• 제목/요약/키워드: Interference regulation

검색결과 121건 처리시간 0.026초

345KV 송전선에 의한 CORONA 잡음 전파장해 연구 (A Study on the Radio Interference due to the Corona Noise of 345 KV Transmission Line)

  • 최기호
    • 한국통신학회논문지
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    • 제4권1호
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    • pp.32-37
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    • 1979
  • 신설된 345KV 송전선에 의해 야기되는 corona 잡음은 송전선 직하 10m 지점에서 주파수 1MHz시 相間의 간섭을 무시하면 최대 강우시 72dB, 젖은 도체는 63dB이고, 3상 전체의 corona noise 합성시는 제일 level이 큰 相이 지배적이다. 측정 결과 직각 거리 특성은 이론치와 잘 일치하고 기후 특성으로는 강우, 강설시 corona level이 제일 높았고 비온 전후로 수 시간이 경과해야 안정한 상태와 같아진다. 주파수 특성은 측정치와 보정식이 비교적 잘 일치한다. 측정된 corona 잡음으로 수신장해 정도를 나타내기 위해서는 통계적인 방법의 S/N 비 정량화가 필요하다. ITU, IEEE 위원회, 일본 NHK 등은 장시간에 걸친 시험 평가로 각각 품질등급에 따라 평가기준을 정의하고 있는데 우리나라에서도 수신품질에 대한 평가기준을 확립할 필요가 있다.

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Down-regulation of EZH2 by RNA Interference Inhibits Proliferation and Invasion of ACHN Cells via the Wnt/β-catenin Pathway

  • Yuan, Jun-Bin;Yang, Luo-Yan;Tang, Zheng-Yan;Zu, Xiong-Bing;Qi, Lin
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권12호
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    • pp.6197-6201
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    • 2012
  • Although enhancer of zeste homolog 2 (EZH2) has been reported as an independent prognostic factor in renal cell carcinoma (RCC), little is known about the exact mechanism of EZH2 in promoting the genesis of RCC. However, several studies have shown that dysregulation of the Wnt/${\beta}$-catenin signaling pathway plays a crucial role. Therefore, we determined whether EZH2 could affect ACHN human RCC cell proliferation and invasion via the Wnt/${\beta}$-catenin pathway. In the present study, we investigated the effects of short interfering RNA (siRNA)-mediated EZH2 gene silencing on Wnt/${\beta}$-catenin signaling in ACHN cells. EZH2-siRNA markedly inhibited the proliferation and invasion capabilities of ACHN, while also reducing the expression of EZH2, Wnt3a and ${\beta}$-catenin. In contrast, cellular expression of GSK-$3{\beta}$ (glycogen synthase kinase-$3{\beta}$), an inhibitor of the Wnt/${\beta}$-catenin pathway, was conspicuously higher after transfection of EZH2 siRNA. These preliminary findings suggest EZH2 may promote proliferation and invasion of ACHN cells via action on the Wnt/${\beta}$-catenin signaling pathway.

Changes in gene expression associated with oocyte meiosis after $Obox4$ RNAi

  • Lee, Hyun-Seo;Kim, Eun-Young;Lee, Kyung-Ah
    • Clinical and Experimental Reproductive Medicine
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    • 제38권2호
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    • pp.68-74
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    • 2011
  • Objective: Previously, we found that oocyte specific homeobox (Obox) 4 plays significant role in completion of meiosis specifically at meiosis I-meiosis II (MI-MII) transition. The purpose of this study was to determine the mechanism of action of $Obox4$ in oocyte maturation by evaluating downstream signal networking. Methods: The $Obox4$ dsRNA was prepared by $in$ $vitro$ transcription and microinjected into the cytoplasm of germinal vesicle oocytes followed by $in$ $vitro$ maturation in the presence or absence of 0.2 mM 3-isobutyl-1-metyl-xanthine. Total RNA was extracted from 200 oocytes of each group using a PicoPure RNA isolation kit then amplified two-rounds. The probe hybridization and data analysis were used by Affymetrix Gene-Chip$^{(R)}$ Mouse Genome 430 2.0 array and GenPlex 3.0 (ISTECH, Korea) software, respectively. Results: Total 424 genes were up (n=80) and down (n=344) regulated after $Obox4$ RNA interference (RNAi). Genes mainly related to metabolic pathways and mitogen-activated protein kinase (MAPK) signaling pathway was changed. Among the protein kinase C (PKC) isoforms, PKC-alpha, beta, gamma were down-regulated and especially the MAPK signaling pathway PKC-gamma was dramatically decreased by $Obox4$ RNAi. In the cell cycle pathway, we evaluated the expression of genes involved in regulation of chromosome separation, and found that these genes were down-regulated. It may cause the aberrant chromosome segregation during MI-MII transition. Conclusion: From the results of this study, it is concluded that $Obox4$ is important upstream regulator of the PKC and anaphase-promoting complex action for maintaining intact germinal vesicle.

