• The Journal of Korean Medicine
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• v.38 no.3
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• pp.103-110
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• 2017

Objectives: The purpose of this study was to examine trends in duplicate publication in Korean medical articles indexed in the Oriental Medicine Advanced Searching Integrated System(OASIS). Methods: We searched the list of papers published in Korean medical journals by using OASIS. We randomly extracted 10% of total articles (n=1,162). We searched using OASIS by entering keywords from the title and names of the first and last authors of each indexed article. After the librarian selected the candidates of duplicate publication, three authors reviewed the full texts of the articles independently. When their opinions were not in agreement, reconciliation was made by discussion. The patterns of duplicate publication, such as copy, salami slicing (fragmentation), and aggregation (imalas), were also determined. Results: A total of 1162 articles were evaluated, 24 (2.1%) index articles of which were duplicate articles. Among 24 index articles, Two were triple publications and 22 were double publications. The patterns of duplication publication were as follows; (1) copy (n=8, 33.3%); (2) salami (9, 37.5%), (3) imalas (5, 20.8%) (4) others (2, 8.3%). Conclusion: Duplicate publications have appeared in Korean medical journals in a small proportion. Education on publication ethics and authors'ethical awareness is needed.

• The Journal of the Korea Contents Association
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• v.14 no.9
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• pp.218-226
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• 2014

China has become a G-2 Superpower country as result of rapid economic growth through the reform and opening-up in these days. It expressed its confidence by helding a few big international events, such as Bejing Olympic Games. Shanghai Expo. Though most Chinese people give their agreement and support to the government, there are serious, ill-concealed political problems behind the curtain in China. As a multi-ethnic nation, China has repeated experience of fragmentation and integration of various ethnic groups through her long history. In spite of top-level political leaders of communist party always concern the issues of separatism very sensitively, China has suffered occasional bloodshed terrorism because of erupting ethnic and religious conflicts. Especially there are many disruption and fear due to the bloodshed and terrorism by a minority race-seperatists of Uighur tribe in Xinjiang province. The Uighur in Xinjiang province is very different from major Chinese Han ethnically and culturally. Although Chinese government has presented various policies in order to suppress the Uighus's desire for seperation, they have not been able to offer a fundamental, satisfying solution. Because we, Korean people face the expansion of possibility of conflicts, such as increasing of foreign workers, multi-cultural families and extremists. At this point, I believe we can learn valuable lessons from Chinese experiences for anti-terrorism.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.1
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• pp.19-27
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• 1999

Apoptosis has been implicated in the pathophysiological mechanisms of various neurodegenerative diseases. In a variety of cell types, oxidative stress has been demonstrated to play an important role in the apoptotic cell death. However, the exact mechanism of oxidative stress-induced apoptosis in neuronal cells is not known. In this study, we induced oxidative stress in IMR-32 human neuroblastoma cells with tert- butylhydroperoxide (TBHP), which was confirmed by significantly reduced glutathione content and glutathione reductase activity, and increased glutathione peroxidase activity. TBHP induced decrease in cell viability and increase in DNA fragmentation, a hallmark of apoptosis, in a dose-dependent manner. TBHP also induced a sustained increase in intracellular $Ca^{2+}$ concentration, which was completely prevented either by EGTA, an extracellular $Ca^{2+}$ chelator or by flufenamic acid (FA), a non-selective cation channel (NSCC) blocker. These results indicate that the TBHP-induced intracellular $Ca^{2+}$ increase may be due to $Ca^{2+}$ influx through the activation of NSCCs. In addition, treatment with either an intracellular $Ca^{2+}$ chelator (BAPTA/AM) or FA significantly suppressed the TBHP-induced apoptosis. Moreover, TBHP increased the expression of p53 gene but decreased c-myc gene expression. Taken together, these results suggest that the oxidative stress-induced apoptosis in neuronal cells may be mediated through the activation of intracellular $Ca^{2+}$ signals and altered expression of p53 and c-myc.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.5
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• pp.163-169
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• 2007

