Asthma is a chronic inflammatory disorder of the airways, which characterized by bronchial hyperresponsiveness, reversible airflow limitation and respiratory symptoms. Internationally, the prevalence of asthma has been increased over last 3 decades. Recently, several studies of asthma have been reported with gradually increasing importance. To tesify the hypothesis that interleukin (IL)-4 and IL-10 may be an important determinant of the severity of airway inflammation, their expression was studied in mouse model of asthma. BALB/c mouse, IL-4 Knockout (KO) mouse and IL-10 KO mouse were sensitized with intraperitoneal injection of ovalbumin adsorbed to aluminum potassium sulfate, followed by challenges with intranasal ovalbumin on 3 consecutive days. The severity of pulmonary inflammation was assessed by eosinophilia in BAL fluid, number of total BAL cells, histopathological changes in lung tissues, and immunohistochemical staining against IL-4 and IL-10. In BAL fluid, the number of total cells was significantly increased in asthma induced mouse compare to the control. In asthma induced mouse, eosinophil was increased to 56% and neutrophil was 0.2%. In H &E stains, eosinophilic infiltration and epithelium hyperplasia were clearly noticed in asthma induced mouse. In immunohistochemical staining for IL-4 and IL-10, there was no positive reaction in control group. However, very strong reactions were appeared in asthma induced group. In this research, IL-4 and IL-10, which seem to play a central role in allergic asthma, KO mouse was utilized to test the causative relationship between airway inflammation and role of specific cytokine. Asthma induced IL-4 and IL-10 KO mice showed much decreased inflammatory reactions in the number of total BAL cells, in eosinophilic infiltration, and in immunohistochemical stains against diverse inflammatory proteins. These results suggest that IL-4 and IL-10 increase the asthmatic reactions in vivo mice model.
Kim, I.A.;Jin, E.J.;Cho, E.J.;Sohn, S.H.;Lee, C.Y.
Journal of Animal Science and Technology
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v.46
no.4
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pp.563-570
/
2004
The insulin-like growth factor(IGF) system, consisting of IGFs-I and -II ligands and their receptors and six IGF-binding proteins(IGFBPs), plays an important role in survival, proliferation and differentiation of a variety of cell types. Lithium is a known modulator of survival and proliferation of many cell types in vitro. The present study was undertaken to investigate the relationship between LiCI-induced changes in cell survival and growth and the expression of the IGF system components in C6 rat glioma cell line which, besides IGF-I and its receptor, is known to express IGFBP-3 as its major IGF carrier. When C6 cells were cultured for 24h in the absence or presence of 2mM or 5mM LiCl in a 10% serwn-containing medium, the viability and the number of cells were not affected by added lithium. In 72-h culture, however, C6 cells clearly exhibited a dose-dependent response to added LiCl. The cells cultured for 72h in the presence of 0, 2mM and 5mM LiCl exhibited a typical mitotic, a growth-arrested and an apoptotic appearances, respectively. Moreover, the apoptotic cells were accompanied by reduced expression of IGF-I, IGF-I receptor and IGFBP-3 as examined by semi-quantitative reverse transcription-polymerase chain reaction. Interestingly, blockade of IGFBP-3 mRNA translation by addition of 101${\mu}M$ IGFBP-3 anti-sense oligodeoxyribonucleotide in serum-free, 24-h culture resulted in a decrease in the number of cells as well as relative abundance of the target mRNA. In summary, results suggest that the cytotoxic effect of lithium in C6 cell is likely to be mediated, in part, by suppression by this agent of the expression of the IGF system components. In this regard, IGFBP-3 may play at least a 'permissive' role in normal proliferation of this cell.
Korean Journal of Agricultural and Forest Meteorology
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v.5
no.2
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pp.70-80
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2003
We report the first direct measurement of $CO_2$ flux over Kwangneung broadleaf deciduous forest, one of the tower flux sites in KoFlux network. Eddy covariance system was installed on a 30 m tower along with other meteorological instruments from June to August in 2002. Although the study site was non-ideal (with valley-like terrain), turbulence characteristics from limited wind directions (i.e., 90$\pm$45$^{\circ}$) was not significantly different from those obtained at simple, homogeneous terrains with an ideal fetch. Despite very low rate of data retrieval, preliminary results from our analysis are encouraging and worthy of further investigation. Ignoring the role of advection terms, the averaged net ecosystem exchange (NEE) of $CO_2$ ranged from -1.2 to 0.7 mg m$^{-2}$ s$^{-1}$ from June to August in 2002. The effect of weak turbulence on nocturnal NEE was examined in terms of friction velocity (u*) along with the estimation of storage term. The effect of low uf u* NEE was obvious with a threshold value of about 0.2 m s$^{-1}$ . The contribution of storage term to nocturnal NEE was insignificant; suggesting that the $CO_2$ stored within the forest canopy at night was probably removed by the drainage flow along the hilly terrain. This could be also an artifact of uncertainty in calculations of storage term based on a single-level concentration. The hyperbolic light response curves explained >80% of variation in the observed NEE, indicating that $CO_2$ exchange at the site was notably light-dependent. Such a relationship can be used effectively in filling up the missing gaps in NEE data through the season. Finally, a simple scaling analysis based on a linear flow model suggested that advection might play a significant role in NEE evaluation at this site.