Suppression of Rice Stripe Virus Replication in Laodelphax striatellus Using Vector Insect-Derived Double-Stranded RNAs

  • Fang, Ying;Choi, Jae Young;Park, Dong Hwan;Park, Min Gu;Kim, Jun Young;Wang, Minghui;Kim, Hyun Ji;Kim, Woo Jin;Je, Yeon Ho
    • The Plant Pathology Journal
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    • 제36권3호
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    • pp.280-288
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    • 2020
  • RNA interference (RNAi) has attracted attention as a promising approach to control plant viruses in their insect vectors. In the present study, to suppress replication of the rice stripe virus (RSV) in its vector, Laodelphax striatellus, using RNAi, dsRNAs against L. striatellus genes that are strongly upregulated upon RSV infection were delivered through a rice leaf-mediated method. RNAi-based silencing of peroxiredoxin, cathepsin B, and cytochrome P450 resulted in significant down regulation of the NS3 gene of RSV, achieving a transcriptional reduction greater than 73.6% at a concentration of 100 ng/μl and, possibly compromising viral replication. L. striatellus genes might play crucial roles in the transmission of RSV; transcriptional silencing of these genes could suppress viral replication in L. striatellus. These results suggest effective RNAi-based approaches for controlling RSV and provide insight into RSV-L. striatellus interactions.

전파관리방식의 변화에 대비한 제도 개선 방안에 대한 조사 (Domestic Radio Waves Propagate Management and Control Systems Investigate the System Status)

  • 최우진;석경휴
    • 한국전자통신학회논문지
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    • 제13권6호
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    • pp.1145-1154
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    • 2018
  • 주파수의 혼신 간섭 방지를 위해 실제 공중에 방사되는 복사전력 중심으로 규제기준 전환이 요구된다. 복사전력 규제는 기술기준, 허가, 검사 등 전파관리 전반에 관련되는 사항이므로 적용 용이성, 시급성 등을 고려해 점진적으로 도입하고, 주요국의 복사전력 관련 법제도 현황 조사를 통해 국내 환경에 적합한 복사전력 방식에 따른 측정, 검사, 인증 등의 무선설비 출력관리 방식을 마련한다. 국내는 현재 안테나 공급 전력의 비중이 높고, 유럽의 경우는 복사전력의 비중이 높음. 향후 무선국의 수가 점점 증가하고 다양해지므로 공간 관리인 복사전력 기반을 병행하여 측정이 가능하도록 제도개선 마련 필요하고, 복사전력 관리체계로 전환하기 위해서는 관련 전파 제도(기술기준, 인증, 무선국 검사, 사후 관리 등)에 대한 제도개선 필요하다.

Effects of Down-regulation of HDAC6 Expression on Proliferation, Cell Cycling and Migration of Esophageal Squamous Cell Carcinoma Cells and Related Molecular Mechanisms

