• 제목/요약/키워드: Reporter

검색결과 935건 처리시간 0.035초

경호무도 구성원리의 미학적 탐색 (A Study of Aesthetical Value of Composition Principle on Security Guard Martial Arts)

  • 김평수;임대용;손진
    • 시큐리티연구
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    • 제25호
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    • pp.131-146
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    • 2010
  • 본 연구의 목적은 그간 사회의 요구로 인하여 발전을 거듭하고 있는 경호 경비학의 전공과목으로서 무도의 역사와 함께하는 경호무도의 학문적 체계 정립이 부족함을 인식하고 경호무도의 철학적 가치 연구를 위하여 그 한 방법으로 경호무도 구성원리 내에서 발견될 수 있는 미학적 가치를 탐색해보고자 하였다. 본 연구의 목적을 달성하기 위해 경호무도관련 학위논문 및 무도와 미학 관련 문헌을 광범위하게 조사였으며 이를 바탕으로 미학의 개념과 무도에서의 미학을 살피고 이를 토대로 경호무도 수련자의 반복 수련을 통한 기술습득과 경호원의 실제현장에서의 기술구사능력이 미학적 구성요소에 대한 체험을 가능하게 하고 심미적 감흥을 획득할 수 있음을 확인하였다. 궁극적으로 경호무도는 상대성 반복성 정신수양 신체일치성 힘의 방향 충격의 강화 및 완화 힘의 극대화 중심자세와 타격점 호흡조절 및 정신집중 등 그 구성원리를 따라 완성되어가는 기술연마 과정 속의 심미적 요소들로 인하여 미학적 가치를 구현할 수 있다고 여겨진다.

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토끼에서 D-luciferin의 관절강 주입에 의한 연골세포의 자연발광 영상 (Bioluminescence Imaging of Chondrocytes in Rabbits by Intraarticular Injection of D-Luciferin)

  • 문성민;민정준;오석중;강한샘;김영호;김성미;김광윤;범희승
    • Nuclear Medicine and Molecular Imaging
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    • 제41권1호
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    • pp.54-58
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    • 2007
  • 목적: Firefly luciferase (이하 Fluc)는 분자영상 분야에 가장 널리 쓰이는 리포터 유전자 중 하나이다. 발광반응의 기질로 사용되는 D-luciferin 은 가격이 비싸고 실험동물의 무게에 비례해서 기질을 주입 하므로 마우스나 렛트와 같은 소동물을 대상으로 전임상 연구가 이루어지고 있다. 본 실험실에서는 중동물인 토끼의 관절강에 D-luciferin을 국소 주입하여 발광영상을 획득하였다. 대상 및 방법: 연골세포를 일주일 동안 배양한 후 Fluc 아데노바이러스에 감염시켰다. 감염된 연골세포를 토끼의 관절강에 주입 또는 이식하였다. 착상된 무릎의 관절강부위에 D-luciferin을 국소 주입한 후 본 실험실서 보유하고 있는 CCD 카메라가 장착된 실시간 영상장비를 이용하여 날짜 별로 분자영상을 획득하였다. 결과: 착상되어진 토끼의 관절강 부위에 기질을 국소주입하여 영상을 성공적으로 획득하였다. 연골세포 주입 및 이식 후 1일째부터 토끼의 관절강에서 빛이 방출되었으며 토끼의 관절강에 주입하는 것보다 이식하는 방법이 강한 빛을 방출함을 알 수 있었다. 또한 7일째까지 토끼의 관절강에 연골세포를 이식한 것이 주입한 것보다 총 광량이 5배에서 10배까지 강하게 나타남을 확인하였고 9일째에는 약 10배정도 강하게 나타났다. 결론: 중동물인 토끼를 이용하여 Fluc을 발현하는 연골세포를 주입 또는 이식한 관절강에 D-luciferin을 국소 주입하여 영상을 성공적으로 획득하였으며, 이러한 결과를 통해 중동물에 소량의 D-luciferin 국소주입하여도 발광영상을 얻는데 충분함을 알 수 있었다.

