• Journal of Magnetics
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• 제7권3호
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• pp.63-71
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• 2002

Three fabrication techniques for forming thin barrier layer with uniform thickness and large barrier height in magnetic tunnel junction (MTJ) are discussed. First, the effect of immiscible element addition to Cu layer, a high conducting layer generally placed under the MTJ, is investigated in order to reduce the surface roughness of the bottom ferromagnetic layer, on which the barrier is formed. The Ag addition to the Cu layer successfully realizes the smooth surface of the ferromagnetic layer because of the suppression of the grain growth of Cu. Second, a new plasma source, characterized as low electron energy of 1 eV and high density of $10^{12}$ $cm^{-3}$, is introduced to the Al oxidation process in MTJ fabrication in order to reduce damages to the barrier layer by the ion-bombardment. The magnetotransport properties of the MTJs are investigated as a function of the annealing temperature. As a peculiar feature, the monotonous decrease of resistance area product (RA) is observed with increasing the annealing temperature. The decrease of the RA is due to the decrease of the effective barrier width. Third, the influence of the mixed inert gas species for plasma oxidization process of metallic Al layer on the tunnel magnetoresistance (TMR) was investigated. By the use of Kr-O$_2$ plasma for Al oxidation process, a 58.8 % of MR ratio was obtained at room temperature after annealing the junction at $300{^{\circ}C}$, while the achieved TMR ratio of the MTJ fabricated with usual Ar-$0_2$ plasma remained 48.4%. A faster oxidization rate of the Al layer by using Kr-O$_2$ plasma is a possible cause to prevent the over oxidization of Al layer and to realize a large magnetoresistance.

• 대한한방내과학회지
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• 제27권1호
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• pp.208-220
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• 2006

Objective: Eosinophils are typically characterized by a bilobar nucleus with highly condensed chromatin and cytoplasm containing two major types of granules, specific and primary granules, and lipid bodies. The role of inflammation in asthma and other allergic diseases of the airways is widely appreciated, and airway inflammation is now included as a defining feature of asthma. The importance of the presence of eosinophils in the airways of patients with fetal asthma has long been recognized, but the mechanism by which these cells are recruited and retained in the lungs are only now being elucidated. Eotaxin is a potent and specific eosinophil chemoattractant that is mobilized in the respiratory epithelium after allergic stimulation. Methods : Water extracts of Armeniacae Amarum Semen(AAS) and pulmonary epithelial cell lines A549(alveolar typeII epithelial cells) and human eosinophils were used. Cytotoxic effects of AAS and MIS assay were estimated, as well as the effects of AAS on chemokines from prestimulated A549 cells by sandwich ELISA and RI-PCR. Chemotaxis assay was conducted on prestimulated eosinophils treated with AAS. Results : In this study it is demonstrated that $TGF-{\alpha}$, IL-4 and $IL-1{\beta}$ induced the accumulation of chemokine mRNAs in the alveolar epithelial cell lines A549 in dose-dependent manner. Eotaxin and IL-8 were inhibited by AAS in dose-dependent manner(p<0.05). Eosinophil migration was inhibited at high concentrations of AAS(p<0.05). Conculusions : These findings are indicative of suppression of eotaxin and IL-8, and suggest that this is accomplished through AAS treatment. This raises the possibility that AAS is of therapeutic value in diseases such as asthma.

• 대한임베디드공학회논문지
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• 제15권5호
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• pp.227-234
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• 2020

In this paper, we propose wav-U-Net to improve speech enhancement in heavy noisy environments, and it has implemented three principal techniques. First, as input data, we use 128 modified Mel-scale filter banks which can reduce computational burden instead of 512 frequency bins. Mel-scale aims to mimic the non-linear human ear perception of sound by being more discriminative at lower frequencies and less discriminative at higher frequencies. Therefore, Mel-scale is the suitable feature considering both performance and computing power because our proposed network focuses on speech signals. Second, we add a simple ResNet as pre-processing that helps our proposed network make estimated speech signals clear and suppress high-frequency noises. Finally, the proposed U-Net model shows significant performance regardless of the kinds of noise. Especially, despite using a single channel, we confirmed that it can well deal with non-stationary noises whose frequency properties are dynamically changed, and it is possible to estimate speech signals from noisy speech signals even in extremely noisy environments where noises are much lauder than speech (less than SNR 0dB). The performance on our proposed wav-U-Net was improved by about 200% on SDR and 460% on NSDR compared to the conventional Jansson's wav-U-Net. Also, it was confirmed that the processing time of out wav-U-Net with 128 modified Mel-scale filter banks was about 2.7 times faster than the common wav-U-Net with 512 frequency bins as input values.

