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A Study on the Mechanism of Immunomodulating Effects of Moxifloxacin in Oleic Acid-Induced Acute Lung Injury

  • Lee, Young-Man
    • Tuberculosis and Respiratory Diseases
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    • v.71 no.2
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    • pp.97-105
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    • 2011
  • Background: It was hypothesized that the immunomodulating effects of moxifloxacin contribute to ameliorate oleic acid (OA)-induced acute lung injury (ALI) by suppression of cytosolic phospholipase A2 (cPLA2). This was based on observations from experiments on rats associated with neutrophilic respiratory burst, cPLA2 activity, and expressions of cPLA2, $TNF{\alpha}$, and COX-II in the lung. Methods: ALI was induced by intravenous injection of OA in male Sprague-Dawley rats. Five hours after OA injection, protein content in bronchoalveolar lavage (BAL), lung myeloperoxidase (MPO) activity, and numbers of BAL neutrophils were measured. As an index of oxidative stress-induced lung injury, the content of malondialdehyde (MDA) in lung tissues was also determined. Lung histology, immunohistochemistry and determination of activity of cPLA2 in lung tissues were carried out. In addition, Western blotting of $TNF{\alpha}$ and COX-II in lung tissues was performed. Results: The accumulation of neutrophils in the lungs was observed after OA injection. BAL protein was increased along with neutrophilic infiltration and migration by OA. Moxifloxacin decreased all of these parameters of ALI and ameliorated ALI histologically. The increased malondialdehyde (MDA) in the lung by OA was also decreased by moxifloxacin. Moxifloxacin not only suppressed cPLA2 expression in the lungs and neutrophils but also decreased cPLA2 activity in lung tissues of rats given OA. The enhanced expressions of $TNF{\alpha}$ and COX-2 in the lung tissues of rats given OA were also suppressed by moxifloxacin. Conclusion: Moxifloxacin inhibited cPLA2 and down-regulated $TNF{\alpha}$ and COX-2 in the lungs of rats given OA, which resulted in the attenuation of inflammatory lung injury.

Expression of Tumor Necrosis Factor Receptor-associated Factor 6 in Lung Cancer Tissues

  • Zhang, Xiu-Ling;Dang, Yi-Wu;Li, Ping;Rong, Min-Hua;Hou, Xin-Xi;Luo, Dian-Zhong;Chen, Gang
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.24
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    • pp.10591-10596
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    • 2015
  • Background: Tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) has been reported to be associated with the development of various cancers. However, the role of TRAF6 in lung cancer remains unclear. Objective: To explore the expression and clinicopathological significance of TRAF6 protein in lung cancer tissues. Materials and Methods: Three hundred and sixty-five lung cancer samples and thirty normal lung tissues were constructed into 3 microarrays. The expression of TRAF6 protein was determined using immunohistochemistry (IHC). Furthermore, correlations between the expression of TRAF6 and clinicopathological parameters were investigated. Results: The expression of TRAF6 in total lung cancer tissues (365 cases), as well as in small cell lung cancer (SCLC, 26 cases) and non-small cell lung cancer (NSCLC, 339 cases) was significantly higher compared with that in normal lung tissues. The ROC curve showed that the area under curve of TRAF6 was 0.663 (95%CI 0.570~0.756) for lung cancer. The diagnostic sensitivity and specificity of TRAF6 were 52.6% and 80%, respectively. In addition, the expression of TRAF6 was correlated with clinical TNM stage, tumor size and lymph node metastasis in all lung cancers. Consistent correlations were also observed for NSCLCs. Conclusions: TRAF6 might be an oncogene and the expression of TRAF6 protein is related to the progression of lung cancer. Thus, TRAF6 might become a target for diagnosis and gene therapy for lung cancer patients.