한국 고유의 품종을 이용한 제초제 저항성 유채 개발 (Development of herbicide-tolerant Korean rapeseed (Brassica napus L.) cultivars)

  • 김효진;이혜진;고영삼;노경희;이영화;장영석;서미정
    • Journal of Plant Biotechnology
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    • 제37권3호
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    • pp.319-326
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    • 2010
  • 화석에너지의 고갈과 지구 온난화 현상으로 인해 재생 가능한 식물자원으로부터 바이오에너지를 얻고자 하는 관심이 높아지고 있다. 이에 바이오디젤의 원료로 사용 되기 적합한 형질전환이 된 유채를 개발하기 위한 첫 단계로 한국 고유 유채 품종을 이용한 형질전환 체계를 구축하였다. 내한, 영산, 탐미, 한라 유채의 종자를 분양 받아 지방산 분석을 실시한 결과, 종자의 약 32-40% 식물성 오일이 포함되어 있었고, 그 중 올레인산의 함량은 60mole% 이상 존재하는 것으로 확인되었다. 그 중 오일 함량 및 올레인산 함량이 높고, 형질전환 효율이 비교적 높은 한라 유채품종이 그리고 $\beta$-glucuronidase (GUS)와 phosphinothricin acetyltransferase (PAT) 유전자가 포함된 pCAM-BIA3301 벡터가 도입된 Agrobacterium tumefaciens GV3101균주가 형질전환에 사용되었다. 형질전환이 된 유채 식물체는 제초제에 대한 내성, PCR을 이용한 PAT 유전자의 도입 여부 및 GUS 활성 분석을 통하여 선별하였다. 그 결과 한라 유채의 경우, 10. 4% 형질전환 효율을 보였고, 제초제 저항성이 다음 세대 ($T_1$ 식물체)로 안정되게 유전됨을 확인하였다. 이러한 연구는 바이오디젤 원료로 사용될 다양한 유채 품종에 교배를 통해 제초제 저항성 유전자를 쉽게 도입할 수 있는 가능성을 제시하였다.

조협의 부위에 따른 항산화 전사인자 Nrf2 활성 효과 (Identification of the Plant Part of Gleditsia sinensis that Activates Nrf2, an Anti-oxidative Transcription Factor)

  • 최지연;김균하;최준용;한창우;하기태;정한솔;주명수
    • 동의생리병리학회지
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    • 제28권3호
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    • pp.303-309
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    • 2014
  • The fruit of Gleditsia sinensis has been extensively used as a key ingredient of an herbal remedy for the treatment of various inflammatory diseases in traditional Korean Medicine. However, the reason of using the fruit of G. sinensis for the remedy is unclear. Since Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a key anti-inflammatory transcription factor, which is activated by the fruit of G. sinesis, we examined whether other plant parts of G. sinensis are also capable of suppressing inflammatory responses by activating Nrf2. Water extracts of various parts of G. sinensis were prepared and tested for Nrf2 activation by reporter assay and western blot analysis. Our results show that the hull of G. sinensis is the most potent in activating Nrf2. Sequential organic solvent extraction of the hull show that all the fractions had a higher potency in activating Nrf2 than the water extract, albeit differential degrees. The hull originated from Korea in general activated Nrf2 strongly compared to that of China. Chloroform fraction of the hull was further examined, showing that the fraction induced nuclear localization of Nrf2, indicative of activated Nrf2, and Nrf2-dependent gene expression including NAD(P)H dehydrogenase quinone 1 (NQO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and heme oxygenase - 1 (HO-1). Therefore, our results show that, among other plant parts examined in this study, the hull of G. sinensis is the most potent, providing the experimental basis for the use of the hull of G. sinensis as an active ingredient for an anti-inflammatory remedy.