• 대한전자공학회논문지TC
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• 제42권11호
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• pp.93-100
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• 2005

본 논문에서는 차량 내에서 음성인식 인터페이스를 이용한 오비오, 비디오와 같은 응용서비스 처리를 위해 임베디드형 음성인식 시스템을 구현한다. 임베디드형 음성인식 시스템은 DSP 보드로 제작 포팅된다. 이는 음성 인식률이 마이크, 음성 코덱 등의 H/W의 영향을 받기 때문이다. 또한 차량 내 잡음을 효율적으로 제거하기 위한 최적의 환경을 구축하고, 이에 따른 테스트 환경을 최적화한다. 본 논문에서 제안된 시스템은 차량 내에서의 신뢰적인 음성인식을 위해 잡음제거 및 특징보상 기술을 적용하고 임베디드 환경에서의 속도 및 성능 향상을 위한 문맥 종속 믹스쳐 공유 음향 모델링을 적용한다. 성능평가는 일반 실험실 환경에서의 인식률과 실제 차량 내에서의 실차 테스트를 통해 검증되었다.

• 센서학회지
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• 제29권1호
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• pp.7-13
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• 2020

Dielectric capacitors are integral components in electronic devices that protect the electric circuit by providing modulated steady voltage. Explosive growth of the electric automobile market has resulted in an increasing demand for dielectric capacitors that can operate at temperatures as high as 400 ℃. To surpass the operation temperature limit of currently available commercial capacitors that operate in temperatures up to 125 ℃, Bi_1/2Na_1/2TiO₃ (BNT), which has a large temperature-insensitive dielectric response with a maximum dielectric permittivity temperature of 300 ℃, was selected. By introducing an intentional A-site cation deficiency and post-heat treatment, we successfully manage to control the dielectric properties of BNT to use it for high-temperature applications. The key feature of this new BNT is remarkable reduction in dielectric loss (0.36 to 0.018) at high temperature (300 ℃). Structural, dielectric, and electrical properties of this newly developed BNT were systematically investigated to understand the underlying mechanism.

• Biomolecules & Therapeutics
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• 제28권4호
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• pp.337-343
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• 2020

Activation of osteoclast and inactivation of osteoblast result in loss of bone mass with bone resorption, leading to the pathological progression of osteoporosis. The receptor activator of NF-κB ligand (RANKL) is a member of the TNF superfamily, and is a key mediator of osteoclast differentiation. A flavanone glycoside isolated from the fruit of Poncirus trifoliata, poncirin has anti-allergic, hypocholesterolemic, anti-inflammatory and anti-platelet activities. The present study investigates the effect of poncirin on osteoclast differentiation of RANKL-stimulated RAW264.7 cells. We observed reduced formation of RANKL-stimulated TRAP-positive multinucleated cells (a morphological feature of osteoclasts) after poncirin exposure. Real-time qPCR analysis showed suppression of the RANKL-mediated induction of key osteoclastogenic molecules such as NFATc1, TRAP, c-Fos, MMP9 and cathepsin K after poncirin treatment. Poncirin also inhibited the RANKL-mediated activation of NF-κB and, notably, JNK, without changes in ERK and p38 expression in RAW264.7 cells. Furthermore, we assessed the in vivo efficacy of poncirin in the lipopolysaccharide (LPS)-induced bone erosion model. Evaluating the micro-CT of femurs revealed that bone erosion in poncirin treated mice was markedly attenuated. Our results indicate that poncirin exerts anti-osteoclastic effects in vitro and in vivo by suppressing osteoclast differentiation. We believe that poncirin is a promising candidate for inflammatory bone loss therapeutics.

• IMMUNE NETWORK
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• 제11권1호
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• pp.59-67
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• 2011

Background: Insulin resistance is an integral feature of metabolic syndromes, including obesity, hyperglycemia, and hyperlipidemia. In this study, we evaluated whether the aloe component could reduce obesity-induced inflammation and the occurrence of metabolic disorders such as blood glucose and insulin resistance. Methods: Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of aloe formula (PAG, ALS, Aloe QDM, and Aloe QDM complex) or pioglitazone (PGZ) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. Results: Aloe QDM lowered fasting blood glucose and plasma insulin compared with HFD. Obesity-induced inflammatory cytokine (IL-$1{\beta}$, -6, -12, TNF-${\alpha}$) and chemokine (CX3CL1, CCL5) mRNA and protein were decreased markedly, as was macrophage infiltration and hepatic triglycerides by Aloe QDM. At the same time, Aloe QDM decreased the mRNA and protein of $PPAR{\gamma}/LXR{\alpha}$ and $11{\beta}$-HSD1 both in the liver and WAT. Conclusion: Dietary aloe formula reduces obesity-induced glucose tolerance not only by suppressing inflammatory responses but also by inducing anti-inflammatory cytokines in the WAT and liver, both of which are important peripheral tissues affecting insulin resistance. The effect of Aloe QDM complex in the WAT and liver are related to its dual action on $PPAR{\gamma}$ and $11{\beta}$-HSD1 ression and its use as a nutritional intervention against T2D and obesity-related inflammation is suggested.