The neurotoxicity of amyloid $\beta(A\beta)$ is associated with an increased production of reactive oxygen species and apoptosis, and it has been implicated in the development of Alzheimer's disease. While(-)-epigallocatechin-3-gallate(EGCG) suppresses $A\beta$-induced apoptosis, the mechanisms underlying this process have yet to be completely clarified. This study was designed to investigate whether EGCG plays a neuroprotective role by activating cell survival system such as protein kinase C(PKC), extracellular-signal-related kinase(ERK), c-Jun N-terminal kinase(JNK), and anti-apoptotic and pro-apoptotic genes in SH-SY5Y human neuroblastoma cells. One ${\mu}M\;A{\beta}_{1-42}$ decreased cell viability, which was correlated with increased DNA fragmentation evidenced by DAPI staining. Pre-treatment of SH-SY5Y neuroblastoma cells with EGCG($1{\mu}M$) significantly attenuated $A{\beta}_{1-42}$-induced cytotoxicity. Potential cell signaling candidates involved in this neuroprotective effects were further examined. EGCG restored the reduced PKC, ERK, and JNK activities caused by $A{\beta}_{1-42}$ toxicity. In addition, gene expression analysis revealed that EGCG prevented both the $A{\beta}_{1-42}$-induced expression of a pro-apoptotic gene mRNA, Bad and Bax, and the decrease of an anti-apoptotic gene mRNA, Bcl-2 and Bcl-xl. These results suggest that the neuroprotective mechanism of EGCG against $A{\beta}_{1-42}$-induced apoptotic cell death includes stimulation of PKC, ERK, and JNK, and modulation of cell survival and death genes.

• Journal of Microbiology and Biotechnology
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• v.6 no.6
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• pp.432-438
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• 1996

Native crystalline chitin was hydrolyzed in an agitated bead reaction system using crude chitinase excreted from Aspergillus fumigatus JC-19. The reaction was enhanced significantly, and the concentration and yield of reducing sugar after 48 hours were measured to be 35.42 g/I (w/v) and 0.64, respectively, around 1.86 times higher than those of the conventional system that was carried out without glass beads. The effect of reaction conditions, such as the amounts of chitin, chitinase and glass beads, and the size of glass bead, were examined. Ball milled chitin was also hydrolyzed in the agitated bead reaction system, the conversion yield and reaction rate of ball milled chitin for 24 hours increased up to 0.87 and 48.02 g/I, respectively. Chitinase showed relatively high stability in the agitated bead reaction system, particularly in the presence of enzyme stabilizer, $Ca^{++}$, which played a critical role in preventing the deactivation of chitinase by the physical impact of glass beads. The variations of the structural features of chitin during the reaction were followed by SEM and X-ray diffraction, and the enhanced hydrolysis reaction was caused by both the fragmentation of chitin particles and the destruction of the crystalline structure owing to the synergic effects of the attrition of glass beads and the hydrolytic action of chitinase.

• Journal of Microbiology and Biotechnology
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• v.23 no.2
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• pp.237-245
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• 2013

Canthaxanthin (cx) is a potent antioxidant that is chemically synthesized at the industrial scale and has imperative applications in the cosmetic and feed industries. An orange pigmented mesophilic bacterium, designated as K44, was isolated from soil samples of Kargil, India. Biochemical tests, 16S rRNA gene sequencing, and FAME analysis of the bacterium indicated it to belong in the genus Dietzia and is distinct from human isolates. The strain showed 98% 16S rRNA gene sequence homology with Dietzia maris DSM 43102. High-performance liquid chromatography profile of the pigments isolated from K44 showed two major peaks absorbing at 465.3 and 475 nm. The liquid chromatography-mass spectrometry (LC-MS) analysis of both these peaks revealed their m/z to be 564. The molecular weights, LC-MS/MS fragmentation patterns, and ${\lambda}_{max}$ of these fractions corresponded to all-trans- (475 nm) and 9-cis-(465.3 nm) cx isomers. The antioxidant activities of cis- and trans-cx isomers isolated from this bacterium were found to differ, where the cis-isomer showed higher free radical, superoxide radical, and reactive oxygen species scavenging activities than the alltrans- isomer, suggesting that 9-cis-cx is more effective as an antioxidant than the all-trans-cx.

• Environmental Analysis Health and Toxicology
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• v.21 no.1 s.52
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• pp.71-79
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• 2006

Epidemiologic studies have showed a close correlation between arsenic exposure and heart disease such as, cardiovascular problem, ischemic heart disease, infarction, atherosclerosis and hypertension in human. It may increase the mortality of high risk group with heart disease. Regarding the mechanism studies of heart failure, blood vessel, vascular smooth muscle cells and endothelial cells have long been focused as the primary targets in arsenic exposure but there are only a few studies on the cardiomyocytes. In this study, the generation of oxidative stress by low dose of arsenic trioxide was investigated in rat cardiomyocytes. By direct measurement of reactive oxygen species and fluorescent microscopic observation using fluorescent dye 2',7'-dichlorofluorescin diacetate, reactive oxygen species were found to be generated without cell death, where cells are treated with 0.1 ppm arsenic for 24 hours. With the induction of reactive oxygen species, GSH level was decreased by the same treatment. However, DNA damage did not seem to be serious by DAPI staining, while high dose of arsenic (2 ppm for 24 hrs) caused fragmentation of DNA. To identify the molecular biomarkers of low-dose arsenic exposure, gene expression was also investigated with whole genome microarray. As results, 9,022 genes were up-regulated including heme oxygenase-l and glutathione S-transrerase, which are well-known biomarkers of oxidative stress. 9,404 genes were down-regulated including endothelial type gp 91-phox gene by the treatment of 0.1 ppm arsenic for 24 hours. This means that biological responses of cardiomyocytes may be altered by ROS induced by low level arsenic without cell death, and this alteration may be detected clearly by molecular biomarkers such as heme oxygenase-1.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2018.04a
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• pp.68-68
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• 2018

