• Tuberculosis and Respiratory Diseases
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• v.40 no.6
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• pp.653-658
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• 1993

Background: Recent advancement of molecular genetics has revealed that malignant transformation of a cell may be a complex multistep process and this process is grouped, in general, into two distinct categories, activation of protooncogenes and inactivation of tumor suppressor genes. This study was focused on the mutation of p53 tumor suppressor gene, because p53 gene mutation is now generally accepted to be one of the most frequent genetic changes in a variety of human cancers. Although lung cancer is one of the common cancers in Korea, the genetic change in the carcinogenesis process is not yet known clearly. To investigate the role of p53 gene mutation in lung cancer, we examined the mutations of exon 4-8 of the p53 gene in humna lung cancer cell lines, because most of the mutations of p53 gene have been reported to develop in exon 4-8. Method: Genomic DNA was obtained by the digestion of proteinase K and the extraction by phenol-chloroform-ethanol method from two human pulmonary adenocarcinoma cell lines, PC-9 and PC-14, and one human small cell lung cancer cell line, H69. To detect the mutations of exon 4-8 of the p53 gene, polymerase chain reaction single-strand conformation polymorphism(PCR-SSCP) analysis was performed with the DNA extracted from the cells. Results: The mutation of p53 gene was present in all three cell lines tested. In PC-9, PC-14 and H69, the altered mobility was detected in exon 7, 7 and 5, respectively. Conclusion: These results suggest that p53 gene mutation plays an important role in certain steps of the carcinogenesis of human non-small cell and small cell lung cancer.

• Tuberculosis and Respiratory Diseases
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• v.56 no.3
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• pp.261-268
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• 2004

Background : The resurgence of tuberculosis and outbreaks of multidrug resistant (MDR) tuberculosis have increased the emphasis for the development of new susceptibility testing of the Mycobacterium tuberculosis for the effective treatment and control of the disease. Conventional drug susceptibility testings, such as those using egg-based or agar-based media have some limits, such as the time required and difficulties in determining critical inhibitory concentrations, but these are still being used in many diagnostic laboratories because of no better lternatives, considering cost and accuracy. To overcome these limits, a rapid and simple method for new susceptibility testing, using live and dead assays, was applied for a bacterial cell viability assay to distinguish dead from live bacterial cells based on two-color fluorescence. Materials and Methods Strains : Forty strains were used in this study, 20 susceptible to all antituberculosis drugs and the other 20 resistant to the four first line antituberculosis drugs isoniazid, rifampicin, streptomycin and ethambutol. Antibiotics : The four antibiotics were dissolved in 7H9 broth to make the following solutions: $0.1{\mu}g\;isoniazid(INH)/m{\ell}$, $0.4{\mu}g\;rifampicin(RMP)/m{\ell}$, $4.0{\mu}g\;streptomycin(SM)/m{\ell}$ and $4.0{\mu}g\;ethambutol(EMB)/m{\ell}$. Results : Live and dead Mycobacterium tuberculosis cells fluoresced green and red with the acridin (Syto 9) and propidium treatments, respectively. These results are very well accorded with conventional drug susceptibility testing by proportional method on Lowensen-Jensen media (L-J) containing 4 drugs (INH, RMP, EMB and SM), showing a 93.7 % accordance rate in susceptible strains and 95% in resistant strains. Conclusion : The results of the drug susceptibility testing using the live and dead bacterial cell assay showed high accordance rates compared with the conventional proportion method on L-J. This finding suggests that the live and dead bacterial cell assay can be used as an alternative to conventional drug susceptibility testing for M. tuberculosis strains.

