• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
• /
• 2000.10a
• /
• pp.190-195
• /
• 2000

This paper presents the fabrication of the LNA which is operating at 2.13∼2.16 GHz for IMT-2000 lot-end receiver using series feedback and resistive decoupling circuit. Series feedback added to the source lead of a transistor keep the low noise characteristics and drop the input reflection coefficient of amplifier simultaneously. Also, it increases the stability of the LNA. Resistive decoupling circuit is suitable for input stage matching because a signal at low frequency is dissipated by a resistor in the matching network The amplifier consist of GaAs FET ATF-10136 for low noise stage and VNA-25 which is internally matched MMIC for high gain stage. The amplifier is fabricated with both the RF circuits and self bias circuit on the Teflon substrate with 3.5 permittivity. The measured results of the LNA which is fabricated using above design technique are presented more than 30 dB in gain P$\_$ldB/ 17 dB and less than 0.7 dB in noise figure, 1.5 in input$.$output SWR(Standing Wave Ratio).

• Journal of the Korean Institute of Navigation
• /
• v.25 no.1
• /
• pp.53-60
• /
• 2001

This paper presents the fabrication of the LNA which is operating at 2.13 ~ 2.16 GHz for IMT-2000 front-end receiver using series feedback and resistive decoupling circuit. Series feedback added to the source lead of a GaAs FET keeps the low noise characteristics and drops the input reflection coefficient of a low noise amplifier simultaneously. Also, it increases the stability of the LNA. Resistive decoupling circuit is suitable for input stage matching because a signal at low frequency is dissipated by a resistor in the matching network. The amplifier consists of GaAs FET ATF-10136 for low noise stage and VNA-25 which is internally matched MMIC for high gain stage. The amplifier is fabricated with both the RF circuits and self bias circuit on the Teflon substrate with 3.5 permittivity. The measured results of the LNA which is fabricated using the above design technique are presented more than 30 dB in gain, PldB 17 dB and less than 0.7 dB in noise figure, 1.5 in inputㆍoutput SWR(Standing Wave Ratio).

• Journal of Life Science
• /
• v.25 no.7
• /
• pp.773-779
• /
• 2015

This study examined extracts from five different kinds of lees and nuruk and their organic solvent fractions in terms of several biological functions, such as anti-adipogenic, anti-inflammatory, and anti-proliferative activities. The anti-adipogenic activity was investigated by treating mouse pre-adipocyte 3T3-L1 cells with one extract (YE) and four organic solvent fractions (YAc, PAc, RAc, and WPAc) during adipogenesis. Among the treated samples, the ethyl acetate fraction of W-Ju lees (WPAc) showed the strongest anti-adipogenic effect, which was confirmed with oil red O staining and down-regulation of pro-adipogenic genes such as PPAR-gamma and SCD-1. Treatment with WPAc also reduced the expression of PPAR-gamma in a time-dependent manner. The effects of five different extracts were examined on nitric oxide (NO) production in mouse RAW 264.7 cells to determine anti-inflammatory activity. The ethyl acetate fraction of B-Ju lees (PAc) significantly decreased NO production in LPS-stimulated RAW 264.7 cells and it also inhibited NO production in a dose-dependent manner. The PAc fraction also dramatically decreased the viability of human colorectal cancer HCT116 cells in a dose-dependent manner. In addition, PAc increased the expression of NAG-1 and ATF3 genes in a dose dependent manner. Overall, these results indicate that lees and nuruk have several biological functions, including anti-adipogenic, anti-inflammatory, and anti-proliferative activities.

• Journal of the Korea Institute of Information and Communication Engineering
• /
• v.7 no.8
• /
• pp.1591-1597
• /
• 2003

In this paper, Active Resonator Oscillator using active inductor and active capacitor with HEMTs(agilent ATF­34143) is designed and fabricated. Active inductor with ­25$\Omega$ and 2.4nH in 5.5GHz frequency band and Active capacitor with ­14$\Omega$ and 0.35pF is designed. Active Resonator Oscillator for LO in ISM band(5.8GHz) is designed with active inductor and active capacitor. Active Resonator Oscillator has been simulated by Agilent ADS 2002C. Active Resonator oscillator implemented on the substrate which has the relative dielectric constant of 3.38, the height of 0.508mm, and metal thickness of 0.018mm. This Active Resonator Oscillator shows the oscillation frequency of 5.68GHz with the output power of ­3.6㏈m and phase noise of ­81㏈c/Hz at the offset frequency of 100KHz.