In this study, we investigated whether S. baicalensis rhizome ethanol extract (SBRE) has antioxidant capacities against oxidative stress induced cellular damage in the HaCaT keratinocytes. Our results revealed that treatment with SBRE prior to hydrogen peroxide ($H_2O_2$) exposure significantly increased the HaCaT cell viability. SBRE also effectively attenuated $H_2O_2$ induced comet tail formation, and inhibited the $H_2O_2$ induced phosphorylation levels of the histone ${\gamma}H2AX$, as well as the number of apoptotic bodies and Annexin V positive cells. In addition, SBRE exhibited scavenging activity against intracellular ROS generation and restored the mitochondria membrane potential loss induced by $H_2O_2$. Moreover, $H_2O_2$ enhanced the cleavage of caspase-3 and degradation of poly (ADP-ribose)-polymerase as well as DNA fragmentation; however, these events were almost totally reversed by pretreatment with SBRE. Furthermore, SBRE increased the levels of HO-1 associated with the induction of Nrf2. Therefore, we believed that SBRE may potentially serve as an agent for the treatment and prevention of neurodegenerative diseases caused by oxidative stress.

• Archives of Pharmacal Research
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• v.23 no.5
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• pp.518-524
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• 2000

We examined the modulation of protein kinase C (PKC) subtypes during apoptosis induced by ginsenoside Rh2 (G-Rh2) in human neuroblastoma SK-N-Bl(2) and rat glioma C6Bu-1 cells. Apoptosis induced by C-Rh2 in both cell lines was confirmed, as indicated by DNA fragmentation and in situ strand breaks, and characteristic morphological changes. During apoptosis induced by G-Rh2 in SK-N-BE(2) cells, PKC subtypes $\alpha$, $\beta$ and $\gamma$ were progressively increased with prolonged treatment, whereas PKC $\delta$ increased transiently at 3 and 6 h and PKC $\varepsilon$ was gradually down-regulated after 6 h following the treatment. On the other hand, PKC subtype $\beta$ markedly increased at 24 h when maximal apoptosis was achieved. In C6Bu-l cells, no significant changes in PKC subtypes $\alpha$, $\gamma$, $\delta$, $\varepsilon$ and $\beta$ were observed during apoptosis induced by G-Rh2. These results suggest the evidence for a possible role of PKC subtype in apoptosis induced by G-Rh2 in SK-N-BE(2) cells but not in C6Bu-1 cells, and raise the possibility that G-Rh2 may induce apoptosis via different pathways interacting with or without PKC in different cell types.

• Archives of Pharmacal Research
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• v.22 no.4
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• pp.404-409
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• 1999

The inhibitory effects of the constituents of Gastrodia elata Bl. (GE) on glutamate-induced apoptosis in human neuronal cells were investigated using IMR32 human neuroblastoma cells. Glutamate (GLU) induced DNA fragmentation, a hallmark of apoptosis, in a dose-dependent manner. GLU also induced a slow and sustained increase in intracellular $Ca^{2+}$ concentration. Treatment with EGTA, an extracellular $Ca^{2+}$ chelator, in a nominal $Ca^{2+}$ -free buffer solution abolished the GLU-induced intracellular $Ca^{2+}$ increase, indicating that GLU stimulated Ca2+ influx pathway in the IMR32 cells. BAPTA, an intracellualr $Ca^{2+}$ chelator, significantly inhibited the GLU-induced apoptosis assessed by the flow cytometry measuring hypodiploid DNA content indicative of apoptosis, implying that intracellular $Ca^{2+}$ rise may mediate the apoptotic action of GLU. Vanillin (VAN) and p-hydroxybenzaldehyde(p-HB), known constituents of GE, significantly inhibited both intracellular $Ca^{2+}$ rise and apoptosis induced by GLU. These results suggest that the apoptosis-inhibitory actions of the constituents of GE may account, at least in part, for the basis of their antiepileptic activities. These results further suggest that intracelluarl $Ca^{2+}$ signaling pathway may be a molecular target of the constituents of GE.