• Journal of Korean Theatre Studies Association
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• no.52
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• pp.319-357
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• 2014

Formation of 'body schema' is the start for actor to create role and becomes the root and the foundation of existing as a role on the stage. For this, an actor needs to form 'scheme of role' with escaping from own 'body schema.' 'Schema of role' is formed by acquiring through synthesizing daily basic actions, namely, walking, standing, sitting, hand stretching, bending, and touching. The body schema, which was made with simple and usual actions, has fundamental significance in a sense of becoming the body in which the past traces in a role are habituated while energy as a role flows. As for the process of forming body schema, an actor first needs to obtain the visualized materials like photo, magazine, picture and image available for seeing a role specifically and clearly based on what analyzed a character. An actor needs to have three-dimensional image available for always recalling it in the head during acting. To do this, image data available for fundamentally capturing routine actions along with body structure are still more useful. Next, the body schema is formed by interaction with environment. Thus, there is a need of passing through the two-time process of forming body schema. Firstly, the body schema is made on routine actions in a role as physical condition of a role in actor's own everyday life. Secondly, the body schema is made on routine actions available for moving efficiently and economically in line with the environment of performance. A theatrical stage is the temporal space of rhythm and rule different from routine space. What forms body schema immediately in the second phase without body schema in the first phase ultimately becomes what exists as actor's own body, not the body of a role. The body schema, which was formed as the second process, is what truly has identity as a role in the ontological aspect, comes to experience the oppositional force in muscle, a qualitative change in energy, and emotional agitation in the physical aspect, and experiences perception, thinking, volition, and even consciousness with the entire body in the cognitive dimension. Thus, the formation of body schema can be known to be just a method of changing even spiritual and emotional layer. Body schema cannot be made if there is no process of embodiment and habit. Embodiment and habit are not simply the repeated, empty and mechanical action in the body. But, habit itself has very important meanings for forming body schema for role creating. First, habit allows the body itself to learn and understand a meaning. Second, habit relies upon environment, thereby allowing an actor of making the habituated body schema to recognize environment. Third, habit makes the mind. The habituated body schema is just the mind and the ego of a person who possesses the body schema. Fourth, habit comes to experience the expansion in energy and the expansion in existence. It may be experienced through interrelation among actor's body, tool, and environment. Fifth, habit makes identity of the body. Hence, this just becomes what secures identity of a role. These implications of habit are the formation of body schema, which is maintained with the body of being remembered firmly through being closely connected with the process of neural adaptation. Finally, it sought for possibility of practice as one method of forming body schema for role creating through Deleuze's '-becoming' theory. As 'actual animal-becoming' is real '-becoming' of forming structural transformation in the physical dimension, it meets with what the formation of body schema pursues actuality and reality. This was explained with a concept as saying of 'all '-becoming' molecular' by Deleuze/Guattari. 'Animal of having imitated animal's characteristic- becoming' is formed by which the body schema relies upon environment. In this way, relationship among the body, tool and environment has influence even upon a change in consciousness, thinking, and emotion, thereby being able to be useful for forming body schema in a sense of possibly experiencing ultimately expansion in role, namely, expansion in existence.

• Journal of Life Science
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• v.29 no.6
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• pp.679-687
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• 2019

Litsea populifolia, a plant species of the Lauraceae family, is widely distributed in the tropical and subtropical areas of Asia. The phylogenetic relationships and botanical characteristics of L. populifolia have been reported; however, its anti-oxidative and anti-cancer activities remain unclear. In this study, we evaluated the anti-oxidative and anti-cancer effects of ethanol extracts of L. populifolia (EELP) together with the molecular mechanism of its anti-cancer activity in human lung adenocarcinoma A549 cells. EELP showed significant anti-oxidative effects with a 50% inhibitory concentration at $11.71{\mu}g/ml$, which was measured by the 2,2-diphenyl-1-picrylhydrazyl radical scavenging assay. EELP exhibited cytotoxic activity and induced cell cycle arrest at the G1 phase in A549 cells in a dose-dependent manner, whereas EELP did not have the cytotoxic effect on the normal human lung cell line IMR90. Treatment with EELP also resulted in a decreased expression of G1/S transition-related molecules-including cyclin-dependent kinase (CDK) 2, CDK6, cyclin D1, and cyclin E-both for the transcription and translation levels. EELP-induced G1 arrest was associated with the phosphorylation of checkpoint kinase 2 (CHK2), p53, cell division cycle 25 homolog A (CDC25A), and the reduction of CDC25A expression in A549 cells. Collectively, these results suggest that EELP may exert an anti-cancer effect by cell cycle arrest at the G1 phase through both p53-dependent and p53-independent (ATM/CHK2/CDC25A/CDK2) pathways in A549 cells.