• JSTS:Journal of Semiconductor Technology and Science
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• 제14권1호
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• pp.8-22
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• 2014

In the past few decades, CMOS logic technologies and devices have been successfully developed with the steady miniaturization of the feature size. At the sub-30-nm CMOS technology nodes, one of the main hurdles for continuously and successfully scaling down CMOS devices is the parametric failure caused by random variations such as line edge roughness (LER), random dopant fluctuation (RDF), and work-function variation (WFV). The characteristics of each random variation source and its effect on advanced device structures such as multigate and ultra-thin-body devices (vs. conventional planar bulk MOSFET) are discussed in detail. Further, suggested are suppression methods for the LER-, RDF-, and WFV-induced threshold voltage (VTH) variations in advanced CMOS logic technologies including the double-patterning and double-etching (2P2E) technique and in advanced device structures including the fully depleted silicon-on-insulator (FD-SOI) MOSFET and FinFET/tri-gate MOSFET at the sub-30-nm nodes. The segmented-channel MOSFET (SegFET) and junctionless transistor (JLT) that can suppress the random variations and the SegFET-/JLT-based static random access memory (SRAM) cell that enhance the read and write margins at a time, though generally with a trade-off between the read and the write margins, are introduced.

• Clinical and Experimental Reproductive Medicine
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• 제47권2호
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• pp.108-113
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• 2020

Objective: Endometrial fibrosis, the primary pathological feature of intrauterine adhesion, may lead to disruption of endometrial tissue structure, menstrual abnormalities, infertility, and recurrent pregnancy loss. At present, no ideal therapeutic strategy exists for this fibrotic disease. Eupatilin, a major pharmacologically active flavone from Artemisia, has been previously reported to act as a potent inducer of dedifferentiation of fibrotic tissue in the liver and lung. However, the effects of eupatilin on endometrial fibrosis have not yet been investigated. In this study, we present the first report on the impact of eupatilin treatment on transforming growth factor beta (TGF-β)-induced endometrial fibrosis. Methods: The efficacy of eupatilin on TGF-β-induced endometrial fibrosis was assessed by examining changes in morphology and the expression levels of fibrosis markers using immunofluorescence staining and quantitative real-time reverse-transcription polymerase chain reaction. Results: Eupatilin treatment significantly reduced the fibrotic activity of TGF-β-induced endometrial fibrosis in Ishikawa cells, which displayed more circular shapes and formed more colonies. Additionally, the effects of eupatilin on fibrotic markers including alpha-smooth muscle actin, hypoxia-inducible factor 1 alpha, collagen type I alpha 1 chain, and matrix metalloproteinase-2, were evaluated in TGF-β-induced endometrial fibrosis. The expression of these markers was highly upregulated by TGF-β pretreatment and recovered to the levels of control cells in response to eupatilin treatment. Conclusion: Our findings suggest that suppression of TGF-β-induced signaling by eupatilin might be an effective therapeutic strategy for the treatment of endometrial fibrosis.

• Biomolecules & Therapeutics
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• 제29권2호
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• pp.127-134
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• 2021

Neuroinflammation―a common pathological feature of neurodegenerative disorders such as Alzheimer's disease―is mediated by microglial activation. Thus, inhibiting microglial activation is vital for treating various neurological disorders. 7,3',4'-Trihydroxyisoflavone (THIF)―a secondary metabolite of the soybean compound daidzein―possesses antioxidant and anticancer properties. However, the effects of 7,3',4'-THIF on microglial activation have not been explored. In this study, antineuroinflammatory effects of 7,3',4'-THIF in lipopolysaccharide (LPS)-stimulated BV2 microglial cells were examined. 7,3',4'-THIF significantly suppressed the production of the proinflammatory mediators nitric oxide (NO), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) as well as of the proinflammatory cytokine interleukin-6 (IL-6) in LPS-stimulated BV2 microglial cells. Moreover, 7,3',4'-THIF markedly inhibited reactive oxygen species (ROS) generation. Western blotting revealed that 7,3',4'-THIF diminished LPS-induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), glycogen synthase kinase-3β (GSK-3β), and nuclear factor kappa B (NF-κB). Overall, 7,3',4'-THIF exerts antineuroinflammatory effects against LPS-induced microglial activation by suppressing mitogen-activated protein kinase (MAPK) and NF-κB signaling, ultimately reducing proinflammatory responses. Therefore, these antineuroinflammatory effects of 7,3',4'-THIF suggest its potential as a therapeutic agent for neurodegenerative disorders.