• Journal of Advanced Navigation Technology
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• v.21 no.3
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• pp.220-229
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• 2017

In this paper, To take advantage a variety of DC power as the boost DC-DC converter design specifications through the inductor L and capacitor C through PSPICE to calculate the best estimate of the value. Boost DC-DC converter with a switch device using IRF840 and reverse recovery time Schottky diodes with excellent with constant current controller using D10SC6M and resistance can be configured to considering the Power LED Module was driven by the production. Converter's switching frequency is 50 kHz, the first Duty Rate was made to increase gradually depending on the value of the detection were, 10 % in the output voltage. As a result, the simulated Boost Power LED driver characteristics is in comparison with the design specifications, 5% or less as the error was approximated. Finally, when input 15 V were offered, a stable output 24 V were obtained. and Dimming Control through the adjustment of brightness and current consumption were possible.

• The Journal of the Institute of Internet, Broadcasting and Communication
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• v.20 no.3
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• pp.9-14
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• 2020

In this paper, Qualification Model of frequency synthesizer is designed for X-band SAR system and performed electrical and environment test. Designed frequency synthesizer generate 13.65 GHz with very low phase noise performance. The integrated phase noise from 10Hz to 1MHz is -37.91 dBc. IRF performances are analyzed according to phase noise and jitter. Also, thermal and structure analysis are achieved for stable operation in space environment. Designed frequency synthesizer is consist of 2 modules of 6U size and generate L-band, C-band, Ku-band. The result of this study would enhance the design ability of RF module and help the frequency synthesizer design for SAR payload system.

• Journal of the Korean Society for Aeronautical & Space Sciences
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• v.50 no.2
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• pp.119-125
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• 2022

In this paper, we present design, implementation and test results of CTM (Chirp Transceiver Module) EM (Engineering Model) for C-Band SAR (Synthetic Aperture Radar) Payload. The CTM is designed to operate dual frequency scan method that simultaneously operate two frequencies in each 50MHz bandwidth to achieve 120Km swath with 10m resolution at about 500Km altitude. The CTM used radiation tolerant RTG4 FPGA for space environment, and implemented with the Parallel DDS (PDDS) method which uses a small memory capacity compared to the memory-map method. Test results show high purity chirp signal generation and excellent IRF performance from received chirp signal after direct digital conversion.

• Experimental and Molecular Medicine
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• v.50 no.11
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• pp.1.1-1.10
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• 2018

Bone marrow-derived mesenchymal stem cells (BMMSCs) are used extensively for cardiac repair and interact with immune cells in the damaged heart. Macrophages are known to be modulated by stem cells, and we hypothesized that priming macrophages with BMMSCs would enhance their therapeutic efficacy. Rat bone marrow-derived macrophages (BMDMs) were stimulated by lipopolysaccharide (LPS) with or without coculture with rat BMCs. In the LPS-stimulated BMDMs, induction of the inflammatory marker iNOS was attenuated, and the anti-inflammatory marker Arg1 was markedly upregulated by coculture with BMMSCs. Myocardial infarction (MI) was induced in rats. One group was injected with BMMSCs, and a second group was injected with MIX (a mixture of BMMSCs and BMDMs after coculture). The reduction in cardiac fibrosis was greater in the MIX group than in the BMC group. Cardiac function was improved in the BMMSC group and was substantially improved in the MIX group. Angiogenesis was better in the MIX group, and anti-inflammatory macrophages were more abundant in the MIX group than in the BMMSC group. In the BMMSCs, interferon regulatory factor 5 (IRF5) was exclusively induced by coculture with macrophages. IRF5 knockdown in BMMSCs failed to suppress inflammatory marker induction in the macrophages. In this study, we demonstrated the successful application of BMDMs primed with BMMSCs as an adjuvant to cell therapy for cardiac repair.