• Korean Journal of Clinical Laboratory Science
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• v.51 no.1
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• pp.71-77
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• 2019

Menadione is known as an anti-tumor factor. Many studies have reported the potential anti-cancer role of menadione against a range of cancer cell lines. In this study, the anti-cancer effects of menadione and the underlying molecular signaling involved in apoptosis was investigated in gastric cancer cell lines. The menadione treatment decreased the cell viability of MKN45 gastric cancer cells. The decreased cell viability was attributed to the induction of apoptosis, which was confirmed by the results indicating the activation of caspase-3 and -7 and the cleavage of PARP in Western blotting. The upstream regulatory molecules involved in apoptosis were investigated further and it was discovered that menadione reduced the expression of survivin, an inhibitor of upstream apoptosis proteins. In addition, a transcription factor ${\beta}$-catenin, which is known to regulate survivin expression, was down-regulated by menadione. A previous report showed that menadione inhibited XIAP expression to induce apoptosis and induced G2/M cell cycle arrest in AGS cells. This study elucidated another inhibitory mechanism of menadione against gastric cancer cells in a different cell line. Although further studies will be needed, the inhibitory mechanism demonstrated in this study will help better understand the anti-cancer effects of menadione.

• The Sea:JOURNAL OF THE KOREAN SOCIETY OF OCEANOGRAPHY
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• v.26 no.1
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• pp.37-48
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• 2021

A new high speed rotation type-passive sampling device (HSR-PSD), which can rotate seawater at high speed and absorb easily and quickly the freely dissolved hydrophobic organic contaminants from seawater, was developed and then applied around the Korean Peninsula. Freely dissolved concentrations (Cfree) of polycyclic aromatic hydrocarbons (PAHs) were determined using the HSR-PSD with low density polyethylene (LDPE) sheets as a passive sampler. Furthermore, dissolved concentrations (Cdissolved) of PAHs in seawater were also obtained from high volume water sampling as a conventional method to account for actual bioavailability. When the LDPE sheets were rotated in the HSR-PSD at 900 rpm, PAHs with log KOW 3.4 ~ 5.2 were equilibrated between the LDPE and water in 5 hours. Although the high molecular weight PAHs with log KOW 5.6 ~ 6.8 was expected to be 2 to 30 days to reach the equilibrium, the Cfree of the PAHs at equilibrium could be corrected using performance reference compounds in 5 hours. Meanwhile, the total Cfree of PAHs were from 0.32 to 1.2 ng/L, which were higher than reported values in other oceans, but lower than in coastal water such as estuary, harbor, or shore. A bioavailability from the detected PAHs was highest at the sampling line near the dumping site of the Yellow Sea. Predicted residual concentrations in biota were relatively higher in offshore including the dumping site than in coastal regions.

• Molecules and Cells
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• v.45 no.12
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• pp.896-910
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• 2022

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible and potentially fatal virus. So far, most comprehensive analyses encompassing clinical and transcriptional manifestation have concentrated on the lungs. Here, we confirmed evident signs of viral infection in the lungs and spleen of SARS-CoV-2-infected K18-hACE2 mice, which replicate the phenotype and infection symptoms in hospitalized humans. Seven days post viral detection in organs, infected mice showed decreased vital signs, leading to death. Bronchopneumonia due to infiltration of leukocytes in the lungs and reduction in the spleen lymphocyte region were observed. Transcriptome profiling implicated the meticulous regulation of distress and recovery from cytokine-mediated immunity by distinct immune cell types in a time-dependent manner. In lungs, the chemokine-driven response to viral invasion was highly elevated at 2 days post infection (dpi). In late infection, diseased lungs, post the innate immune process, showed recovery signs. The spleen established an even more immediate line of defense than the lungs, and the cytokine expression profile dropped at 7 dpi. At 5 dpi, spleen samples diverged into two distinct groups with different transcriptome profile and pathophysiology. Inhibition of consecutive host cell viral entry and massive immunoglobulin production and proteolysis inhibition seemed that one group endeavored to survive, while the other group struggled with developmental regeneration against consistent viral intrusion through the replication cycle. Our results may contribute to improved understanding of the longitudinal response to viral infection and development of potential therapeutics for hospitalized patients affected by SARS-CoV-2.