Bak, Sang Myeon;Park, Soo Yeon;Hur, Gyu Young;Lee, Seung Heon;Kim, Je Hyeong;Lee, Sang Yeub;Shin, Chol;Shim, Jae Jeong;In, Kwang Ho;Kang, Kyung Ho;Yoo, Se Hwa
Tuberculosis and Respiratory Diseases
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v.54
no.1
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pp.80-90
/
2003
Background : Goblet cell hyperplasia is a critical pathological feature in hypersecretory diseases of the airways. A bacterial infection of the lung is also known to induce inflammatory responses, which can lead to the overproduction of mucus. Recently, mucin synthesis in the airways has been reported to be regulated by neutrophilic inflammation-induced epidermal growth factor receptor (EGFR) expression and activation. In addition, it was reported that migration of the activated neutrophils is dependent on the matrix metalloproteinases (MMPs), especially MMP-9. In this study, bacterial lipopolysaccharide (LPS)-induced goblet cell hyperplasia and mucus hypersecretion by EGFR cascade, resulting from the MMPs-dependent neutrophilic inflammation were investigated in the rat airways. Methods : Pathogen-free Sprague-Dawley rats were studied in vivo. Various concentrations of LPS were instilled into the trachea in $300{\mu}{\ell}$ PBS (LPS group). Sterile PBS ($300{\mu}{\ell}$) was instilled into the trachea of the control animals (control group). The airways were examined on different days after instilling LPS. For an examination of the relationship between the LPS-induced goblet cell hyperplasia and MMPs, the animals were pretreated 3 days prior to the LPS instillation and daily thereafter with the matrix metalloproteinase inhibitor (MMPI; 20 mg/Kg/day of CMT-3; Collagenex Pharmaceuticals, USA). The neutrophilic infiltration was quantified as a number in five high power fields (HPF). The alcian blue/periodic acid-Schiff (AB/PAS) stain were performed for the mucus glycoconjugates and the immunohistochemical stains were performed for MUC5AC, EGFR and MMP-9. Their expressions were quantified by an image analysis program and were expressed by the percentage of the total bronchial epithelial area. Results : The instillation of LPS induced AB/PAS and MUC5AC staining in the airway epithelium in a time- and dose-dependent manner. Treatment with the MMPI prevented the LPS-induced goblet cell hyperplasia significantly. The instillation of LPS into the trachea induced also EGFR expression in the airway epithelium. The control airway epithelium contained few leukocytes, but the intratracheal instillation of LPS resulted in a neutrophilic recruitment. A pretreatment with MMPI prevented neutrophilic recruitment, EGFR expression, and goblet cell hyperplasia in the LPS-instilled airway epithelium. Conclusion : Matrix metalloproteinase is involved in LPS-induced mucus hypersecretion, resulting from a neutrophilic inflammation and EGFR cascade. These results suggest a potential therapeutic role of MMPI in the treatment of mucus hypersecretion that were associated with a bacterial infection of the airways.
Kim, Bo-Min;Kim, Guen-Tae;Kim, Eun-Ji;Lim, Eun-Gyeong;Kim, Sang-Yong;Kim, Young-Min
Journal of Life Science
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v.26
no.8
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pp.887-894
/
2016
The extract from Artemisia annuain L.(AAE) is known as a medicinal herb that is effective against cancer. Apoptosis is the process of programmed cell death, and mitochondria are known to play a central role in cell death control. In this study, we evaluated the p53-independent apoptosis of extract of AAE through downregulation of Bcl-2 and the mitochondrial pathway in A549 (lung cancer cells). AAE may exert cancer cell apoptosis through regulating p-Akt, Cox-2, p53 and mitochondria-mediated apoptotic proteins. p-Akt/cox-2 is known to play an important role in cell proliferation and cell survival. The Bcl-2 pro-apoptotic proteins (such as Bax, Bak and Bim) mediate the permeabilization of the mitochondrial outer membrane. Treatment of AAE reduces p-Akt, p-Mdm2, cox-2 and anti-apoptotic proteins (such as Bcl-2), while tumor suppressor p53 and pro-apoptotic proteins. Activation of Bax/Bak releases cytochrome c from mitochondria to the cytosol to activate a caspase. Caspase-3 is the major effector caspase associated with apoptotic pathways. Caspase-3 generally exists in cytoplasm in the form of a pro-enzyme. In the initiation stage of apoptosis, caspase-3 is activated by proteolytic cleavage and activated caspase-3 cleaves poly (ADP-ribose) polymerase (PARP). We treated Pifithrin-α (p53 inhibitor) and Celecoxib (Cox-2 inhibitor) to learn the relationship between the signal transduction of proteins associated with apoptosis. These results suggest that AAE induces apoptosis through a p53-independent pathway in A549.