Regulation of Vacuolar $H^+-ATPase$ c Gene Expression by Oxidative Stress

  • Kwak, Whan-Jong;Kim, Seong-Mook;Kim, Min-Sung;Kang, Jung-Hoon;Kim, Dong-Jin;Kim, Ho-Shik;Kown, Oh-Joo;Kim, In-Kyung;Jeong, Seong-Whan
    • The Korean Journal of Physiology and Pharmacology
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    • 제9권5호
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    • pp.275-282
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    • 2005
  • By using differential display, we identified one of the genes encoding the multi-subunit complex protein V-ATPase, c subunit gene (ATP6L), and showed alterations of the gene expression by oxidative stresses. Expression of the ATP6L gene in Neuro-2A cells was increased by the treatment with $H_2O_2$ and incubation in hypoxic chamber, implying that the expression of the ATP6L gene is regulated by oxidative stresses. To examine mechanisms involved in the regulation of the gene expression by oxidative stresses, the transcriptional activity of the rat ATP6L promoter was studied. Transcription initiation site was determined by primer extension analysis and DNA sequencing, and promoter of the rat ATP6L and its deletion clones were constructed in reporter assay vector. Significant changes of the promoter activities in Neuro-2A cells were observed in two regions within the proximal 1 kbp promoter, and one containing a suppressor was in -195 to -220, which contains GC box that is activated by binding of Sp1 protein. The suppression of promoter activity was lost in mutants of the GC box. We confirmed by electrophoretic mobility shift and supershift assays that Sp1 protein specifically binds to the GC box. The promoter activity was not changed by the $H_2O_2$ treatment and incubation in hypoxic chamber, however, $H_2O_2$ increased the stability of ATP6L mRNA. These data suggest that the expression of the ATP6L gene by oxidative stresses is regulated at posttranscriptional level, whereas the GC box is important in basal activities of the promoter.

Expression characterization and transcription regulation analysis of porcine Yip1 domain family member 3 gene

  • Ni, Dongjiao;Huang, Xiang;Wang, Zhibo;Deng, Lin;Zeng, Li;Zhang, Yiwei;Lu, Dongdong;Zou, Xinhua
    • Asian-Australasian Journal of Animal Sciences
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    • 제33권3호
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    • pp.398-407
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    • 2020
  • Objective: The Yip1 domain family (YIPF) proteins were proposed to function in endoplasmic reticulum (ER) to Golgi transport and maintenance of the morphology of the Golgi, which were homologues of yeast Yip1p and Yif1p. YIPF3, the member 3 of YIPF family was a homolog of Yif1p. The aim of present study was to investigate the expression and regulation mechanism of porcine YIPF3. Methods: Quantitative realtime polymerase chain reaction (qPCR) was used to analyze porcine YIPF3 mRNA expression pattern in different tissues and pig kidney epithelial (PK15) cells stimulated by polyinosine-polycytidylic acid (poly [I:C]). Site-directed mutations combined with dual luciferase reporter assays and electrophoretic mobility shift assay (EMSA) were employed to reveal transcription regulation mechanism of porcine YIPF3. Results: Results showed that the mRNA of porcine YIPF3 (pYIPF3) was widely expressed with the highest levels in lymph and lung followed by spleen and liver, while weak in heart and skeletal muscle. Subcellular localization results indicated that it expressed in Golgi apparatus and plasma membranes. Upon stimulation with poly (I:C), the level of this gene was dramatically up-regulated in a time- and concentration-dependent manner. pYIPF3 core promoter region harbored three cis-acting elements which were bound by ETS proto-oncogene 2 (ETS2), zinc finger and BTB domain containing 4 (ZBTB4), and zinc finger and BTB domain containing 14 (ZBTB14), respectively. In which, ETS2 and ZBTB4 both promoted pYIPF3 transcription activity while ZBTB14 inhibited it, and these three transcription factors all played important regulation roles in tumorigenesis and apoptosis. Conclusion: The pYIPF3 mRNA expression was regulated by ETS2, ZBTB4, and ZBTB14, and its higher expression in immune organs might contribute to enhancing ER to Golgi transport of proteins, thus adapting to the immune response.

