• Title/Summary/Keyword: IRF10

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Performance Analysis of SAR System Using Radar Target Simulation Equipment (표적모의장치를 이용한 SAR 장비의 성능 분석)

  • Kweon, Soon-Koo;Yeo, Hwan-Yong;Park, Sung-Min;Han, Ji-Hoon;Jung, Chang-Sik;Kim, Ki-Wan;Shin, Hyun-Ik
    • The Journal of Korean Institute of Electromagnetic Engineering and Science
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    • v.29 no.2
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    • pp.118-127
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    • 2018
  • In this work, we have designed and manufactured radar target simulation equipment for the performance analysis of synthetic aperture radar(SAR) systems. First, we have explained the function and performance specification of the target simulation equipment and point target scenario generation for validation of the SAR system. In addition, we have developed a simple and accurate calibration method for the time delay of the SAR system using the manufactured target simulation equipment. We have analyzed the point target impulse response function of the SAR image acquired using the SAR system and the target simulation equipment. It was observed that the measured peak to side lobe ratio(=-13.25 dB) and resolution(=0.49 m) are in good agreement with the corresponding theoretical values.

CKD-712, (S)-1-(${\alpha}$-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, Inhibits the NF-${\kappa}B$ Activation and Augments Akt Activation during TLR4 Signaling

  • Lee, Jeong-Gi;Yang, Eun-Jeong;Shin, Jeon-Soo;Kim, Dal-Hyun;Lee, Sung-Sook;Choi, In-Hong
    • IMMUNE NETWORK
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    • v.11 no.6
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    • pp.420-423
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    • 2011
  • Since CKD-712 has been developed as an anti-inflammatory agent, we examined the effect of CKD-712 during TLR4 signaling. Using HEK293 cells expressing TLR4, CKD-712 was pre-treated 1 hr before LPS stimulation. Activation of NF-${\kappa}B$ was assessed by promoter assay. The activation of ERK, JNK, p38, IRF3 and Akt was measured by western blotting. CKD-712 inhibited the NF-${\kappa}B$ signaling triggered by LPS. The activation of ERK, JNK, p38 or IRF3 was not inhibited by CKD-712. On the contrary the activation of these molecules was augmented slightly. The activation of Akt with stimulation of LPS was also enhanced with CKD-712 pre-treatment at lower concentration, but was inhibited at higher concentration. We suggest that during TLR4 signaling CKD-712 inhibits NF-${\kappa}B$ activation. However, CKD-712 augmented the activation of Akt as well as Map kinases. Therefore, we suggest that CKD-712 might have a role as an immunomodulator.

Induction of pro-inflammatory cytokines by 29-kDa FN-f via cGAS/STING pathway

  • Hwang, Hyun Sook;Lee, Mi Hyun;Choi, Min Ha;Kim, Hyun Ah
    • BMB Reports
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    • v.52 no.5
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    • pp.336-341
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    • 2019
  • The cGAS-STING pathway plays an important role in pathogen-induced activation of the innate immune response. The 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) found predominantly in the synovial fluid of osteoarthritis (OA) patients increases the expression of catabolic factors via the toll-like receptor-2 (TLR-2) signaling pathway. In this study, we investigated whether 29-kDa FN-f induces inflammatory responses via the cyclic GMP-AMP synthase (cGAS)/stimulator of interferon gene (STING) pathway in human primary chondrocytes. The levels of cGAS and STING were elevated in OA cartilage compared with normal cartilage. Long-term treatment of chondrocytes with 29-kDa FN-f activated the cGAS/STING pathway together with the increased level of gamma-H2AX, a marker of DNA breaks. In addition, the expression of pro-inflammatory cytokines, including granulocyte-macrophage colony-stimulating factor (GM-CSF/CSF-2), granulocyte colony-stimulating factor (G-CSF/CSF-3), and type I interferon ($IFN-{\alpha}$), was increased more than 100-fold in 29-kDa FN-f-treated chondrocytes. However, knockdown of cGAS and STING suppressed 29-kDa FN-f-induced expression of GM-CSF, G-CSF, and $IFN-{\alpha}$ together with the decreased activation of TANK-binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), and inhibitor protein ${\kappa}B{\alpha}$ ($I{\kappa}B{\alpha}$). Furthermore, NOD2 or TLR-2 knockdown suppressed the expression of GM-CSF, G-CSF, and $IFN-{\alpha}$ as well as decreased the activation of the cGAS/STING pathway in 29-kDa FN-f-treated chondrocytes. These data demonstrate that the cGAS/STING/TBK1/IRF3 pathway plays a critical role in 29-kDa FN-f-induced expression of pro-inflammatory cytokines.