Loss of Imprinting of Insulin-Like Growth Factor 2 is Associated with Increased Risk of Primary Lung Cancer in the Central China Region

  • Zhang, Ming;Wu, Cui-Huan;Zhu, Xiao-Ling;Wang, You-Jie
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.18
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    • pp.7799-7803
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    • 2014
  • Background: To determine the imprinting status of the IGF2 in Chinese patients with primary lung cancer and to analyze the clinical significance of the loss of imprinting (LOI) of IGF2. Materials and Methods: PCRRFLP and RT-PCR-RFLP were carried out to select heterozygous cases for the ApaI polymorphism within exon 9 of the IGF2 gene and further analyze IGF2 LOI in 64 lung cancer patients, respectively. Results: Of 64 lung cancer patients, 31 were heterozygous for IGF2. The positive rates of IGF2 LOI of lung cancer foci, matched paracancer tissues, and normal lung tissues were 77.4% (24/31), 61.3% (19/31), and 29.0% (9/31), respectively. The LOI differences for IGF2 among the three groups were statistically significant (${\chi}^2=15.267$, p=0.000), and the LOI frequency of IGF2 in normal lung tissue was significantly lower than that in lung cancer foci and paracancer tissues (${\chi}^2=14.577$, p=0.000; ${\chi}^2=6.513$, p=0.011). No statistical difference was observed between the lung tumor group and the matched paracancer group (${\chi}^2=1.897$, p=0.168). The prevalence of advanced clinical stages (${\chi}^2=2.379$; p=0.017) and lymph node metastasis (${\chi}^2=5.552$; p=0.018) was significantly higher for LOI-positive paracancer tissues than for LOI-negative paracancer tissues. Conclusions: IGF2 LOI is highly frequent in Chinese primary lung cancer patients, especially those with increased risk of lymph node metastasis and advanced clinical stages. IGF2 LOI may be an early epigenetic event in human lung carcinogenesis.

Structural and Quantitative Expression Analyses of HERV Gene Family in Human Tissues

  • Ahn, Kung;Kim, Heui-Soo
    • Molecules and Cells
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    • v.28 no.2
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    • pp.99-103
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    • 2009
  • Human endogenous retroviruses (HERVs) have been implicated in the pathogenesis of several human diseases as multi-copy members in the human genome. Their gene expression profiling could provide us with important insights into the pathogenic relationship between HERVs and cancer. In this study, we have evaluated the genomic structure and quantitatively determined the expression patterns in the env gene of a variety of HERV family members located on six specific loci by the RetroTector 10 program, as well as real-time RT-PCR amplification. The env gene transcripts evidenced significant differences in the human tumor/normal adjacent tissues (colon, liver, uterus, lung and testis). As compared to the adjacent normal tissues, high levels of expression were noted in testis tumor tissues for HERV-K, in liver and lung tumor tissues for HERV-R, in liver, lung, and testis tumor tissues for HERV-H, and in colon and liver tumor tissues for HERV-P. These data warrant further studies with larger groups of patients to develop biomarkers for specific human cancers.

Down-regulation of Protease-activated Receptor 4 in Lung Adenocarcinoma is Associated with a More Aggressive Phenotype

  • Jiang, Ping;Yu, Guo-Yu;Zhang, Yong;Xiang, Yang;Hua, Hai-Rong;Bian, Li;Wang, Chun-Yan;Lee, Wen-Hui;Zhang, Yun
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.6
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    • pp.3793-3798
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    • 2013
  • The role of protease-activated receptors (PARs) in lung tumors is controversial. Although PAR4 is preferentially expressed in human lung tissues, its possible significance in lung cancer has not been defined. The studies reported herein used a combination of clinical observations and molecular methods. Surgically resected lung adenocarcinomas and associated adjacent normal lung tissues were collected and BEAS-2B and NCI-H157 cell lines were grown in tissue culture. PAR4 expression was evaluated by RT-PCR, RT-qPCR, Western blotting and immunohistochemistry analysis. The results showed that PAR4 mRNA expression was generally decreased in lung adenocarcinoma tissues as compared with matched noncancerous tissues (67.7%) and was associated with poor differentiation (p=0.017) and metastasis (p=0.04). Western blotting and immunohistochemical analysis also showed that PAR4 protein levels were mostly decreased in lung adenocarcinoma tissues (61.3%), and were also associated with poor differentiation (p=0.035) and clinical stage (p=0.027). Moreover, PAR4 expression was decreased in NCI-H157 cells as compared with BEAS-2B cells. In conclusion, PAR4 expression is significantly decreased in lung adenocarcinoma, and down-regulation of PAR4 is associated with a more clinically aggressive phenotype. PAR4 may acts as a tumor suppressor in lung adenocarcinoma.

