• Proceedings of the IEEK Conference
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• 2003.07b
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• pp.979-982
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• 2003

Due to the differential transmission technique and low voltage swing, LVDS has been widely used for high speed transmission with low power consumption. This paper presents the design and implementation of interface circuits for 1.5Gb/s operation in 0.35um CMOS technology. The interface circuit ate fully compatible with the low-voltage differential signaling(LVDS) standard. The LVDS proposed in this paper utilizes a sense amplifiers instead of the conventional differential pre-amplifier, which provides a 1.5Gb/s transmission speed with further reduced driver output voltage. Furthermore, the reduced driver output voltage results in reducing the power consumption.

• ETRI Journal
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• v.37 no.3
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• pp.637-645
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• 2015

Common-mode noise (CMN) is an unresolved problem in wireless capsule endoscopy (WCE) systems. In a WCE system, CMN originates from various electric currents found within the human body or external interference sources and causes critical demodulation performance degradation. The differential operation, a typical method for the removal of CMN rejection, can remove CMN by subtracting two signals simultaneously received by two reception sensors attached to a human body. However, when there is impedance mismatching between the two reception sensors, the differential operation method cannot completely remove CMN. Therefore, to overcome this problem, we propose an enhanced CMN rejection method. The proposed method performs not only subtraction but also addition between two received signals. Then a CMN ratio can be estimated by sufficient accumulation of division operation outcomes between the subtraction and addition outputs during the guard period. Finally, we can reject the residual CMN by combining the subtraction and addition outputs.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.19 no.7
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• pp.1639-1645
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• 2015

In UHD high-speed video transmission system, when a signal within certain frequency region coincides electrically and structurally, the system becomes unstable because the energy is concentrated, and signal flux is interfered and distorted. For the instability, power integrity analysis should be conducted. To remove the signal distortion for MLB, using a high-frequency design technique for EMI phenomenon, EMI which radiates electromagnetic energy fluxed into power layer was analyzed considering system stabilization. In this paper, we proposed an adaptive MLB design method which minimizes high-frequency noise in MLB structure, enhances signal integrity and power integrity, and suppresses EMI. The characteristic impedance for multi-layer circuit board proposed in this study were High-Speed Video Differential Signaling(HSVDS) line width w = 0.203, line gap d = 0.203, beta layer height h = 0.145, line thickness t = 0.0175, dielectric constant ε_r = 4.3, and characteristic impedance Zdiff = 100.186Ω. When high-speed video differential signal interface board was tested with optimized parameters, the magnitude of Eye diagram output was 672mV, jittering was 6.593ps, transmission frequency was 1.322GHz, signal to noise was 29.62dB showing transmission quality improvement of 10dB compared to previous system.

• Journal of the Institute of Electronics Engineers of Korea SC
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• v.45 no.2
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• pp.26-36
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• 2008

Due to the differential and low voltage swing, Low Voltage Differential Signaling(LVDS) has been widely used for high speed data transmission with low power consumption. This paper proposes new LVDS I/O interface circuits for more than 1.3 Gb/s operation. The LVDS receiver proposed in this paper utilizes a sense amp for the pre-amp instead of a conventional differential pre-amp. The proposed LVDS allows more than 1.3 Gb/s transmission speed with significantly reduced driver output voltage. Also, in order to further improve the power consumption and noise performance, this paper introduces an inductance impedance matching technique which can eliminate the termination resistor. A new form of unfolded impedance matching method has been developed to accomplish the impedance matching for LVDS receivers with a sense amplifier as well as with a differential amplifier. The proposed LVDS I/O circuits have been extensively simulated using HSPICE based on 0.35um TSMC CMOS technology. The simulation results show improved power gain and transmission rate by ${\sim}12%$ and ${\sim}18%$, respectively.