• Molecules and Cells
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• v.45 no.10
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• pp.702-717
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• 2022

Hepatitis C virus (HCV) infection can lead to chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. HCV employs diverse strategies to evade host antiviral innate immune responses to mediate a persistent infection. In the present study, we show that nonstructural protein 5A (NS5A) interacts with an NF-κB inhibitor immunomodulatory kinase, IKKε, and subsequently downregulates beta interferon (IFN-β) promoter activity. We further demonstrate that NS5A inhibits DDX3-mediated IKKε and interferon regulatory factor 3 (IRF3) phosphorylation. We also note that hyperphosphorylation of NS5A mediates protein interplay between NS5A and IKKε, thereby contributing to NS5A mediated modulation of IFN-β signaling. Lastly, NS5A inhibits IKKε-dependent p65 phosphorylation and NF-κB activation. Based on these findings, we propose NS5A as a novel regulator of IFN signaling events, specifically by inhibiting IKKε downstream signaling cascades through its interaction with IKKε. Taken together, these data suggest an additional mechanistic means by which HCV modulates host antiviral innate immune responses to promote persistent viral infection.

• Journal of Ginseng Research
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• v.40 no.4
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• pp.437-444
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• 2016

Background: Although Korean Red Ginseng (KRG) has been traditionally used for a long time, its anti-inflammatory role and underlying molecular and cellular mechanisms have been poorly understood. In this study, the anti-inflammatory roles of KRG-derived components, namely, water extract (KRG-WE), saponin fraction (KRG-SF), and nonsaponin fraction (KRG-NSF), were investigated. Methods: To check saponin levels in the test fractions, KRG-WE, KRG-NSF, and KRG-SF were analyzed using high-performance liquid chromatography. The anti-inflammatory roles and underlying cellular and molecular mechanisms of these components were investigated using a macrophage-like cell line (RAW264.7 cells) and an acute gastritis model in mice. Results: Of the tested fractions, KGR-SF (but not KRG-NSF and KRG-WE) markedly inhibited the viability of RAW264.7 cells, and splenocytes at more than 500 mg/mL significantly suppressed NO production at $100{\mu}g/mL$, diminished mRNA expression of inflammatory genes such as inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-${\alpha}$, and interferon-${\beta}$ at $200{\mu}g/mL$, and completely blocked phagocytic uptake by RAW264.7 cells. All three fractions suppressed luciferase activity triggered by interferon regulatory factor 3 (IRF3), but not that triggered by activator protein-1 and nuclear factor-kappa B. Phospho-IRF3 and phospho-TBK1 were simultaneously decreased in KRG-SF. Interestingly, all these fractions, when orally administered, clearly ameliorated the symptoms of gastric ulcer in HCl/ethanol-induced gastritis mice. Conclusion: These results suggest that KRG-WE, KRG-NSF, and KRG-SF might have anti-inflammatory properties, mostly because of the suppression of the IRF3 pathway.

• KSCE Journal of Civil and Environmental Engineering Research
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• v.33 no.1
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• pp.207-218
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• 2013

One of the input parameters in the evaluation of seismic performance of rockfill dams is shear-wave velocity of rock debris and clay core. Reliable evaluation of shear-wave velocity by surface-wave methods requires overcoming the problems of rock-debris discontinuity, material inhomogeneity and sloping boundary. In this paper, for the shear-wave velocity investigation of rockfill dams, SBF (Short-Array Beamforming) technique was proposed using the principles of conventional beamforming technique and adopted to solve limitations of the conventional surface-wave techniques. SBF technique utilizes a 3- to 9-m long measurement array and a far-field source, which allowed the technique to eliminate problems of near-field effects and investigate local anomalies. This paper describes the procedure to investigate shear-wave velocity profile of rockfill dams by SBF technique and IRF (Impulse-response filtration) technique with accuracy and reliability. Validity of the proposed SBF technique was verified by comparisons with downhole tests and CapSASW (Common-Array-Profiling Spectral-Analysis-of-Surface-Waves) tests at a railroad embankment compacted with rock debris.