A study on the isozyme alterations of lactic dehydrogenase in the tissues of albino rat by the exposure in sulfur dioxide (아황산가스에 노출된 백서조직 lactic dehydrogenase의 isozyme변화에 관한 연구)

  • 권숙표
    • YAKHAK HOEJI
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    • v.13 no.4
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    • pp.101-110
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    • 1969
  • The isozyme alteration of lactic dehydrogenase in the tissues of albino rat inhaled SO$_{2}$ were studied in vivo and in vitro, with the following results: (1) The H-type of LDH activity relatively dominated in the normal brain, heart and kidney tissues of rat, M-type in the normal lung, liver, and muscle tissues of the animal. (2) When rats inhale SO$_{2}$ in the concentration of 250 ppm, it appears that the M-type tends to predominate in the anaerobic tissues such as liver, kidney and muscle tissues and the H-type in the aerobic tissues such as brain and heart tissues. (3) When 5% SO$_{2}$ is introduced into tissue homogenates, LDH activities in the heart, lung, liver and muscle tissues are increased more than that of introducing room-air only. With sam treatment, LDH activity is decreased in the kidney tissue and no alteration is observed in the brain tissue. (4) Although, after the aeration of SO$_{2}$, the oxygen tension seems to bring decreases in the level of LDH activity in the anerobic tissues such as liver and muscle tissues, while, on the other hand, increases in the level of the activity in the aerobic tissues, such as the brain, heart and lung tissues. (5) Accordinglly, SO$_{2}$ affects LDH activities, its isozyme pattern of each organs, and their metabolic pathway by its absorption of the gas.

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Evaluation of different media for ex vivo porcine lung culture model

  • Yang, Myeon-Sik;Zhou, Zixiong;Khatun, Amina;Nazki, Salik;Jeong, Chang Gi;Kim, Won Il;Lee, Sang Myeong;Kang, Seog-Jin;Lim, Chae Woong;Kim, Bumseok
    • Korean Journal of Veterinary Service
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    • v.41 no.4
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    • pp.263-269
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    • 2018
  • Developing drugs targeting respiratory pathogen is essential to control respiratory diseases. Many experiments have been performed under in vivo situation. However, in vivo experiments have economical and ethical issues. The objective of this study was to determine the possibility of developing an ex vivo lung culture system with possible application for respiratory infection studies. After isolating lungs from naïve pigs, agarose-inflated lung tissues were prepared and sliced manually. These sliced lung tissues were then subsequently placed on 24-well plates. Eight different combinations of media were used to determine the optimum ex vivo lung culture condition. In addition, lung tissues were infected with porcine reproductive and respiratory syndrome (PRRS) virus at a titer of $1{\times}10^4\;TCID_{50}/mL$. Virus growth was confirmed by titration in MARC-145 cells at 2, 4, 6 days post infection (dpi). We found that ex vivo lung culture in physiological environment was not media specific based on histopathology and cytotoxicity. However, under virus-infected condition, thickened alveolar walls in the lung tissues and stable virus titers at 2, 4, 6 dpi were shown in F12K medium suggesting that it was useful for tissue maintenance and virus infection using PRRS virus infected lung tissues. The present study shows the possibility of using porcine ex vivo lung model for respiratory infection studies.

MCPH1 Protein Expression in Normal and Neoplastic Lung Tissues

  • Zhang, Ji;Wu, Xiao-Bin;Fan, Jian-Jun;Mai, Li;Cai, Wei;Li, Dan;Yuan, Cheng-Fu;Bu, You-Quan;Song, Fang-Zhou
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.12
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    • pp.7295-7300
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    • 2013
  • Lung cancer is the most common cause of cancer-related death in the world. The main types are small-cell lung carcinoma (SCLC) and non-small-cell lung carcinoma (NSCLC), the latter including squamous cell carcinoma (SCC), adenocarcinoma and large cell carcinoma. NSCLCs account for about 80% of all lung cancer cases. Microcephalin (MCPH1), also called BRIT1 (BRCT-repeat inhibitor of hTERT expression), plays an important role in the maintenance of genomic stability. Recently, several studies have provided evidence that the expression of MCPH1 gene is decreased in several different types of human cancers. We evaluated the expression of protein MCPH1 in 188 lung cancer and 20 normal lung tissues by immunohistochemistry. Positive MCPH1 staining was found in all normal lung samples and only some cancerous tissues. MCPH1-positive cells were significantly lower in lung carcinoma compared with normal tissues. Furthermore, we firstly found that MCPH1 expression in lung adenocarcinoma is higher than its expression in squamous cell carcinoma. Change in MCPH1 protein expression may be associated with lung tumorigenesis and may be a useful biomarker for identification of pathological types of lung cancer.