Recent studies say that informal learning is influential to students as much as formal teaming. Nowadays we can see various informal teaming inside and outside of the country. In 2004, it was the first attempt in Korea that engineer had gone to the elementary school fur activity that included scientific experiment and engineering work with students. National Academy of Engineering of Korea (NAEK) progressed activity with companies and elementary schools for students' making sense of engineer and what they are doing. To do that, NAEK had developed the network that company could support its local school's science education circumstance by engineers' visiting program. In 2004, seventeen companies including both large and small ones took part in the program called' Korea Junior Engineering Achievement (KJEA)'. In this program, engineers played the role of teacher (we call them company teacher), elementary school teachers played the role of organizing classes as a mediator. Elementary school teachers and company teachers' recognition is very important to make students' activity meaningful. The aim of this study was to give implication for informal science education activity for which engineers visit their local school. We got the result by survey and interview of company teachers and elementary school teachers. This study's result shows that almost company teachers and school teachers were in favor of purpose of this informal science education activity and satisfied with their participation. But some company teachers were not satisfied with worksheets, materials provided and relationship between school and company). Elementary school teachers and company teachers, both of them believed students' program as the key factor of success of informal science education activity. To make informal science education grow, school administrator and teacher need to have a will to utilize the activities more actively.
Journal of the Korean Institute of Landscape Architecture
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v.40
no.3
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pp.42-50
/
2012
City squares are public open spaces which are closely related to the peoples daily lives. Most squares are located in the center of the city, and they are usually used for community gatherings and they are suitable for open markets, music concerts, political rallies, and other events. City squares also play an important role as a grand public place operating in multi functions that require involvement of more people. The purpose of this study is to examine satisfaction on the spatial components, characteristics, and the user satisfaction in City Squares. The slady also analyzed the relationship between the satisfaction about spatial components, characteristics and it also shows that the user satisfaction is followed. This study sites are made in 3 grand public places in the center of Seoul including the Seoul plaza, Cheonggye Plaza, and Gwanghwarnun Square. Data were analyzed using several statistical methods such as descriptive statistics, factor analysis, ANOVA, correlation and regression. Results of the study are as follows: First, factor analysis carried out to extract the various factors of satisfaction on the sites; spatial components, usability, amenity/security, and spatial characteristics. User satisfaction concerning usability factor was higher than the satisfaction of the other factors. This result represented that the slady sites play an important role to the public open spaces in the city. Second, users showed high user satisfaction to study sites, and user satisfaction rate toward the Gwanghwarnun Square is the highest because of its facility planuing. Finally, user satisfactim was strongly correlated on the usability factor of spatial planning. Also, the significant correlations between the user satisfaction and the other factors such as spatial components, security, and spatial characteristics of spatial planning are presented. Results of this study can help guide the planning and management of the city square as a public open space based on the understanding of user perception and satisfaction.
Journal of the Korean Institute of Traditional Landscape Architecture
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v.34
no.3
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pp.98-114
/
2016
The this study aimed to expand urban heritage using Public Goods and to suggest the assemblage of urban heritage and urban spaces in order to improve landscape conservation and management scheme of urban heritage exposed to a rapidly changing urban environment. The results obtained in this study were summarized as follows: First, in order to improve understanding of the heritage in urban spaces, urban heritage were illustrated on a 1:1000 map with all the public facilities surrounding it using a cultural heritage conservation map listed on the Cultural Heritage Administration's web site, standards for changing present condition, and a topographic map. Second, the status and changes of urban heritage and surroundings were analyzed using the minutes of Historical Cultural Heritage Division Committee for 10 years from 2005 to 2014 to create a status map of urban heritage. Land uses surrounding the urban heritage were investigated the areas of conservation potential and the places that can enhance the to find out values of urban heritage. Also, a profile was created to examine the site characteristics surrounding urban heritage, and photos were taken at important heritage areas and public facilities in order to record the field. Third, analyzed were the relationship of the distance, location, function, and distribution between urban heritage and public facilities surrounding the heritage. using visual features and moving routes in order to identify their impacts on urban heritage and their functions as potential resources. In addition, the role of Public Goods in urban spaces and the plan for revitalizing surrounding areas asset were examined. Fourth, selections were made on Public Goods that have direct or indirect effects on urban heritage. The role of public asset was investigated through visual, areal, and linear elements. The results were summarized to suggest improvement landscape and management mauser on of urban heritage.