Pan-Caspase Inhibitor zVAD Induces Necroptotic and Autophagic Cell Death in TLR3/4-Stimulated Macrophages

  • Chen, Yuan-Shen;Chuang, Wei-Chu;Kung, Hsiu-Ni;Cheng, Ching-Yuan;Huang, Duen-Yi;Sekar, Ponarulselvam;Lin, Wan-Wan
    • Molecules and Cells
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    • v.45 no.4
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    • pp.257-272
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    • 2022
  • In addition to inducing apoptosis, caspase inhibition contributes to necroptosis and/or autophagy depending on the cell type and cellular context. In macrophages, necroptosis can be induced by co-treatment with Toll-like receptor (TLR) ligands (lipopolysaccharide [LPS] for TLR4 and polyinosinic-polycytidylic acid [poly I:C] for TLR3) and a cell-permeable pan-caspase inhibitor zVAD. Here, we elucidated the signaling pathways and molecular mechanisms of cell death. We showed that LPS/zVAD- and poly I:C/zVAD-induced cell death in bone marrow-derived macrophages (BMDMs) was inhibited by receptor-interacting protein kinase 1 (RIP1) inhibitor necrostatin-1 and autophagy inhibitor 3-methyladenine. Electron microscopic images displayed autophagosome/autolysosomes, and immunoblotting data revealed increased LC3II expression. Although zVAD did not affect LPS- or poly I:C-induced activation of IKK, JNK, and p38, it enhanced IRF3 and STAT1 activation as well as type I interferon (IFN) expression. In addition, zVAD inhibited ERK and Akt phosphorylation induced by LPS and poly I:C. Of note, zVAD-induced enhancement of the IRF3/IFN/STAT1 axis was abolished by necrostatin-1, while zVAD-induced inhibition of ERK and Akt was not. Our data further support the involvement of autocrine IFNs action in reactive oxygen species (ROS)-dependent necroptosis, LPS/zVAD-elicited ROS production was inhibited by necrostatin-1, neutralizing antibody of IFN receptor (IFNR) and JAK inhibitor AZD1480. Accordingly, both cell death and ROS production induced by TLR ligands plus zVAD were abrogated in STAT1 knockout macrophages. We conclude that enhanced TRIF-RIP1-dependent autocrine action of IFNβ, rather than inhibition of ERK or Akt, is involved in TLRs/zVAD-induced autophagic and necroptotic cell death via the JAK/STAT1/ROS pathway.

Multi-channel analyzer based on a novel pulse fitting analysis method

  • Wang, Qingshan;Zhang, Xiongjie;Meng, Xiangting;Wang, Bao;Wang, Dongyang;Zhou, Pengfei;Wang, Renbo;Tang, Bin
    • Nuclear Engineering and Technology
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    • v.54 no.6
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    • pp.2023-2030
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    • 2022
  • A novel pulse fitting analysis (PFA) method is presented for the acquisition of nuclear spectra. The charging process of the feedback capacitor in the resistive feedback charge-sensitive preamplifier is equivalent to the impulsive pulse, and its impulse response function (IRF) can be obtained by non-linear fitting of the falling edge of the nuclear pulse. The integral of the IRF excluding the baseline represents the energy deposition of the particles in the detector. In addition, since the non-linear fitting process in PFA method is difficult to achieve in the conventional architecture of spectroscopy system, a new multi-channel analyzer (MCA) based on Zynq SoC is proposed, which transmits all the data of nuclear pulses from the programmable logic (PL) to the processing system (PS) by high-speed AXI-Stream in order to implement PFA method with precision. The linearity of new MCA has been tested. The spectrum of 137Cs was obtained using LaBr3(Ce) scintillator detector, and was compared with commercial MCA by ORTEC. The results of tests indicate that the MCA based on PFA method has the same performance as the commercial MCA based on pulse height analysis (PHA) method and excellent linearity for γ-rays with different energies, which infers that PFA method is an effective and promising method for the acquisition of spectra. Furthermore, it provides a new solution for nuclear pulse processing algorithms involving regression and iterative processes.