• Journal of the Institute of Electronics and Information Engineers
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• v.51 no.4
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• pp.49-58
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• 2014

A low-swing differential near-ground signaling (NGS) transceiver for low-power high-speed mobile I/O interface is presented. The proposed transmitter adopts an on-chip regulated programmable-swing voltage-mode driver and a pre-driver with asymmetric rising/falling time. The proposed receiver utilizes a new multiple gain-path differential amplifier with feed-forward capacitors that boost high-frequency gain. Also, the receiver incorporates a new adaptive bias generator to compensate the input common-mode variation due to the variable output swing of the transmitter and to minimize the current mismatch of the receiver's input stage amplifier. The use of the new simple and effective impedance matching techniques applied in the transmitter and receiver results in good signal integrity and high power efficiency. The proposed transceiver designed in a 65-nm CMOS technology achieves a data rate of 13 Gbps/channel and 0.3 pJ/bit (= 0.3 mW/Gbps) high power efficiency over a 10 cm FR4 printed circuit board.

• Molecules and Cells
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• v.41 no.9
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• pp.853-867
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• 2018

As the most common type of endocrine malignancy, papillary thyroid cancer (PTC) accounts for 85-90% of all thyroid cancers. In this study, we presented the hypothesis that SDC4 gene silencing could effectively attenuate epithelial mesenchymal transition (EMT), and promote cell apoptosis via the $Wnt/{\beta}-catenin$ signaling pathway in human PTC cells. Bioinformatics methods were employed to screen the determined differential expression levels of SDC4 in PTC and adjacent normal samples. PTC tissues and adjacent normal tissues were prepared and their respective levels of SDC4 protein positive expression, in addition to the mRNA and protein levels of SDC4, $Wnt/{\beta}-catenin$ signaling pathway, EMT and apoptosis related genes were all detected accordingly. Flow cytometry was applied in order to detect cell cycle entry and apoptosis. Finally, analyses of PTC migration and invasion abilities were assessed by using a Transwell assay and scratch test. In PTC tissues, activated $Wnt/{\beta}-catenin$ signaling pathway, increased EMT and repressed cell apoptosis were determined. Moreover, the PTC K1 and TPC-1 cell lines exhibiting the highest SDC4 expression were selected for further experiments. In vitro experiments revealed that SDC4 gene silencing could suppress cell migration, invasion and EMT, while acting to promote the apoptosis of PTC cells by inhibiting the activation of the $Wnt/{\beta}-catenin$ signaling pathway. Besides, $si-{\beta}-catenin$ was observed to inhibit the promotion of PTC cell migration and invasion caused by SDC4 overexpression. Our study revealed that SDC4 gene silencing represses EMT, and enhances cell apoptosis by suppressing the activation of the $Wnt/{\beta}-catenin$ signaling pathway in human PTC.

• Journal of the Institute of Electronics Engineers of Korea SD
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• v.42 no.4 s.334
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• pp.45-52
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• 2005

This paper presents the characterization of through hole vias on printed circuit board (PCB) through the time domain and frequency domain measurements. The time domain measurement was performed on a single via using the TDR, and the model parameters were extracted by the fitting simulation using HSPICE. The frequency domain measurement was also performed by using 2 port VNA, and the model parameters were extracted by fitting simulation with ADS. Using the ABCD matrices, the do-embedding equations were derived probing in the same plane in the VNA measurement. Based on the single via characterization, the differential via characterization was also performed by using TDR measurements. The time domain measurements were performed by using the odd mode and even mode sources in TDR module, and the Parameter values were extracted by fitting with HSPICE. Comparing measurements with simulations, the maximum calculated differences were $14\%$ for single vias and $17\%$ for differential vias.