Kim, Jong-Hyeon;Kim, Jong-Suk;Yoo, Wan-Hee;Hur, Hyeon
Journal of Food Hygiene and Safety
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v.21
no.4
/
pp.213-217
/
2006
The halophilic bacterium Vibrio vulnificus is known to be a foodborne pathogen that causes septicemia in human. V. vulnificus infection is characterized by the high fatality rates and the primary attack against a person who have underlying diseases such as liver cirrhosis. However, there is no effective treatment for V. vulnificus septicemia except for classical treatments such as antibiotics. Recently, it has been known that lipoprotein (LDL) plays a major role in the protection against infection and inflammation. Consequently in this paper we analyzed the effects of LDL on V. vulnificus septicemia. We purified V. vulnificus cytolysin, a major virulent factor of V. vulnificus infection and measured inhibitory effects of mouse serum, cholesterol, and LDL on its hemolytic activity. Next experiments were performed to investigate whether LDL has a protective role against septicemia induced by V. vulnificus in mice. Intraperitoneal injection of LDL (1mg as protein) into mice 3hr before V. vulnificus $(1\times10^6\;CFU)$ injection, and V. vulnificus -induced lethality was determined. For the determination the relationship between LDL or cholesterol and prognosis, we determined serum levels of cholesterol and lipoprotein from V. vulnificus septicemia patients (n=15) who had visited the Chonbuk National University Hospital in Chonju. V. vulnificus cytolysin -induced hemolysis of mice erythrocytes was completely inhibited by serum, cholesterol, and low-density lipoprotein. V. vulnificus- induced lethality of mice injected with LDL showed only 40% compared to 100% of control. In survival groups (n=4) of V. vulnificus septicemia patients (n=15), their serum LDL and cholesterol revealed normal levels ($153.3{\pm}40.7,\;LDL;\;190.8{\pm}16.3$, Total cholesterol). However, in death groups (n=11) showed very low levels ($35.6{\pm}13.9,\;LDL;\;59.2{\pm}15.1$, Total cholesterol). Our study indicates that cholesterol and LDL are a prognosis indicator of V. vulnificus septicemia as well as an inhibitor of virulent action of V. vulnificus cytolysin. We suggested that the serum levels of cholesterol or LDL would be major index in the treatment and prevention of V. vulnificus septicemia.
Background: Cyclin-dependent kinase (CDK) inhibitors are family of molecules that regulate the cell cycle. The CDKN2, a CDK4 inhibitor, also called p16, has been implicated in human tumorigenesis. The CDKN2 inhibits the cyclin/CDK complexes which regulate the transition from G1 to S phase of cell cycle. There is a previous report that homozygous deletion of CDKN2 region on chromosome 9p21 was detected frequently in astrocytoma, glioma and osteosarcoma, less frequently in lung cancer, leukemia and ovarian cancer, but not detected in colon cancer and neuroblastoma. However, little is known about the relationship between CDKN2 and laryngeal cancer. Therefore this study was initiated to investigate the role of CDKN2 in human laryngeal squamous cell carcinoma development.1) Materials and methods: We used 5 human laryngeal carcinoma cell lines whether they have deletions or losses of CDKN2 gene expression by DNA-PCR or RT-PCR, respectively. We examined 8 fresh frozen human laryngeal cancer tissues to detect the loss of heterozygosity (LOH) of CDKN2. PCR was performed by using microsatellite markers of short arm of human chromosome 9 (D9S126, D9S144, D9S156, D9S161, D9S162, D9S166, D9S171, D9S200 and D9SIFNA). For informative cases, allelic loss was scored if the signal of one allele was significantly decreased in tumor DNA when compared to the same allele in normal DNA. Results: The CDKN2 DNA deletion was observed in 3 cell lines. The CDKN2 mRNA expression was observed in only one cell line, which was very weak. LOH was detected in 7 cases (87.5%). Conclusion: These results suggest that CDKN2 plays a role in the carcinogenesis of human laryngeal squamous cell carcinoma.
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