An Analysis on the Decoupling between Energy Consumption and Economic Growth in South Korea (한국의 에너지 소비와 경제성장의 탈동조화에 대한 분석)

  • Hyun-Soo Kang
    • Asia-Pacific Journal of Business
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    • v.14 no.4
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    • pp.305-318
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    • 2023
  • Purpose - This study analyzed the decoupling phenomenon between energy consumption and economic growth in Korea from 1990 to 2021. The main purpose of this study is to suggest policy implications for achieving a low-carbon society and decoupling that Korea must move forward in the face of the climate change crisis. Design/methodology/approach - This study investigated the relationship between energy consumption and economic growth by energy source and sector using the energy-EKC (EEKC) hypothesis which included the energy consumption on the traditional Environmental Kuznets Curve (EKC), and the impulse response function (IRF) model based on Bayesian vector auto-regression (BVAR). Findings - During the analysis period, the trend of decoupling of energy consumption and economic growth in Korea is confirmed starting from 1996. However, the decoupling tendency appeared differently depending on the differences in energy consumption by sources and fields. The results of the IRF model using data on energy consumption by source showed that the impact of GDP and renewable energy consumption resulted in an increase in energy consumption of bio and waste, but a decrease in energy consumption by sources, and the impact of trade dependence was found to increase the consumption of petroleum products. Research implications or Originality - According to the main results, efficient distribution by existing energy source is required through expansion of development of not only renewable energy but also alternative energy. Additionally, in order to increase the effectiveness of existing energy policies to achieve carbon neutrality, more detailed strategies by source and sector of energy consumption are needed.

Study on Numerical Sensitivity and Uncertainty in the Analysis of Parametric Roll (파라메트릭 횡동요 수치해석의 민감도 및 불확실성에 대한 연구)

  • Park, Dong-Min;Kim, Tae-Young;Kim, Yong-Hwan
    • Journal of the Society of Naval Architects of Korea
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    • v.49 no.1
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    • pp.60-67
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    • 2012
  • This study considers the numerical analysis on parametric roll for container ships. As a method of numerical simulation, an impulse-response-function approach is applied in time domain. A systematic study is carried out for the parametric roll of two container ships, particularly observing the sensitivity of computational results to some parameters which can affect the analysis of parametric roll. The parameters to be considered are metacentric height (GM), simulation time window, and the discretization of wave spectrum. Based on the result of parametric roll simulation, numerical sensitivity and uncertainty in computational analysis are discussed.

Debt Investment Outflows and Inflows in Korea and Covered Interest Parity Deviation (채권시장 자본유출입과 무위험 금리평형 이탈)

  • Gab-Je Jo
    • Korea Trade Review
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    • v.47 no.1
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    • pp.181-198
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    • 2022
  • This paper investigates the arbitrage effect by the covered interest parity (CIP) deviation, as well as other push or pull factor effect on capital inflows and ouflows in the Korean bond market, by utilizing OLS, TSLS, IRF and VDC in EC model. The sample period covers February 2002 to December 2020. It is found that, the swap basis reflecting the CIP deviations have the significant effects on both debt investment inflows and debt investment outflows. Also, it is found that, the Korean risk factors have decreasing effects on foreigner's investment in the Korean bonds, while the global risk factors have decreasing effects on Korean resident's investment in the foreign bonds.

