunity. Upon activation by DCs, CD4+ helper T cells can cross-prime CD8+ CTLs via IL-12. However, recently activated DCs were described to prime in vitro strong T helper cell type 1 $(Th_1)$ responses, whereas at later time points, they preferentially prime $Th_2$ cells. Therfore, we examined in this study the optimum kinetic state of DCs activation impacted on in vivo priming of tumor-specific CTLs by using ovalbumin (OVA) tumor antigen model. Bone-marrow-derived DCs showed an appropriate expression of surface MHC and costimulatory molecules after 6 or 7-day differentiation. The 6-day differentiated DCs pulsed with OVA antigen for 8 h (8-h DC) and followed by restimulation with LPS for 24 h maintained high interleukin (IL)-12 production potential, accompanying the decreased level in their secretion by delayed re-exposure time to LPS. Furthermore, immunization with 8-h DC induced higher intracellular $interferon(IFN)-{\gamma}+/CD8+T$ cells and elicited more powerful cytotoxicity of splenocytes to EG7 cells, a clone of EL4 cells transfected with an OVA cDNA, than immunization with 24-h DC. In the animal study for the evaluation of therapeutic or protective antitumor immunity, immunization with 8-h DC induced an effective antitumor immunity against tumor of EG7 cells and completely protected mice from tumor formation and prolonged survival, respectively. The most commonly used and clinically applied DC-based vaccine is based on in vitro antigen loading for 24 h. However, our data indicated that antigen stimulation over 8 h decreased antitumor immunity with functional exhaustion of DCs, and that the 8-h DC would be an optimum activation state impacted on in vivo priming of tumor-specific CTLs and subsequently lead to induction of strong antitumor immunity.

• Journal of Life Science
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• v.21 no.7
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• pp.961-968
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• 2011

The formation of reactive lipid aldehydes, 4-hydroxynonenal (HNE) is shown to be derived from fatty acid hydroperoxides through the oxidative process. Among its known effects in cytotoxicity, HNE has been implicated in apoptotic cell death. To delineate its putative role as a potential mediator, we investigated the mechanism by which HNE induces apoptosis of endothelial cells (ECs). The anti-proliferative effects of HNE were tested through MTT assay after exposure to various concentrations ($5\sim15\;{\mu}M$) of HNE. We observed apoptotic bodies with propidium iodide staining, and measured the HNE induction of endothelial apoptosis by flow cytometry assay. We observed that cells exposed to HNE for 24 hr resulted in increased poly(ADP-ribose) polymerase cleavage and up-regulation of Bax. Data on the HNE action strongly indicated the involvement of reactive species, namely, intracellular ROS, nitrite, and peroxynitrite. To obtain evidence on the implication of ROS and peroxynitrite in HNE-induced apoptosis, a ROS scavenger, N-acetylcysteine (NAC), and a peroxynitrite scavenger, penicillamine, were tested. Results clearly indicate that the induction of apoptosis by HNE was effectively inhibited by NAC and penicillamine. Based on the present data, we conclude that the endothelial apoptosis induced by HNE involves both ROS generation and peroxynitrite activity. Our new data could lead to a redefinition of HNE action on apoptosis in ECs.

• Journal of Oral Medicine and Pain
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• v.34 no.3
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• pp.261-276
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• 2009

Lactacystin, a microbial natural product synthesized by Streptomyces, has been commonly used as a selective proteasome inhibitor in many studies. Proteasome inhibitors is known to be preventing the proliferation of cancer cells in vivo as well as in vitro. Furthermore, proteasome inhibitors, as single or combined with other anticancer agents, are suggested as a new class of potential anticancer agents. This study was undertaken to examine in vitro effects of cytotoxicity and growth inhibition, and the molecular mechanism underlying induction of apoptosis in SCC25 human tongue sqaumous cell carcinoma cell line treated with lactacystin. The viability of SCC25 cells, human normal keratinocytes (HaCaT cells) and human gingiva fibroblasts (HGF-1 cells), and the growth inhibition of SCC25 cells were assessed by MTT assay and clonogenic assay respectively. The hoechst staining, hemacolor staining and TUNEL staining were conducted to observe SCC25 cells undergoing apoptosis. SCC25 cells were treated with lactacystin, and Western blotting, immunocytochemistry, confocal microscopy, FAScan flow cytometry, MMP activity, and proteasome activity were performed. Lactacystin treatment of SCC25 cells resulted in a time- and does-dependent decrease of cell viability and a does-dependent inhibition of cell growth, and induced apoptotic cell death. Interestingly, lactacytin remarkably revealed cytotoxicity in SCC25 cells but not normal cells. And tested SCC25 cells showed several lines of apoptotic manifestation such as nuclear condensation, DNA fragmentation, the reduction of MMP and proteasome activity, the decrease of DNA contents, the release of cytochrome c into cytosol, the translocation of AIF and DFF40 (CAD) onto nuclei, the up-regulation of Bax, and the activation of caspase-7, caspase-3, PARP, lamin A/C and DFF45 (ICAD). Flow cytometric analysis revealed that lactacystin resulted in G1 arrest in cell cycle progression which was associated with up-regulation in the protein expression of CDK inhibitors, $p21^{WAF1/CIP1}$ and $p27^{KIP1}$. We presented data indicating that lactacystin induces G1 cell cycle arrest and apoptois via proteasome, mitochondria and caspase pathway in SCC25 cells. Therefore our data provide the possibility that lactacystin could be as a novel therapeutic strategy for human tongue squamous cell carcinoma.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.27 no.5
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• pp.373-384
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• 2001