Polymorphisms and Functional Analysis of the Intact Human Papillomavirus16 E2 Gene

  • Ekalaksananan, Tipaya;Jungpol, Watcharapol;Prasitthimay, Chuthamas;Wongjampa, Weerayut;Kongyingyoes, Bunkerd;Pientong, Chamsai
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권23호
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    • pp.10255-10262
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    • 2015
  • High risk human papillomavirus (HR-HPV) E2 proteins play roles in transcriptional regulation and are commonly functionally disrupted when the HPV genome integrates into host chromosomes. Some 15-40% of cancer cases, however, contain an intact E2 gene or episomal HPV. In these cases, polymorphism of the E2 gene might be involved. This study aimed to determine polymorphisms of the E2 gene in episomal HPV16 detected in high grade squamous intraepithelial lesions and squamous cell carcinomas and altered functions compared to the E2 prototype. The E2 gene was amplified and sequenced. Two expression vectors containing E2 gene polymorphisms were constructed and transfected in SiHa and C33A cells, then E6 gene as well as Il-10 and TNF-${\alpha}$ expression was determined by quantitative RT-PCR. Expression vectors and reporter vectors containing the HPV16 long control region (LCR) were co-transfected and transcriptional activity was determined. The results showed that a total of 32 nucleotides and 23 amino acids were changed in all 20 cases of study, found in the transactivation (TA) domain, hinge (H) region and DNA binding (DB) domain with 14, 5 and 13 nucleotide positions. They mostly caused amino acid change. The expressing vectors containing different E2 gene polymorphisms showed E6 mRNA suppression, TNF-${\alpha}$ mRNA suppression and IL-10 induction but no statistically significant differences when compared to the E2 prototype. Moreover, promoter activity in HPV16 LCR was not affected by E2 protein with different gene polymorphisms, in contrast to nucleotide variations in LCR that showed an effect on transcription activity. These results demonstrated that E2 gene polymorphisms of episomal HPV16 did not affect transcriptional regulation and suggested that nucleotide variation as well as epigenetic modification of the LCR might play a role in inducing malignant transformation of cells containing episomal HPV16.

miR-340 Reverses Cisplatin Resistance of Hepatocellular Carcinoma Cell Lines by Targeting Nrf2-dependent Antioxidant Pathway

  • Shi, Liang;Chen, Zhan-Guo;Wu, Li-li;Zheng, Jian-Jian;Yang, Jian-Rong;Chen, Xiao-Fei;Chen, Zeng-Qiang;Liu, Cun-Li;Chi, Sheng-Ying;Zheng, Jia-Ying;Huang, Hai-Xia;Lin, Xiang-Yang;Zheng, Fang
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권23호
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    • pp.10439-10444
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    • 2015
  • Many chemotherapeutic agents have been successfully used to treat hepatocellular carcinoma (HCC); however, the development of chemoresistance in liver cancer cells usually results in a relapse and worsening of prognosis. It has been demonstrated that DNA methylation and histone modification play crucial roles in chemotherapy resistance. Currently, extensive research has shown that there is another potential mechanism of gene expression control, which is mediated through the function of short noncoding RNAs, especially for microRNAs (miRNAs), but little is known about their roles in cancer cell drug resistance. In present study, by taking advantage of miRNA effects on the resistance of human hepatocellular carcinoma cells line to cisplatin, it has been demonstrated that miR-340 were significantly downregulated whereas Nrf2 was upregulated in HepG2/CDDP (cisplatin) cells, compared with parental HepG2 cells. Bioinformatics analysis and luciferase assays of Nrf2-3'-untranslated region-based reporter constructor indicated that Nrf2 was the direct target gene of miR-340, miR-340 mimics suppressing Nrf2-dependent antioxidant pathway and enhancing the sensitivity of HepG2/CDDP cells to cisplatin. Interestingly, transfection with miR-340 mimics combined with miR-340 inhibitors reactivated the Nrf2 related pathway and restored the resistance of HepG2/CDDP cells to CDDP. Collectively, the results first suggested that lower expression of miR-340 is involved in the development of CDDP resistance in hepatocellular carcinoma cell line, at least partly due to regulating Nrf2-dependent antioxidant pathway.