• Journal of the Korean Applied Science and Technology
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• v.40 no.2
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• pp.223-232
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• 2023

Oxidative stress plays a significant role in the pathogenesis of various skin conditions, resulting in cellular and tissue damage that can contribute to the development of skin tone unevenness, roughness and wrinkles. In this study, we found that Trifolium pratense L. extract (TE) attenuated oxidative-induced damage in HaCaT cells and elucidated the underlying molecular mechanism. Our finding demonstrated that TE effectively protected HaCaT cells against H₂O₂-induced cell death by inhibiting caspase-3 activation, downregulating Bax and upregulating Bcl-2, and attenuating the activation of three mitogen-activated protein kinases (MAPKs). Our results suggest that TE has remarkable cytoprotective properties against oxidative damage in HaCaT cells and could serve as a complementary or alternative approach to prevent and treat skin damage.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.861-869
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• 1998

Backgrounds: The injury of a tissue results in the infalmmation, and the imflammed tissue is replaced by the normal parenchymal cells during the process of repair. But, constitutional or repetitive damage of a tissue causes the deposition of collagen resulting in the loss of its function. These lesions are found in the lung of patients with idiopathic pulmonary fibrosis, complicated fibrosis after diffuse alveolar damage (DAD) and inorganic dust-induced lung fibrosis. The tissue from lungs of patients undergoing episodes of active and/or end-stage pulmonary fibrosis shows the accumulation of inflammatory cells, such as mononuclear cells, neutrophils, mast cells and eosinophils, and fibroblast hyperplasia. In this regard, it appears that the inflammation triggers fibroblast activation and proliferation with enhanced matrix synthesis, stimulated by inflammatory mediators such as interleukin-1 (IL-1) and/or tumor necrosis factor (TNF). It has been well known that TGF-$\beta$ enhance the proliferation of fibroblasts and the production of collagen and fibronectin, and inhibit the degradation of collagen. In this regard, It is likely that TGF-$\beta$ undergoes important roles in the pathogenesis of pulmonary fibrosis. Nevertheless, this single cytokine is not the sole regulator of the pulmonary fibrotic response. It is likely that the balance of many cytokines including TGF-$\beta$, IL-1, IL-6 and TNF-$\alpha$ regulates the pathogenesis of pulmonary fibrosis. In this study, we investigate the interaction of TGF-$\beta$, IL-1$\beta$, IL-6 and TNF-$\alpha$ and their effect on the proliferation of fibroblasts. Methods: We used a human fibroblast cell line, MRC-5 (ATCC). The culture of MRC-5 was confirmed by immunofluorecent staining. First, we determined the concentration of serum in cuture medium, in which the proliferation of MRC-5 is supressed but the survival of MRC-5 is retained. Second, we measured optical density after staining the cytokine-stimulated cells with 0.5% naphthol blue black in order to detect the effect of cytokines on the proliferation of MRC-5. Result: In the medium containing 0.5% fetal calf serum, the proliferation of MRC-5 increased by 50%, and it was maintained for 6 days. IL-1$\beta$, TNF-$\alpha$ and IL-6 induced the proliferation of MRC-5 by 45%, 160% and 120%, respectively. IL-1$\beta$ and TNF-$\alpha$ enhanced TGF-$\beta$-induced proliferation of MRC-5 by 64% and 159%, but IL-6 did not affect the TGF-$\beta$-induced proliferation. And lNF-$\alpha$-induced proliferation of MRC-5 was reduced by IL-1$\beta$ in 50%. TGF-$\beta$, TNF-$\alpha$ and both induced the proliferation of MRC-5 to 89%, 135% and 222%, respectively. Conclusions: TNF-$\alpha$, TGF-$\beta$ and IL-1$\beta$, in the order of the effectiveness, showed the induction of MRC-5 proliferation of MRC-5. TNF-$\alpha$ and IL-1$\beta$ enhance the TGF-$\beta$-induced proliferation of MRC-5, but IL-6 did not have any effect TNF-$\alpha$-induced proliferation of MRC-5 is diminished by IL-1, and TNF-$\alpha$ and TGF-$\beta$ showed a additive effect.