Cellular proliferation is an intricately regulated process mediated by the coordinated interactions of critical growth control genes. Two of these factors in mammalian cells are the p53 and mdm-2 genes. A protein product of the mem-2 oncogene has been recently shown to associate with the protein encoded by the tumor suppressor gene p53. The p53 tumor suppressor protein is stabilized in response to DNA damage and other stress signals and causes the cell to undergo growth arrest or apoptosis, thus preventing the establishment of mutations in future cellular generations. Mutation or loss of p53 is a very common event in tumor progression. It occurs in about 50% of all tumors analysed including of colon, lung, breast and liver. The cellular mdm-2 gene, which has potential transforming activity that can be activated by overexpression, is amplified in a significant percentage of human sarcoma and in other mammalian tumors. Proteins encoded by the mdm-2 gene are able to bind to the p53 protein and, when overexpressed, can inhibit p53's transcriptional activation function, thus mdm-2 can act as a negative regulator of p53 function. Experimental study was performed to observe the relationship between p53 gene mutation and mdm-2 protein expression and apply the results to the clinical activity. 36 golden syrian hamster each weighing $60{\sim}80g$ were used and painted with 0.5% DMBA by 3 times weekly on the right buccal cheek(experimental side) for 6, 8, 10, 12, 14 and 16 weeks. Left buccal cheek(control side) was treated with mineral oil as the same manner to the right side. The hamsters were sacrificed on the 6, 8, 10, 12, 14 & 16 weeks. Normal and tumor tissues from paraffin block were examined for histology and immunohistochemistry observation, and were completely dissected by microdissection and DNA from both tissue were isolated by proteins K/phenol/chloroform extraction. Segments of the hamster p53 exons 5, 6, 7 and 8 were amplified by PCR using the oligonucleotide primers, and then confirmational change was observed by SSCP respectively. The results were as follows : 1. Dysplasia at 6 weeks, carcinoma in situ at 8 weeks and invasive carcinoma from 10 weeks could be observed in experimental groups. 2. p53 mutations were detected in 10 of the 36(28%) and the exons 6(6 of the 10 : 60%) was the most hot spot area among the highy conserved region(exons 5, 6, 7 & 8). 3. Immunohistochemical study confirmed 22 of the 36(61%) of p53 expression involving 10 of p53 mutations. 4. mdm-2 expression of was showed in 3 of the 36(8%) involving 1 of the 22 of p53 expression and 2 of the 14 of p53 non-expression. From the above results, mutation of p53 gene or expression of p53 protein may have the influence of the DMBA induced carcinoma of hamster buccal pouch but the expression of mdm-2 protein may not have relationship with tumorigenesis.

• Journal of Life Science
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• v.25 no.3
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• pp.293-298
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• 2015

Muscle atrophy, known as a sarcopenia, is defined as a loss of muscle mass resulting from a reduction in the muscle fiber area or density due to a decrease in muscle protein synthesis and an increase in protein breakdown. Schisandrae fructus (SF) extract of the fruits of Schisandra chinensis (Turcz) Baillon has been used as a tonic in traditional medicine for thousands of years. Although a great deal of work has been carried out on the therapeutic potential of SF, its pharmacological mechanisms of action in muscle diseases actions remain unclear. In the present study, we investigated the inhibitory effects of SF ethanol extracts on the production of muscle atrophy factors in C2C12 myotubes stimulated with 5-aminoimidazole-4-carboxamide-ribonucleotide (AICAR), an AMP-activated kinase (AMPK) activator, and sought to determine the underlying mechanisms of action. AICAR upregulated atrophy-related ubiquitin ligase muscle RING finger-1 (MuRF-1) and stimulated the levels of the forkhead box O3a (FoxO3a) transcription factor in the C2C12 myotubes. SF supplementation effectively and concentration- dependently counteracted AICAR-induced muscle cell atrophy and reversed the increased expression of MuRF-1 and FoxO3a. Our study demonstrates that SF can reverse the muscle cell atrophy caused by AICAR through regulation of the AMPK and FoxO3a signaling pathways, followed by inhibition of MuRF-1.