Adverse Effects of Kerosene Cleaning on the Formation of DNA Adducts in Skin and Lung of Mice Dermally Exposed to Used Gasoline Engine Oil (피부에 폭로된 폐가솔린엔진오일의 표적장기 DNA adducts형성과 케로신의 세척효과에 관한 연구)

  • Lee, Jin Heon;Talaska, Glenn
    • Journal of Korean Society of Occupational and Environmental Hygiene
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    • v.8 no.2
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    • pp.289-295
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    • 1998
  • Used gasoline engine oils(UGEO) are carcinogenic in long term studies and capable of increasing the number of carcinogen-DNA adducts in short term studies when dermally applied to mice. The carcinogenic risk of UGEO has been attributed to the concentration of polycyclic aromatic hydrocarbons(PAH) which accumulate in the lubricating system during the combustion of gasoline. When dermally exposed to UGEO, the use of hand cleanser was commonly recommended for removing it. But generally workers who dermally exposed oils, use kerosene as cleaner which make skin trouble. During this study, female mice aged 4-6 weeks were utilized to evaluate the efficiency of kerosene, as solvent-based cleanser, following dermal exposure to UGEO. DNA adduct were detected at skin and lung tissues by using the $^{32}P$-postlabeling method. Washing with cleansers were done at two different interval times following dermal application of UGEO. The total DNA adducts in skin and lung tissues were statistically significantly increased in positive control groups, and of which the total adduct level in skin tissues was statistically significant higher than those in lung tissues(p=0.005). When washing kerosene, the DNA adduct level in skin tissues was statistically significantly decreased(p=0.0001). But DNA adducts in lung tissue was statistically increased(p=0.0039), and that washed at 8hr post exposure was more severly increase(p<0.05). The slope of regression between DNA adducts of lung between skin tissues was 1.0802. In conclusion, skin cleaning with kerosene facilitates passage of carcinogens to the lungs of animals dermally treated with used gasoline engine oils(UGEO).

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Trace Element Analysis by Neutron Activastion Analysis in the Human Cancer Tissue (폐암조직에서 중성자 방사화 분석법을 이용한 미량 원소 분석)

  • Lim, Sang-Moo;Zo, Jae-Il;Shim, Young-Mog;Chung, Young-Ju;Cho, Seung-Yeon;Chung, Yong-Sam
    • The Korean Journal of Nuclear Medicine
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    • v.27 no.1
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    • pp.104-111
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    • 1993
  • Trace elements are important components in the biological system, as a structural material and metabolic controller. Neutron activation analysis (NAA) with high neutron flux and high energy resolution Ge (Li) detector coupled to multichannel analyzer (MCA) has been one of the most accurate method for the determination of ultra-trace level components, and is applicable to biological material. In human body, the NAA can be used for quantitation of trace elements in various organs and tissue with endocrinological and metabolic disease and industrial metal poisoning. In this study, Triga Mark III nuclear reactor in Korea Atomic Research Institute was used for quantitation of trace eleement in human lung cancer tissues by neutron activation analysis. In the squamous cell carcinoma tissues, Br, Hg, La, Sb, Sc, Cl, Fe and I content were lower than normal lung tissues, and K, Rb and Se content were higher. In the adenocarcinoma tissues, Fe, Au, La, Sc and Zn content were lower than normal lung tissues, and Rb, Co and Se content were higher. Rb content was higher in the adenocarcinoma tissues than in the squamous cell carcinoma tissues. Fe and Na content were higher in the squamous cell carcinoma tissues than in the adenocarcinoma tissues.

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