• Journal of Chest Surgery
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• v.53 no.5
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• pp.250-257
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• 2020

Background: Lung adenocarcinoma (LUAD) with ground-glass opacity (GGO) can become aggravated, but the reasons for this aggravation are not fully understood. The goal of this study was to analyze the genetic features and causes of progression of GGO LUAD. Methods: LUAD tumor samples and normal tissues were analyzed using an Illumina HiSeq 4000 system. After the tumor mutational burden (TMB) was calculated, the identified mutations were classified as those found only in GGO LUAD, those present only in nonGGO LUAD, and those common to both tissue types. Ten high-frequency genes were selected from each domain, after which protein interaction network analysis was conducted. Results: Overall, 227 mutations in GGO LUAD, 212 in non-GGO LUAD, and 48 that were common to both tumor types were found. The TMB was 8.8 in GGO and 7.8 in non-GGO samples. In GGO LUAD, mutations of FCGBP and SFTPA1 were identified. FOXQ1, IRF5, and MAGEC1 mutations were common to both types, and CDC27 and NOTCH4 mutations were identified in the non-GGO LUAD. Protein interaction network analysis indicated that IRF5 (common to both tissue types) and CDC27 (found in the non-GGO LUAD) had significant biological functions related to the cell cycle and proliferation. Conclusion: In conclusion, GGO LUAD exhibited a higher TMB than non-GGO LUAD. No clinically meaningful mutations were found to be specific to GGO LUAD, but mutations involved in the epithelial-mesenchymal transition or cell cycle were found in both tumor types and in non-GGO tissue alone. These findings could explain the non-invasiveness of GGO-type LUAD.

• Journal of Microbiology and Biotechnology
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• v.29 no.12
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• pp.2014-2021
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• 2019

Middle East respiratory syndrome coronavirus (MERS-CoV) belongs to the genus Betacoronavirus and causes severe morbidity and mortality in humans especially when infected patients have underlying diseases such as chronic obstructive pulmonary disease (COPD). Previously, we demonstrated that MERS-CoV-encoded ORF8b strongly inhibits MDA5- and RIG-I-mediated induction of the interferon beta (IFN-β) promoter activities. Here, we report that ORF8b seemed to regulate MDA5 or RIG-I differentially as protein levels of MDA5 were significantly down-regulated while those of RIG-I were largely unperturbed. In addition, ORF8b seemed to efficiently suppress phosphorylation of IRF3 at the residues of 386 and 396 in cells transfected with RIG-I while total endogenous levels of IRF3 remained largely unchanged. Furthermore, ORF8b was able to inhibit all forms of RIG-I; full-length, RIG-I-1-734, and RIG-I-1-228, the last of which contains only the CARD domains. Taken together, it is tempting to postulate that ORF8b may interfere with the CARD-CARD interactions between RIG-I and MAVS. Further detailed analysis is required to delineate the mechanisms of how ORF8b inhibits the MDA5/RIG-I receptor signaling pathway.

• IMMUNE NETWORK
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• v.12 no.3
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• pp.113-117
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• 2012

FasL, perforin, $TNF{\alpha}$, IL-1 and NO have been considered as effector molecule(s) leading to ${\beta}$-cell death in autoimmune diabetes. However, the real culprit(s) of ${\beta}$-cell destruction have long been elusive despite intense investigation. Previously we have suggested $IFN{\gamma}/TNF{\alpha}$ synergism as the final effector molecules in autoimmune diabetes of NOD mice. A combination of $IFN{\gamma}$ and $TNF{\alpha}$ but neither cytokine alone, induced classical caspase-dependent apoptosis in murine insulinoma and pancreatic islet cells. $IFN{\gamma}$ treatment conferred susceptibility to $TNF{\alpha}$-induced apoptosis on otherwise resistant murine insulinoma cells by STAT1 activation followed by IRF-1 induction. Here we report that $IFN{\gamma}/TNF{\alpha}$ synergism induces apoptosis of human pancreatic islet cells. We also observed STAT1 activation followed by IRF-1 induction by $IFN{\gamma}$ treatment in human islet cells. Taken together, we suggest that $IFN{\gamma}/TNF{\alpha}$ synergism could be involved in human islet cell death in type 1 diabetes, similar to murine type 1 diabetes.