• Journal of Nutrition and Health
• /
• v.52 no.2
• /
• pp.176-184
• /
• 2019

Purpose: Protein overloading in the endoplasmic reticulum (ER) leads to endoplasmic reticulum stress, which exacerbates various disease conditions. Emodin, an anthraquinone compound, is known to have several health benefits. The effect of emodin against palmitic acid (PA) - induced ER stress in HepG2 cells was investigated. Methods: HepG2 cells were treated with varying concentrations of palmitic acid to determine the working concentration that induced ER stress. ER stress associated genes such as ATF4, XBP1s, CHOP and GRP78 were checked using RT- PCR. In addition, the expression levels of unfolded protein response (UPR) associated proteins such as $IRE1{\alpha}$, $eIF2{\alpha}$ and CHOP were checked using immunoblotting to confirm the induction of ER stress. The effect of emodin on ER stress was analyzed by treating HepG2 cells with $750{\mu}M$ palmitic acid and varying concentrations of emodin, then analyzing the expression of UPR associated genes. Results: It was evident from the mRNA and protein expression results that palmitic acid significantly increased the expression of UPR associated genes and thereby induced ER stress. Subsequent treatment with emodin reduced the mRNA expression of ATF4, GRP78, and XBP1s. Furthermore, the protein levels of $p-IRE1{\alpha}$, $p-eIF2{\alpha}$ and CHOP were also reduced by the treatment of emodin. Analysis of sirtuin mRNA expression showed that emodin increased the levels of SIRT4 and SIRT7, indicating a possible role in decreasing the expression of UPR-related genes. Conclusion: Altogether, the results suggest that emodin could exert a protective effect against fatty acid-induced ER stress and could be an agent for the management of various ER stress related diseases.

• Journal of Life Science
• /
• v.22 no.12
• /
• pp.1672-1679
• /
• 2012

The effect of high stocking density (HSD) on the expression of stress and lipid metabolism associated genes in the liver of broiler chickens was examined by chicken genome array analysis. The chickens in a control group were randomly assigned to a $495cm^2/bird$ stocking density, whereas the chickens in a HSD group were arranged in a $245cm^2/bird$ stocking density with feeding ad libitum for 35 days. The chickens assigned to the HSD group had a significantly lower body weight, weight gain, and feed intake compared with those of the control group (p<0.05). The mortality of chickens was higher in the HSD group than in the control group. The microarray analysis indicated up-regulation of stress associated genes such as HMGCR, $HSP90{\alpha}$, HSPA5 (GRP78/Bip), DNAJC3 and ATF4, and down-regulation of interferon-${\gamma}$ and PDCD4 genes. The endoplasmic reticulum stress associated genes, HSPA5 (GRP78/Bip), DNAJC3 and ATF4, were highly expressed in the HSD group. The genes, ACSL5, TMEM195 and ELOVL6, involved in fatty acid synthesis, were elevated in the HSD group. The genes, ACAA1, ACOX1, EHHADH, LOC423347 and CPT1A, related to fatty acid oxidation, were also activated in the HSD group. These results suggest that a HSD rearing system stimulates the genes associated with fatty acid synthesis as well as fatty acid oxidation in the liver of broiler chickens.

• Journal of Nutrition and Health
• /
• v.53 no.6
• /
• pp.583-595
• /
• 2020

Purpose: This study examined the effects of Sargassum horneri extracts on palmitic acid (PA)-induced endoplasmic reticulum (ER) stress in HepG2 cells. Methods: HepG2 cells were treated with varying concentrations of S. horneri extract or PA, and the cell viability was measured by water soluble tetrazolium salts analysis. The effective induction of ER stress and the effects of S. horneri were investigated through an examination of the ER stress-related genes, such as activating transcription factor 4 (ATF4), X-box binding protein (XBP1s), C/EBP homologous protein (CHOP), and 78-kDa glucose-regulated protein (GRP78) by quantitative reverse transcription polymerase chain reaction. The expression and activation levels of unfolded protein response (UPR) associated proteins, such as inositol-requiring enzyme-1α (IRE1α), eukaryotic translation initiation factor 2 alpha submit (eIF2α), and CHOP were examined by western blot analysis. Results: The treatment with PA increased the expression of UPR associated genes significantly and induced ER stress in a 12-hour treatment. Subsequent treatment with S. horneri reduced mRNA expression of ATF4, GRP78, and XBP1s. In addition, the protein levels of phosphate (p)-IRE1α, p-elF2α, and CHOP were also reduced by a treatment with S. horneri. An analysis of sirtuin (SIRT) mRNA expression in the S. horneri and PA-treated HepG2 cells showed that S. horneri increased the levels of SIRT2, SIRT6, and SIRT7, which indicates a possible role in reducing the expression of ER stress-related genes. Conclusion: These data indicate that S. horneri can exert an inhibitory effect on ER stress caused by PA and highlight its potential as an agent for managing various ER stress-related diseases.