Zika Virus Proteins NS2A and NS4A Are Major Antagonists that Reduce IFN-β Promoter Activity Induced by the MDA5/RIG-I Signaling Pathway

  • Ngan, Nguyen Thi Thuy;Kim, Seong-Jun;Lee, Jeong Yoon;Myoung, Jinjong
    • Journal of Microbiology and Biotechnology
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    • v.29 no.10
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    • pp.1665-1674
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    • 2019
  • Zika virus (ZIKV) is a mosquito-transmitted, emerging Flavivirus that causes Guillain-$Barr{\acute{e}}$ syndrome and microcephaly in adults and fetuses, respectively. Since ZIKV was first isolated in 1947, severe outbreaks have occurred at various places worldwide, including Yap Island in 2007, French Polynesia in 2013, and Brazil in 2015. Although incidences of ZIKV infection and dissemination have drastically increased, the mechanisms underlying the pathogenesis of ZIKV have not been sufficiently studied. In addition, despite extensive research, the exact roles of individual ZIKV genes in the viral evasion of the host innate immune responses remain elusive. Besides, it is still possible that more than one ZIKV-encoded protein may negatively affect type I interferon (IFN) induction. Hence, in this study, we aimed to determine the modulations of the IFN promoter activity, induced by the MDA5/RIG-I signaling pathway, by over-expressing individual ZIKV genes. Our results show that two nonstructural proteins, NS2A and NS4A, significantly down-regulated the promoter activity of IFN-${\beta}$ by inhibiting multiple signaling molecules involved in the activation of IFN-${\beta}$. Interestingly, while NS2A suppressed both full-length and constitutively active RIG-I, NS4A had inhibitory activity only on full-length RIG-I. In addition, while NS2A inhibited all forms of IRF3 (full-length, regulatory domain-deficient, and constitutively active), NS4A could not inhibit constitutively active IRF3-5D. Taken together, our results showed that NS2A and NS4A play major roles as antagonists of MDA5/RIG-I-mediated IFN-${\beta}$ induction and more importantly, these two viral proteins seem to inhibit induction of the type I IFN responses in differential mechanisms. We believe this study expands our understanding regarding the mechanisms via which ZIKV controls the innate immune responses in cells and may pave the way to development of ZIKV-specific therapeutics.

TLR-1, TLR-2, and TLR-6 MYD88-dependent signaling pathway: A potential factor in the interaction of high-DNA fragmentation human sperm with fallopian tube epithelial cells

  • Zahra Zandieh;Azam Govahi;Azin Aghamajidi;Ehsan Raoufi;Fatemehsadat Amjadi;Samaneh Aghajanpour;Masoomeh Golestan;Reza Aflatoonian
    • Clinical and Experimental Reproductive Medicine
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    • v.50 no.1
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    • pp.44-52
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    • 2023
  • Objective: The DNA integrity of spermatozoa that attach to fallopian tube (FT) cells is higher than spermatozoa that do not attach. FT epithelial cells can distinguish normal and abnormal sperm chromatin. This study investigated the effects of sperm with a high-DNA fragmentation index (DFI) from men with unexplained repeated implantation failure (RIF) on the Toll-like receptor (TLR) signaling pathway in human FT cells in vitro. Methods: Ten men with a RIF history and high-DFI and 10 healthy donors with low-DFI comprised the high-DFI (>30%) and control (<30%) groups, respectively. After fresh semen preparation, sperm were co-cultured with a human FT epithelial cell line (OE-E6/E7) for 24 hours. RNA was extracted from the cell line and the human innate and adaptive immune responses were tested using an RT2 profiler polymerase chain reaction (PCR) array. Results: The PCR array data showed significantly higher TLR-1, TLR-2, TLR-3, TLR-6, interleukin 1α (IL-1α), IL-1β, IL-6, IL-12, interferon α (IFN-α), IFN-β, tumor necrosis factor α (TNF-α), CXCL8, GM-CSF, G-CSF, CD14, ELK1, IRAK1, IRAK2, IRAK4, IRF1, IRF3, LY96, MAP2K3, MAP2K4, MAP3K7, MAP4K4, MAPK8, MAPK8IP3, MYD88, NFKB1, NFKB2, REL, TIRAP, and TRAF6 expression in the high-DFI group than in the control group. These factors are all involved in the TLR-MyD88 signaling pathway. Conclusion: The MyD88-dependent pathway through TLR-1, TLR-2, and TLR-6 activation may be one of the main inflammatory pathways activated by high-DFI sperm from men with RIF. Following activation of this pathway, epithelial cells produce inflammatory cytokines, resulting in neutrophil infiltration, activation, phagocytosis, neutrophil extracellular trap formation, and apoptosis.