MiRNA-15a Mediates Cell Cycle Arrest and Potentiates Apoptosis in Breast Cancer Cells by Targeting Synuclein-γ

  • Li, Ping;Xie, Xiao-Bing;Chen, Qian;Pang, Guo-Lian;Luo, Wan;Tu, Jian-Cheng;Zheng, Fang;Liu, Song-Mei;Han, Lu;Zhang, Jian-Kun;Luo, Xian-Yong;Zhou, Xin
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권16호
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    • pp.6949-6954
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    • 2014
  • Background: Recent studies have indicated that microRNA-15a (miR-15a) is dysregulated in breast cancer (BC). We aimed to evaluate the expression of miR-15a in BC tissues and corresponding para-carcinoma tissues. We also focused on effects of miR-15a on cellular behavior of MDA-MB-231 and expression of its target gene synuclein-${\gamma}$ (SNCG). Materials and Methods: The expression levels of miR-15a were analysed in BC formalin fixed paraffin embedded (FFPE) tissues by microarray and quantitative real-time PCR. CCK-8 assays, cell cycle and apoptosis assays were used to explore the potential functions of miR-15a in MDA-MB-231 human BC cells. A luciferase reporter assay confirmed direct targets. Results: Downregulation of miR-15a was detected in most primary BCs. Ectopic expression of miR-15a promoted proliferation and suppressed apoptosis in vivo. Further studies indicated that miR-15a may directly interact with the 3'-untranslated region (3'-UTR) of SNCG mRNA, downregulating its mRNA and protein expression levels. SNCG expression was negatively correlated with miR-15a expression. Conclusions: MiR-15a has a critical role in mediating cell cycle arrest and promoting cell apoptosis of BC, probably by directly targeting SNCG. Thus, it may be involved in development and progression of BC.

Mutant p53-Notch1 Signaling Axis Is Involved in Curcumin-Induced Apoptosis of Breast Cancer Cells

  • Bae, Yun-Hee;Ryu, Jong Hyo;Park, Hyun-Joo;Kim, Kwang Rok;Wee, Hee-Jun;Lee, Ok-Hee;Jang, Hye-Ock;Bae, Moon-Kyoung;Kim, Kyu-Won;Bae, Soo-Kyung
    • The Korean Journal of Physiology and Pharmacology
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    • 제17권4호
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    • pp.291-297
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    • 2013
  • Notch1 has been reported to be highly expressed in triple-negative and other subtypes of breast cancer. Mutant p53 (R280K) is overexpressed in MDA-MB-231 triple-negative human breast cancer cells. The present study aimed to determine whether the mutant p53 can be a potent transcriptional activator of the Notch1 in MDA-MB-231 cells, and explore the role of this mutant p53-Notch1 axis in curcumin-induced apoptosis. We found that curcumin treatment resulted in an induction of apoptosis in MDA-MB-231 cells, together with downregulation of Notch1 and its downstream target, Hes1. This reduction in Notch1 expression was determined to be due to the decreased activity of endogenous mutant p53. We confirmed the suppressive effect of curcumin on Notch1 transcription by performing a Notch1 promoter-driven reporter assay and identified a putative p53-binding site in the Notch1 promoter by EMSA and chromatin immunoprecipitation analysis. Overexpression of mutant p53 increased Notch1 promoter activity, whereas knockdown of mutant p53 by small interfering RNA suppressed Notch1 expression, leading to the induction of cellular apoptosis. Moreover, curcumin-induced apoptosis was further enhanced by the knockdown of Notch1 or mutant p53, but it was decreased by the overexpression of active Notch1. Taken together, our results demonstrate, for the first time, that Notch1 is a transcriptional target of mutant p53 in breast cancer cells and suggest that the targeting of mutant p53 and/or Notch1 may be combined with a chemotherapeutic strategy to improve the response of breast cancer cells to curcumin.