• Molecular & Cellular Toxicology
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• v.5 no.3
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• pp.187-192
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• 2009

Toll-like receptors (TLRs) play an important role in host defense by sensing invading microbial pathogens. The stimulation of TLRs by microbial components triggers the activation of the myeloid differential factor 88 (MyD88)- and toll-interleukin-1 receptor domain-containing adapter inducing interferon-$\beta$ (TRIF)-dependent downstream signaling pathways. TLR/MyD88 signaling pathway induces the activation of nuclear factor-kappa B (NF-${\kappa}B$) and the expression of inflammatory cytokine genes, including tumor necrosis factor-alpha, interleukin (IL)-6, IL-12, and IL-$1{\beta}$. On the other hand, TLR/TRIF signaling pathway induces the delayed-activation of NF-${\kappa}B$ and interferon regulatory factor 3 (IRF3), and the expression of type I interferons (IFNs) and IFN-inducible genes. The divalent heavy metal cadmium (Cd) is clearly toxic to most mammalian organ systems, especially the immune system. Yet, the underlying toxic mechanism(s) remain unclear. Cd inhibits the MyD88-dependent pathway by ceasing the activity of inhibitor-${\kappa}B$ kinase. However, it is not known whether Cd inhibits the TRIF-dependent pathway. Presently, Cd inhibited NF-${\kappa}B$ and IRF3 activation induced by lipopolysaccharide (LPS) and polyinosinic-polycytidylic acid. Cd inhibited LPS-induced IRF3 phosphorylation and IFN-inducible genes such as interferon inducible protein-10 and regulated on activation normal T-cell expressed and secreted (RANTES). These results suggest that Cd can modulate TRIF-dependent signaling pathways of TLRs.

• Journal of the Korean Society of Physical Medicine
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• v.13 no.3
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• pp.141-150
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• 2018

PURPOSE: This study was conducted to understand the adaptive responses of different modes of physical exercises utilizing skeletal muscle and the comprehensive relevance of AMPK signaling that can be activated by physical exercise as a potential molecular target in human health problems such as neuromuscular disorders (NMDs). METHODS: Most of the contents in this review article are based on recent publications concerning the main topics of interest. The reference literatures cited were obtained by basic searches of overseas academic databases such as PubMed and ScienceDirect using EndNote X7.8. RESULTS: The phenotypic adaptive responses of skeletal muscle during endurance- and resistance-based exercise training (ET and RT respectively) appear to be distinct. To explain the adaptive responses in each single mode of exercises (ET, RT) along with combined exercise training (CT), AMPK signaling is proposed as an important molecular link among those differential modes of exercise and a promising molecular target of NMDs. CONCLUSION: Based on the available evidence, intracellular AMPK signaling activated by diverse stimuli including physical exercise can be a potential and promising therapeutic target for the prevention, amelioration or cure of various human health problems including NMDs and may also be beneficial for physical rehabilitation and emergency situations that may elicit acute metabolic stresses.

• BMB Reports
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• v.50 no.6
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• pp.281-282
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• 2017

Advances in the understanding of the Hippo signaling as a key regulatory pathway of proliferation and apoptosis have provided mechanical insights for controlling organ size and tumorigenicity. Recently, much attention has been directed to the regulation of LATS1/2 (large tumor suppressor) kinases that phosphorylate YAP/TAZ, a transcriptional co-activator in the Hippo pathway, and control the level and nuclear localization of YAP/TAZ. In our recent work, we showed that deubiquitinase YOD1 stabilizes ITCH, and facilitates ITCH-mediated LATS1/2 ubiquitination and degradation, resulting in increased YAP/TAZ level. Furthermore, we found that the YOD1-ITCH-LATS1/2-YAP/TAZ signaling axis is controlled by the differential expression of miR-21 in a cell-density-dependent manner. Using a transgenic mouse model, we showed that the inducible expression of YOD1 enhances the proliferation of hepatocytes and leads to hepatomegaly in a YAP/TAZ-activity-dependent manner. Moreover, a strong correlation was observed between YOD1 and YAP expression in liver cancer patients. Overall, our data suggest that YOD1 is a novel regulator of the Hippo pathway, and thereby a potential therapeutic target for liver cancer.