  • Li, Ning;Tie, Xiao-Jing;Liu, Pei-Jie;Zhang, Yan;Ren, Hong-Zheng;Gao, Xin;Xu, Zhi-Qiao
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권2호
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    • pp.685-689
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    • 2013
  • Objective: To study the effects of down-regulation of HDAC6 expression on proliferation, cell cycling and migration of esophageal squamous cell carcinoma (ESCC) cells and related molecular mechanisms. Methods: ESCC cell line EC9706 cells were randomly divided into untreated (with no transfection), control siRNA (transfected with control siRNA) and HDAC6 siRNA (transfected with HDAC6 small interfering RNA) groups. Effects of HDAC6 siRNA interference on expression of HDAC6 mRNA and protein in EC9706 cells were investigated by semi-quantitative RT-PCR, Western blotting and immunocytochemistry methods. Effects of down-regulation of HDAC6 expression on cell proliferation, cell cycle, and cell migration were studied using a CCK-8 kit, flow cytometry and Boyden chambers, respectively. Changes of mRNA and protein expression levels of cell cycle related factor (p21) and cell migration related factor (E-cadherin) were investigated by semi-quantitative RT-PCR and Western blotting methods. Results: After transfection of HDAC6 siRNA, the expression of HDAC6 mRNA and protein in EC9706 cells was significantly downregulated. In the HDAC6 siRNA group, cell proliferation was markedly inhibited, the percentage of cells in G0/G1 phase evidently increased and the percentage of cells in S phase decreased, and the number of migrating cells significantly and obviously decreased. The mRNA and protein expression levels of p21 and E-cadherin in the HDAC6 siRNA group were significantly higher than those in the untreated group and the control siRNA group, respectively. Conclusions: HDAC6 siRNA can effectively downregulate the expression of HDAC6 mRNA and protein in EC9706 cells. Down-regulation of HDAC6 expression can obviously inhibit cell proliferation, arrest cell cycling in the G0/G1 phase and reduce cell migration. The latter two functions may be closely related with the elevation of mRNA and protein expression of p21 and E-cadherin.

Characterization of TNNC1 as a Novel Tumor Suppressor of Lung Adenocarcinoma

  • Kim, Suyeon;Kim, Jaewon;Jung, Yeonjoo;Jun, Yukyung;Jung, Yeonhwa;Lee, Hee-Young;Keum, Juhee;Park, Byung Jo;Lee, Jinseon;Kim, Jhingook;Lee, Sanghyuk;Kim, Jaesang
    • Molecules and Cells
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    • 제43권7호
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    • pp.619-631
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    • 2020
  • In this study, we describe a novel function of TNNC1 (Troponin C1, Slow Skeletal and Cardiac Type), a component of actin-bound troponin, as a tumor suppressor of lung adenocarcinoma (LUAD). First, the expression of TNNC1 was strongly down-regulated in cancer tissues compared to matched normal lung tissues, and down-regulation of TNNC1 was shown to be strongly correlated with increased mortality among LUAD patients. Interestingly, TNNC1 expression was enhanced by suppression of KRAS, and ectopic expression of TNNC1 in turn inhibited KRASG12D-mediated anchorage independent growth of NIH3T3 cells. Consistently, activation of KRAS pathway in LUAD patients was shown to be strongly correlated with down-regulation of TNNC1. In addition, ectopic expression of TNNC1 inhibited colony formation of multiple LUAD cell lines and induced DNA damage, cell cycle arrest and ultimately apoptosis. We further examined potential correlations between expression levels of TNNC1 and various clinical parameters and found that low-level expression is significantly associated with invasiveness of the tumor. Indeed, RNA interference-mediated down-regulation of TNNC1 led to significant enhancement of invasiveness in vitro. Collectively, our data indicate that TNNC1 has a novel function as a tumor suppressor and is targeted for down-regulation by KRAS pathway during the carcinogenesis of LUAD.

siRNA-mediated Silencing of Survivin Inhibits Proliferation and Enhances Etoposide Chemosensitivity in Acute Myeloid Leukemia Cells

  • Karami, Hadi;Baradaran, Behzad;Esfahani, Ali;Estiar, Mehrdad Asghari;Naghavi-Behzad, Mohammad;Sakhinia, Masoud;Sakhinia, Ebrahim
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권12호
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    • pp.7719-7724
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    • 2013
  • Background: Overexpression of survivin, a known inhibitor of apoptosis, is associated with tumor progression and drug resistance in numerous malignancies, including leukemias. The aim of this study was to investigate the effect of a specific survivin small interference RNA (siRNA) on proliferation and the sensitivity of HL-60 acute myeloid leukemia (AML) cells to the chemotherapeutic drug etoposide. Materials and Methods: The cells were transfected with siRNAs using Lipofectamine $^{TM}2000$ transfection reagent. Relative survivin mRNA and protein levels were measured by quantitative real-time PCR and Western blotting, respectively. Trypan blue exclusion assays were performed to monitor tumor cell proliferation after siRNA transfection. The cytotoxic effects of etoposide and survivin siRNA, alone and in combination, on leukemic cells were determined using MTT assay. Apoptosis was assessed by ELISA cell death assay. Results: Survivin siRNA markedly reduced both mRNA and protein expression levels in a time-dependent manner, leading to distinct inhibition of cell proliferation and increased spontaneous apoptosis. Surprisingly, survivin siRNA synergistically increased the cell toxic effects of etoposide. Moreover, survivin down-regulation significantly enhanced its induction of apoptosis. Conclusions: Our study suggests that down-regulation of survivin by siRNA can trigger apoptosis and overcome drug resistance of leukemia cells. Therefore, survivin siRNA may be an effective adjuvant in AML chemotherapy.