• Genomics & Informatics
• /
• v.7 no.2
• /
• pp.97-106
• /
• 2009

Epigallocatechin gallate (EGCG), a well-known antioxidant molecule, has been reported to cause hepatotoxicity when used in excess. However, the mechanism underlying EGCG-induced hepatotoxicity is still unclear. To better understand the mode of action of EGCG-induced hepatotoxicity, we examined the effect of EGCG on human hepatic gene expression in HepG2 cells using microarrays. Analyses of microarray data revealed more than 1300 differentially expressed genes with a variety of biological processes. Upregulated genes showed a primary involvement with protein-related biological processes, such as protein synthesis, protein modification, and protein trafficking, while downregulated genes demonstrated a strong association with lipid transport. Genes involved in cellular stress responses were highly upregulated by EGCG treatment, in particular genes involved in endoplasmic reticulum (ER) stress, such as GADD153, GADD34, and ATF3. In addition, changes in genes responsible for cholesterol synthesis and lipid transport were also observed, which explains the high accumulation of EGCG-induced lipids. We also identified other regulatory genes that might aid in clarifying the molecular mechanism underlying EGCG-induced hepatotoxicity.

• Korean Journal of Exercise Nutrition
• /
• v.17 no.2
• /
• pp.35-42
• /
• 2013

The purpose of this study was to identify the effects of gene expression of endoplasmic reticulum (ER) stress in skeletal muscle and adipose tissue on acute exhaustive exercise. Thirty-five Sparague Dawley male rats were divided into a control group (CON, n = 7) and a exhaustive exercise group (n = 28), immediately after exhaustive exercise group (n = 7), after 30 minutes exhaustive exercise group (n = 7), after 60 minutes exhaustive exercise group (n = 7), after 180 minutes exhaustive exercise group (n = 7). As a result, changes in the composition of the blood serum triglyceride concentration increased significantly in immediately after exhaustive exercise group, On the contrary, blood glucose showed a significantly decreased (p < .05). Homeostasis of energy metabolism due to exhaustive exercise as a result of the mechanism of action of skeletal muscle in the glycogenolysis and absorption, which indicates that the process of means. On the other hand, a result of examining changes in endoplasmic reticulum stress-related proteins in skeletal muscle and adipose tissue, JNK1 except in skeletal muscle BiP, ATF4, CHOP, GRP78 mRNA increased significantly immediately after exercise, and after 30 minutes returned to normal levels that could be confirmed (p < .05). BiP mRNA in adipose tissue show a similar pattern and skeletal muscle increased significantly immediately after exercise, but other changes in the specificity of the endoplasmic reticulum stress-related proteins also did not appear. In conclusion, Exercise applies and exercise training duration and exercise intensity as well as research on the interaction of the endoplasmic reticulum stress-related genes should be study continuously, to be more clear.

• YAKHAK HOEJI
• /
• v.60 no.3
• /
• pp.128-134
• /
• 2016

L1 cell adhesion molecule (L1CAM) is a cell surface molecule to initiate a variety of cellular responses through interacting with other cell adhesion molecules in a homophilic or heterophilic manner. Although its expression was found to be upregulated in some tumor cells, including cholangiocarcinomas, and ovarian cancers, and many studies have investigated the role of L1CAM in these cancers, its role in inflammatory responses has been poorly understood. In this study, we explored the role of L1CAM in macrophage-mediated inflammatory responses. L1CAM significantly suppressed the production of nitric oxide (NO), but induced cell proliferation in RAW264.7 cells. L1CAM expression was detectable, but its expression was markedly decreased by lipopolysaccharide (LPS) in RAW264.7 cells. In addition, the expression of pro-inflammatory genes, such as tumor necrosis factor (TNF)-${\alpha}$, cyclooxygenase (COX)-2, and inducible nitric oxide synthase (iNOS) induced by LPS was dramatically suppressed by L1CAM in RAW264.7 cells. L1CAM inhibited the transcriptional activities of NF-${\kappa}B$ and AP-1 while its cytoplasmic domain deletion form, $L1{\Delta}CD$ did not suppressed their activities in RAW264.7 cells. Moreover, L1CAM suppressed nuclear translocation of p65 and p50 as well as c-Jun, c-Fos and p-ATF2 which are transcription factors of NF-${\kappa}B$ and AP-1, respectively. In conclusion, L1CAM suppressed inflammatory responses in macrophages through inhibiting NF-${\kappa}B$ and AP-1 pathways.