RNA Interference-Mediated Knockdown of Astrocyte Elevated Gene-1 Inhibits Growth, Induces Apoptosis, and Increases the Chemosensitivity to 5-Fluorouracil in Renal Cancer Caki-1 Cells

  • Wang, Peng;Yin, Bo;Shan, Liping;Zhang, Hui;Cui, Jun;Zhang, Mo;Song, Yongsheng
    • Molecules and Cells
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    • 제37권12호
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    • pp.857-864
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    • 2014
  • Astrocyte elevated gene-1 (AEG-1) is a recently discovered oncogene that has been reported to be highly expressed in various types of malignant tumors, including renal cell carcinoma. However, the precise role of AEG-1 in renal cancer cell proliferation and apoptosis has not been clarified. In this study, we transfected the renal cancer cell line Caki-1 with a plasmid expressing AEG-1 short hairpin RNA (shRNA) and obtained cell colonies with stable knockdown of AEG-1. We found that AEG-1 down-regulation inhibited cell proliferation and colony formation and arrested cell cycle progression at the sub-G1 and G0/G1 phase. Western blot analysis indicated that the expression of proliferating cell nuclear antigen (PCNA), cyclin D1 and cyclin E were significantly reduced following AEG-1 down-regulation. In addition, AEG-1 knockdown led to the appearance of apoptotic bodies in renal cancer cells, and the ratio of apoptotic cells significantly increased. Expression of the antiapoptotic factor Bcl-2 was dramatically reduced, whereas the pro-apoptotic factors Bax, caspase-3 and poly (ADPribose) polymerase (PARP) were significantly activated. Finally, AEG-1 knockdown in Caki-1 cells remarkably suppressed cell proliferation and enhanced cell apoptosis in response to 5-fluorouracil (5-FU) treatment, suggesting that AEG-1 inhibition sensitizes Caki-1 cells to 5-FU. Taken together, our data suggest that AEG-1 plays an important role in renal cancer formation and development and may be a potential target for future gene therapy for renal cell carcinoma.

Down-regulation of FRα Inhibits Proliferation and Promotes Apoptosis of Cervical Cancer Cells in Vitro

  • Bai, Li-Xia;Ding, Ling;Jiang, Shi-Wen;Kang, Hui-Jie;Gao, Chen-Fei;Chen, Chen;Zhou, Qin;Wang, Jin-Tao
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권14호
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    • pp.5667-5672
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    • 2014
  • Folate receptor alpha ($FR{\alpha}$) mediates folate uptake by endocytosis, and while folate is essential to DNA methylation and synthesis and may have an important role in proliferating cells. $FR{\alpha}$ is known to be expressed in rapidly proliferating cells, including many cancer cell lines, but there has been no systematic assessment of expression in cervical cancer cell lines. The aim of the present study was to evaluate the effects of $FR{\alpha}$ on proliferation and apoptosis of cervical cells and correlation mechanism. In this study, we investigated the biological function of $FR{\alpha}$ in Hela cells using RNA interference. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK8) assay, while cell cycling and apoptosis were assessed by flow cytometry, mRNA levels by real time-PCR and protein levels of $FR{\alpha}$, c-Fos and c-Jun by Western blotting. The results revealed that $FR{\alpha}$ was highly expressed in Hela cells and its silencing with a small interfering RNA (siRNA) inhibited cell proliferation and induced cell apoptosis, arresting the cell cycle in G0/G1 stages while decreasing the proportion in S and G2/M stages, and suppressed the expression levels of c-Fos and c-Jun. In conclusion, the results of this study indicated that $FR{\alpha}$ down-regulation might be capable of suppressing cervical cancer cell proliferation and promoting apoptosis. It suggested that $FR{\alpha}$ might be a novel therapeutic target for cervical cancer.